TY - JOUR T1 - Novel Microtubule-Targeting 7-Deazahypoxanthines Derived from Marine Alkaloid Rigidins with Potent in Vitro and in Vivo Anticancer Activities. AN - 1760867733; 26641132 AB - Docking studies of tubulin-targeting C2-substituted 7-deazahypoxanthine analogues of marine alkaloid rigidins led to the design and synthesis of compounds containing linear C2-substituents. The C2-alkynyl analogue was found to have double- to single-digit nanomolar antiproliferative IC50 values and showed statistically significant tumor size reduction in a colon cancer mouse model at nontoxic concentrations. These results provide impetus and further guidance for the development of these rigidin analogues as anticancer agents. JF - Journal of medicinal chemistry AU - Medellin, Derek C AU - Zhou, Qiong AU - Scott, Robert AU - Hill, R Matthew AU - Frail, Sarah K AU - Dasari, Ramesh AU - Ontiveros, Steven J AU - Pelly, Stephen C AU - van Otterlo, Willem A L AU - Betancourt, Tania AU - Shuster, Charles B AU - Hamel, Ernest AU - Bai, Ruoli AU - LaBarbera, Daniel V AU - Rogelj, Snezna AU - Frolova, Liliya V AU - Kornienko, Alexander AD - Department of Chemistry and Biochemistry, Texas State University , San Marcos, Texas 78666, United States. ; Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus , Aurora, Colorado 80045, United States. ; Departments of Chemistry and Biology, New Mexico Tech , Socorro, New Mexico 87801, United States. ; Department of Biology, New Mexico State University , Las Cruces, New Mexico 88003, United States. ; Department of Chemistry and Polymer Science, Stellenbosch University , Stellenbosch, Western Cape, South Africa. ; Screening Technologies Branch, Developmental Therapeutics Program, National Cancer Institute, Frederick National Laboratory of Cancer Research, National Institutes of Health, Frederick, Maryland 21702, United States. Y1 - 2016/01/14/ PY - 2016 DA - 2016 Jan 14 SP - 480 EP - 485 VL - 59 IS - 1 KW - Antineoplastic Agents KW - 0 KW - Marine Toxins KW - Tubulin KW - Tubulin Modulators KW - Xanthines KW - Colchicine KW - SML2Y3J35T KW - Index Medicus KW - Cell Proliferation -- drug effects KW - Animals KW - Drug Screening Assays, Antitumor KW - Models, Molecular KW - Humans KW - Tubulin -- metabolism KW - Cell Line, Tumor KW - Mice KW - Mice, Nude KW - Drug Design KW - Structure-Activity Relationship KW - Colchicine -- metabolism KW - Tubulin -- drug effects KW - Molecular Docking Simulation KW - Tubulin Modulators -- pharmacology KW - Colonic Neoplasms -- drug therapy KW - Female KW - Marine Toxins -- pharmacology KW - Antineoplastic Agents -- chemical synthesis KW - Xanthines -- chemical synthesis KW - Antineoplastic Agents -- pharmacology KW - Xanthines -- pharmacology KW - Marine Toxins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1760867733?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+medicinal+chemistry&rft.atitle=Novel+Microtubule-Targeting+7-Deazahypoxanthines+Derived+from+Marine+Alkaloid+Rigidins+with+Potent+in+Vitro+and+in+Vivo+Anticancer+Activities.&rft.au=Medellin%2C+Derek+C%3BZhou%2C+Qiong%3BScott%2C+Robert%3BHill%2C+R+Matthew%3BFrail%2C+Sarah+K%3BDasari%2C+Ramesh%3BOntiveros%2C+Steven+J%3BPelly%2C+Stephen+C%3Bvan+Otterlo%2C+Willem+A+L%3BBetancourt%2C+Tania%3BShuster%2C+Charles+B%3BHamel%2C+Ernest%3BBai%2C+Ruoli%3BLaBarbera%2C+Daniel+V%3BRogelj%2C+Snezna%3BFrolova%2C+Liliya+V%3BKornienko%2C+Alexander&rft.aulast=Medellin&rft.aufirst=Derek&rft.date=2016-01-14&rft.volume=59&rft.issue=1&rft.spage=480&rft.isbn=&rft.btitle=&rft.title=Journal+of+medicinal+chemistry&rft.issn=1520-4804&rft_id=info:doi/10.1021%2Facs.jmedchem.5b01426 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-18 N1 - Date created - 2016-01-14 N1 - Date revised - 2017-01-24 N1 - Last updated - 2017-01-25 DO - http://dx.doi.org/10.1021/acs.jmedchem.5b01426 ER - TY - JOUR T1 - Biochemical evidence of a role for matrix trimerization in HIV-1 envelope glycoprotein incorporation. AN - 1760855409; 26711999 AB - The matrix (MA) domain of HIV Gag has important functions in directing the trafficking of Gag to sites of assembly and mediating the incorporation of the envelope glycoprotein (Env) into assembling particles. HIV-1 MA has been shown to form trimers in vitro; however, neither the presence nor the role of MA trimers has been documented in HIV-1 virions. We developed a cross-linking strategy to reveal MA trimers in virions of replication-competent HIV-1. By mutagenesis of trimer interface residues, we demonstrated a correlation between loss of MA trimerization and loss of Env incorporation. Additionally, we found that truncating the long cytoplasmic tail of Env restores incorporation of Env into MA trimer-defective particles, thus rescuing infectivity. We therefore propose a model whereby MA trimerization is required to form a lattice capable of accommodating the long cytoplasmic tail of HIV-1 Env; in the absence of MA trimerization, Env is sterically excluded from the assembling particle. These findings establish MA trimerization as an obligatory step in the assembly of infectious HIV-1 virions. As such, the MA trimer interface may represent a novel drug target for the development of antiretrovirals. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Tedbury, Philip R AU - Novikova, Mariia AU - Ablan, Sherimay D AU - Freed, Eric O AD - Virus-Cell Interaction Section, HIV Dynamics and Replication Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702-1201. ; Virus-Cell Interaction Section, HIV Dynamics and Replication Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702-1201 efreed@nih.gov. Y1 - 2016/01/12/ PY - 2016 DA - 2016 Jan 12 SP - E182 EP - E190 VL - 113 IS - 2 KW - Cross-Linking Reagents KW - 0 KW - Disulfides KW - Viral Matrix Proteins KW - env Gene Products, Human Immunodeficiency Virus KW - gag Gene Products, Human Immunodeficiency Virus KW - Threonine KW - 2ZD004190S KW - Index Medicus KW - retrovirus KW - matrix KW - envelope KW - HIV KW - trimerization KW - Virus Replication KW - gag Gene Products, Human Immunodeficiency Virus -- chemistry KW - Threonine -- genetics KW - Models, Molecular KW - HeLa Cells KW - Humans KW - Cross-Linking Reagents -- pharmacology KW - Mutation -- genetics KW - Virion -- metabolism KW - Protein Structure, Tertiary KW - gag Gene Products, Human Immunodeficiency Virus -- metabolism KW - Disulfides -- metabolism KW - HIV-1 -- metabolism KW - env Gene Products, Human Immunodeficiency Virus -- metabolism KW - Viral Matrix Proteins -- chemistry KW - Protein Multimerization KW - Viral Matrix Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1760855409?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Biochemical+evidence+of+a+role+for+matrix+trimerization+in+HIV-1+envelope+glycoprotein+incorporation.&rft.au=Tedbury%2C+Philip+R%3BNovikova%2C+Mariia%3BAblan%2C+Sherimay+D%3BFreed%2C+Eric+O&rft.aulast=Tedbury&rft.aufirst=Philip&rft.date=2016-01-12&rft.volume=113&rft.issue=2&rft.spage=E182&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=1091-6490&rft_id=info:doi/10.1073%2Fpnas.1516618113 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-13 N1 - Date created - 2016-01-13 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: AIDS Res Hum Retroviruses. 1991 Jun;7(6):511-9 [1657072] EMBO J. 1996 Jul 1;15(13):3267-74 [8670827] J Mol Biol. 1994 Nov 25;244(2):198-223 [7966331] J Virol. 1995 Mar;69(3):1984-9 [7853546] Protein Sci. 1996 Dec;5(12):2391-8 [8976548] J Mol Biol. 1996 Dec 20;264(5):1117-31 [9000634] J Virol. 1997 Jun;71(6):4409-18 [9151831] Science. 2013 Dec 20;342(6165):1484-90 [24179160] Trends Microbiol. 2014 Jul;22(7):372-8 [24933691] EMBO J. 1997 Oct 1;16(19):5819-26 [9312040] J Virol. 1998 Apr;72(4):2855-64 [9525605] J Mol Biol. 1998 Jun 19;279(4):921-8 [9642071] Virology. 1998 Nov 10;251(1):1-15 [9813197] J Virol. 2007 Feb;81(3):1472-8 [17108052] Biochemistry. 2008 Feb 19;47(7):1977-83 [18198900] Biochemistry. 2008 Feb 19;47(7):1928-37 [18220420] Virology. 2009 May 10;387(2):466-72 [19327811] Nature. 2011 Jan 20;469(7330):424-7 [21248851] AIDS Res Hum Retroviruses. 2011 Mar;27(3):239-47 [21247353] Retrovirology. 2011;8:15 [21385335] J Mol Biol. 2011 Jul 22;410(4):582-608 [21762802] J Virol. 2012 Feb;86(4):2347-59 [22156517] Cold Spring Harb Perspect Med. 2012 Jul;2(7):a006924 [22762019] Nature. 2012 Jul 19;487(7407):385-9 [22722831] PLoS Pathog. 2013;9(4):e1003278 [23592992] Nature. 2013 May 30;497(7451):643-6 [23719463] PLoS Pathog. 2013;9(11):e1003739 [24244165] Science. 2013 Dec 20;342(6165):1477-83 [24179159] Retrovirology. 2013;10:64 [23800358] Proc Natl Acad Sci U S A. 2000 Jan 4;97(1):343-8 [10618420] J Virol. 2000 May;74(10):4891-3 [10775630] J Cell Biol. 2000 Oct 16;151(2):F9-14 [11038194] Structure. 2002 Dec;10(12):1627-36 [12467570] EMBO J. 2003 Apr 1;22(7):1707-15 [12660176] Virology. 1986 Apr 30;150(2):503-8 [3485855] Cell. 1986 May 9;45(3):375-85 [2421920] J Virol. 1986 Aug;59(2):284-91 [3016298] J Virol. 1988 Jan;62(1):139-47 [3257102] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5743-7 [2762293] AIDS Res Hum Retroviruses. 1994 Dec;10(12):1651-8 [7888224] Prog Mol Biol Transl Sci. 2015;129:253-84 [25595807] Nature. 2015 Jan 22;517(7535):505-8 [25363765] J Mol Biol. 2015 Mar 27;427(6 Pt B):1413-27 [25659909] Virology. 2015 May;479-480:403-17 [25816761] Proc Natl Acad Sci U S A. 2015 Jun 16;112(24):7575-80 [26034275] Science. 2015 Jul 3;349(6243):99-103 [26044298] Nat Rev Microbiol. 2015 Aug;13(8):484-96 [26119571] J Virol. 1995 Jun;69(6):3824-30 [7745730] Nature. 1995 Dec 14;378(6558):743-7 [7501025] Proc Natl Acad Sci U S A. 1996 Apr 2;93(7):3099-104 [8610175] J Virol. 1994 Aug;68(8):5311-20 [8035531] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1073/pnas.1516618113 ER - TY - JOUR T1 - Effect of Renal Dysfunction on Toxicity in Three Decades of Cancer Therapy Evaluation Program-Sponsored Single-Agent Phase I Studies. AN - 1754524082; 26392101 AB - Alterations in renal clearance of anticancer drugs can affect the occurrence of toxicities related to drug exposure. The National Cancer Institute and the US Food and Drug Administration (FDA) use different criteria to classify renal dysfunction. We examined those discrepancies and their potential association with the incidence of toxicities in patients enrolled onto Cancer Therapy Evaluation Program-sponsored single-agent phase I studies over three decades (1979 to 2010). Data to estimate creatinine clearance according to the Cockcroft-Gault and Jelliffe formulas were available from 10,236 patients, and data to estimate creatinine clearance according to the six- and four-variable Modification of Diet in Renal Disease formulas were available from a subset (n = 4,084). Patients were classified according to National Cancer Institute and FDA criteria, and the rates of clinically relevant toxicities were evaluated within groups and compared among groups. Cockcroft-Gault estimated renal function improved over time, which may be attributed to an increase in weight of patients in the same time frame. Approximately 36% of patients enrolled onto phase I trials had mild renal dysfunction by FDA criteria. Relative to normal function, mild renal dysfunction was associated with a statistically significant but small increase in grade 3 or 4 nonhematologic toxicity and any relevant toxicities. Patients with mild renal dysfunction by FDA criteria have routinely been enrolled onto phase I studies of antineoplastics without clinically meaningful increase in the risk of toxicity. In future oncology renal dysfunction trials based on the FDA classification, the FDA mild group may only need to be activated when the moderate and normal groups differ substantially in tolerability or pharmacokinetics. © 2015 by American Society of Clinical Oncology. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Beumer, Jan H AU - Ding, Fei AU - Tawbi, Hussein AU - Lin, Yan AU - Viluh, Diana AU - Chatterjee, Indrani AU - Rinker, Matthew AU - Chow, Selina L AU - Ivy, S Percy AD - Jan H. Beumer, Fei Ding, Hussein Tawbi, Yan Lin, and Selina L. Chow, University of Pittsburgh Cancer Institute; Jan H. Beumer, University of Pittsburgh School of Pharmacy; Jan H. Beumer and Hussein Tawbi, University of Pittsburgh School of Medicine; Yan Lin, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA; Diana Viluh, Indrani Chatterjee, and Matthew Rinker, Theradex, Princeton, NJ; and S. Percy Ivy, Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, MD. beumerj@gmail.com. ; Jan H. Beumer, Fei Ding, Hussein Tawbi, Yan Lin, and Selina L. Chow, University of Pittsburgh Cancer Institute; Jan H. Beumer, University of Pittsburgh School of Pharmacy; Jan H. Beumer and Hussein Tawbi, University of Pittsburgh School of Medicine; Yan Lin, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, PA; Diana Viluh, Indrani Chatterjee, and Matthew Rinker, Theradex, Princeton, NJ; and S. Percy Ivy, Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, MD. Y1 - 2016/01/10/ PY - 2016 DA - 2016 Jan 10 SP - 110 EP - 116 VL - 34 IS - 2 KW - Antineoplastic Agents KW - 0 KW - Biomarkers KW - Creatinine KW - AYI8EX34EU KW - Index Medicus KW - United States KW - Severity of Illness Index KW - Aged, 80 and over KW - Humans KW - Adult KW - Databases, Factual KW - Biomarkers -- metabolism KW - Aged KW - Middle Aged KW - Male KW - Female KW - Kidney -- metabolism KW - Creatinine -- metabolism KW - Clinical Trials, Phase I as Topic -- statistics & numerical data KW - Antineoplastic Agents -- administration & dosage KW - Antineoplastic Agents -- pharmacokinetics KW - Kidney -- drug effects KW - Renal Insufficiency, Chronic -- blood KW - Patient Selection KW - Renal Insufficiency, Chronic -- metabolism KW - Renal Insufficiency, Chronic -- chemically induced KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1754524082?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Effect+of+Renal+Dysfunction+on+Toxicity+in+Three+Decades+of+Cancer+Therapy+Evaluation+Program-Sponsored+Single-Agent+Phase+I+Studies.&rft.au=Beumer%2C+Jan+H%3BDing%2C+Fei%3BTawbi%2C+Hussein%3BLin%2C+Yan%3BViluh%2C+Diana%3BChatterjee%2C+Indrani%3BRinker%2C+Matthew%3BChow%2C+Selina+L%3BIvy%2C+S+Percy&rft.aulast=Beumer&rft.aufirst=Jan&rft.date=2016-01-10&rft.volume=34&rft.issue=2&rft.spage=110&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=1527-7755&rft_id=info:doi/10.1200%2FJCO.2014.59.7302 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-02 N1 - Date created - 2016-01-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Comment In: J Clin Oncol. 2016 Jan 10;34(2):103-4 [26628472] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1200/JCO.2014.59.7302 ER - TY - JOUR T1 - Incidence and mortality risks for circulatory diseases in US radiologic technologists who worked with fluoroscopically guided interventional procedures, 1994-2008 AN - 1808683384; PQ0003417594 AB - ObjectivesAlthough fluoroscopically guided interventional procedures (FGIP) have provided major advances in the treatment of various common diseases, radiation exposures associated with these procedures may cause adverse health effects in workers. We assess risk of circulatory disease incidence and mortality in medical radiation workers performing FGIP.MethodsA US nationwide prospective cohort study of 90957 radiologic technologists who completed a cohort survey during 1994-1998 was followed until completion of a subsequent survey during 2003-2005 for circulatory disease incidence, or until 31 December 2008 for mortality. Incidence analyses were restricted to the 63482 technologists who completed both the second survey (1994-1998) and the third survey (2003-2005). Cox proportional hazards models were used to assess adjusted HR and 95% CIs for mortality from all causes, all circulatory diseases, all heart diseases, ischaemic heart disease, stroke, acute myocardial infarction and hypertension in participants who reported ever performing FGIP compared to technologists who never performed FGIP procedures. Adjusted HRs were calculated for self-reported hypertension, stroke and myocardial infarction.ResultsWe observed a 34% increase in stroke incidence (HR=1.34, 95% CI 1.10 to 1.64) in technologists who performed FGIP compared to those who never performed these procedures. Mortality from stroke was also modestly elevated, although not statistically significant (HR=1.22, 95% CI 0.85 to 1.73). We observed no statistically significant excess risks of incidence or mortality from any other outcome evaluated.ConclusionsOur finding of elevated risk of stroke in workers performing FGIP needs to be confirmed in studies with individual radiation dose data, but nonetheless underlines the need to keep radiation exposure as low as reasonably achievable without compromising key diagnostic information. JF - Occupational and Environmental Medicine AU - Rajaraman, Preetha AU - Doody, Michele M AU - Yu, Chu Ling AU - Preston, Dale L AU - Miller, Jeremy S AU - Sigurdson, Alice J AU - Freedman, D Michal AU - Alexander, Bruce H AU - Little, Mark P AU - Miller, Donald L AU - Linet, Martha S AD - Center for Global Health, National Cancer Institute, NIH, DHHS, Rockville, Maryland, USA Y1 - 2016/01/08/ PY - 2016 DA - 2016 Jan 08 SP - 21 EP - 27 PB - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom VL - 73 IS - 1 SN - 1351-0711, 1351-0711 KW - Health & Safety Science Abstracts KW - Risk assessment KW - Mortality KW - Radiation KW - Stroke KW - Occupational exposure KW - Myocardial infarction KW - Hypertension KW - Heart diseases KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808683384?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+Environmental+Medicine&rft.atitle=Incidence+and+mortality+risks+for+circulatory+diseases+in+US+radiologic+technologists+who+worked+with+fluoroscopically+guided+interventional+procedures%2C+1994-2008&rft.au=Rajaraman%2C+Preetha%3BDoody%2C+Michele+M%3BYu%2C+Chu+Ling%3BPreston%2C+Dale+L%3BMiller%2C+Jeremy+S%3BSigurdson%2C+Alice+J%3BFreedman%2C+D+Michal%3BAlexander%2C+Bruce+H%3BLittle%2C+Mark+P%3BMiller%2C+Donald+L%3BLinet%2C+Martha+S&rft.aulast=Rajaraman&rft.aufirst=Preetha&rft.date=2016-01-08&rft.volume=73&rft.issue=1&rft.spage=21&rft.isbn=&rft.btitle=&rft.title=Occupational+and+Environmental+Medicine&rft.issn=13510711&rft_id=info:doi/10.1136%2Foemed-2015-102888 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Risk assessment; Mortality; Radiation; Stroke; Myocardial infarction; Occupational exposure; Heart diseases; Hypertension DO - http://dx.doi.org/10.1136/oemed-2015-102888 ER - TY - JOUR T1 - Metabolic profile of mephedrone: Identification of nor-mephedrone conjugates with dicarboxylic acids as a new type of xenobiotic phase II metabolites. AN - 1737475353; 26541208 AB - Metabolic profile of mephedrone (4-methylmethcathinone, 4-MMC), a frequently abused recreational drug, was determined in rats in vivo. The urine of rats dosed with a subcutaneous bolus dose of 20mg 4-MMC/kg was analysed by LC/MS. Ten phase I and five phase II metabolites were identified by comparison of their retention times and MS(2) spectra with those of authentic reference standards and/or with the MS(2) spectra of previously identified metabolites. The main metabolic pathway was N-demethylation leading to normephedrone (4-methylcathinone, 4-MC) which was further conjugated with succinic, glutaric and adipic acid. Other phase I metabolic pathways included oxidation of the 4-methyl group, carbonyl reduction leading to dihydro-metabolites and ω-oxidation at the position 3'. Five of the metabolites detected, namely, 4-carboxynormephedrone (4-carboxycathinone, 4-CC), 4-carboxydihydronormephedrone (4-carboxynorephedrine, 4-CNE), hydroxytolyldihydro-normephedrone (4-hydroxymethylnorephedrine, 4-OH-MNE) and conjugates of 4-MC with glutaric and adipic acid, have not been reported as yet. The last two conjugates represent a novel, hitherto unexploited, type of phase II metabolites in mammals together with an analogous succinic acid conjugate of 4-MC identified by Pozo et al. (2015). These conjugates might be potentially of great importance in the metabolism of other psychoactive amines. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. JF - Toxicology letters AU - Linhart, Igor AU - Himl, Michal AU - Židková, Monika AU - Balíková, Marie AU - Lhotková, Eva AU - Páleníček, Tomáš AD - Department of Organic Chemistry, Faculty of Chemical Technology, University of Chemistry and Technology, Prague, Czech Republic. Electronic address: linharti@vscht.cz. ; Department of Organic Chemistry, Faculty of Chemical Technology, University of Chemistry and Technology, Prague, Czech Republic. ; Institute of Forensic Medicine and Toxicology, 1st Faculty of Medicine, Charles University in Prague, Czech Republic. ; National Institute of Mental Health, Klecany, Czech Republic. Y1 - 2016/01/05/ PY - 2016 DA - 2016 Jan 05 SP - 114 EP - 121 VL - 240 IS - 1 KW - Adipates KW - 0 KW - Dicarboxylic Acids KW - Glutarates KW - Xenobiotics KW - Methamphetamine KW - 44RAL3456C KW - adipic acid KW - 76A0JE0FKJ KW - mephedrone KW - 8BA8T27317 KW - Succinic Acid KW - AB6MNQ6J6L KW - glutaric acid KW - H849F7N00B KW - Index Medicus KW - Dicarboxylic acid conjugates KW - Mephedron metabolism KW - Designer drugs KW - Rats KW - Mass Spectrometry KW - Animals KW - Metabolome KW - Glutarates -- metabolism KW - Adipates -- metabolism KW - Dose-Response Relationship, Drug KW - Rats, Wistar KW - Chromatography, Liquid KW - Male KW - Succinic Acid -- metabolism KW - Xenobiotics -- urine KW - Methamphetamine -- urine KW - Methamphetamine -- chemistry KW - Xenobiotics -- toxicity KW - Methamphetamine -- analogs & derivatives KW - Xenobiotics -- chemistry KW - Methamphetamine -- toxicity KW - Dicarboxylic Acids -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1737475353?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+letters&rft.atitle=Metabolic+profile+of+mephedrone%3A+Identification+of+nor-mephedrone+conjugates+with+dicarboxylic+acids+as+a+new+type+of+xenobiotic+phase+II+metabolites.&rft.au=Linhart%2C+Igor%3BHiml%2C+Michal%3B%C5%BDidkov%C3%A1%2C+Monika%3BBal%C3%ADkov%C3%A1%2C+Marie%3BLhotkov%C3%A1%2C+Eva%3BP%C3%A1len%C3%AD%C4%8Dek%2C+Tom%C3%A1%C5%A1&rft.aulast=Linhart&rft.aufirst=Igor&rft.date=2016-01-05&rft.volume=240&rft.issue=1&rft.spage=114&rft.isbn=&rft.btitle=&rft.title=Toxicology+letters&rft.issn=1879-3169&rft_id=info:doi/10.1016%2Fj.toxlet.2015.10.025 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-28 N1 - Date created - 2015-11-28 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.toxlet.2015.10.025 ER - TY - JOUR T1 - Synthesis, antitumor screening and cell cycle analysis of novel benzothieno[3,2-b]pyran derivatives. AN - 1851271905; 27590401 AB - Three series of benzothiophene derivatives were designed and synthesized as cytotoxic agents. The compounds were subjected to in vitro antitumor screening at the National Cancer Institute (NCI), Bethesda, MD. The results of the single dose screening indicated that only the benzothieno[3,2-b]pyran series 3a-f exhibited potent and broad spectrum cytotoxic activity and was subjected to five dose cytotoxic screening. The most active compound in this study was 2-amino-6-bromo-4-(4-nitrophenyl)-4H-[1]benzothieno[3,2-b]pyran-3-carbonitrile (3e) with MG-MID GI50, TGI, and LC50 values of 0.11, 7.94 and 42.66 μM, respectively. Compound 3e exhibited broad spectrum anticancer activity against a panel of 59 cell lines. To elucidate the underlying mechanism of compound 3e cytotoxic activity, we examined its effect on cell cycle progression and its ability to induce apoptosis using human colon adenocarcinoma cell line (HCT-116). The effect of compound 3e on the cell cycle progression indicated that exposure of HCT-116 cells to compound 3e for 24 and 48 h, induced a significant disruption in the cell cycle profile including time dependent decrease in cell population at G1 phase with concomitant increase in pre-G and G2/M cell population. Moreover, compound 3e induced time dependent increase in the percentage of early and late apoptotic and necrotic cell population. In conclusion, we were able to successfully design a new series of benzothieno[3,2-b]pyran derivatives with potent cytotoxic activity and their mechanism of cytotoxicity was examined. JF - Journal of enzyme inhibition and medicinal chemistry AU - Zaher, Ashraf F AU - Abuel-Maaty, Suzan M AU - El-Nassan, Hala B AU - Amer, Samir A S AU - Abdelghany, Tamer M AD - a Department of Pharmaceutical Organic Chemistry, Faculty of Pharmacy , Cairo University , Cairo , Egypt. ; b Department of Pathology, Molecular Pathology Unit , National Cancer Institute, Cairo University , Cairo , Egypt , and. ; c Department of Pharmacology and Toxicology, Faculty of Pharmacy , Al-Azhar University , Cairo , Egypt. Y1 - 2016 PY - 2016 DA - 2016 SP - 145 EP - 153 VL - 31 KW - cell cycle analysis KW - apoptosis KW - benzothieno[3,2-b]pyran KW - Antitumor activity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1851271905?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+enzyme+inhibition+and+medicinal+chemistry&rft.atitle=Synthesis%2C+antitumor+screening+and+cell+cycle+analysis+of+novel+benzothieno%5B3%2C2-b%5Dpyran+derivatives.&rft.au=Zaher%2C+Ashraf+F%3BAbuel-Maaty%2C+Suzan+M%3BEl-Nassan%2C+Hala+B%3BAmer%2C+Samir+A+S%3BAbdelghany%2C+Tamer+M&rft.aulast=Zaher&rft.aufirst=Ashraf&rft.date=2016-01-01&rft.volume=31&rft.issue=&rft.spage=145&rft.isbn=&rft.btitle=&rft.title=Journal+of+enzyme+inhibition+and+medicinal+chemistry&rft.issn=1475-6374&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2016-09-03 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - The effect of different sets of critical values on type I error rates in tiled regression for genome-wide association studies AN - 1846410501; PQ0003818858 AB - The effects of different sets of critical values on type I error rates in tiled regression were investigated using genome-wide association data from the Trinity Student Study. 200 simulated null traits from the standard normal distribution were analysed using four different sets of critical values for stepwise regression within tiled regression. We observed that (1) the multicollinearity among SNPs considered and the aggregate type I error rates decreased through three levels of tiled regression; (2) the region-specific type I error rates were slightly lower than the 'nominal' critical values at the tile level; and (3) the critical value at the tile level is between the two aggregate type I error rates defined under two different assumptions about the number of tests (the number of SNPs and the number of tiles). The choice of critical value at each stage of tiled regression affects the overall type I error rate. JF - International Journal of Data Mining and Bioinformatics AU - Sung, Heejong AU - Sabourin, Jeremy A AU - Sorant, Alexa JM AU - Wilson, Alexander F AD - Genometrics Section, Computational and Statistical Genomics Branch, National Human Genome Research Institute, National Institutes of Health, 333 Cassell Drive, Suite 1200, Baltimore, MD 21224, USA Y1 - 2016///0, PY - 2016 DA - 0, 2016 SP - 111 EP - 120 PB - Inderscience Publishers Ltd., PO Box 735 Olney Bucks MK46 5WB United Kingdom VL - 16 IS - 2 SN - 1748-5673, 1748-5673 KW - Biotechnology and Bioengineering Abstracts KW - HEALTHCARE AND BIOSCIENCES KW - COMPUTING AND MATHEMATICS KW - Biosciences and Bioinformatics KW - Computing Science, Applications and Software KW - Healthcare and Medical Engineering KW - Data processing KW - Single-nucleotide polymorphism KW - Bioinformatics KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1846410501?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Data+Mining+and+Bioinformatics&rft.atitle=The+effect+of+different+sets+of+critical+values+on+type+I+error+rates+in+tiled+regression+for+genome-wide+association+studies&rft.au=Sung%2C+Heejong%3BSabourin%2C+Jeremy+A%3BSorant%2C+Alexa+JM%3BWilson%2C+Alexander+F&rft.aulast=Sung&rft.aufirst=Heejong&rft.date=2016-01-01&rft.volume=16&rft.issue=2&rft.spage=111&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Data+Mining+and+Bioinformatics&rft.issn=17485673&rft_id=info:doi/10.1504%2FIJDMB.2016.080030 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-12-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Data processing; Single-nucleotide polymorphism; Bioinformatics DO - http://dx.doi.org/10.1504/IJDMB.2016.080030 ER - TY - JOUR T1 - Polycyclic aromatic hydrocarbons: determinants of residential carpet dust levels and risk of non-Hodgkin lymphoma AN - 1842513800; PQ0002586008 AB - To investigate the risk of non-Hodgkin lymphoma (NHL) associated with residential carpet dust measurements of polycyclic aromatic hydrocarbons (PAHs). We evaluated the relationship between residential carpet dust PAH concentrations (benz(a)anthracene, benzo(a)pyrene, benzo(b)fluoranthene, benzo(k)fluoranthene, chrysene, dibenz(a,h)anthracene, and indeno(1,2,3-c,d)pyrene, and their sum) and risk of NHL (676 cases, 511 controls) in the National Cancer Institute Surveillance Epidemiology and End Results multicenter case-control study. As a secondary aim, we investigated determinants of dust PAH concentrations. We computed odds ratios (OR) and 95 % confidence interval (CI) for associations between NHL and concentrations of individual and summed PAHs using unconditional logistic regression, adjusting for age, gender, and study center. Determinants of natural log-transformed PAHs were investigated using multivariate least-squares regression. We observed some elevated risks for NHL overall and B cell lymphoma subtypes in association with quartiles or tertiles of PAH concentrations, but without a monotonic trend, and there was no association comparing the highest quartile or tertile to the lowest. In contrast, risk of T cell lymphoma was significantly increased among participants with the highest tertile of summed PAHs (OR = 3.04; 95 % CI, 1.09-8.47) and benzo(k)fluoranthene (OR = 3.20; 95 % CI, 1.13-9.11) compared with the lowest tertile. Predictors of PAH dust concentrations in homes included ambient air PAH concentrations and the proportion of developed land within 2 km of a residence. Older age, more years of education, and white race were also predictive of higher levels in homes. Our results suggest a potential link between PAH exposure and risk of T cell lymphoma and demonstrate the importance of analyzing risk by NHL histologic type. JF - Cancer Causes & Control AU - DellaValle, Curt T AU - Deziel, Nicole C AU - Jones, Rena R AU - Colt, Joanne S AU - De Roos, Anneclaire J AU - Cerhan, James R AU - Cozen, Wendy AU - Severson, Richard K AU - Flory, Abigail R AU - Morton, Lindsay M AU - Ward, Mary H AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health (NIH), Department of Health and Human Services (DHHS), 9609 Medical Center Dr, Room 6E138 MSC 9771, Bethesda, MD, 20892, USA, wardm@mail.nih.gov Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 1 EP - 13 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 27 IS - 1 SN - 0957-5243, 0957-5243 KW - Toxicology Abstracts KW - Polycyclic aromatic hydrocarbons KW - B-cell lymphoma KW - Age KW - Dust KW - Chrysene KW - Epidemiology KW - Carpets KW - Risk factors KW - Geriatrics KW - Benzo(a)pyrene KW - T-cell lymphoma KW - Races KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1842513800?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Causes+%26+Control&rft.atitle=Polycyclic+aromatic+hydrocarbons%3A+determinants+of+residential+carpet+dust+levels+and+risk+of+non-Hodgkin+lymphoma&rft.au=DellaValle%2C+Curt+T%3BDeziel%2C+Nicole+C%3BJones%2C+Rena+R%3BColt%2C+Joanne+S%3BDe+Roos%2C+Anneclaire+J%3BCerhan%2C+James+R%3BCozen%2C+Wendy%3BSeverson%2C+Richard+K%3BFlory%2C+Abigail+R%3BMorton%2C+Lindsay+M%3BWard%2C+Mary+H&rft.aulast=DellaValle&rft.aufirst=Curt&rft.date=2016-01-01&rft.volume=27&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-015-0660-y LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-11-01 N1 - Number of references - 48 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Chrysene; Age; B-cell lymphoma; Polycyclic aromatic hydrocarbons; Epidemiology; Carpets; Risk factors; Geriatrics; Benzo(a)pyrene; T-cell lymphoma; Races; Dust DO - http://dx.doi.org/10.1007/s10552-015-0660-y ER - TY - JOUR T1 - AMPK Activation Prevents and Reverses Drug-Induced Mitochondrial and Hepatocyte Injury by Promoting Mitochondrial Fusion and Function. AN - 1835685140; 27792760 AB - Mitochondrial damage is the major factor underlying drug-induced liver disease but whether conditions that thwart mitochondrial injury can prevent or reverse drug-induced liver damage is unclear. A key molecule regulating mitochondria quality control is AMP activated kinase (AMPK). When activated, AMPK causes mitochondria to elongate/fuse and proliferate, with mitochondria now producing more ATP and less reactive oxygen species. Autophagy is also triggered, a process capable of removing damaged/defective mitochondria. To explore whether AMPK activation could potentially prevent or reverse the effects of drug-induced mitochondrial and hepatocellular damage, we added an AMPK activator to collagen sandwich cultures of rat and human hepatocytes exposed to the hepatotoxic drugs, acetaminophen or diclofenac. In the absence of AMPK activation, the drugs caused hepatocytes to lose polarized morphology and have significantly decreased ATP levels and viability. At the subcellular level, mitochondria underwent fragmentation and had decreased membrane potential due to decreased expression of the mitochondrial fusion proteins Mfn1, 2 and/or Opa1. Adding AICAR, a specific AMPK activator, at the time of drug exposure prevented and reversed these effects. The mitochondria became highly fused and ATP production increased, and hepatocytes maintained polarized morphology. In exploring the mechanism responsible for this preventive and reversal effect, we found that AMPK activation prevented drug-mediated decreases in Mfn1, 2 and Opa1. AMPK activation also stimulated autophagy/mitophagy, most significantly in acetaminophen-treated cells. These results suggest that activation of AMPK prevents/reverses drug-induced mitochondrial and hepatocellular damage through regulation of mitochondrial fusion and autophagy, making it a potentially valuable approach for treatment of drug-induced liver injury. JF - PloS one AU - Kang, Sun Woo Sophie AU - Haydar, Ghada AU - Taniane, Caitlin AU - Farrell, Geoffrey AU - Arias, Irwin M AU - Lippincott-Schwartz, Jennifer AU - Fu, Dong AD - Faculty of Pharmacy, The University of Sydney, Sydney, NSW, Australia. ; Liver Research Group, Australian National University Medical School, Canberra, Australia. ; National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America. ; Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, Virginia, United States of America. Y1 - 2016 PY - 2016 DA - 2016 SP - 1 VL - 11 IS - 10 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1835685140?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=AMPK+Activation+Prevents+and+Reverses+Drug-Induced+Mitochondrial+and+Hepatocyte+Injury+by+Promoting+Mitochondrial+Fusion+and+Function.&rft.au=Kang%2C+Sun+Woo+Sophie%3BHaydar%2C+Ghada%3BTaniane%2C+Caitlin%3BFarrell%2C+Geoffrey%3BArias%2C+Irwin+M%3BLippincott-Schwartz%2C+Jennifer%3BFu%2C+Dong&rft.aulast=Kang&rft.aufirst=Sun+Woo&rft.date=2016-01-01&rft.volume=11&rft.issue=10&rft.spage=e0165638&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0165638 LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2016-10-28 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0165638 ER - TY - JOUR T1 - Degradation Rate of 5-Fluorouracil in Metastatic Colorectal Cancer: A New Predictive Outcome Biomarker? AN - 1835434204; 27656891 AB - 5-FU based chemotherapy is the most common first line regimen used for metastatic colorectal cancer (mCRC). Identification of predictive markers of response to chemotherapy is a challenging approach for drug selection. The present study analyzes the predictive role of 5-FU degradation rate (5-FUDR) and genetic polymorphisms (MTHFR, TSER, DPYD) on survival. Genetic polymorphisms of MTHFR, TSER and DPYD, and the 5-FUDR of homogenous patients with mCRC were retrospectively studied. Genetic markers and the 5-FUDR were correlated with clinical outcome. 133 patients affected by mCRC, treated with fluoropyrimidine-based chemotherapy from 2009 to 2014, were evaluated. Patients were classified into three metabolic classes, according to normal distribution of 5-FUDR in more than 1000 patients, as previously published: poor-metabolizer (PM) with 5-FU-DR ≤ 0,85 ng/ml/106 cells/min (8 pts); normal metabolizer with 0,85 < 5-FU-DR < 2,2 ng/ml/106 cells/min (119 pts); ultra-rapid metabolizer (UM) with 5-FU-DR ≥ 2,2 ng/ml/106 cells/min (6 pts). PM and UM groups showed a longer PFS respect to normal metabolizer group (14.5 and 11 months respectively vs 8 months; p = 0.029). A higher G3-4 toxicity rate was observed in PM and UM, respect to normal metabolizer (50% in both PM and UM vs 18%; p = 0.019). No significant associations between genes polymorphisms and outcomes or toxicities were observed. 5-FUDR seems to be significantly involved in predicting survival of patients who underwent 5-FU based CHT for mCRC. Although our findings require confirmation in large prospective studies, they reinforce the concept that individual genetic variation may allow personalized selection of chemotherapy to optimize clinical outcomes. JF - PloS one AU - Botticelli, Andrea AU - Borro, Marina AU - Onesti, Concetta Elisa AU - Strigari, Lidia AU - Gentile, Giovanna AU - Cerbelli, Bruna AU - Romiti, Adriana AU - Occhipinti, Mario AU - Sebastiani, Claudia AU - Lionetto, Luana AU - Marchetti, Luca AU - Simmaco, Maurizio AU - Marchetti, Paolo AU - Mazzuca, Federica AD - Department of Clinical and Molecular Medicine, "Sapienza" University of Rome, Rome, Italy. ; Department of Neurosciences, Mental Health and Sensory Organs (NESMOS), "Sapienza" University of Rome, Rome, Italy. ; Medical Oncology Unit, Sant'Andrea Hospital, Rome, Italy. ; Laboratory of Medical Physics and Expert Systems, Regina Elena National Cancer Institute, Rome, Italy. ; Istituto Dermopatico dell'Immacolata-IRCCS, Rome, Italy. ; Department of Radiological Oncological and Pathological Sciences, "Sapienza" University of Rome, Rome, Italy. ; Department of Medical Oncology, Policlinico Umberto I, Rome, Italy. PY - 2016 SP - 1 VL - 11 IS - 9 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1835434204?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Degradation+Rate+of+5-Fluorouracil+in+Metastatic+Colorectal+Cancer%3A+A+New+Predictive+Outcome+Biomarker%3F&rft.au=Botticelli%2C+Andrea%3BBorro%2C+Marina%3BOnesti%2C+Concetta+Elisa%3BStrigari%2C+Lidia%3BGentile%2C+Giovanna%3BCerbelli%2C+Bruna%3BRomiti%2C+Adriana%3BOcchipinti%2C+Mario%3BSebastiani%2C+Claudia%3BLionetto%2C+Luana%3BMarchetti%2C+Luca%3BSimmaco%2C+Maurizio%3BMarchetti%2C+Paolo%3BMazzuca%2C+Federica&rft.aulast=Botticelli&rft.aufirst=Andrea&rft.date=2016-01-01&rft.volume=11&rft.issue=9&rft.spage=e0163105&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0163105 LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2016-09-22 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0163105 ER - TY - JOUR T1 - Advancing toxicology research using in vivo high throughput toxicology with small fish models. AN - 1826701099; 27328013 AB - Small freshwater fish models, especially zebrafish, offer advantages over traditional rodent models, including low maintenance and husbandry costs, high fecundity, genetic diversity, physiology similar to that of traditional biomedical models, and reduced animal welfare concerns. The Collaborative Workshop on Aquatic Models and 21st Century Toxicology was held at North Carolina State University on May 5-6, 2014, in Raleigh, North Carolina, USA. Participants discussed the ways in which small fish are being used as models to screen toxicants and understand mechanisms of toxicity. Workshop participants agreed that the lack of standardized protocols is an impediment to broader acceptance of these models, whereas development of standardized protocols, validation, and subsequent regulatory acceptance would facilitate greater usage. Given the advantages and increasing application of small fish models, there was widespread interest in follow-up workshops to review and discuss developments in their use. In this article, we summarize the recommendations formulated by workshop participants to enhance the utility of small fish species in toxicology studies, as well as many of the advances in the field of toxicology that resulted from using small fish species, including advances in developmental toxicology, cardiovascular toxicology, neurotoxicology, and immunotoxicology. We alsoreview many emerging issues that will benefit from using small fish species, especially zebrafish, and new technologies that will enable using these organisms to yield results unprecedented in their information content to better understand how toxicants affect development and health. JF - ALTEX AU - Planchart, Antonio AU - Mattingly, Carolyn J AU - Allen, David AU - Ceger, Patricia AU - Casey, Warren AU - Hinton, David AU - Kanungo, Jyotshna AU - Kullman, Seth W AU - Tal, Tamara AU - Bondesson, Maria AU - Burgess, Shawn M AU - Sullivan, Con AU - Kim, Carol AU - Behl, Mamta AU - Padilla, Stephanie AU - Reif, David M AU - Tanguay, Robert L AU - Hamm, Jon AD - Department of Biological Sciences, North Carolina State University, Raleigh, NC, USA. ; Integrated Laboratory Systems, Inc., Research Triangle Park, NC, USA. ; National Toxicology Program Interagency Center for the Evaluation of Alternative Toxicological Methods, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. ; Nicholas School of the Environment, Duke University, Durham, NC, USA. ; National Center for Toxicological Research, U.S. Food and Drug Administration, Jefferson, AR, USA. ; Integrated Systems Toxicology Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC, USA. ; Department of Pharmacological and Pharmaceutical Sciences, University of Houston, Houston, TX, USA. ; National Human Genome Research Institute, Bethesda, MD, USA. ; Department of Molecular & Biomedical Sciences, University of Maine, Orono, ME, USA. ; Division of National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. ; Department of Environmental & Molecular Toxicology, Oregon State University, Corvallis, OR, USA. Y1 - 2016 PY - 2016 DA - 2016 SP - 435 EP - 452 VL - 33 IS - 4 SN - 1868-596X, 1868-596X KW - Hazardous Substances KW - 0 KW - Index Medicus KW - aquatic models KW - alternatives KW - 21st century toxicology KW - Animals KW - Humans KW - Whole Body Imaging KW - Cardiovascular Diseases -- chemically induced KW - Animals, Genetically Modified KW - Genome KW - Genomics KW - Fishes KW - Animal Experimentation KW - Toxicity Tests -- methods KW - Hazardous Substances -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826701099?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=ALTEX&rft.atitle=Advancing+toxicology+research+using+in+vivo+high+throughput+toxicology+with+small+fish+models.&rft.au=Planchart%2C+Antonio%3BMattingly%2C+Carolyn+J%3BAllen%2C+David%3BCeger%2C+Patricia%3BCasey%2C+Warren%3BHinton%2C+David%3BKanungo%2C+Jyotshna%3BKullman%2C+Seth+W%3BTal%2C+Tamara%3BBondesson%2C+Maria%3BBurgess%2C+Shawn+M%3BSullivan%2C+Con%3BKim%2C+Carol%3BBehl%2C+Mamta%3BPadilla%2C+Stephanie%3BReif%2C+David+M%3BTanguay%2C+Robert+L%3BHamm%2C+Jon&rft.aulast=Planchart&rft.aufirst=Antonio&rft.date=2016-01-01&rft.volume=33&rft.issue=4&rft.spage=435&rft.isbn=&rft.btitle=&rft.title=ALTEX&rft.issn=1868596X&rft_id=info:doi/10.14573%2Faltex.1601281 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2017-01-17 N1 - Date created - 2016-06-21 N1 - Date revised - 2017-01-30 N1 - Last updated - 2017-01-30 DO - http://dx.doi.org/10.14573/altex.1601281 ER - TY - JOUR T1 - HIV-1 Induced CNS Dysfunction: Current Overview and Research Priorities. AN - 1826666905; 27009096 AB - Over the past three decades, the clinical presentation of HIV infection of the Central Nervous System (CNS) has evolved. Prior to wide spread use of effective antiretroviral therapy (ART), more than a third of infected individuals exhibited a range of neurocognitive and motor deficits that frequently progressed to severe dementia and paralysis. However, the use of ART has significantly decreased the prevalence of severe forms of HIV-1 associated neurocognitive disorders (HAND). Studies of neurocognitive dysfunction have reported variable prevalence, ranging from 21% to 77.6%, defined primarily by mild to moderate neurocognitive impairment. HIV-associated chronic inflammation and associated neurotoxicity of long term ART, as well as the aging of the HIV-infected population, likely influence the pathogenesis of HAND. Despite significant research efforts directed towards a better understanding of the mechanisms underlying HIV neuropathogenesis, definitive causal pathophysiology of HAND and thus effective prevention or treatment remain elusive. Furthermore, HIV therapeutic research now includes efforts to effect a cure, by eliminating or silencing HIV within infected cells, which must include efforts to target the latently infected cells within the CNS. Prevention and treatment of the neurological complications of HIV, and eradication of persistent virus from the CNS compartment are major priorities for the HIV-CNS research. Here we give an overview of the progress of research on HIV-CNS disease, define new challenges and research areas, and highlight domestic and global priorities. JF - Current HIV research AU - Joseph, Jeymohan AU - Colosi, Deborah A AU - Rao, Vasudev R AD - HIV Neuropathogenesis, Genetics, and Therapeutics Branch, Division of AIDS Research, National Institute of Mental Health, Bethesda, MD-20892, USA. jjeymoha@mail.nih.gov. Y1 - 2016 PY - 2016 DA - 2016 SP - 389 EP - 399 VL - 14 IS - 5 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826666905?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+HIV+research&rft.atitle=HIV-1+Induced+CNS+Dysfunction%3A+Current+Overview+and+Research+Priorities.&rft.au=Joseph%2C+Jeymohan%3BColosi%2C+Deborah+A%3BRao%2C+Vasudev+R&rft.aulast=Joseph&rft.aufirst=Jeymohan&rft.date=2016-01-01&rft.volume=14&rft.issue=5&rft.spage=389&rft.isbn=&rft.btitle=&rft.title=Current+HIV+research&rft.issn=1873-4251&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2016-03-24 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - Clinical Performance of a Matrix-Assisted Laser Desorption Ionization-Time of Flight Mass Spectrometry Method for Detection of Certain blaKPC-Containing Plasmids AN - 1819147191; PQ0002453121 AB - Rapid detection of blaKPC-containing organisms can significantly impact infection control and clinical practices, as well as therapeutic choices. Current molecular and phenotypic methods to detect these organisms, however, require additional testing beyond routine organism identification. In this study, we evaluated the clinical performance of matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) to detect pKpQIL_p019 (p019)-an similar to 11,109-Da protein associated with certain blaKPC-containing plasmids that was previously shown to successfully track a clonal outbreak of blaKPC-pKpQIL-Klebsiella pneumoniae in a proof-of-principle study (A. F. Lau, H. Wang, R. A. Weingarten, S. K. Drake, A. F. Suffredini, M. K. Garfield, Y. Chen, M. Gucek, J. H. Youn, F. Stock, H. Tso, J. DeLeo, J. J. Cimino, K. M. Frank, and J. P. Dekker, J Clin Microbiol 52:2804-2812, 2014, http://dx.doi.org/10.1128/JCM.00694-14). PCR for the p019 gene was used as the reference method. Here, blind analysis of 140 characterized Enterobacteriaceae isolates using two protein extraction methods (plate extraction and tube extraction) and two peak detection methods (manual and automated) showed sensitivities and specificities ranging from 96% to 100% and from 95% to 100%, respectively (2,520 spectra analyzed). Feasible laboratory implementation methods (plate extraction and automated analysis) demonstrated 96% sensitivity and 99% specificity. All p019-positive isolates (n = 26) contained blaKPC and were carbapenem resistant. Retrospective analysis of an additional 720 clinical Enterobacteriaceae spectra found an similar to 11,109-Da signal in nine spectra (1.3%), including seven from p019-containing, carbapenem-resistant isolates (positive predictive value [PPV], 78%). Instrument tuning had a significant effect on assay sensitivity, highlighting important factors that must be considered as MALDI-TOF MS moves into applications beyond microbial identification. Using a large blind clinical data set, we have shown that spectra acquired for routine organism identification can also be analyzed automatically in real time at high throughput, at no additional expense to the laboratory, to enable rapid detection of potentially blaKPC-containing carbapenem-resistant isolates, providing early and clinically actionable results. JF - Journal of Clinical Microbiology AU - Youn, Jung-Ho AU - Drake, Steven K AU - Weingarten, Rebecca A AU - Frank, Karen M AU - Dekker, John P AU - Lau, Anna F AD - << + $0, Anna.Lau@nih.gov. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 35 EP - 42 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 54 IS - 1 SN - 0095-1137, 0095-1137 KW - Microbiology Abstracts A: Industrial & Applied Microbiology KW - Data processing KW - Polymerase chain reaction KW - Carbapenems KW - Lasers KW - Plasmids KW - Infection KW - Enterobacteriaceae KW - Mass spectroscopy KW - A 01350:Microbial Resistance UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1819147191?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=Clinical+Performance+of+a+Matrix-Assisted+Laser+Desorption+Ionization-Time+of+Flight+Mass+Spectrometry+Method+for+Detection+of+Certain+blaKPC-Containing+Plasmids&rft.au=Youn%2C+Jung-Ho%3BDrake%2C+Steven+K%3BWeingarten%2C+Rebecca+A%3BFrank%2C+Karen+M%3BDekker%2C+John+P%3BLau%2C+Anna+F&rft.aulast=Youn&rft.aufirst=Jung-Ho&rft.date=2016-01-01&rft.volume=54&rft.issue=1&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/10.1128%2FJCM.01643-15 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-09-01 N1 - Number of references - 22 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Data processing; Carbapenems; Polymerase chain reaction; Lasers; Infection; Plasmids; Mass spectroscopy; Enterobacteriaceae DO - http://dx.doi.org/10.1128/JCM.01643-15 ER - TY - JOUR T1 - Chemical Screens Identify Drugs that Enhance or Mitigate Cellular Responses to Antibody-Toxin Fusion Proteins. AN - 1814659494; 27556570 AB - The intersection of small molecular weight drugs and antibody-based therapeutics is rarely studied in large scale. Both types of agents are currently part of the cancer armamentarium. However, very little is known about how to combine them in optimal ways. Immunotoxins are antibody-toxin gene fusion proteins engineered to target cancer cells via antibody binding to surface antigens. For fusion proteins derived from Pseudomonas exotoxin (PE), potency relies on the enzymatic domain of the toxin which catalyzes the ADP-ribosylation of EF2 causing inhibition of protein synthesis leading to cell death. Candidate immunotoxins have demonstrated clear value in clinical trials but generally have not been curative as single agents. Therefore we undertook three screens to discover effective combinations that could act synergistically. From the MIPE-3 library of compounds we identified various enhancers of immunotoxin action and at least one major class of inhibitor. Follow-up experiments confirmed the screening data and suggested that immunotoxins when administered with everolimus or nilotinib exhibit favorable combinatory activity and would be candidates for preclinical development. Mechanistic studies revealed that everolimus-immunotoxin combinations acted synergistically on elements of the protein synthetic machinery, including S61 kinase and 4E-BP1 of the mTORC1 pathway. Conversely, PARP inhibitors antagonized immunotoxins and also blocked the toxicity due to native ADP-ribosylating toxins. Thus, our goal of investigating a chemical library was justified based on the identification of several approved compounds that could be developed preclinically as 'enhancers' and at least one class of mitigator to be avoided. JF - PloS one AU - Antignani, Antonella AU - Mathews Griner, Lesley AU - Guha, Rajarshi AU - Simon, Nathan AU - Pasetto, Matteo AU - Keller, Jonathan AU - Huang, Manjie AU - Angelus, Evan AU - Pastan, Ira AU - Ferrer, Marc AU - FitzGerald, David J AU - Thomas, Craig J AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-4264, United States of America. ; Division of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, Maryland, 20850, United States of America. Y1 - 2016 PY - 2016 DA - 2016 SP - 1 VL - 11 IS - 8 KW - Index Medicus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1814659494?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Chemical+Screens+Identify+Drugs+that+Enhance+or+Mitigate+Cellular+Responses+to+Antibody-Toxin+Fusion+Proteins.&rft.au=Antignani%2C+Antonella%3BMathews+Griner%2C+Lesley%3BGuha%2C+Rajarshi%3BSimon%2C+Nathan%3BPasetto%2C+Matteo%3BKeller%2C+Jonathan%3BHuang%2C+Manjie%3BAngelus%2C+Evan%3BPastan%2C+Ira%3BFerrer%2C+Marc%3BFitzGerald%2C+David+J%3BThomas%2C+Craig+J&rft.aulast=Antignani&rft.aufirst=Antonella&rft.date=2016-01-01&rft.volume=11&rft.issue=8&rft.spage=e0161415&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0161415 LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2016-08-25 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0161415 ER - TY - JOUR T1 - Gene Therapy Restores Hair Cell Stereocilia Morphology in Inner Ears of Deaf Whirler Mice AN - 1808739204; PQ0003354305 AB - Hereditary deafness is one of the most common disabilities affecting newborns. Many forms of hereditary deafness are caused by morphological defects of the stereocilia bundles on the apical surfaces of inner ear hair cells, which are responsible for sound detection. We explored the effectiveness of gene therapy in restoring the hair cell stereocilia architecture in the whirlin mouse model of human deafness, which is deaf due to dysmorphic, short stereocilia. Wild-type whirlin cDNA was delivered via adeno-associated virus (AAV8) by injection through the round window of the cochleas in neonatal whirler mice. Subsequently, whirlin expression was detected in infected hair cells (IHCs), and normal stereocilia length and bundle architecture were restored. Whirlin gene therapy also increased inner hair cell survival in the treated ears compared to the contralateral nontreated ears. These results indicate that a form of inherited deafness due to structural defects in cochlear hair cells is amenable to restoration through gene therapy. JF - Molecular Therapy AU - Chien, Wade W AU - Isgrig, Kevin AU - Roy, Soumen AU - Belyantseva, Inna A AU - Drummond, Meghan C AU - May, Lindsey A AU - Fitzgerald, Tracy S AU - Friedman, Thomas B AU - Cunningham, Lisa L AD - Neurotology Program, National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health, Bethesda, Maryland, USA, wade.chien@nih.gov Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 17 EP - 25 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 24 IS - 1 SN - 1525-0016, 1525-0016 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Cochlea KW - Cell survival KW - Deafness KW - Hair cells KW - Gene therapy KW - Animal models KW - Sound KW - Cytology KW - Neonates KW - Inner ear KW - Adeno-associated virus KW - W 30905:Medical Applications KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808739204?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Therapy&rft.atitle=Gene+Therapy+Restores+Hair+Cell+Stereocilia+Morphology+in+Inner+Ears+of+Deaf+Whirler+Mice&rft.au=Chien%2C+Wade+W%3BIsgrig%2C+Kevin%3BRoy%2C+Soumen%3BBelyantseva%2C+Inna+A%3BDrummond%2C+Meghan+C%3BMay%2C+Lindsey+A%3BFitzgerald%2C+Tracy+S%3BFriedman%2C+Thomas+B%3BCunningham%2C+Lisa+L&rft.aulast=Chien&rft.aufirst=Wade&rft.date=2016-01-01&rft.volume=24&rft.issue=1&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2015.150 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Cell survival; Cochlea; Deafness; Gene therapy; Hair cells; Sound; Animal models; Cytology; Neonates; Inner ear; Adeno-associated virus DO - http://dx.doi.org/10.1038/mt.2015.150 ER - TY - JOUR T1 - R- Modafinil attenuates nicotine- taking and nicotineseeking behavior in rats AN - 1808671994; PQ0003477990 AB - OBJECTIVE (+ or -)Modafinil(MOD)is amild psychostimulant used in humans for treatment ofsleep disorders and has been investigated as a potentialmedication for the treatment of psychostimulant addic-tion. However,the therapeutic efficacy of(+ or -)MOD foraddiction has been inconclusive. METHODS Herein weused animal models of self-administration and in vivo mi-crodialysis to study the pharmacological action and themechanisms of the R-enantiomer of modafinil(R-MOD)and its S- enantiomer(S- MOD)on nicotine- taking andnicotine- seeking behavior. RESULTS We found thatsystemic injections of R-MOD(10-30 mg[middot]kg-1,ip)inhibit-ed nicotine self-administration in Long-Evans rats,whilea higher dose(100 mg[middot]kg-1)of S-MOD was required. Asalcohol-preferring rats(P-rats)display more robust nico-tine taking and nicotine seeking than Long- Evans rats,we used P-rats to further study the effects of R-MOD onnicotine- seeking behavior. We found that R- MOD(30-100 mg[middot]kg-1)not only inhibited intravenous nicotine selfadministration,but also inhibited nicotine- induced rein-statement of drug seeking after extinction and cue- in-duced nicotine seeking(assessed in an extinction test)after 3 weeks of withdrawal. Further, in vivo brain micro-dialysis assays demonstrated that pretreatment with RMOD(30 and 100 mg[middot]kg- 1)increased basal extracellu-lar dopamine (DA) levels in the nucleus accumbens(NAc),but decreased nicotine-induced increases in ex-tracellular DA,suggesting that a DA-dependent mecha-nism may in part underlie mitigation of nicotine's effectsproduced by R-MOD. CONCLUSION These data sug-gest that R-MOD is more potent than S-MOD in attenuat-ing nicotine-taking and nicotine-seeking behavior in rats,and warrants further investigation for treatment of nico-tine dependence in humans. JF - Zhongguo Yaolixue yu Dulixue Zazhi - Chinese Journal of Pharmacology and Toxicology AU - Wang, Xiao-fei AU - Bi, Guo-hua AU - Yang, Hong-ju AU - Gardner, Eliot L AU - Xi, Zheng-xiong Y1 - 2016///0, PY - 2016 DA - 0, 2016 SP - 452 EP - 453 PB - Zhongguo Duli Xuehui VL - 30 IS - 4 SN - 1000-3002, 1000-3002 KW - Animal Behavior Abstracts; Toxicology Abstracts KW - R-(-)-modafinil KW - nicotine KW - dopamine KW - selfadministration KW - reinstatement KW - alcohol-preferring rats KW - Intravenous administration KW - Dopamine KW - Data processing KW - Extinction KW - Nicotine KW - Withdrawal KW - modafinil KW - Brain KW - Animal models KW - Drug addiction KW - Drug self-administration KW - Y 25150:General/Miscellaneous KW - X 24380:Social Poisons & Drug Abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808671994?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Zhongguo+Yaolixue+yu+Dulixue+Zazhi+-+Chinese+Journal+of+Pharmacology+and+Toxicology&rft.atitle=R-+Modafinil+attenuates+nicotine-+taking+and+nicotineseeking+behavior+in+rats&rft.au=Wang%2C+Xiao-fei%3BBi%2C+Guo-hua%3BYang%2C+Hong-ju%3BGardner%2C+Eliot+L%3BXi%2C+Zheng-xiong&rft.aulast=Wang&rft.aufirst=Xiao-fei&rft.date=2016-01-01&rft.volume=30&rft.issue=4&rft.spage=452&rft.isbn=&rft.btitle=&rft.title=Zhongguo+Yaolixue+yu+Dulixue+Zazhi+-+Chinese+Journal+of+Pharmacology+and+Toxicology&rft.issn=10003002&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Intravenous administration; Data processing; Dopamine; Extinction; Nicotine; Withdrawal; modafinil; Animal models; Brain; Drug addiction; Drug self-administration ER - TY - JOUR T1 - Genomic Diversity of Enterotoxigenic Strains of Bacteroides fragilis. AN - 1800403320; 27348220 AB - Enterotoxigenic (ETBF) strains of Bacteroides fragilis are the subset of strains that secrete a toxin called fragilysin (Bft). Although ETBF strains are known to cause diarrheal disease and have recently been associated with colorectal cancer, they have not been well characterized. By sequencing the complete genome of four ETBF strains, we found that these strains exhibit considerable variation at the genomic level. Only a small number of genes that are located primarily in the Bft pathogenicity island (BFT PAI) and the flanking CTn86 conjugative transposon are conserved in all four strains and a fifth strain whose genome was previously sequenced. Interestingly, phylogenetic analysis strongly suggests that the BFT PAI was acquired by non-toxigenic (NTBF) strains multiple times during the course of evolution. At the phenotypic level, we found that the ETBF strains were less fit than the NTBF strain NCTC 9343 and were susceptible to a growth-inhibitory protein that it produces. The ETBF strains also showed a greater tendency to form biofilms, which may promote tumor formation, than NTBF strains. Although the genomic diversity of ETBF strains raises the possibility that they vary in their pathogenicity, our experimental results also suggest that they share common properties that are conferred by different combinations of non-universal genetic elements. JF - PloS one AU - Pierce, Jessica V AU - Bernstein, Harris D AD - Genetics and Biochemistry Branch, National Institute for Diabetes and Digestive and Kidney Disease, National Institutes of Health, Bethesda, MD, 20892, United States of America. Y1 - 2016 PY - 2016 DA - 2016 SP - 1 VL - 11 IS - 6 KW - Index Medicus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1800403320?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Genomic+Diversity+of+Enterotoxigenic+Strains+of+Bacteroides+fragilis.&rft.au=Pierce%2C+Jessica+V%3BBernstein%2C+Harris+D&rft.aulast=Pierce&rft.aufirst=Jessica&rft.date=2016-01-01&rft.volume=11&rft.issue=6&rft.spage=e0158171&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0158171 LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2016-06-28 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0158171 ER - TY - JOUR T1 - CRISPR-Mediated Triple Knockout of SLAMF1, SLAMF5 and SLAMF6 Supports Positive Signaling Roles in NKT Cell Development. AN - 1794472184; 27258160 AB - The SLAM family receptors contribute to diverse aspects of lymphocyte biology and signal via the small adaptor molecule SAP. Mutations affecting SAP lead to X-linked lymphoproliferative syndrome Type 1, a severe immunodysregulation characterized by fulminant mononucleosis, dysgammaglobulinemia, and lymphoproliferation/lymphomas. Patients and mice having mutations affecting SAP also lack germinal centers due to a defect in T:B cell interactions and are devoid of invariant NKT (iNKT) cells. However, which and how SLAM family members contribute to these phenotypes remains uncertain. Three SLAM family members: SLAMF1, SLAMF5 and SLAMF6, are highly expressed on T follicular helper cells and germinal center B cells. SLAMF1 and SLAMF6 are also implicated in iNKT development. Although individual receptor knockout mice have limited iNKT and germinal center phenotypes compared to SAP knockout mice, the generation of multi-receptor knockout mice has been challenging, due to the genomic linkage of the genes encoding SLAM family members. Here, we used Cas9/CRISPR-based mutagenesis to generate mutations simultaneously in Slamf1, Slamf5 and Slamf6. Genetic disruption of all three receptors in triple-knockout mice (TKO) did not grossly affect conventional T or B cell development and led to mild defects in germinal center formation post-immunization. However, the TKO worsened defects in iNKT cells development seen in SLAMF6 single gene-targeted mice, supporting data on positive signaling and potential redundancy between these receptors. JF - PloS one AU - Huang, Bonnie AU - Gomez-Rodriguez, Julio AU - Preite, Silvia AU - Garrett, Lisa J AU - Harper, Ursula L AU - Schwartzberg, Pamela L AD - Genetic Disease Research Branch, National Human Genome Research Institute, Bethesda, Maryland, United States of America. ; Embryonic Stem Cell and Transgenic Mouse Core, National Human Genome Research Institute, Bethesda, Maryland, United States of America. ; Genomics Core, National Human Genome Research Institute, National Human Genome Research Institute, Bethesda, Maryland, United States of America. Y1 - 2016 PY - 2016 DA - 2016 SP - 1 VL - 11 IS - 6 KW - Index Medicus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1794472184?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=CRISPR-Mediated+Triple+Knockout+of+SLAMF1%2C+SLAMF5+and+SLAMF6+Supports+Positive+Signaling+Roles+in+NKT+Cell+Development.&rft.au=Huang%2C+Bonnie%3BGomez-Rodriguez%2C+Julio%3BPreite%2C+Silvia%3BGarrett%2C+Lisa+J%3BHarper%2C+Ursula+L%3BSchwartzberg%2C+Pamela+L&rft.aulast=Huang&rft.aufirst=Bonnie&rft.date=2016-01-01&rft.volume=11&rft.issue=6&rft.spage=e0156072&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0156072 LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2016-06-04 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0156072 ER - TY - JOUR T1 - Influence of Coding Variability in APP-Aβ Metabolism Genes in Sporadic Alzheimer's Disease. AN - 1793901036; 27249223 AB - The cerebral deposition of Aβ42, a neurotoxic proteolytic derivate of amyloid precursor protein (APP), is a central event in Alzheimer's disease (AD)(Amyloid hypothesis). Given the key role of APP-Aβ metabolism in AD pathogenesis, we selected 29 genes involved in APP processing, Aβ degradation and clearance. We then used exome and genome sequencing to investigate the single independent (single-variant association test) and cumulative (gene-based association test) effect of coding variants in these genes as potential susceptibility factors for AD, in a cohort composed of 332 sporadic and mainly late-onset AD cases and 676 elderly controls from North America and the UK. Our study shows that common coding variability in these genes does not play a major role for the disease development. In the single-variant association analysis, the main hits, none of which statistically significant after multiple testing correction (1.9e-450 million quantitative high-throughput screening (qHTS) data points. A library of several thousands of compounds, including environmental chemicals and drugs, is screened against a panel of nuclear receptor (NR) and stress response (SR) pathway assays. The National Center for Advancing Translational Sciences (NCATS) has organized an international data challenge in order to "crowd-source" data and build predictive toxicity models. This Challenge asks a "crowd" of researchers to use these data to elucidate the extent to which the interference of biochemical and cellular pathways by compounds can be inferred from chemical structure data. The data generated against the Tox21 library served as the training set for this modeling Challenge. The competition attracted participants from 18 different countries to develop computational models aimed at better predicting chemical toxicity. The winning models from nearly 400 model submissions all achieved >80% accuracy. Several models exceeded 90% accuracy, which was measured by area under the receiver operating characteristic curve (AUC-ROC). Combining the winning models with the knowledge already gained from Tox21 screening data are expected to improve the community's ability to prioritize novel chemicals with respect to potential human health concern. JF - Frontiers in Environmental Science AU - Huang, Ruili AU - Xia, Menghang AU - Nguyen, Dac-Trung AU - Zhao, Tongan AU - Sakamuru, Srilatha AU - Zhao, Jinghua AU - Shahane, Sampada A AU - Rossoshek, Anna AU - Simeonov, Anton AD - Division of Pre-clinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, MD, USA, huangru@mail.nih.gov Y1 - 2016/01// PY - 2016 DA - January 2016 PB - Frontiers Research Foundation, P O Box 110 1015 Lausanne Switzerland VL - 3 KW - Environment Abstracts KW - Tox21 KW - HTS KW - nuclear receptor KW - stress response KW - predictive model KW - QSAR KW - in vitro assay KW - Chemicals KW - Biochemistry KW - Economics KW - Prediction models KW - Stress KW - Toxicity KW - Drugs KW - Competition KW - Toxicity testing KW - Side effects KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1776665188?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvabstractsmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Frontiers+in+Environmental+Science&rft.atitle=Tox21Challenge+to+Build+Predictive+Models+of+Nuclear+Receptor+and+Stress+Response+Pathways+as+Mediated+by+Exposure+to+Environmental+Chemicals+and+Drugs&rft.au=Huang%2C+Ruili%3BXia%2C+Menghang%3BNguyen%2C+Dac-Trung%3BZhao%2C+Tongan%3BSakamuru%2C+Srilatha%3BZhao%2C+Jinghua%3BShahane%2C+Sampada+A%3BRossoshek%2C+Anna%3BSimeonov%2C+Anton&rft.aulast=Huang&rft.aufirst=Ruili&rft.date=2016-01-01&rft.volume=3&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Frontiers+in+Environmental+Science&rft.issn=2296-665X&rft_id=info:doi/10.3389%2Ffenvs.2015.00085 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-07-07 N1 - SubjectsTermNotLitGenreText - Chemicals; Biochemistry; Economics; Prediction models; Stress; Toxicity; Toxicity testing; Competition; Drugs; Side effects DO - http://dx.doi.org/10.3389/fenvs.2015.00085 ER - TY - JOUR T1 - Relationship between diffusion parameters derived from intravoxel incoherent motion MRI and perfusion measured by dynamic contrast-enhanced MRI of soft tissue tumors AN - 1776658501; PQ0002807225 AB - Our aim was to evaluate the link between diffusion parameters measured by intravoxel incoherent motion (IVIM) diffusion-weighted imaging (DWI) and the perfusion metrics obtained with dynamic contrast-enhanced (DCE) MRI in soft tissue tumors (STTs). Twenty-eight patients affected by histopathologically confirmed STT were included in a prospective study. All patients underwent both DCE MRI and IVIM DWI. The perfusion fraction f, diffusion coefficient D and perfusion-related diffusion coefficient D* were estimated using a bi-exponential function to fit the DWI data. DCE MRI was acquired with a temporal resolution of 3-5s. Maps of the initial area under the gadolinium concentration curve (IAUGC), time to peak (TTP) and maximum slope of increase (MSI) were derived using commercial software. The relationships between the DCE MRI and IVIM DWI measurements were assessed by Spearman's test. To exclude false positive results under multiple testing, the false discovery rate (FDR) procedure was applied. The Mann-Whitney test was used to evaluate the differences between all variables in patients with non-myxoid and myxoid STT. No significant relationship was found between IVIM parameters and any DCE MRI parameters. Higher f and D*f values were found in non-myxoid tumors compared with myxoid tumors (p=0.004 and p=0.003, respectively). MSI was significantly higher in non-myxoid tumors than in myxoid tumors (p=0.029). From the visual assessments of single clinical cases, both f and D*f maps were in satisfactory agreement with DCE maps in the extreme cases of an avascular mass and a highly vascularized mass, whereas, for tumors with slight vascularity or with a highly heterogeneous perfusion pattern, this association was not straightforward. Although IVIM DWI was demonstrated to be feasible in STT, our data did not support evident relationships between perfusion-related IVIM parameters and perfusion measured by DCE MRI. Although intravoxel incoherent motion (IVIM) diffusion-weighted imaging (DWI) was demonstrated to be feasible in soft tissue tumors (STTs), no significant relationship was found between IVIM parameters and any diffusion contrast-enhanced (DCE) MRI parameters. From the visual assessments of single clinical cases, both f and D*f maps were in satisfactory agreement with DCE maps in the extreme cases of an avascular mass and a highly vascularized mass, whereas, for tumors with a slight vascularity or with a highly heterogeneous perfusion pattern, a clear association was lacking. JF - NMR in Biomedicine AU - Marzi, Simona AU - Stefanetti, Linda AU - Sperati, Francesca AU - Anelli, Vincenzo AD - Medical Physics Laboratory, Regina Elena National Cancer Institute, Rome, Italy. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 6 EP - 14 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 29 IS - 1 SN - 0952-3480, 0952-3480 KW - Biotechnology and Bioengineering Abstracts KW - Computer programs KW - software KW - Perfusion KW - Data processing KW - Magnetic resonance imaging KW - Gadolinium KW - N.M.R. KW - Tumors KW - Diffusion coefficient KW - Maps KW - Soft tissues KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1776658501?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NMR+in+Biomedicine&rft.atitle=Relationship+between+diffusion+parameters+derived+from+intravoxel+incoherent+motion+MRI+and+perfusion+measured+by+dynamic+contrast-enhanced+MRI+of+soft+tissue+tumors&rft.au=Marzi%2C+Simona%3BStefanetti%2C+Linda%3BSperati%2C+Francesca%3BAnelli%2C+Vincenzo&rft.aulast=Marzi&rft.aufirst=Simona&rft.date=2016-01-01&rft.volume=29&rft.issue=1&rft.spage=6&rft.isbn=&rft.btitle=&rft.title=NMR+in+Biomedicine&rft.issn=09523480&rft_id=info:doi/10.1002%2Fnbm.3446 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Computer programs; software; Data processing; Perfusion; Gadolinium; Magnetic resonance imaging; N.M.R.; Diffusion coefficient; Tumors; Maps; Soft tissues DO - http://dx.doi.org/10.1002/nbm.3446 ER - TY - JOUR T1 - A Phase II trial of tandutinib (MLN 518) in combination with bevacizumab for patients with recurrent glioblastoma. AN - 1775633102; 26860632 AB - A Phase II trial of bevacizumab plus tandutinib. We enrolled 41 recurrent, bevacizumab-naive glioblastoma patients for a trial of bevacizumab plus tandutinib. Median age was 55 and 71% were male. Treatment consisted of tandutinib 500 mg two-times a day (b.i.d.) and bevacizumab 10 mg/kg every 2 weeks starting day 15. Of 37 (90%) evaluable, nine (24%) had partial response. Median overall and progression-free survival was 11 and 4.1 months; progression-free survival at 6 months was 23%. All patients suffered treatment-related toxicities; common grade ≥3 toxicities were hypertension (17.1%), muscle weakness (17.1%), lymphopenia (14.6%) and hypophosphatemia (9.8%). Four of six with grade ≥3 tandutinib-related myasthenic-like muscle weakness had electromyography-proven neuromuscular junction pathology. Tandutinib with bevacizumab was as effective but more toxic than bevacizumab monotherapy. JF - CNS oncology AU - Odia, Yazmin AU - Sul, Joohee AU - Shih, Joanna H AU - Kreisl, Teri N AU - Butman, John A AU - Iwamoto, Fabio M AU - Fine, Howard A AD - Neuro-Oncology Division, Neurological Institute of New York, Columbia University College of Physicians & Surgeons, 710 West 168th Street, 9th Floor, New York, NY 10032, USA. ; US FDA, 10903 New Hampshire Ave, Bldg WO22 Rm 2331, Silver Spring, MD 20993, USA. ; Biometric Research Branch, Division of Cancer Treatment & Diagnosis, NCI, 9609 Medical Center Drive, Room 5W124, Rockville, MD 20850, USA. ; Department of Radiology, National Institutes of Health Clinical Center, Building 10, Clinical Center 10 Center Drive, MSC 1074, Bethesda, MD 20892, USA. ; Division of Neuro-Oncology, Director of the Brain Tumor Center, New York-Presbyterian Hospital/Weill Cornell Medical Center, 1305 York Avenue, 9th Floor, New York, NY 10021, USA. Y1 - 2016 PY - 2016 DA - 2016 SP - 59 EP - 67 VL - 5 IS - 2 KW - Piperazines KW - 0 KW - Quinazolines KW - Bevacizumab KW - 2S9ZZM9Q9V KW - tandutinib KW - E1IO3ICJ9A KW - Index Medicus KW - bevacizumab KW - glioblastoma KW - Kaplan-Meier Estimate KW - Disease-Free Survival KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Bevacizumab -- therapeutic use KW - Bevacizumab -- adverse effects KW - Brain Neoplasms -- drug therapy KW - Neoplasm Recurrence, Local -- drug therapy KW - Piperazines -- therapeutic use KW - Quinazolines -- therapeutic use KW - Glioblastoma -- drug therapy KW - Quinazolines -- adverse effects KW - Piperazines -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1775633102?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=CNS+oncology&rft.atitle=A+Phase+II+trial+of+tandutinib+%28MLN+518%29+in+combination+with+bevacizumab+for+patients+with+recurrent+glioblastoma.&rft.au=Odia%2C+Yazmin%3BSul%2C+Joohee%3BShih%2C+Joanna+H%3BKreisl%2C+Teri+N%3BButman%2C+John+A%3BIwamoto%2C+Fabio+M%3BFine%2C+Howard+A&rft.aulast=Odia&rft.aufirst=Yazmin&rft.date=2016-01-01&rft.volume=5&rft.issue=2&rft.spage=59&rft.isbn=&rft.btitle=&rft.title=CNS+oncology&rft.issn=2045-0915&rft_id=info:doi/10.2217%2Fcns-2015-0010 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-10-26 N1 - Date created - 2016-03-23 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00667394; ClinicalTrials.gov N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.2217/cns-2015-0010 ER - TY - JOUR T1 - Association of Cytomegalovirus End-Organ Disease with Stroke in People Living with HIV/AIDS: A Nationwide Population-Based Cohort Study. AN - 1774531603; 26986005 AB - Cytomegalovirus (CMV) infection might increase the risk of cardiovascular event. However, data on the link between incident stroke and co-infections of CMV and human immunodeficiency virus (HIV) are limited and inconsistent. This nationwide population-based cohort study analyzed the association of CMV end-organ disease and stroke among people living with HIV/AIDS (PLWHA). From January 1, 1998, this study identified adult HIV individuals with and without CMV end-organ disease in the Taiwan National Health Insurance Research Database. All patients were observed for incident stroke and were followed until December 31, 2012. Time-dependent analysis was used to evaluate associations of CMV end-organ disease with stroke. Of the 22,581 PLWHA identified (439 with CMV end-organ disease and 22,142 without CMV end-organ disease), 228 (1.01%) had all-cause stroke during a mean follow-up period of 4.85 years, including 169 (0.75%) with ischemic stroke and 59 (0.26%) with hemorrhagic stroke. After adjusting for age, sex, comorbidities, opportunistic infections after HIV diagnosis, and antiretroviral treatment, CMV end-organ disease was found to be an independent risk factor for incident all-cause stroke (adjusted hazard ratio [AHR], 3.07; 95% confidence interval [CI], 1.70 to 5.55). When stroke type was considered, CMV end-organ disease was significantly positively associated with the risk of ischemic stroke (AHR, 3.14; 95% CI, 1.49 to 6.62) but not hemorrhagic stroke (AHR, 2.52; 95% CI, 0.64 to 9.91). This study suggested that CMV end-organ disease was an independent predictor of ischemic stroke among PLWHA. JF - PloS one AU - Yen, Yung-Feng AU - Jen, Ian AU - Chen, Marcelo AU - Chuang, Pei-Hung AU - Liu, Yen-Ling AU - Sharp, Gerald B AU - Chen, Yi-Ming Arthur AD - Section of Infectious Diseases, Taipei City Hospital, Taipei City Government, Taipei, Taiwan. ; Center for Infectious Disease and Cancer Research, Kaohsiung Medical University, Kaohsiung, Taiwan. ; Department of Urology, Mackay Memorial Hospital, Taipei, Taiwan. ; Epidemiology Branch, Basic Sciences Program, Division of AIDS, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America. Y1 - 2016 PY - 2016 DA - 2016 SP - 1 VL - 11 IS - 3 KW - Index Medicus KW - Young Adult KW - Humans KW - Aged KW - Comorbidity KW - Aged, 80 and over KW - Taiwan -- epidemiology KW - Adult KW - Cohort Studies KW - Health Surveys KW - Incidence KW - Middle Aged KW - Adolescent KW - Female KW - Male KW - Coinfection KW - Stroke -- epidemiology KW - Cytomegalovirus Infections -- epidemiology KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - HIV Infections -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1774531603?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Association+of+Cytomegalovirus+End-Organ+Disease+with+Stroke+in+People+Living+with+HIV%2FAIDS%3A+A+Nationwide+Population-Based+Cohort+Study.&rft.au=Yen%2C+Yung-Feng%3BJen%2C+Ian%3BChen%2C+Marcelo%3BChuang%2C+Pei-Hung%3BLiu%2C+Yen-Ling%3BSharp%2C+Gerald+B%3BChen%2C+Yi-Ming+Arthur&rft.aulast=Yen&rft.aufirst=Yung-Feng&rft.date=2016-01-01&rft.volume=11&rft.issue=3&rft.spage=e0151684&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0151684 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-26 N1 - Date created - 2016-03-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Vasa. 2005 Aug;34(3):163-9 [16184834] J Formos Med Assoc. 2005 Mar;104(3):157-63 [15818428] Cardiovasc Res. 2006 Feb 1;69(2):502-11 [16316638] Blood. 2008 Jan 1;111(1):175-82 [17895402] J Exp Med. 2008 Jan 21;205(1):19-24 [18180307] Curr Top Microbiol Immunol. 2008;325:397-415 [18637518] J Neurovirol. 2010 Mar;16(2):179-84 [20370600] Infect Disord Drug Targets. 2010 Apr;10(2):105-11 [20166970] Pharmacoepidemiol Drug Saf. 2011 Mar;20(3):236-42 [21351304] AIDS. 2011 Aug 24;25(13):1637-46 [21646903] CNS Neurosci Ther. 2011 Dec;17(6):590-8 [22117799] CNS Neurosci Ther. 2012 Jun;18(6):457-60 [22672297] J Acquir Immune Defic Syndr. 2012 Aug 1;60(4):351-8 [22580566] JAMA. 2012 Nov 14;308(18):1906-14 [23162861] Lancet. 2012 Dec 15;380(9859):2197-223 [23245608] Clin Infect Dis. 2013 Nov;57(9):1351-61 [23899681] J Infect Dis. 2015 Jan 15;211(2):178-86 [25081936] J Clin Psychiatry. 2015 Apr;76(4):e505-11 [25919843] BMC Neurol. 2015;15:86 [26045186] J Acquir Immune Defic Syndr. 2015 Jul 1;69(3):e117-8 [25886920] Health Aff (Millwood). 2003 May-Jun;22(3):61-76 [12757273] Proc Natl Acad Sci U S A. 1993 Feb 1;90(3):1107-11 [8381532] Circ Res. 1998 Jul 27;83(2):210-6 [9686761] N Engl J Med. 2004 Dec 16;351(25):2611-8 [15602021] Stroke. 2006 Jan;37(1):63-8 [16306469] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0151684 ER - TY - JOUR T1 - The Role of miRNAs in the Regulation of Pancreatic Cancer Stem Cells AN - 1773833203; PQ0002731474 AB - Pancreatic ductal adenocarcinoma is currently one of the deadliest cancers with low overall survival rate. This disease leads to an aggressive local invasion and early metastases and is poorly responsive to treatment with chemotherapy or chemoradiotherapy. Several studies have shown that pancreatic cancer stem cells (PCSCs) play different roles in the regulation of drug resistance and recurrence in pancreatic cancer. MicroRNA (miRNA), a class of newly emerging small noncoding RNAs, is involved in the modulation of several biological activities ranging from invasion to metastases development, as well as drug resistance of pancreatic cancer. In this review, we synthesize the latest findings on the role of miRNAs in regulating different biological properties of pancreatic cancer stem cells. JF - Stem Cells International AU - Bimonte, Sabrina AU - Barbieri, Antonio AU - Leongito, Maddalena AU - Palma, Giuseppe AU - del Vecchio, Vitale AU - Falco, Michela AU - Palaia, Raffaele AU - Albino, Vittorio AU - Piccirillo, Mauro AU - Amore, Alfonso AU - Petrillo, Antonella AU - Granata, Vincenza AU - Izzo, Francesco AD - Division of Abdominal Surgical Oncology, Hepatobiliary Unit, National Cancer Institute "G. Pascale Foundation", IRCCS, 80131 Naples, Italy, s.bimonte@istitutotumori.na.it Y1 - 2016/01// PY - 2016 DA - January 2016 PB - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States VL - 2016 SN - 1687-966X, 1687-966X KW - Biotechnology and Bioengineering Abstracts KW - Metastases KW - Stem cells KW - Drug resistance KW - Chemotherapy KW - miRNA KW - Pancreatic cancer KW - Adenocarcinoma KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1773833203?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+Cells+International&rft.atitle=The+Role+of+miRNAs+in+the+Regulation+of+Pancreatic+Cancer+Stem+Cells&rft.au=Bimonte%2C+Sabrina%3BBarbieri%2C+Antonio%3BLeongito%2C+Maddalena%3BPalma%2C+Giuseppe%3Bdel+Vecchio%2C+Vitale%3BFalco%2C+Michela%3BPalaia%2C+Raffaele%3BAlbino%2C+Vittorio%3BPiccirillo%2C+Mauro%3BAmore%2C+Alfonso%3BPetrillo%2C+Antonella%3BGranata%2C+Vincenza%3BIzzo%2C+Francesco&rft.aulast=Bimonte&rft.aufirst=Sabrina&rft.date=2016-01-01&rft.volume=2016&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Stem+Cells+International&rft.issn=1687966X&rft_id=info:doi/10.1155%2F2016%2F8352684 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Metastases; Stem cells; Chemotherapy; Drug resistance; miRNA; Pancreatic cancer; Adenocarcinoma DO - http://dx.doi.org/10.1155/2016/8352684 ER - TY - JOUR T1 - Impact of NOx emissions on air quality simulations with the Bulgarian WRF-CMAQ modelling system AN - 1773832056; PQ0002717866 AB - The WRF-CMAQ modelling system was applied for air quality simulation over Europe in the frame of the air quality model evaluation international initiative (AQMEII), phase 2. The models were run for the year 2010 for a domain of 5,000 5,000 km super(2) with a horizontal grid resolution of 25 km. A preliminary evaluation of model results vs. EU surface measurements was conducted using JRC web-based ENSEMBLE platform. Model performance was characterised by overestimation for ozone and underestimation for NO2. Trying to understand this fact, another set of NOx emissions, a more complete one, was prepared and the simulations were repeated for the entire year (BG1 and BG2 sets). The increase of NOx emissions with 30% slightly increase the quality of the simulation - the overestimation of O3 decreases by a few percent and NO2 concentrations increase and reach observed levels at rural sites, while they still remain underpredicted at urban sites. JF - International Journal of Environment and Pollution AU - Syrakov, Dimiter AU - Prodanova, Maria AU - Georgieva, Emilia AU - Etropolska, Iglika AU - Slavov, Kiril AD - National Institute of Meteorology and Hydrology (NIMH), Bulgarian Academy of Sciences (BAS), Tsarigradsko shose Blvd., 66, 1784 Sofia, Bulgaria Y1 - 2016///0, PY - 2016 DA - 0, 2016 SP - 285 EP - 296 PB - Inderscience Publishers Ltd., PO Box 735 Olney Bucks MK46 5WB United Kingdom VL - 57 IS - 3-4 SN - 0957-4352, 0957-4352 KW - Environment Abstracts; Pollution Abstracts; Meteorological & Geoastrophysical Abstracts; Sustainability Science Abstracts KW - ENERGY AND ENVIRONMENT KW - Environment and Sustainable Development KW - Ozone measurements KW - Atmospheric pollution KW - Atmospheric pollution models KW - Simulation KW - Air quality KW - Air quality models KW - Numerical simulations KW - ANE, Europe KW - Emissions KW - Emission measurements KW - Rural areas KW - Urban areas KW - Ozone KW - M2 551.510.42:Air Pollution (551.510.42) KW - P 0000:AIR POLLUTION KW - M3 1010:Issues in Sustainable Development KW - ENA 01:Air Pollution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1773832056?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Assamodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Environment+and+Pollution&rft.atitle=Impact+of+NOx+emissions+on+air+quality+simulations+with+the+Bulgarian+WRF-CMAQ+modelling+system&rft.au=Syrakov%2C+Dimiter%3BProdanova%2C+Maria%3BGeorgieva%2C+Emilia%3BEtropolska%2C+Iglika%3BSlavov%2C+Kiril&rft.aulast=Syrakov&rft.aufirst=Dimiter&rft.date=2016-01-01&rft.volume=57&rft.issue=3-4&rft.spage=285&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Environment+and+Pollution&rft.issn=09574352&rft_id=info:doi/10.1504%2FIJEP.2015.074511 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-06-22 N1 - SubjectsTermNotLitGenreText - Ozone measurements; Atmospheric pollution models; Atmospheric pollution; Numerical simulations; Air quality; Air quality models; Ozone; Emission measurements; Emissions; Simulation; Urban areas; Rural areas; ANE, Europe DO - http://dx.doi.org/10.1504/IJEP.2015.074511 ER - TY - JOUR T1 - Evaluating the performance of WRF-CMAQ air quality modelling system in Bulgaria by means of the DELTA tool AN - 1773830906; PQ0002717510 AB - Model evaluation is performed based on comparison of simulated and observed air pollution concentrations at 25 background stations of the Bulgarian national air quality monitoring network for the year 2013. The DELTA software package, developed within the forum for air quality modelling in Europe - FAIRMODE, is used to analyse model results focusing on maximum daily eight-hour mean ozone concentrations, hourly nitrogen dioxide (NO2) and daily particulate matter (PM10) concentrations. Ozone is overestimated by 38%, minimum daily values are overestimated by a factor of 3. NO2 and PM10 are underestimated by a factor of, respectively, 4 and (5 to 9). The main DELTA model quality objective is respected at 26% of the stations for ozone, 58% of the stations for NO2, and nowhere for PM10. The best model performance is for ozone at rural sites during summer. Possible ways for improvement of model results are discussed. JF - International Journal of Environment and Pollution AU - Georgieva, Emilia AU - Syrakov, Dimiter AU - Prodanova, Maria AU - Etropolska, Iglika AU - Slavov, Kiril AD - National Institute of Meteorology and Hydrology (NIMH), Bulgarian Academy of Sciences (BAS), Tsarigradsko shose Blvd., 66, 1784 Sofia, Bulgaria Y1 - 2016///0, PY - 2016 DA - 0, 2016 SP - 272 EP - 284 PB - Inderscience Publishers Ltd., PO Box 735 Olney Bucks MK46 5WB United Kingdom VL - 57 IS - 3-4 SN - 0957-4352, 0957-4352 KW - Environment Abstracts; Pollution Abstracts; Meteorological & Geoastrophysical Abstracts; Sustainability Science Abstracts KW - ENERGY AND ENVIRONMENT KW - Environment and Sustainable Development KW - Pollution monitoring KW - Atmospheric pollution KW - Atmospheric pollution models KW - Atmospheric pollution monitoring KW - MED, Bulgaria KW - Summer KW - Air quality KW - Particulates KW - Particulate atmospheric pollution KW - Air quality models KW - Air pollution KW - Nitrogen dioxide KW - Computer programs KW - Ozone in troposphere KW - Particulate matter in atmosphere KW - ANE, Europe KW - Ozone concentration KW - Atmospheric pollution networks KW - Ozone KW - Rural areas KW - M2 551.510.42:Air Pollution (551.510.42) KW - P 0000:AIR POLLUTION KW - M3 1010:Issues in Sustainable Development KW - ENA 01:Air Pollution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1773830906?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Assamodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Environment+and+Pollution&rft.atitle=Evaluating+the+performance+of+WRF-CMAQ+air+quality+modelling+system+in+Bulgaria+by+means+of+the+DELTA+tool&rft.au=Georgieva%2C+Emilia%3BSyrakov%2C+Dimiter%3BProdanova%2C+Maria%3BEtropolska%2C+Iglika%3BSlavov%2C+Kiril&rft.aulast=Georgieva&rft.aufirst=Emilia&rft.date=2016-01-01&rft.volume=57&rft.issue=3-4&rft.spage=272&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Environment+and+Pollution&rft.issn=09574352&rft_id=info:doi/10.1504%2FIJEP.2015.074512 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-06-22 N1 - SubjectsTermNotLitGenreText - Particulate matter in atmosphere; Ozone in troposphere; Atmospheric pollution models; Atmospheric pollution; Atmospheric pollution monitoring; Ozone concentration; Air quality; Atmospheric pollution networks; Particulate atmospheric pollution; Air quality models; Nitrogen dioxide; Air pollution; Computer programs; Pollution monitoring; Summer; Particulates; Rural areas; Ozone; MED, Bulgaria; ANE, Europe DO - http://dx.doi.org/10.1504/IJEP.2015.074512 ER - TY - JOUR T1 - S values for 131I based on the ICRP adult voxel phantoms AN - 1773830018; PQ0002692838 AB - The aim of this paper is to improve the estimates of organ doses from nuclear medicine procedures using 131I, the authors calculated a comprehensive set of 131I S values, defined as absorbed doses in target tissues per unit of nuclear transition in source regions, for different source and target combinations. The authors used the latest reference adult male and female voxel phantoms published by the International Commission on Radiological Protection (ICRP Publication 110) and the 131I photon and electron spectra from the ICRP Publication 107 to perform Monte Carlo radiation transport calculations using MCNPX2.7 to compute the S values. For each phantom, the authors simulated 55 source regions with an assumed uniform distribution of 131I. They computed the S values for 42 target tissues directly, without calculating specific absorbed fractions. The new set of S values can be applied prospectively or retrospectively to the calculation of radiation doses in adults internally exposed to 131I, including nuclear medicine patients treated for thyroid cancer or hyperthyroidism. JF - Radiation Protection Dosimetry AU - Lamart, Stephanie AU - Simon, Steven L AU - Bouville, Andre AU - Moroz, Brian E AU - Lee, Choonsik AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA, leechoonsik@mail.nih.gov Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 92 EP - 110 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 168 IS - 1 SN - 0144-8420, 0144-8420 KW - Environment Abstracts KW - Monte Carlo simulation KW - Radiation KW - Dosimetry KW - Commissions KW - Thyroid KW - Organs KW - Cancer KW - ENA 14:Radiological Contamination UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1773830018?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvabstractsmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Radiation+Protection+Dosimetry&rft.atitle=S+values+for+131I+based+on+the+ICRP+adult+voxel+phantoms&rft.au=Lamart%2C+Stephanie%3BSimon%2C+Steven+L%3BBouville%2C+Andre%3BMoroz%2C+Brian+E%3BLee%2C+Choonsik&rft.aulast=Lamart&rft.aufirst=Stephanie&rft.date=2016-01-01&rft.volume=168&rft.issue=1&rft.spage=92&rft.isbn=&rft.btitle=&rft.title=Radiation+Protection+Dosimetry&rft.issn=01448420&rft_id=info:doi/10.1093%2Frpd%2Fncv016 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Monte Carlo simulation; Radiation; Commissions; Dosimetry; Thyroid; Organs; Cancer DO - http://dx.doi.org/10.1093/rpd/ncv016 ER - TY - JOUR T1 - Intersection of toxicogenomics and high throughput screening in the Tox21 program: an NIEHS perspective AN - 1773827913; PQ0002717533 AB - Humans are exposed to thousands of chemicals with inadequate toxicological data. Advances in computational toxicology, robotic high throughput screening (HTS), and genome-wide expression have been integrated into the Tox21 program to better predict the toxicological effects of chemicals. Tox21 is a collaboration among US Government agencies initiated in 2008 that aims to shift chemical hazard assessment from traditional animal toxicology to target-specific, mechanism-based, biological observations using in vitro assays and lower organism models. HTS uses biocomputational methods for probing thousands of chemicals in in vitro assays for gene-pathway response patterns predictive of adverse human health outcomes. In 1999, NIEHS began exploring the application of toxicogenomics to toxicology and recent advances in NextGen sequencing should greatly enhance the biological content obtained from HTS platforms. We foresee an intersection of new technologies in toxicogenomics and HTS as an innovative development in Tox21. Tox21 goals, priorities, progress, and challenges will be reviewed. JF - International Journal of Biotechnology AU - Merrick, BAlex AU - Paules, Richard S AU - Tice, Raymond R AD - Biomolecular Screening Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA Y1 - 2016///0, PY - 2016 DA - 0, 2016 SP - 7 EP - 27 PB - Inderscience Publishers Ltd., PO Box 735 Olney Bucks MK46 5WB United Kingdom VL - 14 IS - 1 SN - 0963-6048, 0963-6048 KW - Biotechnology and Bioengineering Abstracts KW - HEALTHCARE AND BIOSCIENCES KW - ENERGY AND ENVIRONMENT KW - Biosciences and Bioinformatics KW - Environment and Sustainable Development KW - Data processing KW - Reviews KW - high-throughput screening KW - robotics KW - Computer applications KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1773827913?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Biotechnology&rft.atitle=Intersection+of+toxicogenomics+and+high+throughput+screening+in+the+Tox21+program%3A+an+NIEHS+perspective&rft.au=Merrick%2C+BAlex%3BPaules%2C+Richard+S%3BTice%2C+Raymond+R&rft.aulast=Merrick&rft.aufirst=BAlex&rft.date=2016-01-01&rft.volume=14&rft.issue=1&rft.spage=7&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Biotechnology&rft.issn=09636048&rft_id=info:doi/10.1504%2FIJBT.2015.074797 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Data processing; Reviews; robotics; high-throughput screening; Computer applications DO - http://dx.doi.org/10.1504/IJBT.2015.074797 ER - TY - JOUR T1 - Abnormal Hypermethylation at Imprinting Control Regions in Patients with S-Adenosylhomocysteine Hydrolase (AHCY) Deficiency. AN - 1773810630; 26974671 AB - S-adenosylhomocysteine hydrolase (AHCY) deficiency is a rare autosomal recessive disorder in methionine metabolism caused by mutations in the AHCY gene. Main characteristics are psychomotor delay including delayed myelination and myopathy (hypotonia, absent tendon reflexes etc.) from birth, mostly associated with hypermethioninaemia, elevated serum creatine kinase levels and increased genome wide DNA methylation. The prime function of AHCY is to hydrolyse and efficiently remove S-adenosylhomocysteine, the by-product of transmethylation reactions and one of the most potent methyltransferase inhibitors. In this study, we set out to more specifically characterize DNA methylation changes in blood samples from patients with AHCY deficiency. Global DNA methylation was increased in two of three analysed patients. In addition, we analysed the DNA methylation levels at differentially methylated regions (DMRs) of six imprinted genes (MEST, SNRPN, LIT1, H19, GTL2 and PEG3) as well as Alu and LINE1 repetitive elements in seven patients. Three patients showed a hypermethylation in up to five imprinted gene DMRs. Abnormal methylation in Alu and LINE1 repetitive elements was not observed. We conclude that DNA hypermethylation seems to be a frequent but not a constant feature associated with AHCY deficiency that affects different genomic regions to different degrees. Thus AHCY deficiency may represent an ideal model disease for studying the molecular origins and biological consequences of DNA hypermethylation due to impaired cellular methylation status. JF - PloS one AU - Motzek, Antje AU - Knežević, Jelena AU - Switzeny, Olivier J AU - Cooper, Alexis AU - Barić, Ivo AU - Beluzić, Robert AU - Strauss, Kevin A AU - Puffenberger, Erik G AU - Mudd, S Harvey AU - Vugrek, Oliver AU - Zechner, Ulrich AD - Institute of Human Genetics, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. ; Institute Ruđer Bošković, Division of Molecular Medicine, Zagreb, Croatia. ; Institute for Toxicology, University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany. ; Department of Pediatrics, University Hospital Center Zagreb & University of Zagreb, School of Medicine, Zagreb, Croatia. ; Clinic for Special Children, Strasburg, Pennsylvania, United States of America. ; Laboratory of Molecular Biology, National Institute of Mental Health, Bethesda, Maryland, United States of America. Y1 - 2016 PY - 2016 DA - 2016 SP - 1 VL - 11 IS - 3 KW - Glycine N-Methyltransferase KW - EC 2.1.1.20 KW - Creatine KW - MU72812GK0 KW - Index Medicus KW - Infant KW - Creatine -- blood KW - Humans KW - Infant, Newborn KW - Male KW - Female KW - Amino Acid Metabolism, Inborn Errors -- blood KW - Glycine N-Methyltransferase -- deficiency KW - Long Interspersed Nucleotide Elements KW - DNA Methylation KW - Alu Elements KW - Glycine N-Methyltransferase -- blood KW - Glycine N-Methyltransferase -- genetics KW - Amino Acid Metabolism, Inborn Errors -- genetics KW - Genomic Imprinting UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1773810630?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Abnormal+Hypermethylation+at+Imprinting+Control+Regions+in+Patients+with+S-Adenosylhomocysteine+Hydrolase+%28AHCY%29+Deficiency.&rft.au=Motzek%2C+Antje%3BKne%C5%BEevi%C4%87%2C+Jelena%3BSwitzeny%2C+Olivier+J%3BCooper%2C+Alexis%3BBari%C4%87%2C+Ivo%3BBeluzi%C4%87%2C+Robert%3BStrauss%2C+Kevin+A%3BPuffenberger%2C+Erik+G%3BMudd%2C+S+Harvey%3BVugrek%2C+Oliver%3BZechner%2C+Ulrich&rft.aulast=Motzek&rft.aufirst=Antje&rft.date=2016-01-01&rft.volume=11&rft.issue=3&rft.spage=e0151261&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0151261 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-01 N1 - Date created - 2016-03-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2006 Nov 14;103(46):17308-12 [17101998] J Inherit Metab Dis. 2006 Aug;29(4):538-45 [16736098] Biol Reprod. 2008 Oct;79(4):618-23 [18562706] PLoS Genet. 2010;6(12):e1001252 [21203497] Am J Med Genet C Semin Med Genet. 2011 Feb 15;157C(1):3-32 [21308989] PLoS One. 2011;6(4):e19464 [21559330] Environ Health Perspect. 2011 Nov;119(11):1528-33 [21669556] Acta Biochim Biophys Sin (Shanghai). 2012 Oct;44(10):866-75 [23017835] Epigenetics. 2012 Sep;7(9):1020-8 [22869041] Mol Genet Metab. 2012 Nov;107(3):611-3 [22959829] Biochim Biophys Acta. 2013 Jan;1832(1):204-15 [23017368] Epigenetics. 2013 Jan;8(1):28-33 [23257959] Diabetes. 2013 Apr;62(4):1320-8 [23209187] Proc Natl Acad Sci U S A. 2013 Dec 17;110(51):20693-8 [24297921] Mol Cell Biochem. 2014 Feb;387(1-2):55-61 [24213682] Mol Genet Metab. 2015 Sep-Oct;116(1-2):44-52 [26095522] Mol Genet Metab. 2015 Dec;116(4):269-74 [26527160] Curr Opin Chem Biol. 2016 Feb;30:52-60 [26629854] Acta Biochim Biophys Sin (Shanghai). 2007 Sep;39(9):657-67 [17805460] Blood. 2007 Nov 15;110(10):3648-55 [17698632] J Biol Chem. 2007 Dec 21;282(51):37082-90 [17971455] Proc Natl Acad Sci U S A. 1999 Dec 7;96(25):14412-7 [10588719] Nature. 1999 Nov 11;402(6758):187-91 [10647011] Nat Genet. 2000 Jul;25(3):338-42 [10888886] J Biol Chem. 2000 Sep 22;275(38):29318-23 [10884384] Hum Mol Genet. 2001 Mar 1;10(5):433-43 [11181567] Nat Rev Genet. 2001 Jan;2(1):21-32 [11253064] J Nutr. 2001 Nov;131(11):2811-8 [11694601] Nat Rev Genet. 2002 May;3(5):370-9 [11988762] Nature. 2003 May 15;423(6937):293-8 [12714972] Science. 2003 Jun 27;300(5628):2055 [12702809] Mol Cell Biol. 2003 Aug;23(15):5293-300 [12861015] Mol Cell Proteomics. 2003 Aug;2(8):525-40 [12872006] Nucleic Acids Res. 2004;32(3):e38 [14973332] Proc Natl Acad Sci U S A. 2004 Mar 23;101(12):4234-9 [15024124] J Biol Chem. 1980 Nov 25;255(22):10822-7 [7430157] Biochim Biophys Acta. 1987 Dec 8;910(3):203-12 [2445384] J Biol Chem. 1988 Dec 15;263(35):19024-33 [2461933] Hum Mutat. 2009 Apr;30(4):E555-65 [19177456] J Inherit Metab Dis. 2009 Aug;32(4):459-71 [19585268] Development. 2009 Oct;136(20):3413-21 [19762426] J Inherit Metab Dis. 2010 Dec;33(6):705-13 [20852937] J Cell Sci Suppl. 1992;16:9-14 [1297654] EMBO J. 1994 Apr 15;13(8):1806-16 [8168479] J Clin Invest. 1996 Jan 1;97(1):146-53 [8550827] Science. 1996 Apr 12;272(5259):258-62 [8602509] Trends Genet. 1997 Aug;13(8):335-40 [9260521] Nat Genet. 1998 Jun;19(2):187-91 [9620779] Mol Cell Biol. 1999 Nov;19(11):7327-35 [10523621] Mutat Res. 2006 Jan 29;593(1-2):80-7 [16144704] J Inherit Metab Dis. 2005;28(6):885-902 [16435181] J Nutr. 2006 Jun;136(6 Suppl):1636S-1640S [16702333] Genesis. 2006 Sep;44(9):401-6 [16868943] Dev Cell. 2006 Nov;11(5):711-22 [17084362] Mol Cell Proteomics. 2011 Jan;10(1):M110.000976 [20930037] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0151261 ER - TY - JOUR T1 - Alcohol Consumption-Related Metabolites in Relation to Colorectal Cancer and Adenoma: Two Case-Control Studies Using Serum Biomarkers. AN - 1773430405; 26967509 AB - Alcohol is a known carcinogen that may be associated with colorectal cancer. However, most epidemiologic studies assess alcoholic beverage consumption using self-reported data, leading to potential exposure misclassification. Biomarkers of alcohol consumption may provide an alternative, complementary approach that reduces misclassification and incorporates individual differences in alcohol metabolism. Therefore, we evaluated the relationship between previously identified alcohol consumption-related metabolites and colorectal cancer and adenoma using serum metabolomics data from two studies. Data on colorectal cancer were obtained from a nested case-control study of 502 US adults (252 cases, 250 controls) within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Data on colorectal adenoma were obtained from a case-control study of 197 US adults (120 cases, 77 controls) from the Navy Colon Adenoma Study. Unconditional multivariable logistic regression models were fit to calculate odds ratios (OR) and 95% confidence intervals (CI) for eight alcohol consumption-related metabolites identified in a previous analysis: ethyl glucuronide; 4-androstene-3beta,17beta-diol disulfate 1; 5-alpha-androstan-3beta,17beta-diol disulfate; 16-hydroxypalmitate; bilirubin (E,Z or Z,E); cyclo (-leu-pro); dihomo-linoleate (20:2n6); and palmitoleate (16:1n7). We found no clear association between these alcohol consumption-related metabolites and either endpoint. However, we did observe an inverse association between cyclo (-leu-pro) and colorectal adenoma that was only observed in the highest metabolite quantile (OR 4th vs. 1st Quantile = 0.30, 95% CI: 0.12-0.78; P-trend = 0.047), but no association for colorectal cancer. In conclusion, there were no adverse associations between alcohol consumption-related metabolites and colorectal cancer or adenoma. JF - PloS one AU - Troche, Jose Ramon AU - Mayne, Susan T AU - Freedman, Neal D AU - Shebl, Fatma M AU - Guertin, Kristin A AU - Cross, Amanda J AU - Abnet, Christian C AD - Yale School of Public Health, New Haven, Connecticut, United States of America. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland, United States of America. ; Department of Public Health Sciences, University of Virginia, Charlottesville, Virginia, United States of America. ; Department of Epidemiology and Biostatistics, School of Public Health, Faculty of Medicine, Imperial College London, St. Mary's Campus, Norfolk Place, London, United Kingdom. Y1 - 2016 PY - 2016 DA - 2016 SP - 1 VL - 11 IS - 3 KW - Biomarkers KW - 0 KW - Dipeptides KW - Fatty Acids, Monounsaturated KW - Glucuronates KW - Palmitic Acids KW - Peptides, Cyclic KW - cyclo(leucyl-prolyl) KW - ethyl glucuronide KW - 17685-04-0 KW - palmitoleic acid KW - 209B6YPZ4I KW - Androstane-3,17-diol KW - 25126-76-5 KW - Ethanol KW - 3K9958V90M KW - 16-hydroxypalmitic acid KW - 7IPP3U0F3I KW - androstane-3,7-diol disulfate KW - 89453-66-7 KW - Linoleic Acid KW - 9KJL21T0QJ KW - Bilirubin KW - RFM9X3LJ49 KW - Index Medicus KW - Fatty Acids, Monounsaturated -- blood KW - Odds Ratio KW - Humans KW - Peptides, Cyclic -- blood KW - Palmitic Acids -- blood KW - Aged KW - Androstane-3,17-diol -- analogs & derivatives KW - Glucuronates -- blood KW - Linoleic Acid -- blood KW - Case-Control Studies KW - Middle Aged KW - Androstane-3,17-diol -- blood KW - Bilirubin -- blood KW - Biomarkers -- blood KW - Male KW - Female KW - Dipeptides -- blood KW - Alcohol Drinking -- adverse effects KW - Colorectal Neoplasms -- blood KW - Alcoholic Beverages -- adverse effects KW - Ethanol -- metabolism KW - Adenoma -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1773430405?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Alcohol+Consumption-Related+Metabolites+in+Relation+to+Colorectal+Cancer+and+Adenoma%3A+Two+Case-Control+Studies+Using+Serum+Biomarkers.&rft.au=Troche%2C+Jose+Ramon%3BMayne%2C+Susan+T%3BFreedman%2C+Neal+D%3BShebl%2C+Fatma+M%3BGuertin%2C+Kristin+A%3BCross%2C+Amanda+J%3BAbnet%2C+Christian+C&rft.aulast=Troche&rft.aufirst=Jose&rft.date=2016-01-01&rft.volume=11&rft.issue=3&rft.spage=e0150962&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0150962 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-12-13 N1 - Date created - 2016-03-12 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Int J Epidemiol. 1993 Jun;22(3):398-402 [8359954] Nutr Cancer. 1992;18(2):97-111 [1437657] Addiction. 1994 Apr;89(4):407-12 [8025493] Epidemiol Rev. 1994;16(2):273-97 [7713180] J Natl Cancer Inst. 1998 Jan 7;90(1):57-62 [9428784] Cancer Res. 1999 Sep 1;59(17):4320-4 [10485479] Cancer Epidemiol Biomarkers Prev. 2006 May;15(5):892-6 [16702366] Int J Cancer. 2007 Feb 1;120(3):664-71 [17096321] Cancer Control. 2007 Jan;14(1):78-85 [17242674] Alcohol Res Health. 2007;30(1):5-13 [17718394] Br J Cancer. 2009 Mar 10;100(5):803-6 [19223903] Cancer Epidemiol. 2009 Nov;33(5):347-54 [19932648] Anal Chem. 2009 Aug 15;81(16):6656-67 [19624122] Cancer Epidemiol Biomarkers Prev. 2010 Aug;19(8):1893-907 [20647400] Ann Oncol. 2011 Sep;22(9):1958-72 [21307158] Nature. 2011 Sep 1;477(7362):54-60 [21886157] Cancer Epidemiol Biomarkers Prev. 2013 Apr;22(4):631-40 [23396963] Cancer Causes Control. 2013 Jul;24(7):1375-83 [23619609] Carcinogenesis. 2014 Jul;35(7):1516-22 [24648381] Br J Cancer. 2015 Feb 3;112(3):580-93 [25422909] Am J Clin Nutr. 2014 Jul;100(1):208-17 [24740205] Dig Dis Sci. 2000 Mar;45(3):487-93 [10749322] Cancer Causes Control. 2000 May;11(5):403-11 [10877333] Control Clin Trials. 2000 Dec;21(6 Suppl):251S-272S [11189683] Control Clin Trials. 2000 Dec;21(6 Suppl):273S-309S [11189684] J Natl Cancer Inst. 2001 May 2;93(9):710-5 [11333294] Gut. 2002 Jan;50(1):38-42 [11772965] Ann Intern Med. 2004 Apr 20;140(8):603-13 [15096331] Br J Addict. 1982 Dec;77(4):357-82 [6762224] Am J Epidemiol. 1988 Nov;128(5):1007-15 [3189277] Gut. 1991 Jan;32(1):70-2 [1991640] Cancer Causes Control. 1990 Jul;1(1):59-68 [2151680] Ann Epidemiol. 1993 May;3(3):239-44 [8275195] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0150962 ER - TY - JOUR T1 - Exposure Estimation for Risk Assessment of the Phthalate Incident in Taiwan. AN - 1772835730; 26960145 AB - In May 2011, di(2-ethylhexyl) phthalates (DEHP) and, to a lesser extent, di-iso-nonyl phthalate (DiNP) were found to have been illegally used for many years in Taiwan as clouding agents in foods including sports drinks, juice beverages, tea drinks, fruit jam/nectar/jelly, and health or nutrient supplements. To estimate the DEHP exposure for the study participants for the follow-up epidemiological study and health risk assessment. A total of 347 individuals possibly highly exposed to phthalate-tainted foods participated in the study. Exposure assessment was performed based on the participants' responses to a structured questionnaire, self-report of exposure history, urinary metabolite concentrations, and DEHP concentration information in 2449 food records. A Bayesian statistical approach using Markov chain Monte Carlo simulation was employed to deal with the uncertainties in the DEHP concentrations of the contaminated foods and the participants' likelihood of being exposed. An estimated 37% and 15% of children younger than 12 years old were exposed to DEHP at medium (20-50 μg / kg_bw / day) and high AvDIs (50-100 μg / kg_bw / day), respectively, prior to the episode (9% and 3% in adults, respectively). Moreover, 11% of children and 1% of adults were highly exposed (> 100 μg / kg_bw / day), with a maximum of 414.1 μg / kg_bw / day and 126.4 μg / kg_bw / day, respectively. The phthalate exposure-associated adverse health effects for these participants warrant further investigation. The estimation procedure may be applied to other exposure assessment with various sources of uncertainties. JF - PloS one AU - Chen, Chu-Chih AU - Wang, Shu-Li AU - Wu, Ming-Tsang AU - Wang, Yin-Han AU - Huang, Po-Chin AU - Chen, Bai-Hsiun AU - Sun, Chien-Wen AU - Ho, Chi-Kung AU - Shih, Yang-Chih AU - Shiu, Ming-Neng AU - Pan, Wen-Harn AU - Chen, Mei-Lien AU - Lee, Ching-Chang AU - Hsiung, Chao A AD - Division of Biostatistics and Bioinformatics, Institute of Population Health Sciences, National Health Research Institutes, Miaoli, Taiwan. ; National Institute of Environmental Health Sciences, National Health Research Institutes, Miaoli, Taiwan. ; Department of Public Health, College of Health Sciences, Kaohsiung Medical University, Kaohsiung, Taiwan. ; Department of Laboratory Medicine and Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan. ; Department of Public Health, Kaohsiung Medical University, Kaohsiung, Taiwan. ; Ministry of Health and Welfare, Taipei, Taiwan. ; Division of Preventive Medicine and Health Services Research, Institute of Population Health Sciences, National Health Research Institutes, Miaoli, Taiwan. ; Institute of Environmental and Occupational Health Sciences, College of Medicine, National Yang Ming University, Taipei, Taiwan. ; Department of Environmental and Occupational Health, College of Medicine, National Cheng Kung University, Tainan, Taiwan. Y1 - 2016 PY - 2016 DA - 2016 SP - 1 VL - 11 IS - 3 KW - Environmental Pollutants KW - 0 KW - Phthalic Acids KW - phthalic acid KW - 6O7F7IX66E KW - Index Medicus KW - Young Adult KW - Humans KW - Bayes Theorem KW - Infant, Newborn KW - Child KW - Environmental Pollutants -- analysis KW - Risk Assessment KW - Child, Preschool KW - Infant KW - Taiwan -- epidemiology KW - Adult KW - Surveys and Questionnaires KW - Follow-Up Studies KW - Adolescent KW - Environmental Exposure -- adverse effects KW - Male KW - Female KW - Environmental Monitoring KW - Beverages -- analysis KW - Phthalic Acids -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1772835730?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Exposure+Estimation+for+Risk+Assessment+of+the+Phthalate+Incident+in+Taiwan.&rft.au=Chen%2C+Chu-Chih%3BWang%2C+Shu-Li%3BWu%2C+Ming-Tsang%3BWang%2C+Yin-Han%3BHuang%2C+Po-Chin%3BChen%2C+Bai-Hsiun%3BSun%2C+Chien-Wen%3BHo%2C+Chi-Kung%3BShih%2C+Yang-Chih%3BShiu%2C+Ming-Neng%3BPan%2C+Wen-Harn%3BChen%2C+Mei-Lien%3BLee%2C+Ching-Chang%3BHsiung%2C+Chao+A&rft.aulast=Chen&rft.aufirst=Chu-Chih&rft.date=2016-01-01&rft.volume=11&rft.issue=3&rft.spage=e0151070&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0151070 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-01 N1 - Date created - 2016-03-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Food Chem Toxicol. 2012 Jul;50(7):2575-83 [22554646] Environ Int. 2008 Jan;34(1):79-85 [17765308] Environ Health Perspect. 2013 Apr;121(4):473-94 [23461894] Food Chem Toxicol. 2013 Aug;58:362-8 [23684997] Environ Int. 2013 Sep;59:469-77 [23955327] Environ Sci Technol. 2013 Dec 3;47(23):13754-62 [24191740] Environ Int. 2014 Dec;73:259-69 [25173060] Environ Health. 2008;7:9 [18307757] J Expo Sci Environ Epidemiol. 2010 Jan;20(1):38-53 [19127283] J Toxicol Environ Health B Crit Rev. 2009 Apr;12(4):225-49 [20183522] PLoS One. 2015;10(6):e0131910 [26121592] PLoS One. 2015;10(7):e0133782 [26207744] Am J Clin Nutr. 2002 Mar;75(3):561-9 [11864864] Environ Health Perspect. 2004 May;112(6):751-3 [15121520] Annu Rev Public Health. 2010;31:179-94 [20070188] Pediatr Neonatol. 2010 Apr;51(2):69-79 [20417456] Int Arch Occup Environ Health. 2010 Aug;83(6):639-51 [20143083] Indoor Air. 2010 Dec;20(6):494-501 [21070375] Mol Nutr Food Res. 2011 Jan;55(1):7-31 [20564479] J Expo Sci Environ Epidemiol. 2011 Mar-Apr;21(2):133-41 [20010977] Chemosphere. 2011 May;83(8):1192-9 [21272909] Int J Occup Med Environ Health. 2011 Jun;24(2):115-41 [21594692] Food Chem Toxicol. 2011 Sep;49(9):2022-9 [21609750] J Formos Med Assoc. 2011 Nov;110(11):671-84 [22118310] Environ Int. 2012 Sep;44:75-9 [22361240] Int J Hyg Environ Health. 2007 Jan;210(1):35-42 [17185035] PLoS One. 2013;8(1):e55005 [23383031] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0151070 ER - TY - JOUR T1 - Risk of Gastrointestinal Cancers among Patients with Appendectomy: A Large-Scale Swedish Register-Based Cohort Study during 1970-2009. AN - 1772831235; 26959234 AB - Removal of the appendix might induce physiological changes in the gastrointestinal tract, and subsequently play a role in carcinogenesis. Therefore, we conducted a nationwide register-based cohort study in Sweden to investigate whether appendectomy is associated with altered risks of gastrointestinal cancers. A population-based cohort study was conducted using the Swedish national registries, including 480,382 eligible patients followed during the period of 1970-2009 for the occurrence of site-specific gastrointestinal cancer (esophageal/gastric/colon/rectal cancer). Outcome and censoring information was collected by linkage to health and demography registers. We examined the incidence of appendectomy in Sweden using data from 1987-2009. We also calculated standardized incidence ratios (SIRs) with 95% confidence intervals (CIs) to estimate the relative gastrointestinal cancer risk through comparison to the general population. We noted an overall decrease in the age-standardized incidence of appendectomy among the entire Swedish population from 189.3 to 105.6 per 100,000 individuals between 1987 and 2009. Grouped by different discharge diagnosis, acute appendicitis, incidental appendectomy, and entirely negative appendectomy continuously decreased over the study period, while the perforation ratio (18%-23%) stayed relatively constant. Compared to the general population, no excess cancer risk was observed for gastrointestinal cancers under study with the exception of a marginally elevated risk for esophageal adenocarcinoma (SIR 1.32, 95% CI 1.09-1.58). In Sweden, the incidence of appendectomy and acute appendicitis has decreased during 1987-2009. No excess gastrointestinal cancer risks were observed among these appendectomized patients, with the possible exception of esophageal adenocarcinoma. JF - PloS one AU - Song, Huan AU - Abnet, Christian C AU - Andrén-Sandberg, Åke AU - Chaturvedi, Anil K AU - Ye, Weimin AD - Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, United States of America. ; Department of Digestive Diseases, Karolinska University Hospital, Huddinge, Stockholm, Sweden. Y1 - 2016 PY - 2016 DA - 2016 SP - 1 VL - 11 IS - 3 KW - Index Medicus KW - Young Adult KW - Humans KW - Infant, Newborn KW - Child KW - Child, Preschool KW - Infant KW - Appendicitis -- surgery KW - Adult KW - Cohort Studies KW - Middle Aged KW - Adolescent KW - Female KW - Male KW - Sweden KW - Gastrointestinal Neoplasms -- epidemiology KW - Appendectomy -- adverse effects KW - Gastrointestinal Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1772831235?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Risk+of+Gastrointestinal+Cancers+among+Patients+with+Appendectomy%3A+A+Large-Scale+Swedish+Register-Based+Cohort+Study+during+1970-2009.&rft.au=Song%2C+Huan%3BAbnet%2C+Christian+C%3BAndr%C3%A9n-Sandberg%2C+%C3%85ke%3BChaturvedi%2C+Anil+K%3BYe%2C+Weimin&rft.aulast=Song&rft.aufirst=Huan&rft.date=2016-01-01&rft.volume=11&rft.issue=3&rft.spage=e0151262&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0151262 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-01 N1 - Date created - 2016-03-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Gut. 1994 Jun;35(6):742-5 [8020796] JAMA. 2015 Jun 16;313(23):2340-8 [26080338] Cancer Causes Control. 1998 Mar;9(2):183-7 [9578295] J Clin Epidemiol. 1998 Oct;51(10):859-65 [9762879] Gut. 1998 Oct;43(4):451 [9824564] Lancet. 1999 Jan 30;353(9150):379 [9950450] J Natl Cancer Inst. 1999 May 5;91(9):786-90 [10328109] Lancet. 2005 Nov 19;366(9499):1784-93 [16298215] J Theor Biol. 2007 Dec 21;249(4):826-31 [17936308] Radiology. 2002 Oct;225(1):131-6 [12354996] Pediatrics. 2003 Jun;111(6 Pt 1):1343-50 [12777551] Gut. 2003 Jul;52(7):938-41 [12801947] Am J Obstet Gynecol. 2003 Dec;189(6):1563-7; discussion 1567-8 [14710065] N Engl J Med. 1986 Dec 11;315(24):1546-7 [3785311] Can J Surg. 1988 Nov;31(6):448-51 [3179856] Am J Epidemiol. 1990 Nov;132(5):910-25 [2239906] Cancer Res. 1990 Dec 1;50(23):7549-51 [2253203] Dig Surg. 2009;26(5):406-12 [19923829] Int J Cancer. 2011 Jan 1;128(1):157-65 [20209500] BMC Public Health. 2011;11:450 [21658213] AJR Am J Roentgenol. 2011 Oct;197(4):861-6 [21940573] J Surg Res. 2012 Jun 15;175(2):185-90 [22099604] World J Surg. 2012 Dec;36(12):2787-94 [22948195] Pediatrics. 2013 Jan;131(1):e37-44 [23266930] MBio. 2013;4(1). pii: e00366-12. doi: 10.1128/mBio.00366-12 [23322636] World J Surg. 2013 May;37(5):974-81 [23192168] Int J Colorectal Dis. 2014 Aug;29(8):1009-12 [24986137] PLoS One. 2015;10(2):e0118411 [25710790] Am J Gastroenterol. 1995 Jun;90(6):906-9 [7771418] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0151262 ER - TY - JOUR T1 - Induction of intrinsic and extrinsic apoptosis through oxidative stress in drug-resistant cancer by a newly synthesized Schiff base copper chelate. AN - 1770221473; 26733073 AB - Multidrug resistance (MDR) in cancer represents a variety of strategies employed by tumor cells to evade the beneficial cytotoxic effects of structurally different anticancer drugs and thus confers impediments to the successful treatment of cancers. Efflux of drugs by MDR protein-1, functional P-glycoprotein and elevated level of reduced glutathione confer resistance to cell death or apoptosis and thus provide a possible therapeutic target for overcoming MDR in cancer. Previously, we reported that a Schiff base ligand, potassium-N-(2-hydroxy 3-methoxy-benzaldehyde)-alaninate (PHMBA) overcomes MDR in both in vivo and in vitro by targeting intrinsic apoptotic/necrotic pathway through induction of reactive oxygen species (ROS). The present study describes the synthesis and spectroscopic characterization of a copper chelate of Schiff base, viz., copper (II)-N-(2-hydroxy-3-methoxy-benzaldehyde)-alaninate (CuPHMBA) and the underlying mechanism of cell death induced by CuPHMBA in vitro. CuPHMBA kills both the drug-resistant and sensitive cell types irrespective of their drug resistance phenotype. The cell death induced by CuPHMBA follows apoptotic pathway and moreover, the cell death is associated with intrinsic mitochondrial and extrinsic receptor-mediated pathways. Oxidative stress plays a pivotal role in the process as proved by the fact that antioxidant enzyme; polyethylene glycol conjugated-catalase completely blocked CuPHMBA-induced ROS generation and abrogated cell death. To summarize, the present work provides a compelling rationale for the future clinical use of CuPHMBA, a redox active copper chelate in the treatment of cancer patients, irrespective of their drug-resistance status. JF - Free radical research AU - Banerjee, Kaushik AU - Basu, Soumya AU - Das, Satyajit AU - Sinha, Abhinaba AU - Biswas, Manas Kumar AU - Choudhuri, Soumitra Kumar AD - a Department of In Vitro Carcinogenesis and Cellular Chemotherapy , Chittaranjan National Cancer Institute , Kolkata , West Bengal , India ; ; b Department of Chemistry , Ramakrishna Mission Residential College , Kolkata , West Bengal , India. Y1 - 2016 PY - 2016 DA - 2016 SP - 426 EP - 446 VL - 50 IS - 4 KW - Antineoplastic Agents KW - 0 KW - Benzaldehydes KW - Chelating Agents KW - Coordination Complexes KW - Reactive Oxygen Species KW - Schiff Bases KW - Polyethylene Glycols KW - 30IQX730WE KW - Copper KW - 789U1901C5 KW - Catalase KW - EC 1.11.1.6 KW - Alanine KW - OF5P57N2ZX KW - Index Medicus KW - mitochondria KW - Apoptosis KW - cancer multidrug resistance KW - reactive oxygen species KW - copper (II)-N-(2-hydroxy-3-methoxy-benzaldehyde)-alaninate KW - Animals KW - Humans KW - Carcinoma, Ehrlich Tumor -- pathology KW - Primary Cell Culture KW - Drug Resistance, Multiple -- drug effects KW - Mice KW - Cell Line, Tumor KW - Catalase -- pharmacology KW - Oxidation-Reduction KW - Alanine -- analogs & derivatives KW - Carcinoma, Ehrlich Tumor -- metabolism KW - Cell Survival -- drug effects KW - Polyethylene Glycols -- chemistry KW - Leukocytes, Mononuclear -- metabolism KW - Apoptosis -- drug effects KW - Benzaldehydes -- chemistry KW - Leukocytes, Mononuclear -- drug effects KW - Leukocytes, Mononuclear -- cytology KW - Drug Resistance, Neoplasm -- drug effects KW - Schiff Bases -- antagonists & inhibitors KW - Reactive Oxygen Species -- metabolism KW - Reactive Oxygen Species -- agonists KW - Chelating Agents -- pharmacology KW - Coordination Complexes -- chemical synthesis KW - Coordination Complexes -- antagonists & inhibitors KW - Coordination Complexes -- pharmacology KW - Chelating Agents -- chemical synthesis KW - Antineoplastic Agents -- chemical synthesis KW - Schiff Bases -- pharmacology KW - Antineoplastic Agents -- pharmacology KW - Schiff Bases -- chemical synthesis KW - Copper -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1770221473?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Epigenetic+modification+of+histone+3+lysine+27%3A+mediator+subunit+MED25+is+required+for+the+dissociation+of+polycomb+repressive+complex+2+from+the+promoter+of+cytochrome+P450+2C9.&rft.au=Englert%2C+Neal+A%3BLuo%2C+George%3BGoldstein%2C+Joyce+A%3BSurapureddi%2C+Sailesh&rft.aulast=Englert&rft.aufirst=Neal&rft.date=2015-01-23&rft.volume=290&rft.issue=4&rft.spage=2264&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.579474 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-12-13 N1 - Date created - 2016-03-02 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3109/10715762.2015.1136062 ER - TY - JOUR T1 - Lipoprotein X Causes Renal Disease in LCAT Deficiency. AN - 1769626356; 26919698 AB - Human familial lecithin:cholesterol acyltransferase (LCAT) deficiency (FLD) is characterized by low HDL, accumulation of an abnormal cholesterol-rich multilamellar particle called lipoprotein-X (LpX) in plasma, and renal disease. The aim of our study was to determine if LpX is nephrotoxic and to gain insight into the pathogenesis of FLD renal disease. We administered a synthetic LpX, nearly identical to endogenous LpX in its physical, chemical and biologic characteristics, to wild-type and Lcat-/- mice. Our in vitro and in vivo studies demonstrated an apoA-I and LCAT-dependent pathway for LpX conversion to HDL-like particles, which likely mediates normal plasma clearance of LpX. Plasma clearance of exogenous LpX was markedly delayed in Lcat-/- mice, which have low HDL, but only minimal amounts of endogenous LpX and do not spontaneously develop renal disease. Chronically administered exogenous LpX deposited in all renal glomerular cellular and matrical compartments of Lcat-/- mice, and induced proteinuria and nephrotoxic gene changes, as well as all of the hallmarks of FLD renal disease as assessed by histological, TEM, and SEM analyses. Extensive in vivo EM studies revealed LpX uptake by macropinocytosis into mouse glomerular endothelial cells, podocytes, and mesangial cells and delivery to lysosomes where it was degraded. Endocytosed LpX appeared to be degraded by both human podocyte and mesangial cell lysosomal PLA2 and induced podocyte secretion of pro-inflammatory IL-6 in vitro and renal Cxl10 expression in Lcat-/- mice. In conclusion, LpX is a nephrotoxic particle that in the absence of Lcat induces all of the histological and functional hallmarks of FLD and hence may serve as a biomarker for monitoring recombinant LCAT therapy. In addition, our studies suggest that LpX-induced loss of endothelial barrier function and release of cytokines by renal glomerular cells likely plays a role in the initiation and progression of FLD nephrosis. JF - PloS one AU - Ossoli, Alice AU - Neufeld, Edward B AU - Thacker, Seth G AU - Vaisman, Boris AU - Pryor, Milton AU - Freeman, Lita A AU - Brantner, Christine A AU - Baranova, Irina AU - Francone, Nicolás O AU - Demosky, Stephen J AU - Vitali, Cecilia AU - Locatelli, Monica AU - Abbate, Mauro AU - Zoja, Carlamaria AU - Franceschini, Guido AU - Calabresi, Laura AU - Remaley, Alan T AD - Centro Grossi Paoletti, Dipartimento di Scienze Farmacologiche e Biomolecolari, Università degli Studi di Milano, Milano, Italy. ; Lipoprotein Metabolism Section, Cardiovascular and Pulmonary Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; NHLBI Electron Microscopy Core Facility, National Institutes of Health, Bethesda, Maryland, United States of America. ; Clinical Center, National Institutes of Health, Bethesda, Maryland, United States of America. ; IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Centro Anna Maria Astori, Science and Technology Park Kilometro Rosso, Bergamo, Italy. Y1 - 2016 PY - 2016 DA - 2016 SP - 1 VL - 11 IS - 2 KW - Apolipoprotein A-I KW - 0 KW - Interleukin-6 KW - Lipoprotein-X KW - Lipoproteins, HDL KW - interleukin-6, mouse KW - Phosphatidylcholine-Sterol O-Acyltransferase KW - EC 2.3.1.43 KW - Phospholipases A2 KW - EC 3.1.1.4 KW - Index Medicus KW - Animals KW - Extracellular Matrix -- metabolism KW - Interleukin-6 -- secretion KW - Humans KW - Lysosomes -- metabolism KW - Lipoproteins, HDL -- metabolism KW - Cytoskeleton -- drug effects KW - Phospholipases A2 -- metabolism KW - Phosphatidylcholine-Sterol O-Acyltransferase -- metabolism KW - Podocytes -- pathology KW - Pinocytosis KW - Glomerular Mesangium -- pathology KW - Endothelial Cells -- pathology KW - Endothelial Cells -- metabolism KW - Podocytes -- metabolism KW - Glomerular Basement Membrane -- pathology KW - Metabolic Clearance Rate KW - Human Umbilical Vein Endothelial Cells KW - Mice KW - Gene Expression Profiling KW - Glomerular Mesangium -- cytology KW - Glomerular Basement Membrane -- drug effects KW - Cells, Cultured KW - Apolipoprotein A-I -- metabolism KW - Mice, Inbred C57BL KW - Cytoskeleton -- ultrastructure KW - Glomerular Mesangium -- metabolism KW - Lipoprotein-X -- pharmacokinetics KW - Lipoprotein-X -- toxicity KW - Lecithin Cholesterol Acyltransferase Deficiency -- pathology KW - Proteinuria -- genetics KW - Lipoprotein-X -- metabolism KW - Kidney Glomerulus -- drug effects KW - Proteinuria -- pathology KW - Lecithin Cholesterol Acyltransferase Deficiency -- metabolism KW - Kidney Glomerulus -- pathology KW - Proteinuria -- etiology KW - Proteinuria -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1769626356?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Lipoprotein+X+Causes+Renal+Disease+in+LCAT+Deficiency.&rft.au=Ossoli%2C+Alice%3BNeufeld%2C+Edward+B%3BThacker%2C+Seth+G%3BVaisman%2C+Boris%3BPryor%2C+Milton%3BFreeman%2C+Lita+A%3BBrantner%2C+Christine+A%3BBaranova%2C+Irina%3BFrancone%2C+Nicol%C3%A1s+O%3BDemosky%2C+Stephen+J%3BVitali%2C+Cecilia%3BLocatelli%2C+Monica%3BAbbate%2C+Mauro%3BZoja%2C+Carlamaria%3BFranceschini%2C+Guido%3BCalabresi%2C+Laura%3BRemaley%2C+Alan+T&rft.aulast=Ossoli&rft.aufirst=Alice&rft.date=2016-01-01&rft.volume=11&rft.issue=2&rft.spage=e0150083&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0150083 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-19 N1 - Date created - 2016-02-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biochim Biophys Acta. 2000 Dec 15;1529(1-3):245-56 [11111093] J Biol Chem. 2001 May 4;276(18):15090-8 [11278414] Nephron. 2001 Jul;88(3):268-72 [11423760] Am J Pathol. 2004 Oct;165(4):1269-78 [15466392] Scand J Gastroenterol. 1975;10(8):785-9 [173014] Clin Chim Acta. 1977 Feb 15;75(1):117-21 [844192] J Cell Biol. 1979 Apr;81(1):137-53 [90048] Q J Med. 1982;51(204):411-26 [7156322] Am J Nephrol. 1986;6(1):66-70 [3963061] Clin Nephrol. 2008 Mar;69(3):213-8 [18397721] Nat Protoc. 2008;3(6):1101-8 [18546601] Methods Enzymol. 1986;128:223-46 [3088390] Kidney Int. 1991 Oct;40(4):597-605 [1745007] J Lipid Res. 1995 Nov;36(11):2344-54 [8656072] Mol Cell Biochem. 1997 Aug;173(1-2):17-24 [9278250] Mol Cell Biochem. 1997 Oct;175(1-2):187-94 [9350051] Kidney Int. 1999 Oct;56(4):1366-77 [10504489] Arterioscler Thromb Vasc Biol. 2005 Sep;25(9):1972-8 [15994445] N Engl J Med. 2006 Mar 30;354(13):1387-401 [16571882] Virchows Arch. 2006 Apr;448(4):485-92 [16418842] Arterioscler Thromb Vasc Biol. 2006 Jun;26(6):1370-5 [16543491] J Lipid Res. 2007 Mar;48(3):592-9 [17183024] Trends Cell Biol. 2007 Mar;17(3):107-17 [17275303] Nephrol Dial Transplant. 2007 Jul;22(7):2084-8 [17452402] J Am Soc Nephrol. 2009 Jun;20(6):1179-87 [19470685] Atherosclerosis. 2009 Aug;205(2):528-32 [19230892] Am J Physiol Renal Physiol. 2010 Mar;298(3):F557-67 [19955187] J Pharmacol Exp Ther. 2010 Oct;335(1):140-8 [20605907] Adv Drug Deliv Rev. 2010 Nov 30;62(14):1337-43 [20828589] Nutr Metab Cardiovasc Dis. 2011 Feb;21(2):79-85 [21186102] Ultrastruct Pathol. 2011 May;35(3):139-45 [21323422] Clin Exp Nephrol. 2011 Jun;15(3):424-9 [21327698] Lipids Health Dis. 2011;10:70 [21554699] Nat Rev Mol Cell Biol. 2011 Jul;12(7):413-26 [21697900] Immunol Cell Biol. 2011 Nov;89(8):836-43 [21423264] Clin Nephrol. 2011 Dec;76(6):492-8 [22105454] J Lipid Res. 2012 Jan;53(1):158-67 [22039582] J Pathol. 2012 Mar;226(4):562-74 [22102407] Curr Opin Nephrol Hypertens. 2012 May;21(3):258-63 [22388551] Exp Cell Res. 2012 May 15;318(9):979-85 [22414873] Exp Cell Res. 2012 May 15;318(9):964-72 [22465480] PLoS One. 2012;7(12):e50745 [23236390] Biochim Biophys Acta. 2013 Mar;1831(3):602-11 [22960355] Am J Physiol Renal Physiol. 2013 Feb 15;304(4):F333-47 [23235479] Atherosclerosis. 2013 May;228(1):193-7 [23522979] Kidney Int. 2014 Jan;85(1):72-81 [23903370] Kidney Int. 2014 Jan;85(1):8-11 [24380900] Curr Opin Nephrol Hypertens. 2014 Jul;23(4):420-30 [24867674] Nat Rev Nephrol. 2014 Jul;10(7):379-88 [24861084] Eur J Cell Biol. 2014 Oct;93(10-12):367-79 [25457677] Nat Commun. 2015;6:6250 [25727495] J Cell Biol. 2015 Apr 27;209(2):199-210 [25918223] J Clin Invest. 2015 Jun;125(6):2307-16 [25915582] Circ Res. 2016 Jan 8;118(1):73-82 [26628614] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0150083 ER - TY - JOUR T1 - Gene Therapy: The View from NCATS AN - 1768575470; PQ0002673072 JF - Human Gene Therapy AU - Brooks, Philip J AU - Yang, NNora AU - Austin, Christopher P AD - Division of Clinical Innovation and Office of Rare Diseases Research, National Center for Advancing Translational Sciences (NCATS), National Institutes of Health, Bethesda, Maryland. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 7 EP - 13 PB - Mary Ann Liebert, Inc., 2 Madison Ave Larchmont NY 10538 United States VL - 27 IS - 1 SN - 1043-0342, 1043-0342 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768575470?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+Gene+Therapy&rft.atitle=Gene+Therapy%3A+The+View+from+NCATS&rft.au=Brooks%2C+Philip+J%3BYang%2C+NNora%3BAustin%2C+Christopher+P&rft.aulast=Brooks&rft.aufirst=Philip&rft.date=2016-01-01&rft.volume=27&rft.issue=1&rft.spage=7&rft.isbn=&rft.btitle=&rft.title=Human+Gene+Therapy&rft.issn=10430342&rft_id=info:doi/10.1089%2Fhum.2016.29018.pjb LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Number of references - 46 N1 - Last updated - 2016-02-29 DO - http://dx.doi.org/10.1089/hum.2016.29018.pjb ER - TY - JOUR T1 - Nuclear receptors and drug metabolism for the personalization of cancer therapy. AN - 1768166968; 26789519 AB - A remarkable inter-individual variability in the occurrence of severe side effects represents an ongoing challenge in cancer treatment. Significant research efforts have focused on elucidating the contribution of the host genetic variability, but only a few markers have been identified for use in clinical practice. Several studies demonstrated that PXR and CAR activation can affect the expression of genes involved in absorption, distribution, metabolism and excretion (ADME) of antineoplastic drugs. The study of the host genetic background of Pregnane X Receptor (PXR; NR1I2) and Constitutive Androstane Receptor (CAR; NR1I3 and NR1I4), represents a new and attractive strategy to discern variability in ADME of antineoplastic drugs. An update of the most important findings about investigational CAR and PXR pharmacogenetic markers of anti-cancer drugs toxicity is provided. A differential activation of PXR and CAR can affect the pharmacokinetics and pharmacodynamics of antineoplastic drugs. Pharmacogenetics studies published up to date provide encouraging even if exploratory results. Future large and prospective studies will clarify the clinical value of PXR and CAR genetic markers in treatment personalization. JF - Expert opinion on drug metabolism & toxicology AU - Cecchin, Erika AU - De Mattia, Elena AU - Toffoli, Giuseppe AD - a Experimental and Clinical Pharmacology , Centro di Riferimento Oncologico- National Cancer Institute , Aviano , Italy. Y1 - 2016 PY - 2016 DA - 2016 SP - 291 EP - 306 VL - 12 IS - 3 KW - Antineoplastic Agents KW - 0 KW - Receptors, Cytoplasmic and Nuclear KW - Receptors, Steroid KW - constitutive androstane receptor KW - pregnane X receptor KW - Index Medicus KW - nuclear receptors KW - PXR KW - toxicity KW - CAR KW - Cancer KW - Gene Expression Regulation, Neoplastic KW - Animals KW - Precision Medicine KW - Humans KW - Receptors, Steroid -- metabolism KW - Receptors, Steroid -- genetics KW - Pharmacogenetics KW - Neoplasms -- drug therapy KW - Neoplasms -- pathology KW - Antineoplastic Agents -- administration & dosage KW - Receptors, Cytoplasmic and Nuclear -- metabolism KW - Antineoplastic Agents -- pharmacokinetics KW - Receptors, Cytoplasmic and Nuclear -- genetics KW - Antineoplastic Agents -- pharmacology KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768166968?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Expert+opinion+on+drug+metabolism+%26+toxicology&rft.atitle=Nuclear+receptors+and+drug+metabolism+for+the+personalization+of+cancer+therapy.&rft.au=Cecchin%2C+Erika%3BDe+Mattia%2C+Elena%3BToffoli%2C+Giuseppe&rft.aulast=Cecchin&rft.aufirst=Erika&rft.date=2016-01-01&rft.volume=12&rft.issue=3&rft.spage=291&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+drug+metabolism+%26+toxicology&rft.issn=1744-7607&rft_id=info:doi/10.1517%2F17425255.2016.1141196 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-10-31 N1 - Date created - 2016-02-24 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1517/17425255.2016.1141196 ER - TY - JOUR T1 - Long-term toxicity of naturally occurring asbestos in male Fischer 344 rats. AN - 1766266271; 26818398 AB - Naturally occurring asbestos (NOA) fibers are found in geologic deposits that may be disturbed by mining, earthworks, or natural processes, resulting in adverse health risks to exposed individuals. The toxicities of Libby amphibole and NOA samples including Sumas Mountain chrysotile (SM), El Dorado tremolite (ED), and Ontario ferroactinolite cleavage fragments (ON) were compared in male Fischer 344 (F344) rats 15 mo after exposure. Rat-respirable fractions of LA and SM displayed greater mean lengths and aspect ratios than ED and ON. After a single intratracheal (IT) instillation (0.5 or 1.5 mg/rat), persistent changes in ventilatory parameters and a significant increase in lung resistance at baseline and after methacholine aerosol dosing were found only in rats exposed to 1.5 mg SM. High-dose ED significantly elevated bronchoalveolar lavage lactate dehydrogenase (LDH) activity and protein levels, while high-dose SM increased γ-glutamyl transferase and LDH activities. A moderate degree of lung interstitial fibrosis after exposure to 1.5 mg SM persisted 15 mo after exposure, unchanged from previous findings at 3 mo. LA induced mild fibrosis, while ED and ON produced minimal and no apparent fibrosis, respectively. Bronchioloalveolar carcinoma was observed 15 mo after exposure to LA or ED. Data demonstrated that SM, given by bolus IT dosing on an equivalent mass basis, induced greater pulmonary function deficits, airway hyperresponsiveness, and interstitial fibrosis than other NOA, although unlike LA and ED, no apparent evidence for carcinogenicity was found. All NOA samples except ON cleavage fragments produced some degree of long-term toxicity. JF - Journal of toxicology and environmental health. Part A AU - Cyphert, Jaime M AU - McGee, Marie A AU - Nyska, Abraham AU - Schladweiler, Mette C AU - Kodavanti, Urmila P AU - Gavett, Stephen H AD - a Curriculum in Toxicology , University of North Carolina School of Medicine , Chapel Hill , North Carolina , USA. ; b Oak Ridge Institute for Science and Education , Oak Ridge , Tennessee , USA. ; c National Institute of Environmental Health Sciences, National Institutes of Health , Research Triangle Park , North Carolina , USA. ; e Environmental Public Health Division , National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency , Research Triangle Park , North Carolina , USA. Y1 - 2016 PY - 2016 DA - 2016 SP - 49 EP - 60 VL - 79 IS - 2 SN - 1528-7394, 1528-7394 KW - Asbestos, Amphibole KW - 0 KW - Asbestos, Serpentine KW - Bronchoconstrictor Agents KW - Carcinogens KW - Methacholine Chloride KW - 0W5ETF9M2K KW - ferroactinolite KW - 12172-67-7 KW - Asbestos KW - 1332-21-4 KW - tremolite KW - 14567-73-8 KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - gamma-Glutamyltransferase KW - EC 2.3.2.2 KW - Index Medicus KW - Respiratory Function Tests KW - Methacholine Chloride -- pharmacology KW - Animals KW - Bronchial Hyperreactivity -- chemically induced KW - Bronchoconstrictor Agents -- pharmacology KW - L-Lactate Dehydrogenase -- analysis KW - gamma-Glutamyltransferase -- metabolism KW - Intubation, Intratracheal KW - Rats KW - Methacholine Chloride -- administration & dosage KW - Rats, Inbred F344 KW - Airway Resistance -- drug effects KW - Bronchoalveolar Lavage Fluid -- chemistry KW - Asbestosis -- pathology KW - Inhalation Exposure KW - Male KW - L-Lactate Dehydrogenase -- metabolism KW - Bronchial Hyperreactivity -- pathology KW - Survival Analysis KW - Carcinogens -- toxicity KW - Asbestos -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1766266271?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+toxicology+and+environmental+health.+Part+A&rft.atitle=Long-term+toxicity+of+naturally+occurring+asbestos+in+male+Fischer+344+rats.&rft.au=Cyphert%2C+Jaime+M%3BMcGee%2C+Marie+A%3BNyska%2C+Abraham%3BSchladweiler%2C+Mette+C%3BKodavanti%2C+Urmila+P%3BGavett%2C+Stephen+H&rft.aulast=Cyphert&rft.aufirst=Jaime&rft.date=2016-01-01&rft.volume=79&rft.issue=2&rft.spage=49&rft.isbn=&rft.btitle=&rft.title=Journal+of+toxicology+and+environmental+health.+Part+A&rft.issn=15287394&rft_id=info:doi/10.1080%2F15287394.2015.1099123 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-29 N1 - Date created - 2016-02-17 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1080/15287394.2015.1099123 ER - TY - JOUR T1 - My Winding Road: From Microbiology to Toxicology and Environmental Health AN - 1765976906; PQ0002580264 AB - I would certainly never have predicted that I would become the director of the National Institute of Environmental Health Sciences (NIEHS) and the National Toxicology Program (NTP) when I was a Jewish girl growing up in Teaneck, New Jersey. My family stressed the importance of education. Yet for a girl there were many not-so-subtle suggestions that the appropriate careers were in teaching or nursing, and the most important thing was to be a wife and mother. Well, I can't disagree with the latter, although I would have to add grandmother to that list of achievements. My parents were both college graduates, but my mom only taught high school English for one year before leaving the field to start our family. My dad returned from World War II and joined his brother in accounting. After my first sister was born, my father joined my mother's family jewelry business and helped to open a second retail store. My mother helped my dad out during the busy times-Christmas and wedding season-but otherwise focused on our growing family of three girls and one boy. This became increasingly challenging when it became clear that my little brother was severely retarded and would require extra care. JF - Annual Review of Pharmacology and Toxicology AU - Birnbaum, Linda S AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, birnbaumls@niehs.nih.gov Y1 - 2016///0, PY - 2016 DA - 0, 2016 SP - 1 EP - 17 PB - Annual Reviews, Inc., 4139 El Camino Way Palo Alto CA 94303-0139 United States VL - 56 SN - 0362-1642, 0362-1642 KW - Environment Abstracts; Toxicology Abstracts KW - autobiography KW - Birnbaum KW - EPA KW - NIEHS KW - NTP KW - Linda S. Birnbaum KW - Education KW - ANW, USA, New Jersey KW - Reviews KW - Nursing KW - Microbiology KW - Careers KW - Environmental health KW - Accounting KW - Toxicology KW - X 24310:Pharmaceuticals KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765976906?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annual+Review+of+Pharmacology+and+Toxicology&rft.atitle=My+Winding+Road%3A+From+Microbiology+to+Toxicology+and+Environmental+Health&rft.au=Birnbaum%2C+Linda+S&rft.aulast=Birnbaum&rft.aufirst=Linda&rft.date=2016-01-01&rft.volume=56&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Annual+Review+of+Pharmacology+and+Toxicology&rft.issn=03621642&rft_id=info:doi/10.1146%2Fannurev-pharmtox-010715-103255 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-04-29 N1 - SubjectsTermNotLitGenreText - Nursing; Reviews; Education; Microbiology; Careers; Environmental health; Accounting; Toxicology; ANW, USA, New Jersey DO - http://dx.doi.org/10.1146/annurev-pharmtox-010715-103255 ER - TY - JOUR T1 - Radiocarbon-Based Assessment of Heterotrophic Soil Respiration in Two Mediterranean Forests AN - 1765974938; PQ0002538660 AB - The amount of soil organic carbon (SOC) released into the atmosphere as carbon dioxide (CO sub(2)), which is referred to as heterotrophic respiration (Rh), is technically difficult to measure despite its necessity to the understanding of how to protect and increase soil carbon stocks. Within this context, the aim of this study is to determine Rh in two Mediterranean forests dominated by pine and oak using radiocarbon measurements of the bulk SOC from different soil layers. The annual Rh was 3.22 Mg C ha super(-1) y super(-1) under pine and 3.13 Mg C ha super(-1) y super(-1) under oak, corresponding to 38 and 31% of the annual soil respiration, respectively. The accuracy of the Rh values was evaluated by determining the net primary production (NPP), as the sum of the Rh and the net ecosystem production measured by eddy covariance, then comparing it with the NPP obtained through independent biometric measurements. No significant differences were observed, which suggested the suitability of our methodology to infer Rh. Assuming the C inputs to soil to consist exclusively of the aboveground and belowground litter and the C output exclusively of the Rh, both soils were C sinks, which is consistent with a previous modeling study that was performed in the same stands. In conclusion, radiocarbon analysis of bulk SOC provided a reliable estimate of the average annual amount of soil carbon released to the atmosphere; hence, its application is convenient for calculating Rh because it utilizes only a single soil sampling and no time-consuming monitoring activities. JF - Ecosystems AU - Chiti, Tommaso AU - Certini, Giacomo AU - Forte, Claudia AU - Papale, Dario AU - Valentini, Riccardo AD - Dipartimento per l'Innovazione nei Sistemi Biologici, Agroalimentari e Forestali (DIBAF), Universita della Tuscia, Via San C. De Lellis s.n.c., 01100, Viterbo, Italy, tommaso.chiti@unitus.it Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 62 EP - 72 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 19 IS - 1 SN - 1432-9840, 1432-9840 KW - Ecology Abstracts; Sustainability Science Abstracts; Environment Abstracts KW - Litter KW - Ecosystems KW - Respiration KW - Organic carbon KW - Forests KW - Soils (organic) KW - Biometrics KW - Atmosphere KW - Primary production KW - Soil KW - Carbon KW - MED KW - Sampling KW - Carbon dioxide KW - M3 1010:Issues in Sustainable Development KW - D 04040:Ecosystem and Ecology Studies KW - ENA 01:Air Pollution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765974938?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Ecosystems&rft.atitle=Radiocarbon-Based+Assessment+of+Heterotrophic+Soil+Respiration+in+Two+Mediterranean+Forests&rft.au=Chiti%2C+Tommaso%3BCertini%2C+Giacomo%3BForte%2C+Claudia%3BPapale%2C+Dario%3BValentini%2C+Riccardo&rft.aulast=Chiti&rft.aufirst=Tommaso&rft.date=2016-01-01&rft.volume=19&rft.issue=1&rft.spage=62&rft.isbn=&rft.btitle=&rft.title=Ecosystems&rft.issn=14329840&rft_id=info:doi/10.1007%2Fs10021-015-9915-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Number of references - 71 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Soil; Litter; Carbon; Respiration; Forests; Soils (organic); Biometrics; Sampling; Carbon dioxide; Primary production; Atmosphere; Ecosystems; Organic carbon; MED DO - http://dx.doi.org/10.1007/s10021-015-9915-4 ER - TY - JOUR T1 - Toward a Better Understanding of the Complexity of Cancer Drug Resistance AN - 1765973185; PQ0002580269 AB - Resistance to anticancer drugs is a complex process that results from alterations in drug targets; development of alternative pathways for growth activation; changes in cellular pharmacology, including increased drug efflux; regulatory changes that alter differentiation pathways or pathways for response to environmental adversity; and/or changes in the local physiology of the cancer, such as blood supply, tissue hydrodynamics, behavior of neighboring cells, and immune system response. All of these specific mechanisms are facilitated by the intrinsic hallmarks of cancer, such as tumor cell heterogeneity, redundancy of growth-promoting pathways, increased mutation rate and/or epigenetic alterations, and the dynamic variation of tumor behavior in time and space. Understanding the relative contribution of each of these factors is further complicated by the lack of adequate in vitro models that mimic clinical cancers. Several strategies to use current knowledge of drug resistance to improve treatment of cancer are suggested. JF - Annual Review of Pharmacology and Toxicology AU - Gottesman, Michael M AU - Lavi, Orit AU - Hall, Matthew D AU - Gillet, Jean-Pierre AD - Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, mgottesman@nih.gov Y1 - 2016///0, PY - 2016 DA - 0, 2016 SP - 85 EP - 102 PB - Annual Reviews, Inc., 4139 El Camino Way Palo Alto CA 94303-0139 United States VL - 56 SN - 0362-1642, 0362-1642 KW - Toxicology Abstracts KW - ABCB1 KW - P-glycoprotein KW - chemotherapy KW - platinum compounds KW - multidrug resistance KW - Hydrodynamics KW - Pharmacology KW - Immune system KW - Drug resistance KW - Drug development KW - Tumors KW - Mutation rates KW - Antitumor agents KW - Immunosuppressive agents KW - Tumor cells KW - Cancer KW - Differentiation KW - Blood KW - epigenetics KW - Reviews KW - X 24310:Pharmaceuticals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765973185?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annual+Review+of+Pharmacology+and+Toxicology&rft.atitle=Toward+a+Better+Understanding+of+the+Complexity+of+Cancer+Drug+Resistance&rft.au=Gottesman%2C+Michael+M%3BLavi%2C+Orit%3BHall%2C+Matthew+D%3BGillet%2C+Jean-Pierre&rft.aulast=Gottesman&rft.aufirst=Michael&rft.date=2016-01-01&rft.volume=56&rft.issue=&rft.spage=85&rft.isbn=&rft.btitle=&rft.title=Annual+Review+of+Pharmacology+and+Toxicology&rft.issn=03621642&rft_id=info:doi/10.1146%2Fannurev-pharmtox-010715-103111 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Hydrodynamics; Pharmacology; Drug resistance; Immune system; Drug development; Tumors; Mutation rates; Tumor cells; Immunosuppressive agents; Antitumor agents; Cancer; Blood; Differentiation; epigenetics; Reviews DO - http://dx.doi.org/10.1146/annurev-pharmtox-010715-103111 ER - TY - JOUR T1 - Tissue time course and bioavailability of the pyrethroid insecticide bifenthrin in the Long-Evans rat. AN - 1765107841; 26367082 AB - 1. Pyrethroids are neurotoxic and parent pyrethroid appears to be toxic entity. This study evaluated the oral disposition and bioavailability of bifenthrin in the adult male Long-Evans rat. 2. In the disposition study, rats were administered bifenthrin (0.3 or 3 mg/kg) by oral gavage and serially sacrificed (0.25 h to 21 days). Blood, liver, brain and adipose tissue were removed. In the bioavailability study, blood was collected serially from jugular vein cannulated rats (0.25 to 24 h) following oral (0.3 or 3 mg/kg) or intravenous (0.3 mg/kg) administration of bifenthrin. Tissues were extracted and analyzed for bifenthrin by high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). 3. Bifenthrin concentration in blood and liver peaked 1-2-h postoral administration and were approximately 90 ng/ml (or g) and 1000 ng/ml (or g) for both tissues at 0.3 and 3 mg/kg, respectively. Bifenthrin was rapidly cleared from both blood and liver. Brain concentrations peaked at 4-6 h and were lower than in blood at both doses (12 and 143 ng/g). Bifenthrin in adipose tissue peaked at the collected time points of 8 (157 ng/g) and 24 (1145 ng/g) h for the 0.3 and 3 mg/kg doses, respectively and was retained 21 days postoral administration. Following intravenous administration, the blood bifenthrin concentration decreased bi-exponentially, with a distribution half-life of 0.2 h and an elimination half-life of 8 h. Bifenthrin bioavailability was approximately 30%. These disposition and kinetic bifenthrin data may decrease uncertainties in the risk assessment for this pyrethroid insecticide. JF - Xenobiotica; the fate of foreign compounds in biological systems AU - Hughes, Michael F AU - Ross, David G AU - Edwards, Brenda C AU - DeVito, Michael J AU - Starr, James M AD - a U.S. Environmental Protection Agency, Office of Research and Development, National Health and Environmental Effects Research Laboratory, Research Triangle Park , NC , USA . ; b National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park , NC , USA , and. ; c U.S. Environmental Protection Agency, Office of Research and Development, National Exposure Research Laboratory, Research Triangle Park , NC , USA. Y1 - 2016 PY - 2016 DA - 2016 SP - 430 EP - 438 VL - 46 IS - 5 KW - Insecticides KW - 0 KW - Pyrethrins KW - bifenthrin KW - 6B66JED0KN KW - Index Medicus KW - pyrethroids KW - Bifenthrin KW - pharmacokinetics KW - disposition KW - Administration, Oral KW - Animals KW - Rats, Long-Evans KW - Brain -- drug effects KW - Blood -- drug effects KW - Tissue Distribution KW - Tandem Mass Spectrometry KW - Administration, Intravenous KW - Chromatography, High Pressure Liquid KW - Risk Assessment KW - Rats KW - Liver -- drug effects KW - Adipose Tissue -- drug effects KW - Time Factors KW - Male KW - Pyrethrins -- administration & dosage KW - Insecticides -- administration & dosage KW - Insecticides -- pharmacokinetics KW - Pyrethrins -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765107841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Xenobiotica%3B+the+fate+of+foreign+compounds+in+biological+systems&rft.atitle=Tissue+time+course+and+bioavailability+of+the+pyrethroid+insecticide+bifenthrin+in+the+Long-Evans+rat.&rft.au=Hughes%2C+Michael+F%3BRoss%2C+David+G%3BEdwards%2C+Brenda+C%3BDeVito%2C+Michael+J%3BStarr%2C+James+M&rft.aulast=Hughes&rft.aufirst=Michael&rft.date=2016-01-01&rft.volume=46&rft.issue=5&rft.spage=430&rft.isbn=&rft.btitle=&rft.title=Xenobiotica%3B+the+fate+of+foreign+compounds+in+biological+systems&rft.issn=1366-5928&rft_id=info:doi/10.3109%2F00498254.2015.1081710 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-11-07 N1 - Date created - 2016-02-11 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3109/00498254.2015.1081710 ER - TY - JOUR T1 - Chemopreventive Effects of Eryngium foetidum L. Leaves on COX-2 Reduction in Mice Induced Colorectal Carcinogenesis. AN - 1762965715; 26771664 AB - To investigate the potential effects of Eryngium foetidum Linn. leaves (EF) in colitis-induced colorectal carcinogenesis in mice by azoxymethane (AOM) and dextran sulfate sodium (DSS), 39 ICR male mice were studied and divided into 6 groups. The mice were received a modified AIN-76 diet in Group 1, whereas Group 2 was given an AOM, DSS, and AIN-76 diet. Groups 3 and 4 were fed with 0.8% and 3.2% freeze-dried EF with AIN-76 diets, for 5 wk. Groups 5 and 6 were fed with 0.8% and 3.2% EF diets for 5 wk during AOM/DSS administration. The mice were necropsied at Week 20 and their colons were collected. The results indicated that the incidences of tumors in Groups 2, 5, and 6 was 100%, 75%, and 88%, with multiplicities (mean ±SE) of 3.75 ±0.92, 2.38 ± 0.96 and 4.25 ± 0.79, respectively. Interestingly, there was a significant difference in COX-2 expression in mice received 3.2% EF in their diet, but the proliferative cell nuclear antigen index and iNOS protein expression were not significantly different. We concluded that EF at a dose level of 3.2% in their diet had a preventive effect on colorectal carcinogenesis via the proinflammatory cytokine, COX-2. JF - Nutrition and cancer AU - Promtes, Kamonwan AU - Kupradinun, Piengchai AU - Rungsipipat, Anudep AU - Tuntipopipat, Siriporn AU - Butryee, Chaniphun AD - a Institute of Nutrition, Mahidol University , Nakhon Pathom , Thailand. ; b Laboratory Animal Section, National Cancer Institute , Bangkok , Thailand. ; c Companion Animal Cancer Research Unit, Department of Veterinary Pathology, Faculty of Veterinary Science, Chulalongkorn University , Bangkok , Thailand. Y1 - 2016 PY - 2016 DA - 2016 SP - 144 EP - 153 VL - 68 IS - 1 KW - Proliferating Cell Nuclear Antigen KW - 0 KW - Nitric Oxide Synthase Type II KW - EC 1.14.13.39 KW - Nos2 protein, mouse KW - Ptgs2 protein, mouse KW - EC 1.14.99.- KW - Cyclooxygenase 2 KW - EC 1.14.99.1 KW - Index Medicus KW - Body Weight KW - Animals KW - Mice, Inbred ICR KW - Plant Leaves KW - Proliferating Cell Nuclear Antigen -- analysis KW - Nitric Oxide Synthase Type II -- metabolism KW - Mice KW - Male KW - Phytotherapy KW - Colorectal Neoplasms -- pathology KW - Eryngium KW - Cyclooxygenase 2 -- metabolism KW - Colorectal Neoplasms -- enzymology KW - Colorectal Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1762965715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nutrition+and+cancer&rft.atitle=Chemopreventive+Effects+of+Eryngium+foetidum+L.+Leaves+on+COX-2+Reduction+in+Mice+Induced+Colorectal+Carcinogenesis.&rft.au=Promtes%2C+Kamonwan%3BKupradinun%2C+Piengchai%3BRungsipipat%2C+Anudep%3BTuntipopipat%2C+Siriporn%3BButryee%2C+Chaniphun&rft.aulast=Promtes&rft.aufirst=Kamonwan&rft.date=2016-01-01&rft.volume=68&rft.issue=1&rft.spage=144&rft.isbn=&rft.btitle=&rft.title=Nutrition+and+cancer&rft.issn=1532-7914&rft_id=info:doi/10.1080%2F01635581.2016.1115103 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-12-13 N1 - Date created - 2016-02-04 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1080/01635581.2016.1115103 ER - TY - JOUR T1 - Lung deposition and clearance of microparticle and nanoparticle C60 fullerene aggregates in B6C3F1 mice and Wistar Han rats following nose-only inhalation for 13 weeks AN - 1762367806; PQ0002517943 AB - C60 fullerenes (C60) are spherical structures consisting of 60 carbon atoms that are generated via combustion from both natural and anthropogenic sources. C60 are also synthesized intentionally for industrial applications. Individual C60 structures have an approximate diameter of 1nm; however, C60 readily forms aggregates and typically exist as larger particles that range from nanometers to micrometers in diameter. In this report, lung and extrapulmonary tissue deposition and lung clearance of C60 nanoparticles (nano-C60, 50nm) and microparticles (micro-C60, 1 mu m) were examined in Wistar Han rats and B6C3F1/N mice after nose-only inhalation for 90 days. Exposure concentrations were 0.5 and 2mg/m3 (nano-C60) and 2, 15, and 30mg/m3 (micro-C60). For both C60 particle sizes, the C60 lung burden increased proportionally to exposure concentration. The C60 lung burden was greater in both species at all time points following exposure to nano-C60 particle exposure compared to micro-C60 exposure at the common exposure concentration 2mg/m3. The calculated C60 particle lung retention half-times were similar for both nano-C60 and micro-C60 exposure at 2mg/m3 in male mice (15-16 days). In contrast, in male rats, the half-time of C60 particles following nano-C60 exposure (61 days) was roughly twice as long as the half-time following micro-C60 exposure (27 days) at the same exposure concentration (2mg/m3) and was similar to the clearance following micro-C60 exposure at higher exposure concentrations (15 and 30mg/m3). C60 was detected in bronchial lymph nodes but the burden was not quantified due to the high variability in the data. C60 concentrations were below the experimental limit of quantitation (ELOQ) in liver, spleen, blood, brain and kidney tissues. These tissue burden data provide information for comparison between nanometer and micrometer sized C60 particle exposure and will aid in the interpretation of toxicity data. JF - Toxicology AU - Sayers, Brian C AU - Walker, Nigel J AU - Roycroft, Joseph H AU - Germolec, Dori R AU - Baker, Gregory L AU - Clark, Mark L AU - Hayden, Barry K AU - DeFord, Henry AU - Dill, Jeffrey A AU - Gupta, Amit AU - Stout, Matthew D AD - Division of the National Toxicology Program, National Institute of Environmental Health Sciences, 111 Alexander Drive, Research Triangle Park, NC 27709, USA Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 87 EP - 96 PB - Elsevier B.V., P.O. Box 85 Limerick Ireland VL - 339 SN - 0300-483X, 0300-483X KW - Toxicology Abstracts KW - C60 fullerene KW - Nanoparticle KW - Inhalation KW - Lung deposition KW - Lung clearance KW - Data processing KW - microparticles KW - Brain KW - Spleen KW - Toxicity KW - Lymph nodes KW - Combustion KW - Blood KW - Carbon KW - Fullerenes KW - Industrial applications KW - Lung KW - Liver KW - Kidney KW - nanoparticles KW - Quantitation KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1762367806?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology&rft.atitle=Lung+deposition+and+clearance+of+microparticle+and+nanoparticle+C60+fullerene+aggregates+in+B6C3F1+mice+and+Wistar+Han+rats+following+nose-only+inhalation+for+13+weeks&rft.au=Sayers%2C+Brian+C%3BWalker%2C+Nigel+J%3BRoycroft%2C+Joseph+H%3BGermolec%2C+Dori+R%3BBaker%2C+Gregory+L%3BClark%2C+Mark+L%3BHayden%2C+Barry+K%3BDeFord%2C+Henry%3BDill%2C+Jeffrey+A%3BGupta%2C+Amit%3BStout%2C+Matthew+D&rft.aulast=Sayers&rft.aufirst=Brian&rft.date=2016-01-01&rft.volume=339&rft.issue=&rft.spage=87&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=0300483X&rft_id=info:doi/10.1016%2Fj.tox.2015.11.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-07-07 N1 - SubjectsTermNotLitGenreText - Inhalation; Data processing; microparticles; Brain; Spleen; Toxicity; Lymph nodes; Combustion; Blood; Carbon; Industrial applications; Fullerenes; Lung; Kidney; Liver; Quantitation; nanoparticles DO - http://dx.doi.org/10.1016/j.tox.2015.11.003 ER - TY - JOUR T1 - A Small RNA-Based Immune System Defends Germ Cells against Mobile Genetic Elements AN - 1762354335; PQ0002408265 AB - Transposons are mobile genetic elements that threaten the survival of species by destabilizing the germline genomes. Limiting the spread of these selfish elements is imperative. Germ cells employ specialized small regulatory RNA pathways to restrain transposon activity. PIWI proteins and Piwi-interacting RNAs (piRNAs) silence transposons at the transcriptional and posttranscriptional level with loss-of-function mutant animals universally exhibiting sterility often associated with germ cell defects. This short review aims to illustrate basic strategies of piRNA-guided defense against transposons. Mechanisms of piRNA silencing are most readily studied in Drosophila melanogaster , which serves as a model to delineate molecular concepts and as a reference for mammalian piRNA systems. PiRNA pathways utilize two major strategies to handle the challenges of transposon control: (1) the hard-wired molecular memory of prior transpositions enables recognition of mobile genetic elements and discriminates transposons from host genes; (2) a feed-forward adaptation mechanism shapes piRNA populations to selectively combat the immediate threat of transposon transcripts. In flies, maternally contributed PIWI-piRNA complexes bolster both of these lines of defense and ensure transgenerational immunity. While recent studies have provided a conceptual framework of what could be viewed as an ancient immune system, we are just beginning to appreciate its many molecular innovations. JF - Stem Cells International AU - Haase, Astrid D AD - Laboratory of Cell and Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA, astrid.haase@nih.gov Y1 - 2016/01// PY - 2016 DA - January 2016 PB - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States VL - 2016 SN - 1687-966X, 1687-966X KW - Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - Genomes KW - Molecular modelling KW - Adaptations KW - Immune system KW - Sterility KW - Transposition KW - Germ cells KW - Transcription KW - Immunity KW - Transposons KW - Stem cells KW - RNA KW - Reviews KW - Drosophila melanogaster KW - Post-transcription KW - W 30925:Genetic Engineering KW - N 14830:RNA KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1762354335?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+Cells+International&rft.atitle=A+Small+RNA-Based+Immune+System+Defends+Germ+Cells+against+Mobile+Genetic+Elements&rft.au=Haase%2C+Astrid+D&rft.aulast=Haase&rft.aufirst=Astrid&rft.date=2016-01-01&rft.volume=2016&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Stem+Cells+International&rft.issn=1687966X&rft_id=info:doi/10.1155%2F2016%2F7595791 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Genomes; Molecular modelling; Adaptations; Immune system; Germ cells; Transposition; Sterility; Transcription; Immunity; Transposons; Stem cells; RNA; Reviews; Post-transcription; Drosophila melanogaster DO - http://dx.doi.org/10.1155/2016/7595791 ER - TY - JOUR T1 - One Hundred False-Positive Amphetamine Specimens Characterized by Liquid Chromatography Time-of-Flight Mass Spectrometry. AN - 1760930472; 26342055 AB - Some amphetamine (AMP) and ecstacy (MDMA) urine immunoassay (IA) kits are prone to false-positive results due to poor specificity of the antibody. We employed two techniques, high-resolution mass spectrometry (HRMS) and an in silico structure search, to identify compounds likely to cause false-positive results. Hundred false-positive IA specimens for AMP and/or MDMA were analyzed by an Agilent 6230 time-of-flight (TOF) mass spectrometer. Separately, SciFinder (Chemical Abstracts) was used as an in silico structure search to generate a library of compounds that are known to cross-react with AMP/MDMA IAs. Chemical formulas and exact masses of 145 structures were then compared against masses identified by TOF. Compounds known to have cross-reactivity with the IAs were identified in the structure-based search. The chemical formulas and exact masses of 145 structures (of 20 chemical formulas) were compared against masses identified by TOF. Urine analysis by HRMS correlates accurate mass with chemical formulae, but provides little information regarding compound structure. Structural data of targeted antigens can be utilized to correlate HRMS-derived chemical formulas with structural analogs. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Journal of analytical toxicology AU - Marin, Stephanie J AU - Doyle, Kelly AU - Chang, Annie AU - Concheiro-Guisan, Marta AU - Huestis, Marilyn A AU - Johnson-Davis, Kamisha L AD - ARUP Institute for Clinical and Experimental Pathology, 500 Chipeta Way, Salt Lake City, UT 84108-1221, USA stephanie.marin@aruplab.com. ; ARUP Laboratories, Inc., 500 Chipeta Way, Salt Lake City, UT 84108-1221, USA Department of Pathology, University of Utah Health Science Center, Salt Lake City, UT, USA. ; University of California, Berkeley, CA, USA. ; National Institute on Drug Abuse, Baltimore, MD, USA Department of Sciences, City University of New York, John Jay College, New York, NY, USA. ; National Institute on Drug Abuse, Baltimore, MD, USA. PY - 2016 SP - 37 EP - 42 VL - 40 IS - 1 KW - Reagent Kits, Diagnostic KW - 0 KW - Amphetamine KW - CK833KGX7E KW - N-Methyl-3,4-methylenedioxyamphetamine KW - KE1SEN21RM KW - Index Medicus KW - Humans KW - Reagent Kits, Diagnostic -- standards KW - Cross Reactions KW - Immunoassay KW - False Positive Reactions KW - Chromatography, Liquid -- methods KW - Amphetamine -- urine KW - N-Methyl-3,4-methylenedioxyamphetamine -- chemistry KW - Mass Spectrometry -- methods KW - N-Methyl-3,4-methylenedioxyamphetamine -- urine KW - Amphetamine -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1760930472?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+analytical+toxicology&rft.atitle=One+Hundred+False-Positive+Amphetamine+Specimens+Characterized+by+Liquid+Chromatography+Time-of-Flight+Mass+Spectrometry.&rft.au=Marin%2C+Stephanie+J%3BDoyle%2C+Kelly%3BChang%2C+Annie%3BConcheiro-Guisan%2C+Marta%3BHuestis%2C+Marilyn+A%3BJohnson-Davis%2C+Kamisha+L&rft.aulast=Marin&rft.aufirst=Stephanie&rft.date=2016-01-01&rft.volume=40&rft.issue=1&rft.spage=37&rft.isbn=&rft.btitle=&rft.title=Journal+of+analytical+toxicology&rft.issn=1945-2403&rft_id=info:doi/10.1093%2Fjat%2Fbkv101 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-26 N1 - Date created - 2016-01-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Chem. 1994 Oct;40(10):1898-903 [7923769] J Anal Toxicol. 2010 Nov;34(9):587-9 [21073812] Obstet Gynecol. 2011 Feb;117(2 Pt 2):503-6 [21252805] J Anal Toxicol. 2011 Apr;35(3):183-7 [21439156] Ther Drug Monit. 2011 Jun;33(3):366-8 [21436763] J Med Toxicol. 2011 Jun;7(2):105-8 [21191682] J Anal Toxicol. 2011 Jul;35(6):364-8 [21740694] Pharmacotherapy. 2012 May;32(5):e98-102 [22499397] J Anal Toxicol. 2012 Sep;36(7):477-86 [22802572] Ther Drug Monit. 2012 Oct;34(5):493-5 [22972534] Pharmacotherapy. 2013 May;33(5):e88-9 [23065913] Anal Bioanal Chem. 2013 Nov;405(29):9437-48 [24196122] Drug Test Anal. 2014 May;6(5):492-9 [24665024] J Anal Toxicol. 2014 Sep;38(7):387-96 [24986836] Clin Chim Acta. 2015 Jan 1;438:307-8 [25242739] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/jat/bkv101 ER - TY - JOUR T1 - A multicenter retrospective survey of poisoning after ingestion of herbicides containing glyphosate potassium salt or other glyphosate salts in Japan. AN - 1760920038; 26691886 AB - A multicenter retrospective survey of patients poisoned by herbicides containing glyphosate salts in Japan was conducted to identify differences in symptoms and outcome of poisoning. Participants were patients who were transported to emergency facilities between October 2006 and March 2014 after consuming herbicides containing glyphosate potassium salt (GlyK(+)) (the K-group) or other glyphosate salts (the O-group). Questionnaires were mailed to 38 emergency facilities that agreed to participate in the study. Serum potassium levels upon arrival were significantly higher (p < 0.01), and abnormal electrocardiogram findings were significantly more common (p < 0.01) in the K-group (n = 55) than in the O-group (n = 62). Conversely, acute lung injury (ALI) including acute respiratory distress syndrome (ARDS) (p = 0.05) and liver injury (LI) (p < 0.01) were significantly more common during hospitalization in the O-group, although no significant differences in the duration of hospital stay (p = 0.92) or outcomes (p = 0.95) were observed between the two groups. The ingestion of products containing glyphosate isopropylamine or ammonium salts, and polyoxyethyleneamine (POEA) as a surfactant, can cause severe organ injury. Physicians should note that the ingestion of products containing glyphosate potassium salt and surfactants other than POEA can cause hyperkalemia, potentially leading to fatal arrhythmias or cardiac arrest. JF - Clinical toxicology (Philadelphia, Pa.) AU - Kamijo, Yoshito AU - Takai, Michiko AU - Sakamoto, Tetsuya AD - a Emergency Medical Center & Poison Center, Saitama Medical University Hospital , Iruma-gun , Saitama , Japan ; ; b Center for Suicide Prevention, National Institute of Mental Health, National Center of Neurology and Psychiatry , Tokyo , Japan ; ; c Department of Emergency Medicine , School of Medicine, Teikyo University , Tokyo , Japan. Y1 - 2016 PY - 2016 DA - 2016 SP - 147 EP - 151 VL - 54 IS - 2 KW - Herbicides KW - 0 KW - Propylamines KW - Surface-Active Agents KW - polyoxyethyleneamine KW - Polyethylene Glycols KW - 30IQX730WE KW - glyphosate KW - 4632WW1X5A KW - 2-propylamine KW - P8W26T4MTD KW - Potassium KW - RWP5GA015D KW - Glycine KW - TE7660XO1C KW - Abridged Index Medicus KW - Index Medicus KW - hyperkalemia KW - cardiac arrest KW - Arrhythmia KW - glyphosate-surfactant herbicide KW - Young Adult KW - Surface-Active Agents -- administration & dosage KW - Chemical and Drug Induced Liver Injury -- pathology KW - Dose-Response Relationship, Drug KW - Humans KW - Retrospective Studies KW - Aged KW - Surface-Active Agents -- poisoning KW - Respiratory Distress Syndrome, Adult -- pathology KW - Polyethylene Glycols -- administration & dosage KW - Respiratory Distress Syndrome, Adult -- chemically induced KW - Polyethylene Glycols -- poisoning KW - Chemical and Drug Induced Liver Injury -- etiology KW - Acute Lung Injury -- pathology KW - Aged, 80 and over KW - Propylamines -- poisoning KW - Propylamines -- administration & dosage KW - Adult KW - Surveys and Questionnaires KW - Middle Aged KW - Acute Lung Injury -- chemically induced KW - Female KW - Japan KW - Male KW - Herbicides -- administration & dosage KW - Herbicides -- poisoning KW - Potassium -- blood KW - Poisoning -- pathology KW - Poisoning -- etiology KW - Glycine -- analogs & derivatives KW - Potassium -- administration & dosage KW - Glycine -- administration & dosage KW - Glycine -- poisoning KW - Glycine -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1760920038?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+toxicology+%28Philadelphia%2C+Pa.%29&rft.atitle=A+multicenter+retrospective+survey+of+poisoning+after+ingestion+of+herbicides+containing+glyphosate+potassium+salt+or+other+glyphosate+salts+in+Japan.&rft.au=Kamijo%2C+Yoshito%3BTakai%2C+Michiko%3BSakamoto%2C+Tetsuya&rft.aulast=Kamijo&rft.aufirst=Yoshito&rft.date=2016-01-01&rft.volume=54&rft.issue=2&rft.spage=147&rft.isbn=&rft.btitle=&rft.title=Clinical+toxicology+%28Philadelphia%2C+Pa.%29&rft.issn=1556-9519&rft_id=info:doi/10.3109%2F15563650.2015.1121271 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-07 N1 - Date created - 2016-01-22 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3109/15563650.2015.1121271 ER - TY - JOUR T1 - Ribonuclease H/DNA Polymerase HIV-1 Reverse Transcriptase Dual Inhibitor: Mechanistic Studies on the Allosteric Mode of Action of Isatin-Based Compound RMNC6. AN - 1760914188; 26800261 AB - The DNA polymerase and ribonuclease H (RNase H) activities of human immunodeficiency virus type 1 (HIV-1) are needed for the replication of the viral genome and are validated drug targets. However, there are no approved drugs inhibiting RNase H and the efficiency of DNA polymerase inhibitors can be diminished by the presence of drug resistance mutations. In this context, drugs inhibiting both activities could represent a significant advance towards better anti-HIV therapies. We report on the mechanisms of allosteric inhibition of a newly synthesized isatin-based compound designated as RMNC6 that showed IC50 values of 1.4 and 9.8 μM on HIV-1 RT-associated RNase H and polymerase activities, respectively. Blind docking studies predict that RMNC6 could bind two different pockets in the RT: one in the DNA polymerase domain (partially overlapping the non-nucleoside RT inhibitor [NNRTI] binding pocket), and a second one close to the RNase H active site. Enzymatic studies showed that RMNC6 interferes with efavirenz (an approved NNRTI) in its binding to the RT polymerase domain, although NNRTI resistance-associated mutations such as K103N, Y181C and Y188L had a minor impact on RT susceptibility to RMNC6. In addition, despite being naturally resistant to NNRTIs, the polymerase activity of HIV-1 group O RT was efficiently inhibited by RMNC6. The compound was also an inhibitor of the RNase H activity of wild-type HIV-1 group O RT, although we observed a 6.5-fold increase in the IC50 in comparison with the prototypic HIV-1 group M subtype B enzyme. Mutagenesis studies showed that RT RNase H domain residues Asn474 and Tyr501, and in a lesser extent Ala502 and Ala508, are critical for RMNC6 inhibition of the endonuclease activity of the RT, without affecting its DNA polymerization activity. Our results show that RMNC6 acts as a dual inhibitor with allosteric sites in the DNA polymerase and the RNase H domains of HIV-1 RT. JF - PloS one AU - Corona, Angela AU - Meleddu, Rita AU - Esposito, Francesca AU - Distinto, Simona AU - Bianco, Giulia AU - Masaoka, Takashi AU - Maccioni, Elias AU - Menéndez-Arias, Luis AU - Alcaro, Stefano AU - Le Grice, Stuart F J AU - Tramontano, Enzo AD - Department of Life and Environmental Sciences, University of Cagliari, Cagliari, Italy. ; National Cancer Institute, Frederick, Maryland, United States of America. ; Centro de Biología Molecular "Severo Ochoa" (Consejo Superior de Investigaciones Científicas & Universidad Autónoma de Madrid), Madrid, Spain. ; Dipartimento di Scienze della Salute, Università Magna Graecia di Catanzaro, Campus "S. Venuta", Viale Europa, 88100, Catanzaro, Italy. Y1 - 2016 PY - 2016 DA - 2016 SP - 1 VL - 11 IS - 1 KW - 4-(2-(2-(2-oxoindolin-3-ylidene)hydrazinyl)thiazol-4-yl)benzonitrile KW - 0 KW - Anti-HIV Agents KW - Benzoxazines KW - Enzyme Inhibitors KW - Hydrazones KW - Reverse Transcriptase Inhibitors KW - Isatin KW - 82X95S7M06 KW - reverse transcriptase, Human immunodeficiency virus 1 KW - EC 2.7.7.- KW - HIV Reverse Transcriptase KW - EC 2.7.7.49 KW - Ribonuclease H, Human Immunodeficiency Virus KW - EC 3.1.26.4 KW - efavirenz KW - JE6H2O27P8 KW - Index Medicus KW - Molecular Docking Simulation KW - Virus Replication -- drug effects KW - Humans KW - HIV-1 -- enzymology KW - Protein Structure, Tertiary KW - Microbial Sensitivity Tests KW - Benzoxazines -- antagonists & inhibitors KW - Binding Sites KW - Benzoxazines -- pharmacology KW - Isatin -- pharmacology KW - Ribonuclease H, Human Immunodeficiency Virus -- antagonists & inhibitors KW - Reverse Transcriptase Inhibitors -- pharmacology KW - Anti-HIV Agents -- pharmacology KW - Hydrazones -- pharmacology KW - HIV Reverse Transcriptase -- antagonists & inhibitors KW - Enzyme Inhibitors -- pharmacology KW - Isatin -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1760914188?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Ribonuclease+H%2FDNA+Polymerase+HIV-1+Reverse+Transcriptase+Dual+Inhibitor%3A+Mechanistic+Studies+on+the+Allosteric+Mode+of+Action+of+Isatin-Based+Compound+RMNC6.&rft.au=Corona%2C+Angela%3BMeleddu%2C+Rita%3BEsposito%2C+Francesca%3BDistinto%2C+Simona%3BBianco%2C+Giulia%3BMasaoka%2C+Takashi%3BMaccioni%2C+Elias%3BMen%C3%A9ndez-Arias%2C+Luis%3BAlcaro%2C+Stefano%3BLe+Grice%2C+Stuart+F+J%3BTramontano%2C+Enzo&rft.aulast=Corona&rft.aufirst=Angela&rft.date=2016-01-01&rft.volume=11&rft.issue=1&rft.spage=e0147225&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0147225 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-01 N1 - Date created - 2016-01-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Antiviral Res. 2005 Feb;65(2):117-24 [15708638] Biochemistry. 2002 Apr 16;41(15):4856-65 [11939780] J Comput Chem. 2005 Jul 15;26(9):915-31 [15841474] J Biomol Screen. 2006 Oct;11(7):854-63 [16943390] ACS Chem Biol. 2006 Dec 20;1(11):702-12 [17184135] J Virol. 2007 Aug;81(15):7852-9 [17507476] Proc Natl Acad Sci U S A. 2008 Feb 5;105(5):1466-71 [18230722] J Antimicrob Chemother. 2008 May;61(5):973-5 [18325896] Virus Res. 2008 Jun;134(1-2):124-46 [18272247] Methods Mol Biol. 2008;426:299-318 [18542872] J Mol Biol. 2009 Oct 2;392(4):872-84 [19651140] J Med Chem. 2009 Oct 22;52(20):6413-20 [19827836] Structure. 2009 Dec 9;17(12):1625-35 [20004166] J Virol. 2010 Aug;84(15):7625-33 [20484498] Chem Biol Drug Des. 2011 Jan;77(1):39-47 [21114787] J Med Chem. 2011 Apr 28;54(8):2727-37 [21446702] J Chem Inf Model. 2011 Aug 22;51(8):1986-98 [21714567] FEBS J. 2011 May;278(9):1444-57 [21348941] J Biol Chem. 2012 Feb 3;287(6):4066-75 [22105069] Eur J Med Chem. 2012 Apr;50:216-29 [22361685] Chem Biol Drug Des. 2012 Nov;80(5):706-16 [22846652] Curr Pharm Des. 2013;19(10):1850-9 [23092286] Nucleic Acids Res. 2013 Apr;41(8):4601-12 [23444139] Biochem J. 2013 Oct 15;455(2):179-84 [23927736] Future Med Chem. 2013 Dec;5(18):2127-39 [24261890] J Med Chem. 2013 Jul 11;56(13):5436-45 [23631411] ChemMedChem. 2014 Aug;9(8):1869-79 [24850787] BMC Infect Dis. 2014;14:407 [25047543] Antimicrob Agents Chemother. 2014 Oct;58(10):6101-10 [25092689] J Med Chem. 2015 Jan 22;58(2):651-64 [25522204] Nucleic Acids Res. 2015 Feb 27;43(4):2259-70 [25662223] Acc Chem Res. 2000 Dec;33(12):889-97 [11123888] J Microbiol. 2015 Apr;53(4):288-93 [25740376] Proc Natl Acad Sci U S A. 2002 Jul 9;99(14):9515-20 [12093908] Proc Natl Acad Sci U S A. 2004 Jul 20;101(29):10548-53 [15249669] Methods Enzymol. 1982;87:500-9 [6757651] Science. 1983 May 20;220(4599):868-71 [6189183] N Engl J Med. 1984 Nov 15;311(20):1292-7 [6208484] Proc Natl Acad Sci U S A. 1988 Feb;85(4):1218-22 [2448794] Proc Natl Acad Sci U S A. 1992 Nov 15;89(22):10763-7 [1279694] Proc Natl Acad Sci U S A. 1993 Jul 1;90(13):6320-4 [7687065] Nat Struct Biol. 1995 Apr;2(4):293-302 [7540934] Nucleic Acids Res. 2000 Jan 1;28(1):235-42 [10592235] J Biol Chem. 2000 May 12;275(19):14316-20 [10799511] Methods Enzymol. 1995;262:130-44 [8594344] J Biol Chem. 1997 Apr 25;272(17):11157-64 [9111014] Virology. 1997 Sep 29;236(2):364-73 [9325244] Biochemistry. 2005 Feb 8;44(5):1595-606 [15683243] Eur J Med Chem. 2015 Mar 26;93:452-60 [25728026] Nucleic Acids Res. 2005;33(4):1249-56 [15741178] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0147225 ER - TY - JOUR T1 - Introduction to the Theme "Cancer Pharmacology". AN - 1760896545; 26551200 JF - Annual review of pharmacology and toxicology AU - Insel, Paul A AU - Amara, Susan G AU - Blaschke, Terrence F AU - Meyer, Urs A AD - Departments of Pharmacology and Medicine, University of California, San Diego, La Jolla, California 92093. ; National Institute of Mental Health, Bethesda, Maryland 20892. ; Departments of Medicine and Molecular Pharmacology, Stanford University School of Medicine, Stanford, California 94305. ; Division of Pharmacology and Neurobiology, University of Basel, Basel CH-4056, Switzerland. Y1 - 2016 PY - 2016 DA - 2016 SP - 19 EP - 22 VL - 56 KW - Antineoplastic Agents KW - 0 KW - Carcinogens, Environmental KW - Index Medicus KW - Pharmacology -- methods KW - Humans KW - Neoplasms -- drug therapy KW - Carcinogens, Environmental -- adverse effects KW - Neoplasms -- chemically induced KW - Antineoplastic Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1760896545?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annual+review+of+pharmacology+and+toxicology&rft.atitle=Introduction+to+the+Theme+%22Cancer+Pharmacology%22.&rft.au=Insel%2C+Paul+A%3BAmara%2C+Susan+G%3BBlaschke%2C+Terrence+F%3BMeyer%2C+Urs+A&rft.aulast=Insel&rft.aufirst=Paul&rft.date=2016-01-01&rft.volume=56&rft.issue=&rft.spage=19&rft.isbn=&rft.btitle=&rft.title=Annual+review+of+pharmacology+and+toxicology&rft.issn=1545-4304&rft_id=info:doi/10.1146%2Fannurev-pharmtox-102015-123106 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-30 N1 - Date created - 2016-01-07 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1146/annurev-pharmtox-102015-123106 ER - TY - JOUR T1 - Oxidative stress in oral diseases. AN - 1760890890; 25417961 AB - Oxidative species, including reactive oxygen species (ROS), are components of normal cellular metabolism and are required for intracellular processes as varied as proliferation, signal transduction, and apoptosis. In the situation of chronic oxidative stress, however, ROS contribute to various pathophysiologies and are involved in multiple stages of carcinogenesis. In head and neck cancers specifically, many common risk factors contribute to carcinogenesis via ROS-based mechanisms, including tobacco, areca quid, alcohol, and viruses. Given their widespread influence on the process of carcinogenesis, ROS and their related pathways are attractive targets for intervention. The effects of radiation therapy, a central component of treatment for nearly all head and neck cancers, can also be altered via interfering with oxidative pathways. These pathways are also relevant to the development of many benign oral diseases. In this review, we outline how ROS contribute to pathophysiology with a focus toward head and neck cancers and benign oral diseases, describing potential targets and pathways for intervention that exploit the role of oxidative species in these pathologic processes. Published 2014. This article is a U.S. Government work and is in the public domain in the USA. JF - Oral diseases AU - Kesarwala, A H AU - Krishna, M C AU - Mitchell, J B AD - Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 9 EP - 18 VL - 22 IS - 1 KW - Dentistry KW - radiation KW - oxidative species KW - reactive oxygen species KW - reactive nitrogen species KW - cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1760890890?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oral+diseases&rft.atitle=Oxidative+stress+in+oral+diseases.&rft.au=Kesarwala%2C+A+H%3BKrishna%2C+M+C%3BMitchell%2C+J+B&rft.aulast=Kesarwala&rft.aufirst=A&rft.date=2016-01-01&rft.volume=22&rft.issue=1&rft.spage=9&rft.isbn=&rft.btitle=&rft.title=Oral+diseases&rft.issn=1601-0825&rft_id=info:doi/10.1111%2Fodi.12300 LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2016-01-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Res. 2008 Mar 1;68(5):1303-9 [18316592] Cell Death Differ. 2008 Apr;15(4):660-6 [18219320] Cancer Lett. 2008 Jul 18;266(1):73-83 [18367325] J Biol Chem. 2008 Jul 4;283(27):18582-90 [18474597] Int J Environ Res Public Health. 2009 Feb;6(2):445-62 [19440393] Alcohol Alcohol. 2009 Jul-Aug;44(4):353-7 [19451660] Cancer Lett. 2010 Sep 28;295(2):154-66 [20363070] J Toxicol Environ Health A. 2002 Feb;65(3-4):327-36 [11911495] Toxicol Lett. 2002 Jun 24;132(3):221-47 [12044705] J Biol Chem. 2002 Nov 22;277(47):44784-90 [12237311] Cancer Biol Ther. 2003 May-Jun;2(3):233-5 [12878854] Curr Med Chem. 2003 Dec;10(23):2495-505 [14529465] Antioxid Redox Signal. 2003 Dec;5(6):771-80 [14588150] Annu Rev Pharmacol Toxicol. 2004;44:239-67 [14744246] Am J Physiol Regul Integr Comp Physiol. 2004 Mar;286(3):R431-44 [14761864] Mol Cell Biochem. 2004 Jan;255(1-2):67-78 [14971647] J Urol. 2004 Apr;171(4):1533-6 [15017214] Neurochem Res. 2004 Mar;29(3):617-28 [15038609] Semin Radiat Oncol. 2004 Jul;14(3):259-66 [15254869] Cancer Lett. 2004 Oct 8;214(1):69-79 [15331175] J Biol Chem. 1969 Nov 25;244(22):6049-55 [5389100] Biochem J. 1972 Jul;128(3):617-30 [4404507] Clin Exp Immunol. 1982 Jul;49(1):247-55 [7127901] Food Chem Toxicol. 1986 Feb;24(2):129-37 [3957160] Chem Rev. 2011 Oct 12;111(10):5944-72 [21861450] J Virol. 2012 Jan;86(1):382-94 [22013061] Free Radic Res. 2012 Feb;46(2):141-6 [22126431] Carcinogenesis. 2012 Apr;33(4):848-58 [22266465] Cochrane Database Syst Rev. 2012;5:CD005005 [22592699] Int J Radiat Oncol Biol Phys. 2012 Jul 15;83(4):1284-90 [22197226] Oxid Med Cell Longev. 2012;2012:976753 [22829965] Clin Chim Acta. 2012 Oct 9;413(19-20):1446-53 [22683781] Free Radic Biol Med. 2012 Oct 1;53(7):1500-13 [22824861] Target Oncol. 2012 Dec;7(4):233-42 [23054400] Invest Ophthalmol Vis Sci. 2013 Jan;54(1):201-10 [23150615] Free Radic Res. 2013 Feb;47(2):71-3 [23153390] Arch Oral Biol. 2013 May;58(5):500-4 [23453083] Phytother Res. 2013 Apr;27(4):493-8 [22627996] PLoS One. 2013;8(6):e67603 [23840748] PLoS One. 2013;8(7):e67985 [23874481] Int J Oncol. 2013 Oct;43(4):1141-50 [23917396] Immunol Cell Biol. 2013 Sep;91(8):503-10 [23897119] Org Lett. 2013 Jul 19;15(14):3582-5 [23808624] PLoS One. 2013;8(9):e75625 [24086592] J Endod. 2013 Nov;39(11):1401-6 [24139262] Biochim Biophys Acta. 2014 Feb;1840(2):809-17 [23541987] Mass Spectrom Rev. 2014 Mar-Apr;33(2):79-97 [23832618] Cell Death Dis. 2014;5:e1056 [24525732] Oral Dis. 2014 Apr;20(3):e49-56 [23679350] J Biol Chem. 2014 Jun 6;289(23):16176-89 [24764302] J Virol. 2014 Jun;88(12):6751-61 [24696478] Curr Opin Cell Biol. 2015 Apr;33:8-13 [25305438] Head Neck. 2015 Aug;37(8):1187-92 [24797795] Circ Res. 2000 Mar 17;86(5):494-501 [10720409] Am J Med. 2000 Jun 1;108(8):652-9 [10856414] Am J Physiol Lung Cell Mol Physiol. 2000 Dec;279(6):L1005-28 [11076791] Free Radic Biol Med. 2001 Jun 1;30(11):1191-212 [11368918] Nature. 2001 Dec 13;414(6865):813-20 [11742414] Cell Biochem Biophys. 2001;35(2):141-70 [11892789] Int J Radiat Oncol Biol Phys. 2005 Nov 15;63(4):985-90 [16253773] Int J Radiat Oncol Biol Phys. 2006 Mar 1;64(3):784-91 [16198504] Chem Biol Interact. 2006 Mar 10;160(1):1-40 [16430879] Mol Cell. 2006 Mar 17;21(6):732-4 [16543142] Cancer Cell. 2006 Sep;10(3):241-52 [16959615] Int J Dent Hyg. 2006 Sep;4 Suppl 1:15-21; discussion 50-2 [16965529] Antioxid Redox Signal. 2006 Sep-Oct;8(9-10):1791-806 [16987032] Proc Natl Acad Sci U S A. 1990 Jun;87(12):4533-7 [2352934] Proc Soc Exp Biol Med. 1991 Nov;198(2):675-82 [1656469] Xenobiotica. 1991 Aug;21(8):1053-65 [1723229] Chem Res Toxicol. 1991 Nov-Dec;4(6):592-604 [1807442] Proc Soc Exp Biol Med. 1993 Jan;202(1):1-8 [8424089] Arch Biochem Biophys. 1993 Jun;303(2):339-48 [8390220] Free Radic Biol Med. 1993 Dec;15(6):621-7 [8138188] Proc Natl Acad Sci U S A. 1995 Jun 6;92(12):5258-65 [7777494] Free Radic Biol Med. 1995 Oct;19(4):499-504 [7590400] Diabetes Care. 1996 Mar;19(3):257-67 [8742574] Exp Physiol. 1997 Mar;82(2):291-5 [9129943] Oncogene. 1999 Jan 7;18(1):173-80 [9926932] Annu Rev Pharmacol Toxicol. 1999;39:67-101 [10331077] Cancer Res. 2005 Feb 1;65(3):1105-11 [15705913] Mol Carcinog. 2005 Mar;42(3):127-41 [15584022] Cell. 2005 Feb 25;120(4):483-95 [15734681] Nature. 2005 Jul 7;436(7047):123-7 [16001073] Int J Radiat Biol. 2005 May;81(5):397-408 [16076755] Br J Dermatol. 2005 Sep;153(3):526-30 [16120137] J Clin Periodontol. 2005 Oct;32(10):1062-8 [16174269] J Biol Chem. 2005 Oct 28;280(43):36088-98 [16135518] J Oral Maxillofac Surg. 2010 Aug;68(8):1732-9 [20493616] Autophagy. 2010 Aug;6(6):725-37 [20523123] Oral Oncol. 2010 Nov;46(11):822-8 [20920876] PLoS One. 2011;6(1):e14558 [21283807] Environ Sci Technol. 2011 Apr 1;45(7):2818-25 [21375262] Mol Carcinog. 2011 Sep;50(9):732-7 [21520294] Cutan Ocul Toxicol. 2011 Sep;30(3):217-20 [21345164] Free Radic Biol Med. 2006 Nov 15;41(10):1521-33 [17045920] PLoS Med. 2006 Oct;3(10):e420 [17020408] Biochim Biophys Acta. 2006 Dec;1763(12):1755-66 [17034877] Cancer Metastasis Rev. 2006 Dec;25(4):695-705 [17160708] Antioxid Redox Signal. 2007 Mar;9(3):343-53 [17184177] Free Radic Biol Med. 2007 Jun 1;42(11):1632-50 [17462532] Proc Natl Acad Sci U S A. 2007 May 1;104(18):7540-5 [17456604] J Dent Res. 2007 Aug;86(8):718-22 [17652198] Cell Mol Life Sci. 2007 Sep;64(17):2202-10 [17605000] Biochem Biophys Res Commun. 2007 Nov 3;362(4):816-21 [17822677] Hepatogastroenterology. 2007 Sep;54(78):1701-4 [18019698] Br J Cancer. 2008 Feb 12;98(3):580-6 [18231107] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/odi.12300 ER - TY - JOUR T1 - Success rates for consent and collection of prenatal biological specimens in an epidemiologic survey of child health. AN - 1760888029; 26407522 AB - The National Children's Study (NCS) Vanguard Study began enrollment in January 2009 as an initial pilot study for a planned large-scale, longitudinal U.S. cohort study of the effect of environmental influences on child health and development, with biological and environmental sample collection conducted in seven locations from April 2009 to October 2010. We sought to determine rates of consent for, and success of collection of, maternal and paternal biospecimens before and during pregnancy in the NCS Vanguard Study. Samples of blood, saliva, vaginal swabs, urine, hair, and nails were collected before and during pregnancy. All specimens were sent to a central repository for processing, storage, and quality assessment. Of 780 pregnant women asked to consent to sample collection, 773 (>99%) agreed, and of 295 nonpregnant women, 292 (99%) agreed. Of 440 fathers asked to consent to sample collection, 435 (99%) agreed. Frequency of successful collection of biospecimens varied depending on sample and visit type. In descending order, the ranges over all visit types of the proportion of expected samples successfully collected from women were: urine, 92.5 to 95.7%; hair, 89.6 to 92.5%; vaginal swab, 84.2 to 88.5%; blood, 74.9 to 78.5%; 2-day saliva, 65.8 to 81.6%; and nails, 76.4 to 76.7%. For fathers, rates were highest for urine (94.9%) and lowest for hair (63.0%). High rates of consent for and collection of a wide variety of biospecimens can be achieved in prospective epidemiologic cohort studies of pregnant women. Ease of sample collection may be a primary factor influencing successful biospecimen collection. © 2015 Wiley Periodicals, Inc. JF - Birth defects research. Part A, Clinical and molecular teratology AU - Abdul-Rahman, Omar A AU - Rodriguez, Beatriz AU - Wadlinger, Sandra R AU - Slutsman, Julia AU - Boyle, Elizabeth B AU - Merrill, Lori S AU - Botkin, Jeffrey AU - Moye, Jack AD - Department of Pediatrics, University of Mississippi Medical Center, Jackson, Mississippi. ; University of Hawaii, Honolulu, Hawaii. ; The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania. ; National Children's Study Program Office, NICHD, NIH, Bethesda, Maryland. ; Westat, Rockville, Maryland. ; University of Utah, Salt Lake City, Utah. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 47 EP - 54 VL - 106 IS - 1 KW - Index Medicus KW - consent rate KW - genetic samples KW - biological specimens KW - epidemiologic research methods KW - biospecimens KW - United States KW - Family Characteristics KW - Epidemiologic Studies KW - Humans KW - Health Surveys KW - Adult KW - Pregnancy Trimesters KW - Child KW - Male KW - Female KW - Pregnancy KW - Specimen Handling -- statistics & numerical data KW - Informed Consent -- statistics & numerical data KW - Prenatal Diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1760888029?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Birth+defects+research.+Part+A%2C+Clinical+and+molecular+teratology&rft.atitle=Success+rates+for+consent+and+collection+of+prenatal+biological+specimens+in+an+epidemiologic+survey+of+child+health.&rft.au=Abdul-Rahman%2C+Omar+A%3BRodriguez%2C+Beatriz%3BWadlinger%2C+Sandra+R%3BSlutsman%2C+Julia%3BBoyle%2C+Elizabeth+B%3BMerrill%2C+Lori+S%3BBotkin%2C+Jeffrey%3BMoye%2C+Jack&rft.aulast=Abdul-Rahman&rft.aufirst=Omar&rft.date=2016-01-01&rft.volume=106&rft.issue=1&rft.spage=47&rft.isbn=&rft.btitle=&rft.title=Birth+defects+research.+Part+A%2C+Clinical+and+molecular+teratology&rft.issn=1542-0760&rft_id=info:doi/10.1002%2Fbdra.23455 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-10-11 N1 - Date created - 2016-01-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Int J Epidemiol. 2002 Dec;31(6):1235-9 [12540728] Int J Epidemiol. 2015 Aug;44(4):1249-62 [25906783] JAMA. 1998 Dec 9;280(22):1951-8 [9851484] Environ Health Perspect. 2006 Oct;114(10):1617-21 [17035153] Acta Obstet Gynecol Scand. 2006;85(12):1420-5 [17260215] Cult Med Psychiatry. 2007 Dec;31(4):445-72 [17968637] Epidemiology. 2008 Mar;19(2):251-7 [18223485] Paediatr Perinat Epidemiol. 2009 Jul;23 Suppl 1:39-50 [19490444] Dimens Crit Care Nurs. 2010 Sep-Oct;29(5):242-5 [20703134] Mt Sinai J Med. 2011 Jan-Feb;78(1):1-10 [21259259] Transfusion. 2011 Feb;51(2):234-6 [21309775] Clin Chem. 2011 Apr;57(4):540-4 [21205881] BMC Med Ethics. 2011;12:11 [21672210] Paediatr Perinat Epidemiol. 2011 Sep;25(5):413-24 [21819423] Theor Med Bioeth. 2011 Oct;32(5):315-26 [21850398] N Engl J Med. 2011 Oct 6;365(14):1304-14 [21991952] Thyroid. 2013 Aug;23(8):927-37 [23488982] Environ Health Perspect. 2013 Oct;121(10):A298-303 [24218659] Clin Chem Lab Med. 2013 Dec;51(12):2287-94 [23924524] Environ Res. 2014 Feb;129:32-8 [24529000] Chemosphere. 2014 Jul;106:20-7 [24485817] Fertil Steril. 2014 May;101(5):1359-66 [24534276] Am J Epidemiol. 2014 Jun 1;179(11):1366-74 [24793429] Nutrients. 2014 Jun;6(6):2165-78 [24892374] BMC Biotechnol. 2014;14:60 [24980254] Genome Biol. 2014;15(2):R22 [24490717] JAMA Pediatr. 2014 Nov;168(11):1063-9 [25265089] Acta Odontol Scand. 1972 Mar;30(1):49-66 [4504438] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/bdra.23455 ER - TY - JOUR T1 - Prospects for gene-engineered T cell immunotherapy for solid cancers. AN - 1760880329; 26735408 AB - Adoptive transfer of receptor-engineered T cells has produced impressive results in treating patients with B cell leukemias and lymphomas. This success has captured public imagination and driven academic and industrial researchers to develop similar 'off-the-shelf' receptors targeting shared antigens on epithelial cancers, the leading cause of cancer-related deaths. However, the successful treatment of large numbers of people with solid cancers using this strategy is unlikely to be straightforward. Receptor-engineered T cells have the potential to cause lethal toxicity from on-target recognition of normal tissues, and there is a paucity of truly tumor-specific antigens shared across tumor types. Here we offer our perspective on how expanding the use of genetically redirected T cells to treat the majority of patients with solid cancers will require major technical, manufacturing and regulatory innovations centered around the development of autologous gene therapies targeting private somatic mutations. JF - Nature medicine AU - Klebanoff, Christopher A AU - Rosenberg, Steven A AU - Restifo, Nicholas P AD - Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 26 EP - 36 VL - 22 IS - 1 KW - Antigens, Neoplasm KW - 0 KW - Receptors, Antigen, T-Cell KW - Index Medicus KW - Adoptive Transfer KW - Humans KW - Antigens, Neoplasm -- immunology KW - Receptors, Antigen, T-Cell -- immunology KW - Genetic Engineering -- methods KW - Immunotherapy, Adoptive -- methods KW - Neoplasms -- therapy KW - Receptors, Antigen, T-Cell -- genetics KW - T-Lymphocytes KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1760880329?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+medicine&rft.atitle=Prospects+for+gene-engineered+T+cell+immunotherapy+for+solid+cancers.&rft.au=Klebanoff%2C+Christopher+A%3BRosenberg%2C+Steven+A%3BRestifo%2C+Nicholas+P&rft.aulast=Klebanoff&rft.aufirst=Christopher&rft.date=2016-01-01&rft.volume=22&rft.issue=1&rft.spage=26&rft.isbn=&rft.btitle=&rft.title=Nature+medicine&rft.issn=1546-170X&rft_id=info:doi/10.1038%2Fnm.4015 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-24 N1 - Date created - 2016-01-07 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nm.4015 ER - TY - JOUR T1 - Novel technologies and emerging biomarkers for personalized cancer immunotherapy. AN - 1760878932; 26788324 AB - The culmination of over a century's work to understand the role of the immune system in tumor control has led to the recent advances in cancer immunotherapies that have resulted in durable clinical responses in patients with a variety of malignancies. Cancer immunotherapies are rapidly changing traditional treatment paradigms and expanding the therapeutic landscape for cancer patients. However, despite the current success of these therapies, not all patients respond to immunotherapy and even those that do often experience toxicities. Thus, there is a growing need to identify predictive and prognostic biomarkers that enhance our understanding of the mechanisms underlying the complex interactions between the immune system and cancer. Therefore, the Society for Immunotherapy of Cancer (SITC) reconvened an Immune Biomarkers Task Force to review state of the art technologies, identify current hurdlers, and make recommendations for the field. As a product of this task force, Working Group 2 (WG2), consisting of international experts from academia and industry, assembled to identify and discuss promising technologies for biomarker discovery and validation. Thus, this WG2 consensus paper will focus on the current status of emerging biomarkers for immune checkpoint blockade therapy and discuss novel technologies as well as high dimensional data analysis platforms that will be pivotal for future biomarker research. In addition, this paper will include a brief overview of the current challenges with recommendations for future biomarker discovery. JF - Journal for immunotherapy of cancer AU - Yuan, Jianda AU - Hegde, Priti S AU - Clynes, Raphael AU - Foukas, Periklis G AU - Harari, Alexandre AU - Kleen, Thomas O AU - Kvistborg, Pia AU - Maccalli, Cristina AU - Maecker, Holden T AU - Page, David B AU - Robins, Harlan AU - Song, Wenru AU - Stack, Edward C AU - Wang, Ena AU - Whiteside, Theresa L AU - Zhao, Yingdong AU - Zwierzina, Heinz AU - Butterfield, Lisa H AU - Fox, Bernard A AD - Memorial Sloan-Kettering Cancer Center, 1275 New York Ave Box 386, New York, NY 10065 USA. ; Genentech, Inc., 1 DNA Way South, San Francisco, CA 94080 USA. ; Bristol-Myers Squibb, 3551 Lawrenceville Road, Princeton, NJ 08648 USA. ; Center of Experimental Therapeutics and Ludwig Institute of Cancer Research, University Hospital of Lausanne, Rue du Bugnon 21, 1011 Lausanne, Switzerland ; Department of Pathology, University of Athens Medical School, "Attikon" University Hospital, 1st Rimini St, 12462 Haidari, Greece. ; Center of Experimental Therapeutics and Ludwig Institute of Cancer Research, University Hospital of Lausanne, Rue du Bugnon 21, 1011 Lausanne, Switzerland. ; Epiontis GmbH, Rudower Chaussee 29, 12489 Berlin, Germany. ; Netherlands Cancer Institute, Postbus 90203, 1006 BE Amsterdam, Netherlands. ; Italian Network for Biotherapy of Tumors (NIBIT)-Laboratory, c/o Medical Oncology and Immunotherapy, University Hospital of Siena, V.le Bracci,16, Siena, 53100 Italy. ; Stanford University Medical Center, 299 Campus Drive, Stanford, CA 94303 USA. ; Earle A. Chiles Research Institute, Providence Cancer Center, 4805 NE Glisan Street, Portland, OR 97213 USA. ; Adaptive Technologies, Inc., 1551 Eastlake Avenue East Suite 200, Seattle, WA 98102 USA. ; AstraZeneca, One MedImmune Way, Gaithersburg, MD 20878 USA. ; PerkinElmer, 68 Elm Street, Hopkinton, MA 01784 USA. ; Sidra Medical and Research Center, PO Box 26999, Doha, Qatar. ; University of Pittsburgh Cancer Institute, 5117 Centre Ave, Suite 1.27, Pittsburgh, PA 15213 USA. ; National Cancer Institute, 9609 Medical Center Drive, Rockville, MD 20850 USA. ; Innsbruck Medical University, Medizinische Klinik, Anichstrasse 35, Innsbruck, A-6020 Austria. ; Department of Medicine, Surgery and Immunology, University of Pittsburgh Cancer Institute, 5117 Centre Avenue, Pittsburgh, PA 15213 USA. Y1 - 2016 PY - 2016 DA - 2016 SP - 3 VL - 4 KW - Task Force KW - Immune monitoring KW - Immune checkpoint blockade KW - Cancer immunotherapy KW - Biomarkers KW - Bioinformatics KW - Technology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1760878932?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+for+immunotherapy+of+cancer&rft.atitle=Novel+technologies+and+emerging+biomarkers+for+personalized+cancer+immunotherapy.&rft.au=Yuan%2C+Jianda%3BHegde%2C+Priti+S%3BClynes%2C+Raphael%3BFoukas%2C+Periklis+G%3BHarari%2C+Alexandre%3BKleen%2C+Thomas+O%3BKvistborg%2C+Pia%3BMaccalli%2C+Cristina%3BMaecker%2C+Holden+T%3BPage%2C+David+B%3BRobins%2C+Harlan%3BSong%2C+Wenru%3BStack%2C+Edward+C%3BWang%2C+Ena%3BWhiteside%2C+Theresa+L%3BZhao%2C+Yingdong%3BZwierzina%2C+Heinz%3BButterfield%2C+Lisa+H%3BFox%2C+Bernard+A&rft.aulast=Yuan&rft.aufirst=Jianda&rft.date=2016-01-01&rft.volume=4&rft.issue=&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=Journal+for+immunotherapy+of+cancer&rft.issn=&rft_id=info:doi/10.1186%2Fs40425-016-0107-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-20 N1 - Date created - 2016-01-20 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/s40425-016-0107-3 ER - TY - JOUR T1 - Evaluation in Cameroon of a Novel, Simplified Methodology to Assist Molecular Microbiological Analysis of V. cholerae in Resource-Limited Settings. AN - 1760863624; 26735969 AB - Vibrio cholerae is endemic in South Asia and Africa where outbreaks of cholera occur widely and are particularly associated with poverty and poor sanitation. Knowledge of the genetic diversity of toxigenic V. cholerae isolates, particularly in Africa, remains scarce. The constraints in improving this understanding is not only the lack of regular cholera disease surveillance, but also the lack of laboratory capabilities in endemic countries to preserve, store and ship isolates in a timely manner. We evaluated the use of simplified sample preservation methods for molecular characterization using multi-locus variable-number tandem-repeat analysis (MLVA) for differentiation of Vibrio cholerae genotypes. Forty-seven V. cholerae isolates and 18 enriched clinical specimens (e.g. stool specimens after enrichment in broth) from cholera outbreaks in Cameroon were preserved on Whatman filter paper for DNA extraction. The samples were collected from two geographically distinct outbreaks in the Far North of Cameroon (FNC) in June 2014 and October 2014. In addition, a convenience sample of 14 isolates from the Philippines and 8 from Mozambique were analyzed. All 87 DNAs were successfully analyzed including 16 paired samples, one a cultured isolate and the other the enriched specimen from which the isolate was collected. Genotypic results were identical between 15 enriched specimens and their culture isolates and the other pair differed at single locus. Two closely related, but distinct clonal complexes were identified among the Cameroonian specimens from 2014. Collecting V. cholerae using simplified laboratory methods in remote and low-resource settings allows for subsequent advanced molecular characterization of V. cholerae O1. These simplified DNA preservation methods identify V. cholerae and make possible timely information regarding the genetic diversity of V. cholerae; our results set the stage for continued molecular epidemiological research to better understand the transmission and dissemination of V. cholerae in Africa and elsewhere worldwide. JF - PLoS neglected tropical diseases AU - Debes, Amanda K AU - Ateudjieu, Jerome AU - Guenou, Etienne AU - Guenou, Etiene AU - Lopez, Anna Lena AU - Bugayong, Mark Philip AU - Retiban, Pearl Joy AU - Garrine, Marcelino AU - Mandomando, Inacio AU - Li, Shan AU - Stine, O Colin AU - Sack, David A AD - Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, United States of America. ; Department of Biomedical Sciences, University of Dschang, Dschang, Cameroon. ; M.A. SANTE (Meilleur Accès aux Soins de Santé), Yaoundé, Cameroon. ; University of the Philippines Manila-National Institutes of Health, Manila, Philippines. ; Centro de Investigação em Saúde de Manhiça (CISM), Maputo, Mozambique. ; University of Maryland School of Medicine, Baltimore, Maryland, United States of America. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 1 VL - 10 IS - 1 KW - Index Medicus KW - Paper KW - Mozambique -- epidemiology KW - Infant KW - Genotype KW - Genetic Variation KW - Cameroon -- epidemiology KW - Humans KW - Infant, Newborn KW - Molecular Epidemiology -- methods KW - Philippines -- epidemiology KW - Child, Preschool KW - Minisatellite Repeats KW - Vibrio cholerae -- genetics KW - Cholera -- microbiology KW - Cholera -- epidemiology KW - Molecular Typing -- methods KW - Vibrio cholerae -- isolation & purification KW - Specimen Handling -- methods KW - Vibrio cholerae -- classification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1760863624?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+neglected+tropical+diseases&rft.atitle=Evaluation+in+Cameroon+of+a+Novel%2C+Simplified+Methodology+to+Assist+Molecular+Microbiological+Analysis+of+V.+cholerae+in+Resource-Limited+Settings.&rft.au=Debes%2C+Amanda+K%3BAteudjieu%2C+Jerome%3BGuenou%2C+Etienne%3BGuenou%2C+Etiene%3BLopez%2C+Anna+Lena%3BBugayong%2C+Mark+Philip%3BRetiban%2C+Pearl+Joy%3BGarrine%2C+Marcelino%3BMandomando%2C+Inacio%3BLi%2C+Shan%3BStine%2C+O+Colin%3BSack%2C+David+A&rft.aulast=Debes&rft.aufirst=Amanda&rft.date=2016-01-01&rft.volume=10&rft.issue=1&rft.spage=e0004307&rft.isbn=&rft.btitle=&rft.title=PLoS+neglected+tropical+diseases&rft.issn=1935-2735&rft_id=info:doi/10.1371%2Fjournal.pntd.0004307 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-02 N1 - Date created - 2016-01-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: FEMS Microbiol Lett. 2008 Nov;288(2):196-201 [18811655] PLoS One. 2015;10(5):e0119824 [25973880] J Clin Microbiol. 2000 Nov;38(11):4145-51 [11060082] Biochim Biophys Acta. 2003 Oct 15;1639(2):65-79 [14559113] J Clin Microbiol. 1991 Jun;29(6):1171-4 [1864936] FEMS Immunol Med Microbiol. 1998 Mar;20(3):201-7 [9566491] Appl Environ Microbiol. 2006 Jun;72(6):4096-104 [16751520] J Clin Microbiol. 2007 Mar;45(3):736-46 [17182751] Infect Immun. 2007 May;75(5):2645-7 [17283087] Lett Appl Microbiol. 2007 Oct;45(4):371-5 [17897378] Emerg Infect Dis. 2008 May;14(5):831-3 [18439375] J Bacteriol. 2010 Sep;192(17):4367-76 [20585059] Epidemiol Infect. 2012 Mar;140(3):510-8 [21676349] Emerg Infect Dis. 2012 Jun;18(6):925-31 [22607971] BMC Microbiol. 2012;12:82 [22624829] Clin Infect Dis. 2012 Dec;55 Suppl 4:S294-302 [23169941] Lancet. 2013 Jul 20;382(9888):209-22 [23680352] PLoS One. 2013;8(9):e74829 [24066154] Emerg Infect Dis. 2014 Jan;20(1):54-60 [24377372] PLoS Negl Trop Dis. 2014 Jun;8(6):e2898 [24901522] MBio. 2014;5(6). pii: e01824-14. doi: 10.1128/mBio.01824-14 [25538191] Erratum In: PLoS Negl Trop Dis. 2016 Mar;10(3):e0004573 [26999288] PLoS Negl Trop Dis. 2016 Mar 08;10(3):e0004537 [26954780] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pntd.0004307 ER - TY - JOUR T1 - Expression of Human NSAID Activated Gene 1 in Mice Leads to Altered Mammary Gland Differentiation and Impaired Lactation. AN - 1760857082; 26745373 AB - Transgenic mice expressing human non-steroidal anti-inflammatory drug activated gene 1 (NAG-1) have less adipose tissue, improved insulin sensitivity, lower insulin levels and are resistant to dietary induced obesity. The hNAG-1 expressing mice are more metabolically active with a higher energy expenditure. This study investigates female reproduction in the hNAG-1 transgenic mice and finds the female mice are fertile but have reduced pup survival after birth. Examination of the mammary glands in these mice suggests that hNAG-1 expressing mice have altered mammary epithelial development during pregnancy, including reduced occupancy of the fat pad and increased apoptosis via TUNEL positive cells on lactation day 2. Pups nursing from hNAG-1 expressing dams have reduced milk spots compared to pups nursing from WT dams. When CD-1 pups were cross-fostered with hNAG-1 or WT dams; reduced milk volume was observed in pups nursing from hNAG-1 dams compared to pups nursing from WT dams in a lactation challenge study. Milk was isolated from WT and hNAG-1 dams, and the milk was found to have secreted NAG-1 protein (approximately 25 ng/mL) from hNAG-1 dams. The WT dams had no detectable hNAG-1 in the milk. A decrease in non-esterified free fatty acids in the milk of hNAG-1 dams was observed. Altered milk composition suggests that the pups were receiving inadequate nutrients during perinatal development. To examine this hypothesis serum was isolated from pups and clinical chemistry points were measured. Male and female pups nursing from hNAG-1 dams had reduced serum triglyceride concentrations. Microarray analysis revealed that genes involved in lipid metabolism are differentially expressed in hNAG-1 mammary glands. Furthermore, the expression of Cidea/CIDEA that has been shown to regulate milk lipid secretion in the mammary gland was reduced in hNAG-1 mammary glands. This study suggests that expression of hNAG-1 in mice leads to impaired lactation and reduces pup survival due to altered milk quality and quantity. JF - PloS one AU - Binder, April K AU - Kosak, Justin P AU - Janardhan, Kyathanahalli S AU - Janhardhan, Kyathanahalli S AU - Moser, Glenda AU - Eling, Thomas E AU - Korach, Kenneth S AD - Reproductive and Developmental Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America. ; Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America. ; Integrated Laboratory Systems Incorporated, Research Triangle Park, North Carolina, United States of America. Y1 - 2016 PY - 2016 DA - 2016 SP - 1 VL - 11 IS - 1 KW - Apoptosis Regulatory Proteins KW - 0 KW - Cidea protein, mouse KW - GDF15 protein, human KW - Growth Differentiation Factor 15 KW - Index Medicus KW - Animals KW - Humans KW - Adiposity KW - Apoptosis Regulatory Proteins -- metabolism KW - Gene Expression KW - Cell Differentiation KW - Mice, Transgenic KW - Male KW - Lipid Metabolism KW - Female KW - Mammary Glands, Animal -- cytology KW - Mammary Glands, Animal -- physiology KW - Growth Differentiation Factor 15 -- biosynthesis KW - Growth Differentiation Factor 15 -- genetics KW - Lactation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1760857082?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Expression+of+Human+NSAID+Activated+Gene+1+in+Mice+Leads+to+Altered+Mammary+Gland+Differentiation+and+Impaired+Lactation.&rft.au=Binder%2C+April+K%3BKosak%2C+Justin+P%3BJanardhan%2C+Kyathanahalli+S%3BJanhardhan%2C+Kyathanahalli+S%3BMoser%2C+Glenda%3BEling%2C+Thomas+E%3BKorach%2C+Kenneth+S&rft.aulast=Binder&rft.aufirst=April&rft.date=2016-01-01&rft.volume=11&rft.issue=1&rft.spage=e0146518&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0146518 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-06 N1 - Date created - 2016-01-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Int J Obes (Lond). 2014 Dec;38(12):1555-64 [24531647] J Mammary Gland Biol Neoplasia. 1997 Oct;2(4):343-54 [10935022] Braz J Med Biol Res. 2002 May;35(5):617-22 [12011949] Cancer Res. 2002 May 15;62(10):2798-805 [12019156] Nat Genet. 2003 Sep;35(1):49-56 [12910269] Development. 2004 Jul;131(13):3047-55 [15163627] Physiol Rev. 1980 Oct;60(4):1049-106 [7001510] Cancer Res. 1987 Nov 15;47(22):6052-7 [3664507] Development. 1995 Jul;121(7):2079-90 [7635053] Fundam Appl Toxicol. 1996 Nov;34(1):56-66 [8937892] Res Commun Mol Pathol Pharmacol. 1997 May;96(2):179-92 [9226752] Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11514-9 [9326641] J Mammary Gland Biol Neoplasia. 1999 Jan;4(1):79-88 [10219908] Cell Tissue Res. 1999 Jul;297(1):103-10 [10398887] J Lipid Res. 2006 Apr;47(4):734-44 [16449762] Mol Cancer Ther. 2006 May;5(5):1352-61 [16731769] Gastroenterology. 2006 Nov;131(5):1553-60 [17101328] Nat Med. 2007 Nov;13(11):1333-40 [17982462] Lancet. 2008 Jan 19;371(9608):243-60 [18207566] J Cell Physiol. 2009 Apr;219(1):57-68 [19086032] Mol Endocrinol. 2009 Mar;23(3):402-11 [19131506] Reprod Toxicol. 2009 Jun;27(3-4):365-72 [19429407] Mol Endocrinol. 1997 Jun;11(6):801-11 [9171243] Environ Health Perspect. 2009 Jul;117(7):1155-61 [19654927] J Nutr. 2009 Dec;139(12):2257-65 [19812223] J Clin Invest. 2010 Apr;120(4):963-72 [20364094] Wiley Interdiscip Rev Syst Biol Med. 2010 Jan-Feb;2(1):117-25 [20836015] Handb Exp Pharmacol. 2010;(198):3-27 [20839083] FASEB J. 2010 Dec;24(12):4660-7 [20667977] Cold Spring Harb Perspect Biol. 2011 Jan;3(1):a003277 [20810549] PLoS One. 2011;6(6):e20895 [21698114] Environ Health Perspect. 2011 Aug;119(8):1070-6 [21501981] Nat Med. 2012 Feb;18(2):235-43 [22245780] PLoS One. 2012;7(4):e34868 [22514681] Biochem Pharmacol. 2013 Mar 1;85(5):597-606 [23220538] PLoS One. 2013;8(2):e55174 [23468844] Mediators Inflamm. 2013;2013:641851 [23737651] Wiley Interdiscip Rev Dev Biol. 2012 Jul-Aug;1(4):533-57 [22844349] Pediatrics. 2013 Sep;132(3):e796-809 [23979084] Obesity (Silver Spring). 2014 May;22(5):1256-63 [24124102] Ther Drug Monit. 2014 Oct;36(5):590-6 [24695355] Erratum In: PLoS One. 2016;11(3):e0151504 [26963910] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0146518 ER - TY - JOUR T1 - Protein dynamics and the all-ferrous [Fe4 S4 ] cluster in the nitrogenase iron protein. AN - 1760855666; 26271353 AB - In nitrogen fixation by Azotobacter vinelandii nitrogenase, the iron protein (FeP) binds to and subsequently transfers electrons to the molybdenum-FeP, which contains the nitrogen fixation site, along with hydrolysis of two ATPs. However, the nature of the reduced state cluster is not completely clear. While reduced FeP is generally thought to contain an [Fe4 S4 ](1+) cluster, evidence also exists for an all-ferrous [Fe4 S4 ](0) cluster. Since the former indicates a single electron is transferred per two ATPs hydrolyzed while the latter indicates two electrons could be transferred per two ATPs hydrolyzed, an all-ferrous [Fe4 S4 ](0) cluster in FeP is potenially two times more efficient. However, the 1+/0 reduction potential has been measured in the protein at both 460 and 790 mV, causing the biological significance to be questioned. Here, "density functional theory plus Poisson Boltzmann" calculations show that cluster movement relative to the protein surface observed in the crystal structures could account for both measured values. In addition, elastic network mode analysis indicates that such movement occurs in low frequency vibrations of the protein, implying protein dynamics might lead to variations in reduction potential. Furthermore, the different reductants used in the conflicting measurements of the reduction potential could be differentially affecting the protein dynamics. Moreover, even if the all-ferrous cluster is not the biologically relevant cluster, mutagenesis to stabilize the conformation with the more exposed cluster may be useful for bioengineering more efficient enzymes. © 2015 The Authors Protein Science published by Wiley Periodicals, Inc. on behalf of The Protein Society. JF - Protein science : a publication of the Protein Society AU - Tan, Ming-Liang AU - Perrin, B Scott AU - Niu, Shuqiang AU - Huang, Qi AU - Ichiye, Toshiko AD - Department of Chemistry, Georgetown University, Washington, District of Columbia, 20057. ; Laboratory of Computational Biology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, 20892. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 12 EP - 18 VL - 25 IS - 1 KW - Iron-Sulfur Proteins KW - 0 KW - Nitrogenase KW - EC 1.18.6.1 KW - Index Medicus KW - metalloprotein KW - elastic network mode analysis KW - reduction potentials KW - iron-sulfur proteins KW - Azotobacter vinelandii -- enzymology KW - Electron Transport KW - Models, Molecular KW - Protein Conformation KW - Iron-Sulfur Proteins -- chemistry KW - Nitrogenase -- chemistry KW - Nitrogenase -- metabolism KW - Iron-Sulfur Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1760855666?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Protein+science+%3A+a+publication+of+the+Protein+Society&rft.atitle=Protein+dynamics+and+the+all-ferrous+%5BFe4+S4+%5D+cluster+in+the+nitrogenase+iron+protein.&rft.au=Tan%2C+Ming-Liang%3BPerrin%2C+B+Scott%3BNiu%2C+Shuqiang%3BHuang%2C+Qi%3BIchiye%2C+Toshiko&rft.aulast=Tan&rft.aufirst=Ming-Liang&rft.date=2016-01-01&rft.volume=25&rft.issue=1&rft.spage=12&rft.isbn=&rft.btitle=&rft.title=Protein+science+%3A+a+publication+of+the+Protein+Society&rft.issn=1469-896X&rft_id=info:doi/10.1002%2Fpro.2772 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-30 N1 - Date created - 2016-01-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nucleic Acids Res. 2000 Jan 1;28(1):235-42 [10592235] Biochemistry. 2000 Feb 1;39(4):641-8 [10651628] Curr Opin Chem Biol. 2000 Oct;4(5):559-66 [11006545] Biochemistry. 2001 Jan 23;40(3):651-6 [11170381] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10037-41 [11517324] J Am Chem Soc. 2002 Oct 16;124(41):12100-1 [12371842] J Am Chem Soc. 2003 Feb 19;125(7):1923-36 [12580620] Crit Rev Biochem Mol Biol. 2003;38(4):351-84 [14551236] Proc Natl Acad Sci U S A. 2003 Nov 11;100(23):13253-8 [14585932] Science. 1983 Aug 19;221(4612):709-13 [6879170] Biochemistry. 1991 Sep 24;30(38):9201-10 [1892829] Biochemistry. 1994 Jun 7;33(22):6739-49 [8204609] Biochemistry. 1997 Dec 23;36(51):16065-73 [9405040] Biophys J. 2005 Jul;89(1):167-78 [15879477] Science. 2005 Aug 26;309(5739):1377-80 [16123301] Proc Natl Acad Sci U S A. 2006 Nov 14;103(46):17131-6 [17085583] Inorg Chem. 2009 Apr 6;48(7):2735-47 [19326927] Proteins. 2010 Oct;78(13):2798-808 [20635418] Inorg Chem. 2011 May 16;50(10):4322-6 [21476577] J Biol Inorg Chem. 2013 Jan;18(1):103-10 [23229112] J Comput Chem. 2013 Mar 15;34(7):576-82 [23115132] Biochemistry. 2013 May 7;52(18):3022-4 [23607577] Biochemistry. 2013 Jul 16;52(28):4791-9 [23815521] J Am Chem Soc. 2015 Jan 14;137(1):146-9 [25522159] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/pro.2772 ER - TY - JOUR T1 - Cardiovascular toxicity after antiangiogenic therapy in persons older than 65 years with advanced renal cell carcinoma. AN - 1760855628; 26439451 AB - Sorafenib and sunitinib are oral vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) approved in 2005 and 2006, respectively, for the treatment of patients with renal cell carcinoma (RCC). A population-based, observational cohort study of the cardiovascular risk of VEGFR TKI therapy in elderly RCC patients was conducted. Using the Surveillance, Epidemiology, and End Results-Medicare database, this study analyzed patients who were 66 years old or older and were diagnosed with RCC from 2000 to 2009. The incidence of cardiovascular adverse events, including congestive heart failure and cardiomyopathy (CHF/CM), acute myocardial infarction (AMI), stroke, and cardiovascular deaths, was examined through December 2010. A Cox proportional hazards model was created to calculate the hazard ratio (HR), and adjustments were made for age, sex, comorbidity, and the use of other systemic therapy. A total of 171 of 670 patients who received sunitinib or sorafenib had cardiovascular events. The incidence rates for CHF/CM, AMI, and stroke were 0.87, 0.14, and 0.14 per 1000 person-days, respectively. Sunitinib or sorafenib use was associated with an increased risk of cardiovascular events (HR, 1.38; 95% confidence interval [CI], 1.02-1.87) and especially stroke (HR, 2.84; 95% CI, 1.52-5.31) in comparison with 788 patients diagnosed with advanced RCC from 2007 to 2009 who were eligible for Part D but did not receive either agent. In subgroup analyses, patients who were 66 to 74 years old at diagnosis had the highest increased risk of stroke associated with the use of either or both drugs. Sunitinib and sorafenib might be associated with an increased risk of cardiovascular events and particularly stroke. © 2015 American Cancer Society. JF - Cancer AU - Jang, Sekwon AU - Zheng, Chaoyi AU - Tsai, Huei-Ting AU - Fu, Alex Z AU - Barac, Ana AU - Atkins, Michael B AU - Freedman, Andrew N AU - Minasian, Lori AU - Potosky, Arnold L AD - Division of Oncology, Inova Dwight and Martha Schar Cancer Institute, Fairfax, Virginia. ; Department of Biostatistics, Bioinformatics, and Biomathematics, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC. ; Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC. ; Division of Cardiology, MedStar Washington Hospital Center, Washington, DC. ; Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, Maryland. ; Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland. Y1 - 2016/01/01/ PY - 2016 DA - 2016 Jan 01 SP - 124 EP - 130 VL - 122 IS - 1 KW - Angiogenesis Inhibitors KW - 0 KW - Indoles KW - Phenylurea Compounds KW - Pyrroles KW - Niacinamide KW - 25X51I8RD4 KW - sorafenib KW - 9ZOQ3TZI87 KW - sunitinib KW - V99T50803M KW - Abridged Index Medicus KW - Index Medicus KW - stroke KW - renal cell carcinoma KW - cardiovascular toxicity KW - Aged, 80 and over KW - Risk Factors KW - Humans KW - SEER Program KW - Incidence KW - Aged KW - United States -- epidemiology KW - Male KW - Female KW - Survival Analysis KW - Proportional Hazards Models KW - Pyrroles -- adverse effects KW - Kidney Neoplasms -- drug therapy KW - Kidney Neoplasms -- blood supply KW - Niacinamide -- administration & dosage KW - Indoles -- adverse effects KW - Niacinamide -- analogs & derivatives KW - Kidney Neoplasms -- epidemiology KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Carcinoma, Renal Cell -- drug therapy KW - Cardiovascular Diseases -- chemically induced KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Phenylurea Compounds -- administration & dosage KW - Angiogenesis Inhibitors -- administration & dosage KW - Carcinoma, Renal Cell -- epidemiology KW - Pyrroles -- administration & dosage KW - Cardiovascular Diseases -- epidemiology KW - Niacinamide -- adverse effects KW - Indoles -- administration & dosage KW - Angiogenesis Inhibitors -- adverse effects KW - Phenylurea Compounds -- adverse effects KW - Carcinoma, Renal Cell -- blood supply UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1760855628?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Cardiovascular+toxicity+after+antiangiogenic+therapy+in+persons+older+than+65+years+with+advanced+renal+cell+carcinoma.&rft.au=Jang%2C+Sekwon%3BZheng%2C+Chaoyi%3BTsai%2C+Huei-Ting%3BFu%2C+Alex+Z%3BBarac%2C+Ana%3BAtkins%2C+Michael+B%3BFreedman%2C+Andrew+N%3BMinasian%2C+Lori%3BPotosky%2C+Arnold+L&rft.aulast=Jang&rft.aufirst=Sekwon&rft.date=2016-01-01&rft.volume=122&rft.issue=1&rft.spage=124&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=1097-0142&rft_id=info:doi/10.1002%2Fcncr.29728 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-06 N1 - Date created - 2016-01-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Epidemiol. 2000 Dec;53(12):1258-67 [11146273] Med Care. 1993 Aug;31(8):732-48 [8336512] N Engl J Med. 2007 Jan 11;356(2):115-24 [17215529] N Engl J Med. 2007 Jan 11;356(2):125-34 [17215530] Br J Cancer. 2007 Jun 18;96(12):1788-95 [17519900] J Clin Oncol. 2008 Nov 10;26(32):5204-12 [18838713] Nat Immunol. 2009 Apr;10(4):356-60 [19295632] J Clin Oncol. 2010 May 1;28(13):2280-5 [20351323] J Clin Oncol. 2011 Sep 1;29(25):3450-6 [21810682] Nat Rev Nephrol. 2014 Mar;10(3):135-45 [24419566] Acta Oncol. 2009;48(1):9-17 [18752081] J Am Heart Assoc. 2014;3(2):e000665 [24755151] Med Care. 2014 May;52(5):e30-8 [22643199] Comment In: Nat Rev Urol. 2015 Nov;12(11):597 [26502989] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/cncr.29728 ER - TY - JOUR T1 - Alkyl Amine Bevirimat Derivatives Are Potent and Broadly Active HIV-1 Maturation Inhibitors AN - 1758248556; PQ0002452972 AB - Concomitant with the release of human immunodeficiency virus type 1 (HIV-1) particles from the infected cell, the viral protease cleaves the Gag polyprotein precursor at a number of sites to trigger virus maturation. We previously reported that a betulinic acid-derived compound, bevirimat (BVM), blocks HIV-1 maturation by disrupting a late step in protease-mediated Gag processing: the cleavage of the capsid-spacer peptide 1 (CA-SP1) intermediate to mature CA. BVM was shown in multiple clinical trials to be safe and effective in reducing viral loads in HIV-1-infected patients. However, naturally occurring polymorphisms in the SP1 region of Gag (e.g., SP1-V7A) led to a variable response in some BVM-treated patients. The reduced susceptibility of SP1-polymorphic HIV-1 to BVM resulted in the discontinuation of its clinical development. To overcome the loss of BVM activity induced by polymorphisms in SP1, we carried out an extensive medicinal chemistry campaign to develop novel maturation inhibitors. In this study, we focused on alkyl amine derivatives modified at the C-28 position of the BVM scaffold. We identified a set of derivatives that are markedly more potent than BVM against an HIV-1 clade B clone (NL4-3) and show robust antiviral activity against a variant of NL4-3 containing the V7A polymorphism in SP1. One of the most potent of these compounds also strongly inhibited a multiclade panel of primary HIV-1 isolates. These data demonstrate that C-28 alkyl amine derivatives of BVM can, to a large extent, overcome the loss of susceptibility imposed by polymorphisms in SP1. JF - Antimicrobial Agents & Chemotherapy AU - Urano, Emiko AU - Ablan, Sherimay D AU - Mandt, Rebecca AU - Pauly, Gary T AU - Sigano, Dina M AU - Schneider, Joel P AU - Martin, David E AU - Nitz, Theodore J AU - Wild, Carl T AU - Freed, Eric O AD - << + $0, efreed@nih.gov. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 190 EP - 197 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 60 IS - 1 SN - 0066-4804, 0066-4804 KW - Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Sp1 protein KW - amines KW - polyproteins KW - Data processing KW - Human immunodeficiency virus KW - Human immunodeficiency virus 1 KW - Proteinase KW - Antiviral activity KW - Clinical trials KW - Gag protein KW - scaffolds KW - A 01340:Antibiotics & Antimicrobials KW - V 22360:AIDS and HIV UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1758248556?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Alkyl+Amine+Bevirimat+Derivatives+Are+Potent+and+Broadly+Active+HIV-1+Maturation+Inhibitors&rft.au=Urano%2C+Emiko%3BAblan%2C+Sherimay+D%3BMandt%2C+Rebecca%3BPauly%2C+Gary+T%3BSigano%2C+Dina+M%3BSchneider%2C+Joel+P%3BMartin%2C+David+E%3BNitz%2C+Theodore+J%3BWild%2C+Carl+T%3BFreed%2C+Eric+O&rft.aulast=Urano&rft.aufirst=Emiko&rft.date=2016-01-01&rft.volume=60&rft.issue=1&rft.spage=190&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.02121-15 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Number of references - 47 N1 - Last updated - 2016-02-29 N1 - SubjectsTermNotLitGenreText - Sp1 protein; polyproteins; amines; Data processing; Proteinase; Antiviral activity; Clinical trials; scaffolds; Gag protein; Human immunodeficiency virus; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1128/AAC.02121-15 ER - TY - JOUR T1 - Diversity of Cyclic Di-GMP-Binding Proteins and Mechanisms AN - 1758248367; PQ0002453076 AB - Cyclic di-GMP (c-di-GMP) synthetases and hydrolases (GGDEF, EAL, and HD-GYP domains) can be readily identified in bacterial genome sequences by using standard bioinformatic tools. In contrast, identification of c-di-GMP receptors remains a difficult task, and the current list of experimentally characterized c-di-GMP-binding proteins is likely incomplete. Several classes of c-di-GMP-binding proteins have been structurally characterized; for some others, the binding sites have been identified; and for several potential c-di-GMP receptors, the binding sites remain to be determined. We present here a comparative structural analysis of c-di-GMP-protein complexes that aims to discern the common themes in the binding mechanisms that allow c-di-GMP receptors to bind it with (sub)micromolar affinities despite the 1,000-fold excess of GTP. The available structures show that most receptors use their Arg and Asp/Glu residues to bind c-di-GMP monomers, dimers, or tetramers with stacked guanine bases. The only exception is the EAL domains that bind c-di-GMP monomers in an extended conformation. We show that in c-di-GMP-binding signature motifs, Arg residues bind to the O-6 and N-7 atoms at the Hoogsteen edge of the guanine base, while Asp/Glu residues bind the N-1 and N-2 atoms at its Watson-Crick edge. In addition, Arg residues participate in stacking interactions with the guanine bases of c-di-GMP and the aromatic rings of Tyr and Phe residues. This may account for the presence of Arg residues in the active sites of every receptor protein that binds stacked c-di-GMP. We also discuss the implications of these structural data for the improved understanding of the c-di-GMP signaling mechanisms. JF - Journal of Bacteriology AU - Chou, Shan-Ho AU - Galperin, Michael Y AD - << + $0, galperin@ncbi.nlm.nih.gov. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 32 EP - 46 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 198 IS - 1 SN - 0021-9193, 0021-9193 KW - Microbiology Abstracts B: Bacteriology KW - Monomers KW - hydrolase KW - Genomes KW - Guanine KW - Data processing KW - Stacking KW - GTP KW - Bioinformatics KW - Aromatics KW - J 02310:Genetics & Taxonomy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1758248367?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=Diversity+of+Cyclic+Di-GMP-Binding+Proteins+and+Mechanisms&rft.au=Chou%2C+Shan-Ho%3BGalperin%2C+Michael+Y&rft.aulast=Chou&rft.aufirst=Shan-Ho&rft.date=2016-01-01&rft.volume=198&rft.issue=1&rft.spage=32&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/10.1128%2FJB.00333-15 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Number of references - 94 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Genomes; hydrolase; Monomers; Guanine; Data processing; Stacking; GTP; Bioinformatics; Aromatics DO - http://dx.doi.org/10.1128/JB.00333-15 ER - TY - JOUR T1 - Priming of the Respiratory Tract with Immunobiotic Lactobacillus plantarum Limits Infection of Alveolar Macrophages with Recombinant Pneumonia Virus of Mice (rK2-PVM) AN - 1758246920; PQ0002453252 AB - Pneumonia virus of mice (PVM) is a natural rodent pathogen that replicates in bronchial epithelial cells and reproduces many clinical and pathological features of the more severe forms of disease associated with human respiratory syncytial virus. In order to track virus-target cell interactions during acute infection in vivo, we developed rK2-PVM, bacterial artificial chromosome-based recombinant PVM strain J3666 that incorporates the fluorescent tag monomeric Katushka 2 (mKATE2). The rK2-PVM pathogen promotes lethal infection in BALB/c mice and elicits characteristic cytokine production and leukocyte recruitment to the lung parenchyma. Using recombinant virus, we demonstrate for the first time PVM infection of both dendritic cells (DCs; CD11c+ major histocompatibility complex class II+) and alveolar macrophages (AMs; CD11c+ sialic acid-binding immunoglobulin-like lectin F+) in vivo and likewise detect mKATE2+ DCs in mediastinal lymph nodes from infected mice. AMs support both active virus replication and production of infectious virions. Furthermore, we report that priming of the respiratory tract with immunobiotic Lactobacillus plantarum, a regimen that results in protection against the lethal inflammatory sequelae of acute respiratory virus infection, resulted in differential recruitment of neutrophils, DCs, and lymphocytes to the lungs in response to rK2-PVM and a reduction from similar to 40% to <10% mKATE2+ AMs in association with a 2-log drop in the release of infectious virions. In contrast, AMs from L. plantarum-primed mice challenged with virus ex vivo exhibited no differential susceptibility to rK2-PVM. Although the mechanisms underlying Lactobacillus-mediated viral suppression remain to be fully elucidated, this study provides insight into the cellular basis of this response. IMPORTANCE Pneumonia virus of mice (PVM) is a natural mouse pathogen that serves as a model for severe human respiratory syncytial virus disease. We have developed a fully functional recombinant PVM strain with a fluorescent reporter protein (rK2-PVM) that permits us to track infection of target cells in vivo. With rK2-PVM, we demonstrate infection of leukocytes in the lung, notably, dendritic cells and alveolar macrophages. Alveolar macrophages undergo productive infection and release infectious virions. We have shown previously that administration of immunobiotic Lactobacillus directly to the respiratory mucosa protects mice from the lethal sequelae of PVM infection in association with profound suppression of the virus-induced inflammatory response. We show here that Lactobacillus administration also limits infection of leukocytes in vivo and results in diminished release of infectious virions from alveolar macrophages. This is the first study to provide insight into the cellular basis of the antiviral impact of immunobiotic L. plantarum. JF - Journal of Virology AU - Dyer, Kimberly D AU - Drummond, Rebecca A AU - Rice, Tyler A AU - Percopo, Caroline M AU - Brenner, Todd A AU - Barisas, Derek AG AU - Karpe, Kendal A AU - Moore, Martin L AU - Rosenberg, Helene F AD - << + $0, hrosenberg@niaid.nih.gov. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 979 EP - 991 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 90 IS - 2 SN - 0022-538X, 0022-538X KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts; Genetics Abstracts; Virology & AIDS Abstracts KW - Macrophages KW - Virions KW - Epithelial cells KW - Plant protection KW - Lactobacillus plantarum KW - Mucosa KW - Animal models KW - Major histocompatibility complex KW - Lymphocytes KW - Infection KW - CD11c antigen KW - Leukocyte migration KW - Dendritic cells KW - Lactobacillus KW - Cytokines KW - Pneumonia virus of mice KW - Respiratory tract KW - Parenchyma KW - Replication KW - Complications KW - Leukocytes (neutrophilic) KW - Lectins KW - Pathogens KW - Human respiratory syncytial virus KW - Lymph nodes KW - Alveoli KW - Inflammation KW - Lung KW - Cell interactions KW - Plant viruses KW - Pneumonia KW - G 07800:Plants and Algae KW - V 22320:Replication KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1758246920?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Priming+of+the+Respiratory+Tract+with+Immunobiotic+Lactobacillus+plantarum+Limits+Infection+of+Alveolar+Macrophages+with+Recombinant+Pneumonia+Virus+of+Mice+%28rK2-PVM%29&rft.au=Dyer%2C+Kimberly+D%3BDrummond%2C+Rebecca+A%3BRice%2C+Tyler+A%3BPercopo%2C+Caroline+M%3BBrenner%2C+Todd+A%3BBarisas%2C+Derek+AG%3BKarpe%2C+Kendal+A%3BMoore%2C+Martin+L%3BRosenberg%2C+Helene+F&rft.aulast=Dyer&rft.aufirst=Kimberly&rft.date=2016-01-01&rft.volume=90&rft.issue=2&rft.spage=979&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.02279-15 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Number of references - 75 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Virions; Macrophages; Epithelial cells; Plant protection; Mucosa; Animal models; Major histocompatibility complex; Lymphocytes; Infection; CD11c antigen; Leukocyte migration; Dendritic cells; Cytokines; Respiratory tract; Parenchyma; Complications; Replication; Leukocytes (neutrophilic); Lectins; Pathogens; Alveoli; Lymph nodes; Inflammation; Lung; Cell interactions; Plant viruses; Pneumonia; Lactobacillus; Lactobacillus plantarum; Pneumonia virus of mice; Human respiratory syncytial virus DO - http://dx.doi.org/10.1128/JVI.02279-15 ER - TY - JOUR T1 - Clinicopathological and prognostic significance of RECQL5 helicase expression in breast cancers. AN - 1754521796; 26586793 AB - RECQL5 is a member of the RecQ family of DNA helicases and has key roles in homologous recombination, base excision repair, replication and transcription. The clinicopathological significance of RECQL5 expression in breast cancer is unknown. In this study, we have evaluated RECQL5 mRNA expression in 1977 breast cancers, and RECQL5 protein level in 1902 breast cancers [Nottingham Tenovus series (n = 1650) and ER- cohort (n = 252)]. Expression levels were correlated to aggressive phenotypes and survival outcomes. High RECQL5 mRNA expression was significantly associated with high histological grade (P = 0.007), HER2 overexpression (P = 0.032), ER+/HER2-/high proliferation genefu subtype (P < 0.0001), integrative molecular clusters (intClust 1and 9) (P < 0.0001) and poor survival (P < 0.0001). In subgroup analysis, high RECQL5 mRNA level remains significantly associated with poor BCSS in ER+ cohort (P < 0.0001) but not in ER- cohort (P = 0.116). At the protein level, in tumours with low RAD51, high RECQL5 level was significantly associated with high histological grade (P < 0.0001), higher mitotic index (P = 0.008), dedifferentiation (P = 0.025), pleomorphism (P = 0.027) and poor survival (P = 0.003). In subgroup analysis, high RECQL5/low RAD51 remains significantly associated with poor BCSS in ER+ cohort (P = 0.010), but not in ER- cohort (P = 0.628). In multivariate analysis, high RECQL5 mRNA and high RECQL5/low RAD51 nuclear protein coexpression independently influenced survival (P = 0.022) in whole cohort and in the ER+ subgroup. Preclinically, we show that exogenous expression of RECQL5 in MCF10A cells can drive proliferation supporting an oncogenic function for RECQL5 in breast cancer. We conclude that RECQL5 is a promising biomarker in breast cancer. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Carcinogenesis AU - Arora, Arvind AU - Abdel-Fatah, Tarek M A AU - Agarwal, Devika AU - Doherty, Rachel AU - Croteau, Deborah L AU - Moseley, Paul M AU - Hameed, Khalid AU - Green, Andrew AU - Aleskandarany, Mohammed A AU - Rakha, Emad A AU - Patterson, Karl AU - Ball, Graham AU - Chan, Stephen Y T AU - Ellis, Ian O AU - Bohr, Vilhelm A AU - Bryant, Helen E AU - Madhusudan, Srinivasan AD - Academic Unit of Oncology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham NG51PB, UK, Department of Oncology, Nottingham University Hospitals, Nottingham NG51PB, UK. ; Department of Oncology, Nottingham University Hospitals, Nottingham NG51PB, UK. ; School of Science and Technology, Nottingham Trent University, Clifton campus, Nottingham NG11 8NS, UK. ; Academic Unit of Oncology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham NG51PB, UK. ; Laboratory of Molecular Gerontology, Biomedical Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MA 21224-6825, USA. ; Department of Pathology, School of Medicine, University of Nottingham, Nottingham NG51PB, UK and. ; Academic Unit of Molecular Oncology, Department of Oncology, Medical School Sheffield Cancer Research Centre, University of Sheffield, Sheffield S10 2RX, UK. ; Academic Unit of Oncology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham NG51PB, UK, Department of Oncology, Nottingham University Hospitals, Nottingham NG51PB, UK, srinivasan.madhusudan@nottingham.ac.uk. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 63 EP - 71 VL - 37 IS - 1 KW - Antigens, Neoplasm KW - 0 KW - Biomarkers, Tumor KW - DNA-Binding Proteins KW - RECQL5 protein, human KW - RNA, Messenger KW - RAD51 protein, human KW - EC 2.7.7.- KW - Rad51 Recombinase KW - RecQ Helicases KW - EC 3.6.4.12 KW - DNA Topoisomerases, Type II KW - EC 5.99.1.3 KW - DNA topoisomerase II alpha KW - Index Medicus KW - DNA Topoisomerases, Type II -- biosynthesis KW - Neoplasm Invasiveness KW - Biomarkers, Tumor -- genetics KW - DNA Topoisomerases, Type II -- genetics KW - Antigens, Neoplasm -- biosynthesis KW - Humans KW - Prognosis KW - DNA-Binding Proteins -- biosynthesis KW - DNA-Binding Proteins -- genetics KW - RNA, Messenger -- genetics KW - RNA, Messenger -- biosynthesis KW - Gene Knockdown Techniques KW - Tissue Array Analysis KW - MCF-7 Cells KW - Antigens, Neoplasm -- genetics KW - Rad51 Recombinase -- genetics KW - Immunohistochemistry KW - Biomarkers, Tumor -- biosynthesis KW - Female KW - Rad51 Recombinase -- biosynthesis KW - Breast Neoplasms -- genetics KW - Breast Neoplasms -- pathology KW - RecQ Helicases -- biosynthesis KW - RecQ Helicases -- genetics KW - Breast Neoplasms -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1754521796?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Clinicopathological+and+prognostic+significance+of+RECQL5+helicase+expression+in+breast+cancers.&rft.au=Arora%2C+Arvind%3BAbdel-Fatah%2C+Tarek+M+A%3BAgarwal%2C+Devika%3BDoherty%2C+Rachel%3BCroteau%2C+Deborah+L%3BMoseley%2C+Paul+M%3BHameed%2C+Khalid%3BGreen%2C+Andrew%3BAleskandarany%2C+Mohammed+A%3BRakha%2C+Emad+A%3BPatterson%2C+Karl%3BBall%2C+Graham%3BChan%2C+Stephen+Y+T%3BEllis%2C+Ian+O%3BBohr%2C+Vilhelm+A%3BBryant%2C+Helen+E%3BMadhusudan%2C+Srinivasan&rft.aulast=Arora&rft.aufirst=Arvind&rft.date=2016-01-01&rft.volume=37&rft.issue=1&rft.spage=63&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgv163 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-15 N1 - Date created - 2016-01-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nucleic Acids Res. 2010 May;38(9):2904-16 [20081208] DNA Repair (Amst). 2010 Sep 4;9(9):964-75 [20643585] DNA Repair (Amst). 2010 Mar 2;9(3):345-53 [20080450] J Biol Chem. 2010 May 21;285(21):15739-45 [20348101] Nucleic Acids Res. 2012 Feb;40(4):1621-35 [22013166] DNA Repair (Amst). 2012 Jul 1;11(7):624-35 [22633600] Nature. 2012 Jun 21;486(7403):346-52 [22522925] J Biol Chem. 2012 Jul 6;287(28):23808-18 [22645136] Mol Biol Cell. 2012 Nov;23(21):4273-85 [22973052] Crit Rev Biochem Mol Biol. 2013 May-Jun;48(3):289-99 [23627586] Nat Rev Cancer. 2013 Aug;13(8):542-58 [23842644] Biosci Rep. 2011 Oct;31(5):363-9 [21210765] Tumour Biol. 2014 Mar;35(3):2669-73 [24213927] Tumour Biol. 2014 Apr;35(4):3255-9 [24287950] Cell. 2014 May 22;157(5):1037-49 [24836610] Antioxid Redox Signal. 2014 Dec 1;21(16):2262-8 [25111287] Neoplasia. 2014 Nov;16(11):982-91 [25425972] Tumour Biol. 2014 Dec;35(12):12201-4 [25394896] Nat Rev Cancer. 2015 Mar;15(3):137-51 [25693836] Mol Oncol. 2015 Mar;9(3):569-85 [25468710] Mol Cancer Ther. 2015 Apr;14(4):1057-65 [25673821] Cancer Res. 1999 Aug 1;59(15):3547-51 [10446958] Nucleic Acids Res. 2000 Apr 1;28(7):1647-55 [10710432] Genet Mol Res. 2015;14(1):1899-902 [25867335] Clin Cancer Res. 2004 Nov 1;10(21):7252-9 [15534099] Mol Cell Biol. 2005 May;25(9):3431-42 [15831450] J Natl Cancer Inst. 2005 Aug 17;97(16):1180-4 [16106022] Nucleic Acids Res. 2006;34(18):5217-31 [17003056] Cell Mol Life Sci. 2007 Sep;64(17):2306-22 [17571213] Genes Dev. 2007 Dec 1;21(23):3073-84 [18003859] Biochem J. 2008 Aug 1;413(3):505-16 [18419580] Mol Biol Cell. 2009 Jan;20(1):114-23 [18987339] Nucleic Acids Res. 2009 May;37(8):2645-57 [19270065] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgv163 ER - TY - JOUR T1 - Common genetic variation and survival after colorectal cancer diagnosis: a genome-wide analysis. AN - 1754521661; 26586795 AB - Genome-wide association studies have identified several germline single nucleotide polymorphisms (SNPs) significantly associated with colorectal cancer (CRC) incidence. Common germline genetic variation may also be related to CRC survival. We used a discovery-based approach to identify SNPs related to survival outcomes after CRC diagnosis. Genome-wide genotyping arrays were conducted for 3494 individuals with invasive CRC enrolled in six prospective cohort studies (median study-specific follow-up = 4.2-8.1 years). In pooled analyses, we used Cox regression to assess SNP-specific associations with CRC-specific and overall survival, with additional analyses stratified by stage at diagnosis. Top findings were followed-up in independent studies. A P value threshold of P < 5×10(-8) in analyses combining discovery and follow-up studies was required for genome-wide significance. Among individuals with distant-metastatic CRC, several SNPs at 6p12.1, nearest the ELOVL5 gene, were statistically significantly associated with poorer survival, with the strongest associations noted for rs209489 [hazard ratio (HR) = 1.8, P = 7.6×10(-10) and HR = 1.8, P = 3.7×10(-9) for CRC-specific and overall survival, respectively). No SNPs were statistically significantly associated with survival among all cases combined or in cases without distant-metastases. SNPs in 6p12.1/ELOVL5 were associated with survival outcomes in individuals with distant-metastatic CRC, and merit further follow-up for functional significance. Findings from this genome-wide association study highlight the potential importance of genetic variation in CRC prognosis and provide clues to genomic regions of potential interest. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Carcinogenesis AU - Phipps, Amanda I AU - Passarelli, Michael N AU - Chan, Andrew T AU - Harrison, Tabitha A AU - Jeon, Jihyoun AU - Hutter, Carolyn M AU - Berndt, Sonja I AU - Brenner, Hermann AU - Caan, Bette J AU - Campbell, Peter T AU - Chang-Claude, Jenny AU - Chanock, Stephen J AU - Cheadle, Jeremy P AU - Curtis, Keith R AU - Duggan, David AU - Fisher, David AU - Fuchs, Charles S AU - Gala, Manish AU - Giovannucci, Edward L AU - Hayes, Richard B AU - Hoffmeister, Michael AU - Hsu, Li AU - Jacobs, Eric J AU - Jansen, Lina AU - Kaplan, Richard AU - Kap, Elisabeth J AU - Maughan, Timothy S AU - Potter, John D AU - Schoen, Robert E AU - Seminara, Daniela AU - Slattery, Martha L AU - West, Hannah AU - White, Emily AU - Peters, Ulrike AU - Newcomb, Polly A AD - Epidemiology Department, University of Washington, Seattle, WA 98195, USA, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, aiphipps@u.washington.edu. ; Epidemiology Department, University of Washington, Seattle, WA 98195, USA, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. ; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA, Channing Division of Network Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA. ; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg 69120, Germany, German Cancer Consortium (DKTK), Heidelberg 69120, Germany. ; Division of Research, Kaiser Permanente Medical Care Program of Northern California, Oakland, CA 94612, USA. ; Epidemiology Research Program, American Cancer Society, Atlanta, GA 30303, USA. ; Division of Cancer Epidemiology, Unit of Genetic Epidemiology, German Cancer Research Center (DKFZ), Heidelberg 69120, Germany. ; Institute of Cancer and Genetics, School of Medicine, Cardiff University, Cardiff CF14 4XN, UK. ; Translational Genomics Research Institute, Phoenix, AZ 85004, USA. ; MRC Clinical Trials Unit, University College London, Aviation House, London WC2B 6NH, UK. ; Channing Division of Network Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA, Department of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215, USA. ; Harvard School of Public Health, Boston, MA 02115, USA. ; Channing Division of Network Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA, Harvard School of Public Health, Boston, MA 02115, USA. ; Division of Epidemiology, Department of Population Health, New York University School of Medicine, New York, NY 10016, USA. ; German Cancer Consortium (DKTK), Heidelberg 69120, Germany. ; Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, Biostatistics Department, University of Washington, Seattle, WA 98195, USA. ; Division of Clinical Epidemiology and Aging Research, German Cancer Research Center (DKFZ), Heidelberg 69120, Germany. ; Gray Institute for Radiation Oncology and Biology, University of Oxford, Oxford OX3 7DQ, UK. ; Epidemiology Department, University of Washington, Seattle, WA 98195, USA, Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA, Centre for Public Health Research, Massey University, Wellington 6140, New Zealand. ; Department of Medicine and Epidemiology, University of Pittsburgh Medical Center, Pittsburgh, PA 15213, USA. ; Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA, and. ; Department of Internal Medicine, University of Utah Health Sciences Center, Salt Lake City, UT 84132, USA. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 87 EP - 95 VL - 37 IS - 1 KW - Index Medicus KW - Genetic Variation KW - Prospective Studies KW - Aged, 80 and over KW - Humans KW - Cohort Studies KW - Prognosis KW - Aged KW - Middle Aged KW - Male KW - Female KW - Genome-Wide Association Study KW - Colorectal Neoplasms -- diagnosis KW - Colorectal Neoplasms -- mortality KW - Colorectal Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1754521661?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Common+genetic+variation+and+survival+after+colorectal+cancer+diagnosis%3A+a+genome-wide+analysis.&rft.au=Phipps%2C+Amanda+I%3BPassarelli%2C+Michael+N%3BChan%2C+Andrew+T%3BHarrison%2C+Tabitha+A%3BJeon%2C+Jihyoun%3BHutter%2C+Carolyn+M%3BBerndt%2C+Sonja+I%3BBrenner%2C+Hermann%3BCaan%2C+Bette+J%3BCampbell%2C+Peter+T%3BChang-Claude%2C+Jenny%3BChanock%2C+Stephen+J%3BCheadle%2C+Jeremy+P%3BCurtis%2C+Keith+R%3BDuggan%2C+David%3BFisher%2C+David%3BFuchs%2C+Charles+S%3BGala%2C+Manish%3BGiovannucci%2C+Edward+L%3BHayes%2C+Richard+B%3BHoffmeister%2C+Michael%3BHsu%2C+Li%3BJacobs%2C+Eric+J%3BJansen%2C+Lina%3BKaplan%2C+Richard%3BKap%2C+Elisabeth+J%3BMaughan%2C+Timothy+S%3BPotter%2C+John+D%3BSchoen%2C+Robert+E%3BSeminara%2C+Daniela%3BSlattery%2C+Martha+L%3BWest%2C+Hannah%3BWhite%2C+Emily%3BPeters%2C+Ulrike%3BNewcomb%2C+Polly+A&rft.aulast=Phipps&rft.aufirst=Amanda&rft.date=2016-01-01&rft.volume=37&rft.issue=1&rft.spage=87&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgv161 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-15 N1 - Date created - 2016-01-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Am J Public Health. 2012 Sep;102(9):1791-7 [22873481] Lancet. 2011 Jun 18;377(9783):2103-14 [21641636] Gastroenterology. 2013 Apr;144(4):799-807.e24 [23266556] Hepatogastroenterology. 2013 Jul-Aug;60(125):1164-8 [23803379] Lancet Oncol. 2014 May;15(6):631-9 [24703531] Mol Biol Rep. 2014 May;41(5):2989-97 [24449368] Clin Res Hepatol Gastroenterol. 2012 Feb;36(1):78-83 [22133576] JAMA. 2009 Aug 12;302(6):649-58 [19671906] Cancer Epidemiol Biomarkers Prev. 2009 Sep;18(9):2492-500 [19690179] Clin Cancer Res. 2010 Jul 15;16(14):3754-9 [20628028] Am J Physiol Gastrointest Liver Physiol. 2009 Oct;297(4):G632-40 [19696144] Nat Genet. 2010 Nov;42(11):973-7 [20972440] Genet Epidemiol. 2010 Dec;34(8):816-34 [21058334] Cancer Epidemiol Biomarkers Prev. 2010 Dec;19(12):3131-9 [20978172] Ann Intern Med. 2011 Jan 4;154(1):22-30 [21200035] BMC Cancer. 2010;10:670 [21129217] Cancer Res. 1997 Jan 1;57(1):75-80 [8988044] J Womens Health. 1997 Feb;6(1):49-62 [9065374] Control Clin Trials. 1998 Feb;19(1):61-109 [9492970] PLoS Genet. 2011 Jun;7(6):e1002105 [21655089] J Lipid Res. 2009 Mar;50(3):412-23 [18838740] Eur J Cancer. 2011 Jul;47(11):1699-707 [21402474] Genes Chromosomes Cancer. 2011 Nov;50(11):875-86 [21910156] Pharmacogenomics. 2011 Sep;12(9):1257-67 [21919605] J Gastroenterol Hepatol. 2012 Jan;27(1):91-5 [21679251] Hum Genet. 2012 Feb;131(2):217-34 [21761138] J Cell Physiol. 2000 Apr;183(1):129-39 [10699974] Control Clin Trials. 2000 Dec;21(6 Suppl):251S-272S [11189683] Control Clin Trials. 2000 Dec;21(6 Suppl):273S-309S [11189684] Control Clin Trials. 2000 Dec;21(6 Suppl):400S-406S [11189691] Biometrics. 1999 Dec;55(4):997-1004 [11315092] Cancer. 2002 May 1;94(9):2490-501 [12015775] Ann Epidemiol. 2003 Oct;13(9 Suppl):S122-8 [14575944] Am J Epidemiol. 2004 Jan 1;159(1):83-93 [14693663] J Clin Oncol. 2004 Sep 15;22(18):3758-65 [15365072] J Natl Cancer Inst. 2004 Oct 6;96(19):1420-5 [15467030] Am J Nurs. 1978 Jun;78(6):1039-40 [248266] Am J Nurs. 1980 Jul;80(7):1333 [6901582] N Engl J Med. 1989 Jul 20;321(3):129-35 [2664509] Lancet. 1991 Aug 24;338(8765):464-8 [1678444] N Engl J Med. 1996 Dec 5;335(23):1727-32 [8929264] Gastroenterology. 2012 Jul;143(1):51-4.e4 [22580541] Cancer Epidemiol Biomarkers Prev. 2006 Jan;15(1):99-107 [16434594] Oncogene. 2006 Mar 13;25(11):1639-48 [16550164] Int J Cancer. 2007 May 15;120(10):2226-32 [17290389] Hum Mutat. 2007 Oct;28(10):968-77 [17492639] Gastroenterology. 2007 Dec;133(6):2045-9 [18054576] Nat Genet. 2008 May;40(5):623-30 [18372905] Nat Genet. 2008 Dec;40(12):1426-35 [19011631] Nat Genet. 2013 Feb;45(2):191-6 [23263487] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgv161 ER - TY - JOUR T1 - Occupational Lead Exposure and Associations with Selected Cancers: The Shanghai Men's and Women's Health Study Cohorts. AN - 1754093789; 26091556 AB - Epidemiologic studies of occupational lead exposure have suggested increased risks of cancers of the stomach, lung, kidney, brain, and meninges; however, the totality of the evidence is inconsistent. We investigated the relationship between occupational lead exposure and cancer incidence at the five abovementioned sites in two prospective cohorts in Shanghai, China. Annual job/industry-specific estimates of lead fume and lead dust exposure, derived from a statistical model combining expert lead intensity ratings with inspection measurements, were applied to the lifetime work histories of participants from the Shanghai Women's Health Study (SWHS; n = 73,363) and the Shanghai Men's Health Study (SMHS; n = 61,379) to estimate cumulative exposure to lead fume and lead dust. These metrics were then combined into an overall occupational lead exposure variable. Cohort-specific relative hazard rate ratios (RRs) and 95% confidence intervals (CIs) comparing exposed and unexposed participants were estimated using Cox proportional hazards regression and combined by meta-analysis. The proportions of SWHS and SMHS participants with estimated occupational lead exposure were 8.9% and 6.9%, respectively. Lead exposure was positively associated with meningioma risk in women only (n = 38 unexposed and 9 exposed cases; RR = 2.4; 95% CI: 1.1, 5.0), particularly with above-median cumulative exposure (RR = 3.1; 95% CI: 1.3, 7.4). However, all 12 meningioma cases among men were classified as unexposed to lead. We also observed non-significant associations with lead exposure for cancers of the kidney (n = 157 unexposed and 17 ever exposed cases; RR = 1.4; 95% CI: 0.9, 2.3) and brain (n = 67 unexposed and 10 ever exposed cases; RR = 1.8; 95% CI: 0.7, 4.8) overall. Our findings, though limited by small numbers of cases, suggest that lead is associated with the risk of several cancers in women and men. Liao LM, Friesen MC, Xiang YB, Cai H, Koh DH, Ji BT, Yang G, Li HL, Locke SJ, Rothman N, Zheng W, Gao YT, Shu XO, Purdue MP. 2016. Occupational lead exposure and associations with selected cancers: the Shanghai Men's and Women's Health Study cohorts. Environ Health Perspect 124:97-103; http://dx.doi.org/10.1289/ehp.1408171. JF - Environmental health perspectives AU - Liao, Linda M AU - Friesen, Melissa C AU - Xiang, Yong-Bing AU - Cai, Hui AU - Koh, Dong-Hee AU - Ji, Bu-Tian AU - Yang, Gong AU - Li, Hong-Lan AU - Locke, Sarah J AU - Rothman, Nathaniel AU - Zheng, Wei AU - Gao, Yu-Tang AU - Shu, Xiao-Ou AU - Purdue, Mark P AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 97 EP - 103 VL - 124 IS - 1 KW - Lead KW - 2P299V784P KW - Index Medicus KW - Prospective Studies KW - Meningioma -- epidemiology KW - Humans KW - China -- epidemiology KW - Adult KW - Confidence Intervals KW - Aged KW - Middle Aged KW - Male KW - Female KW - Proportional Hazards Models KW - Lead -- toxicity KW - Occupational Exposure -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1754093789?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Occupational+Lead+Exposure+and+Associations+with+Selected+Cancers%3A+The+Shanghai+Men%27s+and+Women%27s+Health+Study+Cohorts.&rft.au=Liao%2C+Linda+M%3BFriesen%2C+Melissa+C%3BXiang%2C+Yong-Bing%3BCai%2C+Hui%3BKoh%2C+Dong-Hee%3BJi%2C+Bu-Tian%3BYang%2C+Gong%3BLi%2C+Hong-Lan%3BLocke%2C+Sarah+J%3BRothman%2C+Nathaniel%3BZheng%2C+Wei%3BGao%2C+Yu-Tang%3BShu%2C+Xiao-Ou%3BPurdue%2C+Mark+P&rft.aulast=Liao&rft.aufirst=Linda&rft.date=2016-01-01&rft.volume=124&rft.issue=1&rft.spage=97&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1408171 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-12-13 N1 - Date created - 2016-01-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Expo Sci Environ Epidemiol. 2014 Jan-Feb;24(1):9-16 [22910004] Occup Environ Med. 2013 Mar;70(3):164-70 [23322922] Am J Ind Med. 2000 Sep;38(3):295-9 [10940967] J Occup Environ Med. 2002 Jul;44(7):663-8 [12134530] Environ Health Perspect. 2000 Aug;108(8):719-22 [10964791] Am J Ind Med. 2000 Sep;38(3):330-4 [10940972] Am J Ind Med. 2002 Sep;42(3):214-27 [12210690] Mutat Res. 2003 Dec 10;533(1-2):121-33 [14643416] Mutat Res. 1993 Jan;285(1):117-24 [7678125] Regul Toxicol Pharmacol. 1995 Oct;22(2):162-71 [8577951] J Occup Environ Med. 1996 Feb;38(2):131-6 [8673517] Epidemiol Rev. 1995;17(2):382-414 [8654518] Scand J Work Environ Health. 1995 Dec;21(6):460-9 [8824752] J Occup Environ Med. 1998 Nov;40(11):937-42 [9830598] Am J Ind Med. 1999 Jul;36(1):70-4 [10361589] Am J Epidemiol. 2005 Dec 1;162(11):1123-31 [16236996] Int J Cancer. 2006 Sep 1;119(5):1136-44 [16570286] Cancer Epidemiol Biomarkers Prev. 2006 Dec;15(12):2514-20 [17164378] Environ Res. 2007 May;104(1):85-95 [16996054] Am J Epidemiol. 2007 Nov 1;166(9):1005-14 [17690218] Cancer Epidemiol Biomarkers Prev. 2009 Jun;18(6):1841-8 [19505917] Environ Health Perspect. 2010 Oct;118(10):1355-62 [20562050] J Occup Environ Hyg. 2011 Sep;8(9):520-32 [21793732] PLoS One. 2011;6(7):e20432 [21799727] Occup Environ Med. 2011 Oct;68(10):723-8 [21217163] Cancer Epidemiol Biomarkers Prev. 2012 Jan;21(1):191-201 [22086884] Occup Environ Med. 2012 Feb;69(2):87-92 [22039095] Ann Epidemiol. 2012 Apr;22(4):270-6 [22285868] Int J Epidemiol. 2015 Jun;44(3):810-8 [25733578] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1289/ehp.1408171 ER - TY - JOUR T1 - hERG Blockade by Iboga Alkaloids. AN - 1754092385; 25636206 AB - The iboga alkaloids are a class of naturally occurring and synthetic compounds, some of which modify drug self-administration and withdrawal in humans and preclinical models. Ibogaine, the prototypic iboga alkaloid that is utilized clinically to treat addictions, has been associated with QT prolongation, torsades de pointes and fatalities. hERG blockade as IKr was measured using the whole-cell patch clamp technique in HEK 293 cells. This yielded the following IC50 values: ibogaine manufactured by semisynthesis via voacangine (4.09 ± 0.69 µM) or by extraction from T. iboga (3.53 ± 0.16 µM); ibogaine's principal metabolite noribogaine (2.86 ± 0.68 µM); and voacangine (2.25 ± 0.34 µM). In contrast, the IC50 of 18-methoxycoronaridine, a product of rational synthesis and current focus of drug development was >50 µM. hERG blockade was voltage dependent for all of the compounds, consistent with low-affinity blockade. hERG channel binding affinities (K i) for the entire set of compounds, including 18-MC, ranged from 0.71 to 3.89 µM, suggesting that 18-MC binds to the hERG channel with affinity similar to the other compounds, but the interaction produces substantially less hERG blockade. In view of the extended half-life of noribogaine, these results may relate to observations of persistent QT prolongation and cardiac arrhythmia at delayed intervals of days following ibogaine ingestion. The apparent structure-activity relationships regarding positions of substitutions on the ibogamine skeleton suggest that the iboga alkaloids might provide an informative paradigm for investigation of the structural biology of the hERG channel. JF - Cardiovascular toxicology AU - Alper, Kenneth AU - Bai, Rong AU - Liu, Nian AU - Fowler, Steven J AU - Huang, Xi-Ping AU - Priori, Silvia G AU - Ruan, Yanfei AD - Departments of Psychiatry and Neurology, New York University School of Medicine, New York, NY, 10016, USA. ; National Clinical Research Center for Cardiovascular Diseases and Department of Cardiology, Beijing An Zhen Hospital, Capital Medical University, Beijing, 100029, China. ; Division of Cardiology, Department of Medicine, New York University School of Medicine, New York, NY, 10016, USA. ; National Institute of Mental Health Psychoactive Drug Screening Program (NIMH PDSP), Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC, 27599, USA. ; National Clinical Research Center for Cardiovascular Diseases and Department of Cardiology, Beijing An Zhen Hospital, Capital Medical University, Beijing, 100029, China. ruanyanfei@hotmail.com. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 14 EP - 22 VL - 16 IS - 1 KW - 18-methoxycoronaridine KW - 0 KW - Alkaloids KW - Ether-A-Go-Go Potassium Channels KW - Plant Extracts KW - Potassium Channel Blockers KW - noribogaine KW - Ibogaine KW - 3S814I130U KW - voacangine KW - 510-22-5 KW - Index Medicus KW - 18-Methoxycoronaridine (18-MC) KW - hERG KW - Noribogaine KW - Iboga alkaloid KW - Toxicology KW - Ibogaine -- toxicity KW - Patch-Clamp Techniques KW - Ibogaine -- chemical synthesis KW - Dose-Response Relationship, Drug KW - Humans KW - HEK293 Cells KW - Ibogaine -- chemistry KW - Plant Extracts -- chemistry KW - Ibogaine -- analogs & derivatives KW - Ibogaine -- pharmacology KW - Ibogaine -- pharmacokinetics KW - Structure-Activity Relationship KW - Potassium Channel Blockers -- pharmacology KW - Tabernaemontana -- chemistry KW - Alkaloids -- pharmacology KW - Ether-A-Go-Go Potassium Channels -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1754092385?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cardiovascular+toxicology&rft.atitle=hERG+Blockade+by+Iboga+Alkaloids.&rft.au=Alper%2C+Kenneth%3BBai%2C+Rong%3BLiu%2C+Nian%3BFowler%2C+Steven+J%3BHuang%2C+Xi-Ping%3BPriori%2C+Silvia+G%3BRuan%2C+Yanfei&rft.aulast=Alper&rft.aufirst=Kenneth&rft.date=2016-01-01&rft.volume=16&rft.issue=1&rft.spage=14&rft.isbn=&rft.btitle=&rft.title=Cardiovascular+toxicology&rft.issn=1559-0259&rft_id=info:doi/10.1007%2Fs12012-015-9311-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-30 N1 - Date created - 2016-01-05 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s12012-015-9311-5 ER - TY - JOUR T1 - Establishing the "Biological Relevance" of Dipentyl Phthalate Reductions in Fetal Rat Testosterone Production and Plasma and Testis Testosterone Levels. AN - 1754085634; 26454885 AB - Phthalate esters (PEs) constitute a large class of compounds that are used for many consumer product applications. Many of the C2-C7 di-ortho PEs reduce fetal testicular hormone and gene expression levels in rats resulting in adverse effects seen later in life but it appears that relatively large reductions in fetal testosterone (T) levels and testis gene expression may be required to adversely affect reproductive development (Hannas, B. R., Lambright, C. S., Furr, J., Evans, N., Foster, P. M., Gray, E. L., and Wilson, V. S. (2012). Genomic biomarkers of phthalate-induced male reproductive developmental toxicity: a targeted RT-PCR array approach for defining relative potency. Toxicol. Sci. 125, 544-557). The objectives of this study were (1) to model the relationships between changes in fetal male rat plasma testosterone (PT), T levels in the testis (TT), T production (PROD), and testis gene expression with the reproductive malformation rates, and (2) to quantify the "biologically relevant reductions" (BRRs) in fetal T necessary to induce adverse effects in the offspring. In the fetal experiment, Harlan Sprague-Dawley rats were dosed with dipentyl phthalate (DPeP) at 0, 11, 33, 100, and 300 mg/kg/day from gestational days (GD) 14-18 and fetal testicular T, PT levels, and T Prod and gene expression were assessed on GD 18. In the postnatal experiment, rats were dosed with DPeP from GD 8-18 and reproductive development was monitored through adulthood. The dose-response curves for TT levels (ED(50) = 53 mg/kg) and T PROD (ED(50) = 45 mg/kg) were similar, whereas PT was reduced at ED50 = 19 mg/kg. When the reductions in TPROD and Insl3 mRNA were compared with the postnatal effects of in utero DPeP, dose-related reproductive alterations were noted when T PROD and Insl3 mRNA were reduced by >45% and 42%, respectively. The determination of BRR levels may enable risk assessors to utilize fetal endocrine data to help establish points of departure for quantitative risk assessments. Published by Oxford University Press on behalf of the Society of Toxicology 2015. This work is written by US Government employees and is in the public domain in the US. JF - Toxicological sciences : an official journal of the Society of Toxicology AU - Gray, Leon Earl AU - Furr, Johnathan AU - Tatum-Gibbs, Katoria R AU - Lambright, Christy AU - Sampson, Hunter AU - Hannas, Bethany R AU - Wilson, Vickie S AU - Hotchkiss, Andrew AU - Foster, Paul M D AD - *Reproductive Toxicology Branch, Toxicology Assessment Division, National Health and Environmental Effects Laboratory, Office of Research and Development, U.S. Environmental Protection Agency (US EPA), Research Triangle Park, North Carolina 27711; gray.earl@epa.gov. ; *Reproductive Toxicology Branch, Toxicology Assessment Division, National Health and Environmental Effects Laboratory, Office of Research and Development, U.S. Environmental Protection Agency (US EPA), Research Triangle Park, North Carolina 27711; ; NCEA, ORD, USEPA, Washington, District of Columbia; and. ; National Toxicology Program, NIEHS, NIH, DHHS, Research Triangle Park, North Carolina 27709. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 178 EP - 191 VL - 149 IS - 1 KW - Esters KW - 0 KW - Phthalic Acids KW - Testosterone KW - 3XMK78S47O KW - Index Medicus KW - fetal male rat endocrine KW - risk assessment KW - dipentyl phthalate KW - anti-androgen KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Reproduction -- drug effects KW - Dose-Response Relationship, Drug KW - Esters -- toxicity KW - Male KW - Female KW - Prenatal Exposure Delayed Effects KW - Pregnancy KW - Fetus -- drug effects KW - Testis -- metabolism KW - Testis -- drug effects KW - Testosterone -- blood KW - Testosterone -- biosynthesis KW - Testosterone -- analysis KW - Testis -- chemistry KW - Fetus -- metabolism KW - Phthalic Acids -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1754085634?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.atitle=Establishing+the+%22Biological+Relevance%22+of+Dipentyl+Phthalate+Reductions+in+Fetal+Rat+Testosterone+Production+and+Plasma+and+Testis+Testosterone+Levels.&rft.au=Gray%2C+Leon+Earl%3BFurr%2C+Johnathan%3BTatum-Gibbs%2C+Katoria+R%3BLambright%2C+Christy%3BSampson%2C+Hunter%3BHannas%2C+Bethany+R%3BWilson%2C+Vickie+S%3BHotchkiss%2C+Andrew%3BFoster%2C+Paul+M+D&rft.aulast=Gray&rft.aufirst=Leon&rft.date=2016-01-01&rft.volume=149&rft.issue=1&rft.spage=178&rft.isbn=&rft.btitle=&rft.title=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.issn=1096-0929&rft_id=info:doi/10.1093%2Ftoxsci%2Fkfv224 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-11-02 N1 - Date created - 2016-01-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Toxicol Sci. 2000 May;55(1):143-51 [10788569] Toxicol Sci. 2014 Aug 1;140(2):403-24 [24798384] Toxicol Appl Pharmacol. 2000 Oct 15;168(2):174-5 [11032775] Toxicol Sci. 2001 Aug;62(2):236-49 [11452136] J Toxicol Sci. 2002 Feb;27(1):19-33 [11915366] Biol Reprod. 1973 Jun;8(5):560-5 [4713164] Endocrinology. 1978 Apr;102(4):999-1007 [744029] Environ Health Perspect. 1982 Nov;45:3-9 [6754362] Arch Androl. 1987;18(3):215-24 [2823733] Endocrinology. 1989 Jun;124(6):3043-9 [2498065] J Toxicol Sci. 1993 May;18(2):111-24 [8331691] Toxicol Appl Pharmacol. 1994 Nov;129(1):46-52 [7974495] Biol Reprod. 1998 Feb;58(2):520-5 [9475409] Toxicol Sci. 1998 May;43(1):47-60 [9629619] Toxicol Ind Health. 1999 Jan-Mar;15(1-2):80-93 [10188193] Toxicol Appl Pharmacol. 1999 Apr 15;156(2):81-95 [10198273] Birth Defects Res B Dev Reprod Toxicol. 2005 Jun;74(3):277-85 [15954088] Toxicol Sci. 2006 Sep;93(1):189-95 [16763070] Toxicol Sci. 2009 Aug;110(2):411-25 [19482887] Toxicol Sci. 2010 Aug;116(2):640-6 [20484383] Reprod Toxicol. 2010 Sep;30(2):261-70 [20558277] Toxicol Sci. 2011 Mar;120(1):184-93 [21177253] Toxicol Sci. 2011 Apr;120(2):460-74 [21266533] Toxicol Sci. 2011 Sep;123(1):206-16 [21633115] Toxicol Sci. 2012 Feb;125(2):544-57 [22112501] Reprod Toxicol. 2013 Jan;35:1-6 [23146716] Reprod Toxicol. 2013 Dec;42:192-202 [24055997] Toxicol Lett. 2013 Dec 16;223(3):315-21 [23542816] Toxicol Lett. 2013 Dec 16;223(3):271-9 [23558297] Regul Toxicol Pharmacol. 2000 Aug;32(1):42-50 [11029267] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/toxsci/kfv224 ER - TY - JOUR T1 - How Can Mutations Thermostabilize G-Protein-Coupled Receptors? AN - 1753230501; 26547284 AB - Structures of over 30 different G-protein-coupled receptors (GPCRs) have advanced our understanding of cell signaling and have provided a foundation for structure-guided drug design. This exciting progress has required the development of three complementary methods to facilitate GPCR crystallization, one of which is the thermostabilization of receptors by systematic mutagenesis. However, the reason why a particular mutation, or combination of mutations, stabilizes the receptor is not always evident from a static crystal structure. Molecular dynamics (MD) simulations have been used to identify and estimate the energetic factors that affect thermostability through comparing the dynamics of the thermostabilized receptors with structure-based models of the wild-type receptor. The data indicate that receptors are stabilized through a combination of factors, including an increase in receptor rigidity, a decrease in collective motion, reduced stress at specific residues, and the presence of ordered water molecules. Predicting thermostabilizing mutations computationally represents a major challenge for the field. Copyright © 2015 Elsevier Ltd. All rights reserved. JF - Trends in pharmacological sciences AU - Vaidehi, Nagarajan AU - Grisshammer, Reinhard AU - Tate, Christopher G AD - Division of Immunology, Beckman Research Institute of the City of Hope, 1500 East Duarte Road, Duarte, CA 91010, USA. Electronic address: NVaidehi@coh.org. ; Membrane Protein Structure Function Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH), Department of Health and Human Services, Rockville, MD 20852, USA. ; Medical Research Council (MRC) Laboratory of Molecular Biology, Cambridge Biomedical Campus, Francis Crick Avenue, Cambridge CB2 0QH, UK. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 37 EP - 46 VL - 37 IS - 1 KW - Receptors, G-Protein-Coupled KW - 0 KW - Index Medicus KW - structure KW - dynamics KW - thermostability KW - GPCR KW - Heating KW - Protein Stability KW - Humans KW - Molecular Dynamics Simulation KW - Structure-Activity Relationship KW - Protein Conformation KW - Receptors, G-Protein-Coupled -- chemistry KW - Receptors, G-Protein-Coupled -- metabolism KW - Receptors, G-Protein-Coupled -- genetics KW - Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753230501?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+pharmacological+sciences&rft.atitle=How+Can+Mutations+Thermostabilize+G-Protein-Coupled+Receptors%3F&rft.au=Vaidehi%2C+Nagarajan%3BGrisshammer%2C+Reinhard%3BTate%2C+Christopher+G&rft.aulast=Vaidehi&rft.aufirst=Nagarajan&rft.date=2016-01-01&rft.volume=37&rft.issue=1&rft.spage=37&rft.isbn=&rft.btitle=&rft.title=Trends+in+pharmacological+sciences&rft.issn=1873-3735&rft_id=info:doi/10.1016%2Fj.tips.2015.09.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-10-27 N1 - Date created - 2016-01-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nature. 2011 Jun 23;474(7352):521-5 [21593763] Science. 2013 Sep 20;341(6152):1387-90 [24030490] Structure. 2011 Sep 7;19(9):1283-93 [21885291] Nature. 2011 Sep 29;477(7366):549-55 [21772288] Chem Rev. 2006 May;106(5):1616-23 [16683747] J Mol Biol. 2007 Oct 5;372(5):1179-88 [17825322] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15682-7 [17905872] Science. 2007 Nov 23;318(5854):1266-73 [17962519] Proc Natl Acad Sci U S A. 2008 Jan 22;105(3):877-82 [18192400] Biophys J. 2008 Mar 15;94(6):2027-42 [18065472] J Mol Biol. 2008 Aug 29;381(2):478-86 [18585736] Nature. 2008 Jul 24;454(7203):486-91 [18594507] J Mol Biol. 2008 Oct 3;382(2):539-55 [18638482] Nature. 2009 May 21;459(7245):356-63 [19458711] Proc Natl Acad Sci U S A. 2009 May 26;106(21):8555-60 [19433801] J Mol Biol. 2009 Jul 10;390(2):262-77 [19422831] Curr Opin Struct Biol. 2009 Aug;19(4):386-95 [19682887] Mol Membr Biol. 2009 Dec;26(8):385-96 [19883298] Biophys J. 2010 Jul 21;99(2):568-77 [20643076] Neuropharmacology. 2011 Jan;60(1):36-44 [20624408] Nature. 2011 Jan 13;469(7329):241-4 [21228877] Proc Natl Acad Sci U S A. 2011 May 17;108(20):8228-32 [21540331] J Mol Biol. 2011 Jun 10;409(3):298-310 [21501622] J Mol Biol. 2011 Oct 28;413(3):628-38 [21907721] J Med Chem. 2012 Mar 8;55(5):1898-903 [22220592] J Med Chem. 2012 Mar 8;55(5):1904-9 [22250781] J Am Chem Soc. 2010 Apr 14;132(14):5205-14 [20235532] Trends Pharmacol Sci. 2012 May;33(5):249-60 [22465153] Structure. 2012 May 9;20(5):841-9 [22579251] Structure. 2012 Jun 6;20(6):967-76 [22681902] Proc Natl Acad Sci U S A. 2012 Aug 14;109(33):13284-9 [22847407] Trends Biochem Sci. 2012 Sep;37(9):343-52 [22784935] Nature. 2012 Oct 25;490(7421):508-13 [23051748] Trends Pharmacol Sci. 2013 Jan;34(1):67-84 [23245528] Annu Rev Pharmacol Toxicol. 2013;53:531-56 [23140243] Nature. 2013 Oct 24;502(7472):575-9 [24056936] Nature. 2013 Nov 7;503(7474):85-90 [24037379] Proc Natl Acad Sci U S A. 2014 Feb 11;111(6):E655-62 [24453215] Science. 2014 Feb 14;343(6172):795-8 [24531972] Biochim Biophys Acta. 2014 May;1837(5):606-13 [24055285] J Phys Chem B. 2014 Mar 27;118(12):3355-65 [24579769] Biophys J. 2014 Jul 15;107(2):422-34 [25028884] Nature. 2014 Jul 31;511(7511):557-62 [25042998] Science. 2014 Aug 29;345(6200):1021-6 [25103405] Nature. 2014 Sep 4;513(7516):124-7 [25043059] Nat Commun. 2014;5:4733 [25203160] J Phys Chem B. 2015 Apr 16;119(15):4917-28 [25807267] Nat Commun. 2015;6:7895 [26205105] Cell. 2013 Jan 31;152(3):532-42 [23374348] Nature. 2013 Feb 14;494(7436):185-94 [23407534] Biochim Biophys Acta. 2013 Apr;1828(4):1293-301 [23337476] J Med Chem. 2013 May 9;56(9):3446-55 [23517028] J Phys Chem B. 2013 Jun 20;117(24):7283-91 [23697892] Nature. 2013 Jul 25;499(7459):438-43 [23863939] Curr Opin Struct Biol. 2011 Aug;21(4):567-72 [21782416] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.tips.2015.09.005 ER - TY - JOUR T1 - Prevalence, prescribed quantities, and trajectory of multiple prescriber episodes for benzodiazepines: A 2-year cohort study. AN - 1753010688; 26652896 AB - Little is known about the use of multiple prescribers for benzodiazepines, which might reflect fragmented patient care and increases the risk of hospital admission for drug dependence or poisoning. Therefore, we aimed to identify the prevalence, prescribed quantities, and trajectory of multiple prescriber episodes for benzodiazepines. We conducted a 2-year cohort study of 1178,361 recipients aged 0-74 years using a large health insurance claims database in Japan. We quantified multiple prescriber episodes for benzodiazepines occurring in ambulatory care settings in a baseline and subsequent year by (1) counting the number of unique providers within a 12-month period, (2) calculating the maximum number of unique providers within a single month, and (3) identifying consecutive overlapping prescriptions of over 30 days duration. Among 58,314 patients with a benzodiazepine prescription during the baseline year, 282 (0.5%) filled prescriptions from four or more providers within a 12-month period, 439 (0.8%) filled prescriptions from three or more providers within a single month, and 757 (1.3%) filled consecutive overlapping prescriptions. The odds for multiple prescriber episodes were significantly higher among patients with multiple chronic conditions. Consecutive overlapping prescriptions had the best accuracy to detect patients with potentially questionable prescribed quantities as well as to predict those with multiple prescriber episodes in the subsequent year. These results highlight the need for pharmacists to increase their involvement in prescription oversight and for health insurance agencies to implement a prescription monitoring program to screen for patients with multiple prescriber episodes for benzodiazepines. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. JF - Drug and alcohol dependence AU - Okumura, Yasuyuki AU - Shimizu, Sayuri AU - Matsumoto, Toshihiko AD - Research Department, Institute for Health Economics and Policy, Association for Health Economics Research and Social Insurance and Welfare, 11 Toyo Kaiji Bldg. 2F, 1-5-11 Nishishimbashi, Minato-ku, Tokyo 105-0003, Japan. Electronic address: yokumura@blue.zero.jp. ; Research Department, Institute for Health Economics and Policy, Association for Health Economics Research and Social Insurance and Welfare, 11 Toyo Kaiji Bldg. 2F, 1-5-11 Nishishimbashi, Minato-ku, Tokyo 105-0003, Japan. ; Department of Drug Dependence Research/Center for Suicide Prevention, National Institute of Mental Health, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-Higashi cho, Kodaira, Tokyo 187-8553, Japan. Y1 - 2016/01/01/ PY - 2016 DA - 2016 Jan 01 SP - 118 EP - 125 VL - 158 KW - Benzodiazepines KW - 12794-10-4 KW - Index Medicus KW - Doctor shopping KW - Prescription monitoring KW - Pharmacoepidemiology KW - Diversion KW - Abuse KW - Young Adult KW - Humans KW - Infant, Newborn KW - Aged KW - Child KW - Child, Preschool KW - Infant KW - Japan -- epidemiology KW - Substance-Related Disorders -- diagnosis KW - Adult KW - Cohort Studies KW - Middle Aged KW - Adolescent KW - Time Factors KW - Female KW - Male KW - Substance-Related Disorders -- epidemiology KW - Prevalence KW - Insurance, Health -- trends KW - Databases, Factual -- trends KW - Benzodiazepines -- adverse effects KW - Benzodiazepines -- administration & dosage KW - Drug Prescriptions UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753010688?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+and+alcohol+dependence&rft.atitle=Prevalence%2C+prescribed+quantities%2C+and+trajectory+of+multiple+prescriber+episodes+for+benzodiazepines%3A+A+2-year+cohort+study.&rft.au=Okumura%2C+Yasuyuki%3BShimizu%2C+Sayuri%3BMatsumoto%2C+Toshihiko&rft.aulast=Okumura&rft.aufirst=Yasuyuki&rft.date=2016-01-01&rft.volume=158&rft.issue=&rft.spage=118&rft.isbn=&rft.btitle=&rft.title=Drug+and+alcohol+dependence&rft.issn=1879-0046&rft_id=info:doi/10.1016%2Fj.drugalcdep.2015.11.010 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-18 N1 - Date created - 2016-01-01 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.drugalcdep.2015.11.010 ER - TY - JOUR T1 - High-Resolution Mass Spectrometry for Characterizing the Metabolism of Synthetic Cannabinoid THJ-018 and Its 5-Fluoro Analog THJ-2201 after Incubation in Human Hepatocytes. AN - 1753009548; 26430074 AB - Despite increasing prevalence of novel psychoactive substances, no human metabolism data are currently available, complicating laboratory documentation of intake in urine samples and assessment of the drugs' pharmacodynamic, pharmacokinetic, and toxicological properties. In 2014, THJ-018 and THJ-2201, synthetic cannabinoid indazole analogs of JWH-018 and AM-2201, were identified, with the National Forensic Laboratory Information System containing 220 THJ-2201 reports. Because of numerous adverse events, the Drug Enforcement Administration listed THJ-2201 as Schedule I in January 2015. We used high-resolution mass spectrometry (HR-MS) (TripleTOF 5600(+)) to identify optimal metabolite markers after incubating 10 μmol/L THJ-018 and THJ-2201 in human hepatocytes for 3 h. Data were acquired via full scan and information-dependent acquisition triggered product ion scans with mass defect filter. In silico metabolite predictions were performed with MetaSite and compared with metabolites identified in human hepatocytes. Thirteen THJ-018 metabolites were detected, with the major metabolic pathways being hydroxylation on the N-pentyl chain and further oxidation or glucuronidation. For THJ-2201, 27 metabolites were observed, predominantly oxidative defluorination plus subsequent carboxylation or glucuronidation, and glucuronidation of hydroxylated metabolites. Dihydrodiol formation on the naphthalene moiety was observed for both compounds. MetaSite prediction matched well with THJ-018 hepatocyte metabolites but underestimated THJ-2201 oxidative defluorination. With HR-MS for data acquisition and processing, we characterized THJ-018 and THJ-2201 metabolism in human hepatocytes and suggest appropriate markers for laboratories to identify THJ-018 and THJ-2201 intake and link observed adverse events to these new synthetic cannabinoids. © 2015 American Association for Clinical Chemistry. JF - Clinical chemistry AU - Diao, Xingxing AU - Wohlfarth, Ariane AU - Pang, Shaokun AU - Scheidweiler, Karl B AU - Huestis, Marilyn A AD - Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, NIH, Baltimore, MD; ; SCIEX, Redwood City, CA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, NIH, Baltimore, MD; mhuestis@intra.nida.nih.gov. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 157 EP - 169 VL - 62 IS - 1 KW - Cannabinoids KW - 0 KW - Index Medicus KW - Molecular Structure KW - Humans KW - Mass Spectrometry KW - Cannabinoids -- metabolism KW - Cannabinoids -- chemistry KW - Cannabinoids -- chemical synthesis KW - Hepatocytes -- metabolism KW - Cannabinoids -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753009548?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+chemistry&rft.atitle=High-Resolution+Mass+Spectrometry+for+Characterizing+the+Metabolism+of+Synthetic+Cannabinoid+THJ-018+and+Its+5-Fluoro+Analog+THJ-2201+after+Incubation+in+Human+Hepatocytes.&rft.au=Diao%2C+Xingxing%3BWohlfarth%2C+Ariane%3BPang%2C+Shaokun%3BScheidweiler%2C+Karl+B%3BHuestis%2C+Marilyn+A&rft.aulast=Diao&rft.aufirst=Xingxing&rft.date=2016-01-01&rft.volume=62&rft.issue=1&rft.spage=157&rft.isbn=&rft.btitle=&rft.title=Clinical+chemistry&rft.issn=1530-8561&rft_id=info:doi/10.1373%2Fclinchem.2015.243535 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-20 N1 - Date created - 2015-12-31 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Comment In: Clin Chem. 2016 Jan;62(1):4-5 [26546634] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1373/clinchem.2015.243535 ER - TY - JOUR T1 - Identification of genotoxic compounds using isogenic DNA repair deficient DT40 cell lines on a quantitative high throughput screening platform. AN - 1753008153; 26243743 AB - DNA repair pathways play a critical role in maintaining cellular homeostasis by repairing DNA damage induced by endogenous processes and xenobiotics, including environmental chemicals. Induction of DNA damage may lead to genomic instability, disruption of cellular homeostasis and potentially tumours. Isogenic chicken DT40 B-lymphocyte cell lines deficient in DNA repair pathways can be used to identify genotoxic compounds and aid in characterising the nature of the induced DNA damage. As part of the US Tox21 program, we previously optimised several different DT40 isogenic clones on a high-throughput screening platform and confirmed the utility of this approach for detecting genotoxicants by measuring differential cytotoxicity in wild-type and DNA repair-deficient clones following chemical exposure. In the study reported here, we screened the Tox21 10K compound library against two isogenic DNA repair-deficient DT40 cell lines (KU70 (-/-) /RAD54 (-/-) and REV3 (-/-) ) and the wild-type cell line using a cell viability assay that measures intracellular adenosine triphosphate levels. KU70 and RAD54 are genes associated with DNA double-strand break repair processes, and REV3 is associated with translesion DNA synthesis pathways. Active compounds identified in the primary screening included many well-known genotoxicants (e.g. adriamycin, melphalan) and several compounds previously untested for genotoxicity. A subset of compounds was further evaluated by assessing their ability to induce micronuclei and phosphorylated H2AX. Using this comprehensive approach, three compounds with previously undefined genotoxicity-2-oxiranemethanamine, AD-67 and tetraphenylolethane glycidyl ether-were identified as genotoxic. These results demonstrate the utility of this approach for identifying and prioritising compounds that may damage DNA. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society 2015. JF - Mutagenesis AU - Nishihara, Kana AU - Huang, Ruili AU - Zhao, Jinghua AU - Shahane, Sampada A AU - Witt, Kristine L AU - Smith-Roe, Stephanie L AU - Tice, Raymond R AU - Takeda, Shunichi AU - Xia, Menghang AD - Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshidakonoe, Sakyo, Kyoto 606-8501, Japan, National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, MSC: 3375 Bethesda, MD 20892, USA and. ; National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, MSC: 3375 Bethesda, MD 20892, USA and. ; Division of the National Toxicology Program, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, National Institutes of Health, Research Triangle Park, NC 27709, USA. ; Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshidakonoe, Sakyo, Kyoto 606-8501, Japan. ; National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, MSC: 3375 Bethesda, MD 20892, USA and mxia@mail.nih.gov. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 69 EP - 81 VL - 31 IS - 1 KW - Antigens, Nuclear KW - 0 KW - DNA-Binding Proteins KW - Mutagens KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Ku Autoantigen KW - EC 4.2.99.- KW - Index Medicus KW - B-Lymphocytes -- drug effects KW - Animals KW - Chickens KW - DNA Repair KW - DNA-Binding Proteins -- genetics KW - Mutation KW - Antigens, Nuclear -- genetics KW - DNA-Directed DNA Polymerase -- genetics KW - Mutagenicity Tests -- methods KW - High-Throughput Screening Assays -- methods KW - Mutagens -- toxicity KW - DNA Breaks, Double-Stranded KW - Cell Line UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753008153?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutagenesis&rft.atitle=Identification+of+genotoxic+compounds+using+isogenic+DNA+repair+deficient+DT40+cell+lines+on+a+quantitative+high+throughput+screening+platform.&rft.au=Nishihara%2C+Kana%3BHuang%2C+Ruili%3BZhao%2C+Jinghua%3BShahane%2C+Sampada+A%3BWitt%2C+Kristine+L%3BSmith-Roe%2C+Stephanie+L%3BTice%2C+Raymond+R%3BTakeda%2C+Shunichi%3BXia%2C+Menghang&rft.aulast=Nishihara&rft.aufirst=Kana&rft.date=2016-01-01&rft.volume=31&rft.issue=1&rft.spage=69&rft.isbn=&rft.btitle=&rft.title=Mutagenesis&rft.issn=1464-3804&rft_id=info:doi/10.1093%2Fmutage%2Fgev055 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-10-18 N1 - Date created - 2015-12-31 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11473-8 [16864780] Chem Res Toxicol. 2006 Dec;19(12):1580-94 [17173371] Cell Mol Life Sci. 2014 Oct;71(20):3951-67 [24947324] Nat Protoc. 2007;2(5):1084-104 [17546000] Cell Res. 2008 Jan;18(1):174-83 [18157155] Nat Rev Cancer. 2008 Mar;8(3):193-204 [18256616] Environ Health Perspect. 2008 Mar;116(3):284-91 [18335092] Toxicol In Vitro. 2008 Jun;22(4):1099-106 [18400464] Nat Rev Cancer. 2008 Dec;8(12):957-67 [19005492] Mutagenesis. 2009 Nov;24(6):465-9 [19762349] Mutat Res. 2007 Jun 15;630(1-2):1-13 [17446119] Cell Cycle. 2010 Feb 15;9(4):662-9 [20139725] Mol Cell. 2010 Oct 22;40(2):179-204 [20965415] DNA Repair (Amst). 2010 Dec 10;9(12):1292-8 [21030320] Drugs. 2011 Feb 12;71(3):331-47 [21319870] Int J Oncol. 2011 Jul;39(1):263-70 [21491084] Environ Health Perspect. 2011 Aug;119(8):1142-8 [21543282] Environ Mol Mutagen. 2011 Aug;52(7):547-61 [21538559] Genes Dev. 2012 Jul 1;26(13):1393-408 [22751496] Cancer Res. 2012 Nov 1;72(21):5588-99 [23118055] Environ Mol Mutagen. 2012 Dec;53(9):725-40 [23065650] J Appl Toxicol. 2013 Jun;33(6):399-409 [23339022] Adv Genet. 2013;82:1-45 [23721719] Environ Health Perspect. 2013 Jul;121(7):756-65 [23603828] Drug Discov Today. 2013 Aug;18(15-16):716-23 [23732176] Biochim Biophys Acta. 2014 Jan;1845(1):84-9 [24361676] Ecotoxicol Environ Saf. 2014 Jul;105:13-21 [24780228] Toxicol Sci. 2014 Jul;140(1):103-17 [24743697] Plant Physiol. 1995 Sep;109(1):213-9 [7480323] Environ Mol Mutagen. 1992;19 Suppl 21:2-141 [1541260] Mutat Res. 1986 Mar;169(3):123-7 [3512995] Exp Hematol. 1985 Nov;13(10):1014-7 [4054240] Science. 1984 Oct 26;226(4673):466-8 [6093249] Chem Biol Interact. 1982 Mar 1;39(1):1-15 [7037214] EMBO J. 2003 Jun 16;22(12):3188-97 [12805232] Mutat Res. 2002 May 27;517(1-2):123-34 [12034314] Cancer Res. 2005 Dec 15;65(24):11704-11 [16357182] Genetics. 2005 Feb;169(2):575-82 [15520252] Biochim Biophys Acta. 1998 Oct 1;1400(1-3):155-71 [9748552] EMBO J. 1998 Sep 15;17(18):5497-508 [9736627] Proc Natl Acad Sci U S A. 1998 Jun 9;95(12):6876-80 [9618506] Cell. 1997 Apr 18;89(2):185-93 [9108474] Mutat Res. 1996 Aug 17;355(1-2):13-40 [8781575] Mutat Res. 1995 Oct;335(2):201-6 [7477051] Environ Health Perspect. 2009 Nov;117(11):1737-44 [20049126] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/mutage/gev055 ER - TY - JOUR T1 - Protocol for Detection of HIV-Tat Protein in Cerebrospinal Fluid by a Sandwich Enzyme-Linked Immunosorbent Assay. AN - 1752787402; 26714723 AB - The human immunodeficiency virus (HIV) transactivator of transcription (Tat) is a virally produced protein that is required for efficient viral replication. Once formed inside an infected cell, Tat is secreted into the extracellular space where it has pathophysiological consequences on cells it interacts with. Tat has been demonstrated to be neurotoxic and is produced even under the pressures of anti-retroviral therapy; therefore Tat is suspected to contribute to the development of HIV-associated neurocognitive disorders. In this chapter, we describe a sandwich enzyme-linked immunosorbent assay protocol for the detection of Tat from cerebrospinal fluid samples. JF - Methods in molecular biology (Clifton, N.J.) AU - Johnson, Tory P AU - Nath, Avindra AD - Section of Infections of the Nervous System, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Room 7C-103, Bldg 10; 10 Center Drive, Bethesda, MD, 20892, USA. tory.johnson@nih.gov. ; Section of Infections of the Nervous System, National Institute of Neurological Diseases and Stroke, National Institutes of Health, Room 7C-103, Bldg 10; 10 Center Drive, Bethesda, MD, 20892, USA. Y1 - 2016 PY - 2016 DA - 2016 SP - 343 EP - 352 VL - 1354 KW - tat Gene Products, Human Immunodeficiency Virus KW - 0 KW - Index Medicus KW - CSF KW - Protein detection KW - Transactivator of transcription KW - Tat KW - Cell lysates KW - ELISA KW - HIV KW - Humans KW - Enzyme-Linked Immunosorbent Assay -- methods KW - HIV-1 -- isolation & purification KW - tat Gene Products, Human Immunodeficiency Virus -- cerebrospinal fluid KW - HIV Infections -- cerebrospinal fluid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1752787402?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.atitle=Protocol+for+Detection+of+HIV-Tat+Protein+in+Cerebrospinal+Fluid+by+a+Sandwich+Enzyme-Linked+Immunosorbent+Assay.&rft.au=Johnson%2C+Tory+P%3BNath%2C+Avindra&rft.aulast=Johnson&rft.aufirst=Tory&rft.date=2016-01-01&rft.volume=1354&rft.issue=&rft.spage=343&rft.isbn=&rft.btitle=&rft.title=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.issn=1940-6029&rft_id=info:doi/10.1007%2F978-1-4939-3046-3_23 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-10-13 N1 - Date created - 2015-12-30 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/978-1-4939-3046-3_23 ER - TY - JOUR T1 - F344/NTac Rats Chronically Exposed to Bromodichloroacetic Acid Develop Mammary Adenocarcinomas With Mixed Luminal/Basal Phenotype and Tgfβ Dysregulation. AN - 1752587108; 25732176 AB - Breast cancer is the most common cancer and the second-leading cause of cancer mortality in women in the United States. A recent 2-year National Toxicology Program carcinogenicity study showed an increased incidence of proliferative mammary lesions (hyperplasia, fibroadenoma, adenocarcinoma) in F344/NTac rats exposed to bromodichloroacetic acid (BDCA), a disinfection by-product in finished drinking water with widespread human exposure. We hypothesized that the increase in mammary tumors observed in BDCA-exposed F344/NTac rats may be due to underlying molecular changes relevant for human breast cancer. The objective of the study was to compare (1) gene and protein expression and (2) mutation spectra of relevant human breast cancer genes between normal untreated mammary gland and mammary tumors from control and BDCA-exposed animals to identify molecular changes relevant for human cancer. Histologically, adenocarcinomas from control and BDCA-exposed animals were morphologically very similar, were estrogen/progesterone receptor positive, and displayed a mixed luminal/basal phenotype. Gene expression analysis showed a positive trend in the number of genes associated with human breast cancer, with proportionally more genes represented in the BDCA-treated tumor group. Additionally, a 5-gene signature representing possible Tgfβ pathway activation in BDCA-treated adenocarcinomas was observed, suggesting that this pathway may be involved in the increased incidence of mammary tumors in BDCA-exposed animals. © The Author(s) 2015. JF - Veterinary pathology AU - Harvey, J B AU - Hong, H-H L AU - Bhusari, S AU - Ton, T-V AU - Wang, Y AU - Foley, J F AU - Peddada, S D AU - Hooth, M AU - DeVito, M AU - Nyska, A AU - Pandiri, A R AU - Hoenerhoff, M J AD - Investigative Pathology Group, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA North Carolina State University College of Veterinary Medicine, Raleigh, NC, USA. ; Investigative Pathology Group, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. ; Investigative Pathology Group, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA Special Techniques Group, Cellular and Molecular Pathology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. ; Biostatistics Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. ; Program Operations Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. ; General Toxicology Group, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. ; Integrated Laboratory Systems, Inc., Research Triangle Park, NC, USA. ; Investigative Pathology Group, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA Experimental Pathology Laboratories, Research Triangle Park, NC, USA. ; Investigative Pathology Group, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA hoenerho@med.umich.edu. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 170 EP - 181 VL - 53 IS - 1 KW - Acetates KW - 0 KW - Transforming Growth Factor beta KW - bromodichloroacetic acid KW - 71133-14-7 KW - Index Medicus KW - breast cancer KW - transforming growth factor beta KW - environmental pollutants KW - gene expression KW - luminal KW - basal KW - F344/NTac rat KW - Rats KW - Phenotype KW - Animals KW - Rats, Inbred F344 KW - Humans KW - Female KW - Mammary Neoplasms, Experimental -- chemically induced KW - Acetates -- adverse effects KW - Adenocarcinoma -- chemically induced KW - Transforming Growth Factor beta -- metabolism KW - Mammary Neoplasms, Experimental -- pathology KW - Adenocarcinoma -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1752587108?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Veterinary+pathology&rft.atitle=F344%2FNTac+Rats+Chronically+Exposed+to+Bromodichloroacetic+Acid+Develop+Mammary+Adenocarcinomas+With+Mixed+Luminal%2FBasal+Phenotype+and+Tgf%CE%B2+Dysregulation.&rft.au=Harvey%2C+J+B%3BHong%2C+H-H+L%3BBhusari%2C+S%3BTon%2C+T-V%3BWang%2C+Y%3BFoley%2C+J+F%3BPeddada%2C+S+D%3BHooth%2C+M%3BDeVito%2C+M%3BNyska%2C+A%3BPandiri%2C+A+R%3BHoenerhoff%2C+M+J&rft.aulast=Harvey&rft.aufirst=J&rft.date=2016-01-01&rft.volume=53&rft.issue=1&rft.spage=170&rft.isbn=&rft.btitle=&rft.title=Veterinary+pathology&rft.issn=1544-2217&rft_id=info:doi/10.1177%2F0300985815571680 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-12-13 N1 - Date created - 2015-12-29 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/0300985815571680 ER - TY - JOUR T1 - A Genomic Study of DNA Alteration Events Caused by Ionizing Radiation in Human Embryonic Stem Cells via Next-Generation Sequencing. AN - 1752355317; 26709353 AB - Ionizing radiation (IR) is a known mutagen that is widely employed for medical diagnostic and therapeutic purposes. To study the extent of genetic variations in DNA caused by IR, we used IR-sensitive human embryonic stem cells (hESCs). Four hESC cell lines, H1, H7, H9, and H14, were subjected to IR at 0.2 or 1 Gy dose and then maintained in culture for four days before being harvested for DNA isolation. Irradiation with 1 Gy dose resulted in significant cell death, ranging from 60% to 90% reduction in cell population. Since IR is often implicated as a risk for inducing cancer, a primer pool targeting genomic "hotspot" regions that are frequently mutated in human cancer genes was used to generate libraries from irradiated and control samples. Using a semiconductor-based next-generation sequencing approach, we were able to consistently sequence these samples with deep coverage for reliable data analysis. A possible rare nucleotide variant was identified in the KIT gene (chr4:55593481) exclusively in H1 hESCs irradiated with 1 Gy dose. More extensive further studies are warranted to assess the extent and distribution of genetic changes in hESCs after IR exposure. JF - Stem cells international AU - Nguyen, Van AU - Panyutin, Irina V AU - Panyutin, Igor G AU - Neumann, Ronald D AD - Nuclear Medicine Division, Department of Radiology and Imaging Sciences, Clinical Center, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA. Y1 - 2016 PY - 2016 DA - 2016 SP - 1346521 VL - 2016 SN - 1687-966X, 1687-966X UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1752355317?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+cells+international&rft.atitle=A+Genomic+Study+of+DNA+Alteration+Events+Caused+by+Ionizing+Radiation+in+Human+Embryonic+Stem+Cells+via+Next-Generation+Sequencing.&rft.au=Nguyen%2C+Van%3BPanyutin%2C+Irina+V%3BPanyutin%2C+Igor+G%3BNeumann%2C+Ronald+D&rft.aulast=Nguyen&rft.aufirst=Van&rft.date=2016-01-01&rft.volume=2016&rft.issue=&rft.spage=1346521&rft.isbn=&rft.btitle=&rft.title=Stem+cells+international&rft.issn=1687966X&rft_id=info:doi/10.1155%2F2016%2F1346521 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-28 N1 - Date created - 2015-12-28 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1155/2016/1346521 ER - TY - JOUR T1 - Tea polyphenols epigallocatechin gallete and theaflavin restrict mouse liver carcinogenesis through modulation of self-renewal Wnt and hedgehog pathways. AN - 1751997048; 26386739 AB - The aim of this study is to evaluate chemopreventive and therapeutic efficacy of tea polyphenols epigallocatechin gallete (EGCG) and theaflavin (TF) on self-renewal Wnt and Hedgehog (Hh) pathways during CCl4/N-nitosodiethylamine-induced mouse liver carcinogenesis. For this purpose, the effect of EGCG/TF was investigated in liver lesions of different groups at pre-, continuous and post initiation stages of carcinogenesis. Comparatively increased body weights were evident due to EGCG/TF treatment than carcinogen control mice. Both EGCG and TF could restrict the development of hepatocellular carcinoma at 30th week of carcinogen application showing potential chemoprevention in continuous treated group (mild dysplasia) followed by pretreated (moderate dysplasia) and therapeutic efficacy in posttreated group (mild dysplasia). This restriction was associated with significantly reduced proliferation, increased apoptosis, decreased prevalence of hepatocyte progenitor cell (AFP) and stem cell population (CD44) irrespective of EGCG/TF treatments. The EGCG/TF could modulate the Wnt pathway by reducing β-catenin and phospho-β-catenin-Y-654 expressions along with up-regulation of sFRP1 (secreted frizzled-related protein 1) and adenomatosis polyposis coli during the restriction. In case of the Hh pathway, EGCG/TF could also reduce expressions of glioma-associated oncogene homolog 1 (Gli1) and SMO (smoothened homolog) along with up-regulation of PTCH1 (patched homolog 1). As a result, in Wnt/Hh regulatory pathways decreased expressions of β-catenin/Gli1 target genes like CyclinD1, cMyc and EGFR/phospho-EGFR-Y-1173 and up-regulation of E-cadherin were seen during the restriction. Thus, the restriction of liver carcinogenesis by EGCG/TF was due to reduction in hepatocyte progenitor cell/stem cell population along with modulation of Wnt/Hh and other regulatory pathways. Copyright © 2015 Elsevier Inc. All rights reserved. JF - The Journal of nutritional biochemistry AU - Sur, Subhayan AU - Pal, Debolina AU - Mandal, Syamsundar AU - Roy, Anup AU - Panda, Chinmay Kumar AD - Dept. of Oncogene Regulation, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata 700 026, West Bengal, India. Electronic address: subhayansur18@gmail.com. ; Dept. of Oncogene Regulation, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata 700 026, West Bengal, India. Electronic address: dbln.pl@gmail.com. ; Department of Epidemiology and Biostatistics, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata 700 026, India. ; North Bengal Medical College and Hospital, West Bengal, India. ; Dept. of Oncogene Regulation, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata 700 026, West Bengal, India. Electronic address: ckpanda.cnci@gmail.com. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 32 EP - 42 VL - 27 KW - Antigens, CD44 KW - 0 KW - Biflavonoids KW - Hedgehog Proteins KW - Tea KW - Wnt Proteins KW - alpha-Fetoproteins KW - theaflavin KW - 1IA46M0D13 KW - Catechin KW - 8R1V1STN48 KW - epigallocatechin gallate KW - BQM438CTEL KW - Index Medicus KW - TF KW - CD44 KW - β-Catenin KW - EGCG KW - Hepatocellular carcinoma KW - Gli1 KW - Animals KW - Liver -- pathology KW - Mice KW - Antigens, CD44 -- metabolism KW - alpha-Fetoproteins -- metabolism KW - Female KW - Wnt Proteins -- metabolism KW - Hedgehog Proteins -- metabolism KW - Liver Neoplasms, Experimental -- metabolism KW - Catechin -- analogs & derivatives KW - Biflavonoids -- pharmacology KW - Tea -- chemistry KW - Liver Neoplasms, Experimental -- prevention & control KW - Catechin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751997048?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+nutritional+biochemistry&rft.atitle=Tea+polyphenols+epigallocatechin+gallete+and+theaflavin+restrict+mouse+liver+carcinogenesis+through+modulation+of+self-renewal+Wnt+and+hedgehog+pathways.&rft.au=Sur%2C+Subhayan%3BPal%2C+Debolina%3BMandal%2C+Syamsundar%3BRoy%2C+Anup%3BPanda%2C+Chinmay+Kumar&rft.aulast=Sur&rft.aufirst=Subhayan&rft.date=2016-01-01&rft.volume=27&rft.issue=&rft.spage=32&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+nutritional+biochemistry&rft.issn=1873-4847&rft_id=info:doi/10.1016%2Fj.jnutbio.2015.08.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-10-20 N1 - Date created - 2015-12-25 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jnutbio.2015.08.016 ER - TY - JOUR T1 - Oleanolic acid acetate inhibits rheumatoid arthritis by modulating T cell immune responses and matrix-degrading enzymes. AN - 1751993824; 26570984 AB - Rheumatoid arthritis (RA) is a chronic autoimmune disease associated with a combination of synovium joint inflammation, synovium hyperplasia, and destruction of cartilage and bone. Oleanolic acid acetate (OAA), a compound isolated from Vigna angularis, has been known to possess pharmacological activities, including anti-inflammation and anti-bone destruction. In this study, we investigated the effects of OAA on RA and the underlying mechanisms of action by using a type-II collagen-induced arthritis (CIA) mouse model and tumor necrosis factor (TNF)-α-stimulated RA synovial fibroblasts. Oral administration of OAA decreased the clinical arthritis symptoms, paw thickness, histologic and radiologic changes, and serum total and anti-type II collagen IgG, IgG1, and IgG2a levels. OAA administration reduced Th1/Th17 phenotype CD4(+) T lymphocyte expansions and inflammatory cytokine productions in T cell activated draining lymph nodes and spleen. OAA reduced the expression and production of inflammatory mediators, such as cytokines and matrix metalloproteinase (MMP)-1/3, in the ankle joint tissue and RA synovial fibroblasts by down-regulating Akt, mitogen-activated protein kinases, and nuclear factor-κB. Our results clearly support that OAA plays a therapeutic role in RA pathogenesis by modulating helper T cell immune responses and matrix-degrading enzymes. The immunosuppressive effects of OAA were comparable to dexamethasone and ketoprofen. We provide evidences that OAA could be a potential therapeutic candidate for RA. Copyright © 2015 Elsevier Inc. All rights reserved. JF - Toxicology and applied pharmacology AU - Choi, Jin Kyeong AU - Kim, Sung-Wan AU - Kim, Duk-Sil AU - Lee, Jong Yeong AU - Lee, Soyoung AU - Oh, Hyun-Mee AU - Ha, Yeong Su AU - Yoo, Jeongsoo AU - Park, Pil-Hoon AU - Shin, Tae-Yong AU - Kwon, Taeg Kyu AU - Rho, Mun-Chual AU - Kim, Sang-Hyun AD - Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 700-422, Republic of Korea; Molecular Immunology Section, Laboratory of Immunology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Department of Thoracic and Cardiovascular Surgery, CHA Gumi Medical Center, CHA University, Gumi 730-040, Republic of Korea. ; Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 700-422, Republic of Korea. ; Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 700-422, Republic of Korea; Bio-Materials Research Institute, Korea Research Institute of Bioscience and Biotechnology, Jeongeup 580-185, Republic of Korea. ; Bio-Materials Research Institute, Korea Research Institute of Bioscience and Biotechnology, Jeongeup 580-185, Republic of Korea. ; Department of Molecular Medicine, School of Medicine, Kyungpook National University, Daegu 700-422, Republic of Korea. ; College of Pharmacy, Yeungnam University, Gyeongbuk 712-749, Republic of Korea. ; College of Pharmacy, Woosuk University, Jeonju 565-701, Republic of Korea. ; Department of Immunology, School of Medicine, Keimyung University, Daegu 704-701, Republic of Korea. ; Bio-Materials Research Institute, Korea Research Institute of Bioscience and Biotechnology, Jeongeup 580-185, Republic of Korea. Electronic address: rho-m@kribb.re.kr. ; Department of Pharmacology, School of Medicine, Kyungpook National University, Daegu 700-422, Republic of Korea. Electronic address: shkim72@knu.ac.kr. Y1 - 2016/01/01/ PY - 2016 DA - 2016 Jan 01 SP - 1 EP - 9 VL - 290 KW - Immunoglobulin G KW - 0 KW - NF-kappa B KW - Triterpenes KW - Tumor Necrosis Factor-alpha KW - oleanolic acid 3-acetate KW - 4339-72-4 KW - Dexamethasone KW - 7S5I7G3JQL KW - Ketoprofen KW - 90Y4QC304K KW - Mitogen-Activated Protein Kinases KW - EC 2.7.11.24 KW - Matrix Metalloproteinase 13 KW - EC 3.4.24.- KW - Mmp13 protein, mouse KW - Matrix Metalloproteinase 3 KW - EC 3.4.24.17 KW - Mmp3 protein, mouse KW - Index Medicus KW - Synovial fibroblasts KW - Oleanolic acid acetate KW - Collagen-induced arthritis KW - Matrix metalloproteinase KW - Lymph nodes KW - Inflammatory cytokine KW - Animals KW - Arthritis, Experimental -- drug therapy KW - Dexamethasone -- pharmacology KW - Humans KW - Disease Models, Animal KW - Matrix Metalloproteinase 3 -- metabolism KW - Ketoprofen -- pharmacology KW - Matrix Metalloproteinase 13 -- metabolism KW - Matrix Metalloproteinase 3 -- genetics KW - Down-Regulation KW - Cell Survival -- drug effects KW - Adult KW - Mitogen-Activated Protein Kinases -- genetics KW - Synovial Membrane -- metabolism KW - Male KW - Fibroblasts -- drug effects KW - Mitogen-Activated Protein Kinases -- metabolism KW - Tumor Necrosis Factor-alpha -- pharmacology KW - Mice KW - Bone and Bones -- metabolism KW - Fibroblasts -- metabolism KW - NF-kappa B -- genetics KW - Mice, Inbred DBA KW - Immunoglobulin G -- blood KW - Cells, Cultured KW - Cartilage -- metabolism KW - Bone and Bones -- drug effects KW - Cartilage -- drug effects KW - Synovial Membrane -- drug effects KW - Middle Aged KW - Matrix Metalloproteinase 13 -- genetics KW - NF-kappa B -- metabolism KW - Arthritis, Rheumatoid -- drug therapy KW - T-Lymphocytes -- cytology KW - Triterpenes -- pharmacology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751993824?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Oleanolic+acid+acetate+inhibits+rheumatoid+arthritis+by+modulating+T+cell+immune+responses+and+matrix-degrading+enzymes.&rft.au=Choi%2C+Jin+Kyeong%3BKim%2C+Sung-Wan%3BKim%2C+Duk-Sil%3BLee%2C+Jong+Yeong%3BLee%2C+Soyoung%3BOh%2C+Hyun-Mee%3BHa%2C+Yeong+Su%3BYoo%2C+Jeongsoo%3BPark%2C+Pil-Hoon%3BShin%2C+Tae-Yong%3BKwon%2C+Taeg+Kyu%3BRho%2C+Mun-Chual%3BKim%2C+Sang-Hyun&rft.aulast=Choi&rft.aufirst=Jin&rft.date=2016-01-01&rft.volume=290&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2015.11.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-10 N1 - Date created - 2015-12-26 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.taap.2015.11.005 ER - TY - JOUR T1 - Phase 2 Randomized Controlled Trial of Radiation Therapy Plus Concurrent Interferon-Alpha and Retinoic Acid Versus Cisplatin for Stage III Cervical Carcinoma. AN - 1751991457; 26700705 AB - Because a combination of retinoic acid, interferon-alpha, and radiation therapy demonstrated synergistic action and effectiveness to treat advanced cervical cancers in earlier studies, we designed this randomized phase 2 open-label trial to assess efficacy and safety of interferon alpha-2b (IFN) and 13-cis-retinoic acid (RA) administered concomitantly with radiation therapy (IFN-RA-radiation) to treat stage III cervical cancer. Stage III cervical cancer patients were randomized to study and control groups in a 1:1 ratio. All patients were treated with radiation therapy; study arm patients received IFN (3 × 10(6) IU subcutaneously) 3 times a week for 4 weeks and daily RA (40 mg orally) for 30 days starting on day 1 of radiation, whereas control arm patients received weekly cisplatinum (40 mg/m(2)) for 5 weeks during radiation. Patients were followed for 3 years. The primary endpoint was overall survival at 3 years. Patients in the study (n=104) and control (n=105) groups were comparable for clinicopathological characteristics, radiation therapy-related variables and treatment response. Proportions of disease-free patients in the study and control groups were 38.5% and 44.8%, respectively, after median follow-up of 29.2 months. Hazard ratios were 0.67 (95% confidence interval [CI]: 0.44-1.01) and 0.69 (95% CI: 0.44-1.06) for overall and disease-fee survival, respectively, comparing the study group to control, and demonstrated an inferior outcome with RA-IFN-radiation, although differences were statistically nonsignificant. Kaplan-Meier curves of disease-free and overall survival probabilities also showed inferior survival in the study group compared to those in the control. Acute toxicities of chemoradiation were significantly higher with 2 acute toxicity-related deaths. Treatment with RA-IFN-radiation did not demonstrate survival advantage over chemoradiation despite being less toxic. The trends predicted an inferior outcome with the RA-IFN combination. Copyright © 2016 Elsevier Inc. All rights reserved. JF - International journal of radiation oncology, biology, physics AU - Basu, Partha AU - Jenson, Alfred Bennett AU - Majhi, Tapas AU - Choudhury, Prabir AU - Mandal, Ranajit AU - Banerjee, Dipanwita AU - Biswas, Jaydip AU - Pan, Jianmin AU - Rai, Shesh Nath AU - Ghim, Shin Je AU - Miller, Donald AD - Screening Group, Early Detection and Prevention Section, International Agency for Research on Cancer, Lyon, France. Electronic address: BasuP@iarc.fr. ; James Graham Brown Cancer Center, University of Louisville, Louisville, Kentucky. ; Department of Radiation Oncology, Chittaranjan National Cancer Institute, Kolkata, India. ; Department of Gynecological Oncology, Chittaranjan National Cancer Institute, Kolkata, India. ; Department of Surgical Oncology, Chittaranjan National Cancer Institute, Kolkata, India. Y1 - 2016/01/01/ PY - 2016 DA - 2016 Jan 01 SP - 102 EP - 110 VL - 94 IS - 1 KW - Antineoplastic Agents KW - 0 KW - Interferon-alpha KW - Recombinant Proteins KW - interferon alfa-2b KW - 43K1W2T1M6 KW - Tretinoin KW - 5688UTC01R KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Disease-Free Survival KW - Drug Administration Schedule KW - Interferon-alpha -- administration & dosage KW - Humans KW - Tretinoin -- administration & dosage KW - Aged KW - Cisplatin -- administration & dosage KW - Kaplan-Meier Estimate KW - Brachytherapy KW - Prospective Studies KW - Radiotherapy Dosage KW - Middle Aged KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Recombinant Proteins -- administration & dosage KW - Female KW - Chemoradiotherapy -- methods KW - Uterine Cervical Neoplasms -- therapy KW - Chemoradiotherapy -- adverse effects KW - Uterine Cervical Neoplasms -- mortality KW - Antineoplastic Agents -- therapeutic use KW - Uterine Cervical Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751991457?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.atitle=Phase+2+Randomized+Controlled+Trial+of+Radiation+Therapy+Plus+Concurrent+Interferon-Alpha+and+Retinoic+Acid+Versus+Cisplatin+for+Stage+III+Cervical+Carcinoma.&rft.au=Basu%2C+Partha%3BJenson%2C+Alfred+Bennett%3BMajhi%2C+Tapas%3BChoudhury%2C+Prabir%3BMandal%2C+Ranajit%3BBanerjee%2C+Dipanwita%3BBiswas%2C+Jaydip%3BPan%2C+Jianmin%3BRai%2C+Shesh+Nath%3BGhim%2C+Shin+Je%3BMiller%2C+Donald&rft.aulast=Basu&rft.aufirst=Partha&rft.date=2016-01-01&rft.volume=94&rft.issue=1&rft.spage=102&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.issn=1879-355X&rft_id=info:doi/10.1016%2Fj.ijrobp.2015.09.040 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-27 N1 - Date created - 2015-12-24 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT01276730; ClinicalTrials.gov N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ijrobp.2015.09.040 ER - TY - JOUR T1 - Phenethyl isothiocyanate, by virtue of its antioxidant activity, inhibits invasiveness and metastatic potential of breast cancer cells: HIF-1α as a putative target. AN - 1751672331; 26480821 AB - Hypoxia-inducible factor 1α (HIF-1α) plays a crucial role in facilitating tumor progression and metastasis. Reducing the levels of HIF-1α might therefore be an important anticancer strategy. This could be achieved by understanding the key cellular events involved in HIF-1α activation. Present study explored the effect of phenethyl isothiocyanate (PEITC), a natural isothiocyanate, found in cruciferous vegetables on the expression of HIF-1α and HSP90 in breast adenocarcinoma cell lines (MCF-7 and MDA-MB-231) under both normoxia and hypoxia. This study established the possible role of ROS in the up-regulation of these markers in breast cancer cells. PEITC-induced nuclear accumulation of Nrf2, increased the activities of several antioxidant enzymes, and thus reduced the ROS burden of the tumor cells by acting as an indirect antioxidant. This resulted in the down-regulation of HSP90 and thereby HIF-1α expression. HSP90 was also found to be involved in the regulation of HIF-1α. A probable link between down-regulation of HIF-1α with reduction of ROS by PEITC through induction of Nrf2 was determined. Finally, our study demonstrated that modulation of HIF-1α by PEITC retarded adhesion, aggregation, migration and invasion of the breast cancer cells, thereby showing anti-metastatic effect. Activities of MMPs (2 & 9) and expression of VEGF were also altered by PEITC. JF - Free radical research AU - Sarkar, Ruma AU - Mukherjee, Sutapa AU - Biswas, Jaydip AU - Roy, Madhumita AD - a Department of Environmental Carcinogenesis & Toxicology , Chittaranjan National Cancer Institute , Kolkata , West Bengal , India ; ; b Department of Surgical Oncology , Chittaranjan National Cancer Institute , Kolkata , West Bengal , India. Y1 - 2016 PY - 2016 DA - 2016 SP - 84 EP - 100 VL - 50 IS - 1 KW - Antioxidants KW - 0 KW - HSP90 Heat-Shock Proteins KW - Hypoxia-Inducible Factor 1, alpha Subunit KW - Isothiocyanates KW - phenethyl isothiocyanate KW - 6U7TFK75KV KW - Index Medicus KW - HIF-1α KW - ROS KW - PEITC KW - Nrf2 KW - HSP90 KW - Gene Expression Regulation, Neoplastic KW - Neoplasm Invasiveness KW - Humans KW - Neoplasm Metastasis KW - HSP90 Heat-Shock Proteins -- drug effects KW - Cell Line, Tumor KW - HSP90 Heat-Shock Proteins -- genetics KW - Female KW - Breast Neoplasms -- drug therapy KW - Isothiocyanates -- pharmacology KW - Hypoxia-Inducible Factor 1, alpha Subunit -- drug effects KW - Hypoxia-Inducible Factor 1, alpha Subunit -- genetics KW - Down-Regulation KW - Breast Neoplasms -- pathology KW - Antioxidants -- pharmacology KW - Breast Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751672331?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Free+radical+research&rft.atitle=Phenethyl+isothiocyanate%2C+by+virtue+of+its+antioxidant+activity%2C+inhibits+invasiveness+and+metastatic+potential+of+breast+cancer+cells%3A+HIF-1%CE%B1+as+a+putative+target.&rft.au=Sarkar%2C+Ruma%3BMukherjee%2C+Sutapa%3BBiswas%2C+Jaydip%3BRoy%2C+Madhumita&rft.aulast=Sarkar&rft.aufirst=Ruma&rft.date=2016-01-01&rft.volume=50&rft.issue=1&rft.spage=84&rft.isbn=&rft.btitle=&rft.title=Free+radical+research&rft.issn=1029-2470&rft_id=info:doi/10.1016%2Fj.reprotox.2015.01.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-10-24 N1 - Date created - 2015-12-23 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3109/10715762.2015.1108520 ER - TY - JOUR T1 - Vanadium(III)-L-cysteine protects cisplatin-induced nephropathy through activation of Nrf2/HO-1 pathway. AN - 1751672277; 26573721 AB - Cisplatin (CDDP) is one of the first-line anticancer drugs; however, the major limitation of CDDP therapy is development of nephrotoxicity (25-35% cases), whose precise mechanism mainly involves oxidative stress, inflammation and cell death. Therefore, in search of a potential chemoprotectant, an organovanadium complex, viz., vanadium(III)-L-cysteine (VC-III) was evaluated against CDDP-induced nephropathy in mice. CDDP was administered intraperitoneally (5 mg/kg b.w.) and VC-III was given by oral gavage (1 mg/kg b.w.) in concomitant and pre-treatment schedule. The results showed that VC-III administration reduced (p < 0.001) serum creatinine and blood urea nitrogen levels, suggesting amelioration of renal dysfunction. VC-III treatment also significantly (p < 0.001) prevented CDDP-induced generation of reactive oxygen species, reactive nitrogen species, and onset of lipid peroxidation in kidney tissues of the experimental mice. In addition, VC-III also substantially (p < 0.001) restored CDDP-induced depleted activities of the renal antioxidant enzymes such as, superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, and glutathione (reduced) level. Furthermore, histopathological study also confirmed the renoprotective efficacy of VC-III. Western blotting analysis appended by immunohistochemical data showed that VC-III treatment quite effectively reduced the expression of proinflammatory mediators such as, NFκβ, COX-2 and IL-6. VC-III administration also stimulated Nrf2-mediated antioxidant defense system by promotion of downstream antioxidant enzymes, such as HO-1. Moreover, treatment with VC-III significantly (p < 0.001) enhanced CDDP-mediated cytotoxicity in MCF-7 and NCI-H520 human cancer cell lines. Thus, VC-III can serve as a suitable chemoprotectant and increase the therapeutic window of CDDP in cancer patients. JF - Free radical research AU - Basu, Abhishek AU - Singha Roy, Somnath AU - Bhattacharjee, Arin AU - Bhuniya, Avishek AU - Baral, Rathindranath AU - Biswas, Jaydip AU - Bhattacharya, Sudin AD - a Department of Cancer Chemoprevention , Chittaranjan National Cancer Institute , West Bengal , India. ; b Department of Immunoregulation and Immunodiagnostics , Chittaranjan National Cancer Institute , West Bengal , India. ; c Department of Translational Research , Chittaranjan National Cancer Institute , West Bengal , India. Y1 - 2016 PY - 2016 DA - 2016 SP - 39 EP - 55 VL - 50 IS - 1 KW - Antineoplastic Agents KW - 0 KW - Antioxidants KW - Coordination Complexes KW - NF-E2-Related Factor 2 KW - NFE2L2 protein, human KW - Protective Agents KW - vanadium(III)-cysteine KW - Creatinine KW - AYI8EX34EU KW - Heme Oxygenase-1 KW - EC 1.14.14.18 KW - Cysteine KW - K848JZ4886 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - inflammation KW - Antioxidant KW - ARE pathway KW - free radicals KW - chemotherapy KW - Animals KW - Antioxidants -- metabolism KW - Humans KW - Oxidative Stress -- drug effects KW - Mice KW - Cell Line, Tumor KW - Protective Agents -- pharmacology KW - Blood Urea Nitrogen KW - Creatinine -- blood KW - Signal Transduction KW - Female KW - Cysteine -- therapeutic use KW - Coordination Complexes -- therapeutic use KW - Kidney Diseases -- blood KW - Cysteine -- analogs & derivatives KW - NF-E2-Related Factor 2 -- metabolism KW - Kidney Diseases -- metabolism KW - Cysteine -- chemistry KW - Cisplatin -- toxicity KW - Heme Oxygenase-1 -- metabolism KW - Antineoplastic Agents -- toxicity KW - Coordination Complexes -- chemistry KW - Kidney Diseases -- drug therapy KW - Kidney Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751672277?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Free+radical+research&rft.atitle=Vanadium%28III%29-L-cysteine+protects+cisplatin-induced+nephropathy+through+activation+of+Nrf2%2FHO-1+pathway.&rft.au=Basu%2C+Abhishek%3BSingha+Roy%2C+Somnath%3BBhattacharjee%2C+Arin%3BBhuniya%2C+Avishek%3BBaral%2C+Rathindranath%3BBiswas%2C+Jaydip%3BBhattacharya%2C+Sudin&rft.aulast=Basu&rft.aufirst=Abhishek&rft.date=2016-01-01&rft.volume=50&rft.issue=1&rft.spage=39&rft.isbn=&rft.btitle=&rft.title=Free+radical+research&rft.issn=1029-2470&rft_id=info:doi/10.3109%2F10715762.2015.1102908 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-10-24 N1 - Date created - 2015-12-23 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3109/10715762.2015.1102908 ER - TY - JOUR T1 - Modulation of Tamoxifen Cytotoxicity by Caffeic Acid Phenethyl Ester in MCF-7 Breast Cancer Cells. AN - 1751669297; 26697130 AB - Although Tamoxifen (TAM) is one of the most widely used drugs in managing breast cancer, many women still relapse after long-term therapy. Caffeic acid phenethyl ester (CAPE) is a polyphenolic compound present in many medicinal plants and in propolis. The present study examined the effect of CAPE on TAM cytotoxicity in MCF-7 cells. MCF-7 cells were treated with different concentrations of TAM and/or CAPE for 48 h. This novel combination exerted synergistic cytotoxic effects against MCF-7 cells via induction of apoptotic machinery with activation of caspases and DNA fragmentation, along with downregulation of Bcl-2 and Beclin 1 expression levels. However, the mammalian microtubule-associated protein light chain LC 3-II level was unchanged. Vascular endothelial growth factor level was also decreased, whereas levels of glutathione and nitric oxide were increased. In conclusion, CAPE augmented TAM cytotoxicity via multiple mechanisms, providing a novel therapeutic approach for breast cancer treatment that can overcome resistance and lower toxicity. This effect provides a rationale for further investigation of this combination. JF - Oxidative medicine and cellular longevity AU - Motawi, Tarek K AU - Abdelazim, Samy A AU - Darwish, Hebatallah A AU - Elbaz, Eman M AU - Shouman, Samia A AD - Department of Biochemistry, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt. ; Department of Cancer Biology, National Cancer Institute, Cairo University, Cairo 11796, Egypt. Y1 - 2016 PY - 2016 DA - 2016 SP - 3017108 VL - 2016 KW - Apoptosis Regulatory Proteins KW - 0 KW - BCL2 protein, human KW - BECN1 protein, human KW - Beclin-1 KW - Caffeic Acids KW - Membrane Proteins KW - Microtubule-Associated Proteins KW - Proto-Oncogene Proteins c-bcl-2 KW - light chain 3, human KW - Tamoxifen KW - 094ZI81Y45 KW - caffeic acid phenethyl ester KW - G960R9S5SK KW - Phenylethyl Alcohol KW - ML9LGA7468 KW - Index Medicus KW - Tamoxifen -- pharmacology KW - Microtubule-Associated Proteins -- metabolism KW - Phenylethyl Alcohol -- pharmacology KW - Phenylethyl Alcohol -- analogs & derivatives KW - Membrane Proteins -- metabolism KW - Humans KW - Caffeic Acids -- pharmacology KW - Proto-Oncogene Proteins c-bcl-2 -- metabolism KW - Apoptosis Regulatory Proteins -- metabolism KW - MCF-7 Cells KW - Female KW - Breast Neoplasms -- drug therapy KW - Breast Neoplasms -- pathology KW - Breast Neoplasms -- metabolism KW - Antineoplastic Combined Chemotherapy Protocols -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751669297?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oxidative+medicine+and+cellular+longevity&rft.atitle=Modulation+of+Tamoxifen+Cytotoxicity+by+Caffeic+Acid+Phenethyl+Ester+in+MCF-7+Breast+Cancer+Cells.&rft.au=Motawi%2C+Tarek+K%3BAbdelazim%2C+Samy+A%3BDarwish%2C+Hebatallah+A%3BElbaz%2C+Eman+M%3BShouman%2C+Samia+A&rft.aulast=Motawi&rft.aufirst=Tarek&rft.date=2016-01-01&rft.volume=2016&rft.issue=&rft.spage=3017108&rft.isbn=&rft.btitle=&rft.title=Oxidative+medicine+and+cellular+longevity&rft.issn=1942-0994&rft_id=info:doi/10.1155%2F2016%2F3017108 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-12 N1 - Date created - 2015-12-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Res. 1983 Aug;43(8):3583-5 [6861130] Anal Biochem. 1976 May 7;72:248-54 [942051] J Clin Invest. 1986 Sep;78(3):790-7 [3745439] J Immunol. 1988 Apr 15;140(8):2829-38 [2451695] J Natl Cancer Inst. 1990 Jul 4;82(13):1107-12 [2359136] Biochem Biophys Res Commun. 1991 Aug 30;179(1):442-8 [1652957] J Biol Chem. 1994 Dec 9;269(49):30761-4 [7983002] Arch Biochem Biophys. 1995 Nov 10;323(2):373-81 [7487101] Cancer Lett. 1998 Jan 9;122(1-2):67-75 [9464493] J Control Release. 1998 Feb 12;51(2-3):193-9 [9685917] Toxicol Lett. 1999 Sep 20;109(1-2):87-95 [10514034] Arch Biochem Biophys. 1959 May;82(1):70-7 [13650640] Cancer Res. 2005 Jan 15;65(2):516-25 [15695394] Neuropharmacology. 2005 Mar;48(3):435-47 [15721176] Cell. 2005 Sep 23;122(6):927-39 [16179260] Biol Pharm Bull. 2005 Oct;28(10):1928-33 [16204948] Proc Natl Acad Sci U S A. 2006 May 16;103(20):7670-5 [16679408] Anticancer Drugs. 2006 Aug;17(7):753-62 [16926625] Pharmacol Rev. 2006 Sep;58(3):621-81 [16968952] Surgery. 2006 Oct;140(4):607-14; discussion 614-5 [17011908] Carcinogenesis. 2006 Dec;27(12):2424-33 [16785249] Braz J Med Biol Res. 2007 Aug;40(8):1011-24 [17665037] Cell Res. 2007 Oct;17(10):839-49 [17893711] Oncogene. 2008 Feb 28;27(10):1472-7 [17767197] Oncogene. 2008 Oct 27;27(50):6398-406 [18955968] Pancreatology. 2008;8(6):566-76 [18824880] Breast Cancer Res Treat. 2008 Dec;112(3):389-403 [18172760] Biopharm Drug Dispos. 2009 Jul;30(5):221-8 [19544289] CA Cancer J Clin. 2009 Jul-Aug;59(4):225-49 [19474385] Ann Oncol. 2009 Aug;20(8):1319-29 [19535820] Chem Biol Interact. 2010 Jul 30;186(2):152-6 [20433813] Biometals. 2010 Dec;23(6):997-1013 [20524045] Cell Death Dis. 2010;1:e18 [21364619] Cancer Lett. 2011 Sep 1;308(1):43-53 [21570765] J Clin Invest. 2011 Oct;121(10):3797-803 [21965336] Mol Biol Rep. 2014 Jan;41(1):85-94 [24190489] Redox Biol. 2015;4:184-92 [25590798] Exp Cell Res. 2000 Apr 10;256(1):12-8 [10739646] Proc Natl Acad Sci U S A. 2001 Mar 27;98(7):4202-8 [11259671] Oncogene. 2001 Jul 12;20(31):4188-97 [11464285] Apoptosis. 2001 Dec;6(6):469-77 [11595837] J Agric Food Chem. 2002 Jan 30;50(3):468-72 [11804514] Methods. 2001 Dec;25(4):402-8 [11846609] J Biol Chem. 2004 Feb 13;279(7):6017-26 [14625298] J Radiat Res. 2004 Jun;45(2):253-60 [15304968] Clin Exp Immunol. 2004 Sep;137(3):546-51 [15320904] Chem Pharm Bull (Tokyo). 1985 May;33(5):2028-34 [4053225] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1155/2016/3017108 ER - TY - JOUR T1 - In vitro, in vivo and in silico metabolic profiling of α-pyrrolidinopentiothiophenone, a novel thiophene stimulant. AN - 1750429791; 26648097 AB - Little or no pharmacological or toxicological data are available for novel psychoactive substances when they first emerge, making their identification and interpretation in biological matrices challenging. A new synthetic cathinone, α-pyrrolidinopentiothiophenone (α-PVT), was incubated with hepatocytes and samples were analyzed using liquid chromatography coupled to a Q Exactive™ Orbitrap mass spectrometer. Authentic urine specimens from suspected α-PVT cases were also analyzed. Scans were data mined with Compound Discoverer™ for identification and structural elucidation of metabolites. Seven α-PVT metabolites were identified in hepatocyte incubations, and in the authentic urine samples, also with an additional monohydroxylated product and a glucuronide of low intensity. α-PVT dihydroxypyrrolidinyl, α-PVT 2-ketopyrrolidinyl, α-PVT hydroxythiophenyl and α-PVT thiophenol had the most intense in vivo signals. JF - Bioanalysis AU - Swortwood, Madeleine J AU - Carlier, Jeremy AU - Ellefsen, Kayla N AU - Wohlfarth, Ariane AU - Diao, Xingxing AU - Concheiro-Guisan, Marta AU - Kronstrand, Robert AU - Huestis, Marilyn A AD - Chemistry & Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, NIH, Baltimore, MD 21224, USA. ; Department of Forensic Genetics & Forensic Toxicology, National Board of Forensic Medicine, Linköping, Sweden. Y1 - 2016 PY - 2016 DA - 2016 SP - 65 EP - 82 VL - 8 IS - 1 KW - Central Nervous System Stimulants KW - 0 KW - Pyrrolidines KW - Thiophenes KW - alpha-pyrrolidinopentiothiophenone KW - Index Medicus KW - high-resolution MS KW - metabolism KW - novel psychoactive substances KW - hepatocytes KW - α-PVT KW - synthetic cathinone KW - Mass Spectrometry KW - Data Mining KW - Microsomes, Liver -- metabolism KW - Humans KW - Hepatocytes -- metabolism KW - Thiophenes -- urine KW - Metabolomics -- methods KW - Pyrrolidines -- urine KW - Computer Simulation KW - Central Nervous System Stimulants -- metabolism KW - Thiophenes -- metabolism KW - Central Nervous System Stimulants -- urine KW - Pyrrolidines -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1750429791?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioanalysis&rft.atitle=In+vitro%2C+in+vivo+and+in+silico+metabolic+profiling+of+%CE%B1-pyrrolidinopentiothiophenone%2C+a+novel+thiophene+stimulant.&rft.au=Swortwood%2C+Madeleine+J%3BCarlier%2C+Jeremy%3BEllefsen%2C+Kayla+N%3BWohlfarth%2C+Ariane%3BDiao%2C+Xingxing%3BConcheiro-Guisan%2C+Marta%3BKronstrand%2C+Robert%3BHuestis%2C+Marilyn+A&rft.aulast=Swortwood&rft.aufirst=Madeleine&rft.date=2016-01-01&rft.volume=8&rft.issue=1&rft.spage=65&rft.isbn=&rft.btitle=&rft.title=Bioanalysis&rft.issn=1757-6199&rft_id=info:doi/10.4155%2Fbio.15.237 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-26 N1 - Date created - 2015-12-18 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.4155/bio.15.237 ER - TY - JOUR T1 - Chemotherapy-induced nausea and vomiting: an overview and comparison of three consensus guidelines. AN - 1750429769; 26561590 AB - Chemotherapy-induced nausea and vomiting (CINV) remains one of the most debilitating toxicities associated with cancer treatment. In recent decades, significant strides have been made in our understanding of the pathophysiology of CINV, making way to more effective targeted pharmacotherapies, especially 5-hydroxytryptamine3 receptor antagonists and neurokinin-1 (NK-1) receptor antagonists. As much as 70%-80% of CINV can be prevented with appropriate administration of available antiemetics. Nevertheless, fear of CINV still may diminish cancer treatment adherence. To assimilate and summarise the rapidly growing body of clinical research literature on CINV, three professional organisations-the Multinational Association of Supportive Care in Cancer/European Society for Medical Oncology, the American Society of Clinical Oncology and the National Comprehensive Cancer Network-have created CINV management guidelines. While these respective guidelines are developed from similar consensus processes using similar clinical research literature, their results demonstrate several key differences in recommended strategies. This article aims to provide an overview of CINV pathophysiology, compare and contrast three expert guidelines and offer considerations for future clinical and research challenges. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/ JF - Postgraduate medical journal AU - Tageja, Nishant AU - Groninger, Hunter AD - Medical Oncology Branch, National Cancer Institute, Bethesda, Maryland, USA. ; Section of Palliative Care, Department of Medicine, MedStar Washington Hospital Center, Washington DC, USA. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 34 EP - 40 VL - 92 IS - 1083 KW - Antiemetics KW - 0 KW - Antineoplastic Agents KW - Index Medicus KW - ONCOLOGY KW - PALLIATIVE CARE KW - Humans KW - Drug-Related Side Effects and Adverse Reactions KW - Practice Guidelines as Topic KW - Nausea -- chemically induced KW - Neoplasms -- drug therapy KW - Antiemetics -- therapeutic use KW - Vomiting -- prevention & control KW - Neoplasms -- complications KW - Nausea -- prevention & control KW - Guideline Adherence KW - Vomiting -- chemically induced KW - Consensus KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1750429769?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Postgraduate+medical+journal&rft.atitle=Chemotherapy-induced+nausea+and+vomiting%3A+an+overview+and+comparison+of+three+consensus+guidelines.&rft.au=Tageja%2C+Nishant%3BGroninger%2C+Hunter&rft.aulast=Tageja&rft.aufirst=Nishant&rft.date=2016-01-01&rft.volume=92&rft.issue=1083&rft.spage=34&rft.isbn=&rft.btitle=&rft.title=Postgraduate+medical+journal&rft.issn=1469-0756&rft_id=info:doi/10.1136%2Fpostgradmedj-2014-132969 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-28 N1 - Date created - 2015-12-17 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1136/postgradmedj-2014-132969 ER - TY - JOUR T1 - CYP2C8 Is a Novel Target of Peroxisome Proliferator-Activated Receptor α in Human Liver. AN - 1750013287; 26467040 AB - Human cytochrome P450 (CYP) 2C enzymes metabolize ∼30% of clinically prescribed drugs and various environmental chemicals. CYP2C8, an important member of this subfamily, metabolizes the anticancer drug paclitaxel, certain antidiabetic drugs, and endogenous substrates, including arachidonic acid, to physiologically active epoxyeicosatrienoic acids. Previous studies from our laboratory showed that microRNA 107 (miR107) and microRNA 103 downregulate CYP2C8 post-transcriptionally. miR107 is located in intron 5 of the pantothenate kinase 1 (PANK1) gene. p53 has been reported to coregulate the induction of PANK1 and miR107. Here, we examine the possible downregulation of CYP2C8 by drugs capable of inducing miR107. Hypolipidemic drugs, such as bezafibrate, known activators of the peroxisome proliferator-activated receptor α (PPARα), induce both the PANK1 gene and miR107 (∼2.5-fold) in primary human hepatocytes. Surprisingly, CYP2C8 mRNA and protein levels were induced by bezafibrate. CYP2C8 promoter activity was increased by ectopic expression of PPARα in HepG2 cells, with a further increase after bezafibrate (∼18-fold), 4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio acetic acid (∼10-fold) treatment, or the antidiabetic drug rosiglitazone, all known PPAR activators. Promoter sequence analyses, deletion studies, mutagenesis studies, and electrophoretic mobility shift assays identified a PPARα response element located at position -2109 base pair relative to the translation start site of CYP2C8. Chromatin immunopreciptation assay analysis confirmed recruitment of PPARα to this PPARα response element after bezafibrate treatment of human hepatocytes. Thus, we show for the first time that CYP2C8 is transcriptionally regulated by PPARα, suggesting the potential for drug-drug interactions due to upregulation of CYP2C8 by PPAR activators. U.S. Government work not protected by U.S. copyright. JF - Molecular pharmacology AU - Makia, Ngome L AU - Goldstein, Joyce A AD - Human Metabolism Group, Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina. ; Human Metabolism Group, Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina goldste1@niehs.nih.gov. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 154 EP - 164 VL - 89 IS - 1 KW - Hypolipidemic Agents KW - 0 KW - PPAR alpha KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - CYP2C8 protein, human KW - Cytochrome P-450 CYP2C8 KW - Index Medicus KW - Hepatocytes -- drug effects KW - Hep G2 Cells KW - Humans KW - Hepatocytes -- metabolism KW - Aryl Hydrocarbon Hydroxylases -- metabolism KW - Drug Delivery Systems -- trends KW - Liver -- drug effects KW - Liver -- metabolism KW - PPAR alpha -- metabolism KW - Cytochrome P-450 CYP2C8 -- metabolism KW - Hypolipidemic Agents -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1750013287?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=CYP2C8+Is+a+Novel+Target+of+Peroxisome+Proliferator-Activated+Receptor+%CE%B1+in+Human+Liver.&rft.au=Makia%2C+Ngome+L%3BGoldstein%2C+Joyce+A&rft.aulast=Makia&rft.aufirst=Ngome&rft.date=2016-01-01&rft.volume=89&rft.issue=1&rft.spage=154&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=1521-0111&rft_id=info:doi/10.1124%2Fmol.115.100255 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-14 N1 - Date created - 2015-12-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Pharmacogenomics. 2006 Jun;7(4):575-85 [16753005] Drug Metab Dispos. 2007 Apr;35(4):682-8 [17220242] Mol Genet Metab. 2007 Jul;91(3):209-17 [17521938] Drug Metab Rev. 2007;39(2-3):515-38 [17786636] Exp Physiol. 2008 Jan;93(1):148-54 [17872966] J Pharmacol Exp Ther. 2009 Apr;329(1):192-201 [19164466] Arterioscler Thromb Vasc Biol. 2010 May;30(5):894-9 [20393155] Nucleic Acids Res. 2011 Jan;39(2):440-53 [20833636] PLoS One. 2011;6(1):e14629 [21304969] Nature. 2011 Jun 30;474(7353):649-53 [21654750] Mol Pharmacol. 2012 Apr;81(4):598-609 [22266374] Trends Endocrinol Metab. 2012 Jul;23(7):351-63 [22704720] Mol Pharmacol. 2012 Sep;82(3):529-40 [22723340] Mol Pharmacol. 2012 Oct;82(4):601-13 [22740640] Mol Pharmacol. 2013 Mar;83(3):709-18 [23295386] Nature. 2013 Mar 21;495(7441):394-8 [23485969] Cell Rep. 2013 Aug 29;4(4):724-37 [23972989] Hepatology. 2014 Mar;59(3):1030-42 [24122873] Mol Pharmacol. 2014 Aug;86(2):125-37 [24830941] J Biol Chem. 2014 Jul 11;289(28):19279-93 [24876382] J Pharmacol Exp Ther. 2002 Aug;302(2):475-82 [12130704] Mol Endocrinol. 2002 May;16(5):1013-28 [11981036] J Biol Chem. 2001 Sep 28;276(39):36059-62 [11451964] Nat Med. 2001 May;7(5):584-90 [11329060] Drug Metab Dispos. 2001 Mar;29(3):242-51 [11181490] Proc Natl Acad Sci U S A. 2010 Apr 6;107(14):6334-9 [20308559] Drug Metab Dispos. 2010 Apr;38(4):591-9 [20086032] Curr Drug Metab. 2009 Nov;10(9):1009-47 [20214592] J Biochem Mol Toxicol. 1999;13(6):289-95 [10487415] PLoS One. 2009;4(8):e6796 [19710929] Curr Drug Metab. 2009 Jul;10(6):567-78 [19702536] Annu Rev Pharmacol Toxicol. 2003;43:149-73 [12171978] J Biol Chem. 2003 Apr 18;278(16):13975-83 [12582161] J Biol Chem. 2003 Aug 29;278(35):32852-60 [12810707] J Lipid Res. 2004 Jan;45(1):17-31 [14523052] Cell. 2004 Jan 23;116(2):281-97 [14744438] Nature. 1992 Aug 27;358(6389):771-4 [1324435] Proc Natl Acad Sci U S A. 1994 Nov 8;91(23):11012-6 [7971999] Biochem J. 1995 Mar 1;306 ( Pt 2):473-9 [7887901] J Biol Chem. 1995 Jul 7;270(27):16114-21 [7608174] Biochim Biophys Acta. 1996 Jul 26;1302(2):93-109 [8695669] J Biol Chem. 1997 Oct 3;272(40):25252-9 [9312141] Arch Biochem Biophys. 1999 Sep 1;369(1):11-23 [10462436] Nature. 1999 Sep 30;401(6752):493-7 [10519554] Gastroenterology. 2004 Nov;127(5):1436-45 [15521013] Pharm Res. 2005 Jan;22(1):71-8 [15771232] Mol Pharmacol. 2005 Apr;67(4):1257-67 [15635043] Clin Pharmacol Ther. 2005 May;77(5):341-52 [15900280] Mol Pharmacol. 2005 Sep;68(3):747-57 [15933212] Drug Metab Dispos. 2006 Jan;34(1):138-44 [16243957] J Pharmacol Exp Ther. 2006 May;317(2):537-45 [16467456] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/mol.115.100255 ER - TY - JOUR T1 - Pesticide use and risk of end-stage renal disease among licensed pesticide applicators in the Agricultural Health Study. AN - 1749622602; 26177651 AB - Experimental studies suggest a relationship between pesticide exposure and renal impairment, but epidemiological evidence is limited. We evaluated the association between exposure to 39 specific pesticides and end-stage renal disease (ESRD) incidence in the Agricultural Health Study, a prospective cohort study of licensed pesticide applicators in Iowa and North Carolina. Via linkage to the US Renal Data System, we identified 320 ESRD cases diagnosed between enrolment (1993-1997) and December 2011 among 55 580 male licensed pesticide applicators. Participants provided information on use of pesticides via self-administered questionnaires. Lifetime pesticide use was defined as the product of duration and frequency of use and then modified by an intensity factor to account for differences in pesticide application practices. Cox proportional hazards models, adjusted for age and state, were used to estimate associations between ESRD and: (1) ordinal categories of intensity-weighted lifetime use of 39 pesticides, (2) poisoning and high-level pesticide exposures and (3) pesticide exposure resulting in a medical visit or hospitalisation. Positive exposure-response trends were observed for the herbicides alachlor, atrazine, metolachlor, paraquat, and pendimethalin, and the insecticide permethrin. More than one medical visit due to pesticide use (HR=2.13; 95% CI 1.17 to 3.89) and hospitalisation due to pesticide use (HR=3.05; 95% CI 1.67 to 5.58) were significantly associated with ESRD. Our findings support an association between ESRD and chronic exposure to specific pesticides, and suggest pesticide exposures resulting in medical visits may increase the risk of ESRD. Clinicaltrials.gov NCT00352924. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/ JF - Occupational and environmental medicine AU - Lebov, Jill F AU - Engel, Lawrence S AU - Richardson, David AU - Hogan, Susan L AU - Hoppin, Jane A AU - Sandler, Dale P AD - Department of Epidemiology, University of North Carolina, Chapel Hill, North Carolina, USA. ; Department of Medicine, Division of Nephrology and Hypertension, University of North Carolina, Chapel Hill, North Carolina, USA. ; Department of Biological Sciences, Center for Human Health and the Environment, North Carolina State University, Raleigh, North Carolina, USA. ; Epidemiology Branch/Chronic Disease Epidemiology Group, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 3 EP - 12 VL - 73 IS - 1 KW - Herbicides KW - 0 KW - Pesticides KW - Index Medicus KW - Herbicides -- adverse effects KW - Prospective Studies KW - Risk Factors KW - Humans KW - North Carolina KW - Incidence KW - Occupations KW - Iowa KW - Male KW - Proportional Hazards Models KW - Agriculture KW - Occupational Diseases -- etiology KW - Occupational Exposure -- adverse effects KW - Kidney Failure, Chronic -- etiology KW - Pesticides -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1749622602?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+environmental+medicine&rft.atitle=Pesticide+use+and+risk+of+end-stage+renal+disease+among+licensed+pesticide+applicators+in+the+Agricultural+Health+Study.&rft.au=Lebov%2C+Jill+F%3BEngel%2C+Lawrence+S%3BRichardson%2C+David%3BHogan%2C+Susan+L%3BHoppin%2C+Jane+A%3BSandler%2C+Dale+P&rft.aulast=Lebov&rft.aufirst=Jill&rft.date=2016-01-01&rft.volume=73&rft.issue=1&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=Occupational+and+environmental+medicine&rft.issn=1470-7926&rft_id=info:doi/10.1136%2Foemed-2014-102615 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-07 N1 - Date created - 2015-12-15 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00352924; ClinicalTrials.gov N1 - SuppNotes - Comment In: Occup Environ Med. 2016 Jan;73(1):1-2 [26403530] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1136/oemed-2014-102615 ER - TY - JOUR T1 - The danger-associated molecular pattern HMGB1 mediates the neuroinflammatory effects of methamphetamine. AN - 1749616122; 26254235 AB - Methamphetamine (METH) induces neuroinflammatory effects, which may contribute to the neurotoxicity of METH. However, the mechanism by which METH induces neuroinflammation has yet to be clarified. A considerable body of evidence suggests that METH induces cellular damage and distress, particularly in dopaminergic neurons. Damaged neurons release danger-associated molecular patterns (DAMPs) such as high mobility group box-1 (HMGB1), which induces pro-inflammatory effects. Therefore, we explored the notion here that METH induces neuroinflammation indirectly through the release of HMGB1 from damaged neurons. Adult male Sprague-Dawley rats were injected IP with METH (10mg/kg) or vehicle (0.9% saline). Neuroinflammatory effects of METH were measured in nucleus accumbens (NAcc), ventral tegmental area (VTA) and prefrontal cortex (PFC) at 2h, 4h and 6h after injection. To assess whether METH directly induces pro-inflammatory effects in microglia, whole brain or striatal microglia were isolated using a Percoll density gradient and exposed to METH (0, 0.1, 1, 10, 100, or 1000μM) for 24h and pro-inflammatory cytokines measured. The effect of METH on HMGB1 and IL-1β in striatal tissue was then measured. To determine the role of HMGB1 in the neuroinflammatory effects of METH, animals were injected intra-cisterna magna with the HMGB1 antagonist box A (10μg) or vehicle (sterile water). 24h post-injection, animals were injected IP with METH (10mg/kg) or vehicle (0.9% saline) and 4h later neuroinflammatory effects measured in NAcc, VTA, and PFC. METH induced robust pro-inflammatory effects in NAcc, VTA, and PFC as a function of time and pro-inflammatory analyte measured. In particular, METH induced profound effects on IL-1β in NAcc (2h) and PFC (2h and 4h). Exposure of microglia to METH in vitro failed to induce a pro-inflammatory response, but rather induced significant cell death as well as a decrease in IL-1β. METH treatment increased HMGB1 in parallel with IL-1β in striatum. Pre-treatment with the HMGB1 antagonist box A blocked the neuroinflammatory effects (IL-1β) of METH in NAcc, VTA and PFC. The present results suggest that HMGB1 mediates, in part, the neuroinflammatory effects of METH and thus may alert CNS innate immune cells to the toxic effects of METH. Copyright © 2015 Elsevier Inc. All rights reserved. JF - Brain, behavior, and immunity AU - Frank, Matthew G AU - Adhikary, Sweta AU - Sobesky, Julia L AU - Weber, Michael D AU - Watkins, Linda R AU - Maier, Steven F AD - Department of Psychology and Neuroscience, and the Center for Neuroscience, University of Colorado, Boulder, CO, USA. Electronic address: matt.frank@colorado.edu. ; National Institute on Drug Abuse, National Institutes of Health, USA. ; Department of Psychology and Neuroscience, and the Center for Neuroscience, University of Colorado, Boulder, CO, USA. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 99 EP - 108 VL - 51 KW - HMGB1 Protein KW - 0 KW - Hbp1 protein, rat KW - Inflammation Mediators KW - Methamphetamine KW - 44RAL3456C KW - Index Medicus KW - DAMP KW - HMGB1 KW - Neurotoxicity KW - Neuroinflammation KW - Microglia KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Prefrontal Cortex -- metabolism KW - Nucleus Accumbens -- drug effects KW - Corpus Striatum -- metabolism KW - Nucleus Accumbens -- metabolism KW - Corpus Striatum -- drug effects KW - Ventral Tegmental Area -- metabolism KW - Ventral Tegmental Area -- drug effects KW - Prefrontal Cortex -- drug effects KW - Microglia -- drug effects KW - Male KW - Microglia -- metabolism KW - Methamphetamine -- administration & dosage KW - Brain -- drug effects KW - Brain -- metabolism KW - Encephalitis -- chemically induced KW - Encephalitis -- metabolism KW - HMGB1 Protein -- metabolism KW - Inflammation Mediators -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1749616122?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain%2C+behavior%2C+and+immunity&rft.atitle=The+danger-associated+molecular+pattern+HMGB1+mediates+the+neuroinflammatory+effects+of+methamphetamine.&rft.au=Frank%2C+Matthew+G%3BAdhikary%2C+Sweta%3BSobesky%2C+Julia+L%3BWeber%2C+Michael+D%3BWatkins%2C+Linda+R%3BMaier%2C+Steven+F&rft.aulast=Frank&rft.aufirst=Matthew&rft.date=2016-01-01&rft.volume=51&rft.issue=&rft.spage=99&rft.isbn=&rft.btitle=&rft.title=Brain%2C+behavior%2C+and+immunity&rft.issn=1090-2139&rft_id=info:doi/10.1016%2Fj.bbi.2015.08.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2017-01-10 N1 - Date created - 2015-12-15 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbi.2015.08.001 ER - TY - JOUR T1 - Clinically Relevant Pharmacological Strategies That Reverse MDMA-Induced Brain Hyperthermia Potentiated by Social Interaction. AN - 1749612555; 26105141 AB - MDMA-induced hyperthermia is highly variable, unpredictable, and greatly potentiated by the social and environmental conditions of recreational drug use. Current strategies to treat pathological MDMA-induced hyperthermia in humans are palliative and marginally effective, and there are no specific pharmacological treatments to counteract this potentially life-threatening condition. Here, we tested the efficacy of mixed adrenoceptor blockers carvedilol and labetalol, and the atypical antipsychotic clozapine, in reversing MDMA-induced brain and body hyperthermia. We injected rats with a moderate non-toxic dose of MDMA (9 mg/kg) during social interaction, and we administered potential treatment drugs after the development of robust hyperthermia (>2.5 °C), thus mimicking the clinical situation of acute MDMA intoxication. Brain temperature was our primary focus, but we also simultaneously recorded temperatures from the deep temporal muscle and skin, allowing us to determine the basic physiological mechanisms of the treatment drug action. Carvedilol was modestly effective in attenuating MDMA-induced hyperthermia by moderately inhibiting skin vasoconstriction, and labetalol was ineffective. In contrast, clozapine induced a marked and immediate reversal of MDMA-induced hyperthermia via inhibition of brain metabolic activation and blockade of skin vasoconstriction. Our findings suggest that clozapine, and related centrally acting drugs, might be highly effective for reversing MDMA-induced brain and body hyperthermia in emergency clinical situations, with possible life-saving results. JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology AU - Kiyatkin, Eugene A AU - Ren, Suelynn AU - Wakabayashi, Ken T AU - Baumann, Michael H AU - Shaham, Yavin AD - National Institute on Drug Abuse-Intramural Research Program, NIH, Baltimore, MD, USA. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 549 EP - 559 VL - 41 IS - 2 KW - Antipsychotic Agents KW - 0 KW - Carbazoles KW - Hallucinogens KW - Propanolamines KW - Sympathomimetics KW - Vasodilator Agents KW - carvedilol KW - 0K47UL67F2 KW - Clozapine KW - J60AR2IKIC KW - N-Methyl-3,4-methylenedioxyamphetamine KW - KE1SEN21RM KW - Labetalol KW - R5H8897N95 KW - Index Medicus KW - Animals KW - Skin -- physiopathology KW - Rats, Long-Evans KW - Body Temperature -- drug effects KW - Antipsychotic Agents -- pharmacology KW - Sympathomimetics -- pharmacology KW - Homeostasis -- physiology KW - Homeostasis -- drug effects KW - Vasodilator Agents -- pharmacology KW - Skin -- drug effects KW - Carbazoles -- pharmacology KW - Clozapine -- pharmacology KW - Labetalol -- pharmacology KW - Propanolamines -- pharmacology KW - Male KW - Fever -- chemically induced KW - Brain -- physiopathology KW - N-Methyl-3,4-methylenedioxyamphetamine -- adverse effects KW - Brain -- drug effects KW - Social Behavior KW - Hallucinogens -- pharmacology KW - Hallucinogens -- adverse effects KW - N-Methyl-3,4-methylenedioxyamphetamine -- pharmacology KW - Fever -- physiopathology KW - Fever -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1749612555?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.atitle=Clinically+Relevant+Pharmacological+Strategies+That+Reverse+MDMA-Induced+Brain+Hyperthermia+Potentiated+by+Social+Interaction.&rft.au=Kiyatkin%2C+Eugene+A%3BRen%2C+Suelynn%3BWakabayashi%2C+Ken+T%3BBaumann%2C+Michael+H%3BShaham%2C+Yavin&rft.aulast=Kiyatkin&rft.aufirst=Eugene&rft.date=2016-01-01&rft.volume=41&rft.issue=2&rft.spage=549&rft.isbn=&rft.btitle=&rft.title=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.issn=1740-634X&rft_id=info:doi/10.1038%2Fnpp.2015.182 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-20 N1 - Date created - 2015-12-15 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/npp.2015.182 ER - TY - JOUR T1 - Polyphenols as Modulator of Oxidative Stress in Cancer Disease: New Therapeutic Strategies. AN - 1747311089; 26649142 AB - Cancer onset and progression have been linked to oxidative stress by increasing DNA mutations or inducing DNA damage, genome instability, and cell proliferation and therefore antioxidant agents could interfere with carcinogenesis. It is well known that conventional radio-/chemotherapies influence tumour outcome through ROS modulation. Since these antitumour treatments have important side effects, the challenge is to develop new anticancer therapeutic strategies more effective and less toxic for patients. To this purpose, many natural polyphenols have emerged as very promising anticancer bioactive compounds. Beside their well-known antioxidant activities, several polyphenols target epigenetic processes involved in cancer development through the modulation of oxidative stress. An alternative strategy to the cytotoxic treatment is an approach leading to cytostasis through the induction of therapy-induced senescence. Many anticancer polyphenols cause cellular growth arrest through the induction of a ROS-dependent premature senescence and are considered promising antitumour therapeutic tools. Furthermore, one of the most innovative and interesting topics is the evaluation of efficacy of prooxidant therapies on cancer stem cells (CSCs). Several ROS inducers-polyphenols can impact CSCs metabolisms and self-renewal related pathways. Natural polyphenol roles, mainly in chemoprevention and cancer therapies, are described and discussed in the light of the current literature data. JF - Oxidative medicine and cellular longevity AU - Mileo, Anna Maria AU - Miccadei, Stefania AD - Regina Elena National Cancer Institute, 00144 Rome, Italy. Y1 - 2016 PY - 2016 DA - 2016 SP - 6475624 VL - 2016 KW - Antioxidants KW - 0 KW - Polyphenols KW - Reactive Oxygen Species KW - Index Medicus KW - Animals KW - Humans KW - Reactive Oxygen Species -- metabolism KW - Neoplasms -- drug therapy KW - Polyphenols -- therapeutic use KW - Antioxidants -- therapeutic use KW - Oxidative Stress -- drug effects KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1747311089?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oxidative+medicine+and+cellular+longevity&rft.atitle=Polyphenols+as+Modulator+of+Oxidative+Stress+in+Cancer+Disease%3A+New+Therapeutic+Strategies.&rft.au=Mileo%2C+Anna+Maria%3BMiccadei%2C+Stefania&rft.aulast=Mileo&rft.aufirst=Anna&rft.date=2016-01-01&rft.volume=2016&rft.issue=&rft.spage=6475624&rft.isbn=&rft.btitle=&rft.title=Oxidative+medicine+and+cellular+longevity&rft.issn=1942-0994&rft_id=info:doi/10.1155%2F2016%2F6475624 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-08 N1 - Date created - 2015-12-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Pancreas. 2001 Jan;22(1):1-7 [11138960] Cancer Res. 2001 Apr 15;61(8):3299-307 [11309284] Drugs Aging. 2001;18(9):685-716 [11599635] Biomed Pharmacother. 2002 Mar;56(2):84-7 [12000139] Int J 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STAT3 activity delays obesity-induced thyroid carcinogenesis in a mouse model. AN - 1738481720; 26552408 AB - Compelling epidemiologic studies indicate that obesity is a risk factor for many human cancers, including thyroid cancer. In recent decades, the incidence of thyroid cancer has dramatically increased along with a marked rise in obesity prevalence. We previously demonstrated that a high fat diet (HFD) effectively induced the obese phenotype in a mouse model of thyroid cancer (Thrb(PV/PV)Pten(+/-) mice). Moreover, HFD activates the STAT3 signal pathway to promote more aggressive tumor phenotypes. The aim of the present study was to evaluate the effect of S3I-201, a specific inhibitor of STAT3 activity, on HFD-induced aggressive cancer progression in the mouse model of thyroid cancer. WT and Thrb(PV/PV)Pten(+/-) mice were treated with HFD together with S3I-201 or vehicle-only as controls. We assessed the effects of S3I-201 on HFD-induced thyroid cancer progression, the leptin-JAK2-STAT3 signaling pathway, and key regulators of epithelial-mesenchymal transition (EMT). S3I-201 effectively inhibited HFD-induced aberrant activation of STAT3 and its downstream targets to markedly inhibit thyroid tumor growth and to prolong survival. Decreased protein levels of cyclins D1 and B1, cyclin dependent kinase 4 (CDK4), CDK6, and phosphorylated retinoblastoma protein led to the inhibition of tumor cell proliferation in S3I-201-treated Thrb(PV/PV)Pten(+/-) mice. Reduced occurrence of vascular invasion and blocking of anaplasia and lung metastasis in thyroid tumors of S3I-201-treated Thrb(PV/PV)Pten(+/-) mice were mediated via decreased expression of vimentin and matrix metalloproteinases, two key effectors of EMT. The present findings suggest that inhibition of the STAT3 activity would be a novel treatment strategy for obesity-induced thyroid cancer. © 2016 Society for Endocrinology. JF - Endocrine-related cancer AU - Park, Jeong Won AU - Han, Cho Rong AU - Zhao, Li AU - Willingham, Mark C AU - Cheng, Sheue-yann AD - Laboratory of Molecular BiologyCenter for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Dr, Room 5128, Bethesda, Maryland 20892-6264, USA. ; Laboratory of Molecular BiologyCenter for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Dr, Room 5128, Bethesda, Maryland 20892-6264, USA chengs@mail.nih.gov. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 53 EP - 63 VL - 23 IS - 1 KW - Aminosalicylic Acids KW - 0 KW - Benzenesulfonates KW - NSC 74859 KW - STAT3 Transcription Factor KW - Stat3 protein, mouse KW - Thyroid Hormone Receptors beta KW - PTEN Phosphohydrolase KW - EC 3.1.3.67 KW - Pten protein, mouse KW - Index Medicus KW - thyroid hormone receptor β mutant KW - JAK2-STAT3 signaling KW - Pten-deficiency KW - thyroid cancer KW - obesity KW - STAT3 inhibitor KW - preclinical mouse model KW - Cell Proliferation -- drug effects KW - Animals KW - Thyroid Gland -- pathology KW - Disease Models, Animal KW - Epithelial-Mesenchymal Transition -- drug effects KW - Mice KW - Diet, High-Fat KW - Mice, Transgenic KW - PTEN Phosphohydrolase -- genetics KW - Aminosalicylic Acids -- pharmacology KW - Thyroid Gland -- drug effects KW - Cell Proliferation -- genetics KW - Epithelial-Mesenchymal Transition -- genetics KW - Thyroid Hormone Receptors beta -- genetics KW - Down-Regulation -- drug effects KW - STAT3 Transcription Factor -- antagonists & inhibitors KW - Benzenesulfonates -- pharmacology KW - Obesity -- pathology KW - Thyroid Neoplasms -- genetics KW - Carcinogenesis -- drug effects KW - Thyroid Neoplasms -- pathology KW - Thyroid Neoplasms -- etiology KW - STAT3 Transcription Factor -- metabolism KW - Thyroid Neoplasms -- mortality KW - Obesity -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1738481720?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrine-related+cancer&rft.atitle=Inhibition+of+STAT3+activity+delays+obesity-induced+thyroid+carcinogenesis+in+a+mouse+model.&rft.au=Park%2C+Jeong+Won%3BHan%2C+Cho+Rong%3BZhao%2C+Li%3BWillingham%2C+Mark+C%3BCheng%2C+Sheue-yann&rft.aulast=Park&rft.aufirst=Jeong&rft.date=2016-01-01&rft.volume=23&rft.issue=1&rft.spage=53&rft.isbn=&rft.btitle=&rft.title=Endocrine-related+cancer&rft.issn=1479-6821&rft_id=info:doi/10.1530%2FERC-15-0417 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-26 N1 - Date created - 2015-11-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Int Med Res. 2012;40(6):2041-50 [23321160] Thyroid. 2014 Feb;24(2):190-9 [23879222] Endocrinology. 2013 Aug;154(8):2936-47 [23748362] Biochem Biophys Res Commun. 2001 Mar 9;281(4):907-12 [11237746] Nat Rev Mol Cell Biol. 2014 Mar;15(3):178-96 [24556840] Oncogene. 2003 Jan 23;22(3):319-29 [12545153] Oncogene. 2004 Apr 29;23(20):3550-60 [15116091] Science. 1992 Oct 16;258(5081):424-9 [1411535] J Biol Chem. 1996 May 3;271(18):10441-4 [8631837] Cell. 1999 Aug 6;98(3):295-303 [10458605] Mol Cell Biol. 2005 Jan;25(1):124-35 [15601836] Cancer Res. 2005 Jun 15;65(12):5054-62 [15958548] Biochem Biophys Res Commun. 2006 Jan 20;339(3):923-31 [16329991] Int J Oncol. 2007 Feb;30(2):437-42 [17203226] Cancer Epidemiol Biomarkers Prev. 2008 Sep;17(9):2286-90 [18768494] Oncogene. 2009 Jan 29;28(4):509-17 [18997818] Biol Cell. 2010 Jan;102(1):1-12 [19566485] J Clin Endocrinol Metab. 2009 Nov;94(11):4423-32 [19820016] Asian J Surg. 2009 Oct;32(4):216-23 [19892624] Am J Epidemiol. 2010 Jan 15;171(2):242-52 [19951937] J Cell Physiol. 2010 Apr;223(1):14-26 [20049846] J Obstet Gynaecol Res. 2009 Oct;35(5):918-25 [20149042] Surgery. 2010 Jun;147(6):847-53 [20045163] Cancer Epidemiol Biomarkers Prev. 2011 Mar;20(3):464-72 [21266520] Int J Clin Exp Pathol. 2011 Apr;4(4):356-62 [21577321] Thyroid. 2011 Sep;21(9):957-63 [21767143] Pathol Oncol Res. 2012 Jan;18(1):17-23 [21681602] Mol Cancer Res. 2011 Dec;9(12):1658-67 [21976712] Proc Natl Acad Sci U S A. 2012 Jan 10;109(2):600-5 [22190485] J Biol Chem. 2012 Feb 17;287(8):5819-32 [22205702] Proc Natl Acad Sci U S A. 2012 Jun 12;109(24):9623-8 [22623533] Clin Cancer Res. 2012 Jun 15;18(12):3396-406 [22634319] Int J Biol Markers. 2012 Apr-Jun;27(2):e132-8 [22467101] Clin Endocrinol (Oxf). 2013 Jan;78(1):134-40 [22812676] World J Surg. 2014 Oct;38(10):2621-7 [24867470] Neoplasia. 2014 Sep;16(9):757-69 [25246276] CA Cancer J Clin. 2012 Mar-Apr;62(2):118-28 [22281605] Annu Rev Med. 2015;66:311-28 [25587654] Endocrinology. 2015 Mar;156(3):1181-93 [25555091] Cardiovasc Res. 2015 Jun 1;106(3):365-74 [25784694] Clin Endocrinol (Oxf). 2015 Aug;83(2):261-7 [25158596] Proc Natl Acad Sci U S A. 2007 May 1;104(18):7391-6 [17463090] Oral Oncol. 2007 Sep;43(8):785-90 [17169602] Lancet. 2008 Feb 16;371(9612):569-78 [18280327] Oncogene. 2000 May 15;19(21):2474-88 [10851046] Tumour Biol. 2014 Aug;35(8):7335-42 [24880591] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1530/ERC-15-0417 ER - TY - JOUR T1 - microRNAs in Cancer Chemoprevention: Method to Isolate Them from Fresh Tissues. AN - 1737479759; 26608287 AB - microRNAs are 22-nucleotide-long double-strand small RNAs, able to modulate gene expression at posttranscriptional level, degrading mRNA and/or impairing translation. They have been shown to regulate mRNA and protein abundance and to participate in many regulatory circuits controlling developmental timing, cell proliferation and differentiation, apoptosis and stress response. Notably, microRNA activity has been correlated to the pathogenesis of cancer; they are aberrantly expressed in solid and hematological tumors, suggesting that they could function as oncogenes or tumor suppressors. The emerging role of miRNAs in the carcinogenesis and tumor progression has provided opportunities for their clinical application in the capacity of cancer detection, diagnosis, and prognosis prediction. Here, we describe the experimental protocol used to isolate microRNAs from human tissues coming from head and neck, mesothelioma, and thymoma tumors in order to perform microarray and RT-qPCR experiments. JF - Methods in molecular biology (Clifton, N.J.) AU - Ganci, Federica AU - Blandino, Giovanni AD - Translational Oncogenomics Unit, Italian National Cancer Institute "Regina Elena", 53 Via Elio Chianesi, 00144, Rome, Italy. ; Laboratory of Translational Oncogenomics, Molecular Medicine Department, Regina Elena National Cancer Institute, Rome, Italy. blandino@ifo.it. Y1 - 2016 PY - 2016 DA - 2016 SP - 21 EP - 29 VL - 1379 KW - MicroRNAs KW - 0 KW - Index Medicus KW - RNA extraction KW - HNSCC KW - Thymoma KW - Mesothelioma KW - microRNA KW - Fresh tissues KW - Humans KW - MicroRNAs -- genetics KW - Neoplasms -- prevention & control KW - MicroRNAs -- isolation & purification KW - Chemoprevention KW - Chemical Fractionation -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1737479759?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.atitle=microRNAs+in+Cancer+Chemoprevention%3A+Method+to+Isolate+Them+from+Fresh+Tissues.&rft.au=Ganci%2C+Federica%3BBlandino%2C+Giovanni&rft.aulast=Ganci&rft.aufirst=Federica&rft.date=2016-01-01&rft.volume=1379&rft.issue=&rft.spage=21&rft.isbn=&rft.btitle=&rft.title=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.issn=1940-6029&rft_id=info:doi/10.1007%2F978-1-4939-3191-0_3 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-07 N1 - Date created - 2015-11-26 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/978-1-4939-3191-0_3 ER - TY - JOUR T1 - Computational Methods for Structural and Functional Studies of Alzheimer's Amyloid Ion Channels. AN - 1721353487; 26453217 AB - Aggregation can be studied by a range of methods, experimental and computational. Aggregates form in solution, across solid surfaces, and on and in the membrane, where they may assemble into unregulated leaking ion channels. Experimental probes of ion channel conformations and dynamics are challenging. Atomistic molecular dynamics (MD) simulations are capable of providing insight into structural details of amyloid ion channels in the membrane at a resolution not achievable experimentally. Since data suggest that late stage Alzheimer's disease involves formation of toxic ion channels, MD simulations have been used aiming to gain insight into the channel shapes, morphologies, pore dimensions, conformational heterogeneity, and activity. These can be exploited for drug discovery. Here we describe computational methods to model amyloid ion channels containing the β-sheet motif at atomic scale and to calculate toxic pore activity in the membrane. JF - Methods in molecular biology (Clifton, N.J.) AU - Jang, Hyunbum AU - Arce, Fernando Teran AU - Lee, Joon AU - Gillman, Alan L AU - Ramachandran, Srinivasan AU - Kagan, Bruce L AU - Lal, Ratnesh AU - Nussinov, Ruth AD - Cancer and Inflammation Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, National Cancer Institute at Frederick, 1050 Boyles Street, Frederick, MD, 21702, USA. jangh2@mail.nih.gov. ; Department of Bioengineering, Materials Science Program, University of California, San Diego, La Jolla, CA, 92093, USA. ; Department of Mechanical and Aerospace Engineering, Materials Science Program, University of California, San Diego, La Jolla, CA, 92093, USA. ; Department of Psychiatry, David Geffen School of Medicine, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA, 90024, USA. ; Cancer and Inflammation Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, National Cancer Institute at Frederick, 1050 Boyles Street, Frederick, MD, 21702, USA. nussinor@helix.nih.gov. Y1 - 2016 PY - 2016 DA - 2016 SP - 251 EP - 268 VL - 1345 KW - Amyloid beta-Peptides KW - 0 KW - Ion Channels KW - Peptide Fragments KW - Index Medicus KW - Amyloid channel KW - NAMD KW - Lipid bilayer KW - β-Sheet channel KW - CHARMM KW - Molecular dynamics simulations KW - Protein Structure, Secondary KW - Peptide Fragments -- chemistry KW - Humans KW - Molecular Dynamics Simulation KW - Ion Channels -- chemistry KW - Alzheimer Disease -- genetics KW - Amyloid beta-Peptides -- metabolism KW - Computational Biology -- methods KW - Amyloid beta-Peptides -- chemistry KW - Ion Channels -- metabolism KW - Alzheimer Disease -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1721353487?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.atitle=Computational+Methods+for+Structural+and+Functional+Studies+of+Alzheimer%27s+Amyloid+Ion+Channels.&rft.au=Jang%2C+Hyunbum%3BArce%2C+Fernando+Teran%3BLee%2C+Joon%3BGillman%2C+Alan+L%3BRamachandran%2C+Srinivasan%3BKagan%2C+Bruce+L%3BLal%2C+Ratnesh%3BNussinov%2C+Ruth&rft.aulast=Jang&rft.aufirst=Hyunbum&rft.date=2016-01-01&rft.volume=1345&rft.issue=&rft.spage=251&rft.isbn=&rft.btitle=&rft.title=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.issn=1940-6029&rft_id=info:doi/10.1007%2F978-1-4939-2978-8_16 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-07 N1 - Date created - 2015-10-10 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/978-1-4939-2978-8_16 ER - TY - JOUR T1 - Enhanced Chemotherapeutic Behavior of Open-Caged DNA@Doxorubicin Nanostructures for Cancer Cells. AN - 1718078488; 26031628 AB - In cancer therapy, it is imperative to increase the efficacy and reduce side effects of chemotherapeutic drugs. Nanotechnology offers the unique opportunity to overcome these barriers. In particular, in the last few years, DNA nanostructures have gained attention for their biocompatibility, easy customized synthesis and ability to deliver drugs to cancer cells. Here, an open-caged pyramidal DNA@Doxorubicin (Py-Doxo) nanostructure was constructed with 10 DNA sequences of 26-28 nucleotides for drug delivery to cancer cells. The synthesized DNA nanostructures are sufficiently stable in biological medium. Py-Doxo exhibited significantly enhanced cytotoxicity of the delivered doxorubicin to breast and liver cancer cells up to twofold compared to free doxorubicin. This study demonstrates the importance of the shape and structure of the designed transporter DNA nanostructures for biomedical applications. © 2015 Wiley Periodicals, Inc. JF - Journal of cellular physiology AU - Kumar, Vinit AU - Bayda, Samer AU - Hadla, Mohamad AU - Caligiuri, Isabella AU - Russo Spena, Concetta AU - Palazzolo, Stefano AU - Kempter, Susanne AU - Corona, Giuseppe AU - Toffoli, Giuseppe AU - Rizzolio, Flavio AD - Clinical Pharmacology, Department of Molecular Biology and Translational Research, National Cancer Institute and Center for Molecular Biomedicine, PN, Italy. ; Faculty of Physics and Center for Nanoscience, Ludwig-Maximilians-Universität München, München, Germany. Y1 - 2016/01// PY - 2016 DA - January 2016 SP - 106 EP - 110 VL - 231 IS - 1 KW - DNA Adducts KW - 0 KW - doxorubicin-DNA KW - Doxorubicin KW - 80168379AG KW - Index Medicus KW - Humans KW - Drug Delivery Systems -- methods KW - Cell Line, Tumor KW - Female KW - Breast Neoplasms -- genetics KW - Breast Neoplasms -- drug therapy KW - Doxorubicin -- therapeutic use KW - DNA Adducts -- therapeutic use KW - Nanostructures UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1718078488?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+physiology&rft.atitle=Enhanced+Chemotherapeutic+Behavior+of+Open-Caged+DNA%40Doxorubicin+Nanostructures+for+Cancer+Cells.&rft.au=Kumar%2C+Vinit%3BBayda%2C+Samer%3BHadla%2C+Mohamad%3BCaligiuri%2C+Isabella%3BRusso+Spena%2C+Concetta%3BPalazzolo%2C+Stefano%3BKempter%2C+Susanne%3BCorona%2C+Giuseppe%3BToffoli%2C+Giuseppe%3BRizzolio%2C+Flavio&rft.aulast=Kumar&rft.aufirst=Vinit&rft.date=2016-01-01&rft.volume=231&rft.issue=1&rft.spage=106&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+physiology&rft.issn=1097-4652&rft_id=info:doi/10.1002%2Fjcp.25057 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-19 N1 - Date created - 2015-09-29 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/jcp.25057 ER - TY - JOUR T1 - Pre-clinical immunotoxicity studies of nanotechnology-formulated drugs: Challenges, considerations and strategy. AN - 1751195234; 26348388 AB - Assorted challenges in physicochemical characterization, sterilization, depyrogenation, and in the assessment of pharmacology, safety, and efficacy profiles accompany pre-clinical development of nanotechnology-formulated drugs. Some of these challenges are not unique to nanotechnology and are common in the development of other pharmaceutical products. However, nanoparticle-formulated drugs are biochemically sophisticated, which causes their translation into the clinic to be particularly complex. An understanding of both the immune compatibility of nanoformulations and their effects on hematological parameters is now recognized as an important step in the (pre)clinical development of nanomedicines. An evaluation of nanoparticle immunotoxicity is usually performed as a part of a traditional toxicological assessment; however, it often requires additional in vitro and in vivo specialized immuno- and hematotoxicity tests. Herein, I review literature examples and share the experience with the NCI Nanotechnology Characterization Laboratory assay cascade used in the early (discovery-level) phase of pre-clinical development to summarize common challenges in the immunotoxicological assessment of nanomaterials, highlight considerations and discuss solutions to overcome problems that commonly slow or halt the translation of nanoparticle-formulated drugs toward clinical trials. Special attention will be paid to the grand-challenge related to detection, quantification and removal of endotoxin from nanoformulations, and practical considerations related to this challenge. Copyright © 2015 Elsevier B.V. All rights reserved. JF - Journal of controlled release : official journal of the Controlled Release Society AU - Dobrovolskaia, Marina A AD - Nanotechnology Characterization Laboratory, Cancer Research Technology Program, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, NCI at Frederick, Frederick, MD 21702, United States. Electronic address: marina@mail.nih.gov. Y1 - 2015/12/28/ PY - 2015 DA - 2015 Dec 28 SP - 571 EP - 583 VL - 220 KW - Index Medicus KW - Endotoxin KW - Coagulopathy KW - Anaphylaxis KW - Nanoparticles KW - Thrombosis KW - Protein binding KW - Pre-clinical KW - Immunotoxicity KW - Complement activation KW - Hemolysis KW - Cytokines KW - Phagocytosis KW - Animals KW - Chemistry, Pharmaceutical KW - Risk Factors KW - Humans KW - Risk Assessment KW - Immune System -- metabolism KW - Immune System -- drug effects KW - Nanomedicine -- methods KW - Toxicology -- methods KW - Immunologic Techniques KW - Immune System -- immunology KW - Nanoparticles -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751195234?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+controlled+release+%3A+official+journal+of+the+Controlled+Release+Society&rft.atitle=Pre-clinical+immunotoxicity+studies+of+nanotechnology-formulated+drugs%3A+Challenges%2C+considerations+and+strategy.&rft.au=Dobrovolskaia%2C+Marina+A&rft.aulast=Dobrovolskaia&rft.aufirst=Marina&rft.date=2015-12-28&rft.volume=220&rft.issue=&rft.spage=571&rft.isbn=&rft.btitle=&rft.title=Journal+of+controlled+release+%3A+official+journal+of+the+Controlled+Release+Society&rft.issn=1873-4995&rft_id=info:doi/10.1016%2Fj.jconrel.2015.08.056 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-10-05 N1 - Date created - 2015-12-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Liposome Res. 2012 Sep;22(3):177-92 [22332871] Part Fibre Toxicol. 2012;9:20 [22697169] 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[20001600] Mol Ther. 2010 Jan;18(1):171-80 [19738601] Wiley Interdiscip Rev Nanomed Nanobiotechnol. 2010 Jan-Feb;2(1):99-112 [20049834] J Toxicol Environ Health A. 2010;73(11):748-56 [20391117] Nanomedicine (Lond). 2010 Jun;5(4):555-62 [20528451] J Drug Target. 2010 Aug;18(7):489-98 [20192653] J Control Release. 2010 Sep 1;146(2):164-74 [20385183] Nanotoxicology. 2010 Mar;4(1):52-72 [20795902] Clin Cancer Res. 2010 Dec 15;16(24):6139-49 [20876255] Nat Nanotechnol. 2011 Jan;6(1):39-44 [21170037] J Immunotoxicol. 2011 Jan-Mar;8(1):56-67 [21288165] Int J Immunopathol Pharmacol. 2011 Jan-Mar;24(1 Suppl):65S-71S [21329568] J Control Release. 2012 Jul 20;161(2):403-8 [22306428] J Control Release. 2012 Jul 20;161(2):164-74 [22516097] Swiss Med Wkly. 2012;142:w13609 [22736064] Nanomedicine. 2012 Aug;8(6):987-95 [22100755] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jconrel.2015.08.056 ER - TY - JOUR T1 - Hepatocyte Nuclear Factor 4α Controls Iron Metabolism and Regulates Transferrin Receptor 2 in Mouse Liver. AN - 1751992720; 26527688 AB - Iron is an essential element in biological systems, but excess iron promotes the formation of reactive oxygen species, resulting in cellular toxicity. Several iron-related genes are highly expressed in the liver, a tissue in which hepatocyte nuclear factor 4α (HNF4α) plays a critical role in controlling gene expression. Therefore, the role of hepatic HNF4α in iron homeostasis was examined using liver-specific HNF4α-null mice (Hnf4a(ΔH) mice). Hnf4a(ΔH) mice exhibit hypoferremia and a significant change in hepatic gene expression. Notably, the expression of transferrin receptor 2 (Tfr2) mRNA was markedly decreased in Hnf4a(ΔH) mice. Promoter analysis of the Tfr2 gene showed that the basal promoter was located at a GC-rich region upstream of the transcription start site, a region that can be transactivated in an HNF4α-independent manner. HNF4α-dependent expression of Tfr2 was mediated by a proximal promoter containing two HNF4α-binding sites located between the transcription start site and the translation start site. Both the GC-rich region of the basal promoter and the HNF4α-binding sites were required for maximal transactivation. Moreover, siRNA knockdown of HNF4α suppressed TFR2 expression in human HCC cells. These results suggest that Tfr2 is a novel target gene for HNF4α, and hepatic HNF4α plays a critical role in iron homeostasis. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Matsuo, Shunsuke AU - Ogawa, Masayuki AU - Muckenthaler, Martina U AU - Mizui, Yumiko AU - Sasaki, Shota AU - Fujimura, Takafumi AU - Takizawa, Masayuki AU - Ariga, Nagayuki AU - Ozaki, Hiroaki AU - Sakaguchi, Masakiyo AU - Gonzalez, Frank J AU - Inoue, Yusuke AD - From the Division of Molecular Science, Graduate School of Science and Technology, Gunma University, Kiryu, Gunma 376-8515, Japan. ; the Department of Pediatric Oncology, Hematology and Immunology, University of Heidelberg, 69120 Heidelberg, Germany. ; the Department of Cell Biology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama 700-8558, Japan, and. ; the Laboratory of Metabolism, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20852. ; From the Division of Molecular Science, Graduate School of Science and Technology, Gunma University, Kiryu, Gunma 376-8515, Japan, yinoue@gunma-u.ac.jp. Y1 - 2015/12/25/ PY - 2015 DA - 2015 Dec 25 SP - 30855 EP - 30865 VL - 290 IS - 52 KW - Hepatocyte Nuclear Factor 4 KW - 0 KW - Receptors, Transferrin KW - Trfr2 protein, mouse KW - Iron KW - E1UOL152H7 KW - Index Medicus KW - transferrin KW - transferrin receptor 2 KW - liver KW - nuclear receptor KW - hepcidin KW - transcription regulation KW - hypoferremia KW - HNF4α KW - iron metabolism KW - Transcription Initiation Site KW - Animals KW - Promoter Regions, Genetic KW - Mice KW - Male KW - Female KW - Mice, Knockout KW - Binding Sites KW - Receptors, Transferrin -- genetics KW - Hepatocyte Nuclear Factor 4 -- genetics KW - Liver -- metabolism KW - Gene Expression Regulation KW - Hepatocyte Nuclear Factor 4 -- metabolism KW - Iron -- metabolism KW - Receptors, Transferrin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751992720?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Hepatocyte+Nuclear+Factor+4%CE%B1+Controls+Iron+Metabolism+and+Regulates+Transferrin+Receptor+2+in+Mouse+Liver.&rft.au=Matsuo%2C+Shunsuke%3BOgawa%2C+Masayuki%3BMuckenthaler%2C+Martina+U%3BMizui%2C+Yumiko%3BSasaki%2C+Shota%3BFujimura%2C+Takafumi%3BTakizawa%2C+Masayuki%3BAriga%2C+Nagayuki%3BOzaki%2C+Hiroaki%3BSakaguchi%2C+Masakiyo%3BGonzalez%2C+Frank+J%3BInoue%2C+Yusuke&rft.aulast=Matsuo&rft.aufirst=Shunsuke&rft.date=2015-12-25&rft.volume=290&rft.issue=52&rft.spage=30855&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M115.694414 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-10 N1 - Date created - 2015-12-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 1999 Jul 23;274(30):20826-32 [10409623] Blood. 2004 Nov 15;104(10):3136-47 [15297311] Science. 2004 Dec 17;306(5704):2090-3 [15514116] Gut. 2005 Jul;54(7):980-6 [15951546] J Lipid Res. 2006 Jan;47(1):215-27 [16264197] Biochim Biophys Acta. 2006 Jul;1763(7):668-89 [16872694] Blood. 2009 Jan 15;113(3):688-95 [18997172] Cell Metab. 2009 Mar;9(3):217-27 [19254567] Biochem J. 2011 Mar 15;434(3):365-81 [21348856] J Clin Pathol. 2011 Apr;64(4):281-6 [21177266] Free Radic Biol Med. 2012 Jan 1;52(1):59-69 [22064361] Antioxid Redox Signal. 2012 Jun 1;16(11):1323-67 [22146081] Biometals. 2012 Aug;25(4):677-86 [22294463] Physiol Rev. 2013 Oct;93(4):1721-41 [24137020] Crit Rev Oncol Hematol. 2015 Jul;95(1):12-25 [25737209] Gastroenterology. 2007 Jan;132(1):301-10 [17241880] Nat Genet. 2000 May;25(1):14-5 [10802645] J Biol Chem. 2000 Dec 8;275(49):38135-8 [11027676] Mol Cell Biol. 2001 Feb;21(4):1393-403 [11158324] Blood. 2001 Sep 15;98(6):1949-54 [11535534] Biochemistry. 2002 Jan 29;41(4):1217-28 [11802721] Pharmacol Rev. 2002 Mar;54(1):129-58 [11870262] J Biol Chem. 2002 Jul 12;277(28):25257-65 [11994307] Biotechniques. 2002 Sep;33(3):620-8, 630 [12238772] J Biol Chem. 2002 Oct 25;277(43):41163-70 [12183449] Blood. 2003 May 1;101(9):3690-8 [12393473] Nat Genet. 2003 May;34(1):102-7 [12704390] J Biol Chem. 2004 Jan 23;279(4):2480-9 [14583614] Pharmacol Rev. 2004 Jun;56(2):291-330 [15169930] Mol Endocrinol. 2004 Aug;18(8):1975-87 [15155787] Int J Biochem Cell Biol. 2004 Nov;36(11):2137-43 [15313461] J Biol Chem. 2004 Oct 22;279(43):44740-8 [15292250] J Lab Clin Med. 1987 Dec;110(6):690-705 [3681112] Nature. 1991 Jan 17;349(6306):257-60 [1987478] Am J Hum Genet. 1993 Jul;53(1):201-13 [8317485] J Biol Chem. 1993 Nov 5;268(31):23399-408 [8226864] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M115.694414 ER - TY - JOUR T1 - A Library of Plasmodium vivax Recombinant Merozoite Proteins Reveals New Vaccine Candidates and Protein-Protein Interactions AN - 1762356596; PQ0002480823 AB - Plasmodium vivax causes malaria in millions of people each year, primarily in Southeast Asia and Central and South America. P. vivax has a dormant liver stage, which can lead to disease recurrence in infected individuals even in the absence of mosquito transmission. The development of vaccines that target blood-stage P. vivax parasites is therefore likely to be an essential component of any worldwide effort to eradicate malaria. Studying P. vivax is very difficult as this parasite grows poorly in the laboratory and invades only small numbers of young red blood cells in patients. Due to these and other challenges, only a handful of P. vivax proteins have been tested as potential vaccines. To generate more vaccine candidates, we expressed the entire ectodomains of 37 proteins that are predicted to be involved in P. vivax invasion of red blood cells. Antibodies from Cambodian patients with P. vivax malaria recognized heat-sensitive epitopes in the majority of these proteins, suggesting that they are natively folded. We also used the proteins to screen for both predicted and novel protein-protein interactions, confirming that the proteins are functional and further supporting their potential as vaccine candidates. As a new community resource, this P. vivax recombinant protein library will facilitate future studies of P. vivax pathogenesis and immunity, and greatly expands the list of candidate vaccine antigens. JF - PLoS Neglected Tropical Diseases AU - Hostetler, Jessica B AU - Sharma, Sumana AU - Bartholdson, SJosefin AU - Wright, Gavin J AU - Fairhurst, Rick M AU - Rayner, Julian C AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America Y1 - 2015/12/23/ PY - 2015 DA - 2015 Dec 23 PB - Public Library of Science, 185 Berry Street San Francisco CA 94107 United States VL - 9 IS - 12 SN - 1935-2727, 1935-2727 KW - Genetics Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources KW - Parasites KW - Human diseases KW - Erythrocytes KW - Disease control KW - Plasmodium vivax KW - Malaria KW - Immunity KW - Public health KW - Disease transmission KW - Recombinants KW - ASW, South America KW - Antibodies KW - Merozoites KW - Vaccines KW - ISEW, Southeast Asia KW - Protein interaction KW - Epitopes KW - K 03400:Human Diseases KW - Q1 08604:Stock assessment and management KW - G 07730:Development & Cell Cycle KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1762356596?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+Neglected+Tropical+Diseases&rft.atitle=A+Library+of+Plasmodium+vivax+Recombinant+Merozoite+Proteins+Reveals+New+Vaccine+Candidates+and+Protein-Protein+Interactions&rft.au=Hostetler%2C+Jessica+B%3BSharma%2C+Sumana%3BBartholdson%2C+SJosefin%3BWright%2C+Gavin+J%3BFairhurst%2C+Rick+M%3BRayner%2C+Julian+C&rft.aulast=Hostetler&rft.aufirst=Jessica&rft.date=2015-12-23&rft.volume=9&rft.issue=12&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+Neglected+Tropical+Diseases&rft.issn=19352727&rft_id=info:doi/10.1371%2Fjournal.pntd.0004264 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Recombinants; Parasites; Human diseases; Erythrocytes; Disease control; Malaria; Vaccines; Disease transmission; Public health; Antibodies; Merozoites; Immunity; Epitopes; Protein interaction; Plasmodium vivax; ASW, South America; ISEW, Southeast Asia DO - http://dx.doi.org/10.1371/journal.pntd.0004264 ER - TY - JOUR T1 - Rosuvastatin Alters the Proteome of High Density Lipoproteins: Generation of alpha-1-antitrypsin Enriched Particles with Anti-inflammatory Properties AN - 1808679508; PQ0003416735 AB - Statins lower plasma cholesterol by as much as 50%, thus reducing future cardiovascular events. However, the physiological effects of statins are diverse and not all are related to low density lipoprotein cholesterol (LDL-C) lowering. We performed a small clinical pilot study to assess the impact of statins on lipoprotein-associated proteins in healthy individuals (n = 10) with normal LDL-C (<130 mg/dL), who were treated with rosuvastatin (20 mg/day) for 28 days. Proteomic analysis of size-exclusion chromatography isolated LDL, large high density lipoprotein (HDL-L), and small HDL (HDL-S) fractions and spectral counting was used to compare relative protein detection before and after statin therapy. Significant protein changes were found in each lipoprotein pool and included both increases and decreases in several proteins involved in lipoprotein metabolism, complement regulation and acute phase response. The most dramatic effect of the rosuvastatin treatment was an increase in alpha -1-antirypsin (A1AT) spectral counts associated with HDL-L particles. Quantitative measurement by ELISA confirmed an average 5.7-fold increase in HDL-L associated A1AT. Molecular modeling predictions indicated that the hydrophobic reactive center loop of A1AT, the functional domain responsible for its protease inhibitor activity, is likely involved in lipid binding and association with HDL was found to protect A1AT against oxidative inactivation. Cell culture experiments, using J774 macrophages, demonstrated that the association of A1AT with HDL enhances its antiprotease activity, preventing elastase induced production of tumor necrosis factor alpha . In conclusion, we show that statins can significantly alter the protein composition of both LDL and HDL and our studies reveal a novel functional relationship between A1AT and HDL. The up-regulation of A1AT on HDL enhances its anti-inflammatory functionality, which may contribute to the non-lipid lowering beneficial effects of statins. JF - Molecular and Cellular Proteomics AU - Gordon, Scott M AU - McKenzie, Benjamin AU - Kemeh, Georgina AU - Sampson, Maureen AU - Perl, Shira AU - Young, Neal S AU - Fessler, Michael B AU - Remaley, Alan T AD - From the Lipoprotein Metabolism Section, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland; , scott.gordon@nih.gov Y1 - 2015/12/19/ PY - 2015 DA - 2015 Dec 19 SP - 3247 EP - 3257 PB - American Society for Biochemistry and Molecular Biology, 9650 Rockville Pike Bethesda MD 20814-3996 United States VL - 14 IS - 12 SN - 1535-9476, 1535-9476 KW - Biotechnology and Bioengineering Abstracts KW - Macrophages KW - Enzyme-linked immunosorbent assay KW - Chromatography KW - Lipids KW - Lipoproteins (high density) KW - Proteinase inhibitors KW - Elastase KW - statins KW - Cell culture KW - Hydrophobicity KW - Cholesterol KW - Lipoproteins (low density) KW - Inflammation KW - Lipoproteins KW - Protein composition KW - Protein turnover KW - Tumor necrosis factor- alpha KW - proteomics KW - Antiinflammatory agents KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808679508?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+Cellular+Proteomics&rft.atitle=Rosuvastatin+Alters+the+Proteome+of+High+Density+Lipoproteins%3A+Generation+of+alpha-1-antitrypsin+Enriched+Particles+with+Anti-inflammatory+Properties&rft.au=Gordon%2C+Scott+M%3BMcKenzie%2C+Benjamin%3BKemeh%2C+Georgina%3BSampson%2C+Maureen%3BPerl%2C+Shira%3BYoung%2C+Neal+S%3BFessler%2C+Michael+B%3BRemaley%2C+Alan+T&rft.aulast=Gordon&rft.aufirst=Scott&rft.date=2015-12-19&rft.volume=14&rft.issue=12&rft.spage=3247&rft.isbn=&rft.btitle=&rft.title=Molecular+and+Cellular+Proteomics&rft.issn=15359476&rft_id=info:doi/10.1074%2Fmcp.M115.054031 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Macrophages; Enzyme-linked immunosorbent assay; Chromatography; Lipids; Elastase; Proteinase inhibitors; Lipoproteins (high density); statins; Hydrophobicity; Cell culture; Cholesterol; Inflammation; Lipoproteins (low density); Lipoproteins; Protein composition; Protein turnover; proteomics; Tumor necrosis factor- alpha; Antiinflammatory agents DO - http://dx.doi.org/10.1074/mcp.M115.054031 ER - TY - JOUR T1 - CCR 20th Anniversary Commentary: Autologous T Cells-The Ultimate Personalized Drug for the Immunotherapy of Human Cancer AN - 1808634892; PQ0003450241 AB - The article by Rosenberg and colleagues, which was published in the July 1, 2011, issue of Clinical Cancer Research, demonstrated the power of the adoptive transfer of autologous antitumor T cells to mediate the complete, durable, and likely curative regression of cancer in patients with heavily pretreated metastatic melanoma. It also provided a stimulus to the development of cell transfer approaches for other cancer types using both natural and genetically engineered lymphocytes. Clin Cancer Res; 21(24); 5409-11. copyright 2015 AACR.See related article by Rosenberg et al., Clin Cancer Res 2011; 17(13) July 1, 2011; 4550-7 JF - Clinical Cancer Research AU - Rosenberg, Steven A AD - Surgery Branch, NCI, NIH, Bethesda, Maryland, sar@nih.gov Y1 - 2015/12/15/ PY - 2015 DA - 2015 Dec 15 SP - 5409 EP - 5411 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 24 SN - 1078-0432, 1078-0432 KW - Biotechnology and Bioengineering Abstracts KW - Metastases KW - Immunotherapy KW - Genetic engineering KW - Lymphocytes T KW - Adoptive transfer KW - Cancer KW - Melanoma KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808634892?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Cancer+Research&rft.atitle=CCR+20th+Anniversary+Commentary%3A+Autologous+T+Cells-The+Ultimate+Personalized+Drug+for+the+Immunotherapy+of+Human+Cancer&rft.au=Rosenberg%2C+Steven+A&rft.aulast=Rosenberg&rft.aufirst=Steven&rft.date=2015-12-15&rft.volume=21&rft.issue=24&rft.spage=5409&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-3131 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Metastases; Genetic engineering; Immunotherapy; Adoptive transfer; Lymphocytes T; Cancer; Melanoma DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-3131 ER - TY - JOUR T1 - CRISPR-STAT: an easy and reliable PCR-based method to evaluate target-specific sgRNA activity. AN - 1750001012; 26253739 AB - CRISPR/Cas9 has emerged as a versatile genome-engineering tool that relies on a single guide RNA (sgRNA) and the Cas9 enzyme for genome editing. Simple, fast and economical methods to generate sgRNAs have made targeted mutagenesis routine in cultured cells, mice, zebrafish and other model systems. Pre-screening of sgRNAs for target efficacy is desirable both for successful mutagenesis and minimizing wasted animal husbandry on targets with poor activity. Here, we describe an easy, quick and cost-effective fluorescent polymerase chain reaction (PCR)-based method, CRISPR Somatic Tissue Activity Test (CRISPR-STAT), to determine target-specific efficiency of sgRNA. As a proof of principle, we validated our method using 28 sgRNAs with known and varied levels of germline transmission efficiency in zebrafish by analysis of their somatic activity in injected embryos. Our data revealed a strong positive correlation between the fluorescent PCR profiles of the injected embryos and the germline transmission efficiency. Furthermore, the assay was sensitive enough to evaluate multiplex gene targeting. This method is easy to implement by laboratories with access to a capillary sequencer. Although we validated the method using CRISPR/Cas9 and zebrafish, it can be applied to other model systems and other genome targeting nucleases. Published by Oxford University Press on behalf of Nucleic Acids Research 2015. This work is written by (a) US Government employee(s) and is in the public domain in the US. JF - Nucleic acids research AU - Carrington, Blake AU - Varshney, Gaurav K AU - Burgess, Shawn M AU - Sood, Raman AD - Zebrafish Core, Translational and Functional Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Developmental Genomics Section, Translational and Functional Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Zebrafish Core, Translational and Functional Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA rsood@mail.nih.gov. Y1 - 2015/12/15/ PY - 2015 DA - 2015 Dec 15 SP - 1 VL - 43 IS - 22 KW - RNA KW - 63231-63-0 KW - Index Medicus KW - Animals KW - Fluorescence KW - Zebrafish -- genetics KW - RNA -- metabolism KW - Polymerase Chain Reaction -- methods KW - CRISPR-Cas Systems KW - INDEL Mutation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1750001012?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=CRISPR-STAT%3A+an+easy+and+reliable+PCR-based+method+to+evaluate+target-specific+sgRNA+activity.&rft.au=Carrington%2C+Blake%3BVarshney%2C+Gaurav+K%3BBurgess%2C+Shawn+M%3BSood%2C+Raman&rft.aulast=Carrington&rft.aufirst=Blake&rft.date=2015-12-15&rft.volume=43&rft.issue=22&rft.spage=e157&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=1362-4962&rft_id=info:doi/10.1093%2Fnar%2Fgkv802 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-21 N1 - Date created - 2015-12-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biotechniques. 2004 Apr;36(4):702-7 [15088388] Genome Res. 2015 Jul;25(7):1030-42 [26048245] PLoS One. 2009;4(2):e4348 [19198653] Genome Res. 2009 Jul;19(7):1279-88 [19470664] Nat Methods. 2011 Jan;8(1):67-9 [21151135] Nucleic Acids Res. 2011 Jul;39(12):e82 [21493687] Nat Biotechnol. 2011 Aug;29(8):697-8 [21822241] Nat Biotechnol. 2011 Aug;29(8):699-700 [21822242] Nat Biotechnol. 2012 May;30(5):460-5 [22484455] PLoS Genet. 2012;8(8):e1002861 [22916025] Nature. 2012 Nov 1;491(7422):114-8 [23000899] Science. 2013 Feb 15;339(6121):819-23 [23287718] Science. 2013 Feb 15;339(6121):823-6 [23287722] PLoS One. 2013;8(2):e57239 [23451191] Nat Biotechnol. 2013 Mar;31(3):227-9 [23360964] Trends Biotechnol. 2013 Jul;31(7):397-405 [23664777] Genetics. 2013 Aug;194(4):1029-35 [23709638] Nucleic Acids Res. 2013 Aug;41(14):e141 [23748566] Proc Natl Acad Sci U S A. 2013 Aug 20;110(34):13904-9 [23918387] Nat Methods. 2013 Oct;10(10):957-63 [24076990] Nat Biotechnol. 2014 Mar;32(3):279-84 [24463574] PLoS One. 2014;9(5):e98186 [24873830] PLoS One. 2014;9(6):e98282 [24901507] Cell. 2014 Jun 5;157(6):1262-78 [24906146] Bioinformatics. 2014 Oct 15;30(20):2968-70 [24990609] BMC Genomics. 2014;15:1002 [25409780] Genome Res. 2014 Dec;24(12):2059-65 [25373145] Zebrafish. 2014 Dec;11(6):583-5 [25470533] Nat Biotechnol. 2014 Dec;32(12):1262-7 [25184501] Nucleic Acids Res. 2014 Dec 16;42(22):e168 [25300484] Sci Rep. 2015;5:8841 [25740433] Nat Methods. 2015 Jun;12(6):535-40 [25867848] Nat Biotechnol. 2008 Jun;26(6):702-8 [18500334] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/nar/gkv802 ER - TY - JOUR T1 - Induction of Inhibitory Receptors on T Cells During Plasmodium vivax Malaria Impairs Cytokine Production. AN - 1736412060; 26019284 AB - The function and regulation of the immune response triggered during malaria is complex and poorly understood, and there is a particular paucity of studies conducted in humans infected with Plasmodium vivax. While it has been proposed that T-cell-effector responses are crucial for protection against blood-stage malaria in mice, the mechanisms behind this in humans remain poorly understood. Experimental models of malaria have shown that the regulatory molecules, cytotoxic T-lymphocyte attenuator-4 (CTLA-4), lymphocyte activation gene-3 (LAG-3), and programmed death-1 (PD-1) are involved in the functional impairment of T cells during infection. Our goal was to define the role of these molecules during P. vivax malaria. We demonstrate that infection triggers the expression of regulatory molecules on T cells. The pattern of expression differs in CD4(+) and CD8(+) T cells. Higher frequencies of CD4(+) express more than 1 regulatory molecule compared to CD8(+) T cells. Moreover, lower proportions of CD4(+) T cells coexpress regulatory molecules, but are still able to proliferate. Importantly, simultaneously blockade of the CLTA-4, PD-1, and T-cell immunoglobulin and mucin-3 signaling restores the cytokine production by antigen-specific cells. These data support the hypothesis that upregulation of inhibitory receptors on T cells during P. vivax malaria impairs parasite-specific T-cell effector function. © The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. JF - The Journal of infectious diseases AU - Costa, Pedro A C AU - Leoratti, Fabiana M S AU - Figueiredo, Maria M AU - Tada, Mauro S AU - Pereira, Dhelio B AU - Junqueira, Caroline AU - Soares, Irene S AU - Barber, Daniel L AU - Gazzinelli, Ricardo T AU - Antonelli, Lis R V AD - Laboratório de Immunopatologia, Centro de Pesquisas René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, Minas Gerais. ; Centro de Pesquisas em Medicina Tropical de Rondônia, Porto Velho. ; Departamento de Análises Clínicas e Toxicológicas, Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, Brazil. ; T Lymphocyte Biology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland. ; Laboratório de Immunopatologia, Centro de Pesquisas René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, Minas Gerais Departamento de Bioquímica e Imunologia, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil. Y1 - 2015/12/15/ PY - 2015 DA - 2015 Dec 15 SP - 1999 EP - 2010 VL - 212 IS - 12 KW - Cytokines KW - 0 KW - Receptors, Antigen, T-Cell KW - Abridged Index Medicus KW - Index Medicus KW - malaria KW - T cells KW - Plasmodium vivax KW - regulatory molecules KW - Young Adult KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Female KW - Receptors, Antigen, T-Cell -- metabolism KW - Cytokines -- antagonists & inhibitors KW - Plasmodium vivax -- immunology KW - Malaria, Vivax -- immunology KW - Malaria, Vivax -- parasitology KW - Immune Tolerance KW - T-Lymphocytes -- immunology KW - Host-Pathogen Interactions UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1736412060?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=Induction+of+Inhibitory+Receptors+on+T+Cells+During+Plasmodium+vivax+Malaria+Impairs+Cytokine+Production.&rft.au=Costa%2C+Pedro+A+C%3BLeoratti%2C+Fabiana+M+S%3BFigueiredo%2C+Maria+M%3BTada%2C+Mauro+S%3BPereira%2C+Dhelio+B%3BJunqueira%2C+Caroline%3BSoares%2C+Irene+S%3BBarber%2C+Daniel+L%3BGazzinelli%2C+Ricardo+T%3BAntonelli%2C+Lis+R+V&rft.aulast=Costa&rft.aufirst=Pedro+A&rft.date=2015-12-15&rft.volume=212&rft.issue=12&rft.spage=1999&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=1537-6613&rft_id=info:doi/10.1093%2Finfdis%2Fjiv306 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-08 N1 - Date created - 2015-11-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1992 Apr 15;89(8):3200-3 [1565611] J Exp Med. 2002 Apr 1;195(7):881-92 [11927632] Nature. 2006 Sep 21;443(7109):350-4 [16921384] J Leukoc Biol. 2007 May;81(5):1258-68 [17307864] Microbes Infect. 2007 May;9(6):687-94 [17398134] Infect Immun. 2007 Jul;75(7):3621-32 [17470539] Nat Immunol. 2008 Jul;9(7):725-32 [18563083] Immunol Rev. 2008 Jun;223:317-33 [18613845] J Immunol. 2008 Nov 15;181(10):6738-46 [18981091] Biochim Biophys Acta. 2008 Dec;1779(12):811-9 [18771758] J Exp Med. 2008 Nov 24;205(12):2763-79 [19001139] Nat Immunol. 2009 Jan;10(1):29-37 [19043418] PLoS Pathog. 2009 Feb;5(2):e1000313 [19247441] PLoS One. 2010;5(2):e9245 [20169070] Malar J. 2010;9:13 [20070895] Nat Med. 2010 Apr;16(4):452-9 [20208540] PLoS Negl Trop Dis. 2010;4(8):e774 [20689816] J Infect Dis. 2010 Aug 15;202(4):638-47 [20617923] J Exp Med. 2010 Sep 27;207(10):2175-86 [20819923] J Exp Med. 2010 Sep 27;207(10):2187-94 [20819927] J Clin Invest. 2010 Dec;120(12):4546-57 [21084749] Infect Immun. 2011 May;79(5):1873-81 [21357717] Blood. 2011 May 5;117(18):4805-15 [21398582] Proc Natl Acad Sci U S A. 2011 May 31;108(22):9196-201 [21576466] Nat Immunol. 2012 Feb;13(2):188-95 [22157630] PLoS Pathog. 2012 Feb;8(2):e1002504 [22319445] PLoS One. 2012;7(7):e40798 [22844411] J Immunol. 2013 Feb 1;190(3):1038-47 [23264654] Trends Parasitol. 2013 Jun;29(6):286-94 [23623759] J Immunol. 2013 Dec 1;191(11):5542-50 [24154626] Cell Rep. 2013 Dec 12;5(5):1204-13 [24316071] J Infect Dis. 2014 Jan 15;209(2):290-9 [23922369] Nature. 2002 Feb 7;415(6872):673-9 [11832955] Nature. 2006 Feb 9;439(7077):682-7 [16382236] Clin Exp Immunol. 2003 Aug;133(2):145-52 [12869017] Nat Rev Immunol. 2004 Mar;4(3):169-80 [15039754] Clin Microbiol Rev. 2004 Jul;17(3):509-39, table of contents [15258091] J Immunol. 1984 Oct;133(4):1710-5 [6206131] Science. 1987 Sep 4;237(4819):1210-2 [3306918] Trans R Soc Trop Med Hyg. 1987;81(1):25-8 [3328333] Annu Rev Immunol. 2014;32:157-87 [24655294] Nat Rev Immunol. 2014 Nov;14(11):744-57 [25324127] Infect Immun. 2000 May;68(5):3061-3 [10769016] J Infect Dis. 2001 Mar 1;183(5):796-804 [11181157] Eur J Immunol. 2001 Oct;31(10):2970-8 [11592073] Am J Trop Med Hyg. 1994 Sep;51(3):372-9 [7524374] Infect Immun. 1996 Mar;64(3):913-8 [8641800] Immunogenetics. 1998 Jul;48(2):116-24 [9634475] J Exp Med. 2006 Jun 12;203(6):1427-33 [16754719] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/infdis/jiv306 ER - TY - JOUR T1 - Serological response to Helicobacter pylori infection among Latin American populations with contrasting risks of gastric cancer. AN - 1721346887; 26178251 AB - Gastric cancer is a rare outcome of chronic Helicobacter pylori infection. Serologic profiles may reveal bacterial, environmental and/or host factors associated with cancer risk. We therefore compared specific anti-H. pylori antibodies among populations with at least twofold differences in gastric cancer mortality from Mexico, Colombia and Chile. Our study included 1,776 adults (mean age 42 years) from three nationally representative surveys, equally divided between residents of high- and low-risk areas. Antibodies to 15 immunogenic H. pylori antigens were measured by fluorescent bead-based multiplex assays; results were summarized to identify overall H. pylori seropositivity. We used logistic regression to model associations between antibody seroreactivity and regional cancer risk (high vs. low), adjusting for country, age and sex. Both risk areas had similar H. pylori seroprevalence. Residents in high- and low-risk areas were seroreactive to a similar number of antigens (means 8.2 vs. 7.9, respectively; adjusted odds ratio, OR: 1.02, p = 0.05). Seroreactivities to Catalase and the known virulence proteins CagA and VacA were each significantly (p < 0.05) associated with residence in high-risk areas, but ORs were moderate (1.26, 1.42 and 1.41, respectively) and their discriminatory power was low (area under the curve < 0.6). The association of Catalase was independent from effects of either CagA or VacA. Sensitivity analyses for antibody associations restricted to H. pylori-seropositive individuals generally replicated significant associations. Our findings suggest that humoral responses to H. pylori are insufficient to distinguish high and low gastric cancer risk in Latin America. Factors determining population variation of gastric cancer burden remain to be identified. © 2015 UICC. JF - International journal of cancer AU - Camargo, M Constanza AU - Beltran, Mauricio AU - Conde-Glez, Carlos J AU - Harris, Paul R AU - Michel, Angelika AU - Waterboer, Tim AU - Carolina Flórez, Astrid AU - Torres, Javier AU - Ferreccio, Catterina AU - Sampson, Joshua N AU - Pawlita, Michael AU - Rabkin, Charles S AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD. ; Dirección de Redes en Salud Pública, Instituto Nacional de Salud, Bogotá, Colombia. ; Centro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública, Cuernavaca, Morelos, México. ; Departamento de Gastroenterología y Nutrición Pediátrica, Pontificia Universidad Católica de Chile, Santiago, Chile. ; Division of Genome Modifications and Carcinogenesis, Infection and Cancer Program, German Cancer Research Center (DFKZ), Heidelberg, Germany. ; Laboratorio de Parasitología, Dirección de Redes en Salud Pública, Laboratorio Nacional de Referencia, Instituto Nacional de Salud, Bogotá, Colombia. ; Unidad de Investigación en Enfermedades Infecciosas, UMAE Pediatría, CMN SXXI, Instituto Mexicano del Seguro Social, México City, México. ; Crónicas Advanced Center for Chronic Diseases, Departamento de Salud Pública, Pontificia Universidad Católica de Chile, Santiago, Chile. Y1 - 2015/12/15/ PY - 2015 DA - 2015 Dec 15 SP - 3000 EP - 3005 VL - 137 IS - 12 KW - Antibodies, Bacterial KW - 0 KW - Index Medicus KW - H. pylori KW - gastric cancer KW - Latin America KW - serology KW - Sensitivity and Specificity KW - Risk KW - Hispanic Americans KW - Humans KW - Adult KW - Male KW - Female KW - Survival Analysis KW - Stomach Neoplasms -- microbiology KW - Stomach Neoplasms -- immunology KW - Helicobacter Infections -- immunology KW - Helicobacter Infections -- mortality KW - Helicobacter pylori -- immunology KW - Stomach Neoplasms -- mortality KW - Helicobacter Infections -- blood KW - Antibodies, Bacterial -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1721346887?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Serological+response+to+Helicobacter+pylori+infection+among+Latin+American+populations+with+contrasting+risks+of+gastric+cancer.&rft.au=Camargo%2C+M+Constanza%3BBeltran%2C+Mauricio%3BConde-Glez%2C+Carlos+J%3BHarris%2C+Paul+R%3BMichel%2C+Angelika%3BWaterboer%2C+Tim%3BCarolina+Fl%C3%B3rez%2C+Astrid%3BTorres%2C+Javier%3BFerreccio%2C+Catterina%3BSampson%2C+Joshua+N%3BPawlita%2C+Michael%3BRabkin%2C+Charles+S&rft.aulast=Camargo&rft.aufirst=M&rft.date=2015-12-15&rft.volume=137&rft.issue=12&rft.spage=3000&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.29678 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-25 N1 - Date created - 2015-10-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Environ Health Perspect. 2003 Nov;111(15):1819-26 [14630514] Epidemiology. 2005 Jul;16(4):586-90 [15951682] Int J Cancer. 2004 Jan 20;108(3):456-63 [14648714] Gastroenterology. 2003 Dec;125(6):1636-44 [14724815] Proteomics. 2004 Oct;4(10):2843-8 [15378757] Cancer Epidemiol Biomarkers Prev. 1993 Jan-Feb;2(1):37-40 [8420610] Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):662-7 [17416755] Cancer Res. 2009 Apr 1;69(7):2973-80 [19318564] Cancer Res. 2009 Aug 1;69(15):6164-70 [19602590] Helicobacter. 2009 Dec;14(6):525-35 [19889070] Tohoku J Exp Med. 2010 Jan;220(1):3-14 [20046046] Proc Natl Acad Sci U S A. 2011 May 31;108(22):9238-43 [21562218] Microbes Infect. 2011 Sep;13(10):799-807 [21477660] Cancer Epidemiol Biomarkers Prev. 2012 Dec;21(12):2185-92 [23035179] Cancer Causes Control. 2013 Feb;24(2):217-31 [23224270] Cancer Causes Control. 2013 Feb;24(2):249-56 [23224271] FEBS Lett. 2013 Jun 19;587(12):1823-8 [23684642] BMC Gastroenterol. 2013;13:104 [23800201] Int J Cancer. 2014 Jun 15;134(12):2942-50 [24259284] Cancer Epidemiol Biomarkers Prev. 2002 Oct;11(10 Pt 1):1091-4 [12376512] Proteomics. 2002 Mar;2(3):313-24 [11921447] Helicobacter. 2003 Dec;8(6):613-25 [14632677] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ijc.29678 ER - TY - JOUR T1 - Clinical validity of a DPYD-based pharmacogenetic test to predict severe toxicity to fluoropyrimidines. AN - 1721346834; 26099996 AB - Pre-therapeutic DPYD pharmacogenetic test to prevent fluoropyrimidines (FL)-related toxicities is not yet common practice in medical oncology. We aimed at investigating the clinical validity of DPYD genetic analysis in a large series of oncological patients. Six hundred three cancer patients, treated with FL, have been retrospectively tested for eight DPYD polymorphisms (DPYD-rs3918290, DPYD-rs55886062, DPYD-rs67376798, DPYD-rs2297595, DPYD-rs1801160, DPYD-rs1801158, DPYD-rs1801159, DPYD-rs17376848) for association with Grade ≥3 toxicity, developed within the first three cycles of therapy. DPYD-rs3918290 and DPYD-rs67376798 were associated to Grade ≥3 toxicity after bootstrap validation and Bonferroni correction (p = 0.003, p = 0.048). DPYD-rs55886062 was not significant likely due to its low allelic frequency, nonetheless one out of two heterozygous patients (compound heterozygous with DPYD-rs3918290) died from toxicity after one cycle. Test specificity for the analysis of DPYD-rs3918290, DPYD-rs55886062 and DPYD-rs67376798 was assessed to 99%. Among the seven patients carrying one variant DPYD-rs3918290, DPYD-rs55886062 or DPYD-rs67376798 allele, not developing Grade ≥3 toxicity, 57% needed a FL dose or schedule modification for moderate chronic toxicity. No other DPYD polymorphism was associated with Grade ≥3 toxicity. Our data demonstrate the clinical validity and specificity of the DPYD-rs3918290, DPYD-rs55886062, DPYD-rs67376798 genotyping test to prevent FL-related Grade ≥3 toxicity and to preserve treatment compliance, and support its introduction in the clinical practice. © 2015 UICC. JF - International journal of cancer AU - Toffoli, Giuseppe AU - Giodini, Luciana AU - Buonadonna, Angela AU - Berretta, Massimiliano AU - De Paoli, Antonino AU - Scalone, Simona AU - Miolo, Gianmaria AU - Mini, Enrico AU - Nobili, Stefania AU - Lonardi, Sara AU - Pella, Nicoletta AU - Lo Re, Giovanni AU - Montico, Marcella AU - Roncato, Rossana AU - Dreussi, Eva AU - Gagno, Sara AU - Cecchin, Erika AD - Experimental and Clinical Pharmacology, Centro Di Riferimento Oncologico-National Cancer Institute, 2-33081, Aviano, Italy. ; Medical Oncology Unit B, Centro Di Riferimento Oncologico-National Cancer Institute, 2-33081, Aviano, Italy. ; Medical Oncology Unit A, Centro Di Riferimento Oncologico-National Cancer Institute, 2-33081, Aviano, Italy. ; Department of Radiation Oncology, Centro Di Riferimento Oncologico-National Cancer Institute, 2-33081, Aviano, Italy. ; Section of Internal Medicine, Department of Experimental and Clinical Medicine, University of Florence, 6-50139, Florence, Italy. ; Section of Clinical Pharmacology and Oncology, Department of Health Sciences, University of Florence, 6-50139, Florence, Italy. ; Medical Oncology Unit 1, Istituto Oncologico Veneto- IRCCS, 64-35128, Padua, Italy. ; Medical Oncology Unit, University Hospital, 15-33100, Udine, Italy. ; Oncology Unit, "Azienda Ospedaliera Santa Maria degli Angeli", Pordenone, Italy. Y1 - 2015/12/15/ PY - 2015 DA - 2015 Dec 15 SP - 2971 EP - 2980 VL - 137 IS - 12 KW - Antimetabolites, Antineoplastic KW - 0 KW - Dihydrouracil Dehydrogenase (NADP) KW - EC 1.3.1.2 KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - dihydropyrimidine dehydrogenase KW - polymorphism KW - toxicity KW - pharmacogenetics KW - fluoropyrimidines KW - chemotherapy KW - cancer KW - Young Adult KW - Genetic Testing KW - Polymorphism, Single Nucleotide KW - Aged, 80 and over KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Fluorouracil -- therapeutic use KW - Neoplasms -- drug therapy KW - Fluorouracil -- adverse effects KW - Antimetabolites, Antineoplastic -- adverse effects KW - Antimetabolites, Antineoplastic -- therapeutic use KW - Dihydrouracil Dehydrogenase (NADP) -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1721346834?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Clinical+validity+of+a+DPYD-based+pharmacogenetic+test+to+predict+severe+toxicity+to+fluoropyrimidines.&rft.au=Toffoli%2C+Giuseppe%3BGiodini%2C+Luciana%3BBuonadonna%2C+Angela%3BBerretta%2C+Massimiliano%3BDe+Paoli%2C+Antonino%3BScalone%2C+Simona%3BMiolo%2C+Gianmaria%3BMini%2C+Enrico%3BNobili%2C+Stefania%3BLonardi%2C+Sara%3BPella%2C+Nicoletta%3BLo+Re%2C+Giovanni%3BMontico%2C+Marcella%3BRoncato%2C+Rossana%3BDreussi%2C+Eva%3BGagno%2C+Sara%3BCecchin%2C+Erika&rft.aulast=Toffoli&rft.aufirst=Giuseppe&rft.date=2015-12-15&rft.volume=137&rft.issue=12&rft.spage=2971&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.29654 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-25 N1 - Date created - 2015-10-10 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ijc.29654 ER - TY - JOUR T1 - A gene-expression screen identifies a non-toxic sumoylation inhibitor that mimics SUMO-less human LRH-1 in liver. AN - 1761082030; 26653140 AB - SUMO-modification of nuclear proteins has profound effects on gene expression. However, non-toxic chemical tools that modulate sumoylation in cells are lacking. Here, to identify small molecule sumoylation inhibitors we developed a cell-based screen that focused on the well-sumoylated substrate, human Liver Receptor Homolog-1 (hLRH-1, NR5A2). Our primary gene-expression screen assayed two SUMO-sensitive transcripts, APOC3 and MUC1, that are upregulated by SUMO-less hLRH-1 or by siUBC9 knockdown, respectively. A polyphenol, tannic acid (TA) emerged as a potent sumoylation inhibitor in vitro (IC50 = 12.8 µM) and in cells. TA also increased hLRH-1 occupancy on SUMO-sensitive transcripts. Most significantly, when tested in humanized mouse primary hepatocytes, TA inhibits hLRH-1 sumoylation and induces SUMO-sensitive genes, thereby recapitulating the effects of expressing SUMO-less hLRH-1 in mouse liver. Our findings underscore the benefits of phenotypic screening for targeting post-translational modifications, and illustrate the potential utility of TA for probing the cellular consequences of sumoylation. JF - eLife AU - Suzawa, Miyuki AU - Miranda, Diego A AU - Ramos, Karmela A AU - Ang, Kenny K-H AU - Faivre, Emily J AU - Wilson, Christopher G AU - Caboni, Laura AU - Arkin, Michelle R AU - Kim, Yeong-Sang AU - Fletterick, Robert J AU - Diaz, Aaron AU - Schneekloth, John S AU - Ingraham, Holly A AD - Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, United States. ; Small Molecule Discovery Center, Department of Pharmaceutical Chemistry, University of California, San Francisco, San Francisco, United States. ; Department of Biochemistry and Biophysics, University of California, San Francisco, San Francisco, United States. ; Chemical Biology Laboratory, National Cancer Institute, Frederick, United States. ; Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, United States. Y1 - 2015/12/11/ PY - 2015 DA - 2015 Dec 11 VL - 4 KW - Enzyme Inhibitors KW - 0 KW - NR5A2 protein, human KW - Receptors, Cytoplasmic and Nuclear KW - Tannins KW - Index Medicus KW - primary hepatocytes KW - phenotypic screen KW - sumoylation KW - mouse KW - NR5As KW - human biology KW - cell biology KW - tannic acid KW - medicine KW - human KW - NASH KW - Gene Expression Profiling KW - Animals KW - Cells, Cultured KW - Humans KW - Mice KW - Mice, SCID KW - Inhibitory Concentration 50 KW - Drug Evaluation, Preclinical -- methods KW - Tannins -- metabolism KW - Hepatocytes -- drug effects KW - Tannins -- isolation & purification KW - Receptors, Cytoplasmic and Nuclear -- metabolism KW - Enzyme Inhibitors -- metabolism KW - Enzyme Inhibitors -- isolation & purification KW - Hepatocytes -- enzymology KW - Sumoylation -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1761082030?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=eLife&rft.atitle=A+gene-expression+screen+identifies+a+non-toxic+sumoylation+inhibitor+that+mimics+SUMO-less+human+LRH-1+in+liver.&rft.au=Suzawa%2C+Miyuki%3BMiranda%2C+Diego+A%3BRamos%2C+Karmela+A%3BAng%2C+Kenny+K-H%3BFaivre%2C+Emily+J%3BWilson%2C+Christopher+G%3BCaboni%2C+Laura%3BArkin%2C+Michelle+R%3BKim%2C+Yeong-Sang%3BFletterick%2C+Robert+J%3BDiaz%2C+Aaron%3BSchneekloth%2C+John+S%3BIngraham%2C+Holly+A&rft.aulast=Suzawa&rft.aufirst=Miyuki&rft.date=2015-12-11&rft.volume=4&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=eLife&rft.issn=2050-084X&rft_id=info:doi/10.7554%2FeLife.09003 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-29 N1 - Date created - 2016-01-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Endocrinol. 2008 Jan;22(1):78-90 [17885207] J Antibiot (Tokyo). 2014 Apr;67(4):335-8 [24424345] Cancer Cell. 2014 Jun 16;25(6):748-61 [24835590] Nat Commun. 2014;5:4234 [24953629] Genome Biol. 2012;13(10):R98 [23068444] Nucleic Acids Res. 2014 Jul;42(13):8310-9 [24981513] EMBO Rep. 2014 Aug;15(8):878-85 [24891386] Cell Metab. 2014 Oct 7;20(4):603-13 [25176150] Kidney Int. 2014 Dec;86(6):1161-73 [24940800] Hepatology. 2015 Jan;61(1):15-7 [24975580] EMBO J. 2015 Jan 13;34(2):184-99 [25425577] J Clin Invest. 2000 Jan;105(2):151-9 [10642593] Biochem Biophys Res Commun. 2001 Jul 13;285(2):372-7 [11444852] Bioinformatics. 2002 Feb;18(2):333-4 [11847087] Nucleic Acids Res. 2003 Jul 1;31(13):3651-3 [12824386] J Clin Invest. 2003 Jul;112(1):91-100 [12840063] Mol Endocrinol. 2004 Oct;18(10):2451-62 [15192080] Blood Coagul Fibrinolysis. 1997 Dec;8 Suppl 2:S23-30 [9607110] Mol Cell Biol. 2005 Mar;25(5):1879-90 [15713642] Ann Hepatol. 2008 Jan-Mar;7(1):67-71 [18376369] Mol Endocrinol. 2008 Jun;22(6):1345-56 [18323469] Mol Endocrinol. 2008 Sep;22(9):2061-75 [18562626] Mol Cell Biol. 2008 Dec;28(24):7476-86 [18838537] Genome Biol. 2008;9(9):R137 [18798982] Methods Mol Biol. 2009;497:167-86 [19107417] Methods Mol Biol. 2009;497:225-39 [19107421] FEBS J. 2009 Jan;276(2):425-36 [19125815] Chem Biol. 2009 Feb 27;16(2):133-40 [19246003] J Antibiot (Tokyo). 2009 Apr;62(4):221-4 [19265871] Toxicol Lett. 2009 Jun 22;187(3):131-6 [19429255] J Gastroenterol Hepatol. 2009 Oct;24(10):1669-76 [19788607] Genes Dev. 2010 Feb 15;24(4):381-95 [20159957] Mol Cell. 2010 Apr 23;38(2):191-201 [20417598] Nat Rev Mol Cell Biol. 2010 Dec;11(12):861-71 [21102611] Bioinformatics. 2011 Jun 15;27(12):1696-7 [21486936] Nature. 2011 Jun 23;474(7352):506-10 [21614002] Proc Natl Acad Sci U S A. 2008 Mar 25;105(12):4721-6 [18347329] Assay Drug Dev Technol. 2013 Jun;11(5):308-25 [23772552] Nat Struct Mol Biol. 2013 Jul;20(7):876-83 [23728292] J Hepatol. 2014 Jan;60(1):143-51 [23978713] PLoS Genet. 2013;9(12):e1003992 [24348269] ACS Chem Biol. 2013 Dec 20;8(12):2635-42 [24143955] Nucleic Acids Res. 2014 Feb;42(3):1575-92 [24194604] Nat Rev Drug Discov. 2011 Jul;10(7):507-19 [21701501] Prostate. 2011 Sep;71(12):1299-308 [21308711] Dev Cell. 2011 Aug 16;21(2):315-27 [21820362] Nature. 2011 Dec 1;480(7375):94-8 [22012259] Nat Med. 2012 Mar;18(3):388-95 [22344295] PLoS One. 2012;7(3):e33286 [22428010] Hepatology. 2012 Jun;55(6):1711-21 [22213086] J Clin Invest. 2012 Aug;122(8):2817-26 [22772466] Molecules. 2012;17(9):10774-90 [22960870] Proc Natl Acad Sci U S A. 2012 Dec 18;109(51):20859-64 [23185012] Chem Biol. 2013 Apr 18;20(4):604-13 [23601649] J Chem Inf Model. 2013 Apr 22;53(4):809-20 [23544417] Annu Rev Biochem. 2013;82:357-85 [23746258] Mol Cell Biol. 2005 Jun;25(12):5095-105 [15923626] Curr Opin Genet Dev. 2005 Oct;15(5):536-41 [16095902] Dev Cell. 2005 Dec;9(6):769-79 [16326389] Mol Cell. 2006 Feb 3;21(3):349-57 [16455490] FEBS Lett. 2006 Dec 11;580(28-29):6623-8 [17118359] Nat Protoc. 2006;1(2):550-3 [17191086] Mol Nutr Food Res. 2007 Aug;51(8):962-8 [17628875] Mol Cell Biol. 2007 Dec;27(23):8330-9 [17908794] J Neurosci. 2007 Dec 12;27(50):13624-34 [18077674] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.7554/eLife.09003 ER - TY - JOUR T1 - Repression of Hox genes by LMP1 in nasopharyngeal carcinoma and modulation of glycolytic pathway genes by HoxC8. AN - 1749620562; 25745994 AB - Epstein-Barr virus (EBV) causes human lymphoid malignancies, and the EBV product latent membrane protein 1 (LMP1) has been identified as an oncogene in epithelial carcinomas such as nasopharyngeal carcinoma (NPC). EBV can epigenetically reprogram lymphocyte-specific processes and induce cell immortalization. However, the interplay between LMP1 and the NPC host cell remains largely unknown. Here, we report that LMP1 is important to establish the Hox gene expression signature in NPC cell lines and tumor biopsies. LMP1 induces repression of several Hox genes in part via stalling of RNA polymerase II (RNA Pol II). Pol II stalling can be overcome by irradiation involving the epigenetic regulator TET3. Furthermore, we report that HoxC8, one of the genes silenced by LMP1, has a role in tumor growth. Ectopic expression of HoxC8 inhibits NPC cell growth in vitro and in vivo, modulates glycolysis and regulates the expression of tricarboxylic acid (TCA) cycle-related genes. We propose that viral latency products may repress via stalling key mediators that in turn modulate glycolysis. JF - Oncogene AU - Jiang, Y AU - Yan, B AU - Lai, W AU - Shi, Y AU - Xiao, D AU - Jia, J AU - Liu, S AU - Li, H AU - Lu, J AU - Li, Z AU - Chen, L AU - Chen, X AU - Sun, L AU - Muegge, K AU - Cao, Y AU - Tao, Y AD - Cancer Research Institute, Central South University, Changsha, Hunan, China. ; Department of Pathology, Xiangya Hospital, Central South University, Changsha, Hunan, China. ; Center for Medicine Research, Xiangya Hospital, Central South University, Changsha, Hunan, China. ; Center for Molecular Medicine, Xiangya Hospital, Central South University, Changsha, China. ; Mouse Cancer Genetics Program, National Cancer Institute, Basic Science Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA. Y1 - 2015/12/10/ PY - 2015 DA - 2015 Dec 10 SP - 6079 EP - 6091 VL - 34 IS - 50 KW - EBV-associated membrane antigen, Epstein-Barr virus KW - 0 KW - HOXC8 protein, human KW - Homeodomain Proteins KW - Viral Matrix Proteins KW - TET3 protein, human KW - EC 1.- KW - Dioxygenases KW - EC 1.13.11.- KW - RNA Polymerase II KW - EC 2.7.7.- KW - Index Medicus KW - RNA Polymerase II -- metabolism KW - DNA Methylation KW - Cells, Cultured KW - Humans KW - Glycolysis KW - Dioxygenases -- physiology KW - Citric Acid Cycle KW - Genes, Homeobox -- physiology KW - Homeodomain Proteins -- physiology KW - Nasopharyngeal Neoplasms -- genetics KW - Viral Matrix Proteins -- physiology KW - Nasopharyngeal Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1749620562?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Repression+of+Hox+genes+by+LMP1+in+nasopharyngeal+carcinoma+and+modulation+of+glycolytic+pathway+genes+by+HoxC8.&rft.au=Jiang%2C+Y%3BYan%2C+B%3BLai%2C+W%3BShi%2C+Y%3BXiao%2C+D%3BJia%2C+J%3BLiu%2C+S%3BLi%2C+H%3BLu%2C+J%3BLi%2C+Z%3BChen%2C+L%3BChen%2C+X%3BSun%2C+L%3BMuegge%2C+K%3BCao%2C+Y%3BTao%2C+Y&rft.aulast=Jiang&rft.aufirst=Y&rft.date=2015-12-10&rft.volume=34&rft.issue=50&rft.spage=6079&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2015.53 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-12 N1 - Date created - 2015-12-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Cell. 2008 Jun 20;30(6):755-66 [18514006] Oncogene. 2008 Oct 23;27(49):6356-64 [18679416] Science. 2008 Dec 19;322(5909):1845-8 [19056941] Nat Genet. 2007 Apr;39(4):457-66 [17334365] Nat Rev Mol Cell Biol. 2009 Apr;10(4):243-54 [19277046] Curr Biol. 2009 Apr 28;19(8):688-93 [19345103] Semin Cancer Biol. 2009 Jun;19(3):158-64 [19429479] Science. 2009 May 15;324(5929):930-5 [19372391] Genes Dev. 2009 Jul 1;23(13):1505-9 [19515973] Genome Res. 2009 Nov;19(11):1974-82 [19652013] PLoS One. 2010;5(2):e9163 [20161795] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499] J Virol. 2002 Apr;76(8):4080-6 [11907247] Biochem Biophys Res Commun. 2004 Aug 6;320(4):1253-61 [15249225] Science. 1999 Oct 8;286(5438):300-3 [10514374] Oncogene. 2007 Feb 26;26(9):1297-305 [17322915] Proc Natl Acad Sci U S A. 2007 Mar 27;104(13):5521-6 [17376869] Nature. 2010 Feb 25;463(7284):1101-5 [20098412] Nat Rev Cancer. 2010 May;10(5):361-71 [20357775] Proc Natl Acad Sci U S A. 2010 May 11;107(19):8689-94 [20395551] Science. 2010 May 14;328(5980):916-9 [20395474] PLoS Pathog. 2010;6(6):e1000951 [20548956] Science. 2010 Jul 2;329(5987):78-82 [20595612] Nat Rev Cancer. 2011 Feb;11(2):85-95 [21258394] Proc Natl Acad Sci U S A. 2011 Feb 1;108(5):2130-5 [21245294] Nature. 2011 Feb 17;470(7334):419-23 [21278727] Cell. 2011 May 13;145(4):502-11 [21565610] Nature. 2011 May 19;473(7347):343-8 [21490601] EMBO J. 2011 Jun 1;30(11):2115-29 [21527913] PLoS One. 2011;6(6):e21176 [21701587] Cell. 2011 Jul 8;146(1):67-79 [21722948] Br J Cancer. 2011 Jul 12;105(2):288-95 [21712827] J Virol. 2011 Nov;85(21):10999-1006 [21865393] Cell Host Microbe. 2011 Oct 20;10(4):324-35 [22018233] PLoS Pathog. 2011 Oct;7(10):e1002334 [22046134] PLoS One. 2011;6(11):e24647 [22096476] Nucleic Acids Res. 2011 Dec;39(22):9508-20 [21880597] Int J Oncol. 2012 Apr;40(4):1180-8 [22227861] Cell. 2012 Mar 16;148(6):1132-44 [22424225] Mol Biol Rep. 2012 May;39(5):6179-85 [22203491] Cancer Sci. 2012 Jun;103(6):993-9 [22417000] Semin Cell Dev Biol. 2012 Jun;23(4):370-80 [22306135] Genes Dev. 2012 Jun 15;26(12):1326-38 [22677546] Carcinogenesis. 2012 Aug;33(8):1468-78 [22581837] Oncogene. 2012 Aug 23;31(34):3901-12 [22139084] J Pathol. 2012 Oct;228(2):230-40 [22374749] Cell. 2012 Sep 14;150(6):1135-46 [22980977] Biol Rev Camb Philos Soc. 2013 Feb;88(1):40-8 [22765520] Oncogene. 2013 Jan 31;32(5):663-9 [22391558] Cancer Lett. 2013 Apr 28;330(2):217-24 [23219899] Curr Med Chem. 2013 Feb 1;20(6):833-9 [23276138] Biochim Biophys Acta. 2013 Apr;1835(2):155-63 [23262191] J Biol Chem. 2013 Mar 29;288(13):9153-64 [23408428] Nat Rev Mol Cell Biol. 2013 Jun;14(6):341-56 [23698584] Cell. 2013 Jul 18;154(2):311-24 [23830207] Nat Rev Drug Discov. 2013 Nov;12(11):829-46 [24113830] Cell Host Microbe. 2014 Mar 12;15(3):266-82 [24629334] J Surg Res. 2014 May 15;188(2):442-50 [24525058] Oncotarget. 2014 May 15;5(9):2596-607 [24810778] Radiother Oncol. 2014 May;111(2):168-77 [24861629] Oncogene. 2014 Sep 11;33(37):4568-78 [24662831] Nat Protoc. 2006;1(1):23-9 [17406208] Cell. 2007 May 18;129(4):823-37 [17512414] Cell Mol Immunol. 2007 Jun;4(3):185-96 [17601372] Cell. 2007 Jul 13;130(1):77-88 [17632057] Nat Genet. 2007 Dec;39(12):1507-11 [17994021] Science. 2008 Jun 13;320(5882):1496-501 [18497260] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/onc.2015.53 ER - TY - JOUR T1 - Potential of the Lectin/Inhibitor Isolated from Crataeva tapia Bark (CrataBL) for Controlling Callosobruchus maculatus Larva Development. AN - 1747307041; 26568149 AB - Callosobruchus maculatus is an important predator of cowpeas. Due to infestation during storage, this insect affects the quality of seed and crop yield. This study aimed to investigate the effects of CrataBL, a multifunction protein isolated from Crataeva tapia bark, on C. maculatus larva development. The protein, which is stable even in extreme pH conditions, showed toxic activity, reducing the larval mass 45 and 70% at concentrations of 0.25 and 1.0% (w/w), respectively. Acting as an inhibitor, CrataBL decreased by 39% the activity of cysteine proteinases from larval gut. Conversely, the activity of serine proteinases was increased about 8-fold. The toxic properties of CrataBL may also be attributed to its capacity of binding to glycoproteins or glycosaminoglycans. Such binding interferes with larval metabolism, because CrataBL-FITC was found in the fat body, Malpighian tubules, and feces of larvae. These results demonstrate the potential of this protein for controlling larva development. JF - Journal of agricultural and food chemistry AU - Nunes, Natalia N S AU - Ferreira, Rodrigo S AU - Silva-Lucca, Rosemeire A AU - de Sá, Leonardo F R AU - de Oliveira, Antônia Elenir A AU - Correia, Maria Tereza dos S AU - Paiva, Patrícia Maria G AU - Wlodawer, Alexander AU - Oliva, Maria Luiza V AD - Departamento de Bioquı́mica, Universidade Federal de São Paulo-UNIFESP-EPM , 04044-020 São Paulo, SP, Brazil. ; Centro de Engenharia e Ciências Exatas, Universidade Estadual do Oeste do Paraná , Toledo, Paraná, Brazil. ; Laboratório de Quı́mica e Função de Proteínas e Peptídeos, Centro de Biociências e Biotecnologia-CBB, Universidade Estadual do Norte Fluminense Darcy Ribeiro-UENF , Campos dos Goytacazes, RJ, Brazil. ; Departamento de Bioquı́mica, Universidade Federal de Pernambuco , Recife, PE, Brazil. ; Macromolecular Crystallography Laboratory, Center for Cancer Research, National Cancer Institute , Frederick, Maryland 21702, United States. Y1 - 2015/12/09/ PY - 2015 DA - 2015 Dec 09 SP - 10431 EP - 10436 VL - 63 IS - 48 KW - Cysteine Proteinase Inhibitors KW - 0 KW - Insect Proteins KW - Lectins KW - Plant Extracts KW - Cysteine Proteases KW - EC 3.4.- KW - Index Medicus KW - C. maculatus KW - bioinsecticide KW - lectin KW - inhibitor KW - glycosaminoglycan KW - Crataeva tapia KW - Cysteine Proteinase Inhibitors -- pharmacology KW - Cysteine Proteases -- metabolism KW - Animals KW - Insect Proteins -- metabolism KW - Plant Extracts -- pharmacology KW - Beetles -- enzymology KW - Beetles -- growth & development KW - Larva -- enzymology KW - Plant Bark -- chemistry KW - Larva -- growth & development KW - Larva -- drug effects KW - Lectins -- pharmacology KW - Capparaceae -- chemistry KW - Beetles -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1747307041?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+agricultural+and+food+chemistry&rft.atitle=Potential+of+the+Lectin%2FInhibitor+Isolated+from+Crataeva+tapia+Bark+%28CrataBL%29+for+Controlling+Callosobruchus+maculatus+Larva+Development.&rft.au=Nunes%2C+Natalia+N+S%3BFerreira%2C+Rodrigo+S%3BSilva-Lucca%2C+Rosemeire+A%3Bde+S%C3%A1%2C+Leonardo+F+R%3Bde+Oliveira%2C+Ant%C3%B4nia+Elenir+A%3BCorreia%2C+Maria+Tereza+dos+S%3BPaiva%2C+Patr%C3%ADcia+Maria+G%3BWlodawer%2C+Alexander%3BOliva%2C+Maria+Luiza+V&rft.aulast=Nunes&rft.aufirst=Natalia+N&rft.date=2015-12-09&rft.volume=63&rft.issue=48&rft.spage=10431&rft.isbn=&rft.btitle=&rft.title=Journal+of+agricultural+and+food+chemistry&rft.issn=1520-5118&rft_id=info:doi/10.1021%2Facs.jafc.5b03634 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-10 N1 - Date created - 2015-12-09 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/acs.jafc.5b03634 ER - TY - JOUR T1 - Occupational ionising radiation and risk of basal cell carcinoma in US radiologic technologists (1983-2005) AN - 1808671243; PQ0003414885 AB - ObjectiveTo determine risk for incident basal cell carcinoma from cumulative low-dose ionising radiation in the US radiologic technologist cohort.MethodsWe analysed 65719 Caucasian technologists who were cancer-free at baseline (1983-1989 or 1994-1998) and answered a follow-up questionnaire (2003-2005). Absorbed radiation dose to the skin in mGy for estimated cumulative occupational radiation exposure was reconstructed for each technologist based on badge dose measurements, questionnaire-derived work history and protection practices, and literature information. Radiation-associated risk was assessed using Poisson regression and included adjustment for several demographic, lifestyle, host and sun exposure factors.ResultsCumulative mean absorbed skin dose (to head/neck/arms) was 55.8mGy (range 0-1735mGy). For lifetime cumulative dose, we did not observe an excess radiation-related risk (excess relative risk/Gy=-0.01 (95% CI -0.43 to 0.52). However, we observed that basal cell carcinoma risk was increased for radiation dose received before age 30 (excess relative risk/Gy=0.59, 95% CI -0.11 to 1.42) and before 1960 (excess relative risk/Gy=2.92, 95% CI 1.39 to 4.45).ConclusionsBasal cell carcinoma risk was unrelated to low-dose radiation exposure among radiologic technologists. Because of uncertainties in dosimetry and sensitivity to model specifications, both our null results and our findings of excess risk for dose received before age 30 and exposure before 1960 should be interpreted with caution. JF - Occupational and Environmental Medicine AU - Lee, Terrence AU - Sigurdson, Alice J AU - Preston, Dale L AU - Cahoon, Elizabeth K AU - Freedman, D Michal AU - Simon, Steven L AU - Nelson, Kenrad AU - Matanoski, Genevieve AU - Kitahara, Cari M AU - Liu, Jason J AU - Wang, Timothy AU - Alexander, Bruce H AU - Doody, Michele M AU - Linet, Martha S AU - Little, Mark P AD - Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA Y1 - 2015/12/08/ PY - 2015 DA - 2015 Dec 08 SP - 862 EP - 869 PB - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom VL - 72 IS - 12 SN - 1351-0711, 1351-0711 KW - Toxicology Abstracts; Health & Safety Science Abstracts KW - Risk assessment KW - Historical account KW - Age KW - Demography KW - Radiation KW - Risk factors KW - Sun KW - Occupational exposure KW - Sensitivity KW - Inventories KW - Skin KW - Dosimetry KW - Neck KW - Carcinoma KW - Basal cells KW - Ionizing radiation KW - H 1000:Occupational Safety and Health KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808671243?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+Environmental+Medicine&rft.atitle=Occupational+ionising+radiation+and+risk+of+basal+cell+carcinoma+in+US+radiologic+technologists+%281983-2005%29&rft.au=Lee%2C+Terrence%3BSigurdson%2C+Alice+J%3BPreston%2C+Dale+L%3BCahoon%2C+Elizabeth+K%3BFreedman%2C+D+Michal%3BSimon%2C+Steven+L%3BNelson%2C+Kenrad%3BMatanoski%2C+Genevieve%3BKitahara%2C+Cari+M%3BLiu%2C+Jason+J%3BWang%2C+Timothy%3BAlexander%2C+Bruce+H%3BDoody%2C+Michele+M%3BLinet%2C+Martha+S%3BLittle%2C+Mark+P&rft.aulast=Lee&rft.aufirst=Terrence&rft.date=2015-12-08&rft.volume=72&rft.issue=12&rft.spage=862&rft.isbn=&rft.btitle=&rft.title=Occupational+and+Environmental+Medicine&rft.issn=13510711&rft_id=info:doi/10.1136%2Foemed-2015-102880 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Demography; Risk assessment; Inventories; Age; Basal cells; Skin; Radiation; Sun; Dosimetry; Neck; Occupational exposure; Carcinoma; Historical account; Sensitivity; Ionizing radiation; Risk factors DO - http://dx.doi.org/10.1136/oemed-2015-102880 ER - TY - JOUR T1 - The role of reproductive hormones in epithelial ovarian carcinogenesis AN - 1859477232; PQ0002561326 AB - Epithelial ovarian cancer comprises ~85% of all ovarian cancer cases. Despite acceptance regarding the influence of reproductive hormones on ovarian cancer risk and considerable advances in the understanding of epithelial ovarian carcinogenesis on a molecular level, complete understanding of the biologic processes underlying malignant transformation of ovarian surface epithelium is lacking. Various hypotheses have been proposed over the past several decades to explain the etiology of the disease. The role of reproductive hormones in epithelial ovarian carcinogenesis remains a key topic of research. Primary questions in the field of ovarian cancer biology center on its developmental cell of origin, the positive and negative effects of each class of hormones on ovarian cancer initiation and progression, and the role of the immune system in the ovarian cancer microenvironment. The development of the female reproductive tract is dictated by the hormonal milieu during embryogenesis. Intensive research efforts have revealed that ovarian cancer is a heterogenous disease that may develop from multiple extra-ovarian tissues, including both Mullerian (fallopian tubes, endometrium) and non-Mullerian structures (gastrointestinal tissue), contributing to its heterogeneity and distinct histologic subtypes. The mechanism underlying ovarian localization, however, remains unclear. Here, we discuss the role of reproductive hormones in influencing the immune system and tipping the balance against or in favor of developing ovarian cancer. We comment on animal models that are critical for experimentally validating existing hypotheses in key areas of endocrine research and useful for preclinical drug development. Finally, we address emerging therapeutic trends directed against ovarian cancer. JF - Endocrine-Related Cancer AU - Gharwan, Helen AU - Bunch, Kristen P AU - Annunziata, Christina M AD - National Cancer Institute, National Institutes of Health, 10 Center Drive, Building 10, 12N226, Bethesda, Maryland 20892-1906, USA, hgh7@hotmail.com Y1 - 2015/12// PY - 2015 DA - December 2015 SP - R339 EP - R363 PB - BioScientifica Ltd., Euro House, 22 Apex Ct, Woodlands Bristol, BS32 4JT United Kingdom VL - 22 IS - 6 SN - 1351-0088, 1351-0088 KW - Toxicology Abstracts KW - ovarian cancer KW - hormone action KW - reproductive KW - immune KW - endocrine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1859477232?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrine-Related+Cancer&rft.atitle=The+role+of+reproductive+hormones+in+epithelial+ovarian+carcinogenesis&rft.au=Gharwan%2C+Helen%3BBunch%2C+Kristen+P%3BAnnunziata%2C+Christina+M&rft.aulast=Gharwan&rft.aufirst=Helen&rft.date=2015-12-01&rft.volume=22&rft.issue=6&rft.spage=R339&rft.isbn=&rft.btitle=&rft.title=Endocrine-Related+Cancer&rft.issn=13510088&rft_id=info:doi/10.1530%2FERC-14-0550 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2017-01-01 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1530/ERC-14-0550 ER - TY - JOUR T1 - PubChemRDF: towards the semantic annotation of PubChem compound and substance databases AN - 1837308139; PQ0003733475 AB - PubChem is an open repository for chemical structures, biological activities and biomedical annotations. Semantic Web technologies are emerging as an increasingly important approach to distribute and integrate scientific data. Exposing PubChem data to Semantic Web services may help enable automated data integration and management, as well as facilitate interoperable web applications. This work, one of a series covering the PubChemRDF project, describes an approach to translate PubChem Substance and Compound information into Resource Description Framework (RDF) format. Basic examples are provided to demonstrate its use. The aim of this effort is to provide two new primary benefits to researchers in a cost-effective manner. Firstly, we aim to remove the inherent limitations of using the web-based resource PubChem by allowing a researcher to use readily available semantic technologies (namely, RDF triple stores and their corresponding SPARQL query engines) to query and analyze PubChem data on local computing resources. Secondly, this work intends to help improve data sharing, analysis, and integration of PubChem data to resources external to NCBI and across scientific domains, by means of the association of PubChem data to existing ontological frameworks, including CHEMical INFormation ontology, Semanticscience Integrated Ontology, and others. With the goal of semantically describing information available in the PubChem archive, pre-existing ontological frameworks were used, rather than creating new ones. Semantic relationships between compounds and substances, chemical descriptors associated with compounds and substances, interrelationships between chemicals, as well as provenance and attribute metadata of substances are described. Conclusions: [Figure not available: see fulltext. Caption: Schematic representation of the semantic links for PubChem compounds and substances.] JF - Journal of Cheminformatics AU - Fu, Gang AU - Batchelor, Colin AU - Dumontier, Michel AU - Hastings, Janna AU - Willighagen, Egon AU - Bolton, Evan AD - grid.94365.3d, 0000000122975165, National Center for Biotechnology Information, National Library of Medicine, National Institute of Health, Bethesda, MD, USA, gang.fu@nih.gov Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1 EP - 15 PB - Springer-Verlag (Heidelberg), Tiergartenstrasse 17 Heidelberg 69121 Germany VL - 7 IS - 1 KW - Biotechnology and Bioengineering Abstracts KW - Integration KW - Databases KW - Data processing KW - Informatics KW - Internet KW - Semantics KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1837308139?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Cheminformatics&rft.atitle=PubChemRDF%3A+towards+the+semantic+annotation+of+PubChem+compound+and+substance+databases&rft.au=Fu%2C+Gang%3BBatchelor%2C+Colin%3BDumontier%2C+Michel%3BHastings%2C+Janna%3BWillighagen%2C+Egon%3BBolton%2C+Evan&rft.aulast=Fu&rft.aufirst=Gang&rft.date=2015-12-01&rft.volume=7&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+Cheminformatics&rft.issn=1758-2946&rft_id=info:doi/10.1186%2Fs13321-015-0084-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-11-01 N1 - Number of references - 57 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Databases; Integration; Data processing; Informatics; Internet; Semantics DO - http://dx.doi.org/10.1186/s13321-015-0084-4 ER - TY - JOUR T1 - PubChem structure-activity relationship (SAR) clusters AN - 1837306032; PQ0003733462 AB - Developing structure-activity relationships (SARs) of molecules is an important approach in facilitating hit exploration in the early stage of drug discovery. Although information on millions of compounds and their bioactivities is freely available to the public, it is very challenging to infer a meaningful and novel SAR from that information. Research discussed in the present paper employed a bioactivity-centered clustering approach to group 843,845 non-inactive compounds stored in PubChem according to both structural similarity and bioactivity similarity, with the aim of mining bioactivity data in PubChem for useful SAR information. The compounds were clustered in three bioactivity similarity contexts: (1) non-inactive in a given bioassay, (2) non-inactive against a given protein, and (3) non-inactive against proteins involved in a given pathway. In each context, these small molecules were clustered according to their two-dimensional (2-D) and three-dimensional (3-D) structural similarities. The resulting 18 million clusters, named "PubChem SAR clusters", were delivered in such a way that each cluster contains a group of small molecules similar to each other in both structure and bioactivity. The PubChem SAR clusters, pre-computed using publicly available bioactivity information, make it possible to quickly navigate and narrow down the compounds of interest. Each SAR cluster can be a useful resource in developing a meaningful SAR or enable one to design or expand compound libraries from the cluster. It can also help to predict the potential therapeutic effects and pharmacological actions of less-known compounds from those of well-known compounds (i.e., drugs) in the same cluster. [Figure not available: see fulltext.] JF - Journal of Cheminformatics AU - Kim, Sunghwan AU - Han, Lianyi AU - Yu, Bo AU - Haehnke, Volker D AU - Bolton, Evan E AU - Bryant, Stephen H AD - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Department of Health and Human Services, 8600 Rockville Pike, Bethesda, MD, 20894, USA, bolton@ncbi.nlm.nih.gov Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1 EP - 22 PB - Springer-Verlag (Heidelberg), Tiergartenstrasse 17 Heidelberg 69121 Germany VL - 7 IS - 1 KW - Biotechnology and Bioengineering Abstracts KW - Drug discovery KW - Data processing KW - Informatics KW - Structure-activity relationships KW - Drugs KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1837306032?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Cheminformatics&rft.atitle=PubChem+structure-activity+relationship+%28SAR%29+clusters&rft.au=Kim%2C+Sunghwan%3BHan%2C+Lianyi%3BYu%2C+Bo%3BHaehnke%2C+Volker+D%3BBolton%2C+Evan+E%3BBryant%2C+Stephen+H&rft.aulast=Kim&rft.aufirst=Sunghwan&rft.date=2015-12-01&rft.volume=7&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+Cheminformatics&rft.issn=1758-2946&rft_id=info:doi/10.1186%2Fs13321-015-0070-x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-11-01 N1 - Number of references - 59 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Drug discovery; Data processing; Informatics; Drugs; Structure-activity relationships DO - http://dx.doi.org/10.1186/s13321-015-0070-x ER - TY - JOUR T1 - Analysis of the Zidovudine Resistance Mutations T215Y, M41L, and L210W in HIV-1 Reverse Transcriptase AN - 1832245718; PQ0002380943 AB - Although anti-human immunodeficiency virus type 1 (HIV-1) therapies have become more sophisticated and more effective, drug resistance continues to be a major problem. Zidovudine (azidothymidine; AZT) was the first nucleoside reverse transcriptase (RT) inhibitor (NRTI) approved for the treatment of HIV-1 infections and is still being used, particularly in the developing world. This drug targets the conversion of single-stranded RNA to double-stranded DNA by HIV-1 RT. However, resistance to the drug quickly appeared both in viruses replicating in cells in culture and in patients undergoing AZT monotherapy. The primary resistance pathway selects for mutations of T215 that change the threonine to either a tyrosine or a phenylalanine (T215Y/F); this resistance pathway involves an ATP-dependent excision mechanism. The pseudo-sugar ring of AZT lacks a 3' OH; RT incorporates AZT monophosphate (AZTMP), which blocks the end of the viral DNA primer. AZT-resistant forms of HIV-1 RT use ATP in an excision reaction to unblock the 3' end of the primer strand, allowing its extension by RT. The T215Y AZT resistance mutation is often accompanied by two other mutations, M41L and L210W. In this study, the roles of these mutations, in combination with T215Y, were examined to determine whether they affect polymerization and excision by HIV-1 RT. The M41L mutation appears to help restore the DNA polymerization activity of RT containing the T215Y mutation and also enhances AZTMP excision. The L210W mutation plays a similar role, but it enhances excision by RTs that carry the T215Y mutation when ATP is present at a low concentration. JF - Antimicrobial Agents & Chemotherapy AU - Boyer, Paul L AU - Das, Kalyan AU - Arnold, Eddy AU - Hughes, Stephen H AD - << + $0, hughesst@mail.nih.gov. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 7184 EP - 7196 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 59 IS - 12 SN - 0066-4804, 0066-4804 KW - Virology & AIDS Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Polymerization KW - Drug resistance KW - Double-stranded RNA KW - ATP KW - Zidovudine KW - Tyrosine KW - Cell culture KW - Infection KW - Phenylalanine KW - Lentivirus KW - RNA KW - nucleosides KW - DNA KW - RNA-directed DNA polymerase KW - Primers KW - Threonine KW - Mutation KW - A 01340:Antibiotics & Antimicrobials KW - V 22360:AIDS and HIV KW - N 14830:RNA UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1832245718?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Analysis+of+the+Zidovudine+Resistance+Mutations+T215Y%2C+M41L%2C+and+L210W+in+HIV-1+Reverse+Transcriptase&rft.au=Boyer%2C+Paul+L%3BDas%2C+Kalyan%3BArnold%2C+Eddy%3BHughes%2C+Stephen+H&rft.aulast=Boyer&rft.aufirst=Paul&rft.date=2015-12-01&rft.volume=59&rft.issue=12&rft.spage=7184&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.05069-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-10-01 N1 - Number of references - 34 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Polymerization; Double-stranded RNA; Drug resistance; Tyrosine; Zidovudine; ATP; Cell culture; Infection; Phenylalanine; RNA; nucleosides; DNA; RNA-directed DNA polymerase; Primers; Mutation; Threonine; Lentivirus DO - http://dx.doi.org/10.1128/AAC.05069-14 ER - TY - JOUR T1 - How to perform transcaval access and closure for transcatheter aortic valve implantation AN - 1815711583; PQ0002333077 AB - Transcaval, or caval-aortic, access is a promising approach for fully percutaneous transcatheter aortic valve implantation in patients without good conventional access options. This tutorial review provides step-by-step guidance to planning and executing the procedure, along with approaches to remedy complications. JF - Catheterization and Cardiovascular Interventions AU - Lederman, Robert J AU - Babaliaros, Vasilis C AU - Greenbaum, Adam B AD - Cardiovascular and Pulmonary Branch, Division of Intramural Research, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1242 EP - 1254 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 86 IS - 7 SN - 1522-1946, 1522-1946 KW - Biotechnology and Bioengineering Abstracts KW - Catheterization KW - Aortic valve KW - W 30950:Waste Treatment & Pollution Clean-up UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1815711583?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Catheterization+and+Cardiovascular+Interventions&rft.atitle=How+to+perform+transcaval+access+and+closure+for+transcatheter+aortic+valve+implantation&rft.au=Lederman%2C+Robert+J%3BBabaliaros%2C+Vasilis+C%3BGreenbaum%2C+Adam+B&rft.aulast=Lederman&rft.aufirst=Robert&rft.date=2015-12-01&rft.volume=86&rft.issue=7&rft.spage=1242&rft.isbn=&rft.btitle=&rft.title=Catheterization+and+Cardiovascular+Interventions&rft.issn=15221946&rft_id=info:doi/10.1002%2Fccd.26141 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-08-01 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Catheterization; Aortic valve DO - http://dx.doi.org/10.1002/ccd.26141 ER - TY - JOUR T1 - Genome Analysis of Latin American Cervical Cancer: Frequent Activation of the PIK3CA Pathway AN - 1808657362; PQ0003459017 AB - Purpose: Cervical cancer is one of the most common causes of cancer mortality for women living in poverty, causing more than 28,000 deaths annually in Latin America and 266,000 worldwide. To better understand the molecular basis of the disease, we ascertained blood and tumor samples from Guatemala and Venezuela and performed genomic characterization.Experimental Design: We performed human papillomavirus (HPV) typing and identified somatically mutated genes using exome and ultra-deep targeted sequencing with confirmation in samples from Mexico. Copy number changes were also assessed in the exome sequence.Results: Cervical cancer cases in Guatemala and Venezuela have an average age of diagnosis of 50 years and 5.6 children. Analysis of 675 tumors revealed activation of PIK3CA and other PI3K/AKT pathway genes in 31% of squamous carcinomas and 24% of adeno- and adenosquamous tumors, predominantly at two sites (E542K, E545K) in the helical domain of the PIK3CA gene. This distribution of PIK3CA mutations is distinct from most other cancer types and does not result in the in vitro phosphorylation of AKT. Somatic mutations were more frequent in squamous carcinomas diagnosed after the age of 50 years. Frequent gain of chromosome 3q was found, and low PIK3CA mutation fractions in many tumors suggest that PI3K mutation can be a late event in tumor progression.Conclusions: PI3K pathway mutation is important to cervical carcinogenesis in Latin America. Therapeutic agents that directly target PI3K could play a role in the therapy of this common malignancy. Clin Cancer Res; 21(23); 5360-70. copyright 2015 AACR. JF - Clinical Cancer Research AU - Lou, Hong AU - Villagran, Guillermo AU - Boland, Joseph F AU - Im, Kate M AU - Polo, Sarita AU - Zhou, Weiyin AU - Odey, Ushie AU - Juarez-Torres, Eligia AU - Medina-Martinez, Ingrid AU - Roman-Basaure, Edgar AU - Mitchell, Jason AU - Roberson, David AU - Sawitzke, Julie AU - Garland, Lisa AU - Rodriguez-Herrera, Maria AU - Wells, David AU - Troyer, Jennifer AU - Pinto, Francisco Castillo AU - Bass, Sara AU - Zhang, Xijun AU - Castillo, Miriam AU - Gold, Bert AU - Morales, Hesler AU - Yeager, Meredith AU - Berumen, Jaime AU - Alvirez, Enrique AU - Gharzouzi, Eduardo AU - Dean, Michael AD - Basic Science Program, Leidos Biomedical Research, Inc., Frederick, Maryland, deanm@mail.nih.gov Y1 - 2015/12/01/ PY - 2015 DA - 2015 Dec 01 SP - 5360 EP - 5370 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 23 SN - 1078-0432, 1078-0432 KW - Biotechnology and Bioengineering Abstracts KW - Mortality KW - Age KW - Cervical cancer KW - Adenosquamous KW - Tumors KW - chromosome 3 KW - Children KW - Carcinoma KW - copy number KW - Blood KW - 1-Phosphatidylinositol 3-kinase KW - Malignancy KW - Typing KW - Phosphorylation KW - Carcinogenesis KW - AKT protein KW - genomics KW - Cervix KW - Mutation KW - Human papillomavirus KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808657362?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Cancer+Research&rft.atitle=Genome+Analysis+of+Latin+American+Cervical+Cancer%3A+Frequent+Activation+of+the+PIK3CA+Pathway&rft.au=Lou%2C+Hong%3BVillagran%2C+Guillermo%3BBoland%2C+Joseph+F%3BIm%2C+Kate+M%3BPolo%2C+Sarita%3BZhou%2C+Weiyin%3BOdey%2C+Ushie%3BJuarez-Torres%2C+Eligia%3BMedina-Martinez%2C+Ingrid%3BRoman-Basaure%2C+Edgar%3BMitchell%2C+Jason%3BRoberson%2C+David%3BSawitzke%2C+Julie%3BGarland%2C+Lisa%3BRodriguez-Herrera%2C+Maria%3BWells%2C+David%3BTroyer%2C+Jennifer%3BPinto%2C+Francisco+Castillo%3BBass%2C+Sara%3BZhang%2C+Xijun%3BCastillo%2C+Miriam%3BGold%2C+Bert%3BMorales%2C+Hesler%3BYeager%2C+Meredith%3BBerumen%2C+Jaime%3BAlvirez%2C+Enrique%3BGharzouzi%2C+Eduardo%3BDean%2C+Michael&rft.aulast=Lou&rft.aufirst=Hong&rft.date=2015-12-01&rft.volume=21&rft.issue=23&rft.spage=5360&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-1837 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Mortality; Age; Cervical cancer; Adenosquamous; chromosome 3; Tumors; Children; copy number; Carcinoma; Blood; Malignancy; 1-Phosphatidylinositol 3-kinase; Typing; Phosphorylation; Carcinogenesis; AKT protein; genomics; Cervix; Mutation; Human papillomavirus DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-1837 ER - TY - JOUR T1 - Socioeconomic disadvantage and neural development from infancy through early childhood AN - 1785235313; PQ0002904622 AB - Background: Early social experiences are believed to shape neurodevelopment, with potentially lifelong consequences. Yet minimal evidence exists regarding the role of the social environment on children's neural functioning, a core domain of neurodevelopment.Methods: We analysed data from 36443 participants in the United States Collaborative Perinatal Project, a socioeconomically diverse pregnancy cohort conducted between 1959 and 1974. Study outcomes included: physician (neurologist or paediatrician)-rated neurological abnormality neonatally and thereafter at 4 months and 1 and 7 years; indicators of neurological hard signs and soft signs; and indicators of autonomic nervous system function.Results: Children born to socioeconomically disadvantaged parents were more likely to exhibit neurological abnormalities at 4 months [odds ratio (OR)=1.20; 95% confidence interval (CI)=1.06, 1.37], 1 year (OR=1.35; CI=1.17, 1.56), and 7 years (OR=1.67; CI=1.48, 1.89), and more likely to exhibit neurological hard signs (OR=1.39; CI=1.10, 1.76), soft signs (OR=1.26; CI=1.09, 1.45) and autonomic nervous system dysfunctions at 7 years. Pregnancy and delivery complications, themselves associated with socioeconomic disadvantage, did not account for the higher risks of neurological abnormalities among disadvantaged children.Conclusions: Parental socioeconomic disadvantage was, independently from pregnancy and delivery complications, associated with abnormal child neural development during the first 7 years of life. These findings reinforce the importance of the early environment for neurodevelopment generally, and expand knowledge regarding the domains of neurodevelopment affected by environmental conditions. Further work is needed to determine the mechanisms linking socioeconomic disadvantage with children's neural functioning, the timing of such mechanisms and their potential reversibility. JF - International Journal of Epidemiology AU - Chin-Lun Hung, Galen AU - Hahn, Jill AU - Alamiri, Bibi AU - Buka, Stephen L AU - Goldstein, Jill M AU - Laird, Nan AU - Nelson, Charles A AU - Smoller, Jordan W AU - Gilman, Stephen E AD - *Corresponding author. Eunice Kennedy Shriver National Institute of Child Health and Human Development; 6100 Executive Blvd., Room 7B13M, Rockville, MD 20852, USA. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1889 EP - 1899 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 44 IS - 6 SN - 0300-5771, 0300-5771 KW - CSA Neurosciences Abstracts; Health & Safety Science Abstracts KW - Neural development KW - soft signs KW - neurological abnormality KW - socioeconomic status KW - Autonomic nervous system KW - Data processing KW - Complications KW - Socioeconomics KW - Neurological complications KW - Development KW - Children KW - Pregnancy KW - Socio-economic aspects KW - USA KW - Risk factors KW - Social environment KW - Environmental conditions KW - N3 11003:Developmental neuroscience KW - H 12000:Epidemiology and Public Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1785235313?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Epidemiology&rft.atitle=Socioeconomic+disadvantage+and+neural+development+from+infancy+through+early+childhood&rft.au=Chin-Lun+Hung%2C+Galen%3BHahn%2C+Jill%3BAlamiri%2C+Bibi%3BBuka%2C+Stephen+L%3BGoldstein%2C+Jill+M%3BLaird%2C+Nan%3BNelson%2C+Charles+A%3BSmoller%2C+Jordan+W%3BGilman%2C+Stephen+E&rft.aulast=Chin-Lun+Hung&rft.aufirst=Galen&rft.date=2015-12-01&rft.volume=44&rft.issue=6&rft.spage=1889&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Epidemiology&rft.issn=03005771&rft_id=info:doi/10.1093%2Fije%2Fdyv303 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Socio-economic aspects; Data processing; Autonomic nervous system; Risk factors; Social environment; Development; Environmental conditions; Children; Pregnancy; Complications; Neurological complications; Socioeconomics; USA DO - http://dx.doi.org/10.1093/ije/dyv303 ER - TY - JOUR T1 - Functional Niche Competition Between Normal Hematopoietic Stem and Progenitor Cells and Myeloid Leukemia Cells AN - 1780528560; PQ0002832003 AB - Abstract Hematopoietic stem and progenitor cells (HSPCs) reside in a specialized niche that regulates their proliferative capacity and their fate. There is increasing evidence for similar roles of marrow niches on controlling the behavior of leukemic cells; however, whether normal hematopoietic stem cell (HSC) and leukemic cells reside in or functionally compete for the same marrow niche is unclear. We used the mixed lineage leukemia-AF9 (MLL-AF9) murine acute myeloid leukemia (AML) in a competitive repopulation model to investigate whether normal HSPC and leukemic cells functionally compete for the same marrow niches. Irradiated recipient mice were transplanted with fixed numbers of MLL-AF9 cells mixed with increasing doses of normal syngeneic whole bone marrow (WBM) or with purified HSPC (LSK). Survival was significantly increased and leukemic progression was delayed proportional to increasing doses of normal WBM or normal LSK cells in multiple independent experiments, with all doses of WBM or LSK cells studied above the threshold for rapid and complete hematopoietic reconstitution in the absence of leukemia. Confocal microscopy demonstrated nests of either leukemic cells or normal hematopoietic cells but not both in the marrow adjacent to endosteum. Early following transplantation, leukemic cells from animals receiving lower LSK doses were cycling more actively than in those receiving higher doses. These results suggest that normal HSPC and AML cells compete for the same functional niche. Manipulation of the niche could impact on response to antileukemic therapies, and the numbers of normal HSPC could impact on leukemia outcome, informing approaches to cell dose in the context of stem cell transplantation. Stem Cells 2015; 33:3635-3642 JF - Stem Cells AU - Glait-Santar, Chen AU - Desmond, Ronan AU - Feng, Xingmin AU - Bat, Taha AU - Chen, Jichun AU - Heuston, Elisabeth AU - Mizukawa, Benjamin AU - Mulloy, James C AU - Bodine, David M AU - Larochelle, Andre AU - Dunbar, Cynthia E AD - Hematology Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 3635 EP - 3642 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 33 IS - 12 SN - 1066-5099, 1066-5099 KW - Biotechnology and Bioengineering Abstracts KW - Cell survival KW - Stem cells KW - Syngeneic grafts KW - Acute myeloid leukemia KW - Myeloid leukemia KW - stem cell transplantation KW - Confocal microscopy KW - Bone marrow KW - Animal models KW - Hemopoiesis KW - Nests KW - W 30920:Tissue Engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780528560?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+Cells&rft.atitle=Functional+Niche+Competition+Between+Normal+Hematopoietic+Stem+and+Progenitor+Cells+and+Myeloid+Leukemia+Cells&rft.au=Glait-Santar%2C+Chen%3BDesmond%2C+Ronan%3BFeng%2C+Xingmin%3BBat%2C+Taha%3BChen%2C+Jichun%3BHeuston%2C+Elisabeth%3BMizukawa%2C+Benjamin%3BMulloy%2C+James+C%3BBodine%2C+David+M%3BLarochelle%2C+Andre%3BDunbar%2C+Cynthia+E&rft.aulast=Glait-Santar&rft.aufirst=Chen&rft.date=2015-12-01&rft.volume=33&rft.issue=12&rft.spage=3635&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.2208 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Cell survival; Syngeneic grafts; Stem cells; Myeloid leukemia; Acute myeloid leukemia; stem cell transplantation; Confocal microscopy; Animal models; Bone marrow; Hemopoiesis; Nests DO - http://dx.doi.org/10.1002/stem.2208 ER - TY - JOUR T1 - Transcriptome Dynamics of Developing Photoreceptors in Three-Dimensional Retina Cultures Recapitulates Temporal Sequence of Human Cone and Rod Differentiation Revealing Cell Surface Markers and Gene Networks AN - 1780522456; PQ0002832006 AB - The derivation of three-dimensional (3D) stratified neural retina from pluripotent stem cells has permitted investigations of human photoreceptors. We have generated a H9 human embryonic stem cell subclone that carries a green fluorescent protein (GFP) reporter under the control of the promoter of cone-rod homeobox (CRX), an established marker of postmitotic photoreceptor precursors. The CRXp-GFP reporter replicates endogenous CRX expression in vitro when the H9 subclone is induced to form self-organizing 3D retina-like tissue. At day 37, CRX+ photoreceptors appear in the basal or middle part of neural retina and migrate to apical side by day 67. Temporal and spatial patterns of retinal cell type markers recapitulate the predicted sequence of development. Cone gene expression is concomitant with CRX, whereas rod differentiation factor neural retina leucine zipper protein (NRL) is first observed at day 67. At day 90, robust expression of NRL and its target nuclear receptor NR2E3 is evident in many CRX+ cells, while minimal S-opsin and no rhodopsin or L/M-opsin is present. The transcriptome profile, by RNA-seq, of developing human photoreceptors is remarkably concordant with mRNA and immunohistochemistry data available for human fetal retina although many targets of CRX, including phototransduction genes, exhibit a significant delay in expression. We report on temporal changes in gene signatures, including expression of cell surface markers and transcription factors; these expression changes should assist in isolation of photoreceptors at distinct stages of differentiation and in delineating coexpression networks. Our studies establish the first global expression database of developing human photoreceptors, providing a reference map for functional studies in retinal cultures. Stem Cells 2015; 33:3504-3518 JF - Stem Cells AU - Kaewkhaw, Rossukon AU - Kaya, Koray Dogan AU - Brooks, Matthew AU - Homma, Kohei AU - Zou, Jizhong AU - Chaitankar, Vijender AU - Rao, Mahendra AU - Swaroop, Anand AD - Neurobiology-Neurodegeneration & Repair Laboratory, National Eye Institute, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 3504 EP - 3518 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 33 IS - 12 SN - 1066-5099, 1066-5099 KW - CSA Neurosciences Abstracts; Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Cell surface KW - Cones KW - Data processing KW - Retina KW - Phototransduction KW - Nuclear receptors KW - Green fluorescent protein KW - Cell culture KW - Photoreceptors KW - Gene expression KW - Computer programs KW - Promoters KW - Differentiation KW - Stem cells KW - Rhodopsin KW - Transcription factors KW - Cell migration KW - Leucine zipper proteins KW - Neural stem cells KW - N3 11023:Neurogenetics KW - W 30910:Imaging KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780522456?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+Cells&rft.atitle=Transcriptome+Dynamics+of+Developing+Photoreceptors+in+Three-Dimensional+Retina+Cultures+Recapitulates+Temporal+Sequence+of+Human+Cone+and+Rod+Differentiation+Revealing+Cell+Surface+Markers+and+Gene+Networks&rft.au=Kaewkhaw%2C+Rossukon%3BKaya%2C+Koray+Dogan%3BBrooks%2C+Matthew%3BHomma%2C+Kohei%3BZou%2C+Jizhong%3BChaitankar%2C+Vijender%3BRao%2C+Mahendra%3BSwaroop%2C+Anand&rft.aulast=Kaewkhaw&rft.aufirst=Rossukon&rft.date=2015-12-01&rft.volume=33&rft.issue=12&rft.spage=3504&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.2122 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Cell surface; Data processing; Cones; Phototransduction; Retina; Nuclear receptors; Green fluorescent protein; Cell culture; Photoreceptors; Gene expression; Differentiation; Promoters; Computer programs; Stem cells; Rhodopsin; Transcription factors; Leucine zipper proteins; Cell migration; Neural stem cells DO - http://dx.doi.org/10.1002/stem.2122 ER - TY - JOUR T1 - Spectral fitting using basis set modified by measured B sub(0) field distribution AN - 1780522367; PQ0002828094 AB - This study sought to demonstrate and evaluate a novel spectral fitting method to improve quantification accuracy in the presence of large magnetic field distortion, especially with high fields. MRS experiments were performed using a point-resolved spectroscopy (PRESS)-type sequence at 7T. A double-echo gradient echo (GRE) sequence was used to acquire B sub(0) maps following MRS experiments. The basis set was modified based on the measured B sub(0) distribution within the MRS voxel. Quantification results were obtained after fitting the measured MRS data using the modified basis set. The proposed method was validated using numerical Monte Carlo simulations, phantom measurements, and comparison of occipital lobe MRS measurements under homogeneous and inhomogeneous magnetic field conditions. In vivo results acquired from voxels placed in thalamus and prefrontal cortex regions close to the frontal sinus agreed well with published values. Instead of noise-amplifying complex division, the proposed method treats field variations as part of the signal model, thereby avoiding inherent statistical bias associated with regularization. Simulations and experiments showed that the proposed approach reliably quantified results in the presence of relatively large magnetic field distortion. Linear combination fitting plots from homogeneous and inhomogeneous field acquisitions from the same voxel located in the occipital lobe (indicated by the yellow boxes on the T1-weighted images) of a healthy volunteer. The proposed spectral fitting method used a signal model distorted by the measured B0 field map to fit the observed data. This novel approach provides reliable metabolite quantifications in the presence of large magnetic field distortion, especially with high fields. JF - NMR in Biomedicine AU - Li, Ningzhi AU - An, Li AU - Shen, Jun AD - Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1707 EP - 1715 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 28 IS - 12 SN - 0952-3480, 0952-3480 KW - Biotechnology and Bioengineering Abstracts KW - Monte Carlo simulation KW - Statistics KW - Data processing KW - Statistical analysis KW - Metabolites KW - Sinus KW - Spectroscopy KW - Maps KW - Thalamus KW - Models KW - Magnetic fields KW - N.M.R. KW - Occipital lobe KW - Cortex (prefrontal) KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780522367?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NMR+in+Biomedicine&rft.atitle=Spectral+fitting+using+basis+set+modified+by+measured+B+sub%280%29+field+distribution&rft.au=Li%2C+Ningzhi%3BAn%2C+Li%3BShen%2C+Jun&rft.aulast=Li&rft.aufirst=Ningzhi&rft.date=2015-12-01&rft.volume=28&rft.issue=12&rft.spage=1707&rft.isbn=&rft.btitle=&rft.title=NMR+in+Biomedicine&rft.issn=09523480&rft_id=info:doi/10.1002%2Fnbm.3430 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Monte Carlo simulation; Data processing; Statistics; Statistical analysis; Sinus; Metabolites; Maps; Spectroscopy; Thalamus; Models; Magnetic fields; N.M.R.; Occipital lobe; Cortex (prefrontal) DO - http://dx.doi.org/10.1002/nbm.3430 ER - TY - JOUR T1 - Simultaneous calcium fluorescence imaging and MR of ex vivo organotypic cortical cultures: a new test bed for functional MRI AN - 1780521487; PQ0002828104 AB - Recently, several new functional (f)MRI contrast mechanisms including diffusion, phase imaging, proton density, etc. have been proposed to measure neuronal activity more directly and accurately than blood-oxygen-level dependent (BOLD) fMRI. However, these approaches have proved difficult to reproduce, mainly because of the dearth of reliable and robust test systems to vet and validate them. Here we describe the development and testing of such a test bed for non-BOLD fMRI. Organotypic cortical cultures were used as a stable and reproducible biological model of neuronal activity that shows spontaneous activity similar to that of in vivo brain cortex without any hemodynamic confounds. An open-access, single-sided magnetic resonance (MR) "profiler" consisting of four permanent magnets with magnetic field of 0.32 T was used in this study to perform MR acquisition. A fluorescence microscope with long working distance objective was mounted on the top of a custom-designed chamber that keeps the organotypic culture vital, and the MR system was mounted on the bottom of the chamber to achieve real-time simultaneous calcium fluorescence optical imaging and MR acquisition on the same specimen. In this study, the reliability and performance of the proposed test bed were demonstrated by a conventional CPMG MR sequence acquired simultaneously with calcium imaging, which is a well-characterized measurement of neuronal activity. This experimental design will make it possible to correlate directly the other candidate functional MR signals to the optical indicia of neuronal activity in the future. Here we describe the development and testing of a new test bed for non-BOLD functional MRI aimed at detecting neuronal activity directly and accurately. This test bed enables simultaneous calcium fluorescence optical imaging and MR acquisition on a stable and reproducible biological model of neuronal activity without hemodynamic related artifacts. This experimental design makes it possible to directly correlate the candidate functional MR signals to optical indicators of neuronal activity. JF - NMR in Biomedicine AU - Bai, Ruiliang AU - Klaus, Andreas AU - Bellay, Tim AU - Stewart, Craig AU - Pajevic, Sinisa AU - Nevo, Uri AU - Merkle, Hellmut AU - Plenz, Dietmar AU - Basser, Peter J AD - Section on Tissue Biophysics and Biomimetics, PPITS, NICHD, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1726 EP - 1738 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 28 IS - 12 SN - 0952-3480, 0952-3480 KW - Biotechnology and Bioengineering Abstracts KW - Brain mapping KW - Neuroimaging KW - Fluorescence KW - Protons KW - Functional magnetic resonance imaging KW - Microscopes KW - Calcium imaging KW - Hemodynamics KW - Magnetic fields KW - Cortex KW - N.M.R. KW - Diffusion KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780521487?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NMR+in+Biomedicine&rft.atitle=Simultaneous+calcium+fluorescence+imaging+and+MR+of+ex+vivo+organotypic+cortical+cultures%3A+a+new+test+bed+for+functional+MRI&rft.au=Bai%2C+Ruiliang%3BKlaus%2C+Andreas%3BBellay%2C+Tim%3BStewart%2C+Craig%3BPajevic%2C+Sinisa%3BNevo%2C+Uri%3BMerkle%2C+Hellmut%3BPlenz%2C+Dietmar%3BBasser%2C+Peter+J&rft.aulast=Bai&rft.aufirst=Ruiliang&rft.date=2015-12-01&rft.volume=28&rft.issue=12&rft.spage=1726&rft.isbn=&rft.btitle=&rft.title=NMR+in+Biomedicine&rft.issn=09523480&rft_id=info:doi/10.1002%2Fnbm.3424 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Brain mapping; Magnetic fields; Neuroimaging; Cortex; Fluorescence; Protons; Microscopes; Functional magnetic resonance imaging; Hemodynamics; Calcium imaging; Diffusion; N.M.R. DO - http://dx.doi.org/10.1002/nbm.3424 ER - TY - JOUR T1 - Pressure-induced structural transition of mature HIV-1 protease from a combined NMR/MD simulation approach AN - 1780507199; PQ0002831891 AB - We investigate the pressure-induced structural changes in the mature human immunodeficiency virus type 1 protease dimer, using residual dipolar coupling (RDC) measurements in a weakly oriented solution. super(1)D sub(NH) RDCs were measured under high-pressure conditions for an inhibitor-free PR and an inhibitor-bound complex, as well as for an inhibitor-free multidrug resistant protease bearing 20 mutations (PR20). While PR20 and the inhibitor-bound PR were little affected by pressure, inhibitor-free PR showed significant differences in the RDCs measured at 600 bar compared with 1 bar. The structural basis of such changes was investigated by MD simulations using the experimental RDC restraints, revealing substantial conformational perturbations, specifically a partial opening of the flaps and the penetration of water molecules into the hydrophobic core of the subunits at high pressure. This study highlights the exquisite sensitivity of RDCs to pressure-induced conformational changes and illustrates how RDCs combined with MD simulations can be used to determine the structural properties of metastable intermediate states on the folding energy landscape. Proteins 2015; 83:2117-2123. JF - Proteins: Structure, Function and Bioinformatics AU - Roche, Julien AU - Louis, John M AU - Bax, Ad AU - Best, Robert B AD - Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, 20892. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 2117 EP - 2123 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030 United States VL - 83 IS - 12 SN - 0887-3585, 0887-3585 KW - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts KW - Protein structure KW - Energy KW - Human immunodeficiency virus 1 KW - Proteinase KW - Hydrophobicity KW - N.M.R. KW - Multidrug resistance KW - Bioinformatics KW - Pressure KW - Mutation KW - V 22360:AIDS and HIV KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780507199?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.atitle=Pressure-induced+structural+transition+of+mature+HIV-1+protease+from+a+combined+NMR%2FMD+simulation+approach&rft.au=Roche%2C+Julien%3BLouis%2C+John+M%3BBax%2C+Ad%3BBest%2C+Robert+B&rft.aulast=Roche&rft.aufirst=Julien&rft.date=2015-12-01&rft.volume=83&rft.issue=12&rft.spage=2117&rft.isbn=&rft.btitle=&rft.title=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.issn=08873585&rft_id=info:doi/10.1002%2Fprot.24931 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Protein structure; Energy; Multidrug resistance; N.M.R.; Hydrophobicity; Proteinase; Bioinformatics; Pressure; Mutation; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1002/prot.24931 ER - TY - JOUR T1 - Near-ultraviolet laser diodes for brilliant ultraviolet fluorophore excitation AN - 1776648981; PQ0002793842 AB - Although multiple lasers are now standard equipment on most modern flow cytometers, ultraviolet (UV) lasers (325-365 nm) remain an uncommon excitation source for cytometry. Nd:YVO sub(4) frequency-tripled diode pumped solid-state lasers emitting at 355 nm are now the primary means of providing UV excitation on multilaser flow cytometers. Although a number of UV excited fluorochromes are available for flow cytometry, the cost of solid-state UV lasers remains prohibitively high, limiting their use to all but the most sophisticated multilaser instruments. The recent introduction of the brilliant ultraviolet (BUV) series of fluorochromes for cell surface marker detection and their importance in increasing the number of simultaneous parameters for high-dimensional analysis has increased the urgency of including UV sources in cytometer designs; however, these lasers remain expensive. Near-UV laser diodes (NUVLDs), a direct diode laser source emitting in the 370-380 nm range, have been previously validated for flow cytometric analysis of most UV-excited probes, including quantum nanocrystals, the Hoechst dyes, and 4',6-diamidino-2-phenylindole. However, they remain a little-used laser source for cytometry, despite their significantly lower cost. In this study, the ability of NUVLDs to excite the BUV dyes was assessed, along with their compatibility with simultaneous brilliant violet (BV) labeling. A NUVLD emitting at 375 nm was found to excite most of the available BUV dyes at least as well as a UV 355 nm source. This slightly longer wavelength did produce some unwanted excitation of BV dyes, but at sufficiently low levels to require minimal additional compensation. NUVLDs are compact, relatively inexpensive lasers that have higher power levels than the newest generation of small 355 nm lasers. They can, therefore, make a useful, cost-effective substitute for traditional UV lasers in multicolor analysis involving the BUV and BV dyes. Published 2015 Wiley Periodicals, Inc. This article is a US Government work and is in the public domain in the United States of America. JF - Cytometry Part A AU - Telford, William G AD - Experimental Transplantation and Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, 20892. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1127 EP - 1137 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 87 IS - 12 SN - 1552-4922, 1552-4922 KW - Biotechnology and Bioengineering Abstracts KW - Flow cytometry KW - Cell surface KW - U.V. radiation KW - Dyes KW - 4',6-Diamidino-2-phenylindole KW - Probes KW - Lasers KW - fluorochromes KW - Crystals KW - Wavelength KW - fluorophores KW - W 30945:Fermentation & Cell Culture UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1776648981?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cytometry+Part+A&rft.atitle=Near-ultraviolet+laser+diodes+for+brilliant+ultraviolet+fluorophore+excitation&rft.au=Telford%2C+William+G&rft.aulast=Telford&rft.aufirst=William&rft.date=2015-12-01&rft.volume=87&rft.issue=12&rft.spage=1127&rft.isbn=&rft.btitle=&rft.title=Cytometry+Part+A&rft.issn=15524922&rft_id=info:doi/10.1002%2Fcyto.a.22686 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Flow cytometry; Cell surface; U.V. radiation; 4',6-Diamidino-2-phenylindole; Dyes; Probes; Lasers; fluorophores; Wavelength; Crystals; fluorochromes DO - http://dx.doi.org/10.1002/cyto.a.22686 ER - TY - JOUR T1 - Modeling Human Bone Marrow Failure Syndromes Using Pluripotent Stem Cells and Genome Engineering AN - 1773836728; PQ0002725871 AB - The combination of epigenetic reprogramming with advanced genome editing technologies opened a new avenue to study disease mechanisms, particularly of disorders with depleted target tissue. Bone marrow failure syndromes (BMFS) typically present with a marked reduction of peripheral blood cells due to a destroyed or dysfunctional bone marrow compartment. Somatic and germline mutations have been etiologically linked to many cases of BMFS. However, without the ability to study primary patient material, the exact pathogenesis for many entities remained fragmentary. Capturing the pathological genotype in induced pluripotent stem cells (iPSCs) allows studying potential developmental defects leading to a particular phenotype. The lack of hematopoietic stem and progenitor cells in these patients can also be overcome by differentiating patient-derived iPSCs into hematopoietic lineages. With fast growing genome editing techniques, such as CRISPR/Cas9, correction of disease-causing mutations in iPSCs or introduction of mutations in cells from healthy individuals enable comparative studies that may identify other genetic or epigenetic events contributing to a specific disease phenotype. In this review, we present recent progresses in disease modeling of inherited and acquired BMFS using reprogramming and genome editing techniques. We also discuss the challenges and potential shortcomings of iPSC-based models for hematological diseases. JF - Molecular Therapy AU - Jung, Moonjung AU - Dunbar, Cynthia E AU - Winkler, Thomas AD - Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA, winklert@nhlbi.nih.gov Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1832 EP - 1842 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 23 IS - 12 SN - 1525-0016, 1525-0016 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Genomes KW - Stem cells KW - epigenetics KW - Inhibitory postsynaptic potentials KW - Bone marrow KW - Hemopoiesis KW - Peripheral blood KW - Genotypes KW - Mutation KW - Hematological diseases KW - G 07880:Human Genetics KW - W 30920:Tissue Engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1773836728?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Therapy&rft.atitle=Modeling+Human+Bone+Marrow+Failure+Syndromes+Using+Pluripotent+Stem+Cells+and+Genome+Engineering&rft.au=Jung%2C+Moonjung%3BDunbar%2C+Cynthia+E%3BWinkler%2C+Thomas&rft.aulast=Jung&rft.aufirst=Moonjung&rft.date=2015-12-01&rft.volume=23&rft.issue=12&rft.spage=1832&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2015.180 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Genomes; Stem cells; epigenetics; Inhibitory postsynaptic potentials; Bone marrow; Hemopoiesis; Peripheral blood; Genotypes; Hematological diseases; Mutation DO - http://dx.doi.org/10.1038/mt.2015.180 ER - TY - JOUR T1 - Association of 4p14 TLR locus with antibodies to Helicobacter pylori AN - 1765958791; PQ0002595391 AB - A genome-wide association study among Europeans related polymorphisms of the Toll-like receptor (TLR) locus at 4p14 and the Fc gamma receptor 2a locus at 1q23.3 to Helicobacter pylori serologic status. We replicated associations of 4p14 but not 1q23.3 with anti-Helicobacter pylori antibodies in 1402 Finnish males. Importantly, our analysis clarified that the phenotype affected by 4p14 is quantitative level of these antibodies rather than association with seropositivity per se. In addition, we annotated variants at 4p14 as expression quantitative trait loci (eQTL) associated with TLR6/10 and FAM114A1. Our findings suggest that 4p14 polymorphisms are linked to host immune response to H. pylori infection but not to its acquisition. JF - Genes and Immunity AU - Sung, H AU - Camargo, M C AU - Yu, K AU - Weinstein, S J AU - Morgan, D R AU - Albanes, D AU - Rabkin, C S AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 567 EP - 570 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 16 IS - 8 SN - 1466-4879, 1466-4879 KW - Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Immunology Abstracts KW - Helicobacter pylori KW - Quantitative trait loci KW - Antibodies KW - Chromosome 1 KW - Immune response KW - chromosome 4 KW - Infection KW - Toll-like receptors KW - Fc receptors KW - J 02350:Immunology KW - G 07770:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765958791?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genes+and+Immunity&rft.atitle=Association+of+4p14+TLR+locus+with+antibodies+to+Helicobacter+pylori&rft.au=Sung%2C+H%3BCamargo%2C+M+C%3BYu%2C+K%3BWeinstein%2C+S+J%3BMorgan%2C+D+R%3BAlbanes%2C+D%3BRabkin%2C+C+S&rft.aulast=Sung&rft.aufirst=H&rft.date=2015-12-01&rft.volume=16&rft.issue=8&rft.spage=567&rft.isbn=&rft.btitle=&rft.title=Genes+and+Immunity&rft.issn=14664879&rft_id=info:doi/10.1038%2Fgene.2015.33 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Quantitative trait loci; Antibodies; Chromosome 1; Immune response; Infection; chromosome 4; Toll-like receptors; Fc receptors; Helicobacter pylori DO - http://dx.doi.org/10.1038/gene.2015.33 ER - TY - JOUR T1 - Time for a prepublication culture in clinical research? AN - 1762370222; PQ0002493886 JF - Lancet AU - Lauer, Michael S AU - Krumholz, Harlan M AU - Topol, Eric J AD - Office of Extramural Research, National Institutes of Health, Bethesda, MD 20892, USA Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 2447 EP - 2449 PB - Elsevier B.V., Radarweg 29 Amsterdam 1043 NX Netherlands VL - 386 IS - 10012 SN - 0140-6736, 0140-6736 KW - Health & Safety Science Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1762370222?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lancet&rft.atitle=Time+for+a+prepublication+culture+in+clinical+research%3F&rft.au=Lauer%2C+Michael+S%3BKrumholz%2C+Harlan+M%3BTopol%2C+Eric+J&rft.aulast=Lauer&rft.aufirst=Michael&rft.date=2015-12-01&rft.volume=386&rft.issue=10012&rft.spage=2447&rft.isbn=&rft.btitle=&rft.title=Lancet&rft.issn=01406736&rft_id=info:doi/10.1016%2FS0140-6736%2815%2901177-0 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Number of references - 11 N1 - Last updated - 2016-02-04 DO - http://dx.doi.org/10.1016/S0140-6736(15)01177-0 ER - TY - JOUR T1 - Identification of novel anti-hepatitis C virus agents by a quantitative high throughput screen in a cell-based infection assay AN - 1753461841; PQ0002417767 AB - Hepatitis C virus (HCV) poses a major health threat to the world. The recent development of direct-acting antivirals (DAAs) against HCV has markedly improved the response rate of HCV and reduced the side effects in comparison to the interferon-based therapy. Despite this therapeutic advance, there is still a need to develop new inhibitors that target different stages of the HCV life cycle because of various limitations of the current regimens. In this study, we performed a quantitative high throughput screening of the Molecular Libraries Small Molecule Repository (MLSMR) of 350,000 chemicals for novel HCV inhibitors using our previously developed cell-based HCV infection assay. Following confirmation and structural clustering analysis, we narrowed down to 158 compounds from the initial 3000 molecules that showed inhibitory activity for further structural and functional analyses. We were able to assign the majority of these compounds to specific stage(s) in the HCV life cycle. Three of them are direct inhibitors of NS3/4A protease. Most of the compounds appear to act on novel targets in HCV life cycle. Four compounds with novel structure and excellent drug-like properties, three targeting HCV entry and one targeting HCV assembly/secretion, were advanced for further development as lead hits. These compounds represent diverse chemotypes that are potential lead compounds for further optimization and may offer promising candidates for the development of novel therapeutics against HCV infection. In addition, they represent novel molecular probes to explore the complex interactions between HCV and the cells. JF - Antiviral Research AU - Hu, Zongyi AU - Hu, Xin AU - He, Shanshan AU - Yim, Hyung Joon AU - Xiao, Jingbo AU - Swaroop, Manju AU - Tanega, Cordelle AU - Zhang, Ya-qin AU - Yi, Guanghui AU - Kao, CCheng AU - Marugan, Juan AU - Ferrer, Marc AU - Zheng, Wei AU - Southall, Noel AU - Liang, TJake AD - Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 20 EP - 29 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 124 SN - 0166-3542, 0166-3542 KW - Biotechnology and Bioengineering Abstracts; Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Antiviral KW - HCV inhibitors KW - High throughput screening KW - Cell-based assay KW - Viral life cycle KW - Hepatitis C virus KW - Structure-function relationships KW - Secretion KW - Probes KW - Life cycle KW - Proteinase KW - Drug development KW - high-throughput screening KW - Infection KW - Side effects KW - A 01340:Antibiotics & Antimicrobials KW - W 30940:Products KW - V 22320:Replication UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753461841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antiviral+Research&rft.atitle=Identification+of+novel+anti-hepatitis+C+virus+agents+by+a+quantitative+high+throughput+screen+in+a+cell-based+infection+assay&rft.au=Hu%2C+Zongyi%3BHu%2C+Xin%3BHe%2C+Shanshan%3BYim%2C+Hyung+Joon%3BXiao%2C+Jingbo%3BSwaroop%2C+Manju%3BTanega%2C+Cordelle%3BZhang%2C+Ya-qin%3BYi%2C+Guanghui%3BKao%2C+CCheng%3BMarugan%2C+Juan%3BFerrer%2C+Marc%3BZheng%2C+Wei%3BSouthall%2C+Noel%3BLiang%2C+TJake&rft.aulast=Hu&rft.aufirst=Zongyi&rft.date=2015-12-01&rft.volume=124&rft.issue=&rft.spage=20&rft.isbn=&rft.btitle=&rft.title=Antiviral+Research&rft.issn=01663542&rft_id=info:doi/10.1016%2Fj.antiviral.2015.10.018 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Last updated - 2016-02-29 N1 - SubjectsTermNotLitGenreText - Structure-function relationships; Secretion; Probes; Life cycle; high-throughput screening; Drug development; Proteinase; Infection; Side effects; Hepatitis C virus DO - http://dx.doi.org/10.1016/j.antiviral.2015.10.018 ER - TY - JOUR T1 - New insights into heterogeneity of peritoneal B-1a cells AN - 1753460667; PQ0002420664 AB - Peritoneal B-1a cells are characterized by their expression of CD5 and enrichment for germline-encoded IgM B cell receptors. Early studies showing expression of a diverse array of VDJ sequences among purified B-1a cells provided a molecular basis for understanding the heterogeneity of the B-1a cell repertoire. Antigen-driven positive selection and the identification of B-1a specific progenitors suggest multiple origins of B-1a cells. The introduction of new markers such as PD-L2, CD25, CD73, and PC1 (plasma cell alloantigen 1, also known as ectonucleotide phosphodiesterase/pyrophosphatase 1) further helped to identify phenotypically and functionally distinct B-1a subsets. Among many B-1a subsets defined by these new markers, PC1 is unique in that it subdivides B-1a cells into PC1 super(hi) and PC1 super(lo) subpopulations with distinct functions, such as production of natural IgM and gut IgA, response to the pneumococcal antigen PPS-3, secretion of interleukin-10, and support for T helper 1 (T sub(H)1) cell differentiation. RNA sequencing of these subsets revealed differential expression of genes involved in cellular movement and immune cell trafficking. We will discuss these new insights underlying the heterogeneous nature of the B-1a cell repertoire. JF - Annals of the New York Academy of Sciences AU - Wang, Hongsheng AU - Lin, Jian-xin AU - Li, Peng AU - Skinner, Jeff AU - Leonard, Warren J AU - Morse, Herbert C AD - The Virology and Cellular Immunology Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 68 EP - 76 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 1362 IS - 1 SN - 0077-8923, 0077-8923 KW - Environment Abstracts KW - Streptococcus pneumoniae KW - Subpopulations KW - Cell differentiation KW - Trafficking KW - ENA 18:Transportation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753460667?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvabstractsmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=New+insights+into+heterogeneity+of+peritoneal+B-1a+cells&rft.au=Wang%2C+Hongsheng%3BLin%2C+Jian-xin%3BLi%2C+Peng%3BSkinner%2C+Jeff%3BLeonard%2C+Warren+J%3BMorse%2C+Herbert+C&rft.aulast=Wang&rft.aufirst=Hongsheng&rft.date=2015-12-01&rft.volume=1362&rft.issue=1&rft.spage=68&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/10.1111%2Fnyas.12791 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Subpopulations; Cell differentiation; Trafficking; Streptococcus pneumoniae DO - http://dx.doi.org/10.1111/nyas.12791 ER - TY - JOUR T1 - Particle-based platforms for malaria vaccines AN - 1753457547; PQ0002418103 AB - Recombinant subunit vaccines in general are poor immunogens likely due to the small size of peptides and proteins, combined with the lack or reduced presentation of repetitive motifs and missing complementary signal(s) for optimal triggering of the immune response. Therefore, recombinant subunit vaccines require enhancement by vaccine delivery vehicles in order to attain adequate protective immunity. Particle-based delivery platforms, including particulate antigens and particulate adjuvants, are promising delivery vehicles for modifying the way in which immunogens are presented to both the innate and adaptive immune systems. These particle delivery platforms can also co-deliver non-specific immunostimodulators as additional adjuvants. This paper reviews efforts and advances of the Particle-based delivery platforms in development of vaccines against malaria, a disease that claims over 600,000 lives per year, most of them are children under 5 years of age in sub-Sahara Africa. JF - Vaccine AU - Wu, Yimin AU - Narum, David L AU - Fleury, Sylvain AU - Jennings, Gary AU - Yadava, Anjali AD - Laboratory Malaria Immunology and Vaccinology, National Institute of Allergy and Infectious Diseases, 5640 Fishers Lane, Rockville, MD, USA Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 7518 EP - 7524 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 33 IS - 52 SN - 0264-410X, 0264-410X KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Immunology Abstracts KW - Malaria KW - Vaccine KW - Particle KW - Delivery KW - Adjuvant KW - Age KW - Human diseases KW - Disease control KW - Adjuvants KW - Immunity KW - Children KW - Public health KW - Recombinants KW - Antigens KW - Combined vaccines KW - Africa KW - Immune response KW - Vaccines KW - K 03400:Human Diseases KW - Q1 08423:Behaviour KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753457547?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=Particle-based+platforms+for+malaria+vaccines&rft.au=Wu%2C+Yimin%3BNarum%2C+David+L%3BFleury%2C+Sylvain%3BJennings%2C+Gary%3BYadava%2C+Anjali&rft.aulast=Wu&rft.aufirst=Yimin&rft.date=2015-12-01&rft.volume=33&rft.issue=52&rft.spage=7518&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/10.1016%2Fj.vaccine.2015.09.097 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Number of references - 69 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Recombinants; Human diseases; Antigens; Disease control; Malaria; Immunity; Vaccines; Public health; Age; Combined vaccines; Immune response; Adjuvants; Children; Africa DO - http://dx.doi.org/10.1016/j.vaccine.2015.09.097 ER - TY - JOUR T1 - Utilizing Whole Slide Images for Pathology Peer Review and Working Groups AN - 1751215513; PQ0002364291 AB - This article describes the results of comparisons of digitally scanned whole slide images (WSIs) and glass microscope slides for diagnosis of tissues under peer review by the National Toxicology Program. Findings in this article were developed as a result of the data collected from 6 pathology working groups (PWGs), 1 pathology peer review, and survey comments from over 25 participating pathologists. For each PWG, 6-14 pathologists examined 10-143 tissues per study from 6- and 9-month perinatal studies and 2-year carcinogenicity studies. Overall it was found that evaluation of WSIs is generally equivalent to using glass slides. Concordance of PWG consensus diagnoses based upon review of WSIs versus glass slides ranged from 74% to 100% (median 86%). The intra- and interobserver diagnostic variation did not appear to influence the conclusions of any study. Based upon user opinions collected from surveys, WSIs may be less optimal than glass slides for evaluation of subtle lesions, large complex lesions, small lesions in a large section of tissue, and foci of altered hepatocytes. These results indicate that, although there may be some limitations, the use of WSIs can effectively accomplish the objectives of a conventional glass slide review and definitely serves as a useful adjunct to the conduct of PWGs. JF - Toxicologic Pathology AU - Malarkey, David E AU - Willson, Gabrielle A AU - Willson, Cynthia J AU - Adams, ETerence AU - Olson, Greg R AU - Witt, William M AU - Elmore, Susan A AU - Hardisty, Jerry F AU - Boyle, Michael C AU - Crabbs, Torrie A AU - Miller, Rodney A AD - 1 .Cellular and Molecular Pathology Branch, National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, malarkey@niehs.nih.gov Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1149 EP - 1157 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 43 IS - 8 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - digital images KW - digital pathology KW - digital slides KW - pathology working group KW - peer review KW - whole slide images KW - whole slide imaging KW - Data processing KW - Hepatocytes KW - Carcinogenicity KW - Reviews KW - Microscopes KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751215513?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Utilizing+Whole+Slide+Images+for+Pathology+Peer+Review+and+Working+Groups&rft.au=Malarkey%2C+David+E%3BWillson%2C+Gabrielle+A%3BWillson%2C+Cynthia+J%3BAdams%2C+ETerence%3BOlson%2C+Greg+R%3BWitt%2C+William+M%3BElmore%2C+Susan+A%3BHardisty%2C+Jerry+F%3BBoyle%2C+Michael+C%3BCrabbs%2C+Torrie+A%3BMiller%2C+Rodney+A&rft.aulast=Malarkey&rft.aufirst=David&rft.date=2015-12-01&rft.volume=43&rft.issue=8&rft.spage=1149&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623315605933 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 6 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Data processing; Carcinogenicity; Hepatocytes; Microscopes; Reviews DO - http://dx.doi.org/10.1177/0192623315605933 ER - TY - JOUR T1 - Genomic Profiling Reveals Unique Molecular Alterations in Hepatoblastomas and Adjacent Hepatocellular Carcinomas in B6C3F1 Mice AN - 1751213458; PQ0002364300 AB - The cell of origin of hepatoblastoma (HB) in humans and mice is unknown; it is hypothesized to be a transformed hepatocyte, oval cell, or hepatic progenitor cell. In mice, current dogma is that HBs arise from preexisting hepatocellular neoplasms as a result of further neoplastic transformation. However, there is little evidence supporting this direct relationship. To better understand the relationship between hepatocellular carcinoma (HCC) and HB and determine molecular similarities between mouse and human HB, global gene expression analysis and targeted mutation analysis were performed using HB, HCC, and adjacent liver from the same animals in a recent National Toxicology Program bioassay. There were significant differences in Hras and Ctnnb1 mutation spectra, and by microarray, HBs showed dysregulation of embryonic development, stem cell pluripotency, and genomic imprinting compared to HCC. Meta-analysis showed similarities between HB, early mouse embryonic liver, and hepatocyte-derived stem/progenitor cells compared to HCC. Our data show that there are striking differences between HB and HCC and suggest that HB is a significantly different entity that may arise from a hepatic precursor cell. Furthermore, mouse HB is similar to the human disease at the pathway level and therefore is likely a relevant model for evaluating human cancer hazard. JF - Toxicologic Pathology AU - Bhusari, Sachin AU - Pandiri, Arun R AU - Nagai, Hiroaki AU - Wang, Yu AU - Foley, Julie AU - Hong, Hue-Hua L AU - Ton, Thai-Vu AU - DeVito, Michael AU - Shockley, Keith R AU - Peddada, Shyamal D AU - Gerrish, Kevin E AU - Malarkey, David E AU - Hooth, Michelle J AU - Sills, Robert C AU - Hoenerhoff, Mark J AD - 1 .Cellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, hoenerho@med.umich.edu Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1114 EP - 1126 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 43 IS - 8 SN - 0192-6233, 0192-6233 KW - Genetics Abstracts; Toxicology Abstracts KW - carcinogenesis KW - liver KW - genomics KW - microarray KW - molecular pathology KW - rodent pathology KW - toxicologic pathology KW - Transformation KW - Genomic imprinting KW - Data processing KW - Hepatocytes KW - Animal models KW - Gene expression KW - Embryogenesis KW - Stem cells KW - Embryo cells KW - Reviews KW - Mutation KW - Hepatocellular carcinoma KW - G 07730:Development & Cell Cycle KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751213458?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Genomic+Profiling+Reveals+Unique+Molecular+Alterations+in+Hepatoblastomas+and+Adjacent+Hepatocellular+Carcinomas+in+B6C3F1+Mice&rft.au=Bhusari%2C+Sachin%3BPandiri%2C+Arun+R%3BNagai%2C+Hiroaki%3BWang%2C+Yu%3BFoley%2C+Julie%3BHong%2C+Hue-Hua+L%3BTon%2C+Thai-Vu%3BDeVito%2C+Michael%3BShockley%2C+Keith+R%3BPeddada%2C+Shyamal+D%3BGerrish%2C+Kevin+E%3BMalarkey%2C+David+E%3BHooth%2C+Michelle+J%3BSills%2C+Robert+C%3BHoenerhoff%2C+Mark+J&rft.aulast=Bhusari&rft.aufirst=Sachin&rft.date=2015-12-01&rft.volume=43&rft.issue=8&rft.spage=1114&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623315599853 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 49 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Transformation; Genomic imprinting; Data processing; Hepatocytes; Animal models; Gene expression; Stem cells; Embryogenesis; Embryo cells; Reviews; genomics; Mutation; Hepatocellular carcinoma DO - http://dx.doi.org/10.1177/0192623315599853 ER - TY - JOUR T1 - Uterine Carcinomas in Tetrabromobisphenol A-exposed Wistar Han Rats Harbor Increased Tp53 Mutations and Mimic High-grade Type I Endometrial Carcinomas in Women AN - 1751213453; PQ0002364292 AB - Endometrial carcinoma is the most common gynecologic malignancy is the United States and accounts for 6% of all cancers in women. The disease is classified as type I or type II based on clinicopathologic and molecular features. It is a multifactorial disease with a number of risk factors, including environmental exposures. How environmental exposures, such as flame retardants, may affect the incidence of endometrial cancer is a topic of current and ongoing interest. Tetrabromobisphenol A (TBBPA) is a widely used brominated flame retardant found in a variety of household products. A recent 2-year National Toxicology Program carcinogenicity study found that exposure to TBBPA was associated with a marked increase in the development of uterine tumors, specifically uterine carcinomas, in Wistar Han rats. Molecularly, TBBPA-induced uterine carcinomas in Wistar Han rats were characterized by a marked increase in tumor protein 53 mutation compared to spontaneous uterine carcinomas, as well as overexpression of human epidermal growth factor receptor 2 . Similar to spontaneous carcinomas, tumors in TBBPA-exposed rats were estrogen receptor-alpha positive and progesterone receptor negative by immunohistochemistry. The morphologic and molecular features of uterine carcinomas in TBBPA-exposed rats resemble those of high-grade type I tumors in women, and these data suggest that exposure to TBBPA may pose an increased cancer risk. JF - Toxicologic Pathology AU - Harvey, Janice B AU - Osborne, Tanasa S AU - Hong, Hue-Hua L AU - Bhusari, Sachin AU - Ton, Tai-Vu AU - Pandiri, Arun R AU - Masinde, Tiwanda AU - Dunnick, June AU - Peddada, Shyamal AU - Elmore, Susan AU - Hoenerhoff, Mark J AD - 1 .Cellular and Molecular Pathology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, osbornet@niehs.nih.gov Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1103 EP - 1113 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 43 IS - 8 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - tetrabromobisphenol A KW - dometrial carcinoma KW - Tp53 KW - Ctnnb1 KW - Kras KW - Ccnd1 KW - Her2 KW - Cdh1 KW - Wistar Han rats KW - Endometrium KW - Uterus KW - Data processing KW - Epidermal growth factor receptors KW - Fire retardant chemicals KW - Tumors KW - p53 protein KW - Carcinoma KW - Progesterone receptors KW - Malignancy KW - Household products KW - Carcinogenicity KW - Risk factors KW - Uterine cancer KW - Estrogen receptors KW - Mutation KW - Immunohistochemistry KW - X 24340:Cosmetics, Toiletries & Household Products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751213453?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Uterine+Carcinomas+in+Tetrabromobisphenol+A-exposed+Wistar+Han+Rats+Harbor+Increased+Tp53+Mutations+and+Mimic+High-grade+Type+I+Endometrial+Carcinomas+in+Women&rft.au=Harvey%2C+Janice+B%3BOsborne%2C+Tanasa+S%3BHong%2C+Hue-Hua+L%3BBhusari%2C+Sachin%3BTon%2C+Tai-Vu%3BPandiri%2C+Arun+R%3BMasinde%2C+Tiwanda%3BDunnick%2C+June%3BPeddada%2C+Shyamal%3BElmore%2C+Susan%3BHoenerhoff%2C+Mark+J&rft.aulast=Harvey&rft.aufirst=Janice&rft.date=2015-12-01&rft.volume=43&rft.issue=8&rft.spage=1103&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623315599256 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 42 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Uterus; Endometrium; Data processing; Epidermal growth factor receptors; Tumors; Fire retardant chemicals; Carcinoma; p53 protein; Progesterone receptors; Malignancy; Household products; Carcinogenicity; Risk factors; Uterine cancer; Immunohistochemistry; Mutation; Estrogen receptors DO - http://dx.doi.org/10.1177/0192623315599256 ER - TY - JOUR T1 - A framework for addressing ethical issues in citizen science AN - 1751206389; PQ0002338382 AB - The collaboration between laypeople and professional scientists known as "citizen science" is an important trend in research and data gathering. Citizen science offers important benefits to science and society. For example, citizens can help scientists with data collection and provide advice on research design and implementation. Citizens can also gain a better understanding of scientific concepts and methods. Additionally, citizens can help scientists better understand and address issues of concern to their families and communities. However, citizen science also raises ethical issues that should be addressed when projects begin and throughout the course of scientific investigation. To promote ethical research, scientists should develop guidelines for involvement of citizens in research, communicate effectively with participants and local communities at the outset of their involvement in research projects, carefully oversee their work, develop appropriate publication practices, and provide lay-volunteers with education and training on the responsible conduct of research. Researchers also need to be cognizant of clarifying these roles and responsibilities as well as promoting appropriate and safe citizen participation and transparency of the study methods, data analysis, and communication of results. JF - Environmental Science & Policy AU - Resnik, David B AU - Elliott, Kevin C AU - Miller, Aubrey K AD - National Institute of Environmental Health Sciences, National Institutes of Health, United States Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 475 EP - 481 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 54 SN - 1462-9011, 1462-9011 KW - Environment Abstracts KW - Citizen science KW - Ethics KW - Public KW - Collaboration KW - Data collection KW - Community-based research KW - Transparency KW - Education KW - Communications KW - Training KW - Responsibility KW - Community involvement KW - Guidelines KW - Research design KW - Local communities KW - ENA 04:Environmental Education UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751206389?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvabstractsmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Science+%26+Policy&rft.atitle=A+framework+for+addressing+ethical+issues+in+citizen+science&rft.au=Resnik%2C+David+B%3BElliott%2C+Kevin+C%3BMiller%2C+Aubrey+K&rft.aulast=Resnik&rft.aufirst=David&rft.date=2015-12-01&rft.volume=54&rft.issue=&rft.spage=475&rft.isbn=&rft.btitle=&rft.title=Environmental+Science+%26+Policy&rft.issn=14629011&rft_id=info:doi/10.1016%2Fj.envsci.2015.05.008 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Transparency; Data collection; Education; Communications; Responsibility; Training; Community involvement; Ethics; Guidelines; Research design; Local communities DO - http://dx.doi.org/10.1016/j.envsci.2015.05.008 ER - TY - JOUR T1 - Organ Dose Estimates for Hyperthyroid Patients Treated with (131)I: An Update of the Thyrotoxicosis Follow-Up Study. AN - 1750436540; 26579944 AB - The Thyrotoxicosis Therapy Follow-up Study (TTFUS) is comprised of 35,593 hyperthyroid patients treated from the mid-1940s through the mid-1960s. One objective of the TTFUS was to evaluate the long-term effects of high-dose iodine-131 ((131)I) treatment (1-4). In the TTFUS cohort, 23,020 patients were treated with (131)I, including 21,536 patients with Graves disease (GD), 1,203 patients with toxic nodular goiter (TNG) and 281 patients with unknown disease. The study population constituted the largest group of hyperthyroid patients ever examined in a single health risk study. The average number (± 1 standard deviation) of (131)I treatments per patient was 1.7 ± 1.4 for the GD patients and 2.1 ± 2.1 for the TNG patients. The average total (131)I administered activity was 380 ± 360 MBq for GD patients and 640 ± 550 MBq for TNG patients. In this work, a biokinetic model for iodine was developed to derive organ residence times and to reconstruct the radiation-absorbed doses to the thyroid gland and to other organs resulting from administration of (131)I to hyperthyroid patients. Based on (131)I data for a small, kinetically well-characterized sub-cohort of patients, multivariate regression equations were developed to relate the numbers of disintegrations of (131)I in more than 50 organs and tissues to anatomical (thyroid mass) and clinical (percentage thyroid uptake and pulse rate) parameters. These equations were then applied to estimate the numbers of (131)I disintegrations in the organs and tissues of all other hyperthyroid patients in the TTFUS who were treated with (131)I. The reference voxel phantoms adopted by the International Commission on Radiological Protection (ICRP) were then used to calculate the absorbed doses in more than 20 organs and tissues of the body. As expected, the absorbed doses were found to be highest in the thyroid (arithmetic means of 120 and 140 Gy for GD and TNG patients, respectively). Absorbed doses in organs other than the thyroid were much smaller, with arithmetic means of 1.6 Gy, 1.5 Gy and 0.65 Gy for esophagus, thymus and salivary glands, respectively. The arithmetic mean doses to all other organs and tissues were more than 100 times less than those to the thyroid gland. To our knowledge, this work represents the most comprehensive study to date of the doses received by persons treated with (131)I for hyperthyroidism. JF - Radiation research AU - Melo, Dunstana R AU - Brill, Aaron B AU - Zanzonico, Pat AU - Vicini, Paolo AU - Moroz, Brian AU - Kwon, Deukwoo AU - Lamart, Stephanie AU - Brenner, Alina AU - Bouville, André AU - Simon, Steven L AD - a  Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892; ; b  Vanderbilt University, Nashville, Tennessee 37232; ; c  Memorial Sloan-Kettering Cancer Center, New York, New York 10021; ; d  Department of Bioengineering, University of Washington, Seattle, Washington 98195; and. ; e  Sylvester Comprehensive Cancer Center, University of Miami, Miami, Florida 33136. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 595 EP - 610 VL - 184 IS - 6 KW - Iodine Radioisotopes KW - 0 KW - Radiopharmaceuticals KW - Index Medicus KW - Space life sciences KW - Young Adult KW - Radiopharmaceuticals -- pharmacokinetics KW - Computer Simulation KW - Humans KW - Aged KW - Child KW - Organ Specificity KW - Radiopharmaceuticals -- therapeutic use KW - Aged, 80 and over KW - Radiotherapy Dosage KW - Adult KW - Middle Aged KW - Adolescent KW - Viscera KW - Female KW - Male KW - Iodine Radioisotopes -- therapeutic use KW - Hyperthyroidism -- radiotherapy KW - Whole-Body Counting -- methods KW - Absorption, Radiation KW - Hyperthyroidism -- metabolism KW - Models, Biological KW - Iodine Radioisotopes -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1750436540?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Radiation+research&rft.atitle=Organ+Dose+Estimates+for+Hyperthyroid+Patients+Treated+with+%28131%29I%3A+An+Update+of+the+Thyrotoxicosis+Follow-Up+Study.&rft.au=Melo%2C+Dunstana+R%3BBrill%2C+Aaron+B%3BZanzonico%2C+Pat%3BVicini%2C+Paolo%3BMoroz%2C+Brian%3BKwon%2C+Deukwoo%3BLamart%2C+Stephanie%3BBrenner%2C+Alina%3BBouville%2C+Andr%C3%A9%3BSimon%2C+Steven+L&rft.aulast=Melo&rft.aufirst=Dunstana&rft.date=2015-12-01&rft.volume=184&rft.issue=6&rft.spage=595&rft.isbn=&rft.btitle=&rft.title=Radiation+research&rft.issn=1938-5404&rft_id=info:doi/10.1667%2FRR14160.1 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-20 N1 - Date created - 2015-12-18 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1667/RR14160.1 ER - TY - JOUR T1 - High levels of tobacco-specific N-nitrosamines and nicotine in Chaini Khaini, a product marketed as snus. AN - 1750013232; 25217658 AB - Recently, a tobacco product, Chaini Khaini, identified as snus appeared in India. The product marketing emphasises its discreet nature and explicitly claims safety by referring to the existing evidence on Swedish snus. We analysed tobacco-specific nitrosamines and nicotine in 12 samples of Chaini Khaini purchased in 2013 at open markets in India. Samples were purchased twice: in March 2013 from Mumbai and in November 2013 from Mumbai and Ahmedabad. Chemical constituents were measured by our routine validated methods. Levels of carcinogenic nitrosamines NNN, NNK and NNAL averaged 22.9 (±4.9), 2.6 (±1.0) and 3.1 (±1.5) µg/g tobacco (wet weight), respectively. The levels of NAB, which is normally present in trace levels in tobacco products, ranged from 3.9 to 12.9 µg/g tobacco. Total nicotine levels in all samples averaged 10.0 mg/g tobacco and unprotonated nicotine accounted for an average 95.4% of the total nicotine content. Chaini Khaini, which is labelled as snus and is marketed as a safe alternative to other tobacco products contains very high levels of carcinogenic nitrosamines and biologically available nicotine. Interventions are urgently needed to educate current and potential consumers of this product. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/ JF - Tobacco control AU - Stepanov, Irina AU - Gupta, Prakash C AU - Dhumal, Gauri AU - Yershova, Katrina AU - Toscano, William AU - Hatsukami, Dorothy AU - Parascandola, Mark AD - Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA Division of Environmental Health Sciences, University of Minnesota, Minneapolis, Minnesota, USA. ; Healis-Sekhsaria Institute for Public Health, Mumbai, Maharashtra, India. ; Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA. ; Division of Environmental Health Sciences, University of Minnesota, Minneapolis, Minnesota, USA. ; Tobacco Control Research Branch, National Cancer Institute, Bethesda, Maryland, USA. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - e271 EP - e274 VL - 24 KW - Carcinogens KW - 0 KW - Nitrates KW - Nitrites KW - Nitrosamines KW - Nicotine KW - 6M3C89ZY6R KW - N'-nitrosonornicotine KW - X656TZ86DX KW - Index Medicus KW - Harm Reduction KW - Packaging and Labelling KW - Nitrites -- analysis KW - Humans KW - Nicotine -- analysis KW - Nitrates -- analysis KW - India KW - Inhalation Exposure -- analysis KW - Carcinogens -- analysis KW - Nitrosamines -- analysis KW - Tobacco, Smokeless -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1750013232?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Tobacco+control&rft.atitle=High+levels+of+tobacco-specific+N-nitrosamines+and+nicotine+in+Chaini+Khaini%2C+a+product+marketed+as+snus.&rft.au=Stepanov%2C+Irina%3BGupta%2C+Prakash+C%3BDhumal%2C+Gauri%3BYershova%2C+Katrina%3BToscano%2C+William%3BHatsukami%2C+Dorothy%3BParascandola%2C+Mark&rft.aulast=Stepanov&rft.aufirst=Irina&rft.date=2015-12-01&rft.volume=12&rft.issue=1&rft.spage=200&rft.isbn=&rft.btitle=&rft.title=Neurotherapeutics+%3A+the+journal+of+the+American+Society+for+Experimental+NeuroTherapeutics&rft.issn=1878-7479&rft_id=info:doi/10.1007%2Fs13311-014-0315-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-15 N1 - Date created - 2015-12-15 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1136/tobaccocontrol-2014-051744 ER - TY - JOUR T1 - Cytotoxic, genotoxic, and neurotoxic effects of Mg, Pb, and Fe on pheochromocytoma (PC-12) cells AN - 1746876342; PQ0002309435 AB - Metals such as lead (Pb), magnesium (Mg), and iron (Fe) are ubiquitous in the environment as a result of natural occurrence and anthropogenic activities. Although Mg, Fe, and others are considered essential elements, high level of exposure has been associated with severe adverse health effects including cardiovascular, hematological, nephrotoxic, hepatotoxic, and neurologic abnormalities in humans. In the present study we hypothesized that Mg, Pb, and Fe are cytotoxic, genotoxic and neurotoxic, and their toxicity is mediated through oxidative stress and alteration in protein expression. To test the hypothesis, we used the pheochromocytoma (PC-12) cell line as a neuro cell model and performed the LDH assay for cell viability, Comet assay for DNA damage, Western blot for oxidative stress, and HPLC-MS to assess the concentration levels of neurological biomarkers such as glutamate, dopamine (DA), and 3-methoxytyramine (3-MT). The results of this study clearly show that Mg, Pb, and Fe, respectively in the form of MgSO sub(4), Pb(NO sub(3)) sub(2), FeCl sub(2), and FeCl sub(3) induce cytotoxicity, oxidative stress, and genotoxicity in PC-12 cells. In addition, exposure to these metallic compounds caused significant changes in the concentration levels of glutamate, dopamine, and 3-MT in PC-12 cells. Taken together the findings suggest that MgSO sub(4), Pb(NO sub(3)) sub(2), FeCl sub(2), and FeCl sub(3) have the potential to induce substantial toxicity to PC-12 cells. Environ Toxicol 30: 1445-1458, 2015. JF - Environmental Toxicology AU - Sanders, Talia AU - Liu, Yi-Ming AU - Tchounwou, Paul B AD - Cellomics and Toxicogenomics Research Laboratory, NIH/NIMHD-RCMI Center for Environmental Health, Jackson State University, 1400 Lynch Street, Box18750, Jackson, Mississippi, 39217, USA. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1445 EP - 1458 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 30 IS - 12 SN - 1520-4081, 1520-4081 KW - Toxicology Abstracts; Environment Abstracts; Pollution Abstracts KW - Heavy metals KW - Anthropogenic factors KW - Cell culture KW - Lead KW - Pheochromocytoma KW - Dopamine KW - Oxidative stress KW - Hematology KW - Hepatotoxicity KW - Bioindicators KW - Metals KW - Western blotting KW - Genotoxicity KW - Toxicity KW - biomarkers KW - DNA damage KW - Cytotoxicity KW - Neurotoxicity KW - DNA KW - Proteins KW - Comet assay KW - Glutamic acid KW - Magnesium KW - Iron KW - X 24360:Metals KW - P 6000:TOXICOLOGY AND HEALTH KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746876342?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Toxicology&rft.atitle=Cytotoxic%2C+genotoxic%2C+and+neurotoxic+effects+of+Mg%2C+Pb%2C+and+Fe+on+pheochromocytoma+%28PC-12%29+cells&rft.au=Sanders%2C+Talia%3BLiu%2C+Yi-Ming%3BTchounwou%2C+Paul+B&rft.aulast=Sanders&rft.aufirst=Talia&rft.date=2015-12-01&rft.volume=30&rft.issue=12&rft.spage=1445&rft.isbn=&rft.btitle=&rft.title=Environmental+Toxicology&rft.issn=15204081&rft_id=info:doi/10.1002%2Ftox.22014 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Western blotting; Heavy metals; Genotoxicity; Cell culture; biomarkers; Pheochromocytoma; Lead; DNA damage; Cytotoxicity; Dopamine; Oxidative stress; Neurotoxicity; Glutamic acid; Comet assay; Magnesium; Iron; Bioindicators; Metals; Anthropogenic factors; Toxicity; DNA; Proteins; Hematology; Hepatotoxicity DO - http://dx.doi.org/10.1002/tox.22014 ER - TY - JOUR T1 - Scientific and Regulatory Policy Committee (SRPC) Points to Consider: Histopathology Evaluation of the Pubertal Development and Thyroid Function Assay (OPPTS 890.1450, OPPTS 890.1500) in Rats to Screen for Endocrine Disruptors. AN - 1744659364; 25948506 AB - The U.S. Environmental Protection Agency Endocrine Disruptor Screening Program (EDSP) is a multitiered approach to determine the potential for environmental chemicals to alter the endocrine system. The Pubertal Development and Thyroid Function in Intact Juvenile/Peripubertal Female and Male Rats (OPPTS 890.1450, 890.1500) are 2 of the 9 EDSP tier 1 test Guidelines, which assess upstream mechanistic pathways along with downstream morphological end points including histological evaluation of the kidneys, thyroid, and select male/female reproductive tissues (ovaries, uterus, testes, and epididymides). These assays are part of a battery of in vivo and in vitro screens used for initial detection of test article endocrine activity. In this Points to Consider article, we describe tissue processing, evaluation, and nomenclature to aid in standardization of assay results across laboratories. Pubertal assay end points addressed include organ weights, estrous cyclicity, clinical pathology, hormonal assays, and histological evaluation. Potential treatment-related findings that may indicate endocrine disruption are reviewed. Additional tissues that may be useful in assessment of endocrine disruption (vagina, mammary glands, and liver) are discussed. This Points to Consider article is intended to provide information for evaluating peripubertal tissues within the context of individual assay end points, the overall pubertal assay, and tier I assays of the EDSP program. © 2015 by The Author(s). JF - Toxicologic pathology AU - Keane, Kevin A AU - Parker, George A AU - Regan, Karen S AU - Picut, Catherine AU - Dixon, Darlene AU - Creasy, Dianne AU - Giri, Dipak AU - Hukkanen, Renee R AD - Novo Nordisk, Beijing, China. ; WIL Research, Hillsborough, North Carolina, USA george.parker@wilresearch.com. ; Regan Path/Tox Services, Inc, Ashland, Ohio, USA. ; WIL Research, Hillsborough, North Carolina, USA. ; National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, North Carolina, USA. ; Dianne Creasy Consulting LLC, Pipersville, Pennsylvania, USA. ; Integrated Laboratory Systems, Raleigh-Durham, North Carolina, USA. ; The Dow Chemical Company, Midland, Michigan, USA Department of Comparative Medicine, University of Washington, Seattle, Washington, USA. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1047 EP - 1063 VL - 43 IS - 8 KW - Endocrine Disruptors KW - 0 KW - Index Medicus KW - pubertal development KW - EPA KW - OPPTS 890.1450 KW - OPPTS 890.1500 KW - thyroid function KW - endocrine disruptor screening program KW - Rats KW - Animals KW - Body Weight -- drug effects KW - Male KW - Female KW - Organ Size -- drug effects KW - Endocrine Disruptors -- toxicity KW - Thyroid Gland -- drug effects KW - Puberty -- drug effects KW - Toxicity Tests -- methods KW - Thyroid Function Tests -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1744659364?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Scientific+and+Regulatory+Policy+Committee+%28SRPC%29+Points+to+Consider%3A+Histopathology+Evaluation+of+the+Pubertal+Development+and+Thyroid+Function+Assay+%28OPPTS+890.1450%2C+OPPTS+890.1500%29+in+Rats+to+Screen+for+Endocrine+Disruptors.&rft.au=Keane%2C+Kevin+A%3BParker%2C+George+A%3BRegan%2C+Karen+S%3BPicut%2C+Catherine%3BDixon%2C+Darlene%3BCreasy%2C+Dianne%3BGiri%2C+Dipak%3BHukkanen%2C+Renee+R&rft.aulast=Keane&rft.aufirst=Kevin&rft.date=2015-12-01&rft.volume=43&rft.issue=8&rft.spage=1047&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623315579943 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-27 N1 - Date created - 2015-12-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Toxicol Sci. 1999 Dec;52(2):269-77 [10630580] Crit Rev Toxicol. 2000 Mar;30(2):135-96 [10759430] Crit Rev Toxicol. 2000 Mar;30(2):197-252 [10759431] Eur J Pharmacol. 2000 Jun 16;398(2):317-22 [10854845] Arch Toxicol. 2000 May;74(3):127-32 [10876997] Steroids. 2002 Feb;67(2):137-44 [11755178] Toxicol Pathol. 2002 Jan-Feb;30(1):59-65 [11892727] Toxicol Sci. 2002 Apr;66(2):216-25 [11896288] Arch Toxicol. 2002 May;76(4):194-202 [12029382] Toxicol Pathol. 2002 Jul-Aug;30(4):507-20 [12187942] Toxicol Pathol. 2002 Jul-Aug;30(4):524-33 [12187944] Exp Toxicol Pathol. 2003 Sep;55(2-3):91-106 [14620530] Toxicol Sci. 2004 Jan;77(1):91-100 [14514955] Toxicol Pathol. 2004 Jan-Feb;32(1):91-9 [14713553] Birth Defects Res B Dev Reprod Toxicol. 2003 Oct;68(5):408-15 [14745990] Birth Defects Res B Dev Reprod Toxicol. 2003 Dec;68(6):479-91 [14745982] Exp Toxicol Pathol. 2004 Jul;55(6):413-31 [15384248] J Endocrinol. 1968 Apr;40(4):485-91 [5643421] Endocrinology. 1972 Feb;90(2):466-72 [5009330] Endocrinology. 1976 Jun;98(6):1365-9 [819250] Anat Rec. 1977 Mar;187(3):347-66 [851237] Biol Reprod. 1977 Sep;17(2):298-303 [889997] J Endocrinol. 1979 Aug;82(2):293-303 [490085] Pharmacol Ther B. 1979;5(1-3):305-18 [386373] Fed Proc. 1980 May 15;39(7):2365-71 [6989642] J Steroid Biochem. 1985 Sep;23(3):253-7 [2995728] J Endocrinol. 1989 Jun;121(3):409-17 [2547009] Toxicol Appl Pharmacol. 1990 Sep 1;105(2):271-87 [2171157] Biol Reprod. 1990 Sep;43(3):517-24 [2271733] Vet Pathol. 1991 Mar;28(2):139-45 [1676552] Arch Toxicol. 2012 Dec;86(12):1899-910 [22811025] Clin Exp Obstet Gynecol. 2012;39(3):362-4 [23157045] Toxicol Sci. 2011 Feb;119(2):380-90 [21059795] Biol Reprod. 2011 Feb;84(2):207-17 [20926801] Toxicol Pathol. 2012 Aug;40(6 Suppl):40S-121S [22949412] Toxicol Pathol. 2012 Aug;40(6 Suppl):7S-39S [22949413] Toxicol Pathol. 2012 Oct;40(7):1063-78 [22552397] Regul Toxicol Pharmacol. 2013 Apr;65(3):334-43 [23422911] Toxicol Pathol. 2013;41(4):560-614 [23475558] Toxicol Pathol. 2013 Aug;41(6):921-34 [23334695] Toxicol Pathol. 2013;41(7):1011-5 [23416960] Toxicol Pathol. 2014;42(2):403-13 [23599412] Toxicol Pathol. 2015 Apr;43(3):343-53 [25107574] Toxicol Pathol. 2015 Apr;43(3):326-42 [25217330] Reprod Toxicol. 1991;5(4):379-83 [1806143] Endocrinology. 1993 Jun;132(6):2726-8 [8504773] Environ Health Perspect. 1993 Oct;101(5):378-84 [8080506] Biol Reprod. 1994 Jul;51(1):82-91 [7918878] Toxicol Pathol. 1997 Jan-Feb;25(1):39-48 [9061850] Endocrinology. 1998 Feb;139(2):753-64 [9449650] Toxicol Pathol. 1998 May-Jun;26(3):316-8 [9608636] Am J Physiol. 1998 Sep;275(3 Pt 1):E380-5 [9725802] Toxicol Sci. 1998 Nov;46(1):45-60 [9928668] Toxicol Sci. 1999 Sep;51(1):54-70 [10496677] Toxicol Sci. 2006 May;91(1):93-103 [16443925] Toxicol Pathol. 2007 Feb;35(2):199-207 [17366314] Toxicol Pathol. 2007 Aug;35(5):751-5 [17849358] Toxicol Sci. 2007 Nov;100(1):194-202 [17728285] Toxicol Pathol. 2008 Apr;36(3):375-84 [18441260] Toxicol Pathol. 2008 Jul;36(5):674-9 [18467674] Toxicol Pathol. 2009 Aug;37(5):679-93 [19454599] Toxicol Pathol. 2010 Jun;38(4):568-82 [20460440] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/0192623315579943 ER - TY - JOUR T1 - Sexual health in hematopoietic stem cell transplant recipients. AN - 1738821172; 26372459 AB - Hematopoietic stem cell transplantation (HSCT) plays a central role in patients with malignant and, increasingly, nonmalignant conditions. As the number of transplants increases and the survival rate improves, long-term complications are important to recognize and treat to maintain quality of life. Sexual dysfunction is a commonly described but relatively often underestimated complication after HSCT. Conditioning regimens, generalized or genital graft-versus-host disease, medications, and cardiovascular complications as well as psychosocial problems are known to contribute significantly to physical and psychological sexual dysfunction. Moreover, it is often a difficult topic for patients, their significant others, and health care providers to discuss. Early recognition and management of sexual dysfunction after HSCT can lead to improved quality of life and outcomes for patients and their partners. This review focuses on the risk factors for and treatment of sexual dysfunction after transplantation and provides guidance concerning how to approach and manage a patient with sexual dysfunction after HSCT. © 2015 American Cancer Society. JF - Cancer AU - Li, Zhuoyan AU - Mewawalla, Prerna AU - Stratton, Pamela AU - Yong, Agnes S M AU - Shaw, Bronwen E AU - Hashmi, Shahrukh AU - Jagasia, Madan AU - Mohty, Mohamad AU - Majhail, Navneet S AU - Savani, Bipin N AU - Rovó, Alicia AD - Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee. ; Department of Hematology, Western Pennsylvania Cancer Institute, Pittsburgh, Pennsylvania. ; Program in Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland. ; Department of Haematology, SA Pathology, and School of Medicine, University of Adelaide, Adelaide, South Australia, Australia. ; Center for International Blood and Marrow Transplant Research, Froedtert and the Medical College of Wisconsin, Milwaukee, Wisconsin. ; Division of Hematology, Mayo Clinic, Rochester, Minnesota. ; Hematology and Stem Cell Transplantation Section, Division of Hematology/Oncology, Department of Medicine, Vanderbilt University Medical Center and Veterans Affairs Medical Center, Nashville, Tennessee. ; INSERM (National Institute of Health and Medical Research) 938, Paris, France. ; Blood and Marrow Transplant Program, Cleveland Clinic, Cleveland, Ohio. ; Department of Hematology, University Hospital of Bern, Bern, Switzerland. Y1 - 2015/12/01/ PY - 2015 DA - 2015 Dec 01 SP - 4124 EP - 4131 VL - 121 IS - 23 KW - Abridged Index Medicus KW - Index Medicus KW - sexual health KW - survivorship KW - toxicity KW - transplantation KW - late effects KW - Risk Factors KW - Humans KW - Disease Management KW - Reproductive Health KW - Practice Guidelines as Topic KW - Health Personnel KW - Quality of Life KW - Spouses -- psychology KW - Male KW - Hematopoietic Stem Cell Transplantation -- adverse effects KW - Female KW - Sexual Dysfunction, Physiological -- psychology KW - Transplantation Conditioning -- adverse effects KW - Sexual Dysfunction, Physiological -- etiology KW - Sexual Dysfunctions, Psychological -- etiology KW - Sexual Dysfunction, Physiological -- therapy KW - Sexual Dysfunctions, Psychological -- therapy KW - Sexual Dysfunctions, Psychological -- psychology KW - Graft vs Host Disease -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1738821172?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Sexual+health+in+hematopoietic+stem+cell+transplant+recipients.&rft.au=Li%2C+Zhuoyan%3BMewawalla%2C+Prerna%3BStratton%2C+Pamela%3BYong%2C+Agnes+S+M%3BShaw%2C+Bronwen+E%3BHashmi%2C+Shahrukh%3BJagasia%2C+Madan%3BMohty%2C+Mohamad%3BMajhail%2C+Navneet+S%3BSavani%2C+Bipin+N%3BRov%C3%B3%2C+Alicia&rft.aulast=Li&rft.aufirst=Zhuoyan&rft.date=2015-12-01&rft.volume=121&rft.issue=23&rft.spage=4124&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=1097-0142&rft_id=info:doi/10.1002%2Fcncr.29675 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-22 N1 - Date created - 2015-12-02 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/cncr.29675 ER - TY - JOUR T1 - Allergic reactions and antiasparaginase antibodies in children with high-risk acute lymphoblastic leukemia: A children's oncology group report. AN - 1738820785; 26308766 AB - The objectives of this study were to assess the incidence of clinical allergy and end-induction antiasparaginase (anti-ASNase) antibodies in children with high-risk acute lymphoblastic leukemia treated with pegylated (PEG) Escherichia coli ASNase and to determine whether they carry any prognostic significance. Of 2057 eligible patients, 1155 were allocated to augmented arms in which PEG ASNase replaced native ASNase postinduction. Erwinia chrysanthemi (Erwinia) ASNase could be used to replace native ASNase after allergy, if available. Allergy and survival data were complete for 990 patients. End-induction antibody titers were available for 600 patients. During the consolidation phase, 289 of 990 patients (29.2%) had an allergic reaction. There were fewer allergic reactions to Erwinia ASNase than to native ASNase (odds ratio, 4.33; P < .0001) or PEG ASNase (odds ratio, 3.08; P < .0001) only during phase 1 of interim maintenance. There was no significant difference in 5-year event-free survival (EFS) between patients who received PEG ASNase throughout the entire study postinduction versus those who developed an allergic reaction to PEG ASNase during consolidation phase and subsequently received Erwinia ASNase (80.8% ± 2.8% and 81.6% ± 3.8%, respectively; P = .66). Patients who had positive antibody titers postinduction were more likely to have an allergic reaction to PEG ASNase (odds ratio, 2.4; P < .001). The 5-year EFS rate between patients who had negative versus positive antibody titers (80% ± 2.6% and 77.7% ± 4.3%, respectively; P = .68) and between patients who did not receive any ASNase postconsolidation and those who received PEG ASNase throughout the study (P = .22) were significantly different. The current results demonstrate differences in the incidence rates of toxicity between ASNase preparations but not in EFS. The presence of anti-ASNase antibodies did not affect EFS. © 2015 American Cancer Society. JF - Cancer AU - Ko, Richard H AU - Jones, Tamekia L AU - Radvinsky, David AU - Robison, Nathan AU - Gaynon, Paul S AU - Panosyan, Eduard H AU - Avramis, Ioannis A AU - Avramis, Vassilios I AU - Rubin, Joan AU - Ettinger, Lawrence J AU - Seibel, Nita L AU - Dhall, Girish AD - Children's Center for Cancer and Blood Diseases, Children's Hospital Los Angeles, Los Angeles, California. ; Department of Preventive Medicine, University of Tennessee Health Science Center, Memphis, Tennessee. ; State University of New York of New York Downstate Medical Center, Brooklyn New York. ; Division of Pediatric Hematology and Oncology, Harbor-University of California Los Angeles Medical Center, Torrance, California. ; Department of Pediatrics, St. Peter's University Hospital, New Brunswick, New Jersey. ; Children's Oncology Group, Monrovia, California. ; Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, Maryland. Y1 - 2015/12/01/ PY - 2015 DA - 2015 Dec 01 SP - 4205 EP - 4211 VL - 121 IS - 23 KW - Antibodies KW - 0 KW - Antineoplastic Agents KW - Polyethylene Glycols KW - 30IQX730WE KW - Asparaginase KW - EC 3.5.1.1 KW - Abridged Index Medicus KW - Index Medicus KW - childhood acute lymphoblastic leukemia KW - asparaginase KW - survival KW - drug hypersensitivity KW - Pectobacterium chrysanthemi -- enzymology KW - Infant KW - Escherichia coli -- immunology KW - Antibodies -- blood KW - Polyethylene Glycols -- chemistry KW - Pectobacterium chrysanthemi -- immunology KW - Induction Chemotherapy KW - Humans KW - Treatment Outcome KW - Escherichia coli -- enzymology KW - Child KW - Survival Analysis KW - Child, Preschool KW - Asparaginase -- chemistry KW - Asparaginase -- adverse effects KW - Antineoplastic Agents -- immunology KW - Drug Hypersensitivity -- immunology KW - Drug Hypersensitivity -- epidemiology KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- immunology KW - Asparaginase -- immunology KW - Antineoplastic Agents -- chemistry KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- drug therapy KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- complications KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1738820785?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Allergic+reactions+and+antiasparaginase+antibodies+in+children+with+high-risk+acute+lymphoblastic+leukemia%3A+A+children%27s+oncology+group+report.&rft.au=Ko%2C+Richard+H%3BJones%2C+Tamekia+L%3BRadvinsky%2C+David%3BRobison%2C+Nathan%3BGaynon%2C+Paul+S%3BPanosyan%2C+Eduard+H%3BAvramis%2C+Ioannis+A%3BAvramis%2C+Vassilios+I%3BRubin%2C+Joan%3BEttinger%2C+Lawrence+J%3BSeibel%2C+Nita+L%3BDhall%2C+Girish&rft.aulast=Ko&rft.aufirst=Richard&rft.date=2015-12-01&rft.volume=121&rft.issue=23&rft.spage=4205&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=1097-0142&rft_id=info:doi/10.1002%2Fcncr.29641 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-22 N1 - Date created - 2015-12-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Leuk Lymphoma. 2010 Aug;51(8):1464-72 [20545581] Pediatr Blood Cancer. 2010 Feb;54(2):199-205 [19672973] Blood Cancer J. 2014;4:e203 [24769644] J Clin Oncol. 2000 Apr;18(7):1525-32 [10735901] Br J Haematol. 2001 Sep;114(4):794-9 [11564065] Blood. 2001 Mar 1;97(5):1211-8 [11222362] J Immunol Methods. 2000 May 26;239(1-2):75-83 [10821949] Blood. 2002 Mar 15;99(6):1986-94 [11877270] Blood. 2002 Apr 15;99(8):2734-9 [11929760] Leukemia. 2003 Aug;17(8):1583-8 [12886246] Pharmacotherapy. 2003 Aug;23(8 Pt 2):3S-8S [12921216] J Pediatr Hematol Oncol. 2004 Apr;26(4):217-26 [15087948] Cancer. 1966 Dec;19(12):1813-9 [4959138] JAMA. 1967 Nov 27;202(9):882-8 [5234350] Cancer Res. 1967 Dec;27(12):2619-31 [5237354] Cancer Res. 1969 Feb;29(2):426-34 [4975316] J Clin Invest. 1971 May;50(5):1080-90 [4101590] Pediatr Blood Cancer. 2006 Sep;47(3):299-304 [16302217] Blood. 2007 Feb 1;109(3):896-904 [17003366] Oncologist. 2007 Aug;12(8):991-8 [17766659] Blood. 2008 Mar 1;111(5):2548-55 [18039957] Clin Exp Med. 2009 Jun;9(2):113-6 [19184328] Br J Haematol. 2013 Sep;162(5):710-3 [23750892] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/cncr.29641 ER - TY - JOUR T1 - EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals. AN - 1738820481; 26544531 AB - The Endocrine Society's first Scientific Statement in 2009 provided a wake-up call to the scientific community about how environmental endocrine-disrupting chemicals (EDCs) affect health and disease. Five years later, a substantially larger body of literature has solidified our understanding of plausible mechanisms underlying EDC actions and how exposures in animals and humans-especially during development-may lay the foundations for disease later in life. At this point in history, we have much stronger knowledge about how EDCs alter gene-environment interactions via physiological, cellular, molecular, and epigenetic changes, thereby producing effects in exposed individuals as well as their descendants. Causal links between exposure and manifestation of disease are substantiated by experimental animal models and are consistent with correlative epidemiological data in humans. There are several caveats because differences in how experimental animal work is conducted can lead to difficulties in drawing broad conclusions, and we must continue to be cautious about inferring causality in humans. In this second Scientific Statement, we reviewed the literature on a subset of topics for which the translational evidence is strongest: 1) obesity and diabetes; 2) female reproduction; 3) male reproduction; 4) hormone-sensitive cancers in females; 5) prostate; 6) thyroid; and 7) neurodevelopment and neuroendocrine systems. Our inclusion criteria for studies were those conducted predominantly in the past 5 years deemed to be of high quality based on appropriate negative and positive control groups or populations, adequate sample size and experimental design, and mammalian animal studies with exposure levels in a range that was relevant to humans. We also focused on studies using the developmental origins of health and disease model. No report was excluded based on a positive or negative effect of the EDC exposure. The bulk of the results across the board strengthen the evidence for endocrine health-related actions of EDCs. Based on this much more complete understanding of the endocrine principles by which EDCs act, including nonmonotonic dose-responses, low-dose effects, and developmental vulnerability, these findings can be much better translated to human health. Armed with this information, researchers, physicians, and other healthcare providers can guide regulators and policymakers as they make responsible decisions. JF - Endocrine reviews AU - Gore, A C AU - Chappell, V A AU - Fenton, S E AU - Flaws, J A AU - Nadal, A AU - Prins, G S AU - Toppari, J AU - Zoeller, R T AD - Pharmacology and Toxicology (A.C.G.), College of Pharmacy, The University of Texas at Austin, Austin, Texas 78734; Division of the National Toxicology Program (V.A.C., S.E.F.), National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709; Department of Comparative Biosciences (J.A.F.), University of Illinois at Urbana-Champaign, Urbana, Illinois 61802; Institute of Bioengineering and CIBERDEM (A.N.), Miguel Hernandez University of Elche, 03202 Elche, Alicante, Spain; Departments of Urology, Pathology, and Physiology & Biophysics (G.S.P.), College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612; Departments of Physiology and Pediatrics (J.T.), University of Turku and Turku University Hospital, 20520 Turku, Finland; and Biology Department (R.T.Z.), University of Massachusetts at Amherst, Amherst, Massachusetts 01003. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - E1 EP - E150 VL - 36 IS - 6 KW - Benzhydryl Compounds KW - 0 KW - Endocrine Disruptors KW - Herbicides KW - Pesticides KW - Phenols KW - Phthalic Acids KW - phthalic acid KW - 6O7F7IX66E KW - bisphenol A KW - MLT3645I99 KW - Index Medicus KW - Animals KW - Reproduction -- drug effects KW - Humans KW - Diabetes Mellitus -- chemically induced KW - Prostatic Neoplasms -- chemically induced KW - Diabetes Mellitus -- epidemiology KW - Cardiovascular Diseases -- chemically induced KW - Phthalic Acids -- toxicity KW - Cardiovascular Diseases -- epidemiology KW - Societies, Medical KW - Male KW - Prostatic Neoplasms -- epidemiology KW - Neurosecretory Systems -- drug effects KW - Obesity -- epidemiology KW - Neoplasms, Hormone-Dependent -- epidemiology KW - Neurodevelopmental Disorders -- epidemiology KW - Thyroid Gland -- drug effects KW - Endocrinology KW - Neurodevelopmental Disorders -- chemically induced KW - Environmental Exposure KW - Obesity -- chemically induced KW - Female KW - Endocrine Disruptors -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1738820481?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrine+reviews&rft.atitle=EDC-2%3A+The+Endocrine+Society%27s+Second+Scientific+Statement+on+Endocrine-Disrupting+Chemicals.&rft.au=Gore%2C+A+C%3BChappell%2C+V+A%3BFenton%2C+S+E%3BFlaws%2C+J+A%3BNadal%2C+A%3BPrins%2C+G+S%3BToppari%2C+J%3BZoeller%2C+R+T&rft.aulast=Gore&rft.aufirst=A&rft.date=2015-12-01&rft.volume=36&rft.issue=6&rft.spage=E1&rft.isbn=&rft.btitle=&rft.title=Endocrine+reviews&rft.issn=1945-7189&rft_id=info:doi/10.1210%2Fer.2015-1010 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-14 N1 - Date created - 2015-12-01 N1 - Date revised - 2017-01-14 N1 - 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Chemicals. AN - 1738817869; 26414233 AB - This Executive Summary to the Endocrine Society's second Scientific Statement on environmental endocrine-disrupting chemicals (EDCs) provides a synthesis of the key points of the complete statement. The full Scientific Statement represents a comprehensive review of the literature on seven topics for which there is strong mechanistic, experimental, animal, and epidemiological evidence for endocrine disruption, namely: obesity and diabetes, female reproduction, male reproduction, hormone-sensitive cancers in females, prostate cancer, thyroid, and neurodevelopment and neuroendocrine systems. EDCs such as bisphenol A, phthalates, pesticides, persistent organic pollutants such as polychlorinated biphenyls, polybrominated diethyl ethers, and dioxins were emphasized because these chemicals had the greatest depth and breadth of available information. The Statement also included thorough coverage of studies of developmental exposures to EDCs, especially in the fetus and infant, because these are critical life stages during which perturbations of hormones can increase the probability of a disease or dysfunction later in life. A conclusion of the Statement is that publications over the past 5 years have led to a much fuller understanding of the endocrine principles by which EDCs act, including nonmonotonic dose-responses, low-dose effects, and developmental vulnerability. These findings will prove useful to researchers, physicians, and other healthcare providers in translating the science of endocrine disruption to improved public health. JF - Endocrine reviews AU - Gore, A C AU - Chappell, V A AU - Fenton, S E AU - Flaws, J A AU - Nadal, A AU - Prins, G S AU - Toppari, J AU - Zoeller, R T AD - Pharmacology and Toxicology (A.C.G.), College of Pharmacy, The University of Texas at Austin, Austin, Texas 78734; Division of the National Toxicology Program (V.A.C., S.E.F.), National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709; Department of Comparative Biosciences (J.A.F.), University of Illinois at Urbana-Champaign, Urbana, Illinois 61802; Institute of Bioengineering and CIBERDEM (A.N.), Miguel Hernandez University of Elche, 03202 Elche, Alicante, Spain; Departments of Urology, Pathology and Physiology & Biophysics (G.S.P.), College of Medicine, University of Illinois at Chicago, Chicago, Illinois, 60612; Departments of Physiology and Pediatrics (J.T.), University of Turku and Turku University Hospital, 20520 Turku, Finland; and Biology Department (R.T.Z.), University of Massachusetts at Amherst, Amherst, Massachusetts 01003. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 593 EP - 602 VL - 36 IS - 6 KW - Benzhydryl Compounds KW - 0 KW - Endocrine Disruptors KW - Herbicides KW - Pesticides KW - Phenols KW - Phthalic Acids KW - phthalic acid KW - 6O7F7IX66E KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - bisphenol A KW - MLT3645I99 KW - Index Medicus KW - Animals KW - Reproduction -- drug effects KW - Humans KW - Diabetes Mellitus -- chemically induced KW - Prostatic Neoplasms -- chemically induced KW - Diabetes Mellitus -- epidemiology KW - Phthalic Acids -- toxicity KW - Pesticides -- toxicity KW - Societies, Medical KW - Male KW - Prostatic Neoplasms -- epidemiology KW - Polychlorinated Biphenyls -- toxicity KW - Neurosecretory Systems -- drug effects KW - Phenols -- toxicity KW - Neoplasms, Hormone-Dependent -- chemically induced KW - Epigenesis, Genetic KW - Obesity -- epidemiology KW - Neoplasms, Hormone-Dependent -- epidemiology KW - Neurodevelopmental Disorders -- epidemiology KW - Benzhydryl Compounds -- toxicity KW - Thyroid Gland -- drug effects KW - Endocrinology KW - Neurodevelopmental Disorders -- chemically induced KW - Environmental Exposure KW - Herbicides -- toxicity KW - Gene-Environment Interaction KW - Obesity -- chemically induced KW - Female KW - Endocrine Disruptors -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1738817869?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrine+reviews&rft.atitle=Executive+Summary+to+EDC-2%3A+The+Endocrine+Society%27s+Second+Scientific+Statement+on+Endocrine-Disrupting+Chemicals.&rft.au=Gore%2C+A+C%3BChappell%2C+V+A%3BFenton%2C+S+E%3BFlaws%2C+J+A%3BNadal%2C+A%3BPrins%2C+G+S%3BToppari%2C+J%3BZoeller%2C+R+T&rft.aulast=Gore&rft.aufirst=A&rft.date=2015-12-01&rft.volume=36&rft.issue=6&rft.spage=593&rft.isbn=&rft.btitle=&rft.title=Endocrine+reviews&rft.issn=1945-7189&rft_id=info:doi/10.1210%2Fer.2015-1093 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-14 N1 - Date created - 2015-12-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Environ Health Perspect. 2002 Sep;110(9):917-21 [12204827] Environ Health Perspect. 1997 Jan;105(1):70-6 [9074884] Endocr Rev. 2009 Jun;30(4):293-342 [19502515] Endocr Rev. 2015 Dec;36(6):593-602 [26414233] PLoS Genet. 2012;8(11):e1003072 [23166518] J Dev Orig Health Dis. 2015 Apr;6(2):55-64 [25471238] Endocrinology. 2012 Sep;153(9):4097-110 [22733974] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1210/er.2015-1093 ER - TY - JOUR T1 - Modulation by aspirin and naproxen of nucleotide alterations and tumors in the lung of mice exposed to environmental cigarette smoke since birth. AN - 1738006006; 26464196 AB - Chemoprevention provides an important strategy for cancer control in passive smokers. Due to the crucial role played by smoke-related chronic inflammation in lung carcinogenesis, of special interest are extensively used pharmacological agents, such as nonsteroidal anti-inflammatory drugs (NSAIDs). We evaluated the ability of aspirin and naproxen, inhibitors of both cyclooxygenase-1 and cyclooxygenase -2, to modulate environmental cigarette smoke (ECS)-induced lung carcinogenesis in A/J mice of both genders. Based on a subchronic toxicity study in 180 postweaning mice, we used 1600 mg/kg diet aspirin and 320 mg/kg diet naproxen. In the tumor chemoprevention study, using 320 mice, exposure to ECS started soon after birth and administration of NSAIDs started after weaning. At 10 weeks of life, the NSAIDs did not affect the presence of occult blood in feces. As assessed in a subset of 40 mice, bulky DNA adducts and 8-hydroxy-2'-deoxyguanosine levels were considerably increased in ECS-exposed mice and, irrespective of gender, both NSAIDs remarkably inhibited these nucleotide alterations. After exposure for 4 months followed by 5 months in filtered air, ECS induced a significant increase in the yield of surface lung tumors, the 43.7% of which were adenomas and the 56.3% were adenocarcinomas. Oct-4 (octamer-binding transcription factor 4), a marker of cell stemness, was detected in some adenocarcinoma cells. The NAIDs attenuated the yield of lung tumors, but prevention of ECS-induced lung adenomas was statistically significant only in female mice treated with aspirin, which supports a role for estrogens in ECS-related lung carcinogenesis and highlights the antiestrogenic properties of NSAIDs. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Carcinogenesis AU - La Maestra, Sebastiano AU - D'Agostini, Francesco AU - Izzotti, Alberto AU - Micale, Rosanna T AU - Mastracci, Luca AU - Camoirano, Anna AU - Balansky, Roumen AU - Trosko, James E AU - Steele, Vernon E AU - De Flora, Silvio AD - Department of Surgical and Diagnostic Sciences, University of Genoa, 16132 Genoa, Italy. ; National Center of Oncology, Sofia 1756, Bulgaria. ; National Food Safety Toxicological Center, Department of Pediatrics and Human Development, Michigan State University, East Lansing, MI 48824, USA. ; National Cancer Institute, Division of Cancer Prevention, Chemopreventive Agent Development Research Group, Bethesda, MD 20892, USA. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1531 EP - 1538 VL - 36 IS - 12 KW - Anticarcinogenic Agents KW - 0 KW - Octamer Transcription Factor-3 KW - Pou5f1 protein, mouse KW - Tobacco Smoke Pollution KW - Naproxen KW - 57Y76R9ATQ KW - Aspirin KW - R16CO5Y76E KW - Index Medicus KW - Animals KW - DNA Damage KW - Mice KW - Octamer Transcription Factor-3 -- metabolism KW - Lung -- pathology KW - Lung -- metabolism KW - Drug Evaluation, Preclinical KW - Male KW - Female KW - Lung Neoplasms -- prevention & control KW - Lung Neoplasms -- etiology KW - Anticarcinogenic Agents -- therapeutic use KW - Naproxen -- pharmacology KW - Aspirin -- therapeutic use KW - Anticarcinogenic Agents -- pharmacology KW - Tobacco Smoke Pollution -- adverse effects KW - Lung Neoplasms -- genetics KW - Naproxen -- toxicity KW - Aspirin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1738006006?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Modulation+by+aspirin+and+naproxen+of+nucleotide+alterations+and+tumors+in+the+lung+of+mice+exposed+to+environmental+cigarette+smoke+since+birth.&rft.au=La+Maestra%2C+Sebastiano%3BD%27Agostini%2C+Francesco%3BIzzotti%2C+Alberto%3BMicale%2C+Rosanna+T%3BMastracci%2C+Luca%3BCamoirano%2C+Anna%3BBalansky%2C+Roumen%3BTrosko%2C+James+E%3BSteele%2C+Vernon+E%3BDe+Flora%2C+Silvio&rft.aulast=La+Maestra&rft.aufirst=Sebastiano&rft.date=2015-12-01&rft.volume=36&rft.issue=12&rft.spage=1531&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgv149 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-24 N1 - Date created - 2015-11-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Appl Toxicol. 1999 Nov-Dec;19(6):389-94 [10547619] Exp Toxicol Pathol. 2005 Jul;57 Suppl 1:171-81 [16092725] Tob Control. 2005 Dec;14(6):396-404 [16319363] Contrib Microbiol. 2006;13:45-65 [16627958] Inhal Toxicol. 2006 Aug;18(9):667-77 [16864557] J Biol Chem. 2006 Nov 3;281(44):33554-65 [16951404] Int J Cancer. 2008 Feb 1;122(3):653-7 [17935128] Cancer Sci. 2008 Apr;99(4):696-705 [18377422] Lancet Oncol. 2008 Jul;9(7):657-66 [18598930] Antioxid Redox Signal. 2009 Feb;11(2):297-307 [18834329] Recent Results Cancer Res. 2009;181:231-51 [19213573] Lancet Oncol. 2009 May;10(5):501-7 [19410194] Stem Cells. 2009 Jun;27(6):1265-75 [19489092] Oncol Rep. 2009 Sep;22(3):469-74 [19639190] Oncol Res. 2009;17(11-12):505-18 [19806781] Cancer Prev Res (Phila). 2009 Nov;2(11):951-6 [19892664] Cancer Prev Res (Phila). 2010 Jan;3(1):73-81 [20051374] Cancer Cell. 2010 Jan 19;17(1):89-97 [20129250] J Urol. 2010 Apr;183(4):1598-603 [20172542] Cancer Prev Res (Phila). 2010 Jun;3(6):707-17 [20515954] Lancet. 2011 Jan 1;377(9759):31-41 [21144578] Ann Oncol. 2011 Nov;22(11):2456-65 [21385885] Cancer Causes Control. 2011 Dec;22(12):1709-20 [21987079] Cancer Prev Res (Phila). 2011 Nov;4(11):1895-902 [21764859] Int J Cancer. 2012 Mar 1;130(5):1001-10 [21484788] Clin Lung Cancer. 2012 Jan;13(1):44-51 [21813335] Carcinogenesis. 2013 Apr;34(4):909-15 [23276798] Arch Toxicol. 2013 May;87(5):915-8 [23423711] J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2014;32(2):105-20 [24875440] BMC Cancer. 2014;14:406 [24902960] MMWR Morb Mortal Wkly Rep. 2015 Feb 6;64(4):103-8 [25654612] Int J Oncol. 2001 Mar;18(3):607-15 [11179494] Cancer Res. 2001 Mar 15;61(6):2472-9 [11289117] Toxicon. 2002 Mar;40(3):273-82 [11711124] Biochem Biophys Res Commun. 2002 May 3;293(2):705-9 [12054526] Mutat Res. 2003 Nov;544(2-3):441-9 [14644347] JAMA. 2004 May 26;291(20):2433-40 [15161893] IARC Monogr Eval Carcinog Risks Hum. 2004;83:1-1438 [15285078] Adv Cancer Res. 1975;21:1-58 [1108612] Cancer Lett. 1992 Sep 14;66(1):21-8 [1451092] Arch Toxicol. 1996;70(3-4):244-8 [8825684] Carcinogenesis. 1997 Mar;18(3):575-86 [9067559] Carcinogenesis. 1997 Nov;18(11):2035-42 [9395199] Free Radic Res. 1998 Feb;28(2):165-78 [9645393] Carcinogenesis. 2005 Feb;26(2):495-502 [15513931] J Biol Chem. 2005 Aug 5;280(31):28337-46 [15964853] QJM. 2005 Oct;98(10):711-8 [16170203] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgv149 ER - TY - JOUR T1 - Gene-expression profiling of buccal epithelium among non-smoking women exposed to household air pollution from smoky coal. AN - 1738005814; 26468118 AB - In China's rural counties of Xuanwei and Fuyuan, lung cancer rates are among the highest in the world. While the elevated disease risk in this population has been linked to the usage of smoky (bituminous) coal as compared to smokeless (anthracite) coal, the underlying molecular changes associated with this exposure remains unclear. To understand the physiologic effects of smoky coal exposure, we analyzed the genome-wide gene-expression profiles in buccal epithelial cells collected from healthy, non-smoking female residents of Xuanwei and Fuyuan who burn smoky (n = 26) and smokeless (n = 9) coal. Gene-expression was profiled via microarrays, and changes associated with coal type were correlated to household levels of fine particulate matter (PM2.5) and polycyclic aromatic hydrocarbons (PAHs). Expression levels of 282 genes were altered with smoky versus smokeless coal exposure (P < 0.005), including the 2-fold increase of proinflammatory IL8 and decrease of proapoptotic CASP3. This signature was more correlated with carcinogenic PAHs (e.g. Benzo[a]pyrene; r = 0.41) than with non-carcinogenic PAHs (e.g. Fluorene; r = 0.08) or PM2.5 (r = 0.05). Genes altered with smoky coal exposure were concordantly enriched with tobacco exposure in previously profiled buccal biopsies of smokers and non-smokers (GSEA, q < 0.05). This is the first study to identify a signature of buccal epithelial gene-expression that is associated with smoky coal exposure, which in part is similar to the molecular response to tobacco smoke, thereby lending biologic plausibility to prior epidemiological studies that have linked this exposure to lung cancer risk. Published by Oxford University Press 2015. JF - Carcinogenesis AU - Wang, Teresa W AU - Vermeulen, Roel C H AU - Hu, Wei AU - Liu, Gang AU - Xiao, Xiaohui AU - Alekseyev, Yuriy AU - Xu, Jun AU - Reiss, Boris AU - Steiling, Katrina AU - Downward, George S AU - Silverman, Debra T AU - Wei, Fusheng AU - Wu, Guoping AU - Li, Jihua AU - Lenburg, Marc E AU - Rothman, Nathaniel AU - Spira, Avrum AU - Lan, Qing AD - Division of Computational Biomedicine, Boston University School of Medicine, Boston, MA 02118, USA, Bioinformatics Program, Boston University, Boston, MA 02215, USA. ; Division of Environmental Epidemiology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD 20850, USA. ; Division of Computational Biomedicine, Boston University School of Medicine, Boston, MA 02118, USA. ; Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118, USA. ; School of Public Health, The University of Hong Kong, Hong Kong, China. ; Division of Environmental Epidemiology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands, School of Public Health, University of Washington, Seattle, WA 98195, USA. ; China National Environmental Monitoring Center, Beijing, China and. ; Qujing Center for Diseases Control and Prevention, Qujing, China. ; Division of Computational Biomedicine, Boston University School of Medicine, Boston, MA 02118, USA, Bioinformatics Program, Boston University, Boston, MA 02215, USA, Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118, USA. ; Division of Computational Biomedicine, Boston University School of Medicine, Boston, MA 02118, USA, Bioinformatics Program, Boston University, Boston, MA 02215, USA, Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118, USA, aspira@bu.edu. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1494 EP - 1501 VL - 36 IS - 12 KW - Coal KW - 0 KW - Smoke KW - Index Medicus KW - Gene Expression Profiling KW - Multigene Family KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Female KW - Air Pollution, Indoor KW - Inhalation Exposure KW - Transcriptome KW - Mouth Mucosa -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1738005814?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Gene-expression+profiling+of+buccal+epithelium+among+non-smoking+women+exposed+to+household+air+pollution+from+smoky+coal.&rft.au=Wang%2C+Teresa+W%3BVermeulen%2C+Roel+C+H%3BHu%2C+Wei%3BLiu%2C+Gang%3BXiao%2C+Xiaohui%3BAlekseyev%2C+Yuriy%3BXu%2C+Jun%3BReiss%2C+Boris%3BSteiling%2C+Katrina%3BDownward%2C+George+S%3BSilverman%2C+Debra+T%3BWei%2C+Fusheng%3BWu%2C+Guoping%3BLi%2C+Jihua%3BLenburg%2C+Marc+E%3BRothman%2C+Nathaniel%3BSpira%2C+Avrum%3BLan%2C+Qing&rft.aulast=Wang&rft.aufirst=Teresa&rft.date=2015-12-01&rft.volume=36&rft.issue=12&rft.spage=1494&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgv150 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-24 N1 - Date created - 2015-11-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Toxicol Appl Pharmacol. 2005 Feb 15;203(1):45-52 [15694463] Am J Respir Crit Care Med. 2013 May 1;187(9):933-42 [23471465] Clin Cancer Res. 2005 Mar 15;11(6):2097-105 [15788654] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517] Nucleic Acids Res. 2005;33(20):e175 [16284200] Nat Med. 2007 Mar;13(3):361-6 [17334370] Chest. 2007 Apr;131(4):1149-56 [17426222] Environ Health Perspect. 2007 Jun;115(6):848-55 [17589590] Genome Biol. 2007;8(9):R201 [17894889] Genome Inform. 2007;18:247-57 [18546492] Nat Protoc. 2008;3(6):1101-8 [18546601] BMC Genomics. 2008;9:259 [18513428] Br J Cancer. 2008 Dec 2;99(11):1934-9 [19034286] Int J Cancer. 2009 Feb 1;124(3):511-5 [19003982] J Surg Res. 2009 May 15;153(2):347-58 [19027922] Nature. 2009 Nov 5;462(7269):108-12 [19847166] Physiol Genomics. 2010 Mar 3;41(1):1-8 [19952278] Cancer Prev Res (Phila). 2010 Mar;3(3):266-78 [20179299] Cancer Prev Res (Phila). 2011 Jun;4(6):803-17 [21636547] Lung Cancer. 2014 Apr;84(1):31-5 [24506909] Environ Int. 2014 Jul;68:94-104 [24721117] Environ Pollut. 2014 Aug;191:63-9 [24811947] Environ Sci Technol. 2014;48(15):8456-64 [25003800] Clin Exp Allergy. 2014 Sep;44(9):1100-18 [25040251] Environ Sci Technol. 2014 Dec 16;48(24):14632-41 [25393345] N Engl J Med. 2015 Jul 16;373(3):243-51 [25981554] Cancer Res. 2001 Sep 15;61(18):6679-81 [11559534] Nucleic Acids Res. 2002 Jan 1;30(1):207-10 [11752295] J Natl Cancer Inst. 2002 Jun 5;94(11):826-35 [12048270] Environ Health Perspect. 2002 Nov;110(11):1057-68 [12417475] Am J Respir Crit Care Med. 2003 Jun 1;167(11):1528-33 [12637344] J Med Genet. 2004 Mar;41(3):e27 [14985398] Biotechniques. 2004 Mar;36(3):484-7 [15038164] Proc Natl Acad Sci U S A. 2004 Jul 6;101(27):10143-8 [15210990] Genome Biol. 2004;5(10):R80 [15461798] Science. 1987 Jan 9;235(4785):217-20 [3798109] Arch Environ Health. 1988 Mar-Apr;43(2):180-5 [3377554] Am J Public Health. 1988 Aug;78(8):975-7 [3389438] Environ Health Perspect. 1993 Mar;99:83-7 [8319664] Am J Physiol. 1997 Mar;272(3 Pt 1):L504-11 [9124608] Lung Cancer. 2005 Sep;49(3):317-23 [15921821] Toxicol Appl Pharmacol. 2012 Jun 15;261(3):255-62 [22521606] J Natl Cancer Inst. 2012 Jun 6;104(11):855-68 [22393209] BMJ. 2012;345:e5414 [22936785] Drug Metab Dispos. 2012 Oct;40(10):1953-65 [22798553] Cold Spring Harb Perspect Biol. 2013 Apr;5(4):a008656 [23545416] BMC Bioinformatics. 2013;14:128 [23586463] J Clin Oncol. 2005 Feb 10;23(5):1011-27 [15585754] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgv150 ER - TY - JOUR T1 - Immunoconjugates in the management of hairy cell leukemia. AN - 1738005379; 26614902 AB - Hairy cell leukemia (HCL) is an indolent B-cell malignancy effectively treated but not often cured by purine analog therapy; after multiple courses of purine analogs, patients can become purine analog resistant and in need of alternative therapies. Complete remission to single-agent purine analog is often accompanied by minimal residual disease (MRD), residual HCL cells detectable by immunologic methods, considered a risk factor for eventual relapse. Several different non-chemotherapy approaches are being used to target relapsed and refractory HCL, including inhibitors of BRAF, but so far only monoclonal antibody (MAb)-based approaches have been reported to eliminate MRD in a high percentage of patients. One of the MAb-based options for HCL currently under clinical investigation involves recombinant immunotoxins, containing a fragment of a MAb and a bacterial toxin. The bacterial toxin, a highly potent fragment from Pseudomonas exotoxin, catalytically ADP-ribosylates elongation factor 2 (EF2), resulting in protein synthesis inhibition and apoptotic cell death. Recombinant immunotoxins tested in HCL patients include LMB-2, targeting CD25, and BL22, targeting CD22. An affinity matured version of BL22, termed moxetumomab pasudotox (formerly HA22 or CAT-8015) achieved high CR rates in phase I, and is currently undergoing multicenter Phase 3 testing. Phase I testing was without dose-limiting toxicity, although 2 patients had grade 2 hemolytic uremic syndrome (HUS) with transient grade 1 abnormalities in platelets and creatinine. Preclinical work is underway to identify residues on moxetumomab pasudotox leading to immunogenicity. Moxetumomab pasudotox is undergoing pivotal testing for relapsed and refractory HCL. Published by Elsevier Ltd. JF - Best practice & research. Clinical haematology AU - Kreitman, Robert J AU - Pastan, Ira AD - The Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, 37/5124b, 9000 Rockville Pike Bethesda, MD 20892-4255, USA. Electronic address: kreitmar@mail.nih.gov. ; The Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, 37/5124b, 9000 Rockville Pike Bethesda, MD 20892-4255, USA. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 236 EP - 245 VL - 28 IS - 4 KW - Antibodies, Monoclonal KW - 0 KW - Antineoplastic Agents KW - B3(Fv)-PE38KDEL recombinant immunotoxin KW - Bacterial Toxins KW - Exotoxins KW - Immunoconjugates KW - Peptide Elongation Factor 2 KW - immunotoxin HA22 KW - Pentostatin KW - 395575MZO7 KW - Cladribine KW - 47M74X9YT5 KW - BRAF protein, human KW - EC 2.7.11.1 KW - Proto-Oncogene Proteins B-raf KW - Index Medicus KW - Recombinant immunotoxin KW - CD22 KW - CD25 KW - Moxetumomab pasudotox KW - BL22 KW - Pseudomonas exotoxin KW - Neoplasm, Residual KW - Proto-Oncogene Proteins B-raf -- immunology KW - Humans KW - Cladribine -- therapeutic use KW - Peptide Elongation Factor 2 -- genetics KW - Proto-Oncogene Proteins B-raf -- antagonists & inhibitors KW - Clinical Trials as Topic KW - Peptide Elongation Factor 2 -- immunology KW - Pentostatin -- therapeutic use KW - Peptide Elongation Factor 2 -- antagonists & inhibitors KW - Proto-Oncogene Proteins B-raf -- genetics KW - Mutation KW - Survival Analysis KW - Remission Induction KW - Leukemia, Hairy Cell -- mortality KW - Leukemia, Hairy Cell -- pathology KW - Bacterial Toxins -- therapeutic use KW - Leukemia, Hairy Cell -- drug therapy KW - Exotoxins -- therapeutic use KW - Antineoplastic Agents -- therapeutic use KW - Leukemia, Hairy Cell -- immunology KW - Immunoconjugates -- therapeutic use KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1738005379?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Best+practice+%26+research.+Clinical+haematology&rft.atitle=Immunoconjugates+in+the+management+of+hairy+cell+leukemia.&rft.au=Kreitman%2C+Robert+J%3BPastan%2C+Ira&rft.aulast=Kreitman&rft.aufirst=Robert&rft.date=2015-12-01&rft.volume=28&rft.issue=4&rft.spage=236&rft.isbn=&rft.btitle=&rft.title=Best+practice+%26+research.+Clinical+haematology&rft.issn=1532-1924&rft_id=info:doi/10.1016%2Fj.beha.2015.09.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-07 N1 - Date created - 2015-11-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biochemistry. 1994 May 10;33(18):5451-9 [7910034] Biochemistry. 1994 May 17;33(19):5894-900 [8180218] J Biol Chem. 1994 Jul 8;269(27):18167-76 [8027078] Bioconjug Chem. 1993 Mar-Apr;4(2):112-20 [7873642] J Clin Oncol. 1995 Apr;13(4):974-82 [7707126] Biochem J. 1995 Apr 1;307 ( Pt 1):29-37 [7717988] Proc Natl Acad Sci U S A. 1995 Oct 24;92(22):10427-31 [7479798] J Clin Pathol. 1995 Oct;48(10):955-60 [8537498] Bioconjug Chem. 1996 Sep-Oct;7(5):557-63 [8889017] Biochem Soc Trans. 1997 May;25(2):709-14 [9191188] Blood. 1997 Sep 1;90(5):2020-6 [9292538] Biochemistry. 1997 Nov 25;36(47):14577-82 [9398176] Leuk Res. 1997 Oct;21(10):997-9 [9403010] Immunopharmacology. 1997 Oct;37(2-3):117-32 [9403331] J Neurosci Res. 1998 Jan 15;51(2):162-73 [9469570] Blood. 1998 Sep 15;92(6):1918-26 [9731048] J Clin Oncol. 1998 Sep;16(9):3007-15 [9738569] Int J Cancer. 1999 Mar 31;81(1):148-55 [10077166] Blood. 1958 Jul;13(7):609-30 [13560561] Blood. 2005 Jul 1;106(1):241-6 [15761021] J Clin Oncol. 2005 Sep 20;23(27):6719-29 [16061911] Clin Cancer Res. 2006 May 1;12(9):2804-11 [16675574] Hematol Oncol Clin North Am. 2006 Oct;20(5):1023-49 [16990105] Hematol Oncol Clin North Am. 2006 Oct;20(5):1051-63 [16990106] Cancer Res. 2008 Aug 1;68(15):6300-5 [18676854] J Cell Sci. 2008 Oct 1;121(Pt 19):3140-5 [18765564] Clin Cancer Res. 2009 Feb 1;15(3):832-9 [19188153] J Clin Oncol. 2009 Jun 20;27(18):2983-90 [19414673] Br J Haematol. 2009 Jun;145(6):733-40 [19344416] Blood. 2009 Nov 19;114(21):4687-95 [19745070] Mol Cell Biol. 2010 Jul;30(14):3444-52 [20457813] Cancer Treat Rev. 2011 Feb;37(1):3-10 [20558005] Cytometry B Clin Cytom. 2011 Mar;80(2):83-90 [20872890] Am J Clin Pathol. 2011 Oct;136(4):625-30 [21917686] Blood. 2012 Apr 5;119(14):3330-2 [22210875] J Clin Oncol. 2012 May 20;30(15):1822-8 [22355053] Leuk Res. 2013 Apr;37(4):401-9 [23347903] Clin Cancer Res. 2013 Nov 15;19(22):6313-21 [24097860] Clin Cancer Res. 2013 Dec 15;19(24):6873-81 [24277451] Blood. 2014 Jan 9;123(2):177-83 [24192579] Proc Natl Acad Sci U S A. 2014 Jun 10;111(23):8571-6 [24799704] Leuk Res. 2014 Oct;38(10):1224-9 [25127689] CA Cancer J Clin. 2015 Jan-Feb;65(1):5-29 [25559415] J Clin Oncol. 2000 Apr;18(8):1622-36 [10764422] Blood. 1999 Nov 15;94(10):3340-8 [10552943] Biochemistry. 1999 Dec 14;38(50):16507-13 [10600112] Clin Cancer Res. 2000 Feb;6(2):693-700 [10690555] Clin Cancer Res. 2000 Apr;6(4):1476-87 [10778980] Int J Cancer. 2000 Jul 1;87(1):86-94 [10861457] Blood. 2000 Nov 1;96(9):2981-6 [11049974] N Engl J Med. 2001 Jul 26;345(4):241-7 [11474661] Clin Cancer Res. 2002 Apr;8(4):995-1002 [11948105] J Clin Oncol. 2003 Mar 1;21(5):891-6 [12610190] Best Pract Res Clin Haematol. 2003 Mar;16(1):41-56 [12670464] Best Pract Res Clin Haematol. 2003 Mar;16(1):101-16 [12670469] Blood. 2004 Apr 1;103(7):2718-26 [14525789] Cell. 1978 Sep;15(1):245-50 [699044] J Biol Chem. 1980 Nov 25;255(22):10717-20 [7000782] Leuk Res. 1980;4(6):547-59 [7206776] J Clin Invest. 1984 Sep;74(3):966-71 [6432853] Blood. 1985 Jun;65(6):1416-21 [2986744] Cell. 1986 Dec 5;47(5):641-8 [3536124] N Engl J Med. 1987 Apr 2;316(14):825-30 [2434850] J Biol Chem. 1987 Apr 25;262(12):5908-12 [3571242] J Biol Chem. 1987 Jun 25;262(18):8707-11 [2885323] Leukemia. 1987 Apr;1(4):405 [3669765] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1922-6 [3126499] Nature. 1989 Jun 1;339(6223):394-7 [2498664] N Engl J Med. 1990 Apr 19;322(16):1117-21 [1969613] J Biol Chem. 1991 Nov 5;266(31):21118-24 [1939154] Infect Immun. 1992 Feb;60(2):497-502 [1730481] Blood. 1992 Nov 1;80(9):2344-52 [1421405] J Biol Chem. 1992 Dec 15;267(35):25396-401 [1460035] Cancer Res. 1993 Feb 15;53(4):819-25 [8428363] Leukemia. 1993 Apr;7(4):553-62 [8464234] Blood. 1993 Aug 15;82(4):1277-87 [7688993] Proc Natl Acad Sci U S A. 1993 Aug 15;90(16):7774-8 [8356083] Cancer Res. 1994 Feb 15;54(4):1059-64 [8313362] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.beha.2015.09.003 ER - TY - JOUR T1 - Dorzolamide synergizes the antitumor activity of mitomycin C against Ehrlich's carcinoma grown in mice: role of thioredoxin-interacting protein. AN - 1737480507; 26264806 AB - The antitumor activity of carbonic anhydrase (CA) inhibitors is attributed to their ability to induce a state of intracellular acidification. In fact, acidic intracellular pH was demonstrated to upregulate several tumor suppressor proteins and increase the activity of many chemotherapies. The present study aimed to investigate the antitumor activity of the CA inhibitor, dorzolamide, in combination with mitomycin C and to study the effect of these drugs on tumoral thioredoxin-interacting protein (TXNIP) as well as tumor cell proliferation and apoptosis. Solid tumors were induced by subcutaneous inoculation of Ehrlich's ascites carcinoma (EAC) cells in female mice. Mice were treated with dorzolamide (3, 10, or 30 mg/kg/day, i.p.) and/or mitomycin C (1 mg/kg, i.p.) weekly for 3 weeks. Treatment with mitomycin C increased TXNIP level in EAC solid tumors in mice. Likewise, treatment with dorzolamide upregulated TXNIP and p53 while downregulated bcl-2. Both drug therapies increased tumoral caspase 9, caspase 3, and PARP-1 cleavage in addition to decreasing the proliferative Ki-67-stained nuclear fraction. Indeed, a synergistic effect was detected between mitomycin C and dorzolamide. The current data demonstrated that the antitumor activity of mitomycin C and dorzolamide was, at least in part, mediated through stimulating tumoral expression of TXNIP and enhancing tumor apoptosis. JF - Naunyn-Schmiedeberg's archives of pharmacology AU - Ali, Belal M AU - Zaitone, Sawsan A AU - Shouman, Samia A AU - Moustafa, Yasser M AD - Department of Pharmacology and Toxicology, Faculty of Pharmacy and Pharmaceutical Industries, Sinai University, Arish, Egypt. ; Department of Pharmacology and Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia, 41522, Egypt. Sawsan_zaytoon@pharm.suez.edu.eg. ; Department of Tumor Cell Biology, National Cancer Institute, Cairo University, Cairo, Egypt. ; Department of Pharmacology and Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia, 41522, Egypt. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1271 EP - 1282 VL - 388 IS - 12 KW - Antibiotics, Antineoplastic KW - 0 KW - Carrier Proteins KW - Sulfonamides KW - Thiophenes KW - Txnip protein, mouse KW - Mitomycin KW - 50SG953SK6 KW - Thioredoxins KW - 52500-60-4 KW - dorzolamide KW - 9JDX055TW1 KW - Index Medicus KW - TXNIP KW - Anticancer KW - Carbonic anhydrase KW - Mitomycin C KW - Ehrlich’s ascites carcinoma KW - Dorzolamide KW - Animals KW - Dose-Response Relationship, Drug KW - Mice KW - Cell Line, Tumor KW - Drug Synergism KW - Female KW - Thiophenes -- therapeutic use KW - Thioredoxins -- physiology KW - Carcinoma, Ehrlich Tumor -- pathology KW - Carcinoma, Ehrlich Tumor -- drug therapy KW - Mitomycin -- therapeutic use KW - Carrier Proteins -- physiology KW - Sulfonamides -- therapeutic use KW - Antibiotics, Antineoplastic -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1737480507?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Naunyn-Schmiedeberg%27s+archives+of+pharmacology&rft.atitle=Dorzolamide+synergizes+the+antitumor+activity+of+mitomycin+C+against+Ehrlich%27s+carcinoma+grown+in+mice%3A+role+of+thioredoxin-interacting+protein.&rft.au=Ali%2C+Belal+M%3BZaitone%2C+Sawsan+A%3BShouman%2C+Samia+A%3BMoustafa%2C+Yasser+M&rft.aulast=Ali&rft.aufirst=Belal&rft.date=2015-12-01&rft.volume=388&rft.issue=12&rft.spage=1271&rft.isbn=&rft.btitle=&rft.title=Naunyn-Schmiedeberg%27s+archives+of+pharmacology&rft.issn=1432-1912&rft_id=info:doi/10.1007%2Fs00210-015-1163-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-12 N1 - Date created - 2015-11-28 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00210-015-1163-9 ER - TY - JOUR T1 - Reproductive toxicity of low level bisphenol A exposures in a two-generation zebrafish assay: Evidence of male-specific effects. AN - 1737478057; 26562050 AB - Bisphenol A (BPA), a high-volume chemical used to make polycarbonate plastic and epoxy resins, is a ubiquitous contaminant in environment and human body. To investigate the reproductive effects of long-term exposure to low concentrations of BPA, a two-generation study was conducted using the aquatic model species of zebrafish. Our findings revealed that exposure to 1nM (0.228μg/L) BPA for continuous two generations resulted in female-biased sex ratio in both F1 and F2 adult population, decreased sperm density, and decreased sperm quality as measured by motility, velocity, ATP content and lipid peroxidation in F1 and F2 males. Females were less sensitive to BPA exposures than males as no adverse effects were found in female gonads or gametes. Delayed hatching at 48hpf and increased malformation and mortality were found in the offspring from BPA exposed F2, but not F1 parents. Most importantly, the adverse effect on larval development and survival from BPA exposed F2 parents was paternal-specific, resulting mainly from BPA exposed males. Subsequent transcription analysis of F2 male gonads revealed dysregulated mitochondrial biogenesis and significant activation of non-canonical Wnt/planar cell polarity and Wnt/Calcium signaling pathways. Gene expression analysis of larvae from BPA exposed F2 parents showed significant reduced expression of DNA methyltransferases such as dnmt1, dnmt3, and dnmt5. In conclusion, low level BPA exposures for continuous two generations not only affects sex ratio and sperm quantity/quality in F1 and F2 adults, reproductive success in offspring from F2 parents, but also perturbs various molecular pathways potentially contributing to these BPA induced male-specific reproductive defects. Copyright © 2015 Elsevier B.V. All rights reserved. JF - Aquatic toxicology (Amsterdam, Netherlands) AU - Chen, Jiangfei AU - Xiao, Yanyan AU - Gai, Zengxin AU - Li, Rong AU - Zhu, Zixu AU - Bai, Chenglian AU - Tanguay, Robert L AU - Xu, Xiaojiang AU - Huang, Changjiang AU - Dong, Qiaoxiang AD - Zhejiang Provincial Key Laboratory for Technology and Application of Model Organisms, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou 325035, China; Institute of Environmental Safety and Human Health, Wenzhou Medical University, Wenzhou 325035, China. ; Environmental and Molecular Toxicology, The Sinnhuber Aquatic Research Laboratory and the Environmental Health Sciences Center, Oregon State, University, Corvallis, OR 97333, USA. ; Integrated Bioinformatics, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. ; Zhejiang Provincial Key Laboratory for Technology and Application of Model Organisms, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou 325035, China; Institute of Environmental Safety and Human Health, Wenzhou Medical University, Wenzhou 325035, China. Electronic address: cjhuang5711@163.com. ; Zhejiang Provincial Key Laboratory for Technology and Application of Model Organisms, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou 325035, China; Institute of Environmental Safety and Human Health, Wenzhou Medical University, Wenzhou 325035, China. Electronic address: dqxdong@163.com. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 204 EP - 214 VL - 169 KW - Benzhydryl Compounds KW - 0 KW - Phenols KW - Water Pollutants, Chemical KW - Methyltransferases KW - EC 2.1.1.- KW - bisphenol A KW - MLT3645I99 KW - Index Medicus KW - Wnt signaling KW - Chronic exposure KW - BPA KW - Sperm KW - Zebrafish KW - Mitochondrial biogenesis KW - Methyltransferases -- genetics KW - Animals KW - Sex Factors KW - Gene Expression Regulation, Enzymologic -- drug effects KW - Gonads -- drug effects KW - Sex Ratio KW - Male KW - Female KW - Benzhydryl Compounds -- toxicity KW - Reproduction -- drug effects KW - Water Pollutants, Chemical -- toxicity KW - Phenols -- toxicity KW - Zebrafish -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1737478057?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Aquatic+toxicology+%28Amsterdam%2C+Netherlands%29&rft.atitle=Reproductive+toxicity+of+low+level+bisphenol+A+exposures+in+a+two-generation+zebrafish+assay%3A+Evidence+of+male-specific+effects.&rft.au=Chen%2C+Jiangfei%3BXiao%2C+Yanyan%3BGai%2C+Zengxin%3BLi%2C+Rong%3BZhu%2C+Zixu%3BBai%2C+Chenglian%3BTanguay%2C+Robert+L%3BXu%2C+Xiaojiang%3BHuang%2C+Changjiang%3BDong%2C+Qiaoxiang&rft.aulast=Chen&rft.aufirst=Jiangfei&rft.date=2015-12-01&rft.volume=169&rft.issue=&rft.spage=204&rft.isbn=&rft.btitle=&rft.title=Aquatic+toxicology+%28Amsterdam%2C+Netherlands%29&rft.issn=1879-1514&rft_id=info:doi/10.1016%2Fj.aquatox.2015.10.020 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-22 N1 - Date created - 2015-11-27 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.aquatox.2015.10.020 ER - TY - JOUR T1 - Dose Addition Models Based on Biologically Relevant Reductions in Fetal Testosterone Accurately Predict Postnatal Reproductive Tract Alterations by a Phthalate Mixture in Rats. AN - 1737475190; 26350170 AB - Challenges in cumulative risk assessment of anti-androgenic phthalate mixtures include a lack of data on all the individual phthalates and difficulty determining the biological relevance of reduction in fetal testosterone (T) on postnatal development. The objectives of the current study were 2-fold: (1) to test whether a mixture model of dose addition based on the fetal T production data of individual phthalates would predict the effects of a 5 phthalate mixture on androgen-sensitive postnatal male reproductive tract development, and (2) to determine the biological relevance of the reductions in fetal T to induce abnormal postnatal reproductive tract development using data from the mixture study. We administered a dose range of the mixture (60, 40, 20, 10, and 5% of the top dose used in the previous fetal T production study consisting of 300 mg/kg per chemical of benzyl butyl (BBP), di(n)butyl (DBP), diethyl hexyl phthalate (DEHP), di-isobutyl phthalate (DiBP), and 100 mg dipentyl (DPP) phthalate/kg; the individual phthalates were present in equipotent doses based on their ability to reduce fetal T production) via gavage to Sprague Dawley rat dams on GD8-postnatal day 3. We compared observed mixture responses to predictions of dose addition based on the previously published potencies of the individual phthalates to reduce fetal T production relative to a reference chemical and published postnatal data for the reference chemical (called DAref). In addition, we predicted DA (called DAall) and response addition (RA) based on logistic regression analysis of all 5 individual phthalates when complete data were available. DA ref and DA all accurately predicted the observed mixture effect for 11 of 14 endpoints. Furthermore, reproductive tract malformations were seen in 17-100% of F1 males when fetal T production was reduced by about 25-72%, respectively. Published by Oxford University Press on behalf of of the Society of Toxicology 2015. This work is written by US Government employees and is in the public domain in the US. JF - Toxicological sciences : an official journal of the Society of Toxicology AU - Howdeshell, Kembra L AU - Rider, Cynthia V AU - Wilson, Vickie S AU - Furr, Johnathan R AU - Lambright, Christy R AU - Gray, L Earl AD - *Division of the National Toxicology Program (NTP), National Institute of Environmental Health Sciences (NIEHS), PO Box 12233, Research Triangle Park (RTP), North Carolina 27709 and howdeshellkl@niehs.nih.gov. ; *Division of the National Toxicology Program (NTP), National Institute of Environmental Health Sciences (NIEHS), PO Box 12233, Research Triangle Park (RTP), North Carolina 27709 and. ; Reproductive Toxicology Branch, Toxicology Assessment Division (TAD), National Health and Environmental Effects Research Laboratories, Office of Research and Development, US Environmental Protection Agency (US EPA), RTP, North Carolina 27711. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 488 EP - 502 VL - 148 IS - 2 KW - Androgen Antagonists KW - 0 KW - Endocrine Disruptors KW - Phthalic Acids KW - Testosterone KW - 3XMK78S47O KW - Index Medicus KW - phthalates KW - dose addition KW - endocrine disruptors KW - mixture models KW - postnatal developmental toxicity KW - male reproductive tract KW - Animals KW - Rats, Sprague-Dawley KW - Age Factors KW - Down-Regulation KW - Logistic Models KW - Dose-Response Relationship, Drug KW - Gestational Age KW - Male KW - Female KW - Risk Assessment KW - Prenatal Exposure Delayed Effects KW - Pregnancy KW - Endocrine Disruptors -- toxicity KW - Androgen Antagonists -- toxicity KW - Genitalia, Male -- metabolism KW - Genitalia, Male -- embryology KW - Testosterone -- metabolism KW - Reproduction -- drug effects KW - Genitalia, Male -- drug effects KW - Toxicity Tests -- methods KW - Models, Biological KW - Phthalic Acids -- toxicity KW - Genitalia, Male -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1737475190?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.atitle=Dose+Addition+Models+Based+on+Biologically+Relevant+Reductions+in+Fetal+Testosterone+Accurately+Predict+Postnatal+Reproductive+Tract+Alterations+by+a+Phthalate+Mixture+in+Rats.&rft.au=Howdeshell%2C+Kembra+L%3BRider%2C+Cynthia+V%3BWilson%2C+Vickie+S%3BFurr%2C+Johnathan+R%3BLambright%2C+Christy+R%3BGray%2C+L+Earl&rft.aulast=Howdeshell&rft.aufirst=Kembra&rft.date=2015-12-01&rft.volume=148&rft.issue=2&rft.spage=488&rft.isbn=&rft.btitle=&rft.title=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.issn=1096-0929&rft_id=info:doi/10.1093%2Ftoxsci%2Fkfv196 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-08 N1 - Date created - 2015-11-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Fertil Steril. 2008 Feb;89(2 Suppl):e33-8 [18308057] Int J Androl. 2012 Jun;35(3):303-16 [22372636] Toxicol Lett. 2013 Dec 16;223(3):315-21 [23542816] Reproduction. 2014;147(4):465-76 [24287426] Reproduction. 2014;147(4):489-501 [24298046] Toxicol Sci. 2014 Aug 1;140(2):403-24 [24798384] J Expo Sci Environ Epidemiol. 2015 Jul-Aug;25(4):343-53 [25944701] Reprod Toxicol. 2000 Jan-Feb;14(1):13-9 [10689199] Toxicol Sci. 2000 May;55(1):143-51 [10788569] Environ Health Perspect. 2000 Oct;108(10):979-82 [11049818] Reprod Toxicol. 2000 Nov-Dec;14(6):513-32 [11099877] Toxicol Sci. 2000 Dec;58(2):339-49 [11099646] Toxicol Sci. 2000 Dec;58(2):350-65 [11099647] Toxicol Lett. 2004 Feb 2;146(3):207-15 [14687758] Reprod Toxicol. 2004 Mar-Apr;18(2):241-64 [15019722] Toxicol Sci. 2004 Sep;81(1):60-8 [15141095] Bull Environ Contam Toxicol. 2004 Jun;72(6):1226-31 [15362453] Environ Health Perspect. 1997 Jan;105(1):102-7 [9074889] Toxicol Sci. 1998 May;43(1):47-60 [9629619] Toxicol Sci. 1998 Oct;45(2):212-24 [9848128] Toxicol Appl Pharmacol. 1999 Apr 15;156(2):81-95 [10198273] Mol Endocrinol. 1999 May;13(5):681-91 [10319319] Biol Reprod. 2004 Dec;71(6):1852-61 [15286035] Biol Reprod. 2005 Jul;73(1):180-92 [15728792] Environ Health Perspect. 2005 Aug;113(8):1056-61 [16079079] Toxicol Sci. 2005 Oct;87(2):520-8 [16002478] Int J Androl. 2006 Feb;29(1):96-104; discussion 105-8 [16466529] Int J Androl. 2006 Feb;29(1):140-7; discussion 181-5 [16102138] Biol Reprod. 2002 Sep;67(3):699-705 [12193374] J Toxicol Sci. 2005 Dec;30 Spec No.:39-58 [16641542] Toxicol Lett. 2006 Aug 1;165(1):39-46 [16516415] Toxicol Sci. 2006 Sep;93(1):189-95 [16763070] Toxicol Sci. 2007 Sep;99(1):190-202 [17400582] Environ Health Perspect. 2007 Dec;115 Suppl 1:122-8 [18174960] Int J Androl. 2008 Apr;31(2):249-62 [18205796] Toxicol Sci. 2008 Sep;105(1):153-65 [18411233] Environ Health Perspect. 2008 Aug;116(8):1092-7 [18709157] Reprod Toxicol. 2008 Oct;26(2):107-15 [18706996] Environ Res. 2008 Oct;108(2):168-76 [18949836] Toxicol Pathol. 2009 Jan;37(1):100-13 [19147833] Toxicol Sci. 2009 Aug;110(2):411-25 [19482887] Environ Health Perspect. 2009 Dec;117(12):1839-46 [20049201] Int J Androl. 2010 Apr;33(2):443-62 [20487044] Int J Androl. 2010 Apr;33(2):463-74 [20487045] Toxicol Sci. 2010 Aug;116(2):640-6 [20484383] Reprod Toxicol. 2010 Sep;30(2):261-70 [20558277] Crit Rev Toxicol. 2011 May;41(5):369-83 [21309635] Int J Hyg Environ Health. 2011 Jun;214(3):188-95 [21371937] Toxicol Sci. 2012 Feb;125(2):544-57 [22112501] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/toxsci/kfv196 ER - TY - JOUR T1 - Broad targeting of angiogenesis for cancer prevention and therapy. AN - 1736411253; 25600295 AB - Deregulation of angiogenesis--the growth of new blood vessels from an existing vasculature--is a main driving force in many severe human diseases including cancer. As such, tumor angiogenesis is important for delivering oxygen and nutrients to growing tumors, and therefore considered an essential pathologic feature of cancer, while also playing a key role in enabling other aspects of tumor pathology such as metabolic deregulation and tumor dissemination/metastasis. Recently, inhibition of tumor angiogenesis has become a clinical anti-cancer strategy in line with chemotherapy, radiotherapy and surgery, which underscore the critical importance of the angiogenic switch during early tumor development. Unfortunately the clinically approved anti-angiogenic drugs in use today are only effective in a subset of the patients, and many who initially respond develop resistance over time. Also, some of the anti-angiogenic drugs are toxic and it would be of great importance to identify alternative compounds, which could overcome these drawbacks and limitations of the currently available therapy. Finding "the most important target" may, however, prove a very challenging approach as the tumor environment is highly diverse, consisting of many different cell types, all of which may contribute to tumor angiogenesis. Furthermore, the tumor cells themselves are genetically unstable, leading to a progressive increase in the number of different angiogenic factors produced as the cancer progresses to advanced stages. As an alternative approach to targeted therapy, options to broadly interfere with angiogenic signals by a mixture of non-toxic natural compound with pleiotropic actions were viewed by this team as an opportunity to develop a complementary anti-angiogenesis treatment option. As a part of the "Halifax Project" within the "Getting to know cancer" framework, we have here, based on a thorough review of the literature, identified 10 important aspects of tumor angiogenesis and the pathological tumor vasculature which would be well suited as targets for anti-angiogenic therapy: (1) endothelial cell migration/tip cell formation, (2) structural abnormalities of tumor vessels, (3) hypoxia, (4) lymphangiogenesis, (5) elevated interstitial fluid pressure, (6) poor perfusion, (7) disrupted circadian rhythms, (8) tumor promoting inflammation, (9) tumor promoting fibroblasts and (10) tumor cell metabolism/acidosis. Following this analysis, we scrutinized the available literature on broadly acting anti-angiogenic natural products, with a focus on finding qualitative information on phytochemicals which could inhibit these targets and came up with 10 prototypical phytochemical compounds: (1) oleanolic acid, (2) tripterine, (3) silibinin, (4) curcumin, (5) epigallocatechin-gallate, (6) kaempferol, (7) melatonin, (8) enterolactone, (9) withaferin A and (10) resveratrol. We suggest that these plant-derived compounds could be combined to constitute a broader acting and more effective inhibitory cocktail at doses that would not be likely to cause excessive toxicity. All the targets and phytochemical approaches were further cross-validated against their effects on other essential tumorigenic pathways (based on the "hallmarks" of cancer) in order to discover possible synergies or potentially harmful interactions, and were found to generally also have positive involvement in/effects on these other aspects of tumor biology. The aim is that this discussion could lead to the selection of combinations of such anti-angiogenic compounds which could be used in potent anti-tumor cocktails, for enhanced therapeutic efficacy, reduced toxicity and circumvention of single-agent anti-angiogenic resistance, as well as for possible use in primary or secondary cancer prevention strategies. Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved. JF - Seminars in cancer biology AU - Wang, Zongwei AU - Dabrosin, Charlotta AU - Yin, Xin AU - Fuster, Mark M AU - Arreola, Alexandra AU - Rathmell, W Kimryn AU - Generali, Daniele AU - Nagaraju, Ganji P AU - El-Rayes, Bassel AU - Ribatti, Domenico AU - Chen, Yi Charlie AU - Honoki, Kanya AU - Fujii, Hiromasa AU - Georgakilas, Alexandros G AU - Nowsheen, Somaira AU - Amedei, Amedeo AU - Niccolai, Elena AU - Amin, Amr AU - Ashraf, S Salman AU - Helferich, Bill AU - Yang, Xujuan AU - Guha, Gunjan AU - Bhakta, Dipita AU - Ciriolo, Maria Rosa AU - Aquilano, Katia AU - Chen, Sophie AU - Halicka, Dorota AU - Mohammed, Sulma I AU - Azmi, Asfar S AU - Bilsland, Alan AU - Keith, W Nicol AU - Jensen, Lasse D AD - Department of Urology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: zwang0@partners.org. ; Department of Oncology, Linköping University, Linköping, Sweden; Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden. ; Medicine and Research Services, Veterans Affairs San Diego Healthcare System & University of California, San Diego, San Diego, CA, USA. ; Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC, USA. ; Molecular Therapy and Pharmacogenomics Unit, AO Isituti Ospitalieri di Cremona, Cremona, Italy. ; Department of Hematology and Medical Oncology, Emory University, Atlanta, GA, USA. ; Department of Basic Medical Sciences, Neurosciences and Sensory Organs, University of Bari Medical School, Bari, Italy; National Cancer Institute Giovanni Paolo II, Bari, Italy. ; Department of Biology, Alderson Broaddus University, Philippi, WV, USA. ; Department of Orthopedic Surgery, Arthroplasty and Regenerative Medicine, Nara Medical University, Nara, Japan. ; Physics Department, School of Applied Mathematics and Physical Sciences, National Technical University of Athens, Athens, Greece. ; Mayo Graduate School, Mayo Clinic College of Medicine, Rochester, MN, USA. ; Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy. ; Department of Biology, College of Science, United Arab Emirate University, United Arab Emirates; Faculty of Science, Cairo University, Cairo, Egypt. ; Department of Chemistry, College of Science, United Arab Emirate University, United Arab Emirates. ; University of Illinois at Urbana Champaign, Urbana, IL, USA. ; School of Chemical and Bio Technology, SASTRA University, Thanjavur, India. ; Department of Biology, University of Rome "Tor Vergata", Rome, Italy. ; Ovarian and Prostate Cancer Research Trust Laboratory, Guilford, Surrey, UK. ; New York Medical College, New York City, NY, USA. ; Department of Comparative Pathobiology, Purdue University Center for Cancer Research, West Lafayette, IN, USA. ; School of Medicine, Wayne State University, Detroit, MI, USA. ; Institute of Cancer Sciences, University of Glasgow, Glasgow, UK. ; Department of Medical, and Health Sciences, Linköping University, Linköping, Sweden; Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden. Electronic address: lasse.jensen@liu.se. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - S224 EP - S243 VL - 35 Suppl KW - Angiogenesis Inhibitors KW - 0 KW - Antineoplastic Agents, Phytogenic KW - Index Medicus KW - Angiogenesis KW - Anti-angiogenic KW - Phytochemicals KW - Treatment KW - Cancer KW - Cell Proliferation -- drug effects KW - Immunotherapy KW - Humans KW - Blood Vessels -- growth & development KW - Blood Vessels -- drug effects KW - Blood Vessels -- pathology KW - Angiogenesis Inhibitors -- therapeutic use KW - Antineoplastic Agents, Phytogenic -- therapeutic use KW - Neoplasms -- prevention & control KW - Neovascularization, Pathologic -- prevention & control KW - Neoplasms -- therapy KW - Neovascularization, Pathologic -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1736411253?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Performance+of+self-collected+cervical+samples+in+screening+for+future+precancer+using+human+papillomavirus+DNA+testing.&rft.au=Porras%2C+Carolina%3BHildesheim%2C+Allan%3BGonz%C3%A1lez%2C+Paula%3BSchiffman%2C+Mark%3BRodr%C3%ADguez%2C+Ana+Cecilia%3BWacholder%2C+Sholom%3BJim%C3%A9nez%2C+Silvia%3BQuint%2C+Wim%3BGuillen%2C+Diego%3BKreimer%2C+Aim%C3%A9e+R%3BHerrero%2C+Rolando%3BCVT+Vaccine+Group&rft.aulast=Porras&rft.aufirst=Carolina&rft.date=2015-01-01&rft.volume=107&rft.issue=1&rft.spage=400&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdju400 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-07 N1 - Date created - 2015-11-23 N1 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[24486850] Cancer Prev Res (Phila). 2014 Apr;7(4):466-74 [24550143] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.semcancer.2015.01.001 ER - TY - JOUR T1 - Explanation of timing of botulinum neurotoxin effects, onset and duration, and clinical ways of influencing them. AN - 1736411224; 26220801 AB - While the steps in the action of botulinum neurotoxin (BoNT) are well known, the factors underlying the timing of these steps are not fully understood. After toxin is injected into a muscle, it resides in the extracellular space and must be taken up into the nerve terminals. More toxin will be taken up if near the endplate. Toxin is distributed mainly by convection and there is likely little diffusion. Toxin that is not taken up will go into the general circulation where it may have a slight systemic effect. The uptake is activity and temperature dependent. Encouraging the unwanted muscle contractions after injection should be helpful. Cooling will decrease the uptake. The times for washout from the extracellular space and uptake of the toxin are not well established, but are likely measured in minutes. Toxin in the general circulation has a long half time. The time from injection to weakness is determined by how long it takes to get sufficient damage of the SNARE proteins to interfere with synaptic release. Toxins are zinc dependent proteases, and supplemental zinc may produce a greater effect. There will be weakness as long as there is residual toxin in the nerve ending. Published by Elsevier Ltd. JF - Toxicon : official journal of the International Society on Toxinology AU - Hallett, Mark AD - Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Building 10, Room 7D37, 10 Center Drive, Bethesda, MD 20892-1428, USA. Electronic address: hallettm@ninds.nih.gov. Y1 - 2015/12/01/ PY - 2015 DA - 2015 Dec 01 SP - 64 EP - 67 VL - 107 KW - Botulinum Toxins KW - EC 3.4.24.69 KW - Index Medicus KW - Duration of action KW - Muscle activity KW - Zinc KW - Uptake KW - Cooling KW - Endplate KW - Animals KW - Paralysis -- chemically induced KW - Humans KW - Action Potentials -- drug effects KW - Time Factors KW - Muscle, Skeletal -- drug effects KW - Botulinum Toxins -- pharmacology KW - Botulinum Toxins -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1736411224?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicon+%3A+official+journal+of+the+International+Society+on+Toxinology&rft.atitle=Explanation+of+timing+of+botulinum+neurotoxin+effects%2C+onset+and+duration%2C+and+clinical+ways+of+influencing+them.&rft.au=Hallett%2C+Mark&rft.aulast=Hallett&rft.aufirst=Mark&rft.date=2015-12-01&rft.volume=107&rft.issue=&rft.spage=64&rft.isbn=&rft.btitle=&rft.title=Toxicon+%3A+official+journal+of+the+International+Society+on+Toxinology&rft.issn=1879-3150&rft_id=info:doi/10.1016%2Fj.toxicon.2015.07.013 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-19 N1 - Date created - 2015-11-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Arch Phys Med Rehabil. 2009 Jan;90(1):9-16.e2 [19154823] Eur J Neurol. 2014 Dec;21(12):1486-e98 [25060697] Clin Neurophysiol. 2011 Aug;122(8):1611-6 [21195024] J Drugs Dermatol. 2012 Apr;11(4):507-12 [22453589] Toxicon. 2013 Jun;68:40-59 [23518040] Nat Rev Microbiol. 2014 Aug;12(8):535-49 [24975322] J Cosmet Laser Ther. 2014 Oct;16(5):258-62 [25105993] J Neurol Sci. 2014 Sep 15;344(1-2):76-9 [25023196] J Electromyogr Kinesiol. 2014 Dec;24(6):923-7 [25138645] Ann Plast Surg. 2015 Sep;75(3):272-4 [25536197] J Nutr. 2000 May;130(5S Suppl):1367S-73S [10801945] Toxicon. 2003 Oct;42(5):461-9 [14529727] J Pharmacol Exp Ther. 1980 Jan;212(1):16-21 [6243359] J Physiol. 1982 Jan;322:197-210 [7069613] Laryngoscope. 1991 Sep;101(9):960-4 [1886444] Neurosci Lett. 1992 May 25;139(2):289-92 [1608558] Nutrition. 1993 May-Jun;9(3):218-24 [8353362] Mov Disord. 1997 Jan;12(1):89-94 [8990059] Food Chem Toxicol. 1998 Jan;36(1):7-12 [9487359] Mov Disord. 1999 Mar;14(2):307-12 [10091625] J Physiol. 1962 Feb;160:221-33 [14449824] Muscle Nerve. 2009 Sep;40(3):374-80 [19618426] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.toxicon.2015.07.013 ER - TY - JOUR T1 - Critical role of c-jun N-terminal protein kinase in promoting mitochondrial dysfunction and acute liver injury. AN - 1735909684; 26491845 AB - The mechanism by which c-Jun N-terminal protein kinase (JNK) promotes tissue injury is poorly understood. Thus we aimed at studying the roles of JNK and its phospho-target proteins in mouse models of acute liver injury. Young male mice were exposed to a single dose of CCl4 (50mg/kg, IP) and euthanized at different time points. Liver histology, blood alanine aminotransferase, and other enzyme activities were measured in CCl4-exposed mice without or with the highly-specific JNK inhibitors. Phosphoproteins were purified from control or CCl4-exposed mice and analyzed by differential mass-spectrometry followed by further characterizations of immunoprecipitation and activity measurements. JNK was activated within 1h while liver damage was maximal at 24h post-CCl4 injection. Markedly increased phosphorylation of many mitochondrial proteins was observed between 1 and 8h following CCl4 exposure. Pretreatment with the selective JNK inhibitor SU3327 or the mitochondria-targeted antioxidant mito-TEMPO markedly reduced the levels of p-JNK, mitochondrial phosphoproteins and liver damage in CCl4-exposed mice. Differential proteomic analysis identified many phosphorylated mitochondrial proteins involved in anti-oxidant defense, electron transfer, energy supply, fatty acid oxidation, etc. Aldehyde dehydrogenase, NADH-ubiquinone oxidoreductase, and α-ketoglutarate dehydrogenase were phosphorylated in CCl4-exposed mice but dephosphorylated after SU3327 pretreatment. Consistently, the suppressed activities of these enzymes were restored by SU3327 pretreatment in CCl4-exposed mice. These data provide a novel mechanism by which JNK, rapidly activated by CCl4, promotes mitochondrial dysfunction and acute hepatotoxicity through robust phosphorylation of numerous mitochondrial proteins. Published by Elsevier B.V. JF - Redox biology AU - Jang, Sehwan AU - Yu, Li-Rong AU - Abdelmegeed, Mohamed A AU - Gao, Yuan AU - Banerjee, Atrayee AU - Song, Byoung-Joon AD - Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892-9410, USA. Electronic address: sehwan.jang@upr.edu. ; Biomarkers and Alternative Models Branch, Division of Systems Biology, National Center for Toxicological Research, Food and Drug Administration, Jefferson, AR 72079, USA. Electronic address: Lirong.Yu@fda.hhs.gov. ; Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892-9410, USA. Electronic address: abdelmegeedm@mail.nih.gov. ; Biomarkers and Alternative Models Branch, Division of Systems Biology, National Center for Toxicological Research, Food and Drug Administration, Jefferson, AR 72079, USA. Electronic address: yuangao2000@gmail.com. ; Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892-9410, USA. Electronic address: atrayee.liver@gmail.com. ; Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD 20892-9410, USA. Electronic address: bj.song@nih.gov. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 552 EP - 564 VL - 6 KW - Bax protein, mouse KW - 0 KW - Mitochondrial Proteins KW - bcl-2-Associated X Protein KW - Cytochrome P-450 CYP2E1 KW - EC 1.14.13.- KW - JNK Mitogen-Activated Protein Kinases KW - EC 2.7.11.24 KW - Index Medicus KW - JNK KW - Carbon tetrachloride KW - Protein phosphorylation KW - Acute liver injury KW - Differential proteomics KW - Mitochondria KW - Mice, 129 Strain KW - Animals KW - Phosphorylation KW - Enzyme Activation KW - Protein Processing, Post-Translational KW - Cytochrome P-450 CYP2E1 -- physiology KW - Mitochondrial Proteins -- metabolism KW - Mice, Transgenic KW - Male KW - bcl-2-Associated X Protein -- metabolism KW - Mitochondria, Liver -- enzymology KW - JNK Mitogen-Activated Protein Kinases -- physiology KW - Acute Lung Injury -- enzymology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1735909684?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Redox+biology&rft.atitle=Critical+role+of+c-jun+N-terminal+protein+kinase+in+promoting+mitochondrial+dysfunction+and+acute+liver+injury.&rft.au=Jang%2C+Sehwan%3BYu%2C+Li-Rong%3BAbdelmegeed%2C+Mohamed+A%3BGao%2C+Yuan%3BBanerjee%2C+Atrayee%3BSong%2C+Byoung-Joon&rft.aulast=Jang&rft.aufirst=Sehwan&rft.date=2015-12-01&rft.volume=6&rft.issue=&rft.spage=552&rft.isbn=&rft.btitle=&rft.title=Redox+biology&rft.issn=2213-2317&rft_id=info:doi/10.1016%2Fj.redox.2015.09.040 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-05 N1 - Date created - 2015-11-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Ann Intern Med. 1986 Mar;104(3):399-404 [3511825] Redox Biol. 2014;3:109-23 [25465468] Antioxid Redox Signal. 2015 Mar 1;22(7):572-86 [25365698] Hepatology. 1991 Dec;14(6):1209-16 [1959871] Lancet. 1992 Aug 15;340(8816):384-7 [1353554] Science. 1995 Nov 24;270(5240):1326-31 [7481820] Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):12908-13 [8917518] Chem Res Toxicol. 1997 Aug;10(8):895-905 [9282839] Biochem Pharmacol. 1998 Sep 15;56(6):773-9 [9751083] Toxicol Appl Pharmacol. 1998 Nov;153(1):109-18 [9875305] Toxicol Pathol. 2005;33(1):155-64 [15805067] J Hepatol. 2005 Jun;42(6):850-9 [15885356] Gastroenterology. 2006 Jul;131(1):165-78 [16831600] J Biol Chem. 2006 Jul 28;281(30):21256-65 [16709574] Exp Mol Med. 2006 Aug 31;38(4):408-16 [16953120] Hepatology. 2006 Nov;44(5):1218-30 [17058263] Microbiol Mol Biol Rev. 2006 Dec;70(4):1061-95 [17158707] Hepatology. 2007 Feb;45(2):412-21 [17366662] Gut. 2007 Jul;56(7):982-90 [17185352] Arch Toxicol. 2007 Jul;81(7):489-93 [17285312] Biochem J. 2007 Dec 15;408(3):297-315 [17850214] J Biol Chem. 2008 May 16;283(20):13565-77 [18337250] Proteomics. 2008 Sep;8(18):3906-18 [18780394] Proc Natl Acad Sci U S A. 2008 Oct 28;105(43):16809-13 [18922779] Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):E18; author reply E19 [19204298] J Med Chem. 2009 Apr 9;52(7):1943-52 [19271755] Expert Rev Proteomics. 2010 Feb;7(1):39-53 [20121475] Free Radic Biol Med. 2010 Feb 1;48(3):391-8 [19922789] Oncogene. 2010 Mar 18;29(11):1702-16 [20062077] EMBO J. 2011 Jan 19;30(2):249-62 [21131905] J Nutr. 2011 Apr 1;141(4):603-10 [21346097] J Biol Chem. 2000 Jan 7;275(1):322-7 [10617621] Toxicol Sci. 2001 Aug;62(2):212-20 [11452133] Mol Pharmacol. 2001 Oct;60(4):847-56 [11562448] Toxicol Appl Pharmacol. 2001 Dec 1;177(2):112-20 [11740910] Toxicol Sci. 2002 Feb;65(2):166-76 [11812920] Addiction. 2002 Jul;97(7):773-83 [12133112] Mol Pharmacol. 2003 Feb;63(2):401-8 [12527812] Biochem J. 2003 Apr 1;371(Pt 1):199-204 [12534346] Crit Rev Toxicol. 2003;33(2):105-36 [12708612] Biochem J. 2003 Jun 1;372(Pt 2):359-69 [12614194] Methods Mol Biol. 2004;282:103-15 [15105559] Hepatology. 2004 Jul;40(1):6-9 [15239078] JAMA. 1980 Jul 18;244(3):251-3 [7382090] Biochem Pharmacol. 1981 Dec 15;30(24):3265-75 [7034733] J Biol Chem. 2011 May 6;286(18):16052-62 [21454558] ACS Chem Biol. 2011 Aug 19;6(8):808-18 [21563797] J Biol Chem. 2011 Oct 7;286(40):35071-8 [21844199] J Proteomics. 2011 Nov 18;74(12):2745-59 [21884834] Drug Metab Rev. 2012 Feb;44(1):34-87 [21892896] Gastroenterology. 2012 Aug;143(2):307-20 [22705006] Gastroenterology. 2012 Sep;143(3):e1-7 [22796239] Hepatology. 2012 Nov;56(5):1599-601 [22729522] Free Radic Biol Med. 2013 Jul;60:211-22 [23454065] Free Radic Biol Med. 2013 Dec;65:1238-45 [24064383] Oxid Med Cell Longev. 2014;2014:149627 [24876909] Pharmacol Ther. 1989;43(1):139-54 [2675128] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.redox.2015.09.040 ER - TY - JOUR T1 - Lack of Gαi2 leads to dilative cardiomyopathy and increased mortality in β1-adrenoceptor overexpressing mice. AN - 1735327516; 26464333 AB - Inhibitory G (Gi) proteins have been proposed to be cardioprotective. We investigated effects of Gαi2 knockout on cardiac function and survival in a murine heart failure model of cardiac β1-adrenoceptor overexpression. β1-transgenic mice lacking Gαi2 (β1-tg/Gαi2 (-/-)) were compared with wild-type mice and littermates either overexpressing cardiac β1-adrenoceptors (β1-tg) or lacking Gαi2 (Gαi2 (-/-)). At 300 days, mortality of mice only lacking Gαi2 was already higher compared with wild-type or β1-tg, but similar to β1-tg/Gαi2 (-/-), mice. Beyond 300 days, mortality of β1-tg/Gαi2 (-/-) mice was enhanced compared with all other genotypes (mean survival time: 363 ± 21 days). At 300 days of age, echocardiography revealed similar cardiac function of wild-type, β1-tg, and Gαi2 (-/-) mice, but significant impairment for β1-tg/Gαi2 (-/-) mice (e.g. ejection fraction 14 ± 2 vs. 40 ± 4% in wild-type mice). Significantly increased ventricle-to-body weight ratio (0.71 ± 0.06 vs. 0.48 ± 0.02% in wild-type mice), left ventricular size (length 0.82 ± 0.04 vs. 0.66 ± 0.03 cm in wild types), and atrial natriuretic peptide and brain natriuretic peptide expression (mRNA: 2819 and 495% of wild-type mice, respectively) indicated hypertrophy. Gαi3 was significantly up-regulated in Gαi2 knockout mice (protein compared with wild type: 340 ± 90% in Gαi2 (-/-) and 394 ± 80% in β1-tg/Gαi2 (-/-), respectively). Gαi2 deficiency combined with cardiac β1-adrenoceptor overexpression strongly impaired survival and cardiac function. At 300 days of age, β1-adrenoceptor overexpression alone had not induced cardiac hypertrophy or dysfunction while there was overt cardiomyopathy in mice additionally lacking Gαi2. We propose an enhanced effect of increased β1-adrenergic drive by the lack of protection via Gαi2. Gαi3 up-regulation was not sufficient to compensate for Gαi2 deficiency, suggesting an isoform-specific or a concentration-dependent mechanism. Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2015. For permissions please email: journals.permissions@oup.com. JF - Cardiovascular research AU - Keller, Kirsten AU - Maass, Martina AU - Dizayee, Sara AU - Leiss, Veronika AU - Annala, Suvi AU - Köth, Jessica AU - Seemann, Wiebke K AU - Müller-Ehmsen, Jochen AU - Mohr, Klaus AU - Nürnberg, Bernd AU - Engelhardt, Stefan AU - Herzig, Stefan AU - Birnbaumer, Lutz AU - Matthes, Jan AD - Department of Pharmacology, University of Cologne, Gleueler Strasse 24, 50931 Cologne, Germany. ; Department of Internal Medicine III, University Hospital of Cologne, Cologne, Germany. ; Department of Pharmacology and Experimental Therapy, Institute of Experimental and Clinical Pharmacology and Toxicology, Eberhard Karls University Hospitals and Clinics, and Interfaculty Center of Pharmacogenomics and Drug Research, Tuebingen, Germany. ; Asklepios Klinik Altona, Hamburg, Germany. ; Pharmacology and Toxicology Section, Institute of Pharmacy, University of Bonn, Bonn, Germany. ; Institute of Pharmacology and Toxicology, Technische Universität München, Munich, Germany. ; Laboratory of Neurobiology, NIEHS, NIH (Department of Health and Human Services), Durham, USA. ; Department of Pharmacology, University of Cologne, Gleueler Strasse 24, 50931 Cologne, Germany jan.matthes@uni-koeln.de. Y1 - 2015/12/01/ PY - 2015 DA - 2015 Dec 01 SP - 348 EP - 356 VL - 108 IS - 3 KW - Adrb1 protein, mouse KW - 0 KW - Receptors, Adrenergic, beta-1 KW - Natriuretic Peptide, Brain KW - 114471-18-0 KW - Atrial Natriuretic Factor KW - 85637-73-6 KW - Cyclic AMP KW - E0399OZS9N KW - Cyclic AMP-Dependent Protein Kinases KW - EC 2.7.11.11 KW - GTP-Binding Protein alpha Subunit, Gi2 KW - EC 3.6.5.1 KW - GTP-Binding Protein alpha Subunits, Gi-Go KW - Gnai2 protein, mouse KW - Gnai3 protein, mouse KW - Index Medicus KW - Cardiomyopathy KW - Cardioprotection KW - Heart failure KW - Adrenergic receptor KW - Inhibitory G protein KW - Ventricular Remodeling KW - Cyclic AMP-Dependent Protein Kinases -- metabolism KW - Ventricular Function, Left KW - Animals KW - GTP-Binding Protein alpha Subunits, Gi-Go -- metabolism KW - Atrial Natriuretic Factor -- genetics KW - GTP-Binding Protein alpha Subunits, Gi-Go -- genetics KW - Natriuretic Peptide, Brain -- genetics KW - Disease Models, Animal KW - Ultrasonography KW - Mice, Knockout KW - Phenotype KW - Mice, 129 Strain KW - Natriuretic Peptide, Brain -- metabolism KW - Atrial Natriuretic Factor -- metabolism KW - Cyclic AMP -- metabolism KW - Mice, Inbred C57BL KW - Gene Expression Regulation KW - Genetic Predisposition to Disease KW - Time Factors KW - Stroke Volume KW - Receptors, Adrenergic, beta-1 -- metabolism KW - GTP-Binding Protein alpha Subunit, Gi2 -- genetics KW - Cardiomyopathy, Dilated -- diagnostic imaging KW - Heart Failure -- diagnostic imaging KW - Heart Failure -- metabolism KW - Myocytes, Cardiac -- pathology KW - Heart Failure -- genetics KW - Cardiomyopathy, Dilated -- physiopathology KW - GTP-Binding Protein alpha Subunit, Gi2 -- deficiency KW - Receptors, Adrenergic, beta-1 -- genetics KW - Cardiomyopathy, Dilated -- genetics KW - Heart Failure -- physiopathology KW - Cardiomyopathy, Dilated -- metabolism KW - Myocytes, Cardiac -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1735327516?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cardiovascular+research&rft.atitle=Lack+of+G%CE%B1i2+leads+to+dilative+cardiomyopathy+and+increased+mortality+in+%CE%B21-adrenoceptor+overexpressing+mice.&rft.au=Keller%2C+Kirsten%3BMaass%2C+Martina%3BDizayee%2C+Sara%3BLeiss%2C+Veronika%3BAnnala%2C+Suvi%3BK%C3%B6th%2C+Jessica%3BSeemann%2C+Wiebke+K%3BM%C3%BCller-Ehmsen%2C+Jochen%3BMohr%2C+Klaus%3BN%C3%BCrnberg%2C+Bernd%3BEngelhardt%2C+Stefan%3BHerzig%2C+Stefan%3BBirnbaumer%2C+Lutz%3BMatthes%2C+Jan&rft.aulast=Keller&rft.aufirst=Kirsten&rft.date=2015-12-01&rft.volume=108&rft.issue=3&rft.spage=348&rft.isbn=&rft.btitle=&rft.title=Cardiovascular+research&rft.issn=1755-3245&rft_id=info:doi/10.1093%2Fcvr%2Fcvv235 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-13 N1 - Date created - 2015-11-20 N1 - Date revised - 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Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/cvr/cvv235 ER - TY - JOUR T1 - Estimation of tetrabromobisphenol A (TBBPA) percutaneous uptake in humans using the parallelogram method. AN - 1735327349; 26387765 AB - Tetrabromobisphenol A (TBBPA) is currently the world's highest production volume brominated flame retardant. Humans are frequently exposed to TBBPA by the dermal route. In the present study, a parallelogram approach was used to make predictions of internal dose in exposed humans. Human and rat skin samples received 100 nmol of TBBPA/cm(2) skin and absorption and penetrance were determined using a flow-through in vitro system. TBBPA-derived [(14)C]-radioactivity was determined at 6h intervals in the media and at 24h post-dosing in the skin. The human skin and media contained an average of 3.4% and 0.2% of the total dose at the terminal time point, respectively, while the rat skin and media contained 9.3% and 3.5%, respectively. In the intact rat, 14% of a dermally-administered dose of ~100 nmol/cm(2) remained in the skin at the dosing site, with an additional 8% reaching systemic circulation by 24h post-dosing. Relative absorption and penetrance were less (10% total) at 24h following dermal administration of a ten-fold higher dose (~1000 nmol/cm(2)) to rats. However, by 72 h, 70% of this dose was either absorbed into the dosing-site skin or had reached systemic circulation. It is clear from these results that TBBPA can be absorbed by the skin and dermal contact with TBBPA may represent a small but important route of exposure. Together, these in vitro data in human and rat skin and in vivo data from rats may be used to predict TBBPA absorption in humans following dermal exposure. Based on this parallelogram calculation, up to 6% of dermally applied TBBPA may be bioavailable to humans exposed to TBBPA. Published by Elsevier Inc. JF - Toxicology and applied pharmacology AU - Knudsen, Gabriel A AU - Hughes, Michael F AU - McIntosh, Katelyn L AU - Sanders, J Michael AU - Birnbaum, Linda S AD - NCI at NIEHS, 111 T W Alexander Dr., Research Triangle Park, NC, USA. Electronic address: gabriel.knudsen@nih.gov. ; Integrated Systems Toxicology Division, National Health and Environmental Effects Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, USA. ; NCI at NIEHS, 111 T W Alexander Dr., Research Triangle Park, NC, USA. Y1 - 2015/12/01/ PY - 2015 DA - 2015 Dec 01 SP - 323 EP - 329 VL - 289 IS - 2 KW - Flame Retardants KW - 0 KW - Polybrominated Biphenyls KW - tetrabromobisphenol A KW - FQI02RFC3A KW - Index Medicus KW - Tetrabromobisphenol A KW - Tetrabromobisphenol A (PubChem CID: 6618) KW - Dermal bioavailability KW - Parallelogram method KW - Brominated flame retardant KW - Persistent organic pollutant KW - Animals KW - Administration, Cutaneous KW - Humans KW - Body Burden KW - In Vitro Techniques KW - Rats, Wistar KW - Environmental Exposure KW - Aged KW - Male KW - Female KW - Risk Assessment KW - Biological Availability KW - Polybrominated Biphenyls -- metabolism KW - Flame Retardants -- metabolism KW - Polybrominated Biphenyls -- pharmacokinetics KW - Skin Absorption KW - Skin -- metabolism KW - Polybrominated Biphenyls -- administration & dosage KW - Flame Retardants -- pharmacokinetics KW - Polybrominated Biphenyls -- toxicity KW - Models, Biological KW - Flame Retardants -- administration & dosage KW - Flame Retardants -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1735327349?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Estimation+of+tetrabromobisphenol+A+%28TBBPA%29+percutaneous+uptake+in+humans+using+the+parallelogram+method.&rft.au=Knudsen%2C+Gabriel+A%3BHughes%2C+Michael+F%3BMcIntosh%2C+Katelyn+L%3BSanders%2C+J+Michael%3BBirnbaum%2C+Linda+S&rft.aulast=Knudsen&rft.aufirst=Gabriel&rft.date=2015-12-01&rft.volume=289&rft.issue=2&rft.spage=323&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2015.09.012 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-08 N1 - Date created - 2015-11-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Environ Int. 2015 Oct;83:183-91 [26177148] Chemosphere. 2002 Feb;46(5):709-16 [11999794] J Invest Dermatol. 2003 Feb;120(2):285-91 [12542534] Hum Exp Toxicol. 2004 Aug;23(9):421-30 [15497817] Mutat Res. 1977 Aug;46(4):245-60 [331104] J Pharm Sci. 1985 Jan;74(1):64-7 [3981421] Toxicol Appl Pharmacol. 1989 Jul;99(3):522-33 [2749737] Food Chem Toxicol. 1993 Sep;31(9):615-21 [8406237] J Dermatol Sci. 1995 Jan;9(1):48-58 [7727354] Toxicol Sci. 2005 Feb;83(2):215-23 [15509665] Toxicol Sci. 2006 May;91(1):49-58 [16481339] Toxicol Sci. 2007 Apr;96(2):237-45 [17234645] Toxicology. 2008 Mar 12;245(1-2):76-89 [18255212] Environ Sci Technol. 2008 Sep 15;42(18):6910-6 [18853808] Toxicol Sci. 2010 Jun;115(2):344-53 [20176623] Sci Total Environ. 2010 Jul 1;408(15):2885-918 [19815253] Chemosphere. 2011 Jan;82(3):424-30 [21030062] J Toxicol Environ Health A. 2011;74(6):351-63 [21271436] Toxicol Lett. 2012 Sep 18;213(3):305-8 [22796587] Environ Sci Technol. 2012 Dec 18;46(24):13056-66 [23185960] Int J Toxicol. 2013 Mar-Apr;32(2):130-5 [23493903] Xenobiotica. 2000 Sep;30(9):881-90 [11055266] Gastroenterology. 2001 Feb;120(2):525-33 [11159893] Food Chem Toxicol. 2001 Dec;39(12):1263-70 [11696400] Environ Int. 2013 Sep;59:124-32 [23797055] Environ Sci Technol. 2013 Dec 3;47(23):13848-56 [24195753] Toxicol Sci. 2013 Dec;136(2):382-91 [24014645] Environ Sci Pollut Res Int. 2014 Jun;21(12):7656-67 [24622986] Sci Rep. 2014;4:5251 [24918694] Chemosphere. 2014 Oct;112:481-6 [25048943] Chemosphere. 2014 Dec;116:54-60 [24485814] J Appl Toxicol. 2015 Jan;35(1):1-10 [25345378] Ecotoxicol Environ Saf. 2014 Dec;110:136-42 [25238485] Environ Int. 2015 Jan;74:13-22 [25310507] Toxicology. 2015 Mar 2;329:49-59 [25523853] Toxicol Pathol. 2015 Jun;43(4):464-73 [25476797] Environ Toxicol Pharmacol. 2015 May;39(3):997-1007 [25863327] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.taap.2015.09.012 ER - TY - JOUR T1 - Urine Mescaline Screening With a Biochip Array Immunoassay and Quantification by Gas Chromatography-Mass Spectrometry. AN - 1733194929; 25992796 AB - Mescaline, the primary psychoactive chemical in peyote cactus, has been consumed for thousands of years in ancient religious ceremonies. The US military wanted to determine if mescaline intake was a problem for personnel readiness. Twenty thousand seventeen urine specimens negative for cannabinoids, cocaine, opiates, and amphetamines were tested for mescaline with the Randox Drugs of Abuse V (DOA-V) biochip array immunoassay at the manufacturer's recommended cutoff of 6 mcg/L. A sensitive and specific method for mescaline quantification in urine was developed and fully validated. Extracted analytes were derivatized with pentafluoropropionic anhydride and pentafluoropropanol and quantified by gas chromatography-mass spectrometry (GC/MS) with electron impact ionization. Standard curves, using linear least squares regression with 1/x weighting, were linear from 1 to 250 mcg/L with coefficients of determination >0.994. Intra- and inter-assay imprecision was 90.4%. Mean extraction efficiencies were >92.0% across the linear range. This fully validated method was applied for the confirmation of urinary mescaline in 526 presumptive-positive specimens and 198 randomly selected presumptive-negative specimens at the manufacturer's 6 mcg/L cutoff. No specimen confirmed positive at the GC/MS limit of quantification of 1 mcg/L. Results indicated that during this time frame, there was insufficient mescaline drug use in the military to warrant routine screening in the drug testing program. However, mescaline stability, although assessed, could have contributed to lower prevalence. We also present a validated GC/MS method for mescaline quantification in urine for reliable confirmation of suspected mescaline intake. JF - Therapeutic drug monitoring AU - Battal, Dilek AU - Barnes, Allan J AU - Castaneto, Marisol S AU - Martin, Thomas M AU - Klette, Kevin L AU - Huestis, Marilyn A AD - *Department of Toxicology, Faculty of Pharmacy, Mersin University, Turkey; †Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland; and ‡Drug Testing and Program Policy, Office of the Secretary of Defense, Operational Readiness and Safety, Washington, District of Columbia. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 805 EP - 811 VL - 37 IS - 6 KW - Mescaline KW - RHO99102VC KW - Index Medicus KW - Sensitivity and Specificity KW - Immunoassay -- methods KW - Humans KW - Limit of Detection KW - Mescaline -- urine KW - Substance-Related Disorders -- diagnosis KW - Gas Chromatography-Mass Spectrometry -- methods KW - Substance Abuse Detection -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1733194929?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Therapeutic+drug+monitoring&rft.atitle=Urine+Mescaline+Screening+With+a+Biochip+Array+Immunoassay+and+Quantification+by+Gas+Chromatography-Mass+Spectrometry.&rft.au=Battal%2C+Dilek%3BBarnes%2C+Allan+J%3BCastaneto%2C+Marisol+S%3BMartin%2C+Thomas+M%3BKlette%2C+Kevin+L%3BHuestis%2C+Marilyn+A&rft.aulast=Battal&rft.aufirst=Dilek&rft.date=2015-12-01&rft.volume=37&rft.issue=6&rft.spage=805&rft.isbn=&rft.btitle=&rft.title=Therapeutic+drug+monitoring&rft.issn=1536-3694&rft_id=info:doi/10.1097%2FFTD.0000000000000220 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-06 N1 - Date created - 2015-11-13 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/FTD.0000000000000220 ER - TY - JOUR T1 - Estimating retrospective exposure of household humidifier disinfectants. AN - 1731783137; 25557769 AB - We conducted a comprehensive humidifier disinfectant exposure characterization for 374 subjects with lung disease who presumed their disease was related to humidifier disinfectant use (patient group) and for 303 of their family members (family group) for an ongoing epidemiological study. We visited the homes of the registered patients to investigate disinfectant use characteristics. Probability of exposure to disinfectants was determined from the questionnaire and supporting evidence from photographs demonstrating the use of humidifier disinfectant, disinfectant purchase receipts, any residual disinfectant, and the consistency of their statements. Exposure duration was estimated as cumulative disinfectant use hours from the questionnaire. Airborne disinfectant exposure intensity (μg/m(3)) was estimated based on the disinfectant volume (ml) and frequency added to the humidifier per day, disinfectant bulk level (μg/ml), the volume of the room (m(3)) with humidifier disinfectant, and the degree of ventilation. Overall, the distribution patterns of the intensity, duration, and cumulative exposure to humidifier disinfectants for the patient group were higher than those of the family group, especially for pregnant women and patients ≤6 years old. Further study is underway to evaluate the association between the disinfectant exposures estimated here with clinically diagnosed lung disease. Retrospective exposure to household humidifier disinfectant as estimated here can be used to evaluate associations with clinically diagnosed lung disease due to the use of humidifier disinfectant in Korea. The framework, with modifications to account for dispersion and use patterns, can also be potentially adapted to assessment of other household chemical exposures. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. JF - Indoor air AU - Park, D U AU - Friesen, M C AU - Roh, H S AU - Choi, Y Y AU - Ahn, J J AU - Lim, H K AU - Kim, S K AU - Koh, D H AU - Jung, H J AU - Lee, J H AU - Cheong, H K AU - Lim, S Y AU - Leem, J H AU - Kim, Y H AU - Paek, D M AD - Department of Environmental Health, Korea National Open University, Seoul, South Korea. ; Division of Cancer Epidemiology and Genetics, Occupational and Environmental Epidemiology Branch, National Cancer Institute, National Institutes of Health, DHHS, Bethesda, MD, USA. ; Data Analytics Team, Tiny Labs, Seoul, South Korea. ; Asian Citizen's Center for Environment and Health, Seoul, South Korea. ; Department of Occupational and Environmental Medicine, International St. Mary's Hospital, Catholic Kwandong University, Incheon, South Korea. ; Institute of Environmental Safety and Protection, NeoEnBiz Co., Bucheon, South Korea. ; Department of Social and Preventive Medicine, Sungkyunkwan University School of Medicine, Suwon, Korea. ; Department of Occupational & Environmental Medicine, College of Medicine, Kyung Hee University, Seoul, Korea. ; Department of Occupational & Environmental Medicine, Inha University Hospital, Incheon, South Korea. ; Korea Institute of Toxicology, Daejeon, South Korea. ; School of Public Health, Seoul National University, Seoul, South Korea. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 631 EP - 640 VL - 25 IS - 6 KW - Disinfectants KW - 0 KW - Index Medicus KW - Humidifier disinfectant KW - Aerosol KW - PHMG KW - PGH KW - Exposure assessment KW - Nano-particle KW - Young Adult KW - Lung Diseases -- etiology KW - Republic of Korea -- epidemiology KW - Humans KW - Retrospective Studies KW - Aged KW - Lung Diseases -- epidemiology KW - Child KW - Pregnancy KW - Child, Preschool KW - Aged, 80 and over KW - Adult KW - Middle Aged KW - Adolescent KW - Female KW - Male KW - Air Pollution, Indoor -- adverse effects KW - Disinfectants -- adverse effects KW - Air Pollution, Indoor -- analysis KW - Humidifiers KW - Disinfectants -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731783137?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Indoor+air&rft.atitle=Estimating+retrospective+exposure+of+household+humidifier+disinfectants.&rft.au=Park%2C+D+U%3BFriesen%2C+M+C%3BRoh%2C+H+S%3BChoi%2C+Y+Y%3BAhn%2C+J+J%3BLim%2C+H+K%3BKim%2C+S+K%3BKoh%2C+D+H%3BJung%2C+H+J%3BLee%2C+J+H%3BCheong%2C+H+K%3BLim%2C+S+Y%3BLeem%2C+J+H%3BKim%2C+Y+H%3BPaek%2C+D+M&rft.aulast=Park&rft.aufirst=D&rft.date=2015-12-01&rft.volume=25&rft.issue=6&rft.spage=631&rft.isbn=&rft.btitle=&rft.title=Indoor+air&rft.issn=1600-0668&rft_id=info:doi/10.1111%2Fina.12180 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-12-13 N1 - Date created - 2015-11-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Sci Total Environ. 1995 Jun 16;168(2):109-17 [7481728] Chest. 1995 Mar;107(3):711-7 [7874942] Am J Ind Med. 1994 Sep;26(3):313-26 [7977405] N Y State J Med. 1990 May;90(5):263-5 [2348946] Am J Epidemiol. 2006 Aug 1;164(3):212-21 [16760223] Environ Health Perspect. 2007 Dec;115(12):1787-93 [18087601] J Environ Public Health. 2013;2013:129470 [23840228] Environ Health Perspect. 2011 Dec;119(12):1760-5 [21813367] PLoS One. 2013;8(6):e64430 [23755124] J Korean Med Sci. 2013 Jun;28(6):915-23 [23772158] J Expo Anal Environ Epidemiol. 2004 Nov;14(6):466-72 [15026776] Thorax. 2014 Aug;69(8):694-702 [24473332] Environ Health. 2014;13:70 [25178403] Environ Health. 2010;9:40 [20646273] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/ina.12180 ER - TY - JOUR T1 - Safety, pharmacokinetics and neutralization of the broadly neutralizing HIV-1 human monoclonal antibody VRC01 in healthy adults. AN - 1730022102; 26332605 AB - VRC-HIVMAB060-00-AB (VRC01) is a broadly neutralizing HIV-1 monoclonal antibody (mAb) isolated from the B cells of an HIV-infected patient. It is directed against the HIV-1 CD4 binding site and is capable of potently neutralizing the majority of diverse HIV-1 strains. This Phase I dose-escalation study in healthy adults was conducted at the National Institutes of Health (NIH) Clinical Center (Bethesda, MD, USA). Primary objectives were the safety, tolerability and pharmacokinetics (PK) of VRC01 intravenous (i.v.) infusion at 5, 20 or 40 mg/kg, given either once (20 mg/kg) or twice 28 days apart (all doses), and of subcutaneous (s.c.) delivery at 5 mg/kg compared to s.c. placebo given twice, 28 days apart. Cumulatively, 28 subjects received 43 VRC01 and nine received placebo administrations. There were no serious adverse events or dose-limiting toxicities. Mean 28-day serum trough concentrations after the first infusion were 35 and 57 μg/ml for groups infused with 20 mg/kg (n = 8) and 40 mg/kg (n = 5) doses, respectively. Mean 28-day trough concentrations after the second infusion were 56 and 89 μg/ml for the same two doses. Over the 5-40 mg/kg i.v. dose range (n = 18), the clearance was 0.016 l/h and terminal half-life was 15 days. After infusion VRC01 retained expected neutralizing activity in serum, and anti-VRC01 antibody responses were not detected. The human monoclonal antibody (mAb) VRC01 was well tolerated when delivered i.v. or s.c. The mAb demonstrated expected half-life and pharmacokinetics for a human immunoglobulin G. The safety and PK results support and inform VRC01 dosing schedules for planning HIV-1 prevention efficacy studies. © 2015 British Society for Immunology. JF - Clinical and experimental immunology AU - Ledgerwood, J E AU - Coates, E E AU - Yamshchikov, G AU - Saunders, J G AU - Holman, L AU - Enama, M E AU - DeZure, A AU - Lynch, R M AU - Gordon, I AU - Plummer, S AU - Hendel, C S AU - Pegu, A AU - Conan-Cibotti, M AU - Sitar, S AU - Bailer, R T AU - Narpala, S AU - McDermott, A AU - Louder, M AU - O'Dell, S AU - Mohan, S AU - Pandey, J P AU - Schwartz, R M AU - Hu, Z AU - Koup, R A AU - Capparelli, E AU - Mascola, J R AU - Graham, B S AU - VRC 602 Study Team AD - Vaccine Research Center (VRC), National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. ; Department of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC, USA. ; Biostatistics Research Branch, Division of Clinical Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. ; School of Medicine and Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego, San Diego, CA, USA. ; VRC 602 Study Team Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 289 EP - 301 VL - 182 IS - 3 KW - Antibodies, Monoclonal KW - 0 KW - Antibodies, Neutralizing KW - HIV Antibodies KW - VRC01 monoclonal antibody KW - Index Medicus KW - Phase I clinical trial KW - passive immunization KW - pharmacokinetics KW - HIV-1 KW - monoclonal antibody KW - Half-Life KW - Dose-Response Relationship, Drug KW - Humans KW - Adult KW - Middle Aged KW - Adolescent KW - Male KW - Female KW - Antibodies, Neutralizing -- administration & dosage KW - HIV Infections -- blood KW - Antibodies, Monoclonal -- pharmacokinetics KW - HIV Antibodies -- administration & dosage KW - HIV Infections -- drug therapy KW - Antibodies, Neutralizing -- adverse effects KW - Antibodies, Monoclonal -- adverse effects KW - Antibodies, Monoclonal -- administration & dosage KW - HIV Antibodies -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1730022102?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+and+experimental+immunology&rft.atitle=Safety%2C+pharmacokinetics+and+neutralization+of+the+broadly+neutralizing+HIV-1+human+monoclonal+antibody+VRC01+in+healthy+adults.&rft.au=Ledgerwood%2C+J+E%3BCoates%2C+E+E%3BYamshchikov%2C+G%3BSaunders%2C+J+G%3BHolman%2C+L%3BEnama%2C+M+E%3BDeZure%2C+A%3BLynch%2C+R+M%3BGordon%2C+I%3BPlummer%2C+S%3BHendel%2C+C+S%3BPegu%2C+A%3BConan-Cibotti%2C+M%3BSitar%2C+S%3BBailer%2C+R+T%3BNarpala%2C+S%3BMcDermott%2C+A%3BLouder%2C+M%3BO%27Dell%2C+S%3BMohan%2C+S%3BPandey%2C+J+P%3BSchwartz%2C+R+M%3BHu%2C+Z%3BKoup%2C+R+A%3BCapparelli%2C+E%3BMascola%2C+J+R%3BGraham%2C+B+S%3BVRC+602+Study+Team&rft.aulast=Ledgerwood&rft.aufirst=J&rft.date=2015-12-01&rft.volume=182&rft.issue=3&rft.spage=289&rft.isbn=&rft.btitle=&rft.title=Clinical+and+experimental+immunology&rft.issn=1365-2249&rft_id=info:doi/10.1111%2Fcei.12692 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-18 N1 - Date created - 2015-11-03 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT01993706; ClinicalTrials.gov N1 - SuppNotes - Cited By: Pediatrics. 1998 Sep;102(3 Pt 1):531-7 [9738173] Blood. 1990 Aug 15;76(4):849-52 [2383661] Science. 1963 Feb 1;139(3553):418-9 [14012122] Science. 1964 Jul 10;145(3628):170-1 [14171557] J Virol. 2004 Dec;78(23):13232-52 [15542675] Science. 2012 Jul 13;337(6091):183-6 [22798606] Proc Natl Acad Sci U S A. 2012 Jul 24;109(30):E2083-90 [22745174] Immunity. 2012 Sep 21;37(3):412-25 [22999947] Immunol Rev. 2012 Nov;250(1):180-98 [23046130] AIDS. 2013 Jan 28;27(3):337-46 [23296195] AIDS Res Hum Retroviruses. 2013 Mar;29(3):511-5 [23075434] Nat Rev Immunol. 2013 Sep;13(9):693-701 [23969737] Immunity. 2013 Aug 22;39(2):245-58 [23911655] PLoS Med. 2014 Apr;11(4):e1001616 [24714363] Sci Transl Med. 2014 Jul 2;6(243):243ra88 [24990883] J Immunol Methods. 2014 Jul;409:131-46 [24291345] J Virol. 2014 Nov;88(21):12669-82 [25142607] J Virol. 2015 Apr;89(8):4201-13 [25631091] Cell. 2015 Apr 23;161(3):470-85 [25865483] Nature. 2015 Jun 25;522(7557):487-91 [25855300] Nat Med. 2005 Jun;11(6):615-22 [15880120] J Virol. 2005 Aug;79(16):10103-7 [16051803] J Virol. 2005 Aug;79(16):10108-25 [16051804] Proc Natl Acad Sci U S A. 2005 Oct 18;102(42):14943-8 [16219699] Annu Rev Immunol. 2006;24:739-69 [16551265] Nat Med. 2007 Sep;13(9):1032-4 [17721546] J Immunol Methods. 2008 Jan 1;329(1-2):112-24 [17996249] Nature. 2008 May 29;453(7195):667-71 [18449194] J Virol. 2008 Dec;82(23):11651-68 [18815292] J Virol. 2009 Jul;83(14):7337-48 [19439467] MAbs. 2009 Jul-Aug;1(4):332-8 [20073133] Annu Rev Immunol. 2010;28:413-44 [20192810] Science. 2010 Aug 13;329(5993):811-7 [20616231] Science. 2010 Aug 13;329(5993):856-61 [20616233] Immunity. 2010 Oct 29;33(4):542-54 [21029964] J Virol. 2011 Sep;85(17):8954-67 [21715490] Science. 2011 Sep 16;333(6049):1633-7 [21764753] Science. 2011 Sep 16;333(6049):1593-602 [21835983] Cold Spring Harb Perspect Med. 2012 Jan;2(1):a007039 [22315717] J Virol. 2012 May;86(10):5844-56 [22419808] AIDS. 2002 Oct 18;16(15):2019-25 [12370500] Pediatr Infect Dis J. 2001 Jun;20(6):628-30 [11419509] Clin Infect Dis. 2012 Jun;54(11):1615-7 [22437237] J Antimicrob Chemother. 2004 Nov;54(5):915-20 [15456731] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/cei.12692 ER - TY - JOUR T1 - PTEN expression in benign human endometrial tissue and cancer in relation to endometrial cancer risk factors. AN - 1728674418; 26376893 AB - Clonal loss of PTEN expression occurs frequently in endometrial carcinoma and endometrial hyperplasia. Limited data from immunohistochemical studies suggest that PTEN-null appearing endometrial glands are detectable in women without pathologic abnormalities, but the relationship of PTEN expression to endometrial cancer risk factors has not been extensively explored. We evaluated relationships between endometrial cancer risk factors and loss of PTEN expression in a set of benign endometrial samples prospectively collected from women undergoing hysterectomy and in endometrial cancer tissues from a population-based case-control study. We used a validated PTEN immunohistochemical assay to assess expression in epidemiological studies designed to assess benign endometrium [Benign Reproductive Tissue Evaluation Study (n = 73); Einstein Endometrium Study (n = 19)], and endometrial cancer [Polish Endometrial Cancer Study (n = 148)] tissues. Associations between endometrial cancer risk factors (collected via study-specific risk factor questionnaires) and PTEN expression in endometrial tissues were determined using Fisher's exact tests. PTEN loss was detected in 19% of benign endometrial tissues versus 55% in endometrial cancers. NSAID use was statistically significantly associated with PTEN loss in the benign endometrium (p = 0.02). Our data demonstrate that PTEN loss is detectable in endometrial tissues that are benign and malignant, with substantially more frequent loss in endometrial cancer compared with benign endometrium. However, alterations in expression were unrelated to most risk factors in this analysis, except for the association with NSAID use, which may represent a chance finding or reverse causality among patients with endometriosis who may have PTEN pathway abnormalities in eutopic endometrium. Further evaluation of factors associated with PTEN loss and long-term follow-up of women with PTEN-null endometrial glands may be useful in understanding early events in endometrial carcinogenesis. JF - Cancer causes & control : CCC AU - Yang, Hannah P AU - Meeker, Alan AU - Guido, Richard AU - Gunter, Marc J AU - Huang, Gloria S AU - Luhn, Patricia AU - d'Ambrosio, Lori AU - Wentzensen, Nicolas AU - Sherman, Mark E AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Room #7E238, Bethesda, MD, 20892-9774, USA. yanghan@mail.nih.gov. ; Johns Hopkins University, Baltimore, MD, USA. ; Magee Women's Hospital of the UPMC System, Pittsburgh, PA, USA. ; Imperial College London, London, UK. ; Obstetrics and Gynecology and Women's Health; and Molecular Pharmacology, Albert Einstein Cancer Center, Albert Einstein College of Medicine and Montefiore Medical Center, Bronx, NY, USA. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Room #7E238, Bethesda, MD, 20892-9774, USA. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1729 EP - 1736 VL - 26 IS - 12 KW - PTEN Phosphohydrolase KW - EC 3.1.3.67 KW - PTEN protein, human KW - Index Medicus KW - Risk factors KW - Endometrial cancer KW - PTEN KW - Risk Factors KW - Humans KW - Adult KW - Case-Control Studies KW - Aged KW - Middle Aged KW - Female KW - Endometrial Neoplasms -- pathology KW - PTEN Phosphohydrolase -- genetics KW - Endometrium -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1728674418?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+causes+%26+control+%3A+CCC&rft.atitle=PTEN+expression+in+benign+human+endometrial+tissue+and+cancer+in+relation+to+endometrial+cancer+risk+factors.&rft.au=Yang%2C+Hannah+P%3BMeeker%2C+Alan%3BGuido%2C+Richard%3BGunter%2C+Marc+J%3BHuang%2C+Gloria+S%3BLuhn%2C+Patricia%3Bd%27Ambrosio%2C+Lori%3BWentzensen%2C+Nicolas%3BSherman%2C+Mark+E&rft.aulast=Yang&rft.aufirst=Hannah&rft.date=2015-12-01&rft.volume=26&rft.issue=12&rft.spage=1729&rft.isbn=&rft.btitle=&rft.title=Cancer+causes+%26+control+%3A+CCC&rft.issn=1573-7225&rft_id=info:doi/10.1007%2Fs10552-015-0666-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-08 N1 - Date created - 2015-10-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Lancet Oncol. 2012 Apr;13(4):385-94 [22361336] Med Oncol. 2012 Mar;29(1):304-10 [21181309] Cancer Epidemiol Biomarkers Prev. 2012 Sep;21(9):1441-9 [22665579] Mod Pathol. 2012 Nov;25(11):1508-15 [22766795] Int J Cancer. 2013 Mar 1;132(5):1146-55 [22777678] Gynecol Oncol. 2013 Jan;128(1):113-9 [23063765] Histopathology. 2013 Jan;62(1):111-23 [23240673] Hum Reprod. 2014 Feb;29(2):324-36 [24154570] Int J Cancer. 2014 Oct 15;135(8):1860-8 [24623538] J Natl Cancer Inst. 2000 Jun 7;92(11):924-30 [10841828] Cancer Res. 2000 Jul 1;60(13):3605-11 [10910075] Cancer Res. 2001 Jun 1;61(11):4311-4 [11389050] Am J Pathol. 2002 Apr;160(4):1481-6 [11943731] J Clin Oncol. 2004 Jul 15;22(14):2954-63 [15254063] Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1563-8 [9990064] Br J Cancer. 2007 May 7;96(9):1450-6 [17426703] Appl Immunohistochem Mol Morphol. 2008 Jul;16(4):329-43 [18528284] Cancer Res. 2008 Jul 15;68(14):6014-20 [18632658] N Engl J Med. 2009 Jan 15;360(3):268-79 [19144942] Cancer. 2009 May 15;115(10):2111-8 [19280590] Maturitas. 2009 May 20;63(1):39-44 [19285814] Hum Reprod. 2009 Aug;24(8):1880-90 [19429661] Clin Cancer Res. 2010 Sep 1;16(17):4325-30 [20622047] Nat Rev Cancer. 2011 Apr;11(4):289-301 [21430697] Clin Cancer Res. 2011 Oct 15;17(20):6563-73 [21878536] Hematol Oncol Clin North Am. 2012 Feb;26(1):1-12 [22244658] Mod Pathol. 2012 May;25(5):699-708 [22301702] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s10552-015-0666-5 ER - TY - JOUR T1 - Differential and Concordant Roles for Poly(ADP-Ribose) Polymerase 1 and Poly(ADP-Ribose) in Regulating WRN and RECQL5 Activities. AN - 1728670246; 26391948 AB - Poly(ADP-ribose) (PAR) polymerase 1 (PARP1) catalyzes the poly(ADP-ribosyl)ation (PARylation) of proteins, a posttranslational modification which forms the nucleic acid-like polymer PAR. PARP1 and PAR are integral players in the early DNA damage response, since PARylation orchestrates the recruitment of repair proteins to sites of damage. Human RecQ helicases are DNA unwinding proteins that are critical responders to DNA damage, but how their recruitment and activities are regulated by PARPs and PAR is poorly understood. Here we report that all human RecQ helicases interact with PAR noncovalently. Furthermore, we define the effects that PARP1, PARylated PARP1, and PAR have on RECQL5 and WRN, using both in vitro and in vivo assays. We show that PARylation is involved in the recruitment of RECQL5 and WRN to laser-induced DNA damage and that RECQL5 and WRN have differential responses to PARylated PARP1 and PAR. Furthermore, we show that the loss of RECQL5 or WRN resulted in increased sensitivity to PARP inhibition. In conclusion, our results demonstrate that PARP1 and PAR actively, and in some instances differentially, regulate the activities and cellular localization of RECQL5 and WRN, suggesting that PARylation acts as a fine-tuning mechanism to coordinate their functions in time and space during the genotoxic stress response. Copyright © 2015, American Society for Microbiology. All Rights Reserved. JF - Molecular and cellular biology AU - Khadka, Prabhat AU - Hsu, Joseph K AU - Veith, Sebastian AU - Tadokoro, Takashi AU - Shamanna, Raghavendra A AU - Mangerich, Aswin AU - Croteau, Deborah L AU - Bohr, Vilhelm A AD - Laboratory of Molecular Gerontology, Biomedical Research Center, National Institute on Aging, NIH, Baltimore, Maryland, USA. ; Molecular Toxicology Group, Department of Biology, University of Konstanz, Konstanz, Germany. ; Laboratory of Molecular Gerontology, Biomedical Research Center, National Institute on Aging, NIH, Baltimore, Maryland, USA vbohr@nih.gov. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 3974 EP - 3989 VL - 35 IS - 23 KW - Poly(ADP-ribose) Polymerase Inhibitors KW - 0 KW - RECQL5 protein, human KW - Poly Adenosine Diphosphate Ribose KW - 26656-46-2 KW - PARP1 protein, human KW - EC 2.4.2.30 KW - Poly (ADP-Ribose) Polymerase-1 KW - Poly(ADP-ribose) Polymerases KW - Exodeoxyribonucleases KW - EC 3.1.- KW - Adenosine Triphosphatases KW - EC 3.6.1.- KW - RecQ Helicases KW - EC 3.6.4.12 KW - WRN protein, human KW - Werner Syndrome Helicase KW - Index Medicus KW - DNA Repair KW - HeLa Cells KW - Poly(ADP-ribose) Polymerase Inhibitors -- pharmacology KW - Humans KW - HEK293 Cells KW - Enzyme Activation -- drug effects KW - Adenosine Triphosphatases -- metabolism KW - DNA Breaks, Double-Stranded KW - Protein Interaction Maps KW - RecQ Helicases -- metabolism KW - Poly(ADP-ribose) Polymerases -- metabolism KW - Poly Adenosine Diphosphate Ribose -- metabolism KW - Exodeoxyribonucleases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1728670246?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biology&rft.atitle=Differential+and+Concordant+Roles+for+Poly%28ADP-Ribose%29+Polymerase+1+and+Poly%28ADP-Ribose%29+in+Regulating+WRN+and+RECQL5+Activities.&rft.au=Khadka%2C+Prabhat%3BHsu%2C+Joseph+K%3BVeith%2C+Sebastian%3BTadokoro%2C+Takashi%3BShamanna%2C+Raghavendra+A%3BMangerich%2C+Aswin%3BCroteau%2C+Deborah+L%3BBohr%2C+Vilhelm+A&rft.aulast=Khadka&rft.aufirst=Prabhat&rft.date=2015-12-01&rft.volume=35&rft.issue=23&rft.spage=3974&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biology&rft.issn=1098-5549&rft_id=info:doi/10.1128%2FMCB.00427-15 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-16 N1 - Date created - 2015-10-31 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Struct Mol Biol. 2013 Mar;20(3):347-54 [23396353] J Biol Chem. 2000 Dec 29;275(52):40974-80 [11016934] Nat Struct Mol Biol. 2013 Apr;20(4):502-7 [23474714] Cancer Cell. 2013 May 13;23(5):693-704 [23680151] DNA Repair (Amst). 2013 Jun 1;12(6):414-21 [23583337] Nat Rev Cancer. 2013 Aug;13(8):542-58 [23842644] Nat Commun. 2013;4:2164 [23917065] Genes Dev. 2013 Aug 15;27(16):1752-68 [23964092] Exp Cell Res. 2004 Jul 15;297(2):521-32 [15212953] Am J Pathol. 2003 May;162(5):1559-69 [12707040] J Mol Biol. 2003 Jun 27;330(1):29-42 [12818200] Aging Cell. 2003 Aug;2(4):191-9 [12934712] FEBS Lett. 2003 Nov 6;554(1-2):55-8 [14596914] Annu Rev Biochem. 2004;73:39-85 [15189136] FEBS J. 2013 Aug;280(15):3491-507 [23711178] EMBO J. 2004 Jul 21;23(14):2882-91 [15241474] Nucleic Acids Res. 2004;32(13):4003-14 [15292449] Mol Cell Biol. 2004 Nov;24(21):9305-16 [15485900] Biochemistry. 1984 Jul 31;23(16):3771-7 [6206890] Nucleic Acids Res. 1999 Sep 1;27(17):3557-66 [10446247] Nature. 2005 Apr 14;434(7035):917-21 [15829967] Genes Dev. 2005 Sep 1;19(17):1951-67 [16140981] Exp Cell Res. 2006 Oct 15;312(17):3443-57 [16949575] J Biol Chem. 2007 Jun 1;282(22):16441-53 [17428792] Genes Dev. 2007 Dec 1;21(23):3073-84 [18003859] Nucleic Acids Res. 2007;35(21):e143 [17991682] Nature. 2008 Jan 3;451(7174):81-5 [18172500] J Biol Chem. 2008 Jan 11;283(2):1197-208 [18025084] Mol Cell Biol. 2008 Jan;28(2):814-24 [17991898] Cell Cycle. 2008 Sep 15;7(18):2902-6 [18769152] EMBO J. 2009 Mar 4;28(5):568-77 [19177149] Nucleic Acids Res. 2009 May;37(8):2645-57 [19270065] Nat Rev Cancer. 2010 Apr;10(4):293-301 [20200537] Mol Cell Biol. 2010 May;30(10):2460-72 [20231364] DNA Repair (Amst). 2010 Jul 1;9(7):796-804 [20451470] Aging Cell. 2010 Jun;9(3):358-71 [20222902] Carcinogenesis. 2010 Dec;31(12):2058-65 [20926829] DNA Repair (Amst). 2011 Jan 2;10(1):73-86 [20970388] Genes Dev. 2011 Mar 1;25(5):409-33 [21363960] Methods Mol Biol. 2011;780:67-82 [21870255] Mol Cell Biol. 2011 Dec;31(23):4832-43 [21969602] Nature. 2012 Jan 19;481(7381):287-94 [22258607] Genes Dev. 2012 Feb 1;26(3):235-40 [22267412] DNA Repair (Amst). 2012 Jul 1;11(7):624-35 [22633600] Nat Rev Mol Cell Biol. 2012 Jul;13(7):411-24 [22713970] J Biol Chem. 2012 Jul 6;287(28):23808-18 [22645136] Aging (Albany NY). 2012 Jun;4(6):417-29 [22713343] Nat Rev Cancer. 2012 Sep;12(9):587-98 [22918414] Oxid Med Cell Longev. 2012;2012:321653 [23050038] Mol Biol Cell. 2012 Nov;23(21):4273-85 [22973052] Cancer Res. 2012 Nov 1;72(21):5588-99 [23118055] ACS Chem Biol. 2013 Jan 18;8(1):179-88 [23082994] Nucleic Acids Res. 2013 Jan;41(2):881-99 [23180761] Mol Aspects Med. 2013 Dec;34(6):1066-87 [23268355] Nucleic Acids Res. 2014 Feb;42(4):2380-90 [24319145] Annu Rev Biochem. 2014;83:519-52 [24606147] Ageing Res Rev. 2015 Sep;23(Pt A):12-28 [25555679] Nat Struct Mol Biol. 2013 Apr;20(4):508-14 [23474712] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/MCB.00427-15 ER - TY - JOUR T1 - Comparative Toxicity by Sex Among Children Treated for Acute Lymphoblastic Leukemia: A Report From the Children's Oncology Group. AN - 1727996039; 26173904 AB - Epidemiologic studies find sex-based differences in incidence, survival, and long-term outcomes for children with cancer. The purpose of this study was to determine whether male and female patients differ with regard to acute treatment-related toxicities. We reviewed data collected on the Children's cancer group (CCG) high-risk acute lymphoblastic leukemia (ALL-HR) study (CCG-1961), and compared male and female patients' toxicity incidence and related variables in the first four phases of treatment. Similar analyses were performed with standard-risk ALL (ALL-SR) patients enrolled in CCG-1991. Among ALL-HR patients, females had significantly more hospital days, delays in therapy, grade 3 or 4 toxicities (e.g., gastrointestinal, liver), and supportive care interventions (e.g., transfusions, intravenous antibiotics) than males. Females were significantly more likely to have died of treatment-related causes than males (Hazard ratio = 2.8, 95%CI = 1.5-5.3, P = 0.002). Five months after beginning the treatment, the cumulative incidence of treatment-related deaths was 2.6% for females and 1.2% for males. Similar disparities were found among ALL-SR patients, with females experiencing significantly more hospital days and treatment-related toxicities than males. This study complements cancer survivorship studies that also report an increase in treatment-related late effects among females. Risk profiles appear to be different for male and female patients, with females having greater risk of developing both acute and long-term treatment-related toxicities. The underlying biological mechanisms for these sex differences are poorly understood and warrant further study in order to determine how sex-based outcome disparities can be addressed in future clinical trials and practice. © 2015 Wiley Periodicals, Inc. JF - Pediatric blood & cancer AU - Meeske, Kathleen A AU - Ji, Lingyun AU - Freyer, David R AU - Gaynon, Paul AU - Ruccione, Kathleen AU - Butturini, Anna AU - Avramis, Vassilios I AU - Siegel, Stuart AU - Matloub, Yousif AU - Seibel, Nita L AU - Sposto, Richard AD - Children's Center for Cancer and Blood Diseases, Children's Hospital Los Angeles, Los Angeles, California. ; Department of Preventive Medicine, Keck School of Medicine, University of Southern California, Los Angeles, California. ; Agensys, Inc., Santa Monica, California. ; Division of Hematology-Oncology, Rainbow Babies & Children's Hospital, Case Western Reserve University, Cleveland, Ohio. ; Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, Maryland. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 2140 EP - 2149 VL - 62 IS - 12 KW - Index Medicus KW - sex KW - acute lymphoblastic leukemia KW - acute toxicities KW - pediatric oncology KW - disparities KW - Infant KW - Disease-Free Survival KW - Survival Rate KW - Humans KW - Adult KW - Retrospective Studies KW - Follow-Up Studies KW - Child KW - Adolescent KW - Male KW - Female KW - Child, Preschool KW - Sex Characteristics KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- therapy KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727996039?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pediatric+blood+%26+cancer&rft.atitle=Comparative+Toxicity+by+Sex+Among+Children+Treated+for+Acute+Lymphoblastic+Leukemia%3A+A+Report+From+the+Children%27s+Oncology+Group.&rft.au=Meeske%2C+Kathleen+A%3BJi%2C+Lingyun%3BFreyer%2C+David+R%3BGaynon%2C+Paul%3BRuccione%2C+Kathleen%3BButturini%2C+Anna%3BAvramis%2C+Vassilios+I%3BSiegel%2C+Stuart%3BMatloub%2C+Yousif%3BSeibel%2C+Nita+L%3BSposto%2C+Richard&rft.aulast=Meeske&rft.aufirst=Kathleen&rft.date=2015-12-01&rft.volume=62&rft.issue=12&rft.spage=2140&rft.isbn=&rft.btitle=&rft.title=Pediatric+blood+%26+cancer&rft.issn=1545-5017&rft_id=info:doi/10.1002%2Fpbc.25628 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-08 N1 - Date created - 2015-10-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: JAMA. 2001 Mar 14;285(10):1322-6 [11255387] J Gen Intern Med. 2001 Apr;16(4):266-75 [11318929] Invest New Drugs. 2001 May;19(2):171-7 [11392451] J Clin Oncol. 2001 Jul 1;19(13):3163-72 [11432882] Int J Toxicol. 2001 May-Jun;20(3):149-52 [11488556] J Womens Health Gend Based Med. 2002 Sep;11(7):617-29 [12396894] Int J Food Sci Nutr. 2003 Nov;54(6):467-71 [14522692] Ann Hematol. 2004 Mar;83(3):176-82 [15064867] J Pediatr Hematol Oncol. 2004 Apr;26(4):217-26 [15087948] Br J Cancer. 2004 Oct 4;91(7):1229-35 [15305188] Am J Physiol. 1984 Oct;247(4 Pt 2):F632-6 [6496691] J Clin Oncol. 1992 Jul;10(7):1171-5 [1607921] J Adolesc Health. 1994 Dec;15(8):619-29 [7696281] N Engl J Med. 1995 Jun 29;332(26):1738-43 [7760889] Cancer Chemother Pharmacol. 1995;36(6):473-6 [7554038] Leukemia. 2009 Jul;23(7):1264-9 [19212332] J Clin Oncol. 2010 Mar 1;28(7):1224-31 [20124180] Trends Pharmacol Sci. 2010 Mar;31(3):108-14 [20117848] Lancet Oncol. 2010 Oct;11(10):950-61 [20850381] Pediatr Blood Cancer. 2011 Apr;56(4):551-9 [21298739] Pediatr Cardiol. 2011 Mar;32(3):342-53 [21221562] Blood. 2011 Jul 14;118(2):243-51 [21562038] Expert Rev Clin Pharmacol. 2011 Jul;4(4):453-66 [22114855] Br J Clin Pharmacol. 2012 Jan;73(1):106-14 [21707700] J Autoimmun. 2012 May;38(2-3):J282-91 [22225601] Pediatr Blood Cancer. 2012 Oct;59(4):611-6 [22180320] Pediatrics. 2013 Jan;131(1):e273-87 [23266919] Drugs. 1995 Jul;50(1):1-6 [7588082] J Clin Oncol. 1996 Jan;14(1):18-24 [8558195] Arch Dis Child. 1996 Feb;74(2):101-7 [8660070] Br J Clin Pharmacol. 1998 Nov;46(5):447-52 [9833597] J Womens Health (Larchmt). 2005 Jan-Feb;14(1):19-29 [15692274] Pharmacol Res. 2007 Feb;55(2):81-95 [17129734] J Clin Oncol. 2007 Oct 1;25(28):4477-89 [17906209] Blood. 2008 Mar 1;111(5):2548-55 [18039957] Int Rev Neurobiol. 2008;83:1-10 [18929073] Nat Rev Immunol. 2008 Sep;8(9):737-44 [18728636] Clin Pharmacokinet. 2009;48(3):143-57 [19385708] Int J Cancer. 2009 Jul 15;125(2):426-31 [19391136] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/pbc.25628 ER - TY - JOUR T1 - Early and delayed intervention with rapamycin prevents NNK-induced lung adenocarcinoma in A/J mice. AN - 1727994767; 26397133 AB - In tobacco-associated lung cancers, the protein kinase B/mammalian target of rapamycin (Akt/mTOR) pathway frequently is activated by nicotine and its metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). The aim of the present study was to examine the effects of early or late intervention with rapamycin in NNK-induced lung adenoma and progression to adenocarcinoma in female A/J mice. At 7 weeks of age, 40 mice/each carcinogen group received one dose of 10 μmol NNK i.p. Three weeks later, the early intervention groups (25/group) were fed diets containing 0, 8 or 16 ppm rapamycin. The mice were sacrificed after 17 or 34 weeks of drug exposure and tumors were evaluated via histopathology. For late intervention (late adenoma and adenocarcinoma stage), groups of 15 mice were administered diets containing 8 or 16 ppm rapamycin starting 20 weeks after NNK treatment and continuing for 17 weeks before evaluation of tumor progression. Administration of 8 or 16 ppm rapamycin as an early or a late stage intervention significantly suppressed lung adenoma and adenocarcinoma formation (p50‑60% tumor inihibition; p2.10 to <~0.75 mm3 (p=0.0056). Lung tumors harvested from mice exposed to rapamycin showed a significant decrease in p-mTOR, p-S6K1, PCNA and Bcl-xL as compared with controls in the early and late stage intervention studies. These observations suggest that rapamycin is highly effective even with administration after dysplastic adenoma or early adenocarcinoma stages and is useful for high-risk lung cancer patients. JF - Oncology reports AU - Patlolla, Jagan M R AU - Kopelovich, Levy AU - Qian, Li AU - Zhang, Yuting AU - Kumar, Gaurav AU - Madka, Venkateshwar AU - Mohammed, Altaf AU - Biddick, Laura AU - Sadeghi, Michael AU - Lightfoot, Stan AU - Rao, Chinthalapally V AD - Center for Chemoprevention and Cancer Drug Development, Department of Medicine, Hem-Onc Section, PCS Oklahoma Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA. ; Chemopreventive Agent Development Research Group, Division of Cancer Prevention, National Cancer Institute, Bethesda, MD 20892-9788, USA. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 2925 EP - 2934 VL - 34 IS - 6 KW - Bcl2l1 protein, mouse KW - 0 KW - Carcinogens KW - Nitrosamines KW - Proliferating Cell Nuclear Antigen KW - bcl-X Protein KW - Nicotine KW - 6M3C89ZY6R KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone KW - 7S395EDO61 KW - MTOR protein, human KW - EC 2.7.1.1 KW - TOR Serine-Threonine Kinases KW - Ribosomal Protein S6 Kinases, 90-kDa KW - EC 2.7.11.1 KW - Rps6ka1 protein, mouse KW - Sirolimus KW - W36ZG6FT64 KW - Index Medicus KW - TOR Serine-Threonine Kinases -- biosynthesis KW - Nitrosamines -- toxicity KW - Animals KW - bcl-X Protein -- biosynthesis KW - Ribosomal Protein S6 Kinases, 90-kDa -- biosynthesis KW - Humans KW - Nicotine -- adverse effects KW - Disease Progression KW - Carcinogens -- toxicity KW - Mice KW - Female KW - Proliferating Cell Nuclear Antigen -- biosynthesis KW - Sirolimus -- administration & dosage KW - Adenocarcinoma -- chemically induced KW - Lung Neoplasms -- drug therapy KW - Lung Neoplasms -- genetics KW - Adenocarcinoma -- genetics KW - Tobacco -- adverse effects KW - Lung Neoplasms -- chemically induced KW - Adenocarcinoma -- drug therapy KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Lung Neoplasms -- pathology KW - Adenocarcinoma -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727994767?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncology+reports&rft.atitle=Early+and+delayed+intervention+with+rapamycin+prevents+NNK-induced+lung+adenocarcinoma+in+A%2FJ+mice.&rft.au=Patlolla%2C+Jagan+M+R%3BKopelovich%2C+Levy%3BQian%2C+Li%3BZhang%2C+Yuting%3BKumar%2C+Gaurav%3BMadka%2C+Venkateshwar%3BMohammed%2C+Altaf%3BBiddick%2C+Laura%3BSadeghi%2C+Michael%3BLightfoot%2C+Stan%3BRao%2C+Chinthalapally+V&rft.aulast=Patlolla&rft.aufirst=Jagan+M&rft.date=2015-12-01&rft.volume=34&rft.issue=6&rft.spage=2925&rft.isbn=&rft.btitle=&rft.title=Oncology+reports&rft.issn=1791-2431&rft_id=info:doi/10.3892%2For.2015.4277 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-08 N1 - Date created - 2015-10-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Rev Cancer. 2004 May;4(5):335-48 [15122205] J Clin Oncol. 2006 Jan 10;24(2):306-14 [16330671] Neoplasia. 2006 Jan;8(1):52-8 [16533426] Int J Cancer. 2006 Oct 1;119(7):1547-52 [16671086] Clin Cancer Res. 2007 Apr 1;13(7):2281-9 [17404113] J Biol Chem. 2007 Apr 27;282(17):13123-32 [17337444] EMBO J. 2007 May 16;26(10):2527-39 [17446862] Science. 2007 Nov 9;318(5852):977-80 [17991864] Apoptosis. 2008 Jan;13(1):1-9 [17990121] J Cell Biol. 2008 Oct 6;183(1):101-16 [18838554] Nat Rev Cancer. 2009 Jul;9(7):476-88 [19550424] Nature. 2009 Jul 16;460(7253):392-5 [19587680] Clin Cancer Res. 2010 Jan 1;16(1):4-10 [20028747] J Biol Chem. 2010 Mar 19;285(12):8621-7 [20048149] J Biol Chem. 2010 May 7;285(19):14071-7 [20231296] Science. 2010 May 28;328(5982):1172-6 [20508131] Nat Cell Biol. 2010 Sep;12(9):831-5 [20811355] Oncotarget. 2010 Nov;1(7):530-43 [21317449] Science. 2011 Jun 10;332(6035):1317-22 [21659604] Cancer Res. 2011 Jul 15;71(14):4955-67 [21622715] Mol Biol Rep. 2012 Jan;39(1):259-67 [21556768] Free Radic Biol Med. 2012 Sep 15;53(6):1358-70 [22841871] J Environ Pathol Toxicol Oncol. 2012;31(4):295-312 [23394443] Mol Med Rep. 2013 May;7(5):1501-5 [23525201] CA Cancer J Clin. 2015 Jan-Feb;65(1):5-29 [25559415] Adv Cancer Res. 2000;78:199-334 [10547671] Cancer Res. 2000 Jul 1;60(13):3504-13 [10910062] Cancer Epidemiol Biomarkers Prev. 2001 Apr;10(4):311-8 [11319170] Cancer Metastasis Rev. 2004 Aug-Dec;23(3-4):367-87 [15197336] J Cell Biochem Suppl. 1993;17F:95-103 [8412213] Carcinogenesis. 2004 Nov;25(11):2053-9 [15240509] Carcinogenesis. 2005 Jul;26(7):1182-95 [15790591] Cancer Res. 2005 Aug 15;65(16):7052-8 [16103051] Cell. 2005 Sep 23;122(6):927-39 [16179260] Oncogene. 2005 Nov 14;24(50):7455-64 [16288292] Cancer Res. 2006 Jan 1;66(1):315-23 [16397245] Cell. 2002 Jan 25;108(2):153-64 [11832206] Cell. 2002 Jul 26;110(2):163-75 [12150925] J Cell Biol. 2002 Oct 28;159(2):217-24 [12403809] J Clin Invest. 2003 Jan;111(1):81-90 [12511591] Nat Cell Biol. 2003 Jan;5(1):28-37 [12510191] J Natl Cancer Inst. 2003 Feb 19;95(4):291-302 [12591985] Cancer Res. 2004 Jan 15;64(2):446-51 [14744754] Br J Cancer. 2004 Mar 8;90(5):1047-52 [14997206] Cancer Res. 2004 Apr 1;64(7):2307-16 [15059877] Oncogene. 2004 Apr 19;23(18):3151-71 [15094765] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3892/or.2015.4277 ER - TY - JOUR T1 - Oxaliplatin/5-fluorouracil-based adjuvant chemotherapy as a standard of care for colon cancer in clinical practice: Outcomes of the ACCElox registry. AN - 1727436623; 26471890 AB - The ACCElox registry was set up to assess therapeutic management of early-stage colon cancer with oxaliplatin/5-fluorouracil (5-FU)-based regimen and the duration of adjuvant chemotherapy in current clinical practice. This prospective observational study was conducted between 2006 and 2008 in 19 countries on 1548 newly diagnosed patients with stage II/III colon cancer, who had complete resection of the primary tumor and treated with at least one dose of oxaliplatin. The patient/disease characteristics, dose intensity, toxicity management, treatment delay and duration of disease-free survival (DFS)/relapse were assessed. About 73 and 27% of the patients were diagnosed with stage III (Dukes C) and stage II (Dukes B2) colon cancer, respectively. Overall, 74.4% patients completed the prescribed chemotherapy (FOLFOX 88%) and 97.6% patients received at least two cycles of oxaliplatin chemotherapy. The median actual dose intensity of oxaliplatin per cycle was 85 mg/m(2) . Relapse within 3 years occurred in 18.4% of patients with similar rate in all three groups (FOLFOX - 18.1%, FLOX - 19%, XELOX - 18.6%). At 3 years follow-up only 72 deaths were reported. The most common adverse events (AEs) at any cycle were neutropenia (63.9%), thrombocytopenia (23.3%), diarrhea (9.7%), sensory neuropathy (4.5%) and infection (2.6%). Disorders of central and peripheral nervous systems were frequently reported AEs at 6 months (54.3%, grade ≥1) and 12 months (36.4%, grade ≥1) of follow-up. Majority of the patients completed the prescribed oxaliplatin/5-FU regimen. There was no significant difference in the DFS among these regimens. Our results confirm the favorable benefit/risk profile of oxaliplatin/5-FU-based regimens in this setting in clinical practice. © 2015 Wiley Publishing Asia Pty Ltd. JF - Asia-Pacific journal of clinical oncology AU - Park, Young Suk AU - Ji, Jiafu AU - Zalcberg, John Raymond AU - El-Serafi, Mostafa AU - Buzaid, Antonio AU - Ghosn, Marwan AD - Samsung Medical Centre, Sungkyunkwan University School of Medicine, Seoul, South Korea. ; Beijing Cancer Hospital, Beijing, China. ; Peter MacCallum Cancer Centre, Melbourne, Victoria, Australia. ; National Cancer Institute, University of Cairo, Giza, Egypt. ; Hospital Sirio Libanes, São Paulo, Brazil. ; Hotel-Dieu de France Hospital, Beirut, Lebanon. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 334 EP - 342 VL - 11 IS - 4 KW - Organoplatinum Compounds KW - 0 KW - oxaliplatin KW - 04ZR38536J KW - Fluorouracil KW - U3P01618RT KW - Index Medicus KW - thrombocytopenia KW - adjuvant chemotherapy KW - sensory neuropathy KW - neutropenia KW - Young Adult KW - Organoplatinum Compounds -- administration & dosage KW - Neoplasm Staging KW - Humans KW - Prognosis KW - Aged KW - Fluorouracil -- administration & dosage KW - Prospective Studies KW - Survival Rate KW - Aged, 80 and over KW - Adult KW - Middle Aged KW - Adolescent KW - Chemotherapy, Adjuvant KW - Female KW - Male KW - Practice Patterns, Physicians' KW - Neoplasm Recurrence, Local -- drug therapy KW - Colonic Neoplasms -- mortality KW - Colonic Neoplasms -- drug therapy KW - Standard of Care KW - Colonic Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Neoplasm Recurrence, Local -- pathology KW - Neoplasm Recurrence, Local -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727436623?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Asia-Pacific+journal+of+clinical+oncology&rft.atitle=Oxaliplatin%2F5-fluorouracil-based+adjuvant+chemotherapy+as+a+standard+of+care+for+colon+cancer+in+clinical+practice%3A+Outcomes+of+the+ACCElox+registry.&rft.au=Park%2C+Young+Suk%3BJi%2C+Jiafu%3BZalcberg%2C+John+Raymond%3BEl-Serafi%2C+Mostafa%3BBuzaid%2C+Antonio%3BGhosn%2C+Marwan&rft.aulast=Park&rft.aufirst=Young&rft.date=2015-12-01&rft.volume=11&rft.issue=4&rft.spage=334&rft.isbn=&rft.btitle=&rft.title=Asia-Pacific+journal+of+clinical+oncology&rft.issn=1743-7563&rft_id=info:doi/10.1111%2Fajco.12409 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-24 N1 - Date created - 2015-10-23 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/ajco.12409 ER - TY - JOUR T1 - Epigenomic profiling of DNA methylation in paired prostate cancer versus adjacent benign tissue. AN - 1722933310; 26383847 AB - Aberrant DNA methylation may promote prostate carcinogenesis. We investigated epigenome-wide DNA methylation profiles in prostate cancer (PCa) compared to adjacent benign tissue to identify differentially methylated CpG sites. The study included paired PCa and adjacent benign tissue samples from 20 radical prostatectomy patients. Epigenetic profiling was done using the Infinium HumanMethylation450 BeadChip. Linear models that accounted for the paired study design and False Discovery Rate Q-values were used to evaluate differential CpG methylation. mRNA expression levels of the genes with the most differentially methylated CpG sites were analyzed. In total, 2,040 differentially methylated CpG sites were identified in PCa versus adjacent benign tissue (Q-value < 0.001), the majority of which were hypermethylated (n = 1,946; 95%). DNA methylation profiles accurately distinguished between PCa and benign tissue samples. Twenty-seven top-ranked hypermethylated CpGs had a mean methylation difference of at least 40% between tissue types, which included 25 CpGs in 17 genes. Furthermore, for 10 genes over 50% of promoter region CpGs were hypermethylated in PCa versus benign tissue. The top-ranked differentially methylated genes included three genes that were associated with both promoter hypermethylation and reduced gene expression: SCGB3A1, HIF3A, and AOX1. Analysis of The Cancer Genome Atlas (TCGA) data provided confirmatory evidence for our findings. This study of PCa versus adjacent benign tissue showed many differentially methylated CpGs and regions in and outside gene promoter regions, which may potentially be used for the development of future epigenetic-based diagnostic tests or as therapeutic targets. © 2015 Wiley Periodicals, Inc. JF - The Prostate AU - Geybels, Milan S AU - Zhao, Shanshan AU - Wong, Chao-Jen AU - Bibikova, Marina AU - Klotzle, Brandy AU - Wu, Michael AU - Ostrander, Elaine A AU - Fan, Jian-Bing AU - Feng, Ziding AU - Stanford, Janet L AD - Division of Public Health Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington. ; Illumina, Inc., San Diego, California. ; Cancer Genetics Branch, National Human Genome Research Institute, NIH, Bethesda, Maryland. ; MD Anderson Cancer Center, Houston, Texas. Y1 - 2015/12// PY - 2015 DA - December 2015 SP - 1941 EP - 1950 VL - 75 IS - 16 KW - Index Medicus KW - mRNA expression KW - benign KW - DNA methylation KW - tumor KW - prostate cancer KW - Promoter Regions, Genetic KW - Humans KW - CpG Islands KW - Middle Aged KW - Male KW - Epigenomics KW - Prostatic Neoplasms -- metabolism KW - Gene Expression Regulation, Neoplastic KW - Prostatic Neoplasms -- pathology KW - DNA Methylation KW - Prostate -- metabolism KW - Prostatic Neoplasms -- genetics KW - Prostate -- pathology KW - Epigenesis, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722933310?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Prostate&rft.atitle=Epigenomic+profiling+of+DNA+methylation+in+paired+prostate+cancer+versus+adjacent+benign+tissue.&rft.au=Geybels%2C+Milan+S%3BZhao%2C+Shanshan%3BWong%2C+Chao-Jen%3BBibikova%2C+Marina%3BKlotzle%2C+Brandy%3BWu%2C+Michael%3BOstrander%2C+Elaine+A%3BFan%2C+Jian-Bing%3BFeng%2C+Ziding%3BStanford%2C+Janet+L&rft.aulast=Geybels&rft.aufirst=Milan&rft.date=2015-12-01&rft.volume=75&rft.issue=16&rft.spage=1941&rft.isbn=&rft.btitle=&rft.title=The+Prostate&rft.issn=1097-0045&rft_id=info:doi/10.1002%2Fpros.23093 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-02 N1 - Date created - 2015-10-16 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/pros.23093 ER - TY - JOUR T1 - Cancer incidence and metolachlor use in the Agricultural Health Study: An update. AN - 1713526837; 26033014 AB - Metolachlor, a widely used herbicide, is classified as a Group C carcinogen by the U.S. Environmental Protection Agency based on increased liver neoplasms in female rats. Epidemiologic studies of the health effects of metolachlor have been limited. The Agricultural Health Study (AHS) is a prospective cohort study including licensed private and commercial pesticide applicators in Iowa and North Carolina enrolled 1993-1997. We evaluated cancer incidence through 2010/2011 (NC/IA) for 49,616 applicators, 53% of whom reported ever using metolachlor. We used Poisson regression to evaluate relations between two metrics of metolachlor use (lifetime days, intensity-weighted lifetime days) and cancer incidence. We saw no association between metolachlor use and incidence of all cancers combined (n = 5,701 with a 5-year lag) or most site-specific cancers. For liver cancer, in analyses restricted to exposed workers, elevations observed at higher categories of use were not statistically significant. However, trends for both lifetime and intensity-weighted lifetime days of metolachor use were positive and statistically significant with an unexposed reference group. A similar pattern was observed for follicular cell lymphoma, but no other lymphoma subtypes. An earlier suggestion of increased lung cancer risk at high levels of metolachlor use in this cohort was not confirmed in this update. This suggestion of an association between metolachlor and liver cancer among pesticide applicators is a novel finding and echoes observation of increased liver neoplasms in some animal studies. However, our findings for both liver cancer and follicular cell lymphoma warrant follow-up to better differentiate effects of metolachlor use from other factors. © 2015 UICC. JF - International journal of cancer AU - Silver, Sharon R AU - Bertke, Steven J AU - Hines, Cynthia J AU - Alavanja, Michael C R AU - Hoppin, Jane A AU - Lubin, Jay H AU - Rusiecki, Jennifer A AU - Sandler, Dale P AU - Beane Freeman, Laura E AD - Division of Surveillance, Hazard Evaluations and Field Studies, National Institute for Occupational Safety and Health, Cincinnati, OH. ; Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD. ; Department of Biological Sciences, North Carolina State University, Raleigh, NC. ; Department of Preventive Medicine and Biostatistics, Uniformed Services University of the Health Sciences, Bethesda, MD. ; Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC. Y1 - 2015/12/01/ PY - 2015 DA - 2015 Dec 01 SP - 2630 EP - 2643 VL - 137 IS - 11 KW - Acetamides KW - 0 KW - Carcinogens KW - Herbicides KW - metolachlor KW - X0I01K05X2 KW - Index Medicus KW - pesticide KW - occupation KW - epidemiology KW - cancer KW - Prospective Studies KW - Humans KW - Cohort Studies KW - Occupational Exposure -- adverse effects KW - Incidence KW - Aged KW - Middle Aged KW - North Carolina -- epidemiology KW - Male KW - Iowa -- epidemiology KW - Female KW - Agricultural Workers' Diseases -- epidemiology KW - Acetamides -- toxicity KW - Agricultural Workers' Diseases -- chemically induced KW - Neoplasms -- epidemiology KW - Carcinogens -- toxicity KW - Herbicides -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1713526837?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Cancer+incidence+and+metolachlor+use+in+the+Agricultural+Health+Study%3A+An+update.&rft.au=Silver%2C+Sharon+R%3BBertke%2C+Steven+J%3BHines%2C+Cynthia+J%3BAlavanja%2C+Michael+C+R%3BHoppin%2C+Jane+A%3BLubin%2C+Jay+H%3BRusiecki%2C+Jennifer+A%3BSandler%2C+Dale+P%3BBeane+Freeman%2C+Laura+E&rft.aulast=Silver&rft.aufirst=Sharon&rft.date=2015-12-01&rft.volume=137&rft.issue=11&rft.spage=2630&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.29621 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-14 N1 - Date created - 2015-09-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Environ Sci Health C Environ Carcinog Ecotoxicol Rev. 2005;23(2):261-78 [16291529] Ecotoxicol Environ Saf. 2006 Mar;63(3):451-5 [16406594] Int J Cancer. 2006 Jun 15;118(12):3118-23 [16425265] Food Chem Toxicol. 2007 May;45(5):871-7 [17207564] Int J Cancer. 2007 Jul 15;121(2):339-46 [17390374] Blood. 2007 Jul 15;110(2):695-708 [17389762] J Biochem Mol Toxicol. 2008 Feb;22(1):41-50 [18273908] Environ Health Perspect. 2010 Jun;118(6):812-7 [20164001] Cancer Causes Control. 2010 Nov;21(11):1759-75 [20730623] Environ Health Perspect. 2000 Dec;108(12):1151-7 [11133395] Epidemiology. 2002 Jan;13(1):94-9 [11805592] Ann Occup Hyg. 2002 Mar;46(2):245-60 [12074034] J Expo Anal Environ Epidemiol. 2002 Sep;12(5):313-8 [12198579] Int J Toxicol. 2003 Jul-Aug;22(4):287-95 [12933323] Am J Epidemiol. 2004 Feb 15;159(4):373-80 [14769641] Am J Epidemiol. 2004 Nov 1;160(9):876-85 [15496540] Environ Health Perspect. 1996 Apr;104(4):362-9 [8732939] Mutat Res. 1997 Dec 12;395(2-3):159-71 [9465927] Mutat Res. 1999 Jul 15;443(1-2):183-221 [10415440] Scand J Work Environ Health. 2005;31 Suppl 1:39-45; discussion 5-7 [16190148] Int J Environ Res Public Health. 2011 Dec;8(12):4608-22 [22408592] J Expo Sci Environ Epidemiol. 2012 Jul;22(4):409-16 [22569205] J Expo Sci Environ Epidemiol. 2012 Nov;22(6):584-92 [22854518] Food Chem Toxicol. 2013 Dec;62:777-81 [24144947] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ijc.29621 ER - TY - JOUR T1 - PubChem atom environments AN - 1712773242; PQ0001973747 AB - Background: Atom environments and fragments find wide-spread use in chemical information and cheminformatics. They are the basis of prediction models, an integral part in similarity searching, and employed in structure search techniques. Most of these methods were developed and evaluated on the relatively small sets of chemical structures available at the time. An analysis of fragment distributions representative of most known chemical structures was published in the 1970s using the Chemical Abstracts Service data system. More recently, advances in automated synthesis of chemicals allow millions of chemicals to be synthesized by a single organization. In addition, open chemical databases are readily available containing tens of millions of chemical structures from a multitude of data sources, including chemical vendors, patents, and the scientific literature, making it possible for scientists to readily access most known chemical structures. With this availability of information, one can now address interesting questions, such as: what chemical fragments are known today? How do these fragments compare to earlier studies? How unique are chemical fragments found in chemical structures? Results: For our analysis, after hydrogen suppression, atoms were characterized by atomic number, formal charge, implicit hydrogen count, explicit degree (number of neighbors), valence (bond order sum), and aromaticity. Bonds were differentiated as single, double, triple or aromatic bonds. Atom environments were created in a circular manner focused on a central atom with radii from 0 (atom types) up to 3 (representative of ECFP_6 fragments). In total, combining atom types and atom environments that include up to three spheres of nearest neighbors, our investigation identified 28,462,319 unique fragments in the 46 million structures found in the PubChem Compound database as of January 2013. We could identify several factors inflating the number of environments involving transition metals, with many seemingly due to erroneous interpretation of structures from patent data. Compared to fragmentation statistics published 40 years ago, the exponential growth in chemistry is mirrored in a nearly eightfold increase in the number of unique chemical fragments; however, this result is clearly an upper bound estimate as earlier studies employed structure sampling approaches and this study shows that a relatively high rate of atom fragments are found in only a single chemical structure (singletons). In addition, the percentage of singletons grows as the size of the chemical fragment is increased. Conclusions: The observed growth of the numbers of unique fragments over time suggests that many chemically possible connections of atom types to larger fragments have yet to be explored by chemists. A dramatic drop in the relative rate of increase of atom environments from smaller to larger fragments shows that larger fragments mainly consist of diverse combinations of a limited subset of smaller fragments. This is further supported by the observed concomitant increase of singleton atom environments. Combined, these findings suggest that there is considerable opportunity for chemists to combine known fragments to novel chemical compounds. The comparison of PubChem to an older study of known chemical structures shows noticeable differences. The changes suggest advances in synthetic capabilities of chemists to combine atoms in new patterns. Log-log plots of fragment incidence show small numbers of fragments are found in many structures and that large numbers of fragments are found in very few structures, with nearly half being novel using the methods in this work. The relative decrease in the count of new fragments as a function of size further suggests considerable opportunity for more novel chemicals exists. Lastly, the differences in atom environment diversity between PubChem Substance and Compound showcase the effect of PubChem standardization protocols, but also indicate that a normalization procedure for atom types, functional groups, and tautomeric/resonance forms based on atom environments is possible. The complete sets of atom types and atom environments are supplied as supporting information. Graphical abstract: [Figure not available: see fulltext.] JF - Journal of Cheminformatics AU - Haehnke, Volker D AU - Bolton, Evan E AU - Bryant, Stephen H AD - Department of Health and Human Services, National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, 8600 Rockville Pike, Bethesda, MD, 20894, USA, bolton@ncbi.nlm.nih.gov Y1 - 2015/12// PY - 2015 DA - Dec 2015 SP - 1 EP - 37 PB - Springer-Verlag (Heidelberg), Tiergartenstrasse 17 Heidelberg 69121 Germany VL - 7 IS - 1 KW - Biotechnology and Bioengineering Abstracts KW - Databases KW - Standardization KW - Data processing KW - Informatics KW - Patents KW - Statistical analysis KW - Transition metals KW - Hydrogen KW - Sampling KW - Aromatics KW - Models KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1712773242?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Cheminformatics&rft.atitle=PubChem+atom+environments&rft.au=Haehnke%2C+Volker+D%3BBolton%2C+Evan+E%3BBryant%2C+Stephen+H&rft.aulast=Haehnke&rft.aufirst=Volker&rft.date=2015-12-01&rft.volume=7&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+Cheminformatics&rft.issn=1758-2946&rft_id=info:doi/10.1186%2Fs13321-015-0076-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Number of references - 80 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Standardization; Databases; Data processing; Informatics; Patents; Statistical analysis; Transition metals; Sampling; Hydrogen; Aromatics; Models DO - http://dx.doi.org/10.1186/s13321-015-0076-4 ER - TY - JOUR T1 - Modeling groundwater nitrate concentrations in private wells in Iowa. AN - 1710652846; 26232757 AB - Contamination of drinking water by nitrate is a growing problem in many agricultural areas of the country. Ingested nitrate can lead to the endogenous formation of N-nitroso compounds, potent carcinogens. We developed a predictive model for nitrate concentrations in private wells in Iowa. Using 34,084 measurements of nitrate in private wells, we trained and tested random forest models to predict log nitrate levels by systematically assessing the predictive performance of 179 variables in 36 thematic groups (well depth, distance to sinkholes, location, land use, soil characteristics, nitrogen inputs, meteorology, and other factors). The final model contained 66 variables in 17 groups. Some of the most important variables were well depth, slope length within 1 km of the well, year of sample, and distance to nearest animal feeding operation. The correlation between observed and estimated nitrate concentrations was excellent in the training set (r-square=0.77) and was acceptable in the testing set (r-square=0.38). The random forest model had substantially better predictive performance than a traditional linear regression model or a regression tree. Our model will be used to investigate the association between nitrate levels in drinking water and cancer risk in the Iowa participants of the Agricultural Health Study cohort. Copyright © 2015 Elsevier B.V. All rights reserved. JF - The Science of the total environment AU - Wheeler, David C AU - Nolan, Bernard T AU - Flory, Abigail R AU - DellaValle, Curt T AU - Ward, Mary H AD - Department of Biostatistics, Virginia Commonwealth University, 830 East Main St, Richmond, VA 23298, United States. Electronic address: dcwheeler@vcu.edu. ; U.S. Geological Survey, Reston, VA, United States. ; Westat, Rockville, MD, United States. ; Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD, United States. Y1 - 2015/12/01/ PY - 2015 DA - 2015 Dec 01 SP - 481 EP - 488 VL - 536 KW - Drinking Water KW - 0 KW - Nitrates KW - Water Pollutants, Chemical KW - Index Medicus KW - Random forest KW - Nitrate KW - Groundwater contamination KW - Environmental Exposure -- statistics & numerical data KW - Humans KW - Drinking Water -- chemistry KW - Models, Chemical KW - Water Supply -- statistics & numerical data KW - Groundwater -- chemistry KW - Water Pollutants, Chemical -- analysis KW - Nitrates -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1710652846?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Science+of+the+total+environment&rft.atitle=Modeling+groundwater+nitrate+concentrations+in+private+wells+in+Iowa.&rft.au=Wheeler%2C+David+C%3BNolan%2C+Bernard+T%3BFlory%2C+Abigail+R%3BDellaValle%2C+Curt+T%3BWard%2C+Mary+H&rft.aulast=Wheeler&rft.aufirst=David&rft.date=2015-12-01&rft.volume=536&rft.issue=&rft.spage=481&rft.isbn=&rft.btitle=&rft.title=The+Science+of+the+total+environment&rft.issn=1879-1026&rft_id=info:doi/10.1016%2Fj.scitotenv.2015.07.080 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-23 N1 - Date created - 2015-09-08 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.scitotenv.2015.07.080 ER - TY - JOUR T1 - Cancer and circulatory disease risks in US radiologic technologists associated with performing procedures involving radionuclides AN - 1808618847; PQ0003422788 AB - ObjectivesThe number of nuclear medicine procedures has increased substantially over the past several decades, with uncertain health risks to the medical workers who perform them. We estimated risks of incidence and mortality from cancer and circulatory disease associated with performing procedures involving the use of radionuclides.MethodsFrom a nationwide cohort of 90955 US radiologic technologists who completed a mailed questionnaire during 1994-1998, 22039 reported ever performing diagnostic radionuclide procedures, brachytherapy, radioactive iodine therapy, or other radionuclide therapy. We calculated multivariable-adjusted HRs and 95% CIs for incidence (through 2003-2005) and mortality (through 2008) associated with performing these procedures.ResultsEver (versus never) performing radionuclide procedures was not associated with risks for most end points examined. However, we observed increased risks for squamous cell carcinoma of the skin (HR=1.29, 95% CI 1.01 to 1.66) with ever performing diagnostic radionuclide procedures, for myocardial infarction incidence (HR=1.37, 95% CI 1.10 to 1.70), all-cause mortality (HR=1.10, 95% CI 1.00 to 1.20) and all-cancer mortality (HR=1.20, 95% CI 1.01 to 1.43) with ever performing brachytherapy, and for mortality from all causes (HR=1.14, 95% CI 1.01 to 1.30), breast cancer (HR=2.68, 95% CI 1.10 to 6.51), and myocardial infarction (HR=1.76, 95% CI 1.02 to 3.04) with ever performing other radionuclide therapy procedures (excluding brachytherapy and radioactive iodine); increasing risks were also observed with greater frequency of performing these procedures, particularly before 1980.ConclusionsThe modest health risks among radiologic technologists performing procedures using radionuclides require further examination in studies with individual dose estimates, more detailed information regarding types of procedures performed and radionuclides used, and longer follow-up. JF - Occupational and Environmental Medicine AU - Kitahara, Cari M AU - Linet, Martha S AU - Drozdovitch, Vladimir AU - Alexander, Bruce H AU - Preston, Dale L AU - Simon, Steven L AU - Freedman, D Michal AU - Brill, Aaron B AU - Miller, Jeremy S AU - Little, Mark P AU - Rajaraman, Preetha AU - Doody, Michele M AD - Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA Y1 - 2015/11/28/ PY - 2015 DA - 2015 Nov 28 SP - 770 EP - 776 PB - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom VL - 72 IS - 11 SN - 1351-0711, 1351-0711 KW - Toxicology Abstracts; Health & Safety Science Abstracts KW - Mortality KW - Inventories KW - Skin KW - squamous cell carcinoma KW - Cancer KW - Medical personnel KW - Myocardial infarction KW - Health risks KW - Workers KW - Brachytherapy KW - Radioisotopes KW - Iodine KW - Nuclear medicine KW - Breast cancer KW - X 24390:Radioactive Materials KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808618847?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+Environmental+Medicine&rft.atitle=Cancer+and+circulatory+disease+risks+in+US+radiologic+technologists+associated+with+performing+procedures+involving+radionuclides&rft.au=Kitahara%2C+Cari+M%3BLinet%2C+Martha+S%3BDrozdovitch%2C+Vladimir%3BAlexander%2C+Bruce+H%3BPreston%2C+Dale+L%3BSimon%2C+Steven+L%3BFreedman%2C+D+Michal%3BBrill%2C+Aaron+B%3BMiller%2C+Jeremy+S%3BLittle%2C+Mark+P%3BRajaraman%2C+Preetha%3BDoody%2C+Michele+M&rft.aulast=Kitahara&rft.aufirst=Cari&rft.date=2015-11-28&rft.volume=72&rft.issue=11&rft.spage=770&rft.isbn=&rft.btitle=&rft.title=Occupational+and+Environmental+Medicine&rft.issn=13510711&rft_id=info:doi/10.1136%2Foemed-2015-102834 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Workers; Inventories; Mortality; Skin; Brachytherapy; Radioisotopes; Breast cancer; Nuclear medicine; Iodine; squamous cell carcinoma; Myocardial infarction; Health risks; Medical personnel; Cancer DO - http://dx.doi.org/10.1136/oemed-2015-102834 ER - TY - JOUR T1 - Sweet and bitter taste in the brain of awake behaving animals. AN - 1737480200; 26580015 AB - Taste is responsible for evaluating the nutritious content of food, guiding essential appetitive behaviours, preventing the ingestion of toxic substances, and helping to ensure the maintenance of a healthy diet. Sweet and bitter are two of the most salient sensory percepts for humans and other animals; sweet taste allows the identification of energy-rich nutrients whereas bitter warns against the intake of potentially noxious chemicals. In mammals, information from taste receptor cells in the tongue is transmitted through multiple neural stations to the primary gustatory cortex in the brain. Recent imaging studies have shown that sweet and bitter are represented in the primary gustatory cortex by neurons organized in a spatial map, with each taste quality encoded by distinct cortical fields. Here we demonstrate that by manipulating the brain fields representing sweet and bitter taste we directly control an animal's internal representation, sensory perception, and behavioural actions. These results substantiate the segregation of taste qualities in the cortex, expose the innate nature of appetitive and aversive taste responses, and illustrate the ability of gustatory cortex to recapitulate complex behaviours in the absence of sensory input. JF - Nature AU - Peng, Yueqing AU - Gillis-Smith, Sarah AU - Jin, Hao AU - Tränkner, Dimitri AU - Ryba, Nicholas J P AU - Zuker, Charles S AD - Howard Hughes Medical Institute, Columbia College of Physicians and Surgeons, Columbia University, New York, New York 10032, USA. ; National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892, USA. Y1 - 2015/11/26/ PY - 2015 DA - 2015 Nov 26 SP - 512 EP - 515 VL - 527 IS - 7579 KW - Index Medicus KW - Animals KW - Brain Mapping KW - Discrimination (Psychology) -- physiology KW - Mice, Inbred C57BL KW - Optogenetics KW - Mice KW - Male KW - Stereotaxic Techniques KW - Cerebral Cortex -- cytology KW - Cerebral Cortex -- physiology KW - Avoidance Learning -- physiology KW - Taste -- physiology KW - Avoidance Learning -- radiation effects KW - Wakefulness -- physiology KW - Cerebral Cortex -- radiation effects KW - Taste Perception -- physiology KW - Appetitive Behavior -- radiation effects KW - Appetitive Behavior -- physiology KW - Taste Perception -- radiation effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1737480200?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Sweet+and+bitter+taste+in+the+brain+of+awake+behaving+animals.&rft.au=Peng%2C+Yueqing%3BGillis-Smith%2C+Sarah%3BJin%2C+Hao%3BTr%C3%A4nkner%2C+Dimitri%3BRyba%2C+Nicholas+J+P%3BZuker%2C+Charles+S&rft.aulast=Peng&rft.aufirst=Yueqing&rft.date=2015-11-26&rft.volume=527&rft.issue=7579&rft.spage=512&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=1476-4687&rft_id=info:doi/10.1038%2Fnature15763 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-14 N1 - Date created - 2015-11-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Front Neural Circuits. 2014;8:86 [25120438] J Neurosci. 2014 Sep 24;34(39):13000-17 [25253848] Cell. 2015 Jan 29;160(3):528-41 [25635460] Cell. 2001 Aug 10;106(3):381-90 [11509186] Nature. 2001 Sep 13;413(6852):219-25 [11557991] Proc Natl Acad Sci U S A. 2002 Apr 2;99(7):4692-6 [11917125] Cell. 2003 Feb 7;112(3):293-301 [12581520] Neuron. 2003 Aug 14;39(4):701-11 [12925283] Cell. 2003 Oct 31;115(3):255-66 [14636554] Brain Res. 1978 Mar 24;143(2):263-79 [630409] Brain Res. 1978 Mar 24;143(2):281-97 [630410] Prog Neurobiol. 1984;23(4):273-315 [6398454] Behav Neurosci. 1996 Aug;110(4):737-45 [8864265] Nature. 2005 Mar 10;434(7030):225-9 [15759003] Nat Neurosci. 2005 Sep;8(9):1263-8 [16116447] Behav Cogn Neurosci Rev. 2005 Sep;4(3):143-91 [16510892] Nat Rev Neurosci. 2006 Nov;7(11):890-901 [17053812] J Neurosci. 2007 Feb 7;27(6):1396-404 [17287514] Neuron. 2010 Dec 9;68(5):991-1001 [21145010] Science. 2010 Dec 17;330(6011):1677-81 [21164015] Nature. 2011 Mar 17;471(7338):358-62 [21389985] Science. 2011 Sep 2;333(6047):1262-6 [21885776] Cell. 2011 Sep 16;146(6):1004-15 [21925321] Nature. 2012 Aug 9;488(7410):172-7 [22801496] Nature. 2012 Nov 8;491(7423):212-7 [23064228] PLoS One. 2014;9(2):e88678 [24520413] J Neurosci. 2014 May 28;34(22):7398-411 [24872546] Comment In: Oral Dis. 2016 May;22(4):251-2 [26859421] Nat Rev Neurosci. 2016 Jan;17(1):1 [26656255] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nature15763 ER - TY - JOUR T1 - An anthrax toxin variant with an improved activity in tumor targeting. AN - 1735909836; 26584669 AB - Anthrax lethal toxin (LT) is an A-B type toxin secreted by Bacillus anthracis, consisting of the cellular binding moiety, protective antigen (PA), and the catalytic moiety, lethal factor (LF). To target cells, PA binds to cell-surface receptors and is then proteolytically processed forming a LF-binding competent PA oligomer where each LF binding site is comprised of three subsites on two adjacent PA monomers. We previously generated PA-U2-R200A, a urokinase-activated PA variant with LF-binding subsite II residue Arg200 mutated to Ala, and PA-L1-I210A, a matrix metalloproteinase-activated PA variant with subsite III residue Ile210 mutated to Ala. PA-U2-R200A and PA-L1-I210A displayed reduced cytotoxicity when used singly. However, when combined, they formed LF-binding competent heterogeneous oligomers by intermolecular complementation, and achieved high specificity in tumor targeting. Nevertheless, each of these proteins, in particular PA-L1-I210A, retained residual LF-binding ability. In this work, we screened a library containing all possible amino acid substitutions for LF-binding site to find variants with activity strictly dependent upon intermolecular complementation. PA-I207R was identified as an excellent replacement for the original clockwise-side variant, PA-I210A. Consequently, the new combination of PA-L1-I207R and PA-U2-R200A showed potent anti-tumor activity and low toxicity, exceeding the performance of the original combination, and warranting further investigation. JF - Scientific reports AU - Wein, Alexander N AU - Peters, Diane E AU - Valivullah, Zaheer AU - Hoover, Benjamin J AU - Tatineni, Aparna AU - Ma, Qian AU - Fattah, Rasem AU - Bugge, Thomas H AU - Leppla, Stephen H AU - Liu, Shihui AD - Microbial Pathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA. ; Proteases and Tissue Remodeling Section, Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/11/20/ PY - 2015 DA - 2015 Nov 20 SP - 16267 VL - 5 KW - Antigens, Bacterial KW - 0 KW - Bacterial Toxins KW - Mutant Proteins KW - anthrax toxin KW - Index Medicus KW - Animals KW - Cell Survival -- drug effects KW - Tumor Burden -- drug effects KW - Dose-Response Relationship, Drug KW - Mice, Inbred C57BL KW - Cell Line, Tumor KW - Time Factors KW - Mutation, Missense KW - Male KW - Female KW - Cell Line KW - Mutant Proteins -- genetics KW - Macrophages -- cytology KW - Bacterial Toxins -- genetics KW - Bacterial Toxins -- pharmacology KW - Antigens, Bacterial -- pharmacology KW - Neoplasms, Experimental -- drug therapy KW - Neoplasms, Experimental -- pathology KW - Mutant Proteins -- pharmacology KW - Macrophages -- drug effects KW - Antigens, Bacterial -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1735909836?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scientific+reports&rft.atitle=An+anthrax+toxin+variant+with+an+improved+activity+in+tumor+targeting.&rft.au=Wein%2C+Alexander+N%3BPeters%2C+Diane+E%3BValivullah%2C+Zaheer%3BHoover%2C+Benjamin+J%3BTatineni%2C+Aparna%3BMa%2C+Qian%3BFattah%2C+Rasem%3BBugge%2C+Thomas+H%3BLeppla%2C+Stephen+H%3BLiu%2C+Shihui&rft.aulast=Wein&rft.aufirst=Alexander&rft.date=2015-11-20&rft.volume=5&rft.issue=&rft.spage=16267&rft.isbn=&rft.btitle=&rft.title=Scientific+reports&rft.issn=2045-2322&rft_id=info:doi/10.1038%2Fsrep16267 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-10-11 N1 - Date created - 2015-11-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2001 May 25;276(21):17976-84 [11278833] Nature. 2001 Nov 8;414(6860):225-9 [11700562] Proc Natl Acad Sci U S A. 2002 May 14;99(10):7045-8 [11997437] Proc Natl Acad Sci U S A. 2002 May 14;99(10):7049-53 [11997439] Proc Natl Acad Sci U S A. 2003 Jan 21;100(2):657-62 [12525700] Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5170-4 [12700348] Expert Opin Biol Ther. 2003 Aug;3(5):843-53 [12880383] J Clin Invest. 2003 Sep;112(5):670-82 [12952916] J Biol Chem. 1989 Nov 15;264(32):19103-7 [2509473] Proc Natl Acad Sci U S A. 1992 Nov 1;89(21):10277-81 [1438214] Annu Rev Cell Biol. 1993;9:541-73 [8280471] Infect Immun. 1994 Nov;62(11):4955-61 [7927776] Science. 1998 May 1;280(5364):734-7 [9563949] APMIS. 1999 Jan;107(1):120-7 [10190288] J Clin Invest. 1999 May;103(9):1237-41 [10225966] Nat Biotechnol. 2005 Jun;23(6):725-30 [15895075] Cell Microbiol. 2007 Apr;9(4):977-87 [17381430] J Biol Chem. 2008 Jan 4;283(1):529-40 [17974567] PLoS Pathog. 2009 May;5(5):e1000456 [19478875] Nat Struct Mol Biol. 2010 Nov;17(11):1383-90 [21037566] Clin Cancer Res. 2011 Jun 1;17(11):3697-705 [21521777] PLoS One. 2011;6(5):e20532 [21655226] Protein Expr Purif. 2011 Nov;80(1):80-90 [21827967] J Biol Chem. 2013 Mar 29;288(13):9058-65 [23393143] Mol Oncol. 2013 Jun;7(3):440-51 [23290417] Nature. 2013 Sep 5;501(7465):63-8 [23995686] Mol Cancer Ther. 2013 Oct;12(10):2273-81 [23945077] Sci Transl Med. 2013 Oct 23;5(208):208ra147 [24154601] Cell Death Dis. 2014;5:e1003 [24434511] Trends Microbiol. 2014 Jun;22(6):317-25 [24684968] Toxicol Appl Pharmacol. 2014 Sep 1;279(2):220-9 [24971906] Cancer Res. 2000 Nov 1;60(21):6061-7 [11085528] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/srep16267 ER - TY - JOUR T1 - Molecular Basis of Spectral Diversity in Near-Infrared Phytochrome-Based Fluorescent Proteins. AN - 1735902778; 26590639 AB - Near-infrared fluorescent proteins (NIR FPs) engineered from bacterial phytochromes (BphPs) are the probes of choice for deep-tissue imaging. Detection of several processes requires spectrally distinct NIR FPs. We developed an NIR FP, BphP1-FP, which has the most blue-shifted spectra and the highest fluorescence quantum yield among BphP-derived FPs. We found that these properties result from the binding of the biliverdin chromophore to a cysteine residue in the GAF domain, unlike natural BphPs and other BphP-based FPs. To elucidate the molecular basis of the spectral shift, we applied biochemical, structural and mass spectrometry analyses and revealed the formation of unique chromophore species. Mutagenesis of NIR FPs of different origins indicated that the mechanism of the spectral shift is general and can be used to design multicolor NIR FPs from other BphPs. We applied pairs of spectrally distinct point cysteine mutants to multicolor cell labeling and demonstrated that they perform well in model deep-tissue imaging. Copyright © 2015 Elsevier Ltd. All rights reserved. JF - Chemistry & biology AU - Shcherbakova, Daria M AU - Baloban, Mikhail AU - Pletnev, Sergei AU - Malashkevich, Vladimir N AU - Xiao, Hui AU - Dauter, Zbigniew AU - Verkhusha, Vladislav V AD - Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA. ; Macromolecular Crystallography Laboratory, Basic Research Program, National Cancer Institute and Leidos Biomedical Research Inc., Argonne, IL 60439, USA. ; Department of Biochemistry, Albert Einstein College of Medicine, Bronx, NY 10461, USA. ; Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA. ; Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA; Department of Biochemistry and Developmental Biology, Faculty of Medicine, University of Helsinki, Helsinki 00029, Finland. Electronic address: vladislav.verkhusha@einstein.yu.edu. Y1 - 2015/11/19/ PY - 2015 DA - 2015 Nov 19 SP - 1540 EP - 1551 VL - 22 IS - 11 KW - Bacterial Proteins KW - 0 KW - Luminescent Proteins KW - Recombinant Proteins KW - Phytochrome KW - 11121-56-5 KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Microscopy, Confocal KW - Animals KW - Cysteine -- metabolism KW - Recombinant Proteins -- biosynthesis KW - HeLa Cells KW - Humans KW - Amino Acid Sequence KW - Mice KW - Spectroscopy, Near-Infrared KW - Mutagenesis KW - Phytochrome -- chemistry KW - Bacteria -- metabolism KW - Recombinant Proteins -- isolation & purification KW - Phytochrome -- metabolism KW - Cysteine -- chemistry KW - Sequence Alignment KW - Rhodopseudomonas -- metabolism KW - Molecular Sequence Data KW - Recombinant Proteins -- chemistry KW - Protein Structure, Tertiary KW - Bacterial Proteins -- genetics KW - Bacterial Proteins -- chemistry KW - Bacterial Proteins -- metabolism KW - Luminescent Proteins -- metabolism KW - Luminescent Proteins -- chemistry KW - Luminescent Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1735902778?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemistry+%26+biology&rft.atitle=Molecular+Basis+of+Spectral+Diversity+in+Near-Infrared+Phytochrome-Based+Fluorescent+Proteins.&rft.au=Shcherbakova%2C+Daria+M%3BBaloban%2C+Mikhail%3BPletnev%2C+Sergei%3BMalashkevich%2C+Vladimir+N%3BXiao%2C+Hui%3BDauter%2C+Zbigniew%3BVerkhusha%2C+Vladislav+V&rft.aulast=Shcherbakova&rft.aufirst=Daria&rft.date=2015-11-19&rft.volume=22&rft.issue=11&rft.spage=1540&rft.isbn=&rft.btitle=&rft.title=Chemistry+%26+biology&rft.issn=1879-1301&rft_id=info:doi/10.1016%2Fj.chembiol.2015.10.007 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-07 N1 - Date created - 2015-11-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nature. 2001 Dec 13;414(6865):776-9 [11742406] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10566-71 [11553807] J Biol Chem. 2003 Sep 5;278(36):33786-92 [12824166] Eur J Biochem. 2004 Mar;271(6):1117-26 [15009190] Biochemistry. 2004 Mar 30;43(12):3659-69 [15035636] J Mol Biol. 1993 Jun 20;231(4):1049-67 [8515464] J Biol Chem. 1997 Apr 11;272(15):9655-60 [9092494] Acta Crystallogr D Biol Crystallogr. 2004 Dec;60(Pt 12 Pt 1):2126-32 [15572765] Proc Natl Acad Sci U S A. 2004 Dec 14;101(50):17334-9 [15548612] Biochem J. 2005 Nov 15;392(Pt 1):103-16 [16004604] Biochemistry. 2005 Nov 22;44(46):15203-15 [16285723] Nature. 2005 Nov 17;438(7066):325-31 [16292304] J Biol Chem. 2007 Apr 20;282(16):12298-309 [17322301] J Biol Chem. 2008 May 2;283(18):12212-26 [18192276] Photosynth Res. 2008 Aug;97(2):141-53 [18612842] Proc Natl Acad Sci U S A. 2008 Sep 23;105(38):14709-14 [18799745] Proc Natl Acad Sci U S A. 2008 Sep 23;105(38):14715-20 [18799746] Science. 2009 May 8;324(5928):804-7 [19423828] Biochemistry. 2009 Jul 14;48(27):6305-17 [19496558] Proc Natl Acad Sci U S A. 2009 Sep 15;106(37):15639-44 [19720999] Chem Biol. 2009 Nov 25;16(11):1169-79 [19942140] Acta Crystallogr D Biol Crystallogr. 2010 Jan;66(Pt 1):22-5 [20057045] Chemphyschem. 2010 Apr 26;11(6):1172-80 [20155775] Crit Rev Biochem Mol Biol. 2011 Feb;46(1):67-88 [21250783] Acta Crystallogr D Biol Crystallogr. 2011 Apr;67(Pt 4):355-67 [21460454] Phys Chem Chem Phys. 2011 Jul 7;13(25):11985-97 [21611667] Nat Biotechnol. 2011 Aug;29(8):757-61 [21765402] J Biol Chem. 2012 Mar 2;287(10):7000-9 [22210774] Structure. 2012 Aug 8;20(8):1436-46 [22795083] Chem Soc Rev. 2013 Apr 21;42(8):3441-52 [23361376] Nature. 2013 May 30;497(7451):628-32 [23624372] Nat Commun. 2013;4:2153 [23842578] Nat Methods. 2013 Aug;10(8):751-4 [23770755] Chem Biol. 2013 Aug 22;20(8):1078-86 [23891149] Mol Imaging Biol. 2013 Oct;15(5):560-8 [23619897] J Biomed Opt. 2014 Jan;19(1):16019 [24474505] Nature. 2014 May 8;509(7499):245-8 [24776794] Exp Anim. 2014;63(3):311-9 [25077761] Proc Natl Acad Sci U S A. 2014 Jul 15;111(28):10179-84 [24982198] Nat Commun. 2014;5:3626 [24832154] J Biol Chem. 2014 Nov 14;289(46):32144-52 [25253687] Acta Crystallogr D Biol Crystallogr. 2015 Mar;71(Pt 3):646-66 [25760612] Nat Methods. 2015 Aug;12(8):763-5 [26098020] Curr Opin Chem Biol. 2015 Aug;27:52-63 [26115447] Biochemistry. 2000 Nov 7;39(44):13487-95 [11063585] Nat Biotechnol. 2001 Apr;19(4):316-7 [11283581] Acta Crystallogr D Biol Crystallogr. 2002 Nov;58(Pt 11):1948-54 [12393927] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.chembiol.2015.10.007 ER - TY - JOUR T1 - Multiplex H. pylori Serology and Risk of Gastric Cardia and Noncardia Adenocarcinomas AN - 1827886252; PQ0003454961 AB - Risk of certain stomach cancers of high incidence in Asia are associated with changes in seropositivity to H. pylori bacterial antigens, with implications for population health management. The reported associations with gastric adenocarcinoma and seropositivity to different Helicobacter pylori antigens using multiplex serology have not been consistent across studies. We aimed to investigate the association between 15 different multiplex serology antigens and the risk of gastric cardia (GCA) and gastric noncardia (GNCA) adenocarcinomas in northeastern Iran, a population with high rates of gastric adenocarcinoma. We included 272 cases of gastric adenocarcinoma (142 GCA, 103 GNCA, and 27 unspecified) and 524 controls who were individually matched to cases for age, sex, and place of residence in a population-based case-control study. Seropositivity to H. pylori was assessed using both multiplex serology and H. pylori IgG ELISA. Ninety-five percent of controls were seropositive to H. pylori. Of the 15 antibodies in the multiplex assay, 11 showed no significant association with gastric adenocarcinomas. CagA and VacA were associated with a significantly increased risk of all gastric adenocarcinoma and GNCA in multivariate models. Surprisingly, GroEL and NapA were significantly associated with a reduced risk of these tumors. Only CagA antigen was associated with significantly elevated risk of GCA. We found no associations between H. pylori seropositivity overall either by whole-cell ELISA test or multiplex serology, likely due to the high prevalence of seropositivity. Individual antigen testing showed that CagA positivity was associated with increased risk of both noncardia and cardia adenocarcinoma, which is similar to some other Asian populations, whereas two antigens were associated with lower risk of gastric cancer. This latter result was unexpected and should be retested in other populations. Cancer Res; 75(22); 4876-83. [copy2015 AACR. JF - Cancer Research AU - Shakeri, Ramin AU - Malekzadeh, Reza AU - Nasrollahzadeh, Dariush AU - Pawilta, Michael AU - Murphy, Gwen AU - Islami, Farhad AU - Sotoudeh, Masoud AU - Michel, Angelika AU - Etemadi, Arash AU - Waterboer, Tim AU - Poustchi, Hossein AU - Brennan, Paul AU - Boffetta, Paolo AU - Dawsey, Sanford M AU - Kamangar, Farin AU - Abnet, Christian C AD - Digestive Oncology Research Center, Digestive Disease Research Institute, Tehran University of Medical Sciences, Tehran, Iran, abnetc@mail.nih.gov Y1 - 2015/11/15/ PY - 2015 DA - 2015 Nov 15 SP - 4876 EP - 4883 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 75 IS - 22 SN - 0008-5472, 0008-5472 KW - Microbiology Abstracts B: Bacteriology KW - Helicobacter pylori KW - Enzyme-linked immunosorbent assay KW - Risk factors KW - Immunoglobulin G KW - Tumors KW - Adenocarcinoma KW - Gastric cancer KW - Serology KW - Models KW - Sex KW - J 02300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1827886252?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Research&rft.atitle=Multiplex+H.+pylori+Serology+and+Risk+of+Gastric+Cardia+and+Noncardia+Adenocarcinomas&rft.au=Shakeri%2C+Ramin%3BMalekzadeh%2C+Reza%3BNasrollahzadeh%2C+Dariush%3BPawilta%2C+Michael%3BMurphy%2C+Gwen%3BIslami%2C+Farhad%3BSotoudeh%2C+Masoud%3BMichel%2C+Angelika%3BEtemadi%2C+Arash%3BWaterboer%2C+Tim%3BPoustchi%2C+Hossein%3BBrennan%2C+Paul%3BBoffetta%2C+Paolo%3BDawsey%2C+Sanford+M%3BKamangar%2C+Farin%3BAbnet%2C+Christian+C&rft.aulast=Shakeri&rft.aufirst=Ramin&rft.date=2015-11-15&rft.volume=75&rft.issue=22&rft.spage=4876&rft.isbn=&rft.btitle=&rft.title=Cancer+Research&rft.issn=00085472&rft_id=info:doi/10.1158%2F0008-5472.CAN-15-0556 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-10-01 N1 - Last updated - 2016-10-12 N1 - SubjectsTermNotLitGenreText - Enzyme-linked immunosorbent assay; Risk factors; Immunoglobulin G; Tumors; Gastric cancer; Adenocarcinoma; Serology; Sex; Models; Helicobacter pylori DO - http://dx.doi.org/10.1158/0008-5472.CAN-15-0556 ER - TY - JOUR T1 - 13C-MR Spectroscopic Imaging with Hyperpolarized [1-13C]pyruvate Detects Early Response to Radiotherapy in SCC Tumors and HT-29 Tumors AN - 1808673589; PQ0003439811 AB - Purpose: X-ray irradiation of tumors causes diverse effects on the tumor microenvironment, including metabolism. Recent developments of hyperpolarized 13C-MRI enabled detecting metabolic changes in tumors using a tracer [1-13C]pyruvate, which participates in important bioenergetic processes that are altered in cancers. Here, we investigated the effects of X-ray irradiation on pyruvate metabolism in squamous cell carcinoma (SCCVII) and colon cancer (HT-29) using hyperpolarized 13C-MRI.Experimental Design: SCCVII and HT-29 tumors were grown by injecting tumor cells into the hind legs of mice. [1-13C]pyruvate was hyperpolarized and injected intravenously into tumor-bearing mice, and 13C-MR signals were acquired using a 4.7 T scanner.Results: [1-13C]pyruvate and [1-13C]lactate were detected in the tumor-bearing legs immediately after hyperpolarized [1-13C]pyruvate administration. The [1-13C]lactate to [1-13C]pyruvate ratio (Lac/Pyr) increased as the tumors grew in nonirradiated SCCVII tumors. The increase in Lac/Pyr was suppressed modestly with a single 10 Gy of irradiation, but it significantly decreased by further irradiation (10 Gy 3). Similar results were obtained in HT-29; Lac/Pyr significantly dropped with fractionated 30 Gy irradiation. Independent ex vivo measurements revealed that the lactate dehydrogenase (LDH) activity and protein level were significantly smaller in the irradiated SCCVII tumors compared with the nonirradiated tumors, indicating that a decrease in LDH activity was one of the main factors responsible for the decrease of Lac/Pyr observed on 13C-MRI.Conclusions: Robust changes of Lac/Pyr observed in the HT-29 after the radiation suggested that lactate conversion from pyruvate monitored with hyperpolarized 13C-MRI could be useful for the evaluation of early response to radiotherapy. Clin Cancer Res; 21(22); 5073-81. copyright 2015 AACR.See related commentary by Lai et al., p. 4996 JF - Clinical Cancer Research AU - Saito, Keita AU - Matsumoto, Shingo AU - Takakusagi, Yoichi AU - Matsuo, Masayuki AU - Morris, HDouglas AU - Lizak, Martin J AU - Munasinghe, Jeeva P AU - Devasahayam, Nallathamby AU - Subramanian, Sankaran AU - Mitchell, James B AU - Krishna, Murali C AD - Radiation Biology Branch, Center for Cancer Research, NCI, NIH, Bethesda, Maryland, murali@helix.nih.gov Y1 - 2015/11/15/ PY - 2015 DA - 2015 Nov 15 SP - 5073 EP - 5081 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 22 SN - 1078-0432, 1078-0432 KW - Biotechnology and Bioengineering Abstracts KW - Bioenergetics KW - Radiotherapy KW - squamous cell carcinoma KW - Colon cancer KW - Tumors KW - Tumor cells KW - imaging KW - L-Lactate dehydrogenase KW - Leg KW - Tracers KW - Pyruvic acid KW - Ionizing radiation KW - Lactic acid KW - Microenvironments KW - Metabolism KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808673589?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Cancer+Research&rft.atitle=13C-MR+Spectroscopic+Imaging+with+Hyperpolarized+%5B1-13C%5Dpyruvate+Detects+Early+Response+to+Radiotherapy+in+SCC+Tumors+and+HT-29+Tumors&rft.au=Saito%2C+Keita%3BMatsumoto%2C+Shingo%3BTakakusagi%2C+Yoichi%3BMatsuo%2C+Masayuki%3BMorris%2C+HDouglas%3BLizak%2C+Martin+J%3BMunasinghe%2C+Jeeva+P%3BDevasahayam%2C+Nallathamby%3BSubramanian%2C+Sankaran%3BMitchell%2C+James+B%3BKrishna%2C+Murali+C&rft.aulast=Saito&rft.aufirst=Keita&rft.date=2015-11-15&rft.volume=21&rft.issue=22&rft.spage=5073&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-1717 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Bioenergetics; Radiotherapy; squamous cell carcinoma; Tumors; Colon cancer; imaging; Tumor cells; L-Lactate dehydrogenase; Leg; Tracers; Pyruvic acid; Ionizing radiation; Lactic acid; Microenvironments; Metabolism DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-1717 ER - TY - JOUR T1 - High Oral Human Papillomavirus Type 16 Load Predicts Long-term Persistence in Individuals With or at Risk for HIV Infection AN - 1776652321; PQ0002734361 AB - The association between oral human papillomavirus 16 (HPV16) DNA load and infection clearance was evaluated among 88 individuals with oral HPV16 infection who were identified within a prospective cohort of 1470 HIV-infected and uninfected individuals. Oral rinse specimens were collected semiannually for up to 5 years. The oral HPV16 load at the time of the first positive test result was significantly associated with the time to clearance of infection (continuous P trends <.01). Notably, clearance rates by 24 months were 41% and 94% in the highest and lowest HPV16 load tertiles (P = .03), respectively. High oral HPV16 load warrants consideration as a biomarker for infection persistence, the presumed precursor of HPV16-associated oropharyngeal cancer. JF - Journal of Infectious Diseases AU - Beachler, Daniel C AU - Guo, Yingshi AU - Xiao, Wiehong AU - Burk, Robert D AU - Minkoff, Howard AU - Strickler, Howard D AU - Cranston, Ross D AU - Wiley, Dorothy J AU - Jacobson, Lisa P AU - Weber, Kathleen M AU - Margolick, Joseph B AU - Sugar, Elizabeth A AU - Reddy, Susheel AU - Gillison, Maura L AU - D'Souza, Gypsyamber AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, gdsouza2@jhu.edu Y1 - 2015/11/15/ PY - 2015 DA - 2015 Nov 15 SP - 1588 EP - 1591 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 212 IS - 10 SN - 0022-1899, 0022-1899 KW - Virology & AIDS Abstracts; Health & Safety Science Abstracts KW - oral HPV KW - viral load KW - persistence KW - oropharyngeal cancer KW - HIV KW - Bioindicators KW - Infection KW - biomarkers KW - Cancer KW - Health risks KW - Infectious diseases KW - Human immunodeficiency virus KW - Human papillomavirus 16 KW - DNA KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - V 22360:AIDS and HIV UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1776652321?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=High+Oral+Human+Papillomavirus+Type+16+Load+Predicts+Long-term+Persistence+in+Individuals+With+or+at+Risk+for+HIV+Infection&rft.au=Beachler%2C+Daniel+C%3BGuo%2C+Yingshi%3BXiao%2C+Wiehong%3BBurk%2C+Robert+D%3BMinkoff%2C+Howard%3BStrickler%2C+Howard+D%3BCranston%2C+Ross+D%3BWiley%2C+Dorothy+J%3BJacobson%2C+Lisa+P%3BWeber%2C+Kathleen+M%3BMargolick%2C+Joseph+B%3BSugar%2C+Elizabeth+A%3BReddy%2C+Susheel%3BGillison%2C+Maura+L%3BD%27Souza%2C+Gypsyamber&rft.aulast=Beachler&rft.aufirst=Daniel&rft.date=2015-11-15&rft.volume=212&rft.issue=10&rft.spage=1588&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiv273 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - DNA; Infection; biomarkers; oropharyngeal cancer; Bioindicators; Health risks; Infectious diseases; Human immunodeficiency virus; Cancer; Human papillomavirus 16 DO - http://dx.doi.org/10.1093/infdis/jiv273 ER - TY - JOUR T1 - T-Cell Depletion in the Colonic Mucosa of Patients With Idiopathic CD4 super(+) Lymphopenia AN - 1776649319; PQ0002734360 AB - Idiopathic CD4 super(+) lymphopenia (ICL) is a rare syndrome characterized by low peripheral CD4 super(+) T-cell counts that can lead to serious opportunistic infections. The pathogenesis of ICL remains unclear, and whether effector sites are also lymphopenic is unknown. In this study, rectosigmoid mucosal biopsy specimens from patients with ICL and healthy controls were evaluated. Significant T-cell lymphopenia was observed in the mucosal tissue of patients with ICL by flow cytometry and immunohistochemistry, compared with healthy controls. Functional capacity of T cells, assessed by production of interferon [gamma] and interleukin 17, was preserved in the mucosa of patients with ICL. In contrast to T lymphocytes, the frequency of myeloid cells (neutrophils and macrophages) was elevated in the colonic mucosa of patients with ICL. Despite the observed mucosal abnormalities, plasma levels of intestinal fatty acid binding protein, a marker of enterocyte turnover and other inflammatory biomarkers, including interleukin 6, C-reactive protein, and tumor necrosis factor, were not elevated in patients with ICL, compared with healthy controls, whereas soluble CD14 levels were minimally elevated. These data suggest that patients with ICL, despite gut mucosal lymphopenia and local tissue inflammation, have preserved enterocyte turnover and T-helper type 17 cells with minimal systemic inflammation. These observations highlight differences from patients with human immunodeficiency virus infection, with or without AIDS, and may partially explain their distinct clinical prognosis. JF - Journal of Infectious Diseases AU - Kovacs, Stephen B AU - Sheikh, Virginia AU - Thompson, William L AU - Morcock, David R AU - Perez-Diez, Ainhoa AU - Yao, Michael D AU - Rupert, Adam W AU - Utay, Netanya S AU - Roby, Gregg AU - Freeman, Alexandra F AU - Estes, Jacob D AU - Sereti, Irini AD - Clinical Research Directorate/Clinical Monitoring Research Program, isereti@niaid.nih.gov Y1 - 2015/11/15/ PY - 2015 DA - 2015 Nov 15 SP - 1579 EP - 1587 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 212 IS - 10 SN - 0022-1899, 0022-1899 KW - Immunology Abstracts; Health & Safety Science Abstracts KW - idiopathic CD4 super(+) KW - lymphopenia KW - HIV/AIDS KW - mucosal immunity KW - biomarkers KW - inflammation KW - Bioindicators KW - Acquired immune deficiency syndrome KW - Infectious diseases KW - Human immunodeficiency virus KW - Fatty acids KW - Proteins KW - Lymphocytes KW - Tumors KW - Infection KW - H 6000:Natural Disasters/Civil Defense/Emergency Management UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1776649319?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=T-Cell+Depletion+in+the+Colonic+Mucosa+of+Patients+With+Idiopathic+CD4+super%28%2B%29+Lymphopenia&rft.au=Kovacs%2C+Stephen+B%3BSheikh%2C+Virginia%3BThompson%2C+William+L%3BMorcock%2C+David+R%3BPerez-Diez%2C+Ainhoa%3BYao%2C+Michael+D%3BRupert%2C+Adam+W%3BUtay%2C+Netanya+S%3BRoby%2C+Gregg%3BFreeman%2C+Alexandra+F%3BEstes%2C+Jacob+D%3BSereti%2C+Irini&rft.aulast=Kovacs&rft.aufirst=Stephen&rft.date=2015-11-15&rft.volume=212&rft.issue=10&rft.spage=1579&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiv282 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Bioindicators; Acquired immune deficiency syndrome; Infectious diseases; Human immunodeficiency virus; Fatty acids; Proteins; Tumors; Lymphocytes; Infection DO - http://dx.doi.org/10.1093/infdis/jiv282 ER - TY - JOUR T1 - A Review of the Effectiveness of Neuroimaging Modalities for the Detection of Traumatic Brain Injury AN - 1746885005; PQ0002315619 AB - The incidence of traumatic brain injury (TBI) in the United States was 3.5 million cases in 2009, according to the Centers for Disease Control and Prevention. It is a contributing factor in 30.5% of injury-related deaths among civilians. Additionally, since 2000, more than 260,000 service members were diagnosed with TBI, with the vast majority classified as mild or concussive (76%). The objective assessment of TBI via imaging is a critical research gap, both in the military and civilian communities. In 2011, the Department of Defense (DoD) prepared a congressional report summarizing the effectiveness of seven neuroimaging modalities (computed tomography [CT], magnetic resonance imaging [MRI], transcranial Doppler [TCD], positron emission tomography, single photon emission computed tomography, electrophysiologic techniques [magnetoencephalography and electroencephalography], and functional near-infrared spectroscopy) to assess the spectrum of TBI from concussion to coma. For this report, neuroimaging experts identified the most relevant peer-reviewed publications and assessed the quality of the literature for each of these imaging technique in the clinical and research settings. Although CT, MRI, and TCD were determined to be the most useful modalities in the clinical setting, no single imaging modality proved sufficient for all patients due to the heterogeneity of TBI. All imaging modalities reviewed demonstrated the potential to emerge as part of future clinical care. This paper describes and updates the results of the DoD report and also expands on the use of angiography in patients with TBI. JF - Journal of Neurotrauma AU - Amyot, Franck AU - Arciniegas, David B AU - Brazaitis, Michael P AU - Curley, Kenneth C AU - Diaz-Arrastia, Ramon AU - Gandjbakhche, Amir AU - Herscovitch, Peter AU - Hinds, Sidney R AU - Manley, Geoffrey T AU - Pacifico, Anthony AU - Razumovsky, Alexander AU - Riley, Jason AU - Salzer, Wanda AU - Shih, Robert AU - Smirniotopoulos, James G AU - Stocker, Derek AD - The Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, Maryland. Y1 - 2015/11/15/ PY - 2015 DA - 2015 Nov 15 SP - 1693 EP - 1721 PB - Mary Ann Liebert, Inc., 140 Huguenot Street, 3rd Floor New Rochelle NY 10801 USA VL - 32 IS - 22 SN - 0897-7151, 0897-7151 KW - Biotechnology and Bioengineering Abstracts; CSA Neurosciences Abstracts KW - electrophysiology KW - imaging KW - spectroscopy KW - tomography KW - ultrasound KW - Magnetoencephalography KW - Neuroimaging KW - I.R. radiation KW - concussion KW - Magnetic resonance imaging KW - Disease control KW - Single photon emission computed tomography KW - Trauma KW - Coma KW - Angiography KW - I.R. spectroscopy KW - Computed tomography KW - Positron emission tomography KW - EEG KW - Traumatic brain injury KW - Ultrasound KW - W 30910:Imaging KW - N3 11027:Neurology & neuropathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746885005?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Neurotrauma&rft.atitle=A+Review+of+the+Effectiveness+of+Neuroimaging+Modalities+for+the+Detection+of+Traumatic+Brain+Injury&rft.au=Amyot%2C+Franck%3BArciniegas%2C+David+B%3BBrazaitis%2C+Michael+P%3BCurley%2C+Kenneth+C%3BDiaz-Arrastia%2C+Ramon%3BGandjbakhche%2C+Amir%3BHerscovitch%2C+Peter%3BHinds%2C+Sidney+R%3BManley%2C+Geoffrey+T%3BPacifico%2C+Anthony%3BRazumovsky%2C+Alexander%3BRiley%2C+Jason%3BSalzer%2C+Wanda%3BShih%2C+Robert%3BSmirniotopoulos%2C+James+G%3BStocker%2C+Derek&rft.aulast=Amyot&rft.aufirst=Franck&rft.date=2015-11-15&rft.volume=32&rft.issue=22&rft.spage=1693&rft.isbn=&rft.btitle=&rft.title=Journal+of+Neurotrauma&rft.issn=08977151&rft_id=info:doi/10.1089%2Fneu.2013.3306 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 344 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Magnetoencephalography; Neuroimaging; I.R. radiation; concussion; Magnetic resonance imaging; Disease control; Trauma; Single photon emission computed tomography; Coma; Angiography; I.R. spectroscopy; Computed tomography; Positron emission tomography; EEG; Traumatic brain injury; Ultrasound DO - http://dx.doi.org/10.1089/neu.2013.3306 ER - TY - JOUR T1 - Maraviroc Pharmacokinetics in HIV-1-Infected Pregnant Women. AN - 1727439064; 26202768 AB - To describe the pharmacokinetics of maraviroc in human immunodeficiency virus (HIV)-infected women during pregnancy and post partum. HIV-infected pregnant women receiving maraviroc as part of clinical care had intensive steady-state 12-hour pharmacokinetic profiles performed during the third trimester and ≥2 weeks after delivery. Cord blood samples and matching maternal blood samples were taken at delivery. The data were collected in 2 studies: P1026 (United States) and PANNA (Europe). Pharmacokinetic parameters were calculated. Eighteen women were included in the analysis. Most women (12; 67%) received 150 mg of maraviroc twice daily with a protease inhibitor, 2 (11%) received 300 mg twice daily without a protease inhibitor, and 4 (22%) had an alternative regimen. The geometric mean ratios for third-trimester versus postpartum maraviroc were 0.72 (90% confidence interval, .60-.88) for the area under the curve over a dosing interval (AUCtau) and 0.70 (0.58-0.85) for the maximum maraviroc concentration. Only 1 patient showed a trough concentration (Ctrough) below the suggested target of 50 ng/mL, both during pregnancy and post partum. The median ratio of maraviroc cord blood to maternal blood was 0.33 (range, 0.03-0.56). The viral load close to delivery was <50 copies/mL in 13 women (76%). All children were HIV negative at testing. Overall maraviroc exposure during pregnancy was decreased, with a reduction in AUCtau and maximum concentration of about 30%. Ctrough was reduced by 15% but exceeded the minimum Ctrough target concentration. Therefore, the standard adult dose seems sufficient in pregnancy. NCT00825929 and NCT000422890. © The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. JF - Clinical infectious diseases : an official publication of the Infectious Diseases Society of America AU - Colbers, Angela AU - Best, Brookie AU - Schalkwijk, Stein AU - Wang, Jiajia AU - Stek, Alice AU - Hidalgo Tenorio, Carmen AU - Hawkins, David AU - Taylor, Graham AU - Kreitchmann, Regis AU - Burchett, Sandra AU - Haberl, Annette AU - Kabeya, Kabamba AU - van Kasteren, Marjo AU - Smith, Elizabeth AU - Capparelli, Edmund AU - Burger, David AU - Mirochnick, Mark AU - PANNA Network and the IMPAACT 1026 Study Team AD - Department of Pharmacy. ; UC San Diego Skaggs School of Pharmacy and Pharmaceutical Sciences & School of Medicine, University of California San Diego. ; Department of Pharmacy Department of Pharmacology and Toxicology, Radboud university medical center, Nijmegen. ; Center for Biostatistics in AIDS Research, Harvard School of Public Health. ; Maternal Child and Adolescent/Adult Center, University of Southern California School of Medicine, Los Angeles. ; Department of Infectious Diseases, Hospital Universitario Virgen de las Nieves Granada, Spain. ; Chelsea and Westminster Hospital. ; Imperial College Healthcare NHS Trust, London, United Kingdom. ; HIV/AIDS Research Department, Irmandade da Santa Casa de Misericordia de Porto Alegre, Brazil. ; Boston Children's Hospital, Harvard Medical School. ; Department of Infectious Diseases, Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany. ; Department of Infectious Diseases, Saint-Pierre University Hospital, Brussels, Belgium. ; Department of Internal Medicine, St Elisabeth Ziekenhuis, Tilburg, The Netherlands. ; Maternal, Adolescent, and Pediatric Research Branch, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland. ; Boston University School of Medicine, Massachusetts. ; PANNA Network and the IMPAACT 1026 Study Team Y1 - 2015/11/15/ PY - 2015 DA - 2015 Nov 15 SP - 1582 EP - 1589 VL - 61 IS - 10 KW - Anti-HIV Agents KW - 0 KW - Cyclohexanes KW - Triazoles KW - maraviroc KW - MD6P741W8A KW - Index Medicus KW - MTCT KW - pregnancy KW - HIV KW - pharmacokinetics KW - United States KW - Young Adult KW - Blood Chemical Analysis KW - Humans KW - Adult KW - Europe KW - Female KW - Pregnancy KW - Anti-HIV Agents -- pharmacokinetics KW - HIV Infections -- drug therapy KW - Anti-HIV Agents -- administration & dosage KW - Cyclohexanes -- administration & dosage KW - Pregnancy Complications, Infectious -- drug therapy KW - Cyclohexanes -- pharmacokinetics KW - Triazoles -- pharmacokinetics KW - Triazoles -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727439064?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+infectious+diseases+%3A+an+official+publication+of+the+Infectious+Diseases+Society+of+America&rft.atitle=Maraviroc+Pharmacokinetics+in+HIV-1-Infected+Pregnant+Women.&rft.au=Colbers%2C+Angela%3BBest%2C+Brookie%3BSchalkwijk%2C+Stein%3BWang%2C+Jiajia%3BStek%2C+Alice%3BHidalgo+Tenorio%2C+Carmen%3BHawkins%2C+David%3BTaylor%2C+Graham%3BKreitchmann%2C+Regis%3BBurchett%2C+Sandra%3BHaberl%2C+Annette%3BKabeya%2C+Kabamba%3Bvan+Kasteren%2C+Marjo%3BSmith%2C+Elizabeth%3BCapparelli%2C+Edmund%3BBurger%2C+David%3BMirochnick%2C+Mark%3BPANNA+Network+and+the+IMPAACT+1026+Study+Team&rft.aulast=Colbers&rft.aufirst=Angela&rft.date=2015-11-15&rft.volume=61&rft.issue=10&rft.spage=1582&rft.isbn=&rft.btitle=&rft.title=Clinical+infectious+diseases+%3A+an+official+publication+of+the+Infectious+Diseases+Society+of+America&rft.issn=1537-6591&rft_id=info:doi/10.1093%2Fcid%2Fciv587 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-27 N1 - Date created - 2015-10-23 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00825929; ClinicalTrials.gov; NCT00422890 N1 - SuppNotes - Cited By: Best Pract Res Clin Obstet Gynaecol. 2001 Dec;15(6):819-26 [11800526] Antimicrob Agents Chemother. 2004 Mar;48(3):824-31 [14982771] Clin Pharmacokinet. 2005;44(10):989-1008 [16176115] AIDS. 2006 Oct 3;20(15):1931-9 [16988514] Am J Obstet Gynecol. 2007 Sep;197(3 Suppl):S33-41 [17825649] Clin Infect Dis. 2008 Jul 15;47(2):236-41 [18532888] Antimicrob Agents Chemother. 2010 Oct;54(10):4059-63 [20696881] Antimicrob Agents Chemother. 2011 May;55(5):2290-6 [21383098] J Antimicrob Chemother. 2012 Mar;67(3):671-4 [22174038] Clin Pharmacokinet. 2012 Jun 1;51(6):365-96 [22515555] Antimicrob Agents Chemother. 2013 Mar;57(3):1415-20 [23295922] Antivir Ther. 2013;18(3):361-75 [23676668] J Antimicrob Chemother. 2013 Aug;68(8):1938-9 [23535879] AIDS. 2014 Apr 24;28(7):1049-57 [24566097] Clin Infect Dis. 2014 Dec 15;59 Suppl 7:S437-44 [25425722] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/cid/civ587 ER - TY - JOUR T1 - Long-term rescue of cone photoreceptor degeneration in retinitis pigmentosa 2 (RP2)-knockout mice by gene replacement therapy. AN - 1727438928; 26358772 AB - Retinal neurodegenerative diseases are especially attractive targets for gene replacement therapy, which appears to be clinically effective for several monogenic diseases. X-linked forms of retinitis pigmentosa (XLRP) are relatively severe blinding disorders, resulting from progressive photoreceptor dysfunction primarily caused by mutations in RPGR or RP2 gene. With a goal to develop gene therapy for the XLRP-RP2 disease, we first performed detailed characterization of the Rp2-knockout (Rp2-KO) mice and observed early-onset cone dysfunction, which was followed by progressive cone degeneration, mimicking cone vision impairment in XLRP patients. The mice also exhibited distinct and significantly delayed falling phase of photopic b-wave of electroretinogram (ERG). Concurrently, we generated a self-complementary adeno-associated viral (AAV) vector carrying human RP2-coding sequence and demonstrated its ability to mediate stable RP2 protein expression in mouse photoreceptors. A long-term efficacy study was then conducted in Rp2-KO mice following AAV-RP2 vector administration. Preservation of cone function was achieved with a wide dose range over 18-month duration, as evidenced by photopic ERG and optomotor tests. The slower b-wave kinetics was also completely restored. Morphologically, the treatment preserved cone viability, corrected mis-trafficking of M-cone opsin and restored cone PDE6 expression. The therapeutic effect was achieved even in mice that received treatment at an advanced disease stage. The highest AAV-RP2 dose group demonstrated retinal toxicity, highlighting the importance of careful vector dosing in designing future human trials. The wide range of effective dose, a broad treatment window and long-lasting therapeutic effects should make the RP2 gene therapy attractive for clinical development. Published by Oxford University Press 2015. This work is written by (a) US Government employee(s) and is in the public domain in the US. JF - Human molecular genetics AU - Mookherjee, Suddhasil AU - Hiriyanna, Suja AU - Kaneshiro, Kayleigh AU - Li, Linjing AU - Li, Yichao AU - Li, Wei AU - Qian, Haohua AU - Li, Tiansen AU - Khanna, Hemant AU - Colosi, Peter AU - Swaroop, Anand AU - Wu, Zhijian AD - National Eye Institute, National Institutes of Health, Bethesda, MD, USA and. ; Department of Ophthalmology, University of Massachusetts Medical School, Worcester, MA, USA. ; National Eye Institute, National Institutes of Health, Bethesda, MD, USA and wuzh@mail.nih.gov swaroopa@nei.nih.gov. Y1 - 2015/11/15/ PY - 2015 DA - 2015 Nov 15 SP - 6446 EP - 6458 VL - 24 IS - 22 KW - Eye Proteins KW - 0 KW - Intracellular Signaling Peptides and Proteins KW - Membrane Proteins KW - RP2 protein, human KW - Pyrophosphatases KW - EC 3.6.1.- KW - RP2 protein, mouse KW - Index Medicus KW - Pyrophosphatases -- genetics KW - Animals KW - Humans KW - HEK293 Cells KW - Genetic Vectors KW - Genetic Diseases, X-Linked -- genetics KW - Pyrophosphatases -- deficiency KW - Mice KW - Mutation KW - Retinal Degeneration -- genetics KW - Mice, Knockout KW - Electroretinography KW - Intracellular Signaling Peptides and Proteins -- biosynthesis KW - Retinal Cone Photoreceptor Cells -- physiology KW - Membrane Proteins -- genetics KW - Retinitis Pigmentosa -- metabolism KW - Intracellular Signaling Peptides and Proteins -- genetics KW - Retinitis Pigmentosa -- therapy KW - Retinal Cone Photoreceptor Cells -- pathology KW - Eye Proteins -- genetics KW - Membrane Proteins -- biosynthesis KW - Genetic Therapy -- methods KW - Retinal Cone Photoreceptor Cells -- metabolism KW - Eye Proteins -- biosynthesis KW - Retinitis Pigmentosa -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727438928?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+molecular+genetics&rft.atitle=Long-term+rescue+of+cone+photoreceptor+degeneration+in+retinitis+pigmentosa+2+%28RP2%29-knockout+mice+by+gene+replacement+therapy.&rft.au=Mookherjee%2C+Suddhasil%3BHiriyanna%2C+Suja%3BKaneshiro%2C+Kayleigh%3BLi%2C+Linjing%3BLi%2C+Yichao%3BLi%2C+Wei%3BQian%2C+Haohua%3BLi%2C+Tiansen%3BKhanna%2C+Hemant%3BColosi%2C+Peter%3BSwaroop%2C+Anand%3BWu%2C+Zhijian&rft.aulast=Mookherjee&rft.aufirst=Suddhasil&rft.date=2015-11-15&rft.volume=24&rft.issue=22&rft.spage=6446&rft.isbn=&rft.btitle=&rft.title=Human+molecular+genetics&rft.issn=1460-2083&rft_id=info:doi/10.1093%2Fhmg%2Fddv354 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-12 N1 - Date created - 2015-10-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Invest Ophthalmol Vis Sci. 2002 Jun;43(6):2015-20 [12037013] Hum Mol Genet. 2002 Nov 15;11(24):3065-74 [12417528] Blood. 2003 Oct 1;102(7):2412-9 [12791653] Am J Hum Genet. 2003 Nov;73(5):1131-46 [14564670] Gene Ther. 2003 Dec;10(26):2105-11 [14625564] Gene Ther. 2003 Dec;10(26):2112-8 [14625565] Nat Genet. 1996 May;13(1):35-42 [8673101] Curr Biol. 1997 Feb 1;7(2):148-51 [9016703] Biochem Biophys Res Commun. 1997 Aug 18;237(2):318-24 [9268708] Nat Genet. 1998 Aug;19(4):327-32 [9697692] Invest Ophthalmol Vis Sci. 2004 Dec;45(12):4611-6 [15557474] Invest Ophthalmol Vis Sci. 2007 Sep;48(9):3954-61 [17724172] J Virol. 2007 Oct;81(20):11372-80 [17699581] Gene Ther. 2008 Mar;15(6):463-7 [18004402] Nat Struct Mol Biol. 2008 Apr;15(4):373-80 [18376416] N Engl J Med. 2008 May 22;358(21):2240-8 [18441370] Exp Eye Res. 2009 Jun 15;89(1):49-62 [19250935] Expert Opin Ther Targets. 2009 Oct;13(10):1239-51 [19702441] Gene Ther. 2010 Jan;17(1):117-31 [19710705] Vis Neurosci. 2005 Sep-Oct;22(5):677-84 [16332278] Exp Eye Res. 2006 Apr;82(4):543-4 [16310188] Lancet. 2006 Nov 18;368(9549):1795-809 [17113430] Invest Ophthalmol Vis Sci. 2007 Jul;48(7):3324-8 [17591905] Nat Genet. 2000 Aug;25(4):462-6 [10932196] Hum Mol Genet. 2000 Aug 12;9(13):1919-26 [10942419] Am J Hum Genet. 2002 Jun;70(6):1545-54 [11992260] Exp Eye Res. 2010 May;90(5):546-54 [20138034] Arch Ophthalmol. 2010 Jul;128(7):915-23 [20625056] Hum Gene Ther. 2010 Aug;21(8):993-1004 [20384479] Sci Transl Med. 2011 Jun 22;3(88):88ra54 [21697530] Proc Natl Acad Sci U S A. 2012 Feb 7;109(6):2132-7 [22308428] Hum Mol Genet. 2012 Aug 15;21(16):3647-54 [22619378] Hum Mol Genet. 2012 Oct 15;21(R1):R111-24 [22843501] Vision Res. 2012 Dec 15;75:2-4 [22884633] Invest Ophthalmol Vis Sci. 2012 Dec;53(13):8232-7 [23150612] Mol Ther. 2013 Mar;21(3):509-19 [23358189] Invest Ophthalmol Vis Sci. 2013 Jul;54(7):4503-11 [23745007] Clin Genet. 2013 Aug;84(2):132-41 [23701314] Curr Gene Ther. 2013 Dec;13(6):434-52 [24195602] Hum Gene Ther. 2014 Jun;25(6):488-97 [24773122] J Gene Med. 2014 May-Jun;16(5-6):122-30 [24962736] N Engl J Med. 2014 Nov 20;371(21):1994-2004 [25409372] JAMA. 2015 Jan 13;313(2):131-2 [25585318] Drugs. 2015 Feb;75(2):175-82 [25559420] N Engl J Med. 2015 Feb 26;372(9):793-5 [25635347] FASEB J. 2015 Mar;29(3):932-42 [25422369] Hum Mol Genet. 2015 Jul 15;24(14):3956-70 [25877300] Hum Mol Genet. 2015 Aug 15;24(16):4648-59 [26034134] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/hmg/ddv354 ER - TY - JOUR T1 - Reformulating the low-carbon green growth strategy in China AN - 1753461886; PQ0002389856 AB - This synthesis article reviews China's efforts and effects concerning low-carbon green growth (LCGG) and explores the policy implications of reformulating the country's LCGG strategy. The article first reviews China's efforts in four major areas - carbon mitigation, market construction, fostering green industries, and managing the negative effects of LCGG - and then reviews China's LCGG effects with respect to the growth effect and the low-carbon effect. The results show that the increasingly stringent low-carbon policy has not diminished the country's economic growth as some had expected. Rather, the policy has fostered green industries and brought impressive quality improvements, including structural change and increased employment. Although the efforts and effects in China are impressive, the global emissions reduction is far from sufficient to achieve the global climate change target. To solve the problem of global climate change and seize the opportunity of green growth, China must reformulate its LCGG strategy, not just enhancing its existing LCGG efforts, but more importantly, rethinking the purpose of development and shifting its development paradigm from one that is highly gross domestic product (GDP)-oriented to one that is well-being-oriented. Policy relevance China must reformulate its LCGG strategy on two levels. First, China must enhance its existing efforts. Second, China should learn lessons from the industrial countries and reformulate its development model to one that is well-being-oriented to establish a more forward-looking green growth model in the new context of the Internet era. The time is now ripe for China to make a strategic transition. The 13th Five-Year Plan (FYP, 2016 to 2020) provides an opportunity for a more fundamental change in LCGG strategy. If China could succeed in exploring LCGG, it would make a significant contribution to the whole world. JF - Climate Policy AU - Zhang, Yongsheng AD - The Development Research Center of the State Council, 225 Chaoyangmen Nei Dajie, Beijing 100010, People's Republic of China Y1 - 2015/11/06/ PY - 2015 DA - 2015 Nov 06 SP - S40 EP - S59 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 15 IS - sup1 SN - 1469-3062, 1469-3062 KW - Sustainability Science Abstracts; Environment Abstracts; Meteorological & Geoastrophysical Abstracts KW - Mitigation KW - Climate change KW - Public policy and climate KW - Emission control KW - Economic growth KW - Employment KW - Environmental policy KW - Growth KW - Reviews KW - China, People's Rep. KW - Internet KW - M2 551.583:Variations (551.583) KW - M3 1010:Issues in Sustainable Development KW - ENA 20:Weather Modification & Geophysical Change UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753461886?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Assamodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Climate+Policy&rft.atitle=Reformulating+the+low-carbon+green+growth+strategy+in+China&rft.au=Zhang%2C+Yongsheng&rft.aulast=Zhang&rft.aufirst=Yongsheng&rft.date=2015-11-06&rft.volume=15&rft.issue=sup1&rft.spage=S40&rft.isbn=&rft.btitle=&rft.title=Climate+Policy&rft.issn=14693062&rft_id=info:doi/10.1080%2F14693062.2015.1094726 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Last updated - 2016-11-09 N1 - SubjectsTermNotLitGenreText - Public policy and climate; Climate change; Internet; Growth; Mitigation; Reviews; Emission control; Employment; Economic growth; Environmental policy; China, People's Rep. DO - http://dx.doi.org/10.1080/14693062.2015.1094726 ER - TY - JOUR T1 - "Clinicopathological features and treatment outcomes of differentiated thyroid cancer in Saudi children and adults". AN - 1732311159; 26546329 AB - Age is an important prognostic factor in differentiated thyroid cancer (DTC). Our aim was to evaluate differences in clinicopathological features and treatment outcomes among children and adult patients with DTC. We studied 27 children (below 18 years) with DTC treated during the period 2000-2012 and were compared with (a) 78 adults aged 19-25 years and (b) 52 adults aged 26-30 years treated during the same period in terms of their clinicopathological features and long term treatment outcomes. Locoregional recurrence (LRR), locoregional control (LRC), distant metastasis (DM), distant metastasis control (DMC), disease free survival (DFS) and overall survival (OS) rates were evaluated. Mean age of children was 13.5 years (range: 5-18), while mean age of adults was 24.6 years (range: 19-30). In children, female: male ratio was 2.85:1, and in adults female: male ratio was 7.1:1 (P = 0.041). No significant difference in tumor size was seen between the two groups (P = 0.653). According to American Thyroid Association (ATA) risk stratification classification, the children (85.2 %) were found to have at high risk as compared to adults P = 0.001. Post-thyroidectomy complications and RAI induced toxicities were observed more in children than adults (P = 0.043 and P = 0.041 respectively). LRR occurred in 6 (22.2 %), 9 (11.5 %) and 3 (5.8 %) in age groups of <18 years, 19-25 years and 26-30 years respectively (P = 0.032); while DM was seen in 10 (37.0 %), 9 (10.3 %) and 5 (9.6 %) in age groups of <18 years, 19-25 years and 26-30 years respectively (P = 0.002). Ten year DFS rates were 67.3 % in age group below 18 years, 82.4 % in age group of 19-25 years and 90.1 % in age group of 26-30 years (P = 0.021). At the time of diagnosis, children with DTC were found to have more aggressive clinicopathological characteristics. Comparatively lower LRC, DMC and DFS rates in children warrants further multi-institutional studies. JF - Journal of otolaryngology - head & neck surgery = Le Journal d'oto-rhino-laryngologie et de chirurgie cervico-faciale AU - Al-Qahtani, Khalid Hussain AU - Tunio, Mutahir A AU - Al Asiri, Mushabbab AU - Aljohani, Naji J AU - Bayoumi, Yasser AU - Riaz, Khalid AU - AlShakweer, Wafa AD - Department of Otolaryngology-Head & Neck Surgery, College of Medicine, King Saud University, Riyadh, Saudi Arabia. kalqahtani@KSU.EDU.SA. ; Radiation Oncology, King Fahad Medical City, Riyadh, Saudi Arabia. drmutahirtonio@hotmail.com. ; Radiation Oncology, Comprehensive Cancer Center, King Fahad Medical City, Riyadh, 59046, Saudi Arabia. masiri@kfmc.med.sa. ; Endocrinology and Thyroid Oncology, King Fahad Medical City, Riyadh, 59046, Saudi Arabia. njaljohani@kfmc.med.sa. ; Radiation Oncology, NCI, Cairo University, Cairo, Egypt. yasserbayoumi777@yahoo.com. ; Radiation Oncology, King Fahad Medical City, Riyadh, Saudi Arabia. kriaz@kfmc.med.sa. ; Histopathology, Comprehensive Cancer Center, King Fahad Medical City, Riyadh, 59046, Saudi Arabia. walshakweer@kfmc.med.sa. Y1 - 2015/11/06/ PY - 2015 DA - 2015 Nov 06 SP - 48 VL - 44 KW - Index Medicus KW - Survival Rate -- trends KW - Young Adult KW - Disease-Free Survival KW - Humans KW - Saudi Arabia -- epidemiology KW - Retrospective Studies KW - Child KW - Child, Preschool KW - Adult KW - Treatment Outcome KW - Follow-Up Studies KW - Adolescent KW - Female KW - Male KW - Neoplasm Staging KW - Thyroidectomy -- methods KW - Thyroid Neoplasms -- pathology KW - Thyroid Neoplasms -- surgery KW - Thyroid Neoplasms -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732311159?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+otolaryngology+-+head+%26+neck+surgery+%3D+Le+Journal+d%27oto-rhino-laryngologie+et+de+chirurgie+cervico-faciale&rft.atitle=%22Clinicopathological+features+and+treatment+outcomes+of+differentiated+thyroid+cancer+in+Saudi+children+and+adults%22.&rft.au=Al-Qahtani%2C+Khalid+Hussain%3BTunio%2C+Mutahir+A%3BAl+Asiri%2C+Mushabbab%3BAljohani%2C+Naji+J%3BBayoumi%2C+Yasser%3BRiaz%2C+Khalid%3BAlShakweer%2C+Wafa&rft.aulast=Al-Qahtani&rft.aufirst=Khalid&rft.date=2015-11-06&rft.volume=44&rft.issue=&rft.spage=48&rft.isbn=&rft.btitle=&rft.title=Journal+of+otolaryngology+-+head+%26+neck+surgery+%3D+Le+Journal+d%27oto-rhino-laryngologie+et+de+chirurgie+cervico-faciale&rft.issn=1916-0216&rft_id=info:doi/10.1186%2Fs40463-015-0102-6 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-06 N1 - Date created - 2015-11-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Pediatr. 2009 May;154(5):708-14 [19167722] CA Cancer J Clin. 2009 Jul-Aug;59(4):225-49 [19474385] J Surg Res. 2009 Sep;156(1):167-72 [19631341] World J Surg. 2010 Jun;34(6):1192-202 [20087589] Ann Surg Oncol. 2010 Oct;17(10):2545-53 [20429037] Clin Nucl Med. 2012 Sep;37(9):850-3 [22889773] Clin Endocrinol (Oxf). 2000 Nov;53(5):635-44 [11106926] J Korean Med Sci. 2013 May;28(5):693-9 [23678260] Hematol Oncol Stem Cell Ther. 2013 Jun;6(2):58-64 [23756719] Acta Med Port. 2013 Sep-Oct;26(5):578-82 [24192098] J Nucl Med. 2014 May;55(5):710-7 [24722527] J Pediatr. 2014 Jun;164(6):1481-5 [24630354] Endocr J. 2014;61(11):1079-86 [25132169] Eur Ann Otorhinolaryngol Head Neck Dis. 2014 Nov;131(5):293-7 [24993783] J Nucl Med. 1997 May;38(5):669-75 [9170425] Endocr Relat Cancer. 2005 Dec;12(4):773-803 [16322322] J Pediatr Surg. 2004 Oct;39(10):1500-5 [15486894] Eur J Cancer. 2004 Jul;40(11):1743-51 [15251165] J Endocrinol Invest. 2002 Jan;25(1):18-24 [11883862] Hormones (Athens). 2007 Jul-Sep;6(3):200-9 [17724004] J Clin Endocrinol Metab. 1996 May;81(5):2006-9 [8626874] Surgery. 1988 Dec;104(6):1157-66 [3194843] Curr Opin Otolaryngol Head Neck Surg. 2013 Apr;21(2):135-42 [23486378] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/s40463-015-0102-6 ER - TY - JOUR T1 - A multi-omic analysis of human naïve CD4+ T cells. AN - 1731791832; 26542228 AB - Cellular function and diversity are orchestrated by complex interactions of fundamental biomolecules including DNA, RNA and proteins. Technological advances in genomics, epigenomics, transcriptomics and proteomics have enabled massively parallel and unbiased measurements. Such high-throughput technologies have been extensively used to carry out broad, unbiased studies, particularly in the context of human diseases. Nevertheless, a unified analysis of the genome, epigenome, transcriptome and proteome of a single human cell type to obtain a coherent view of the complex interplay between various biomolecules has not yet been undertaken. Here, we report the first multi-omic analysis of human primary naïve CD4+ T cells isolated from a single individual. Integrating multi-omics datasets allowed us to investigate genome-wide methylation and its effect on mRNA/protein expression patterns, extent of RNA editing under normal physiological conditions and allele specific expression in naïve CD4+ T cells. In addition, we carried out a multi-omic comparative analysis of naïve with primary resting memory CD4+ T cells to identify molecular changes underlying T cell differentiation. This analysis provided mechanistic insights into how several molecules involved in T cell receptor signaling are regulated at the DNA, RNA and protein levels. Phosphoproteomics revealed downstream signaling events that regulate these two cellular states. Availability of multi-omics data from an identical genetic background also allowed us to employ novel proteogenomics approaches to identify individual-specific variants and putative novel protein coding regions in the human genome. We utilized multiple high-throughput technologies to derive a comprehensive profile of two primary human cell types, naïve CD4+ T cells and memory CD4+ T cells, from a single donor. Through vertical as well as horizontal integration of whole genome sequencing, methylation arrays, RNA-Seq, miRNA-Seq, proteomics, and phosphoproteomics, we derived an integrated and comparative map of these two closely related immune cells and identified potential molecular effectors of immune cell differentiation following antigen encounter. JF - BMC systems biology AU - Mitchell, Christopher J AU - Getnet, Derese AU - Kim, Min-Sik AU - Manda, Srikanth S AU - Kumar, Praveen AU - Huang, Tai-Chung AU - Pinto, Sneha M AU - Nirujogi, Raja Sekhar AU - Iwasaki, Mio AU - Shaw, Patrick G AU - Wu, Xinyan AU - Zhong, Jun AU - Chaerkady, Raghothama AU - Marimuthu, Arivusudar AU - Muthusamy, Babylakshmi AU - Sahasrabuddhe, Nandini A AU - Raju, Rajesh AU - Bowman, Caitlyn AU - Danilova, Ludmila AU - Cutler, Jevon AU - Kelkar, Dhanashree S AU - Drake, Charles G AU - Prasad, T S Keshava AU - Marchionni, Luigi AU - Murakami, Peter N AU - Scott, Alan F AU - Shi, Leming AU - Thierry-Mieg, Jean AU - Thierry-Mieg, Danielle AU - Irizarry, Rafael AU - Cope, Leslie AU - Ishihama, Yasushi AU - Wang, Charles AU - Gowda, Harsha AU - Pandey, Akhilesh AD - McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. cmitch48@jhmi.edu. ; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. dgetnet1@jhmi.edu. ; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. mskim@jhmi.edu. ; Institute of Bioinformatics, International Tech Park, Whitefield, Bangalore, India. srikanth@ibioinformatics.org. ; Institute of Bioinformatics, International Tech Park, Whitefield, Bangalore, India. praveen@ibioinformatics.org. ; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. huang@jhmi.edu. ; Institute of Bioinformatics, International Tech Park, Whitefield, Bangalore, India. pinto@jhmi.edu. ; Institute of Bioinformatics, International Tech Park, Whitefield, Bangalore, India. raja@ibioinformatics.org. ; Department of Molecular & Cellular BioAnalysis, Kyoto University, Kyoto, Japan. omio13@gmail.com. ; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. pshaw@jhsph.edu. ; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. xinyan@jhmi.edu. ; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. jzhong@jhmi.edu. ; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. raghothama@jhmi.edu. ; Institute of Bioinformatics, International Tech Park, Whitefield, Bangalore, India. arivusudar@ibioinformatics.org. ; Institute of Bioinformatics, International Tech Park, Whitefield, Bangalore, India. babylakshmi@ibioinformatics.org. ; Institute of Bioinformatics, International Tech Park, Whitefield, Bangalore, India. nandini@ibioinformatics.org. ; Institute of Bioinformatics, International Tech Park, Whitefield, Bangalore, India. rajesh@ibioinformatics.org. ; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. cbowma14@jhmi.edu. ; Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA. ludmila.danilova@gmail.com. ; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. jevon@jhmi.edu. ; Institute of Bioinformatics, International Tech Park, Whitefield, Bangalore, India. dhanashree@ibioinformatics.org. ; Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA. cdrake@jhmi.edu. ; Institute of Bioinformatics, International Tech Park, Whitefield, Bangalore, India. keshav@ibioinformatics.org. ; Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA. marchion@gmail.com. ; Department of Biostatistics, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA. pmurakam@jhsph.edu. ; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. afscott@jhmi.edu. ; National Center for Toxicological Research, Food and Drug Administration, Jefferson, AR, USA. leming.shi@fda.hhs.gov. ; National Center for Biotechnology Information, National Institutes of Health, Bethesda, MD, USA. mieg@ncbi.nlm.nih.gov. ; Department of Biostatistics and Computational Biology, Dana Farber Cancer Institute, Boston, MA, USA. rafa@jhu.edu. ; Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Lcope1@jhmi.edu. ; Department of Molecular & Cellular BioAnalysis, Kyoto University, Kyoto, Japan. yishiham@pharm.kyoto-u.ac.jp. ; Center for Genomics and Division of Microbiology & Molecular Genetics, Loma Linda University, Loma Linda, CA, USA. chwang@llu.edu. ; Institute of Bioinformatics, International Tech Park, Whitefield, Bangalore, India. harsha@bioinformatics.org. ; McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. pandey@jhmi.edu. Y1 - 2015/11/06/ PY - 2015 DA - 2015 Nov 06 SP - 75 VL - 9 KW - RNA, Messenger KW - 0 KW - Index Medicus KW - Genetic Variation KW - Genome, Human KW - Humans KW - Gene Expression Profiling KW - DNA Methylation KW - Phosphorylation KW - RNA, Messenger -- metabolism KW - Proteomics KW - Signal Transduction -- genetics KW - RNA Editing -- drug effects KW - Transcriptome KW - Epigenomics KW - Genomics KW - High-Throughput Nucleotide Sequencing KW - CD4-Positive T-Lymphocytes -- metabolism KW - Immunity, Innate -- physiology KW - Immunity, Innate -- genetics KW - Models, Biological UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731791832?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+systems+biology&rft.atitle=A+multi-omic+analysis+of+human+na%C3%AFve+CD4%2B+T+cells.&rft.au=Mitchell%2C+Christopher+J%3BGetnet%2C+Derese%3BKim%2C+Min-Sik%3BManda%2C+Srikanth+S%3BKumar%2C+Praveen%3BHuang%2C+Tai-Chung%3BPinto%2C+Sneha+M%3BNirujogi%2C+Raja+Sekhar%3BIwasaki%2C+Mio%3BShaw%2C+Patrick+G%3BWu%2C+Xinyan%3BZhong%2C+Jun%3BChaerkady%2C+Raghothama%3BMarimuthu%2C+Arivusudar%3BMuthusamy%2C+Babylakshmi%3BSahasrabuddhe%2C+Nandini+A%3BRaju%2C+Rajesh%3BBowman%2C+Caitlyn%3BDanilova%2C+Ludmila%3BCutler%2C+Jevon%3BKelkar%2C+Dhanashree+S%3BDrake%2C+Charles+G%3BPrasad%2C+T+S+Keshava%3BMarchionni%2C+Luigi%3BMurakami%2C+Peter+N%3BScott%2C+Alan+F%3BShi%2C+Leming%3BThierry-Mieg%2C+Jean%3BThierry-Mieg%2C+Danielle%3BIrizarry%2C+Rafael%3BCope%2C+Leslie%3BIshihama%2C+Yasushi%3BWang%2C+Charles%3BGowda%2C+Harsha%3BPandey%2C+Akhilesh&rft.aulast=Mitchell&rft.aufirst=Christopher&rft.date=2015-11-06&rft.volume=9&rft.issue=&rft.spage=75&rft.isbn=&rft.btitle=&rft.title=BMC+systems+biology&rft.issn=1752-0509&rft_id=info:doi/10.1186%2Fs12918-015-0225-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-26 N1 - Date created - 2015-11-06 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - PRJNA234019; SRA N1 - SuppNotes - Cited By: J Immunol. 2000 Sep 1;165(5):2458-64 [10946271] Trends Biochem Sci. 2001 Jan;26(1):54-61 [11165518] Nat Immunol. 2000 Jul;1(1):59-64 [10881176] Nat Rev Immunol. 2002 Aug;2(8):547-56 [12154374] J Neuropathol Exp Neurol. 2004 Apr;63(4):350-62 [15099025] RNA. 2012 Sep;18(9):1586-96 [22832026] Genome Res. 2012 Sep;22(9):1626-33 [22955975] Nature. 2012 Oct 4;490(7418):61-70 [23000897] Nat Immunol. 2012 Nov;13(11):1037-44 [23080204] Mol Cell Proteomics. 2005 Jul;4(7):873-86 [15858219] Immunity. 2005 Dec;23(6):561-74 [16356855] Cell Immunol. 2005 Sep;237(1):17-27 [16289056] Nat Protoc. 2006;1(1):139-45 [17406225] Annu Rev Immunol. 2007;25:193-219 [17129180] J Immunol. 2007 Sep 15;179(6):3689-98 [17785805] J Immunol. 2008 Jan 1;180(1):402-8 [18097041] J Biol Chem. 2008 Sep 5;283(36):24392-9 [18583339] Nucleic Acids Res. 2009 Jan;37(Database issue):D767-72 [18988627] PLoS One. 2009;4(1):e4150 [19127300] J Exp Med. 2009 Sep 28;206(10):2111-9 [19770269] J Immunol. 2009 Dec 1;183(11):7362-70 [19917688] Nat Rev Immunol. 2009 Dec;9(12):823-32 [19935802] Mol Cell Biol. 2010 Feb;30(4):922-34 [20008554] J Immunol. 1999 Jan 1;162(1):186-94 [9886385] Mol Cell Proteomics. 2005 May;4(5):637-50 [15723814] Nat Genet. 2010 Apr;42(4):295-302 [20190752] J Cell Sci. 2010 Jul 15;123(Pt 14):2375-80 [20551178] Mol Cell. 2010 Dec 10;40(5):798-809 [21145487] Brief Funct Genomics. 2011 Mar;10(2):98-107 [21436306] J Clin Invest. 2011 Mar;121(3):1191-8 [21393862] Nature. 2011 May 19;473(7347):337-42 [21593866] Mol Syst Biol. 2011;7:522 [21811232] Nat Methods. 2011;8(10):785-6 [21959131] Genome Res. 2011 Nov;21(11):1872-81 [21795387] Mol Cell Proteomics. 2011 Dec;10(12):M111.011627 [21969609] Nucleic Acids Res. 2012 Jan;40(Database issue):D302-5 [22053084] Genome Res. 2012 Jan;22(1):142-50 [21960545] Biochem Soc Trans. 2012 Feb;40(1):79-84 [22260669] J Chromatogr A. 2012 Mar 9;1228:292-7 [22078304] Science. 2012 Feb 17;335(6070):823-8 [22344438] Nat Biotechnol. 2012 Mar;30(3):253-60 [22327324] Cell. 2012 Mar 16;148(6):1293-307 [22424236] Annu Rev Biochem. 2012;81:379-405 [22439968] Proc Natl Acad Sci U S A. 2012 Jun 19;109(25):E1629-37 [22615393] Curr Opin Biotechnol. 2012 Aug;23(4):591-7 [22169889] PLoS One. 2012;7(8):e42775 [22880103] Nature. 2014 May 29;509(7502):575-81 [24870542] J Exp Med. 1994 Apr 1;179(4):1127-35 [8145034] J Immunol. 1995 Apr 1;154(7):3062-77 [7534786] J Mol Med (Berl). 1996 Oct;74(10):589-607 [8912180] J Biol Chem. 1998 Jan 9;273(2):1144-9 [9422780] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/s12918-015-0225-4 ER - TY - JOUR T1 - Posttranslational Regulation of Human DNA Polymerase ι. AN - 1731783190; 26370087 AB - Human DNA polymerases (pols) η and ι are Y-family DNA polymerase paralogs that facilitate translesion synthesis past damaged DNA. Both polη and polι can be monoubiquitinated in vivo. Polη has been shown to be ubiquitinated at one primary site. When this site is unavailable, three nearby lysines may become ubiquitinated. In contrast, mass spectrometry analysis of monoubiquitinated polι revealed that it is ubiquitinated at over 27 unique sites. Many of these sites are localized in different functional domains of the protein, including the catalytic polymerase domain, the proliferating cell nuclear antigen-interacting region, the Rev1-interacting region, and its ubiquitin binding motifs UBM1 and UBM2. Polι monoubiquitination remains unchanged after cells are exposed to DNA-damaging agents such as UV light (generating UV photoproducts), ethyl methanesulfonate (generating alkylation damage), mitomycin C (generating interstrand cross-links), or potassium bromate (generating direct oxidative DNA damage). However, when exposed to naphthoquinones, such as menadione and plumbagin, which cause indirect oxidative damage through mitochondrial dysfunction, polι becomes transiently polyubiquitinated via Lys(11)- and Lys(48)-linked chains of ubiquitin and subsequently targeted for degradation. Polyubiquitination does not occur as a direct result of the perturbation of the redox cycle as no polyubiquitination was observed after treatment with rotenone or antimycin A, which both inhibit mitochondrial electron transport. Interestingly, polyubiquitination was observed after the inhibition of the lysine acetyltransferase KATB3/p300. We hypothesize that the formation of polyubiquitination chains attached to polι occurs via the interplay between lysine acetylation and ubiquitination of ubiquitin itself at Lys(11) and Lys(48) rather than oxidative damage per se. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - McIntyre, Justyna AU - McLenigan, Mary P AU - Frank, Ekaterina G AU - Dai, Xiaoxia AU - Yang, Wei AU - Wang, Yinsheng AU - Woodgate, Roger AD - From the Laboratory of Genomic Integrity, NICHD, National Institutes of Health, Bethesda, Maryland 20892-3371, Institute of Biochemistry and Biophysics, Polish Academy of Sciences, 02-106 Warsaw, Poland. ; From the Laboratory of Genomic Integrity, NICHD, National Institutes of Health, Bethesda, Maryland 20892-3371. ; Department of Chemistry, University of California, Riverside, California 92521-0403, and. ; Laboratory of Molecular Biology, NIDDK, National Institutes of Health, Bethesda, Maryland 20892. ; From the Laboratory of Genomic Integrity, NICHD, National Institutes of Health, Bethesda, Maryland 20892-3371, woodgate@nih.gov. Y1 - 2015/11/06/ PY - 2015 DA - 2015 Nov 06 SP - 27332 EP - 27344 VL - 290 IS - 45 KW - Recombinant Proteins KW - 0 KW - DNA polymerase iota KW - EC 2.7.7.- KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Lysine KW - K3Z4F929H6 KW - Index Medicus KW - mutagenesis KW - DNA polymerase ι KW - posttranslational modification (PTM) KW - DNA repair KW - Y-family DNA polymerase KW - ubiquitin KW - DNA synthesis KW - DNA Repair KW - Lysine -- chemistry KW - DNA Damage KW - Models, Molecular KW - HEK293 Cells KW - Humans KW - Protein Processing, Post-Translational KW - Amino Acid Sequence KW - Tandem Mass Spectrometry KW - Recombinant Proteins -- genetics KW - Mutagenesis, Site-Directed KW - Recombinant Proteins -- metabolism KW - Ubiquitination KW - Molecular Sequence Data KW - Recombinant Proteins -- chemistry KW - Binding Sites -- genetics KW - Amino Acid Substitution KW - Protein Conformation KW - DNA-Directed DNA Polymerase -- genetics KW - DNA-Directed DNA Polymerase -- metabolism KW - DNA-Directed DNA Polymerase -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731783190?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Posttranslational+Regulation+of+Human+DNA+Polymerase+%CE%B9.&rft.au=McIntyre%2C+Justyna%3BMcLenigan%2C+Mary+P%3BFrank%2C+Ekaterina+G%3BDai%2C+Xiaoxia%3BYang%2C+Wei%3BWang%2C+Yinsheng%3BWoodgate%2C+Roger&rft.aulast=McIntyre&rft.aufirst=Justyna&rft.date=2015-11-06&rft.volume=290&rft.issue=45&rft.spage=27332&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M115.675769 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-22 N1 - Date created - 2015-11-07 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 3GV8; PDB; 4GK5; 2KWV; 4FJO; 2ZVM; 2L0F N1 - SuppNotes - Cited By: Mol Cell Biol. 2004 Jan;24(2):936-43 [14701763] Mol Cell. 2004 May 21;14(4):491-500 [15149598] Nature. 2004 Jul 15;430(6997):377-80 [15254543] DNA Repair (Amst). 2004 Nov 2;3(11):1503-14 [15380106] Bioessays. 2005 Apr;27(4):408-15 [15770681] Nat Rev Mol Cell Biol. 2005 Aug;6(8):599-609 [16064136] Nat Cell Biol. 2007 May;9(5):596-603 [17435751] Science. 2005 Dec 16;310(5755):1821-4 [16357261] J Biol Chem. 2006 Dec 29;281(52):40485-92 [17088248] Mutat Res. 1984 Sep-Nov;134(2-3):113-42 [6390190] Arch Biochem Biophys. 1985 Apr;238(1):170-7 [2984995] Carcinogenesis. 1995 Feb;16(2):335-42 [7859366] Cancer Res. 1998 Feb 1;58(3):453-61 [9458089] Chem Biol Interact. 1998 May 15;113(2):133-44 [9717514] Annu Rev Biochem. 1998;67:425-79 [9759494] Mol Cell Biol. 1999 Aug;19(8):5619-30 [10409751] J Biol Chem. 2004 Nov 12;279(46):48360-8 [15342632] Mol Cell Biol. 2005 Feb;25(3):1183-90 [15657443] J Exp Med. 2007 Jan 22;204(1):7-10 [17190841] J Biol Chem. 2007 Aug 24;282(34):24689-96 [17609217] J Cell Biochem. 2007 Sep 1;102(1):98-109 [17372917] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15591-8 [17898175] Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3768-73 [18316726] Cell. 2008 May 16;133(4):653-65 [18485873] Int J Mol Med. 2008 Sep;22(3):381-7 [18698499] Proc Natl Acad Sci U S A. 2008 Aug 26;105(34):12411-6 [18719106] EMBO J. 2008 Nov 5;27(21):2883-95 [18923427] Mol Biol Cell. 2008 Dec;19(12):5193-202 [18799611] J Biol Chem. 2009 Jan 16;284(3):1732-40 [18984581] Genes Cells. 2009 Feb;14(2):101-11 [19170759] Cell. 2009 Apr 3;137(1):133-45 [19345192] Cancer Lett. 2009 Jun 8;278(1):34-40 [19168278] J Biol Chem. 2009 Apr 17;284(16):10552-60 [19208623] EMBO J. 2009 Jun 3;28(11):1644-54 [19440206] J Biol Chem. 2009 Sep 4;284(36):24453-64 [19570987] Mol Cell. 2010 Feb 12;37(3):396-407 [20159558] Arch Biochem Biophys. 2010 Apr 15;496(2):93-100 [20153715] Nat Biotechnol. 2010 Aug;28(8):868-73 [20639865] Mol Cell. 2010 Aug 13;39(3):477-84 [20655260] Biochemistry. 2010 Nov 30;49(47):10198-207 [21049971] J Biol Chem. 2011 Jan 14;286(2):1364-73 [20929865] Mol Cell Proteomics. 2011 Mar;10(3):M110.003590 [21139048] J Biol Chem. 2011 May 20;286(20):17503-11 [21454642] Mol Cell Proteomics. 2011 Oct;10(10):M111.013284 [21890473] Mol Cell. 2011 Oct 21;44(2):325-40 [21906983] Nat Rev Mol Cell Biol. 2012 Mar;13(3):141-52 [22358330] Toxicol Sci. 2012 May;127(1):130-8 [22331492] Annu Rev Biochem. 2012;81:203-29 [22524316] Nat Cell Biol. 2012 Oct;14(10):1089-98 [23000965] Nucleic Acids Res. 2013 Feb 1;41(3):1649-60 [23248005] Mol Cell Proteomics. 2013 Mar;12(3):825-31 [23266961] Nature. 2013 Apr 18;496(7445):372-6 [23503661] Nat Methods. 2013 Jul;10(7):634-7 [23749302] J Proteome Res. 2013 Sep 6;12(9):4167-75 [23978223] Nat Protoc. 2013 Oct;8(10):1950-60 [24051958] J Biol Chem. 2014 Mar 14;289(11):7702-17 [24469461] Nucleic Acids Res. 2015 Jan;43(Database issue):D512-20 [25514926] DNA Repair (Amst). 2015 May;29:139-46 [25733082] DNA Repair (Amst). 2015 May;29:166-79 [25743599] J Biol Chem. 2003 Aug 8;278(32):29649-54 [12777390] Nature. 2000 Apr 27;404(6781):1011-3 [10801132] Genes Dev. 2000 Jul 1;14(13):1642-50 [10887158] Mol Cell Biol. 2000 Oct;20(19):7099-108 [10982826] Science. 2001 Mar 16;291(5511):2156-9 [11251121] J Biol Chem. 2001 Jul 27;276(30):27936-43 [11369780] Mol Cell. 2001 Jul;8(1):7-8 [11515498] Nature. 2002 Sep 12;419(6903):135-41 [12226657] EMBO J. 2002 Nov 15;21(22):6246-56 [12426396] Nucleic Acids Res. 2002 Dec 1;30(23):5284-92 [12466554] J Biol Chem. 2003 Mar 7;278(10):8516-25 [12496265] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M115.675769 ER - TY - JOUR T1 - Perspective: Sustaining the big-data ecosystem AN - 1746880485; PQ0002289512 JF - Nature AU - Bourne, Philip E AU - Lorsch, Jon R AU - Green, Eric D AD - US National Institutes of Health. He was previously associate vice-chancellor for innovation and industry alliances at the Office of Research Affairs at the University of California, San Diego. Y1 - 2015/11/04/ PY - 2015 DA - 2015 Nov 04 SP - S16 EP - S17 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 527 IS - 7576 SN - 0028-0836, 0028-0836 KW - Ecology Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746880485?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Perspective%3A+Sustaining+the+big-data+ecosystem&rft.au=Bourne%2C+Philip+E%3BLorsch%2C+Jon+R%3BGreen%2C+Eric+D&rft.aulast=Bourne&rft.aufirst=Philip&rft.date=2015-11-04&rft.volume=527&rft.issue=7576&rft.spage=S16&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/10.1038%2F527S16a LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Last updated - 2016-06-22 DO - http://dx.doi.org/10.1038/527S16a ER - TY - JOUR T1 - Targeting glycolysis by 3-bromopyruvate improves tamoxifen cytotoxicity of breast cancer cell lines. AN - 1730020281; 26526196 AB - Tamoxifen is the standard endocrine therapy for ER+ breast cancer; however, many women still relapse after long-term therapy. 3-Bromopyruvate, a glycolytic inhibitor, has shown high selective anti-tumor activity in vitro, and in vivo. The aim of this study was to evaluate the possible augmentation of the effect of tamoxifen via reprograming cancer cell metabolism using 3-bromopyruvate. An in vitro screening of antitumor activity as well as the apoptotic, anti-metastatic, and anti-angiogenic potentials of the combination therapy were carried out using different techniques on breast cancer cell lines MCF7and T47D. In addition the antitumor effect of the combined therapy was done on mice bearing tumor. Our results showed modulation in apoptosis, angiogenesis and metastatic potential by either drug alone; however, their combination has surpassed that of the individual one. Combination regimen enhanced activated caspases-3, 7 and 9, as well as oxidative stress, signified by increased malondialdehyde and decreased glutathione level. Additionally, the angiogenesis and metastasis markers, including hypoxia inducing factor-1α, vascular endothelia growth factor, and metaloproteinases-2 and 9 were decreased after using the combination regimen. These results were further confirmed by the in vivo study, which depicted a decrease in the tumor volume and angiogenesis and an increase in oxidative stress as well. 3-bromopyruvate could be a valuable compound when added with tamoxifen in breast cancer treatment. JF - BMC cancer AU - Attia, Yasmin M AU - El-Abhar, Hanan S AU - Al Marzabani, Mahmoud M AU - Shouman, Samia A AD - Pharmacology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Kasr Al Eini Street, Fom El Khalig, Cairo, Egypt, 11796. Yasmin.m.attia@gmail.com. ; Pharmacology and Toxicology Department, Faculty of Pharmacy, Cairo University, Kasr El-Aini St, Cairo, Egypt, 11562. hanan.elabhar@pharma.cu.edu.eg. ; Pharmacology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Kasr Al Eini Street, Fom El Khalig, Cairo, Egypt, 11796. mahmoud.almarzanani@nci.cu.edu.eg. ; Pharmacology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Kasr Al Eini Street, Fom El Khalig, Cairo, Egypt, 11796. samia.shouman@nci.cu.edu.eg. Y1 - 2015/11/03/ PY - 2015 DA - 2015 Nov 03 SP - 838 VL - 15 KW - Pyruvates KW - 0 KW - Tamoxifen KW - 094ZI81Y45 KW - bromopyruvate KW - 63JMV04GRK KW - Index Medicus KW - Cell Proliferation -- drug effects KW - Animals KW - Glycolysis -- drug effects KW - Humans KW - Apoptosis -- drug effects KW - Xenograft Model Antitumor Assays KW - Mice KW - Cell Line, Tumor KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Tamoxifen -- administration & dosage KW - Female KW - Breast Neoplasms -- drug therapy KW - Neovascularization, Pathologic -- drug therapy KW - Neoplasm Recurrence, Local -- drug therapy KW - Breast Neoplasms -- pathology KW - Pyruvates -- administration & dosage KW - Neovascularization, Pathologic -- pathology KW - Neoplasm Recurrence, Local -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1730020281?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+cancer&rft.atitle=Targeting+glycolysis+by+3-bromopyruvate+improves+tamoxifen+cytotoxicity+of+breast+cancer+cell+lines.&rft.au=Attia%2C+Yasmin+M%3BEl-Abhar%2C+Hanan+S%3BAl+Marzabani%2C+Mahmoud+M%3BShouman%2C+Samia+A&rft.aulast=Attia&rft.aufirst=Yasmin&rft.date=2015-11-03&rft.volume=15&rft.issue=&rft.spage=838&rft.isbn=&rft.btitle=&rft.title=BMC+cancer&rft.issn=1471-2407&rft_id=info:doi/10.1186%2Fs12885-015-1850-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-01 N1 - Date created - 2015-11-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Toxicol Lett. 2003 Apr 4;139(2-3):125-33 [12628748] Biomed Pharmacother. 2010 Feb;64(2):88-92 [20005069] J Biol Chem. 2004 Sep 17;279(38):39846-55 [15247300] Biochem Biophys Res Commun. 2004 Nov 5;324(1):269-75 [15465013] Anal Biochem. 1976 May 7;72:248-54 [942051] J Natl Cancer Inst. 1990 Jul 4;82(13):1107-12 [2359136] Methods Enzymol. 1990;186:421-31 [2233309] Growth Factors. 1992;7(1):53-64 [1380254] Tumori. 1993 Aug 31;79(4):268-72 [8249181] J Exp Med. 1996 May 1;183(5):1957-64 [8642305] J Natl Cancer Inst. 1997 Jun 4;89(11):747-9 [9182965] Anticancer Res. 2010 Mar;30(3):923-35 [20393016] Cancer Res. 2011 Jul 1;71(13):4585-97 [21498634] Leuk Res. 2011 Jun;35(6):814-20 [21316758] Nat Rev Cancer. 2012 Jan;12(1):9-22 [22169972] PLoS One. 2012;7(2):e31532 [22384035] Genome Res. 2003 Dec;13(12):2665-73 [14656971] Genetics. 2006 Dec;174(4):2229-43 [17028312] Cancer Res. 2007 Feb 1;67(3):1282-90 [17283165] Breast Cancer Res Treat. 2007 May;102(3):253-61 [17031577] Mol Cancer Ther. 2007 Sep;6(9):2554-62 [17876052] Mitochondrion. 2013 May;13(3):199-208 [22846431] J Vasc Interv Radiol. 2013 May;24(5):737-43 [23489770] Lancet. 2013 Mar 9;381(9869):805-16 [23219286] Life Sci. 2014 Mar 3;97(2):116-22 [24361399] Cell Biol Toxicol. 2000;16(4):207-19 [11101003] Exp Cell Res. 1998 Jun 15;241(2):426-34 [9637784] Arch Biochem Biophys. 1959 May;82(1):70-7 [13650640] Cancer. 2005 Apr 1;103(7):1408-14 [15744746] J Pathol. 2005 Jul;206(3):291-304 [15906272] Mol Endocrinol. 2005 Aug;19(8):2006-19 [15774498] Cancer Res. 2006 May 1;66(9):4789-94 [16651433] Biochim Biophys Acta. 2006 May-Jun;1757(5-6):639-47 [16678785] Oncogene. 2006 Aug 7;25(34):4633-46 [16892078] Surgery. 2006 Oct;140(4):607-14; discussion 614-5 [17011908] Carcinogenesis. 2006 Dec;27(12):2424-33 [16785249] Apoptosis. 2001 Dec;6(6):469-77 [11595837] Genes Dev. 2001 Oct 15;15(20):2675-86 [11641274] Methods. 2001 Dec;25(4):402-8 [11846609] Adv Exp Med Biol. 2007;608:1-22 [17993229] Oncogene. 2008 Feb 28;27(10):1472-7 [17767197] J Bioenerg Biomembr. 2008 Jun;40(3):123-6 [18780167] Mol Cancer Res. 2008 Oct;6(10):1630-8 [18922978] Toxicology. 2009 Jan 8;255(1-2):58-64 [18992300] J Proteome Res. 2009 Jan;8(1):104-12 [18954100] Semin Cancer Biol. 2009 Feb;19(1):17-24 [19101634] Biochim Biophys Acta. 2009 May;1787(5):553-60 [19285479] Biochem Biophys Res Commun. 2009 Jul 24;385(2):251-6 [19460356] FEBS Lett. 2009 Dec 17;583(24):3966-73 [19850042] Med Chem. 2009 Nov;5(6):491-6 [19534685] Curr Opin Genet Dev. 2010 Feb;20(1):51-6 [19942427] Oncol Rep. 2013 Jan;29(1):329-34 [23076497] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/s12885-015-1850-4 ER - TY - JOUR T1 - In-between sprawl and fires: long-term forest expansion and settlement dynamics at the wildland-urban interface in Rome, Italy AN - 1787982334; PQ0002955688 AB - Understanding the intimate dynamics of urban-wildland interfaces in Mediterranean landscapes is particularly challenging because of multiple biophysical factors (dry or arid climate, low-quality soils, poor vegetation cover) determining an increased environmental sensitivity to human pressure. Although dense and compact cities were sprawling rapidly in the most recent decades, many suburban areas in southern Europe still preserve biodiversity-rich habitats, traditional crop mosaics and high-quality relict forest stands. Diachronic forest and settlement maps were analysed over two time intervals (1936-1974 and 1974-2006) representing different socio-economic contexts on a local scale with the aim to assess trends in forest land cover vis a vis urban growth in Rome, central Italy. Forests expanded into agricultural land during the whole time period following cropland abandonment and benefiting from a higher level of land protection from urbanisation, especially during the most recent decades. Although the broadleaved wood dominated the composition of forest fragments at the wildland-urban interface at both the beginning and the end of the study period, coniferous stands showed a slower decrease compared to other wood types, such as those dominated by chestnut or beech. The observed changes in forest composition are the result of a higher disturbance level, possibly triggered by the increase of fire frequency and severity, a higher fragmentation of natural land, intense soil sealing and a larger occurrence of invasive species. Forest diversity increased especially in areas with medium-density settlements, indicating a tendency towards more heterogeneous forest structures at the urban-wildland interface compared to natural landscapes. A long-term monitoring of settlement dynamics and woodland expansion is required to inform a sustainable management of Mediterranean suburban forests. JF - International Journal of Sustainable Development and World Ecology AU - Biasi, Rita AU - Colantoni, Andrea AU - Ferrara, Carlotta AU - Ranalli, Flavia AU - Salvati, Luca AD - Dipartimento per l'Innovazione nei Sistemi Biologici, Agroalimentari e Forestali, Universita degli studi di Viterbo, Via S. Camillo de Lellis snc, I-01100 Viterbo, Italy Y1 - 2015/11/02/ PY - 2015 DA - 2015 Nov 02 SP - 467 EP - 475 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 22 IS - 6 SN - 1350-4509, 1350-4509 KW - Sustainability Science Abstracts KW - MED, Italy KW - Sensitivity KW - Fires KW - Urban sprawl KW - Urbanization KW - Landscape KW - Socioeconomics KW - Wood KW - Forests KW - Crops KW - Soil KW - Vegetation cover KW - Cities KW - MED KW - Invasive species KW - Disturbance KW - M3 1010:Issues in Sustainable Development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1787982334?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Assamodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Sustainable+Development+and+World+Ecology&rft.atitle=In-between+sprawl+and+fires%3A+long-term+forest+expansion+and+settlement+dynamics+at+the+wildland-urban+interface+in+Rome%2C+Italy&rft.au=Biasi%2C+Rita%3BColantoni%2C+Andrea%3BFerrara%2C+Carlotta%3BRanalli%2C+Flavia%3BSalvati%2C+Luca&rft.aulast=Biasi&rft.aufirst=Rita&rft.date=2015-11-02&rft.volume=22&rft.issue=6&rft.spage=467&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Sustainable+Development+and+World+Ecology&rft.issn=13504509&rft_id=info:doi/10.1080%2F13504509.2015.1064488 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-05-01 N1 - Last updated - 2016-07-07 N1 - SubjectsTermNotLitGenreText - Fires; Sensitivity; Urban sprawl; Urbanization; Landscape; Forests; Wood; Socioeconomics; Crops; Soil; Cities; Vegetation cover; Invasive species; Disturbance; MED, Italy; MED DO - http://dx.doi.org/10.1080/13504509.2015.1064488 ER - TY - JOUR T1 - Use of Ciliogenesis to Detect Aneugens: The Role of Primary Cilia. AN - 1730024881; 26523475 AB - Primary cilia arise from the centrosomes of quiescent or post-mitotic cells, and serve as sensory organelles that communicate mechanical and chemical stimuli from the environment to the interior of the cell. Cilium formation may, therefore, become a useful end point signaling exposure to genotoxins or aneugens. Here we have used the aneugen, zidovudine (AZT), an antiretroviral drug that induces DNA replication arrest and centrosomal amplification (>2 centrosomes per quiescent cell), to evaluate cilia formation in retinal epithelial (pigmented) cells. Since cilia are derived from centrosomes, and aneugens can induce centrosomal amplification, the production of multiple cilia arising from multiple centrosomes may reveal the aneugenic nature of the agents. Cells were exposed to AZT to induce centrosomal amplification, cultured without serum to allow the centrioles to develop cilia, and immunostained to visualize cilia and centrosomes. Nuclear DNA was stained with DAPI. Preliminary observations suggest that cells with multiple centrosomes are able to generate extra cilia. Copyright © 2015 John Wiley & Sons, Inc. JF - Current protocols in toxicology AU - Divi, Kathyayini V AU - Ward, Yvona AU - Poirier, Miriam C AU - Olivero, Ofelia A AD - Carcinogen-DNA Interactions Section, LCBG, CCR, NIH, Bethesda, Maryland. ; Cell and Cancer Biology Branch, National Cancer Institute, NIH, Bethesda, Maryland. Y1 - 2015/11/02/ PY - 2015 DA - 2015 Nov 02 SP - 3.13.1 EP - 8 VL - 66 KW - Aneugens KW - 0 KW - Zidovudine KW - 4B9XT59T7S KW - Index Medicus KW - centrosomal amplification KW - aneugens KW - primary cilia KW - AZT KW - Retinal Pigment Epithelium -- cytology KW - Retinal Pigment Epithelium -- ultrastructure KW - Retinal Pigment Epithelium -- drug effects KW - Centrosome -- drug effects KW - Centrosome -- ultrastructure KW - Cell Line KW - Cilia -- drug effects KW - Zidovudine -- toxicity KW - Aneuploidy KW - DNA Damage KW - Aneugens -- toxicity KW - Cilia -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1730024881?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+protocols+in+toxicology&rft.atitle=Use+of+Ciliogenesis+to+Detect+Aneugens%3A+The+Role+of+Primary+Cilia.&rft.au=Divi%2C+Kathyayini+V%3BWard%2C+Yvona%3BPoirier%2C+Miriam+C%3BOlivero%2C+Ofelia+A&rft.aulast=Divi&rft.aufirst=Kathyayini&rft.date=2015-11-02&rft.volume=66&rft.issue=&rft.spage=3.13.1&rft.isbn=&rft.btitle=&rft.title=Current+protocols+in+toxicology&rft.issn=1934-9262&rft_id=info:doi/10.1002%2F0471140856.tx0313s66 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-19 N1 - Date created - 2015-11-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Sci. 2006 Apr;97(4):252-8 [16630116] J Histochem Cytochem. 1985 Aug;33(8):813-20 [3894499] Mutat Res. 1993 May;287(1):3-15 [7683383] Cytometry. 1999 Apr 1;35(4):353-62 [10213201] J Infect Dis. 2013 Jul 15;208(2):244-8 [23559463] J Cell Biol. 2007 Oct 22;179(2):321-30 [17954613] Curr Protoc Neurosci. 2001 May;Chapter 2:Unit 2.1 [18428456] Mutat Res. 2009 Jun 1;665(1-2):67-74 [19427513] J Cell Biol. 1982 Jun;93(3):938-49 [7119006] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/0471140856.tx0313s66 ER - TY - JOUR T1 - CDK4 Amplification Reduces Sensitivity to CDK4/6 Inhibition in Fusion-Positive Rhabdomyosarcoma AN - 1808616943; PQ0003449450 AB - Purpose: Rhabdomyosarcoma (RMS) is the most common pediatric soft tissue sarcoma and includes a PAX3- or PAX7-FOXO1 fusion-positive subtype. Amplification of chromosomal region 12q13-q14, which contains the CDK4 proto-oncogene, was identified in an aggressive subset of fusion-positive RMS. CDK4/6 inhibitors have antiproliferative activity in CDK4-amplified liposarcoma and neuroblastoma, suggesting CDK4/6 inhibition as a potential therapeutic strategy in fusion-positive RMS.Experimental Design: We examined the biologic consequences of CDK4 knockdown, CDK4 overexpression, and pharmacologic CDK4/6 inhibition by LEE011 in fusion-positive RMS cell lines and xenografts.Results: Knockdown of CDK4 abrogated proliferation and transformation of 12q13-14-amplified and nonamplified fusion-positive RMS cells via G1-phase cell-cycle arrest. This arrest was mediated by reduced RB phosphorylation and E2F-responsive gene expression. Significant differences in E2F target expression, cell-cycle distribution, proliferation, or transformation were not observed in RMS cells overexpressing CDK4. Treatment with LEE011 phenocopied CDK4 knockdown, decreasing viability, RB phosphorylation, and E2F-responsive gene expression and inducing G1-phase cell-cycle arrest. Although all fusion-positive cell lines showed sensitivity to CDK4/6 inhibition, there was diminished sensitivity associated with CDK4 amplification and overexpression. This variable responsiveness to LEE011 was recapitulated in xenograft models of CDK4-amplified and nonamplified fusion-positive RMS.Conclusions: Our data demonstrate that CDK4 is necessary but overexpression is not sufficient for RB-E2F-mediated G1-phase cell-cycle progression, proliferation, and transformation in fusion-positive RMS. Our studies indicate that LEE011 is active in the setting of fusion-positive RMS and suggest that low CDK4-expressing fusion-positive tumors may be particularly susceptible to CDK4/6 inhibition. Clin Cancer Res; 21(21); 4947-59. copyright 2015 AACR.See related commentary by Gatz and Shipley, p. 4750 JF - Clinical Cancer Research AU - Olanich, Mary E AU - Sun, Wenyue AU - Hewitt, Stephen M AU - Abdullaev, Zied AU - Pack, Svetlana D AU - Barr, Frederic G AD - Cancer Molecular Pathology Section, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, barrfg@mail.nih.gov Y1 - 2015/11/01/ PY - 2015 DA - 2015 Nov 01 SP - 4947 EP - 4959 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 21 SN - 1078-0432, 1078-0432 KW - Biotechnology and Bioengineering Abstracts KW - Transformation KW - Data processing KW - Pediatrics KW - Retinoblastoma protein KW - Tumors KW - Cyclin-dependent kinase 4 KW - soft tissue sarcoma KW - Neuroblastoma KW - Gene expression KW - Liposarcoma KW - E2F protein KW - Phosphorylation KW - Xenografts KW - Cell proliferation KW - Proto-oncogenes KW - Rhabdomyosarcoma KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808616943?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Cancer+Research&rft.atitle=CDK4+Amplification+Reduces+Sensitivity+to+CDK4%2F6+Inhibition+in+Fusion-Positive+Rhabdomyosarcoma&rft.au=Olanich%2C+Mary+E%3BSun%2C+Wenyue%3BHewitt%2C+Stephen+M%3BAbdullaev%2C+Zied%3BPack%2C+Svetlana+D%3BBarr%2C+Frederic+G&rft.aulast=Olanich&rft.aufirst=Mary&rft.date=2015-11-01&rft.volume=21&rft.issue=21&rft.spage=4947&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-2955 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Transformation; Data processing; Pediatrics; Retinoblastoma protein; Tumors; Cyclin-dependent kinase 4; Neuroblastoma; soft tissue sarcoma; Gene expression; E2F protein; Liposarcoma; Phosphorylation; Xenografts; Cell proliferation; Proto-oncogenes; Rhabdomyosarcoma DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-2955 ER - TY - JOUR T1 - Prevention of cyclophosphamide-induced hepatotoxicity and genotoxicity: Effect of an l-cysteine based oxovanadium(IV) complex on oxidative stress and DNA damage AN - 1785242377; PQ0002384823 AB - Vanadium has been emerged as a promising agent owing to its ability to prevent several types of cancer. This study was aimed to investigate the protective role of an organovanadium complex, viz., oxovanadium(IV)-l-cysteine methyl ester (VC-IV) against cyclophosphamide (CP)-induced hepatotoxicity and genotoxicity in mice. Oral administration of VC-IV quite effectively ameliorated CP-induced histopathological lesions and reduced levels of alanine transaminase, aspartate transaminase and alkaline phosphatase. In addition, VC-IV significantly attenuated CP-induced oxidative stress in the liver as evident from levels of reactive oxygen species, nitric oxide and lipid peroxidation. Restoration of glutathione level and activities of antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase) were also observed upon VC-IV administration. Moreover, VC-IV significantly mitigated CP-induced chromosomal aberrations, micronuclei formation, DNA fragmentation and apoptosis in bone marrow cells and DNA damage in lymphocytes. The present study showed that VC-IV could provide adequate protection against CP-induced hepatotoxicity and genotoxicity in vivo. JF - Environmental Toxicology and Pharmacology AU - Basu, Abhishek AU - Bhattacharjee, Arin AU - Samanta, Amalesh AU - Bhattacharya, Sudin AD - Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, 37, S. P. Mukherjee Road, Kolkata 700026, West Bengal, India Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 747 EP - 757 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 40 IS - 3 SN - 1382-6689, 1382-6689 KW - Toxicology Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Environment Abstracts KW - Chemoprotection KW - Cyclophosphamide KW - Oxidative stress KW - Histopathology KW - DNA damage KW - Apoptosis KW - Antioxidants KW - Lipids KW - Micronuclei KW - Bone marrow KW - Lymphocytes KW - Glutathione transferase KW - DNA fragmentation KW - Reactive oxygen species KW - Glutathione peroxidase KW - Superoxide dismutase KW - Aspartate transaminase KW - Hepatotoxicity KW - Chromosome aberrations KW - Vanadium KW - Peroxidation KW - Genotoxicity KW - Oral administration KW - Enzymes KW - Mice KW - Esters KW - Alanine transaminase KW - Lipid peroxidation KW - Cancer KW - hepatotoxicity KW - Catalase KW - Prevention KW - Alkaline phosphatase KW - DNA KW - Liver KW - Nitric oxide KW - X 24310:Pharmaceuticals KW - N 14820:DNA Metabolism & Structure KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1785242377?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Toxicology+and+Pharmacology&rft.atitle=Prevention+of+cyclophosphamide-induced+hepatotoxicity+and+genotoxicity%3A+Effect+of+an+l-cysteine+based+oxovanadium%28IV%29+complex+on+oxidative+stress+and+DNA+damage&rft.au=Basu%2C+Abhishek%3BBhattacharjee%2C+Arin%3BSamanta%2C+Amalesh%3BBhattacharya%2C+Sudin&rft.aulast=Basu&rft.aufirst=Abhishek&rft.date=2015-11-01&rft.volume=40&rft.issue=3&rft.spage=747&rft.isbn=&rft.btitle=&rft.title=Environmental+Toxicology+and+Pharmacology&rft.issn=13826689&rft_id=info:doi/10.1016%2Fj.etap.2015.08.035 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-05-01 N1 - Last updated - 2016-05-12 N1 - SubjectsTermNotLitGenreText - Apoptosis; Antioxidants; Micronuclei; Bone marrow; Cyclophosphamide; Lymphocytes; Glutathione transferase; DNA fragmentation; Reactive oxygen species; Oxidative stress; Superoxide dismutase; Glutathione peroxidase; Aspartate transaminase; Chromosome aberrations; Vanadium; Genotoxicity; Oral administration; Enzymes; Alanine transaminase; Catalase; hepatotoxicity; Cancer; Lipid peroxidation; DNA damage; Alkaline phosphatase; Liver; Nitric oxide; Peroxidation; Lipids; Mice; Esters; Prevention; DNA; Hepatotoxicity DO - http://dx.doi.org/10.1016/j.etap.2015.08.035 ER - TY - JOUR T1 - Neighbor-directed histidine N ( tau )-alkylation: A route to imidazolium-containing phosphopeptide macrocycles AN - 1776649968; PQ0002784277 AB - Our recently discovered, selective, on-resin route to N( tau )-alkylated imidazolium-containing histidine residues affords new strategies for peptide mimetic design. In this, we demonstrate the use of this chemistry to prepare a series of macrocyclic phosphopeptides, in which imidazolium groups serve as ring-forming junctions. Interestingly, these cationic moieties subsequently serve to charge-mask the phosphoamino acid group that directed their formation. Neighbor-directed histidine N( tau )-alkylation opens the door to new families of phosphopeptidomimetics for use in a range of chemical biology contexts. Biopolymers (Pept Sci) 104: 663-673, 2015. JF - Biopolymers AU - Qian, Wen-Jian AU - Park, Jung-Eun AU - Grant, Robert AU - Lai, Christopher C AU - Kelley, James A AU - Yaffe, Michael B AU - Lee, Kyung S AU - Burke, Terrence R AD - Chemical Biology Laboratory, Center for Cancer Research, National Cancer Institute-Frederick, Frederick, MD, 21702. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 663 EP - 673 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 104 IS - 6 SN - 0006-3525, 0006-3525 KW - Biotechnology and Bioengineering Abstracts KW - New families KW - Histidine KW - Biopolymers KW - W 30935:Food Biotechnology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1776649968?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biopolymers&rft.atitle=Neighbor-directed+histidine+N+%28+tau+%29-alkylation%3A+A+route+to+imidazolium-containing+phosphopeptide+macrocycles&rft.au=Qian%2C+Wen-Jian%3BPark%2C+Jung-Eun%3BGrant%2C+Robert%3BLai%2C+Christopher+C%3BKelley%2C+James+A%3BYaffe%2C+Michael+B%3BLee%2C+Kyung+S%3BBurke%2C+Terrence+R&rft.aulast=Qian&rft.aufirst=Wen-Jian&rft.date=2015-11-01&rft.volume=104&rft.issue=6&rft.spage=663&rft.isbn=&rft.btitle=&rft.title=Biopolymers&rft.issn=00063525&rft_id=info:doi/10.1002%2Fbip.22698 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - New families; Histidine; Biopolymers DO - http://dx.doi.org/10.1002/bip.22698 ER - TY - JOUR T1 - Assay Development for Image-Based Quantification of Intracellular Bacterial Replication and Analysis of the Innate Immune Response to Infection AN - 1768576019; PQ0002687087 AB - Severe bacterial infection can lead to inflammation, host tissue damage, and ultimately disseminated septic shock. The mammalian innate immune system responds to microbial infection through the detection of invariant pathogen-associated molecular patterns (PAMPs) by a range of pattern recognition receptors (PRRs) expressed by the host cell. A successful immune response involves tightly coordinated signaling from these receptors, leading to a robust transcriptional response producing cytokines and antimicrobial effectors. While the PRR-expressing phagocytes of the host innate immune system function to contain and degrade internalized bacteria through pathways such as selective autophagy, pathogenic bacteria may subvert this process to replicate in the host cell. We describe the development of imaging assays to investigate these host-pathogen interactions through gene perturbation screens, which could lead to the identification of novel effectors of the host response to bacterial infection. We identify markers of coordinated initial signaling in macrophages challenged with ligands to PRRs of the toll-like receptor (TLR) family and compare this response to that induced by intact bacteria of the Burkholderia cenocepacia complex (Bcc), an opportunistic pathogen that causes life-threatening infections in patients with cystic fibrosis and chronic granulomatous disease. Bcc has been shown to escape the endocytic pathway, activate selective autophagy, and replicate within human macrophages. We demonstrate robust image-based quantification of multiple stages of Bcc infection of macrophages: ubiquitin tagging of cytosolic bacteria, recruitment of selective autophagy effector proteins, and intracellular bacterial replication, and we show perturbation of bacterial replication using drug treatment or siRNA-based gene knockdown. The described panel of imaging assays can be extended to other bacterial infections and pathogenic ligand combinations where high-content siRNA screening could provide significant new insight into regulation of the innate immune response to infection. JF - Assay and Drug Development Technologies AU - Miller, Alexandra H AU - Vayttaden, Sharat J AU - Al-Khodor, Souhaila AU - Fraser, Iain DC AD - Signaling Systems Unit, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 515 EP - 528 PB - Mary Ann Liebert, Inc., 2 Madison Ave Larchmont NY 10538-1962 United States VL - 13 IS - 9 SN - 1540-658X, 1540-658X KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts; Biotechnology and Bioengineering Abstracts KW - Macrophages KW - Burkholderia KW - Immunosuppressive agents KW - Pattern recognition KW - Phagocytes KW - Cytokines KW - Phagocytosis KW - Cystic fibrosis KW - Ubiquitin KW - Bacteria KW - Replication KW - Transcription KW - Drug development KW - Septic shock KW - Pathogens KW - imaging KW - Opportunist infection KW - Antimicrobial agents KW - Inflammation KW - siRNA KW - Host-pathogen interactions KW - Chronic infection KW - Immune response KW - Chronic granulomatous disease KW - Toll-like receptors KW - Signal transduction KW - J 02350:Immunology KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768576019?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Assay+and+Drug+Development+Technologies&rft.atitle=Assay+Development+for+Image-Based+Quantification+of+Intracellular+Bacterial+Replication+and+Analysis+of+the+Innate+Immune+Response+to+Infection&rft.au=Miller%2C+Alexandra+H%3BVayttaden%2C+Sharat+J%3BAl-Khodor%2C+Souhaila%3BFraser%2C+Iain+DC&rft.aulast=Miller&rft.aufirst=Alexandra&rft.date=2015-11-01&rft.volume=13&rft.issue=9&rft.spage=515&rft.isbn=&rft.btitle=&rft.title=Assay+and+Drug+Development+Technologies&rft.issn=1540658X&rft_id=info:doi/10.1089%2Fadt.2015.664 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Number of references - 22 N1 - Last updated - 2016-06-22 N1 - SubjectsTermNotLitGenreText - Macrophages; Replication; Transcription; Drug development; Pathogens; Septic shock; imaging; Immunosuppressive agents; Inflammation; Antimicrobial agents; Opportunist infection; Pattern recognition; siRNA; Phagocytes; Host-pathogen interactions; Chronic infection; Cytokines; Immune response; Chronic granulomatous disease; Phagocytosis; Cystic fibrosis; Toll-like receptors; Signal transduction; Ubiquitin; Bacteria; Burkholderia DO - http://dx.doi.org/10.1089/adt.2015.664 ER - TY - JOUR T1 - LDlink: a web-based application for exploring population-specific haplotype structure and linking correlated alleles of possible functional variants AN - 1753469191; PQ0002423340 AB - Summary: Assessing linkage disequilibrium (LD) across ancestral populations is a powerful approach for investigating population-specific genetic structure as well as functionally mapping regions of disease susceptibility. Here, we present LDlink, a web-based collection of bioinformatic modules that query single nucleotide polymorphisms (SNPs) in population groups of interest to generate haplotype tables and interactive plots. Modules are designed with an emphasis on ease of use, query flexibility, and interactive visualization of results. Phase 3 haplotype data from the 1000 Genomes Project are referenced for calculating pairwise metrics of LD, searching for proxies in high LD, and enumerating all observed haplotypes. LDlink is tailored for investigators interested in mapping common and uncommon disease susceptibility loci by focusing on output linking correlated alleles and highlighting putative functional variants.Availability and implementation: LDlink is a free and publically available web tool which can be accessed at http://analysistools.nci.nih.gov/LDlink/. JF - Bioinformatics AU - Machiela, Mitchell J AU - Chanock, Stephen J AD - *To whom correspondence should be addressed., mitchell.machiela@nih.gov Y1 - 2015/11/01/ PY - 2015 DA - 2015 Nov 01 SP - 3555 EP - 3557 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 31 IS - 21 SN - 1367-4803, 1367-4803 KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - Linkage disequilibrium KW - Data processing KW - Haplotypes KW - Single-nucleotide polymorphism KW - Bioinformatics KW - Genetic structure KW - Gene mapping KW - N 14810:Methods KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753469191?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioinformatics&rft.atitle=LDlink%3A+a+web-based+application+for+exploring+population-specific+haplotype+structure+and+linking+correlated+alleles+of+possible+functional+variants&rft.au=Machiela%2C+Mitchell+J%3BChanock%2C+Stephen+J&rft.aulast=Machiela&rft.aufirst=Mitchell&rft.date=2015-11-01&rft.volume=31&rft.issue=21&rft.spage=3555&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtv402 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Last updated - 2016-07-20 N1 - SubjectsTermNotLitGenreText - Linkage disequilibrium; Data processing; Haplotypes; Single-nucleotide polymorphism; Bioinformatics; Genetic structure; Gene mapping DO - http://dx.doi.org/10.1093/bioinformatics/btv402 ER - TY - JOUR T1 - Association of Nrf2 with airway pathogenesis: lessons learned from genetic mouse models AN - 1751217298; PQ0002367405 AB - Nrf2 is a key transcription factor for antioxidant response element (ARE)-bearing genes involved in diverse host defense functions including redox balance, cell cycle, immunity, mitochondrial biogenesis, energy metabolism, and carcinogenesis. Nrf2 in the airways is particularly essential as the respiratory system continuously interfaces with environmental stress. Since Nrf2 was determined to be a susceptibility gene for a model of acute lung injury, its protective capacity in the airways has been demonstrated in experimental models of human disorders using Nrf2 mutant mice which were susceptible to supplemental respiratory therapy (e.g., hyperoxia, mechanical ventilation), cigarette smoke, allergens, virus, environmental pollutants, and fibrotic agents compared to wild-type littermates. Recent studies also determined that Nrf2 is indispensable in developmental lung injury. While association studies with genetic NRF2 polymorphisms supported a protective role for murine Nrf2 in oxidative airway diseases, somatic NRF2 mutations enhanced NRF2-ARE responses, and were favorable for lung carcinogenesis and chemoresistance. Bioinformatic tools have elucidated direct Nrf2 targets as well as Nrf2-interacting networks. Moreover, potent Nrf2-ARE agonists protected oxidant-induced lung phenotypes in model systems, suggesting a therapeutic or preventive intervention. Further investigations on Nrf2 should yield greater understanding of its contribution to normal and pathophysiological function in the airways. JF - Archives of Toxicology AU - Cho, Hye-Youn AU - Kleeberger, Steven R AD - Immunity, Inflammation, and Diseases Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, 111 TW Alexander Dr., Building 101, MD D-201, Research Triangle Park, NC, 27709, USA, cho2@niehs.nih.gov Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 1931 EP - 1957 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 89 IS - 11 SN - 0340-5761, 0340-5761 KW - Genetics Abstracts; Toxicology Abstracts KW - Antioxidants KW - Injuries KW - Energy metabolism KW - Regulatory sequences KW - Gene polymorphism KW - Cell cycle KW - Animal models KW - Mitochondria KW - Hyperoxia KW - Respiratory tract diseases KW - Pollutants KW - Lung KW - Transcription factors KW - Allergens KW - Carcinogenesis KW - Environmental stress KW - Bioinformatics KW - Mutation KW - Evolution KW - X 24380:Social Poisons & Drug Abuse KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751217298?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+Toxicology&rft.atitle=Association+of+Nrf2+with+airway+pathogenesis%3A+lessons+learned+from+genetic+mouse+models&rft.au=Cho%2C+Hye-Youn%3BKleeberger%2C+Steven+R&rft.aulast=Cho&rft.aufirst=Hye-Youn&rft.date=2015-11-01&rft.volume=89&rft.issue=11&rft.spage=1931&rft.isbn=&rft.btitle=&rft.title=Archives+of+Toxicology&rft.issn=03405761&rft_id=info:doi/10.1007%2Fs00204-015-1557-y LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 203 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Antioxidants; Energy metabolism; Injuries; Gene polymorphism; Regulatory sequences; Cell cycle; Animal models; Mitochondria; Hyperoxia; Respiratory tract diseases; Pollutants; Lung; Allergens; Transcription factors; Carcinogenesis; Environmental stress; Bioinformatics; Mutation; Evolution DO - http://dx.doi.org/10.1007/s00204-015-1557-y ER - TY - JOUR T1 - Clonal Diversification and Changes in Lipid Traits and Colony Morphology in Mycobacterium abscessus Clinical Isolates AN - 1751215508; PQ0002308841 AB - The smooth-to-rough colony morphology shift in Mycobacterium abscessus has been implicated in loss of glycopeptidolipid (GPL), increased pathogenicity, and clinical decline in cystic fibrosis (CF) patients. However, the evolutionary phenotypic and genetic changes remain obscure. Serial isolates from nine non-CF patients with persistent M. abscessus infection were characterized by colony morphology, lipid profile via thin-layer chromatography and matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS), sequencing of eight genes in the GPL locus, and expression level of fadD23, a key gene involved in the biosynthesis of complex lipids. All 50 isolates were typed as M. abscessus subspecies abscessus and were clonally related within each patient. Rough isolates, all lacking GPL, predominated at later disease stages, some showing variation within rough morphology. While most (77%) rough isolates harbored detrimental mutations in mps1 and mps2, 13% displayed previously unreported mutations in mmpL4a and mmpS4, the latter yielding a putative GPL precursor. Two isolates showed no deleterious mutations in any of the eight genes sequenced. Mixed populations harboring different GPL locus mutations were detected in 5 patients, demonstrating clonal diversification, which was likely overlooked by conventional acid-fast bacillus (AFB) culture methods. Our work highlights applications of MALDI-TOF MS beyond identification, focusing on mycobacterial lipids relevant in virulence and adaptation. Later isolates displayed accumulation of triacylglycerol and reduced expression of fadD23, sometimes preceding rough colony onset. Our results indicate that clonal diversification and a shift in lipid metabolism, including the loss of GPL, occur during chronic lung infection with M. abscessus. GPL loss alone may not account for all traits associated with rough morphology. JF - Journal of Clinical Microbiology AU - Park, In Kwon AU - Hsu, Amy P AU - Tettelin, Herve AU - Shallom, Shamira J AU - Drake, Steven K AU - Ding, Li AU - Wu, Un-In AU - Adamo, Nick AU - Prevots, D Rebecca AU - Olivier, Kenneth N AD - << + $0, azelazny@mail.nih.gov. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 3438 EP - 3447 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 53 IS - 11 SN - 0095-1137, 0095-1137 KW - Microbiology Abstracts B: Bacteriology KW - Clinical isolates KW - Adaptations KW - Mycobacterium KW - Lipids KW - Mass spectroscopy KW - Glycopeptidolipids KW - Lipid metabolism KW - Virulence KW - Gene expression KW - Colonies KW - Mycobacterium abscessus KW - Pathogenicity KW - Lung KW - Triglycerides KW - Chronic infection KW - Lasers KW - Thin-layer chromatography KW - Bacillus KW - Cystic fibrosis KW - Mutation KW - Evolution KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751215508?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=Clonal+Diversification+and+Changes+in+Lipid+Traits+and+Colony+Morphology+in+Mycobacterium+abscessus+Clinical+Isolates&rft.au=Park%2C+In+Kwon%3BHsu%2C+Amy+P%3BTettelin%2C+Herve%3BShallom%2C+Shamira+J%3BDrake%2C+Steven+K%3BDing%2C+Li%3BWu%2C+Un-In%3BAdamo%2C+Nick%3BPrevots%2C+D+Rebecca%3BOlivier%2C+Kenneth+N&rft.aulast=Park&rft.aufirst=In&rft.date=2015-11-01&rft.volume=53&rft.issue=11&rft.spage=3438&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/10.1128%2FJCM.02015-15 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 35 N1 - Last updated - 2016-07-20 N1 - SubjectsTermNotLitGenreText - Clinical isolates; Adaptations; Lipids; Mass spectroscopy; Lipid metabolism; Glycopeptidolipids; Gene expression; Virulence; Colonies; Pathogenicity; Lung; Triglycerides; Chronic infection; Lasers; Thin-layer chromatography; Mutation; Cystic fibrosis; Evolution; Mycobacterium abscessus; Mycobacterium; Bacillus DO - http://dx.doi.org/10.1128/JCM.02015-15 ER - TY - JOUR T1 - New Real-Time PCR Assays for Detection of Inducible and Acquired Clarithromycin Resistance in the Mycobacterium abscessus Group AN - 1751214482; PQ0002308826 AB - Members of the Mycobacterium abscessus group (MAG) cause lung, soft tissue, and disseminated infections. The oral macrolides clarithromycin and azithromycin are commonly used for treatment. MAG can display clarithromycin resistance through the inducible erm(41) gene or via acquired mutations in the rrl (23S rRNA) gene. Strains harboring a truncation or a T28C substitution in erm(41) lose the inducible resistance trait. Phenotypic detection of clarithromycin resistance requires extended incubation (14 days), highlighting the need for faster methods to detect resistance. Two real-time PCR-based assays were developed to assess inducible and acquired clarithromycin resistance and tested on a total of 90 clinical and reference strains. A SYBR green assay was designed to distinguish between a full-length and truncated erm(41) gene by temperature shift in melting curve analysis. Single nucleotide polymorphism (SNP) allele discrimination assays were developed to distinguish T or C at position 28 of erm(41) and 23S rRNA rrl gene mutations at position 2058 and/or 2059. Truncated and full-size erm(41) genes were detected in 21/90 and 69/90 strains, respectively, with 64/69 displaying T at nucleotide position 28 and 5/69 containing C at that position. Fifteen isolates showed rrl mutations conferring clarithromycin resistance, including A2058G (11 isolates), A2058C (3 isolates), and A2059G (1 isolate). Targeted sequencing and phenotypic assessment of resistance concurred with molecular assay results. Interestingly, we also noted cooccurring strains harboring an active erm(41), inactive erm(41), and/or acquired mutational resistance, as well as slowly growing MAG strains and also strains displaying an inducible resistance phenotype within 5 days, long before the recommended 14-day extended incubation. JF - Journal of Clinical Microbiology AU - Shallom, Shamira J AU - Moura, Natalia S AU - Olivier, Kenneth N AU - Sampaio, Elizabeth P AU - Holland, Steven M AU - Zelazny, Adrian M AD - << + $0, azelazny@mail.nih.gov. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 3430 EP - 3437 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 53 IS - 11 SN - 0095-1137, 0095-1137 KW - Microbiology Abstracts B: Bacteriology KW - Temperature effects KW - rRNA 23S KW - Melting curve KW - Disseminated infection KW - rrl gene KW - Clarithromycin KW - rRNA KW - Mycobacterium abscessus KW - Single-nucleotide polymorphism KW - Lung KW - Azithromycin KW - Polymerase chain reaction KW - Soft tissues KW - J 02310:Genetics & Taxonomy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751214482?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Microbiology&rft.atitle=New+Real-Time+PCR+Assays+for+Detection+of+Inducible+and+Acquired+Clarithromycin+Resistance+in+the+Mycobacterium+abscessus+Group&rft.au=Shallom%2C+Shamira+J%3BMoura%2C+Natalia+S%3BOlivier%2C+Kenneth+N%3BSampaio%2C+Elizabeth+P%3BHolland%2C+Steven+M%3BZelazny%2C+Adrian+M&rft.aulast=Shallom&rft.aufirst=Shamira&rft.date=2015-11-01&rft.volume=53&rft.issue=11&rft.spage=3430&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Microbiology&rft.issn=00951137&rft_id=info:doi/10.1128%2FJCM.01714-15 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 30 N1 - Last updated - 2016-07-20 N1 - SubjectsTermNotLitGenreText - Temperature effects; rRNA; Clarithromycin; Lung; rRNA 23S; Single-nucleotide polymorphism; Azithromycin; Disseminated infection; Melting curve; rrl gene; Polymerase chain reaction; Soft tissues; Mycobacterium abscessus DO - http://dx.doi.org/10.1128/JCM.01714-15 ER - TY - JOUR T1 - Analyzing the influence of PEG molecular weight on the separation of PEGylated gold nanoparticles by asymmetric-flow field-flow fractionation AN - 1751214361; PQ0002364438 AB - Polyethylene glycol (PEG) is an important tool for increasing the biocompatibility of nanoparticle therapeutics. Understanding how these potential nanomedicines will react after they have been introduced into the bloodstream is a critical component of the preclinical evaluation process. Hence, it is paramount that better methods for separating, characterizing, and analyzing these complex and polydisperse formulations are developed. We present a method for separating nominal 30-nm gold nanoparticles coated with various molecular weight PEG moieties that uses only phosphate-buffered saline as the mobile phase, without the need for stabilizing surfactants. The optimized asymmetric-flow field-flow fractionation technique using in-line multiangle light scattering, dynamic light scattering, refractive index, and UV-vis detectors allowed successful separation and detection of a mixture of nanoparticles coated with 2-, 5-, 10-, and 20-kDa PEG. The particles coated with the larger PEG species (10 and 20 kDa) were eluted at times significantly earlier than predicted by field-flow fractionation theory. This was attributed to a lower-density PEG shell for the higher molecular weight PEGylated nanoparticles, which allows a more fluid PEG surface that can be greater influenced by external forces. Hence, the apparent particle hydrodynamic size may fluctuate significantly depending on the overall density of the stabilizing surface coating when an external force is applied. This has considerable implications for PEGylated nanoparticles intended for in vivo application, as nanoparticle size is important for determining circulation times, accumulation sites, and routes of excretion, and highlights the importance and value of the use of secondary size detectors when one is working with complex samples in asymmetric-flow field-flow fractionation. JF - Analytical and Bioanalytical Chemistry AU - Hansen, Matthew AU - Smith, Mackensie C AU - Crist, Rachael M AU - Clogston, Jeffrey D AU - McNeil, Scott E AD - Nanotechnology Characterization Laboratory, Cancer Research Technology Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, 21702, USA, jeffrey.clogston@nih.gov Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 8661 EP - 8672 PB - Springer Science+Business Media, Berlin/Heidelberg Germany VL - 407 IS - 29 SN - 1618-2642, 1618-2642 KW - Pollution Abstracts; Water Resources Abstracts; Aqualine Abstracts KW - Hydrodynamics KW - Light scattering KW - Particulates KW - Evaluation KW - Weight KW - Pollutants KW - Gold KW - Particle size KW - Density KW - Fractionation KW - Excretion KW - Accumulation KW - Surfactants KW - Coatings KW - AQ 00001:Water Resources and Supplies KW - P 9999:GENERAL POLLUTION KW - SW 0540:Properties of water UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751214361?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+and+Bioanalytical+Chemistry&rft.atitle=Analyzing+the+influence+of+PEG+molecular+weight+on+the+separation+of+PEGylated+gold+nanoparticles+by+asymmetric-flow+field-flow+fractionation&rft.au=Hansen%2C+Matthew%3BSmith%2C+Mackensie+C%3BCrist%2C+Rachael+M%3BClogston%2C+Jeffrey+D%3BMcNeil%2C+Scott+E&rft.aulast=Hansen&rft.aufirst=Matthew&rft.date=2015-11-01&rft.volume=407&rft.issue=29&rft.spage=8661&rft.isbn=&rft.btitle=&rft.title=Analytical+and+Bioanalytical+Chemistry&rft.issn=16182642&rft_id=info:doi/10.1007%2Fs00216-015-9056-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 47 N1 - Last updated - 2016-02-29 N1 - SubjectsTermNotLitGenreText - Particle size; Hydrodynamics; Fractionation; Light scattering; Excretion; Particulates; Surfactants; Coatings; Evaluation; Pollutants; Weight; Density; Gold; Accumulation DO - http://dx.doi.org/10.1007/s00216-015-9056-9 ER - TY - JOUR T1 - Polymerase δ replicates both strands after homologous recombination-dependent fork restart. AN - 1735334708; 26436826 AB - To maintain genetic stability, DNA must be replicated only once per cell cycle, and replication must be completed even when individual replication forks are inactivated. Because fork inactivation is common, passive convergence of an adjacent fork is insufficient to rescue all inactive forks. Thus, eukaryotic cells have evolved homologous recombination-dependent mechanisms to restart persistent inactive forks. Completing DNA synthesis via homologous recombination-restarted replication (HoRReR) ensures cell survival, but at a cost. One such cost is increased mutagenesis because HoRReR is more error prone than canonical replication. This increased error rate implies the HoRReR mechanism is distinct from that of a canonical fork. Here we demonstrate, in Schizosaccharomyces pombe, that a DNA sequence duplicated by HoRReR during S phase is replicated semiconservatively, but both the leading and lagging strands are synthesized by DNA polymerase δ. JF - Nature structural & molecular biology AU - Miyabe, Izumi AU - Mizuno, Ken'Ichi AU - Keszthelyi, Andrea AU - Daigaku, Yasukazu AU - Skouteri, Meliti AU - Mohebi, Saed AU - Kunkel, Thomas A AU - Murray, Johanne M AU - Carr, Antony M AD - Genome Damage and Stability Centre, University of Sussex, Brighton, UK. ; Frontier Research Institute for Interdisciplinary Sciences, Tohoku University, Sendai, Japan. ; Genome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 932 EP - 938 VL - 22 IS - 11 KW - DNA Polymerase III KW - EC 2.7.7.- KW - Index Medicus KW - Cell Division KW - Homologous Recombination KW - Schizosaccharomyces -- genetics KW - Schizosaccharomyces -- enzymology KW - Schizosaccharomyces -- physiology KW - DNA Polymerase III -- metabolism KW - DNA Replication UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1735334708?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+structural+%26+molecular+biology&rft.atitle=Polymerase+%CE%B4+replicates+both+strands+after+homologous+recombination-dependent+fork+restart.&rft.au=Miyabe%2C+Izumi%3BMizuno%2C+Ken%27Ichi%3BKeszthelyi%2C+Andrea%3BDaigaku%2C+Yasukazu%3BSkouteri%2C+Meliti%3BMohebi%2C+Saed%3BKunkel%2C+Thomas+A%3BMurray%2C+Johanne+M%3BCarr%2C+Antony+M&rft.aulast=Miyabe&rft.aufirst=Izumi&rft.date=2015-11-01&rft.volume=22&rft.issue=11&rft.spage=932&rft.isbn=&rft.btitle=&rft.title=Nature+structural+%26+molecular+biology&rft.issn=1545-9985&rft_id=info:doi/10.1038%2Fnsmb.3100 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-07 N1 - Date created - 2015-11-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Genet. 2013 Nov;45(11):1319-26 [24056715] Nature. 2013 Oct 17;502(7471):389-92 [24025772] Cold Spring Harb Perspect Biol. 2013 Dec;5(12):a010397 [23881940] EMBO Rep. 2000 Aug;1(2):145-50 [11265754] Nature. 2001 Aug 2;412(6846):557-61 [11484058] Genes Dev. 2003 Jan 1;17(1):64-76 [12514100] Methods Enzymol. 1991;194:795-823 [2005825] Nature. 1994 May 19;369(6477):207-12 [7910375] Mol Cell. 1999 May;3(5):679-85 [10360184] Nature. 2005 Apr 14;434(7035):864-70 [15829956] Nature. 2005 Apr 14;434(7035):907-13 [15829965] Cell. 2005 Jun 3;121(5):689-702 [15935756] Genes Dev. 2005 Aug 15;19(16):1905-19 [16103218] Nature. 2006 Nov 30;444(7119):633-7 [17136093] Nature. 2006 Nov 30;444(7119):638-42 [17136094] Nature. 2013 Oct 17;502(7471):393-6 [24025768] Mol Cell. 2015 Aug 6;59(3):462-77 [26166705] Nature. 2007 Mar 8;446(7132):153-8 [17344846] Nature. 2007 May 3;447(7140):102-5 [17410126] Nature. 2007 Jul 26;448(7152):445-51 [17597761] Genome Res. 2007 Sep;17(9):1296-303 [17675364] Genes Dev. 2007 Dec 15;21(24):3331-41 [18079179] Gene. 2008 Jan 15;407(1-2):63-74 [18054176] Genetics. 2008 Sep;180(1):27-39 [18723894] Trends Cell Biol. 2008 Nov;18(11):521-7 [18824354] Genes Dev. 2009 Feb 1;23(3):291-303 [19204116] Genes Dev. 2009 Dec 15;23(24):2876-86 [20008937] Mol Cell. 2010 Feb 26;37(4):492-502 [20188668] Mol Cell. 2010 Aug 13;39(3):346-59 [20705238] PLoS Biol. 2011;9(2):e1000594 [21347245] Cell. 2011 Apr 29;145(3):435-46 [21529715] PLoS Genet. 2011 Dec;7(12):e1002407 [22144917] Crit Rev Biochem Mol Biol. 2012 May-Jun;47(3):222-35 [22324461] Curr Opin Genet Dev. 2012 Jun;22(3):211-20 [22440479] Cancer Cell. 2012 Jul 10;22(1):106-16 [22789542] Mol Biol Cell. 2012 Aug;23(16):3240-53 [22718908] PLoS Genet. 2012;8(10):e1002976 [23093942] Nature. 2013 Jan 10;493(7431):246-9 [23178809] Hum Mol Genet. 2013 Feb 15;22(4):749-56 [23161748] Cell. 2013 Jan 31;152(3):620-32 [23352430] J Cell Biol. 2013 Mar 18;200(6):699-708 [23479741] Chromosoma. 2013 Mar;122(1-2):33-45 [23446515] Curr Opin Genet Dev. 2013 Apr;23(2):132-9 [23267817] Curr Opin Genet Dev. 2013 Jun;23(3):271-9 [23790415] Oncogene. 2013 Aug 8;32(32):3744-53 [22945645] Proc Natl Acad Sci U S A. 2013 Aug 13;110(33):13475-80 [23898170] PLoS One. 2013;8(12):e83800 [24376751] Science. 2014 Jan 3;343(6166):88-91 [24310611] J Genet. 1949 Dec;49(3):264-85 [24536673] Nat Struct Mol Biol. 2014 Aug;21(8):664-70 [24997598] Genome Res. 2014 Nov;24(11):1751-64 [25217194] Nat Commun. 2015;6:6357 [25721418] Nature. 2015 Feb 26;518(7540):502-6 [25624100] Nat Struct Mol Biol. 2015 Mar;22(3):185-91 [25622295] Nat Struct Mol Biol. 2015 Mar;22(3):192-8 [25664722] Elife. 2015;4:e04539 [25806683] J Mol Biol. 2013 Nov 29;425(23):4733-44 [23643490] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nsmb.3100 ER - TY - JOUR T1 - Agent Orange Exposure and Monoclonal Gammopathy of Undetermined Significance: An Operation Ranch Hand Veteran Cohort Study. AN - 1733196429; 26335650 AB - Multiple myeloma has been classified as exhibiting "limited or suggestive evidence" of an association with exposure to herbicides in Vietnam War veterans. Occupational studies have shown that other pesticides (ie, insecticides, herbicides, fungicides) are associated with excess risk of multiple myeloma and its precursor state, monoclonal gammopathy of undetermined significance (MGUS); however, to our knowledge, no studies have uncovered such an association in Vietnam War veterans. To examine the relationship between MGUS and exposure to Agent Orange, including its contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), in Vietnam War veterans. This was a prospective cohort study conducted in 2013 to 2014, testing for MGUS in serum specimens collected and stored in 2002 by the Air Force Health Study (AFHS). The relevant exposure data collected by the AFHS was also used. We tested all specimens in 2013 without knowledge of the exposure status. The AFHS included former US Air Force personnel who participated in Operation Ranch Hand (Ranch Hand veterans) and other US Air Force personnel who had similar duties in Southeast Asia during the same time period (1962 to 1971) but were not involved in herbicide spray missions (comparison veterans). Agent Orange was used by the US Air Force personnel who conducted aerial spray missions of herbicides (Operation Ranch Hand) in Vietnam from 1962 to 1971. We included 479 Ranch Hand veterans and 479 comparison veterans who participated in the 2002 follow-up examination of AFHS. Agent Orange and TCDD. Serum TCDD levels were measured in 1987, 1992, 1997, and 2002. Risk of MGUS measured by prevalence, odds ratios (ORs), and 95% CIs. The 479 Ranch Hand veterans and 479 comparison veterans had similar demographic and lifestyle characteristics and medical histories. The crude prevalence of overall MGUS was 7.1% (34 of 479) in Ranch Hand veterans and 3.1% (15 of 479) in comparison veterans. This translated into a 2.4-fold increased risk for MGUS in Ranch Hand veterans than comparison veterans after adjusting for age, race, BMI in 2002, and the change in BMI between 2002 and the time of blood draw for TCDD measurement (adjusted OR, 2.37; 95% CI, 1.27-4.44; P=.007). Operation Ranch Hand veterans have a significantly increased risk of MGUS, supporting an association between Agent Orange exposure and multiple myeloma. JF - JAMA oncology AU - Landgren, Ola AU - Shim, Youn K AU - Michalek, Joel AU - Costello, Rene AU - Burton, Debra AU - Ketchum, Norma AU - Calvo, Katherine R AU - Caporaso, Neil AU - Raveche, Elizabeth AU - Middleton, Dan AU - Marti, Gerald AU - Vogt, Robert F AD - National Cancer Institute, National Institutes of Health, Bethesda, Maryland2Memorial Sloan Kettering Cancer Center, New York, New York. ; Agency for Toxic Substances and Disease Registry, Atlanta, Georgia. ; Department of Epidemiology and Biostatistics, University of Texas Health Science Center, San Antonio. ; National Cancer Institute, National Institutes of Health, Bethesda, Maryland. ; Clinical Center, National Institutes of Health, Bethesda, Maryland. ; Department of Pathology and Laboratory Medicine, Rutgers New Jersey Medical School, Newark. ; Center for Devices and Radiological Health, Food and Drug Administration, Silver Spring, Maryland. ; National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Georgia. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 1061 EP - 1068 VL - 1 IS - 8 KW - Biomarkers KW - 0 KW - Herbicides KW - Polychlorinated Dibenzodioxins KW - 2,4-Dichlorophenoxyacetic Acid KW - 2577AQ9262 KW - Agent Orange KW - 39277-47-9 KW - 2,4,5-Trichlorophenoxyacetic Acid KW - 9Q963S4YMX KW - Index Medicus KW - Odds Ratio KW - Humans KW - Aged KW - Risk Assessment KW - Prospective Studies KW - Aged, 80 and over KW - Logistic Models KW - Risk Factors KW - Case-Control Studies KW - Middle Aged KW - United States -- epidemiology KW - Time Factors KW - Biomarkers -- blood KW - Male KW - Prevalence KW - Multiple Myeloma -- diagnosis KW - Monoclonal Gammopathy of Undetermined Significance -- chemically induced KW - Polychlorinated Dibenzodioxins -- adverse effects KW - Monoclonal Gammopathy of Undetermined Significance -- blood KW - Monoclonal Gammopathy of Undetermined Significance -- diagnosis KW - Herbicides -- adverse effects KW - Multiple Myeloma -- chemically induced KW - Veterans Health KW - 2,4-Dichlorophenoxyacetic Acid -- adverse effects KW - 2,4,5-Trichlorophenoxyacetic Acid -- adverse effects KW - Monoclonal Gammopathy of Undetermined Significance -- epidemiology KW - Multiple Myeloma -- blood KW - Multiple Myeloma -- epidemiology KW - Vietnam Conflict KW - Occupational Exposure -- adverse effects KW - Polychlorinated Dibenzodioxins -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1733196429?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA+oncology&rft.atitle=Agent+Orange+Exposure+and+Monoclonal+Gammopathy+of+Undetermined+Significance%3A+An+Operation+Ranch+Hand+Veteran+Cohort+Study.&rft.au=Landgren%2C+Ola%3BShim%2C+Youn+K%3BMichalek%2C+Joel%3BCostello%2C+Rene%3BBurton%2C+Debra%3BKetchum%2C+Norma%3BCalvo%2C+Katherine+R%3BCaporaso%2C+Neil%3BRaveche%2C+Elizabeth%3BMiddleton%2C+Dan%3BMarti%2C+Gerald%3BVogt%2C+Robert+F&rft.aulast=Landgren&rft.aufirst=Ola&rft.date=2015-11-01&rft.volume=1&rft.issue=8&rft.spage=1061&rft.isbn=&rft.btitle=&rft.title=JAMA+oncology&rft.issn=2374-2445&rft_id=info:doi/10.1001%2Fjamaoncol.2015.2938 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-29 N1 - Date created - 2015-11-13 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Comment In: JAMA Oncol. 2015 Nov;1(8):1035-6 [26335544] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1001/jamaoncol.2015.2938 ER - TY - JOUR T1 - A torque balance measurement of anisotropy of the magnetic susceptibility in white matter AN - 1732813557; PQ0002211260 AB - Purpose Recent MRI studies have suggested that the magnetic susceptibility of white matter (WM) in the human brain is anisotropic, providing a new contrast mechanism for the visualization of fiber bundles and allowing the extraction of cellular compartment-specific information. This study provides an independent confirmation and quantification of this anisotropy. Methods Anisotropic magnetic susceptibility results in a torque exerted on WM when placed in a uniform magnetic field, tending to align the WM fibers with the field. To quantify the effect, excised spinal cord samples were placed in a torque balance inside the magnet of a 7 T MRI system and the magnetic torque was measured as function of orientation. Results All tissue samples (n=5) showed orienting effects, confirming the presence of anisotropic susceptibility. Analysis of the magnetic torque resulted in reproducible values for the WM volume anisotropy that ranged from 13.6 to 19.2 ppb. Conclusion The independently determined anisotropy values confirm estimates inferred from MRI experiments and validate the use of anisotropy to extract novel information about brain fiber structure and myelination. Magn Reson Med 74:1388-1396, 2015. JF - Magnetic Resonance in Medicine AU - van Gelderen, Peter AU - Mandelkow, Hendrik AU - de Zwart, Jacco A AU - Duyn, Jeff H AD - Advanced MRI section, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/11// PY - 2015 DA - Nov 2015 SP - 1388 EP - 1396 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 74 IS - 5 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Fibers KW - Magnetic fields KW - Anisotropy KW - Spinal cord KW - Information processing KW - Magnetic resonance imaging KW - Brain KW - Magnetic susceptibility KW - Substantia alba KW - N.M.R. KW - Myelination KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732813557?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Magnetic+Resonance+in+Medicine&rft.atitle=A+torque+balance+measurement+of+anisotropy+of+the+magnetic+susceptibility+in+white+matter&rft.au=van+Gelderen%2C+Peter%3BMandelkow%2C+Hendrik%3Bde+Zwart%2C+Jacco+A%3BDuyn%2C+Jeff+H&rft.aulast=van+Gelderen&rft.aufirst=Peter&rft.date=2015-11-01&rft.volume=74&rft.issue=5&rft.spage=1388&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.25524 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-01 N1 - Last updated - 2015-11-13 N1 - SubjectsTermNotLitGenreText - Magnetic fields; Fibers; Anisotropy; Spinal cord; Information processing; Magnetic resonance imaging; Brain; Substantia alba; Magnetic susceptibility; N.M.R.; Myelination DO - http://dx.doi.org/10.1002/mrm.25524 ER - TY - JOUR T1 - Selective inhibition of the p38 alternative activation pathway in infiltrating T cells inhibits pancreatic cancer progression. AN - 1731784968; 26479921 AB - Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive neoplasm characterized by a marked fibro-inflammatory microenvironment, the presence of which can promote both cancer induction and growth. Therefore, selective manipulation of local cytokines is an attractive, although unrealized, therapeutic approach. T cells possess a unique mechanism of p38 mitogen-activated protein kinase (MAPK) activation downstream of T cell receptor (TCR) engagement through the phosphorylation of Tyr323 (pY323). This alternative p38 activation pathway is required for pro-inflammatory cytokine production. Here we show in human PDAC that a high percentage of infiltrating pY323(+) T cells was associated with large numbers of tumor necrosis factor (TNF)-α- and interleukin (IL)-17-producing CD4(+) tumor-infiltrating lymphocytes (TILs) and aggressive disease. The growth of mouse pancreatic tumors was inhibited by genetic ablation of the alternative p38 pathway, and transfer of wild-type CD4(+) T cells, but not those lacking the alternative pathway, enhanced tumor growth in T cell-deficient mice. Notably, a plasma membrane-permeable peptide derived from GADD45-α, the naturally occurring inhibitor of p38 pY323(+) (ref. 7), reduced CD4(+) TIL production of TNF-α, IL-17A, IL-10 and secondary cytokines, halted growth of implanted tumors and inhibited progression of spontaneous KRAS-driven adenocarcinoma in mice. Thus, TCR-mediated activation of CD4(+) TILs results in alternative p38 activation and production of protumorigenic factors and can be targeted for therapeutic benefit. JF - Nature medicine AU - Alam, Muhammad S AU - Gaida, Matthias M AU - Bergmann, Frank AU - Lasitschka, Felix AU - Giese, Thomas AU - Giese, Nathalia A AU - Hackert, Thilo AU - Hinz, Ulf AU - Hussain, S Perwez AU - Kozlov, Serguei V AU - Ashwell, Jonathan D AD - Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. ; Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany. ; Institute of Immunology, University of Heidelberg, Heidelberg, Germany. ; Department of Surgery, University Hospital Heidelberg, Heidelberg, Germany. ; Pancreatic Cancer Unit, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. ; Cancer and Developmental Biology Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, Maryland, USA. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 1337 EP - 1343 VL - 21 IS - 11 KW - Cytokines KW - 0 KW - Interleukin-17 KW - Receptors, Antigen, T-Cell KW - Tumor Necrosis Factor-alpha KW - Interleukin-10 KW - 130068-27-8 KW - p38 Mitogen-Activated Protein Kinases KW - EC 2.7.11.24 KW - Index Medicus KW - Animals KW - Interleukin-10 -- secretion KW - Humans KW - Tumor Necrosis Factor-alpha -- immunology KW - Disease Progression KW - Interleukin-10 -- immunology KW - Cell Line, Tumor KW - MAP Kinase Signaling System -- immunology KW - Mice KW - Tumor Necrosis Factor-alpha -- secretion KW - CD4-Positive T-Lymphocytes KW - MAP Kinase Signaling System -- genetics KW - Interleukin-17 -- secretion KW - Phosphorylation KW - Interleukin-17 -- immunology KW - Lymphocytes, Tumor-Infiltrating -- immunology KW - Pancreatic Neoplasms -- metabolism KW - Carcinoma, Pancreatic Ductal -- immunology KW - p38 Mitogen-Activated Protein Kinases -- genetics KW - Cytokines -- immunology KW - Cytokines -- secretion KW - Receptors, Antigen, T-Cell -- metabolism KW - Carcinoma, Pancreatic Ductal -- genetics KW - Pancreatic Neoplasms -- genetics KW - Receptors, Antigen, T-Cell -- immunology KW - T-Lymphocytes -- secretion KW - Lymphocytes, Tumor-Infiltrating -- secretion KW - p38 Mitogen-Activated Protein Kinases -- immunology KW - p38 Mitogen-Activated Protein Kinases -- antagonists & inhibitors KW - Carcinoma, Pancreatic Ductal -- metabolism KW - T-Lymphocytes -- immunology KW - Pancreatic Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731784968?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+medicine&rft.atitle=Selective+inhibition+of+the+p38+alternative+activation+pathway+in+infiltrating+T+cells+inhibits+pancreatic+cancer+progression.&rft.au=Alam%2C+Muhammad+S%3BGaida%2C+Matthias+M%3BBergmann%2C+Frank%3BLasitschka%2C+Felix%3BGiese%2C+Thomas%3BGiese%2C+Nathalia+A%3BHackert%2C+Thilo%3BHinz%2C+Ulf%3BHussain%2C+S+Perwez%3BKozlov%2C+Serguei+V%3BAshwell%2C+Jonathan+D&rft.aulast=Alam&rft.aufirst=Muhammad&rft.date=2015-11-01&rft.volume=21&rft.issue=11&rft.spage=1337&rft.isbn=&rft.btitle=&rft.title=Nature+medicine&rft.issn=1546-170X&rft_id=info:doi/10.1038%2Fnm.3957 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-16 N1 - Date created - 2015-11-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Lab Invest. 2013 Jul;93(7):844-54 [23752129] Cancer Cell. 2014 Jun 16;25(6):719-34 [24856586] Cell Rep. 2014 Oct 23;9(2):484-94 [25310976] J Neurosci. 2001 Aug 15;21(16):6000-7 [11487623] J Immunol. 2002 May 15;168(10):5342-51 [11994493] Mol Cell Biol. 2003 Jun;23(11):3859-71 [12748288] Cancer Cell. 2003 Dec;4(6):437-50 [14706336] Nat Med. 2004 Mar;10(3):305-9 [14770176] Br J Cancer. 2004 Mar 22;90(6):1279-84 [15026813] Nat Immunol. 2005 Apr;6(4):396-402 [15735649] Nat Immunol. 2005 Apr;6(4):390-5 [15735648] J Gen Virol. 1983 Aug;64 (Pt 8):1689-98 [6875516] J Gastroenterol. 2005 Apr;40(4):402-8 [15870976] Cancer Cell. 2005 May;7(5):469-83 [15894267] Proc Natl Acad Sci U S A. 2005 Dec 20;102(51):18538-43 [16344461] J Clin Invest. 2007 May;117(5):1175-83 [17476347] Int J Cancer. 2007 Aug 15;121(4):699-705 [17534898] Cancer Res. 2008 Mar 1;68(5):1443-50 [18316608] Nature. 2008 Jul 24;454(7203):436-44 [18650914] Nat Rev Cancer. 2009 Aug;9(8):537-49 [19629069] Cell. 2010 Jan 22;140(2):197-208 [20141834] Cell. 2010 Mar 19;140(6):883-99 [20303878] PLoS One. 2010;5(9):e12715 [20856806] Nat Med. 2011 Apr;17(4):500-3 [21460848] Gut. 2011 Jun;60(6):861-8 [20966025] Blood. 2011 Sep 22;118(12):3280-9 [21715315] Neoplasia. 2012 Sep;14(9):778-87 [23019409] Nature. 2012 Nov 8;491(7423):254-8 [23034650] Science. 2013 Jan 18;339(6117):286-91 [23329041] Cancer Cell. 2013 Feb 11;23(2):249-62 [23410977] Br J Cancer. 2013 Mar 19;108(5):997-1003 [23385734] Cancer Immunol Res. 2014 May;2(5):423-35 [24795355] Cancer Cell. 2014 May 12;25(5):621-37 [24823639] J Exp Med. 2014 Jun 2;211(6):1257-70 [24863062] Proc Natl Acad Sci U S A. 2013 Sep 10;110(37):15019-24 [23980171] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nm.3957 ER - TY - JOUR T1 - A Phase 1 Randomized, Blinded Comparison of the Pharmacokinetics and Colonic Distribution of Three Candidate Rectal Microbicide Formulations of Tenofovir 1% Gel with Simulated Unprotected Sex (CHARM-02). AN - 1731784475; 26227279 AB - CHARM-02 is a crossover, double-blind, randomized trial to compare the safety and pharmacokinetics of three rectally applied tenofovir 1% gel candidate rectal microbicides of varying osmolalities: vaginal formulation (VF) (3111 mOsmol/kg), the reduced glycerin vaginal formulation (RGVF) (836 mOsmol/kg), and an isoosmolal rectal-specific formulation (RF) (479 mOsmol/kg). Participants (n = 9) received a single, 4 ml, radiolabeled dose of each gel twice, once with and once without simulated unprotected receptive anal intercourse (RAI). The safety, plasma tenofovir pharmacokinetics, colonic small molecule permeability, and SPECT/CT imaging of lower gastrointestinal distribution of drug and virus surrogate were assessed. There were no Grade 3 or 4 adverse events reported for any of the products. Overall, there were more Grade 2 adverse events in the VF group compared to RF (p = 0.006) and RGVF (p = 0.048). In the absence of simulated unprotected RAI, VF had up to 3.8-fold greater systemic tenofovir exposure, 26- to 234-fold higher colonic permeability of the drug surrogate, and 1.5- to 2-fold greater proximal migration in the colonic lumen, when compared to RF and RGVF. Similar trends were observed with simulated unprotected RAI, but most did not reach statistical significance. SPECT analysis showed 86% (standard deviation 19%) of the drug surrogate colocalized with the virus surrogate in the colonic lumen. There were no significant differences between the RGVF and RF formulation, with the exception of a higher plasma tenofovir concentration of RGVF in the absence of simulated unprotected RAI. VF had the most adverse events, highest plasma tenofovir concentrations, greater mucosal permeability of the drug surrogate, and most proximal colonic luminal migration compared to RF and RGVF formulations. There were no major differences between RF and RGVF formulations. Simultaneous assessment of toxicity, systemic and luminal pharmacokinetics, and colocalization of drug and viral surrogates substantially informs rectal microbicide product development. JF - AIDS research and human retroviruses AU - Hiruy, Hiwot AU - Fuchs, Edward J AU - Marzinke, Mark A AU - Bakshi, Rahul P AU - Breakey, Jennifer C AU - Aung, Wutyi S AU - Manohar, Madhuri AU - Yue, Chen AU - Caffo, Brian S AU - Du, Yong AU - Abebe, Kaleab Z AU - Spiegel, Hans M L AU - Rohan, Lisa C AU - McGowan, Ian AU - Hendrix, Craig W AD - 1 Department of Medicine (Clinical Pharmacology), Johns Hopkins University , Baltimore, Maryland. ; 2 Department of Biostatistics, Johns Hopkins School of Public Health , Baltimore, Maryland. ; 3 Department of Radiology, Johns Hopkins School of Medicine , Baltimore, Maryland. ; 4 Department of Medicine, University of Pittsburgh , Pittsburgh, Pennsylvania. ; 5 HJF-DAIDS, a Division of The Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc., Contractor to National Institute of Allergy and Infectious Diseases, National Institutes of Health , Department of Health and Human Services, Bethesda, Maryland. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 1098 EP - 1108 VL - 31 IS - 11 KW - Anti-HIV Agents KW - 0 KW - Gels KW - Tenofovir KW - 99YXE507IL KW - Index Medicus KW - AIDS/HIV KW - Unsafe Sex KW - Double-Blind Method KW - Humans KW - Drug-Related Side Effects and Adverse Reactions -- pathology KW - Adult KW - Drug-Related Side Effects and Adverse Reactions -- epidemiology KW - Cross-Over Studies KW - Middle Aged KW - Administration, Rectal KW - Plasma -- chemistry KW - Male KW - Gels -- pharmacokinetics KW - Anti-HIV Agents -- pharmacokinetics KW - Tenofovir -- adverse effects KW - HIV Infections -- transmission KW - Gels -- adverse effects KW - HIV Infections -- prevention & control KW - Gels -- administration & dosage KW - Tenofovir -- pharmacokinetics KW - Anti-HIV Agents -- adverse effects KW - Anti-HIV Agents -- administration & dosage KW - Tenofovir -- administration & dosage KW - Disease Transmission, Infectious -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731784475?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+research+and+human+retroviruses&rft.atitle=A+Phase+1+Randomized%2C+Blinded+Comparison+of+the+Pharmacokinetics+and+Colonic+Distribution+of+Three+Candidate+Rectal+Microbicide+Formulations+of+Tenofovir+1%25+Gel+with+Simulated+Unprotected+Sex+%28CHARM-02%29.&rft.au=Hiruy%2C+Hiwot%3BFuchs%2C+Edward+J%3BMarzinke%2C+Mark+A%3BBakshi%2C+Rahul+P%3BBreakey%2C+Jennifer+C%3BAung%2C+Wutyi+S%3BManohar%2C+Madhuri%3BYue%2C+Chen%3BCaffo%2C+Brian+S%3BDu%2C+Yong%3BAbebe%2C+Kaleab+Z%3BSpiegel%2C+Hans+M+L%3BRohan%2C+Lisa+C%3BMcGowan%2C+Ian%3BHendrix%2C+Craig+W&rft.aulast=Hiruy&rft.aufirst=Hiwot&rft.date=2015-11-01&rft.volume=31&rft.issue=11&rft.spage=1098&rft.isbn=&rft.btitle=&rft.title=AIDS+research+and+human+retroviruses&rft.issn=1931-8405&rft_id=info:doi/10.1089%2FAID.2015.0098 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-12 N1 - Date created - 2015-11-07 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT01575418; ClinicalTrials.gov N1 - SuppNotes - Cited By: Biomaterials. 2013 Sep;34(28):6922-9 [23769419] Br J Clin Pharmacol. 2012 Dec;74(6):1013-22 [22404308] AIDS Res Hum Retroviruses. 2013 Nov;29(11):1487-95 [23885722] AIDS. 2013 Nov 13;27(17):2665-78 [23842129] J Nucl Cardiol. 2014 Apr;21(2):329-40 [24366822] Pharm Weekbl Sci. 1989 Feb 24;11(1):9-12 [2540479] J Infect Dis. 2007 Mar 1;195(5):703-10 [17262713] Clin Pharmacol Ther. 2008 Jan;83(1):97-105 [17507921] Med Phys. 2009 Jun;36(6):2021-33 [19610291] Lancet Infect Dis. 2010 Jul;10(7):479-88 [20610330] Science. 2010 Sep 3;329(5996):1168-74 [20643915] Sex Transm Infect. 2012 Dec;88(8):574-80 [22750885] PLoS One. 2013;8(1):e55013 [23383037] PLoS One. 2013;8(4):e60147 [23573238] J Acquir Immune Defic Syndr. 2013 Jun 1;63(2):221-7 [23406978] AIDS. 2013 Mar 13;27(5):825-32 [23169330] J Acquir Immune Defic Syndr. 2013 Apr 15;62(5):584-9 [23334505] Lancet. 2013 Jun 15;381(9883):2083-90 [23769234] N Engl J Med. 2010 Dec 30;363(27):2587-99 [21091279] J Acquir Immune Defic Syndr. 2011 May 1;57(1):77-87 [21297479] PLoS One. 2012;7(5):e38143 [22693590] Zhonghua Liu Xing Bing Xue Za Zhi. 2012 Apr;33(4):368-73 [22781407] N Engl J Med. 2012 Aug 2;367(5):399-410 [22784037] N Engl J Med. 2012 Aug 2;367(5):423-34 [22784038] AIDS Res Hum Retroviruses. 2015 Nov;31(11):1089-97 [26066390] PLoS One. 2015;10(5):e0125363 [25942472] PLoS One. 2012;7(8):e43071 [22937013] Curr Opin HIV AIDS. 2012 Nov;7(6):498-504 [22964888] AIDS Res Hum Retroviruses. 2012 Nov;28(11):1412-21 [22943559] AIDS Res Hum Retroviruses. 2013 Nov;29(11):1443-50 [23600365] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1089/AID.2015.0098 ER - TY - JOUR T1 - Interweaving Knowledge Resources to Address Complex Environmental Health Challenges. AN - 1730020209; 25910282 AB - Complex problems do not respect academic disciplinary boundaries. Environmental health research is complex and often moves beyond these boundaries, integrating diverse knowledge resources to solve such challenges. Here we describe an evolving paradigm for interweaving approaches that integrates widely diverse resources outside of traditional academic environments in full partnerships of mutual respect and understanding. We demonstrate that scientists, social scientists, and engineers can work with government agencies, industry, and communities to interweave their expertise into metaphorical knowledge fabrics to share understanding, resources, and enthusiasm. Our goal is to acknowledge and validate how interweaving research approaches can contribute to research-driven, solution-oriented problem solving in environmental health, and to inspire more members of the environmental health community to consider this approach. The National Institutes of Health's National Institute of Environmental Health Sciences Superfund Research Program (SRP), as mandated by Congress, has evolved to become a program that reaches across a wide range of knowledge resources. SRP fosters interweaving multiple knowledge resources to develop innovative multidirectional partnerships for research and training. Here we describe examples of how motivation, ideas, knowledge, and expertise from different people, institutions, and agencies can integrate to tackle challenges that can be as complex as the resources they bring to bear on it. By providing structure for interweaving science with its stakeholders, we are better able to leverage resources, increase potential for innovation, and proactively ensure a more fully developed spectrum of beneficial outcomes of research investments. Anderson BE, Naujokas MF, Suk WA. 2015. Interweaving knowledge resources to address complex environmental health challenges. Environ Health Perspect 123:1095-1099; http://dx.doi.org/10.1289/ehp.1409525. JF - Environmental health perspectives AU - Anderson, Beth Ellen AU - Naujokas, Marisa F AU - Suk, William A AD - Superfund Research Program, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 1095 EP - 1099 VL - 123 IS - 11 KW - Hazardous Substances KW - 0 KW - Index Medicus KW - United States KW - Population Groups KW - Cooperative Behavior KW - Humans KW - Universities KW - Environmental Pollution -- prevention & control KW - National Institute of Environmental Health Sciences (U.S.) KW - Environmental Health -- methods KW - Environmental Pollution -- adverse effects KW - Community Participation -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1730020209?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Interweaving+Knowledge+Resources+to+Address+Complex+Environmental+Health+Challenges.&rft.au=Anderson%2C+Beth+Ellen%3BNaujokas%2C+Marisa+F%3BSuk%2C+William+A&rft.aulast=Anderson&rft.aufirst=Beth&rft.date=2015-11-01&rft.volume=123&rft.issue=11&rft.spage=1095&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1409525 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-26 N1 - Date created - 2015-11-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Environ Health Perspect. 2002 Apr;110 Suppl 2:155-9 [11929724] Sci Total Environ. 2015 May 1;514:170-7 [25659315] Environ Sci Technol. 2008 Jul 1;42(13):4655-62 [18677987] Nature. 2010 Feb 18;463(7283):876 [20164899] Am J Public Health. 2010 Apr 1;100 Suppl 1:S19-24 [20147662] New Solut. 2010;20(1):49-72 [20359991] Environ Int. 2012 Jan;38(1):10-6 [21982028] Environ Health Perspect. 2012 Jan;120(1):6-10 [21890450] Environ Sci Technol. 2012 Jan 17;46(2):1019-27 [22191663] Environ Health Perspect. 2012 Mar;120(3):326-31 [22147336] Environ Health Perspect. 2012 Jul;120(7):a261-2 [22759358] Environ Sci Technol. 2013 Mar 19;47(6):2457-70 [23360069] Sci Total Environ. 2013 Jun 1;454-455:373-82 [23562690] J Health Soc Behav. 2013 Jun;54(2):145-64 [23598897] Chem Res Toxicol. 2013 Jun 17;26(6):853-5 [23713983] Environ Sci Technol. 2013;47(21):11985-92 [24083557] J Agric Food Chem. 2012 Jul 11;60(27):6899-906 [22690788] Sci Total Environ. 2014 Nov 1;497-498:651-64 [25173762] Sci Total Environ. 2015 Feb 1;505:694-703 [25461072] Am J Prev Med. 2008 Aug;35(2 Suppl):S116-23 [18619391] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1289/ehp.1409525 ER - TY - JOUR T1 - Drug-induced mitochondrial dysfunction and cardiotoxicity. AN - 1729349442; 26386112 AB - Mitochondria has an essential role in myocardial tissue homeostasis; thus deterioration in mitochondrial function eventually leads to cardiomyocyte and endothelial cell death and consequent cardiovascular dysfunction. Several chemical compounds and drugs have been known to directly or indirectly modulate cardiac mitochondrial function, which can account both for the toxicological and pharmacological properties of these substances. In many cases, toxicity problems appear only in the presence of additional cardiovascular disease conditions or develop months/years following the exposure, making the diagnosis difficult. Cardiotoxic agents affecting mitochondria include several widely used anticancer drugs [anthracyclines (Doxorubicin/Adriamycin), cisplatin, trastuzumab (Herceptin), arsenic trioxide (Trisenox), mitoxantrone (Novantrone), imatinib (Gleevec), bevacizumab (Avastin), sunitinib (Sutent), and sorafenib (Nevaxar)], antiviral compound azidothymidine (AZT, Zidovudine) and several oral antidiabetics [e.g., rosiglitazone (Avandia)]. Illicit drugs such as alcohol, cocaine, methamphetamine, ecstasy, and synthetic cannabinoids (spice, K2) may also induce mitochondria-related cardiotoxicity. Mitochondrial toxicity develops due to various mechanisms involving interference with the mitochondrial respiratory chain (e.g., uncoupling) or inhibition of the important mitochondrial enzymes (oxidative phosphorylation, Szent-Györgyi-Krebs cycle, mitochondrial DNA replication, ADP/ATP translocator). The final phase of mitochondrial dysfunction induces loss of mitochondrial membrane potential and an increase in mitochondrial oxidative/nitrative stress, eventually culminating into cell death. This review aims to discuss the mechanisms of mitochondrion-mediated cardiotoxicity of commonly used drugs and some potential cardioprotective strategies to prevent these toxicities. Copyright © 2015 the American Physiological Society. JF - American journal of physiology. Heart and circulatory physiology AU - Varga, Zoltán V AU - Ferdinandy, Peter AU - Liaudet, Lucas AU - Pacher, Pál AD - Laboratory of Cardiovascular Physiology and Tissue Injury, National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland; Cardiometabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary; ; Cardiometabolic Research Group, Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary; Pharmahungary Group, Szeged, Hungary; and. ; Department of Intensive Care Medicine BH 08-621-University Hospital Medical Center, Lausanne, Switzerland. ; Laboratory of Cardiovascular Physiology and Tissue Injury, National Institutes of Health/National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland; pacher@mail.nih.gov. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - H1453 EP - H1467 VL - 309 IS - 9 KW - Antineoplastic Agents KW - 0 KW - Antiviral Agents KW - Hypoglycemic Agents KW - Street Drugs KW - Index Medicus KW - heart KW - drug development KW - reactive oxygen species KW - toxicology KW - cardiomyopathy KW - heart failure KW - Cardiotoxicity -- etiology KW - Humans KW - Oxidative Stress KW - Cardiotoxicity -- metabolism KW - Cardiomyopathies -- metabolism KW - Mitochondrial Diseases -- metabolism KW - Street Drugs -- adverse effects KW - Mitochondrial Diseases -- etiology KW - Hypoglycemic Agents -- adverse effects KW - Cardiomyopathies -- chemically induced KW - Mitochondria, Heart -- metabolism KW - Antiviral Agents -- adverse effects KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1729349442?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+physiology.+Heart+and+circulatory+physiology&rft.atitle=Drug-induced+mitochondrial+dysfunction+and+cardiotoxicity.&rft.au=Varga%2C+Zolt%C3%A1n+V%3BFerdinandy%2C+Peter%3BLiaudet%2C+Lucas%3BPacher%2C+P%C3%A1l&rft.aulast=Varga&rft.aufirst=Zolt%C3%A1n&rft.date=2015-11-01&rft.volume=309&rft.issue=9&rft.spage=H1453&rft.isbn=&rft.btitle=&rft.title=American+journal+of+physiology.+Heart+and+circulatory+physiology&rft.issn=1522-1539&rft_id=info:doi/10.1152%2Fajpheart.00554.2015 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-08 N1 - Date created - 2015-11-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Br J Pharmacol. 2011 Jun;163(3):499-509 [21232044] Curr Med Chem. 2011;18(24):3720-8 [21774756] Circ Res. 2011 Sep 16;109(7):750-7 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Acta. 1999 Apr 21;1411(1):201-5 [10216166] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1152/ajpheart.00554.2015 ER - TY - JOUR T1 - The role of haplotype in 15q25.1 locus in lung cancer risk: results of scanning chromosome 15. AN - 1728674496; 26282330 AB - The role of haplotypes and the interaction of haplotypes and smoking in lung cancer risk have not been well characterized. We analyzed data from an Italian population-based, case-control study with 1815 lung cancer patients and 1959 healthy controls in discovery, and performed a validation using a case-control study with 2983 lung cancer patients and 3553 healthy controls of European ancestry for replication. Sliding window haplotype analysis within chromosome 15, evaluating 4722250 haplotypes and pair-wise haplotype analysis identified that CHRNA5 rs588765-rs16969968 was the most significant haplotype associated with lung cancer risk (omnibus P = 8.35×10(-15) in discovery and 7.26×10(-14) in replication), and improved the prediction of case status over that provided by the individual SNPs rs16969968 or rs588765 (likelihood ratio test P = 0.006 for rs16969968 and 3.83×10(-14) for rs588765 in discovery, 0.009 for rs16969968 and 4.62×10(-13) for rs588765 in replication, compared with rs588765-rs16969968). Compared with the wild-type homozygous diplotype, CA/CA homozygote exhibited an approximately 2-fold increase risk for lung cancer (OR = 2.12; 95% CI 1.46-3.07 in discovery, and OR = 2.01; 95% CI 1.51-2.67 in replication). Even among never-smokers, CA/CA homozygote showed an increased risk of lung cancer with borderline significance in discovery (adjusted OR = 1.75, 95% CI 0.96-3.19) and statistical significance in replication (adjusted OR = 2.10, 95% CI 1.12-3.96), compared with combined genotypes (CG/CG + CG/TG). Accordingly, rs588765-rs16969968 may be a genetic marker to lung cancer risk, even among never-smokers. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Carcinogenesis AU - Ji, Xuemei AU - Gui, Jiang AU - Han, Younghun AU - Brennan, Paul AU - Li, Yafang AU - McKay, James AU - Caporaso, Neil E AU - Bertazzi, Pier Alberto AU - Landi, Maria Teresa AU - Amos, Christopher I AD - International Agency for Research on Cancer, 69372 Lyon, France. ; Department of Health and Human Services, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Department of Clinical Sciences and Community Health, Department of Preventive Medicine, University of Milan, Fondazione IRCCS Ca' Granda Policlinico Hospital, 20122 Milan, Italy. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 1275 EP - 1283 VL - 36 IS - 11 KW - Index Medicus KW - Polymorphism, Single Nucleotide KW - Haplotypes KW - Genetic Loci KW - Humans KW - Genetic Association Studies KW - Case-Control Studies KW - Smoking -- adverse effects KW - Aged KW - Middle Aged KW - Genetic Predisposition to Disease KW - Male KW - Female KW - Carcinoma, Squamous Cell -- genetics KW - Lung Neoplasms -- genetics KW - Adenocarcinoma -- genetics KW - Chromosomes, Human, Pair 15 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1728674496?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=The+role+of+haplotype+in+15q25.1+locus+in+lung+cancer+risk%3A+results+of+scanning+chromosome+15.&rft.au=Ji%2C+Xuemei%3BGui%2C+Jiang%3BHan%2C+Younghun%3BBrennan%2C+Paul%3BLi%2C+Yafang%3BMcKay%2C+James%3BCaporaso%2C+Neil+E%3BBertazzi%2C+Pier+Alberto%3BLandi%2C+Maria+Teresa%3BAmos%2C+Christopher+I&rft.aulast=Ji&rft.aufirst=Xuemei&rft.date=2015-11-01&rft.volume=36&rft.issue=11&rft.spage=1275&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgv118 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-03 N1 - Date created - 2015-10-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Int J Mol Sci. 2014;15(4):5446-57 [24686516] Int J Cancer. 2013 Apr 15;132(8):1811-20 [23011884] Int J Cancer. 1994 Nov 15;59(4):494-504 [7960219] Nature. 2008 Apr 3;452(7187):638-42 [18385739] Nat Genet. 2008 May;40(5):616-22 [18385676] BMC Public Health. 2008;8:203 [18538025] Am J Psychiatry. 2008 Sep;165(9):1163-71 [18519524] Cancer Res. 2008 Nov 15;68(22):9137-40 [19010884] Clin Cancer Res. 2009 Mar 1;15(5):1837-42 [19223495] Hum Mol Genet. 2009 Aug 15;18(16):3125-35 [19443489] Cancer Res. 2009 Aug 15;69(16):6633-41 [19654303] Cancer Res. 2009 Oct 1;69(19):7844-50 [19789337] Nat Genet. 2010 May;42(5):436-40 [20418889] Nat Genet. 2010 May;42(5):441-7 [20418890] J Surg Res. 2010 Jul;162(1):75-8 [19577767] PLoS Genet. 2010 Aug;6(8). pii: e1001053. doi: 10.1371/journal.pgen.1001053 [20700436] J Natl Cancer Inst. 2010 Sep 8;102(17):1366-70 [20733116] PLoS One. 2011;6(4):e19085 [21559498] CA Cancer J Clin. 2011 Jul-Aug;61(4):212-36 [21685461] J Natl Cancer Inst. 2011 Sep 7;103(17):1342-6 [21747048] Cancer Epidemiol Biomarkers Prev. 2011 Dec;20(12):2603-9 [22028403] J Biol Chem. 2012 Mar 2;287(10):7246-55 [22241472] Cancer Epidemiol Biomarkers Prev. 2012 Jul;21(7):1213-21 [22573796] Nat Genet. 2012 Aug;44(8):895-9 [22797725] Cancer Epidemiol Biomarkers Prev. 2013 Feb;22(2):251-60 [23221128] Nat Genet. 2014 Jul;46(7):736-41 [24880342] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgv118 ER - TY - JOUR T1 - Genomic copy number analysis of Chernobyl papillary thyroid carcinoma in the Ukrainian-American Cohort. AN - 1728674212; 26320103 AB - One of the major consequences of the 1986 Chernobyl reactor accident was a dramatic increase in papillary thyroid carcinoma (PTC) incidence, predominantly in patients exposed to the radioiodine fallout at young age. The present study is the first on genomic copy number alterations (CNAs) of PTCs of the Ukrainian-American cohort (UkrAm) generated by array comparative genomic hybridization (aCGH). Unsupervised hierarchical clustering of CNA profiles revealed a significant enrichment of a subgroup of patients with female gender, long latency (>17 years) and negative lymph node status. Further, we identified single CNAs that were significantly associated with latency, gender, radiation dose and BRAF V600E mutation status. Multivariate analysis revealed no interactions but additive effects of parameters gender, latency and dose on CNAs. The previously identified radiation-associated gain of the chromosomal bands 7q11.22-11.23 was present in 29% of cases. Moreover, comparison of our radiation-associated PTC data set with the TCGA data set on sporadic PTCs revealed altered copy numbers of the tumor driver genes NF2 and CHEK2. Further, we integrated the CNA data with transcriptomic data that were available on a subset of the herein analyzed cohort and did not find statistically significant associations between the two molecular layers. However, applying hierarchical clustering on a 'BRAF-like/RAS-like' transcriptome signature split the cases into four groups, one of which containing all BRAF-positive cases validating the signature in an independent data set. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Carcinogenesis AU - Selmansberger, Martin AU - Braselmann, Herbert AU - Hess, Julia AU - Bogdanova, Tetiana AU - Abend, Michael AU - Tronko, Mykola AU - Brenner, Alina AU - Zitzelsberger, Horst AU - Unger, Kristian AD - Institute of Endocrinology and Metabolism, National Academy of Medical Sciences of the Ukraine, 254114 Kiev, Ukraine. ; Bundeswehr Institute of Radiobiology, 80937 Munich, Germany and. ; Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, NCI , Bethesda, MD 20892, USA. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 1381 EP - 1387 VL - 36 IS - 11 KW - Iodine Radioisotopes KW - 0 KW - Radioactive Fallout KW - BRAF protein, human KW - EC 2.7.11.1 KW - Proto-Oncogene Proteins B-raf KW - Index Medicus KW - United States KW - DNA Copy Number Variations KW - Comparative Genomic Hybridization KW - Chernobyl Nuclear Accident KW - Genome, Human KW - Humans KW - Ukraine -- ethnology KW - Mutation, Missense KW - Male KW - Female KW - Proto-Oncogene Proteins B-raf -- genetics KW - Genome-Wide Association Study KW - Thyroid Neoplasms -- genetics KW - Iodine Radioisotopes -- adverse effects KW - Neoplasms, Radiation-Induced -- genetics KW - Carcinoma, Papillary -- genetics KW - Radioactive Fallout -- adverse effects KW - Carcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1728674212?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Genomic+copy+number+analysis+of+Chernobyl+papillary+thyroid+carcinoma+in+the+Ukrainian-American+Cohort.&rft.au=Selmansberger%2C+Martin%3BBraselmann%2C+Herbert%3BHess%2C+Julia%3BBogdanova%2C+Tetiana%3BAbend%2C+Michael%3BTronko%2C+Mykola%3BBrenner%2C+Alina%3BZitzelsberger%2C+Horst%3BUnger%2C+Kristian&rft.aulast=Selmansberger&rft.aufirst=Martin&rft.date=2015-11-01&rft.volume=36&rft.issue=11&rft.spage=1381&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgv119 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-03 N1 - Date created - 2015-10-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Oncogene. 2015 Jul 23;34(30):3917-25 [25284583] Med Pediatr Oncol. 2001 May;36(5):574-82 [11340615] J Biol Chem. 2004 Apr 30;279(18):18559-66 [14981079] Radiat Res. 2004 Sep;162(3):241-8 [15332999] J Clin Endocrinol Metab. 2004 Sep;89(9):4272-9 [15356021] Genome Biol. 2004;5(10):R80 [15461798] Radiat Res. 2005 Feb;163(2):125-36 [15658887] J Natl Cancer Inst. 2005 May 18;97(10):724-32 [15900042] Bioinformatics. 2005 Jul 15;21(14):3193-4 [15879450] Radiat Res. 2006 Jul;166(1 Pt 2):271-86 [16808613] J Natl Cancer Inst. 2006 Jul 5;98(13):897-903 [16818853] BMC Bioinformatics. 2006;7:264 [16716215] Radiat Res. 2006 Aug;166(2):375-86 [16881739] Eur J Endocrinol. 2006 Nov;155(5):645-53 [17062879] Cell Oncol. 2007;29(4):351-9 [17641418] Health Phys. 2007 Nov;93(5):502-11 [18049226] Oncogene. 2008 Jul 31;27(33):4592-602 [18408749] Biometrics. 2009 Mar;65(1):19-29 [18479479] Cancer. 2009 Apr 25;117(2):73-81 [19365829] Nat Rev Cancer. 2009 Aug;9(8):596-604 [19629073] Mol Cell Endocrinol. 2010 May 28;321(1):44-9 [19883730] Thyroid. 2010 May;20(5):475-87 [19725780] Br J Cancer. 2011 Jan 4;104(1):181-7 [21102590] Clin Oncol (R Coll Radiol). 2011 May;23(4):251-60 [21396807] Proc Natl Acad Sci U S A. 2011 Jun 7;108(23):9595-600 [21606360] Environ Health Perspect. 2011 Jul;119(7):933-9 [21406336] J Radiol Prot. 2012 Mar;32(1):N65-9 [22394669] PLoS One. 2012;7(7):e39103 [22848350] BMC Bioinformatics. 2012;13:80 [22559006] Sci Signal. 2013 Apr 2;6(269):pl1 [23550210] Cancer. 2013 May 15;119(10):1792-9 [23436219] Cell Rep. 2013 Aug 29;4(4):776-90 [23972991] Br J Cancer. 2013 Oct 15;109(8):2286-94 [24045656] Cell. 2014 Oct 23;159(3):676-90 [25417114] Mol Cancer Res. 2015 May;13(5):879-90 [25652588] Carcinogenesis. 2015 Jul;36(7):748-56 [25957251] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgv119 ER - TY - JOUR T1 - Strong association between long and heterogeneous telomere length in blood lymphocytes and bladder cancer risk in Egyptian. AN - 1728673106; 26342126 AB - Although it is widely recognized that telomere dysfunction plays an important role in cancer, the relationship between telomere function and bladder cancer risk is not well defined. In a case-control study of bladder cancer in Egypt, we examined relationships between two telomere features and bladder cancer risk. Telomere fluorescent in situ hybridization was used to measure telomere features using short-term cultured blood lymphocytes. Logistic regression was used to estimate the strength of association between telomere features and the risk of urothelial carcinoma of the bladder. High telomere length variation (TLV) across all chromosomal ends was significantly associated with an increased risk of bladder cancer [adjusted odds ratios (OR) = 2.22, 95% confidence interval (CI) = 1.48-3.35], as was long average telomere length (OR = 3.19, 95% CI = 2.07, 4.91). Further, TLV and average telomere length jointly affected bladder cancer risk: when comparing individuals with long telomere length and high TLV to those with short telomere length and low TLV, the adjusted OR was 14.68 (95% CI: 6.74-31.98). These associations were stronger among individuals who are 60 years of age or younger. In summary, long and heterogeneous telomere length in blood lymphocytes was strongly associated with an increased bladder cancer risk in Egyptian and the association was modulated by age. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Carcinogenesis AU - Wang, Hongkun AU - Wang, Ying AU - Kota, Krishna K AU - Kallakury, Bhaskar AU - Mikhail, Nabiel N AU - Sayed, Douaa AU - Mokhtar, Ahmed AU - Maximous, Doaa AU - Yassin, Etemad H AU - Gouda, Iman AU - Sobitan, Adebiyi AU - Sun, Bing AU - Loffredo, Christopher A AU - Zheng, Yun-Ling AD - Department of Biostatistics, Bioinformatics, and Biomathematics. ; Cancer Prevention and Control Program. ; Department of Pathology, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, 3970 Reservoir Road, NW, Research Building, Room W201, Washington DC 20057, USA. ; South Egypt Cancer Institute, Assiut University, Assiut 71515, Egypt and. ; National Cancer Institute, Cairo 11796, Egypt. ; Department of Biostatistics, Bioinformatics, and Biomathematics, Cancer Prevention and Control Program. ; Department of Biostatistics, Bioinformatics, and Biomathematics, Cancer Prevention and Control Program, yz37@georgetown.edu. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 1284 EP - 1290 VL - 36 IS - 11 KW - Biomarkers, Tumor KW - 0 KW - Index Medicus KW - Egypt KW - Biomarkers, Tumor -- genetics KW - Aged, 80 and over KW - Risk Factors KW - Humans KW - Genetic Association Studies KW - Case-Control Studies KW - Aged KW - Middle Aged KW - Genetic Predisposition to Disease KW - Male KW - Female KW - Urinary Bladder Neoplasms -- genetics KW - Telomere -- genetics KW - Lymphocytes -- physiology KW - Telomere Homeostasis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1728673106?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Strong+association+between+long+and+heterogeneous+telomere+length+in+blood+lymphocytes+and+bladder+cancer+risk+in+Egyptian.&rft.au=Wang%2C+Hongkun%3BWang%2C+Ying%3BKota%2C+Krishna+K%3BKallakury%2C+Bhaskar%3BMikhail%2C+Nabiel+N%3BSayed%2C+Douaa%3BMokhtar%2C+Ahmed%3BMaximous%2C+Doaa%3BYassin%2C+Etemad+H%3BGouda%2C+Iman%3BSobitan%2C+Adebiyi%3BSun%2C+Bing%3BLoffredo%2C+Christopher+A%3BZheng%2C+Yun-Ling&rft.aulast=Wang&rft.aufirst=Hongkun&rft.date=2015-11-01&rft.volume=36&rft.issue=11&rft.spage=1284&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgv121 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-03 N1 - Date created - 2015-10-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Genes Dev. 2005 Sep 15;19(18):2100-10 [16166375] Mol Cell Biol. 2004 Nov;24(22):9948-57 [15509797] Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):815-9 [17416776] Cancer Res. 2008 May 15;68(10):3618-23 [18483243] Genes Dev. 2009 Sep 1;23(17):2060-75 [19679647] Lung Cancer. 2009 Nov;66(2):157-61 [19285750] N Engl J Med. 2009 Dec 10;361(24):2353-65 [20007561] J Immunol Methods. 2010 Jan 31;352(1-2):71-80 [19837074] Hum Mol Genet. 2011 Jan 15;20(2):378-86 [20956286] Am J Pathol. 2011 Oct;179(4):1608-15 [21888887] J Allergy Clin Immunol. 2012 Feb;129(2):473-82, 482.e1-3 [22078571] Nat New Biol. 1972 Oct 18;239(94):197-201 [4507727] J Theor Biol. 1973 Sep 14;41(1):181-90 [4754905] Science. 1998 Jan 16;279(5349):334-5 [9454329] Nat Biotechnol. 1998 Aug;16(8):743-7 [9702772] Clin Cancer Res. 2005 Jan 1;11(1):217-25 [15671549] Carcinogenesis. 2005 Jul;26(7):1263-71 [15746160] Cancer Epidemiol Biomarkers Prev. 2012 Mar;21(3):537-46 [22147365] Cancer Epidemiol Biomarkers Prev. 2012 Nov;21(11):2095-100 [23093543] Cancer. 2013 May 15;119(10):1885-91 [23408253] Mod Pathol. 2013 Nov;26(11):1425-32 [23765250] Neoplasia. 2013 Nov;15(11):1301-13 [24339742] Nucleic Acids Res. 2014 Apr;42(7):4391-405 [24500201] Cell Cycle. 2014;13(11):1765-76 [24721976] Cancer Res. 2014 Aug 1;74(15):4090-8 [24853549] Cancer Epidemiol Biomarkers Prev. 2014 Nov;23(11):2439-46 [25234236] Lung Cancer. 2015 Jun;88(3):297-303 [25840848] Cell. 1985 Dec;43(2 Pt 1):405-13 [3907856] Nature. 1990 May 31;345(6274):458-60 [2342578] EMBO J. 1995 Sep 1;14(17):4240-8 [7556065] Annu Rev Biochem. 1996;65:337-65 [8811183] Cell. 1997 Oct 3;91(1):25-34 [9335332] Nat Med. 1997 Nov;3(11):1271-4 [9359704] Br J Haematol. 2000 May;109(2):272-9 [10848812] Nature. 2000 Aug 10;406(6796):641-5 [10949306] Cell. 2001 Sep 21;106(6):661-73 [11572773] Cell. 2001 Oct 5;107(1):67-77 [11595186] Science. 2002 Jul 26;297(5581):565-9 [12142527] Carcinogenesis. 2003 Feb;24(2):269-74 [12584177] J Natl Cancer Inst. 2003 Aug 20;95(16):1211-8 [12928346] Oncogene. 2004 Feb 12;23(6):1221-8 [14716292] Mutat Res. 2004 Sep;567(1):85-104 [15341904] Genes Chromosomes Cancer. 2005 Dec;44(4):339-50 [16052508] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgv121 ER - TY - JOUR T1 - Induction of oxidative stress by Taxol® vehicle Cremophor-EL triggers production of interleukin-8 by peripheral blood mononuclear cells through the mechanism not requiring de novo synthesis of mRNA. AN - 1728670507; 26282378 AB - Understanding the ability of cytotoxic oncology drugs, and their carriers and formulation excipients, to induce pro-inflammatory responses is important for establishing safe and efficacious formulations. Literature data about cytokine response induction by the traditional formulation of paclitaxel, Taxol®, are controversial, and no data are available about the pro-inflammatory profile of the nano-albumin formulation of this drug, Abraxane®. Herein, we demonstrate and explain the difference in the cytokine induction profile between Taxol® and Abraxane®, and describe a novel mechanism of cytokine induction by a nanosized excipient, Cremophor EL, which is not unique to Taxol® and is commonly used in the pharmaceutical industry for delivery of a wide variety of small molecular drugs. Advances in nanotechnology have enabled the production of many nano-formulation drugs. The cellular response to drugs has been reported to be different between traditional and nano-formulations. In this article, the authors investigated and compared cytokine response induction profiles between Taxol® and Abraxane®. The findings here provided further understanding to create drugs with better safety profiles. Copyright © 2015 Elsevier Inc. All rights reserved. JF - Nanomedicine : nanotechnology, biology, and medicine AU - Ilinskaya, Anna N AU - Clogston, Jeffrey D AU - McNeil, Scott E AU - Dobrovolskaia, Marina A AD - Nanotechnology Characterization Laboratory, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Inc., Frederick, MD, USA. ; Nanotechnology Characterization Laboratory, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Inc., Frederick, MD, USA. Electronic address: marina@mail.nih.gov. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 1925 EP - 1938 VL - 11 IS - 8 KW - Albumin-Bound Paclitaxel KW - 0 KW - Antineoplastic Agents KW - IL8 protein, human KW - Interleukin-8 KW - Pharmaceutical Vehicles KW - Polyethylene Glycols KW - 30IQX730WE KW - cremophor KW - 39279-69-1 KW - cremophor EL KW - 6D4M1DAL6O KW - Paclitaxel KW - P88XT4IS4D KW - Glycerol KW - PDC6A3C0OX KW - Index Medicus KW - Abraxane® KW - Immunotoxicity KW - Oxidative stress KW - Cremophor-EL KW - Taxol® KW - Cytokines KW - Interleukin 8 KW - Animals KW - Humans KW - Leukocytes, Mononuclear -- metabolism KW - Mice KW - Leukocytes, Mononuclear -- drug effects KW - Interleukin-8 -- metabolism KW - Interleukin-8 -- blood KW - Cell Line KW - Paclitaxel -- adverse effects KW - Glycerol -- analogs & derivatives KW - Oxidative Stress -- drug effects KW - Pharmaceutical Vehicles -- adverse effects KW - Glycerol -- adverse effects KW - Albumin-Bound Paclitaxel -- adverse effects KW - Polyethylene Glycols -- adverse effects KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1728670507?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nanomedicine+%3A+nanotechnology%2C+biology%2C+and+medicine&rft.atitle=Induction+of+oxidative+stress+by+Taxol%C2%AE+vehicle+Cremophor-EL+triggers+production+of+interleukin-8+by+peripheral+blood+mononuclear+cells+through+the+mechanism+not+requiring+de+novo+synthesis+of+mRNA.&rft.au=Ilinskaya%2C+Anna+N%3BClogston%2C+Jeffrey+D%3BMcNeil%2C+Scott+E%3BDobrovolskaia%2C+Marina+A&rft.aulast=Ilinskaya&rft.aufirst=Anna&rft.date=2015-11-01&rft.volume=11&rft.issue=8&rft.spage=1925&rft.isbn=&rft.btitle=&rft.title=Nanomedicine+%3A+nanotechnology%2C+biology%2C+and+medicine&rft.issn=1549-9642&rft_id=info:doi/10.1016%2Fj.nano.2015.07.012 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-12 N1 - Date created - 2015-10-31 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Eur J Pharm Sci. 2012 Mar 12;45(4):492-8 [21963457] Blood. 2012 Jan 19;119(3):651-65 [22053109] J Immunol. 2013 Aug 15;191(4):1835-44 [23842754] Mol Cancer Ther. 2013 Aug;12(8):1676-87 [23720768] Cancer Lett. 2014 Jun 28;348(1-2):77-87 [24657657] Methods Mol Biol. 2014;1172:285-93 [24908315] Curr Drug Deliv. 2014;11(6):666-86 [24909147] Mol Oncol. 2015 Feb;9(2):377-88 [25306394] J Biol Chem. 2000 Jan 28;275(4):2251-4 [10644670] Free Radic Biol Med. 2000 Feb 1;28(3):463-99 [10699758] Infect Immun. 2000 Apr;68(4):2053-60 [10722601] Chest. 2000 Aug;118(2):503-8 [10936147] J Immunol. 2001 Jan 1;166(1):574-81 [11123339] Cytometry. 2001 Apr 15;46(2):72-8 [11309815] Int Immunopharmacol. 2001 Apr;1(4):721-35 [11357884] Eur J Immunol. 2001 Aug;31(8):2448-57 [11500829] Eur J Cancer. 2001 Sep;37(13):1590-8 [11527683] Cytokine. 2001 Aug 7;15(3):156-65 [11554785] J Endotoxin Res. 2001;7(3):232-6 [11581576] Blood. 2002 Aug 15;100(4):1215-9 [12149200] Metabolism. 2002 Oct;51(10):1340-7 [12370856] J Leukoc Biol. 2002 Nov;72(5):847-55 [12429706] Nature. 2002 Dec 19-26;420(6917):860-7 [12490959] Oncogene. 2003 Jan 16;22(2):256-65 [12527894] FASEB J. 2003 Nov;17(14):2115-7 [12958148] Cell Signal. 2004 Oct;16(10):1113-21 [15240006] Science. 1990 Apr 20;248(4953):370-2 [1970196] J Exp Med. 1993 Aug 1;178(2):695-702 [8101863] J Clin Invest. 1992 Nov;90(5):2123-9 [1331181] J Immunol. 1992 Oct 1;149(7):2459-65 [1356126] J Lab Clin Med. 1993 Oct;122(4):374-81 [7901310] J Immunol. 1995 Apr 15;154(8):4113-22 [7706748] Mol Med. 1995 May;1(4):428-35 [8521300] J Immunol. 1997 May 1;158(9):4422-9 [9127007] J Natl Cancer Inst. 1998 Feb 18;90(4):300-6 [9486816] Urology. 1999 Jan;53(1):139-47 [9886603] J Immunol. 1999 Jan 15;162(2):1077-83 [9916736] J Immunol. 1999 Jun 15;162(12):7335-42 [10358184] Cancer Cell. 2004 Nov;6(5):447-58 [15542429] Clin Cancer Res. 2005 Oct 15;11(20):7490-8 [16243823] J Clin Oncol. 2005 Nov 1;23(31):7794-803 [16172456] Mol Cell Biol. 2006 Mar;26(6):2399-407 [16508014] Cancer Res. 2006 Apr 1;66(7):3859-68 [16585214] Biochim Biophys Acta. 2006 Dec;1763(12):1755-66 [17034877] Biochem Biophys Res Commun. 2007 Jun 1;357(2):402-7 [17420005] Invest Ophthalmol Vis Sci. 2007 Nov;48(11):5000-6 [17962450] Surgery. 2008 Jul;144(1):57-65 [18571585] J Biol Chem. 2008 Oct 10;283(41):27916-26 [18650420] Eur J Clin Invest. 2009 Feb;39(2):157-64 [19200169] Am J Physiol Lung Cell Mol Physiol. 2011 Jan;300(1):L81-7 [20952496] Blood. 2011 Apr 7;117(14):3720-32 [21304099] Cytokine. 2011 Nov;56(2):365-75 [21742513] Biosci Rep. 2012 Feb;32(1):1-15 [21981137] Cell Death Differ. 2013 Feb;20(2):270-80 [22976835] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.nano.2015.07.012 ER - TY - JOUR T1 - Spinal and Bulbar Muscular Atrophy. AN - 1728669484; 26515625 AB - Spinal and bulbar muscular atrophy, or Kennedy disease, is a slowly progressive X-linked neuromuscular disease caused by a trinucleotide (CAG) repeat expansion in the androgen receptor gene. Affected males typically develop weakness in their mid-40s as well as evidence of androgen insensitivity with reduced fertility and gynecomastia. Diagnosis is often delayed because of decreased awareness of the disease, although genetic testing allows for direct diagnosis. Therapeutic strategies to block the toxicity of the mutant androgen receptor have been unsuccessful thus far, and evaluation of additional candidate therapies is underway. Published by Elsevier Inc. JF - Neurologic clinics AU - Grunseich, Christopher AU - Fischbeck, Kenneth H AD - Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, NIH, 35 Convent Drive, Bethesda, MD 20892, USA. Electronic address: Christopher.grunseich@nih.gov. ; Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, NIH, 35 Convent Drive, Bethesda, MD 20892, USA. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 847 EP - 854 VL - 33 IS - 4 KW - Receptors, Androgen KW - 0 KW - Polyglutamic Acid KW - 25513-46-6 KW - Index Medicus KW - Androgen receptor KW - Kennedy disease KW - Motor neuron disease KW - Spinal and bulbar muscular atrophy KW - Animals KW - Humans KW - Disease Progression KW - Middle Aged KW - Male KW - Bulbo-Spinal Atrophy, X-Linked -- genetics KW - Receptors, Androgen -- genetics KW - Polyglutamic Acid -- genetics KW - Bulbo-Spinal Atrophy, X-Linked -- classification KW - Bulbo-Spinal Atrophy, X-Linked -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1728669484?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurologic+clinics&rft.atitle=Spinal+and+Bulbar+Muscular+Atrophy.&rft.au=Grunseich%2C+Christopher%3BFischbeck%2C+Kenneth+H&rft.aulast=Grunseich&rft.aufirst=Christopher&rft.date=2015-11-01&rft.volume=33&rft.issue=4&rft.spage=847&rft.isbn=&rft.btitle=&rft.title=Neurologic+clinics&rft.issn=1557-9875&rft_id=info:doi/10.1016%2Fj.ncl.2015.07.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-08 N1 - Date created - 2015-10-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Neurobiol Dis. 2014 Oct;70:12-20 [24925468] Arch Phys Med Rehabil. 2007 Nov;88(11):1452-64 [17964887] Neuromuscul Disord. 2014 Nov;24(11):978-81 [25047668] Hum Mol Genet. 2009 Jan 1;18(1):27-42 [18824496] Hum Mol Genet. 2000 Sep 1;9(14):2197-202 [10958659] J Neurol. 2001 Oct;248(10):856-60 [11697521] Neurology. 2002 Sep 10;59(5):770-2 [12221177] Clin Genet. 1996 Sep;50(3):133-7 [8946111] Ann Neurol. 1998 Aug;44(2):249-54 [9708548] Brain. 2006 Jun;129(Pt 6):1446-55 [16621916] J Clin Invest. 2006 Oct;116(10):2663-72 [16981011] Hum Mol Genet. 2009 Jun 1;18(11):1937-50 [19279159] Neuron. 2009 Aug 13;63(3):316-28 [19679072] Muscle Nerve. 2009 Nov;40(5):809-14 [19670325] Nature. 1991 Jul 4;352(6330):77-9 [2062380] Nat Genet. 1992 Dec;2(4):301-4 [1303283] J Neurol Neurosurg Psychiatry. 1994 Oct;57(10):1274-5 [7931399] Neurology. 2014 Jun 10;82(23):2077-84 [24814851] Nature. 2007 Jun 14;447(7146):859-63 [17568747] Neurology. 2014 May 20;82(20):1813-21 [24759840] Proc Natl Acad Sci U S A. 2007 Nov 13;104(46):18259-64 [17984063] J Neurol Sci. 2008 Jan 15;264(1-2):100-5 [17854832] Neurology. 2009 Jan 27;72(4):317-23 [19171827] Ann Neurol. 2009 Feb;65(2):140-50 [19259967] Neuron. 2002 Aug 29;35(5):843-54 [12372280] Nat Med. 2003 Jun;9(6):768-73 [12754502] Proc Natl Acad Sci U S A. 2004 Apr 6;101(14):4758-63 [15037741] J Neurosci. 2004 May 19;24(20):4778-86 [15152038] Neurology. 1968 Jul;18(7):671-80 [4233749] Brain. 2009 Dec;132(Pt 12):3242-51 [19846582] J Neurosci. 2010 Apr 21;30(16):5702-12 [20410122] Lancet Neurol. 2010 Sep;9(9):875-84 [20691641] Neuron. 2010 Sep 23;67(6):936-52 [20869592] J Biol Chem. 2010 Nov 12;285(46):35567-77 [20826791] Lancet Neurol. 2011 Feb;10(2):140-7 [21216197] Muscle Nerve. 2012 Feb;45(2):169-74 [22246870] Neurology. 2013 Jun 4;80(23):2095-8 [23645595] Oral Dis. 2014 Jan;20(1):6-9 [23656576] Neuron. 2014 Apr 16;82(2):295-307 [24742458] Cell Rep. 2014 May 8;7(3):774-84 [24746732] Nat Neurosci. 2014 Sep;17(9):1180-9 [25108912] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ncl.2015.07.002 ER - TY - JOUR T1 - Hfqs in Bacillus anthracis: Role of protein sequence variation in the structure and function of proteins in the Hfq family. AN - 1727995914; 26271475 AB - Hfq proteins in Gram-negative bacteria play important roles in bacterial physiology and virulence, mediated by binding of the Hfq hexamer to small RNAs and/or mRNAs to post-transcriptionally regulate gene expression. However, the physiological role of Hfqs in Gram-positive bacteria is less clear. Bacillus anthracis, the causative agent of anthrax, uniquely expresses three distinct Hfq proteins, two from the chromosome (Hfq1, Hfq2) and one from its pXO1 virulence plasmid (Hfq3). The protein sequences of Hfq1 and 3 are evolutionarily distinct from those of Hfq2 and of Hfqs found in other Bacilli. Here, the quaternary structure of each B. anthracis Hfq protein, as produced heterologously in Escherichia coli, was characterized. While Hfq2 adopts the expected hexamer structure, Hfq1 does not form similarly stable hexamers in vitro. The impact on the monomer-hexamer equilibrium of varying Hfq C-terminal tail length and other sequence differences among the Hfqs was examined, and a sequence region of the Hfq proteins that was involved in hexamer formation was identified. It was found that, in addition to the distinct higher-order structures of the Hfq homologs, they give rise to different phenotypes. Hfq1 has a disruptive effect on the function of E. coli Hfq in vivo, while Hfq3 expression at high levels is toxic to E. coli but also partially complements Hfq function in E. coli. These results set the stage for future studies of the roles of these proteins in B. anthracis physiology and for the identification of sequence determinants of phenotypic complementation. © 2015 The Protein Society. JF - Protein science : a publication of the Protein Society AU - Vrentas, Catherine AU - Ghirlando, Rodolfo AU - Keefer, Andrea AU - Hu, Zonglin AU - Tomczak, Aurelie AU - Gittis, Apostolos G AU - Murthi, Athulaprabha AU - Garboczi, David N AU - Gottesman, Susan AU - Leppla, Stephen H AD - NIAID, National Institutes of Health (NIH), 33 North Drive, Bethesda, Maryland. ; NIDDK, NIH, 5 Memorial Drive, Bethesda, Maryland. ; NIAID, NIH, 10 Center Drive, Bethesda, Maryland. ; Structural Biology Section, Research Technologies Branch, NIAID, NIH, Twinbrook II, 12441 Parklawn Drive, Rockville, Maryland. ; NCI, NIH, 37 Convent Drive, Bethesda, MD. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 1808 EP - 1819 VL - 24 IS - 11 KW - Host Factor 1 Protein KW - 0 KW - Recombinant Proteins KW - Index Medicus KW - sRNA KW - small RNA KW - Hfq KW - pXO1 KW - anthrax KW - Bacillus anthracis KW - Sequence Alignment KW - Bacillus anthracis -- genetics KW - Recombinant Proteins -- metabolism KW - Models, Molecular KW - Molecular Sequence Data KW - Escherichia coli -- genetics KW - Amino Acid Sequence KW - Recombinant Proteins -- chemistry KW - Recombinant Proteins -- genetics KW - Host Factor 1 Protein -- metabolism KW - Host Factor 1 Protein -- genetics KW - Host Factor 1 Protein -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727995914?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Protein+science+%3A+a+publication+of+the+Protein+Society&rft.atitle=Hfqs+in+Bacillus+anthracis%3A+Role+of+protein+sequence+variation+in+the+structure+and+function+of+proteins+in+the+Hfq+family.&rft.au=Vrentas%2C+Catherine%3BGhirlando%2C+Rodolfo%3BKeefer%2C+Andrea%3BHu%2C+Zonglin%3BTomczak%2C+Aurelie%3BGittis%2C+Apostolos+G%3BMurthi%2C+Athulaprabha%3BGarboczi%2C+David+N%3BGottesman%2C+Susan%3BLeppla%2C+Stephen+H&rft.aulast=Vrentas&rft.aufirst=Catherine&rft.date=2015-11-01&rft.volume=24&rft.issue=11&rft.spage=1808&rft.isbn=&rft.btitle=&rft.title=Protein+science+%3A+a+publication+of+the+Protein+Society&rft.issn=1469-896X&rft_id=info:doi/10.1002%2Fpro.2773 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-26 N1 - Date created - 2015-10-27 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 1KQ1; PDB; 1KQ2; 1HK9; 3QHS N1 - SuppNotes - Cited By: Biophys J. 2000 Jan;78(1):385-93 [10620302] Biochemistry. 1999 Dec 14;38(50):16424-31 [10600103] Nucleic Acids Res. 2002 Sep 1;30(17):3662-71 [12202750] Nucleic Acids Res. 2003 Jul 15;31(14):4091-8 [12853626] Mol Microbiol. 2004 Mar;51(6):1525-33 [15009882] Biochem Biophys Res Commun. 2004 Oct 22;323(3):1017-23 [15381101] Mol Microbiol. 1994 Jul;13(1):35-49 [7984093] Biophys Chem. 1994 Dec;53(1-2):57-68 [7841332] Trends Biochem Sci. 2005 Sep;30(9):522-8 [16051491] Nat Struct Mol Biol. 2005 Dec;12(12):1031-6 [16327775] BMC Microbiol. 2007;7:10 [17291347] Nucleic Acids Res. 2008 Jan;36(1):133-43 [18000007] Nucleic Acids Res. 2010 Jan;38(3):907-19 [19942685] Curr Opin Microbiol. 2010 Feb;13(1):24-33 [20080057] Methods Mol Biol. 2010;607:11-21 [20204844] Syst Biol. 2010 May;59(3):307-21 [20525638] Acta Crystallogr Sect F Struct Biol Cryst Commun. 2010 Jul 1;66(Pt 7):760-4 [20606268] Mol Microbiol. 2010 Nov;78(3):622-35 [20815822] J Bacteriol. 2011 Apr;193(7):1515-26 [21278292] Nat Rev Microbiol. 2011 Aug;9(8):578-89 [21760622] J Mol Biol. 2012 Apr 13;417(5):406-12 [22326348] Biochimie. 2012 Jul;94(7):1554-9 [22326874] Nucleic Acids Res. 2012 Sep;40(16):8072-84 [22718981] Curr Protoc Protein Sci. 2013 Feb;Chapter 20:Unit20.12 [23377850] J Biol Chem. 2013 Mar 22;288(12):7996-8003 [23362267] RNA Biol. 2013 Apr;10(4):610-8 [23535768] J Mol Biol. 2013 Oct 9;425(19):3678-97 [23318956] BMC Genomics. 2014;15:229 [24661624] Biochemistry (Mosc). 2014 May;79(5):469-77 [24954598] J Bacteriol. 2014 Sep;196(18):3234-48 [24982306] RNA. 2014 Oct;20(10):1567-78 [25147238] Biochim Biophys Acta. 2015 Sep;1850(9):1661-8 [25863287] EMBO J. 2002 Jul 1;21(13):3546-56 [12093755] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/pro.2773 ER - TY - JOUR T1 - Sleep interruption associated with house staff work schedules alters circadian gene expression. AN - 1727988130; 26498241 AB - Epidemiological studies indicate that disruption of circadian rhythm by shift work increases the risk of breast and prostate cancer. Our studies demonstrated that carcinogens disrupt the circadian expression of circadian genes (CGs) and circadian-controlled genes (CCGs) during the early stages of rat mammary carcinogenesis. A chemopreventive regimen of methylselenocysteine (MSC) restored the circadian expression of CGs and CCGs, including PERIOD 2 (PER2) and estrogen receptor β (ERS2), to normal. The present study evaluated whether changes in CG and CCG expression in whole blood can serve as indicators of circadian disruption in shift workers. Fifteen shift workers were recruited to a crossover study. Blood samples were drawn before (6 PM) and after (8 AM) completing a night shift after at least seven days on floating night-shift rotation, and before (8 AM), during (1 PM), and after (6 PM) completing seven days on day shift. The plasma melatonin level and messenger RNA (mRNA) expression of PER2, nuclear receptor subfamily 1, group d, member 1 (NR1D1), and ERS2 were measured, and the changes in levels of melatonin and gene expression were evaluated with statistical analyses. The mRNA expression of PER2 was affected by shift (p = 0.0079); the levels were higher in the evening for the night shift, but higher in the morning for the day shift. Increased PER2 expression (p = 0.034) was observed in the evening on the night versus day shifts. The melatonin level was higher in the morning for both day shifts (p = 0.013) and night shifts (p <0.0001). Changes in the level of PER2 gene expression can serve as a biomarker of disrupted circadian rhythm in blood cells. Therefore, they can be a useful intermediate indicator of efficacy in future MSC-mediated chemoprevention studies. Copyright © 2015 Elsevier B.V. All rights reserved. JF - Sleep medicine AU - Fang, Ming Zhu AU - Ohman-Strickland, Pamela AU - Kelly-McNeil, Kathie AU - Kipen, Howard AU - Crabtree, Benjamin F AU - Lew, Jenny Pan AU - Zarbl, Helmut AD - Department of Environmental and Occupational Medicine, Robert Wood Johnson Medical School, Piscataway, NJ, USA; National Institute for Environmental Health Sciences (NIEHS) Center for Environmental Exposures and Disease, Environmental and Occupational Health Sciences Institute, Piscataway, NJ, USA; Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA. ; National Institute for Environmental Health Sciences (NIEHS) Center for Environmental Exposures and Disease, Environmental and Occupational Health Sciences Institute, Piscataway, NJ, USA; Department of Biostatistics, School of Public Health, Piscataway, NJ, USA. ; Department of Environmental and Occupational Medicine, Robert Wood Johnson Medical School, Piscataway, NJ, USA; National Institute for Environmental Health Sciences (NIEHS) Center for Environmental Exposures and Disease, Environmental and Occupational Health Sciences Institute, Piscataway, NJ, USA. ; Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA; Family Medicine, Robert Wood Johnson Medical School, Piscataway, NJ, USA. ; Children's National Medical Center, Washington, DC 20010, USA. ; Department of Environmental and Occupational Medicine, Robert Wood Johnson Medical School, Piscataway, NJ, USA; National Institute for Environmental Health Sciences (NIEHS) Center for Environmental Exposures and Disease, Environmental and Occupational Health Sciences Institute, Piscataway, NJ, USA; Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA. Electronic address: zarbl@eohsi.rutgers.edu. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 1388 EP - 1394 VL - 16 IS - 11 KW - Biomarkers KW - 0 KW - PER2 protein, human KW - Period Circadian Proteins KW - RNA, Messenger KW - Melatonin KW - JL5DK93RCL KW - Index Medicus KW - PERIOD 2 KW - Shift worker KW - Breast cancer KW - Circadian rhythm KW - Biomarker KW - Rats KW - Young Adult KW - Animals KW - Circadian Clocks KW - RNA, Messenger -- metabolism KW - Humans KW - Adult KW - Cross-Over Studies KW - Biomarkers -- blood KW - Male KW - Female KW - Work Schedule Tolerance KW - Melatonin -- blood KW - Period Circadian Proteins -- genetics KW - Period Circadian Proteins -- metabolism KW - Circadian Rhythm -- physiology KW - Sleep Disorders, Circadian Rhythm -- genetics KW - Internship and Residency KW - Gene Expression UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727988130?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Sleep+medicine&rft.atitle=Sleep+interruption+associated+with+house+staff+work+schedules+alters+circadian+gene+expression.&rft.au=Fang%2C+Ming+Zhu%3BOhman-Strickland%2C+Pamela%3BKelly-McNeil%2C+Kathie%3BKipen%2C+Howard%3BCrabtree%2C+Benjamin+F%3BLew%2C+Jenny+Pan%3BZarbl%2C+Helmut&rft.aulast=Fang&rft.aufirst=Ming&rft.date=2015-11-01&rft.volume=16&rft.issue=11&rft.spage=1388&rft.isbn=&rft.btitle=&rft.title=Sleep+medicine&rft.issn=1878-5506&rft_id=info:doi/10.1016%2Fj.sleep.2015.06.011 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-15 N1 - Date created - 2015-10-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Rev Cancer. 2003 May;3(5):350-61 [12724733] Scand J Work Environ Health. 2014 May 1;40(3):295-304 [24402410] Cancer Lett. 2000 Feb 1;148(2):121-6 [10695987] J Biol Rhythms. 2003 Dec;18(6):513-23 [14667152] J Neural Transm. 1980;47(2):121-30 [6768843] Epidemiology. 2005 Mar;16(2):254-8 [15703542] Ann N Y Acad Sci. 2004 Dec;1031:234-41 [15753149] Cancer Causes Control. 2006 May;17(4):501-7 [16596303] Cell Cycle. 2007 Jun 1;6(11):1329-31 [17534151] Sleep. 2007 Nov;30(11):1427-36 [18041477] JAMA. 2009 Jan 7;301(1):39-51 [19066370] Cancer Prev Res (Phila). 2008 Jul;1(2):119-27 [19122877] Lancet Oncol. 2007 Dec;8(12):1065-6 [19271347] Mol Interv. 2009 Feb;9(1):18-21 [19299660] Integr Cancer Ther. 2009 Dec;8(4):298-302 [20042408] Mutat Res. 2009 Nov-Dec;680(1-2):95-105 [19833225] Cancer Prev Res (Phila). 2010 May;3(5):573-5 [20403999] Cancer Prev Res (Phila). 2010 May;3(5):604-10 [20424130] Cancer Prev Res (Phila). 2010 May;3(5):640-52 [20424134] PLoS One. 2010;5(6):e10995 [20539819] Nat Rev Neurosci. 2010 Aug;11(8):589-99 [20631712] Ann Med. 2010 Sep;42(6):404-15 [20568980] Cancer Epidemiol Biomarkers Prev. 2011 Nov;20(11):2404-12 [21953114] Occup Environ Med. 2012 May;69(5):339-46 [22368032] Scand J Work Environ Health. 2013 Mar 1;39(2):178-86 [22517501] J Biol Regul Homeost Agents. 2013 Jan-Mar;27(1):267-74 [23489707] Sleep Med Rev. 2013 Aug;17(4):273-84 [23137527] Cancer Epidemiol Biomarkers Prev. 2013 Jun;22(6):1079-87 [23563887] Int Arch Occup Environ Health. 2013 Nov;86(8):923-30 [23179107] Ann Oncol. 2013 Nov;24(11):2724-32 [23975662] World J Gastroenterol. 2013 Dec 28;19(48):9231-9 [24409051] J Clin Epidemiol. 2001 Jun;54(6):634-44 [11377125] Occup Environ Med. 2013 Dec;70(12):831-8 [23817841] Psychiatry Res. 2013 Dec 30;210(3):1219-25 [24176594] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.sleep.2015.06.011 ER - TY - JOUR T1 - Why has active immunotherapy not worked in lung cancer? AN - 1727985777; 26232492 AB - Vaccines that rely on active specific stimulation of the host immune system have the potential to trigger durable antitumor responses with minimal toxicity. However, in nonsmall-cell lung cancer (NSCLC), several large phase III trials of vaccines reported within the last year have yielded disappointing results. Compared with placebo, belagenpumatucel-L (an allogenic tumor cell vaccine), tecemotide (a peptide vaccine targeting MUC-1) and melanoma-associated antigen-A3 (a protein-based vaccine) did not improve outcomes in NSCLC. The lack of clinically significant outcomes, despite their ability to prime and expand tumor antigen-specific T cells could at least partly be attributed to the inability of vaccine-induced T-cell responses to overcome the tumoral mechanisms of immune escape which limit the clonal expansion of T cells following vaccination. A number of such mechanisms have been recognized including reduced antigen presentation, antigenic loss, cytokines, immunosuppressive cells and immune checkpoints. Strategies aimed at modulating the immune checkpoints have shown promise and are on the verge of revolutionizing the therapeutic landscape of metastatic NSCLC. Overcoming immune tolerance and improving the activation of antitumor T cells via combinatorial approaches may represent a new and more promising therapeutic application for active immunotherapies in NSCLC. Published by Oxford University Press on behalf of the European Society for Medical Oncology 2015. This work is written by (a) US Government employee(s) and is in the public domain in the US. JF - Annals of oncology : official journal of the European Society for Medical Oncology AU - Thomas, A AU - Giaccone, G AD - Thoracic and GI Oncology Branch, National Cancer Institute, Bethesda. ; Lombardi Comprehensive Cancer Center, Georgetown University, Washington, USA gg496@georgetown.edu. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 2213 EP - 2220 VL - 26 IS - 11 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, Neoplasm KW - Index Medicus KW - nonsmall-cell lung cancer KW - active immunotherapy KW - vaccines KW - tumor-mediated immunosuppression KW - immune checkpoint KW - Animals KW - Humans KW - Clinical Trials, Phase III as Topic -- methods KW - Antigens, Neoplasm -- immunology KW - T-Lymphocytes -- immunology KW - Antibodies, Monoclonal -- immunology KW - Immunotherapy, Active -- trends KW - Lung Neoplasms -- diagnosis KW - Lung Neoplasms -- immunology KW - Lung Neoplasms -- therapy KW - Carcinoma, Non-Small-Cell Lung -- immunology KW - Carcinoma, Non-Small-Cell Lung -- diagnosis KW - Carcinoma, Non-Small-Cell Lung -- therapy KW - Immunotherapy, Active -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727985777?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+oncology+%3A+official+journal+of+the+European+Society+for+Medical+Oncology&rft.atitle=Why+has+active+immunotherapy+not+worked+in+lung+cancer%3F&rft.au=Thomas%2C+A%3BGiaccone%2C+G&rft.aulast=Thomas&rft.aufirst=A&rft.date=2015-11-01&rft.volume=26&rft.issue=11&rft.spage=2213&rft.isbn=&rft.btitle=&rft.title=Annals+of+oncology+%3A+official+journal+of+the+European+Society+for+Medical+Oncology&rft.issn=1569-8041&rft_id=info:doi/10.1093%2Fannonc%2Fmdv323 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-18 N1 - Date created - 2015-10-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Cancer Res. 1999 Apr;5(4):933-6 [10213231] Eur J Cancer. 1994;30A(3):376-81 [8204362] J Immunol. 1999 Nov 1;163(9):5020-8 [10528207] Expert Rev Vaccines. 2005 Jun;4(3):249-57 [16026241] J Clin Oncol. 2005 Sep 20;23(27):6674-81 [16170175] J Clin Oncol. 2006 Oct 10;24(29):4721-30 [16966690] J Immunol. 2007 Mar 1;178(5):2883-92 [17312132] Cancer Res. 2007 May 1;67(9):4507-13 [17483367] Clin Cancer Res. 2007 Aug 1;13(15 Pt 2):s4652-4 [17671159] Cancer Sci. 2007 Sep;98(9):1424-30 [17645781] Cancer Sci. 2007 Nov;98(11):1795-802 [17725806] Cell Death Differ. 2008 Jan;15(1):3-12 [18007663] Clin Cancer Res. 2008 Oct 15;14(20):6674-82 [18927310] Nat Rev Immunol. 2009 Mar;9(3):162-74 [19197294] Nat Rev Immunol. 2009 May;9(5):377-84 [19330016] Blood. 2010 Apr 29;115(17):3520-30 [20197554] Nat Rev Cancer. 2010 Jun;10(6):415-24 [20495575] J Clin Oncol. 2010 Jul 1;28(19):3167-75 [20516446] Clin Cancer Res. 2010 Aug 1;16(15):4046-56 [20562209] N Engl J Med. 2010 Jul 29;363(5):411-22 [20818862] Ann N Y Acad Sci. 2010 Oct;1209:99-108 [20958322] Clin Lung Cancer. 2010 Nov 1;11(6):391-5 [21071331] Semin Immunopathol. 2011 Jul;33(4):369-83 [21611872] J Cancer Res Clin Oncol. 2011 Sep;137(9):1337-42 [21744082] J Thorac Oncol. 2011 Oct;6(10):1763-73 [21876456] Cancer Immunol Immunother. 2012 Apr;61(4):511-21 [21971588] Curr Opin Immunol. 2012 Apr;24(2):207-12 [22236695] J Pharmacol Exp Ther. 2000 Apr;293(1):166-71 [10734166] Cancer. 2001 Mar 1;91(5):964-71 [11251948] J Immunol. 2002 May 1;168(9):4272-6 [11970966] Nat Rev Immunol. 2002 May;2(5):372-7 [12033743] Cell Immunol. 1993 Feb;146(2):391-405 [8174177] Nature. 2014 Nov 27;515(7528):563-7 [25428504] Nat Genet. 1996 Jun;13(2):210-3 [8640228] Int J Cancer. 1996 Nov 27;68(5):629-36 [8938146] J Immunol. 1996 Dec 15;157(12):5512-20 [8955201] Gene Ther. 1997 Oct;4(10):1029-35 [9415308] Cancer Res. 1998 Aug 15;58(16):3660-7 [9721876] Chest. 2002 Jul;122(1):282-8 [12114371] Cancer Res. 2003 Feb 1;63(3):642-6 [12566308] Clin Cancer Res. 2003 Feb;9(2):606-12 [12576425] Proc Natl Acad Sci U S A. 1986 Apr;83(8):2438-42 [2871553] Proc Natl Acad Sci U S A. 1990 Feb;87(4):1486-90 [2137615] J Exp Med. 1993 Feb 1;177(2):265-72 [8426105] J Natl Cancer Inst. 2012 Apr 18;104(8):590-8 [22491345] J Clin Oncol. 2012 Jun 10;30(17):2046-54 [22547592] N Engl J Med. 2012 Jun 28;366(26):2443-54 [22658127] Lancet Oncol. 2012 Jul;13(7):e301-10 [22748269] PLoS One. 2012;7(7):e40677 [22815789] Clin Dev Immunol. 2012;2012:741741 [23118782] J Clin Oncol. 2013 Jul 1;31(19):2396-403 [23715567] Cancer Discov. 2013 Dec;3(12):1355-63 [24078774] Lancet Oncol. 2014 Jan;15(1):59-68 [24331154] Cancer Immunol Res. 2013 Dec;1(6):365-72 [24563870] Cancer Immunol Res. 2013 Aug;1(2):123-33 [24455752] Cancer Cell. 2014 May 12;25(5):590-604 [24794706] Cancer Immunol Res. 2014 Sep;2(9):831-8 [25187273] Ann Oncol. 2014 Oct;25(10):1935-40 [25009014] Science. 2014 Oct 10;346(6206):256-9 [25301631] Immunity. 1999 Aug;11(2):141-51 [10485649] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/annonc/mdv323 ER - TY - JOUR T1 - Geminin is Essential to Prevent DNA Re-Replication-Dependent Apoptosis in Pluripotent Cells, but not in Differentiated Cells AN - 1727671664; PQ0002186629 AB - Geminin is a dual-function protein unique to multicellular animals with roles in modulating gene expression and preventing DNA re-replication. Here, we show that geminin is essential at the beginning of mammalian development to prevent DNA re-replication in pluripotent cells, exemplified by embryonic stem cells, as they undergo self-renewal and differentiation. Embryonic stem cells, embryonic fibroblasts, and immortalized fibroblasts were characterized before and after geminin was depleted either by gene ablation or siRNA. Depletion of geminin under conditions that promote either self-renewal or differentiation rapidly induced DNA re-replication, followed by DNA damage, then a DNA damage response, and finally apoptosis. Once differentiation had occurred, geminin was no longer essential for viability, although it continued to contribute to preventing DNA re-replication induced DNA damage. No relationship was detected between expression of geminin and genes associated with either pluripotency or differentiation. Thus, the primary role of geminin at the beginning of mammalian development is to prevent DNA re-replication-dependent apoptosis, a role previously believed essential only in cancer cells. These results suggest that regulation of gene expression by geminin occurs only after pluripotent cells differentiate into cells in which geminin is not essential for viability. Stem Cells 2015; 33:3239-3253 JF - Stem Cells AU - Huang, Yi-Yuan AU - Kaneko, Kotaro J AU - Pan, Haiyan AU - DePamphilis, Melvin L AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 3239 EP - 3253 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 33 IS - 11 SN - 1066-5099, 1066-5099 KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - Gene expression KW - Differentiation KW - DNA damage KW - Stem cells KW - Apoptosis KW - Embryo cells KW - siRNA KW - Embryo fibroblasts KW - geminin KW - Cancer KW - W 30910:Imaging KW - N 14820:DNA Metabolism & Structure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727671664?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+Cells&rft.atitle=Geminin+is+Essential+to+Prevent+DNA+Re-Replication-Dependent+Apoptosis+in+Pluripotent+Cells%2C+but+not+in+Differentiated+Cells&rft.au=Huang%2C+Yi-Yuan%3BKaneko%2C+Kotaro+J%3BPan%2C+Haiyan%3BDePamphilis%2C+Melvin+L&rft.aulast=Huang&rft.aufirst=Yi-Yuan&rft.date=2015-11-01&rft.volume=33&rft.issue=11&rft.spage=3239&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.2092 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-02-29 N1 - SubjectsTermNotLitGenreText - Gene expression; DNA damage; Differentiation; Stem cells; Apoptosis; siRNA; Embryo cells; Embryo fibroblasts; geminin; Cancer DO - http://dx.doi.org/10.1002/stem.2092 ER - TY - JOUR T1 - Functional and genetic deconstruction of the cellular origin in liver cancer. AN - 1727435859; 26493646 AB - During the past decade, research on primary liver cancers has particularly highlighted the uncommon plasticity of differentiated parenchymal liver cells (that is, hepatocytes and cholangiocytes (also known as biliary epithelial cells)), the role of liver progenitor cells in malignant transformation, the importance of the tumour microenvironment and the molecular complexity of liver tumours. Whereas other reviews have focused on the landscape of genetic alterations that promote development and progression of primary liver cancers and the role of the tumour microenvironment, the crucial importance of the cellular origin of liver cancer has been much less explored. Therefore, in this Review, we emphasize the importance and complexity of the cellular origin in tumour initiation and progression, and attempt to integrate this aspect with recent discoveries in tumour genomics and the contribution of the disrupted hepatic microenvironment to liver carcinogenesis. JF - Nature reviews. Cancer AU - Marquardt, Jens U AU - Andersen, Jesper B AU - Thorgeirsson, Snorri S AD - Department of Medicine I, Johannes Gutenberg University, Langenbeckstrasse 1, 55131 Mainz, Germany. ; Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Ole Maaløes Vej 5, 2200 Copenhagen N, Denmark. ; Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 653 EP - 667 VL - 15 IS - 11 KW - Index Medicus KW - Animals KW - Humans KW - Liver Neoplasms -- pathology KW - Tumor Microenvironment KW - Cell Differentiation KW - Liver Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727435859?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+reviews.+Cancer&rft.atitle=Functional+and+genetic+deconstruction+of+the+cellular+origin+in+liver+cancer.&rft.au=Marquardt%2C+Jens+U%3BAndersen%2C+Jesper+B%3BThorgeirsson%2C+Snorri+S&rft.aulast=Marquardt&rft.aufirst=Jens&rft.date=2015-11-01&rft.volume=15&rft.issue=11&rft.spage=653&rft.isbn=&rft.btitle=&rft.title=Nature+reviews.+Cancer&rft.issn=1474-1768&rft_id=info:doi/10.1038%2Fnrc4017 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-28 N1 - Date created - 2015-10-23 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nrc4017 ER - TY - JOUR T1 - Pharmacodynamics (PD) and pharmacokinetics (PK) of E7389 (eribulin, halichondrin B analog) during a phase I trial in patients with advanced solid tumors: a California Cancer Consortium trial. AN - 1725523192; 26362045 AB - The California Cancer Consortium completed a phase I trial of E7389 (eribulin mesylate), an analog of the marine natural product halichondrin B. This trial was to determine the pharmacodynamics, pharmacokinetics, and MTD of E7389 administered by bolus injection weekly for 3 weeks out of four. This trial included a rapid titration design. Real-time pharmacokinetics were utilized to guide dose escalation. Initially, single-patient cohorts were enrolled with intra- and inter-patient dose doubling. The second phase was a standard 3 + 3 dose escalation schedule. At the MTD, a cohort of patients was enrolled for target validation studies (separate manuscript). The starting dose was 0.125 mg/m(2), and doses were doubled within and between patients in the first phase. Blood and urine sampling for E7389 pharmacokinetics was performed on doses 1 and 3 of cycle 1. Levels were determined using a LC/MS/MS assay. Forty patients were entered. Thirty-eight were evaluable for toxicity and 35 for response. The rapid escalation ended with a grade 3 elevation of alkaline phosphatase at 0.5 mg/m(2)/week. The second phase ended at 2.0 mg/m(2)/week with dose-limiting toxicities of grades 3 and 4 febrile neutropenia. Other toxicities included hypoglycemia, hypophosphatemia, and fatigue. The MTD was 1.4 mg/m(2)/week. Responses included four partial responses (lung cancer [2], urothelial [1], and melanoma [1]). E7389 was well tolerated in this trial with the major toxicity being myelosuppression. PD shows that E7389 induces significant morphologic changes (bundle formation) in the microtubules of peripheral blood mononuclear cells and tumor cells in vivo. The data suggest that lower intra-tumoral levels of β-tubulin III or higher intra-tumoral levels of MAP4 may correlate with response to E7389, while lower intra-tumoral levels of stathmin may be associated with progression. PK data reveal that E7389 exhibits a tri-exponential elimination from the plasma of patients receiving a rapid i.v. infusion. At sub-toxic doses, plasma concentrations of E7389 are maintained well above the levels required for activity in vitro for >72 h. JF - Cancer chemotherapy and pharmacology AU - Morgan, Robert J AU - Synold, Timothy W AU - Longmate, Jeffrey A AU - Quinn, David I AU - Gandara, David AU - Lenz, Heinz-Josef AU - Ruel, Christopher AU - Xi, Bixin AU - Lewis, Michael D AU - Colevas, A Dimitrios AU - Doroshow, James AU - Newman, Edward M AD - Department of Medical Oncology and Therapeutics Research, City of Hope Comprehensive Cancer Center, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. rmorgan@coh.org. ; Department of Cancer Biology, City of Hope Comprehensive Cancer Center, Duarte, CA, 91010, USA. ; Department of Biostatistics, City of Hope Comprehensive Cancer Center, Duarte, CA, 91010, USA. ; Division of Medical Oncology, University of Southern California, Norris Comprehensive Cancer Center, Los Angeles, CA, 90033, USA. ; Division of Medical Oncology, University of California, Davis Cancer Center, Sacramento, CA, USA. ; Eisai Research Institute, Andover, MA, 01810, USA. ; Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, MD, 20892, USA. ; Department of Medical Oncology and Therapeutics Research, City of Hope Comprehensive Cancer Center, 1500 E. Duarte Rd., Duarte, CA, 91010, USA. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 897 EP - 907 VL - 76 IS - 5 KW - Antineoplastic Agents KW - 0 KW - Furans KW - Ketones KW - Tubulin Modulators KW - eribulin KW - LR24G6354G KW - Index Medicus KW - Halichondrin B analog KW - Phase I trial KW - Pharmacokinetics KW - Pharmacodynamics KW - Eribulin KW - Breast Neoplasms -- drug therapy KW - Urologic Neoplasms -- blood KW - Lymphopenia -- chemically induced KW - Injections, Intravenous KW - Dose-Response Relationship, Drug KW - Lung Neoplasms -- blood KW - Humans KW - Urologic Neoplasms -- drug therapy KW - Salvage Therapy KW - Melanoma -- blood KW - Lung Neoplasms -- drug therapy KW - Aged KW - Breast Neoplasms -- blood KW - Ovarian Neoplasms -- drug therapy KW - Aged, 80 and over KW - Febrile Neutropenia -- chemically induced KW - Ovarian Neoplasms -- blood KW - Melanoma -- drug therapy KW - Adult KW - Drug Monitoring KW - Middle Aged KW - Male KW - Female KW - Ketones -- blood KW - Furans -- pharmacokinetics KW - Tubulin Modulators -- blood KW - Antineoplastic Agents -- pharmacokinetics KW - Antineoplastic Agents -- blood KW - Ketones -- therapeutic use KW - Antineoplastic Agents -- adverse effects KW - Furans -- pharmacology KW - Tubulin Modulators -- adverse effects KW - Tubulin Modulators -- pharmacology KW - Ketones -- adverse effects KW - Carcinoma -- drug therapy KW - Furans -- adverse effects KW - Furans -- therapeutic use KW - Furans -- blood KW - Tubulin Modulators -- therapeutic use KW - Ketones -- pharmacokinetics KW - Antineoplastic Agents -- therapeutic use KW - Carcinoma -- blood KW - Tubulin Modulators -- pharmacokinetics KW - Antineoplastic Agents -- pharmacology KW - Ketones -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1725523192?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+chemotherapy+and+pharmacology&rft.atitle=Pharmacodynamics+%28PD%29+and+pharmacokinetics+%28PK%29+of+E7389+%28eribulin%2C+halichondrin+B+analog%29+during+a+phase+I+trial+in+patients+with+advanced+solid+tumors%3A+a+California+Cancer+Consortium+trial.&rft.au=Morgan%2C+Robert+J%3BSynold%2C+Timothy+W%3BLongmate%2C+Jeffrey+A%3BQuinn%2C+David+I%3BGandara%2C+David%3BLenz%2C+Heinz-Josef%3BRuel%2C+Christopher%3BXi%2C+Bixin%3BLewis%2C+Michael+D%3BColevas%2C+A+Dimitrios%3BDoroshow%2C+James%3BNewman%2C+Edward+M&rft.aulast=Morgan&rft.aufirst=Robert&rft.date=2015-11-01&rft.volume=76&rft.issue=5&rft.spage=897&rft.isbn=&rft.btitle=&rft.title=Cancer+chemotherapy+and+pharmacology&rft.issn=1432-0843&rft_id=info:doi/10.1007%2Fs00280-015-2868-7 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-28 N1 - Date created - 2015-10-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biochim Biophys Acta. 2001;1471(2):O1-9 [11342188] Cancer Res. 2001 Feb 1;61(3):1013-21 [11221827] Biol Blood Marrow Transplant. 2001;7(8):414-32 [11569887] Clin Cancer Res. 2002 Jul;8(7):2035-43 [12114401] Cancer Res. 2002 Dec 1;62(23):6864-9 [12460900] Cancer Res. 2003 Mar 15;63(6):1207-13 [12649178] Mol Cancer Ther. 2005 Jul;4(7):1086-95 [16020666] Cancer Treat Rev. 2006 Dec;32(8):619-29 [17069979] Nat Chem Biol. 2006 Dec;2(12):689-700 [17108987] Int J Cancer. 2007 May 15;120(10):2078-85 [17285590] Cancer Res. 2007 Oct 1;67(19):9356-63 [17909044] Mol Cancer Ther. 2008 Jul;7(7):2003-11 [18645010] Clin Cancer Res. 2009 Jun 15;15(12):3903-5 [19509144] Clin Cancer Res. 2009 Jun 15;15(12):4213-9 [19509146] Clin Cancer Res. 2009 Jun 15;15(12):4207-12 [19509177] Mol Cancer Ther. 2009 Aug;8(8):2086-95 [19671735] Biochemistry. 2010 Feb 16;49(6):1331-7 [20030375] Lancet. 2011 Mar 12;377(9769):914-23 [21376385] Cancer Res. 2004 Aug 15;64(16):5760-6 [15313917] Clin Ther. 2012 Jul;34(7):1467-73 [22739019] J Thorac Oncol. 2012 Mar;7(3):574-8 [22198425] J Biol Chem. 1991 Aug 25;266(24):15882-9 [1874739] Pharmacol Ther. 1992;55(1):31-51 [1287674] Biochem Pharmacol. 1993 Jan 26;45(2):421-7 [8435093] Mol Pharmacol. 1993 Oct;44(4):757-66 [8232226] J Natl Cancer Inst. 1997 Aug 6;89(15):1138-47 [9262252] J Exp Ther Oncol. 1996 Mar;1(2):119-25 [9414395] Clin Cancer Res. 2005 Jan 1;11(1):298-305 [15671559] Mol Cancer Ther. 2005 Feb;4(2):333-42 [15713904] J Clin Oncol. 1999 Jun;17(6):1786-93 [10561216] Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2904-9 [10688884] Oncogene. 2000 Jun 22;19(27):3078-85 [10871860] Trends Pharmacol Sci. 2000 Sep;21(9):321-4 [10973074] Cancer Res. 2001 Aug 1;61(15):5803-9 [11479219] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00280-015-2868-7 ER - TY - JOUR T1 - Predictors of survival and effect of short (40 Gy) or standard-course (60 Gy) irradiation plus concomitant temozolomide in elderly patients with glioblastoma: a multicenter retrospective study of AINO (Italian Association of Neuro-Oncology). AN - 1725512545; 26423801 AB - The efficacy of temozolomide (TMZ) plus radiation therapy (RT) in elderly patients with glioblastoma is unclear. We performed a large multicenter retrospective study to analyze prognostic factors and clinical outcome in these patients. Inclusion criteria were age ≥65 years, newly histologically confirmed glioblastoma, ECOG PS 0-2, adjuvant treatment with RT plus TMZ. We enrolled 237 patients; the average age was 71 and ECOG PS was 0-1 in 196 patients; gross total resection was performed in 174 cases. MGMT was analyzed in 151 persons and was methylated in 56 %. IDH1 was assessed in 100 patients and was mutated in 6 %. Seventy-one patients were treated with RT 40 Gy and 166 with RT 60 Gy. Progression-free survival and overall survival (OS) were 11.3 and 17.3 months, respectively. Overall survival was 19.4 vs 13.8 months for patients treated with RT 60 Gy and 40 Gy (p = 0.02); OS was 17.7 versus 16.1 months for patients treated with gross total resection vs partial surgery (p = 0.02); OS was 21.2 versus 13.6 months for methylated and unmethylated MGMT (p < 0.001). On multivariate analysis, gross total resection, RT 60 Gy, methylated MGMT and ECOG PS 0-1 were independent predictors of longer survival. Twenty-five patients (10 %) had grade 3-4 haematological toxicity during the concomitant treatment. We showed that, in elderly patients in good clinical condition treated with concomitant treatment, standard-course irradiation might be more effective than short-course irradiation. Methylated MGMT remains the most important prognostic factor. JF - Journal of neuro-oncology AU - Lombardi, Giuseppe AU - Pace, Andrea AU - Pasqualetti, Francesco AU - Rizzato, Simona AU - Faedi, Marina AU - Anghileri, Elena AU - Nicolotto, Elisa AU - Bazzoli, Elena AU - Bellu, Luisa AU - Villani, Veronica AU - Fabi, Alessandra AU - Ferrazza, Patrizia AU - Gurrieri, Lorena AU - Dall'Agata, Monia AU - Eoli, Marica AU - Della Puppa, Alessandro AU - Pambuku, Ardi AU - D'Avella, Domenico AU - Berti, Franco AU - Rudà, Roberta AU - Zagonel, Vittorina AD - Department of Clinical and Experimental Oncology, Medical Oncology 1, Veneto Institute of Oncology IOV - IRCCS, via Gattamelata, 64, 35128, Padua, Italy. giuseppe.lombardi@ioveneto.it. ; Neuro-Oncology Unit, "Regina Elena" National Cancer Institute, Rome, Italy. ; Department of Radiotherapy, Azienda Ospedaliero-Universitaria Pisana, Pisa, Italy. ; Department of Oncology, Azienda Ospedaliero-Universitaria di Udine, Udine, Italy. ; Department of Medical Oncology, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. ; Unit of Molecular Neuro-Oncology, Fondazione I.R.C.C.S. Istituto Neurologico C. Besta, Milan, Italy. ; Department of Neuro-Oncology, University of Turin and City of Health and Science, University Hospital, Turin, Italy. ; Department of Neurological and Movement Sciences, University of Verona, Verona, Italy. ; Department of Clinical and Experimental Oncology, Medical Oncology 1, Veneto Institute of Oncology IOV - IRCCS, via Gattamelata, 64, 35128, Padua, Italy. ; Division of Medical Oncology, "Regina Elena" National Cancer Institute, Rome, Italy. ; Biostatistics and Clinical Trials Unit, Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori (IRST) IRCCS, Meldola, Italy. ; Neurosurgery Department, Azienda Ospedaliera di Padova, Padua, Italy. ; Neurosurgery Department, University of Padua, Padua, Italy. ; Radiation Therapy and Nuclear Medicine Unit, Veneto Institute of Oncology IOV IRCCS, Padua, Italy. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 359 EP - 367 VL - 125 IS - 2 KW - Antineoplastic Agents, Alkylating KW - 0 KW - Dacarbazine KW - 7GR28W0FJI KW - Isocitrate Dehydrogenase KW - EC 1.1.1.41 KW - IDH1 protein, human KW - EC 1.1.1.42. KW - O(6)-Methylguanine-DNA Methyltransferase KW - EC 2.1.1.63 KW - temozolomide KW - YF1K15M17Y KW - Index Medicus KW - Radiation therapy KW - Glioblastoma KW - Chemotherapy KW - Elderly KW - Temozolomide KW - Magnetic Resonance Imaging KW - Disease-Free Survival KW - Combined Modality Therapy KW - Humans KW - Isocitrate Dehydrogenase -- genetics KW - Retrospective Studies KW - Aged KW - DNA Methylation -- radiation effects KW - Karnofsky Performance Status KW - Italy KW - O(6)-Methylguanine-DNA Methyltransferase -- metabolism KW - Aged, 80 and over KW - Radiotherapy Dosage KW - DNA Methylation -- drug effects KW - Mutation -- genetics KW - Male KW - Female KW - Glioblastoma -- genetics KW - Dacarbazine -- therapeutic use KW - Brain Neoplasms -- therapy KW - Antineoplastic Agents, Alkylating -- therapeutic use KW - Glioblastoma -- mortality KW - Brain Neoplasms -- mortality KW - Brain Neoplasms -- genetics KW - Dacarbazine -- analogs & derivatives KW - Chemoradiotherapy KW - Glioblastoma -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1725512545?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neuro-oncology&rft.atitle=Predictors+of+survival+and+effect+of+short+%2840+Gy%29+or+standard-course+%2860+Gy%29+irradiation+plus+concomitant+temozolomide+in+elderly+patients+with+glioblastoma%3A+a+multicenter+retrospective+study+of+AINO+%28Italian+Association+of+Neuro-Oncology%29.&rft.au=Lombardi%2C+Giuseppe%3BPace%2C+Andrea%3BPasqualetti%2C+Francesco%3BRizzato%2C+Simona%3BFaedi%2C+Marina%3BAnghileri%2C+Elena%3BNicolotto%2C+Elisa%3BBazzoli%2C+Elena%3BBellu%2C+Luisa%3BVillani%2C+Veronica%3BFabi%2C+Alessandra%3BFerrazza%2C+Patrizia%3BGurrieri%2C+Lorena%3BDall%27Agata%2C+Monia%3BEoli%2C+Marica%3BDella+Puppa%2C+Alessandro%3BPambuku%2C+Ardi%3BD%27Avella%2C+Domenico%3BBerti%2C+Franco%3BRud%C3%A0%2C+Roberta%3BZagonel%2C+Vittorina&rft.aulast=Lombardi&rft.aufirst=Giuseppe&rft.date=2015-11-01&rft.volume=125&rft.issue=2&rft.spage=359&rft.isbn=&rft.btitle=&rft.title=Journal+of+neuro-oncology&rft.issn=1573-7373&rft_id=info:doi/10.1007%2Fs11060-015-1923-x LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-25 N1 - Date created - 2015-10-21 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s11060-015-1923-x ER - TY - JOUR T1 - Endocrine disruptors and obesity. AN - 1725024428; 26391979 AB - The increasing incidence of obesity is a serious global public health challenge. Although the obesity epidemic is largely fueled by poor nutrition and lack of exercise, certain chemicals have been shown to potentially have a role in its aetiology. A substantial body of evidence suggests that a subclass of endocrine-disrupting chemicals (EDCs), which interfere with endocrine signalling, can disrupt hormonally regulated metabolic processes, especially if exposure occurs during early development. These chemicals, so-called 'obesogens' might predispose some individuals to gain weight despite their efforts to limit caloric intake and increase levels of physical activity. This Review discusses the role of EDCs in the obesity epidemic, the latest research on the obesogen concept, epidemiological and experimental findings on obesogens, and their modes of action. The research reviewed here provides knowledge that health scientists can use to inform their research and decision-making processes. JF - Nature reviews. Endocrinology AU - Heindel, Jerrold J AU - Newbold, Retha AU - Schug, Thaddeus T AD - Division of Extramural Research and Training, Population Health Branch, National Institute of Environmental Sciences, PO Box 12233, Research Triangle Park, NC 27709, USA. ; Division of the National Toxicology Program, National Institute of Environmental Health Sciences/National Institutes of Health, PO Box 12233, Research Triangle Park, NC 27709, USA. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 653 EP - 661 VL - 11 IS - 11 KW - Endocrine Disruptors KW - 0 KW - Environmental Pollutants KW - Index Medicus KW - Environmental Pollutants -- toxicity KW - Humans KW - Adult KW - Environmental Exposure KW - Smoking -- adverse effects KW - Female KW - Adipogenesis -- drug effects KW - Pregnancy KW - Endocrine Disruptors -- pharmacology KW - Obesity -- physiopathology KW - Obesity -- epidemiology KW - Obesity -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1725024428?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+reviews.+Endocrinology&rft.atitle=Endocrine+disruptors+and+obesity.&rft.au=Heindel%2C+Jerrold+J%3BNewbold%2C+Retha%3BSchug%2C+Thaddeus+T&rft.aulast=Heindel&rft.aufirst=Jerrold&rft.date=2015-11-01&rft.volume=11&rft.issue=11&rft.spage=653&rft.isbn=&rft.btitle=&rft.title=Nature+reviews.+Endocrinology&rft.issn=1759-5037&rft_id=info:doi/10.1038%2Fnrendo.2015.163 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-21 N1 - Date created - 2015-10-20 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nrendo.2015.163 ER - TY - JOUR T1 - Association of Human Papillomavirus 31 DNA Load with Risk of Cervical Intraepithelial Neoplasia Grades 2 and 3. AN - 1722930742; 26292291 AB - The association between human papillomavirus 31 (HPV31) DNA loads and the risk of cervical intraepithelial neoplasia grades 2 and 3 (CIN2-3) was evaluated among women enrolled in the atypical squamous cells of undetermined significance (ASCUS) and low-grade squamous intraepithelial lesion (LSIL) triage study (ALTS), who were monitored semiannually over 2 years and who had HPV31 infections detected at ≥1 visit. HPV31 DNA loads in the first HPV31-positive samples and in a random set of the last positive samples from women with ≥2 HPV31-positive visits were measured by a real-time PCR assay. CIN2-3 was histologically confirmed at the same time as the first detection of HPV31 for 88 (16.6%) of 530 women. After adjustment for HPV31 lineages, coinfection with other oncogenic types, and the timing of the first positive detection, the odds ratio (OR) per 1-log-unit increase in viral loads for the risk of a concurrent diagnosis of CIN2-3 was 1.5 (95% confidence interval [CI], 1.2 to 1.9). Of 373 women without CIN2-3 at the first positive visit who had ≥1 later visit, 44 had subsequent diagnoses of CIN2-3. The initial viral loads were associated with CIN2-3 diagnosed within 6 months after the first positive visit (adjusted OR, 1.5 [95% CI, 1.0 to 2.4]) but were unrelated to CIN2-3 diagnosed later. For a random set of 49 women who were tested for viral loads at the first and last positive visits, changes in viral loads were upward and downward among women with and without follow-up CIN2-3 diagnoses, respectively, although the difference was not statistically significant. Results suggest that HPV31 DNA load levels at the first positive visit signal a short-term but not long-term risk of CIN2-3. Copyright © 2015, American Society for Microbiology. All Rights Reserved. JF - Journal of clinical microbiology AU - Liu, Xia AU - Schiffman, Mark AU - Hulbert, Ayaka AU - He, Zhonghu AU - Shen, Zhenping AU - Koutsky, Laura A AU - Xi, Long Fu AD - Department of Pathology, School of Medicine, University of Washington, Seattle, Washington, USA Department of Obstetrics and Gynecology, Shengjing Hospital, China Medical University, Liaoning, People's Republic of China. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA. ; Department of Pathology, School of Medicine, University of Washington, Seattle, Washington, USA. ; Key Laboratory of Carcinogenesis and Translational Research, Peking University School of Oncology, Beijing, People's Republic of China. ; Department of Epidemiology, School of Public Health, University of Washington, Seattle, Washington, USA. ; Department of Pathology, School of Medicine, University of Washington, Seattle, Washington, USA Department of Epidemiology, School of Public Health, University of Washington, Seattle, Washington, USA longfu@u.washington.edu. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 3451 EP - 3457 VL - 53 IS - 11 KW - Biomarkers, Tumor KW - 0 KW - DNA, Viral KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Biomarkers, Tumor -- genetics KW - Papillomavirus Infections -- diagnosis KW - Humans KW - Papillomavirus Infections -- virology KW - Neoplasm Grading KW - Female KW - Colposcopy KW - Viral Load -- genetics KW - Atypical Squamous Cells of the Cervix -- virology KW - Uterine Cervical Neoplasms -- diagnosis KW - Cervical Intraepithelial Neoplasia -- virology KW - Atypical Squamous Cells of the Cervix -- cytology KW - Cervical Intraepithelial Neoplasia -- diagnosis KW - DNA, Viral -- genetics KW - Uterine Cervical Neoplasms -- virology KW - Human papillomavirus 31 -- genetics KW - Cervical Intraepithelial Neoplasia -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722930742?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+microbiology&rft.atitle=Association+of+Human+Papillomavirus+31+DNA+Load+with+Risk+of+Cervical+Intraepithelial+Neoplasia+Grades+2+and+3.&rft.au=Liu%2C+Xia%3BSchiffman%2C+Mark%3BHulbert%2C+Ayaka%3BHe%2C+Zhonghu%3BShen%2C+Zhenping%3BKoutsky%2C+Laura+A%3BXi%2C+Long+Fu&rft.aulast=Liu&rft.aufirst=Xia&rft.date=2015-11-01&rft.volume=53&rft.issue=11&rft.spage=3451&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+microbiology&rft.issn=1098-660X&rft_id=info:doi/10.1128%2FJCM.01279-15 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-22 N1 - Date created - 2015-10-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: N Engl J Med. 1998 Feb 12;338(7):423-8 [9459645] Int J Cancer. 2014 Apr 15;134(8):1889-98 [24136492] Br J Cancer. 2005 Mar 14;92(5):891-4 [15756259] Br J Cancer. 2005 Jun 20;92(12):2195-200 [15942630] Int J Cancer. 2006 Sep 1;119(5):1102-7 [16570279] Br J Dermatol. 2007 Mar;156(3):596-8 [17300265] Int J Cancer. 2007 Aug 1;121(3):621-32 [17405118] Int J Cancer. 2007 Dec 15;121(12):2787-93 [17722112] J Natl Cancer Inst. 2008 Apr 2;100(7):513-7 [18364507] J Infect Dis. 2008 Aug 1;198(3):324-31 [18627250] Int J Cancer. 2009 Jan 15;124(2):381-6 [19003961] J Infect Dis. 2009 Dec 1;200(11):1789-97 [19848609] BMC Cancer. 2014;14:384 [24885011] BMC Cancer. 2015;15:100 [25885207] Cancer Med. 2015 Aug;4(8):1294-302 [25991420] Int J Cancer. 2002 Apr 1;98(4):590-5 [11920620] J Clin Microbiol. 2000 Jan;38(1):357-61 [10618116] Acta Cytol. 2000 Sep-Oct;44(5):726-42 [11015972] J Clin Pathol. 2002 Apr;55(4):244-65 [11919208] Cancer Epidemiol Biomarkers Prev. 2003 Oct;12(10):1038-44 [14578140] Virology. 2004 Jun 20;324(1):17-27 [15183049] Int J Cancer. 2004 Dec 10;112(5):854-9 [15386375] J Clin Microbiol. 1999 Apr;37(4):1030-4 [10074522] Int J Cancer. 2011 Feb 15;128(4):927-35 [20473886] J Infect Dis. 2011 May 15;203(10):1425-33 [21415020] Int J Cancer. 2012 Nov 15;131(10):2349-59 [22323075] Int J Cancer. 2012 Nov 15;131(10):2300-7 [22396129] Int J Cancer. 2013 Feb 1;132(3):549-55 [22729840] J Cell Mol Med. 2012 Dec;16(12):3096-104 [22978795] Cancer Epidemiol Biomarkers Prev. 2013 Jan;22(1):150-8 [23155137] J Gen Virol. 2013 Aug;94(Pt 8):1850-7 [23677791] Comput Programs Biomed. 1978 Jun;8(2):121-34 [668307] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/JCM.01279-15 ER - TY - JOUR T1 - Primary Treatment Options for High-Risk/Medically Inoperable Early Stage NSCLC Patients. AN - 1722924701; 26027433 AB - Lung cancer is among the most common cancers worldwide and is the leading cause of cancer death in both men and women. For patients with early stage (American Joint Committee on Cancer T1-2, N0) non-small-cell lung cancer, the current standard of care is lobectomy with systematic lymph node evaluation. Unfortunately, patients with lung cancer often have medical comorbities, which may preclude the option of surgical resection. In such cases, a number of minimally invasive to noninvasive treatment options have gained popularity in the treatment of these high-risk patients. These modalities provide significant advantages, including patient convenience, treatment in an outpatient setting, and acceptable toxicities, including reduced impact on lung function and a modest risk of postprocedure chest wall pain. We provide a comprehensive review of the literature, including reported outcomes, complications, and limitations of sublobar resection with or without intraoperative brachytherapy, radiofrequency ablation, microwave ablation, percutaneous cryoablation, photodynamic therapy, and stereotactic body radiotherapy. Published by Elsevier Inc. JF - Clinical lung cancer AU - Jones, Guy C AU - Kehrer, Jason D AU - Kahn, Jenna AU - Koneru, Bobby N AU - Narayan, Ram AU - Thomas, Tarita O AU - Camphausen, Kevin AU - Mehta, Minesh P AU - Kaushal, Aradhana AD - National Cancer Institute, Bethesda, MD. Electronic address: guy.jones@nih.gov. ; National Cancer Institute, Bethesda, MD. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 413 EP - 430 VL - 16 IS - 6 KW - Index Medicus KW - Stereotactic body radiotherapy KW - Photodynamic therapy KW - Percutaneous cryotherapy KW - Radiofrequency ablation KW - SBRT KW - Microwave ablation KW - Intraoperative brachytherapy KW - Risk KW - Humans KW - Treatment Outcome KW - Cryosurgery KW - Pneumonectomy -- contraindications KW - Radiosurgery KW - Ambulatory Care KW - Lung Neoplasms -- radiotherapy KW - Brachytherapy KW - Carcinoma, Non-Small-Cell Lung -- surgery KW - Photochemotherapy KW - Lung Neoplasms -- surgery KW - Catheter Ablation KW - Carcinoma, Non-Small-Cell Lung -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722924701?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+lung+cancer&rft.atitle=Primary+Treatment+Options+for+High-Risk%2FMedically+Inoperable+Early+Stage+NSCLC+Patients.&rft.au=Jones%2C+Guy+C%3BKehrer%2C+Jason+D%3BKahn%2C+Jenna%3BKoneru%2C+Bobby+N%3BNarayan%2C+Ram%3BThomas%2C+Tarita+O%3BCamphausen%2C+Kevin%3BMehta%2C+Minesh+P%3BKaushal%2C+Aradhana&rft.aulast=Jones&rft.aufirst=Guy&rft.date=2015-11-01&rft.volume=16&rft.issue=6&rft.spage=413&rft.isbn=&rft.btitle=&rft.title=Clinical+lung+cancer&rft.issn=1938-0690&rft_id=info:doi/10.1016%2Fj.cllc.2015.04.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-15 N1 - Date created - 2015-10-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Ann Thorac Surg. 2006 Feb;81(2):434-8; 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AN - 1722420033; 25935674 AB - In clinical practice, one objective is to obtain diagnostic information while minimizing the invasiveness of the tests and the pain for the patients. To this end, tests based on the interaction of light with readily available biofluids including blood, urine, or saliva are highly desirable. In this review we examine the state of the art regarding the use of surface-enhanced Raman spectroscopy (SERS) to investigate biofluids, focusing on diagnostic applications. First, a critical evaluation of the experimental aspects involved in the collection of SERS spectra is presented; different substrate types are introduced, with a clear distinction between colloidal and non-colloidal metal nanostructures. Then the effect of the excitation wavelength is discussed, along with anomalous bands and artifacts which might affect SERS spectra of biofluids. The central part of the review examines the literature available on the SERS spectra of blood, plasma, serum, urine, saliva, tears, and semen. Finally, diagnostic applications are critically discussed in the context of the published evidence; this section clearly reveals that SERS of biofluids is most promising as a rapid, cheap, and non-invasive tool for mass screening for cancer. JF - Analytical and bioanalytical chemistry AU - Bonifacio, Alois AU - Cervo, Silvia AU - Sergo, Valter AD - Raman Spectroscopy Laboratory, Department of Engineering and Architecture, University of Trieste, Via Valerio 6a, 34127, Trieste, TS, Italy. abonifacio@units.it. ; CRO-Biobank, CRO Aviano, National Cancer Institute, Via Franco Gallini 2, 33081, Aviano, PN, Italy. ; Raman Spectroscopy Laboratory, Department of Engineering and Architecture, University of Trieste, Via Valerio 6a, 34127, Trieste, TS, Italy. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 8265 EP - 8277 VL - 407 IS - 27 KW - Silver KW - 3M4G523W1G KW - Gold KW - 7440-57-5 KW - Index Medicus KW - Diagnosis KW - Raman KW - Biofluids KW - SERS KW - Silver -- chemistry KW - Animals KW - Tears -- chemistry KW - Nanostructures -- chemistry KW - Saliva -- chemistry KW - Humans KW - Semen Analysis -- methods KW - Gold -- chemistry KW - Neoplasms -- diagnosis KW - Neoplasms -- urine KW - Neoplasms -- blood KW - Mass Screening -- economics KW - Mass Screening -- methods KW - Spectrum Analysis, Raman -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722420033?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+and+bioanalytical+chemistry&rft.atitle=Label-free+surface-enhanced+Raman+spectroscopy+of+biofluids%3A+fundamental+aspects+and+diagnostic+applications.&rft.au=Bonifacio%2C+Alois%3BCervo%2C+Silvia%3BSergo%2C+Valter&rft.aulast=Bonifacio&rft.aufirst=Alois&rft.date=2015-11-01&rft.volume=407&rft.issue=27&rft.spage=8265&rft.isbn=&rft.btitle=&rft.title=Analytical+and+bioanalytical+chemistry&rft.issn=1618-2650&rft_id=info:doi/10.1007%2Fs00216-015-8697-z LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-22 N1 - Date created - 2015-10-14 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00216-015-8697-z ER - TY - JOUR T1 - Paving the road ahead for CD19 CAR T-cell therapy. AN - 1722188226; 26335422 AB - Modern immunotherapies, most notably in the form of anti-CD19 chimeric antigen receptor (CAR) T cells, have produced significant clinical responses in otherwise refractory pre-B-cell acute lymphoblastic leukemia patients. Several groups have simultaneously reported robust response rates in children and adults alike. These early studies indicate an impending shift in paradigm for the treatment of acute lymphoblastic leukemia. Incorporating CD19 CAR T-cell therapy into upfront or salvage regimens has its challenges and opportunities. Most CD19 CAR T-cell products in trial today are excellent at inducing minimal residual disease negative remissions, and most responding patients experience cytokine release syndrome and/or neurotoxicity. The challenges facing the CAR community involve how best to minimize the severity of cytokine release syndrome and neurotoxicity while maximizing antitumor efficacy, determining what role this therapy will play for the prophylaxis and treatment of central nervous system leukemia, and its implications on subsequent hematopoietic stem cell transplant given the emergence of CD19-negative relapses. CD19 CAR T-cell therapy is a powerful new tool in the oncologist's arsenal. How it is incorporated into standard practice and how it will shift survival curves are the exciting questions that are waiting to be answered. JF - Current opinion in hematology AU - Nellan, Anandani AU - Lee, Daniel W AD - Pediatric Oncology Branch, National Cancer Institute, Bethesda, Maryland, USA. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 516 EP - 520 VL - 22 IS - 6 KW - Antigens, CD19 KW - 0 KW - Receptors, Antigen, T-Cell KW - Index Medicus KW - T-Lymphocytes -- transplantation KW - Humans KW - T-Lymphocytes -- immunology KW - Antigens, CD19 -- immunology KW - Precursor B-Cell Lymphoblastic Leukemia-Lymphoma -- therapy KW - Receptors, Antigen, T-Cell -- immunology KW - Precursor B-Cell Lymphoblastic Leukemia-Lymphoma -- immunology KW - Immunotherapy -- trends KW - Precursor B-Cell Lymphoblastic Leukemia-Lymphoma -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722188226?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+hematology&rft.atitle=Paving+the+road+ahead+for+CD19+CAR+T-cell+therapy.&rft.au=Nellan%2C+Anandani%3BLee%2C+Daniel+W&rft.aulast=Nellan&rft.aufirst=Anandani&rft.date=2015-11-01&rft.volume=22&rft.issue=6&rft.spage=516&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+hematology&rft.issn=1531-7048&rft_id=info:doi/10.1097%2FMOH.0000000000000182 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-23 N1 - Date created - 2015-10-13 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Ther. 2010 Apr;18(4):843-51 [20179677] Mol Ther. 2010 Apr;18(4):666-8 [20357779] J Clin Oncol. 2012 May 10;30(14):1663-9 [22412151] Clin Cancer Res. 2012 May 15;18(10):2780-90 [22589486] Blood. 2013 Dec 12;122(25):4129-39 [24055823] Sci Transl Med. 2014 Feb 19;6(224):224ra25 [24553386] Blood. 2014 Jul 10;124(2):188-95 [24876563] N Engl J Med. 2014 Oct 16;371(16):1507-17 [25317870] Lancet. 2015 Feb 7;385(9967):517-28 [25319501] Nat Med. 2015 Jun;21(6):581-90 [25939063] Blood. 2015 Jun 25;125(26):4017-23 [25999455] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/MOH.0000000000000182 ER - TY - JOUR T1 - Triangulating the sexually dimorphic brain through high-resolution neuroimaging of murine sex chromosome aneuploidies AN - 1722183057; PQ0002076154 AB - Murine sex chromosome aneuploidies (SCAs) provide powerful models for charting sex chromosome influences on mammalian brain development. Here, building on prior work in X-monosomic (XO) mice, we use spatially non-biased high-resolution imaging to compare and contrast neuroanatomical alterations in XXY and XO mice relative to their wild-type XX and XY littermates. First, we show that carriage of a supernumerary X chromosome in XXY males (1) does not prevent normative volumetric masculinization of the bed nucleus of the stria terminalis (BNST) and medial amygdala, but (2) causes distributed anatomical alterations relative to XY males, which show a statistically unexpected tendency to be co-localized with and reciprocal to XO-XX differences in anatomy. These overlaps identify the lateral septum, BNST, ventral group thalamic nuclei and periaqueductal gray matter as regions with replicable sensitivity to X chromosome dose across two SCAs. We then harness anatomical variation across all four karyotype groups in our study-XO, XX, XY and XXY-to create an agnostic data-driven segmentation of the mouse brain into five distributed clusters which (1) recover fundamental properties of brain organization with high spatial precision, (2) define two previously uncharacterized systems of relative volume excess in females vs. males ("forebrain cholinergic" and "cerebelo-pontine-thalamo-cortical"), and (3) adopt stereotyped spatial motifs which delineate ordered gradients of sex chromosome and gonadal influences on volumetric brain development. Taken together, these data provide a new framework for the study of sexually dimorphic influences on brain development in health and disrupted brain development in SCA. JF - Brain Structure and Function AU - Raznahan, Armin AU - Lue, YanHe AU - Probst, Frank AU - Greenstein, Deanna AU - Giedd, Jay AU - Wang, Christina AU - Lerch, Jason AU - Swerdloff, Ronald AD - Child Psychiatry Branch, National Institute of Mental Health, National Institutes of Health, Rm 4C108, Building 20, 10 Center Drive, Bethesda, MD, 20815, USA, raznahana@mail.nih.gov Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 3581 EP - 3593 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 220 IS - 6 SN - 1863-2653, 1863-2653 KW - Biotechnology and Bioengineering Abstracts; Genetics Abstracts; CSA Neurosciences Abstracts KW - Stria terminalis KW - Sexual dimorphism KW - Neuroimaging KW - Aneuploidy KW - Data processing KW - X chromosome KW - Brain KW - Functional anatomy KW - Karyotypes KW - Forebrain KW - Structure-function relationships KW - Thalamic nuclei KW - Segmentation KW - bed nucleus KW - Amygdala KW - Septum KW - Periaqueductal gray area KW - Sex chromosomes KW - Supernumerary KW - Brain architecture KW - W 30910:Imaging KW - N3 11003:Developmental neuroscience KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722183057?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+Structure+and+Function&rft.atitle=Triangulating+the+sexually+dimorphic+brain+through+high-resolution+neuroimaging+of+murine+sex+chromosome+aneuploidies&rft.au=Raznahan%2C+Armin%3BLue%2C+YanHe%3BProbst%2C+Frank%3BGreenstein%2C+Deanna%3BGiedd%2C+Jay%3BWang%2C+Christina%3BLerch%2C+Jason%3BSwerdloff%2C+Ronald&rft.aulast=Raznahan&rft.aufirst=Armin&rft.date=2015-11-01&rft.volume=220&rft.issue=6&rft.spage=3581&rft.isbn=&rft.btitle=&rft.title=Brain+Structure+and+Function&rft.issn=18632653&rft_id=info:doi/10.1007%2Fs00429-014-0875-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Number of references - 66 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Stria terminalis; Sexual dimorphism; Neuroimaging; Data processing; Aneuploidy; X chromosome; Brain; Functional anatomy; Karyotypes; Forebrain; Structure-function relationships; Thalamic nuclei; bed nucleus; Segmentation; Amygdala; Septum; Sex chromosomes; Periaqueductal gray area; Supernumerary; Brain architecture DO - http://dx.doi.org/10.1007/s00429-014-0875-9 ER - TY - JOUR T1 - Recovery of dopamine transporters with methamphetamine detoxification is not linked to changes in dopamine release. AN - 1721917825; 26208874 AB - Methamphetamine's widepread abuse and concerns that it might increase Parkinson's disease led us to assess if the reported loss of dopamine transporters (DAT) in methamphetamine abusers (MA) reflected damage to dopamine neurons. Using PET with [(11)C]cocaine to measure DAT, and with [(11)C]raclopride to measure dopamine release (assessed as changes in specific binding of [(11)C]raclopride between placebo and methylphenidate), which was used as a marker of dopamine neuronal function, we show that MA (n=16), tested during early detoxification, had lower DAT (20-30%) but overall normal DA release in striatum (except for a small decrease in left putamen), when compared to controls (n=15). In controls, DAT were positively correlated with DA release (higher DAT associated with larger DA increases), consistent with DAT serving as markers of DA terminals. In contrast, MA showed a trend for a negative correlation (p=0.07) (higher DAT associated with lower DA increases), consistent with reduced DA re-uptake following DAT downregulation. MA who remained abstinent nine-months later (n=9) showed significant increases in DAT (20%) but methylphenidate-induced dopamine increases did not change. In contrast, in controls, DAT did not change when retested 9 months later but methylphenidate-induced dopamine increases in ventral striatum were reduced (p=0.05). Baseline D2/D3 receptors in caudate were lower in MA than in controls and did not change with detoxification, nor did they change in the controls upon retest. The loss of DAT in the MA, which was not associated with a concomitant reduction in dopamine release as would have been expected if DAT loss reflected DA terminal degneration; as well as the recovery of DAT after protracted detoxification, which was not associated with increased dopamine release as would have been expected if DAT increases reflected terminal regeneration, indicate that the loss of DAT in these MA does not reflect degeneration of dopamine terminals. Published by Elsevier Inc. JF - NeuroImage AU - Volkow, Nora D AU - Wang, Gene-Jack AU - Smith, Lisa AU - Fowler, Joanna S AU - Telang, Frank AU - Logan, Jean AU - Tomasi, Dardo AD - Laboratory of Neuroimaging, Intramural Program, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD, USA; Office of Director, National Institute on Drug Abuse, Bethesda, MD, USA. Electronic address: nvolkow@nida.nih.gov. ; Laboratory of Neuroimaging, Intramural Program, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD, USA. ; Department of Psychiatry, University of California, Los Angeles, CA, USA. ; Medical Department, Brookhaven National Laboratory, Upton, NY, USA. Y1 - 2015/11/01/ PY - 2015 DA - 2015 Nov 01 SP - 20 EP - 28 VL - 121 KW - DRD2 protein, human KW - 0 KW - DRD3 protein, human KW - Dopamine Antagonists KW - Dopamine Plasma Membrane Transport Proteins KW - Dopamine Uptake Inhibitors KW - Receptors, Dopamine D2 KW - Receptors, Dopamine D3 KW - Methamphetamine KW - 44RAL3456C KW - Index Medicus KW - Parkinson's disease KW - Neurotoxicity KW - Dopamine terminal KW - Addiction KW - Positron-Emission Tomography KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Female KW - Amphetamine-Related Disorders -- metabolism KW - Caudate Nucleus -- diagnostic imaging KW - Caudate Nucleus -- metabolism KW - Methamphetamine -- adverse effects KW - Amphetamine-Related Disorders -- diagnostic imaging KW - Dopaminergic Neurons -- metabolism KW - Dopaminergic Neurons -- pathology KW - Putamen -- diagnostic imaging KW - Receptors, Dopamine D2 -- metabolism KW - Receptors, Dopamine D3 -- metabolism KW - Putamen -- metabolism KW - Dopamine Plasma Membrane Transport Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1721917825?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NeuroImage&rft.atitle=Recovery+of+dopamine+transporters+with+methamphetamine+detoxification+is+not+linked+to+changes+in+dopamine+release.&rft.au=Volkow%2C+Nora+D%3BWang%2C+Gene-Jack%3BSmith%2C+Lisa%3BFowler%2C+Joanna+S%3BTelang%2C+Frank%3BLogan%2C+Jean%3BTomasi%2C+Dardo&rft.aulast=Volkow&rft.aufirst=Nora&rft.date=2015-11-01&rft.volume=121&rft.issue=&rft.spage=20&rft.isbn=&rft.btitle=&rft.title=NeuroImage&rft.issn=1095-9572&rft_id=info:doi/10.1016%2Fj.neuroimage.2015.07.035 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-20 N1 - Date created - 2015-10-12 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.neuroimage.2015.07.035 ER - TY - JOUR T1 - Beyond the Crystal Structure: Insight into the Function and Vaccine Potential of TbpA Expressed by Neisseria gonorrhoeae. AN - 1721347539; 26351283 AB - Neisseria gonorrhoeae, the causative agent of the sexually transmitted infection gonorrhea, is not preventable by vaccination and is rapidly developing resistance to antibiotics. However, the transferrin (Tf) receptor system, composed of TbpA and TbpB, is an ideal target for novel therapeutics and vaccine development. Using a three-dimensional structure of gonococcal TbpA, we investigated two hypotheses, i.e., that loop-derived antibodies can interrupt ligand-receptor interactions in the native bacterium and that the loop 3 helix is a critical functional domain. Preliminary loop-derived antibodies, as well as optimized second-generation antibodies, demonstrated similar modest ligand-blocking effects on the gonococcal surface but different effects in Escherichia coli. Mutagenesis of loop 3 helix residues was employed, generating 11 mutants. We separately analyzed the mutants' abilities to (i) bind Tf and (ii) internalize Tf-bound iron in the absence of the coreceptor TbpB. Single residue mutations resulted in up to 60% reductions in ligand binding and up to 85% reductions in iron utilization. All strains were capable of growing on Tf as the sole iron source. Interestingly, in the presence of TbpB, only a 30% reduction in Tf-iron utilization was observed, indicating that the coreceptor can compensate for TbpA impairment. Complete deletion of the loop 3 helix of TbpA eliminated the abilities to bind Tf, internalize iron, and grow with Tf as the sole iron source. Our studies demonstrate that while the loop 3 helix is a key functional domain, its function does not exclusively rely on any single residue. Copyright © 2015, American Society for Microbiology. All Rights Reserved. JF - Infection and immunity AU - Cash, Devin R AU - Noinaj, Nicholas AU - Buchanan, Susan K AU - Cornelissen, Cynthia Nau AD - Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, Virginia, USA. ; Laboratory of Molecular Biology, NIDDK, National Institutes of Health, Bethesda, Maryland, USA. ; Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, Virginia, USA cncornel@vcu.edu. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 4438 EP - 4449 VL - 83 IS - 11 KW - Bacterial Proteins KW - 0 KW - Bacterial Vaccines KW - Transferrin KW - Transferrin-Binding Protein A KW - Index Medicus KW - Transferrin -- metabolism KW - Gonorrhea -- genetics KW - Bacterial Vaccines -- metabolism KW - Protein Structure, Secondary KW - Bacterial Vaccines -- chemistry KW - Humans KW - Bacterial Vaccines -- genetics KW - Transferrin -- genetics KW - Gonorrhea -- metabolism KW - Gonorrhea -- microbiology KW - Protein Binding KW - Bacterial Proteins -- genetics KW - Neisseria gonorrhoeae -- metabolism KW - Transferrin-Binding Protein A -- genetics KW - Bacterial Proteins -- chemistry KW - Bacterial Proteins -- metabolism KW - Transferrin-Binding Protein A -- metabolism KW - Neisseria gonorrhoeae -- genetics KW - Neisseria gonorrhoeae -- chemistry KW - Transferrin-Binding Protein A -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1721347539?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+immunity&rft.atitle=Beyond+the+Crystal+Structure%3A+Insight+into+the+Function+and+Vaccine+Potential+of+TbpA+Expressed+by+Neisseria+gonorrhoeae.&rft.au=Cash%2C+Devin+R%3BNoinaj%2C+Nicholas%3BBuchanan%2C+Susan+K%3BCornelissen%2C+Cynthia+Nau&rft.aulast=Cash&rft.aufirst=Devin&rft.date=2015-11-01&rft.volume=83&rft.issue=11&rft.spage=4438&rft.isbn=&rft.btitle=&rft.title=Infection+and+immunity&rft.issn=1098-5522&rft_id=info:doi/10.1128%2FIAI.00762-15 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-30 N1 - Date created - 2015-10-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Immunol. 2011 Mar 15;186(6):3606-14 [21325619] Emerg Infect Dis. 2011 Jan;17(1):148-9 [21192886] MMWR Morb Mortal Wkly Rep. 2011 Jul 8;60(26):873-7 [21734634] Antimicrob Agents Chemother. 2012 Mar;56(3):1273-80 [22155830] Infect Immun. 2000 Dec;68(12):6988-96 [11083823] Infect Immun. 2000 Aug;68(8):4725-35 [10899879] Nature. 2012 Mar 1;483(7387):53-8 [22327295] J Infect Dis. 2001 Dec 15;184(12):1621-3 [11740741] Infect Immun. 2002 Feb;70(2):732-40 [11796606] Infect Immun. 2002 May;70(5):2549-58 [11953395] Prev Med. 2003 Apr;36(4):502-9 [12649059] Biochemistry. 2003 Apr 8;42(13):3701-7 [12667060] Infect Immun. 2004 Jan;72(1):277-83 [14688106] Infect Immun. 2004 Mar;72(3):1775-85 [14977987] Annu Rev Biochem. 1981;50:715-31 [6455965] Infect Immun. 1981 Aug;33(2):555-64 [6792081] Infect Immun. 1982 Mar;35(3):915-20 [6121757] J Bacteriol. 1987 Aug;169(8):3414-21 [3112120] J Bacteriol. 1990 Sep;172(9):5225-35 [2168377] J Bacteriol. 1991 Jun;173(12):3911-3 [1904861] J Bacteriol. 1992 Sep;174(18):5788-97 [1325963] J Gen Microbiol. 1992 Dec;138(12):2475-83 [1487719] J Bacteriol. 1994 Jun;176(11):3162-70 [8195069] J Bacteriol. 1996 Mar;178(5):1437-44 [8631722] Mol Microbiol. 1997 Apr;24(1):169-79 [9140974] Mol Microbiol. 1997 Oct;26(1):25-35 [9383187] Mol Microbiol. 1998 Feb;27(3):611-6 [9489672] J Bacteriol. 1963 Jun;85:1274-9 [14047217] Infect Immun. 2005 Jul;73(7):3945-53 [15972481] Bioinformatics. 2006 Jan 15;22(2):195-201 [16301204] MMWR Morb Mortal Wkly Rep. 2007 Apr 13;56(14):332-6 [17431378] Infect Immun. 2007 Jul;75(7):3220-32 [17438025] Infect Immun. 2007 Aug;75(8):4138-47 [17562775] Infect Immun. 2008 May;76(5):1960-9 [18347046] Future Microbiol. 2008 Jun;3(3):287-98 [18505395] Nat Struct Mol Biol. 2012 Mar;19(3):358-60 [22343719] J Antimicrob Chemother. 2012 Aug;67(8):1858-60 [22566592] Mol Microbiol. 2012 Oct;86(2):246-57 [22957710] Vaccine. 2013 Nov 4;31(46):5451-7 [24035433] N Engl J Med. 2014 Nov 6;371(19):1850-1 [25372111] Infect Immun. 2015 Mar;83(3):1030-8 [25547790] J Infect Dis. 2015 Sep 1;212(5):784-92 [25676468] Antimicrob Agents Chemother. 2011 Jul;55(7):3538-45 [21576437] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/IAI.00762-15 ER - TY - JOUR T1 - Notch signaling in response to excitotoxicity induces neurodegeneration via erroneous cell cycle reentry. AN - 1719420500; 25822340 AB - Neurological disorders such as Alzheimer's disease, stroke and epilepsy are currently marred by the lack of effective treatments to prevent neuronal death. Erroneous cell cycle reentry (CCR) is hypothesized to have a causative role in neurodegeneration. We show that forcing S-phase reentry in cultured hippocampal neurons is sufficient to induce neurodegeneration. We found that kainic-acid treatment in vivo induces erroneous CCR and neuronal death through a Notch-dependent mechanism. Ablating Notch signaling in neurons provides neuroprotection against kainic acid-induced neuronal death. We further show that kainic-acid treatment activates Notch signaling, which increases the bioavailability of CyclinD1 through Akt/GSK3β pathway, leading to aberrant CCR via activation of CyclinD1-Rb-E2F1 axis. In addition, pharmacological blockade of this pathway at critical steps is sufficient to confer resistance to kainic acid-induced neurotoxicity in mice. Taken together, our results demonstrate that excitotoxicity leads to neuronal death in a Notch-dependent manner through erroneous CCR. JF - Cell death and differentiation AU - Marathe, S AU - Liu, S AU - Brai, E AU - Kaczarowski, M AU - Alberi, L AD - Department of Medicine, Institute of Anatomy, University of Fribourg, Fribourg, Switzerland. ; Receptor Biology Section, NINDS/NIH, Bethesda, MD, USA. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 1775 EP - 1784 VL - 22 IS - 11 KW - Receptors, Notch KW - 0 KW - Cyclin D1 KW - 136601-57-5 KW - Glycogen Synthase Kinase 3 beta KW - EC 2.7.11.1 KW - Gsk3b protein, mouse KW - Proto-Oncogene Proteins c-akt KW - Glycogen Synthase Kinase 3 KW - EC 2.7.11.26 KW - Kainic Acid KW - SIV03811UC KW - Index Medicus KW - Proto-Oncogene Proteins c-akt -- metabolism KW - Animals KW - Kainic Acid -- pharmacology KW - Blotting, Western KW - Cyclin D1 -- metabolism KW - Cells, Cultured KW - Signal Transduction -- drug effects KW - Immunoprecipitation KW - Mice KW - Glycogen Synthase Kinase 3 -- metabolism KW - Immunohistochemistry KW - Receptors, Notch -- genetics KW - Neurodegenerative Diseases -- metabolism KW - Receptors, Notch -- metabolism KW - Cell Cycle -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1719420500?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+death+and+differentiation&rft.atitle=Notch+signaling+in+response+to+excitotoxicity+induces+neurodegeneration+via+erroneous+cell+cycle+reentry.&rft.au=Marathe%2C+S%3BLiu%2C+S%3BBrai%2C+E%3BKaczarowski%2C+M%3BAlberi%2C+L&rft.aulast=Marathe&rft.aufirst=S&rft.date=2015-11-01&rft.volume=22&rft.issue=11&rft.spage=1775&rft.isbn=&rft.btitle=&rft.title=Cell+death+and+differentiation&rft.issn=1476-5403&rft_id=info:doi/10.1038%2Fcdd.2015.23 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-09 N1 - Date created - 2015-10-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Neurosci. 2000 May 1;20(9):3104-14 [10777774] Stroke. 2010 Oct;41(10 Suppl):S64-71 [20876509] Neuron. 2011 Feb 10;69(3):437-44 [21315255] Neuron. 2011 Mar 10;69(5):840-55 [21382546] Proc Natl Acad Sci U S A. 2011 Apr 19;108(16):6486-91 [21464312] J Exp Med. 2011 May 9;208(5):937-48 [21482697] Mol Pharmacol. 2011 Jul;80(1):23-31 [21450930] J Neurosci. 2012 Oct 17;32(42):14809-14 [23077065] PLoS One. 2012;7(10):e48180 [23110206] Epilepsia. 2012 Nov;53(11):2026-33 [23145776] Cell Death Dis. 2013;4:e580 [23559014] Stroke. 2013 Jul;44(7):2031-5 [23686980] J Neurosci. 2013 Sep 11;33(37):14645-59 [24027266] Hum Mol Genet. 2001 Apr;10(7):699-703 [11257102] Int Immunol. 2002 Jun;14(6):637-45 [12039915] Curr Opin Cell Biol. 2013 Dec;25(6):711-6 [24055434] Neuroscience. 2014 Aug 22;274:153-61 [24875179] Nat Cell Biol. 2002 Nov;4(11):859-64 [12389032] Am J Pathol. 2003 Mar;162(3):823-35 [12598317] Ann Neurol. 2003 Apr;53(4):454-68 [12666113] J Neurosci. 2003 Apr 1;23(7):2557-63 [12684440] J Biol Chem. 2003 Aug 22;278(34):32227-35 [12794074] J Biol Chem. 2004 Jan 23;279(4):2937-44 [14583609] Brain Res. 1977 May 13;126(3):397-42 [861729] Nature. 1995 Dec 21-28;378(6559):785-9 [8524413] Cell. 1996 Dec 27;87(7):1317-26 [8980237] J Neuropathol Exp Neurol. 1998 Aug;57(8):738-45 [9720489] Genes Dev. 1998 Nov 15;12(22):3499-511 [9832503] Proc Natl Acad Sci U S A. 1999 Mar 2;96(5):2110-5 [10051603] Mol Cancer Ther. 2004 Nov;3(11):1427-38 [15542782] Proc Natl Acad Sci U S A. 2005 Jun 7;102(23):8333-8 [15923260] Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):14080-5 [16166266] Folia Neuropathol. 2005;43(4):322-39 [16416396] BMC Cell Biol. 2006;7:10 [16507111] Nat Med. 2006 Jun;12(6):621-3 [16680150] Nature. 2006 Oct 19;443(7113):796-802 [17051206] Proc Natl Acad Sci U S A. 2007 Feb 27;104(9):3585-90 [17360686] Biochim Biophys Acta. 2007 Apr;1772(4):409-12 [17196375] Biochim Biophys Acta. 2007 Apr;1772(4):484-93 [17241774] Nature. 2007 Sep 20;449(7160):351-5 [17721509] Nat Med. 2007 Oct;13(10):1203-10 [17873882] Cancer Cell. 2007 Nov;12(5):411-3 [17996644] Neurobiol Dis. 2008 Aug;31(2):230-41 [18585919] Neuropathol Appl Neurobiol. 2008 Aug;34(4):457-65 [17995921] Int J Dev Neurosci. 2008 Nov;26(7):665-71 [18768156] Cell. 2009 Apr 17;137(2):216-33 [19379690] J Chem Neuroanat. 2010 Jan;39(1):15-9 [19800401] Cell Stem Cell. 2010 May 7;6(5):445-56 [20452319] Am J Pathol. 2010 Jul;177(1):15-20 [20472889] Cell Mol Life Sci. 2010 Sep;67(18):3187-96 [20454918] Neurobiol Aging. 2000 Nov-Dec;21(6):771-81 [11124421] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/cdd.2015.23 ER - TY - JOUR T1 - Taxonomic distribution of defensive alkaloids in Nearctic oribatid mites (Acari, Oribatida). AN - 1718915121; 26264156 AB - The opisthonotal (oil) glands of oribatid mites are the source of a wide diversity of taxon-specific defensive chemicals, and are likely the location for the more than 90 alkaloids recently identified in oribatids. Although originally recognized in temperate oribatid species, alkaloids have also been detected in related lineages of tropical oribatids. Many of these alkaloids are also present in a worldwide radiation of poison frogs, which are known to sequester these defensive chemicals from dietary arthropods, including oribatid mites. To date, most alkaloid records involve members of the superfamily Oripodoidea (Brachypylina), although few species have been examined and sampling of other taxonomic groups has been highly limited. Herein, we examined adults of more than 60 species of Nearctic oribatid mites, representing 46 genera and 33 families, for the presence of alkaloids. GC-MS analyses of whole body extracts led to the detection of 15 alkaloids, but collectively they occur only in members of the genera Scheloribates (Scheloribatidae) and Protokalumma (Parakalummidae). Most of these alkaloids have also been detected previously in the skin of poison frogs. All examined members of the oripodoid families Haplozetidae and Oribatulidae were alkaloid-free, and no mites outside the Oripodoidea contained alkaloids. Including previous studies, all sampled species of the cosmopolitan oripodoid families Scheloribatidae and Parakalummidae, and the related, mostly tropical families Mochlozetidae and Drymobatidae contain alkaloids. Our findings are consistent with a generalization that alkaloid presence is widespread, but not universal in Oripodoidea. Alkaloid presence in tropical, but not temperate members of some non-oripodoid taxa (in particular Galumnidae) deserves further study. JF - Experimental & applied acarology AU - Saporito, Ralph A AU - Norton, Roy A AU - Garraffo, Martin H AU - Spande, Thomas F AD - Department of Biology, John Carroll University, University Heights, OH, 44118, USA. rsaporito@jcu.edu. ; College of Environmental Science and Forestry, State University of New York, Syracuse, NY, 13210, USA. ; Clinical Mass Spectrometry Core, NIDDK, NIH, DHHS, Bethesda, MD, 20892, USA. ; Laboratory of Medicinal Chemistry, NIDA, NIH, DHHS, Bethesda, MD, 20892, USA. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 317 EP - 333 VL - 67 IS - 3 KW - Alkaloids KW - 0 KW - Index Medicus KW - Opisthonotal (oil) gland KW - Chemical defense KW - Soil mites KW - Scheloribates KW - Poison frogs KW - Protokalumma KW - Dendrobatids KW - United States KW - Spectroscopy, Fourier Transform Infrared KW - Animals KW - Gas Chromatography-Mass Spectrometry KW - Mites -- chemistry KW - Mites -- metabolism KW - Alkaloids -- secretion KW - Alkaloids -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1718915121?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Experimental+%26+applied+acarology&rft.atitle=Taxonomic+distribution+of+defensive+alkaloids+in+Nearctic+oribatid+mites+%28Acari%2C+Oribatida%29.&rft.au=Saporito%2C+Ralph+A%3BNorton%2C+Roy+A%3BGarraffo%2C+Martin+H%3BSpande%2C+Thomas+F&rft.aulast=Saporito&rft.aufirst=Ralph&rft.date=2015-11-01&rft.volume=67&rft.issue=3&rft.spage=317&rft.isbn=&rft.btitle=&rft.title=Experimental+%26+applied+acarology&rft.issn=1572-9702&rft_id=info:doi/10.1007%2Fs10493-015-9962-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-13 N1 - Date created - 2015-10-02 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s10493-015-9962-8 ER - TY - JOUR T1 - Five years' experience treating locally advanced cervical cancer with concurrent chemoradiotherapy: results from a single institution. AN - 1718329090; 25914074 AB - Cervical cancer is the second most common cause of female cancer death. In Morocco it is the second most common cancer, our department recruits more than 500 patients each year and proximally half of the cases are diagnosed at an advanced stage. Between January 2008 and December 2008, all patients with diagnosis of locally advanced cervical cancer referred to our department and treated with concurrent chemoradiotherapy were retrieved. We analyzed outcomes for this particular population; overall survival, local control, and toxicities, we also retrieved prognostic factors influencing outcomes for this population. The overall survival rate for the cohort was 68 % at 2 years, and reached 47 % at 5 years. The overall LC rate was 71 % at 2 years and 58 % at 5 years. The most important prognostic factors for OS and LC were the pretreatment hemoglobin, the tumor size, total duration of treatment, and the use of brachytherapy. For OS, the presence of enlarged lymph nodes was also important. For LC, the number of chemotherapy's courses was important. Of the included patients, 20 % experienced late grade 3 or 4 toxicity. The results of our study have shown that despite all the treatment strategies available, locally advanced cervical cancer is associated with bad outcomes. In this cohort, the most important prognostic factors were the pretreatment hemoglobin level and the tumor size. JF - Archives of gynecology and obstetrics AU - Khalil, J AU - El Kacemi, H AU - Afif, M AU - Kebdani, T AU - Benjaafar, N AD - National Cancer Institute, Mohamed V University, Rabat, Morocco. jihane.khalil@gmail.com. ; National Cancer Institute, Mohamed V University, Rabat, Morocco. elkacemihanan@yahoo.fr. ; National Cancer Institute, Mohamed V University, Rabat, Morocco. afifmed85@gmail.com. ; National Cancer Institute, Mohamed V University, Rabat, Morocco. kebdani2000@yahoo.fr. ; National Cancer Institute, Mohamed V University, Rabat, Morocco. n.benjaafar@um5s.net.ma. Y1 - 2015/11// PY - 2015 DA - November 2015 SP - 1091 EP - 1099 VL - 292 IS - 5 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Concurrent chemoradiotherapy KW - Prognostic factors KW - Locally advanced cervical cancer KW - Disease-Free Survival KW - Neoplasm Staging KW - Combined Modality Therapy KW - Humans KW - Retrospective Studies KW - Aged KW - Survival Rate KW - Morocco -- epidemiology KW - Adult KW - Treatment Outcome KW - Neoplasm Metastasis KW - Middle Aged KW - Female KW - Chemoradiotherapy -- methods KW - Uterine Cervical Neoplasms -- therapy KW - Uterine Cervical Neoplasms -- mortality KW - Brachytherapy -- methods KW - Antineoplastic Agents -- therapeutic use KW - Uterine Cervical Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1718329090?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+gynecology+and+obstetrics&rft.atitle=Five+years%27+experience+treating+locally+advanced+cervical+cancer+with+concurrent+chemoradiotherapy%3A+results+from+a+single+institution.&rft.au=Khalil%2C+J%3BEl+Kacemi%2C+H%3BAfif%2C+M%3BKebdani%2C+T%3BBenjaafar%2C+N&rft.aulast=Khalil&rft.aufirst=J&rft.date=2015-11-01&rft.volume=292&rft.issue=5&rft.spage=1091&rft.isbn=&rft.btitle=&rft.title=Archives+of+gynecology+and+obstetrics&rft.issn=1432-0711&rft_id=info:doi/10.1007%2Fs00404-015-3712-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-25 N1 - Date created - 2015-09-30 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00404-015-3712-3 ER - TY - JOUR T1 - Modification of Occupational Exposures on Bladder Cancer Risk by Common Genetic Polymorphisms. AN - 1713526828; 26374428 AB - Few studies have demonstrated gene/environment interactions in cancer research. Using data on high-risk occupations for 2258 case patients and 2410 control patients from two bladder cancer studies, we observed that three of 16 known or candidate bladder cancer susceptibility variants displayed statistically significant and consistent evidence of additive interactions; specifically, the GSTM1 deletion polymorphism (P interaction ≤ .001), rs11892031 (UGT1A, P interaction = .01), and rs798766 (TMEM129-TACC3-FGFR3, P interaction = .03). There was limited evidence for multiplicative interactions. When we examined detailed data on a prevalent occupational exposure associated with increased bladder cancer risk, straight metalworking fluids, we also observed statistically significant additive interaction for rs798766 (TMEM129-TACC3-FGFR3, P interaction = .02), with the interaction more apparent in patients with tumors positive for FGFR3 expression. All statistical tests were two-sided. The interaction we observed for rs798766 (TMEM129-TACC3-FGFR3) with specific exposure to straight metalworking fluids illustrates the value of integrating germline genetic variation, environmental exposures, and tumor marker data to provide insight into the mechanisms of bladder carcinogenesis. Published by Oxford University Press 2015. This work is written by (a) US Government employee(s) and is in the public domain in the US. JF - Journal of the National Cancer Institute AU - Figueroa, Jonine D AU - Koutros, Stella AU - Colt, Joanne S AU - Kogevinas, Manolis AU - Garcia-Closas, Montserrat AU - Real, Francisco X AU - Friesen, Melissa C AU - Baris, Dalsu AU - Stewart, Patricia AU - Schwenn, Molly AU - Johnson, Alison AU - Karagas, Margaret R AU - Armenti, Karla R AU - Moore, Lee E AU - Schned, Alan AU - Lenz, Petra AU - Prokunina-Olsson, Ludmila AU - Banday, A Rouf AU - Paquin, Ashley AU - Ylaya, Kris AU - Chung, Joon-Yong AU - Hewitt, Stephen M AU - Nickerson, Michael L AU - Tardón, Adonina AU - Serra, Consol AU - Carrato, Alfredo AU - García-Closas, Reina AU - Lloreta, Josep AU - Malats, Núria AU - Fraumeni, Joseph F AU - Chanock, Stephen J AU - Chatterjee, Nilanjan AU - Rothman, Nathaniel AU - Silverman, Debra T AD - Division of Cancer Epidemiology and Genetics (JDF, SK, JSC, MGC, MCF, DB, PS, LEM, LPO, ARB, AP, JFFJr, SJC, NC, NR, DTS), Experimental Pathology Laboratory, Laboratory of Pathology, Center for Cancer Research (KY, JYC, SMH), and Cancer and Inflammation Program (MLN), National Cancer Institute, Bethesda, MD; Usher Institute of Population Health Sciences and Informatics, The University of Edinburgh Medical School, Edinburgh UK (JDF); CIBERESP, CIBER Epidemiologia y Salud Publica, Madrid, Spain (MK, AT, JL); Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain (MK); Municipal Institute of Medical Research (IMIM-Hospital del Mar), Barcelona, Spain (MK); Division of Genetics and Epidemiology, Institute of Cancer Research, London, UK (MGC); Spanish National Cancer Research Centre (CNIO), Madrid, Spain (FXR, NM); Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra, Barcelona, Spain (FXR, CS); Maine Cancer Registry, Augusta, ME (MS); Vermont Cancer Registry, Burlington, VT (AJ); Geisel School of Medicine at Dartmouth, Hanover, NH (MRK, AS); New Hampshire Department of Health and Human Services, Concord, NH (KRA); Clinical Research Directorate/Clinical Monitoring Research Program, Leidos Biomedical Research, Inc. (formerly SAIC-Frederick, Inc.), Frederick National Laboratory for Cancer Research, Frederick, MD (PL); Molecular Epidemiology Group, Instituto Universitario de Oncologia, Universidad de Oviedo, Oviedo, Asturias, Spain (AT); Hospital Ramón y Cajal, Elche, Madrid, Spain (AC); Unidad de Investigación, Hospital Universitario de Canarias, La Laguna, Spain (RGC). Y1 - 2015/11// PY - 2015 DA - November 2015 VL - 107 IS - 11 KW - Microtubule-Associated Proteins KW - 0 KW - TACC3 protein, human KW - TMEM129 protein, human KW - EC 2.3.2.27 KW - Ubiquitin-Protein Ligases KW - UGT1A1 enzyme KW - EC 2.4.1.- KW - Glucuronosyltransferase KW - EC 2.4.1.17 KW - Glutathione Transferase KW - EC 2.5.1.18 KW - glutathione S-transferase M1 KW - FGFR3 protein, human KW - EC 2.7.10.1 KW - Receptor, Fibroblast Growth Factor, Type 3 KW - Index Medicus KW - Glucuronosyltransferase -- genetics KW - Receptor, Fibroblast Growth Factor, Type 3 -- genetics KW - Humans KW - Aged KW - Glutathione Transferase -- genetics KW - Scotland -- epidemiology KW - Gene Deletion KW - Microtubule-Associated Proteins -- genetics KW - Risk Factors KW - Ubiquitin-Protein Ligases -- genetics KW - Adult KW - Surveys and Questionnaires KW - Middle Aged KW - Genetic Predisposition to Disease KW - Germ-Line Mutation KW - Female KW - Male KW - Metallurgy KW - Polymorphism, Single Nucleotide KW - Occupational Diseases -- genetics KW - Urinary Bladder Neoplasms -- etiology KW - Urinary Bladder Neoplasms -- epidemiology KW - Urinary Bladder Neoplasms -- genetics KW - Occupational Diseases -- etiology KW - Occupational Exposure -- adverse effects KW - Occupational Diseases -- epidemiology KW - Gene-Environment Interaction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1713526828?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Modification+of+Occupational+Exposures+on+Bladder+Cancer+Risk+by+Common+Genetic+Polymorphisms.&rft.au=Figueroa%2C+Jonine+D%3BKoutros%2C+Stella%3BColt%2C+Joanne+S%3BKogevinas%2C+Manolis%3BGarcia-Closas%2C+Montserrat%3BReal%2C+Francisco+X%3BFriesen%2C+Melissa+C%3BBaris%2C+Dalsu%3BStewart%2C+Patricia%3BSchwenn%2C+Molly%3BJohnson%2C+Alison%3BKaragas%2C+Margaret+R%3BArmenti%2C+Karla+R%3BMoore%2C+Lee+E%3BSchned%2C+Alan%3BLenz%2C+Petra%3BProkunina-Olsson%2C+Ludmila%3BBanday%2C+A+Rouf%3BPaquin%2C+Ashley%3BYlaya%2C+Kris%3BChung%2C+Joon-Yong%3BHewitt%2C+Stephen+M%3BNickerson%2C+Michael+L%3BTard%C3%B3n%2C+Adonina%3BSerra%2C+Consol%3BCarrato%2C+Alfredo%3BGarc%C3%ADa-Closas%2C+Reina%3BLloreta%2C+Josep%3BMalats%2C+N%C3%BAria%3BFraumeni%2C+Joseph+F%3BChanock%2C+Stephen+J%3BChatterjee%2C+Nilanjan%3BRothman%2C+Nathaniel%3BSilverman%2C+Debra+T&rft.aulast=Figueroa&rft.aufirst=Jonine&rft.date=2015-11-01&rft.volume=107&rft.issue=11&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdjv223 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-06 N1 - Date created - 2015-09-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Genet. 2010 Nov;42(11):978-84 [20972438] Occup Environ Med. 2011 Apr;68(4):239-49 [20864470] Pharmacogenet Genomics. 2011 Apr;21(4):231-6 [20739907] J Natl Cancer Inst. 2011 Jul 6;103(13):1037-48 [21705679] Hum Mol Genet. 2011 Nov 1;20(21):4268-81 [21750109] Hum Mol Genet. 2011 Nov 1;20(21):4282-9 [21824976] Hum Mol Genet. 2012 Apr 15;21(8):1918-30 [22228101] Am J Epidemiol. 2012 Dec 1;176(11):1060-7 [23118105] Cancer Res. 2013 Apr 1;73(7):2211-20 [23536561] Hum Mol Genet. 2014 Mar 1;23(5):1387-98 [24163127] Occup Environ Med. 2014 Oct;71(10):667-74 [25201311] Am J Epidemiol. 2002 Jul 15;156(2):95-109 [12117698] Lancet. 2005 Aug 20-26;366(9486):649-59 [16112301] Occup Environ Med. 2008 May;65(5):347-53 [17951336] Nat Genet. 2008 Nov;40(11):1307-12 [18794855] Nat Genet. 2009 Feb;41(2):221-7 [19151717] Nat Genet. 2009 Sep;41(9):991-5 [19648920] J Natl Cancer Inst. 2009 Nov 18;101(22):1553-61 [19917915] Nat Genet. 2010 May;42(5):415-9 [20348956] Pharmacogenet Genomics. 2009 Nov;19(11):903-6 [19801959] Comment In: J Natl Cancer Inst. 2016 Mar;108(3). pii: djv441. doi: 10.1093/jnci/djv441 [26857138] J Natl Cancer Inst. 2016 Mar;108(3). pii: djv440. doi: 10.1093/jnci/djv440 [26857137] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/jnci/djv223 ER - TY - JOUR T1 - A retrospective cohort study of cause-specific mortality and incidence of hematopoietic malignancies in Chinese benzene-exposed workers AN - 1709165654; PQ0001901473 AB - Benzene exposure has been causally linked with acute myeloid leukemia (AML), but inconsistently associated with other hematopoietic, lymphoproliferative and related disorders (HLD) or solid tumors in humans. Many neoplasms have been described in experimental animals exposed to benzene. We used Poisson regression to estimate adjusted relative risks (RR) and the likelihood ratio statistic to derive confidence intervals for cause-specific mortality and HLD incidence in 73,789 benzene-exposed compared with 34,504 unexposed workers in a retrospective cohort study in 12 cities in China. Follow-up and outcome assessment was based on factory, medical and other records. Benzene-exposed workers experienced increased risks for all-cause mortality (RR=1.1, 95% CI=1.1, 1.2) due to excesses of all neoplasms (RR=1.3, 95% CI=1.2, 1.4), respiratory diseases (RR=1.7, 95% CI=1.2, 2.3) and diseases of blood forming organs (RR=[infin], 95% CI=3.4, [infin]). Lung cancer mortality was significantly elevated (RR=1.5, 95% CI=1.2, 1.9) with similar RRs for males and females, based on three-fold more cases than in our previous follow-up. Significantly elevated incidence of all myeloid disorders reflected excesses of myelodysplastic syndrome/acute myeloid leukemia (RR=2.7, 95% CI=1.2, 6.6) and chronic myeloid leukemia (RR=2.5, 95% CI=0.8, 11), and increases of all lymphoid disorders included excesses of non-Hodgkin lymphoma (RR=3.9, 95%CI=1.5, 13) and all lymphoid leukemia (RR=5.4, 95%CI=1.0, 99). The 28-year follow-up of Chinese benzene-exposed workers demonstrated increased risks of a broad range of myeloid and lymphoid neoplasms, lung cancer, and respiratory diseases and suggested possible associations with other malignant and non-malignant disorders. What's new? More than two million workers worldwide are exposed to benzene each year. In this long-term study of Chinese workers, the authors found that chronic benzene exposure was associated with a substantial increase in the risk of myeloid and lymphoid neoplasms, lung cancer, and respiratory diseases. The results also suggest possible associations with other malignant and non-malignant disorders. JF - International Journal of Cancer AU - Linet, Martha S AU - Yin, Song-Nian AU - Gilbert, Ethel S AU - Dores, Graca M AU - Hayes, Richard B AU - Vermeulen, Roel AU - Tian, Hao-Yuan AU - Lan, Qing AU - Portengen, Lutzen AU - Ji, Bu-Tian AU - Li, Gui-Lan AU - Rothman, Nathaniel AD - Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Rockville, MD. Y1 - 2015/11// PY - 2015 DA - Nov 2015 SP - 2184 EP - 2197 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 137 IS - 9 SN - 0020-7136, 0020-7136 KW - Risk Abstracts; Toxicology Abstracts; Health & Safety Science Abstracts KW - Risk assessment KW - Chronic myeloid leukemia KW - Acute myeloid leukemia KW - Lymphatic leukemia KW - Respiratory diseases KW - Lymphocytes KW - Benzene KW - Cities KW - Factories KW - Leukemia KW - Workers KW - Malignancy KW - Risk factors KW - Lymphoma KW - Occupational exposure KW - Lung cancer KW - Mortality KW - Solid tumors KW - Tumors KW - Organs KW - Cancer KW - Health risks KW - Blood KW - Myelodysplastic syndrome KW - Hemopoiesis KW - China, People's Rep. KW - R2 23060:Medical and environmental health KW - H 1000:Occupational Safety and Health KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709165654?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=A+retrospective+cohort+study+of+cause-specific+mortality+and+incidence+of+hematopoietic+malignancies+in+Chinese+benzene-exposed+workers&rft.au=Linet%2C+Martha+S%3BYin%2C+Song-Nian%3BGilbert%2C+Ethel+S%3BDores%2C+Graca+M%3BHayes%2C+Richard+B%3BVermeulen%2C+Roel%3BTian%2C+Hao-Yuan%3BLan%2C+Qing%3BPortengen%2C+Lutzen%3BJi%2C+Bu-Tian%3BLi%2C+Gui-Lan%3BRothman%2C+Nathaniel&rft.aulast=Linet&rft.aufirst=Martha&rft.date=2015-11-01&rft.volume=137&rft.issue=9&rft.spage=2184&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.29591 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-09-30 N1 - SubjectsTermNotLitGenreText - Chronic myeloid leukemia; Risk assessment; Mortality; Solid tumors; Acute myeloid leukemia; Lymphatic leukemia; Lymphocytes; Benzene; Myelodysplastic syndrome; Workers; Blood; Malignancy; Hemopoiesis; Lymphoma; Occupational exposure; Lung cancer; Tumors; Respiratory diseases; Organs; Cancer; Health risks; Leukemia; Factories; Cities; Risk factors; China, People's Rep. DO - http://dx.doi.org/10.1002/ijc.29591 ER - TY - JOUR T1 - Design Issues in Randomized Clinical Trials of Maintenance Therapies. AN - 1705735671; 26286730 AB - A potential therapeutic strategy for patients who respond (or have stable disease) on a fixed-duration induction therapy is to receive maintenance therapy, typically given for a prolonged period of time. To enable patients and clinicians to make informed treatment decisions, the designs of phase III randomized clinical trials (RCTs) assessing maintenance strategies need to be such that their results will provide clear assessment of the relevant risks and benefits of these strategies. We review the key aspects of maintenance RCT designs. Important design considerations include choice of first-line and second-line therapies, minimizing between-arm differences in follow-up schedules, and choice of the primary endpoint. In order to change clinical practice, RCTs should be designed to accurately isolate and quantify the clinical benefit of maintenance as compared with the standard approach of fixed-duration induction followed by the second-line treatment at progression. To accomplish this, RCTs need to utilize an overall survival (or quality of life) endpoint or, in settings where this is not feasible, endpoints that incorporate the effects of the subsequent line of therapy (eg, time from randomization to second progression or death). Toxicity and symptom information over both the study treatment (maintenance) and the second-line treatment should also be collected and reported. Published by Oxford University Press 2015. This work is written by (a) US Government employee(s) and is in the public domain in the US. JF - Journal of the National Cancer Institute AU - Freidlin, Boris AU - Little, Richard F AU - Korn, Edward L AD - Biometric Research Branch (BF, ELK) and Clinical Investigations Branch, Cancer Therapy Evaluation Program (RFL), Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, MD. freidlinb@ctep.nci.nih.gov. ; Biometric Research Branch (BF, ELK) and Clinical Investigations Branch, Cancer Therapy Evaluation Program (RFL), Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, MD. Y1 - 2015/11// PY - 2015 DA - November 2015 VL - 107 IS - 11 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Induction Chemotherapy KW - Humans KW - Salvage Therapy KW - Quality of Life KW - Antineoplastic Agents -- administration & dosage KW - Randomized Controlled Trials as Topic -- trends KW - Disease Progression KW - Randomized Controlled Trials as Topic -- standards KW - Maintenance Chemotherapy KW - Research Design KW - Randomized Controlled Trials as Topic -- methods KW - Survival Analysis KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1705735671?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Design+Issues+in+Randomized+Clinical+Trials+of+Maintenance+Therapies.&rft.au=Freidlin%2C+Boris%3BLittle%2C+Richard+F%3BKorn%2C+Edward+L&rft.aulast=Freidlin&rft.aufirst=Boris&rft.date=2015-11-01&rft.volume=107&rft.issue=11&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdjv225 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-06 N1 - Date created - 2015-08-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Oncologist. 2014 Aug;19(8):829-44 [25063227] Lancet Oncol. 2014 Jul;15(8):852-61 [24882434] J Clin Oncol. 2015 Mar 20;33(9):1008-14 [25667291] Stat Med. 2005 Jan 30;24(2):163-82 [15515150] Eur J Cancer. 2011 Sep;47 Suppl 3:S76-84 [21944033] J Clin Oncol. 2011 Nov 1;29(31):4199-204 [21969501] Nat Rev Clin Oncol. 2012 Jan;9(1):41-7 [22009075] N Engl J Med. 2011 Dec 29;365(26):2473-83 [22204724] J Clin Oncol. 2012 Feb 20;30(6):667-71 [22271475] J Clin Oncol. 2012 Apr 1;30(10):1030-3 [22370321] Lung Cancer. 2012 Jun;76(3):269-79 [22266040] J Clin Oncol. 2013 Mar 10;31(8):1009-20 [23401441] J Clin Oncol. 2013 May 1;31(13):1624-30 [23547078] Clin Cancer Res. 2013 May 15;19(10):2613-20 [23669421] J Clin Oncol. 2013 Nov 1;31(31):3987-96 [24101047] Lancet Oncol. 2015 Mar;16(3):241-3 [25752545] J Clin Oncol. 2014 Oct 1;32(28):3096-102 [25154829] Lancet. 2015 May 9;385(9980):1843-52 [25862517] Nat Rev Clin Oncol. 2015 Jun;12(6):358-70 [25754949] J Clin Oncol. 2015 Aug 10;33(23):2563-77 [26101248] Stat Med. 2005 May 30;24(10):1455-81 [15586395] J Clin Oncol. 2006 Jul 1;24(19):3121-7 [16754935] J Natl Cancer Inst. 2007 Mar 21;99(6):428-32 [17374832] J Clin Oncol. 2007 May 20;25(15):2122-6 [17513819] J Clin Oncol. 2007 Aug 20;25(24):3572-5 [17704403] J Natl Cancer Inst. 2007 Nov 7;99(21):1613-22 [17971530] J Clin Oncol. 2008 Apr 20;26(12):1922-3 [18421044] J Clin Oncol. 2009 Feb 1;27(4):591-8 [19075278] J Clin Oncol. 2009 Jun 10;27(17):2874-80 [19414672] J Clin Oncol. 2010 Jan 1;28(1):49-55 [19917841] J Clin Oncol. 2010 Apr 10;28(11):1835-42 [20212250] Lancet Oncol. 2010 Jun;11(6):521-9 [20493771] Lancet Oncol. 2010 Oct;11(10):934-41 [20739218] J Clin Oncol. 2010 Dec 1;28(34):5116-23 [21041704] Oncologist. 2010;15(12):1344-51 [21148614] Lancet. 2011 Jan 1;377(9759):42-51 [21176949] Lancet. 2011 Jan 1;377(9759):4-6 [21176951] Lancet. 2011 Apr 2;377(9772):1151; author reply 1151-2 [21459205] J Clin Oncol. 2011 Jun 10;29(17):2439-42 [21555691] Blood. 2011 Sep 22;118(12):3205-11 [21791430] J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437] Biometrics. 2002 Mar;58(1):48-57 [11890326] J Clin Oncol. 2003 Jul 1;21(13):2451-3 [12829660] J Clin Oncol. 2003 Jul 1;21(13):2460-5 [12829663] J Clin Oncol. 1991 Jan;9(1):116-22 [1985160] Cancer. 1997 Dec 15;80(12):2222-9 [9404698] BMJ. 1998 Sep 19;317(7161):771-5 [9740561] J Natl Cancer Inst. 2013 Nov 6;105(21):1594-5 [24108810] Clin Genitourin Cancer. 2014 Feb;12(1):1-12 [24220221] J Clin Oncol. 2014 Oct 1;32(28):3093-5 [25154826] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/jnci/djv225 ER - TY - JOUR T1 - Metabolomic analysis of prostate cancer risk in a prospective cohort: The alpha-tocolpherol, beta-carotene cancer prevention (ATBC) study. AN - 1704352165; 25904191 AB - Despite decades of concerted epidemiological research, relatively little is known about the etiology of prostate cancer. As genome-wide association studies have identified numerous genetic variants, so metabolomic profiling of blood and other tissues represents an agnostic, "broad-spectrum" approach for examining potential metabolic biomarkers of prostate cancer risk. To this end, we conducted a prospective analysis of prostate cancer within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort based on 200 cases (100 aggressive) and 200 controls (age- and blood collection date-matched) with fasting serum collected up to 20 years prior to case diagnoses. Ultrahigh performance liquid chromatography/mass spectroscopy and gas chromatography/mass spectroscopy identified 626 compounds detected in >95% of the men and the odds ratio per 1-standard deviation increase in log-metabolite levels and risk were estimated using conditional logistic regression. We observed strong inverse associations between energy and lipid metabolites and aggressive cancer (p = 0.018 and p = 0.041, respectively, for chemical class over-representation). Inositol-1-phosphate showed the strongest association (OR = 0.56, 95% CI = 0.39-0.81, p = 0.002) and glycerophospholipids and fatty acids were heavily represented; e.g., oleoyl-linoleoyl-glycerophosphoinositol (OR = 0.64, p = 0.004), 1-stearoylglycerophosphoglycerol (OR=0.65, p = 0.025), stearate (OR=0.65, p = 0.010) and docosadienoate (OR = 0.66, p = 0.014). Both alpha-ketoglutarate and citrate were associated with aggressive disease risk (OR = 0.69, 95% CI = 0.51-0.94, p = 0.02; OR = 0.69, 95% CI = 0.50-0.95, p = 0.02), as were elevated thyroxine and trimethylamine oxide (OR = 1.65, 95% CI = 1.08-2.54, p = 0.021; and OR = 1.36, 95% CI = 1.02-1.81, p = 0.039). Serum PSA adjustment did not alter the findings. Our data reveal several metabolomic leads that may have pathophysiological relevance to prostate carcinogenesis and should be examined through additional research. © 2015 The Authors. Published by Wiley Periodicals, Inc. on behalf of UICC. JF - International journal of cancer AU - Mondul, Alison M AU - Moore, Steven C AU - Weinstein, Stephanie J AU - Karoly, Edward D AU - Sampson, Joshua N AU - Albanes, Demetrius AD - Department of Epidemiology, University of Michigan School of Public Health, Ann Arbor, MI. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, MD. ; Metabolon, Morrisville, NC. Y1 - 2015/11/01/ PY - 2015 DA - 2015 Nov 01 SP - 2124 EP - 2132 VL - 137 IS - 9 KW - Biomarkers, Tumor KW - 0 KW - beta Carotene KW - 01YAE03M7J KW - alpha-Tocopherol KW - H4N855PNZ1 KW - Index Medicus KW - TCA cycle KW - TMAO KW - Warburg KW - energy metabolism KW - serology KW - prostate cancer KW - lipid metabolism KW - thyroxine KW - biomarkers KW - metabolomics KW - Prospective Studies KW - Humans KW - Middle Aged KW - Metabolomics KW - Male KW - Adenocarcinoma -- blood KW - Metabolome KW - beta Carotene -- therapeutic use KW - Prostatic Neoplasms -- blood KW - Prostatic Neoplasms -- prevention & control KW - Adenocarcinoma -- prevention & control KW - Biomarkers, Tumor -- blood KW - alpha-Tocopherol -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1704352165?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Metabolomic+analysis+of+prostate+cancer+risk+in+a+prospective+cohort%3A+The+alpha-tocolpherol%2C+beta-carotene+cancer+prevention+%28ATBC%29+study.&rft.au=Mondul%2C+Alison+M%3BMoore%2C+Steven+C%3BWeinstein%2C+Stephanie+J%3BKaroly%2C+Edward+D%3BSampson%2C+Joshua+N%3BAlbanes%2C+Demetrius&rft.aulast=Mondul&rft.aufirst=Alison&rft.date=2015-11-01&rft.volume=137&rft.issue=9&rft.spage=2124&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.29576 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-29 N1 - Date created - 2015-08-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2007 Oct 5;282(40):29584-93 [17635910] Carcinogenesis. 2014 Jul;35(7):1516-22 [24648381] Cell Rep. 2014 Jun 12;7(5):1679-90 [24857658] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517] Chem Biol. 2011 Jul 29;18(7):846-56 [21802006] Science. 1956 Feb 24;123(3191):309-14 [13298683] Biochim Biophys Acta. 2014 Aug;1841(8):1060-84 [24440821] Bioanalysis. 2012 Feb;4(4):431-51 [22394143] Cell. 2010 Jan 8;140(1):49-61 [20079333] Urol Oncol. 2011 Sep-Oct;29(5):572-81 [21930089] Nat Med. 2014 Oct;20(10):1193-8 [25261994] J Cheminform. 2010 Oct 18;2(1):9 [20955607] Nature. 2008 Oct 23;455(7216):1054-6 [18948945] Adv Enzyme Regul. 2010;50(1):324-37 [20006638] Cancer Res. 2014 Dec 15;74(24):7442-52 [25336191] Cancer Epidemiol Biomarkers Prev. 2013 Apr;22(4):631-40 [23396963] Nat Rev Cancer. 2013 Apr;13(4):227-32 [23446547] Ann Epidemiol. 1994 Jan;4(1):1-10 [8205268] Trends Endocrinol Metab. 2005 Aug;16(6):273-9 [16002302] Int J Cancer. 2008 Aug 15;123(4):899-904 [18491405] Eur Radiol. 2015 May;25(5):1247-56 [25749786] Am J Epidemiol. 1998 Oct 15;148(8):775-85 [9786232] FEBS J. 2012 Aug;279(15):2610-23 [22621751] Metabolomics. 2014 Oct 1;10(5):1036-1041 [25254003] Mol Cancer Ther. 2014 Oct;13(10):2361-71 [25122071] Oncology. 2000 Nov;59(4):269-82 [11096338] Nat Rev Mol Cell Biol. 2014 Apr;15(4):243-56 [24651542] Ann Intern Med. 1993 May 15;118(10):793-803 [8470854] Mitochondrion. 2005 Jun;5(3):143-53 [16050980] Anal Chem. 2009 Aug 15;81(16):6656-67 [19624122] NMR Biomed. 2014 Jan;27(1):53-66 [23904127] Nat Genet. 2014 Oct;46(10):1103-9 [25217961] Nat Med. 2013 May;19(5):576-85 [23563705] World J Urol. 2012 Apr;30(2):195-200 [22476558] Eur J Radiol. 2010 Feb;73(2):345-51 [19070978] J Natl Cancer Inst. 2014 Sep;106(9). pii: dju240. doi: 10.1093/jnci/dju240 [25210201] Biochim Biophys Acta. 2010 Mar;1801(3):381-91 [19782152] Expert Opin Drug Saf. 2010 Jul;9(4):603-21 [20377474] Int J Mol Sci. 2015;16(1):924-49 [25561239] PLoS One. 2012;7(10):e47730 [23118893] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ijc.29576 ER - TY - JOUR T1 - A dual-specific anti-IGF-1/IGF-2 human monoclonal antibody alone and in combination with temsirolimus for therapy of neuroblastoma. AN - 1704347991; 25924852 AB - The insulin-like growth factors (IGFs), IGF-1 and IGF-2, have been implicated in the growth, survival and metastasis of a broad range of malignancies including pediatric tumors. They bind to the IGF receptor type 1 (IGF-1R) and the insulin receptor (IR) which are overexpressed in many types of solid malignancies. Activation of the IR by IGF-2 results in increased survival of tumor cells. We have previously identified a novel human monoclonal antibody, m708.5, which binds with high (pM) affinity to both human IGF-1 and IGF-2, and potently inhibits phosphorylation of the IGF-1R and the IR in tumor cells. m708.5 exhibited strong antitumor activity as a single agent against most cell lines derived from neuroblastoma, Ewing family of tumor, rhabdomyosarcoma and osteosarcoma. When tested in neuroblastoma cell lines, it showed strong synergy with temsirolimus and synergy with chemotherapeutic agents in vitro. In xenograft models, the combination of m708.5 and temsirolimus significantly inhibited neuroblastoma growth and prolonged mouse survival. Taken together, these results support the clinical development of m708.5 for pediatric solid tumors with potential for synergy with chemotherapy and mTOR inhibitors. © 2015 UICC. JF - International journal of cancer AU - Zhao, Qi AU - Tran, Hoa AU - Dimitrov, Dimiter S AU - Cheung, Nai-Kong V AD - Department of Pediatrics, Memorial Sloan-Kettering Cancer Center, New York, NY. ; Protein Interaction Section, Laboratory of Experimental Immunology, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute-Frederick, National Institutes of Health, Frederick, MD, USA. Y1 - 2015/11/01/ PY - 2015 DA - 2015 Nov 01 SP - 2243 EP - 2252 VL - 137 IS - 9 KW - Antibodies, Monoclonal KW - 0 KW - m708.5 monoclonal antibody KW - temsirolimus KW - 624KN6GM2T KW - Insulin-Like Growth Factor I KW - 67763-96-6 KW - Insulin-Like Growth Factor II KW - 67763-97-7 KW - Sirolimus KW - W36ZG6FT64 KW - Index Medicus KW - IGF-2 KW - IGF-1 KW - neuroblastoma KW - chemotherapy KW - Cell Proliferation -- drug effects KW - Sirolimus -- administration & dosage KW - Animals KW - Insulin-Like Growth Factor II -- antagonists & inhibitors KW - Cricetulus KW - Humans KW - Cell Line, Tumor KW - Antibodies, Monoclonal -- chemistry KW - Protein Binding KW - Insulin-Like Growth Factor I -- immunology KW - Antibodies, Monoclonal -- administration & dosage KW - Insulin-Like Growth Factor II -- immunology KW - Insulin-Like Growth Factor I -- antagonists & inhibitors KW - Xenograft Model Antitumor Assays KW - CHO Cells KW - Mice, SCID KW - Drug Synergism KW - Sirolimus -- analogs & derivatives KW - Cricetinae KW - Neuroblastoma -- pathology KW - Neuroblastoma -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- pharmacology KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1704347991?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=A+dual-specific+anti-IGF-1%2FIGF-2+human+monoclonal+antibody+alone+and+in+combination+with+temsirolimus+for+therapy+of+neuroblastoma.&rft.au=Zhao%2C+Qi%3BTran%2C+Hoa%3BDimitrov%2C+Dimiter+S%3BCheung%2C+Nai-Kong+V&rft.aulast=Zhao&rft.aufirst=Qi&rft.date=2015-11-01&rft.volume=137&rft.issue=9&rft.spage=2243&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.29588 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-29 N1 - Date created - 2015-08-15 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ijc.29588 ER - TY - CPAPER T1 - Importance of community engagement: Contributions from Centers for Children's Environmental Healtlh T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731771929; 6365864 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - O'Fallon, Liam AU - Gray, Kimberly Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Community involvement KW - Children UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731771929?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Importance+of+community+engagement%3A+Contributions+from+Centers+for+Children%27s+Environmental+Healtlh&rft.au=O%27Fallon%2C+Liam%3BGray%2C+Kimberly&rft.aulast=O%27Fallon&rft.aufirst=Liam&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - NIAID's Role in the United States Government (USG) Research Response to the 2014-15 Ebola Outbreak T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731771701; 6365485 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - McNay, Laura Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - USA KW - Viruses KW - Outbreaks UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731771701?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=NIAID%27s+Role+in+the+United+States+Government+%28USG%29+Research+Response+to+the+2014-15+Ebola+Outbreak&rft.au=McNay%2C+Laura&rft.aulast=McNay&rft.aufirst=Laura&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Integrating Disaster Mental Health and Resiliency Training into Existing Occupational Health and Safety Programs T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731771069; 6365704 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - Hughes, Joseph AU - Eagin, Betsy Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Mental disorders KW - Training KW - Safety KW - Disasters KW - Health and safety KW - Occupational health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731771069?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Integrating+Disaster+Mental+Health+and+Resiliency+Training+into+Existing+Occupational+Health+and+Safety+Programs&rft.au=Hughes%2C+Joseph%3BEagin%2C+Betsy&rft.aulast=Hughes&rft.aufirst=Joseph&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Gulf Coast Health Alliance: Health risks related to the Macondo Spill - Using a CBPR Approach to Developing Tools & Techniques That Communicate Risk and Increase Environmental Health Literacy in Gulf Coast Communities Affected by the DWH Oil Disaster T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731770986; 6365583 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - Sullivan, John Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Health risks KW - Coastal zone KW - Disasters KW - Environmental health KW - Oil pollution KW - Oil spills UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731770986?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Gulf+Coast+Health+Alliance%3A+Health+risks+related+to+the+Macondo+Spill+-+Using+a+CBPR+Approach+to+Developing+Tools+%26amp%3B+Techniques+That+Communicate+Risk+and+Increase+Environmental+Health+Literacy+in+Gulf+Coast+Communities+Affected+by+the+DWH+Oil+Disaster&rft.au=Sullivan%2C+John&rft.aulast=Sullivan&rft.aufirst=John&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Building Capacity for Ebola and Infectious Disease Training in the US: The NIEHS WTP Ebola Biosafety Worker Training Program T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731769379; 6365029 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - Hughes Jr, Joseph AU - Weinstock, Deborah Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Infectious diseases KW - Training KW - Viruses UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731769379?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Building+Capacity+for+Ebola+and+Infectious+Disease+Training+in+the+US%3A+The+NIEHS+WTP+Ebola+Biosafety+Worker+Training+Program&rft.au=Hughes+Jr%2C+Joseph%3BWeinstock%2C+Deborah&rft.aulast=Hughes+Jr&rft.aufirst=Joseph&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Understanding youth and parent perceived neighborhood environments and the association to health behaviors T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731768257; 6366726 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - Patel, Minal Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Behavior KW - Perception UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731768257?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Understanding+youth+and+parent+perceived+neighborhood+environments+and+the+association+to+health+behaviors&rft.au=Patel%2C+Minal&rft.aulast=Patel&rft.aufirst=Minal&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Work Flow and Timeliness in Task Distribution and Response Collection for a Public Health Clinical Research Liaison Office T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731768068; 6366533 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - Weiss, Susanna AU - Li, Yin Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Clinical trials KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731768068?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Work+Flow+and+Timeliness+in+Task+Distribution+and+Response+Collection+for+a+Public+Health+Clinical+Research+Liaison+Office&rft.au=Weiss%2C+Susanna%3BLi%2C+Yin&rft.aulast=Weiss&rft.aufirst=Susanna&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - National Toxicology Program's role in shaping public health policies for a healthier tomorrow T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731767673; 6364845 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - Wolfe, Mary Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Toxicology KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731767673?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=National+Toxicology+Program%27s+role+in+shaping+public+health+policies+for+a+healthier+tomorrow&rft.au=Wolfe%2C+Mary&rft.aulast=Wolfe&rft.aufirst=Mary&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Beyond the camp crier: Tribal data dissemination using video-teleconference technology T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731766997; 6364837 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - Brockie, Teresa AU - Around Him, Deana AU - Ricker, Adriann AU - Wetsit, Lawrence AU - Wallen, Gwenyth Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Data processing KW - Cyclic AMP KW - Technology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731766997?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Beyond+the+camp+crier%3A+Tribal+data+dissemination+using+video-teleconference+technology&rft.au=Brockie%2C+Teresa%3BAround+Him%2C+Deana%3BRicker%2C+Adriann%3BWetsit%2C+Lawrence%3BWallen%2C+Gwenyth&rft.aulast=Brockie&rft.aufirst=Teresa&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Feasibility of mobile technology for monitoring dietary intake in resource-limited communities: Investigating the use of digital food records in the Cardiovascular Health and Needs Assessment in Washington, D.C T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731765483; 6366205 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - Yingling, Leah Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Feasibility studies KW - Diets KW - USA, Washington KW - Food KW - Ingestion KW - Dietary intake KW - Technology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731765483?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Feasibility+of+mobile+technology+for+monitoring+dietary+intake+in+resource-limited+communities%3A+Investigating+the+use+of+digital+food+records+in+the+Cardiovascular+Health+and+Needs+Assessment+in+Washington%2C+D.C&rft.au=Yingling%2C+Leah&rft.aulast=Yingling&rft.aufirst=Leah&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Analyzing the health co-benefits of renewable energy deployment in the United States T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731765454; 6365580 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - Balbus, John AU - Bast, Elizabeth Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Resource management KW - USA KW - Renewable energy KW - Conservation KW - Environment management UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731765454?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Analyzing+the+health+co-benefits+of+renewable+energy+deployment+in+the+United+States&rft.au=Balbus%2C+John%3BBast%2C+Elizabeth&rft.aulast=Balbus&rft.aufirst=John&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Mobile Screenings - Opening Doors to Improving Cardiovascular Health in High-Risk Communities T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731765226; 6365203 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - Powell-Wiley, Tiffany Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Screening KW - Risk groups UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731765226?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Mobile+Screenings+-+Opening+Doors+to+Improving+Cardiovascular+Health+in+High-Risk+Communities&rft.au=Powell-Wiley%2C+Tiffany&rft.aulast=Powell-Wiley&rft.aufirst=Tiffany&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Banning tobacco price promotions, smoking-related beliefs and behavior: Findings from the International Tobacco Control four-country cohort survey T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731764647; 6366974 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - El-Toukhy, Sherine AU - Choi, Kelvin Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Behavior KW - Tobacco UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731764647?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Banning+tobacco+price+promotions%2C+smoking-related+beliefs+and+behavior%3A+Findings+from+the+International+Tobacco+Control+four-country+cohort+survey&rft.au=El-Toukhy%2C+Sherine%3BChoi%2C+Kelvin&rft.aulast=El-Toukhy&rft.aufirst=Sherine&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Developing a population definition and screening tool to identify Adults with Chronic Healthcare Needs (ACHCN): Findings from an expert measurement panel T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731764506; 6364576 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - Gulley, Stephen AU - Rasch, Elizabeth AU - Chan, Leighton Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Screening KW - Health care UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731764506?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Developing+a+population+definition+and+screening+tool+to+identify+Adults+with+Chronic+Healthcare+Needs+%28ACHCN%29%3A+Findings+from+an+expert+measurement+panel&rft.au=Gulley%2C+Stephen%3BRasch%2C+Elizabeth%3BChan%2C+Leighton&rft.aulast=Gulley&rft.aufirst=Stephen&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Shared Decision-Making Process and PSA Testing Among Black Men T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731764177; 6366036 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - Jackson, Devlon AU - Hollander, Roberta AU - Stroman, Carolyn Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Decision making UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731764177?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Shared+Decision-Making+Process+and+PSA+Testing+Among+Black+Men&rft.au=Jackson%2C+Devlon%3BHollander%2C+Roberta%3BStroman%2C+Carolyn&rft.aulast=Jackson&rft.aufirst=Devlon&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Asian American & Pacific Islanders Health Disparities Research with the National Institute on Aging T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731762888; 6364865 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - Hill, Carl Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Aging KW - Pacific UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731762888?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Asian+American+%26amp%3B+Pacific+Islanders+Health+Disparities+Research+with+the+National+Institute+on+Aging&rft.au=Hill%2C+Carl&rft.aulast=Hill&rft.aufirst=Carl&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Geographic disparities in willingness to engage in mobile health information exchange T2 - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AN - 1731762629; 6366921 JF - 143rd American Public Health Association Annual Meeting and Exposition (APHA 2015) AU - Serrano, Katrina AU - Atienza, Audie Y1 - 2015/10/31/ PY - 2015 DA - 2015 Oct 31 KW - Information exchange UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731762629?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.atitle=Geographic+disparities+in+willingness+to+engage+in+mobile+health+information+exchange&rft.au=Serrano%2C+Katrina%3BAtienza%2C+Audie&rft.aulast=Serrano&rft.aufirst=Katrina&rft.date=2015-10-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=143rd+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/143am/webprogram/meeting.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - JOUR T1 - Harnessing Intracellular Biochemical Pathways for In Vitro Synthesis of Designer Tellurium Nanorods. AN - 1725513832; 26313741 AB - Synthesizing nanomaterials of desired properties is a big challenge, which requires extremely harsh conditions and/or use of toxic materials. More recently developed in vivo methods have brought a different set of problems such as separation and purification of nanomaterials made in vivo. Here, a novel approach that harnesses cellular pathways for in vitro synthesis of high-quality tellurium nanorods with tunable lengths and optical properties is reported. It is first demonstrated that in vivo biochemical pathways could be used to synthesize Te nanorods via the intracellular reduction of TeO3(2-) in living Staphylococcus aureus cells. The pathways to set up a quasi-biological system for Te precursor formation are then utilized, which could further synthesize Te nanorods in vitro. This allows to successfully synthesize in vitro, under routine laboratory conditions, Te nanorods with uniform and tunable lengths, ranging from about 10 to 200 nm, and controllable optical properties with high molar extinction coefficients. The approach here should open new avenues for controllable, facile, and efficient synthesis of designer nanomaterials for diverse industrial and biomedical applications. © 2015 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. JF - Small (Weinheim an der Bergstrasse, Germany) AU - Xiong, Ling-Hong AU - Cui, Ran AU - Zhang, Zhi-Ling AU - Tu, Jia-Wei AU - Shi, Yun-Bo AU - Pang, Dai-Wen AD - Key Laboratory of Analytical Chemistry for Biology and Medicine (Ministry of Education), College of Chemistry and Molecular Sciences, State Key Laboratory of Virology, The Institute for Advanced Studies and Wuhan Institute of Biotechnology, Wuhan University, Wuhan, 430072, P. R. China. ; Section on Molecular Morphogenesis, PCRM, NICHD, NIH, Bethesda, MD, 20892-5431, USA. Y1 - 2015/10/28/ PY - 2015 DA - 2015 Oct 28 SP - 5416 EP - 5422 VL - 11 IS - 40 KW - Tellurium KW - NQA0O090ZJ KW - Index Medicus KW - nanorods KW - Staphylococcus aureus KW - in vitro synthesis KW - designer nanomaterials KW - intracellular biochemical pathways KW - Nanotubes -- chemistry KW - Nanostructures -- chemistry KW - Tellurium -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1725513832?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Small+%28Weinheim+an+der+Bergstrasse%2C+Germany%29&rft.atitle=Harnessing+Intracellular+Biochemical+Pathways+for+In+Vitro+Synthesis+of+Designer+Tellurium+Nanorods.&rft.au=Xiong%2C+Ling-Hong%3BCui%2C+Ran%3BZhang%2C+Zhi-Ling%3BTu%2C+Jia-Wei%3BShi%2C+Yun-Bo%3BPang%2C+Dai-Wen&rft.aulast=Xiong&rft.aufirst=Ling-Hong&rft.date=2015-10-28&rft.volume=11&rft.issue=40&rft.spage=5416&rft.isbn=&rft.btitle=&rft.title=Small+%28Weinheim+an+der+Bergstrasse%2C+Germany%29&rft.issn=1613-6829&rft_id=info:doi/10.1002%2Fsmll.201500816 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-29 N1 - Date created - 2015-10-21 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/smll.201500816 ER - TY - JOUR T1 - Asp1 from Schizosaccharomyces pombe binds a [2Fe-2S](2+) cluster which inhibits inositol pyrophosphate 1-phosphatase activity. AN - 1727993113; 26422458 AB - Iron-sulfur (Fe-S) clusters are widely distributed protein cofactors that are vital to cellular biochemistry and the maintenance of bioenergetic homeostasis, but to our knowledge, they have never been identified in any phosphatase. Here, we describe an iron-sulfur cluster in Asp1, a dual-function kinase/phosphatase that regulates cell morphogenesis in Schizosaccharomyces pombe. Full-length Asp1, and its phosphatase domain (Asp1(371-920)), were each heterologously expressed in Escherichia coli. The phosphatase activity is exquisitely specific: it hydrolyzes the 1-diphosphate from just two members of the inositol pyrophosphate (PP-InsP) signaling family, namely, 1-InsP7 and 1,5-InsP8. We demonstrate that Asp1 does not hydrolyze either InsP6, 2-InsP7, 3-InsP7, 4-InsP7, 5-InsP7, 6-InsP7, or 3,5-InsP8. We also recorded 1-phosphatase activity in a human homologue of Asp1, hPPIP5K1, which was heterologously expressed in Drosophila S3 cells with a biotinylated N-terminal tag, and then isolated from cell lysates with avidin beads. Purified, recombinant Asp1(371-920) contained iron and acid-labile sulfide, but the stoichiometry (0.8 atoms of each per protein molecule) indicates incomplete iron-sulfur cluster assembly. We reconstituted the Fe-S cluster in vitro under anaerobic conditions, which increased the stoichiometry to approximately 2 atoms of iron and acid-labile sulfide per Asp1 molecule. The presence of a [2Fe-2S](2+) cluster in Asp1(371-920) was demonstrated by UV-visible absorption, resonance Raman spectroscopy, and electron paramagnetic resonance spectroscopy. We determined that this [2Fe-2S](2+) cluster is unlikely to participate in redox chemistry, since it rapidly degraded upon reduction by dithionite. Biochemical and mutagenic studies demonstrated that the [2Fe-2S](2+) cluster substantially inhibits the phosphatase activity of Asp1, thereby increasing its net kinase activity. JF - Biochemistry AU - Wang, Huanchen AU - Nair, Vasudha S AU - Holland, Ashley A AU - Capolicchio, Samanta AU - Jessen, Henning J AU - Johnson, Michael K AU - Shears, Stephen B AD - Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health , 101 T. W. Alexander Drive, Research Triangle Park, North Carolina 27709, United States. ; Department of Chemistry and Center for Metalloenzyme Studies, University of Georgia , Athens, Georgia 30602, United States. ; Department of Chemistry, University of Zurich (UZH) , Winterthurerstrasse 190, 8057 Zurich, Switzerland. Y1 - 2015/10/27/ PY - 2015 DA - 2015 Oct 27 SP - 6462 EP - 6474 VL - 54 IS - 42 KW - Asp1 protein, S pombe KW - 0 KW - Cytoskeletal Proteins KW - Inositol Phosphates KW - Iron-Sulfur Proteins KW - Recombinant Proteins KW - Schizosaccharomyces pombe Proteins KW - Phosphoric Monoester Hydrolases KW - EC 3.1.3.2 KW - inositol-1,4-bisphosphate 1-phosphatase KW - EC 3.1.3.57 KW - Index Medicus KW - Phosphoric Monoester Hydrolases -- chemistry KW - Inositol Phosphates -- metabolism KW - Models, Molecular KW - Schizosaccharomyces -- metabolism KW - Humans KW - Iron-Sulfur Proteins -- genetics KW - Phosphoric Monoester Hydrolases -- genetics KW - Amino Acid Sequence KW - Spectrum Analysis, Raman KW - Recombinant Proteins -- genetics KW - Phosphoric Monoester Hydrolases -- metabolism KW - Iron-Sulfur Proteins -- metabolism KW - Iron-Sulfur Proteins -- chemistry KW - Mutagenesis, Site-Directed KW - Schizosaccharomyces -- genetics KW - Recombinant Proteins -- metabolism KW - Electron Spin Resonance Spectroscopy KW - Molecular Sequence Data KW - Recombinant Proteins -- chemistry KW - Sequence Homology, Amino Acid KW - Protein Structure, Tertiary KW - Inositol Phosphates -- chemistry KW - Schizosaccharomyces pombe Proteins -- genetics KW - Schizosaccharomyces pombe Proteins -- metabolism KW - Cytoskeletal Proteins -- chemistry KW - Cytoskeletal Proteins -- metabolism KW - Schizosaccharomyces pombe Proteins -- chemistry KW - Cytoskeletal Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727993113?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Asp1+from+Schizosaccharomyces+pombe+binds+a+%5B2Fe-2S%5D%282%2B%29+cluster+which+inhibits+inositol+pyrophosphate+1-phosphatase+activity.&rft.au=Wang%2C+Huanchen%3BNair%2C+Vasudha+S%3BHolland%2C+Ashley+A%3BCapolicchio%2C+Samanta%3BJessen%2C+Henning+J%3BJohnson%2C+Michael+K%3BShears%2C+Stephen+B&rft.aulast=Wang&rft.aufirst=Huanchen&rft.date=2015-10-27&rft.volume=54&rft.issue=42&rft.spage=6462&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=1520-4995&rft_id=info:doi/10.1021%2Facs.biochem.5b00532 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-12 N1 - Date created - 2015-10-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Pharmacol. 2008 Aug;74(2):527-36 [18460607] J Biol Chem. 1992 Aug 5;267(22):15502-10 [1639790] Biochim Biophys Acta. 1992 Dec 7;1140(2):175-83 [1280165] Bioorg Med Chem Lett. 2007 Jan 1;17(1):183-8 [17045478] Science. 2007 Apr 6;316(5821):106-9 [17412958] Science. 2007 Apr 6;316(5821):109-12 [17412959] Proc Natl Acad Sci U S A. 2007 Sep 25;104(39):15305-10 [17873058] J Biol Chem. 2007 Oct 19;282(42):30754-62 [17690096] J Biol Chem. 2007 Oct 19;282(42):30763-75 [17702752] Science. 2007 Nov 23;318(5854):1299-302 [18033884] Nat Chem Biol. 2008 Jan;4(1):25-32 [18059263] Biochem J. 2008 Jan 15;409(2):333-48 [18092946] Inorg Chem. 2008 Jun 16;47(12):5394-416 [18491857] Protein Expr Purif. 2008 Oct;61(2):142-8 [18595733] Biochemistry. 2009 Jun 9;48(22):4946-58 [19385603] Mol Pharmacol. 2009 Aug;76(2):236-52 [19439500] Nature. 2009 Aug 13;460(7257):831-8 [19675643] Biochemistry. 2009 Oct 13;48(40):9569-81 [19715344] Blood. 2010 Jan 28;115(4):860-9 [19965627] Mol Cell Biol. 2010 Sep;30(18):4535-47 [20624911] Cell. 2010 Dec 10;143(6):897-910 [21145457] Biochem J. 2011 Mar 15;434(3):415-26 [21222653] Sci Signal. 2011 Aug 30;4(188):re1 [21878680] Biochemistry. 2011 Nov 8;50(44):9641-50 [21977977] Science. 2011 Nov 11;334(6057):802-5 [22076377] Genetics. 2011 Nov;189(3):695-704 [22084421] Curr Opin Struct Biol. 2012 Feb;22(1):94-100 [22169085] Nucleic Acids Res. 2012 May;40(10):4247-60 [22287629] Biochem J. 2013 Jun 15;452(3):369-79 [23725456] Gene. 2013 Jul 25;524(2):341-6 [23590984] Angew Chem Int Ed Engl. 2013 Jul 1;52(27):6912-6 [23712702] Biochem J. 2013 Aug 1;453(3):413-26 [23682967] Biochem J. 2013 Oct 1;455(1):27-35 [23834247] J Mol Biol. 2014 Jan 23;426(2):301-8 [24144619] Biosci Rep. 2013;33(2):e00022 [23240582] Proc Natl Acad Sci U S A. 2014 Mar 18;111(11):4043-8 [24591629] Angew Chem Int Ed Engl. 2014 Sep 1;53(36):9508-11 [25044992] J Biol Chem. 2014 Aug 29;289(35):24032-42 [25023283] PLoS Genet. 2014 Sep;10(9):e1004586 [25254656] Proc Natl Acad Sci U S A. 1994 Jan 4;91(1):316-20 [7904068] Biochemistry. 1994 Jan 18;33(2):403-7 [8286370] Cytotechnology. 1994;15(1-3):139-44 [7534468] Methods Enzymol. 1995;246:416-60 [7752933] Science. 1997 Aug 1;277(5326):653-9 [9235882] Biochemistry. 1998 Jul 21;37(29):10429-37 [9671512] Genetics. 1999 Jul;152(3):895-908 [10388810] J Biol Chem. 1963 Dec;238:3899-913 [14086723] Science. 2004 Dec 17;306(5704):2101-5 [15604408] Blood Cells Mol Dis. 2005 Sep-Oct;35(2):177-81 [16009582] Biochemistry. 2000 Jul 11;39(27):7856-62 [10891064] J Bacteriol. 2000 Oct;182(19):5309-16 [10986231] Cell. 2003 Sep 5;114(5):559-72 [13678580] Biochemistry. 2004 Feb 24;43(7):2007-21 [14967041] Biochem Biophys Res Commun. 1966 Jun 21;23(6):822-7 [5962494] Biochim Biophys Acta. 1979 Jul 25;579(1):107-21 [465523] J Biochem Biophys Methods. 1989 Aug-Sep;19(2-3):249-51 [2555407] Proc Natl Acad Sci U S A. 1990 Jan;87(2):598-602 [2153958] Proc Natl Acad Sci U S A. 1990 Nov;87(22):8965-9 [2174169] J Biol Chem. 1991 Sep 5;266(25):16499-506 [1653239] Proc Natl Acad Sci U S A. 1991 Oct 15;88(20):9210-3 [1924383] Mol Cell Biol. 2015 Jan;35(2):370-8 [25368382] Nat Rev Mol Cell Biol. 2015 Jan;16(1):45-55 [25425402] Proteins. 2015 Mar;83(3):411-27 [25546158] Open Biol. 2015 Mar;5(3):150014 [25808508] J Am Chem Soc. 2015 Apr 8;137(13):4567-80 [25790339] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/acs.biochem.5b00532 ER - TY - JOUR T1 - Novel 3-Substituted 7-Phenylpyrrolo[3,2-f]quinolin-9(6H)-ones as Single Entities with Multitarget Antiproliferative Activity. AN - 1728053215; 26418966 AB - A series of chemically modified 7-phenylpyrrolo[3,2-f]quinolinones was synthesized and evaluated as anticancer agents. Among them, the most cytotoxic (subnanomolar GI50 values) amidic derivative 5f was shown to act as an inhibitor of tubulin polymerization (IC50, 0.99 μM) by binding to the colchicine site with high affinity. Moreover, 5f induced cell cycle arrest in the G2/M phase of the cell cycle in a concentration dependent manner, followed by caspase-dependent apoptotic cell death. Compound 5f also showed lower toxicity in nontumoral cells, suggesting selectivity toward cancer cells. Additional experiments revealed that 5f inhibited the enzymatic activity of multiple kinases, including AURKA, FLT3, GSK3A, MAP3K, MEK, RSK2, RSK4, PLK4, ULK1, and JAK1. Computational studies showed that 5f can be properly accommodated in the colchicine binding site of tubulin as well as in the ATP binding clefts of all examined kinases. Our data indicate that the excellent antiproliferative profile of 5f may be derived from its interactions with multiple cellular targets. JF - Journal of medicinal chemistry AU - Carta, Davide AU - Bortolozzi, Roberta AU - Hamel, Ernest AU - Basso, Giuseppe AU - Moro, Stefano AU - Viola, Giampietro AU - Ferlin, Maria Grazia AD - Department of Pharmaceutical and Pharmacological Sciences, University of Padova , Via Marzolo, 5, 35131 Padova, Italy. ; Laboratory of Oncohematology, Department of Women's and Children's Health, University of Padova , 35128 Padova, Italy. ; Screening Technologies Branch, Developmental Therapeutics Program, Division of Cancer Treatment and Diagnosis, Frederick National Laboratory for Cancer Research, National Cancer Institute, National Institutes of Health , Frederick, Maryland 21702, United States. Y1 - 2015/10/22/ PY - 2015 DA - 2015 Oct 22 SP - 7991 EP - 8010 VL - 58 IS - 20 KW - 3-(cyclopropylmethanone)-7-phenyl-H-pyrrolo(3,2-f)quinolin-9(6H)-one KW - 0 KW - Antineoplastic Agents KW - Protein Kinase Inhibitors KW - Pyrroles KW - Quinolones KW - Tubulin KW - Tubulin Modulators KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Colchicine KW - SML2Y3J35T KW - Index Medicus KW - Cell Proliferation -- drug effects KW - Animals KW - Drug Interactions KW - Protein Kinase Inhibitors -- pharmacology KW - HeLa Cells KW - Humans KW - Cell Line, Tumor KW - Tubulin -- biosynthesis KW - Structure-Activity Relationship KW - Colchicine -- metabolism KW - Tubulin -- drug effects KW - Binding Sites -- drug effects KW - Adenosine Triphosphate -- metabolism KW - Apoptosis -- drug effects KW - Protein Kinase Inhibitors -- chemical synthesis KW - Cell Cycle -- drug effects KW - Tubulin Modulators -- chemical synthesis KW - Tubulin Modulators -- pharmacology KW - Antineoplastic Agents -- chemical synthesis KW - Quinolones -- chemical synthesis KW - Pyrroles -- pharmacology KW - Pyrroles -- chemical synthesis KW - Antineoplastic Agents -- pharmacology KW - Quinolones -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1728053215?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+medicinal+chemistry&rft.atitle=Novel+3-Substituted+7-Phenylpyrrolo%5B3%2C2-f%5Dquinolin-9%286H%29-ones+as+Single+Entities+with+Multitarget+Antiproliferative+Activity.&rft.au=Carta%2C+Davide%3BBortolozzi%2C+Roberta%3BHamel%2C+Ernest%3BBasso%2C+Giuseppe%3BMoro%2C+Stefano%3BViola%2C+Giampietro%3BFerlin%2C+Maria+Grazia&rft.aulast=Carta&rft.aufirst=Davide&rft.date=2015-10-22&rft.volume=58&rft.issue=20&rft.spage=7991&rft.isbn=&rft.btitle=&rft.title=Journal+of+medicinal+chemistry&rft.issn=1520-4804&rft_id=info:doi/10.1021%2Facs.jmedchem.5b00805 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-02 N1 - Date created - 2015-10-22 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 4AFJ; PDB; 1RJB; 4JXF; 4EL9; 1SA0; 4E4N N1 - SuppNotes - Cited By: Nature. 2011 Mar 3;471(7336):110-4 [21368834] Oncotarget. 2010 Nov;1(7):530-43 [21317449] Mol Interv. 2011 Apr;11(2):141-50 [21540474] Curr Med Chem. 2011;18(18):2686-714 [21649578] J Med Chem. 2011 Jul 28;54(14):5144-53 [21663319] Biochem Pharmacol. 2012 Jan 1;83(1):16-26 [21964343] Mol Biol Cell. 2012 Feb;23(4):567-76 [22171325] J Med Chem. 2012 Jun 28;55(12):5901-21 [22591402] Biochemistry. 2012 Aug 21;51(33):6499-510 [22846040] Cell Death Differ. 2012 Nov;19(11):1733-40 [22935609] Pharm Res. 2012 Nov;29(11):2943-71 [22814904] J Cell Biol. 2012 Dec 10;199(6):871-81 [23229895] Angiogenesis. 2013 Jul;16(3):647-62 [23456551] CA Cancer J Clin. 2014 Jan-Feb;64(1):9-29 [24399786] Trends Cell Biol. 2009 Mar;19(3):89-98 [19168356] Anticancer Agents Med Chem. 2008 Dec;8(8):832-6 [19075565] Biochim Biophys Acta. 2008 Jan;1784(1):159-85 [17997386] Med Res Rev. 2008 Jan;28(1):155-83 [17464966] J Med Chem. 2007 Nov 1;50(22):5509-13 [17915851] Pharmacol Rev. 2006 Sep;58(3):621-81 [16968952] J Med Chem. 2006 Mar 23;49(6):1910-5 [16539377] J Med Chem. 2005 May 5;48(9):3417-27 [15857148] Proteins. 1998 Nov 15;33(3):367-82 [9829696] Mol Pharmacol. 1998 Jan;53(1):62-76 [9443933] Cancer Res. 1997 Jan 15;57(2):229-33 [9000560] Oncotarget. 2014 Aug 15;5(15):5978-91 [24980813] DNA Repair (Amst). 2004 Aug-Sep;3(8-9):959-67 [15279782] Oncogene. 2004 Apr 12;23(16):2825-37 [15077146] Nature. 2004 Mar 11;428(6979):198-202 [15014504] Mol Cell. 2004 Jan 30;13(2):169-78 [14759363] Apoptosis. 2003 Oct;8(5):413-50 [12975575] EMBO Rep. 2003 Jul;4(7):671-7 [12835754] Cell Biochem Biophys. 2003;38(1):1-22 [12663938] Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13103-7 [11069302] Nucleic Acids Res. 2000 Jan 1;28(1):235-42 [10592235] Biochemistry. 1989 Aug 22;28(17):6984-91 [2819042] Cancer Res. 2010 Jan 15;70(2):440-6 [20068163] ChemMedChem. 2010 Aug 2;5(8):1373-85 [20629070] Biochem J. 2010 Sep 1;430(2):199-205 [20704571] Bioorg Med Chem. 2011 Jan 1;19(1):448-57 [21145750] Methods Mol Biol. 2011;731:237-45 [21516412] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/acs.jmedchem.5b00805 ER - TY - JOUR T1 - Targeted Proteomics-Driven Computational Modeling of Macrophage S1P Chemosensing AN - 1808618258; PQ0003421844 AB - Osteoclasts are monocyte-derived multinuclear cells that directly attach to and resorb bone. Sphingosine-1-phosphate (S1P) regulates bone resorption by functioning as both a chemoattractant and chemorepellent of osteoclast precursors through two G-protein coupled receptors that antagonize each other in an S1P-concentration-dependent manner. To quantitatively explore the behavior of this chemosensing pathway, we applied targeted proteomics, transcriptomics, and rule-based pathway modeling using the Simmune toolset. RAW264.7 cells (a mouse monocyte/macrophage cell line) were used as model osteoclast precursors, RNA-seq was used to identify expressed target proteins, and selected reaction monitoring (SRM) mass spectrometry using internal peptide standards was used to perform absolute abundance measurements of pathway proteins. The resulting transcript and protein abundance values were strongly correlated. Measured protein abundance values, used as simulation input parameters, led to in silico pathway behavior matching in vitro measurements. Moreover, once model parameters were established, even simulated responses toward stimuli that were not used for parameterization were consistent with experimental findings. These findings demonstrate the feasibility and value of combining targeted mass spectrometry with pathway modeling for advancing biological insight. JF - Molecular and Cellular Proteomics AU - Manes, Nathan P AU - Angermann, Bastian R AU - Koppenol-Raab, Marijke AU - An, Eunkyung AU - Sjoelund, Virginie H AU - Sun, Jing AU - Ishii, Masaru AU - Germain, Ronald N AU - Meier-Schellersheim, Martin AU - Nita-Lazar, Aleksandra AD - From the Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 9000 Rockville Pike, Bethesda, Maryland, 20892-0421; , nitalazarau@niaid.nih.gov Y1 - 2015/10/21/ PY - 2015 DA - 2015 Oct 21 SP - 2661 EP - 2681 PB - American Society for Biochemistry and Molecular Biology, 9650 Rockville Pike Bethesda MD 20814-3996 United States VL - 14 IS - 10 SN - 1535-9476, 1535-9476 KW - Biotechnology and Bioengineering Abstracts KW - Macrophages KW - Osteoclasts KW - Animal models KW - Transcription KW - Sphingosine 1-phosphate KW - Computer applications KW - Mass spectroscopy KW - G protein-coupled receptors KW - Chemotactic factors KW - Osteoprogenitor cells KW - Bone resorption KW - proteomics KW - Monocytes KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808618258?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+Cellular+Proteomics&rft.atitle=Targeted+Proteomics-Driven+Computational+Modeling+of+Macrophage+S1P+Chemosensing&rft.au=Manes%2C+Nathan+P%3BAngermann%2C+Bastian+R%3BKoppenol-Raab%2C+Marijke%3BAn%2C+Eunkyung%3BSjoelund%2C+Virginie+H%3BSun%2C+Jing%3BIshii%2C+Masaru%3BGermain%2C+Ronald+N%3BMeier-Schellersheim%2C+Martin%3BNita-Lazar%2C+Aleksandra&rft.aulast=Manes&rft.aufirst=Nathan&rft.date=2015-10-21&rft.volume=14&rft.issue=10&rft.spage=2661&rft.isbn=&rft.btitle=&rft.title=Molecular+and+Cellular+Proteomics&rft.issn=15359476&rft_id=info:doi/10.1074%2Fmcp.M115.048918 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Macrophages; Osteoclasts; Animal models; Transcription; Sphingosine 1-phosphate; Computer applications; Mass spectroscopy; G protein-coupled receptors; Chemotactic factors; Osteoprogenitor cells; Bone resorption; Monocytes; proteomics DO - http://dx.doi.org/10.1074/mcp.M115.048918 ER - TY - JOUR T1 - Phase I Study of Single-Agent AZD1775 (MK-1775), a Wee1 Kinase Inhibitor, in Patients With Refractory Solid Tumors. AN - 1724258992; 25964244 AB - Wee1 tyrosine kinase phosphorylates and inactivates cyclin-dependent kinase (Cdk) 1/2 in response to DNA damage. AZD1775 is a first-in-class inhibitor of Wee1 kinase with single-agent antitumor activity in preclinical models. We conducted a phase I study of single-agent AZD1775 in adult patients with refractory solid tumors to determine its maximum-tolerated dose (MTD), pharmacokinetics, and modulation of phosphorylated Tyr15-Cdk (pY15-Cdk) and phosphorylated histone H2AX (γH2AX) levels in paired tumor biopsies. AZD1775 was administered orally twice per day over 2.5 days per week for up to 2 weeks per 21-day cycle (3 + 3 design). At the MTD, paired tumor biopsies were obtained at baseline and after the fifth dose to determine pY15-Cdk and γH2AX levels. Six patients with BRCA-mutant solid tumors were also enrolled at the MTD. Twenty-five patients were enrolled. The MTD was established as 225 mg twice per day orally over 2.5 days per week for 2 weeks per 21-day cycle. Confirmed partial responses were observed in two patients carrying BRCA mutations: one with head and neck cancer and one with ovarian cancer. Common toxicities were myelosuppression and diarrhea. Dose-limiting toxicities were supraventricular tachyarrhythmia and myelosuppression. Accumulation of drug (t1/2 approximately 11 hours) was observed. Reduction in pY15-Cdk levels (two of five paired biopsies) and increases in γH2AX levels (three of five paired biopsies) were demonstrated. This is the first report of AZD1775 single-agent activity in patients carrying BRCA mutations. Proof-of-mechanism was demonstrated by target modulation and DNA damage response in paired tumor biopsies. © 2015 by American Society of Clinical Oncology. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Do, Khanh AU - Wilsker, Deborah AU - Ji, Jiuping AU - Zlott, Jennifer AU - Freshwater, Tomoko AU - Kinders, Robert J AU - Collins, Jerry AU - Chen, Alice P AU - Doroshow, James H AU - Kummar, Shivaani AD - Khanh Do, Jennifer Zlott, Jerry Collins, Alice P. Chen, James H. Doroshow, and Shivaani Kummar, National Cancer Institute, Bethesda, MD; Deborah Wilsker, Jiuping Ji, and Robert J. Kinders, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, MD; and Tomoko Freshwater, Merck Research Laboratories-Oncology, Boston, MA. ; Khanh Do, Jennifer Zlott, Jerry Collins, Alice P. Chen, James H. Doroshow, and Shivaani Kummar, National Cancer Institute, Bethesda, MD; Deborah Wilsker, Jiuping Ji, and Robert J. Kinders, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research, Frederick, MD; and Tomoko Freshwater, Merck Research Laboratories-Oncology, Boston, MA. kummars@mail.nih.gov. Y1 - 2015/10/20/ PY - 2015 DA - 2015 Oct 20 SP - 3409 EP - 3415 VL - 33 IS - 30 KW - Antineoplastic Agents KW - 0 KW - Cell Cycle Proteins KW - MK 1775 KW - Nuclear Proteins KW - Protein Kinase Inhibitors KW - Pyrazoles KW - Pyrimidines KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - WEE1 protein, human KW - EC 2.7.10.2 KW - Index Medicus KW - Administration, Oral KW - Young Adult KW - Cell Cycle Proteins -- antagonists & inhibitors KW - Drug Administration Schedule KW - Dose-Response Relationship, Drug KW - Humans KW - Aged KW - Protein-Tyrosine Kinases -- metabolism KW - Cell Cycle Proteins -- metabolism KW - Nuclear Proteins -- antagonists & inhibitors KW - Protein-Tyrosine Kinases -- antagonists & inhibitors KW - Adult KW - Middle Aged KW - Nuclear Proteins -- metabolism KW - Female KW - Male KW - Pyrazoles -- administration & dosage KW - Pyrimidines -- adverse effects KW - Neoplasms -- drug therapy KW - Neoplasms -- enzymology KW - Antineoplastic Agents -- administration & dosage KW - Antineoplastic Agents -- pharmacokinetics KW - Neoplasms -- blood KW - Protein Kinase Inhibitors -- administration & dosage KW - Protein Kinase Inhibitors -- pharmacokinetics KW - Pyrazoles -- adverse effects KW - Pyrimidines -- blood KW - Antineoplastic Agents -- blood KW - Pyrimidines -- pharmacokinetics KW - Pyrazoles -- blood KW - Pyrimidines -- administration & dosage KW - Pyrazoles -- pharmacokinetics KW - Antineoplastic Agents -- adverse effects KW - Protein Kinase Inhibitors -- adverse effects KW - Protein Kinase Inhibitors -- blood KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1724258992?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Phase+I+Study+of+Single-Agent+AZD1775+%28MK-1775%29%2C+a+Wee1+Kinase+Inhibitor%2C+in+Patients+With+Refractory+Solid+Tumors.&rft.au=Do%2C+Khanh%3BWilsker%2C+Deborah%3BJi%2C+Jiuping%3BZlott%2C+Jennifer%3BFreshwater%2C+Tomoko%3BKinders%2C+Robert+J%3BCollins%2C+Jerry%3BChen%2C+Alice+P%3BDoroshow%2C+James+H%3BKummar%2C+Shivaani&rft.aulast=Do&rft.aufirst=Khanh&rft.date=2015-10-20&rft.volume=33&rft.issue=30&rft.spage=3409&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=1527-7755&rft_id=info:doi/10.1200%2FJCO.2014.60.4009 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-02 N1 - Date created - 2015-10-19 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT01748825; ClinicalTrials.gov N1 - SuppNotes - Cited By: Clin Cancer Res. 2010 Nov 15;16(22):5447-57 [20924131] Curr Clin Pharmacol. 2010 Aug;5(3):186-91 [20406171] Clin Cancer Res. 2011 May 1;17(9):2799-806 [21389100] J Cell Biol. 2011 Aug 22;194(4):567-79 [21859861] Clin Cancer Res. 2011 Sep 1;17(17):5638-48 [21799033] Mol Cancer Ther. 2012 Jan;11(1):174-82 [22084170] Mol Cell Biol. 2012 Oct;32(20):4226-36 [22907750] Cancer Res. 2013 Jan 15;73(2):776-84 [23135916] Mol Cancer Ther. 2013 Aug;12(8):1442-52 [23699655] Nat Commun. 2013;4:2993 [24356582] Leukemia. 2015 Jan;29(1):27-37 [24791855] Oncotarget. 2015 Feb 20;6(5):3394-408 [25428911] Cancer Biol Ther. 2010 Apr 1;9(7):514-22 [20107315] Science. 2003 Oct 24;302(5645):639-42 [14576433] Proc Natl Acad Sci U S A. 2004 Apr 27;101(17):6484-9 [15096610] EMBO J. 1995 May 1;14(9):1878-91 [7743995] J Biol Chem. 2006 Nov 17;281(46):34759-67 [16968694] Eur J Cancer. 2009 Jan;45(2):228-47 [19097774] Mol Cancer Ther. 2009 Nov;8(11):2992-3000 [19887545] PLoS One. 2010;5(2):e9197 [20169205] Comment In: J Clin Oncol. 2015 Oct 20;33(30):3485-7 [26215953] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1200/JCO.2014.60.4009 ER - TY - JOUR T1 - Elimination of murine and human T-cell epitopes in recombinant immunotoxin eliminates neutralizing and anti-drug antibodies in vivo. AN - 1826627683; 26477977 AB - Antibodies against the toxin portion of recombinant immunotoxins (RIT) reduce their efficacy and pose a potential safety risk. To overcome this problem we mutated the very immunogenic immunotoxin SS1P to produce LMB-T20, a de-immunized RIT that has the eight human T-cell epitopes in SS1P modified or removed. To determine the effect of T-cell epitope removal in vivo we mapped the T-cell epitopes in immune-competent BALB/c mice and found that these mice recognize two epitopes. One corresponds to the human immunodominant T-cell epitope and the other to a human subdominant epitope; both were eliminated in LMB-T20. We found that mice immunized with LMB-T20 did not have T-cell activation and did not develop anti-drug antibodies (ADA), whereas mice immunized with SS1P, showed T-cell activation, and developed ADA detected by both ELISA and drug neutralizing assays. The ability of the mice treated with LMB-T20 to respond to other antigens was not compromised. We conclude that elimination of T-cell epitopes is sufficient to prevent formation of antibodies to an immunogenic foreign protein.Cellular & Molecular Immunology advance online publication, 19 October 2015; doi:10.1038/cmi.2015.91. JF - Cellular & molecular immunology AU - Mazor, Ronit AU - Crown, Devorah AU - Addissie, Selamawit AU - Jang, Youjin AU - Kaplan, Gilad AU - Pastan, Ira AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Leidos Biomedical Research, Inc., National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2015/10/19/ PY - 2015 DA - 2015 Oct 19 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826627683?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cellular+%26+molecular+immunology&rft.atitle=Elimination+of+murine+and+human+T-cell+epitopes+in+recombinant+immunotoxin+eliminates+neutralizing+and+anti-drug+antibodies+in+vivo.&rft.au=Mazor%2C+Ronit%3BCrown%2C+Devorah%3BAddissie%2C+Selamawit%3BJang%2C+Youjin%3BKaplan%2C+Gilad%3BPastan%2C+Ira&rft.aulast=Mazor&rft.aufirst=Ronit&rft.date=2015-10-19&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Cellular+%26+molecular+immunology&rft.issn=2042-0226&rft_id=info:doi/10.1038%2Fcmi.2015.91 LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2015-10-19 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/cmi.2015.91 ER - TY - JOUR T1 - Host Cell-catalyzed S-Palmitoylation Mediates Golgi Targeting of the Legionella Ubiquitin Ligase GobX. AN - 1722929724; 26316537 AB - The facultative intracellular pathogen Legionella pneumophila, the causative agent of Legionnaires disease, infects and replicates within human alveolar macrophages. L. pneumophila delivers almost 300 effector proteins into the besieged host cell that alter signaling cascades and create conditions that favor intracellular bacterial survival. In order for the effectors to accomplish their intracellular mission, their activity needs to be specifically directed toward the correct host cell protein or target organelle. Here, we show that the L. pneumophila effector GobX possesses E3 ubiquitin ligase activity that is mediated by a central region homologous to mammalian U-box domains. Furthermore, we demonstrate that GobX exploits host cell S-palmitoylation to specifically localize to Golgi membranes. The hydrophobic palmitate moiety is covalently attached to a cysteine residue at position 175, which is part of an amphipathic α-helix within the C-terminal region of GobX. Site-directed mutagenesis of cysteine 175 or residues on the hydrophobic face of the amphipathic helix strongly attenuated palmitoylation and Golgi localization of GobX. Together, our study provides evidence that the L. pneumophila effector GobX exploits two post-translational modification pathways of host cells, ubiquitination and S-palmitoylation. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Lin, Yi-Han AU - Doms, Alexandra G AU - Cheng, Eric AU - Kim, Byoungkwan AU - Evans, Timothy R AU - Machner, Matthias P AD - From the Unit on Microbial Pathogenesis, Cell Biology and Metabolism Program, Eunice Kennedy Shriver NICHD, National Institutes of Health, Bethesda, Maryland 20892. ; From the Unit on Microbial Pathogenesis, Cell Biology and Metabolism Program, Eunice Kennedy Shriver NICHD, National Institutes of Health, Bethesda, Maryland 20892 machnerm@mail.nih.gov. Y1 - 2015/10/16/ PY - 2015 DA - 2015 Oct 16 SP - 25766 EP - 25781 VL - 290 IS - 42 KW - Ubiquitin-Protein Ligases KW - EC 2.3.2.27 KW - Index Medicus KW - Legionella pneumophila KW - ubiquitylation (ubiquitination) KW - protein palmitoylation KW - translocated effector KW - bacterial pathogenesis KW - DHHC protein KW - Golgi KW - click chemistry KW - Protein Transport KW - Biocatalysis KW - Legionella pneumophila -- enzymology KW - Ubiquitin-Protein Ligases -- metabolism KW - Golgi Apparatus -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722929724?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Host+Cell-catalyzed+S-Palmitoylation+Mediates+Golgi+Targeting+of+the+Legionella+Ubiquitin+Ligase+GobX.&rft.au=Lin%2C+Yi-Han%3BDoms%2C+Alexandra+G%3BCheng%2C+Eric%3BKim%2C+Byoungkwan%3BEvans%2C+Timothy+R%3BMachner%2C+Matthias+P&rft.aulast=Lin&rft.aufirst=Yi-Han&rft.date=2015-10-16&rft.volume=290&rft.issue=42&rft.spage=25766&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M115.637397 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-16 N1 - Date created - 2015-10-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Microbiol. 1979 Oct;10(4):437-41 [393713] Nat Genet. 2004 Nov;36(11):1165-73 [15467720] Neuron. 2004 Dec 16;44(6):987-96 [15603741] J Biol Chem. 2005 Apr 15;280(15):14620-7 [15710609] Trends Biochem Sci. 2011 May;36(5):245-53 [21388813] Cell Microbiol. 2011 Feb;13(2):227-45 [20880356] Nucleic Acids Res. 2005 Jul 1;33(Web Server issue):W244-8 [15980461] Cell Host Microbe. 2011 Jul 21;10(1):9-20 [21767808] Science. 2011 Jul 22;333(6041):453-6 [21680813] Proc Natl Acad Sci U S A. 2011 Sep 6;108(36):14733-40 [21873199] Cell Microbiol. 2011 Dec;13(12):1870-80 [21981078] Nat Methods. 2012 Jan;9(1):84-9 [22056678] Future Microbiol. 2012 Feb;7(2):241-57 [22324993] J Bacteriol. 2005 Nov;187(22):7716-26 [16267296] Biochim Biophys Acta. 2006 Apr;1761(4):474-83 [16647879] PLoS Pathog. 2006 May;2(5):e46 [16710455] Dev Cell. 2006 Jul;11(1):47-56 [16824952] Nat Cell Biol. 2006 Sep;8(9):971-7 [16906144] Nat Chem Biol. 2006 Nov;2(11):584-90 [17051234] Bioinformatics. 2007 Nov 1;23(21):2947-8 [17846036] Curr Protoc Cell Biol. 2001 May;Chapter 3:Unit 3.9 [18228361] Mol Microbiol. 2008 Mar;67(6):1307-19 [18284575] PLoS Pathog. 2008;4(8):e1000117 [18670632] Cell Microbiol. 2008 Dec;10(12):2416-33 [18673369] Traffic. 2009 Jan;10(1):76-87 [18980612] Nat Methods. 2009 Feb;6(2):135-8 [19137006] J Biol Chem. 2009 Feb 20;284(8):4846-56 [19095644] Curr Opin Microbiol. 2009 Feb;12(1):67-73 [19157961] J Am Chem Soc. 2009 Apr 8;131(13):4967-75 [19281244] J Biol Chem. 2009 Jun 5;284(23):15867-79 [19346252] Curr Opin Chem Biol. 2009 Oct;13(4):382-91 [19699139] Int J Med Microbiol. 2009 Nov;299(7):489-508 [19482547] Nat Chem Biol. 2010 Jun;6(6):449-56 [20418879] Infect Immun. 2010 Sep;78(9):3905-19 [20547746] Annu Rev Cell Dev Biol. 2010;26:261-83 [20929312] J Biol Chem. 2010 Nov 5;285(45):34686-98 [20813839] J Cell Sci. 2010 Dec 1;123(Pt 23):4007-10 [21084560] J Bacteriol. 2012 Mar;194(6):1389-400 [22228731] Mol Biol Cell. 2012 Dec;23(23):4543-51 [23034182] PLoS Pathog. 2012;8(12):e1003082 [23271971] Curr Opin Chem Biol. 2013 Feb;17(1):20-6 [23287289] Curr Opin Chem Biol. 2013 Feb;17(1):27-33 [23332315] ACS Chem Biol. 2013 Sep 20;8(9):1912-7 [23844586] Nat Commun. 2014;5:3552 [24675427] Proc Natl Acad Sci U S A. 2014 Mar 25;111(12):4560-5 [24616501] J Cell Biol. 2014 Apr 14;205(1):113-26 [24711504] PLoS One. 2014;9(4):e95021 [24751652] Proc Natl Acad Sci U S A. 2014 Jul 22;111(29):10538-43 [25006264] Proc Natl Acad Sci U S A. 2014 Aug 26;111(34):E3514-23 [25114243] Infect Immun. 2015 Oct;83(10):3989-4002 [26216420] J Biol Chem. 2000 Jan 7;275(1):261-70 [10617614] Cell. 2000 May 12;101(4):353-63 [10830163] J Biol Chem. 2001 Aug 31;276(35):33111-20 [11435423] Nature. 2002 Apr 18;416(6882):703-9 [11961546] J Cell Biol. 2002 Oct 14;159(1):23-8 [12370247] Mol Microbiol. 2003 Apr;48(2):305-21 [12675793] Proc Natl Acad Sci U S A. 2004 Jan 20;101(3):841-6 [14715899] Infect Immun. 2004 May;72(5):3048-53 [15102819] J Exp Med. 2004 May 3;199(9):1201-11 [15117975] Mol Microbiol. 1993 Jan;7(1):7-19 [8382332] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M115.637397 ER - TY - JOUR T1 - Treatment with Ibrutinib Inhibits BTK- and VLA-4-Dependent Adhesion of Chronic Lymphocytic Leukemia Cells In Vivo AN - 1808629563; PQ0003449985 AB - Purpose: Ibrutinib leads to a transient lymphocytosis in patients with chronic lymphocytic leukemia (CLL) that develops within hours of starting drug and is due to the efflux of cells from lymphoid tissues into the blood. We therefore sought to investigate the in vivo effect of ibrutinib on migration and adhesion of CLL cells.Experimental Design: Patients received single-agent ibrutinib (420 mg daily) on an investigator-initiated phase II trial. Serial blood samples were collected pretreatment and during treatment for ex vivo functional assays.Results: Adhesion of CLL cells to fibronectin was rapidly (within hours) and almost completely inhibited (median reduction 98% on day 28, P < 0.001), while the effect on migration to chemokines was more moderate (median reduction 64%, P = 0.008) and less uniform. Although cell surface expression of key adhesion molecules such as CD49d, CD29, and CD44 were modestly reduced, this was only apparent after weeks of treatment. Stimulation of CLL cells from patients on ibrutinib with PMA, which activates PKC independent of BTK, restored the ability of the cells to adhere to fibronectin in a VLA-4-dependent manner. Finally, the addition of ibrutinib to CLL cells adhered to fibronectin in vitro caused the detachment of 17% of the cells, on average; consisten t with in vivo observations of an increasing lymphocytosis within 4 hours of starting ibrutinib.Conclusions: Inhibition of BTK and VLA-4-dependent adhesion of CLL cells to stroma and stromal components provides a mechanistic explanation for the treatment-induced lymphocytosis and may reduce CD49d-dependent prosurvival signals in the tissue microenvironment. Clin Cancer Res; 21(20); 4642-51. copyright 2015 AACR. JF - Clinical Cancer Research AU - Herman, Sarah EM AU - Mustafa, Rashida Z AU - Jones, Jade AU - Wong, Deanna H AU - Farooqui, Mohammed AU - Wiestner, Adrian AD - Hematology Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, wiestnea@nhlbi.nih.gov Y1 - 2015/10/15/ PY - 2015 DA - 2015 Oct 15 SP - 4642 EP - 4651 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 20 SN - 1078-0432, 1078-0432 KW - Immunology Abstracts; Biotechnology and Bioengineering Abstracts KW - Protein kinase C KW - CD49d antigen KW - Stroma KW - Cell surface KW - Chemokines KW - Phorbol esters KW - Fibronectin KW - CD44 antigen KW - Clinical trials KW - Cancer KW - Lymphoid tissue KW - Lymphocytosis KW - Microenvironments KW - CD29 antigen KW - Cell migration KW - Chronic lymphatic leukemia KW - Cell adhesion molecules KW - Bruton's tyrosine kinase KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808629563?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Cancer+Research&rft.atitle=Treatment+with+Ibrutinib+Inhibits+BTK-+and+VLA-4-Dependent+Adhesion+of+Chronic+Lymphocytic+Leukemia+Cells+In+Vivo&rft.au=Herman%2C+Sarah+EM%3BMustafa%2C+Rashida+Z%3BJones%2C+Jade%3BWong%2C+Deanna+H%3BFarooqui%2C+Mohammed%3BWiestner%2C+Adrian&rft.aulast=Herman&rft.aufirst=Sarah&rft.date=2015-10-15&rft.volume=21&rft.issue=20&rft.spage=4642&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-15-0781 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-10-26 N1 - SubjectsTermNotLitGenreText - Stroma; CD49d antigen; Protein kinase C; Cell surface; Chemokines; Phorbol esters; CD44 antigen; Fibronectin; Clinical trials; Lymphoid tissue; Cancer; Lymphocytosis; Microenvironments; CD29 antigen; Cell migration; Chronic lymphatic leukemia; Bruton's tyrosine kinase; Cell adhesion molecules DO - http://dx.doi.org/10.1158/1078-0432.CCR-15-0781 ER - TY - JOUR T1 - super(18)F-fluorodeoxyglucose Positron Emission Tomography in Kaposi Sarcoma Herpesvirus-Associated Multicentric Castleman Disease: Correlation With Activity, Severity, Inflammatory and Virologic Parameters AN - 1773909524; PQ0002721040 AB - Background.?Kaposi sarcoma herpesvirus (KSHV)-associated multicentric Castleman disease (MCD) is a lymphoproliferative inflammatory disorder commonly associated with human immunodeficiency virus (HIV). Its presentation may be difficult to distinguish from HIV and its complications, including lymphoma. Novel imaging strategies could address these problems. Methods.?We prospectively characterized super(18)F-fluorodeoxyglucose positron emission tomography (PET) findings in 27 patients with KSHV-MCD. Patients were imaged with disease activity and at remission with scans evaluated blind to clinical status. Symptoms, C-reactive protein level, and HIV and KSHV loads were assessed in relation to imaging findings. Results.?KSHV-MCD activity was associated with hypermetabolic symmetric lymphadenopathy (median maximal standardized uptake value [SUV sub(max)], 6.0; range, 2.0-8.0) and splenomegaly (3.4; 1.2-11.0), with increased metabolism also noted in the marrow (2.1; range, 1.0-3.5) and salivary glands (3.0; range, 2.0-6.0). The super(18)F-fluorodeoxyglucose PET abnormalities improved at remission, with significant SUV sub(max) decreases in the lymph nodes (P = .004), spleen (P = .008), marrow (P = .004), and salivary glands (P = .004). Nodal SUV sub(max) correlated with symptom severity (P = .005), C-reactive protein level (R = 0.62; P = .004), and KSHV load (R = 0.54; P = .02) but not HIV load (P = .52). Conclusions.?KSHV-MCD activity is associated with super(18)F-FDG PET abnormalities of the lymph nodes, spleen, marrow, and salivary glands. These findings have clinical implications for the diagnosis and monitoring of KSHV-MCD and shed light on its pathobiologic mechanism. JF - Journal of Infectious Diseases AU - Polizzotto, Mark N AU - Millo, Corina AU - Uldrick, Thomas S AU - Aleman, Karen AU - Whatley, Millie AU - Wyvill, Kathleen M AU - O'Mahony, Deirdre AU - Marshall, Vickie AU - Whitby, Denise AU - Maass-Moreno, Roberto AU - Steinberg, Seth M AU - Little, Richard F AU - Yarchoan, Robert AD - HIV and AIDS Malignancy Branch, robert.yarchoan@nih.gov Y1 - 2015/10/15/ PY - 2015 DA - 2015 Oct 15 SP - 1250 EP - 1260 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 212 IS - 8 SN - 0022-1899, 0022-1899 KW - Virology & AIDS Abstracts; Health & Safety Science Abstracts KW - Castleman disease KW - human herpesvirus 8 (HHV-8)/Kaposi sarcoma herpesvirus (KSHV) KW - HIV KW - 18F-FDG positron emission tomography KW - Herpesvirus KW - Lymphocytes KW - Salivary gland KW - Infectious diseases KW - Inflammatory diseases KW - Emissions KW - Positron emission tomography KW - Lymphoma KW - Complications KW - Kaposi's sarcoma-associated herpesvirus KW - Spleen KW - Remission KW - Lymph nodes KW - Inflammation KW - Lymphadenopathy KW - Human immunodeficiency virus KW - Sarcoma KW - Proteins KW - Uptake KW - Standards KW - Splenomegaly KW - Metabolism KW - C-reactive protein KW - V 22360:AIDS and HIV KW - H 2000:Transportation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1773909524?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=super%2818%29F-fluorodeoxyglucose+Positron+Emission+Tomography+in+Kaposi+Sarcoma+Herpesvirus-Associated+Multicentric+Castleman+Disease%3A+Correlation+With+Activity%2C+Severity%2C+Inflammatory+and+Virologic+Parameters&rft.au=Polizzotto%2C+Mark+N%3BMillo%2C+Corina%3BUldrick%2C+Thomas+S%3BAleman%2C+Karen%3BWhatley%2C+Millie%3BWyvill%2C+Kathleen+M%3BO%27Mahony%2C+Deirdre%3BMarshall%2C+Vickie%3BWhitby%2C+Denise%3BMaass-Moreno%2C+Roberto%3BSteinberg%2C+Seth+M%3BLittle%2C+Richard+F%3BYarchoan%2C+Robert&rft.aulast=Polizzotto&rft.aufirst=Mark&rft.date=2015-10-15&rft.volume=212&rft.issue=8&rft.spage=1250&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiv204 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Remission; Spleen; Lymphocytes; Salivary gland; Lymph nodes; Inflammation; Lymphadenopathy; Inflammatory diseases; Positron emission tomography; Sarcoma; Splenomegaly; Lymphoma; Metabolism; C-reactive protein; Infectious diseases; Complications; Human immunodeficiency virus; Emissions; Uptake; Proteins; Standards; Herpesvirus; Kaposi's sarcoma-associated herpesvirus DO - http://dx.doi.org/10.1093/infdis/jiv204 ER - TY - JOUR T1 - Prospective study of Helicobacter pylori antigens and gastric noncardia cancer risk in the nutrition intervention trial cohort. AN - 1702653858; 25845708 AB - Helicobacter pylori (H. pylori) infection is the strongest known risk factor for gastric noncardia adenocarcinoma (GNCA). We used multiplex serology to determine whether seropositivity to 15 H. pylori proteins is associated with the subsequent development of noncardia gastric cancer in Linxian, China. We included 448 GNCA cases and 1242 controls from two time points within the Linxian General Population Nutrition Intervention Trial, Linxian. H. pylori multiplex seropositivity was defined as positivity to ≥4 of the 15 included antigens. Odds ratios (ORs) and 95% confidence intervals (CIs) were adjusted for major GNCA risk factors. In addition, we undertook a meta-analysis combining H. pylori multiplex serology data from both time points. H. pylori multiplex seropositivity was associated with a significant increase in risk of GNCA at one time point (1985; OR: 3.44, 95% CI: 1.91, 6.19) and this association remained significant following adjustment for H. pylori or CagA ELISA seropositivity (OR: 2.92, 95% CI: 1.56, 5.47). Combining data from both time points in a meta-analysis H. pylori multiplex seropositivity was associated with an increased risk of GNCA, as were six individual antigens: GroEL, HP0305, CagA, VacA, HcpC and Omp. CagM was inversely associated with risk of GNCA. We identified six individual antigens that confer an increase in risk of GNCA within this population of high H. pylori seroprevalence, as well as a single antigen that may be inversely associated with GNCA risk. We further determined that the H. pylori multiplex assay provides additional information to the conventional ELISA methods on risk of GNCA. © 2015 UICC. JF - International journal of cancer AU - Murphy, Gwen AU - Freedman, Neal D AU - Michel, Angelika AU - Fan, Jin-Hu AU - Taylor, Philip R AU - Pawlita, Michael AU - Qiao, You-Lin AU - Zhang, Han AU - Yu, Kai AU - Abnet, Christian C AU - Dawsey, Sanford M AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD. ; Division of Genome Modifications and Carcinogenesis, Infection and Cancer Program, German Cancer Research Center (DKFZ), Heidelberg, Germany. ; Department of Epidemiology, Cancer Institute, Chinese Academy of Medical Sciences, Beijing, People's Republic of China. Y1 - 2015/10/15/ PY - 2015 DA - 2015 Oct 15 SP - 1938 EP - 1946 VL - 137 IS - 8 KW - Antigens, Bacterial KW - 0 KW - Index Medicus KW - gastric cancer KW - Helicobacter pylori KW - multiplex serology KW - esophageal cancer KW - Prospective Studies KW - Risk Factors KW - Humans KW - Seroepidemiologic Studies KW - Aged KW - Middle Aged KW - Male KW - Female KW - Stomach Neoplasms -- microbiology KW - Helicobacter Infections -- immunology KW - Adenocarcinoma -- epidemiology KW - Adenocarcinoma -- blood KW - Helicobacter pylori -- immunology KW - Adenocarcinoma -- microbiology KW - Stomach Neoplasms -- blood KW - Helicobacter Infections -- blood KW - Antigens, Bacterial -- immunology KW - Stomach Neoplasms -- epidemiology KW - Helicobacter Infections -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1702653858?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Prospective+study+of+Helicobacter+pylori+antigens+and+gastric+noncardia+cancer+risk+in+the+nutrition+intervention+trial+cohort.&rft.au=Murphy%2C+Gwen%3BFreedman%2C+Neal+D%3BMichel%2C+Angelika%3BFan%2C+Jin-Hu%3BTaylor%2C+Philip+R%3BPawlita%2C+Michael%3BQiao%2C+You-Lin%3BZhang%2C+Han%3BYu%2C+Kai%3BAbnet%2C+Christian+C%3BDawsey%2C+Sanford+M&rft.aulast=Murphy&rft.aufirst=Gwen&rft.date=2015-10-15&rft.volume=137&rft.issue=8&rft.spage=1938&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.29543 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-24 N1 - Date created - 2015-08-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2000 Feb 1;97(3):1263-8 [10655519] Am J Pathol. 2001 Feb;158(2):647-54 [11159201] J Natl Cancer Inst. 2001 Feb 7;93(3):226-33 [11158192] N Engl J Med. 2001 Sep 13;345(11):784-9 [11556297] Mol Microbiol. 2001 Dec;42(5):1337-48 [11886563] Proteomics. 2002 Mar;2(3):313-24 [11921447] Int J Cancer. 2004 Jan 20;108(3):456-63 [14648714] Nat Rev Cancer. 2004 Sep;4(9):688-94 [15343275] J Natl Cancer Inst. 1993 Sep 15;85(18):1483-92 [8360931] Ann Epidemiol. 1993 Nov;3(6):577-85 [7921303] J Biol Chem. 1995 Jul 28;270(30):17771-7 [7629077] J Natl Cancer Inst. 1995 Dec 6;87(23):1777-80 [7473834] Infect Immun. 1998 Mar;66(3):1023-7 [9488391] Int J Cancer. 2005 Jan 20;113(3):456-63 [15455378] Infect Immun. 2005 Aug;73(8):4732-42 [16040986] Clin Chem. 2005 Oct;51(10):1845-53 [16099939] Infect Immun. 2006 Jan;74(1):425-34 [16368998] J Chromatogr B Analyt Technol Biomed Life Sci. 2006 Mar 20;833(1):63-79 [16483854] J Natl Cancer Inst. 2006 Oct 18;98(20):1445-52 [17047193] Br J Cancer. 2007 Jan 15;96(1):172-6 [17179990] J Natl Cancer Inst. 2009 Apr 1;101(7):507-18 [19318634] Cancer Res. 2009 Apr 1;69(7):2973-80 [19318564] Cancer Res. 2009 Aug 1;69(15):6164-70 [19602590] Helicobacter. 2009 Dec;14(6):525-35 [19889070] Nat Rev Microbiol. 2009 Dec;7(12):887-94 [19898491] Cancer Epidemiol Biomarkers Prev. 2012 Dec;21(12):2185-92 [23035179] Am J Clin Nutr. 2013 Nov;98(5):1289-97 [24025629] Hepatology. 2014 Dec;60(6):1963-71 [24797247] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ijc.29543 ER - TY - JOUR T1 - Prefusion F-specific antibodies determine the magnitude of RSV neutralizing activity in human sera AN - 1808673135; PQ0003213361 AB - Respiratory syncytial virus (RSV) is estimated to claim more lives among infants 90% of NT activity and depleted binding antibodies to both F conformations. In contrast, adsorption with post-F removed ~30% of NT activity, and binding antibodies to pre-F were retained. These findings were consistent across all age groups. Protein competition neutralization assays with pre-F mutants in which sites O or II were altered to knock out binding of antibodies to the corresponding sites showed that these sites accounted for ~35 and <10% of NT activity, respectively. Binding competition assays with monoclonal antibodies (mAbs) indicated that the amount of site O-specific antibodies correlated with NT activity, whereas the magnitude of binding competed by site II mAbs did not correlate with neutralization. Our results indicate that RSV NT activity in human sera is primarily derived from pre-F-specific antibodies, and therefore, inducing or boosting NT activity by vaccination will be facilitated by using pre-F antigens that preserve site O. JF - Science Translational Medicine AU - Ngwuta, Joan O AU - Chen, Man AU - Modjarrad, Kayvon AU - Joyce, M Gordon AU - Kanekiyo, Masaru AU - Kumar, Azad AU - Yassine, Hadi M AU - Moin, Syed M AU - Killikelly, April M AU - Chuang, Gwo-Yu AD - Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA Y1 - 2015/10/14/ PY - 2015 DA - 2015 Oct 14 PB - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States VL - 7 IS - 309 SN - 1946-6234, 1946-6234 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources KW - Respiratory syncytial virus KW - Antibodies KW - Antigens KW - Monoclonal antibodies KW - Respiration KW - Man-induced effects KW - Age groups KW - Pathogens KW - Metabolism KW - Public health KW - Q1 08423:Behaviour KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808673135?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+Translational+Medicine&rft.atitle=Prefusion+F-specific+antibodies+determine+the+magnitude+of+RSV+neutralizing+activity+in+human+sera&rft.au=Ngwuta%2C+Joan+O%3BChen%2C+Man%3BModjarrad%2C+Kayvon%3BJoyce%2C+M+Gordon%3BKanekiyo%2C+Masaru%3BKumar%2C+Azad%3BYassine%2C+Hadi+M%3BMoin%2C+Syed+M%3BKillikelly%2C+April+M%3BChuang%2C+Gwo-Yu&rft.aulast=Ngwuta&rft.aufirst=Joan&rft.date=2015-10-14&rft.volume=7&rft.issue=309&rft.spage=309ra162&rft.isbn=&rft.btitle=&rft.title=Science+Translational+Medicine&rft.issn=19466234&rft_id=info:doi/10.1126%2Fscitranslmed.aac4241 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Antibodies; Antigens; Monoclonal antibodies; Respiration; Man-induced effects; Age groups; Pathogens; Metabolism; Public health; Respiratory syncytial virus DO - http://dx.doi.org/10.1126/scitranslmed.aac4241 ER - TY - JOUR T1 - Genetic Landscape of Human Papillomavirus-Associated Head and Neck Cancer and Comparison to Tobacco-Related Tumors. AN - 1721349692; 26351353 AB - Head and neck cancer is the fifth most common cancer worldwide. It is often amenable to curative intent therapy when localized to the head and neck region, but it carries a poor prognosis when it is recurrent or metastatic. Therefore, initial treatment decisions are critical to improve patient survival. However, multimodality therapy used with curative intent is toxic. The balance between offering intensive versus tolerable and function-preserving therapy has been thrown into sharp relief with the recently described epidemic of human papillomavirus-associated head and neck squamous cell carcinomas characterized by improved clinical outcomes compared with smoking-associated head and neck tumors. Model systems and clinical trials have been slow to address the clinical questions that face the field to date. With this as a background, a host of translational studies have recently reported the somatic alterations in head and neck cancer and have highlighted the distinct genetic and biologic differences between viral and tobacco-associated tumors. This review seeks to summarize the main findings of studies, including The Cancer Genome Atlas, for the clinician scientist, with a goal of leveraging this new knowledge toward the betterment of patients with head and neck cancer. © 2015 by American Society of Clinical Oncology. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Hayes, D Neil AU - Van Waes, Carter AU - Seiwert, Tanguy Y AD - D. Neil Hayes, The University of North Carolina, Chapel Hill, NC; Carter Van Waes, National Institute on Deafness and Other Communication Disorders, Bethesda, MD; and Tanguy Y. Seiwert, The University of Chicago, Chicago, IL. hayes@med.unc.edu. ; D. Neil Hayes, The University of North Carolina, Chapel Hill, NC; Carter Van Waes, National Institute on Deafness and Other Communication Disorders, Bethesda, MD; and Tanguy Y. Seiwert, The University of Chicago, Chicago, IL. Y1 - 2015/10/10/ PY - 2015 DA - 2015 Oct 10 SP - 3227 EP - 3234 VL - 33 IS - 29 KW - Index Medicus KW - Humans KW - Prognosis KW - Disease Progression KW - Papillomavirus Infections -- epidemiology KW - Carcinoma, Squamous Cell -- etiology KW - Carcinoma, Squamous Cell -- epidemiology KW - Head and Neck Neoplasms -- etiology KW - Papillomavirus Infections -- complications KW - Head and Neck Neoplasms -- virology KW - Carcinoma, Squamous Cell -- genetics KW - Smoking -- adverse effects KW - Papillomavirus Infections -- genetics KW - Head and Neck Neoplasms -- genetics KW - Head and Neck Neoplasms -- epidemiology KW - Carcinoma, Squamous Cell -- virology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1721349692?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Genetic+Landscape+of+Human+Papillomavirus-Associated+Head+and+Neck+Cancer+and+Comparison+to+Tobacco-Related+Tumors.&rft.au=Hayes%2C+D+Neil%3BVan+Waes%2C+Carter%3BSeiwert%2C+Tanguy+Y&rft.aulast=Hayes&rft.aufirst=D&rft.date=2015-10-10&rft.volume=33&rft.issue=29&rft.spage=3227&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=1527-7755&rft_id=info:doi/10.1200%2FJCO.2015.62.1086 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-11 N1 - Date created - 2015-10-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Otolaryngol Head Neck Surg. 2014 Sep;151(3):375-80 [24925311] Cancer Discov. 2013 Jul;3(7):770-81 [23619168] Clin Cancer Res. 2014 Dec 15;20(24):6551-8 [25294908] Cancer Biol Ther. 2014;15(12):1613-21 [25535896] BMC Cancer. 2014;14:968 [25515630] Nature. 2015 Jan 29;517(7536):576-82 [25631445] Lancet Oncol. 2015 Jan;16(1):25-35 [25524798] Clin Cancer Res. 2015 Feb 1;21(3):632-41 [25056374] J Clin Invest. 2015 Feb;125(2):462-8 [25642706] Clin Cancer Res. 2015 Feb 15;21(4):870-81 [25492084] J Clin Oncol. 2015 Mar 10;33(8):836-45 [25667292] Lancet Oncol. 2015 Mar;16(3):257-65 [25704439] Cancer Med. 2015 Apr;4(4):596-607 [25644715] Ann Oncol. 2015 Jun;26(6):1216-23 [25712460] Clin Cancer Res. 2015 Jul 15;21(14):3307-17 [25609060] Cancer Cell. 2004 May;5(5):489-500 [15144956] Cancer Res. 1996 Oct 15;56(20):4620-4 [8840974] Oncogene. 1996 Nov 21;13(10):2243-54 [8950992] Nature. 2006 Jan 12;439(7073):208-11 [16306936] N Engl J Med. 2006 Feb 9;354(6):567-78 [16467544] Oncogene. 2006 Apr 20;25(17):2558-64 [16314836] Nat Rev Genet. 2006 Aug;7(8):606-19 [16847462] Proc Natl Acad Sci U S A. 2007 Mar 27;104(13):5569-74 [17376864] J Clin Oncol. 2007 Jun 1;25(16):2191-7 [17538164] N Engl J Med. 2008 Sep 11;359(11):1116-27 [18784101] Gastroenterology. 2008 Oct;135(4):1358-1368, 1368.e1-4 [18692501] Lancet Oncol. 2010 Jan;11(1):21-8 [19897418] N Engl J Med. 2010 Jul 1;363(1):24-35 [20530316] Sci Signal. 2010;3(130):ra52 [20628156] Nat Rev Genet. 2010 Oct;11(10):685-96 [20847746] Nat Rev Immunol. 2011 Jul;11(7):457-68 [21660053] Science. 2011 Aug 26;333(6046):1157-60 [21798893] Science. 2011 Aug 26;333(6046):1154-7 [21798897] Mod Pathol. 2011 Oct;24(10):1295-305 [21572401] J Cell Biol. 2011 Nov 28;195(5):855-71 [22105346] Cancer J. 2011 Nov-Dec;17(6):451-64 [22157289] Dev Cell. 2012 Mar 13;22(3):669-77 [22364861] J Clin Oncol. 2012 Jun 10;30(17):2102-11 [22565003] Am J Surg Pathol. 2012 Jul;36(7):945-54 [22743284] Nature. 2012 Sep 27;489(7417):519-25 [22960745] Cancer Res. 2012 Oct 1;72(19):5004-13 [22991304] Clin Cancer Res. 2012 Nov 15;18(22):6169-77 [23014527] Nat Genet. 2013 Mar;45(3):253-61 [23354438] Nature. 2013 Jul 4;499(7456):43-9 [23792563] Lancet Oncol. 2013 Jul;14(8):697-710 [23746666] Nat Genet. 2013 Sep;45(9):977-83 [23852168] Nat Genet. 2013 Sep;45(9):970-6 [23852170] J Pathol. 2013 Nov;231(3):311-22 [23868181] Ann Oncol. 2013 Nov;24(11):2711-3 [24170608] Genome Res. 2014 Feb;24(2):185-99 [24201445] Am J Otolaryngol. 2014 Mar-Apr;35(2):147-53 [24209992] Cancer Causes Control. 2014 Apr;25(4):461-71 [24474236] Ann Surg Oncol. 2014 Jul;21(7):2347-52 [24599410] Cell Rep. 2014 Jun 26;7(6):1833-41 [24910434] Nat Genet. 2014 Sep;46(9):939-43 [25086664] PLoS One. 2013;8(2):e56823 [23451093] Virchows Arch. 2013 Apr;462(4):381-9 [23503925] PLoS Pathog. 2013;9(5):e1003384 [23717208] Proc Natl Acad Sci U S A. 2014 Oct 28;111(43):15544-9 [25313082] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1200/JCO.2015.62.1086 ER - TY - JOUR T1 - Scoring the SF-36 in Orthopaedics: A Brief Guide AN - 1811877664; PQ0003422314 AB - Abstract:The Short Form-36 (SF-36) is the most widely used health-related quality-of-life measure in research to date. There are currently two sources for the SF-36 and scoring instructions: licensing them from Optum, Inc., or obtaining them from publicly available documentation from the RAND Corporation. The SF-36 yields eight scale scores and two summary scores. The physical component summary (PCS) and mental component summary (MCS) scores were derived using an orthogonal-factor analytic model that forced the PCS and MCS to be uncorrelated, and it has been shown to contribute to an inflation of the MCS in patients with substantial physical disability. Oblique scoring can reduce this inflation of the MCS in orthopaedic studies. Spreadsheets to score the SF-36, along with a copy of the questionnaire, are provided. JF - Journal of Bone and Joint Surgery (American) AU - Laucis, Nicholas C AU - Hays, Ron D AU - Bhattacharyya, Timothy AD - Clinical and Investigative Orthopedics Surgery Unit, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, 10 Center Drive, Building 10-CRC, Room 4-2339, MSC1498, Bethesda, MD. E-mail address for T. Bhattacharyya:, bhattacharyyat@mail.nih.gov Y1 - 2015/10/07/ PY - 2015 DA - 2015 Oct 07 SP - 1628 EP - 1634 PB - The Journal of Bone and Joint Surgery, Inc., 20 Pickering St. Needham MA 02492-3157 United States VL - 97 IS - 19 SN - 0021-9355, 0021-9355 KW - Physical Education Index KW - Handicapped KW - Teaching KW - Bones KW - Surgery KW - Surveys KW - Patients KW - Joints KW - PE 090:Sports Medicine & Exercise Sport Science UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1811877664?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bone+and+Joint+Surgery+%28American%29&rft.atitle=Scoring+the+SF-36+in+Orthopaedics%3A+A+Brief+Guide&rft.au=Laucis%2C+Nicholas+C%3BHays%2C+Ron+D%3BBhattacharyya%2C+Timothy&rft.aulast=Laucis&rft.aufirst=Nicholas&rft.date=2015-10-07&rft.volume=97&rft.issue=19&rft.spage=1628&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bone+and+Joint+Surgery+%28American%29&rft.issn=00219355&rft_id=info:doi/10.2106%2FJBJS.O.00030 LA - English DB - Physical Education Index N1 - Date revised - 2016-08-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Handicapped; Bones; Teaching; Surgery; Surveys; Patients; Joints DO - http://dx.doi.org/10.2106/JBJS.O.00030 ER - TY - JOUR T1 - Outer membrane protein biogenesis in Gram-negative bacteria AN - 1808617740; PQ0003420844 AB - Gram-negative bacteria contain a double membrane which serves for both protection and for providing nutrients for viability. The outermost of these membranes is called the outer membrane (OM), and it contains a host of fully integrated membrane proteins which serve essential functions for the cell, including nutrient uptake, cell adhesion, cell signalling and waste export. For pathogenic strains, many of these outer membrane proteins (OMPs) also serve as virulence factors for nutrient scavenging and evasion of host defence mechanisms. OMPs are unique membrane proteins in that they have a beta -barrel fold and can range in size from 8 to 26 strands, yet can still serve many different functions for the cell. Despite their essential roles in cell survival and virulence, the exact mechanism for the biogenesis of these OMPs into the OM has remained largely unknown. However, the past decade has witnessed significant progress towards unravelling the pathways and mechanisms necessary for moulding a nascent polypeptide into a functional OMP within the OM. Here, we will review some of these recent discoveries that have advanced our understanding of the biogenesis of OMPs in Gram-negative bacteria, starting with synthesis in the cytoplasm to folding and insertion into the OM. JF - Philosophical Transactions of the Royal Society of London, Series B: Biological Sciences AU - Rollauer, Sarah E AU - Sooreshjani, Moloud A AU - Noinaj, Nicholas AU - Buchanan, Susan K AD - National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, , Bethesda, MD 20892, USA, nnoinaj@purdue.edu Y1 - 2015/10/05/ PY - 2015 DA - 2015 Oct 05 SP - 20150023 PB - Royal Society of London, 6 Carlton House Terrace London SW1Y 5AG United Kingdom VL - 370 IS - 1679 SN - 0962-8436, 0962-8436 KW - Ecology Abstracts KW - beta -barrel membrane protein KW - outer membrane KW - protein folding KW - beta -barrel assembly machinery complex KW - insertase KW - lateral gate KW - Cell survival KW - Bacteria KW - outer membrane proteins KW - virulence factors KW - Wastes KW - Nutrients KW - Membrane proteins KW - Cell adhesion KW - Gram-negative bacteria KW - Reviews KW - Cytoplasm KW - Nutrient uptake KW - Signal transduction KW - D 04040:Ecosystem and Ecology Studies UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808617740?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Philosophical+Transactions+of+the+Royal+Society+of+London%2C+Series+B%3A+Biological+Sciences&rft.atitle=Outer+membrane+protein+biogenesis+in+Gram-negative+bacteria&rft.au=Rollauer%2C+Sarah+E%3BSooreshjani%2C+Moloud+A%3BNoinaj%2C+Nicholas%3BBuchanan%2C+Susan+K&rft.aulast=Rollauer&rft.aufirst=Sarah&rft.date=2015-10-05&rft.volume=370&rft.issue=1679&rft.spage=20150023&rft.isbn=&rft.btitle=&rft.title=Philosophical+Transactions+of+the+Royal+Society+of+London%2C+Series+B%3A+Biological+Sciences&rft.issn=09628436&rft_id=info:doi/10.1098%2Frstb.2015.0023 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Cell survival; outer membrane proteins; virulence factors; Cytoplasm; Reviews; Gram-negative bacteria; Wastes; Nutrients; Membrane proteins; Nutrient uptake; Signal transduction; Cell adhesion; Bacteria DO - http://dx.doi.org/10.1098/rstb.2015.0023 ER - TY - JOUR T1 - Radiation-Induced Alteration of the Brain Proteome: Understanding the Role of the Sirtuin 2 Deacetylase in a Murine Model. AN - 1718906148; 26373435 AB - Whole brain radiotherapy (WBRT) produces unwanted sequelae, albeit via unknown mechanisms. A deacetylase expressed in the central nervous system, Sirtuin 2 (SIRT2), has been linked to neurodegeneration. Therefore, we sought to challenge the notion that a single disease pathway is responsible for radiation-induced brain injury in Sirt2 wild-type (WT) and knockout (KO) mice at the proteomic level. We utilized isobaric tag for relative and absolute quantitation to analyze brain homogenates from Sirt2 WT and KO mice with and without WBRT. Selected proteins were independently verified, followed by ingenuity pathway analysis. Canonical pathways for Huntington's, Parkinson's, and Alzheimer's were acutely affected by radiation within 72 h of treatment. Although loss of Sirt2 preferentially affected both Huntington's and Parkinson's pathways, WBRT most significantly affected Huntington's-related proteins in the absence of Sirt2. Identical protein expression patterns were identified in Mog following WBRT in both Sirt2 WT and KO mice, revealing a proteomic radiation signature; however, long-term radiation effects were found to be associated with altered levels of a small number of key neurodegeneration-related proteins, identified as Mapt, Mog, Snap25, and Dnm1. Together, these data demonstrate the principle that the presence of Sirt2 can have significant effects on the brain proteome and its response to ionizing radiation. JF - Journal of proteome research AU - Shukla, Sudhanshu AU - Shankavaram, Uma T AU - Nguyen, Phuongmai AU - Stanley, Bruce A AU - Smart, DeeDee K AD - Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institute of Health , 10 Center Drive, Bethesda, Maryland 20892, United States. ; Proteomics and Mass Spectrometry Core Facility, Penn State College of Medicine , 500 University Drive, MC: H093, Hershey, Pennsylvania 17033, United States. Y1 - 2015/10/02/ PY - 2015 DA - 2015 Oct 02 SP - 4104 EP - 4117 VL - 14 IS - 10 KW - Mapt protein, mouse KW - 0 KW - Mog protein, mouse KW - Myelin-Oligodendrocyte Glycoprotein KW - Proteome KW - Snap25 protein, mouse KW - Synaptosomal-Associated Protein 25 KW - tau Proteins KW - Sirt2 protein, mouse KW - EC 3.5.1.- KW - Sirtuin 2 KW - Dynamin I KW - EC 3.5.1.50 KW - Index Medicus KW - iTRAQ KW - radiation KW - neurotoxicity KW - neurodegeneration KW - brain KW - SIRT2 KW - Animals KW - tau Proteins -- metabolism KW - Myelin-Oligodendrocyte Glycoprotein -- genetics KW - Brain Chemistry KW - Humans KW - Neurodegenerative Diseases -- pathology KW - Disease Models, Animal KW - Myelin-Oligodendrocyte Glycoprotein -- metabolism KW - Mice KW - Dynamin I -- genetics KW - Mice, Knockout KW - Molecular Sequence Annotation KW - Dynamin I -- metabolism KW - Neurodegenerative Diseases -- genetics KW - Gene Expression Profiling KW - Synaptosomal-Associated Protein 25 -- metabolism KW - Neurodegenerative Diseases -- metabolism KW - tau Proteins -- genetics KW - Synaptosomal-Associated Protein 25 -- genetics KW - Gene Expression Regulation KW - Proteome -- genetics KW - Sirtuin 2 -- deficiency KW - Sirtuin 2 -- genetics KW - Metabolic Networks and Pathways -- radiation effects KW - Gamma Rays KW - Brain -- radiation effects KW - Proteome -- metabolism KW - Brain -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1718906148?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+proteome+research&rft.atitle=Radiation-Induced+Alteration+of+the+Brain+Proteome%3A+Understanding+the+Role+of+the+Sirtuin+2+Deacetylase+in+a+Murine+Model.&rft.au=Shukla%2C+Sudhanshu%3BShankavaram%2C+Uma+T%3BNguyen%2C+Phuongmai%3BStanley%2C+Bruce+A%3BSmart%2C+DeeDee+K&rft.aulast=Shukla&rft.aufirst=Sudhanshu&rft.date=2015-10-02&rft.volume=14&rft.issue=10&rft.spage=4104&rft.isbn=&rft.btitle=&rft.title=Journal+of+proteome+research&rft.issn=1535-3907&rft_id=info:doi/10.1021%2Facs.jproteome.5b00083 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-08 N1 - Date created - 2015-10-02 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/acs.jproteome.5b00083 ER - TY - JOUR T1 - Screening a mouse liver gene expression compendium identifies modulators of the aryl hydrocarbon receptor (AhR). AN - 1711540400; 26215100 AB - The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that mediates the biological and toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), dioxin-like compounds (DLC) as well as some drugs and endogenous tryptophan metabolites. Short-term activation of AhR can lead to hepatocellular steatosis, and chronic activation can lead to liver cancer in mice and rats. Analytical approaches were developed to identify biosets in a genomic database in which AhR activity was altered. A set of 63 genes was identified (the AhR gene expression biomarker) that was dependent on AhR for regulation after exposure to TCDD or benzo[a]pyrene and includes the known AhR targets Cyp1a1 and Cyp1b1. A fold-change rank-based test (Running Fisher's test; p-value ≤ 10(-4)) was used to evaluate the similarity between the AhR biomarker and a test set of 37 and 41 biosets positive or negative, respectively for AhR activation. The test resulted in a balanced accuracy of 95%. The rank-based test was used to identify factors that activate or suppress AhR in an annotated mouse liver/mouse primary hepatocyte gene expression database of ∼ 1850 comparisons. In addition to the expected activation of AhR by TCDD and DLC, AhR was activated by AP20189 and phenformin. AhR was suppressed by phenobarbital and 1,4-Bis[2-(3,5-dichloropyridyloxy)] benzene (TCPOBOP) in a constitutive activated receptor (CAR)-dependent manner and pregnenolone-16α-carbonitrile in a pregnane X receptor (PXR)-dependent manner. Inactivation of individual genes in nullizygous models led to AhR activation (Pxr, Ghrhr, Taf10) or suppression (Ahr, Ilst6st, Hnf1a). This study describes a novel screening strategy for identifying factors in mouse liver that perturb AhR in a gene expression compendium. Published by Elsevier Ireland Ltd. JF - Toxicology AU - Oshida, Keiyu AU - Vasani, Naresh AU - Thomas, Russell S AU - Applegate, Dawn AU - Gonzalez, Frank J AU - Aleksunes, Lauren M AU - Klaassen, Curtis D AU - Corton, J Christopher AD - NHEERL, US-EPA, Research Triangle Park, NC 27711, United States. ; The Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709, United States. ; RegeneMed, San Diego, CA 92121, United States. ; National Cancer Institute, NIH, Bethesda, MD 20892, United States. ; Rutgers University, Piscataway, NJ 08854, United States. ; University of Kansas Medical Center, Kansas City, KS 66160, United States. ; NHEERL, US-EPA, Research Triangle Park, NC 27711, United States. Electronic address: corton.chris@epa.gov. Y1 - 2015/10/02/ PY - 2015 DA - 2015 Oct 02 SP - 99 EP - 112 VL - 336 KW - Genetic Markers KW - 0 KW - Receptors, Aryl Hydrocarbon KW - Index Medicus KW - Peroxisome proliferator-activated receptor KW - Liver cancer KW - Aryl hydrocarbon receptor KW - Keap1 KW - Nrf2 KW - Transcript profiling KW - Pregnane X receptor KW - Constitutive activated receptor KW - Real-Time Polymerase Chain Reaction KW - Protein Array Analysis KW - Animals KW - High-Throughput Screening Assays -- methods KW - Enzyme Activation -- drug effects KW - Mice KW - Mice, Inbred BALB C KW - Male KW - Mice, Knockout KW - Enzyme Activation -- genetics KW - Receptors, Aryl Hydrocarbon -- drug effects KW - Gene Expression -- drug effects KW - Liver -- metabolism KW - Receptors, Aryl Hydrocarbon -- metabolism KW - Receptors, Aryl Hydrocarbon -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1711540400?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology&rft.atitle=Screening+a+mouse+liver+gene+expression+compendium+identifies+modulators+of+the+aryl+hydrocarbon+receptor+%28AhR%29.&rft.au=Oshida%2C+Keiyu%3BVasani%2C+Naresh%3BThomas%2C+Russell+S%3BApplegate%2C+Dawn%3BGonzalez%2C+Frank+J%3BAleksunes%2C+Lauren+M%3BKlaassen%2C+Curtis+D%3BCorton%2C+J+Christopher&rft.aulast=Oshida&rft.aufirst=Keiyu&rft.date=2015-10-02&rft.volume=336&rft.issue=&rft.spage=99&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=1879-3185&rft_id=info:doi/10.1016%2Fj.tox.2015.07.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-15 N1 - Date created - 2015-09-12 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - GSE55756; GEO; GSE55084; GSE55746 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.tox.2015.07.005 ER - TY - JOUR T1 - Novel cystathionine beta -synthase gene mutations in a Filipino patient with classic homocystinuria AN - 1815696216; PQ0002246083 AB - Abstract Background Classic homocystinuria due to cystathionine beta -synthase (CBS) deficiency is an autosomal recessive disorder of sulfur metabolism. Clinical manifestations include mental retardation, dislocation of the optic lens (ectopia lentis), skeletal abnormalities and a tendency to thromboembolic episodes. We present the first mutational analysis of CBS in a Filipino patient with classic homocystinuria. Methods Genomic DNA was extracted from peripheral blood collected from a diagnosed Filipino patient with classic homocystinuria. The entire coding region of CBS (17 exons) was amplified using polymerase chain reaction and bidirectionally sequenced using standard protocols. Results The patient was found to be compound heterozygous for two novel mutations, g.13995G>A [c.982G>A; p.D328K] and g.15860-15868dupGCAGGAGCT [c.1083-1091dupGCAGGAGCT; p. Q362-L364dupQEL]. Four known single-nucleotide polymorphisms (rs234706, rs1801181, rs706208 and rs706209) were also detected in the present patient's CBS. The patient was heterozygous for all the identified alleles. Conclusions This is the first mutational analysis of CBS done in a Filipino patient with classic homocystinuria who presented with a novel duplication mutation and a novel missense mutation. Homocystinuria due to CBS deficiency is a heterogeneous disorder at the molecular level. JF - Pediatrics International AU - Silao, Catherine Lynn T AU - Fabella, Terence Diane F AU - Rama, Kahlil Izza D AU - Estrada, Sylvia C AD - Institute of Human Genetics, National Institutes of Health Philippines. Y1 - 2015/10// PY - 2015 DA - October 2015 SP - 884 EP - 887 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 57 IS - 5 SN - 1328-8067, 1328-8067 KW - Toxicology Abstracts KW - Sulfur KW - Optics KW - Missense mutation KW - Hereditary diseases KW - Exons KW - Cystathionine beta -synthase KW - Point mutation KW - Homocystinuria KW - Peripheral blood KW - Thromboembolism KW - Dislocation KW - Single-nucleotide polymorphism KW - Polymerase chain reaction KW - Mental retardation KW - genomics KW - Metabolism KW - X 24310:Pharmaceuticals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1815696216?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pediatrics+International&rft.atitle=Novel+cystathionine+beta+-synthase+gene+mutations+in+a+Filipino+patient+with+classic+homocystinuria&rft.au=Silao%2C+Catherine+Lynn+T%3BFabella%2C+Terence+Diane+F%3BRama%2C+Kahlil+Izza+D%3BEstrada%2C+Sylvia+C&rft.aulast=Silao&rft.aufirst=Catherine+Lynn&rft.date=2015-10-01&rft.volume=57&rft.issue=5&rft.spage=884&rft.isbn=&rft.btitle=&rft.title=Pediatrics+International&rft.issn=13288067&rft_id=info:doi/10.1111%2Fped.12666 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-08-01 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Sulfur; Optics; Missense mutation; Hereditary diseases; Exons; Cystathionine beta -synthase; Point mutation; Homocystinuria; Peripheral blood; Thromboembolism; Dislocation; Single-nucleotide polymorphism; Polymerase chain reaction; genomics; Mental retardation; Metabolism DO - http://dx.doi.org/10.1111/ped.12666 ER - TY - JOUR T1 - Targeting of HPV-16+ Epithelial Cancer Cells by TCR Gene Engineered T Cells Directed against E6 AN - 1808641885; PQ0003441518 AB - Purpose: The E6 and E7 oncoproteins of HPV-associated epithelial cancers are in principle ideal immunotherapeutic targets, but evidence that T cells specific for these antigens can recognize and kill HPV+ tumor cells is limited. We sought to determine whether TCR gene engineered T cells directed against an HPV oncoprotein can successfully target HPV+ tumor cells.Experimental Design: T-cell responses against the HPV-16 oncoproteins were investigated in a patient with an ongoing 22-month disease-free interval after her second resection of distant metastatic anal cancer. T cells genetically engineered to express an oncoprotein-specific TCR from this patient's tumor-infiltrating T cells were tested for specific reactivity against HPV+ epithelial tumor cells.Results: We identified, from an excised metastatic anal cancer tumor, T cells that recognized an HLA-A*02:01-restricted epitope of HPV-16 E6. The frequency of the dominant T-cell clonotype from these cells was approximately 400-fold greater in the patient's tumor than in her peripheral blood. T cells genetically engineered to express the TCR from this clonotype displayed high avidity for an HLA-A*02:01-restricted epitope of HPV-16, and they showed specific recognition and killing of HPV-16+ cervical, and head and neck cancer cell lines.Conclusions: These findings demonstrate that HPV-16+ tumors can be targeted by E6-specific TCR gene engineered T cells, and they provide the foundation for a novel cellular therapy directed against HPV-16+ malignancies, including cervical, oropharyngeal, anal, vulvar, vaginal, and penile cancers. Clin Cancer Res; 21(19); 4431-9. copyright 2015 AACR. JF - Clinical Cancer Research AU - Draper, Lindsey M AU - Kwong, Mei Li M AU - Gros, Alena AU - Stevanovic, Sanja AU - Tran, Eric AU - Kerkar, Sid AU - Raffeld, Mark AU - Rosenberg, Steven A AU - Hinrichs, Christian S AD - Surgery Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, Hinrichs@nih.gov Y1 - 2015/10/01/ PY - 2015 DA - 2015 Oct 01 SP - 4431 EP - 4439 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 19 SN - 1078-0432, 1078-0432 KW - Virology & AIDS Abstracts; Immunology Abstracts; Biotechnology and Bioengineering Abstracts KW - Histocompatibility antigen HLA KW - T-cell receptor KW - Peripheral blood KW - Penis KW - Tumor cells KW - Cancer KW - Metastases KW - Malignancy KW - Avidity KW - Genetic engineering KW - Vagina KW - Lymphocytes T KW - Head and neck cancer KW - Cervix KW - Epitopes KW - Human papillomavirus KW - V 22350:Immunology KW - W 30945:Fermentation & Cell Culture UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808641885?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Cancer+Research&rft.atitle=Targeting+of+HPV-16%2B+Epithelial+Cancer+Cells+by+TCR+Gene+Engineered+T+Cells+Directed+against+E6&rft.au=Draper%2C+Lindsey+M%3BKwong%2C+Mei+Li+M%3BGros%2C+Alena%3BStevanovic%2C+Sanja%3BTran%2C+Eric%3BKerkar%2C+Sid%3BRaffeld%2C+Mark%3BRosenberg%2C+Steven+A%3BHinrichs%2C+Christian+S&rft.aulast=Draper&rft.aufirst=Lindsey&rft.date=2015-10-01&rft.volume=21&rft.issue=19&rft.spage=4431&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-3341 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-11-09 N1 - SubjectsTermNotLitGenreText - Histocompatibility antigen HLA; T-cell receptor; Peripheral blood; Tumor cells; Penis; Cancer; Metastases; Malignancy; Avidity; Genetic engineering; Vagina; Lymphocytes T; Head and neck cancer; Cervix; Epitopes; Human papillomavirus DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-3341 ER - TY - JOUR T1 - An Improved Reverse Genetics System to Overcome Cell-Type-Dependent Ebola Virus Genome Plasticity AN - 1780501123; PQ0002879690 AB - Reverse genetics systems represent a key technique for studying replication and pathogenesis of viruses, including Ebola virus (EBOV). During the rescue of recombinant EBOV from Vero cells, a high frequency of mutations was observed throughout the genomes of rescued viruses, including at the RNA editing site of the glycoprotein gene. The influence that such genomic instability could have on downstream uses of rescued virus may be detrimental, and we therefore sought to improve the rescue system. Here we report an improved EBOV rescue system with higher efficiency and genome stability, using a modified full-length EBOV clone in Huh7 cells. Moreover, by evaluating a variety of cells lines, we revealed that EBOV genome instability is cell-type dependent, a fact that has significant implications for the preparation of standard virus stocks. Thus, our improved rescue system will have an impact on both basic and translational research in the filovirus field. JF - Journal of Infectious Diseases AU - Tsuda, Yoshimi AU - Hoenen, Thomas AU - Banadyga, Logan AU - Weisend, Carla AU - Ricklefs, Stacy M AU - Porcella, Stephen F AU - Ebihara, Hideki AD - Molecular Virology and Host-Pathogen Interaction Unit, ebiharah@niaid.nih.gov Y1 - 2015/10/01/ PY - 2015 DA - 2015 Oct 01 SP - S129 EP - S137 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 212 SN - 0022-1899, 0022-1899 KW - Virology & AIDS Abstracts; Health & Safety Science Abstracts KW - Ebola virus KW - reverse genetics system KW - mutation KW - RNA editing site KW - Genomes KW - Translation KW - Vero cells KW - Replication KW - Viruses KW - Genetics KW - Genomic instability KW - Infectious diseases KW - Filovirus KW - Emergency preparedness KW - RNA editing KW - Downstream KW - Glycoproteins KW - Mutation KW - Search and rescue KW - V 22320:Replication KW - H 0500:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780501123?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=An+Improved+Reverse+Genetics+System+to+Overcome+Cell-Type-Dependent+Ebola+Virus+Genome+Plasticity&rft.au=Tsuda%2C+Yoshimi%3BHoenen%2C+Thomas%3BBanadyga%2C+Logan%3BWeisend%2C+Carla%3BRicklefs%2C+Stacy+M%3BPorcella%2C+Stephen+F%3BEbihara%2C+Hideki&rft.aulast=Tsuda&rft.aufirst=Yoshimi&rft.date=2015-10-01&rft.volume=212&rft.issue=&rft.spage=S129&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiu681 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Genomes; Translation; Genomic instability; Vero cells; Replication; RNA editing; Glycoproteins; Mutation; Genetics; Infectious diseases; Emergency preparedness; Viruses; Downstream; Search and rescue; Filovirus; Ebola virus DO - http://dx.doi.org/10.1093/infdis/jiu681 ER - TY - JOUR T1 - State-of-the-Art Workshops on Medical Countermeasures Potentially Available for Human Use Following Accidental Exposures to Ebola Virus AN - 1780500942; PQ0002879685 AB - The ongoing outbreak of Ebola in West Africa has raised a general awareness that at present there are no Ebola-specific medical countermeasures (MCMs) with proven effectiveness. This paper recapitulates discussions held at the 6th International Filovirus Symposium in March 2014 as well as the subsequent design of a randomized clinical trial design for treating Ebola virus-infected patients evacuated from West Africa to the United States. A number of different drugs or biologics were critically reviewed and 3 different postexposure strategies were identified as being farthest along in development; passive immunotherapy with monoclonal antibodies, postexposure vaccination with constructs involving viral vectors (such as vesicular stomatitis virus), and antisense compounds directly targeting the viral genome such as modified phosphorodiamidate morpholino oligomer-based compounds and small interfering RNA products. At the time of the meetings, there were no investigational new drugs (INDs) in place for the candidate MCMs. Developers and sponsors of these candidate products were strongly encouraged to prepare pre-IND packets and submit pre-IND meeting requests to the Food and Drug Administration. Some of these investigational products have already been used under emergency authorizations to treat patients in Africa as well as patients evacuated to the United States or Western Europe. JF - Journal of Infectious Diseases AU - Jahrling, Peter B AU - Hensley, Lisa E AU - Barrett, Kevin AU - Lane, Henry Clifford AU - Davey, Richard T AD - Integrated Research Facility, jahrlingp@niaid.nih.gov Y1 - 2015/10/01/ PY - 2015 DA - 2015 Oct 01 SP - S84 EP - S90 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 212 SN - 0022-1899, 0022-1899 KW - Virology & AIDS Abstracts; Health & Safety Science Abstracts KW - antisense KW - Ebola virus KW - medical countermeasures KW - monoclonal antibody KW - randomized clinical trial KW - siRNA KW - Genomes KW - Immunotherapy KW - Viruses KW - Clinical trials KW - Antisense KW - Infectious diseases KW - ANE, Europe KW - Filovirus KW - Drugs KW - Vesicular stomatitis virus KW - Conferences KW - Monoclonal antibodies KW - Drug development KW - Food contamination KW - Vaccination KW - USA KW - Reviews KW - Africa KW - Vaccines KW - Outbreaks KW - V 22420:Plant Diseases KW - H 4000:Food and Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780500942?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=State-of-the-Art+Workshops+on+Medical+Countermeasures+Potentially+Available+for+Human+Use+Following+Accidental+Exposures+to+Ebola+Virus&rft.au=Jahrling%2C+Peter+B%3BHensley%2C+Lisa+E%3BBarrett%2C+Kevin%3BLane%2C+Henry+Clifford%3BDavey%2C+Richard+T&rft.aulast=Jahrling&rft.aufirst=Peter&rft.date=2015-10-01&rft.volume=212&rft.issue=&rft.spage=S84&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiv115 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Genomes; Antisense; siRNA; Conferences; Monoclonal antibodies; Immunotherapy; Drug development; Vaccination; Clinical trials; Infectious diseases; Reviews; Viruses; Outbreaks; Vaccines; Food contamination; Drugs; Filovirus; Ebola virus; Vesicular stomatitis virus; USA; ANE, Europe; Africa DO - http://dx.doi.org/10.1093/infdis/jiv115 ER - TY - JOUR T1 - Stat1-Deficient Mice Are Not an Appropriate Model for Efficacy Testing of Recombinant Vesicular Stomatitis Virus-Based Filovirus Vaccines AN - 1780500160; PQ0002879726 AB - Stat1-/- mice lack a response to interferon alpha , beta , and gamma , allowing for replication of nonadapted wild-type (wt) Ebolavirus and Marburgvirus. We sought to establish a mouse model for efficacy testing of live attenuated recombinant vesicular stomatitis virus (rVSV)-based filovirus vaccine vectors using wt Ebolavirus and Marburgvirus challenge strains. While infection of immunocompetent mice with different rVSV-based filovirus vectors did not cause disease, infection of Stat1-/- mice with the same vectors resulted in systemic infection and lethal outcome for the majority of tested rVSVs. Despite differences in viral loads, organ tropism was remarkably similar between rVSV filovirus vaccine vectors and rVSVwt, with the exception of the brain. In conclusion, Stat1-/- mice are not an appropriate immunocompromised mouse model for efficacy testing of live attenuated, replication-competent rVSV vaccine vectors. JF - Journal of Infectious Diseases AU - Marzi, Andrea AU - Kercher, Lisa AU - Marceau, Joshua AU - York, Anthony AU - Callsion, Julie AU - Gardner, Donald J AU - Geisbert, Thomas W AU - Feldmann, Heinz AD - Laboratory of Virology, marzia@niaid.nih.gov Y1 - 2015/10/01/ PY - 2015 DA - 2015 Oct 01 SP - S404 EP - S409 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 212 SN - 0022-1899, 0022-1899 KW - Immunology Abstracts; Virology & AIDS Abstracts; Health & Safety Science Abstracts KW - Vesicular stomatitis virus KW - Ebolavirus KW - Marburgvirus KW - vaccine KW - Stat1-deficient mice KW - beta -Interferon KW - Replication KW - Tropism KW - Disseminated infection KW - Animal models KW - Brain KW - Mice KW - Infection KW - Organs KW - Vesicular stomatitis KW - Infectious diseases KW - Filovirus KW - alpha -Interferon KW - Vaccines KW - V 22320:Replication KW - H 4000:Food and Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780500160?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Stat1-Deficient+Mice+Are+Not+an+Appropriate+Model+for+Efficacy+Testing+of+Recombinant+Vesicular+Stomatitis+Virus-Based+Filovirus+Vaccines&rft.au=Marzi%2C+Andrea%3BKercher%2C+Lisa%3BMarceau%2C+Joshua%3BYork%2C+Anthony%3BCallsion%2C+Julie%3BGardner%2C+Donald+J%3BGeisbert%2C+Thomas+W%3BFeldmann%2C+Heinz&rft.aulast=Marzi&rft.aufirst=Andrea&rft.date=2015-10-01&rft.volume=212&rft.issue=&rft.spage=S404&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiv188 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - beta -Interferon; Vesicular stomatitis; Replication; Disseminated infection; alpha -Interferon; Tropism; Brain; Animal models; Vaccines; Infectious diseases; Mice; Infection; Organs; Filovirus; Vesicular stomatitis virus DO - http://dx.doi.org/10.1093/infdis/jiv188 ER - TY - JOUR T1 - Natural Immunity to Ebola Virus in the Syrian Hamster Requires Antibody Responses AN - 1780498716; PQ0002879708 AB - Most ebolaviruses can cause severe disease in humans and other primates, with high case fatality rates during human outbreaks. Although these viruses have been studied for almost 4 decades, little is know regarding the mechanisms by which they cause disease and what is important for protection or treatment after infection. Because of the sporadic nature of the outbreaks and difficulties accessing the populations affected by ebolaviruses, little is also known about what constitutes an appropriate immune response to infection in humans that survive infection. Such knowledge would allow a targeted approach to therapies. In contrast to humans, rodents are protected from disease on infection with ebolaviruses, although adapted versions of some of the viruses are lethal in mice, hamsters and guinea pigs. Using the recently described hamster model, along with T-cell depletion strategies, we show that CD4+ T cells are required for natural immunity to Ebola virus infection and that CD4-dependent antibody responses are required for immunity in this model. JF - Journal of Infectious Diseases AU - Prescott, Joseph AU - Falzarano, Darryl AU - Feldmann, Heinz AD - Laboratory of Virology, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, feldmannh@niaid.nih.gov Y1 - 2015/10/01/ PY - 2015 DA - 2015 Oct 01 SP - S271 EP - S276 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 212 SN - 0022-1899, 0022-1899 KW - Immunology Abstracts; Virology & AIDS Abstracts; Health & Safety Science Abstracts KW - Ebola virus KW - immune response KW - antibody T cell KW - Mortality KW - Viruses KW - Animal models KW - Mice KW - Immunity KW - Infection KW - Primates KW - Antibodies KW - CD4 antigen KW - Infectious diseases KW - Lymphocytes T KW - Outbreaks KW - Immune response KW - Rodents KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - V 22350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780498716?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Natural+Immunity+to+Ebola+Virus+in+the+Syrian+Hamster+Requires+Antibody+Responses&rft.au=Prescott%2C+Joseph%3BFalzarano%2C+Darryl%3BFeldmann%2C+Heinz&rft.aulast=Prescott&rft.aufirst=Joseph&rft.date=2015-10-01&rft.volume=212&rft.issue=&rft.spage=S271&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiv203 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - CD4 antigen; Antibodies; Lymphocytes T; Animal models; Immunity; Immune response; Infection; Mortality; Infectious diseases; Viruses; Mice; Outbreaks; Primates; Rodents; Ebola virus DO - http://dx.doi.org/10.1093/infdis/jiv203 ER - TY - JOUR T1 - Soluble Glycoprotein Is Not Required for Ebola Virus Virulence in Guinea Pigs AN - 1780498354; PQ0002879705 AB - Ebola virus (EBOV) uses transcriptional editing to express several glycoproteins (GPs), including secreted soluble GP (sGP) and structural GP1,2, from a single gene. Recombinant viruses predominantly expressing GP1,2 are known to rapidly mutate and acquire an editing site predominantly expressing sGP in vivo, suggesting an important role of this protein during infection. Therefore, we generated a recombinant virus that is no longer able to express sGP and assessed its virulence in the EBOV guinea pig model. Surprisingly, although this virus remained genetically stable, it did not show any significant attenuation in vivo, showing that sGP is not required for virulence in this model. JF - Journal of Infectious Diseases AU - Hoenen, Thomas AU - Marzi, Andrea AU - Scott, Dana P AU - Feldmann, Friederike AU - Callison, Julie AU - Safronetz, David AU - Ebihara, Hideki AU - Feldmann, Heinz AD - Laboratory of Virology, thomas.hoenen@nih.gov Y1 - 2015/10/01/ PY - 2015 DA - 2015 Oct 01 SP - S242 EP - S246 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 212 SN - 0022-1899, 0022-1899 KW - Virology & AIDS Abstracts; Health & Safety Science Abstracts KW - ebola virus KW - soluble glycoprotein KW - sGP KW - virulence KW - guinea pigs KW - recombinant virus KW - reverse genetics KW - mRNA editing KW - Viruses KW - Animal models KW - Transcription KW - Ebola virus KW - Infection KW - Models KW - Virulence KW - Infectious diseases KW - Proteins KW - Glycoproteins KW - V 22410:Animal Diseases KW - H 0500:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780498354?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Soluble+Glycoprotein+Is+Not+Required+for+Ebola+Virus+Virulence+in+Guinea+Pigs&rft.au=Hoenen%2C+Thomas%3BMarzi%2C+Andrea%3BScott%2C+Dana+P%3BFeldmann%2C+Friederike%3BCallison%2C+Julie%3BSafronetz%2C+David%3BEbihara%2C+Hideki%3BFeldmann%2C+Heinz&rft.aulast=Hoenen&rft.aufirst=Thomas&rft.date=2015-10-01&rft.volume=212&rft.issue=&rft.spage=S242&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiv111 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Virulence; Animal models; Transcription; Glycoproteins; Infection; Models; Infectious diseases; Viruses; Proteins; Ebola virus DO - http://dx.doi.org/10.1093/infdis/jiv111 ER - TY - JOUR T1 - Significant increase in detection of prostate cancer recurrence following radical prostatectomy with an early imaging acquisition protocol with super(18)F-fluorocholine positron emission tomography/computed tomography AN - 1768588917; PQ0002078661 AB - Purpose: To highlight a new imaging acquisition protocol during super(18)F-fluorocholine PET/CT in patients with biochemical recurrence after RP. Methods: A total of 146 patients with PSA levels between 0.2 and 1 ng/ml with negative conventional imaging who did not receive salvage treatment were prospectively enrolled. Imaging acquisition protocol included an early dynamic phase (1-8 min), a conventional whole body (10-20 min), and a late phase (30-40 min). Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were measured. Univariable and multivariable analyses were performed to identify independent predictors of positive PET/CT. Results: The median trigger PSA was 0.6 ng/ml (IQR 0.43-0.76). Median PSA doubling time (PSA DT) was 7.91 months (IQR 4.42-11.3); median PSA velocity (PSAV) was 0.02 ng/ml per month (IQR 0.02-0.04). Overall, super(18)F-fluorocholine PET/CT was positive in 111 of 146 patients (76 %). Out of 111 positive examinations, 80 (72.1 %) were positive only in the early dynamic phase. Sensitivity, specificity, PPV, NPV, and accuracy were 78.9, 76.9, 97.2, 26.3, and 78.7 %, respectively. At multivariable logistic regression, trigger PSA greater than or equal to 0.6 ng/ml [odds ratio (OR) 3.13; p = 0.001] and PSAV greater than or equal to 0.04 ng/ml per month (OR 4.95; p = 0.004) were independent predictors of positive PET/CT. The low NPV remains the main limitation of PET/CT in this setting of patients. Conclusions: The increased sensitivity, thanks to the early imaging acquisition protocol, makes super(18)F-fluorocholine PET/CT an attractive tool to detect prostate cancer recurrences in patients with a PSA level <1 ng/ml. JF - World Journal of Urology AU - Simone, Giuseppe AU - Pierro, Giovanni Battista AU - Papalia, Rocco AU - Sciuto, Rosa AU - Rea, Sandra AU - Ferriero, Mariaconsiglia AU - Guaglianone, Salvatore AU - Maini, Carlo Ludovico AU - Gallucci, Michele AD - Department of Urology, "Regina Elena" National Cancer Institute, Via Elio Chianesi 53, 00144, Rome, Italy, puldet@gmail.com Y1 - 2015/10// PY - 2015 DA - October 2015 SP - 1511 EP - 1518 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 33 IS - 10 SN - 0724-4983, 0724-4983 KW - Biotechnology and Bioengineering Abstracts KW - Prostate cancer KW - Computed tomography KW - Positron emission tomography KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768588917?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=World+Journal+of+Urology&rft.atitle=Significant+increase+in+detection+of+prostate+cancer+recurrence+following+radical+prostatectomy+with+an+early+imaging+acquisition+protocol+with+super%2818%29F-fluorocholine+positron+emission+tomography%2Fcomputed+tomography&rft.au=Simone%2C+Giuseppe%3BPierro%2C+Giovanni+Battista%3BPapalia%2C+Rocco%3BSciuto%2C+Rosa%3BRea%2C+Sandra%3BFerriero%2C+Mariaconsiglia%3BGuaglianone%2C+Salvatore%3BMaini%2C+Carlo+Ludovico%3BGallucci%2C+Michele&rft.aulast=Simone&rft.aufirst=Giuseppe&rft.date=2015-10-01&rft.volume=33&rft.issue=10&rft.spage=1511&rft.isbn=&rft.btitle=&rft.title=World+Journal+of+Urology&rft.issn=07244983&rft_id=info:doi/10.1007%2Fs00345-015-1481-z LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Number of references - 21 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Prostate cancer; Computed tomography; Positron emission tomography DO - http://dx.doi.org/10.1007/s00345-015-1481-z ER - TY - JOUR T1 - Pioglitazone for Hepatic Steatosis in HIV/Hepatitis C Virus Coinfection AN - 1768582639; PQ0002687205 AB - Chronic hepatitis C infection frequently coexists with human immunodeficiency virus (HIV) and together are associated with increased hepatic steatosis. Steatosis is a risk factor for progression of liver disease and may persist despite a sustained virologic response to hepatitis C treatment. Therefore, therapies to target hepatic steatosis are important for individuals with HIV and hepatitis C virus (HCV) coinfection. We completed a 48-week, randomized, double-blind, placebo-controlled trial of pioglitazone (45mg/day) in 13 subjects with HIV/HCV coinfection. The primary outcome variable was hepatic fat content, measured by magnetic resonance spectroscopy (MRS) imaging. Individuals randomized to pioglitazone had a significant decrease in hepatic fat content measured by MRS from baseline (15.1 plus or minus 7.0%) to week 48 (7.6 plus or minus 3.9%), with a mean difference of -7.4% (p=0.02, n=5). There was no significant change in hepatic fat content with placebo. Glycemic control as measured by oral glucose challenge improved significantly with pioglitazone (p=0.047). Though not statistically significant, there were trends toward improved alanine aminotransferase (ALT) and histopathologic grade of steatosis in subjects who received pioglitazone. Pioglitazone was well tolerated and no one discontinued due to side effects. This study demonstrates that 48 weeks of pioglitazone therapy, and not placebo, results in significant reductions in hepatic fat content as measured by MRS in subjects with HIV and HCV coinfection and hepatic steatosis. This small study shows that pioglitazone helps ameliorate steatosis in the context of HIV/HCV coinfection. JF - AIDS Research and Human Retroviruses AU - Matthews, Lindsay AU - Kleiner, David E AU - Chairez, Cheryl AU - McManus, Maryellen AU - Nettles, Mary Jane AU - Zemanick, Kira AU - Morse, Caryn Gee AU - Benator, Debra AU - Kovacs, Joseph A AU - Hadigan, Colleen AD - Critical Care Medicine Department, NIH Clinical Center, National Institutes of Health, Bethesda, Maryland. Y1 - 2015/10// PY - 2015 DA - October 2015 SP - 961 EP - 966 PB - Mary Ann Liebert, Inc., 140 Huguenot Street New Rochelle NY 10801 United States VL - 31 IS - 10 SN - 0889-2229, 0889-2229 KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Acquired immune deficiency syndrome KW - Statistical analysis KW - Glucose KW - Spectroscopy KW - Infection KW - Clinical trials KW - pioglitazone KW - Retrovirus KW - Risk factors KW - Magnetic resonance spectroscopy KW - Hepatitis C KW - Liver diseases KW - steatosis KW - Alanine transaminase KW - imaging KW - Hepatitis C virus KW - Human immunodeficiency virus KW - Chronic infection KW - Liver KW - Fatty liver KW - Side effects KW - V 22360:AIDS and HIV KW - H 4000:Food and Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1768582639?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS+Research+and+Human+Retroviruses&rft.atitle=Pioglitazone+for+Hepatic+Steatosis+in+HIV%2FHepatitis+C+Virus+Coinfection&rft.au=Matthews%2C+Lindsay%3BKleiner%2C+David+E%3BChairez%2C+Cheryl%3BMcManus%2C+Maryellen%3BNettles%2C+Mary+Jane%3BZemanick%2C+Kira%3BMorse%2C+Caryn+Gee%3BBenator%2C+Debra%3BKovacs%2C+Joseph+A%3BHadigan%2C+Colleen&rft.aulast=Matthews&rft.aufirst=Lindsay&rft.date=2015-10-01&rft.volume=31&rft.issue=10&rft.spage=961&rft.isbn=&rft.btitle=&rft.title=AIDS+Research+and+Human+Retroviruses&rft.issn=08892229&rft_id=info:doi/10.1089%2Faid.2015.0093 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Number of references - 27 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Liver diseases; steatosis; Glucose; Statistical analysis; Alanine transaminase; imaging; pioglitazone; Magnetic resonance spectroscopy; Risk factors; Chronic infection; Fatty liver; Hepatitis C; Side effects; Acquired immune deficiency syndrome; Human immunodeficiency virus; Liver; Infection; Spectroscopy; Clinical trials; Retrovirus; Hepatitis C virus DO - http://dx.doi.org/10.1089/aid.2015.0093 ER - TY - JOUR T1 - Primary HIV infection presenting as limbic encephalitis and rhabdomyolysis AN - 1765977211; PQ0002583936 AB - Recognising the initial clinical presentation of acute HIV infection could enable earlier initiation of antiretroviral therapy and appropriate counselling to reduce the risk of transmission to others. Herein, we describe an unusual case of acute HIV infection presenting as limbic encephalitis and rhabdomyolysis. JF - International Journal of STD & AIDS AU - Ferrada, Marcela A AU - Xie, Yingda AU - Nuermberger, Eric AD - 1 .Division of Infectious Diseases, The Johns Hopkins University School of Medicine, Baltimore, MD, USA, marcela.ferrada@nih.gov Y1 - 2015/10// PY - 2015 DA - October 2015 SP - 835 EP - 836 PB - Sage Publications, Inc., 2455 Teller Road Thousand Oaks CA 91320 United States VL - 26 IS - 11 SN - 0956-4624, 0956-4624 KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - HIV KW - AIDS KW - epidemiology KW - primary HIV infection KW - limbic encephalitis KW - rhabdomyolysis KW - seroconversion KW - North America KW - Acquired immune deficiency syndrome KW - Rhabdomyolysis KW - Human immunodeficiency virus KW - antiretroviral therapy KW - Risk reduction KW - Infection KW - Antiretroviral agents KW - Sexually transmitted diseases KW - Encephalitis KW - V 22360:AIDS and HIV KW - H 11000:Diseases/Injuries/Trauma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1765977211?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+STD+%26+AIDS&rft.atitle=Primary+HIV+infection+presenting+as+limbic+encephalitis+and+rhabdomyolysis&rft.au=Ferrada%2C+Marcela+A%3BXie%2C+Yingda%3BNuermberger%2C+Eric&rft.aulast=Ferrada&rft.aufirst=Marcela&rft.date=2015-10-01&rft.volume=26&rft.issue=11&rft.spage=835&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+STD+%26+AIDS&rft.issn=09564624&rft_id=info:doi/10.1177%2F0956462414560777 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-02-01 N1 - Number of references - 8 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Rhabdomyolysis; antiretroviral therapy; Infection; Encephalitis; Acquired immune deficiency syndrome; Human immunodeficiency virus; Risk reduction; Antiretroviral agents; Sexually transmitted diseases DO - http://dx.doi.org/10.1177/0956462414560777 ER - TY - JOUR T1 - Oral prenylation inhibition with lonafarnib in chronic hepatitis D infection: a proof-of-concept randomised, double-blind, placebo-controlled phase 2A trial AN - 1746880828; PQ0002171989 AB - Background Therapies for chronic hepatitis delta virus (HDV) infection are unsatisfactory. Prenylation is essential for HDV and inhibition abrogates HDV production in experimental models. In a proof-of-concept study, we aimed to assess the effect on HDV RNA levels, safety, and tolerability of the prenylation inhibitor lonafarnib in patients with chronic delta hepatitis. Methods In this phase 2A double-blind, randomised, placebo-controlled study, patients aged 18 years or older with chronic HDV infection were randomly assigned (3:1 in group 1 and 2:1 in group 2) to receive lonafarnib 100 mg (group 1) or lonafarnib 200 mg (group 2) twice daily for 28 days with 6 months' follow-up. Participants were randomised by random-number tables blocked in groups of four without stratification. Both groups enrolled six treatment participants and two placebo participants. Group 1 placebo patients received open-label lonafarnib as group 2 participants. The primary therapeutic endpoint was a decrease in HDV RNA viral titre in serum and the primary safety endpoint was the ability to tolerate the drug at the prescribed dose for the full 4-week duration, defined as drug discontinuation due to intolerance or grade 3/4 adverse events. This trial is registered with ClinicalTrials.gov, number NCT01495585. Findings Between Jan 19, 2012, and April 28, 2014, 14 patients were enrolled, of whom eight were assigned to group 1 and six were assigned to group 2. At day 28, compared with placebo, mean log HDV RNA declines from baseline were -0.73 log IU/mL in group 1 (95% CI 0.17-1.31; p=0.03) and -1.54 log IU/mL in group 2 (1.21-1.93; p<0.0001). Lonafarnib serum concentrations correlated with HDV RNA change (r2=0.78, p<0.0001). Model fits show that hepatitis B surface antigen (HBsAg) remained stable after a short pharmacological delay (0.75 days [SE 0.24]), lonafarnib effectiveness in blocking HDV production was greater in group 2 than in group 1 (0.952 [SE 0.06] vs 0.739 [0.05], p<0.001), and the HDV half-life was 1.62 days (0.07). There was no evidence of virological resistance. Adverse events were mainly mild to moderate with group 1 patients experiencing diarrhoea in three patients (50%) and nausea in two patients (33%) and in group 2 with all patients (100%) experiencing nausea, diarrhoea, abdominal bloating, and weight loss greater than 2 kg (mean of 4 kg). No treatment discontinuations occurred in any treatment groups. Interpretation Treatment of chronic HDV with lonafarnib significantly reduces virus levels. The decline in virus levels significantly correlated with serum drug levels, providing further evidence for the efficacy of prenylation inhibition in chronic HDV. Funding National Institute of Diabetes and Digestive and Kidney Diseases and National Cancer Institute, National Institutes of Health, and Eiger Biopharmaceuticals Inc. JF - Lancet Infectious Diseases AU - Koh, Christopher AU - Canini, Laetitia AU - Dahari, Harel AU - Zhao, Xiongce AU - Uprichard, Susan L AU - Haynes-Williams, Vanessa AU - Winters, Mark A AU - Subramanya, Gitanjali AU - Cooper, Stewart L AU - Pinto, Peter AU - Wolff, Erin F AU - Bishop, Rachel AU - Ai Thanda Han, Ma AU - Cotler, Scott J AU - Kleiner, David E AU - Keskin, Onur AU - Idilman, Ramazan AU - Yurdaydin, Cihan AU - Glenn, Jeffrey S AU - Heller, Theo AD - Translational Hepatology Unit, Liver Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA Y1 - 2015/10// PY - 2015 DA - October 2015 SP - 1167 EP - 1174 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 15 IS - 10 SN - 1473-3099, 1473-3099 KW - Toxicology Abstracts; Virology & AIDS Abstracts KW - Diarrhea KW - Hepatitis B virus KW - Kidney diseases KW - Hepatitis B surface antigen KW - Clinical trials KW - Models KW - Diabetes mellitus KW - Hepatitis KW - RNA KW - Chronic infection KW - Pharmaceuticals KW - Nausea KW - Hepatitis D virus KW - Drugs KW - Intolerance KW - X 24310:Pharmaceuticals KW - V 22400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746880828?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lancet+Infectious+Diseases&rft.atitle=Oral+prenylation+inhibition+with+lonafarnib+in+chronic+hepatitis+D+infection%3A+a+proof-of-concept+randomised%2C+double-blind%2C+placebo-controlled+phase+2A+trial&rft.au=Koh%2C+Christopher%3BCanini%2C+Laetitia%3BDahari%2C+Harel%3BZhao%2C+Xiongce%3BUprichard%2C+Susan+L%3BHaynes-Williams%2C+Vanessa%3BWinters%2C+Mark+A%3BSubramanya%2C+Gitanjali%3BCooper%2C+Stewart+L%3BPinto%2C+Peter%3BWolff%2C+Erin+F%3BBishop%2C+Rachel%3BAi+Thanda+Han%2C+Ma%3BCotler%2C+Scott+J%3BKleiner%2C+David+E%3BKeskin%2C+Onur%3BIdilman%2C+Ramazan%3BYurdaydin%2C+Cihan%3BGlenn%2C+Jeffrey+S%3BHeller%2C+Theo&rft.aulast=Koh&rft.aufirst=Christopher&rft.date=2015-10-01&rft.volume=15&rft.issue=10&rft.spage=1167&rft.isbn=&rft.btitle=&rft.title=Lancet+Infectious+Diseases&rft.issn=14733099&rft_id=info:doi/10.1016%2FS1473-3099%2815%2900074-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Diarrhea; Kidney diseases; Hepatitis B surface antigen; Clinical trials; Models; Hepatitis; Diabetes mellitus; RNA; Chronic infection; Pharmaceuticals; Nausea; Drugs; Intolerance; Hepatitis B virus; Hepatitis D virus DO - http://dx.doi.org/10.1016/S1473-3099(15)00074-2 ER - TY - JOUR T1 - Identification of Genes Expressed in Hyperpigmented Skin Using Meta-Analysis of Microarray Data Sets AN - 1732820043; PQ0002241900 AB - More than 375 genes have been identified that are involved in regulating skin pigmentation and these act during development, survival, differentiation, and/or responses of melanocytes to the environment. Many of these genes have been cloned, and disruptions of their functions are associated with various pigmentary diseases; however, many remain to be identified. We have performed a series of microarray analyses of hyperpigmented compared with less pigmented skin to identify genes responsible for these differences. The rationale and goal for this study was to perform a meta-analysis on these microarray databases to identify genes that may be significantly involved in regulating skin phenotype either directly or indirectly that might not have been identified due to subtle differences by any of these individual studies alone. The meta-analysis demonstrates that 1,271 probes representing 921 genes are differentially expressed at significant levels in the 5 microarray data sets compared, providing new insights into the variety of genes involved in determining skin phenotype. Immunohistochemistry was used to validate two of these markers at the protein level (TRIM63 and QPCT), and we discuss the possible functions of these genes in regulating skin physiology. JF - Journal of Investigative Dermatology AU - Yin, Lanlan AU - Coelho, Sergio G AU - Valencia, Julio C AU - Ebsen, Dominik AU - Mahns, Andre AU - Smuda, Christoph AU - Miller, Sharon A AU - Beer, Janusz Z AU - Kolbe, Ludger AU - Hearing, Vincent J AD - Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA Y1 - 2015/10// PY - 2015 DA - October 2015 SP - 2455 EP - 2463 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 135 IS - 10 SN - 0022-202X, 0022-202X KW - Biotechnology and Bioengineering Abstracts; Genetics Abstracts KW - Differentiation KW - Pigmentation KW - Databases KW - Skin KW - Data processing KW - Reviews KW - Probes KW - Survival KW - Melanocytes KW - Immunohistochemistry KW - G 07730:Development & Cell Cycle KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732820043?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Investigative+Dermatology&rft.atitle=Identification+of+Genes+Expressed+in+Hyperpigmented+Skin+Using+Meta-Analysis+of+Microarray+Data+Sets&rft.au=Yin%2C+Lanlan%3BCoelho%2C+Sergio+G%3BValencia%2C+Julio+C%3BEbsen%2C+Dominik%3BMahns%2C+Andre%3BSmuda%2C+Christoph%3BMiller%2C+Sharon+A%3BBeer%2C+Janusz+Z%3BKolbe%2C+Ludger%3BHearing%2C+Vincent+J&rft.aulast=Yin&rft.aufirst=Lanlan&rft.date=2015-10-01&rft.volume=135&rft.issue=10&rft.spage=2455&rft.isbn=&rft.btitle=&rft.title=Journal+of+Investigative+Dermatology&rft.issn=0022202X&rft_id=info:doi/10.1038%2Fjid.2015.179 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Databases; Pigmentation; Differentiation; Data processing; Skin; Reviews; Probes; Survival; Melanocytes; Immunohistochemistry DO - http://dx.doi.org/10.1038/jid.2015.179 ER - TY - JOUR T1 - Systematic Identification of Cyclic-di-GMP Binding Proteins in Vibrio cholerae Reveals a Novel Class of Cyclic-di-GMP-Binding ATPases Associated with Type II Secretion Systems. AN - 1728256070; 26506097 AB - Cyclic-di-GMP (c-di-GMP) is a ubiquitous bacterial signaling molecule that regulates a variety of complex processes through a diverse set of c-di-GMP receptor proteins. We have utilized a systematic approach to identify c-di-GMP receptors from the pathogen Vibrio cholerae using the Differential Radial Capillary Action of Ligand Assay (DRaCALA). The DRaCALA screen identified a majority of known c-di-GMP binding proteins in V. cholerae and revealed a novel c-di-GMP binding protein, MshE (VC0405), an ATPase associated with the mannose sensitive hemagglutinin (MSHA) type IV pilus. The known c-di-GMP binding proteins identified by DRaCALA include diguanylate cyclases, phosphodiesterases, PilZ domain proteins and transcription factors VpsT and VpsR, indicating that the DRaCALA-based screen of open reading frame libraries is a feasible approach to uncover novel receptors of small molecule ligands. Since MshE lacks the canonical c-di-GMP-binding motifs, a truncation analysis was utilized to locate the c-di-GMP binding activity to the N-terminal T2SSE_N domain. Alignment of MshE homologs revealed candidate conserved residues responsible for c-di-GMP binding. Site-directed mutagenesis of these candidate residues revealed that the Arg9 residue is required for c-di-GMP binding. The ability of c-di-GMP binding to MshE to regulate MSHA dependent processes was evaluated. The R9A allele, in contrast to the wild type MshE, was unable to complement the ΔmshE mutant for the production of extracellular MshA to the cell surface, reduction in flagella swimming motility, attachment to surfaces and formation of biofilms. Testing homologs of MshE for binding to c-di-GMP identified the type II secretion ATPase of Pseudomonas aeruginosa (PA14_29490) as a c-di-GMP receptor, indicating that type II secretion and type IV pili are both regulated by c-di-GMP. JF - PLoS pathogens AU - Roelofs, Kevin G AU - Jones, Christopher J AU - Helman, Sarah R AU - Shang, Xiaoran AU - Orr, Mona W AU - Goodson, Jonathan R AU - Galperin, Michael Y AU - Yildiz, Fitnat H AU - Lee, Vincent T AD - Department of Cell Biology and Molecular Genetics, University of Maryland at College Park, Maryland, United States of America. ; Department of Microbiology and Environmental Toxicology, University of California, Santa Cruz, Santa Cruz, California, United States of America. ; National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, Maryland, United States of America. Y1 - 2015/10// PY - 2015 DA - October 2015 SP - 1 VL - 11 IS - 10 KW - Mannose-Binding Lectin KW - 0 KW - MshA protein, Vibrio cholerae KW - Type II Secretion Systems KW - Fimbriae Proteins KW - 147680-16-8 KW - bis(3',5')-cyclic diguanylic acid KW - 61093-23-0 KW - Adenosine Triphosphatases KW - EC 3.6.1.- KW - Cyclic GMP KW - H2D2X058MU KW - Index Medicus KW - Mannose-Binding Lectin -- metabolism KW - Open Reading Frames KW - Fimbriae, Bacterial -- physiology KW - Cyclic GMP -- metabolism KW - Fimbriae Proteins -- metabolism KW - Type II Secretion Systems -- physiology KW - Adenosine Triphosphatases -- metabolism KW - Vibrio cholerae -- metabolism KW - Cyclic GMP -- analogs & derivatives UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1728256070?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+pathogens&rft.atitle=Systematic+Identification+of+Cyclic-di-GMP+Binding+Proteins+in+Vibrio+cholerae+Reveals+a+Novel+Class+of+Cyclic-di-GMP-Binding+ATPases+Associated+with+Type+II+Secretion+Systems.&rft.au=Roelofs%2C+Kevin+G%3BJones%2C+Christopher+J%3BHelman%2C+Sarah+R%3BShang%2C+Xiaoran%3BOrr%2C+Mona+W%3BGoodson%2C+Jonathan+R%3BGalperin%2C+Michael+Y%3BYildiz%2C+Fitnat+H%3BLee%2C+Vincent+T&rft.aulast=Roelofs&rft.aufirst=Kevin&rft.date=2015-10-01&rft.volume=11&rft.issue=10&rft.spage=e1005232&rft.isbn=&rft.btitle=&rft.title=PLoS+pathogens&rft.issn=1553-7374&rft_id=info:doi/10.1371%2Fjournal.ppat.1005232 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-11 N1 - Date created - 2015-10-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl 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[18790873] Nature. 1987 Jan 15-21;325(6101):279-81 [18990795] Mol Plant Pathol. 2008 Nov;9(6):819-24 [19019010] J Bacteriol. 2009 Jan;191(1):169-77 [18952786] Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3461-6 [19218451] Nat Rev Microbiol. 2009 Apr;7(4):263-73 [19287449] Proc Natl Acad Sci U S A. 2009 May 12;106(19):7997-8002 [19416883] Nature. 2009 Jun 18;459(7249):1015-8 [19536266] Structure. 2009 Aug 12;17(8):1104-16 [19679088] Nat Rev Microbiol. 2009 Oct;7(10):724-35 [19756011] J Bacteriol. 2009 Nov;191(21):6632-42 [19734314] J Mol Biol. 2009 Nov 6;393(4):848-66 [19646999] J Bacteriol. 2009 Nov;191(22):7121-2 [19633082] J Bacteriol. 2010 Feb;192(4):1020-9 [20008070] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.ppat.1005232 ER - TY - JOUR T1 - A 7T spine array based on electric dipole transmitters AN - 1722177657; PQ0002019190 AB - Purpose The goal of this study was to explore the feasibility of using an array of electric dipole antennas for RF transmission in spine MRI at high fields. Method A two-channel transmit array based on an electric dipole design was quantitatively optimized for 7T spine imaging and integrated with a receive array combining eight loop coils. Using [Formulaomitted] mapping, the transmit efficiency of the dipole array was compared with a design using quadrature loop pairs. The radiofrequency energy deposition for each array was measured using a home-built dielectric phantom and MR thermometry. The performance of the proposed array was qualitatively demonstrated in human studies. Results The results indicate dramatically improved transmit efficiency for the dipole design compared with the loop excitation. A gain of up to 76% was achieved within the spinal region. Conclusion For imaging of the spine, electric dipole-based transmitters provide an attractive alternative to the traditional loop-based design. Easy integration with existing receive array technology facilitates practical use at high fields. Magn Reson Med 74:1189-1197, 2015. Published 2015. This article is a U.S. Government work and is in the public domain in the USA. JF - Magnetic Resonance in Medicine AU - Duan, Qi AU - Nair, Govind AU - Gudino, Natalia AU - de Zwart, Jacco A AU - van Gelderen, Peter AU - Murphy-Boesch, Joe AU - Reich, Daniel S AU - Duyn, Jeff H AU - Merkle, Hellmut AD - Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/10// PY - 2015 DA - Oct 2015 SP - 1189 EP - 1197 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 74 IS - 4 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Integration KW - Spine KW - Energy KW - Magnetic resonance imaging KW - N.M.R. KW - Mapping KW - Antennae KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722177657?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Magnetic+Resonance+in+Medicine&rft.atitle=A+7T+spine+array+based+on+electric+dipole+transmitters&rft.au=Duan%2C+Qi%3BNair%2C+Govind%3BGudino%2C+Natalia%3Bde+Zwart%2C+Jacco+A%3Bvan+Gelderen%2C+Peter%3BMurphy-Boesch%2C+Joe%3BReich%2C+Daniel+S%3BDuyn%2C+Jeff+H%3BMerkle%2C+Hellmut&rft.aulast=Duan&rft.aufirst=Qi&rft.date=2015-10-01&rft.volume=74&rft.issue=4&rft.spage=1189&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.25817 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Integration; Spine; Energy; Magnetic resonance imaging; N.M.R.; Mapping; Antennae DO - http://dx.doi.org/10.1002/mrm.25817 ER - TY - JOUR T1 - Variation in vervet (Chlorocebus aethiops) hair cortisol concentrations reflects ecological disturbance by humans AN - 1722170581; PQ0002079155 AB - Vervet monkeys (Chlorocebus aethiops) often live in close proximity to humans. Vervets are known to raid crops, homes and gardens in suburban areas leading to human-vervet conflict. In general, primate groups with access to human foods experience increased population densities and intra-group aggression. This suggests high stress loads for vervets living in environments with high levels of human habitat disturbance and close proximity to humans. We tested the hypothesis that populations characterized by high levels of human impact are more physiologically stressed than low human impact populations, and that this increased stress would be reflected in higher concentrations of hair cortisol. We predicted that because females would be less likely to engage in high risk foraging activities, and hence keep more distance from humans than males, their hair cortisol levels should be lower than those in males. We quantified cortisol in the hair of wild caught individuals from populations that experienced different degrees of human habitat disturbance and differences in access to human food. We found that males in high human impact groups had significantly higher hair cortisol concentrations than those in low human impact groups, although this difference was not observed in female vervets. Human impacts on vervet behavioral ecology appear to be a significant source of stress for male animals in particular. JF - Primates AU - Fourie, Nicolaas H AU - Turner, Trudy R AU - Brown, Janine L AU - Pampush, James D AU - Lorenz, Joseph G AU - Bernstein, Robin M AD - Biobehavioral Branch, Division of Intramural Research, National Institute of Nursing Research, National Institutes of Health, Room 2N104, 10 Center Drive, Bethesda, MD, 20892, USA, fourienh@mail.nih.gov Y1 - 2015/10// PY - 2015 DA - October 2015 SP - 365 EP - 373 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 56 IS - 4 SN - 0032-8332, 0032-8332 KW - Risk Abstracts; Ecology Abstracts; Sustainability Science Abstracts; Animal Behavior Abstracts KW - Hydrocortisone KW - Food KW - Physiology KW - Population density KW - Crops KW - Human impact KW - Ecology KW - Risk factors KW - Aggression KW - Foraging behavior KW - Aggressive behavior KW - Stress KW - Habitat KW - Primates KW - Hair KW - Ecosystem disturbance KW - Disturbance KW - Human factors KW - Conflicts KW - Y 25040:Behavioral Ecology KW - M3 1010:Issues in Sustainable Development KW - D 04040:Ecosystem and Ecology Studies KW - R2 23110:Psychological aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722170581?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Primates&rft.atitle=Variation+in+vervet+%28Chlorocebus+aethiops%29+hair+cortisol+concentrations+reflects+ecological+disturbance+by+humans&rft.au=Fourie%2C+Nicolaas+H%3BTurner%2C+Trudy+R%3BBrown%2C+Janine+L%3BPampush%2C+James+D%3BLorenz%2C+Joseph+G%3BBernstein%2C+Robin+M&rft.aulast=Fourie&rft.aufirst=Nicolaas&rft.date=2015-10-01&rft.volume=56&rft.issue=4&rft.spage=365&rft.isbn=&rft.btitle=&rft.title=Primates&rft.issn=00328332&rft_id=info:doi/10.1007%2Fs10329-015-0486-y LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Number of references - 56 N1 - Last updated - 2016-02-29 N1 - SubjectsTermNotLitGenreText - Foraging behavior; Hydrocortisone; Risk factors; Food; Population density; Stress; Aggression; Habitat; Hair; Crops; Human impact; Physiology; Aggressive behavior; Primates; Ecosystem disturbance; Ecology; Human factors; Disturbance; Conflicts DO - http://dx.doi.org/10.1007/s10329-015-0486-y ER - TY - JOUR T1 - Posterior subcapsular prostate cancer: identification with mpMRI and MRI/TRUS fusion-guided biopsy AN - 1722168932; PQ0002078847 AB - Purpose: The posterior subcapsular region of the prostate is often undersampled by transrectal ultrasound (TRUS)-guided biopsy. The close proximity of these lesions to the posterior capsular wall of the prostate makes them difficult to localize while increasing the need for early detection because of their increased risk for extracapsular extension. We retrospectively evaluated the multiparametric MRI (mpMRI) features of subcapsular prostate cancers to make radiologists more aware of this condition. Materials and Methods: Between January 2010 and July 2014, all patients referred for 3T mpMRI and subsequent MR-US Fusion-guided biopsy (FgBx) and systematic 12-core sextant biopsy (SBx) under an IRB approved protocol, were reviewed, and imaging confirmed subcapsular prostate cancers were identified. Subcapsular lesions were defined as thin lesions that were just inside the prostate capsule. Matching patient demographics and clinical findings including age, PSA, PSA density, whole prostate volume, history of prostate cancer, Gleason score, and clinical management were tabulated. Results: Of 992 eligible patients, 33 patients had subcapsular lesions in the prostate detected by mpMRI. Mean age, PSA, and prostate volume in this group were 63 years (range: 52-76 years), 8.4 ng/mL (range: 1.22-65.20), and 53 mL (range: 12-125 mL), respectively. The combination biopsy (SBx + FgBx) confirmed prostate cancer in 24 of 33 patients (72.7%) and in 9 patients the biopsy was negative. Of the 24 cancers, 19 were confirmed on both FgBx and conventional biopsy; however, 5 cancers were only detected on FgBx. In 4 of the 19 patients in which both biopsy methods were positive, the FgBx yielded a higher Gleason score. Conclusion: Subcapsular lesions on mpMRI are relatively infrequent but are usually malignant. Although the majority are confirmed on conventional 12-core biopsies, about 20% of these lesions require FgBx for diagnosis, and FgBx more accurately grades the lesions in another 20%. Thus, FgBx is of considerable benefit in confirming the diagnosis of subcapsular prostate cancer despite their proximity to the prostatic capsule. JF - Abdominal Imaging AU - Sankineni, Sandeep AU - George, Arvin K AU - Brown, Anna M AU - Rais-Bahrami, Soroush AU - Wood, Bradford J AU - Merino, Maria J AU - Pinto, Peter A AU - Choyke, Peter L AU - Turkbey, Baris AD - Molecular Imaging Program, NCI, NIH, Bethesda, MD, USA, turkbeyi@mail.nih.gov Y1 - 2015/10// PY - 2015 DA - Oct 2015 SP - 2557 EP - 2565 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 40 IS - 7 SN - 0942-8925, 0942-8925 KW - Biotechnology and Bioengineering Abstracts KW - Demography KW - Age KW - Prostate cancer KW - Magnetic resonance imaging KW - Biopsy KW - Ultrasound KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722168932?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Abdominal+Imaging&rft.atitle=Posterior+subcapsular+prostate+cancer%3A+identification+with+mpMRI+and+MRI%2FTRUS+fusion-guided+biopsy&rft.au=Sankineni%2C+Sandeep%3BGeorge%2C+Arvin+K%3BBrown%2C+Anna+M%3BRais-Bahrami%2C+Soroush%3BWood%2C+Bradford+J%3BMerino%2C+Maria+J%3BPinto%2C+Peter+A%3BChoyke%2C+Peter+L%3BTurkbey%2C+Baris&rft.aulast=Sankineni&rft.aufirst=Sandeep&rft.date=2015-10-01&rft.volume=40&rft.issue=7&rft.spage=2557&rft.isbn=&rft.btitle=&rft.title=Abdominal+Imaging&rft.issn=09428925&rft_id=info:doi/10.1007%2Fs00261-015-0426-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Number of references - 17 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Demography; Age; Prostate cancer; Magnetic resonance imaging; Biopsy; Ultrasound DO - http://dx.doi.org/10.1007/s00261-015-0426-8 ER - TY - JOUR T1 - Inhibition of UDP-Glucuronosyltransferases (UGTs) Activity by constituents of Schisandra chinensis. AN - 1721360948; 26084208 AB - Structure-activity relationship for the inhibition of Schisandra chinensis's ingredients toward (Uridine-Diphosphate) UDP-glucuronosyltransferases (UGTs) activity was performed in the present study. In vitro incubation system was employed to screen the inhibition capability of S. chinensis's ingredients, and in silico molecular docking method was carried out to explain possible mechanisms. At 100 μM of compounds, the activity of UGTs was inhibited by less than 90% by schisandrol A, schisandrol B, schisandrin, schisandrin C, schisantherin A, gomisin D, and gomisin G. Schisandrin A exerted strong inhibition toward UGT1A1 and UGT1A3, with the residual activity to be 7.9% and 0% of control activity. Schisanhenol exhibited strong inhibition toward UGT2B7, with the residual activity to be 7.9% of control activity. Gomisin J of 100 μM inhibited 91.8% and 93.1% of activity of UGT1A1 and UGT1A9, respectively. Molecular docking prediction indicated different hydrogen bonds interaction resulted in the different inhibition potential induced by subtle structure alteration among schisandrin A, schisandrin, and schisandrin C toward UGT1A1 and UGT1A3: schisandrin A > schisandrin > schisandrin C. The detailed inhibition kinetic evaluation showed the strong inhibition of gomisin J toward UGT1A9 with the inhibition kinetic parameter (Ki ) to be 0.7 μM. Based on the concentrations of gomisin J in the plasma of the rats given with S. chinensis, high herb-drug interaction existed between S. chinensis and drugs mainly undergoing UGT1A9-mediated metabolism. In conclusion, in silico-in vitro method was used to give the inhibition information and possible inhibition mechanism for S. chinensis's components toward UGTs, which guide the clinical application of S. chinensis. Copyright © 2015 John Wiley & Sons, Ltd. JF - Phytotherapy research : PTR AU - Song, Jin-Hui AU - Cui, Li AU - An, Li-Bin AU - Li, Wen-Tao AU - Fang, Zhong-Ze AU - Zhang, Yan-Yan AU - Dong, Pei-Pei AU - Wu, Xue AU - Wang, Li-Xuan AU - Gonzalez, Frank J AU - Sun, Xiao-Yu AU - Zhao, De-Wei AD - Affiliated Zhongshan Hospital of Dalian University, No.6, Jiefang Street, Zhongshan District, Dalian, 116001, China. ; Dalian University, Dalian, 116622, China. ; Department of Toxicology, School of Public Health, Tianjin Medical University, 22 Qixiangtai Road, Heping District, Tianjin, 300070, China. ; First Affiliated Hospital of Liaoning Medical University, Jinzhou, Liaoning, China. ; Institute of Integrative Medicine, College of Pharmacy, Dalian Medical University, Dalian, 116044, China. ; Personalized Treatment & Diagnosis Center, No.6, Jiefang Street, Zhongshan District, Dalian, 116001, China. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2015/10// PY - 2015 DA - October 2015 SP - 1658 EP - 1664 VL - 29 IS - 10 KW - Cyclooctanes KW - 0 KW - Dioxoles KW - Drugs, Chinese Herbal KW - Lignans KW - Plant Extracts KW - Polycyclic Compounds KW - schisandrol A KW - schizandrol B KW - 58546-54-6 KW - gomisin D KW - 60546-10-3 KW - schizandrin A KW - 61281-38-7 KW - schizandrin C KW - 61301-33-5 KW - schisanhenol KW - 69363-14-0 KW - schizandrin KW - 7432-28-2 KW - schizandrer A KW - 82042-38-4 KW - Glucuronosyltransferase KW - EC 2.4.1.17 KW - gomisin J KW - X13A57600T KW - Index Medicus KW - herb-drug interaction KW - in silico KW - in vitro KW - Schisandra chinensis KW - UDP-glucuronosyltransferases (UGTs) KW - Rats KW - Animals KW - Herb-Drug Interactions KW - Drugs, Chinese Herbal -- pharmacology KW - Structure-Activity Relationship KW - Plant Extracts -- pharmacology KW - Schisandra -- chemistry KW - Glucuronosyltransferase -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1721360948?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Phytotherapy+research+%3A+PTR&rft.atitle=Inhibition+of+UDP-Glucuronosyltransferases+%28UGTs%29+Activity+by+constituents+of+Schisandra+chinensis.&rft.au=Song%2C+Jin-Hui%3BCui%2C+Li%3BAn%2C+Li-Bin%3BLi%2C+Wen-Tao%3BFang%2C+Zhong-Ze%3BZhang%2C+Yan-Yan%3BDong%2C+Pei-Pei%3BWu%2C+Xue%3BWang%2C+Li-Xuan%3BGonzalez%2C+Frank+J%3BSun%2C+Xiao-Yu%3BZhao%2C+De-Wei&rft.aulast=Song&rft.aufirst=Jin-Hui&rft.date=2015-10-01&rft.volume=29&rft.issue=10&rft.spage=1658&rft.isbn=&rft.btitle=&rft.title=Phytotherapy+research+%3A+PTR&rft.issn=1099-1573&rft_id=info:doi/10.1002%2Fptr.5395 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-28 N1 - Date created - 2015-10-09 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ptr.5395 ER - TY - JOUR T1 - Predicting Ovarian Activity in Women Affected by Early Breast Cancer: A Meta-Analysis-Based Nomogram. AN - 1718913566; 26341758 AB - The assessment of ovarian reserve in premenopausal women requiring anticancer gonadotoxic therapy can help clinicians address some challenging issues, including the probability of future pregnancies after the end of treatment. Anti-Müllerian hormone (AMH) and age can reliably estimate ovarian reserve. A limited number of studies have evaluated AMH and age as predictors of residual ovarian reserve following cytotoxic chemotherapy in breast cancer patients. To conduct a meta-analysis of published data on this topic, we searched the medical literature using the key MeSH terms "amenorrhea/chemically induced," "ovarian reserve," "anti-Mullerian hormone/blood," and "breast neoplasms/drug therapy." Preferred Reporting Items for Systematic Reviews and Meta-Analyses statements guided the search strategy. U.K. National Health Service guidelines were used in abstracting data and assessing data quality and validity. Area under the receiver operating characteristic curve (ROC/AUC) analysis was used to evaluate the predictive utility of baseline AMH and age model. The meta-analysis of data pooled from the selected studies showed that both age and serum AMH are reliable predictors of post-treatment ovarian activity in breast cancer patients. Importantly, ROC/AUC analysis indicated AMH was a more reliable predictor of post-treatment ovarian activity in patients aged younger than 40 years (0.753; 95% confidence interval [CI]: 0.602-0.904) compared with those older than 40 years (0.678; 95% CI: 0.491-0.866). We generated a nomogram describing the correlations among age, pretreatment AMH serum levels, and ovarian activity at 1 year from the end of chemotherapy. After the ongoing validation process, the proposed nomogram may help clinicians discern premenopausal women requiring cytotoxic chemotherapy who should be considered high priority for fertility preservation counseling and procedures. ©AlphaMed Press. JF - The oncologist AU - Barnabei, Agnese AU - Strigari, Lidia AU - Marchetti, Paolo AU - Sini, Valentina AU - De Vecchis, Liana AU - Corsello, Salvatore Maria AU - Torino, Francesco AD - Endocrinology Unit, "Regina Elena" National Cancer Institute of Rome, Rome, Italy. ; Laboratory of Medical Physics and Expert Systems, "Regina Elena" National Cancer Institute of Rome, Rome, Italy. ; Department of Clinical and Molecular Medicine, Medical Oncology Division, "Sapienza" University of Rome, Rome, Italy Sant'Andrea Hospital, Rome, Italy IDI-IRCCS, Rome, Italy. ; Department of Clinical and Molecular Medicine, Medical Oncology Division, "Sapienza" University of Rome, Rome, Italy Oncology Unit, "Santo Spirito" Hospital - Lungotevere in Sassia, Rome, Italy. ; Department of Systems Medicine, "Tor Vergata" University of Rome, Rome, Italy. ; Endocrinology Unit, Università Cattolica Roma, Rome, Italy corsello.sm@mclink.it. Y1 - 2015/10// PY - 2015 DA - October 2015 SP - 1111 EP - 1118 VL - 20 IS - 10 KW - Antineoplastic Agents KW - 0 KW - Anti-Mullerian Hormone KW - 80497-65-0 KW - Index Medicus KW - Ovarian toxicity KW - Predictive factors KW - Ovarian reserve KW - Breast cancer KW - Anti-Müllerian hormone KW - Anti-Mullerian Hormone -- blood KW - Age Factors KW - ROC Curve KW - Nomograms KW - Humans KW - Adult KW - Middle Aged KW - Antineoplastic Agents -- therapeutic use KW - Amenorrhea -- chemically induced KW - Ovarian Reserve -- physiology KW - Female KW - Antineoplastic Agents -- adverse effects KW - Breast Neoplasms -- drug therapy KW - Breast Neoplasms -- physiopathology KW - Ovary -- drug effects KW - Ovary -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1718913566?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+oncologist&rft.atitle=Predicting+Ovarian+Activity+in+Women+Affected+by+Early+Breast+Cancer%3A+A+Meta-Analysis-Based+Nomogram.&rft.au=Barnabei%2C+Agnese%3BStrigari%2C+Lidia%3BMarchetti%2C+Paolo%3BSini%2C+Valentina%3BDe+Vecchis%2C+Liana%3BCorsello%2C+Salvatore+Maria%3BTorino%2C+Francesco&rft.aulast=Barnabei&rft.aufirst=Agnese&rft.date=2015-10-01&rft.volume=20&rft.issue=10&rft.spage=1111&rft.isbn=&rft.btitle=&rft.title=The+oncologist&rft.issn=1549-490X&rft_id=info:doi/10.1634%2Ftheoncologist.2015-0183 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-07 N1 - Date created - 2015-10-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Oncol. 1999 Aug;17(8):2365-70 [10561298] Hum Reprod. 2004 Jul;19(7):1612-7 [15205396] Semin Oncol. 1982 Mar;9(1):84-94 [6176028] Biometrics. 1988 Sep;44(3):837-45 [3203132] J Clin Oncol. 1996 May;14(5):1718-29 [8622093] Eur J Cancer. 1998 Apr;34(5):632-40 [9713266] J Clin Oncol. 2006 Aug 20;24(24):4044-6 [16921067] Hum Reprod. 2006 Oct;21(10):2583-92 [16820385] J Clin Oncol. 2006 Dec 20;24(36):5769-79 [17130515] Br J Cancer. 2007 Jun 18;96(12):1808-16 [17533402] J Clin Oncol. 2008 Feb 10;26(5):753-8 [18258983] Cancer Invest. 2008 Apr-May;26(3):286-95 [18317970] PLoS Med. 2009 Jul 21;6(7):e1000097 [19621072] Maturitas. 2009 Aug 20;63(4):280-91 [19631481] Cancer. 2010 Feb 1;116(3):592-9 [19918920] Reprod Biomed Online. 2010 Feb;20(2):280-5 [20113967] Fertil Steril. 2010 Jun;94(1):156-66 [19342041] Cancer. 2010 Jul 1;116(13):3102-11 [20564648] Fertil Steril. 2010 Jul;94(2):638-44 [19409543] J Clin Oncol. 2011 Mar 20;29(9):1110-6 [21300930] J Clin Endocrinol Metab. 2011 May;96(5):1336-43 [21325458] Fertil Steril. 2011 Jun;95(7):2359-63, 2363.e1 [21457958] Ann Clin Biochem. 2011 Jul;48(Pt 4):370-3 [21628625] PLoS One. 2011;6(7):e22024 [21789206] J Clin Endocrinol Metab. 2011 Aug;96(8):2532-9 [21613357] J Natl Cancer Inst. 2012 Mar 7;104(5):386-405 [22271773] Endocr Relat Cancer. 2012 Apr;19(2):R21-33 [22241718] J Clin Endocrinol Metab. 2012 Jun;97(6):2059-67 [22472563] Eur J Obstet Gynecol Reprod Biol. 2012 Aug;163(2):180-4 [22579227] J Clin Endocrinol Metab. 2012 Dec;97(12):4650-5 [22993032] J Cell Mol Med. 2013 Jan;17(1):1-11 [23279634] Fertil Steril. 2013 Mar 15;99(4):963-9 [23312225] PLoS One. 2013;8(3):e57005 [23505417] Eur J Cancer. 2013 Apr;49(6):1374-403 [23485231] Fertil Steril. 2013 May;99(6):1469-75 [23541317] Hum Reprod. 2013 Jun;28(6):1695-706 [23508249] J Clin Oncol. 2013 Jul 1;31(19):2500-10 [23715580] Ann Oncol. 2013 Sep;24(9):2206-23 [23917950] Ann Oncol. 2013 Oct;24 Suppl 6:vi160-70 [23813932] Eur J Cancer. 2013 Nov;49(16):3404-11 [23968732] Semin Reprod Med. 2013 Nov;31(6):399-415 [24101221] Crit Rev Oncol Hematol. 2014 Jan;89(1):27-42 [23953684] Oncologist. 2014 Jan;19(1):68-74 [24319018] Endocr Relat Cancer. 2014 Feb;21(1):R51-65 [24292601] Fertil Steril. 2014 Feb;101(2):523-9 [24220704] Breast Cancer Res Treat. 2014 Apr;144(3):591-7 [24584876] Reprod Biol Endocrinol. 2014;12:26 [24666685] Breast Cancer Res Treat. 2014 May;145(1):113-28 [24671358] Hum Reprod Update. 2014 May-Jun;20(3):370-85 [24430863] Hum Reprod Update. 2014 Sep-Oct;20(5):688-701 [24821925] Climacteric. 2014 Oct;17(5):591-7 [24716733] Cancer. 2014 Dec 1;120(23):3691-8 [25081546] Reprod Biomed Online. 2014 Nov;29(5):573-80 [25246112] CA Cancer J Clin. 2015 Mar;65(2):87-108 [25651787] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1634/theoncologist.2015-0183 ER - TY - JOUR T1 - Occupational Exposure to Benzene and Non-Hodgkin Lymphoma in a Population-Based Cohort: The Shanghai Women's Health Study. AN - 1718904299; 25748391 AB - The association between benzene exposure and non-Hodgkin lymphoma (NHL) has been the subject of debate as a result of inconsistent epidemiologic evidence. An International Agency for Research on Cancer (IARC) working group evaluated benzene in 2009 and noted evidence for a positive association between benzene exposure and NHL risk. We evaluated the association between occupational benzene exposure and NHL among 73,087 women enrolled in the prospective population-based Shanghai Women's Health Study. Benzene exposure estimates were derived using a previously developed exposure assessment framework that combined ordinal job-exposure matrix intensity ratings with quantitative benzene exposure measurements from an inspection database of Shanghai factories collected between 1954 and 2000. Associations between benzene exposure metrics and NHL (n = 102 cases) were assessed using Cox proportional hazard models, with study follow-up occurring from December 1996 through December 2009. Women ever exposed to benzene had a significantly higher risk of NHL [hazard ratio (HR) = 1.87, 95% CI: 1.19, 2.96]. Compared with unexposed women, significant trends in NHL risk were observed for increasing years of benzene exposure (p(trend) = 0.006) and increasing cumulative exposure levels (p(trend) = 0.005), with the highest duration and cumulative exposure tertiles having a significantly higher association with NHL (HR = 2.07, 95% CI: 1.07, 4.01 and HR = 2.16, 95% CI: 1.17, 3.98, respectively). Our findings, using a population-based prospective cohort of women with diverse occupational histories, provide additional evidence that occupational exposure to benzene is associated with NHL risk. JF - Environmental health perspectives AU - Bassig, Bryan A AU - Friesen, Melissa C AU - Vermeulen, Roel AU - Shu, Xiao-Ou AU - Purdue, Mark P AU - Stewart, Patricia A AU - Xiang, Yong-Bing AU - Chow, Wong-Ho AU - Zheng, Tongzhang AU - Ji, Bu-Tian AU - Yang, Gong AU - Linet, Martha S AU - Hu, Wei AU - Zhang, Heping AU - Zheng, Wei AU - Gao, Yu-Tang AU - Rothman, Nathaniel AU - Lan, Qing AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute (NCI), National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Bethesda, Maryland, USA. Y1 - 2015/10// PY - 2015 DA - October 2015 SP - 971 EP - 977 VL - 123 IS - 10 KW - Benzene KW - J64922108F KW - Index Medicus KW - Prospective Studies KW - Women's Health KW - Humans KW - China -- epidemiology KW - Adult KW - Aged KW - Middle Aged KW - Female KW - Risk Assessment KW - Occupational Exposure KW - Lymphoma, Non-Hodgkin -- epidemiology KW - Benzene -- analysis KW - Occupational Diseases -- epidemiology KW - Lymphoma, Non-Hodgkin -- chemically induced KW - Occupational Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1718904299?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Occupational+Exposure+to+Benzene+and+Non-Hodgkin+Lymphoma+in+a+Population-Based+Cohort%3A+The+Shanghai+Women%27s+Health+Study.&rft.au=Bassig%2C+Bryan+A%3BFriesen%2C+Melissa+C%3BVermeulen%2C+Roel%3BShu%2C+Xiao-Ou%3BPurdue%2C+Mark+P%3BStewart%2C+Patricia+A%3BXiang%2C+Yong-Bing%3BChow%2C+Wong-Ho%3BZheng%2C+Tongzhang%3BJi%2C+Bu-Tian%3BYang%2C+Gong%3BLinet%2C+Martha+S%3BHu%2C+Wei%3BZhang%2C+Heping%3BZheng%2C+Wei%3BGao%2C+Yu-Tang%3BRothman%2C+Nathaniel%3BLan%2C+Qing&rft.aulast=Bassig&rft.aufirst=Bryan&rft.date=2015-10-01&rft.volume=123&rft.issue=10&rft.spage=971&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1408307 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-13 N1 - Date created - 2015-10-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Epidemiol Biomarkers Prev. 2007 Mar;16(3):405-8 [17337643] Occup Environ Med. 2003 Sep;60(9):676-9 [12937190] Environ Mol Mutagen. 2007 Jul;48(6):467-74 [17584886] Environ Mol Mutagen. 2008 Jul;49(6):453-7 [18481315] Am J Ind Med. 2008 Nov;51(11):803-11 [18651579] Epidemiology. 2003 Sep;14(5):569-77 [14501272] Int J Occup Environ Health. 2004 Jan-Mar;10(1):13-21 [15070021] Am J Ind Med. 1996 Mar;29(3):236-46 [8833776] Occup Environ Med. 1996 Nov;53(11):773-81 [9038803] J Natl Cancer Inst. 1997 Jul 16;89(14):1065-71 [9230889] Science. 2004 Dec 3;306(5702):1774-6 [15576619] Am J Epidemiol. 2005 Dec 1;162(11):1123-31 [16236996] Lifetime Data Anal. 2007 Jun;13(2):261-72 [17401682] Blood. 2008 Nov 15;112(10):4247-9 [18711000] Toxicol Ind Health. 2008 Jun-Jul;24(5-6):263-398 [19022880] Blood. 2008 Dec 15;112(13):5150-60 [18796628] Am J Epidemiol. 2009 Jan 15;169(2):176-85 [19056833] Toxicol Sci. 2009 Aug;110(2):293-306 [19478238] J Occup Environ Hyg. 2009 Nov;6(11):659-70 [19753498] Lancet Oncol. 2009 Dec;10(12):1143-4 [19998521] Chem Biol Interact. 2010 Mar 19;184(1-2):129-46 [19900422] Occup Environ Med. 2010 May;67(5):341-7 [20447988] Blood. 2010 Nov 18;116(20):e90-8 [20699439] Environ Health Perspect. 2011 Feb;119(2):159-67 [20880796] Ann Occup Hyg. 2012 Jan;56(1):80-91 [21976309] Cancer Res. 2012 Sep 15;72(18):4733-43 [22846913] J Natl Cancer Inst. 2012 Nov 21;104(22):1724-37 [23111193] Blood. 2013 Aug 8;122(6):951-7 [23814017] Cancer Causes Control. 2001 Apr;12(3):201-12 [11405325] Crit Rev Toxicol. 2002 Jan;32(1):1-42 [11846214] Am J Ind Med. 2002 Oct;42(4):275-85 [12271475] Epidemiology. 2006 Sep;17(5):552-61 [16878041] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1289/ehp.1408307 ER - TY - JOUR T1 - Evaluation of the Safety and Benefit of Phase I Oncology Trials for Patients With Primary CNS Tumors. AN - 1718332937; 26282642 AB - Patients with high-grade gliomas (HGG) are frequently excluded from first-in-human solid tumor trials because of perceived poor prognosis, excessive toxicities, concomitant drug interactions, and poor efficacy. We conducted an analysis of outcomes from select, single-agent phase I studies in patients with HGG. We compared outcomes to pooled analysis of published studies in solid tumors with various molecular and cytotoxic drugs evaluated as single agents or as combinations. Individual records of patients with recurrent HGG enrolled onto Adult Brain Tumor Consortium trials of single-agent, cytotoxic or molecular agents from 2000 to 2008 were analyzed for baseline characteristics, toxicities, responses, and survival. Our analysis included 327 patients with advanced, refractory HGG who were enrolled onto eight trials involving targeted molecular (n=5) and cytotoxic (n=3) therapies. At enrollment, patients had a median Karnofsky performance score of 90 and median age of 52 years; 62% were men, 63% had glioblastoma, and the median number of prior systemic chemotherapies was one. Baseline laboratory values were in an acceptable range to meet eligibility criteria. Patients were on the study for a median of two cycles (range, 90% as metabolites within 24h. Using more sensitive methods, our study expands the findings of other human oral pharmacokinetic studies. Conjugation reactions are rapid and nearly complete with unconjugated BPA comprising less than 1% of the total d6-BPA in blood at all times. Elimination of conjugates into urine largely occurs within 24h. Published by Elsevier Ltd. JF - Environment international AU - Thayer, Kristina A AU - Doerge, Daniel R AU - Hunt, Dawn AU - Schurman, Shepherd H AU - Twaddle, Nathan C AU - Churchwell, Mona I AU - Garantziotis, Stavros AU - Kissling, Grace E AU - Easterling, Michael R AU - Bucher, John R AU - Birnbaum, Linda S AD - Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, P.O. Box 12233, Mail Drop K2-02, Research Triangle Park, NC 27709, USA. Electronic address: thayer@niehs.nih.gov. ; Division of Biochemical Toxicology, National Center for Toxicological Research, U.S. Food & Drug Administration, NCTR-53C RM204L HFT-110, 3900 NCTR Road, Jefferson, AR 72079, USA. Electronic address: daniel.doerge@fda.hhs.gov. ; Clinical Research Unit, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, P.O. Box 12233, Mail Drop CU-01, Research Triangle Park, NC 27709, USA. Electronic address: dawnhunt2233@outlook.com. ; Clinical Research Unit, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, P.O. Box 12233, Mail Drop CU-01, Research Triangle Park, NC 27709, USA. Electronic address: schurmansh@niehs.nih.gov. ; Division of Biochemical Toxicology, National Center for Toxicological Research, U.S. Food & Drug Administration, NCTR-53C RM204L HFT-110, 3900 NCTR Road, Jefferson, AR 72079, USA. Electronic address: Nathan.Twaddle@fda.hhs.gov. ; Division of Biochemical Toxicology, National Center for Toxicological Research, U.S. Food & Drug Administration, NCTR-53C RM204L HFT-110, 3900 NCTR Road, Jefferson, AR 72079, USA. Electronic address: Mona.Churchwell@fda.hhs.gov. ; Clinical Research Unit, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, P.O. Box 12233, Mail Drop CU-01, Research Triangle Park, NC 27709, USA. Electronic address: garantziotis@niehs.nih.gov. ; Biostatistics Branch, National Institute of Environmental Health Sciences, P.O. Box 12233, Mail Drop A3-03, Research Triangle Park, NC 27709, USA. Electronic address: kissling@niehs.nih.gov. ; Social & Scientific Systems, Inc., 1009 Slater Rd # 120, Durham, NC 27703, USA. Electronic address: MEasterling@s-3.com. ; Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, P.O. Box 12233, Mail Drop K2-02, Research Triangle Park, NC 27709, USA. Electronic address: bucher@niehs.nih.gov. ; National Cancer Institute, National Institutes of Health, Department of Health and Human Services, P.O. Box 12233, Mail Drop B2-01, Research Triangle Park, NC 27709, USA. Electronic address: birnbaumls@niehs.nih.gov. Y1 - 2015/10// PY - 2015 DA - October 2015 SP - 107 EP - 115 VL - 83 KW - Benzhydryl Compounds KW - 0 KW - Environmental Pollutants KW - Glucuronides KW - Phenols KW - Sulfuric Acid Esters KW - bisphenol A glucuronide KW - bisphenol A KW - MLT3645I99 KW - Index Medicus KW - Bioavailability KW - ADME KW - Endocrine disruptor KW - Excretion KW - Metabolism KW - Deuterated bisphenol A KW - Administration, Oral KW - Sulfuric Acid Esters -- urine KW - Half-Life KW - Area Under Curve KW - Humans KW - North Carolina KW - Adult KW - Middle Aged KW - Glucuronides -- blood KW - Sulfuric Acid Esters -- blood KW - Glucuronides -- urine KW - Male KW - Female KW - Benzhydryl Compounds -- pharmacokinetics KW - Phenols -- blood KW - Phenols -- pharmacokinetics KW - Environmental Pollutants -- urine KW - Benzhydryl Compounds -- blood KW - Phenols -- urine KW - Environmental Pollutants -- blood KW - Environmental Pollutants -- pharmacokinetics KW - Benzhydryl Compounds -- urine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1705735125?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environment+international&rft.atitle=Pharmacokinetics+of+bisphenol+A+in+humans+following+a+single+oral+administration.&rft.au=Thayer%2C+Kristina+A%3BDoerge%2C+Daniel+R%3BHunt%2C+Dawn%3BSchurman%2C+Shepherd+H%3BTwaddle%2C+Nathan+C%3BChurchwell%2C+Mona+I%3BGarantziotis%2C+Stavros%3BKissling%2C+Grace+E%3BEasterling%2C+Michael+R%3BBucher%2C+John+R%3BBirnbaum%2C+Linda+S&rft.aulast=Thayer&rft.aufirst=Kristina&rft.date=2015-10-01&rft.volume=83&rft.issue=&rft.spage=107&rft.isbn=&rft.btitle=&rft.title=Environment+international&rft.issn=1873-6750&rft_id=info:doi/10.1016%2Fj.envint.2015.06.008 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-04 N1 - Date created - 2015-08-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Toxicol Appl Pharmacol. 2010 Oct 1;248(1):1-11 [20655935] Anal Bioanal Chem. 2010 Sep;398(1):571-6 [20623271] Toxicol Appl Pharmacol. 2010 Sep 1;247(2):158-65 [20600215] Xenobiotica. 2010 Feb;40(2):83-92 [19916736] Philos Trans R Soc Lond B Biol Sci. 2009 Jul 27;364(1526):2063-78 [19528056] Environ Health Perspect. 2009 May;117(5):784-9 [19479022] Toxicol Appl Pharmacol. 2015 Oct 15;288(2):131-42 [25620055] NTP CERHR MON. 2008 Sep;(22):v, vii-ix, 1-64 passim [19407859] Birth Defects Res B Dev Reprod Toxicol. 2008 Jun;83(3):157-395 [18613034] Toxicol Appl Pharmacol. 2008 Apr 1;228(1):114-34 [18207480] Environ Health Perspect. 2008 Jan;116(1):39-44 [18197297] Reprod Toxicol. 2007 Aug-Sep;24(2):139-77 [17825522] Chem Res Toxicol. 2002 Oct;15(10):1281-7 [12387626] AIHAJ. 2000 Sep-Oct;61(5):649-57 [11071416] Rapid Commun Mass Spectrom. 2010 Oct 30;24(20):3011-20 [20872634] Environ Health Perspect. 2011 Apr;119(4):422-30 [20855240] Toxicol Lett. 2011 Jul 28;204(2-3):190-8 [21571050] Toxicol Appl Pharmacol. 2011 Sep 15;255(3):261-70 [21820460] Arch Toxicol. 2011 Nov;85(11):1373-81 [21404072] Toxicol Lett. 2011 Dec 15;207(3):298-305 [21983029] Clin Pharmacokinet. 2012 May 1;51(5):319-30 [22439649] J Expo Sci Environ Epidemiol. 2012 Nov;22(6):610-6 [22617719] Environ Health Perspect. 2013 Mar;121(3):283-6 [23458838] J Anal Toxicol. 2007 Apr;31(3):177-8 [17598284] Mol Cell Endocrinol. 2014 Dec;398(1-2):101-13 [25304273] PLoS One. 2014;9(10):e110509 [25337790] Toxicol Sci. 2014 Sep;141(1):292-9 [24980262] Environ Health. 2014;13(1):25 [24690217] Reprod Toxicol. 2014 Jun;45:105-16 [24582107] Environ Health Perspect. 2009 Apr;117(4):639-44 [19440505] Breast Cancer Res. 2013;15(5):403 [24083327] Environ Res. 2014 Feb;129:32-8 [24529000] Food Chem Toxicol. 2013 Dec;62:949-63 [23959105] Environ Sci Technol. 2013;47(21):12477-85 [23941471] Environ Res. 2013 Oct;126:211-4 [23899777] Environ Health Perspect. 2013 Aug;121(8):951-6 [23761051] Rev Environ Health. 2013;28(1):37-58 [23612528] Toxicol Sci. 2014 May;139(1):4-20 [24496641] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.envint.2015.06.008 ER - TY - JOUR T1 - Chemical exposures in the workplace and breast cancer risk: A prospective cohort study AN - 1701481821; PQ0001761735 AB - We investigated the relationship between workplace chemical exposures and breast cancer risk among women enrolled in the Sister Study, a prospective cohort study of US and Puerto Rican women. A total of 47,640 participants reported work outside of the home. Workplace exposure to eleven agents (acids, dyes or inks, gasoline or other petroleum products, glues or adhesives, lubricating oils, metals, paints, pesticides, soldering materials, solvents and stains or varnishes) was characterized based on self-reports of frequency and duration of use. Approximately 14% of the study population reported exposure to only one agent and 11% reported working with two or more of the 11 agents in their lifetime. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated for each agent, adjusting for established breast cancer risk factors. During follow-up, 1,966 cases of breast cancer were reported. Although there were no significant associations between ever use of the eleven agents evaluated and breast cancer risk, women with cumulative exposure to gasoline or petroleum products at or above the highest quartile cutoff had an elevated risk of total (HR: 2.3, 95%CI: 1.1-4.9) and invasive (HR: 2.5, 95%CI: 1.1-5.9) breast cancer compared with women in the lowest quartile group (p sub(trend)=0.03). Workplace exposure to soldering materials was associated with an increased risk of premenopausal breast cancer (HR=1.8, 95% CI=1.1-3.0). Findings support the need for further studies to elucidate the role of occupational chemicals in breast cancer etiology. What's new? There has been widespread interest in the role of chemical exposures in the development of breast cancer, but few occupational studies have prospectively investigated breast cancer risk. The workplace is a setting where there is the potential for greater than background levels of exposure. Here, the authors investigate the association between workplace chemical exposures and incident breast cancer in 47,640 women enrolled in the Sister Study. They observe significant trends in breast cancer risk associated with increased gasoline/petroleum product use, suggesting that additional studies are warranted to examine the influence of occupational chemical exposures on breast cancer etiology. JF - International Journal of Cancer AU - Ekenga, Christine C AU - Parks, Christine G AU - Sandler, Dale P AD - Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC. Y1 - 2015/10// PY - 2015 DA - Oct 2015 SP - 1765 EP - 1774 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 137 IS - 7 SN - 0020-7136, 0020-7136 KW - Toxicology Abstracts; Risk Abstracts; Health & Safety Science Abstracts KW - Soldering KW - Invasiveness KW - Gasoline KW - Stains KW - Petroleum KW - Risk factors KW - Adhesives KW - Occupational exposure KW - Metals KW - Etiology KW - Solvents KW - Oils KW - Population studies KW - Cancer KW - Health risks KW - Dyes KW - Acids KW - Background levels KW - Pesticides KW - Breast cancer KW - Paints KW - R2 23060:Medical and environmental health KW - H 1000:Occupational Safety and Health KW - X 24330:Agrochemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701481821?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=Chemical+exposures+in+the+workplace+and+breast+cancer+risk%3A+A+prospective+cohort+study&rft.au=Ekenga%2C+Christine+C%3BParks%2C+Christine+G%3BSandler%2C+Dale+P&rft.aulast=Ekenga&rft.aufirst=Christine&rft.date=2015-10-01&rft.volume=137&rft.issue=7&rft.spage=1765&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.29545 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2015-09-30 N1 - SubjectsTermNotLitGenreText - Soldering; Metals; Etiology; Invasiveness; Gasoline; Oils; Solvents; Population studies; Stains; Dyes; Risk factors; Acids; Petroleum; Pesticides; Background levels; Breast cancer; Adhesives; Occupational exposure; Paints; Cancer; Health risks DO - http://dx.doi.org/10.1002/ijc.29545 ER - TY - JOUR T1 - Circulating Inflammation Markers, Risk of Lung Cancer, and Utility for Risk Stratification. AN - 1700335051; 26220734 AB - We conducted two independent nested case-control studies to identify circulating inflammation markers reproducibly associated with lung cancer risk and to investigate the utility of replicated markers for lung cancer risk stratification. Nested within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, the previously published discovery study included 526 lung cancer patients and 592 control subjects and the replication study included 526 lung cancer case patients and 625 control subjects. Control subjects were matched by sex, age, smoking, study visit, and years of blood draw and exit. Serum levels of 51 inflammation markers were measured. Odds ratios (ORs) were estimated with conditional logistic regression. All statistical tests were two-sided. Of 11 markers identified in the discovery study, C-reactive protein (CRP) (odds ratio [OR] [highest vs. lowest category] = 1.77, 95% confidence interval [CI] = 1.23 to 2.54), serum amyloid A (SAA) (OR = 1.88, 95% CI = 1.28 to 2.76), soluble tumor necrosis factor receptor-2 (sTNFRII) (OR = 1.70, 95% CI = 1.18 to 2.45), and monokine induced by gamma interferon (CXCL9/MIG) (OR = 2.09, 95% CI = 1.41 to 3.00) were associated with lung cancer risk in the replication study (P trend < .01). In pooled analyses, CRP, SAA, and CXCL9/MIG remained associated with lung cancer more than six years before diagnosis (P trend < .05). The incorporation of an inflammation score combining these four markers did not improve the sensitivity (77.6% vs 75.8%, P = .33) or specificity (56.1% vs 56.1%, P = .98) of risk-based lung cancer models. Circulating levels of CRP, SAA, sTNFRII, and CXCL9/MIG were reproducibly associated with lung cancer risk in two independent studies within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, underscoring an etiologic role for inflammation in lung carcinogenesis, though replication is needed in other populations. Markers did not improve lung cancer risk stratification beyond standard demographic and behavioral characteristics. Published by Oxford University Press 2015. This work is written by (a) US Government employee(s) and is in the public domain in the US. JF - Journal of the National Cancer Institute AU - Shiels, Meredith S AU - Katki, Hormuzd A AU - Hildesheim, Allan AU - Pfeiffer, Ruth M AU - Engels, Eric A AU - Williams, Marcus AU - Kemp, Troy J AU - Caporaso, Neil E AU - Pinto, Ligia A AU - Chaturvedi, Anil K AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD (MSS, HAK, AH, RMP, EAE, NEC, AKC); HPV Immunology Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Inc, Frederick, MD (MW, TJK, LAP). shielsms@mail.nih.gov. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD (MSS, HAK, AH, RMP, EAE, NEC, AKC); HPV Immunology Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Inc, Frederick, MD (MW, TJK, LAP). Y1 - 2015/10// PY - 2015 DA - October 2015 VL - 107 IS - 10 KW - Biomarkers KW - 0 KW - Biomarkers, Tumor KW - CXCL9 protein, human KW - Chemokine CXCL9 KW - Receptors, Tumor Necrosis Factor, Type II KW - Serum Amyloid A Protein KW - C-Reactive Protein KW - 9007-41-4 KW - Index Medicus KW - Sensitivity and Specificity KW - Odds Ratio KW - Reproducibility of Results KW - Humans KW - Smoking -- adverse effects KW - Aged KW - Smoking -- epidemiology KW - Risk Assessment KW - Logistic Models KW - Risk Factors KW - Adult KW - Case-Control Studies KW - Early Detection of Cancer KW - Middle Aged KW - United States -- epidemiology KW - Biomarkers -- blood KW - Female KW - Male KW - Lung Neoplasms -- epidemiology KW - Serum Amyloid A Protein -- metabolism KW - Lung Neoplasms -- blood KW - Inflammation -- blood KW - Chemokine CXCL9 -- blood KW - Receptors, Tumor Necrosis Factor, Type II -- blood KW - Biomarkers, Tumor -- blood KW - C-Reactive Protein -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1700335051?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Circulating+Inflammation+Markers%2C+Risk+of+Lung+Cancer%2C+and+Utility+for+Risk+Stratification.&rft.au=Shiels%2C+Meredith+S%3BKatki%2C+Hormuzd+A%3BHildesheim%2C+Allan%3BPfeiffer%2C+Ruth+M%3BEngels%2C+Eric+A%3BWilliams%2C+Marcus%3BKemp%2C+Troy+J%3BCaporaso%2C+Neil+E%3BPinto%2C+Ligia+A%3BChaturvedi%2C+Anil+K&rft.aulast=Shiels&rft.aufirst=Meredith&rft.date=2015-10-01&rft.volume=107&rft.issue=10&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdjv199 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-26 N1 - Date created - 2015-07-29 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/jnci/djv199 ER - TY - JOUR T1 - Exosomal doxorubicin reduces the cardiac toxicity of doxorubicin. AN - 1826641824; 26420143 AB - To test the efficacy and toxicity of exosomal doxorubicin (exoDOX) compared with free doxorubicin. The cytotoxic effects of exoDOX were tested in vitro and in nude mice by measuring the tumor volume. The toxic effects were evaluated by measuring the bodyweight and through histopathologic analyses. The biodistribution of DOX was assessed by MS. In vitro and in vivo studies showed that exosomes did not decrease the efficacy of DOX. Surprisingly, exoDOX showed no cardiotoxicity as observed in DOX-treated mice and MS studies confirmed that the accumulation of exoDOX in the heart was reduced by about 40 percent. We demonstrated that exoDOX was less toxic than DOX through its altered biodistribution. JF - Nanomedicine (London, England) AU - Toffoli, Giuseppe AU - Hadla, Mohamad AU - Corona, Giuseppe AU - Caligiuri, Isabella AU - Palazzolo, Stefano AU - Semeraro, Sabrina AU - Gamini, Amelia AU - Canzonieri, Vincenzo AU - Rizzolio, Flavio AD - Department of Translational Research, National Cancer Institute - CRO-IRCSS, Aviano, Italy. ; Department of Chemical & Pharmaceutical Sciences, University of Trieste, Italy. Y1 - 2015/09/30/ PY - 2015 DA - 2015 Sep 30 KW - breast cancer KW - toxicity KW - exosomal doxorubicin KW - nanomedicine KW - drug delivery KW - exosome UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826641824?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nanomedicine+%28London%2C+England%29&rft.atitle=Exosomal+doxorubicin+reduces+the+cardiac+toxicity+of+doxorubicin.&rft.au=Toffoli%2C+Giuseppe%3BHadla%2C+Mohamad%3BCorona%2C+Giuseppe%3BCaligiuri%2C+Isabella%3BPalazzolo%2C+Stefano%3BSemeraro%2C+Sabrina%3BGamini%2C+Amelia%3BCanzonieri%2C+Vincenzo%3BRizzolio%2C+Flavio&rft.aulast=Toffoli&rft.aufirst=Giuseppe&rft.date=2015-09-30&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Nanomedicine+%28London%2C+England%29&rft.issn=1748-6963&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2015-09-30 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - The DNA structure and sequence preferences of WRN underlie its function in telomeric recombination events. AN - 1718333325; 26420422 AB - Telomeric abnormalities caused by loss of function of the RecQ helicase WRN are linked to the multiple premature ageing phenotypes that characterize Werner syndrome. Here we examine WRN's role in telomeric maintenance, by comparing its action on a variety of DNA structures without or with telomeric sequences. Our results show that WRN clearly prefers to act on strand invasion intermediates in a manner that favours strand invasion and exchange. Moreover, WRN unwinding of these recombination structures is further enhanced when the invading strand contains at least three G-rich single-stranded telomeric repeats. These selectivities are most pronounced at NaCl concentrations within the reported intranuclear monovalent cation concentration range, and are partly conferred by WRN's C-terminal region. Importantly, WRN's specificity for the G-rich telomeric sequence within this precise structural context is particularly relevant to telomere metabolism and strongly suggests a physiological role in telomeric recombination processes, including T-loop dynamics. JF - Nature communications AU - Edwards, Deanna N AU - Machwe, Amrita AU - Chen, Li AU - Bohr, Vilhelm A AU - Orren, David K AD - Department of Toxicology and Cancer Biology, University of Kentucky College of Medicine, Lexington, Kentucky 40536, USA. ; Markey Cancer Center, University of Kentucky College of Medicine, Lexington, Kentucky 40536, USA. ; Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA. Y1 - 2015/09/30/ PY - 2015 DA - 2015 Sep 30 SP - 8331 VL - 6 KW - DNA KW - 9007-49-2 KW - Exodeoxyribonucleases KW - EC 3.1.- KW - RecQ Helicases KW - EC 3.6.4.12 KW - WRN protein, human KW - Werner Syndrome Helicase KW - Index Medicus KW - Humans KW - Werner Syndrome -- metabolism KW - Telomere -- metabolism KW - Werner Syndrome -- enzymology KW - DNA -- metabolism KW - Recombination, Genetic KW - DNA -- genetics KW - Telomere -- genetics KW - RecQ Helicases -- genetics KW - RecQ Helicases -- chemistry KW - DNA -- chemistry KW - Exodeoxyribonucleases -- genetics KW - Werner Syndrome -- genetics KW - Exodeoxyribonucleases -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1718333325?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+communications&rft.atitle=The+DNA+structure+and+sequence+preferences+of+WRN+underlie+its+function+in+telomeric+recombination+events.&rft.au=Edwards%2C+Deanna+N%3BMachwe%2C+Amrita%3BChen%2C+Li%3BBohr%2C+Vilhelm+A%3BOrren%2C+David+K&rft.aulast=Edwards&rft.aufirst=Deanna&rft.date=2015-09-30&rft.volume=6&rft.issue=&rft.spage=8331&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms9331 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-20 N1 - Date created - 2015-09-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2005 Sep 16;280(37):32069-80 [16030011] Nat Genet. 1998 Oct;20(2):114-6 [9771700] Biochemistry. 2006 Nov 28;45(47):13939-46 [17115688] Proc Natl Acad Sci U S A. 2007 Feb 13;104(7):2205-10 [17284601] Mol Cell Biol. 2008 Mar;28(6):1892-904 [18212065] Annu Rev Genet. 2008;42:301-34 [18680434] Hum Genet. 2008 Nov;124(4):369-77 [18810497] J Am Chem Soc. 2009 Apr 1;131(12):4301-9 [19271707] Trends Cell Biol. 2009 Aug;19(8):414-22 [19589679] Mol Cell Biol. 2009 Oct;29(20):5552-63 [19667071] Structure. 2010 Feb 10;18(2):177-87 [20159463] Nucleic Acids Res. 2010 Jul;38(12):3984-98 [20215438] FEBS J. 2010 Sep;277(17):3470-88 [20670277] Biochemistry. 2011 Aug 16;50(32):6774-88 [21736299] Cell. 1998 Feb 6;92(3):401-13 [9476899] Nucleic Acids Res. 2014 Jul;42(12):7748-61 [24880691] J Biol Chem. 1998 Dec 18;273(51):34139-44 [9852073] Science. 1999 Feb 26;283(5406):1321-5 [10037601] J Biol Chem. 1999 Apr 30;274(18):12797-802 [10212265] Nat Genet. 2000 Jan;24(1):16-7 [10615119] Nature. 2000 Nov 9;408(6809):263-6 [11089984] Nucleic Acids Res. 2001 Jul 1;29(13):2843-9 [11433031] Mech Ageing Dev. 2001 Oct;122(15):1685-94 [11557273] EMBO J. 2001 Oct 1;20(19):5532-40 [11574485] J Biol Chem. 2002 Feb 8;277(6):4492-504 [11717307] Science. 2002 Mar 29;295(5564):2446-9 [11923537] J Biol Chem. 2002 Jun 28;277(26):23236-45 [11956187] J Biol Chem. 2002 Oct 25;277(43):41110-9 [12181313] Biochemistry. 2002 Nov 19;41(46):13483-8 [12427008] Hum Genet. 2003 Sep;113(4):337-47 [12827497] Curr Biol. 2003 Sep 2;13(17):1549-56 [12956959] J Biol Chem. 2003 Dec 26;278(52):52997-3006 [14534320] Oncogene. 2004 Jan 8;23(1):149-56 [14712220] Mol Cell. 2004 Jun 18;14(6):763-74 [15200954] Nat Genet. 2004 Aug;36(8):877-82 [15235603] Mol Cell Biol. 2004 Oct;24(19):8437-46 [15367665] J Biol Chem. 1968 Sep 25;243(18):4661-6 [4234709] J Cell Sci. 1970 Jul;7(1):5-13 [5476863] J Physiol. 1978 Nov;284:37-53 [104029] Methods Enzymol. 1980;65(1):499-560 [6246368] Cell. 1985 Dec;43(2 Pt 1):405-13 [3907856] Am J Med. 1986 Apr 25;80(4A):3-7 [3706350] Cell. 1989 Dec 1;59(5):871-80 [2590943] Methods Enzymol. 1992;211:191-9 [1406307] Proc Natl Acad Sci U S A. 1992 Nov 1;89(21):10114-8 [1438199] J Biol Chem. 1994 Aug 26;269(34):21858-69 [8063830] Science. 1996 Apr 12;272(5259):258-62 [8602509] Nat Genet. 1997 Sep;17(1):100-3 [9288107] Mech Ageing Dev. 1997 Dec;98(3):239-54 [9352493] Cell. 1999 May 14;97(4):503-14 [10338214] Nucleic Acids Res. 1999 Sep 1;27(17):3557-66 [10446247] Science. 2004 Dec 10;306(5703):1951-3 [15591207] J Biol Chem. 2005 Jun 17;280(24):23397-407 [15845538] Semin Cancer Biol. 2011 Dec;21(6):349-53 [22015685] Mutat Res. 2012 Feb 1;730(1-2):12-9 [21945241] Exp Cell Res. 2012 Jul 15;318(12):1456-60 [22391099] Nature. 2013 May 23;497(7450):458-62 [23657261] Curr Opin Genet Dev. 2013 Jun;23(3):271-9 [23790415] Trends Genet. 2013 Sep;29(9):513-20 [23876621] Cell. 2013 Oct 10;155(2):345-56 [24120135] PLoS One. 2014;9(1):e80664 [24454683] Annu Rev Biochem. 2014;83:519-52 [24606147] Genes Dev. 2005 Nov 1;19(21):2560-70 [16264192] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ncomms9331 ER - TY - JOUR T1 - Mechanistic Implications of the Unique Structural Features and Dimerization of the Cytoplasmic Domain of the Pseudomonas Sigma Regulator, PupR. AN - 1718074887; 26313375 AB - Gram-negative bacteria tightly regulate intracellular levels of iron, an essential nutrient. To ensure this strict control, some outer membrane TonB-dependent transporters (TBDTs) that are responsible for iron import stimulate their own transcription in response to extracellular binding by an iron-laden siderophore. This process is mediated by an inner membrane sigma regulator protein (an anti-sigma factor) that transduces an unknown periplasmic signal from the TBDT to release an intracellular sigma factor from the inner membrane, which ultimately upregulates TBDT transcription. Here, we use the Pseudomonas putida ferric-pseudobactin BN7/BN8 sigma regulator, PupR, as a model system to understand the molecular mechanism of this conserved class of sigma regulators. We have determined the X-ray crystal structure of the cytoplasmic anti-sigma domain (ASD) of PupR to 2.0 Å. Size exclusion chromatography, small-angle X-ray scattering, and sedimentation velocity analytical ultracentrifugation all indicate that, in contrast to other ASDs, the PupR-ASD exists as a dimer in solution. Mutagenesis of residues at the dimer interface identified from the crystal structure disrupts dimerization and protein stability, as determined by sedimentation velocity analytical ultracentrifugation and thermal denaturation circular dichroism spectroscopy. These combined results suggest that this type of inner membrane sigma regulator may utilize an unusual mechanism to sequester their cognate sigma factors and prevent transcription activation. JF - Biochemistry AU - Jensen, Jaime L AU - Balbo, Andrea AU - Neau, David B AU - Chakravarthy, Srinivas AU - Zhao, Huaying AU - Sinha, Sangita C AU - Colbert, Christopher L AD - Department of Chemistry and Biochemistry, North Dakota State University , Fargo, North Dakota 58108-6050, United States. ; Biomedical Engineering and Physical Science Shared Resource, National Institute of Biomedical Imaging and Bioengineering, National Institutes of Health , Bethesda, Maryland 20892, United States. ; Department of Chemistry and Chemical Biology, Cornell University, Northeastern Collaborative Access Team, Argonne National Laboratory, Argonne, Illinois 60439, United States. ; Biophysics Collaborative Access Team, Advanced Photon Source, 9700 South Cass Avenue, Bldg. 435B, Argonne, Illinois 60439, United States. ; Dynamics of Macromolecular Assembly Section, Laboratory of Cellular Imaging and Macromolecular Biophysics, National Institute of Biomedical Imaging and Bioengineering, National Institutes of Health , Bethesda, Maryland 20892, United States. Y1 - 2015/09/29/ PY - 2015 DA - 2015 Sep 29 SP - 5867 EP - 5877 VL - 54 IS - 38 KW - Bacterial Proteins KW - 0 KW - Membrane Proteins KW - PupR protein, Pseudomonas putida KW - Index Medicus KW - Models, Molecular KW - Protein Stability KW - Crystallography, X-Ray KW - Protein Structure, Tertiary KW - Protein Multimerization KW - Bacterial Proteins -- chemistry KW - Membrane Proteins -- chemistry KW - Pseudomonas putida -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1718074887?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Mechanistic+Implications+of+the+Unique+Structural+Features+and+Dimerization+of+the+Cytoplasmic+Domain+of+the+Pseudomonas+Sigma+Regulator%2C+PupR.&rft.au=Jensen%2C+Jaime+L%3BBalbo%2C+Andrea%3BNeau%2C+David+B%3BChakravarthy%2C+Srinivas%3BZhao%2C+Huaying%3BSinha%2C+Sangita+C%3BColbert%2C+Christopher+L&rft.aulast=Jensen&rft.aufirst=Jaime&rft.date=2015-09-29&rft.volume=54&rft.issue=38&rft.spage=5867&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=1520-4995&rft_id=info:doi/10.1021%2Facs.biochem.5b00826 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-11 N1 - Date created - 2015-09-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Anal Biochem. 2003 Sep 1;320(1):104-24 [12895474] J Bacteriol. 2000 Feb;182(3):637-46 [10633096] J Mol Biol. 2001 Oct 26;313(3):485-99 [11676534] Anal Biochem. 2001 Dec 15;299(2):271-4 [11730356] Mol Cell. 2003 Apr;11(4):1067-78 [12718891] Mol Microbiol. 2003 Jun;48(6):1467-80 [12791131] J Comput Chem. 2004 Oct;25(13):1605-12 [15264254] EMBO J. 2004 Aug 4;23(15):2952-62 [15257291] Mol Microbiol. 2004 Aug;53(4):1267-77 [15306027] Annu Rev Microbiol. 2004;58:611-47 [15487950] Annu Rev Genet. 1985;19:355-87 [3936407] J Bacteriol. 1990 Dec;172(12):6749-58 [2254251] Anal Biochem. 1992 Nov 1;206(2):215-25 [1443589] J Mol Biol. 1993 Jan 5;229(1):105-24 [7678431] Mol Microbiol. 1993 May;8(3):591-601 [8392140] EMBO J. 1994 Jun 15;13(12):2805-13 [8026465] EMBO J. 1995 Apr 3;14(7):1430-8 [7729419] Mol Microbiol. 1995 Jan;15(1):119-32 [7752886] Mol Microbiol. 1995 Oct;18(1):163-74 [8596456] Methods Enzymol. 1997;276:523-30 [9048379] Microbiol Mol Biol Rev. 1997 Sep;61(3):319-36 [9293185] J Biol Chem. 1997 Nov 7;272(45):28391-7 [9353297] Protein Expr Purif. 1999 Feb;15(1):34-9 [10024467] J Struct Biol. 1999 Apr-May;125(2-3):185-95 [10222274] Genes Dev. 1999 Sep 15;13(18):2449-61 [10500101] Acta Crystallogr D Biol Crystallogr. 2004 Dec;60(Pt 12 Pt 1):2126-32 [15572765] FEMS Microbiol Rev. 2005 Sep;29(4):673-84 [16102597] Biometals. 2005 Oct;18(5):507-17 [16333751] Acta Crystallogr D Biol Crystallogr. 2006 Apr;62(Pt 4):439-50 [16552146] Proc Natl Acad Sci U S A. 2007 Jan 9;104(2):513-8 [17197416] PLoS One. 2014;9(4):e89502 [24727671] J Mol Biol. 2014 Jun 12;426(12):2313-27 [24727125] FEMS Microbiol Rev. 2014 Jul;38(4):569-97 [24923658] Environ Microbiol. 2014 Aug;16(8):2433-43 [24373018] BMC Microbiol. 2014;14:287 [25433393] J Biol Chem. 2015 May 8;290(19):12237-46 [25809487] Biomolecules. 2015;5(3):1245-65 [26131973] Environ Microbiol. 2015 Sep;17(9):3263-77 [25581349] J Mol Biol. 2007 Apr 27;368(2):398-406 [17349657] J Am Chem Soc. 2007 May 2;129(17):5656-64 [17411046] J Mol Biol. 2007 Sep 21;372(3):774-97 [17681537] Mol Cell. 2007 Sep 7;27(5):793-805 [17803943] Acta Crystallogr D Biol Crystallogr. 2008 Jan;64(Pt 1):61-9 [18094468] Curr Protoc Immunol. 2008 May;Chapter 18:Unit 18.15 [18491296] BMC Struct Biol. 2008;8:25 [18477405] Biochim Biophys Acta. 2008 Sep;1778(9):1930-45 [17673165] Proc Natl Acad Sci U S A. 2009 Jan 27;106(4):1045-50 [19144921] Acta Crystallogr D Biol Crystallogr. 2009 Jun;65(Pt 6):582-601 [19465773] Mol Microbiol. 2009 Dec;74(5):1257-71 [19889096] Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):125-32 [20124692] Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):213-21 [20124702] J Mol Biol. 2010 Apr 16;397(5):1199-208 [20184899] Nucleic Acids Res. 2010 Jul;38(Web Server issue):W540-4 [20507903] Annu Rev Microbiol. 2010;64:43-60 [20420522] J Mol Biol. 2011 Apr 8;407(4):477-91 [21295582] Biophys J. 2011 May 4;100(9):2309-17 [21539801] Mol Microbiol. 2011 Dec;82(6):1444-53 [22040024] Anal Chem. 2012 Nov 6;84(21):9513-9 [23020071] J Gen Physiol. 2013 Jun;141(6):747-9 [23855058] Biophys J. 2013 Aug 20;105(4):962-74 [23972848] Acta Crystallogr D Biol Crystallogr. 2014 Apr;70(Pt 4):1026-36 [24699647] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/acs.biochem.5b00826 ER - TY - CPAPER T1 - From Commensalism to Parasitism: Context and Consequences T2 - 48th Annual Meeting of the Society for Leukocyte Biology AN - 1731760051; 6364447 JF - 48th Annual Meeting of the Society for Leukocyte Biology AU - Belkaid, Yasmine Y1 - 2015/09/27/ PY - 2015 DA - 2015 Sep 27 KW - Commensalism KW - Parasitism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731760051?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=48th+Annual+Meeting+of+the+Society+for+Leukocyte+Biology&rft.atitle=From+Commensalism+to+Parasitism%3A+Context+and+Consequences&rft.au=Belkaid%2C+Yasmine&rft.aulast=Belkaid&rft.aufirst=Yasmine&rft.date=2015-09-27&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=48th+Annual+Meeting+of+the+Society+for+Leukocyte+Biology&rft.issn=&rft_id=info:doi/ L2 - http://leukocytebiology.org/PDFs/2015-Conference/SLB-2015-Program-Book-FINAL.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - CPAPER T1 - Genomic Switches and Lymphocyte Identity T2 - 48th Annual Meeting of the Society for Leukocyte Biology AN - 1731759892; 6364441 JF - 48th Annual Meeting of the Society for Leukocyte Biology AU - O'Shea, John Y1 - 2015/09/27/ PY - 2015 DA - 2015 Sep 27 KW - genomics KW - Lymphocytes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731759892?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=48th+Annual+Meeting+of+the+Society+for+Leukocyte+Biology&rft.atitle=Genomic+Switches+and+Lymphocyte+Identity&rft.au=O%27Shea%2C+John&rft.aulast=O%27Shea&rft.aufirst=John&rft.date=2015-09-27&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=48th+Annual+Meeting+of+the+Society+for+Leukocyte+Biology&rft.issn=&rft_id=info:doi/ L2 - http://leukocytebiology.org/PDFs/2015-Conference/SLB-2015-Program-Book-FINAL.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-06 N1 - Last updated - 2015-11-09 ER - TY - JOUR T1 - Origin of eukaryotes from within archaea, archaeal eukaryome and bursts of gene gain: eukaryogenesis just made easier? AN - 1808700701; PQ0003420169 AB - The origin of eukaryotes is a fundamental, forbidding evolutionary puzzle. Comparative genomic analysis clearly shows that the last eukaryotic common ancestor (LECA) possessed most of the signature complex features of modern eukaryotic cells, in particular the mitochondria, the endomembrane system including the nucleus, an advanced cytoskeleton and the ubiquitin network. Numerous duplications of ancestral genes, e.g. DNA polymerases, RNA polymerases and proteasome subunits, also can be traced back to the LECA. Thus, the LECA was not a primitive organism and its emergence must have resulted from extensive evolution towards cellular complexity. However, the scenario of eukaryogenesis, and in particular the relationship between endosymbiosis and the origin of eukaryotes, is far from being clear. Four recent developments provide new clues to the likely routes of eukaryogenesis. First, evolutionary reconstructions suggest complex ancestors for most of the major groups of archaea, with the subsequent evolution dominated by gene loss. Second, homologues of signature eukaryotic proteins, such as actin and tubulin that form the core of the cytoskeleton or the ubiquitin system, have been detected in diverse archaea. The discovery of this 'dispersed eukaryome' implies that the archaeal ancestor of eukaryotes was a complex cell that might have been capable of a primitive form of phagocytosis and thus conducive to endosymbiont capture. Third, phylogenomic analyses converge on the origin of most eukaryotic genes of archaeal descent from within the archaeal evolutionary tree, specifically, the TACK superphylum. Fourth, evidence has been presented that the origin of the major archaeal phyla involved massive acquisition of bacterial genes. Taken together, these findings make the symbiogenetic scenario for the origin of eukaryotes considerably more plausible and the origin of the organizational complexity of eukaryotic cells more readily explainable than they appeared until recently. JF - Philosophical Transactions of the Royal Society of London, Series B: Biological Sciences AU - Koonin, Eugene V AD - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, , Bethesda, MD 20894, USA, koonin@ncbi.nlm.nih.gov Y1 - 2015/09/26/ PY - 2015 DA - 2015 Sep 26 SP - 20140333 PB - Royal Society of London, 6 Carlton House Terrace London SW1Y 5AG United Kingdom VL - 370 IS - 1678 SN - 0962-8436, 0962-8436 KW - Ecology Abstracts KW - endosymbiosis KW - phagocytosis KW - cytoskeleton KW - horizontal gene transfer KW - archaea KW - Archaea KW - Endosymbionts KW - proteasomes KW - Mitochondria KW - Cytoskeleton KW - DNA-directed DNA polymerase KW - Genomic analysis KW - Actin KW - Evolutionary genetics KW - Nuclei KW - Tubulin KW - Phagocytosis KW - Evolution KW - Ubiquitin KW - D 04040:Ecosystem and Ecology Studies UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808700701?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Philosophical+Transactions+of+the+Royal+Society+of+London%2C+Series+B%3A+Biological+Sciences&rft.atitle=Origin+of+eukaryotes+from+within+archaea%2C+archaeal+eukaryome+and+bursts+of+gene+gain%3A+eukaryogenesis+just+made+easier%3F&rft.au=Koonin%2C+Eugene+V&rft.aulast=Koonin&rft.aufirst=Eugene&rft.date=2015-09-26&rft.volume=370&rft.issue=1678&rft.spage=20140333&rft.isbn=&rft.btitle=&rft.title=Philosophical+Transactions+of+the+Royal+Society+of+London%2C+Series+B%3A+Biological+Sciences&rft.issn=09628436&rft_id=info:doi/10.1098%2Frstb.2014.0333 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Endosymbionts; proteasomes; Mitochondria; Cytoskeleton; DNA-directed DNA polymerase; Genomic analysis; Actin; Evolutionary genetics; Phagocytosis; Tubulin; Nuclei; Evolution; Ubiquitin; Archaea DO - http://dx.doi.org/10.1098/rstb.2014.0333 ER - TY - JOUR T1 - Integrative genomics identifies YY1AP1 as an oncogenic driver in EpCAM(+) AFP(+) hepatocellular carcinoma. AN - 1716935143; 25597408 AB - Identification of key drivers and new therapeutic targets is important given the poor prognosis for hepatocellular carcinoma (HCC) patients, particularly those ineligible for surgical resection or liver transplant. However, the approach to identify such driver genes is facing significant challenges due to the genomically heterogenous nature of HCC. Here we tested whether the integrative genomic profiling of a well-defined HCC subset that is classified by an extreme EpCAM(+) AFP(+) gene expression signature and associated with poor prognosis, all attributes of a stem cell-like phenotype, could uncover survival-related driver genes in HCC. Following transcriptomic analysis of the well-defined HCC cases, a Gene Set Enrichment Analysis coupled with genomic copy number alteration assessment revealed that YY1-associated protein 1 (YY1AP1) is a critical oncoprotein specifically activated in EpCAM(+) AFP(+) HCC. YY1AP1 silencing eliminates oncogene addiction by altering the chromatin landscape and triggering massive apoptosis in vitro and tumor suppression in vivo. YY1AP1 expression promotes HCC proliferation and is required for the maintenance of stem cell features. We revealed that YY1AP1 cooperates with YY1 to alter the chromatin landscape and activate transcription of stemness regulators. Thus YY1AP1 may serve as a key molecular target for EpCAM(+) AFP(+) HCC subtype. Our results demonstrate the feasibility and power of a new strategy by utilizing well-defined patient samples and integrative genomics to uncover critical pathways linked to HCC subtypes with prognostic impact. JF - Oncogene AU - Zhao, X AU - Parpart, S AU - Takai, A AU - Roessler, S AU - Budhu, A AU - Yu, Z AU - Blank, M AU - Zhang, Y E AU - Jia, H-L AU - Ye, Q-H AU - Qin, L-X AU - Tang, Z-Y AU - Thorgeirsson, S S AU - Wang, X W AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA. ; Laboratory of Cellular and Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA. ; Liver Cancer Institute, Fudan University, Shanghai, China. ; Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA. Y1 - 2015/09/24/ PY - 2015 DA - 2015 Sep 24 SP - 5095 EP - 5104 VL - 34 IS - 39 KW - Antigens, Neoplasm KW - 0 KW - Cell Adhesion Molecules KW - Chromatin KW - EPCAM protein, human KW - Epithelial Cell Adhesion Molecule KW - Nuclear Proteins KW - Transcription Factors KW - YY1AP1 protein, human KW - alpha-Fetoproteins KW - Index Medicus KW - Chromatin -- metabolism KW - Humans KW - Transcriptome KW - Transcription Factors -- physiology KW - Liver Neoplasms -- metabolism KW - Cell Adhesion Molecules -- genetics KW - Carcinoma, Hepatocellular -- metabolism KW - Nuclear Proteins -- genetics KW - Cell Adhesion Molecules -- metabolism KW - Antigens, Neoplasm -- metabolism KW - Antigens, Neoplasm -- genetics KW - Transcription Factors -- genetics KW - Nuclear Proteins -- physiology KW - alpha-Fetoproteins -- metabolism KW - Genomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1716935143?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Integrative+genomics+identifies+YY1AP1+as+an+oncogenic+driver+in+EpCAM%28%2B%29+AFP%28%2B%29+hepatocellular+carcinoma.&rft.au=Zhao%2C+X%3BParpart%2C+S%3BTakai%2C+A%3BRoessler%2C+S%3BBudhu%2C+A%3BYu%2C+Z%3BBlank%2C+M%3BZhang%2C+Y+E%3BJia%2C+H-L%3BYe%2C+Q-H%3BQin%2C+L-X%3BTang%2C+Z-Y%3BThorgeirsson%2C+S+S%3BWang%2C+X+W&rft.aulast=Zhao&rft.aufirst=X&rft.date=2015-09-24&rft.volume=34&rft.issue=39&rft.spage=5095&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2014.438 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-15 N1 - Date created - 2015-09-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Cell Biol. 2011 Feb;31(4):700-9 [21173166] Nucleic Acids Res. 2011 Jan;39(Database issue):D945-50 [20952405] CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855] N Engl J Med. 2012 Mar 8;366(10):883-92 [22397650] Gastroenterology. 2012 Apr;142(4):957-966.e12 [22202459] Nat Genet. 2012 Jun;44(6):694-8 [22561517] Nature. 2012 Jun 21;486(7403):400-4 [22722201] Nature. 2012 Jul 19;487(7407):330-7 [22810696] Semin Oncol. 2012 Aug;39(4):461-72 [22846863] Nature. 2012 Sep 27;489(7417):519-25 [22960745] Hepatology. 2012 Nov;56(5):1792-803 [22707408] CA Cancer J Clin. 2013 Jan;63(1):11-30 [23335087] Gastroenterology. 2013 May;144(5):1066-1075.e1 [23376425] Gastroenterology. 2001 Jun;120(7):1763-73 [11375957] Hepatology. 2009 Aug;50(2):472-80 [19585654] Cancer Res. 2009 Sep 15;69(18):7385-92 [19723656] Cancer. 2001 Apr 15;91(8):1479-86 [11301395] J Clin Invest. 2013 May;123(5):1911-8 [23635789] Nature. 2002 Jul 4;418(6893):104-8 [12077605] Science. 2002 Jul 5;297(5578):63-4 [12098689] Hepatology. 2007 Jan;45(1):42-52 [17187432] Cancer Res. 2007 Nov 15;67(22):10831-9 [18006828] Cell. 2007 Dec 14;131(6):1084-96 [18083099] Cancer Res. 2008 Mar 1;68(5):1451-61 [18316609] N Engl J Med. 2008 Jul 24;359(4):378-90 [18650514] Cancer Res. 2009 Feb 1;69(3):753-7 [19141643] Gastroenterology. 2009 Mar;136(3):1012-24 [19150350] Nature. 2009 Apr 9;458(7239):719-24 [19360079] Nat Med. 2003 Apr;9(4):416-23 [12640447] J Biol Chem. 2004 Apr 23;279(17):17750-5 [14744866] Clin Cancer Res. 2004 Aug 1;10(15):5131-6 [15297416] Hepatology. 2004 Sep;40(3):667-76 [15349906] Cancer Lett. 1997 Jul 15;117(1):93-8 [9233837] Mol Cell Biol. 2005 Apr;25(8):3305-16 [15798214] Curr Biol. 2005 Aug 23;15(16):1487-93 [16040246] Clin Cancer Res. 2005 Oct 15;11(20):7532-7 [16243828] Nat Med. 2006 Apr;12(4):410-6 [16532004] Genomics. 2006 Aug;88(2):143-51 [16545939] Cancer Cell. 2006 Aug;10(2):99-111 [16904609] Cell. 2009 May 1;137(3):459-71 [19410543] Nature. 2010 Feb 18;463(7283):899-905 [20164920] Cancer Res. 2010 Dec 15;70(24):10202-12 [21159642] Cell. 2011 Mar 4;144(5):646-74 [21376230] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/onc.2014.438 ER - TY - JOUR T1 - Non-Hodgkin Lymphoma in Children and Adolescents: Progress Through Effective Collaboration, Current Knowledge, and Challenges Ahead. AN - 1713951747; 26304908 AB - Non-Hodgkin lymphoma is the fourth most common malignancy in children, has an even higher incidence in adolescents, and is primarily represented by only a few histologic subtypes. Dramatic progress has been achieved, with survival rates exceeding 80%, in large part because of a better understanding of the biology of the different subtypes and national and international collaborations. Most patients with Burkitt lymphoma and diffuse large B-cell lymphoma are cured with short intensive pulse chemotherapy containing cyclophosphamide, cytarabine, and high-dose methotrexate. The benefit of the addition of rituximab has not been established except in the case of primary mediastinal B-cell lymphoma. Lymphoblastic lymphoma is treated with intensive, semi-continuous, longer leukemia-derived protocols. Relapses in B-cell and lymphoblastic lymphomas are rare and infrequently curable, even with intensive approaches. Event-free survival rates of approximately 75% have been achieved in anaplastic large-cell lymphomas with various regimens that generally include a short intensive B-like regimen. Immunity seems to play an important role in prognosis and needs further exploration to determine its therapeutic application. ALK inhibitor therapeutic approaches are currently under investigation. For all pediatric lymphomas, the intensity of induction/consolidation therapy correlates with acute toxicities, but because of low cumulative doses of anthracyclines and alkylating agents, minimal or no long-term toxicity is expected. Challenges that remain include defining the value of prognostic factors, such as early response on positron emission tomography/computed tomography and minimal disseminated and residual disease, using new biologic technologies to improve risk stratification, and developing innovative therapies, both in the first-line setting and for relapse. © 2015 by American Society of Clinical Oncology. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Minard-Colin, Véronique AU - Brugières, Laurence AU - Reiter, Alfred AU - Cairo, Mitchell S AU - Gross, Thomas G AU - Woessmann, Wilhelm AU - Burkhardt, Birgit AU - Sandlund, John T AU - Williams, Denise AU - Pillon, Marta AU - Horibe, Keizo AU - Auperin, Anne AU - Le Deley, Marie-Cécile AU - Zimmerman, Martin AU - Perkins, Sherrie L AU - Raphael, Martine AU - Lamant, Laurence AU - Klapper, Wolfram AU - Mussolin, Lara AU - Poirel, Hélène A AU - Macintyre, Elizabeth AU - Damm-Welk, Christine AU - Rosolen, Angelo AU - Patte, Catherine AD - Véronique Minard-Colin, Laurence Brugières, Anne Auperin, Marie-Cécile Le Deley, and Catherine Patte, Institut Gustave Roussy, Villejuif; Martine Raphael, Centre National de la Recherche Scientifique UMR 8126, Université Paris Sud; Elizabeth Macintyre, Université Paris Descartes Sorbonne Cité, Institut Necker-Enfants Malades, Institut National de Recherche Médicale U1151, and Assistance Publique-Hôpitaux de Paris, Hôpital Necker Enfants-Malades, Paris; Laurence Lamant, Institut Universitaire du Cancer Toulouse Oncopole and Université Paul-Sabatier, Toulouse, France; Alfred Reiter, Wilhelm Woessmann, and Christine Damm-Welk, Justus-Liebig-University Giessen, Giessen; Birgit Burkhardt, Children University Hospital, Münster; Martin Zimmerman, Medizinische Hochschule, Hannover; Wolfram Klapper, Christian-Albrechts-University Kiel, Kiel, Germany; Mitchell S. Cairo, New York Medical College, Valhalla, NY; Thomas G. Gross, National Cancer Institute, Bethesda, MD; John T. Sandlund, St Jude Children's Research Hospital and University of Tennessee Health Science Center, College of Medicine, Memphis, TN; Sherrie L. Perkins, University of Utah Health Sciences, Salt Lake City, UT; Denise Williams, Cambridge University Hospitals Foundation Trust, Cambridge, United Kingdom; Marta Pillon and Angelo Rosolen, University of Padova, Padova; Lara Mussolin, Istituto di Ricerca Pediatrico-Fondazione Cittàdella Speranza and University of Padua, Padua, Italy; Keizo Horibe, National Hospital Organization Nagoya Medical Center, Nagoya, Japan; and Hélène A. Poirel, Center for Human Genetics, Cliniques Universitaires Saint-Luc-Université Catholique de Louvain, Belgium, Brussels. ; Véronique Minard-Colin, Laurence Brugières, Anne Auperin, Marie-Cécile Le Deley, and Catherine Patte, Institut Gustave Roussy, Villejuif; Martine Raphael, Centre National de la Recherche Scientifique UMR 8126, Université Paris Sud; Elizabeth Macintyre, Université Paris Descartes Sorbonne Cité, Institut Necker-Enfants Malades, Institut National de Recherche Médicale U1151, and Assistance Publique-Hôpitaux de Paris, Hôpital Necker Enfants-Malades, Paris; Laurence Lamant, Institut Universitaire du Cancer Toulouse Oncopole and Université Paul-Sabatier, Toulouse, France; Alfred Reiter, Wilhelm Woessmann, and Christine Damm-Welk, Justus-Liebig-University Giessen, Giessen; Birgit Burkhardt, Children University Hospital, Münster; Martin Zimmerman, Medizinische Hochschule, Hannover; Wolfram Klapper, Christian-Albrechts-University Kiel, Kiel, Germany; Mitchell S. Cairo, New York Medical College, Valhalla, NY; Thomas G. Gross, National Cancer Institute, Bethesda, MD; John T. Sandlund, St Jude Children's Research Hospital and University of Tennessee Health Science Center, College of Medicine, Memphis, TN; Sherrie L. Perkins, University of Utah Health Sciences, Salt Lake City, UT; Denise Williams, Cambridge University Hospitals Foundation Trust, Cambridge, United Kingdom; Marta Pillon and Angelo Rosolen, University of Padova, Padova; Lara Mussolin, Istituto di Ricerca Pediatrico-Fondazione Cittàdella Speranza and University of Padua, Padua, Italy; Keizo Horibe, National Hospital Organization Nagoya Medical Center, Nagoya, Japan; and Hélène A. Poirel, Center for Human Genetics, Cliniques Universitaires Saint-Luc-Université Catholique de Louvain, Belgium, Brussels. catherine.patte@gustaveroussy.fr. Y1 - 2015/09/20/ PY - 2015 DA - 2015 Sep 20 SP - 2963 EP - 2974 VL - 33 IS - 27 KW - Index Medicus KW - Disease-Free Survival KW - Cooperative Behavior KW - Age of Onset KW - Risk Factors KW - Humans KW - Diffusion of Innovation KW - Treatment Outcome KW - Forecasting KW - Child KW - Adolescent KW - Time Factors KW - Survivors KW - Lymphoma, Non-Hodgkin -- diagnosis KW - Pediatrics -- trends KW - Lymphoma, Non-Hodgkin -- mortality KW - Lymphoma, Non-Hodgkin -- therapy KW - International Cooperation KW - Interdisciplinary Communication KW - Medical Oncology -- trends UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1713951747?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Non-Hodgkin+Lymphoma+in+Children+and+Adolescents%3A+Progress+Through+Effective+Collaboration%2C+Current+Knowledge%2C+and+Challenges+Ahead.&rft.au=Minard-Colin%2C+V%C3%A9ronique%3BBrugi%C3%A8res%2C+Laurence%3BReiter%2C+Alfred%3BCairo%2C+Mitchell+S%3BGross%2C+Thomas+G%3BWoessmann%2C+Wilhelm%3BBurkhardt%2C+Birgit%3BSandlund%2C+John+T%3BWilliams%2C+Denise%3BPillon%2C+Marta%3BHoribe%2C+Keizo%3BAuperin%2C+Anne%3BLe+Deley%2C+Marie-C%C3%A9cile%3BZimmerman%2C+Martin%3BPerkins%2C+Sherrie+L%3BRaphael%2C+Martine%3BLamant%2C+Laurence%3BKlapper%2C+Wolfram%3BMussolin%2C+Lara%3BPoirel%2C+H%C3%A9l%C3%A8ne+A%3BMacintyre%2C+Elizabeth%3BDamm-Welk%2C+Christine%3BRosolen%2C+Angelo%3BPatte%2C+Catherine&rft.aulast=Minard-Colin&rft.aufirst=V%C3%A9ronique&rft.date=2015-09-20&rft.volume=33&rft.issue=27&rft.spage=2963&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=1527-7755&rft_id=info:doi/10.1200%2FJCO.2014.59.5827 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-15 N1 - Date created - 2015-09-19 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1200/JCO.2014.59.5827 ER - TY - JOUR T1 - Using perturbations to identify the brain circuits underlying active vision AN - 1808662012; PQ0003438437 AB - The visual and oculomotor systems in the brain have been studied extensively in the primate. Together, they can be regarded as a single brain system that underlies active vision-the normal vision that begins with visual processing in the retina and extends through the brain to the generation of eye movement by the brainstem. The system is probably one of the most thoroughly studied brain systems in the primate, and it offers an ideal opportunity to evaluate the advantages and disadvantages of the series of perturbation techniques that have been used to study it. The perturbations have been critical in moving from correlations between neuronal activity and behaviour closer to a causal relation between neuronal activity and behaviour. The same perturbation techniques have also been used to tease out neuronal circuits that are related to active vision that in turn are driving behaviour. The evolution of perturbation techniques includes ablation of both cortical and subcortical targets, punctate chemical lesions, reversible inactivations, electrical stimulation, and finally the expanding optogenetic techniques. The evolution of perturbation techniques has supported progressively stronger conclusions about what neuronal circuits in the brain underlie active vision and how the circuits themselves might be organized. JF - Philosophical Transactions of the Royal Society of London, Series B: Biological Sciences AU - Wurtz, Robert H AD - Laboratory of Sensorimotor Research, National Eye Institute, National Institutes of Health, , Bethesda, MD 20892-4435, USA, bob@lsr.nei.nih.gov Y1 - 2015/09/19/ PY - 2015 DA - 2015 Sep 19 SP - 20140205 PB - Royal Society of London, 6 Carlton House Terrace London SW1Y 5AG United Kingdom VL - 370 IS - 1677 SN - 0962-8436, 0962-8436 KW - CSA Neurosciences Abstracts; Ecology Abstracts KW - brain-circuits KW - behaviour KW - monkeys KW - lesions KW - inactivations KW - optogenetics KW - Optics KW - oculomotor system KW - Retina KW - Eye KW - Brain stem KW - Brain KW - Circuits KW - Electrical stimuli KW - Genetics KW - Visual pathways KW - Vision KW - Information processing KW - Evolution KW - N3 11007:Neurobiology KW - D 04040:Ecosystem and Ecology Studies UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808662012?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Philosophical+Transactions+of+the+Royal+Society+of+London%2C+Series+B%3A+Biological+Sciences&rft.atitle=Using+perturbations+to+identify+the+brain+circuits+underlying+active+vision&rft.au=Wurtz%2C+Robert+H&rft.aulast=Wurtz&rft.aufirst=Robert&rft.date=2015-09-19&rft.volume=370&rft.issue=1677&rft.spage=20140205&rft.isbn=&rft.btitle=&rft.title=Philosophical+Transactions+of+the+Royal+Society+of+London%2C+Series+B%3A+Biological+Sciences&rft.issn=09628436&rft_id=info:doi/10.1098%2Frstb.2014.0205 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Optics; oculomotor system; Eye; Retina; Brain stem; Brain; Circuits; Visual pathways; Genetics; Electrical stimuli; Vision; Information processing; Evolution DO - http://dx.doi.org/10.1098/rstb.2014.0205 ER - TY - JOUR T1 - Discovery of small molecule inhibitors of MyD88-dependent signaling pathways using a computational screen. AN - 1716939606; 26381092 AB - In this study, we used high-throughput computational screening to discover drug-like inhibitors of the host MyD88 protein-protein signaling interaction implicated in the potentially lethal immune response associated with Staphylococcal enterotoxins. We built a protein-protein dimeric docking model of the Toll-interleukin receptor (TIR)-domain of MyD88 and identified a binding site for docking small molecules. Computational screening of 5 million drug-like compounds led to testing of 30 small molecules; one of these molecules inhibits the TIR-TIR domain interaction and attenuates pro-inflammatory cytokine production in human primary cell cultures. Compounds chemically similar to this hit from the PubChem database were observed to be more potent with improved drug-like properties. Most of these 2(nd) generation compounds inhibit Staphylococcal enterotoxin B (SEB)-induced TNF-α, IFN-γ, IL-6, and IL-1β production at 2-10 μM in human primary cells. Biochemical analysis and a cell-based reporter assay revealed that the most promising compound, T6167923, disrupts MyD88 homodimeric formation, which is critical for its signaling function. Furthermore, we observed that administration of a single dose of T6167923 completely protects mice from lethal SEB-induced toxic shock. In summary, our in silico approach has identified anti-inflammatory inhibitors against in vitro and in vivo toxin exposure with promise to treat other MyD88-related pro-inflammatory diseases. JF - Scientific reports AU - Olson, Mark A AU - Lee, Michael S AU - Kissner, Teri L AU - Alam, Shahabuddin AU - Waugh, David S AU - Saikh, Kamal U AD - Department of Cell Biology and Biochemistry and. ; Department of Immunology, Molecular and Translational Sciences Division, U.S. Army Medical Research Institute of Infectious Diseases, Frederick, MD 21702. ; Macromolecular Crystallography Laboratory, National Cancer Institute at Frederick, Frederick, MD 21702. Y1 - 2015/09/18/ PY - 2015 DA - 2015 Sep 18 SP - 14246 VL - 5 KW - Cytokines KW - 0 KW - Enterotoxins KW - Inflammation Mediators KW - Myeloid Differentiation Factor 88 KW - enterotoxin B, staphylococcal KW - 39424-53-8 KW - Index Medicus KW - Animals KW - Enterotoxins -- metabolism KW - Models, Molecular KW - Dose-Response Relationship, Drug KW - Humans KW - Protein Multimerization -- drug effects KW - Cytokines -- metabolism KW - Leukocytes, Mononuclear -- immunology KW - Mice KW - Protein Binding KW - Inflammation Mediators -- metabolism KW - Enterotoxins -- immunology KW - Leukocytes, Mononuclear -- metabolism KW - Inhibitory Concentration 50 KW - Leukocytes, Mononuclear -- drug effects KW - Protein Interaction Domains and Motifs KW - Protein Conformation KW - Myeloid Differentiation Factor 88 -- metabolism KW - Computer Simulation KW - Signal Transduction -- drug effects KW - Computational Biology -- methods KW - Myeloid Differentiation Factor 88 -- chemistry KW - Drug Discovery -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1716939606?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scientific+reports&rft.atitle=Discovery+of+small+molecule+inhibitors+of+MyD88-dependent+signaling+pathways+using+a+computational+screen.&rft.au=Olson%2C+Mark+A%3BLee%2C+Michael+S%3BKissner%2C+Teri+L%3BAlam%2C+Shahabuddin%3BWaugh%2C+David+S%3BSaikh%2C+Kamal+U&rft.aulast=Olson&rft.aufirst=Mark&rft.date=2015-09-18&rft.volume=5&rft.issue=&rft.spage=14246&rft.isbn=&rft.btitle=&rft.title=Scientific+reports&rft.issn=2045-2322&rft_id=info:doi/10.1038%2Fsrep14246 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-08-19 N1 - Date created - 2015-09-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Mol Graph Model. 2005 Apr;23(5):395-407 [15781182] J Comput Chem. 2009 Jul 30;30(10):1545-614 [19444816] Nucleic Acids Res. 2005 Jul 1;33(Web Server issue):W363-7 [15980490] Proteins. 2005 Aug 1;60(2):181-6 [15981262] Nature. 2000 Nov 2;408(6808):111-5 [11081518] J Immunol. 2013 Dec 15;191(12):6101-9 [24198284] Proc Natl Acad Sci U S A. 2006 Jul 18;103(29):10961-6 [16832055] Proteins. 2005 Aug 1;60(2):224-31 [15981269] Protein Sci. 2005 Dec;14(12):2964-71 [16322578] Nat Immunol. 2006 Apr;7(4):375-81 [16491077] Proc Natl Acad Sci U S A. 2006 Feb 21;103(8):2953-8 [16477040] Methods Mol Biol. 2007;363:1-19 [17272834] FEBS Lett. 2007 Feb 20;581(4):629-36 [17258210] Annu Rev Biochem. 2007;76:141-65 [17362201] J Virol. 2007 Aug;81(15):8180-91 [17507480] J Leukoc Biol. 2007 Oct;82(4):801-10 [17548806] J Chem Inf Model. 2007 Nov-Dec;47(6):2140-8 [17985865] Proteins. 2007 Dec 1;69(4):793-800 [17894347] J Biol Chem. 2008 May 2;283(18):11861-5 [18332149] Nucleic Acids Res. 2008 Jul 1;36(Web Server issue):W233-8 [18442991] Proc Natl Acad Sci U S A. 2009 Jun 23;106(25):10260-5 [19506249] J Biol Chem. 2009 Aug 7;284(32):21386-92 [19535337] J Biol Chem. 2005 Apr 22;280(16):15809-14 [15755740] Biochem Soc Trans. 2003 Jun;31(Pt 3):643-7 [12773173] J Biol Chem. 2003 Oct 17;278(42):41443-51 [12888566] J Med Chem. 2004 Jan 15;47(2):337-44 [14711306] Nat Rev Immunol. 2004 Jul;4(7):499-511 [15229469] Nat Immunol. 2004 Oct;5(10):975-9 [15454920] Oncogene. 1996 Dec 5;13(11):2467-75 [8957090] J Biol Chem. 1998 May 15;273(20):12203-9 [9575168] J Chem Inf Model. 2005 Jan-Feb;45(1):177-82 [15667143] Immunology. 2010 Aug;130(4):516-26 [20465563] Drug Discov Today. 2010 Dec;15(23-24):1052-7 [20970519] PLoS One. 2011;6(1):e15985 [21283748] Nat Immunol. 2011 May;12(5):416-24 [21441935] Nat Immunol. 2011 May;12(5):375-6 [21502988] J Biol Chem. 2011 Sep 9;286(36):31385-96 [21693701] PLoS One. 2011;6(8):e23989 [21897866] Innate Immun. 2011 Oct;17(5):451-62 [20699281] Chem Biol Drug Des. 2012 Apr;79(4):530-4 [22188672] PLoS One. 2012;7(7):e40773 [22848400] Proc Natl Acad Sci U S A. 2013 Apr 23;110(17):6985-90 [23569230] J Biol Chem. 2013 Oct 18;288(42):30210-22 [24019529] J Mol Biol. 2008 Sep 12;381(4):1068-87 [18640688] Methods Mol Biol. 2009;498:297-307 [18988033] Immunol Rev. 2009 Jan;227(1):161-75 [19120483] J Comput Chem. 2009 Dec;30(16):2785-91 [19399780] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/srep14246 ER - TY - JOUR T1 - A Mutation in Transmembrane Domain 7 (TM7) of Excitatory Amino Acid Transporters Disrupts the Substrate-dependent Gating of the Intrinsic Anion Conductance and Drives the Channel into a Constitutively Open State. AN - 1713949949; 26203187 AB - In the mammalian central nervous system, excitatory amino acid transporters (EAATs) are responsible for the clearance of glutamate after synaptic release. This energetically demanding activity is crucial for precise neuronal communication and for maintaining extracellular glutamate concentrations below neurotoxic levels. In addition to their ability to recapture glutamate from the extracellular space, EAATs exhibit a sodium- and glutamate-gated anion conductance. Here we show that substitution of a conserved positively charged residue (Arg-388, hEAAT1) in transmembrane domain 7 with a negatively charged amino acid eliminates the ability of glutamate to further activate the anion conductance. When expressed in oocytes, R388D or R388E mutants show large anion currents that display no further increase in amplitude after application of saturating concentrations of Na(+) and glutamate. They also show a substantially reduced transport activity. The mutant transporters appear to exist preferentially in a sodium- and glutamate-independent constitutive open channel state that rarely transitions to complete the transport cycle. In addition, the accessibility of cytoplasmic residues to membrane-permeant modifying reagents supports the idea that this substrate-independent open state correlates with an intermediate outward facing conformation of the transporter. Our data provide additional insights into the mechanism by which substrates gate the anion conductance in EAATs and suggest that in EAAT1, Arg-388 is a critical element for the structural coupling between the substrate translocation and the gating mechanisms of the EAAT-associated anion channel. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Torres-Salazar, Delany AU - Jiang, Jie AU - Divito, Christopher B AU - Garcia-Olivares, Jennie AU - Amara, Susan G AD - From the National Institute of Mental Health, Bethesda, Maryland 20892 and delany.torressalazar@nih.gov. ; the Department of Neurobiology, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15213. ; From the National Institute of Mental Health, Bethesda, Maryland 20892 and. ; From the National Institute of Mental Health, Bethesda, Maryland 20892 and the Department of Neurobiology, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15213 susan.amara@nih.gov. Y1 - 2015/09/18/ PY - 2015 DA - 2015 Sep 18 SP - 22977 EP - 22990 VL - 290 IS - 38 KW - Excitatory Amino Acid Transporter 1 KW - 0 KW - Recombinant Proteins KW - SLC1A3 protein, human KW - Index Medicus KW - synaptic transmission KW - neurotransmitter KW - neurotransmitter transport KW - chloride channel KW - voltage-dependent anion channel (VDAC) KW - glutamate transporter KW - glutamate KW - Xenopus laevis KW - Animals KW - Recombinant Proteins -- metabolism KW - Humans KW - Gene Expression KW - Oocytes KW - Recombinant Proteins -- genetics KW - Protein Structure, Tertiary KW - Ion Transport -- physiology KW - Amino Acid Substitution KW - Ion Channel Gating -- physiology KW - Excitatory Amino Acid Transporter 1 -- metabolism KW - Mutation, Missense KW - Excitatory Amino Acid Transporter 1 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1713949949?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=A+Mutation+in+Transmembrane+Domain+7+%28TM7%29+of+Excitatory+Amino+Acid+Transporters+Disrupts+the+Substrate-dependent+Gating+of+the+Intrinsic+Anion+Conductance+and+Drives+the+Channel+into+a+Constitutively+Open+State.&rft.au=Torres-Salazar%2C+Delany%3BJiang%2C+Jie%3BDivito%2C+Christopher+B%3BGarcia-Olivares%2C+Jennie%3BAmara%2C+Susan+G&rft.aulast=Torres-Salazar&rft.aufirst=Delany&rft.date=2015-09-18&rft.volume=290&rft.issue=38&rft.spage=22977&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M115.660860 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-14 N1 - Date created - 2015-09-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2002 Jul 19;277(29):26074-80 [11994293] Adv Physiol Educ. 2002 Dec;26(1-4):327-41 [12444005] Science. 2003 Apr 4;300(5616):108-12 [12649487] Biochemistry. 2003 Nov 11;42(44):12981-8 [14596613] J Biol Chem. 2003 Dec 12;278(50):50112-9 [14506254] J Biol Chem. 2004 May 14;279(20):20742-51 [14982939] J Biol Chem. 2004 Sep 17;279(38):39505-12 [15265858] Nature. 1995 Feb 9;373(6514):527-31 [7845466] Nature. 1995 Jun 15;375(6532):599-603 [7791878] J Biol Chem. 1995 Jul 28;270(30):17668-71 [7629063] Neuron. 1995 Sep;15(3):721-8 [7546750] Biophys J. 1996 Feb;70(2):733-42 [8789090] Nature. 1996 Oct 17;383(6601):634-7 [8857541] J Gen Physiol. 1996 Oct;108(4):237-50 [8894974] J Biol Chem. 1996 Nov 1;271(44):27715-22 [8910364] J Neurosci. 1998 Oct 1;18(19):7650-61 [9742136] Methods Enzymol. 1998;296:318-31 [9779458] J Neurosci. 1998 Dec 1;18(23):9620-8 [9822723] Neuron. 1998 Dec;21(6):1487-98 [9883740] Clin Exp Pharmacol Physiol. 2005 Jan-Feb;32(1-2):1-6 [15730426] J Gen Physiol. 2005 Dec;126(6):571-89 [16316976] Proc Natl Acad Sci U S A. 2005 Dec 27;102(52):19214-8 [16365297] J Neurosci. 2006 Jul 12;26(28):7513-22 [16837599] J Biol Chem. 2006 Oct 6;281(40):29788-96 [16877378] Nat Neurosci. 2006 Nov;9(11):1388-96 [17041592] Nature. 2007 Jan 25;445(7126):387-93 [17230192] Mol Pharmacol. 2007 May;71(5):1341-8 [17272682] Nat Struct Mol Biol. 2007 May;14(5):365-71 [17435767] Biochemistry. 2007 Aug 28;46(34):9685-92 [17676873] J Biol Chem. 2007 Nov 30;282(48):34719-26 [17908688] J Physiol. 1949 Mar 1;108(1):37-77 [18128147] J Biol Chem. 2008 Oct 17;283(42):28680-90 [18678877] Nature. 2009 Dec 17;462(7275):880-5 [19924125] J Biol Chem. 2010 Jun 4;285(23):17725-33 [20378543] J Biol Chem. 2010 Jul 30;285(31):23676-86 [20519505] Neuropharmacology. 2011 Jan;60(1):172-81 [20708631] J Neurosci. 2011 Apr 20;31(16):6255-62 [21508248] J Biol Chem. 2011 Jul 8;286(27):23780-8 [21572047] Biophys J. 2014 Aug 5;107(3):621-9 [25099801] Cell. 2015 Jan 29;160(3):542-53 [25635461] Proc Natl Acad Sci U S A. 2011 Sep 13;108(37):15141-6 [21876140] Channels (Austin). 2011 Nov-Dec;5(6):468-74 [21849820] Nat Struct Mol Biol. 2012 Mar;19(3):355-7 [22343718] J Biol Chem. 2012 Jun 8;287(24):20016-26 [22532568] J Mol Biol. 2013 May 13;425(9):1461-75 [23357172] Nat Struct Mol Biol. 2013 May;20(5):634-40 [23563139] J Biol Chem. 2014 Jan 17;289(3):1815-24 [24307171] Neuron. 2000 Mar;25(3):695-706 [10774736] Prog Neurobiol. 2001 Sep;65(1):1-105 [11369436] J Gen Physiol. 2001 Jun;117(6):547-62 [11382805] J Biol Chem. 2001 Nov 2;276(44):40396-401 [11479303] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15324-9 [11752470] Nature. 2002 Jan 17;415(6869):287-94 [11796999] J Biol Chem. 2002 Feb 8;277(6):3985-92 [11724778] J Biol Chem. 2002 Apr 19;277(16):13494-500 [11815608] J Biol Chem. 2002 Apr 19;277(16):13501-7 [11823462] Nature. 2004 Oct 14;431(7010):811-8 [15483603] J Physiol. 1990 Jul;426:43-80 [2231407] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M115.660860 ER - TY - JOUR T1 - Peroxisome Proliferator-activated Receptor-D (PPARD) Coordinates Mouse Spermatogenesis by Modulating Extracellular Signal-regulated Kinase (ERK)-dependent Signaling. AN - 1713944208; 26242735 AB - Ppard(-/-) mice exhibit smaller litter size compared with Ppard(+/+) mice. To determine whether peroxisome proliferator-activated receptor-D (PPARD) could possibly influence this phenotype, the role of PPARD in testicular biology was examined. Atrophic testes and testicular degeneration were observed in Ppard(-/-) mice compared with Ppard(+/+) mice, indicating that PPARD modulates spermatogenesis. Higher expression of p27 and decreased expression of proliferating cellular nuclear antigen in Sertoli cells were observed in Ppard(+/+) mice as compared with Ppard(-/-) mice, and these were associated with decreased Sertoli cell number in Ppard(+/+) mice. Cyclin D1 and cyclin D2 expression was lower in Ppard(+/+) as compared with Ppard(-/-) mice. Ligand activation of PPARD inhibited proliferation of a mouse Sertoli cell line, TM4, and an inverse agonist of PPARD (DG172) rescued this effect. Temporal inhibition of extracellular signal-regulated kinase (ERK) activation by PPARD in the testis was observed in Ppard(+/+) mice and was associated with decreased serum follicle-stimulating hormone and higher claudin-11 expression along the blood-testis barrier. PPARD-dependent ERK activation also altered expression of claudin-11, p27, cyclin D1, and cyclin D2 in TM4 cells, causing inhibition of cell proliferation, maturation, and formation of tight junctions in Sertoli cells, thus confirming a requirement for PPARD in accurate Sertoli cell function. Combined, these results reveal for the first time that PPARD regulates spermatogenesis by modulating the function of Sertoli cells during early testis development. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Yao, Pei-Li AU - Chen, LiPing AU - Hess, Rex A AU - Müller, Rolf AU - Gonzalez, Frank J AU - Peters, Jeffrey M AD - From the Department of Veterinary and Biomedical Sciences and The Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802, pxy11@psu.edu. ; From the Department of Veterinary and Biomedical Sciences and The Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802. ; Reproductive Biology and Toxicology, Department of Comparative Biosciences, College of Veterinary Medicine, University of Illinois, Urbana, Illinois 61802. ; Institute of Molecular Biology and Tumor Research, Center for Tumor and Immunobiology, Philipps University, Hans-Meerwein-Strasse 3, 35043 Marburg, Germany, and. ; Laboratory of Metabolism, NCI, National Institutes of Health, Bethesda, Maryland 20892. ; From the Department of Veterinary and Biomedical Sciences and The Center of Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, Pennsylvania 16802, jmp21@psu.edu. Y1 - 2015/09/18/ PY - 2015 DA - 2015 Sep 18 SP - 23416 EP - 23431 VL - 290 IS - 38 KW - Ccnd1 protein, mouse KW - 0 KW - Ccnd2 protein, mouse KW - Claudins KW - Cldn11 protein, mouse KW - Cyclin D2 KW - Ppard protein, mouse KW - Receptors, Cytoplasmic and Nuclear KW - Cyclin D1 KW - 136601-57-5 KW - Extracellular Signal-Regulated MAP Kinases KW - EC 2.7.11.24 KW - Index Medicus KW - Sertoli cells KW - cell proliferation KW - peroxisome proliferator-activated receptor (PPAR) KW - tight junction KW - extracellular signal-regulated kinase KW - testis KW - spermatogenesis KW - Cyclin D2 -- genetics KW - Animals KW - Extracellular Signal-Regulated MAP Kinases -- biosynthesis KW - Claudins -- genetics KW - Claudins -- biosynthesis KW - Mice KW - Cyclin D1 -- genetics KW - Cyclin D1 -- biosynthesis KW - Cyclin D2 -- biosynthesis KW - Male KW - Cell Line KW - Extracellular Signal-Regulated MAP Kinases -- genetics KW - Spermatogenesis -- physiology KW - Sertoli Cells -- cytology KW - MAP Kinase Signaling System -- physiology KW - Cell Proliferation -- physiology KW - Sertoli Cells -- metabolism KW - Receptors, Cytoplasmic and Nuclear -- metabolism KW - Receptors, Cytoplasmic and Nuclear -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1713944208?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Peroxisome+Proliferator-activated+Receptor-D+%28PPARD%29+Coordinates+Mouse+Spermatogenesis+by+Modulating+Extracellular+Signal-regulated+Kinase+%28ERK%29-dependent+Signaling.&rft.au=Yao%2C+Pei-Li%3BChen%2C+LiPing%3BHess%2C+Rex+A%3BM%C3%BCller%2C+Rolf%3BGonzalez%2C+Frank+J%3BPeters%2C+Jeffrey+M&rft.aulast=Yao&rft.aufirst=Pei-Li&rft.date=2015-09-18&rft.volume=290&rft.issue=38&rft.spage=23416&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M115.664508 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-15 N1 - Date created - 2015-09-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biol Reprod. 1976 Jun;14(5):665-9 [1276330] Front Biosci (Elite Ed). 2011;3:1209-20 [21622127] Endocrinology. 1988 Mar;122(3):787-94 [3125042] Proc Natl Acad Sci U S A. 1993 Aug 1;90(15):7225-9 [8394014] Genes Dev. 1996 Jan 1;10(1):80-92 [8557197] Endocrinology. 1999 Apr;140(4):1834-40 [10098522] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4683-8 [10781074] Mol Cell Biol. 2000 Jul;20(14):5119-28 [10866668] Endocrinology. 2000 Aug;141(8):3012-9 [10919290] Biol Reprod. 2000 Dec;63(6):1893-8 [11090462] Biol Reprod. 2001 Feb;64(2):689-95 [11159374] Mol Endocrinol. 2001 Jun;15(6):985-96 [11376116] Oncogene. 2001 Aug 2;20(34):4696-709 [11498792] Cell Transplant. 2002;11(6):499-505 [12428738] Mol Endocrinol. 2002 Dec;16(12):2780-92 [12456799] Bioorg Med Chem Lett. 2003 May 5;13(9):1517-21 [12699745] Nature. 2004 Sep 16;431(7006):320-4 [15372036] Mol Cell Endocrinol. 2004 Oct 15;225(1-2):57-64 [15451568] Endocr Rev. 2004 Oct;25(5):747-806 [15466940] Endocrinology. 1999 Jul;140(7):2968-75 [10385388] Arch Histol Cytol. 2004 Nov;67(4):271-84 [15700535] Biol Reprod. 2005 Mar;72(3):745-54 [15564602] J Cell Physiol. 2005 Jun;203(3):564-72 [15605377] Biol Reprod. 2005 Jun;72(6):1429-36 [15728790] Reproduction. 2005 Jul;130(1):15-28 [15985628] Biol Reprod. 2005 Nov;73(5):951-8 [16014817] J Androl. 2006 May-Jun;27(3):358-64 [16474013] Biol Reprod. 2006 May;74(5):798-806 [16407497] Genes Cells. 2006 Sep;11(9):1125-32 [16923130] Horm Res. 2006;66(4):153-61 [16804315] Mol Reprod Dev. 2007 Mar;74(3):341-59 [16967501] Mol Biol Cell. 2007 Apr;18(4):1457-63 [17314399] Cell Signal. 2007 Jun;19(6):1163-71 [17254750] Reproduction. 2007 Jun;133(6):1169-79 [17636171] Carcinogenesis. 2008 Jan;29(1):169-76 [17893232] Int J Androl. 2008 Apr;31(2):275-87 [18205797] Anim Reprod Sci. 2008 Apr;105(1-2):23-51 [18242891] Clin Sci (Lond). 2008 Aug;115(4):107-27 [18616431] Adv Exp Med Biol. 2008;636:1-15 [19856159] Biol Reprod. 2010 Mar;82(3):516-27 [19828778] Proc Natl Acad Sci U S A. 2010 Apr 6;107(14):6210-5 [20308578] Philos Trans R Soc Lond B Biol Sci. 2010 May 27;365(1546):1593-605 [20403872] Mol Carcinog. 2011 Nov;50(11):884-900 [21400612] Cancer Metastasis Rev. 2011 Dec;30(3-4):619-40 [22037942] J Med Chem. 2012 Mar 22;55(6):2858-68 [22369181] J Androl. 2012 May-Jun;33(3):368-74 [21868750] Science. 2012 Nov 9;338(6108):798-802 [22997133] BMC Genomics. 2012;13:665 [23176727] Adv Exp Med Biol. 2012;763:334-55 [23397633] Adv Exp Med Biol. 2013;786:105-28 [23696354] Dev Biol. 2014 Apr 15;388(2):170-80 [24525297] Mol Cancer Ther. 2014 Apr;13(4):1008-17 [24464939] Semin Cell Dev Biol. 2014 Jun;30:2-13 [24598768] J Biol Chem. 2014 Jul 18;289(29):20102-19 [24898257] Oncogene. 2014 Nov 13;33(46):5348-59 [24213576] Toxicology. 2014 Dec 4;326:62-73 [25456267] Biol Reprod. 2015 Mar;92(3):80 [25673562] Horm Behav. 1981 Sep;15(3):238-45 [7298026] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M115.664508 ER - TY - CPAPER T1 - Vaccines against Ebola Virus T2 - 55th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2015) AN - 1697993776; 6353874 JF - 55th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2015) AU - Feldmann, Heinz Y1 - 2015/09/17/ PY - 2015 DA - 2015 Sep 17 KW - Disease control KW - Vaccines KW - Ebola virus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1697993776?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=55th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2015%29&rft.atitle=Vaccines+against+Ebola+Virus&rft.au=Feldmann%2C+Heinz&rft.aulast=Feldmann&rft.aufirst=Heinz&rft.date=2015-09-17&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=55th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={7A574A80-EAB1-4B50-B343-4695DF14907E} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-06-30 N1 - Last updated - 2015-07-23 ER - TY - CPAPER T1 - Clinical Trial Strategies and New Regimes for XDR TB T2 - 55th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2015) AN - 1697991323; 6353921 JF - 55th Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2015) AU - Clifton III, Barry Y1 - 2015/09/17/ PY - 2015 DA - 2015 Sep 17 KW - Clinical trials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1697991323?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=55th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2015%29&rft.atitle=Clinical+Trial+Strategies+and+New+Regimes+for+XDR+TB&rft.au=Clifton+III%2C+Barry&rft.aulast=Clifton+III&rft.aufirst=Barry&rft.date=2015-09-17&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=55th+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={7A574A80-EAB1-4B50-B343-4695DF14907E} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-06-30 N1 - Last updated - 2015-07-23 ER - TY - JOUR T1 - SLFN11 Is a Transcriptional Target of EWS-FLI1 and a Determinant of Drug Response in Ewing Sarcoma AN - 1808638406; PQ0003458118 AB - Purpose: SLFN11 was identified as a critical determinant of response to DNA-targeted therapies by analyzing gene expression and drug sensitivity of NCI-60 and CCLE datasets. However, how SLFN11 is regulated in cancer cells remained unknown. Ewing sarcoma, which is characterized by the chimeric transcription factor EWS-FLI1, has notably high SLFN11 expression, leading us to investigate whether EWS-FLI1 drives SLFN11 expression and the role of SLFN11 in the drug response of Ewing sarcoma cells.Experimental Design: Binding sites of EWS-FLI1 on the SLFN11 promoter were analyzed by chromatin immunoprecipitation sequencing and promoter-luciferase reporter analyses. The relationship between SLFN11 and EWS-FLI1 were further examined in EWS-FLI1-knockdown or -overexpressing cells and in clinical tumor samples.Results: EWS-FLI1 binds near the transcription start site of SLFN11 promoter and acts as a positive regulator of SLFN11 expression in Ewing sarcoma cells. EWS-FLI1-mediated SLFN11 expression is responsible for high sensitivity of Ewing sarcoma to camptothecin and combinations of PARP inhibitors with temozolomide. Importantly, Ewing sarcoma patients with higher SLFN11 expression showed better tumor-free survival rate. The correlated expression between SLFN11 and FLI1 extends to leukemia, pediatric, colon, breast, and prostate cancers. In addition, expression of other ETS members correlates with SLFN11 in NCI-60 and CCLE datasets, and molecular experiments demonstrate that ETS1 acts as a positive regulator for SLFN11 expression in breast cancer cells.Conclusions: Our results imply the emerging relevance of SLFN11 as an ETS transcription factor response gene and for therapeutic response to topoisomerase I inhibitors and temozolomide-PARP inhibitor combinations in ETS-activated cancers. Clin Cancer Res; 21(18); 4184-93. copyright 2015 AACR.See related commentary by Kovar, p. 4033 JF - Clinical Cancer Research AU - Tang, Sai-Wen AU - Bilke, Sven AU - Cao, Liang AU - Murai, Junko AU - Sousa, Fabricio G AU - Yamade, Mihoko AU - Rajapakse, Vinodh AU - Varma, Sudhir AU - Helman, Lee J AU - Khan, Javed AU - Meltzer, Paul S AU - Pommier, Yves AD - Laboratory of Molecular Pharmacology, Developmental Therapeutics Branch, NCI, NIH, Bethesda, Maryland, pommier@nih.gov Y1 - 2015/09/15/ PY - 2015 DA - 2015 Sep 15 SP - 4184 EP - 4193 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 18 SN - 1078-0432, 1078-0432 KW - Biotechnology and Bioengineering Abstracts KW - Ets-1 protein KW - Chromatin KW - Pediatrics KW - Immunoprecipitation KW - DNA topoisomerase KW - Drug development KW - Tumors KW - Camptothecin KW - ETS protein KW - Gene expression KW - Promoters KW - Leukemia KW - temozolomide KW - Ewing's sarcoma KW - Prostate cancer KW - Colon KW - Transcription factors KW - Poly(ADP-ribose) polymerase KW - Breast cancer KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808638406?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Cancer+Research&rft.atitle=SLFN11+Is+a+Transcriptional+Target+of+EWS-FLI1+and+a+Determinant+of+Drug+Response+in+Ewing+Sarcoma&rft.au=Tang%2C+Sai-Wen%3BBilke%2C+Sven%3BCao%2C+Liang%3BMurai%2C+Junko%3BSousa%2C+Fabricio+G%3BYamade%2C+Mihoko%3BRajapakse%2C+Vinodh%3BVarma%2C+Sudhir%3BHelman%2C+Lee+J%3BKhan%2C+Javed%3BMeltzer%2C+Paul+S%3BPommier%2C+Yves&rft.aulast=Tang&rft.aufirst=Sai-Wen&rft.date=2015-09-15&rft.volume=21&rft.issue=18&rft.spage=4184&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-2112 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Chromatin; Ets-1 protein; Pediatrics; DNA topoisomerase; Immunoprecipitation; Drug development; Tumors; Camptothecin; ETS protein; Gene expression; Leukemia; Promoters; Ewing's sarcoma; temozolomide; Prostate cancer; Colon; Poly(ADP-ribose) polymerase; Transcription factors; Breast cancer DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-2112 ER - TY - JOUR T1 - Inhibition of Survivin with YM155 Induces Durable Tumor Response in Anaplastic Thyroid Cancer AN - 1808636809; PQ0003443372 AB - Purpose: Anaplastic thyroid cancer (ATC) is a rare but lethal malignancy without any effective therapy. The aim of this study is to use a high-throughput drug library screening to identify a novel therapeutic agent that targets dysregulated genes/pathways in ATC.ExperimentalDesign: We performed quantitative high-throughput screening (qHTS) in ATC cell lines using a compound library of 3,282 drugs. Dysregulated genes in ATC were analyzed using genome-wide expression analysis and immunohistochemistry in human ATC tissue samples and ATC cell lines. In vitro and in vivo studies were performed for determining drug activity, effectiveness of targeting, and the mechanism of action.Results: qHTS identified 100 active compounds in three ATC cell lines. One of the most active agents was the first-in-class survivin inhibitor YM155. Genome-wide expression analysis and immunohistochemistry showed overexpression of survivin in human ATC tissue samples, and survivin was highly expressed in all ATC cell lines tested. YM155 significantly inhibited ATC cellular proliferation. Mechanistically, YM155 inhibited survivin expression in ATC cells. Furthermore, YM155 treatment reduced claspin expression, which was associated with S-phase arrest in ATC cells. In vivo, YM155 significantly inhibited growth and metastases and prolonged survival.Conclusions: Our data show that YM155 is a promising anticancer agent for ATC and that its target, survivin, is overexpressed in ATC. Our findings support the use of YM155 in clinical trials as a therapeutic option in advanced and metastatic ATC. Clin Cancer Res; 21(18); 4123-32. copyright 2015 AACR. JF - Clinical Cancer Research AU - Mehta, Amit AU - Zhang, Lisa AU - Boufraqech, Myriem AU - Liu-Chittenden, Yi AU - Zhang, Yaqin AU - Patel, Dhaval AU - Davis, Sean AU - Rosenberg, Avi AU - Ylaya, Kris AU - Aufforth, Rachel AU - Li, Zhuyin AU - Shen, Min AU - Kebebew, Electron AD - Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, kebebewe@mail.nih.gov Y1 - 2015/09/15/ PY - 2015 DA - 2015 Sep 15 SP - 4123 EP - 4132 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 18 SN - 1078-0432, 1078-0432 KW - Biotechnology and Bioengineering Abstracts KW - Data processing KW - survivin KW - Tumors KW - Drug screening KW - Clinical trials KW - Antitumor agents KW - Metastases KW - Malignancy KW - thyroid cancer KW - high-throughput screening KW - Immunohistochemistry KW - Drugs KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808636809?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Cancer+Research&rft.atitle=Inhibition+of+Survivin+with+YM155+Induces+Durable+Tumor+Response+in+Anaplastic+Thyroid+Cancer&rft.au=Mehta%2C+Amit%3BZhang%2C+Lisa%3BBoufraqech%2C+Myriem%3BLiu-Chittenden%2C+Yi%3BZhang%2C+Yaqin%3BPatel%2C+Dhaval%3BDavis%2C+Sean%3BRosenberg%2C+Avi%3BYlaya%2C+Kris%3BAufforth%2C+Rachel%3BLi%2C+Zhuyin%3BShen%2C+Min%3BKebebew%2C+Electron&rft.aulast=Mehta&rft.aufirst=Amit&rft.date=2015-09-15&rft.volume=21&rft.issue=18&rft.spage=4123&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-3251 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Metastases; Malignancy; Data processing; survivin; thyroid cancer; high-throughput screening; Tumors; Drug screening; Antitumor agents; Clinical trials; Drugs; Immunohistochemistry DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-3251 ER - TY - JOUR T1 - Class 3 semaphorins negatively regulate dermal lymphatic network formation AN - 1808611474; PQ0003420839 AB - The development of a patterned lymphatic vascular network is essential for proper lymphatic functions during organ development and homeostasis. Here we report that class 3 semaphorins (SEMA3s), SEMA3F and SEMA3G negatively regulate lymphatic endothelial cell (LEC) growth and sprouting to control dermal lymphatic network formation. Neuropilin2 (NRP2) functions as a receptor for SEMA3F and SEMA3G, as well as vascular endothelial growth factor C (VEGFC). In culture, Both SEMA3F and SEMA3G inhibit VEGFC-mediated sprouting and proliferation of human dermal LECs. In the developing mouse skin, Sema3f is expressed in the epidermis and Sema3g expression is restricted to arteries, whereas their receptor Nrp2 is preferentially expressed by lymphatic vessels. Both Sema3f; Sema3g double mutants and Nrp2 mutants exhibit increased LEC growth in the skin. In contrast, Sema3f; Sema3g double mutants display increased lymphatic branching, while Nrp2 mutants exhibit reduced lymphatic branching. A targeted mutation in PlexinA1 or PlexinA2, signal transducers forming a receptor complex with NRP2 for SEMA3s, exhibits an increase in LEC growth and lymphatic branching as observed in Sema3f; Sema3g double mutants. Our results provide the first evidence that SEMA3F and SEMA3G function as a negative regulator for dermal lymphangiogenesis in vivo. The reciprocal phenotype in lymphatic branching between Sema3f; Sema3g double mutants and Nrp2 mutants suggest a complex NRP2 function that regulates LEC behavior both positively and negatively, through a binding with VEGFC or SEMA3s. JF - Biology Open AU - Uchida, Yutaka AU - James, Jennifer M AU - Suto, Fumikazu AU - Mukouyama, Yoh-suke AD - Laboratory of Stem Cell and Neuro-Vascular Biology, Genetics and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Building 10/6C103, 10 Center Drive, Bethesda, MD 20892, USA, mukoyamay@mail.nih.gov Y1 - 2015/09/15/ PY - 2015 DA - 2015 Sep 15 SP - 1194 EP - 1205 PB - The Company of Biologists Ltd., 140 Cowley Rd Cambridge, CB4 0DL United Kingdom VL - 4 IS - 9 SN - 2046-6390, 2046-6390 KW - Biotechnology and Bioengineering Abstracts KW - SEMA3s KW - NRP2 KW - Dermal lymphangiogenesis KW - LEC sprouting KW - LEC growth KW - Endothelial cells KW - Epidermis KW - Skin KW - vascular endothelial growth factor C KW - Arteries KW - Cell culture KW - Homeostasis KW - semaphorins KW - Mutation KW - Lymphatic system KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808611474?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biology+Open&rft.atitle=Class+3+semaphorins+negatively+regulate+dermal+lymphatic+network+formation&rft.au=Uchida%2C+Yutaka%3BJames%2C+Jennifer+M%3BSuto%2C+Fumikazu%3BMukouyama%2C+Yoh-suke&rft.aulast=Uchida&rft.aufirst=Yutaka&rft.date=2015-09-15&rft.volume=4&rft.issue=9&rft.spage=1194&rft.isbn=&rft.btitle=&rft.title=Biology+Open&rft.issn=20466390&rft_id=info:doi/10.1242%2Fbio.012302 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Endothelial cells; Epidermis; Skin; vascular endothelial growth factor C; Arteries; Cell culture; Homeostasis; Mutation; semaphorins; Lymphatic system DO - http://dx.doi.org/10.1242/bio.012302 ER - TY - JOUR T1 - Plasmonic Vesicles of Amphiphilic Nanocrystals: Optically Active Multifunctional Platform for Cancer Diagnosis and Therapy. AN - 1712775214; 26134093 AB - Vesicular structures with compartmentalized, water-filled cavities, such as liposomes of natural and synthetic amphiphiles, have tremendous potential applications in nanomedicine. When block copolymers self-assemble, the result is polymersomes with tailored structural properties and built-in releasing mechanisms, controlled by stimuli-responsive polymer building blocks. More recently, chemists are becoming interested in multifunctional hybrid vesicles containing inorganic nanocrystals with unique optical, electronic, and magnetic properties. In this Account, we review our recent progress in assembling amphiphilic plasmonic nanostructures to create a new class of multifunctional hybrid vesicles and applying them towards cancer diagnosis and therapy. Localized surface plasmon resonance (LSPR) gives plasmonic nanomaterials a unique set of optical properties that are potentially useful for both biosensing and nanomedicine. For instance, the strong light scattering at their LSPR wavelength opens up the applications of plasmonic nanostructures in single particle plasmonic imaging. Their superior photothermal conversion properties, on the other hand, make them excellent transducers for photothermal ablation and contrast agents for photoacoustic imaging. Of particular note for ultrasensitive detection is that the confined electromagnetic field resulting from excitation of LSPR can give rise to highly efficient surface enhanced Raman scattering (SERS) for molecules in close proximity. We have explored several ways to combine well-defined plasmonic nanocrystals with amphiphilic polymer brushes of diverse chemical functionalities. In multiple systems, we have shown that the polymer grafts impart amphiphilicity-driven self-assembly to the hybrid nanoparticles. This has allowed us to synthesize well-defined vesicles in which we have embedded plasmonic nanocrystals in the shell of collapsed hydrophobic polymers. The hydrophilic brushes extend into external and interior aqueous environment to stabilize the vesicular structure. More importantly, we have demonstrated that strong interparticle coupling greatly enhances the optical properties (scattering, photothermal conversion, and SERS) in plasmonic vesicles. In combination with the loading capacity of the vesicles, this technology can provide unique opportunities for integrated diagnosis and therapy, multimodality combination therapy, and imaging-guided therapy. One key property differentiating the plasmonic vesicles from other vesicular structures containing nanocrystals is that we can tailor the interparticle coupling and disintegration of the plasmonic vesicles by altering structural parameters and conformational changes of the covalently bound polymer brushes. This gives us tremendous flexibility to engineer plasmonic vesicles for ultrasensitive detection and targeted therapy. Through bringing together advances in nanochemistry, polymer chemistry, self-assembly, and nanophotonics, we expect to further expand our capability of tailoring optical and structural characteristics of plasmonic vesicles to address challenges in medical settings. JF - Accounts of chemical research AU - Song, Jibin AU - Huang, Peng AU - Duan, Hongwei AU - Chen, Xiaoyuan AD - Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH) , Bethesda, Maryland 20892, United States. ; School of Chemical and Biomedical Engineering, Nanyang Technological University , 70 Nanyang Drive, 637457 Singapore. Y1 - 2015/09/15/ PY - 2015 DA - 2015 Sep 15 SP - 2506 EP - 2515 VL - 48 IS - 9 KW - Gold KW - 7440-57-5 KW - Index Medicus KW - Microscopy, Electron, Transmission KW - Hydrophobic and Hydrophilic Interactions KW - Drug Delivery Systems KW - Diagnostic Imaging KW - Neoplasms -- diagnosis KW - Metal Nanoparticles -- chemistry KW - Cell Nucleolus -- chemistry KW - Gold -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1712775214?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Accounts+of+chemical+research&rft.atitle=Plasmonic+Vesicles+of+Amphiphilic+Nanocrystals%3A+Optically+Active+Multifunctional+Platform+for+Cancer+Diagnosis+and+Therapy.&rft.au=Song%2C+Jibin%3BHuang%2C+Peng%3BDuan%2C+Hongwei%3BChen%2C+Xiaoyuan&rft.aulast=Song&rft.aufirst=Jibin&rft.date=2015-09-15&rft.volume=48&rft.issue=9&rft.spage=2506&rft.isbn=&rft.btitle=&rft.title=Accounts+of+chemical+research&rft.issn=1520-4898&rft_id=info:doi/10.1021%2Facs.accounts.5b00059 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-24 N1 - Date created - 2015-09-15 N1 - Date revised - 2017-01-24 N1 - Last updated - 2017-01-25 DO - http://dx.doi.org/10.1021/acs.accounts.5b00059 ER - TY - JOUR T1 - Metabolic mapping of A3 adenosine receptor agonist MRS5980. AN - 1710001223; 26212548 AB - (1S,2R,3S,4R,5S)-4-(2-((5-Chlorothiophen-2-yl)ethynyl)-6-(methylamino)-9H-purin-9-yl)-2,3-dihydroxy-N-methylbicyclo[3.1.0]hexane-1-carboxamide (MRS5980) is an A3AR selective agonist containing multiple receptor affinity- and selectivity-enhancing modifications and a therapeutic candidate drug for many inflammatory diseases. Metabolism-related poor pharmacokinetic behavior and toxicities are a major reason for drug R&D failure. Metabolomics with UPLC-MS was employed to profile the metabolism of MRS5980 and MRS5980-induced disruption of endogenous compounds. Recombinant drug-metabolizing enzymes screening experiment were used to determine the enzymes involved in MRS5980 metabolism. Analysis of lipid metabolism-related genes was performed to investigate the reason for MRS5980-induced lipid metabolic disorders. Unsupervised principal components analysis separated the control and MRS5980 treatment groups in feces, urine, and liver samples, but not in bile and serum. The major ions mainly contributing to the separation of feces and urine were oxidized MRS5980, glutathione (GSH) conjugates and cysteine conjugate (degradation product of the GSH conjugates) of MRS5980. The major ions contributing to the group separation of liver samples were phosphatidylcholines. In vitro incubation experiments showed the involvement of CYP3A enzymes in the oxidative metabolism of MRS5980 and direct GSH reactivity of MRS5980. The electrophilic attack by MRS5980 is a minor pathway and did not alter GSH levels in liver or liver histology, and thus may be of minor clinical consequence. Gene expression analysis further showed decreased expression of PC biosynthetic genes choline kinase a and b, which further accelerated conversion of lysophosphatidylcholine to phosphatidylcholines through increasing the expression of lysophosphatidylcholine acyltransferase 3. These data will be useful to guide rational design of drugs targeting A3AR, considering efficacy, metabolic elimination, and electrophilic reactivity. Published by Elsevier Inc. JF - Biochemical pharmacology AU - Fang, Zhong-Ze AU - Tosh, Dilip K AU - Tanaka, Naoki AU - Wang, Haina AU - Krausz, Kristopher W AU - O'Connor, Robert AU - Jacobson, Kenneth A AU - Gonzalez, Frank J AD - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA; Department of Toxicology, School of Public Health, Tianjin Medical University, Tianjin 300070, China. ; Molecular Recognition Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0810, USA. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Molecular Recognition Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0810, USA. Electronic address: kajacobs@helix.nih.gov. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Electronic address: gonzalef@mail.nih.gov. Y1 - 2015/09/15/ PY - 2015 DA - 2015 Sep 15 SP - 215 EP - 223 VL - 97 IS - 2 KW - Adenosine A3 Receptor Agonists KW - 0 KW - Receptor, Adenosine A3 KW - Index Medicus KW - Electrophilies KW - A(3) adenosine receptor (AR) KW - Metabolomics KW - MRS5980 KW - Animals KW - Microsomes, Liver -- metabolism KW - Humans KW - Microsomes, Liver -- drug effects KW - Mice, Inbred C57BL KW - Mice KW - Male KW - Metabolomics -- methods KW - Adenosine A3 Receptor Agonists -- pharmacology KW - Receptor, Adenosine A3 -- metabolism KW - Adenosine A3 Receptor Agonists -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1710001223?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+pharmacology&rft.atitle=Metabolic+mapping+of+A3+adenosine+receptor+agonist+MRS5980.&rft.au=Fang%2C+Zhong-Ze%3BTosh%2C+Dilip+K%3BTanaka%2C+Naoki%3BWang%2C+Haina%3BKrausz%2C+Kristopher+W%3BO%27Connor%2C+Robert%3BJacobson%2C+Kenneth+A%3BGonzalez%2C+Frank+J&rft.aulast=Fang&rft.aufirst=Zhong-Ze&rft.date=2015-09-15&rft.volume=97&rft.issue=2&rft.spage=215&rft.isbn=&rft.btitle=&rft.title=Biochemical+pharmacology&rft.issn=1873-2968&rft_id=info:doi/10.1016%2Fj.bcp.2015.07.007 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-27 N1 - Date created - 2015-09-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Drug Metab Dispos. 2003 Jan;31(1):122-32 [12485961] Drug Metab Dispos. 2004 Jan;32(1):35-42 [14709618] Drug Metab Dispos. 2006 Jul;34(7):1208-19 [16611859] J Pharmacol Exp Ther. 2007 Jul;322(1):391-8 [17442842] J Hepatol. 2009 Jun;50(6):1236-46 [19398233] Br J Clin Pharmacol. 2010 Feb;69(2):193-9 [20233183] Drug Metab Dispos. 2010 Jul;38(7):1238-45 [20382753] Biochem Pharmacol. 2010 Oct 1;80(7):1063-74 [20541539] Annu Rev Pharmacol Toxicol. 2011;51:145-67 [21210745] Hepatology. 2011 Apr;53(4):1282-93 [21480330] Curr Med Chem. 2011;18(20):3116-35 [21651480] FASEB J. 2012 May;26(5):1855-65 [22345405] Br J Pharmacol. 2012 Nov;167(6):1271-86 [22671862] Dig Dis. 2012;30 Suppl 3:85-91 [23295697] J Pharm Pharmacol. 2013 Apr;65(4):521-7 [23488780] Arch Toxicol. 2013 Nov;87(11):1975-87 [23575800] J Lipid Res. 2014 Mar;55(3):455-65 [24343899] Arch Toxicol. 2014 Apr;88(4):983-96 [24385052] Br J Pharmacol. 2014 Apr;171(7):1735-46 [24417285] Anticancer Res. 2014 Apr;34(4):2001-6 [24692738] Arch Toxicol. 2014 Aug;88(8):1491-502 [24710571] Pharmacol Rev. 2015;67(1):74-102 [25387804] J Med Chem. 2014 Dec 11;57(23):9901-14 [25422861] Brain. 2015 Jan;138(Pt 1):28-35 [25414036] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bcp.2015.07.007 ER - TY - JOUR T1 - Human endogenous retrovirus K and cancer: Innocent bystander or tumorigenic accomplice? AN - 1695184060; 24890612 AB - Harbored as relics of ancient germline infections, human endogenous retroviruses (HERVs) now constitute up to 8% of our genome. A proportion of this sequence has been co-opted for molecular and cellular processes, beneficial to human physiology, such as the fusogenic activity of the envelope protein, a vital component of placentogenesis. However, the discovery of high levels of HERV-K mRNA and protein and even virions in a wide array of cancers has revealed that HERV-K may be playing a more sinister role-a role as an etiological agent in cancer itself. Whether the presence of this retroviral material is simply an epiphenomenon, or an actual causative factor, is a hotly debated topic. This review will summarize the current state of knowledge regarding HERV-K and cancer and attempt to outline the potential mechanisms by which HERV-K could be involved in the onset and promotion of carcinogenesis. © 2014 The Authors. Published by Wiley Periodicals, Inc. on behalf of UICC. JF - International journal of cancer AU - Downey, Ronan F AU - Sullivan, Francis J AU - Wang-Johanning, Feng AU - Ambs, Stefan AU - Giles, Francis J AU - Glynn, Sharon A AD - Prostate Cancer Institute, National University of Ireland Galway, Galway, Ireland. ; Center for Cancer and Metabolism, SRI International, Menlo Park, CA. ; Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD. Y1 - 2015/09/15/ PY - 2015 DA - 2015 Sep 15 SP - 1249 EP - 1257 VL - 137 IS - 6 KW - RNA, Messenger KW - 0 KW - RNA, Viral KW - Index Medicus KW - Rec KW - oncogenesis KW - HERV-K activation KW - Np9 KW - melanoma KW - human endogenous retrovirus KW - Env KW - breast cancer KW - carcinogenesis KW - immunomodulation KW - Gag KW - prostate cancer KW - HERV-K KW - Animals KW - Humans KW - RNA, Viral -- genetics KW - RNA, Messenger -- genetics KW - Neoplasms -- virology KW - Carcinogenesis -- genetics KW - Retroviridae -- genetics KW - Neoplasms -- genetics KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1695184060?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Human+endogenous+retrovirus+K+and+cancer%3A+Innocent+bystander+or+tumorigenic+accomplice%3F&rft.au=Downey%2C+Ronan+F%3BSullivan%2C+Francis+J%3BWang-Johanning%2C+Feng%3BAmbs%2C+Stefan%3BGiles%2C+Francis+J%3BGlynn%2C+Sharon+A&rft.aulast=Downey&rft.aufirst=Ronan&rft.date=2015-09-15&rft.volume=137&rft.issue=6&rft.spage=1249&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.29003 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-28 N1 - Date created - 2015-07-09 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ijc.29003 ER - TY - JOUR T1 - Inhibition of autophagy by 3-MA enhances IL-24-induced apoptosis in human oral squamous cell carcinoma cells. AN - 1712524845; 26361755 AB - Interleukin-24(IL-24), also referred to as melanoma differentiation-associated gene-7(mda-7), is a unique member of the IL-10 gene family, which displays nearly ubiquitous cancer-specific toxicity. The most notable feature of IL-24 is selectively induced growth suppression and apoptosis in various cancer cells, with no harmful effects toward normal cells. Autophagy is a self-protective mechanism in many kinds of tumor cells that respond to anticancer treatment. It is reported that autophagy inhibition could enhance the effects of many kinds of anticancer treatments, including gene therapy. However, whether IL-24 is effective to treat oral squamous cell carcinomas (OSCC) and if autophagy inhibition could improve the anticancer effect of IL-24 towards OSCC is has not been detected. MTT assays were carried out to determine the cell proliferation; Transfection was used to gene transfer; Western Blot was performed to detect the protein level of LC3II, P62, Beclin 1, Cleaved caspase-3, β-Tubulin and β-actin; Apoptosis rates and cell cycle alteration were analyzed using flow cytometry; Autophagy induction was confirmed by MDC staining, GFP-LC3 staining and transmission electron microscopy. Amount of IL-24 in the culture medium was quantified by ELISA. Apoptosis in vivo was analyzed by TUNEL assay. HE staining was used to observe the morphology of the samples. In the present study, we proved that IL-24 have a novel anticancer effect towards KB cells and that autophagy inhibition could improve the anticancer effect of IL-24. IL-24 treated cells showed autophagy characteristics and autophagy inhibition by 3-methyladenine (3-MA) significantly enhanced IL-24-induced apoptosis. Similar results were obtained in the KB cells xenograft tumor model. These results suggest that the combination of autophagy inhibitors and IL-24 based on the AdLTR2EF1α-mediated gene transfer could be a promising way to cure OSCC. JF - Journal of experimental & clinical cancer research : CR AU - Li, Jichen AU - Yang, Dezhao AU - Wang, Wei AU - Piao, Songlin AU - Zhou, Jianyu AU - Saiyin, Wuliji AU - Zheng, Changyu AU - Sun, Hongchen AU - Li, Yu AD - School of Life Science and Technology, Harbin Institute of Technology, 2 Yikuang Street, Harbin, 150001, People's Republic of China. lijichen@163.com. ; Department of Oral and Maxillofacial Surgery, School of Dentistry, Harbin Medical University, 141 Yiman Street, Nangang District, Harbin, 150001, People's Republic of China. 264706737@163.com. ; Department of Oral and Maxillofacial Surgery, School of Dentistry, Harbin Medical University, 141 Yiman Street, Nangang District, Harbin, 150001, People's Republic of China. wangwei123www@126.com. ; Department of Oral and Maxillofacial Surgery, School of Dentistry, Harbin Medical University, 141 Yiman Street, Nangang District, Harbin, 150001, People's Republic of China. spiao@umich.edu. ; Department of Oral and Maxillofacial Surgery, School of Dentistry, Harbin Medical University, 141 Yiman Street, Nangang District, Harbin, 150001, People's Republic of China. zjyhmu@126.com. ; Department of Oral and Maxillofacial Surgery, School of Dentistry, Harbin Medical University, 141 Yiman Street, Nangang District, Harbin, 150001, People's Republic of China. 1208401803@qq.com. ; National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA. czheng@dir.nidcr.nih.gov. ; Department of Oral Pathology, School of Stomatology, Jilin University, 1500 Qinghua Road, Changchun, 130021, People's Republic of China. hcsun@mail.jlu.edu.cn. ; School of Life Science and Technology, Harbin Institute of Technology, 2 Yikuang Street, Harbin, 150001, People's Republic of China. liyugene@hit.edu.cn. Y1 - 2015/09/11/ PY - 2015 DA - 2015 Sep 11 SP - 97 VL - 34 KW - Antineoplastic Agents KW - 0 KW - Interleukins KW - interleukin-24 KW - 3-methyladenine KW - 5142-23-4 KW - Adenine KW - JAC85A2161 KW - Index Medicus KW - Autophagy -- drug effects KW - Animals KW - Humans KW - Gene Expression KW - Tumor Burden KW - Cell Line, Tumor KW - Genetic Therapy KW - Mice, Nude KW - Cell Proliferation KW - Mice, Inbred BALB C KW - Cell Survival KW - Transfection KW - Xenograft Model Antitumor Assays KW - Neoplasms, Squamous Cell -- pathology KW - Neoplasms, Squamous Cell -- therapy KW - Apoptosis KW - Mouth Neoplasms -- metabolism KW - Mouth Neoplasms -- therapy KW - Interleukins -- physiology KW - Neoplasms, Squamous Cell -- metabolism KW - Mouth Neoplasms -- pathology KW - Antineoplastic Agents -- pharmacology KW - Adenine -- analogs & derivatives KW - Adenine -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1712524845?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+experimental+%26+clinical+cancer+research+%3A+CR&rft.atitle=Inhibition+of+autophagy+by+3-MA+enhances+IL-24-induced+apoptosis+in+human+oral+squamous+cell+carcinoma+cells.&rft.au=Li%2C+Jichen%3BYang%2C+Dezhao%3BWang%2C+Wei%3BPiao%2C+Songlin%3BZhou%2C+Jianyu%3BSaiyin%2C+Wuliji%3BZheng%2C+Changyu%3BSun%2C+Hongchen%3BLi%2C+Yu&rft.aulast=Li&rft.aufirst=Jichen&rft.date=2015-09-11&rft.volume=34&rft.issue=&rft.spage=97&rft.isbn=&rft.btitle=&rft.title=Journal+of+experimental+%26+clinical+cancer+research+%3A+CR&rft.issn=1756-9966&rft_id=info:doi/10.1186%2Fs13046-015-0211-0 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-23 N1 - Date created - 2015-09-12 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: EMBO J. 1996 Apr 15;15(8):1766-77 [8617221] Eur J Cell Biol. 1995 Jan;66(1):3-14 [7750517] Oncogene. 2005 Nov 17;24(51):7552-66 [16044151] Hum Gene Ther. 2006 Mar;17(3):253-63 [16544975] EMBO J. 2007 May 16;26(10):2527-39 [17446862] Int J Oncol. 2007 Nov;31(5):985-1007 [17912425] Cell. 2008 Jan 11;132(1):27-42 [18191218] Autophagy. 2008 May;4(4):513-5 [18299661] Mol Ther. 2008 Jun;16(6):1089-97 [18388914] Autophagy. 2009 May;5(4):569-70 [19398886] Cell Death Differ. 2009 Jul;16(7):966-75 [19325568] Cancer Cell. 2011 May 17;19(5):613-28 [21575862] Cancer Lett. 2011 Aug 28;307(2):141-8 [21511395] Mol Cell. 2011 Dec 9;44(5):698-709 [22152474] Oncol Rep. 2013 Feb;29(2):481-90 [23135406] J Exp Clin Cancer Res. 2012;31:51 [22640485] J Biol Chem. 2012 Apr 6;287(15):12455-68 [22362782] J Exp Clin Cancer Res. 2013;32:99 [24305604] J Exp Clin Cancer Res. 2014;33:42 [24887205] Gene Ther. 2003 Jun;10(11):955-63 [12756416] Int Immunopharmacol. 2004 May;4(5):649-67 [15120650] Mol Cell Biol. 1990 Aug;10(8):4239-42 [2370865] J Virol. 1999 Jul;73(7):6141-6 [10364373] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/s13046-015-0211-0 ER - TY - JOUR T1 - Microbial growth dynamics and human disease AN - 1811909603; PQ0003420407 AB - How do human-associated microbial communities contribute to health and disease? To answer this, scientists have been exploring changes in the gut microbiota between individuals, and even across generations and continents (1, 2). Large genome sequence data sets are producing tally sheets of bacteria in time and space throughout disease courses (3, 4). One challenge has been to determine the metabolic state of these microbial communities to identify bacteria that are responding to a perturbation and/or driving disease pathogenesis (5, 6). On page 1101 of this issue, Korem et al. (7) explore metagenomic DNA sequence data sets to estimate growth rates (metabolic states) of bacterial taxa in a microbial community. JF - Science AU - Segre, Julia A AD - Microbial Genomics Section, Translational and Functional Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA Y1 - 2015/09/04/ PY - 2015 DA - 2015 Sep 04 SP - 1058 EP - 1059 PB - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States VL - 349 IS - 6252 SN - 0036-8075, 0036-8075 KW - Microbiology Abstracts A: Industrial & Applied Microbiology KW - Genomes KW - Growth rate KW - Data processing KW - Digestive tract KW - Nucleotide sequence KW - A 01300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1811909603?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science&rft.atitle=Microbial+growth+dynamics+and+human+disease&rft.au=Segre%2C+Julia+A&rft.aulast=Segre&rft.aufirst=Julia&rft.date=2015-09-04&rft.volume=349&rft.issue=6252&rft.spage=1058&rft.isbn=&rft.btitle=&rft.title=Science&rft.issn=00368075&rft_id=info:doi/10.1126%2Fscience.aad0781 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-08-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Growth rate; Genomes; Digestive tract; Data processing; Nucleotide sequence DO - http://dx.doi.org/10.1126/science.aad0781 ER - TY - JOUR T1 - Zeta Inhibitory Peptide Disrupts Electrostatic Interactions That Maintain Atypical Protein Kinase C in Its Active Conformation on the Scaffold p62. AN - 1709707797; 26187466 AB - Atypical protein kinase C (aPKC) enzymes signal on protein scaffolds, yet how they are maintained in an active conformation on scaffolds is unclear. A myristoylated peptide based on the autoinhibitory pseudosubstrate fragment of the atypical PKCζ, zeta inhibitory peptide (ZIP), has been extensively used to inhibit aPKC activity; however, we have previously shown that ZIP does not inhibit the catalytic activity of aPKC isozymes in cells (Wu-Zhang, A. X., Schramm, C. L., Nabavi, S., Malinow, R., and Newton, A. C. (2012) J. Biol. Chem. 287, 12879-12885). Here we sought to identify a bona fide target of ZIP and, in so doing, unveiled a novel mechanism by which aPKCs are maintained in an active conformation on a protein scaffold. Specifically, we used protein-protein interaction network analysis, structural modeling, and protein-protein docking to predict that ZIP binds an acidic surface on the Phox and Bem1 (PB1) domain of p62, an interaction validated by peptide array analysis. Using a genetically encoded reporter for PKC activity fused to the p62 scaffold, we show that ZIP inhibits the activity of wild-type aPKC, but not a construct lacking the pseudosubstrate. These data support a model in which the pseudosubstrate of aPKCs is tethered to the acidic surface on p62, locking aPKC in an open, signaling-competent conformation. ZIP competes for binding to the acidic surface, resulting in displacement of the pseudosubstrate of aPKC and re-engagement in the substrate-binding cavity. This study not only identifies a cellular target for ZIP, but also unveils a novel mechanism by which scaffolded aPKC is maintained in an active conformation. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Tsai, Li-Chun Lisa AU - Xie, Lei AU - Dore, Kim AU - Xie, Li AU - Del Rio, Jason C AU - King, Charles C AU - Martinez-Ariza, Guillermo AU - Hulme, Christopher AU - Malinow, Roberto AU - Bourne, Philip E AU - Newton, Alexandra C AD - From the Department of Pharmacology. ; the Department of Computer Science, Hunter College, the City University of New York, New York, New York 10065. ; Department of Neurosciences. ; Skaggs School of Pharmacy, and. ; Pediatric Diabetes Research Center, University of California San Diego, La Jolla, California 92093. ; the Department of Pharmacology and Toxicology, College of Pharmacy, University of Arizona, Tucson, Arizona 85721, and. ; the Office of the Director, the National Institutes of Health, Bethesda, Maryland 20892. ; From the Department of Pharmacology, anewton@ucsd.edu. Y1 - 2015/09/04/ PY - 2015 DA - 2015 Sep 04 SP - 21845 EP - 21856 VL - 290 IS - 36 KW - Adaptor Proteins, Signal Transducing KW - 0 KW - Isoenzymes KW - Pregnancy Proteins KW - Receptors, AMPA KW - SQSTM1 protein, human KW - Sequestosome-1 Protein KW - zeta inhibitor protein 14 kDa, human KW - protein kinase C zeta KW - EC 2.7.11.1 KW - PKC-3 protein KW - EC 2.7.11.13 KW - Protein Kinase C KW - protein kinase C lambda KW - Index Medicus KW - atypical protein kinase C (aPKC) KW - protein-protein interaction KW - enzyme mechanism KW - serine/threonine protein kinase KW - scaffold protein KW - p62 (sequestosome 1(SQSTM1)) KW - Isoenzymes -- chemistry KW - Animals KW - COS Cells KW - Models, Molecular KW - HEK293 Cells KW - Humans KW - Fluorescence Resonance Energy Transfer KW - Amino Acid Sequence KW - Receptors, AMPA -- metabolism KW - Protein Binding KW - Isoenzymes -- genetics KW - Isoenzymes -- metabolism KW - Binding Sites KW - Static Electricity KW - Blotting, Western KW - Binding, Competitive KW - Cercopithecus aethiops KW - Molecular Sequence Data KW - Receptors, AMPA -- genetics KW - Protein Structure, Tertiary KW - Protein Conformation KW - Protein Kinase C -- metabolism KW - Adaptor Proteins, Signal Transducing -- metabolism KW - Adaptor Proteins, Signal Transducing -- chemistry KW - Protein Kinase C -- genetics KW - Pregnancy Proteins -- metabolism KW - Protein Kinase C -- chemistry KW - Adaptor Proteins, Signal Transducing -- genetics KW - Pregnancy Proteins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709707797?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Zeta+Inhibitory+Peptide+Disrupts+Electrostatic+Interactions+That+Maintain+Atypical+Protein+Kinase+C+in+Its+Active+Conformation+on+the+Scaffold+p62.&rft.au=Tsai%2C+Li-Chun+Lisa%3BXie%2C+Lei%3BDore%2C+Kim%3BXie%2C+Li%3BDel+Rio%2C+Jason+C%3BKing%2C+Charles+C%3BMartinez-Ariza%2C+Guillermo%3BHulme%2C+Christopher%3BMalinow%2C+Roberto%3BBourne%2C+Philip+E%3BNewton%2C+Alexandra+C&rft.aulast=Tsai&rft.aufirst=Li-Chun&rft.date=2015-09-04&rft.volume=290&rft.issue=36&rft.spage=21845&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M115.676221 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-04 N1 - Date created - 2015-09-05 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 2KTR; PDB N1 - SuppNotes - Cited By: J Clin Endocrinol Metab. 2002 Feb;87(2):716-23 [11836310] J Mol Biol. 2006 Oct 6;362(5):901-14 [16949603] Annu Rev Neurosci. 2002;25:103-26 [12052905] Proteins. 2003 Jul 1;52(1):80-7 [12784371] J Cell Biol. 2003 Jun 9;161(5):899-909 [12782683] Mol Cell Biol. 2003 Jul;23(14):4892-900 [12832475] J Mol Biol. 2003 Aug 1;331(1):281-99 [12875852] J Biol Chem. 2003 Sep 5;278(36):34568-81 [12813044] J Cell Sci. 2004 Jan 15;117(Pt 2):131-2 [14676268] Microsc Res Tech. 2004 Jan 1;63(1):58-66 [14677134] Front Biosci. 2004 May 1;9:1626-36 [14977573] J Biol Chem. 2004 Jul 23;279(30):31883-90 [15143057] Nucleic Acids Res. 2010 Jul;38(Web Server issue):W445-9 [20444869] Methods Mol Biol. 2011;756:295-310 [21870234] Chem Biol. 2011 Nov 23;18(11):1463-73 [22118680] PLoS Genet. 2012 Feb;8(2):e1002510 [22346764] J Biol Chem. 2012 Apr 13;287(16):12879-85 [22378786] Proteins. 2012 Jul;80(7):1715-35 [22411565] J Biol Chem. 2006 Oct 13;281(41):30947-56 [16901905] J Biol Chem. 2006 Nov 3;281(44):33773-88 [16950780] FEBS Lett. 2007 Jan 23;581(2):175-9 [17188686] Science. 2007 Aug 17;317(5840):951-3 [17702943] Sci STKE. 2007 Aug 28;2007(401):re6 [17726178] J Neurochem. 2008 Jul;106(1):107-20 [18346206] PLoS Biol. 2008 Dec 23;6(12):2698-706 [19108606] Bioorg Med Chem Lett. 2009 Feb 1;19(3):908-11 [19097791] Hippocampus. 2009 Apr;19(4):392-406 [19004011] Nat Rev Mol Cell Biol. 2010 Feb;11(2):103-12 [20094051] Am J Physiol Endocrinol Metab. 2010 Mar;298(3):E395-402 [19934406] Nat Neurosci. 2010 May;13(5):630-4 [20383136] Biochemistry. 2001 Nov 6;40(44):13216-29 [11683630] J Biol Chem. 2012 Jun 15;287(25):21003-11 [22544755] Nature. 2013 Jan 17;493(7432):416-9 [23283171] Nature. 2013 Jan 17;493(7432):420-3 [23283174] Biochem J. 2013 Jun 1;452(2):195-209 [23662807] Mol Cell Proteomics. 2013 Dec;12(12):3498-508 [23788531] Sci China Life Sci. 2014 Jan;57(1):69-80 [24369353] Biochem Pharmacol. 2014 Mar 1;88(1):1-11 [24231509] ACS Nano. 2014 May 27;8(5):4815-26 [24717072] Sci Signal. 2014 Aug 12;7(338):ra75 [25118327] Nat Rev Mol Cell Biol. 2015 Apr;16(4):232-44 [25785716] Mol Biol Cell. 2015 Apr 15;26(8):1523-31 [25694446] Cell Rep. 2015 Aug 25;12(8):1252-60 [26279568] Proc Natl Acad Sci U S A. 1986 Mar;83(6):1613-6 [3456605] Biochem Biophys Res Commun. 1989 Mar 31;159(3):871-7 [2539153] J Biol Chem. 1992 Aug 5;267(22):15263-6 [1639770] J Biol Chem. 1993 Jan 5;268(1):13-6 [8380153] FEBS Lett. 1994 Feb 28;340(1-2):145-50 [8119399] J Biol Chem. 1994 Apr 15;269(15):11590-4 [8157692] FASEB J. 1999 Oct;13(13):1658-76 [10506570] J Biol Chem. 2005 Feb 18;280(7):5581-7 [15583002] Mol Biol Cell. 2006 Jan;17(1):56-66 [16236797] Science. 2006 Aug 25;313(5790):1141-4 [16931766] J Biol Chem. 2006 Sep 22;281(38):28450-9 [16861740] Nat Neurosci. 2002 Apr;5(4):295-6 [11914719] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M115.676221 ER - TY - JOUR T1 - Evidence That Base-pairing Interaction between Intron and mRNA Leader Sequences Inhibits Initiation of HAC1 mRNA Translation in Yeast. AN - 1709707363; 26175153 AB - The Hac1 transcription factor in yeast up-regulates a collection of genes that control protein homeostasis. Base-pairing interactions between sequences in the intron and the 5'-untranslated region (5' UTR) of the HAC1 mRNA represses Hac1 protein production under basal conditions, whereas cytoplasmic splicing of the intron by the Ire1 kinase-endonuclease, activated under endoplasmic reticulum stress conditions, relieves the inhibition and enables Hac1 synthesis. Using a random mutational screen as well as site-directed mutagenesis, we identify point mutations within the 5' UTR-intron interaction site that derepress translation of the unspliced HAC1 mRNA. We also show that insertion of an in-frame AUG start codon upstream of the interaction site releases the translational block, demonstrating that an elongating ribosome can disrupt the interaction. Moreover, overexpression of translation initiation factor eIF4A, a helicase, enhances production of Hac1 from an mRNA containing an upstream AUG start codon at the beginning of the base-paired region. These results suggest that the major block of translation occurs at the initiation stage. Supporting this interpretation, the point mutations that enhanced Hac1 production resulted in an increased percentage of the HAC1 mRNA associating with polysomes versus free ribosomal subunits. Thus, our results provide evidence that the 5' UTR-intron interaction represses translation initiation on the unspliced HAC1 mRNA. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Sathe, Leena AU - Bolinger, Cheryl AU - Mannan, M Amin-ul AU - Dever, Thomas E AU - Dey, Madhusudan AD - From the Department of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53211 and. ; Eunice Kennedy Shriver NICHD, National Institutes of Health, Bethesda, Maryland 20892. ; Eunice Kennedy Shriver NICHD, National Institutes of Health, Bethesda, Maryland 20892 tdever@nih.gov. ; From the Department of Biological Sciences, University of Wisconsin-Milwaukee, Milwaukee, Wisconsin 53211 and deym@uwm.edu. Y1 - 2015/09/04/ PY - 2015 DA - 2015 Sep 04 SP - 21821 EP - 21832 VL - 290 IS - 36 KW - 5' Untranslated Regions KW - 0 KW - Basic-Leucine Zipper Transcription Factors KW - Codon, Initiator KW - HAC1 protein, S cerevisiae KW - RNA, Messenger KW - Repressor Proteins KW - Saccharomyces cerevisiae Proteins KW - Eukaryotic Initiation Factor-4A KW - EC 2.7.7.- KW - Index Medicus KW - unfolded protein response (UPR) KW - translation KW - HAC1 KW - eukaryotic translation initiation KW - eukaryotic initiation factor 4A (eIF4A) KW - ribosome KW - endoplasmic reticulum stress (ER stress) KW - Gene Expression Regulation, Fungal KW - Blotting, Northern KW - Codon, Initiator -- genetics KW - RNA Splicing KW - Eukaryotic Initiation Factor-4A -- genetics KW - Polyribosomes -- metabolism KW - RNA, Messenger -- genetics KW - Saccharomyces cerevisiae -- genetics KW - Mutagenesis, Site-Directed KW - Base Pairing KW - Polyribosomes -- genetics KW - Blotting, Western KW - Eukaryotic Initiation Factor-4A -- metabolism KW - Saccharomyces cerevisiae -- metabolism KW - RNA, Messenger -- metabolism KW - Point Mutation KW - Mutagenesis, Insertional KW - Saccharomyces cerevisiae Proteins -- metabolism KW - Protein Biosynthesis KW - 5' Untranslated Regions -- genetics KW - Saccharomyces cerevisiae Proteins -- genetics KW - Repressor Proteins -- metabolism KW - Basic-Leucine Zipper Transcription Factors -- metabolism KW - Basic-Leucine Zipper Transcription Factors -- genetics KW - Repressor Proteins -- genetics KW - Introns -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709707363?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Evidence+That+Base-pairing+Interaction+between+Intron+and+mRNA+Leader+Sequences+Inhibits+Initiation+of+HAC1+mRNA+Translation+in+Yeast.&rft.au=Sathe%2C+Leena%3BBolinger%2C+Cheryl%3BMannan%2C+M+Amin-ul%3BDever%2C+Thomas+E%3BDey%2C+Madhusudan&rft.aulast=Sathe&rft.aufirst=Leena&rft.date=2015-09-04&rft.volume=290&rft.issue=36&rft.spage=21821&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M115.649335 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-04 N1 - Date created - 2015-09-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Biol Cell. 1997 Sep;8(9):1805-14 [9307975] Cell. 1997 Sep 19;90(6):1031-9 [9323131] Mol Biol Cell. 1997 Oct;8(10):1845-62 [9348528] Mol Cell Biol. 1997 Dec;17(12):6876-86 [9372919] Curr Biol. 1997 Nov 1;7(11):850-9 [9382810] Nature. 1998 Aug 27;394(6696):854-9 [9732867] EMBO J. 1999 Jun 1;18(11):3119-32 [10357823] Cell. 2005 Jan 14;120(1):49-58 [15652481] Cell. 2014 Feb 27;156(5):950-62 [24581494] Annu Rev Biochem. 2014;83:779-812 [24499181] Mol Cell Biol. 2015 Jan;35(1):199-210 [25348718] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4660-5 [10781071] Cell. 2000 Apr 28;101(3):249-58 [10847680] Nat Rev Mol Cell Biol. 2001 Jul;2(7):521-9 [11433366] Cell. 2001 Oct 5;107(1):103-14 [11595189] Science. 2011 Nov 25;334(6059):1081-6 [22116877] Cold Spring Harb Perspect Biol. 2012 Jul;4(7):a012245 [22751153] Cold Spring Harb Perspect Biol. 2012;4(10). pii: a011544. doi: 10.1101/cshperspect.a011544 [22815232] J Mol Biol. 2013 Jun 26;425(12):2083-99 [23541589] J Biol Chem. 2014 Jan 17;289(3):1704-22 [24285537] Genes Dev. 2002 Nov 15;16(22):2906-22 [12435632] PLoS Biol. 2004 Aug;2(8):E246 [15314660] Cell. 1985 Mar;40(3):515-26 [2982496] Proc Natl Acad Sci U S A. 1986 May;83(9):2850-4 [3458245] Genetics. 1989 May;122(1):19-27 [2659436] Mol Cell Biol. 1989 Nov;9(11):5134-42 [2601712] Mol Cell Biol. 1991 Jul;11(7):3463-71 [2046664] J Biol Chem. 1991 Oct 25;266(30):19867-70 [1939050] J Biol Chem. 1992 Jan 25;267(3):1554-62 [1730701] Gene Expr. 1991 May;1(2):111-5 [1820208] EMBO J. 1992 Jul;11(7):2643-54 [1378397] Cell. 1993 Jun 18;73(6):1197-206 [8513503] Genes Dev. 1995 Dec 1;9(23):2997-3007 [7498795] Cell. 1996 Nov 1;87(3):391-404 [8898193] Cell. 1996 Nov 1;87(3):405-13 [8898194] Genes Cells. 1996 Sep;1(9):803-17 [9077435] Proc Natl Acad Sci U S A. 1997 May 13;94(10):5201-6 [9144215] Annu Rev Microbiol. 2005;59:407-50 [16153175] Gene. 2005 Nov 21;361:13-37 [16213112] Nat Rev Mol Cell Biol. 2007 Jul;8(7):519-29 [17565364] Science. 2008 Jun 6;320(5881):1344-9 [18451266] Science. 2009 Apr 10;324(5924):218-23 [19213877] Trends Biochem Sci. 2009 Jul;34(7):324-31 [19535251] Mol Biol Cell. 2010 Nov 1;21(21):3722-34 [20844078] Microbiol Mol Biol Rev. 2011 Sep;75(3):434-67, first page of table of contents [21885680] J Mol Biol. 2011 Sep 30;412(4):674-87 [21840318] RNA Biol. 2011 Jul-Aug;8(4):552-6 [21593604] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M115.649335 ER - TY - JOUR T1 - Adapted Resistance to the Knockdown Effect of shRNA-Derived Srsf3 siRNAs in Mouse Littermates AN - 1753485203; PQ0002149098 AB - Gene silencing techniques are widely used to control gene expression and have potential for RNAi-based therapeutics. In this report, transgenic mouse lines were created for conditional knockdown of Srsf3 (SRp20) expression in liver and mammary gland tissues by expressing Srsf3-specific shRNAs driven by a U6 promoter. Although a small portion of the transgenic mouse littermates were found to produce siRNAs in the targeted tissues, most of the transgenic littermates at two months of age failed to display a knockdown phenotype of Srsf3 expression in their liver and mammary gland tissues where an abundant level of Srsf3 siRNAs remained. We saw only one of four mice with liver/mammary gland expressing Srsf3 siRNA displayed a suppressed level of Srsf3 protein, but not the mRNA. Data indicate that the host resistance to a gene-specific siRNA targeting an essential gene transcript can be developed in animals, presumably as a physiological necessity to cope with the hostile perturbation. JF - International Journal of Biological Sciences AU - Ajiro, Masahiko AU - Jia, Rong AU - Wang, Rui-Hong AU - Deng, Chu-Xia AU - Zheng, Zhi-Ming AD - . Tumor Virus RNA Biology Section, Gene Regulation and Chromosome Biology Laboratory, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, Maryland 21702, USA PY - 2015 SP - 1248 EP - 1256 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 11 IS - 11 KW - Biotechnology and Bioengineering Abstracts KW - Srsf3 KW - shRNAs KW - transgenic mouse KW - Promoters KW - Age KW - Data processing KW - siRNA KW - Mammary gland KW - Liver KW - Transcription KW - Transgenic mice KW - Gene silencing KW - W 30925:Genetic Engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753485203?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Biological+Sciences&rft.atitle=Adapted+Resistance+to+the+Knockdown+Effect+of+shRNA-Derived+Srsf3+siRNAs+in+Mouse+Littermates&rft.au=Ajiro%2C+Masahiko%3BJia%2C+Rong%3BWang%2C+Rui-Hong%3BDeng%2C+Chu-Xia%3BZheng%2C+Zhi-Ming&rft.aulast=Ajiro&rft.aufirst=Masahiko&rft.date=2015-09-03&rft.volume=11&rft.issue=11&rft.spage=1248&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Biological+Sciences&rft.issn=1449-2288&rft_id=info:doi/10.7150%2Fijbs.13011 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Promoters; Age; Data processing; siRNA; Mammary gland; Liver; Transcription; Transgenic mice; Gene silencing DO - http://dx.doi.org/10.7150/ijbs.13011 ER - TY - JOUR T1 - Oxime ether lipids containing hydroxylated head groups are more superior siRNA delivery agents than their nonhydroxylated counterparts AN - 1846415651; PQ0003837172 AB - Aim: To evaluate the structure-activity relationship of oxime ether lipids (OELs) containing modifications in the hydrophobic domains (chain length, degree of unsaturation) and hydrophilic head groups (polar domain hydroxyl groups) toward complex formation with siRNA molecules and siRNA delivery efficiency of resulting complexes to a human breast cancer cell line (MDA-MB-231). Materials & methods: Ability of lipoplex formation between oxime ether lipids with nucleic acids were examined using biophysical techniques. The potential of OELs to deliver nucleic acids and silence green fluorescent protein (GFP) gene was analyzed using MDA-MB-231 and MDA-MB-231/GFP cells, respectively. Results & conclusion: Introduction of hydroxyl groups to the polar domain of the OELs and unsaturation into the hydrophobic domain favor higher transfection and gene silencing in a cell culture system. JF - Nanomedicine AU - Gupta, Kshitij AU - Mattingly, Stephanie J AU - Knipp, Ralph J AU - Afonin, Kirill A AU - Viard, Mathias AU - Bergman, Joseph T AU - Stepler, Marissa AU - Nantz, Michael H AU - Puri, Anu AU - Shapiro, Bruce A AD - super(1)Gene Regulation & Chromosome Biology Lab, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702-1201, USA Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 2805 EP - 2818 PB - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom VL - 10 IS - 18 SN - 1743-5889, 1743-5889 KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - breast cancer cells KW - lipoplexes KW - nonsymmetric hydrophobic domain KW - oxime ether lipids KW - RNA interference KW - structure-activity relationship KW - Lipids KW - Green fluorescent protein KW - Hydrophobicity KW - Cell culture KW - Lipid rafts KW - Tumor cell lines KW - nucleic acids KW - siRNA KW - Transfection KW - oximes KW - Breast cancer KW - Ethers KW - Structure-activity relationships KW - nanotechnology KW - Gene silencing KW - Phospholipids KW - W 30905:Medical Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1846415651?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nanomedicine&rft.atitle=Oxime+ether+lipids+containing+hydroxylated+head+groups+are+more+superior+siRNA+delivery+agents+than+their+nonhydroxylated+counterparts&rft.au=Gupta%2C+Kshitij%3BMattingly%2C+Stephanie+J%3BKnipp%2C+Ralph+J%3BAfonin%2C+Kirill+A%3BViard%2C+Mathias%3BBergman%2C+Joseph+T%3BStepler%2C+Marissa%3BNantz%2C+Michael+H%3BPuri%2C+Anu%3BShapiro%2C+Bruce+A&rft.aulast=Gupta&rft.aufirst=Kshitij&rft.date=2015-09-01&rft.volume=10&rft.issue=18&rft.spage=2805&rft.isbn=&rft.btitle=&rft.title=Nanomedicine&rft.issn=17435889&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-12-01 N1 - Number of references - 48 N1 - Last updated - 2017-02-01 N1 - SubjectsTermNotLitGenreText - Lipids; Green fluorescent protein; Cell culture; Hydrophobicity; Lipid rafts; Tumor cell lines; nucleic acids; siRNA; Transfection; oximes; Breast cancer; Ethers; Structure-activity relationships; Phospholipids; Gene silencing; nanotechnology ER - TY - JOUR T1 - Effect of Functionally Significant Deiodinase Single Nucleotide Polymorphisms on Drinking Behavior in Alcohol Dependence: An Exploratory Investigation AN - 1827893759; PQ0003712084 AB - Background Abnormalities of the hypothalamic-pituitary-thyroid (HPT) axis have been reported in alcoholism; however, there is no definitive agreement on the specific thyroid abnormalities and their underlying mechanisms in alcohol dependence. The biological activity of thyroid hormones or the availability of T3 is regulated by the three deiodinase enzymes: D1, D2, and D3. In the context of alcohol use, functionally significant single nucleotide polymorphisms (SNPs) of these deiodinase genes may play a role in HPT dysfunction. Methods This study explored the effect of three functionally significant SNPs (D1: rs2235544, D2: rs225014, and rs12885300) of deiodinase genes on drinking behavior and thyroid-stimulating hormone (TSH) levels in alcohol-dependent (N = 521) and control subjects (N = 288). Results Rs225014 was associated with significant differences in the amount of naturalistic alcohol drinking assessed by Timeline Follow Back. Alcohol-dependent subjects had significantly higher TSH levels compared to controls; however, there was no effect of genotype on TSH levels for either group. Conclusions These findings extend previous studies on thyroid dysfunction in alcoholism and provide novel, albeit preliminary, information by linking functionally significant genetic polymorphisms of the deiodinase enzymes with alcohol-drinking behavior. JF - Alcoholism: Clinical and Experimental Research AU - Lee, Mary R AU - Schwandt, Melanie L AU - Bollinger, Jared W AU - Dias, Alexandra A AU - Oot, Emily N AU - Goldman, David AU - Hodgkinson, Colin A AU - Leggio, Lorenzo AD - Section on Clinical Psychoneuroendocrinology and Neuropsychopharmacology , National Institute on Alcohol Abuse and Alcoholism and National Institute on Drug Abuse, National Institutes of Health, Bethesda, Maryland. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 1665 EP - 1670 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 39 IS - 9 SN - 0145-6008, 0145-6008 KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - Hypothalamus KW - Gene polymorphism KW - Enzymes KW - Triiodothyronine KW - Hypothalamic-pituitary-thyroid axis KW - Drug abuse KW - Thyroid hormones KW - Drug dependence KW - Single-nucleotide polymorphism KW - Alcoholism KW - Drinking behavior KW - Thyroid-stimulating hormone KW - Iodide peroxidase KW - Ethanol KW - X 24380:Social Poisons & Drug Abuse KW - N 14810:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1827893759?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%3A+Clinical+and+Experimental+Research&rft.atitle=Effect+of+Functionally+Significant+Deiodinase+Single+Nucleotide+Polymorphisms+on+Drinking+Behavior+in+Alcohol+Dependence%3A+An+Exploratory+Investigation&rft.au=Lee%2C+Mary+R%3BSchwandt%2C+Melanie+L%3BBollinger%2C+Jared+W%3BDias%2C+Alexandra+A%3BOot%2C+Emily+N%3BGoldman%2C+David%3BHodgkinson%2C+Colin+A%3BLeggio%2C+Lorenzo&rft.aulast=Lee&rft.aufirst=Mary&rft.date=2015-09-01&rft.volume=39&rft.issue=9&rft.spage=1665&rft.isbn=&rft.btitle=&rft.title=Alcoholism%3A+Clinical+and+Experimental+Research&rft.issn=01456008&rft_id=info:doi/10.1111%2Facer.12814 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-10-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Hypothalamus; Gene polymorphism; Enzymes; Hypothalamic-pituitary-thyroid axis; Triiodothyronine; Drug abuse; Drug dependence; Thyroid hormones; Single-nucleotide polymorphism; Alcoholism; Drinking behavior; Thyroid-stimulating hormone; Iodide peroxidase; Ethanol DO - http://dx.doi.org/10.1111/acer.12814 ER - TY - JOUR T1 - Converging Patterns of Alcohol Use and Related Outcomes Among Females and Males in the United States, 2002 to 2012 AN - 1827893617; PQ0003712085 AB - Background Females in the United States consume less alcohol and cause and experience fewer alcohol-related harms than males. However, recent research suggests such gaps might be narrowing. The purpose of this study was to explore changes in alcohol use and associated outcomes among females and males in the United States between 2002 and 2012. Methods Data from the National Survey on Drug Use and Health were used to assess the prevalence and trends for females and males aged 12+ in lifetime abstinence, age of onset, current drinking, binge drinking, drinking and driving, reaching DSM-IV criteria for an alcohol use disorder, combining alcohol with other drugs such as marijuana, and other variables. Of particular interest was whether differences between females and males narrowed during the decade under study. Results Differences in the drinking patterns of females and males aged 12+ narrowed between 2002 and 2012 for current drinking, number of drinking days per month, past year DSM-IV alcohol abuse, and past-year driving under the influence of alcohol. In addition, convergence was noted in 1 or more age subgroups for the prevalence of binge drinking and DSM-IV alcohol dependence and mean age at drinking onset. Divergence in drinking habits did not occur for any measure in any age subgroups with the exception of a greater increase in the prevalence of combining alcohol with marijuana among young adult male drinkers than female drinkers aged 18 to 25. Conclusions Between 2002 and 2012, differences in alcohol consumption and related outcomes narrowed for females and males. Reasons for converging patterns of alcohol use are unclear and do not appear to be easily explainable by recent trends in employment status, pregnancy status, or marital status. More research is needed to identify the psychosocial and environmental contributors to these changes and to assess implications for prevention and treatment efforts. JF - Alcoholism: Clinical and Experimental Research AU - White, Aaron AU - Castle, I-Jen P AU - Chen, Chiung M AU - Shirley, Mariela AU - Roach, Deidra AU - Hingson, Ralph AD - National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 1712 EP - 1726 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 39 IS - 9 SN - 0145-6008, 0145-6008 KW - Toxicology Abstracts KW - Drug dependence KW - Age KW - Data processing KW - Convergence KW - Alcoholism KW - Cannabis KW - Drinking behavior KW - Drug abuse KW - Ethanol KW - Pregnancy KW - X 24380:Social Poisons & Drug Abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1827893617?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%3A+Clinical+and+Experimental+Research&rft.atitle=Converging+Patterns+of+Alcohol+Use+and+Related+Outcomes+Among+Females+and+Males+in+the+United+States%2C+2002+to+2012&rft.au=White%2C+Aaron%3BCastle%2C+I-Jen+P%3BChen%2C+Chiung+M%3BShirley%2C+Mariela%3BRoach%2C+Deidra%3BHingson%2C+Ralph&rft.aulast=White&rft.aufirst=Aaron&rft.date=2015-09-01&rft.volume=39&rft.issue=9&rft.spage=1712&rft.isbn=&rft.btitle=&rft.title=Alcoholism%3A+Clinical+and+Experimental+Research&rft.issn=01456008&rft_id=info:doi/10.1111%2Facer.12815 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-10-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Drug dependence; Age; Data processing; Convergence; Alcoholism; Cannabis; Drinking behavior; Drug abuse; Pregnancy; Ethanol DO - http://dx.doi.org/10.1111/acer.12815 ER - TY - JOUR T1 - TLR4 mutant mice are protected from renal fibrosis and chronic kidney disease progression AN - 1815694575; PQ0002090133 AB - Chronic kidney disease (CKD) is associated with persistent low-grade inflammation and immunosuppression. In this study we tested the role of Toll-like receptor 4, the main receptor for endotoxin (LPS), in a mouse model of renal fibrosis and in a model of progressive CKD that better resembles the human disease. C3HeJ (TLR4 mutant) mice have a missense point mutation in the TLR4 gene, rendering the receptor nonfunctional. In a model of renal fibrosis after folic acid injection, TLR4 mutant mice developed less interstititial fibrosis in comparison to wild-type (WT) mice. Furthermore, 4 weeks after 5/6 nephrectomy with continuous low-dose angiotensin II infusion, C3HeOuJ (TLR4 WT) mice developed progressive CKD with albuminuria, increased serum levels of BUN and creatinine, glomerulosclerosis, and interstitial fibrosis, whereas TLR4 mutant mice were significantly protected from CKD progression. TLR4 WT mice also developed low-grade systemic inflammation, splenocyte apoptosis and increased expression of the immune inhibitory receptor PD-1 in the spleen, which were not observed in TLR4 mutant mice. In vitro, endotoxin (LPS) directly upregulated NLRP3 inflammasome expression in renal epithelial cells via TLR4. In summary, TLR4 contributes to renal fibrosis and CKD progression, at least in part, via inflammasome activation in renal epithelial cells, and may also participate in the dysregulated immune response that is associated with CKD. TLR4 mutant mice are protected from renal fibrosis and CKD progression in two different mouse models. JF - Physiological Reports AU - Souza, Ana CP AU - Tsuji, Takayuki AU - Baranova, Irina N AU - Bocharov, Alexander V AU - Wilkins, Kenneth J AU - Street, Jonathan M AU - Alvarez-Prats, Alejandro AU - Hu, Xuzhen AU - Eggerman, Thomas AU - Yuen, Peter ST AU - Star, Robert A AD - Renal Diagnostics and Therapeutics Unit, NIDDK, NIH, Bethesda, Maryland. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - [np] PB - Wiley Subscription Services, Inc. VL - 3 IS - 9 SN - 2051-817X, 2051-817X KW - Toxicology Abstracts KW - Endotoxins KW - Epithelial cells KW - Apoptosis KW - Fibrosis KW - Point mutation KW - Kidney diseases KW - Animal models KW - Spleen KW - Angiotensin II KW - Inflammation KW - PD-1 protein KW - Splenocytes KW - Creatinine KW - Nephrectomy KW - Lipopolysaccharides KW - Immune response KW - TLR4 protein KW - Toll-like receptors KW - Immunosuppression KW - X 24370:Natural Toxins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1815694575?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Physiological+Reports&rft.atitle=TLR4+mutant+mice+are+protected+from+renal+fibrosis+and+chronic+kidney+disease+progression&rft.au=Souza%2C+Ana+CP%3BTsuji%2C+Takayuki%3BBaranova%2C+Irina+N%3BBocharov%2C+Alexander+V%3BWilkins%2C+Kenneth+J%3BStreet%2C+Jonathan+M%3BAlvarez-Prats%2C+Alejandro%3BHu%2C+Xuzhen%3BEggerman%2C+Thomas%3BYuen%2C+Peter+ST%3BStar%2C+Robert+A&rft.aulast=Souza&rft.aufirst=Ana&rft.date=2015-09-01&rft.volume=3&rft.issue=9&rft.spage=%5Bnp%5D&rft.isbn=&rft.btitle=&rft.title=Physiological+Reports&rft.issn=2051817X&rft_id=info:doi/10.14814%2Fphy2.12558 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-08-01 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Endotoxins; Epithelial cells; Apoptosis; Fibrosis; Point mutation; Animal models; Kidney diseases; Spleen; Angiotensin II; Inflammation; Splenocytes; PD-1 protein; Creatinine; Nephrectomy; Lipopolysaccharides; Immune response; TLR4 protein; Toll-like receptors; Immunosuppression DO - http://dx.doi.org/10.14814/phy2.12558 ER - TY - JOUR T1 - Superiority of [68Ga]-DOTATATE PET/CT to Other Functional Imaging Modalities in the Localization of SDHB-Associated Metastatic Pheochromocytoma and Paraganglioma AN - 1808682048; PQ0003419730 AB - Purpose: Patients with succinate dehydrogenase subunit B(SDHB) mutation-related pheochromocytoma/paraganglioma (PHEO/PGL) are at a higher risk for metastatic disease than other hereditary PHEOs/PGLs. Current therapeutic approaches are limited, but the best outcomes are based on the early and proper detection of as many lesions as possible. Because PHEOs/PGLs overexpress somatostatin receptor 2 (SSTR2), the goal of our study was to assess the clinical utility of [68Ga]-DOTA(0)-Tyr(3)-octreotate ([68Ga]-DOTATATE) positron emission tomography/computed tomography (PET/CT) and to evaluate its diagnostic utility in comparison with the currently recommended functional imaging modalities [18F]-fluorodopamine ([18F]-FDA), [18F]-fluorodihydroxyphenylalanine ([18F]-FDOPA), [18F]-fluoro-2-deoxy-d-glucose ([18F]- FDG) PET/CT as well as CT/MRI.Experimental Design: [68Ga]-DOTATATE PET/CT was prospectively performed in 17 patients with SDHB-related metastatic PHEOs/PGLs. All patients also underwent [18F]-FDG PET/CT and CT/MRI, with 16 of the 17 patients also receiving [18F]-FDOPA and [18F]-FDA PET/CT scans. Detection rates of metastatic lesions were compared between all these functional imaging studies. A composite synthesis of all used functional and anatomical imaging studies served as the imaging comparator.Results: [68Ga]-DOTATATE PET/CT demonstrated a lesion-based detection rate of 98.6% [95% confidence interval (CI), 96.5%-99.5%], [18F]-FDG, [18F]-FDOPA, [18F]-FDA PET/CT, and CT/MRI showed detection rates of 85.8% (CI, 81.3%-89.4%; P < 0.01), 61.4% (CI, 55.6%-66.9%; P < 0.01), 51.9% (CI, 46.1%-57.7%; P < 0.01), and 84.8% (CI, 80.0%-88.5%; P < 0.01), respectively.Conclusions: [68Ga]-DOTATATE PET/CT showed a significantly superior detection rate to all other functional and anatomical imaging modalities and may represent the preferred future imaging modality in the evaluation of SDHB-related metastatic PHEO/PGL. Clin Cancer Res; 21(17); 3888-95. copyright 2015 AACR.See related commentary by Hofman and Hicks, p. 3815 JF - Clinical Cancer Research AU - Janssen, Ingo AU - Blanchet, Elise M AU - Adams, Karen AU - Chen, Clara C AU - Millo, Corina M AU - Herscovitch, Peter AU - Taieb, David AU - Kebebew, Electron AU - Lehnert, Hendrik AU - Fojo, Antonio T AU - Pacak, Karel AD - Department of Radiology and Nuclear Medicine, Section of Nuclear Medicine, University Hospital Schleswig Holstein, Campus Luebeck, Luebeck, Germany, karel@mail.nih.gov Y1 - 2015/09/01/ PY - 2015 DA - 2015 Sep 01 SP - 3888 EP - 3895 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 17 SN - 1078-0432, 1078-0432 KW - Biotechnology and Bioengineering Abstracts KW - Metastases KW - Paraganglioma KW - Somatostatin receptors KW - Succinate dehydrogenase KW - Risk factors KW - Computed tomography KW - Magnetic resonance imaging KW - Positron emission tomography KW - Pheochromocytoma KW - Cancer KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808682048?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Cancer+Research&rft.atitle=Superiority+of+%5B68Ga%5D-DOTATATE+PET%2FCT+to+Other+Functional+Imaging+Modalities+in+the+Localization+of+SDHB-Associated+Metastatic+Pheochromocytoma+and+Paraganglioma&rft.au=Janssen%2C+Ingo%3BBlanchet%2C+Elise+M%3BAdams%2C+Karen%3BChen%2C+Clara+C%3BMillo%2C+Corina+M%3BHerscovitch%2C+Peter%3BTaieb%2C+David%3BKebebew%2C+Electron%3BLehnert%2C+Hendrik%3BFojo%2C+Antonio+T%3BPacak%2C+Karel&rft.aulast=Janssen&rft.aufirst=Ingo&rft.date=2015-09-01&rft.volume=21&rft.issue=17&rft.spage=3888&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-2751 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Metastases; Paraganglioma; Somatostatin receptors; Risk factors; Succinate dehydrogenase; Magnetic resonance imaging; Computed tomography; Positron emission tomography; Cancer; Pheochromocytoma DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-2751 ER - TY - JOUR T1 - SERS analysis of serum for detection of early and locally advanced breast cancer AN - 1746882133; PQ0002077722 AB - In this contribution, we investigated whether surface-enhanced Raman scattering (SERS) of serum can be a candidate method for detecting "luminal A" breast cancer (BC) at different stages. We selected three groups of participants aged over 50 years: 20 healthy women, 20 women with early localized small BC, and 20 women affected by BC with lymph node involvement. SERS revealed clear spectral differences between these three groups. A predictive model using principal component analysis (PCA) and linear discriminant analysis (LDA) was developed based on spectral data, and its performance was estimated with cross-validation. PCA-LDA of SERS spectra could distinguish healthy from BC subjects (sensitivity, 92 %; specificity, 85 %), as well as subjects with BC at different stages, with a promising diagnostic performance (sensitivity and specificity, greater than or equal to 80 %; overall accuracy, 84 %). Our data suggest that SERS spectroscopy of serum, combined with multivariate data analysis, represents a minimally invasive, easy to use, and fast approach to discriminate healthy from BC subjects and even to distinguish BC at different clinical stages. JF - Analytical and Bioanalytical Chemistry AU - Cervo, Silvia AU - Mansutti, Elena AU - Mistro, Greta AU - Spizzo, Riccardo AU - Colombatti, Alfonso AU - Steffan, Agostino AU - Sergo, Valter AU - Bonifacio, Alois AD - CRO-Biobank, CRO Aviano National Cancer Institute, Via Franco Gallini 2, 33081, Aviano, PN, Italy, abonifacio@units.it PY - 2015 SP - 7503 EP - 7509 PB - Springer Science+Business Media, Berlin/Heidelberg Germany VL - 407 IS - 24 SN - 1618-2642, 1618-2642 KW - Aqualine Abstracts; Water Resources Abstracts KW - Principal Component Analysis KW - Spectroscopy KW - Model Studies KW - AQ 00001:Water Resources and Supplies KW - SW 5010:Network design UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746882133?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+and+Bioanalytical+Chemistry&rft.atitle=SERS+analysis+of+serum+for+detection+of+early+and+locally+advanced+breast+cancer&rft.au=Cervo%2C+Silvia%3BMansutti%2C+Elena%3BMistro%2C+Greta%3BSpizzo%2C+Riccardo%3BColombatti%2C+Alfonso%3BSteffan%2C+Agostino%3BSergo%2C+Valter%3BBonifacio%2C+Alois&rft.aulast=Cervo&rft.aufirst=Silvia&rft.date=2015-09-01&rft.volume=407&rft.issue=24&rft.spage=7503&rft.isbn=&rft.btitle=&rft.title=Analytical+and+Bioanalytical+Chemistry&rft.issn=16182642&rft_id=info:doi/10.1007%2Fs00216-015-8923-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 39 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Principal Component Analysis; Spectroscopy; Model Studies DO - http://dx.doi.org/10.1007/s00216-015-8923-8 ER - TY - JOUR T1 - Individual and Geographic Variation of Skin Alkaloids in Three Swamp-Forest Species of Madagascan Poison Frogs (Mantella) AN - 1727686511; PQ0002127982 AB - Seventy skins of three mantellid frog species from Madagascan swamp-forest habitats, Mantella aurantiaca, M. crocea, and M. milotympanum, were individually examined for skin alkaloids using GC/MS. These poison frogs were found to differ significantly in their alkaloid composition from species of Mantella originating from non-flooded rainforest in eastern Madagascar, which were examined in earlier work. Only 16 of the previously detected 106 alkaloids were represented among the 60 alkaloids from the swamp-forest frogs of the present study. We hypothesize this difference is related mainly to habitat but cannot exclude a phylogenetic component as the three swamp-forest species are a closely related monophyletic group. The paucity of alkaloids with unbranched-carbon skeletons (ant-derived) and the commonness of alkaloids with branched-carbon skeletons (mite-derived) indicate that oribatid mites are a major source of alkaloids in these species of mantellids. Furthermore, most of the alkaloids have an oxygen atom in their formulae. Differences in alkaloids were observed among species, populations of the same species, and habitats. In M. aurantiaca, small geographic distances among populations were associated with differences in alkaloid profiles, with a remote third site illustrating even greater differences. The present study and an earlier study of three other mantellid species suggest that oribatid mites, and not ants, are the major source of alkaloids in the species of mantellids examined thus far. JF - Journal of Chemical Ecology AU - Andriamaharavo, Nirina R AU - Garraffo, HMartin AU - Spande, Thomas F AU - Giddings, Lesley-Ann AU - Vieites, David R AU - Vences, Miguel AU - Saporito, Ralph A AD - Laboratory of Bioorganic Chemistry, NIDDK, NIH, DHHS, Bethesda, MD, 20892, USA, ralph.saporito@gmail.com Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 837 EP - 847 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 41 IS - 9 SN - 0098-0331, 0098-0331 KW - Entomology Abstracts; Chemoreception Abstracts; Ecology Abstracts KW - Phylogeny KW - Skin KW - Anura KW - Formicidae KW - Mantella aurantiaca KW - Mantella KW - Habitat KW - Guanylate cyclase KW - Oxygen KW - Alkaloids KW - Rain forests KW - Oribatida KW - Geographical variations KW - Z 05340:Ecology and Behavior KW - D 04040:Ecosystem and Ecology Studies KW - R 18160:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727686511?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Chemical+Ecology&rft.atitle=Individual+and+Geographic+Variation+of+Skin+Alkaloids+in+Three+Swamp-Forest+Species+of+Madagascan+Poison+Frogs+%28Mantella%29&rft.au=Andriamaharavo%2C+Nirina+R%3BGarraffo%2C+HMartin%3BSpande%2C+Thomas+F%3BGiddings%2C+Lesley-Ann%3BVieites%2C+David+R%3BVences%2C+Miguel%3BSaporito%2C+Ralph+A&rft.aulast=Andriamaharavo&rft.aufirst=Nirina&rft.date=2015-09-01&rft.volume=41&rft.issue=9&rft.spage=837&rft.isbn=&rft.btitle=&rft.title=Journal+of+Chemical+Ecology&rft.issn=00980331&rft_id=info:doi/10.1007%2Fs10886-015-0616-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Number of references - 40 N1 - Last updated - 2016-02-29 N1 - SubjectsTermNotLitGenreText - Phylogeny; Oxygen; Guanylate cyclase; Rain forests; Alkaloids; Skin; Geographical variations; Habitat; Oribatida; Formicidae; Anura; Mantella aurantiaca; Mantella DO - http://dx.doi.org/10.1007/s10886-015-0616-4 ER - TY - JOUR T1 - Recognition of the bacterial alarmone ZMP through long-distance association of two RNA subdomains AN - 1727682665; PQ0002119397 AB - The bacterial alarmone 5-aminoimidazole-4-carboxamide riboside 5'-triphosphate (AICAR triphosphate or ZTP), derived from the monophosphorylated purine precursor ZMP, accumulates during folate starvation. ZTP regulates genes involved in purine and folate metabolism through a cognate riboswitch. The linker connecting this riboswitch's two subdomains varies in length by over 100 nucleotides. We report the cocrystal structure of the Fusobacterium ulcerans riboswitch bound to ZMP, which spans the two subdomains whose interface also comprises a pseudoknot and ribose zipper. The riboswitch recognizes the carboxamide oxygen of ZMP through an unprecedented inner-sphere coordination with a Mg super(2+) ion. We show that the affinity of the riboswitch for ZMP is modulated by the linker length. Notably, ZMP can simultaneously bind to the two subdomains even when they are synthesized as separate RNAs. The ZTP riboswitch demonstrates how specific small-molecule binding can drive association of distant noncoding-RNA domains to regulate gene expression. JF - Nature Structural & Molecular Biology AU - Jones, Christopher P AU - Ferre-D'Amare, Adrian R AD - Biochemistry and Biophysics Center, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA. PY - 2015 SP - 679 EP - 685 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 22 IS - 9 SN - 1545-9993, 1545-9993 KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - Starvation KW - Bacteria KW - Ribose KW - Riboswitches KW - purines KW - Nucleotides KW - Oxygen KW - RNA KW - Fusobacterium KW - Folic acid KW - Magnesium KW - Metabolism KW - J 02320:Cell Biology KW - N 14830:RNA UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727682665?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+Structural+%26+Molecular+Biology&rft.atitle=Recognition+of+the+bacterial+alarmone+ZMP+through+long-distance+association+of+two+RNA+subdomains&rft.au=Jones%2C+Christopher+P%3BFerre-D%27Amare%2C+Adrian+R&rft.aulast=Jones&rft.aufirst=Christopher&rft.date=2015-09-01&rft.volume=22&rft.issue=9&rft.spage=679&rft.isbn=&rft.btitle=&rft.title=Nature+Structural+%26+Molecular+Biology&rft.issn=15459993&rft_id=info:doi/10.1038%2Fnsmb.3073 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Starvation; Oxygen; RNA; Ribose; Riboswitches; Magnesium; Folic acid; Metabolism; Nucleotides; purines; Bacteria; Fusobacterium DO - http://dx.doi.org/10.1038/nsmb.3073 ER - TY - JOUR T1 - Metallothionein gene expression is altered in oral cancer and may predict metastasis and patient outcomes. AN - 1724260292; 25640883 AB - Metallothioneins (MTs) are proteins associated with the carcinogenesis and prognosis of various tumours. Previous studies have shown their potential as biomarkers in oral squamous cell carcinoma (OSCC). Aiming to understand more clearly the function of MTs in OSCC we evaluated, for the first time, the gene expression profile of MTs in this neoplasm. Tissue samples from 35 cases of tongue and/or floor of mouth OSCC, paired with their corresponding non-neoplastic oral mucosa (NNOM), were retrieved (2007-09). All tissues were analysed for the following genes using TaqMan(®) reverse transcription-quantitative polymerase chain reaction (RT-qPCR) assays: MT1A, MT1B, MT1E, MT1F, MT1G, MT1H, MT1X, MT2A, MT3 and MT4. The expression of MT1B and MT1H was seldom detected in both OSCC and NNOM. A significant loss of MT1A, MT1X, MT3 and MT4 expression and gain of MT1F expression was observed in OSCC, compared to NNOM. Cases with MT1G down-regulation exhibited the worst prognoses. The up-regulation of MT1X was restricted to non-metastatic cases, whereas up-regulation of MT3 was related to cases with lymph node metastasis. Metallothionein mRNA expression is altered significantly in oral squamous cell carcinomas. The expression of MT1G, MT1X and MT3 may aid in the prognostic discrimination of OSCC cases. © 2015 John Wiley & Sons Ltd. JF - Histopathology AU - Brazão-Silva, Marco T AU - Rodrigues, Maria Fernandes S AU - Eisenberg, Ana Lúcia A AU - Dias, Fernando L AU - de Castro, Luciana M AU - Nunes, Fábio D AU - Faria, Paulo R AU - Cardoso, Sérgio V AU - Loyola, Adriano M AU - de Sousa, Suzana C O M AD - PhD program in Estomatology and Basic and Applied Pathology, School of Dentistry, University of São Paulo, São Paulo, Brazil. ; Laboratory of Molecular Pathology, School of Dentistry, University of São Paulo, São Paulo, Brazil. ; Department of Pathology, Brazilian National Cancer Institute/INCA, Rio de Janeiro, Brazil. ; Department of Head and Neck Surgery, Brazilian National Cancer Institute/INCA, Rio de Janeiro, Brazil. ; National Tumor Bank, Brazilian National Cancer Institute/INCA, Rio de Janeiro, Brazil. ; Department of Histology and Morphology, Institute of Biomedical Sciences, Federal University of Uberlândia, Uberlândia, Brazil. ; Department of Oral Pathology, School of Dentistry, Federal University of Uberlândia, Uberlândia, Brazil. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 358 EP - 367 VL - 67 IS - 3 KW - Biomarkers, Tumor KW - 0 KW - MMP16 protein, human KW - MT1G protein, human KW - RNA, Messenger KW - RNA, Neoplasm KW - metallothionein1X , human KW - Metallothionein KW - 9038-94-2 KW - Matrix Metalloproteinase 16 KW - EC 3.4.24.- KW - Index Medicus KW - RT-qPCR KW - metastasis KW - metallothionein KW - oral squamous cell carcinoma KW - prognosis KW - Biomarkers, Tumor -- genetics KW - Humans KW - Mouth Mucosa -- enzymology KW - Prognosis KW - Aged KW - RNA, Neoplasm -- genetics KW - RNA, Messenger -- genetics KW - Tongue Neoplasms -- genetics KW - Down-Regulation KW - Tongue Neoplasms -- pathology KW - Middle Aged KW - Up-Regulation KW - Matrix Metalloproteinase 16 -- genetics KW - Female KW - Male KW - Carcinoma, Squamous Cell -- secondary KW - Carcinoma, Squamous Cell -- pathology KW - Carcinoma, Squamous Cell -- genetics KW - Metallothionein -- genetics KW - Mouth Neoplasms -- pathology KW - Mouth Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1724260292?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Histopathology&rft.atitle=Metallothionein+gene+expression+is+altered+in+oral+cancer+and+may+predict+metastasis+and+patient+outcomes.&rft.au=Braz%C3%A3o-Silva%2C+Marco+T%3BRodrigues%2C+Maria+Fernandes+S%3BEisenberg%2C+Ana+L%C3%BAcia+A%3BDias%2C+Fernando+L%3Bde+Castro%2C+Luciana+M%3BNunes%2C+F%C3%A1bio+D%3BFaria%2C+Paulo+R%3BCardoso%2C+S%C3%A9rgio+V%3BLoyola%2C+Adriano+M%3Bde+Sousa%2C+Suzana+C+O+M&rft.aulast=Braz%C3%A3o-Silva&rft.aufirst=Marco&rft.date=2015-09-01&rft.volume=67&rft.issue=3&rft.spage=358&rft.isbn=&rft.btitle=&rft.title=Histopathology&rft.issn=1365-2559&rft_id=info:doi/10.1111%2Fhis.12660 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-10-31 N1 - Date created - 2015-08-12 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/his.12660 ER - TY - JOUR T1 - Persistence of hAQP1 expression in human salivary gland cells following AdhAQP1 transduction is associated with a lack of methylation of hCMV promoter AN - 1722170092; PQ0002109233 AB - In 2012, we reported that 5 out of 11 subjects in a clinical trial (NCT00372320) administering AdhAQP1 to radiation-damaged parotid glands showed increased saliva flow rates and decreased symptoms over the initial 42 days. AdhAQP1 is a first-generation, E1-deleted, replication-defective, serotype 5 adenoviral vector encoding human aquaporin-1 (hAQP1). This vector uses the human cytomegalovirus enhancer/promoter (hCMVp). As subject peak responses were at times much longer (7-42 days) than expected, we hypothesized that the hCMVp may not be methylated in human salivary gland cells to the extent previously observed in rodent salivary gland cells. This hypothesis was supported in human salivary gland primary cultures and human salivary gland cell lines after transduction with AdhAQP1. Importantly, hAQP1 maintained its function in those cells. Conversely, when we transduced mouse and rat cell lines in vitro and submandibular glands in vivo with AdhAQP1, the hCMVp was gradually methylated over time and associated with decreased hAQP1 expression and function in vitro and decreased hAQP1 expression in vivo. These data suggest that the hCMVp in AdhAQP1was probably not methylated in transduced human salivary gland cells of responding subjects, resulting in an unexpectedly longer functional expression of hAQP1. JF - Gene Therapy AU - Zheng, C AU - Baum, B J AU - Liu, X AU - Goldsmith, C M AU - Perez, P AU - Jang, S-I AU - Cotrim, A P AU - McCullagh, L AU - Ambudkar, I S AU - Alevizos, I AD - Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA Y1 - 2015/09// PY - 2015 DA - Sep 2015 SP - 758 EP - 766 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 22 IS - 9 SN - 0969-7128, 0969-7128 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Data processing KW - Serotypes KW - Gene therapy KW - Parotid gland KW - Cell culture KW - Salivary gland KW - Clinical trials KW - Expression vectors KW - Human cytomegalovirus KW - Enhancers KW - Promoters KW - DNA methylation KW - Submandibular gland KW - Saliva KW - W 30905:Medical Applications KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722170092?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene+Therapy&rft.atitle=Persistence+of+hAQP1+expression+in+human+salivary+gland+cells+following+AdhAQP1+transduction+is+associated+with+a+lack+of+methylation+of+hCMV+promoter&rft.au=Zheng%2C+C%3BBaum%2C+B+J%3BLiu%2C+X%3BGoldsmith%2C+C+M%3BPerez%2C+P%3BJang%2C+S-I%3BCotrim%2C+A+P%3BMcCullagh%2C+L%3BAmbudkar%2C+I+S%3BAlevizos%2C+I&rft.aulast=Zheng&rft.aufirst=C&rft.date=2015-09-01&rft.volume=22&rft.issue=9&rft.spage=758&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2015.55 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Serotypes; Data processing; Gene therapy; Parotid gland; Cell culture; Salivary gland; Clinical trials; Expression vectors; Promoters; Enhancers; DNA methylation; Submandibular gland; Saliva; Human cytomegalovirus DO - http://dx.doi.org/10.1038/gt.2015.55 ER - TY - JOUR T1 - A developmental analysis of caregiving modalities across infancy in 38 low- and middle-income countries AN - 1718087011; 4709431 AB - Caregiving is requisite to wholesome child development from the beginning of life. A cross-sectional microgenetic analysis of six caregiving practices across the child's 1st year (0– ;12 months) in 42,539 families from nationally representative samples in 38 low- and middle-income countries is reported. Rates of caregiving varied tremendously within and across countries. However, caregiving practices followed one of two developmental trajectories: (a) greater proportions of caregivers read, told stories, and named, counted, and drew with each additional month of infant age, and (b) proportions of caregivers who played, sang songs, and took their infants outside increased each month from birth but reached an asymptote at 4-5  ;months. Rates and growth functions of caregiving have implications for infant care and development. Reprinted by permission of the University of Chicago Press. © All rights reserved JF - Child development AU - Bradley, Robert H AU - Bornstein, Marc H AU - Putnick, Diane L AU - Lansford, Jennifer E AU - Deater-Deckard, Kirby AD - National Institutes of Health ; Duke University ; Virginia Polytechnic Institute and State University ; Arizona State University Y1 - 2015/09// PY - 2015 DA - Sep 2015 SP - 1571 EP - 1587 VL - 86 IS - 5 SN - 0009-3920, 0009-3920 KW - Sociology KW - Countries KW - Infancy KW - Family KW - Caring KW - Child development KW - Infants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1718087011?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Child+development&rft.atitle=A+developmental+analysis+of+caregiving+modalities+across+infancy+in+38+low-+and+middle-income+countries&rft.au=Bradley%2C+Robert+H%3BBornstein%2C+Marc+H%3BPutnick%2C+Diane+L%3BLansford%2C+Jennifer+E%3BDeater-Deckard%2C+Kirby&rft.aulast=Bradley&rft.aufirst=Robert&rft.date=2015-09-01&rft.volume=86&rft.issue=5&rft.spage=1571&rft.isbn=&rft.btitle=&rft.title=Child+development&rft.issn=00093920&rft_id=info:doi/10.1111%2Fcdev.12402 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-10-01 N1 - Last updated - 2015-11-19 N1 - SubjectsTermNotLitGenreText - 2039 13521; 2197 2212 6075 3483; 6490 2211 652 5676 646 6091 2212; 6495 2212; 4748; 2958 12092 DO - http://dx.doi.org/10.1111/cdev.12402 ER - TY - JOUR T1 - Age and death: a defence of gradualism AN - 1718082106; 4706152 AB - According to standard comparativist views, death is bad in so far as it deprives someone of goods she would otherwise have had. In The Ethics of Killing, Jeff McMahan argues against such views and in favour of a gradualist account according to which how bad it is to die is a function of both the future goods of which the decedent is deprived and her cognitive development when she dies. Comparativists and gradualists therefore disagree about how bad it is to die at different ages. In this article I examine two prominent criticisms of gradualism and show that both misconstrue McMahan. I develop a related criticism that seems to show that a gradualist cannot coherently relate morbidity and mortality. This criticism also fails, but has an instructive implication for how policy-makers setting priorities for health care investments should regard choices between life-saving interventions and interventions against non-fatal diseases in the very young. Reprinted by permission of Cambridge University Press. An electronic version of this article can be accessed via the internet at http://journals.cambridge.org JF - Utilitas AU - Millum, Joseph AD - National Institutes of Health Y1 - 2015/09// PY - 2015 DA - Sep 2015 SP - 279 EP - 297 VL - 27 IS - 3 SN - 0953-8208, 0953-8208 KW - Sociology KW - Ageing KW - Age KW - Death KW - Cognitive development KW - Social policy KW - Analytical philosophy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1718082106?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Utilitas&rft.atitle=Age+and+death%3A+a+defence+of+gradualism&rft.au=Millum%2C+Joseph&rft.aulast=Millum&rft.aufirst=Joseph&rft.date=2015-09-01&rft.volume=27&rft.issue=3&rft.spage=279&rft.isbn=&rft.btitle=&rft.title=Utilitas&rft.issn=09538208&rft_id=info:doi/10.1017%2FS0953820815000047 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-10-01 N1 - Last updated - 2015-11-19 N1 - SubjectsTermNotLitGenreText - 973 9486; 3303; 646; 655; 2450 6075 3483; 11888 10472 DO - http://dx.doi.org/10.1017/S0953820815000047 ER - TY - JOUR T1 - Brief Report: Cryopyrin-Associated Periodic Syndrome Caused by a Myeloid-Restricted Somatic NLRP3 Mutation AN - 1717492452; PQ0001959295 AB - Objective To identify the cause of disease in an adult patient presenting with recent-onset fevers, chills, urticaria, fatigue, and profound myalgia, who was found to be negative for cryopyrin-associated periodic syndrome (CAPS) NLRP3 mutations by conventional Sanger DNA sequencing. Methods We performed whole-exome sequencing and targeted deep sequencing using DNA from the patient's whole blood to identify a possible NLRP3 somatic mutation. We then screened for this mutation in subcloned NLRP3 amplicons from fibroblasts, buccal cells, granulocytes, negatively selected monocytes, and T and B lymphocytes and further confirmed the somatic mutation by targeted sequencing of exon 3. Results We identified a previously reported CAPS-associated mutation, p.Tyr570Cys, with a mutant allele frequency of 15% based on exome data. Targeted sequencing and subcloning of NLRP3 amplicons confirmed the presence of the somatic mutation in whole blood at a ratio similar to the exome data. The mutant allele frequency was in the range of 13.3-16.8% in monocytes and 15.2-18% in granulocytes. Notably, this mutation was either absent or present at a very low frequency in B and T lymphocytes, in buccal cells, and in the patient's cultured fibroblasts. Conclusion Our findings indicate the possibility of myeloid-restricted somatic mosaicism in the pathogenesis of CAPS, underscoring the emerging role of massively parallel sequencing in clinical diagnosis. JF - Arthritis & Rheumatology AU - Zhou, Qing AU - Aksentijevich, Ivona AU - Wood, Geryl M AU - Walts, Avram D AU - Hoffmann, Patrycja AU - Remmers, Elaine F AU - Kastner, Daniel L AU - Ombrello, Amanda K AD - National Human Genome Research Institute, NIH, Bethesda, Maryland. Y1 - 2015/09// PY - 2015 DA - Sep 2015 SP - 2482 EP - 2486 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 67 IS - 9 SN - 2326-5191, 2326-5191 KW - Toxicology Abstracts KW - Fatigue KW - Data processing KW - Exons KW - Lymphocytes B KW - Urticaria KW - Fibroblasts KW - Fever KW - Leukocytes (granulocytic) KW - Blood KW - DNA sequencing KW - Mosaicism KW - Lymphocytes T KW - Gene frequency KW - Monocytes KW - Mutation KW - Myalgia KW - X 24310:Pharmaceuticals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1717492452?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Arthritis+%26+Rheumatology&rft.atitle=Brief+Report%3A+Cryopyrin-Associated+Periodic+Syndrome+Caused+by+a+Myeloid-Restricted+Somatic+NLRP3+Mutation&rft.au=Zhou%2C+Qing%3BAksentijevich%2C+Ivona%3BWood%2C+Geryl+M%3BWalts%2C+Avram+D%3BHoffmann%2C+Patrycja%3BRemmers%2C+Elaine+F%3BKastner%2C+Daniel+L%3BOmbrello%2C+Amanda+K&rft.aulast=Zhou&rft.aufirst=Qing&rft.date=2015-09-01&rft.volume=67&rft.issue=9&rft.spage=2482&rft.isbn=&rft.btitle=&rft.title=Arthritis+%26+Rheumatology&rft.issn=23265191&rft_id=info:doi/10.1002%2Fart.39190 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Data processing; Fatigue; Lymphocytes B; Exons; Urticaria; Fibroblasts; Fever; Blood; Leukocytes (granulocytic); DNA sequencing; Mosaicism; Lymphocytes T; Gene frequency; Monocytes; Myalgia; Mutation DO - http://dx.doi.org/10.1002/art.39190 ER - TY - JOUR T1 - The negative impact of tobacco smoking on survival after prostate cancer diagnosis AN - 1717491043; PQ0001974657 AB - Purpose: Tobacco smoking has been found to increase prostate cancer (PCa) mortality in cohorts of healthy men, but its effects on prognosis of men with PCa are still unclear. This study investigated the role of smoking on long-term survival after PCa diagnosis. Methods: A retrospective cohort including 780 men with incident PCa previously enrolled (between 1995 and 2002) as cases in an Italian case-control study. Information on vital status up to 2013 (median follow-up 13 years) and cause of death were retrieved through health archives. Hazard ratios (HRs) of all-cause and PCa-specific death, and corresponding 95 % confidence intervals (CIs), were calculated using Cox models, adjusting for Gleason score and major confounders. Results: Out of 263 PCa deceased patients, 81 died because of PCa. Smokers at PCa diagnosis reported increased risks of all-cause (HR = 1.5, 95 % CI 1.1-2.2) and PCa death (HR = 2.0, 95 % CI 1.0-3.8), as compared to never smokers. Dose-response effects emerged according to smoking intensity (HRs for >15 cigarettes/day: 1.9, 95 % CI 1.3-3.0, for all causes and 2.3, 95 % CI 1.1-4.9, for PCa) and duration (HRs for >45 years: 1.7, 95 % CI 1.1-2.6, for all causes and 2.6, 95 % CI 1.2-5.5, for PCa). Conversely, former smokers at PCa diagnosis showed no statistically significant higher risks of PCa death. The effects of smoking were consistent in strata of Gleason score. Conclusions: Current smoking at PCa diagnosis negatively impacted PCa-specific, long-term survival, regardless of Gleason score. Our findings suggest that smoking could be a modifiable risk factor to improve prognosis of men diagnosed with PCa. JF - Cancer Causes & Control AU - Polesel, Jerry AU - Gini, Andrea AU - Dal Maso, Luigino AU - Stocco, Carmen AU - Birri, Silvia AU - Taborelli, Martina AU - Serraino, Diego AU - Zucchetto, Antonella AD - Epidemiology and Biostatistics Unit, CRO Aviano National Cancer Institute, IRCCS, via F. Gallini no. 2, 33081, Aviano, Italy, zucchetto.epi@cro.it Y1 - 2015/09// PY - 2015 DA - Sep 2015 SP - 1299 EP - 1305 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 26 IS - 9 SN - 0957-5243, 0957-5243 KW - Toxicology Abstracts KW - Tobacco smoking KW - Mortality KW - Prostate cancer KW - Cigarettes KW - Risk factors KW - Dose-response effects KW - Prognosis KW - Statistical analysis KW - Survival KW - Models KW - X 24380:Social Poisons & Drug Abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1717491043?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Causes+%26+Control&rft.atitle=The+negative+impact+of+tobacco+smoking+on+survival+after+prostate+cancer+diagnosis&rft.au=Polesel%2C+Jerry%3BGini%2C+Andrea%3BDal+Maso%2C+Luigino%3BStocco%2C+Carmen%3BBirri%2C+Silvia%3BTaborelli%2C+Martina%3BSerraino%2C+Diego%3BZucchetto%2C+Antonella&rft.aulast=Polesel&rft.aufirst=Jerry&rft.date=2015-09-01&rft.volume=26&rft.issue=9&rft.spage=1299&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-015-0624-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Number of references - 23 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Mortality; Tobacco smoking; Prostate cancer; Cigarettes; Dose-response effects; Risk factors; Statistical analysis; Prognosis; Survival; Models DO - http://dx.doi.org/10.1007/s10552-015-0624-2 ER - TY - JOUR T1 - Engineering soya bean seeds as a scalable platform to produce cyanovirin-N, a non-ARV microbicide against HIV AN - 1712778129; PQ0001915391 AB - There is an urgent need to provide effective anti-HIV microbicides to resource-poor areas worldwide. Some of the most promising microbicide candidates are biotherapeutics targeting viral entry. To provide biotherapeutics to poorer areas, it is vital to reduce the cost. Here, we report the production of biologically active recombinant cyanovirin-N (rCV-N), an antiviral protein, in genetically engineered soya bean seeds. Pure, biologically active rCV-N was isolated with a yield of 350 mu g/g of dry seed weight. The observed amino acid sequence of rCV-N matched the expected sequence of native CV-N, as did the mass of rCV-N (11 009 Da). Purified rCV-N from soya is active in anti-HIV assays with an EC sub(50) of 0.82-2.7 nM (compared to 0.45-1.8 nM for E. coli-produced CV-N). Standard industrial processing of soya bean seeds to harvest soya bean oil does not diminish the antiviral activity of recovered rCV-N, allowing the use of industrial soya bean processing to generate both soya bean oil and a recombinant protein for anti-HIV microbicide development. JF - Plant Biotechnology Journal AU - O'Keefe, Barry R AU - Murad, Andre M AU - Vianna, Giovanni R AU - Ramessar, Koreen AU - Saucedo, Carrie J AU - Wilson, Jennifer AU - Buckheit, Karen W AU - Cunha, Nicolau B AU - Araujo, Ana Claudia G AU - Lacorte, Cristiano C AU - Madeira, Luisa AU - McMahon, James B AU - Rech, Elibio L AD - Molecular Targets Laboratory, Center for Cancer Research, National Cancer Institute, NIH, Frederick, MD, USA. Y1 - 2015/09// PY - 2015 DA - Sep 2015 SP - 884 EP - 892 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 13 IS - 7 SN - 1467-7644, 1467-7644 KW - Biotechnology and Bioengineering Abstracts KW - Oil KW - Seeds KW - cyanovirin-N KW - Human immunodeficiency virus KW - Genetic engineering KW - Antiviral activity KW - Beans KW - microbicides KW - Amino acid sequence KW - W 30925:Genetic Engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1712778129?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Plant+Biotechnology+Journal&rft.atitle=Engineering+soya+bean+seeds+as+a+scalable+platform+to+produce+cyanovirin-N%2C+a+non-ARV+microbicide+against+HIV&rft.au=O%27Keefe%2C+Barry+R%3BMurad%2C+Andre+M%3BVianna%2C+Giovanni+R%3BRamessar%2C+Koreen%3BSaucedo%2C+Carrie+J%3BWilson%2C+Jennifer%3BBuckheit%2C+Karen+W%3BCunha%2C+Nicolau+B%3BAraujo%2C+Ana+Claudia+G%3BLacorte%2C+Cristiano+C%3BMadeira%2C+Luisa%3BMcMahon%2C+James+B%3BRech%2C+Elibio+L&rft.aulast=O%27Keefe&rft.aufirst=Barry&rft.date=2015-09-01&rft.volume=13&rft.issue=7&rft.spage=884&rft.isbn=&rft.btitle=&rft.title=Plant+Biotechnology+Journal&rft.issn=14677644&rft_id=info:doi/10.1111%2Fpbi.12309 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Oil; cyanovirin-N; Seeds; Genetic engineering; Antiviral activity; Beans; Amino acid sequence; microbicides; Human immunodeficiency virus DO - http://dx.doi.org/10.1111/pbi.12309 ER - TY - JOUR T1 - Bayesian analysis of transverse signal decay with application to human brain AN - 1712563572; PQ0001932689 AB - Purpose Transverse relaxation analysis with several signal models has been used extensively to determine tissue and material properties. However, the derivation of corresponding parameter values is notoriously unreliable. We evaluate improvements in the quality of parameter estimation using Bayesian analysis and incorporating the Rician noise model, as appropriate for magnitude MR images. Theory and Methods Monoexponential, stretched exponential, and biexponential signal models were analyzed using nonlinear least squares (NLLS) and Bayesian approaches. Simulations and phantom and human brain data were analyzed using three different approaches to account for noise. Parameter estimation bias (reflecting accuracy) and dispersion (reflecting precision) were derived for a range of signal-to-noise ratios (SNR) and relaxation parameters. Results All methods performed well at high SNR. At lower SNR, the Bayesian approach yielded parameter estimates of considerably greater precision, as well as greater accuracy, than did NLLS. Incorporation of the Rician noise model greatly improved accuracy and, to a somewhat lesser extent, precision, in derived transverse relaxation parameters. Analyses of data obtained from solution phantoms and from brain were consistent with simulations. Conclusion Overall, estimation of parameters characterizing several different transverse relaxation models was markedly improved through use of Bayesian analysis and through incorporation of the Rician noise model. Magn Reson Med 74:785-802, 2015. JF - Magnetic Resonance in Medicine AU - Bouhrara, Mustapha AU - Reiter, David A AU - Spencer, Richard G AD - Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA. Y1 - 2015/09// PY - 2015 DA - Sep 2015 SP - 785 EP - 802 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 74 IS - 3 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Mathematical models KW - Data processing KW - Bayesian analysis KW - Brain KW - N.M.R. KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1712563572?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Magnetic+Resonance+in+Medicine&rft.atitle=Bayesian+analysis+of+transverse+signal+decay+with+application+to+human+brain&rft.au=Bouhrara%2C+Mustapha%3BReiter%2C+David+A%3BSpencer%2C+Richard+G&rft.aulast=Bouhrara&rft.aufirst=Mustapha&rft.date=2015-09-01&rft.volume=74&rft.issue=3&rft.spage=785&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.25457 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Data processing; Mathematical models; Bayesian analysis; Brain; N.M.R. DO - http://dx.doi.org/10.1002/mrm.25457 ER - TY - JOUR T1 - Prediction of human population responses to toxic compounds by a collaborative competition. AN - 1710985867; 26258538 AB - The ability to computationally predict the effects of toxic compounds on humans could help address the deficiencies of current chemical safety testing. Here, we report the results from a community-based DREAM challenge to predict toxicities of environmental compounds with potential adverse health effects for human populations. We measured the cytotoxicity of 156 compounds in 884 lymphoblastoid cell lines for which genotype and transcriptional data are available as part of the Tox21 1000 Genomes Project. The challenge participants developed algorithms to predict interindividual variability of toxic response from genomic profiles and population-level cytotoxicity data from structural attributes of the compounds. 179 submitted predictions were evaluated against an experimental data set to which participants were blinded. Individual cytotoxicity predictions were better than random, with modest correlations (Pearson's r < 0.28), consistent with complex trait genomic prediction. In contrast, predictions of population-level response to different compounds were higher (r < 0.66). The results highlight the possibility of predicting health risks associated with unknown compounds, although risk estimation accuracy remains suboptimal. JF - Nature biotechnology AU - Eduati, Federica AU - Mangravite, Lara M AU - Wang, Tao AU - Tang, Hao AU - Bare, J Christopher AU - Huang, Ruili AU - Norman, Thea AU - Kellen, Mike AU - Menden, Michael P AU - Yang, Jichen AU - Zhan, Xiaowei AU - Zhong, Rui AU - Xiao, Guanghua AU - Xia, Menghang AU - Abdo, Nour AU - Kosyk, Oksana AU - NIEHS-NCATS-UNC DREAM Toxicogenetics Collaboration AU - Friend, Stephen AU - Dearry, Allen AU - Simeonov, Anton AU - Tice, Raymond R AU - Rusyn, Ivan AU - Wright, Fred A AU - Stolovitzky, Gustavo AU - Xie, Yang AU - Saez-Rodriguez, Julio AD - European Molecular Biology Laboratory, European Bioinformatics Institute (EMBL-EBI), Wellcome Trust Genome Campus, Cambridge, UK. ; Sage Bionetworks, Seattle, Washington, USA. ; Quantitative Biomedical Research Center, Department of Clinical Sciences, University of Texas Southwestern Medical Center, Dallas, Texas, USA. ; Division of Preclinical Innovation, National Institutes of Health Chemical Genomics Center, National Center for Advancing Translational Sciences, Rockville, Maryland, USA. ; Department of Biostatistics, University of Michigan, Ann Arbor, Michigan, USA. ; Department of Environmental Sciences and Engineering, University of North Carolina, Chapel Hill, North Carolina, USA. ; NIEHS-NCATS-UNC DREAM Toxicogenetics Collaboration Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 933 EP - 940 VL - 33 IS - 9 KW - Hazardous Substances KW - 0 KW - Index Medicus KW - Computer Simulation KW - Genetics, Population KW - Dose-Response Relationship, Drug KW - Humans KW - Toxicity Tests -- methods KW - Incidence KW - Risk Assessment -- methods KW - Genetic Predisposition to Disease -- genetics KW - Models, Genetic KW - High-Throughput Screening Assays -- methods KW - Lymphocytes -- cytology KW - Lymphocytes -- physiology KW - Lymphocytes -- drug effects KW - Hazardous Substances -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1710985867?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+biotechnology&rft.atitle=Prediction+of+human+population+responses+to+toxic+compounds+by+a+collaborative+competition.&rft.au=Eduati%2C+Federica%3BMangravite%2C+Lara+M%3BWang%2C+Tao%3BTang%2C+Hao%3BBare%2C+J+Christopher%3BHuang%2C+Ruili%3BNorman%2C+Thea%3BKellen%2C+Mike%3BMenden%2C+Michael+P%3BYang%2C+Jichen%3BZhan%2C+Xiaowei%3BZhong%2C+Rui%3BXiao%2C+Guanghua%3BXia%2C+Menghang%3BAbdo%2C+Nour%3BKosyk%2C+Oksana%3BNIEHS-NCATS-UNC+DREAM+Toxicogenetics+Collaboration%3BFriend%2C+Stephen%3BDearry%2C+Allen%3BSimeonov%2C+Anton%3BTice%2C+Raymond+R%3BRusyn%2C+Ivan%3BWright%2C+Fred+A%3BStolovitzky%2C+Gustavo%3BXie%2C+Yang%3BSaez-Rodriguez%2C+Julio&rft.aulast=Eduati&rft.aufirst=Federica&rft.date=2015-09-01&rft.volume=33&rft.issue=9&rft.spage=933&rft.isbn=&rft.btitle=&rft.title=Nature+biotechnology&rft.issn=1546-1696&rft_id=info:doi/10.1038%2Fnbt.3299 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-29 N1 - Date created - 2015-09-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Toxicol Sci. 2000 Dec;58(2):399-415 [11099651] Nat Methods. 2012 Aug;9(8):796-804 [22796662] Nature. 2012 Nov 1;491(7422):56-65 [23128226] Environ Health Perspect. 2013 Jan;121(1):23-31 [23086705] Vet Pathol. 2013 Mar;50(2):324-33 [22700852] Nat Genet. 2013 Apr;45(4):400-5, 405e1-3 [23455638] Sci Transl Med. 2013 Apr 17;5(181):181re1 [23596205] Blood. 2013 May 23;121(21):4366-76 [23538338] Nature. 2013 Sep 26;501(7468):506-11 [24037378] Nature. 2013 Oct 17;502(7471):377-80 [23995691] Nucleic Acids Res. 2014 Jan;42(Database issue):D199-205 [24214961] Pharmacogenomics. 2014 Feb;15(2):137-46 [24444404] Nat Biotechnol. 2014 Jun;32(6):583-91 [24837663] BMC Syst Biol. 2014;8:13 [24507381] Nat Biotechnol. 2014 Dec;32(12):1202-12 [24880487] Environ Health Perspect. 2015 May;123(5):458-66 [25622337] Adv Drug Deliv Rev. 2001 Mar 1;46(1-3):3-26 [11259830] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517] Biostatistics. 2007 Jan;8(1):118-27 [16632515] Am J Hum Genet. 2007 Sep;81(3):559-75 [17701901] Science. 2008 Feb 15;319(5865):906-7 [18276874] Environ Health Perspect. 2008 Mar;116(3):284-91 [18335092] J Comput Aided Mol Des. 2008 Jun-Jul;22(6-7):403-21 [18253701] PLoS Genet. 2008 Nov;4(11):e1000287 [19043577] Environ Health Perspect. 2009 May;117(5):685-95 [19479008] Toxicology. 2010 Feb 9;268(3):156-64 [19932147] J Chem Inf Model. 2010 May 24;50(5):742-54 [20426451] Nat Genet. 2010 Jul;42(7):570-5 [20562874] Nat Genet. 2010 Jul;42(7):565-9 [20562875] Nature. 2010 Oct 28;467(7319):1061-73 [20981092] Hum Mol Genet. 2011 Apr 15;20(8):1643-52 [21289059] Toxicol Appl Pharmacol. 2011 Sep 15;255(3):297-306 [21784091] Nucleic Acids Res. 2012 Jan;40(Database issue):D1100-7 [21948594] Nucleic Acids Res. 2012 Jan;40(Database issue):D400-12 [22140110] Nat Genet. 2012 Feb;44(2):127-30 [22281773] Erratum In: Nat Biotechnol. 2015 Oct;33(10):1109 [26448092] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nbt.3299 ER - TY - JOUR T1 - Statistical inference for the additive hazards model under outcome-dependent sampling AN - 1710258272; 4703610 AB - Cost-effective study designs and proper inference procedures for data from such designs are always of particular interest to study investigators. In this article, we propose a biased sampling scheme: an outcome-dependent sampling (ODS) design for survival data with right censoring under the additive hazards model. We develop a weighted pseudo-score estimator for the regression parameters for the proposed design and derive the asymptotic properties of the proposed estimator. We also provide some suggestions for using the proposed method by evaluating the relative efficiency of the proposed method against simple random sampling design and derive the optimal allocation of the subsamples for the proposed design. Simulation studies show that the proposed ODS design is more powerful than other existing designs and the proposed estimator is more efficient than other estimators. We apply our method to analyze a cancer study conducted at NIEHS, the Cancer Incidence and Mortality of Uranium Miners Study, to study the risk of radon exposure to cancer. The Canadian Journal of Statistics 43: 436-453; 2015 © 2015 Statistical Society of Canada // ABSTRACT IN : Les plans d'expérience efficients et les procédures d'inférence appropriées pour ceux-ci revêtent toujours de l'intérêt pour les chercheurs. Les auteurs proposent un plan d'expérience biaisé, à savoir un plan dont l'échantillonnage dépend du résultat pour des données de survie censurées à droite sous un modèle à risques additifs. Ils développent un estimateur pondéré du pseudo-score pour les paramètres de régression du plan proposé et en déterminent les propriétés asymptotiques. Ils offrent également quelques suggestions pour l'application de leur méthode en évaluant son efficacité relative par rapport à un échantillon aléatoire simple, et en déterminent l'attribution optimale des sous-é ;chantillons pour le plan proposé. À l'aide de simulations, ils montrent que leur plan est plus puissant que d'autres plans existants et que les estimateurs proposés sont plus efficaces que d'autres. Les auteurs utilisent leur mé ;thode pour l'analyse d'une étude du NIEHS sur l'incidence de cancers et la mortalité associée chez les travailleurs de mine d'uranium, afin d'étudier les risques de cancer liés à l'exposition au radon. La revue canadienne de statistique xx: 1-18; 2015 © 2015 Société statistique du Canada JF - Canadian journal of statistics AU - Yu, Jichang AU - Liu, Yanyan AU - Sandler, Dale P AU - Zhou, Haibo AD - Zhongnan University of Economics and Law ; Wuhan University ; National Institute of Environmental Health Sciences ; University of North Carolina, Chapel Hill Y1 - 2015/09// PY - 2015 DA - Sep 2015 SP - 436 EP - 453 VL - 43 IS - 3 SN - 0319-5724, 0319-5724 KW - Economics KW - Economic models KW - Regression analysis KW - Statistical analysis KW - Simulation KW - Sampling KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1710258272?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Canadian+journal+of+statistics&rft.atitle=Statistical+inference+for+the+additive+hazards+model+under+outcome-dependent+sampling&rft.au=Yu%2C+Jichang%3BLiu%2C+Yanyan%3BSandler%2C+Dale+P%3BZhou%2C+Haibo&rft.aulast=Yu&rft.aufirst=Jichang&rft.date=2015-09-01&rft.volume=43&rft.issue=3&rft.spage=436&rft.isbn=&rft.btitle=&rft.title=Canadian+journal+of+statistics&rft.issn=03195724&rft_id=info:doi/10.1002%2Fcjs.11257 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-09-09 N1 - Last updated - 2015-09-09 N1 - SubjectsTermNotLitGenreText - 12224 971; 11670; 11255 12228 10919; 3969 8163; 1939 3617 6220; 10739 12228 10919 DO - http://dx.doi.org/10.1002/cjs.11257 ER - TY - JOUR T1 - Advancing Symptom Science Through Use of Common Data Elements AN - 1710151776 AB - Background Use of common data elements (CDEs), conceptually defined as variables that are operationalized and measured in identical ways across studies, enables comparison of data across studies in ways that would otherwise be impossible. Although healthcare researchers are increasingly using CDEs, there has been little systematic use of CDEs for symptom science. CDEs are especially important in symptom science because people experience common symptoms across a broad range of health and developmental states, and symptom management interventions may have common outcomes across populations. Purposes The purposes of this article are to (a) recommend best practices for the use of CDEs for symptom science within and across centers; (b) evaluate the benefits and challenges associated with the use of CDEs for symptom science; (c) propose CDEs to be used in symptom science to serve as the basis for this emerging science; and (d) suggest implications and recommendations for future research and dissemination of CDEs for symptom science. Design The National Institute of Nursing Research (NINR)-supported P20 and P30 Center directors applied published best practices, expert advice, and the literature to identify CDEs to be used across the centers to measure pain, sleep, fatigue, and affective and cognitive symptoms. Findings We generated a minimum set of CDEs to measure symptoms. Conclusions The CDEs identified through this process will be used across the NINR Centers and will facilitate comparison of symptoms across studies. We expect that additional symptom CDEs will be added and the list will be refined in future work. Clinical Relevance Symptoms are an important focus of nursing care. Use of CDEs will facilitate research that will lead to better ways to assist people to manage their symptoms. JF - Journal of Nursing Scholarship AU - Redeker, Nancy S AU - Anderson, Ruth AU - Bakken, Suzanne AU - Corwin, Elizabeth AU - Docherty, Sharron AU - Dorsey, Susan G AU - Heitkemper, Margaret AU - McCloskey, Donna Jo AU - Moore, Shirley AU - Pullen, Carol AU - Rapkin, Bruce AU - Schiffman, Rachel AU - Waldrop-Valverde, Drenna AU - Grady, Patricia AD - Beatrice Renfield Term Professor of Nursing, Yale School of Nursing, New Haven, CT, USA. ; Professor and Associate Dean for Research, University of North Carolina–Chapel Hill, Chapel Hill, NC, USA. ; The Alumni Professor of Nursing and Professor of Biomedical Informatics, Columbia University, New York, NY, USA. ; Associate Dean for Research and Professor, Emory University, Atlanta, GA, USA. ; Associate Professor, Duke University, Durham, NC, USA. ; Professor and Chair, Department of Pain and Translational Symptom Science, University of Maryland, Baltimore, MD, USA. ; Professor and Department Chairperson, University of Washington, Seattle, WA, USA. ; Lead Program Director, National Institute of Nursing Research, NIH, Bethesda, MD, USA. ; Edward J. and Louise Mellen Professor of Nursing and Associate Dean for Research, Case Western Reserve University, Cleveland, OH, USA. ; Beatrice Renfield Term Professor of Nursing, Yale School of Nursing, New Haven, CT, USA., Professor, University of Nebraska Medical Center, Omaha, NB, USA. ; Beatrice Renfield Term Professor of Nursing, Yale School of Nursing, New Haven, CT, USA., Professor of Epidemiology and Population Health, Albert Einstein College of Medicine, New York, NY, USA. ; Beatrice Renfield Term Professor of Nursing, Yale School of Nursing, New Haven, CT, USA., Professor and Associate Dean for Research, University of Wisconsin-Milwaukee, Milwaukee, WI, USA. ; Beatrice Renfield Term Professor of Nursing, Yale School of Nursing, New Haven, CT, USA., Associate Professor, Emory University, Atlanta, GA, USA. ; Beatrice Renfield Term Professor of Nursing, Yale School of Nursing, New Haven, CT, USA., Director, National Institute of Nursing Research, NIH, Bethesda, MD, USA. ; Beatrice Renfield Term Professor of Nursing, Yale School of Nursing, New Haven, CT, USA. Y1 - 2015/09// PY - 2015 DA - Sep 2015 SP - 379 EP - 388 CY - Indianapolis PB - Wiley Subscription Services, Inc. VL - 47 IS - 5 SN - 1527-6546 KW - Medical Sciences--Nurses And Nursing KW - Best practice KW - Clinical guidelines KW - Clinical nursing KW - Dissemination KW - Fatigue KW - Health care KW - Interventions KW - Nursing KW - Pain KW - Symptoms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1710151776?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Nursing+Scholarship&rft.atitle=Advancing+Symptom+Science+Through+Use+of+Common+Data+Elements&rft.au=Redeker%2C+Nancy+S%3BAnderson%2C+Ruth%3BBakken%2C+Suzanne%3BCorwin%2C+Elizabeth%3BDocherty%2C+Sharron%3BDorsey%2C+Susan+G%3BHeitkemper%2C+Margaret%3BMcCloskey%2C+Donna+Jo%3BMoore%2C+Shirley%3BPullen%2C+Carol%3BRapkin%2C+Bruce%3BSchiffman%2C+Rachel%3BWaldrop-Valverde%2C+Drenna%3BGrady%2C+Patricia&rft.aulast=Redeker&rft.aufirst=Nancy&rft.date=2015-09-01&rft.volume=47&rft.issue=5&rft.spage=379&rft.isbn=&rft.btitle=&rft.title=Journal+of+Nursing+Scholarship&rft.issn=15276546&rft_id=info:doi/10.1111%2Fjnu.12155 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Name - National Institute of Nursing Research N1 - Date revised - 2015-09-22 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1111/jnu.12155 ER - TY - JOUR T1 - CDK1-Mediated SIRT3 Activation Enhances Mitochondrial Function and Tumor Radioresistance. AN - 1709711452; 26141949 AB - Tumor adaptive resistance to therapeutic radiation remains a barrier for further improvement of local cancer control. SIRT3, a member of the sirtuin family of NAD(+)-dependent protein deacetylases in mitochondria, promotes metabolic homeostasis through regulation of mitochondrial protein deacetylation and plays a key role in prevention of cell aging. Here, we demonstrate that SIRT3 expression is induced in an array of radiation-treated human tumor cells and their corresponding xenograft tumors, including colon cancer HCT-116, glioblastoma U87, and breast cancer MDA-MB231 cells. SIRT3 transcriptional activation is due to SIRT3 promoter activation controlled by the stress transcription factor NF-κB. Posttranscriptionally, SIRT3 enzymatic activity is further enhanced via Thr150/Ser159 phosphorylation by cyclin B1-CDK1, which is also induced by radiation and relocated to mitochondria together with SIRT3. Cells expressing Thr150Ala/Ser159Ala-mutant SIRT3 show a reduction in mitochondrial protein lysine deacetylation, Δψm, MnSOD activity, and mitochondrial ATP generation. The clonogenicity of Thr150Ala/Ser159Ala-mutant transfectants is lower and significantly decreased under radiation. Tumors harboring Thr150Ala/Ser159Ala-mutant SIRT3 show inhibited growth and increased sensitivity to in vivo local irradiation. These results demonstrate that enhanced SIRT3 transcription and posttranslational modifications in mitochondria contribute to adaptive radioresistance in tumor cells. CDK1-mediated SIRT3 phosphorylation is a potential effective target to sensitize tumor cells to radiotherapy. ©2015 American Association for Cancer Research. JF - Molecular cancer therapeutics AU - Liu, Rui AU - Fan, Ming AU - Candas, Demet AU - Qin, Lili AU - Zhang, Xiaodi AU - Eldridge, Angela AU - Zou, June X AU - Zhang, Tieqiao AU - Juma, Shuaib AU - Jin, Cuihong AU - Li, Robert F AU - Perks, Julian AU - Sun, Lun-Quan AU - Vaughan, Andrew T M AU - Hai, Chun-Xu AU - Gius, David R AU - Li, Jian Jian AD - Department of Radiation Oncology, University of California Davis School of Medicine, Sacramento, California. ; Department of Internal Medicine, University of California Davis School of Medicine, Sacramento, California. ; Center for Biophotonics Science and Technology, University of California Davis School of Medicine, Sacramento, California. ; Department of Radiation Oncology, University of California Davis School of Medicine, Sacramento, California. NCI-designated Comprehensive Cancer Center, University of California Davis School of Medicine, Sacramento, California. ; Center for Molecular Imaging, Central South University, Changsha, Hunan, China. ; Department of Toxicology, Fourth Military Medical University, Xian, Shaanxi, China. ; Department of Radiation Oncology, Robert Lurie Cancer Center, Northwestern University, Chicago, Illinois. ; Department of Radiation Oncology, University of California Davis School of Medicine, Sacramento, California. NCI-designated Comprehensive Cancer Center, University of California Davis School of Medicine, Sacramento, California. jijli@ucdavis.edu. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 2090 EP - 2102 VL - 14 IS - 9 KW - Mitochondrial Proteins KW - 0 KW - NF-kappa B KW - CDK1 protein, human KW - EC 2.7.11.22 KW - Cyclin-Dependent Kinases KW - Sirtuin 3 KW - EC 3.5.1.- KW - Index Medicus KW - Animals KW - Acetylation KW - Phosphorylation KW - Enzyme Activation KW - Humans KW - Disease Models, Animal KW - Transcription, Genetic KW - Gene Expression Regulation, Neoplastic -- radiation effects KW - Cell Line, Tumor KW - Mitochondrial Proteins -- metabolism KW - Mutation KW - NF-kappa B -- metabolism KW - Cyclin-Dependent Kinases -- metabolism KW - Neoplasms -- pathology KW - Mitochondria -- radiation effects KW - Neoplasms -- radiotherapy KW - Sirtuin 3 -- metabolism KW - Mitochondria -- metabolism KW - Sirtuin 3 -- genetics KW - Transcriptional Activation KW - Neoplasms -- genetics KW - Radiation Tolerance -- genetics KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709711452?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+cancer+therapeutics&rft.atitle=CDK1-Mediated+SIRT3+Activation+Enhances+Mitochondrial+Function+and+Tumor+Radioresistance.&rft.au=Liu%2C+Rui%3BFan%2C+Ming%3BCandas%2C+Demet%3BQin%2C+Lili%3BZhang%2C+Xiaodi%3BEldridge%2C+Angela%3BZou%2C+June+X%3BZhang%2C+Tieqiao%3BJuma%2C+Shuaib%3BJin%2C+Cuihong%3BLi%2C+Robert+F%3BPerks%2C+Julian%3BSun%2C+Lun-Quan%3BVaughan%2C+Andrew+T+M%3BHai%2C+Chun-Xu%3BGius%2C+David+R%3BLi%2C+Jian+Jian&rft.aulast=Liu&rft.aufirst=Rui&rft.date=2015-09-01&rft.volume=14&rft.issue=9&rft.spage=2090&rft.isbn=&rft.btitle=&rft.title=Molecular+cancer+therapeutics&rft.issn=1538-8514&rft_id=info:doi/10.1158%2F1535-7163.MCT-15-0017 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-07 N1 - Date created - 2015-09-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Methods Enzymol. 2014;543:141-63 [24924131] Cancer Res. 2014 Dec 15;74(24):7498-509 [25377473] J Mol Cell Biol. 2013 Jun;5(3):166-75 [23243068] Biochem Pharmacol. 2000 Oct 15;60(8):1085-9 [11007945] J Biol Chem. 2001 Jan 19;276(3):1993-7 [11067844] Cancer Res. 2001 Oct 15;61(20):7689-96 [11606413] Semin Radiat Oncol. 2001 Oct;11(4):346-51 [11677659] Mol Cell Biol. 2003 Apr;23(7):2362-78 [12640121] J Biol Chem. 2003 Jun 13;278(24):21631-8 [12690099] Mol Cancer Ther. 2003 Nov;2(11):1113-20 [14617784] Proc Natl Acad Sci U S A. 2004 Jul 6;101(27):10137-42 [15220474] Cancer Res. 1979 Apr;39(4):1141-9 [217531] Int J Radiat Oncol Biol Phys. 1994 Aug 30;30(1):229-34 [8083118] N Engl J Med. 1996 May 23;334(21):1356-61 [8614420] Ann N Y Acad Sci. 2004 Dec;1030:1-13 [15659775] Mol Cancer Res. 2006 Dec;4(12):945-55 [17189385] Genes Dev. 2007 Apr 15;21(8):920-8 [17437997] Free Radic Biol Med. 2008 Jan 1;44(1):1-13 [17967430] Biochem J. 2008 Apr 15;411(2):e11-3 [18363549] J Biol Chem. 2008 Jul 25;283(30):21011-23 [18508759] J Mol Biol. 2008 Oct 10;382(3):790-801 [18680753] Int J Biol Sci. 2008;4(5):291-9 [18781224] Proc Natl Acad Sci U S A. 2008 Sep 23;105(38):14447-52 [18794531] Radiat Res. 2009 Jan;171(1):9-21 [19138055] J Mammary Gland Biol Neoplasia. 2009 Mar;14(1):11-7 [19252973] PLoS One. 2009;4(4):e5284 [19384424] Nature. 2009 Jul 30;460(7255):587-91 [19641587] Lancet Oncol. 2010 Jan;11(1):21-8 [19897418] Nature. 2010 Mar 4;464(7285):121-5 [20203611] J Clin Oncol. 2010 May 1;28(13):2181-90 [20351327] Biochim Biophys Acta. 2010 Aug;1804(8):1645-51 [20060508] J Clin Oncol. 2010 Jun 20;28(18):2996-3001 [20479390] Mech Ageing Dev. 2010 Jul-Aug;131(7-8):511-6 [20478325] Trends Biochem Sci. 2010 Dec;35(12):669-75 [20863707] Cell Metab. 2010 Dec 1;12(6):662-7 [21109198] Mol Cell. 2010 Dec 22;40(6):893-904 [21172655] Sci Signal. 2011;4(156):pe2 [21245467] Mol Cell. 2011 Jan 21;41(2):139-49 [21255725] J Cell Physiol. 2011 Apr;226(4):962-7 [20945393] Mol Cancer Ther. 2011 Feb;10(2):292-302 [21216938] Cancer. 2011 Apr 15;117(8):1670-8 [21472714] EMBO Rep. 2011 Jun;12(6):534-41 [21566644] Mol Cell. 2011 Jun 10;42(5):561-8 [21658599] Nat Rev Mol Cell Biol. 2012 Apr;13(4):225-38 [22395773] J Biol Chem. 2012 Apr 20;287(17):14078-86 [22416140] Sci Rep. 2012;2:425 [22645641] Mol Cancer Res. 2012 Jun;10(6):768-77 [22547077] Free Radic Res. 2012 Aug;46(8):1029-43 [22656864] Trends Endocrinol Metab. 2012 Sep;23(9):467-76 [22902903] Cell Rep. 2013 Feb 21;3(2):319-27 [23375372] Cell Death Dis. 2013;4:e731 [23868064] Dev Cell. 2014 Apr 28;29(2):217-32 [24746669] Antioxid Redox Signal. 2014 Aug 1;21(4):551-64 [24252090] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1535-7163.MCT-15-0017 ER - TY - JOUR T1 - Timing of Environmental Exposures as a Critical Element in Breast Cancer Risk. AN - 1709707074; 26214118 AB - The role of the chemical environment in disease initiation or progression is becoming more evident. Endocrine disruption via environmental chemicals is now well documented in humans, rodent research models, and wildlife. Breast cancer is an endocrine-based disease whose risk may be modified by environmental exposures. Our purpose is to encourage more investigation into early life environmental exposures as they relate to breast cancer risk factors and disease over a lifetime. The 2009 President's Cancer Panel, 2012 Institute of Medicine, 2013 Interagency Breast Cancer and the Environment Research Coordinating Committee reports, and research publications dated ≥2012 in PubMed were used to inform our perspective. Literature was reviewed and evidence gathered on the effects of the environment on risk of breast cancer or mammary tumor development in animal research models as it pertained to the influence of timing of exposure on later-life outcomes. Evidence has accumulated for several chemicals that environmental factors have a stronger effect on breast cancer risk when exposure occurred early in life. The insecticide, dichlorodiphenyltrichloroethane, is an excellent example and is just one of several chemicals for which there seems to be both animal and human evidence for the developmental basis of adult disease. The developing breast undergoes many changes in early life, leaving it vulnerable to the effects of epigenetic marks, endocrine disruption, and carcinogens. More research is needed in the area of early beginnings of breast cancer, with prevention of the disease as the ultimate goal. JF - The Journal of clinical endocrinology and metabolism AU - Fenton, Suzanne E AU - Birnbaum, Linda S AD - National Toxicology Program (NTP) Laboratory, Division of the NTP (S.E.F.), National Institute of Environmental Health Sciences (L.S.B.), National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina 27709. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 3245 EP - 3250 VL - 100 IS - 9 KW - Endocrine Disruptors KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Time Factors KW - Endocrine Disruptors -- toxicity KW - Breast Neoplasms -- pathology KW - Environmental Exposure KW - Breast Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709707074?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+endocrinology+and+metabolism&rft.atitle=Timing+of+Environmental+Exposures+as+a+Critical+Element+in+Breast+Cancer+Risk.&rft.au=Fenton%2C+Suzanne+E%3BBirnbaum%2C+Linda+S&rft.aulast=Fenton&rft.aufirst=Suzanne&rft.date=2015-09-01&rft.volume=100&rft.issue=9&rft.spage=3245&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+endocrinology+and+metabolism&rft.issn=1945-7197&rft_id=info:doi/10.1210%2Fjc.2015-2848 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-24 N1 - Date created - 2015-09-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Epidemiology. 1999 Nov;10(6):722-32 [10535787] Reprod Toxicol. 2015 Jul;54:58-65 [25277313] Reprod Toxicol. 2015 Jul;54:136-40 [25554384] Am J Clin Nutr. 2000 May;71(5 Suppl):1344S-52S [10799412] Am J Epidemiol. 2000 Aug 15;152(4):363-70 [10968381] Environ Health Perspect. 2001 Mar;109 Suppl 1:35-47 [11250804] Int J Cancer. 2001 Feb 15;91(4):568-74 [11251983] Toxicol Sci. 2001 Jul;62(1):46-53 [11399792] Toxicol Sci. 2002 May;67(1):63-74 [11961217] Environ Health Perspect. 2002 Jul;110(7):625-8 [12117637] Environ Health Perspect. 2002 Aug;110(8):771-6 [12153757] Environ Health Perspect. 2003 Apr;111(4):389-94 [12676588] Environ Health Perspect. 2004 Feb;112(2):207-14 [14754575] N Engl J Med. 1984 Nov 29;311(22):1393-8 [6493300] Lancet. 1986 May 10;1(8489):1077-81 [2871345] BMJ. 1995 Jul 15;311(6998):171-4 [7613432] Toxicol Appl Pharmacol. 1997 Jan;142(1):192-200 [9007049] Lancet. 1997 Oct 18;350(9085):1131-5 [9343501] Carcinogenesis. 1998 Sep;19(9):1623-9 [9771934] Cad Saude Publica. 1998;14 Suppl 3:125-32 [9819471] J Biochem Mol Toxicol. 1999;13(6):296-302 [10487416] Cancer Epidemiol Biomarkers Prev. 2006 Aug;15(8):1509-14 [16896041] Environ Health Perspect. 2007 Oct;115(10):1406-14 [17938728] Chemosphere. 2008 Oct;73(6):999-1004 [18707752] Pediatrics. 2009 May;123(5):e932-9 [19403485] Endocr Rev. 2009 Jun;30(4):293-342 [19502515] Environ Health Perspect. 2010 May;118(5):596-601 [20435547] Environ Health Perspect. 2011 Aug;119(8):1070-6 [21501981] N Engl J Med. 2011 Oct 6;365(14):1304-14 [21991952] Environ Health Perspect. 2011 Dec;119(12):1700-5 [21810551] Annu Rev Pharmacol Toxicol. 2012;52:455-79 [22017681] Environ Health Perspect. 2012 Aug;120(8):1170-6 [22514210] Occup Environ Med. 2012 Sep;69(9):636-42 [22767868] J Mammary Gland Biol Neoplasia. 2013 Mar;18(1):43-61 [23417729] Birth Defects Res C Embryo Today. 2013 Jun;99(2):134-46 [23897597] Obesity (Silver Spring). 2013 Jun;21(6):1079-80 [23784921] Mol Endocrinol. 2013 Oct;27(10):1666-77 [24002655] J Clin Endocrinol Metab. 2015 Aug;100(8):2865-72 [26079774] Regul Toxicol Pharmacol. 2013 Dec;67(3):421-33 [24021539] Pediatrics. 2013 Dec;132(6):1019-27 [24190685] Breast Cancer Res. 2014;16(2):208 [25032259] J Obstet Gynaecol. 2015 Jan;35(1):60-3 [25020211] Sci Total Environ. 2015 Jul 1;520:106-13 [25804877] Biol Reprod. 2001 Oct;65(4):1215-23 [11566746] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1210/jc.2015-2848 ER - TY - JOUR T1 - Prediagnostic Serum Organochlorine Concentrations and Metastatic Prostate Cancer: A Nested Case-Control Study in the Norwegian Janus Serum Bank Cohort. AN - 1709393655; 25734605 AB - Organochlorine (OC) insecticides and polychlorinated biphenyls (PCBs) have been shown to have estrogenic, antiestrogenic, or antiandrogenic properties; as a result, the impact of exposure to these compounds and risk of hormonal cancers, such as prostate cancer, is a concern. We conducted a nested case-control study, using prospectively collected serum, to estimate associations between OC exposures and metastatic prostate cancer in a population-based cohort from Norway. Sera from 150 cases and 314 controls matched on date of blood draw, age at blood draw, and region was used to determine concentrations of 11 OC pesticide metabolites and 34 PCB congeners. Odds ratios (ORs) and 95% confidence intervals (95% CIs) for quartiles of lipid-corrected metabolite levels were calculated using conditional logistic regression. Metastatic prostate cancer was two times as likely among men with serum concentrations of oxychlordane in the highest quartile compared with those in the lowest quartile (OR = 2.03; 95% CI: 1.03, 4.03; p-trend 0.05). Elevated but nonsignificant ORs were estimated for the highest versus lowest quartile of heptachlor epoxide, HCB, and mirex, although these exposures were correlated with oxychlordane. Findings for specific PCB congeners showed a significant inverse association between natural log-transformed lipid-adjusted PCB 44 and metastatic prostate cancer (OR = 0.74; 95% CI: 0.56, 0.97; p-trend = 0.02). Our study highlights the importance of estimating associations with specific OC chemicals and suggests a possible role of OC insecticides and PCBs in the etiology of metastatic prostate cancer. Koutros S, Langseth H, Grimsrud TK, Barr DB, Vermeulen R, Portengen L, Wacholder S, Beane Freeman LE, Blair A, Hayes RB, Rothman N, Engel LS. 2015. Prediagnostic serum organochlorine concentrations and metastatic prostate cancer: a nested case-control study in the Norwegian Janus Serum Bank cohort. Environ Health Perspect 123:867-872; http://dx.doi.org/10.1289/ehp.1408245. JF - Environmental health perspectives AU - Koutros, Stella AU - Langseth, Hilde AU - Grimsrud, Tom K AU - Barr, Dana Boyd AU - Vermeulen, Roel AU - Portengen, Lützen AU - Wacholder, Sholom AU - Freeman, Laura E Beane AU - Blair, Aaron AU - Hayes, Richard B AU - Rothman, Nathaniel AU - Engel, Lawrence S AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 867 EP - 872 VL - 123 IS - 9 KW - Hydrocarbons, Chlorinated KW - 0 KW - Insecticides KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - Index Medicus KW - Prospective Studies KW - Logistic Models KW - Humans KW - Polychlorinated Biphenyls -- blood KW - Adult KW - Neoplasm Metastasis KW - Case-Control Studies KW - Aged KW - Middle Aged KW - Norway KW - Male KW - Prostatic Neoplasms -- pathology KW - Hydrocarbons, Chlorinated -- blood KW - Prostatic Neoplasms -- blood KW - Prostatic Neoplasms -- chemically induced KW - Insecticides -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709393655?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Prediagnostic+Serum+Organochlorine+Concentrations+and+Metastatic+Prostate+Cancer%3A+A+Nested+Case-Control+Study+in+the+Norwegian+Janus+Serum+Bank+Cohort.&rft.au=Koutros%2C+Stella%3BLangseth%2C+Hilde%3BGrimsrud%2C+Tom+K%3BBarr%2C+Dana+Boyd%3BVermeulen%2C+Roel%3BPortengen%2C+L%C3%BCtzen%3BWacholder%2C+Sholom%3BFreeman%2C+Laura+E+Beane%3BBlair%2C+Aaron%3BHayes%2C+Richard+B%3BRothman%2C+Nathaniel%3BEngel%2C+Lawrence+S&rft.aulast=Koutros&rft.aufirst=Stella&rft.date=2015-09-01&rft.volume=123&rft.issue=9&rft.spage=867&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1408245 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-31 N1 - Date created - 2015-09-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Environ Health Perspect. 2010 Jun;118(6):796-802 [20146964] J Expo Sci Environ Epidemiol. 2010 Jul;20(5):434-45 [19513097] J Clin Oncol. 2010 Jul 20;28(21):3457-62 [20566993] Chemosphere. 2010 Sep;81(4):464-8 [20817259] Am J Epidemiol. 2013 Jan 1;177(1):59-74 [23171882] Lancet Oncol. 2013 Apr;14(4):287-8 [23499544] J Occup Environ Med. 2003 Jul;45(7):692-702 [12855910] Chemosphere. 2004 Mar;54(10):1509-20 [14659953] Environ Health Perspect. 1989 May;81:225-39 [2503374] Environ Health Perspect. 1997 Jan;105(1):13-4 [9074863] Annu Rev Public Health. 1997;18:211-44 [9143718] Environ Health Perspect. 2004 Dec;112(17):1691-6 [15579415] Int Arch Occup Environ Health. 2004 Nov;77(8):559-70 [15688248] Environ Res. 2005 May;98(1):104-13 [15721890] J Occup Environ Med. 2006 Jul;48(7):700-7 [16832227] Environ Health Perspect. 2006 Oct;114(10):1508-14 [17035134] Int J Cancer. 2007 Feb 1;120(3):642-9 [17096337] Cancer Res. 2007 Jun 1;67(11):5545-52 [17545638] Int J Cancer. 2007 Oct 1;121(7):1571-8 [17450530] J Natl Cancer Inst. 2007 Dec 19;99(24):1881-7 [18073376] Endocr Rev. 2009 Jun;30(4):293-342 [19502515] Mol Nutr Food Res. 2009 Nov;53(11):1438-51 [19842105] Environ Health Perspect. 2009 Oct;117(10):1514-9 [20019899] Environ Health Perspect. 2010 Jan;118(1):60-6 [20056587] Acta Oncol. 2010 Apr;49(3):368-77 [20059313] Environ Health Perspect. 2010 May;118(5):659-65 [20435560] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1289/ehp.1408245 ER - TY - JOUR T1 - Therapeutic anti-NLGP monoclonal antibody for carcinoembryonic antigen expressing tumors is nontoxic to Swiss and BALB/c mice. AN - 1708897718; 26283593 AB - A murine monoclonal antibody (mAb), 1C8 was developed against a novel glycoprotein NLGP and its unique property to recognize carcinoembryonic antigen (CEA) was reported. Utilizing this CEA recognizing property, 1C8 is successful to restrict the growth of CEA(+) murine and human cancers both in vitro and in vivo. Here, we have thoroughly evaluated the toxicity profile of this mAb 1C8 on different physiological systems of both tumor-free and tumor-bearing Swiss and BALB/c mice. Effective concentration (25 μg/mice) of 1C8 caused no behavioral changes in animals and no death was recorded. Moreover, little increase in the body and organ weights in all mice groups was noted. MAb 1C8 showed no adverse effect on the hematological system, but little hematostimulation was noticed, as evidenced by increased hemoglobin content, leukocyte count and lymphocyte numbers. Liver enzymes like alkaline phosphatase, SGOT, SGPT and nephrological products like urea and creatinine assessment confirmed no abnormalities in both hepatic and renal functions. Number of T cells, B cells, NK cells, macrophages and dendritic cells was upregulated in vivo by mAb treatment with significant downregulation of regulatory T cells. During this treatment serum levels of type 1 cytokines were upregulated over type 2 cytokines. This mAb 1C8 also did not induce any significant increase in antibody titer following treatment. Accumulated evidences from Swiss and BALB/c mice strongly suggest that this mAb 1C8 is completely safe, thus, can be recommended for further clinical trial for the therapy of CEA(+) tumors. Copyright © 2015 Elsevier B.V. All rights reserved. JF - International immunopharmacology AU - Das, Arnab AU - Mondal, Bipasa AU - Bose, Anamika AU - Biswas, Jaydip AU - Baral, Rathindranath AU - Pal, Smarajit AD - Clinical Biochemistry Unit, Chittaranjan National Cancer Institute (CNCI), 37, S. P. Mukherjee Road, Kolkata 700026, India; Department of Immunoregulation and Immunodiagnostics, Chittaranjan National Cancer Institute (CNCI), 37, S. P. Mukherjee Road, Kolkata 700026, India. ; Department of Immunoregulation and Immunodiagnostics, Chittaranjan National Cancer Institute (CNCI), 37, S. P. Mukherjee Road, Kolkata 700026, India. ; Department of Surgical Oncology and Medical Oncology, Chittaranjan National Cancer Institute (CNCI), 37, S. P. Mukherjee Road, Kolkata 700026, India. ; Clinical Biochemistry Unit, Chittaranjan National Cancer Institute (CNCI), 37, S. P. Mukherjee Road, Kolkata 700026, India. Electronic address: psmarajit@hotmail.com. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 785 EP - 793 VL - 28 IS - 1 KW - Antibodies, Monoclonal, Murine-Derived KW - 0 KW - Antineoplastic Agents KW - Carcinoembryonic Antigen KW - Cytokines KW - Glycoproteins KW - Index Medicus KW - Histology KW - CEA KW - Anti-NLGP mAb KW - Toxicity KW - Antibody response KW - Animals KW - Kidney Function Tests KW - Cytokines -- secretion KW - Cell Line, Tumor KW - Mice KW - Liver Function Tests KW - Mice, Inbred BALB C KW - Neoplasm Transplantation KW - Behavior, Animal -- drug effects KW - Plant Leaves -- immunology KW - Body Weight -- drug effects KW - Female KW - Survival Analysis KW - Organ Size -- drug effects KW - Glycoproteins -- immunology KW - Antibodies, Monoclonal, Murine-Derived -- toxicity KW - Antineoplastic Agents -- administration & dosage KW - Antibodies, Monoclonal, Murine-Derived -- therapeutic use KW - Carcinoembryonic Antigen -- immunology KW - Colonic Neoplasms -- drug therapy KW - Antibodies, Monoclonal, Murine-Derived -- administration & dosage KW - Antineoplastic Agents -- toxicity KW - Colonic Neoplasms -- immunology KW - Antineoplastic Agents -- therapeutic use KW - Azadirachta -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1708897718?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+immunopharmacology&rft.atitle=Therapeutic+anti-NLGP+monoclonal+antibody+for+carcinoembryonic+antigen+expressing+tumors+is+nontoxic+to+Swiss+and+BALB%2Fc+mice.&rft.au=Das%2C+Arnab%3BMondal%2C+Bipasa%3BBose%2C+Anamika%3BBiswas%2C+Jaydip%3BBaral%2C+Rathindranath%3BPal%2C+Smarajit&rft.aulast=Das&rft.aufirst=Arnab&rft.date=2015-09-01&rft.volume=28&rft.issue=1&rft.spage=785&rft.isbn=&rft.btitle=&rft.title=International+immunopharmacology&rft.issn=1878-1705&rft_id=info:doi/10.1016%2Fj.intimp.2015.08.004 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-20 N1 - Date created - 2015-08-31 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.intimp.2015.08.004 ER - TY - JOUR T1 - Optimization of N-aryl-6-methoxy-1,2,3,4-tetrahydroquinolines as tubulin polymerization inhibitors. AN - 1708896778; 26242242 AB - Thirteen new N-aryl 1,2,3,4-tetrahydroquinoline compounds (4a-f, 6a-c, and 8a-d) were synthesized and evaluated for antitumor activity and drug-like properties. Compound 4a exhibited high inhibitory potency with low nanomolar GI50 values of 16-20 nM in cellular assays, including excellent activity against the P-glycoprotein overexpressing cell line KBvin. Compound 4a inhibited colchicine binding to tubulin and tubulin assembly with an IC50 value of 0.85 μM, superior to the reference compound CA4 (1.2 μM) in the same assay. In addition, 4a also exhibited highly improved water solubility (75 μg/mL) and a suitable logP value (3.43) at pH 7.4. With a good balance between antitumor potency and drug-like properties, compound 4a could be a new potential drug candidate for further development. Current results on SAR studies and molecular modeling provided more insight about this class of compounds as tubulin polymerization inhibitors targeting the colchicine site. Copyright © 2015 Elsevier Ltd. All rights reserved. JF - Bioorganic & medicinal chemistry AU - Wang, Sheng-Biao AU - Wang, Xiao-Feng AU - Qin, Bingjie AU - Ohkoshi, Emika AU - Hsieh, Kan-Yen AU - Hamel, Ernest AU - Cui, Mu-Tian AU - Zhu, Dong-Qing AU - Goto, Masuo AU - Morris-Natschke, Susan L AU - Lee, Kuo-Hsiung AU - Xie, Lan AD - Beijing Institute of Pharmacology & Toxicology, 27 Tai-Ping Road, Beijing 100850, China. ; Natural Products Research Laboratories, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, NC 27599, USA. ; Natural Products Research Laboratories, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, NC 27599, USA; Graduate Institute of Natural Products, College of Pharmacy, Kaohsiung Medical University, Kaohsiung, Taiwan. ; Screening Technologies Branch, Developmental Therapeutics Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute, Frederick National Laboratory for Cancer Research, National Institutes of Health, Frederick, MD 21702, USA. ; Natural Products Research Laboratories, UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, NC 27599, USA; Chinese Medicine Research and Development Center, China Medical University and Hospital, Taichung, Taiwan. Electronic address: khlee@unc.edu. ; Beijing Institute of Pharmacology & Toxicology, 27 Tai-Ping Road, Beijing 100850, China. Electronic address: lanxieshi@yahoo.com. Y1 - 2015/09/01/ PY - 2015 DA - 2015 Sep 01 SP - 5740 EP - 5747 VL - 23 IS - 17 KW - Quinolines KW - 0 KW - Tubulin Modulators KW - 1,2,3,4-tetrahydroquinoline KW - CCR50N1Z9G KW - Index Medicus KW - Cytotoxic activity KW - Colchicine binding inhibitors KW - N-Aryl 1,2,3,4-tetrahydroquinolines KW - Tubulin polymerization inhibitors KW - Cell Proliferation -- drug effects KW - Drug Screening Assays, Antitumor KW - Models, Molecular KW - Humans KW - Cell Line, Tumor KW - Structure-Activity Relationship KW - Quinolines -- chemistry KW - Quinolines -- pharmacology KW - Tubulin Modulators -- pharmacology KW - Tubulin Modulators -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1708896778?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioorganic+%26+medicinal+chemistry&rft.atitle=Optimization+of+N-aryl-6-methoxy-1%2C2%2C3%2C4-tetrahydroquinolines+as+tubulin+polymerization+inhibitors.&rft.au=Wang%2C+Sheng-Biao%3BWang%2C+Xiao-Feng%3BQin%2C+Bingjie%3BOhkoshi%2C+Emika%3BHsieh%2C+Kan-Yen%3BHamel%2C+Ernest%3BCui%2C+Mu-Tian%3BZhu%2C+Dong-Qing%3BGoto%2C+Masuo%3BMorris-Natschke%2C+Susan+L%3BLee%2C+Kuo-Hsiung%3BXie%2C+Lan&rft.aulast=Wang&rft.aufirst=Sheng-Biao&rft.date=2015-09-01&rft.volume=23&rft.issue=17&rft.spage=5740&rft.isbn=&rft.btitle=&rft.title=Bioorganic+%26+medicinal+chemistry&rft.issn=1464-3391&rft_id=info:doi/10.1016%2Fj.bmc.2015.07.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-29 N1 - Date created - 2015-08-31 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Res. 2002 Jun 15;62(12):3408-16 [12067983] Cell Biochem Biophys. 2003;38(1):1-22 [12663938] Nature. 2004 Mar 11;428(6979):198-202 [15014504] J Natl Cancer Inst. 1990 Jul 4;82(13):1113-8 [2359137] J Natl Cancer Inst. 1991 Jun 5;83(11):757-66 [2041050] Mol Pharmacol. 1998 Jan;53(1):62-76 [9443933] Nat Rev Cancer. 2005 Jun;5(6):423-35 [15928673] Methods. 2007 Aug;42(4):377-87 [17560325] Med Res Rev. 2008 Jan;28(1):155-83 [17464966] J Med Chem. 2009 Apr 23;52(8):2341-51 [19296653] Proc Natl Acad Sci U S A. 2009 Aug 18;106(33):13775-9 [19666559] Cancer Lett. 2010 Sep 28;295(2):135-43 [20418015] Nat Rev Drug Discov. 2010 Oct;9(10):790-803 [20885410] Cancer Treat Rev. 2011 Feb;37(1):63-74 [20570444] Integr Biol (Camb). 2011 Apr;3(4):375-87 [21321746] J Med Chem. 2011 Sep 8;54(17):6014-27 [21774499] J Med Chem. 2012 Jun 14;55(11):5413-24 [22612652] J Med Chem. 2012 Aug 23;55(16):7219-29 [22856541] Bioorg Med Chem Lett. 2012 Oct 1;22(19):6224-8 [22932313] Bioorg Med Chem. 2013 Feb 1;21(3):632-42 [23274123] Eur J Med Chem. 2013 Sep;67:196-207 [23867604] J Med Chem. 2014 Feb 27;57(4):1390-402 [24502232] Eur J Med Chem. 2014 Jun 10;80:243-53 [24780601] Eur J Med Chem. 2014 Oct 6;85:341-51 [25105922] Eur J Med Chem. 2014 Nov 24;87:89-124 [25240869] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bmc.2015.07.016 ER - TY - JOUR T1 - Deficient vesicular storage: A common theme in catecholaminergic neurodegeneration. AN - 1708895190; 26255205 AB - Several neurodegenerative diseases involve loss of catecholamine neurons--Parkinson's disease (PD) is a prototypical example. Catecholamine neurons are rare in the nervous system, and why they are lost has been mysterious. Accumulating evidence supports the concept of "autotoxicity"--inherent cytotoxicity caused by catecholamine metabolites. Since vesicular sequestration limits the buildup of toxic products of enzymatic and spontaneous oxidation of catecholamines, a vesicular storage defect could play a pathogenic role in the death of catecholaminergic neurons in a variety of neurodegenerative diseases. In putamen, deficient vesicular storage is revealed in vivo by accelerated loss of (18)F-DOPA-derived radioactivity and post-mortem by decreased tissue dopamine (DA):DOPA ratios; in myocardium in vivo by accelerated loss of (18)F-dopamine-derived radioactivity and post-mortem by increased 3,4-dihydroxyphenylglycol:norepinephrine (DHPG:NE) ratios; and in sympathetic noradrenergic nerves overall in vivo by increased plasma F-dihydroxyphenylacetic acid (F-DOPAC):DHPG ratios. We retrospectively analyzed data from 20 conditions with decreased or intact catecholaminergic innervation, involving different etiologies, pathogenetic mechanisms, and lesion locations. All conditions involving parkinsonism had accelerated loss of putamen (18)F-DOPA-derived radioactivity; in those with post-mortem data there were also decreased putamen DA:DOPA ratios. All conditions involving cardiac sympathetic denervation had accelerated loss of myocardial (18)F-dopamine-derived radioactivity; in those with post-mortem data there were increased myocardial DHPG:NE ratios. All conditions involving localized loss of catecholaminergic innervation had evidence of decreased vesicular storage specifically in the denervated regions. Thus, across neurodegenerative diseases, loss of catecholaminergic neurons seems to be associated with decreased vesicular storage in the residual neurons. Copyright © 2015 Elsevier Ltd. All rights reserved. JF - Parkinsonism & related disorders AU - Goldstein, David S AU - Holmes, Courtney AU - Sullivan, Patti AU - Mash, Deborah C AU - Sidransky, Ellen AU - Stefani, Alessandro AU - Kopin, Irwin J AU - Sharabi, Yehonatan AD - Clinical Neurocardiology Section, Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA. Electronic address: goldsteind@ninds.nih.gov. ; Clinical Neurocardiology Section, Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892, USA. ; Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA. ; Medical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, 20892, USA. ; Movement Disorder Center, University of Tor Vergata, Rome, Italy. ; Department of Internal Medicine, Chaim Sheba Medical Center, Tel-HaShomer, and Sackler Faculty of Medicine, Tel-Aviv University School of Medicine, Tel-Avid, Israel. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 1013 EP - 1022 VL - 21 IS - 9 KW - Catecholamines KW - 0 KW - Fluorodeoxyglucose F18 KW - 0Z5B2CJX4D KW - Levodopa KW - 46627O600J KW - Index Medicus KW - Catecholamine KW - Dopamine KW - Parkinson's disease KW - Norepinephrine KW - Neurodegeneration KW - Autopsy KW - Humans KW - Parkinson Disease -- metabolism KW - Fluorodeoxyglucose F18 -- metabolism KW - Levodopa -- metabolism KW - Parkinson Disease -- pathology KW - Putamen -- pathology KW - Neurons -- metabolism KW - Catecholamines -- metabolism KW - Synaptic Vesicles -- metabolism KW - Neurodegenerative Diseases -- metabolism KW - Neurodegenerative Diseases -- pathology KW - Neurons -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1708895190?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Parkinsonism+%26+related+disorders&rft.atitle=Deficient+vesicular+storage%3A+A+common+theme+in+catecholaminergic+neurodegeneration.&rft.au=Goldstein%2C+David+S%3BHolmes%2C+Courtney%3BSullivan%2C+Patti%3BMash%2C+Deborah+C%3BSidransky%2C+Ellen%3BStefani%2C+Alessandro%3BKopin%2C+Irwin+J%3BSharabi%2C+Yehonatan&rft.aulast=Goldstein&rft.aufirst=David&rft.date=2015-09-01&rft.volume=21&rft.issue=9&rft.spage=1013&rft.isbn=&rft.btitle=&rft.title=Parkinsonism+%26+related+disorders&rft.issn=1873-5126&rft_id=info:doi/10.1016%2Fj.parkreldis.2015.07.009 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-23 N1 - Date created - 2015-08-31 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Pharmacol Ther. 2014 Dec;144(3):268-82 [24945828] Neurosci Lett. 2015 Mar 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[18725592] Parkinsonism Relat Disord. 2008 Dec;14(8):600-7 [18325818] Auton Neurosci. 2009 Mar 12;146(1-2):18-21 [19155193] Free Radic Res. 2009 Apr;43(4):417-30 [19291591] J Nucl Med. 2009 Jun;50(6):893-9 [19443601] Clin Auton Res. 2009 Jun;19(3):137-48 [19266158] Chem Res Toxicol. 2009 Jul;22(7):1256-63 [19537779] J Nucl Med. 2009 Sep;50(9):1479-82 [19690020] Clin Auton Res. 2015 Feb;25(1):61-7 [25638582] Parkinsonism Relat Disord. 2015 Jun;21(6):567-72 [25829070] J Neurochem. 2014 Oct;131(2):219-28 [24848581] N Engl J Med. 2000 Feb 24;342(8):541-9 [10684912] Ann Intern Med. 2000 Sep 5;133(5):338-47 [10979878] N Engl J Med. 2000 Oct 5;343(14):1008-14 [11018167] Am J Hum Genet. 2001 Mar;68(3):598-605 [11179008] Ann Neurol. 2001 Mar;49(3):313-9 [11261505] Neurology. 2001 Apr 10;56(7):980-1 [11294945] Brain Res Mol Brain Res. 2001 Sep 10;93(1):1-7 [11532332] Neurology. 2001 Sep 25;57(6):1140-1 [11571358] Ann Intern Med. 2001 Dec 4;135(11):1010-1 [11730415] J Cereb Blood Flow Metab. 2002 Feb;22(2):232-9 [11823721] Naunyn Schmiedebergs Arch Pharmacol. 2002 Jan;365(1):38-49 [11862332] J Neurol Sci. 2002 Aug 15;200(1-2):79-84 [12127681] Clin Auton Res. 2002 Aug;12(4):281-5 [12357282] Circulation. 2002 Oct 29;106(18):2358-65 [12403667] J Neurol Neurosurg Psychiatry. 2002 Dec;73(6):776-7 [12438492] J Neurosci. 2003 Jul 2;23(13):5835-45 [12843288] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.parkreldis.2015.07.009 ER - TY - JOUR T1 - An APOBEC3A hypermutation signature is distinguishable from the signature of background mutagenesis by APOBEC3B in human cancers. AN - 1708162139; 26258849 AB - Elucidation of mutagenic processes shaping cancer genomes is a fundamental problem whose solution promises insights into new treatment, diagnostic and prevention strategies. Single-strand DNA-specific APOBEC cytidine deaminase(s) are major source(s) of mutation in several cancer types. Previous indirect evidence implicated APOBEC3B as the more likely major mutator deaminase, whereas the role of APOBEC3A is not established. Using yeast models enabling the controlled generation of long single-strand genomic DNA substrates, we show that the mutation signatures of APOBEC3A and APOBEC3B are statistically distinguishable. We then apply three complementary approaches to identify cancer samples with mutation signatures resembling either APOBEC. Strikingly, APOBEC3A-like samples have over tenfold more APOBEC-signature mutations than APOBEC3B-like samples. We propose that APOBEC3A-mediated mutagenesis is much more frequent because APOBEC3A itself is highly proficient at generating DNA breaks, whose repair can trigger the formation of single-strand hypermutation substrates. JF - Nature genetics AU - Chan, Kin AU - Roberts, Steven A AU - Klimczak, Leszek J AU - Sterling, Joan F AU - Saini, Natalie AU - Malc, Ewa P AU - Kim, Jaegil AU - Kwiatkowski, David J AU - Fargo, David C AU - Mieczkowski, Piotr A AU - Getz, Gad AU - Gordenin, Dmitry A AD - Genome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, US National Institutes of Health, Research Triangle Park, North Carolina, USA. ; Integrative Bioinformatics Support Group, National Institute of Environmental Health Sciences, US National Institutes of Health, Research Triangle Park, North Carolina, USA. ; Department of Genetics, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina, USA. ; Broad Institute of MIT and Harvard, Cambridge, Massachusetts, USA. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 1067 EP - 1072 VL - 47 IS - 9 KW - Minor Histocompatibility Antigens KW - 0 KW - Proteins KW - APOBEC3A protein, human KW - EC 3.5.4.5 KW - APOBEC3B protein, human KW - Cytidine Deaminase KW - Index Medicus KW - Base Sequence KW - Humans KW - DNA Mutational Analysis KW - DNA Breaks, Double-Stranded KW - Mutation KW - Mutagenesis KW - Cytidine Deaminase -- genetics KW - Proteins -- genetics KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1708162139?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+genetics&rft.atitle=An+APOBEC3A+hypermutation+signature+is+distinguishable+from+the+signature+of+background+mutagenesis+by+APOBEC3B+in+human+cancers.&rft.au=Chan%2C+Kin%3BRoberts%2C+Steven+A%3BKlimczak%2C+Leszek+J%3BSterling%2C+Joan+F%3BSaini%2C+Natalie%3BMalc%2C+Ewa+P%3BKim%2C+Jaegil%3BKwiatkowski%2C+David+J%3BFargo%2C+David+C%3BMieczkowski%2C+Piotr+A%3BGetz%2C+Gad%3BGordenin%2C+Dmitry+A&rft.aulast=Chan&rft.aufirst=Kin&rft.date=2015-09-01&rft.volume=47&rft.issue=9&rft.spage=1067&rft.isbn=&rft.btitle=&rft.title=Nature+genetics&rft.issn=1546-1718&rft_id=info:doi/10.1038%2Fng.3378 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-13 N1 - Date created - 2015-08-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biometrika. 1945 Nov;33:222-5 [21006837] PLoS One. 2009;4(1):e4277 [19169351] Science. 2011 Mar 25;331(6024):1553-8 [21436442] EMBO Rep. 2011 May;12(5):444-50 [21460793] Cell. 2012 May 25;149(5):979-93 [22608084] Mol Cell. 2012 May 25;46(4):424-35 [22607975] PLoS Genet. 2012;8(12):e1003149 [23271983] Genome Res. 2013 Feb;23(2):228-35 [23124520] Nature. 2013 Feb 21;494(7437):366-70 [23389445] J Natl Cancer Inst. 2013 Apr 17;105(8):573-9 [23411593] Elife. 2013;2:e00534 [23599896] Nature. 2013 Jul 11;499(7457):214-8 [23770567] Nature. 2013 Aug 22;500(7463):415-21 [23945592] PLoS One. 2013;8(8):e73641 [23977391] Nat Genet. 2013 Sep;45(9):977-83 [23852168] Nat Genet. 2013 Sep;45(9):970-6 [23852170] Carcinogenesis. 2013 Oct;34(10):2240-3 [23715497] Nucleic Acids Res. 2013 Oct;41(19):8995-9005 [23925127] Elife. 2013;2:e01222 [24171103] DNA Repair (Amst). 2013 Nov;12(11):878-89 [23988736] Nat Methods. 2013 Dec;10(12):1211-2 [24097270] Cancer Res. 2013 Dec 15;73(24):7222-31 [24154874] Mol Biol Evol. 2014 Feb;31(2):330-40 [24162735] Nature. 2014 Mar 20;507(7492):315-22 [24476821] Nat Genet. 2014 May;46(5):487-91 [24728294] Cell Rep. 2014 Jun 12;7(5):1640-8 [24882007] Cancer Cell. 2014 Sep 8;26(3):319-30 [25155756] Nat Commun. 2014;5:5129 [25298230] Science. 2014 Oct 10;346(6206):251-6 [25301630] Nat Genet. 2014 Dec;46(12):1258-63 [25383969] Nature. 2014 Nov 27;515(7528):558-62 [25428503] N Engl J Med. 2014 Dec 4;371(23):2189-99 [25409260] Nat Rev Cancer. 2014 Dec;14(12):786-800 [25568919] Cell. 2015 Jan 15;160(1-2):48-61 [25594174] Proc Natl Acad Sci U S A. 2015 Mar 3;112(9):2841-6 [25730878] Oncotarget. 2015 Feb 20;6(5):3409-19 [25401976] Eur Urol. 2015 May;67(5):876-88 [25466937] Breast Cancer Res. 2015;17:8 [25848704] Biomed J. 2015 Mar-Apr;38(2):102-10 [25566802] Mol Cell. 2002 Nov;10(5):1247-53 [12453430] Nature. 2000 Apr 27;404(6781):1011-3 [10801132] Nat Commun. 2015;6:6997 [25904160] Curr Biol. 2004 Aug 10;14(15):1392-6 [15296758] Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9473-7 [1658784] J Mol Biol. 1994 Jan 14;235(2):625-34 [8289285] Nucleic Acids Res. 1998 Feb 15;26(4):942-7 [9461451] J Biol Chem. 2004 Dec 17;279(51):53379-86 [15466872] Methods Enzymol. 2006;409:329-45 [16793410] J Virol. 2006 Nov;80(21):10522-33 [16920826] DNA Repair (Amst). 2007 Dec 1;6(12):1829-38 [17715002] DNA Repair (Amst). 2011 Mar 7;10(3):344-8 [21227759] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ng.3378 ER - TY - JOUR T1 - Acute and recent air pollution exposure and cardiovascular events at labour and delivery. AN - 1707558434; 26105036 AB - To study the relationship between acute air pollution exposure and cardiovascular events during labour/delivery. The Consortium on Safe Labor (2002-2008), an observational US cohort with 223,502 singleton deliveries provided electronic medical records. Air pollution exposure was estimated by modified Community Multiscale Air Quality models. Cardiovascular events (cardiac failure/arrest, stroke, myocardial infarcts and other events) were recorded in the hospital discharge records for 687 pregnancies (0.3%). Logistic regression with generalised estimating equations estimated the relationship between cardiovascular events and daily air pollutant levels for delivery day and the 7 days preceding delivery. Increased odds of cardiovascular events were observed for each IQR increase in exposure to nitric oxides at 5 and 6 days prior to delivery (OR=1.17, 99% CI 1.04 to 1.30 and OR=1.15, 1.03 to 1.28, respectively). High exposure to toxic air pollution species such as ethylbenzene (OR=1.50, 1.08 to 2.09), m-xylene (OR=1.54, 1.11 to 2.13), o-xylene (OR=1.51, 1.09 to 2.09), p-xylene (OR=1.43, 1.03 to 1.99) and toluene (OR=1.42, 1.02 to 1.97) at 5 days prior to delivery were also associated with cardiovascular events. Decreased odds of events were observed with exposure to ozone. Air pollution in the days prior to delivery, especially nitrogen oxides and some toxic air pollution species, was associated with increased risk of cardiovascular events during the labour/delivery admission. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions. JF - Heart (British Cardiac Society) AU - Männistö, Tuija AU - Mendola, Pauline AU - Laughon Grantz, Katherine AU - Leishear, Kira AU - Sundaram, Rajeshwari AU - Sherman, Seth AU - Ying, Qi AU - Liu, Danping AD - Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Rockville, Maryland, USA Northern Finland Laboratory Centre NordLab, Oulu, Finland Department of Clinical Chemistry, University of Oulu, Oulu, Finland Medical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland Department of Chronic Disease Prevention, National Institute for Health and Welfare, Oulu, Finland. ; Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Rockville, Maryland, USA. ; Glotech Inc., Rockville, Maryland, USA US Food and Drug Administration, Silver Spring, Maryland, USA. ; Biostatistics and Bioinformatics Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Rockville, Maryland, USA. ; The EMMES Corporation, Rockville, Maryland, USA. ; Zachry Department of Civil Engineering, Texas A&M University, College Station, Texas, USA. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 1491 EP - 1498 VL - 101 IS - 18 KW - Nitrogen Oxides KW - 0 KW - Xylenes KW - Ozone KW - 66H7ZZK23N KW - Abridged Index Medicus KW - Index Medicus KW - Electronic Health Records KW - Delivery, Obstetric -- mortality KW - Risk Factors KW - Humans KW - Adult KW - Outcome Assessment (Health Care) KW - Delivery, Obstetric -- methods KW - United States -- epidemiology KW - Male KW - Female KW - Risk Assessment KW - Pregnancy KW - Ozone -- analysis KW - Air Pollution -- analysis KW - Pregnancy Complications, Cardiovascular -- epidemiology KW - Environmental Exposure -- analysis KW - Nitrogen Oxides -- analysis KW - Xylenes -- toxicity KW - Air Pollution -- adverse effects KW - Pregnancy Complications, Cardiovascular -- prevention & control KW - Pregnancy Complications, Cardiovascular -- chemically induced KW - Environmental Exposure -- adverse effects KW - Nitrogen Oxides -- toxicity KW - Xylenes -- analysis KW - Ozone -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1707558434?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Heart+%28British+Cardiac+Society%29&rft.atitle=Acute+and+recent+air+pollution+exposure+and+cardiovascular+events+at+labour+and+delivery.&rft.au=M%C3%A4nnist%C3%B6%2C+Tuija%3BMendola%2C+Pauline%3BLaughon+Grantz%2C+Katherine%3BLeishear%2C+Kira%3BSundaram%2C+Rajeshwari%3BSherman%2C+Seth%3BYing%2C+Qi%3BLiu%2C+Danping&rft.aulast=M%C3%A4nnist%C3%B6&rft.aufirst=Tuija&rft.date=2015-09-01&rft.volume=101&rft.issue=18&rft.spage=1491&rft.isbn=&rft.btitle=&rft.title=Heart+%28British+Cardiac+Society%29&rft.issn=1468-201X&rft_id=info:doi/10.1136%2Fheartjnl-2014-307366 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-16 N1 - Date created - 2015-08-26 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1136/heartjnl-2014-307366 ER - TY - JOUR T1 - High Prevalence of Nonalcoholic Fatty Liver Disease in Adolescents Undergoing Bariatric Surgery. AN - 1707554135; 26026390 AB - Little is known about the prevalence of nonalcoholic fatty liver disease (NAFLD) among severely obese adolescents or factors that determine its development. We investigated the prevalence of NAFLD in a multicenter cohort of adolescents undergoing bariatric surgery and the factors associated with it. We enrolled 242 adolescents undergoing bariatric surgery between March 2007 and February 2012 at 5 tertiary care centers into a multicenter, prospective observational cohort study. Intraoperative core liver biopsies were collected from 165 subjects; 17 were excluded because of insufficient liver tissue or use of hepatotoxic medications, so 148 remained in the study (mean age, 16.8 ± 1.6 years; median body mass index = 52 kg/m(2)). Liver tissues were analyzed by histology using validated criteria. Hepatic gene expression was analyzed in 67 samples. NAFLD was present in 59% of this predominantly female (72%), white (68%), non-Hispanic (91%) cohort. Of subjects with NAFLD, 24% had borderline and 10% had definite nonalcoholic steatohepatitis (NASH). Mild fibrosis (stage 2 or lower) was observed in 18% of liver biopsies and stage 3 was observed in 0.7%, but cirrhosis was not detected. Dyslipidemia was present in 78% of subjects, hypertension in 44%, and diabetes in 14%. More severe NAFLD was associated with increasing levels of alanine aminotransferase, fasting glucose level, hypertension (each P < .01), and white blood cell count (P = .04). Only diabetes was associated with detection of fibrosis (odds ratio = 3.56; 95% confidence interval: 1.93-6.56). Microarray analysis associated presence of NASH with altered expression of genes that regulate macrophage chemotaxis, cholesterol absorption, and fatty acid binding. More than half of adolescents undergoing bariatric surgery in this cohort had NAFLD, yet the prevalence of severe or fibrotic NASH was low. Increasing severity of NAFLD was associated with level of alanine aminotransferase and cardiometabolic risk factors, but not body mass index. Based on gene expression analysis, borderline and definite NASH were associated with abnormal immune function, intestinal cholesterol absorption, and lipid metabolism. Copyright © 2015 AGA Institute. Published by Elsevier Inc. All rights reserved. JF - Gastroenterology AU - Xanthakos, Stavra A AU - Jenkins, Todd M AU - Kleiner, David E AU - Boyce, Tawny W AU - Mourya, Reena AU - Karns, Rebekah AU - Brandt, Mary L AU - Harmon, Carroll M AU - Helmrath, Michael A AU - Michalsky, Marc P AU - Courcoulas, Anita P AU - Zeller, Meg H AU - Inge, Thomas H AU - Teen-LABS Consortium AD - Division of Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio. Electronic address: Stavra.xanthakos@cchmc.org. ; Division of Pediatric Surgery, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio. ; Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. ; University of New Mexico Cancer Center, Biostatistics Shared Resource, Albuquerque, New Mexico. ; Division of Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio. ; Division of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio. ; Division of Pediatric Surgery, Texas Children's Hospital, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas. ; Division of Pediatric Surgery, Women & Children's Hospital of Buffalo, University of Buffalo School of Medicine and Biomedical Sciences, Buffalo, New York. ; Department of Pediatric Surgery, The Ohio State University College of Medicine and Nationwide Children's Hospital, Columbus, Ohio. ; Department of Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. ; Division of Behavioral Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. ; Teen-LABS Consortium Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 623 EP - 34.e8 VL - 149 IS - 3 KW - Biomarkers KW - 0 KW - RNA, Messenger KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Abridged Index Medicus KW - Index Medicus KW - Pediatric KW - Microarray KW - Severe Obesity KW - Inflammation KW - Liver -- enzymology KW - Age Factors KW - Odds Ratio KW - Humans KW - Biopsy KW - Multivariate Analysis KW - Gene Expression Regulation KW - Adolescent KW - Biomarkers -- blood KW - Male KW - Severity of Illness Index KW - Liver -- pathology KW - RNA, Messenger -- analysis KW - Predictive Value of Tests KW - Longitudinal Studies KW - Age Distribution KW - Gene Expression Profiling KW - Alanine Transaminase -- blood KW - Prospective Studies KW - Logistic Models KW - Risk Factors KW - Liver Cirrhosis -- epidemiology KW - United States -- epidemiology KW - Female KW - Prevalence KW - Pediatric Obesity -- diagnosis KW - Non-alcoholic Fatty Liver Disease -- genetics KW - Pediatric Obesity -- surgery KW - Bariatric Surgery KW - Non-alcoholic Fatty Liver Disease -- epidemiology KW - Non-alcoholic Fatty Liver Disease -- blood KW - Non-alcoholic Fatty Liver Disease -- diagnosis KW - Pediatric Obesity -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1707554135?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastroenterology&rft.atitle=High+Prevalence+of+Nonalcoholic+Fatty+Liver+Disease+in+Adolescents+Undergoing+Bariatric+Surgery.&rft.au=Xanthakos%2C+Stavra+A%3BJenkins%2C+Todd+M%3BKleiner%2C+David+E%3BBoyce%2C+Tawny+W%3BMourya%2C+Reena%3BKarns%2C+Rebekah%3BBrandt%2C+Mary+L%3BHarmon%2C+Carroll+M%3BHelmrath%2C+Michael+A%3BMichalsky%2C+Marc+P%3BCourcoulas%2C+Anita+P%3BZeller%2C+Meg+H%3BInge%2C+Thomas+H%3BTeen-LABS+Consortium&rft.aulast=Xanthakos&rft.aufirst=Stavra&rft.date=2015-09-01&rft.volume=149&rft.issue=3&rft.spage=623&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=1528-0012&rft_id=info:doi/10.1053%2Fj.gastro.2015.05.039 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-09 N1 - Date created - 2015-08-25 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00474318; ClinicalTrials.gov N1 - SuppNotes - Cited By: Hepatology. 2014 Feb;59(2):471-82 [23913408] JAMA Pediatr. 2014 Jan;168(1):47-53 [24189578] Semin Liver Dis. 2014 Feb;34(1):98-107 [24782263] Nature. 2014 May 8;509(7499):183-8 [24670636] World J Gastroenterol. 2014 Jul 21;20(27):9026-37 [25083076] PLoS One. 2014;9(11):e112569 [25419656] Lancet. 2015 Mar 14;385(9972):956-65 [25468160] J Pediatr Gastroenterol Nutr. 2015 Apr;60(4):550-61 [25591123] Obesity (Silver Spring). 2009 May;17(5):901-10 [19396070] Hepatology. 2005 Jun;41(6):1313-21 [15915461] Am J Epidemiol. 2005 Aug 1;162(3):199-200 [15987728] Hepatology. 2005 Sep;42(3):641-9 [16116629] Hepatology. 2005 Sep;42(3):665-74 [16116632] Clin Gastroenterol Hepatol. 2006 Feb;4(2):226-32 [16469684] Pediatrics. 2006 Oct;118(4):1388-93 [17015527] Am J Gastroenterol. 2007 Feb;102(2):399-408 [17311652] Clin Gastroenterol Hepatol. 2007 Nov;5(11):1329-32 [17702661] Cell Metab. 2008 May;7(5):410-20 [18460332] Gastroenterology. 2008 Dec;135(6):1961-1971.e2 [19013463] Hepatology. 2009 Mar;49(3):1017-44 [19243014] Diabetes Care. 2009 Jun;32(6):1068-75 [19244087] Nucleic Acids Res. 2009 Jul;37(Web Server issue):W305-11 [19465376] Hepatology. 2009 Oct;50(4):1113-20 [19637190] Gastroenterology. 2010 Apr;138(4):1357-64, 1364.e1-2 [20064512] Am J Gastroenterol. 2010 Sep;105(9):2093-102 [20372110] PLoS One. 2010;5(10):e13577 [21042596] Dig Liver Dis. 2010 Dec;42(12):888-94 [20472517] Hepatology. 2011 Mar;53(3):810-20 [21319198] JAMA. 2011 Apr 27;305(16):1659-68 [21521847] Metabolism. 2011 Jul;60(7):1001-11 [21075404] Hepatology. 1999 Dec;30(6):1356-62 [10573511] Hepatology. 2003 Jul;38(1):244-51 [12830008] Am J Epidemiol. 2004 Apr 1;159(7):702-6 [15033648] Hepatology. 2004 Aug;40(2):475-83 [15368453] Surg Obes Relat Dis. 2012 Jan-Feb;8(1):1-7 [22030146] Gastroenterology. 2012 Jun;142(7):1592-609 [22656328] Hepatology. 2012 Sep;56(3):943-51 [22505194] PLoS One. 2012;7(12):e51131 [23300535] J Clin Endocrinol Metab. 2013 Apr;98(4):E708-12 [23457410] Obesity (Silver Spring). 2014 Feb;22(2):390-400 [23804416] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1053/j.gastro.2015.05.039 ER - TY - JOUR T1 - Identification of microRNAs specific for epithelial cell adhesion molecule-positive tumor cells in hepatocellular carcinoma. AN - 1707553725; 25953724 AB - Therapies that target cancer stem cells (CSCs) hold promise in eliminating cancer burden. However, normal stem cells are likely to be targeted owing to their similarities to CSCs. It is established that epithelial cell adhesion molecule (EpCAM) is a biomarker for normal hepatic stem cells (HpSCs), and EpCAM(+) AFP(+) hepatocellular carcinoma (HCC) cells have enriched hepatic CSCs. We sought to determine whether specific microRNAs (miRNAs) exist in hepatic CSCs that are not expressed in normal HpSCs. We performed a pair-wise comparison of the miRNA transcriptome of EpCAM(+) and corresponding EpCAM(-) cells isolated from two primary HCC specimens, as well as from two fetal livers and three healthy adult liver donors by small RNA deep sequencing. We found that miR-150, miR-155, and miR-223 were preferentially highly expressed in EpCAM(+) HCC cells, which was further validated. Their gene surrogates, identified using miRNA and messenger RNA profiling in a cohort of 292 HCC patients, were associated with patient prognosis. We further demonstrated that miR-155 was highly expressed in EpCAM(+) HCC cells, compared to corresponding EpCAM(-) HCC cells, fetal livers with enriched normal hepatic progenitors, and normal adult livers with enriched mature hepatocytes. Suppressing miR-155 resulted in a decreased EpCAM(+) fraction in HCC cells and reduced HCC cell colony formation, migration, and invasion in vitro. The reduced levels of identified miR-155 targets predicted the shortened overall survival and time to recurrence of HCC patients. miR-155 is highly elevated in EpCAM(+) HCC cells and might serve as a molecular target to eradicate the EpCAM(+) CSC population in human HCCs. © 2015 by the American Association for the Study of Liver Diseases. JF - Hepatology (Baltimore, Md.) AU - Ji, Junfang AU - Zheng, Xin AU - Forgues, Marshonna AU - Yamashita, Taro AU - Wauthier, Eliane L AU - Reid, Lola M AU - Wen, Xinyu AU - Song, Young AU - Wei, Jun S AU - Khan, Javed AU - Thorgeirsson, Snorri S AU - Wang, Xin Wei AD - Life Sciences Institute, Zhejiang University, Hangzhou, China. ; University of Hawaii Cancer Center, Cancer Biology Program (Ji), Epidemiology Program (Zheng), Honolulu, HI. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD. ; Department of Gastroenterology, Kanazawa University Hospital, Kanazawa, Japan. ; Department of Cell Biology and Physiology and Program in Molecular Biology and Biotechnology, UNC School of Medicine, Chapel Hill, NC. ; Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD. ; Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 829 EP - 840 VL - 62 IS - 3 KW - Antigens, Neoplasm KW - 0 KW - Cell Adhesion Molecules KW - EPCAM protein, human KW - Epithelial Cell Adhesion Molecule KW - MicroRNAs KW - Index Medicus KW - Kaplan-Meier Estimate KW - Reference Values KW - Survival Rate KW - Humans KW - Up-Regulation -- genetics KW - Cell Line, Tumor KW - Signal Transduction KW - Gene Expression Regulation, Neoplastic KW - Liver Neoplasms -- pathology KW - Cell Adhesion Molecules -- genetics KW - MicroRNAs -- genetics KW - Neoplastic Stem Cells -- pathology KW - Carcinoma, Hepatocellular -- genetics KW - Liver Neoplasms -- mortality KW - Carcinoma, Hepatocellular -- pathology KW - Antigens, Neoplasm -- genetics KW - Carcinoma, Hepatocellular -- mortality KW - Neoplastic Stem Cells -- metabolism KW - Liver Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1707553725?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hepatology+%28Baltimore%2C+Md.%29&rft.atitle=Identification+of+microRNAs+specific+for+epithelial+cell+adhesion+molecule-positive+tumor+cells+in+hepatocellular+carcinoma.&rft.au=Ji%2C+Junfang%3BZheng%2C+Xin%3BForgues%2C+Marshonna%3BYamashita%2C+Taro%3BWauthier%2C+Eliane+L%3BReid%2C+Lola+M%3BWen%2C+Xinyu%3BSong%2C+Young%3BWei%2C+Jun+S%3BKhan%2C+Javed%3BThorgeirsson%2C+Snorri+S%3BWang%2C+Xin+Wei&rft.aulast=Ji&rft.aufirst=Junfang&rft.date=2015-09-01&rft.volume=62&rft.issue=3&rft.spage=829&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.27886 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-25 N1 - Date created - 2015-08-25 N1 - Date revised - 2017-02-01 N1 - SuppNotes - Cited By: Semin Oncol. 2012 Aug;39(4):461-72 [22846863] Hepatology. 2010 May;51(5):1635-44 [20196115] Gastroenterology. 2013 May;144(5):1066-1075.e1 [23376425] Oncogene. 2013 Dec 12;32(50):5614-24 [23955085] Am J Physiol Heart Circ Physiol. 2014 Apr 15;306(8):H1192-203 [24486510] J Virol. 2010 Jul;84(13):6318-27 [20427544] Nat Rev Gastroenterol Hepatol. 2010 Aug;7(8):448-58 [20628345] Cancer Res. 2010 Dec 15;70(24):10202-12 [21159642] Hepatology. 2011 Mar;53(3):1035-45 [21374667] Gastroenterology. 2012 Apr;142(4):957-966.e12 [22202459] Nat Rev Genet. 2012 May;13(5):358-69 [22510765] Proc Natl Acad Sci U S A. 2012 Jun 26;109(26):E1695-704 [22685206] Cancer Sci. 2003 Oct;94(10):851-7 [14556657] Dev Biol. 2004 Jun 15;270(2):488-98 [15183728] Hepatology. 2004 Jun;39(6):1477-87 [15185286] J Natl Cancer Inst. 1982 May;68(5):771-8 [7040771] Nat Genet. 2004 Dec;36(12):1306-11 [15565109] Nature. 2005 Jun 9;435(7043):834-8 [15944708] Science. 2005 Jul 8;309(5732):310-1 [15919954] N Engl J Med. 2005 Oct 27;353(17):1793-801 [16251535] Nat Med. 2006 Apr;12(4):410-6 [16532004] Histopathology. 2006 Aug;49(2):138-51 [16879391] Nat Rev Cancer. 2006 Nov;6(11):857-66 [17060945] RNA Biol. 2004 Jul;1(2):106-13 [17179747] Gastroenterology. 2007 Jun;132(7):2557-76 [17570226] Cancer Res. 2007 Nov 15;67(22):10831-9 [18006828] Proc Natl Acad Sci U S A. 2008 Feb 19;105(7):2445-50 [18263735] Cancer Res. 2008 Mar 1;68(5):1451-61 [18316609] Hepatology. 2008 Mar;47(3):897-907 [18176954] Oncogene. 2008 Mar 13;27(12):1749-58 [17891174] Stem Cells. 2008 Jun;26(6):1547-55 [18323408] Future Oncol. 2008 Oct;4(5):647-60 [18922122] Stem Cells. 2008 Oct;26(10):2496-505 [18583537] Hepatology. 2008 Nov;48(5):1598-607 [18972441] Gastroenterology. 2009 Mar;136(3):1012-24 [19150350] Clin Cancer Res. 2009 May 15;15(10):3462-71 [19447872] Hepatology. 2009 Aug;50(2):472-80 [19585654] Nat Med. 2009 Sep;15(9):1010-2 [19734877] Hepatology. 2012 Nov;56(5):1792-803 [22707408] Cancer Res. 2008 Jun 1;68(11):4287-95 [18519688] N Engl J Med. 2009 Oct 8;361(15):1437-47 [19812400] Cancer Biol Ther. 2009 Sep;8(18):1686-93 [19901517] Nat Rev Genet. 2010 Jan;11(1):31-46 [19997069] Nat Rev Genet. 2009 Oct;10(10):704-14 [19763153] Comment In: Transl Gastroenterol Hepatol. 2016 Mar 16;1:16 [28138583] N1 - Last updated - 2017-02-01 DO - http://dx.doi.org/10.1002/hep.27886 ER - TY - JOUR T1 - Sharing State Mental Health Data for Research: Building Toward Ongoing Learning in Mental Health Care Systems AN - 1706981463 AB - With the rise of “big data," the opportunities to use administrative and clinical data to evaluate impact of state level program initiatives are greatly expanded. The National Institute of Mental Health has in recent years supported research studies pooling data across states to address state-relevant questions. This commentary summarizes these activities and describes future platforms that may enhance ongoing work in this area. JF - Administration and Policy in Mental Health and Mental Health Services Research AU - Rupp, Agnes AD - Division of Services and Intervention Research, National Institute of Mental Health, Bethesda, MD, USA ; Chambers, David A; Division of Cancer Control and Population Sciences, National Cancer Institute, 9609 Medical Center Drive, Room 4E440, Rockville, MD, 20850, USA Y1 - 2015/09// PY - 2015 DA - Sep 2015 SP - 586 EP - 587 CY - New York PB - Springer Science & Business Media VL - 42 IS - 5 SN - 0894-587X KW - Public Health And Safety KW - Health Care Services KW - Mental Health KW - Health KW - Health Research KW - Mental Health Services KW - Health care KW - Health information KW - Health initiatives KW - Learning KW - Medical research KW - Mental health care KW - Mental health services UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1706981463?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Administration+and+Policy+in+Mental+Health+and+Mental+Health+Services+Research&rft.atitle=Sharing+State+Mental+Health+Data+for+Research%3A+Building+Toward+Ongoing+Learning+in+Mental+Health+Care+Systems&rft.au=Chambers%2C+David+A%3BRupp%2C+Agnes&rft.aulast=Chambers&rft.aufirst=David&rft.date=2015-09-01&rft.volume=42&rft.issue=5&rft.spage=586&rft.isbn=&rft.btitle=&rft.title=Administration+and+Policy+in+Mental+Health+and+Mental+Health+Services+Research&rft.issn=0894587X&rft_id=info:doi/10.1007%2Fs10488-015-0624-2 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Name - National Institute of Mental Health N1 - Date revised - 2015-08-25 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1007/s10488-015-0624-2 ER - TY - JOUR T1 - Olfactomedin 1 Deficiency Leads to Defective Olfaction and Impaired Female Fertility. AN - 1706209309; 26107991 AB - Olfactomedin 1 (OLFM1) is a glycoprotein highly expressed in the brain. Olfm1(-/-) female mice were previously reported to have reduced fertility. Previous microarray analysis revealed Olfm1 among the most highly upregulated genes in the uterine luminal epithelium upon embryo implantation, which was confirmed by in situ hybridization. We hypothesized that Olfm1 deficiency led to defective embryo implantation and thus impaired fertility. Indeed, Olfm1(-/-) females had defective embryo implantation. However, Olfm1(-/-) females rarely mated and those that mated rarely became pregnant. Ovarian histology indicated the absence of corpora lutea in Olfm1(-/-) females, indicating defective ovulation. Superovulation using equine chorionic gonadotropin-human chorionic gonadotropin rescued mating, ovulation, and pregnancy, and equine chorionic gonadotropin alone rescued ovulation in Olfm1(-/-) females. Olfm1(-/-) females had a 13% reduction of hypothalamic GnRH neurons but comparable basal serum LH levels and GnRH-induced LH levels compared with wild-type controls. These results indicated no obvious local defects in the female reproductive system and a functional hypothalamic-pituitary-gonadal axis. Olfm1(-/-) females were unresponsive to the effects of male bedding stimulation on pubertal development and estrous cycle. There were 41% fewer cFos-positive cells in the mitral cell layer of accessory olfactory bulb upon male urine stimulation for 90 minutes. OLFM1 was expressed in the main and accessory olfactory systems including main olfactory epithelium, vomeronasal organ, main olfactory bulb, and accessory olfactory bulb, with the highest expression detected in the axon bundles of olfactory sensory neurons. These data demonstrate that defective fertility in Olfm1(-/-) females is most likely a secondary effect of defective olfaction. JF - Endocrinology AU - Li, Rong AU - Diao, Honglu AU - Zhao, Fei AU - Xiao, Shuo AU - El Zowalaty, Ahmed E AU - Dudley, Elizabeth A AU - Mattson, Mark P AU - Ye, Xiaoqin AD - Department of Physiology and Pharmacology (R.L., H.D., F.Z., S.X., A.E.E.Z., E.A.D., X.Y.), College of Veterinary Medicine, and Interdisciplinary Toxicology Program (R.L., F.Z., S.X., A.E.E.Z., E.A.D., X.Y.), University of Georgia, Athens, Georgia 30602; and Laboratory of Neurosciences (M.P.M.), National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 3344 EP - 3357 VL - 156 IS - 9 KW - Extracellular Matrix Proteins KW - 0 KW - Glycoproteins KW - olfactomedin KW - Luteinizing Hormone KW - 9002-67-9 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Hypothalamus -- physiology KW - Embryo Implantation KW - Random Allocation KW - Uterus -- metabolism KW - Mice, 129 Strain KW - Ovulation KW - Vomeronasal Organ -- metabolism KW - Superovulation KW - Luteinizing Hormone -- blood KW - Olfactory Bulb -- metabolism KW - Olfactory Receptor Neurons -- metabolism KW - Female KW - Male KW - Odorants KW - Sexual Behavior, Animal -- physiology KW - Fertility KW - Extracellular Matrix Proteins -- deficiency KW - Glycoproteins -- deficiency KW - Smell UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1706209309?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrinology&rft.atitle=Olfactomedin+1+Deficiency+Leads+to+Defective+Olfaction+and+Impaired+Female+Fertility.&rft.au=Li%2C+Rong%3BDiao%2C+Honglu%3BZhao%2C+Fei%3BXiao%2C+Shuo%3BEl+Zowalaty%2C+Ahmed+E%3BDudley%2C+Elizabeth+A%3BMattson%2C+Mark+P%3BYe%2C+Xiaoqin&rft.aulast=Li&rft.aufirst=Rong&rft.date=2015-09-01&rft.volume=156&rft.issue=9&rft.spage=3344&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=1945-7170&rft_id=info:doi/10.1210%2Fen.2015-1389 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-17 N1 - Date created - 2015-08-22 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Front Neuroendocrinol. 2013 Oct;34(4):255-67 [23911848] Exp Neurol. 2013 Dec;250:205-18 [24095980] Reprod Sci. 2014 Mar;21(3):351-62 [23885106] J Neuroendocrinol. 2013 Dec;25(12):1273-9 [24028332] Reprod Toxicol. 2014 Apr;44:85-92 [24365114] Proc Natl Acad Sci U S A. 1993 May 15;90(10):4655-9 [8506313] J Exp Zool. 1993 Sep 1;266(6):541-58 [8371097] J Reprod Fertil. 1992 Nov;96(2):649-55 [1339844] Brain Res Mol Brain Res. 1998 Jan;53(1-2):13-23 [9473566] Mol Biol Evol. 1998 Jun;15(6):718-26 [9615453] Microsc Res Tech. 1999 Jan 1;44(1):2-10 [9915559] Neuroscience. 1999;92(4):1165-70 [10426475] J Endocrinol. 1958 Sep;17(3):307-13 [13587836] J Endocrinol. 1959 Jan;18(1):102-7 [13620841] FASEB J. 2005 Jan;19(1):133-5 [15629898] Chem Senses. 2005 Jan;30 Suppl 1:i146-7 [15738083] Nature. 2005 May 5;435(7038):104-8 [15875025] Neuroscience. 2005;133(4):947-57 [15927402] FEBS Lett. 2005 Oct 24;579(25):5443-53 [16212957] Neurosci Lett. 2006 May 1;398(1-2):59-62 [16442731] J Neurosci. 2007 Feb 14;27(7):1519-28 [17301160] Int J Biochem Cell Biol. 2007;39(12):2265-77 [17681868] Physiol Rev. 2007 Oct;87(4):1113-73 [17928582] Endocrinology. 2008 Feb;149(2):597-604 [18006629] Physiol Rev. 2009 Jul;89(3):921-56 [19584317] Fertil Steril. 2011 May;95(6):2087-93 [21371703] Mol Endocrinol. 2011 May;25(5):833-46 [21436260] Proc Natl Acad Sci U S A. 2011 Aug 2;108(31):12898-903 [21768373] Reprod Toxicol. 2011 Dec;32(4):434-41 [21907787] J Clin Endocrinol Metab. 2012 Jan;97(1):E136-44 [22072740] Nat Rev Endocrinol. 2012 Apr;8(4):246-54 [22290357] PLoS One. 2012;7(4):e35538 [22514749] Endocrinology. 2012 Jun;153(6):2839-50 [22454148] Physiol Rev. 2012 Jul;92(3):1235-316 [22811428] Development. 2012 Nov;139(21):3986-96 [22992957] J Biol Chem. 2012 Oct 26;287(44):37171-84 [22923615] Curr Biol. 2012 Nov 6;22(21):1998-2007 [23041191] PLoS One. 2013;8(2):e56757 [23451081] Dis Model Mech. 2013 May;6(3):632-42 [23264563] Horm Behav. 2013 May;63(5):723-41 [23545474] Biol Reprod. 2013 Jun;88(6):142 [23616592] Biol Reprod. 2013 Aug;89(2):31 [23843229] Nat Med. 2013 Sep;19(9):1153-6 [23933983] Neuroscience. 2014 Sep 5;275:170-83 [24931761] Auton Neurosci. 2014 Oct;185:29-35 [25002406] Nat Cell Biol. 2000 Apr;2(4):219-25 [10783240] J Neurochem. 2000 Jul;75(1):1-8 [10854240] J Comp Neurol. 2000 Nov 27;427(4):593-603 [11056466] Reprod Toxicol. 2001 May-Jun;15(3):275-80 [11390172] Int J Dev Biol. 2001;45(3):597-605 [11417904] Toxicol Sci. 2002 May;67(1):63-74 [11961217] Mol Neurobiol. 2009 Oct;40(2):122-38 [19554483] Biol Reprod. 2009 Dec;81(6):1182-8 [19684334] Fertil Steril. 2010 May 15;93(8):2750-3 [20188365] Mol Cell Endocrinol. 2010 Aug 5;324(1-2):12-20 [20083157] Cold Spring Harb Perspect Biol. 2010 Dec;2(12):a003178 [20739412] Hum Reprod. 2011 Jan;26(1):167-75 [21106493] Behav Brain Res. 2011 Mar 1;217(2):347-53 [21070815] J Neurosci. 2011 Jan 12;31(2):426-38 [21228153] Reprod Biol Endocrinol. 2011;9:14 [21272326] J Neurosci. 2011 Feb 23;31(8):2974-82 [21414919] Exp Neurol. 2014 Nov;261:802-11 [25218043] Mol Cell Endocrinol. 2014 Nov;397(1-2):4-14 [25289807] Science. 2002 Jun 21;296(5576):2185-8 [12077405] J Cell Biol. 2003 Feb 17;160(4):597-604 [12591917] J Reprod Fertil. 1969 Jul;19(2):239-45 [5793460] J Reprod Fertil. 1972 Mar;28(3):453-6 [5018060] J Reprod Fertil. 1975 Dec;45(3):437-48 [1206643] Nature. 1976 Dec 2;264(5585):461-3 [794737] Biol Reprod. 1984 Jun;30(5):1135-41 [6733206] Biol Reprod. 1987 Feb;36(1):211-25 [3567276] Biochemistry. 1991 Sep 24;30(38):9143-53 [1892825] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1210/en.2015-1389 ER - TY - JOUR T1 - Under-reporting and Poor Adherence to Monitoring Guidelines for Severe Cases of Isoniazid Hepatotoxicity. AN - 1706208657; 25724701 AB - Isoniazid is a leading cause of liver injury but it is not clear how many cases are reported or how many clinicians and patients adhere to American Thoracic Society (ATS) guidelines. We collected data on cases of isoniazid hepatotoxicity and assessed adherence to ATS guidelines and reports to the Centers for Disease Control's (CDC) isoniazid severe adverse events program. We analyzed Drug-Induced Liver Injury Network (DILIN) cases considered definite, highly likely, or probable for isoniazid injury from 2004 through 2013. We assessed the delays in isoniazid discontinuance according to ATS criteria and hepatotoxicity severity by Severity Index Score. We checked reporting to the CDC by matching cases based on age, latency, indication, reporting period, and comorbidities. Isoniazid was the second most commonly reported agent in the DILIN, with 69 cases; 60 of these met inclusion criteria. The median age of cases was 49 years (range, 4-68 y), 70% were female, 97% had latent tuberculosis, and 62% were hospitalized. Patients took a median of 9 days to stop taking isoniazid (range, 0-99 days). Thirty-three cases (55%) continued taking isoniazid for more than 7 days after the ATS criteria for stopping were met. Twenty-four cases (40%) continued isoniazid for more than 14 days after meeting criteria for stopping. A delay in stopping was associated with more severe injury (P < .05). Of 13 patients who died or underwent liver transplantation, 9 (70%) continued taking isoniazid for more than 7 days after meeting criteria for stopping. Only 1 of 25 cases of isoniazid hepatotoxicity eligible for reporting to the CDC was reported. Poor adherence to ATS guidelines is common in cases of hepatotoxicity and is associated with more severe outcomes including hospitalization, death, and liver transplantation. Isoniazid continues to be a leading cause of DILI in the United States, and its hepatotoxicity is under-reported significantly. Copyright © 2015 AGA Institute. Published by Elsevier Inc. All rights reserved. JF - Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association AU - Hayashi, Paul H AU - Fontana, Robert J AU - Chalasani, Naga P AU - Stolz, Andrew A AU - Talwalkar, Jay A AU - Navarro, Victor J AU - Lee, William M AU - Davern, Timothy J AU - Kleiner, David E AU - Gu, Jiezhun AU - Hoofnagle, Jay H AU - US Drug-Induced Liver Injury Network Investigators AD - Division of Gastroenterology and Hepatology, University of North Carolina, Chapel Hill, North Carolina. Electronic address: paul_hayashi@med.unc.edu. ; Division of Gastroenterology, University of Michigan, Ann Arbor, Michigan. ; Division of Gastroenterology, Indiana University School of Medicine, Indianapolis, Indiana. ; Division of Gastroenterology, University of Southern California, Los Angeles, California. ; Division of Gastroenterology, Mayo Clinic, Rochester, Minnesota. ; Division of Gastroenterology, Einstein Healthcare Network and University of Pennsylvania, Philadelphia, Pennsylvania. ; Division of Gastroenterology, University of Texas, Southwestern Medical Center, Dallas, Texas. ; Division of Gastroenterology, California Pacific Medical Center, San Francisco, California. ; Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. ; Duke Clinical Research Institute, Duke University, Durham, North Carolina. ; Liver Disease Research Branch, Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. ; US Drug-Induced Liver Injury Network Investigators Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 1676 EP - 82.e1 VL - 13 IS - 9 KW - Antitubercular Agents KW - 0 KW - Isoniazid KW - V83O1VOZ8L KW - Index Medicus KW - Drug-Induced Liver Injury KW - Tuberculosis KW - Antibiotics KW - Adverse Reaction KW - Hepatotoxicity KW - United States KW - Young Adult KW - Prospective Studies KW - Humans KW - Adult KW - Retrospective Studies KW - Aged KW - Middle Aged KW - Child KW - Adolescent KW - Male KW - Female KW - Child, Preschool KW - Chemical and Drug Induced Liver Injury -- pathology KW - Chemical and Drug Induced Liver Injury -- epidemiology KW - Guideline Adherence KW - Adverse Drug Reaction Reporting Systems KW - Antitubercular Agents -- administration & dosage KW - Health Services Research KW - Drug-Related Side Effects and Adverse Reactions -- pathology KW - Drug-Related Side Effects and Adverse Reactions -- epidemiology KW - Isoniazid -- adverse effects KW - Antitubercular Agents -- adverse effects KW - Isoniazid -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1706208657?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+gastroenterology+and+hepatology+%3A+the+official+clinical+practice+journal+of+the+American+Gastroenterological+Association&rft.atitle=Under-reporting+and+Poor+Adherence+to+Monitoring+Guidelines+for+Severe+Cases+of+Isoniazid+Hepatotoxicity.&rft.au=Hayashi%2C+Paul+H%3BFontana%2C+Robert+J%3BChalasani%2C+Naga+P%3BStolz%2C+Andrew+A%3BTalwalkar%2C+Jay+A%3BNavarro%2C+Victor+J%3BLee%2C+William+M%3BDavern%2C+Timothy+J%3BKleiner%2C+David+E%3BGu%2C+Jiezhun%3BHoofnagle%2C+Jay+H%3BUS+Drug-Induced+Liver+Injury+Network+Investigators&rft.aulast=Hayashi&rft.aufirst=Paul&rft.date=2015-09-01&rft.volume=13&rft.issue=9&rft.spage=1676&rft.isbn=&rft.btitle=&rft.title=Clinical+gastroenterology+and+hepatology+%3A+the+official+clinical+practice+journal+of+the+American+Gastroenterological+Association&rft.issn=1542-7714&rft_id=info:doi/10.1016%2Fj.cgh.2015.02.024 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-09 N1 - Date created - 2015-08-22 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: BMC Infect Dis. 2013;13:566 [24295439] Am J Respir Crit Care Med. 2003 Aug 15;168(4):443-7 [12746255] Am J Respir Crit Care Med. 2003 Aug 15;168(4):412-3 [12912731] Am Rev Respir Dis. 1972 Sep;106(3):357-65 [5080707] Chest. 1975 Aug;68(2):181-90 [1080096] Ann Intern Med. 1976 Feb;84(2):181-92 [766682] Am J Gastroenterol. 1983 Jun;78(6):378-80 [6859018] MMWR Morb Mortal Wkly Rep. 1993 Jul 23;42(28):545-7 [8326947] JAMA. 1999 Mar 17;281(11):1014-8 [10086436] J Am Med Assoc. 1953 May 2;152(1):38-40 [13034525] Am Rev Respir Dis. 1965 Feb;91:297-8 [14253184] Dis Chest. 1955 Oct;28(4):462-4 [13261870] Am J Respir Crit Care Med. 2006 Apr 15;173(8):927-31 [16424442] Am J Respir Crit Care Med. 2006 Oct 15;174(8):935-52 [17021358] Drug Saf. 2009;32(1):55-68 [19132805] Liver Transpl. 2009 Jul;15(7):719-29 [19562705] Clin Infect Dis. 2010 Mar 15;50(6):833-9 [20156055] MMWR Morb Mortal Wkly Rep. 2010 Mar 5;59(8):224-9 [20203555] Sci Transl Med. 2012 Sep 19;4(152):152ra129 [22993296] Gastroenterology. 2013 Jun;144(7):1419-25, 1425.e1-3; quiz e19-20 [23419359] Comment In: Clin Gastroenterol Hepatol. 2015 Sep;13(9):1683-5 [25929538] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.cgh.2015.02.024 ER - TY - JOUR T1 - Health-related quality-of-life results from PALETTE: A randomized, double-blind, phase 3 trial of pazopanib versus placebo in patients with soft tissue sarcoma whose disease has progressed during or after prior chemotherapy-a European Organization for research and treatment of cancer soft tissue and bone sarcoma group global network study (EORTC 62072). AN - 1706208021; 26033286 AB - Health-related quality of life (HRQoL) was an exploratory endpoint in the PALETTE trial, a global, double-blind, randomized, phase 3 trial of pazopanib 800 mg versus placebo as second-line or later treatment for patients with advanced soft tissue sarcoma (N = 369). In that trial, progression-free survival was significantly improved in the pazopanib arm (median, 4.6 vs 1.6 months; hazard ratio, 0.31; P < .001), and toxicity of pazopanib consisted mainly of fatigue, diarrhea, nausea, weight loss, and hypertension. HRQoL was assessed using the 30-item core European Organization for the Research and Treatment of Cancer (EORTC) Quality-of-Life Questionnaire (EORTC QLQ-C30) at baseline and at weeks 4, 8, and 12 in patients who received treatment on protocol. The primary HRQoL endpoint was the EORTC QLQ-C30 global health status scale. Compliance with HRQoL assessments was good, ranging from 94% at baseline to 81% at week 12. Differences in scores on the EORTC QLQ-C30 global health status subscale between the 2 treatment arms were not statistically significant and did not exceed the predetermined, minimal clinically important difference of 10 points (P = .291; maximum difference, 3.8 points). Among the other subscales, the pazopanib arm reported significantly worse symptom scores for diarrhea (P < .001) loss of appetite (P < .001), nausea/vomiting (P < .001), and fatigue (P = .012). In general, HRQoL scores tended to decline over time in both arms. HRQoL did not improve with the receipt of pazopanib. However, the observed improvement in progression-free survival without impairment of HRQoL was considered a meaningful result. The toxicity profile of pazopanib was reflected in the patients' self-reported symptoms but did not translate into significantly worse overall global health status during treatment. © 2015 American Cancer Society. JF - Cancer AU - Coens, Corneel AU - van der Graaf, Winette T A AU - Blay, Jean-Yves AU - Chawla, Sant P AU - Judson, Ian AU - Sanfilippo, Roberta AU - Manson, Stephanie C AU - Hodge, Rachel A AU - Marreaud, Sandrine AU - Prins, Judith B AU - Lugowska, Iwona AU - Litière, Saskia AU - Bottomley, Andrew AD - Department of Biostatistics, European Organization for Research and Treatment of Cancer, Brussels, Belgium. ; Department of Medical Oncology, Radboud University Medical Center, Nijmegen, the Netherlands. ; Centre Léon Bérard, Université Claude Bernard Lyon, Lyon, France. ; Sarcoma Oncology Center, Santa Monica Oncology Center, Santa Monica, California. ; Sarcoma Unit, Royal Marsden Hospital, London, United Kingdom. ; National Cancer Institute of Milan, Foundation for the Scientific Institute for Research, Hospitalization, and Health Care, Milan, Italy. ; GlaxoSmithKline Oncology, Uxbridge, United Kingdom. ; Medical and Pharmacovigilance Department, European Organization for Research and Treatment of Cancer, Brussels, Belgium. ; Department of Medical Psychology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. ; Maria Sklodowska Curie Memorial Cancer Center and Institute of Oncology, Warsaw, Poland. Y1 - 2015/09/01/ PY - 2015 DA - 2015 Sep 01 SP - 2933 EP - 2941 VL - 121 IS - 17 KW - Angiogenesis Inhibitors KW - 0 KW - Pyrimidines KW - Sulfonamides KW - pazopanib KW - 7RN5DR86CK KW - Abridged Index Medicus KW - Index Medicus KW - randomized clinical trial KW - advanced KW - quality of life KW - soft tissue sarcoma KW - Young Adult KW - Disease-Free Survival KW - Double-Blind Method KW - Humans KW - Quality of Life KW - Aged KW - Drug Resistance, Neoplasm KW - Kaplan-Meier Estimate KW - Aged, 80 and over KW - Adult KW - Treatment Outcome KW - Middle Aged KW - Adolescent KW - Female KW - Male KW - Proportional Hazards Models KW - Angiogenesis Inhibitors -- therapeutic use KW - Sarcoma -- mortality KW - Pyrimidines -- therapeutic use KW - Sarcoma -- drug therapy KW - Sulfonamides -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1706208021?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Health-related+quality-of-life+results+from+PALETTE%3A+A+randomized%2C+double-blind%2C+phase+3+trial+of+pazopanib+versus+placebo+in+patients+with+soft+tissue+sarcoma+whose+disease+has+progressed+during+or+after+prior+chemotherapy-a+European+Organization+for+research+and+treatment+of+cancer+soft+tissue+and+bone+sarcoma+group+global+network+study+%28EORTC+62072%29.&rft.au=Coens%2C+Corneel%3Bvan+der+Graaf%2C+Winette+T+A%3BBlay%2C+Jean-Yves%3BChawla%2C+Sant+P%3BJudson%2C+Ian%3BSanfilippo%2C+Roberta%3BManson%2C+Stephanie+C%3BHodge%2C+Rachel+A%3BMarreaud%2C+Sandrine%3BPrins%2C+Judith+B%3BLugowska%2C+Iwona%3BLiti%C3%A8re%2C+Saskia%3BBottomley%2C+Andrew&rft.aulast=Coens&rft.aufirst=Corneel&rft.date=2015-09-01&rft.volume=121&rft.issue=17&rft.spage=2933&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=1097-0142&rft_id=info:doi/10.1002%2Fcncr.29426 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-04 N1 - Date created - 2015-08-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Comment In: Cancer. 2015 Sep 1;121(17):2868-70 [26033391] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/cncr.29426 ER - TY - JOUR T1 - Curcumin effectively inhibits oncogenic NF-κB signaling and restrains stemness features in liver cancer. AN - 1705476037; 25937435 AB - The cancer stem cells (CSCs) have important therapeutic implications for multi-resistant cancers including hepatocellular carcinoma (HCC). Among the key pathways frequently activated in liver CSCs is NF-κB signaling. We evaluated the CSCs-depleting potential of NF-κB inhibition in liver cancer achieved by the IKK inhibitor curcumin, RNAi and specific peptide SN50. The effects on CSCs were assessed by analysis of side population (SP), sphere formation and tumorigenicity. Molecular changes were determined by RT-qPCR, global gene expression microarray, EMSA, and Western blotting. HCC cell lines exposed to curcumin exhibited differential responses to curcumin and were classified as sensitive and resistant. In sensitive lines, curcumin-mediated induction of cell death was directly related to the extent of NF-κB inhibition. The treatment also led to a selective CSC-depletion as evidenced by a reduced SP size, decreased sphere formation, down-regulation of CSC markers and suppressed tumorigenicity. Similarly, NF-κB inhibition by SN50 and siRNA against p65 suppressed tumor cell growth. In contrast, curcumin-resistant cells displayed a paradoxical increase in proliferation and expression of CSC markers. Mechanistically, an important component of the CSC-depleting activity of curcumin could be attributed to a NF-κB-mediated HDAC inhibition. Co-administration of the class I/II HDAC inhibitor trichostatine sensitized resistant cells to curcumin. Further, integration of a predictive signature of curcumin sensitivity with human HCC database indicated that HCCs with poor prognosis and progenitor features are most likely to benefit from NF-κB inhibition. These results demonstrate that blocking NF-κB can specifically target CSC populations and suggest a potential for combined inhibition of NF-κB and HDAC signaling for treatment of liver cancer patients with poor prognosis. Copyright © 2015 European Association for the Study of the Liver. All rights reserved. JF - Journal of hepatology AU - Marquardt, Jens U AU - Gomez-Quiroz, Luis AU - Arreguin Camacho, Lucrecia O AU - Pinna, Federico AU - Lee, Yun-Han AU - Kitade, Mitsuteru AU - Domínguez, Mayrel Palestino AU - Castven, Darko AU - Breuhahn, Kai AU - Conner, Elizabeth A AU - Galle, Peter R AU - Andersen, Jesper B AU - Factor, Valentina M AU - Thorgeirsson, Snorri S AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Bethesda, USA; Department of Medicine I, Johannes Gutenberg University, Mainz, Germany. Electronic address: marquarj@uni-mainz.de. ; Departamento de Ciencias de la Salud, División de Ciencias Biológicas y de la Salud, Universidad Autónoma Metropolitana-Iztapalapa, Mexico. ; Department of Medicine I, Johannes Gutenberg University, Mainz, Germany. ; Institute of Pathology, University Hospital Heidelberg, Heidelberg, Germany. ; Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Bethesda, USA. ; Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Ole Maaløes Vej 5, 2200 Copenhagen N, Denmark. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 661 EP - 669 VL - 63 IS - 3 KW - Antineoplastic Agents KW - 0 KW - Hydroxamic Acids KW - NF-kappa B KW - trichostatin A KW - 3X2S926L3Z KW - Histone Deacetylases KW - EC 3.5.1.98 KW - Curcumin KW - IT942ZTH98 KW - Index Medicus KW - Liver cancer KW - Histone deacetylases KW - Cancer stem cells KW - NF-κB KW - Hepatocarcinogenesis KW - Animals KW - Humans KW - Histone Deacetylases -- physiology KW - Mice KW - Cell Line, Tumor KW - Hydroxamic Acids -- pharmacology KW - Liver Neoplasms -- pathology KW - Liver Neoplasms -- drug therapy KW - Signal Transduction -- drug effects KW - NF-kappa B -- physiology KW - Antineoplastic Agents -- pharmacology KW - Neoplastic Stem Cells -- drug effects KW - NF-kappa B -- antagonists & inhibitors KW - Curcumin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1705476037?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+hepatology&rft.atitle=Curcumin+effectively+inhibits+oncogenic+NF-%CE%BAB+signaling+and+restrains+stemness+features+in+liver+cancer.&rft.au=Marquardt%2C+Jens+U%3BGomez-Quiroz%2C+Luis%3BArreguin+Camacho%2C+Lucrecia+O%3BPinna%2C+Federico%3BLee%2C+Yun-Han%3BKitade%2C+Mitsuteru%3BDom%C3%ADnguez%2C+Mayrel+Palestino%3BCastven%2C+Darko%3BBreuhahn%2C+Kai%3BConner%2C+Elizabeth+A%3BGalle%2C+Peter+R%3BAndersen%2C+Jesper+B%3BFactor%2C+Valentina+M%3BThorgeirsson%2C+Snorri+S&rft.aulast=Marquardt&rft.aufirst=Jens&rft.date=2015-09-01&rft.volume=63&rft.issue=3&rft.spage=661&rft.isbn=&rft.btitle=&rft.title=Journal+of+hepatology&rft.issn=1600-0641&rft_id=info:doi/10.1016%2Fj.jhep.2015.04.018 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-08 N1 - Date created - 2015-08-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nature. 2004 Oct 28;431(7012):1112-7 [15475948] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517] Nat Med. 2006 Apr;12(4):410-6 [16532004] Eur J Cancer. 2006 Apr;42(6):779-84 [16530406] Cancer Cell. 2010 Apr 13;17(4):333-47 [20385359] J Biol Chem. 2010 Jul 30;285(31):23590-7 [20519513] J Hepatol. 2010 Sep;53(3):568-77 [20646772] Sci Transl Med. 2010 Oct 20;2(54):54ra77 [20962331] Cancer Res. 2010 Nov 1;70(21):8264-9 [20959491] Cell Res. 2011 Jan;21(1):159-68 [21187858] Nat Rev Gastroenterol Hepatol. 2011 Feb;8(2):108-18 [21293511] Gastroenterology. 2011 May;140(5):1410-26 [21406195] J Clin Invest. 2011 Jul;121(7):2781-93 [21701067] J Biol Chem. 2011 Sep 30;286(39):34036-50 [21816815] J Clin Invest. 2011 Oct;121(10):3804-9 [21965337] Breast Cancer Res. 2011;13(4):214 [21867572] Hepatology. 2011 Sep 2;54(3):1031-42 [21618577] Cell. 2012 Mar 30;149(1):36-47 [22464322] Lancet. 2012 Mar 31;379(9822):1245-55 [22353262] Biochim Biophys Acta. 2012 Jun;1822(6):942-51 [22386877] Cell Stem Cell. 2012 Jun 14;10(6):717-28 [22704512] Lancet Oncol. 2013 Jan;14(1):7-8 [23182626] Cancer Prev Res (Phila). 2013 May;6(5):387-400 [23466484] Cancer Cell. 2013 May 13;23(5):647-59 [23602409] J Biol Chem. 2008 May 23;283(21):14581-9 [18348981] Nature. 2008 Jun 5;453(7196):807-11 [18432192] Cancer Lett. 2008 Aug 28;267(2):182-8 [18479806] Nat Med. 2008 Aug;14(8):814 [18685595] Ann N Y Acad Sci. 2009 Feb;1155:206-21 [19250206] Front Biosci (Schol Ed). 2009;1:45-60 [19482682] Hepatology. 2009 Oct;50(4):1251-62 [19670424] Cold Spring Harb Perspect Biol. 2009 Nov;1(5):a000141 [20066113] Mol Cancer. 2009;8:129 [20030852] Cancer Cell. 2010 Mar 16;17(3):286-97 [20227042] N Engl J Med. 2013 Jun 13;368(24):2316-8 [23758237] Cancer Cell. 2013 Oct 14;24(4):423-37 [24054986] Cell. 2013 Nov 7;155(4):750-64 [24209616] J Clin Invest. 2014 Feb;124(2):528-42 [24382349] Cell Stem Cell. 2014 Mar 6;14(3):275-91 [24607403] Stem Cells. 2014 Apr;32(4):844-51 [24214290] Cancer Lett. 2014 May 1;346(2):197-205 [24463298] Nat Rev Cancer. 2002 Apr;2(4):301-10 [12001991] Cancer Res. 2003 Jan 1;63(1):25-30 [12517772] Nature. 2003 Jun 5;423(6940):659-63 [12789343] Hepatology. 2004 Sep;40(3):667-76 [15349906] Nature. 2004 Sep 23;431(7007):461-6 [15329734] Nature. 2006 May 25;441(7092):431-6 [16724054] N Engl J Med. 2006 Sep 21;355(12):1253-61 [16990388] Cancer Res. 2006 Oct 1;66(19):9339-44 [16990346] Hepatology. 2007 Aug;46(2):590-7 [17661407] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jhep.2015.04.018 ER - TY - JOUR T1 - A national multicenter phase 2 study of prostate-specific antigen (PSA) pox virus vaccine with sequential androgen ablation therapy in patients with PSA progression: ECOG 9802. AN - 1705475210; 25533418 AB - E9802 was a phase 2 multi-institution study conducted to evaluate the safety and effectiveness of vaccinia and fowlpox prostate-specific antigen (PSA) vaccine (step 1) followed by combination with androgen ablation therapy (step 2) in patients with PSA progression without visible metastasis. To test the hypothesis that vaccine therapy in this early disease setting will be safe and have a biochemical effect that would support future studies of immunotherapy in patients with minimal disease burden. Patients who had PSA progression following local therapy were treated with PROSTVAC-V (vaccinia)/TRICOM on cycle 1 followed by PROSTVAC-F (fowlpox)/TRICOM for subsequent cycles in combination with granulocyte-macrophage colony-stimulating factor (step 1). Androgen ablation was added on progression (step 2). Step 1 primary end points included progression at 6 mo and characterization of change in PSA velocity pretreatment to post-treatment. Step 2 end points included PSA response with combined vaccine and androgen ablation. In step 1, 25 of 40 eligible patients (63%) were progression free at 6 mo after registration (90% confidence interval [CI], 48-75). The median pretreatment PSA velocity was 0.13 log(PSA)/mo, in contrast to median postregistration velocity of 0.09 log(PSA)/mo (p=0.02), which is an increase in median PSA doubling time from 5.3 mo to 7.7 mo. No grade ≥4 treatment-related toxicity was observed. In the 27 patients eligible and treated for step 2, 20 patients achieved a complete response (CR) at 7 mo (CR rate: 74%; 90% CI, 57-87). Although supportive of larger studies in the cooperative group setting, this study is limited by the small number of patients and the absence of a control group as in a phase 3 study. A viral PSA vaccine can be administered safely in the multi-institutional cooperative group setting to patients with minimal disease volume alone and combined with androgen ablation, supporting the feasibility of future phase 3 studies in this population. These data support consideration of vaccine therapy earlier in the course of prostate cancer progression with minimal disease burden in future studies of vaccine approaches in earlier stages of disease. Copyright © 2014 European Association of Urology. All rights reserved. JF - European urology AU - DiPaola, Robert S AU - Chen, Yu-Hui AU - Bubley, Glenn J AU - Stein, Mark N AU - Hahn, Noah M AU - Carducci, Michael A AU - Lattime, Edmund C AU - Gulley, James L AU - Arlen, Philip M AU - Butterfield, Lisa H AU - Wilding, George AD - Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA. Electronic address: Robert.DiPaola@rutgers.edu. ; Dana-Farber Cancer Institute, Boston, MA, USA. ; Beth Israel Deaconess Medical Center, Boston, MA, USA. ; Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA. ; Indiana University Simon Cancer Center, Indianapolis, IN, USA. ; Johns Hopkins University, Baltimore, MD, USA. ; National Cancer Institute, Bethesda, MD, USA. ; University of Pittsburgh, Pittsburgh, PA, USA. ; UW Carbone Cancer Center, University of Wisconsin, Madison, WI, USA. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 365 EP - 371 VL - 68 IS - 3 KW - Androgen Antagonists KW - 0 KW - Cancer Vaccines KW - PROSTVAC KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Kallikreins KW - EC 3.4.21.- KW - kallikrein-related peptidase 3, human KW - Prostate-Specific Antigen KW - EC 3.4.21.77 KW - Index Medicus KW - Prostate cancer KW - Vaccine KW - PSA KW - Pox virus KW - Vaccinia virus -- immunology KW - Prostatectomy KW - Combined Modality Therapy KW - Humans KW - Disease Progression KW - Aged KW - Middle Aged KW - Fowlpox virus -- immunology KW - Granulocyte-Macrophage Colony-Stimulating Factor -- therapeutic use KW - Male KW - Kallikreins -- immunology KW - Cancer Vaccines -- immunology KW - Kallikreins -- blood KW - Androgen Antagonists -- therapeutic use KW - Prostate-Specific Antigen -- immunology KW - Prostate-Specific Antigen -- blood KW - Cancer Vaccines -- therapeutic use KW - Prostatic Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1705475210?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+urology&rft.atitle=A+national+multicenter+phase+2+study+of+prostate-specific+antigen+%28PSA%29+pox+virus+vaccine+with+sequential+androgen+ablation+therapy+in+patients+with+PSA+progression%3A+ECOG+9802.&rft.au=DiPaola%2C+Robert+S%3BChen%2C+Yu-Hui%3BBubley%2C+Glenn+J%3BStein%2C+Mark+N%3BHahn%2C+Noah+M%3BCarducci%2C+Michael+A%3BLattime%2C+Edmund+C%3BGulley%2C+James+L%3BArlen%2C+Philip+M%3BButterfield%2C+Lisa+H%3BWilding%2C+George&rft.aulast=DiPaola&rft.aufirst=Robert&rft.date=2015-09-01&rft.volume=68&rft.issue=3&rft.spage=365&rft.isbn=&rft.btitle=&rft.title=European+urology&rft.issn=1873-7560&rft_id=info:doi/10.1016%2Fj.eururo.2014.12.010 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-06 N1 - Date created - 2015-08-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Curr Opin Urol. 2004 May;14(3):177-83 [15069309] J Clin Oncol. 2004 Jun 1;22(11):2122-32 [15169798] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11349-53 [8876138] Clin Cancer Res. 1999 Jul;5(7):1738-44 [10430077] Semin Oncol. 2005 Dec;32(6):549-55 [16338420] Adv Immunol. 2006;90:51-81 [16730261] J Clin Oncol. 2006 Aug 20;24(24):3984-90 [16921051] J Clin Oncol. 2009 Jul 20;27(21):3452-8 [19506162] J Clin Oncol. 2010 Mar 1;28(7):1099-105 [20100959] N Engl J Med. 2010 Jul 29;363(5):411-22 [20818862] Oncologist. 2010;15(9):969-75 [20798195] Clin Cancer Res. 2011 Feb 15;17(4):907-17 [21106727] Clin Adv Hematol Oncol. 2012 Nov;10(11):716-22 [23271258] N Engl J Med. 2013 Apr 4;368(14):1314-25 [23550669] Eur Urol. 2014 Mar;65(3):620-7 [23245686] BioDrugs. 2003;17(2):131-8 [12641491] Proc Natl Acad Sci U S A. 2001 Dec 4;98(25):14565-70 [11734652] Prostate. 2002 Oct 1;53(2):109-17 [12242725] Comment In: Eur Urol. 2015 Sep;68(3):372-3 [25766723] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.eururo.2014.12.010 ER - TY - JOUR T1 - Treatment results of pediatric nasopharyngeal carcinoma, NCI, Cairo University experience. AN - 1705007093; 26187402 AB - Investigate treatment outcome, prognostic factors and survival among selected group of Egyptian pediatric nasopharyngeal carcinoma patients. Thirty patients treated from non-metastatic nasopharyngeal carcinoma between 1997 and 2012 were retrospectively evaluated including: TNM staging, chemo-radiotherapy regimens. Survival analysis was done using Kaplan-Meier survival curves. Twenty-three males and 7 females (M:F 3.2:1) with median age of 14 years; 84% with stages III/IV. Neck node enlargement was reported in 90% (27/30). Induction chemotherapy followed by radiotherapy was implemented in 80% of patients. Mucositis (87%) was the commonest treatment related toxicity. Nineteen patients (63%) were in CR with a median FU of 69 months (range 24-160). Eleven patients had treatment local and distant failures (2 local, 7 distant and 2 local/distant) at a median FU of 24 and 34 months respectively. 5-year overall and event-free survival rates were 77% and 63% respectively. Prolonged OAP of RT⩾50 days, Hb<11g% and T4 stage affected EFS and OAS on UVA; while on MVA; prolonged OAP of RT⩾50 days (p=0.002) and T4 stage (p=0.004) affected EFS and only Hb<11g% (p=0.019) affected OAS. Late toxicity was reported in 70% of irradiated patients. Radio-chemotherapy management for pediatric NPC resulted in comparable treatment outcomes with tolerable late effects. Response adapted radio-chemotherapy regimens in addition to the potential use of IMRT should be recommended to decrease treatment related side effects. Prolonged OAP of RT⩾50 days and low Hb level were encountered as adverse prognostic factors; findings that need further investigation. Copyright © 2015 The Authors. Production and hosting by Elsevier B.V. All rights reserved. JF - Journal of the Egyptian National Cancer Institute AU - Khalil, Ehab M AU - Anwar, Manal M AD - Radiation Oncology & Nuclear Medicine Department, NCI, Cairo University, Egypt. Electronic address: Ehab.khalil@nci.cu.edu.eg. ; Public Health & Community Medicine, Faculty of Medicine, Beni-Sueif University, Egypt. Electronic address: M_anwarabdo@yahoo.com. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 119 EP - 128 VL - 27 IS - 3 SN - 1110-0362, 1110-0362 KW - Index Medicus KW - Pediatric KW - Treatment results KW - Nasopharyngeal carcinoma KW - Late toxicity KW - Kaplan-Meier Estimate KW - Disease-Free Survival KW - Hospitals, University KW - Humans KW - Treatment Outcome KW - Retrospective Studies KW - Prognosis KW - Follow-Up Studies KW - Child KW - Adolescent KW - Male KW - Female KW - Nasopharyngeal Neoplasms -- radiotherapy KW - Nasopharyngeal Neoplasms -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1705007093?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+Egyptian+National+Cancer+Institute&rft.atitle=Treatment+results+of+pediatric+nasopharyngeal+carcinoma%2C+NCI%2C+Cairo+University+experience.&rft.au=Khalil%2C+Ehab+M%3BAnwar%2C+Manal+M&rft.aulast=Khalil&rft.aufirst=Ehab&rft.date=2015-09-01&rft.volume=27&rft.issue=3&rft.spage=119&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+Egyptian+National+Cancer+Institute&rft.issn=11100362&rft_id=info:doi/10.1016%2Fj.jnci.2015.06.004 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-23 N1 - Date created - 2015-08-17 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jnci.2015.06.004 ER - TY - JOUR T1 - A Phase II Study of Sorafenib Combined With Cetuximab in EGFR-Expressing, KRAS-Mutated Metastatic Colorectal Cancer. AN - 1704352632; 25861837 AB - Mutations in the KRAS gene predict for resistance to anti-epidermal growth factor receptor (EGFR) therapies, including cetuximab. Upregulation of vascular endothelial growth factor (VEGF)-A has been implicated in resistance to anti-EGFR treatment. Abrogation of the VEGF and RAS/RAF/MEK/ERK pathways has the potential to restore cetuximab sensitivity. Adult patients with histologically documented, measurable, EGFR-expressing, KRAS-mutated metastatic colorectal cancer (mCRC) that had progressed after 5-fluorouracil-based regimens were treated with sorafenib 400 mg orally twice daily and intravenous cetuximab weekly in 28-day cycles. The primary endpoint was the response rate (complete response, partial response, and stable disease at 4 cycles). The secondary endpoints included plasma biomarker analysis of angiogenic cytokines and correlative imaging studies with dynamic contrast-enhanced magnetic resonance imaging and zirconium 89-panitumumab. Of the 30 patients enrolled, 26 were evaluable for response. Of the 26 patients evaluated, 4 had stable disease at 4 cycles and 1 had stable disease at 8 cycles. The median progression-free survival was 1.84 months. The common toxicities were rash, diarrhea, and liver enzyme elevations. Of the angiogenic cytokines evaluated, only the placental growth factor increased significantly with treatment (P < .0001). No pharmacodynamic parameters were associated with the treatment response. We report the results of a trial that combined cetuximab and sorafenib for the treatment of KRAS-mutated mCRC, with correlative imaging studies and pharmacodynamic angiogenic cytokine profiling as downstream markers of EGFR and VEGF receptor (VEGFR) signaling. No objective responses were observed. Additional development of biomarkers for patient selection is needed to evaluate combined EGFR and VEGFR blockade as a therapeutic option in KRAS-mutated CRC. Published by Elsevier Inc. JF - Clinical colorectal cancer AU - Do, Khanh AU - Cao, Liang AU - Kang, Zhigang AU - Turkbey, Baris AU - Lindenberg, Maria L AU - Larkins, Erin AU - Holkova, Beata AU - Steinberg, Seth M AU - Raffeld, Mark AU - Peer, Cody J AU - Figg, William D AU - Eugeni, Michelle AU - Jacobs, Paula AU - Choyke, Peter AU - Wright, John J AU - Doroshow, James H AU - Kummar, Shivaani AD - Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, MD. ; Center for Cancer Research, National Cancer Institute, Bethesda, MD. ; Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, MD. Electronic address: kummars@mail.nih.gov. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 154 EP - 161 VL - 14 IS - 3 KW - KRAS protein, human KW - 0 KW - Phenylurea Compounds KW - Vascular Endothelial Growth Factor A KW - Niacinamide KW - 25X51I8RD4 KW - sorafenib KW - 9ZOQ3TZI87 KW - Receptor, Epidermal Growth Factor KW - EC 2.7.10.1 KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - Cetuximab KW - PQX0D8J21J KW - Index Medicus KW - Antiangiogenic therapy KW - Biomarkers KW - Panitumumab imaging KW - Combination Therapy KW - Pharmacodynamics KW - Young Adult KW - Disease-Free Survival KW - Niacinamide -- administration & dosage KW - Humans KW - Niacinamide -- analogs & derivatives KW - Aged KW - Patient Selection KW - Phenylurea Compounds -- administration & dosage KW - Vascular Endothelial Growth Factor A -- antagonists & inhibitors KW - Aged, 80 and over KW - Adult KW - Cetuximab -- administration & dosage KW - Middle Aged KW - Female KW - Male KW - Receptor, Epidermal Growth Factor -- antagonists & inhibitors KW - Colorectal Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- pharmacology KW - Colorectal Neoplasms -- genetics KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Colorectal Neoplasms -- drug therapy KW - Proto-Oncogene Proteins p21(ras) -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1704352632?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+colorectal+cancer&rft.atitle=A+Phase+II+Study+of+Sorafenib+Combined+With+Cetuximab+in+EGFR-Expressing%2C+KRAS-Mutated+Metastatic+Colorectal+Cancer.&rft.au=Do%2C+Khanh%3BCao%2C+Liang%3BKang%2C+Zhigang%3BTurkbey%2C+Baris%3BLindenberg%2C+Maria+L%3BLarkins%2C+Erin%3BHolkova%2C+Beata%3BSteinberg%2C+Seth+M%3BRaffeld%2C+Mark%3BPeer%2C+Cody+J%3BFigg%2C+William+D%3BEugeni%2C+Michelle%3BJacobs%2C+Paula%3BChoyke%2C+Peter%3BWright%2C+John+J%3BDoroshow%2C+James+H%3BKummar%2C+Shivaani&rft.aulast=Do&rft.aufirst=Khanh&rft.date=2015-09-01&rft.volume=14&rft.issue=3&rft.spage=154&rft.isbn=&rft.btitle=&rft.title=Clinical+colorectal+cancer&rft.issn=1938-0674&rft_id=info:doi/10.1016%2Fj.clcc.2015.02.007 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-19 N1 - Date created - 2015-08-13 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.clcc.2015.02.007 ER - TY - JOUR T1 - Cannabis effects on driving lateral control with and without alcohol. AN - 1704347802; 26144593 AB - Effects of cannabis, the most commonly encountered non-alcohol drug in driving under the influence cases, are heavily debated. We aim to determine how blood Δ(9)-tetrahydrocannabinol (THC) concentrations relate to driving impairment, with and without alcohol. Current occasional (≥1×/last 3 months, ≤3days/week) cannabis smokers drank placebo or low-dose alcohol, and inhaled 500mg placebo, low (2.9%)-THC, or high (6.7%)-THC vaporized cannabis over 10min ad libitum in separate sessions (within-subject design, 6 conditions). Participants drove (National Advanced Driving Simulator, University of Iowa) simulated drives (∼0.8h duration). Blood, oral fluid (OF), and breath alcohol samples were collected before (0.17h, 0.42h) and after (1.4h, 2.3h) driving that occurred 0.5-1.3h after inhalation. We evaluated standard deviations of lateral position (lane weave, SDLP) and steering angle, lane departures/min, and maximum lateral acceleration. In N=18 completers (13 men, ages 21-37years), cannabis and alcohol increased SDLP. Blood THC concentrations of 8.2 and 13.1μg/L during driving increased SDLP similar to 0.05 and 0.08g/210L breath alcohol concentrations, the most common legal alcohol limits. Cannabis-alcohol SDLP effects were additive rather than synergistic, with 5μg/L THC+0.05g/210L alcohol showing similar SDLP to 0.08g/210L alcohol alone. Only alcohol increased lateral acceleration and the less-sensitive lane departures/min parameters. OF effectively documented cannabis exposure, although with greater THC concentration variability than paired blood samples. SDLP was a sensitive cannabis-related lateral control impairment measure. During drive blood THC ≥8.2μg/L increased SDLP similar to notably-impairing alcohol concentrations. Despite OF's screening value, OF variability poses challenges in concentration-based effects interpretation. Published by Elsevier Ireland Ltd. JF - Drug and alcohol dependence AU - Hartman, Rebecca L AU - Brown, Timothy L AU - Milavetz, Gary AU - Spurgin, Andrew AU - Pierce, Russell S AU - Gorelick, David A AU - Gaffney, Gary AU - Huestis, Marilyn A AD - Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, NIH, 251 Bayview Boulevard Ste 200 Rm 05A721, Baltimore, MD, USA; Program in Toxicology, University of Maryland Baltimore, 660 West Redwood Street, Baltimore, MD, USA. ; National Advanced Driving Simulator, University of Iowa, 2401 Oakdale Boulevard, Iowa City, IA, USA. ; College of Pharmacy, University of Iowa, Iowa City, IA, USA. ; Variable Solutions, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, NIH, 251 Bayview Boulevard Ste 200 Rm 05A721, Baltimore, MD, USA; Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA. ; Carver College of Medicine, University of Iowa, Iowa City, IA, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, NIH, 251 Bayview Boulevard Ste 200 Rm 05A721, Baltimore, MD, USA. Electronic address: mhuestis@intra.nida.nih.gov. Y1 - 2015/09/01/ PY - 2015 DA - 2015 Sep 01 SP - 25 EP - 37 VL - 154 KW - Ethanol KW - 3K9958V90M KW - Dronabinol KW - 7J8897W37S KW - Index Medicus KW - Alcohol KW - Driving KW - THC KW - Cannabis KW - Oral fluid KW - Lateral control KW - Young Adult KW - Drug Interactions KW - Computer Simulation KW - Humans KW - Adult KW - Administration, Inhalation KW - Male KW - Female KW - Breath Tests KW - Marijuana Smoking -- blood KW - Psychomotor Performance -- drug effects KW - Ethanol -- pharmacology KW - Marijuana Smoking -- adverse effects KW - Dronabinol -- pharmacology KW - Dronabinol -- blood KW - Dronabinol -- administration & dosage KW - Automobile Driving UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1704347802?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+and+alcohol+dependence&rft.atitle=Cannabis+effects+on+driving+lateral+control+with+and+without+alcohol.&rft.au=Hartman%2C+Rebecca+L%3BBrown%2C+Timothy+L%3BMilavetz%2C+Gary%3BSpurgin%2C+Andrew%3BPierce%2C+Russell+S%3BGorelick%2C+David+A%3BGaffney%2C+Gary%3BHuestis%2C+Marilyn+A&rft.aulast=Hartman&rft.aufirst=Rebecca&rft.date=2015-09-01&rft.volume=154&rft.issue=&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=Drug+and+alcohol+dependence&rft.issn=1879-0046&rft_id=info:doi/10.1016%2Fj.drugalcdep.2015.06.015 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-11 N1 - Date created - 2015-08-13 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Psychopharmacology (Berl). 2002 Mar;160(2):213-9 [11875640] Forensic Sci Int. 2003 Mar 12;132(1):18-25 [12689747] Accid Anal Prev. 2004 Mar;36(2):239-48 [14642878] Drug Alcohol Rev. 2003 Sep;22(3):309-15 [15385225] J Anal Toxicol. 1992 Sep-Oct;16(5):276-82 [1338215] J Pharmacol Exp Ther. 1995 Feb;272(2):560-9 [7853169] Addict Behav. 2005 Mar;30(3):619-26 [15718082] BMJ. 2005 Dec 10;331(7529):1371 [16321993] Drug Alcohol Depend. 2006 Nov 8;85(2):114-22 [16723194] Addiction. 2006 Nov;101(11):1614-21 [17034441] Forensic Sci Int. 2007 Aug 6;170(2-3):105-10 [17658711] Psychol Addict Behav. 2007 Sep;21(3):425-30 [17874895] Addiction. 2007 Dec;102(12):1910-7 [17916224] Addiction. 2008 Mar;103(3):452-61 [18190663] Traffic Inj Prev. 2008 Mar;9(1):11-21 [18338290] Curr Drug Saf. 2006 Jan;1(1):63-71 [18690916] J Anal Toxicol. 2008 Sep;32(7):470-7 [18713514] Am J Addict. 2009 May-Jun;18(3):185-93 [19340636] J Psychopharmacol. 2009 May;23(3):266-77 [18719045] Clin Chem. 2009 Nov;55(11):1910-31 [19745062] J Chromatogr A. 2010 Feb 26;1217(9):1513-21 [20083251] Accid Anal Prev. 2010 May;42(3):859-66 [20380913] J Psychoactive Drugs. 2010 Mar;42(1):19-30 [20464803] Accid Anal Prev. 2010 Nov;42(6):1855-65 [20728636] Psychopharmacology (Berl). 2011 Mar;214(2):391-401 [21049267] Accid Anal Prev. 2011 May;43(3):1197-203 [21376919] Clin Chem. 2011 Jun;57(6):805-10 [21350039] Anal Bioanal Chem. 2011 Sep;401(4):1273-83 [21727996] Epidemiol Rev. 2012;34:65-72 [21976636] Psychopharmacology (Berl). 2012 Feb;219(3):775-81 [21750898] BMJ. 2012;344:e536 [22323502] J Anal Toxicol. 2012 Jul;36(6):418-21 [22577111] Accid Anal Prev. 2013 Jan;50:879-86 [22871272] Clin Chem. 2013 Mar;59(3):478-92 [23220273] Clin Chem. 2013 Mar;59(3):519-26 [23449702] Drug Test Anal. 2013 Mar;5(3):156-65 [22887894] Clin Chem. 2013 Jul;59(7):1108-17 [23519966] Clin Chem. 2014 Apr;60(4):631-43 [24563491] Drug Alcohol Depend. 2014 Jul 1;140:137-44 [24831752] Hum Psychopharmacol. 2014 Jul;29(4):322-9 [24753058] J Drug Educ. 2013;43(2):183-201 [25068170] J Anal Toxicol. 2014 Oct;38(8):575-81 [25217549] Drug Alcohol Depend. 2014 Nov 1;144:231-8 [25287325] Exp Clin Psychopharmacol. 2014 Dec;22(6):484-93 [25347077] Accid Anal Prev. 2015 Jan;74:210-7 [25463962] Traffic Inj Prev. 2015;16(5):440-2 [25375366] Drug Test Anal. 2015 Mar;7(3):178-86 [24753449] Clin Chem. 2015 Jun;61(6):850-69 [26019183] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.drugalcdep.2015.06.015 ER - TY - JOUR T1 - Feasibility Study of a Novel Experimental Induction Protocol Combining B43-PAP (Anti-CD19) Immunotoxin With Standard Induction Chemotherapy in Children and Adolescents With Relapsed B-Lineage ALL: A Report From the Children's Oncology Group. AN - 1703718275; 26261894 AB - B43-pokeweed antiviral protein (B43-PAP) is a high-affinity anti-CD19 immunotoxin that is capable of causing apoptotic death in B-lineage leukemic cells with a drug-resistant phenotype. B43-PAP exhibited in vivo antileukemic activity in preclinical studies as well as on a single-agent phase I clinical trial. This pediatric phase I/II study evaluated the toxicity profile and efficacy of B43-PAP immunotoxin in combination with standard induction chemotherapy in children and adolescents with relapsed CD19-positive B-lineage acute lymphoblastic leukemia (B-ALL). Pharmacokinetic profile and immunogenicity of B43-PAP were assessed. B43-PAP in combination with standard 3 and 4-drug induction chemotherapy was administered on days 9-13 and 21-25 of a 28-day treatment course with vincristine, prednisone, L-asparaginase, daunomycin, and intrathecal methotrexate. Thirty patients with relapsed B-ALL were enrolled on study CCG-0957. Grade III/IV nonhematologic dose-limiting toxicities were encountered in 4 patients evaluable for toxicity and included myalgias, motor dysfunction, pulmonary toxicity, and elevated liver transaminase. Dose-limiting toxicities occurred only with the 4-drug regimen. Fourteen patients achieved a complete remission at the end of induction among the 20 patients evaluable for response. B43-PAP in combination with standard induction chemotherapy can be safely administered and exhibits clinical antileukemic activity against relapsed B-ALL. JF - Journal of immunotherapy (Hagerstown, Md. : 1997) AU - Meany, Holly J AU - Seibel, Nita L AU - Krailo, Mark AU - Villaluna, Doojduen AU - Chen, Zhengjia AU - Gaynon, Paul AU - Neglia, Joseph P AU - Park, Julie R AU - Hutchinson, Raymond AU - Sato, Judith K AU - Wells, Robert J AU - Woods, William G AU - Reaman, Gregory AD - *Department of Pediatric Hematology-Oncology, Children's National Medical Center, George Washington University School of Medicine and Public Health, Washington, DC †Clinical Investigations Branch, Cancer Therapy Evaluation Program, NCI, Bethesda ¶¶Center for Drug Evaluation and Research, US Food and Drug Administration, Silver Spring, MD ‡Keck School of Medicine, University of Southern California ¶Division of Hematology-Oncology, Children's Hospital Los Angeles, Los Angeles §Children's Oncology Group, Arcadia ‡‡Department of Pediatrics, City of Hope National Medical Center, Duarte, CA ∥Department of Biostatistics and Bioinformatics, Emory University ∥∥Aflac Cancer and Blood Disorder Center, Children's Healthcare of Atlanta/Emory University, Atlanta, GA #Department of Pediatrics, University of Minnesota Medical School, Minneapolis, MN **Department of Pediatrics, Seattle Children's Hospital, University of Washington, Seattle, WA ††Pediatric Hematology-Oncology, C.S. Mott Children's Hospital, Ann Arbor, MI §§Division of Pediatrics, Children's Cancer Hospital at the University of Texas M.D. Anderson Cancer Center, Houston, TX. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 299 EP - 305 VL - 38 IS - 7 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD19 KW - Antineoplastic Agents KW - Immunotoxins KW - Ribosome Inactivating Proteins, Type 1 KW - pokeweed antiviral protein KW - EC 3.2.2.22 KW - Index Medicus KW - Feasibility Studies KW - Induction Chemotherapy -- methods KW - Humans KW - Drug Therapy, Combination -- methods KW - Child KW - Adolescent KW - Male KW - Female KW - Child, Preschool KW - Antibodies, Monoclonal -- immunology KW - Antigens, CD19 -- immunology KW - Immunotoxins -- immunology KW - Ribosome Inactivating Proteins, Type 1 -- immunology KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- immunology KW - B-Lymphocytes -- immunology KW - Antineoplastic Agents -- therapeutic use KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1703718275?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunotherapy+%28Hagerstown%2C+Md.+%3A+1997%29&rft.atitle=Feasibility+Study+of+a+Novel+Experimental+Induction+Protocol+Combining+B43-PAP+%28Anti-CD19%29+Immunotoxin+With+Standard+Induction+Chemotherapy+in+Children+and+Adolescents+With+Relapsed+B-Lineage+ALL%3A+A+Report+From+the+Children%27s+Oncology+Group.&rft.au=Meany%2C+Holly+J%3BSeibel%2C+Nita+L%3BKrailo%2C+Mark%3BVillaluna%2C+Doojduen%3BChen%2C+Zhengjia%3BGaynon%2C+Paul%3BNeglia%2C+Joseph+P%3BPark%2C+Julie+R%3BHutchinson%2C+Raymond%3BSato%2C+Judith+K%3BWells%2C+Robert+J%3BWoods%2C+William+G%3BReaman%2C+Gregory&rft.aulast=Meany&rft.aufirst=Holly&rft.date=2015-09-01&rft.volume=38&rft.issue=7&rft.spage=299&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunotherapy+%28Hagerstown%2C+Md.+%3A+1997%29&rft.issn=1537-4513&rft_id=info:doi/10.1097%2FCJI.0000000000000088 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-04 N1 - Date created - 2015-08-12 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Oncol. 2005 Nov 1;23(31):7942-50 [16258094] Br J Haematol. 2005 Jul;130(1):67-75 [15982346] Br J Haematol. 2006 Nov;135(4):500-8 [17061978] Blood. 2007 Feb 1;109(3):926-35 [17003380] J Clin Oncol. 2007 Dec 20;25(36):5800-7 [18089878] Br J Haematol. 2000 Mar;108(3):531-43 [10759711] Eur J Haematol. 2015 Feb;94(2):99-108 [24981395] Curr Opin Pediatr. 2008 Feb;20(1):17-22 [18197034] Blood. 2008 Mar 1;111(5):2548-55 [18039957] Leuk Lymphoma. 2008 Jun;49(6):1142-54 [18569638] J Clin Oncol. 2008 Aug 1;26(22):3756-62 [18669463] J Clin Oncol. 2008 Aug 20;26(24):3971-8 [18711187] Lancet Oncol. 2008 Sep;9(9):873-83 [18760243] Cancer Res. 2008 Oct 1;68(19):8049-57 [18829563] Curr Oncol Rep. 2008 Nov;10(6):453-8 [18928659] Pediatr Blood Cancer. 2009 Feb;52(2):177-81 [18816698] Leukemia. 2008 Dec;22(12):2142-50 [18818707] Semin Hematol. 2009 Jan;46(1):52-63 [19100368] J Clin Oncol. 2010 Feb 1;28(4):648-54 [19841326] Curr Opin Oncol. 2013 Nov;25(6):701-6 [24097105] Leuk Lymphoma. 2014 Apr;55(4):737-48 [23841506] N Engl J Med. 2014 Oct 16;371(16):1507-17 [25317870] Clin Cancer Res. 1999 Dec;5(12):3906-13 [10632319] Clin Cancer Res. 1999 Dec;5(12):3920-7 [10632321] Br J Haematol. 2003 Nov;123(3):396-405 [14616997] Blood. 2004 Jul 1;104(1):178-83 [15001473] J Exp Med. 1986 Feb 1;163(2):347-68 [3511171] Blood. 1988 Jan;71(1):13-29 [3257143] Blood. 1990 Nov 15;76(10):1908-23 [2242419] J Immunol Methods. 1991 Feb 15;136(2):221-37 [1705571] Blood. 1991 Sep 1;78(5):1166-72 [1878583] Blood. 1992 May 15;79(10):2649-61 [1375109] Blood. 1993 Feb 1;81(3):602-9 [8427957] Br J Haematol. 1993 Nov;85(3):435-8 [8136262] Blood. 1995 Dec 1;86(11):4228-33 [7492781] Leuk Lymphoma. 1995 Aug;18(5-6):385-97 [8528044] Haematologica. 1995 Nov-Dec;80(6):546-56 [8647523] J Clin Oncol. 1999 Feb;17(2):445-55 [10080584] Leuk Lymphoma. 1999 Mar;33(1-2):101-6 [10194126] Cancer. 2005 Jan 15;103(2):368-76 [15599932] J Clin Oncol. 2006 Jul 1;24(19):3150-6 [16717292] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/CJI.0000000000000088 ER - TY - JOUR T1 - Model Organisms in G Protein-Coupled Receptor Research. AN - 1703702481; 25979002 AB - The study of G protein-coupled receptors (GPCRs) has benefited greatly from experimental approaches that interrogate their functions in controlled, artificial environments. Working in vitro, GPCR receptorologists discovered the basic biologic mechanisms by which GPCRs operate, including their eponymous capacity to couple to G proteins; their molecular makeup, including the famed serpentine transmembrane unit; and ultimately, their three-dimensional structure. Although the insights gained from working outside the native environments of GPCRs have allowed for the collection of low-noise data, such approaches cannot directly address a receptor's native (in vivo) functions. An in vivo approach can complement the rigor of in vitro approaches: as studied in model organisms, it imposes physiologic constraints on receptor action and thus allows investigators to deduce the most salient features of receptor function. Here, we briefly discuss specific examples in which model organisms have successfully contributed to the elucidation of signals controlled through GPCRs and other surface receptor systems. We list recent examples that have served either in the initial discovery of GPCR signaling concepts or in their fuller definition. Furthermore, we selectively highlight experimental advantages, shortcomings, and tools of each model organism. U.S. Government work not protected by U.S. copyright. JF - Molecular pharmacology AU - Langenhan, Tobias AU - Barr, Maureen M AU - Bruchas, Michael R AU - Ewer, John AU - Griffith, Leslie C AU - Maiellaro, Isabella AU - Taghert, Paul H AU - White, Benjamin H AU - Monk, Kelly R AD - Institute of Physiology, Department of Neurophysiology (T.L.), and Institute of Pharmacology and Toxicology, Rudolf Virchow Center (I.M.), University of Würzburg, Germany, Würzburg, Germany; Department of Genetics, Rutgers, The State University of New Jersey, Piscataway, New Jersey (M.M.B.); Division of Basic Research, Department of Anesthesiology, Washington University Pain Center (M.R.B.), Division of Biological and Biomedical Sciences, Department of Anatomy and Neurobiology (M.R.B., P.H.T.), and Department of Developmental Biology, Hope Center for Neurologic Disorders, (K.R.M.), Washington University School of Medicine, St. Louis, Missouri; Centro Interdisciplinario de Neurociencia, Universidad de Valparaiso, Valparaiso, Chile (J.E.); National Center of Behavioral Genomics, Volen Center for Complex Systems, and Department of Biology, Brandeis University, Waltham, Massachusetts (L.C.G.); and Laboratory of Molecular Biology, National Institutes of Health National Institute of Mental Health, Bethesda, Maryland (B.H.W.) tobias.langenhan@uni-wuerzburg.de monkk@wustl.edu. ; Institute of Physiology, Department of Neurophysiology (T.L.), and Institute of Pharmacology and Toxicology, Rudolf Virchow Center (I.M.), University of Würzburg, Germany, Würzburg, Germany; Department of Genetics, Rutgers, The State University of New Jersey, Piscataway, New Jersey (M.M.B.); Division of Basic Research, Department of Anesthesiology, Washington University Pain Center (M.R.B.), Division of Biological and Biomedical Sciences, Department of Anatomy and Neurobiology (M.R.B., P.H.T.), and Department of Developmental Biology, Hope Center for Neurologic Disorders, (K.R.M.), Washington University School of Medicine, St. Louis, Missouri; Centro Interdisciplinario de Neurociencia, Universidad de Valparaiso, Valparaiso, Chile (J.E.); National Center of Behavioral Genomics, Volen Center for Complex Systems, and Department of Biology, Brandeis University, Waltham, Massachusetts (L.C.G.); and Laboratory of Molecular Biology, National Institutes of Health National Institute of Mental Health, Bethesda, Maryland (B.H.W.). Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 596 EP - 603 VL - 88 IS - 3 KW - Drosophila Proteins KW - 0 KW - Receptors, G-Protein-Coupled KW - Index Medicus KW - Animals KW - Receptors, G-Protein-Coupled -- metabolism KW - Drosophila -- metabolism KW - Receptors, G-Protein-Coupled -- genetics KW - Drosophila Proteins -- genetics KW - Drosophila -- genetics KW - Drosophila Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1703702481?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Model+Organisms+in+G+Protein-Coupled+Receptor+Research.&rft.au=Langenhan%2C+Tobias%3BBarr%2C+Maureen+M%3BBruchas%2C+Michael+R%3BEwer%2C+John%3BGriffith%2C+Leslie+C%3BMaiellaro%2C+Isabella%3BTaghert%2C+Paul+H%3BWhite%2C+Benjamin+H%3BMonk%2C+Kelly+R&rft.aulast=Langenhan&rft.aufirst=Tobias&rft.date=2015-09-01&rft.volume=88&rft.issue=3&rft.spage=596&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=1521-0111&rft_id=info:doi/10.1124%2Fmol.115.098764 LA - 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Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/mol.115.098764 ER - TY - JOUR T1 - Efficient, large-scale synthesis and preclinical studies of MRS5698, a highly selective A3 adenosine receptor agonist that protects against chronic neuropathic pain. AN - 1703244980; 26111639 AB - We reported that 2-(3,4-difluorophenylethynyl)-N (6)-3-chlorobenzyl (N)-methanocarba adenosine derivative 1 (MRS5698) binds selectively to human and mouse A3 adenosine receptors (A3ARs, K i 3 nM). It is becoming an important pharmacological tool for defining A3AR effects and is orally active in a chronic neuropathic pain model. Here, we introduce a new synthetic route for MRS5698 from D-ribose, suitable for a scale-up on a multi-gram scale, and we measure in vitro and in vivo ADME-Tox parameters. MRS5698 was very stable in vitro, failed to inhibit CYPs at <10 μM, and was largely bound to plasma proteins. It was well tolerated in the rat at doses of ≤200 mg/kg i.p. A 1 mg/kg i.p. dose in the mouse displayed t 1/2 of 1.09 h and plasma Cmax of 204 nM at 1 h with an AUC of 213 ng × h/mL. CACO-2 bidirectional transport studies suggested intestinal efflux of MRS5698 (efflux ratio 86). Although the oral %F is only 5 %, the beneficial effect to reverse pain lasted for at least 2 h in the CCI model in rats, using the same vehicle for oral administration of a high dose. The stability, low toxicity, lack of CYP interaction, pharmacokinetic half-life, and in vivo efficacy suggest that MRS5698 is a preferred compound for further consideration as a treatment for neuropathic pain. JF - Purinergic signalling AU - Tosh, Dilip K AU - Padia, Janak AU - Salvemini, Daniela AU - Jacobson, Kenneth A AD - Molecular Recognition Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 371 EP - 387 VL - 11 IS - 3 KW - Adenosine A3 Receptor Agonists KW - 0 KW - Blood Proteins KW - MRS5698 KW - Adenosine KW - K72T3FS567 KW - Index Medicus KW - Animals KW - Microsomes, Liver KW - Humans KW - Caco-2 Cells KW - Biological Transport, Active KW - Protein Binding KW - Rats KW - Rats, Sprague-Dawley KW - Mutagenicity Tests KW - Half-Life KW - In Vitro Techniques KW - Chronic Disease KW - Blood Proteins -- metabolism KW - Constriction, Pathologic -- complications KW - Male KW - Adenosine -- pharmacokinetics KW - Neuralgia -- drug therapy KW - Adenosine -- toxicity KW - Adenosine A3 Receptor Agonists -- toxicity KW - Adenosine A3 Receptor Agonists -- therapeutic use KW - Adenosine -- analogs & derivatives KW - Adenosine A3 Receptor Agonists -- pharmacokinetics KW - Adenosine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1703244980?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Purinergic+signalling&rft.atitle=Efficient%2C+large-scale+synthesis+and+preclinical+studies+of+MRS5698%2C+a+highly+selective+A3+adenosine+receptor+agonist+that+protects+against+chronic+neuropathic+pain.&rft.au=Tosh%2C+Dilip+K%3BPadia%2C+Janak%3BSalvemini%2C+Daniela%3BJacobson%2C+Kenneth+A&rft.aulast=Tosh&rft.aufirst=Dilip&rft.date=2015-09-01&rft.volume=11&rft.issue=3&rft.spage=371&rft.isbn=&rft.btitle=&rft.title=Purinergic+signalling&rft.issn=1573-9546&rft_id=info:doi/10.1007%2Fs11302-015-9459-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-24 N1 - Date created - 2015-08-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Adv Drug Deliv Rev. 2001 Mar 1;46(1-3):3-26 [11259830] J Med Chem. 2002 Jun 6;45(12):2615-23 [12036371] Nat Rev Drug Discov. 2003 Mar;2(3):175-6 [12619637] J Org Chem. 2004 Apr 2;69(7):2634-6 [15049678] J Neurobiol. 2004 Oct;61(1):126-48 [15362157] Annu Rev Pharmacol Toxicol. 1980;20:441-62 [7387124] Acta Anaesthesiol Scand. 1988 Apr;32(3):253-9 [3364150] Pain. 1988 Apr;33(1):87-107 [2837713] Pain. 1995 Sep;62(3):259-74 [8657426] Toxicol In Vitro. 2005 Jun;19(4):491-503 [15826807] J Clin Invest. 2006 Jan;116(1):4-15 [16395396] Minerva Anestesiol. 2006 Mar;72(3):151-69 [16493391] J Pain. 2006 Apr;7(4):281-9 [16618472] Org Lett. 2006 Oct 26;8(22):5081-3 [17048848] Nucleosides Nucleotides Nucleic Acids. 2008 Mar;27(3):279-91 [18260011] Mutat Res. 2008 May 31;653(1-2):130-3 [18514567] Chemistry. 2009 Jun 15;15(25):6244-57 [19441002] Curr Opin Support Palliat Care. 2011 Mar;5(1):1-7 [21192267] Drug Discov Today. 2012 Apr;17(7-8):359-66 [22033198] FASEB J. 2012 May;26(5):1855-65 [22345405] J Med Chem. 2012 May 24;55(10):4847-60 [22559880] Regul Toxicol Pharmacol. 2014 Feb;68(1):16-22 [24239523] PLoS One. 2014;9(5):e97858 [24859150] J Med Chem. 2014 Dec 11;57(23):9901-14 [25422861] Brain Behav Immun. 2015 Feb;44:91-9 [25220279] Brain. 2015 Jan;138(Pt 1):28-35 [25414036] J Med Chem. 2015 Mar 26;58(6):2584-608 [25494650] J Neurosci. 2015 Apr 15;35(15):6057-67 [25878279] J Med Chem. 2015 May 14;58(9):4066-72 [25860834] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s11302-015-9459-2 ER - TY - JOUR T1 - Development of a novel observational measure for anxiety in young children: The Anxiety Dimensional Observation Scale AN - 1703151088 AB - Background Identifying anxiety disorders in preschool-age children represents an important clinical challenge. Observation is essential to clinical assessment and can help differentiate normative variation from clinically significant anxiety. Yet, most anxiety assessment methods for young children rely on parent-reports. The goal of this article is to present and preliminarily test the reliability and validity of a novel observational paradigm for assessing a range of fearful and anxious behaviors in young children, the Anxiety Dimensional Observation Schedule (Anx-DOS). Methods A diverse sample of 403 children, aged 3 to 6 years, and their mothers was studied. Reliability and validity in relation to parent reports (Preschool Age Psychiatric Assessment) and known risk factors, including indicators of behavioral inhibition (latency to touch novel objects) and attention bias to threat (in the dot-probe task) were investigated. Results The Anx-DOS demonstrated good inter-rater reliability and internal consistency. Evidence for convergent validity was demonstrated relative to mother-reported separation anxiety, social anxiety, phobic avoidance, trauma symptoms, and past service use. Finally, fearfulness was associated with observed latency and attention bias toward threat. Conclusions Findings support the Anx-DOS as a method for capturing early manifestations of fearfulness and anxiety in young children. Multimethod assessments incorporating standardized methods for assessing discrete, observable manifestations of anxiety may be beneficial for early identification and clinical intervention efforts. JF - Journal of Child Psychology and Psychiatry AU - Mian, Nicholas D AU - Carter, Alice S AU - Pine, Daniel S AU - Wakschlag, Lauren S AU - Briggs-Gowan, Margaret J AD - Center for Anxiety and Related Disorders, Department of Psychological and Brain Sciences, Boston University, Boston, MA, USA. ; Department of Psychology, University of Massachusetts Boston, Boston, MA, USA. ; National Institute of Mental Health, Division of Intramural Research Programs, Bethesda, MD, USA. ; Department of Medical Social Sciences, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA., Institute for Policy Research, Northwestern University, Chicago, IL, USA. ; Department of Psychiatry, University of Connecticut School of Medicine, Farmington, CT, USA. ; Center for Anxiety and Related Disorders, Department of Psychological and Brain Sciences, Boston University, Boston, MA, USA. Y1 - 2015/09// PY - 2015 DA - Sep 2015 SP - 1017 EP - 1025 CY - Malden PB - Wiley Subscription Services, Inc. VL - 56 IS - 9 KW - Psychology KW - Assessment KW - Inhibition KW - Latency KW - Mothers KW - Preschool children KW - Psychological trauma KW - Reliability KW - Risk assessment KW - Risk factors KW - Separation anxiety KW - Service provision KW - Social anxiety KW - Young children KW - Attentional bias KW - Avoidance KW - Behaviour KW - Child development KW - Children KW - Clinical assessment KW - Convergent validity KW - Early intervention programmes KW - Identification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1703151088?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Child+Psychology+and+Psychiatry&rft.atitle=Development+of+a+novel+observational+measure+for+anxiety+in+young+children%3A+The+Anxiety+Dimensional+Observation+Scale&rft.au=Mian%2C+Nicholas+D%3BCarter%2C+Alice+S%3BPine%2C+Daniel+S%3BWakschlag%2C+Lauren+S%3BBriggs-Gowan%2C+Margaret+J&rft.aulast=Mian&rft.aufirst=Nicholas&rft.date=2015-09-01&rft.volume=56&rft.issue=9&rft.spage=1017&rft.isbn=&rft.btitle=&rft.title=Journal+of+Child+Psychology+and+Psychiatry&rft.issn=&rft_id=info:doi/10.1111%2Fjcpp.12407 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-08-11 N1 - Last updated - 2016-05-16 DO - http://dx.doi.org/10.1111/jcpp.12407 ER - TY - JOUR T1 - The Air We Breathe. AN - 1702653912; 26180966 JF - American journal of public health AU - Fee, Elizabeth AU - Blum, Nava AD - Elizabeth Fee and Nava Blum are with the National Library of Medicine, National Institutes of Health, Bethesda, MD. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 1751 VL - 105 IS - 9 KW - Air Pollutants KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - United States KW - Socioeconomic Factors KW - Humans KW - Lung Diseases -- chemically induced KW - Air Pollution -- adverse effects KW - Air Pollutants -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1702653912?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+public+health&rft.atitle=The+Air+We+Breathe.&rft.au=Fee%2C+Elizabeth%3BBlum%2C+Nava&rft.aulast=Fee&rft.aufirst=Elizabeth&rft.date=2015-09-01&rft.volume=105&rft.issue=9&rft.spage=1751&rft.isbn=&rft.btitle=&rft.title=American+journal+of+public+health&rft.issn=1541-0048&rft_id=info:doi/10.2105%2FAJPH.2015.302700 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-02 N1 - Date created - 2015-08-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Environ Health Perspect. 2000 Aug;108 Suppl 4:713-23 [10931790] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.2105/AJPH.2015.302700 ER - TY - JOUR T1 - Pregnane X Receptor-Humanized Mice Recapitulate Gender Differences in Ethanol Metabolism but Not Hepatotoxicity. AN - 1702086468; 26159875 AB - Both human and rodent females are more susceptible to developing alcoholic liver disease following chronic ethanol (EtOH) ingestion. However, little is known about the relative effects of acute EtOH exposure on hepatotoxicity in female versus male mice. The nuclear receptor pregnane X receptor (PXR; NR1I2) is a broad-specificity sensor with species-specific responses to toxic agents. To examine the effects of the human PXR on acute EtOH toxicity, the responses of male and female PXR-humanized (hPXR) transgenic mice administered oral binge EtOH (4.5 g/kg) were analyzed. Basal differences were observed between hPXR males and females in which females expressed higher levels of two principal enzymes responsible for EtOH metabolism, alcohol dehydrogenase 1 and aldehyde dehydrogenase 2, and two key mediators of hepatocyte replication and repair, cyclin D1 and proliferating cell nuclear antigen. EtOH ingestion upregulated hepatic estrogen receptor α, cyclin D1, and CYP2E1 in both genders, but differentially altered lipid and EtOH metabolism. Consistent with higher basal levels of EtOH-metabolizing enzymes, blood EtOH was more rapidly cleared in hPXR females. These factors combined to provide greater protection against EtOH-induced liver injury in female hPXR mice, as revealed by markers for liver damage, lipid peroxidation, and endoplasmic reticulum stress. These results indicate that female hPXR mice are less susceptible to acute binge EtOH-induced hepatotoxicity than their male counterparts, due at least in part to the relative suppression of cellular stress and enhanced expression of enzymes involved in both EtOH metabolism and hepatocyte proliferation and repair in hPXR females. U.S. Government work not protected by U.S. copyright. JF - The Journal of pharmacology and experimental therapeutics AU - Spruiell, Krisstonia AU - Gyamfi, Afua A AU - Yeyeodu, Susan T AU - Richardson, Ricardo M AU - Gonzalez, Frank J AU - Gyamfi, Maxwell A AD - Julius L. Chambers Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, North Carolina (K.S., A.A.G., S.T.Y., R.M.R., M.A.G.); and Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland (F.J.G.). ; Julius L. Chambers Biomedical/Biotechnology Research Institute, North Carolina Central University, Durham, North Carolina (K.S., A.A.G., S.T.Y., R.M.R., M.A.G.); and Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland (F.J.G.) mgyamfi@nccu.edu. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 459 EP - 470 VL - 354 IS - 3 KW - Estrogen Receptor alpha KW - 0 KW - Receptors, Steroid KW - pregnane X receptor KW - Cyclin D1 KW - 136601-57-5 KW - Ethanol KW - 3K9958V90M KW - Alcohol Dehydrogenase KW - EC 1.1.1.1 KW - Cytochrome P-450 CYP2E1 KW - EC 1.14.13.- KW - ALDH2 protein, mouse KW - EC 1.2.1.3 KW - Aldehyde Dehydrogenase KW - Aldehyde Dehydrogenase, Mitochondrial KW - Index Medicus KW - Animals KW - Alcohol Drinking -- metabolism KW - Sex Characteristics KW - Humans KW - Mice KW - Cytochrome P-450 CYP2E1 -- metabolism KW - Estrogen Receptor alpha -- metabolism KW - Mice, Transgenic KW - Endoplasmic Reticulum Stress -- physiology KW - Lipid Peroxidation -- physiology KW - Liver Diseases, Alcoholic -- metabolism KW - Cyclin D1 -- metabolism KW - Mice, Inbred C57BL KW - Alcohol Dehydrogenase -- metabolism KW - Aldehyde Dehydrogenase -- metabolism KW - Male KW - Female KW - Receptors, Steroid -- metabolism KW - Liver -- metabolism KW - Ethanol -- metabolism KW - Hepatocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1702086468?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=Pregnane+X+Receptor-Humanized+Mice+Recapitulate+Gender+Differences+in+Ethanol+Metabolism+but+Not+Hepatotoxicity.&rft.au=Spruiell%2C+Krisstonia%3BGyamfi%2C+Afua+A%3BYeyeodu%2C+Susan+T%3BRichardson%2C+Ricardo+M%3BGonzalez%2C+Frank+J%3BGyamfi%2C+Maxwell+A&rft.aulast=Spruiell&rft.aufirst=Krisstonia&rft.date=2015-09-01&rft.volume=354&rft.issue=3&rft.spage=459&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=1521-0103&rft_id=info:doi/10.1124%2Fjpet.115.224295 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-06 N1 - Date created - 2015-08-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: World J Gastroenterol. 2010 Mar 21;16(11):1377-84 [20238405] Forensic Sci Int. 2010 Jul 15;200(1-3):1-20 [20304569] Hepatology. 2011 May;53(5):1752-63 [21384408] Alcohol Clin Exp Res. 2012 Sep;36(9):1578-86 [22375794] Transplant Proc. 2013 Mar;45(2):463-73 [23498780] Endocrinology. 2000 Nov;141(11):4021-31 [11089532] Alcohol Clin Exp Res. 2001 May;25(5 Suppl ISBRA):40S-45S [11391047] Comp Biochem Physiol C Toxicol Pharmacol. 2001 Jul;129(3):285-93 [11461843] Am J Physiol Gastrointest Liver Physiol. 2001 Dec;281(6):G1348-56 [11705739] J Clin Invest. 2002 May;109(9):1125-31 [11994399] Alcohol Alcohol. 2013 Nov-Dec;48(6):648-56 [23969550] Am J Physiol Gastrointest Liver Physiol. 2000 Apr;278(4):G652-61 [10762620] Biochem Pharmacol. 1999 May 1;57(9):1067-72 [10796077] Mol Cell Endocrinol. 2002 Jul 31;193(1-2):101-4 [12161008] J Nutr Sci Vitaminol (Tokyo). 2002 Jun;48(3):216-24 [12350080] Endocr Rev. 2002 Oct;23(5):687-702 [12372848] J Clin Lab Anal. 2003;17(3):93-6 [12696080] Hepatology. 2003 Jul;38(1):133-40 [12829995] Life Sci. 2004 Jun 11;75(4):469-83 [15147833] FEBS Lett. 2004 Jun 4;567(2-3):243-7 [15178330] Toxicology. 2013 Dec 15;314(2-3):193-201 [24144995] J Biol Chem. 2014 Feb 7;289(6):3244-61 [24362030] Biochim Biophys Acta. 2014 Jun;1838(6):1477-87 [24184426] Biochem Pharmacol. 2014 Jun 1;89(3):399-412 [24721462] J Hepatol. 2015 Jun;62(6):1375-81 [25543082] Biochem J. 1980 Feb 15;186(2):483-90 [6990919] J Hepatol. 1986;2(1):33-42 [3950362] Gastroenterology. 1987 May;92(5 Pt 1):1169-73 [3557012] Proc Natl Acad Sci U S A. 1989 Aug;86(15):5903-7 [2474823] N Engl J Med. 1990 Jan 11;322(2):95-9 [2248624] Alcohol Clin Exp Res. 1989 Dec;13(6):752-4 [2690657] Gastroenterology. 1991 Dec;101(6):1716-23 [1955136] Biochem Pharmacol. 1992 Apr 1;43(7):1555-61 [1567477] Alcohol Alcohol. 1992 Nov;27(6):641-7 [1292437] Mol Med Today. 1996 Feb;2(2):82-9 [8796861] Alcohol. 1997 Nov-Dec;14(6):527-31 [9401665] Cell. 1998 Apr 17;93(2):241-52 [9568716] J Steroid Biochem Mol Biol. 1998 Apr;65(1-6):65-74 [9699859] J Clin Invest. 1998 Sep 1;102(5):1016-23 [9727070] J Nutr Sci Vitaminol (Tokyo). 1998 Oct;44(5):625-39 [9919483] Clin Cancer Res. 1999 Aug;5(8):2103-7 [10473093] Toxicol Pathol. 2004 Sep-Oct;32(5):567-76 [15603541] Gut. 2005 Oct;54(10):1461-7 [15870229] Mol Cell Biol. 2005 Nov;25(21):9350-9 [16227586] Biochem Biophys Res Commun. 2005 Dec 2;337(4):1324-9 [16236269] J Biol Chem. 2006 May 26;281(21):15013-20 [16556603] Genes Dev. 2006 Aug 15;20(16):2306-14 [16912279] J Pharmacol Exp Ther. 2006 Oct;319(1):360-8 [16829625] Drug Metab Dispos. 2007 Feb;35(2):194-200 [17093002] J Pharmacol Exp Ther. 2007 Jul;322(1):391-8 [17442842] Hepatology. 2007 Dec;46(6):2032-9 [18046720] J Pharmacol Exp Ther. 2008 Feb;324(2):443-53 [17975011] J Pharmacol Exp Ther. 2008 May;325(2):655-64 [18281592] Toxicol Appl Pharmacol. 2008 Dec 1;233(2):193-202 [18789348] Alcohol. 2010 Mar;44(2):157-69 [20116195] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/jpet.115.224295 ER - TY - JOUR T1 - A New Era of Low-Dose Radiation Epidemiology. AN - 1701312840; 26231501 AB - The last decade has introduced a new era of epidemiologic studies of low-dose radiation facilitated by electronic record linkage and pooling of cohorts that allow for more direct and powerful assessments of cancer and other stochastic effects at doses below 100 mGy. Such studies have provided additional evidence regarding the risks of cancer, particularly leukemia, associated with lower-dose radiation exposures from medical, environmental, and occupational radiation sources, and have questioned the previous findings with regard to possible thresholds for cardiovascular disease and cataracts. Integrated analysis of next generation genomic and epigenetic sequencing of germline and somatic tissues could soon propel our understanding further regarding disease risk thresholds, radiosensitivity of population subgroups and individuals, and the mechanisms of radiation carcinogenesis. These advances in low-dose radiation epidemiology are critical to our understanding of chronic disease risks from the burgeoning use of newer and emerging medical imaging technologies, and the continued potential threat of nuclear power plant accidents or other radiological emergencies. JF - Current environmental health reports AU - Kitahara, Cari M AU - Linet, Martha S AU - Rajaraman, Preetha AU - Ntowe, Estelle AU - Berrington de González, Amy AD - Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Rm 7E566, Rockville, MD, 20850, USA, kitaharac@mail.nih.gov. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 236 EP - 249 VL - 2 IS - 3 KW - Index Medicus KW - Cardiovascular Diseases -- etiology KW - Epidemiologic Studies KW - Humans KW - Occupational Exposure -- adverse effects KW - Risk Assessment KW - Radiation, Ionizing KW - Nuclear Power Plants KW - Radiation Exposure -- adverse effects KW - Neoplasms, Radiation-Induced -- etiology KW - Neoplasms, Radiation-Induced -- epidemiology KW - Dose-Response Relationship, Radiation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701312840?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+environmental+health+reports&rft.atitle=A+New+Era+of+Low-Dose+Radiation+Epidemiology.&rft.au=Kitahara%2C+Cari+M%3BLinet%2C+Martha+S%3BRajaraman%2C+Preetha%3BNtowe%2C+Estelle%3BBerrington+de+Gonz%C3%A1lez%2C+Amy&rft.aulast=Kitahara&rft.aufirst=Cari&rft.date=2015-09-01&rft.volume=2&rft.issue=3&rft.spage=236&rft.isbn=&rft.btitle=&rft.title=Current+environmental+health+reports&rft.issn=2196-5412&rft_id=info:doi/10.1007%2Fs40572-015-0055-y LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-26 N1 - Date created - 2015-08-03 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s40572-015-0055-y ER - TY - JOUR T1 - Socioeconomic Differences in the Association Between Competitive Food Laws and the School Food Environment AN - 1701262673 AB - BACKGROUND Schools of low socioeconomic status (SES) tend to sell fewer healthy competitive foods/beverages. This study examined whether state competitive food laws may reduce such disparities. METHODS School administrators for fifth- and eighth grade reported foods and beverages sold in school. Index measures of the food/beverage environments were constructed from these data. Schools were classified into SES tertiles based on median household income of studentsʼ postal zip code. Regression models were used to estimate SES differences in (1) Healthy School Food Environment Index (HSFEI) score, Healthy School Beverage Environment Index (HSBEI) score, and specific food/beverage sales, and (2) associations between state competitive food/beverage laws and HSFEI score, HSBEI score, and specific food/beverage sales. RESULTS Strong competitive food laws were positively associated with HSFEI in eighth grade, regardless of SES. Strong competitive beverage laws were positively associated with HSBEI particularly in low-SES schools in eighth grade. These associations were attributable to schools selling fewer unhealthy items, not providing healthy alternatives. High-SES schools sold more healthy items than low-SES schools regardless of state laws. CONCLUSIONS Strong competitive food laws may reduce access to unhealthy foods/beverages in middle schools, but additional initiatives are needed to provide students with healthy options, particularly in low-SES areas. JF - The Journal of School Health AU - Taber, Daniel R AU - Chriqui, Jamie F AU - Powell, Lisa M AU - Perna, Frank M AU - Robinson, Whitney R AU - Chaloupka, Frank J AD - University of Texas Health Science Center at Houston—Austin Regional Campus, 1616 Guadalupe St, Suite 6.300, Austin, TX 78701. ; University of Illinois at Chicago, 1747 W. Roosevelt Rd, Chicago, IL 60608. ; Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, 9609 Medical Center Dr, Room 3E104, Rockville, MD 20850. ; Gillings School of Global Public Health, University of North Carolina at Chapel Hill, 2104B McGavran-Greenberg Hall, Chapel Hill, NC 27599-7435. ; University of Texas Health Science Center at Houston—Austin Regional Campus, 1616 Guadalupe St, Suite 6.300, Austin, TX 78701. Y1 - 2015/09// PY - 2015 DA - Sep 2015 SP - 578 EP - 586 CY - Kent PB - Wiley Subscription Services, Inc. VL - 85 IS - 9 SN - 0022-4391 KW - Physical Fitness And Hygiene KW - Associations KW - Drinks KW - Food KW - Healthy food KW - Low income people KW - Middle schools KW - Sales KW - School meals KW - Socioeconomic factors KW - Socioeconomic status UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701262673?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+School+Health&rft.atitle=Socioeconomic+Differences+in+the+Association+Between+Competitive+Food+Laws+and+the+School+Food+Environment&rft.au=Taber%2C+Daniel+R%3BChriqui%2C+Jamie+F%3BPowell%2C+Lisa+M%3BPerna%2C+Frank+M%3BRobinson%2C+Whitney+R%3BChaloupka%2C+Frank+J&rft.aulast=Taber&rft.aufirst=Daniel&rft.date=2015-09-01&rft.volume=85&rft.issue=9&rft.spage=578&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+School+Health&rft.issn=00224391&rft_id=info:doi/10.1111%2Fjosh.12288 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-09-22 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1111/josh.12288 ER - TY - JOUR T1 - Reduced Dose Intensity of Chemotherapy may not Lead to Inferior Palliation in Locally Advanced Carcinoma of the Gall Bladder: An Experience from a Regional Cancer Centre in Eastern India. AN - 1700686763; 26116258 AB - To assess impact of relative total dose intensity (RTDI) on clinical benefit among patients with locally advanced carcinoma gall bladder receiving gemcitabine-cisplatin (GemCis). Comparison of clinical benefit among patients receiving variable RTDI was the primary objective. The secondary objective was an impact of RTDI on chemotherapy toxicity. One-hundred twenty-one patients with locally advanced inoperable carcinoma gall bladder undergoing chemotherapy with three weekly gemcitabine-cisplatin chemotherapies (gemcitabine 1000 mg/m(2) on day 1 and 8, cisplatin 70 mg/m(2) on day 1) were studied. Clinical benefit and treatment toxicity was assessed. Total dose of chemotherapy and relative total dose intensity, the proportion of planned dose actually received was calculated. RTDI of at least 50 % conferred substantial clinical benefit compared to lower RTDI (75.49 vs. 21.05 %). RTDI above 50-59 % did not improve clinical benefit; two-tailed p values of RTDI >60 % vs. RTDI >50 % and RTDI >70 % vs. RTDI >50 % were 1.000 and 0.4266, respectively. Subsequent extended cholecystectomy rates did not significantly improve among patients who received RTDI greater than 50-59 %; two-tailed p values of RTDI >60 % vs. RTDI >50 % and RTDI >70 % vs. >50 % were 0.0920 and 0.5648, respectively. Significantly higher neutropenia and anemia of at least grade 2 occurred with RTDI >70 % vs. RTDI 50-59 %; two-tailed p values 0.0019 and 0.0048, respectively. Relative total dose intensity of chemotherapy higher than 60 % among patients with inoperable locally advanced carcinoma gall bladder conferred no significant improvement in clinical benefit and subsequent rates of extended cholecystectomy. Higher RTDI however led to significantly increased toxicity among these patients. JF - Journal of gastrointestinal cancer AU - Gangopadhyay, Aparna AU - Nath, Partha AU - Biswas, Jaydip AD - Department of Medical Oncology, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata, 700026, India, mails7778@gmail.com. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 297 EP - 300 VL - 46 IS - 3 KW - Index Medicus KW - Humans KW - Adult KW - Middle Aged KW - Male KW - Female KW - India KW - Gallbladder Neoplasms -- drug therapy KW - Drug Therapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1700686763?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+gastrointestinal+cancer&rft.atitle=Reduced+Dose+Intensity+of+Chemotherapy+may+not+Lead+to+Inferior+Palliation+in+Locally+Advanced+Carcinoma+of+the+Gall+Bladder%3A+An+Experience+from+a+Regional+Cancer+Centre+in+Eastern+India.&rft.au=Gangopadhyay%2C+Aparna%3BNath%2C+Partha%3BBiswas%2C+Jaydip&rft.aulast=Gangopadhyay&rft.aufirst=Aparna&rft.date=2015-09-01&rft.volume=46&rft.issue=3&rft.spage=297&rft.isbn=&rft.btitle=&rft.title=Journal+of+gastrointestinal+cancer&rft.issn=1941-6636&rft_id=info:doi/10.1007%2Fs12029-015-9742-z LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-11 N1 - Date created - 2015-07-30 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s12029-015-9742-z ER - TY - JOUR T1 - Phase 2 trial of sorafenib in children and young adults with refractory solid tumors: A report from the Children's Oncology Group. AN - 1698964631; 26207356 AB - Sorafenib is an oral small molecule inhibitor of multiple kinases controlling tumor growth and angiogenesis. The purpose of the phase 2 study was to determine the response rate of sorafenib and gain further information on the associated toxicities, pharmacokinetics, and pharmacodynamics of sorafenib in children and young adults with relapsed or refractory tumors including rhabdomyosarcoma, Wilms tumor, hepatocellular carcinoma (HCC), and papillary thyroid carcinoma (PTC). Sorafenib, 200 mg/m(2) /dose, was administered every 12 hr continuously for 28 day cycles using a two-stage design in two primary strata (rhabdomyosarcoma and Wilms tumor) and two secondary strata (HCC and PTC). Correlative studies in consenting patients included determination of sorafenib steady state trough concentrations and assessments of VEGF and sVEGFR2. Twenty patients (median age of 11 years; range, 5-21) enrolled. No objective responses (RECIST) were observed in the 10 evaluable patients enrolled in each of the two primary disease strata of rhabdomyosarcoma and Wilms tumor. No patients with HCC or PTC were enrolled. Sorafenib was not associated with an excessive rate of dose-limiting toxicity (DLT). The mean ± SD steady state concentration during cycle 1 day 15 was 6.5 ± 3.9 μg/ml (n = 10). Sorafenib was well tolerated in children at 200 mg/m(2) /dose twice daily on a continuous regimen with toxicity profile and steady state drug concentrations similar to those previously reported. Single agent sorafenib was inactive in children with recurrent or refractory rhabdomyosarcoma or Wilms tumor. © 2015 Wiley Periodicals, Inc. JF - Pediatric blood & cancer AU - Kim, AeRang AU - Widemann, Brigitte C AU - Krailo, Mark AU - Jayaprakash, Nalini AU - Fox, Elizabeth AU - Weigel, Brenda AU - Blaney, Susan M AD - Children's National Medical Center, Washington, District of Columbia. ; Pediatric Oncology Branch, National Cancer Institute, Bethesda, Maryland. ; Children's Oncology Group Statistics, Monrovia, California. ; Children's Hospital of Philadelphia, Philadelphia, Pennsylvania. ; University of Minnesota Medical Center, Minneapolis, Minnesota. ; Baylor College of Medicine, Houston, Texas. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 1562 EP - 1566 VL - 62 IS - 9 KW - Angiogenesis Inhibitors KW - 0 KW - Antineoplastic Agents KW - Neoplasm Proteins KW - Phenylurea Compounds KW - Protein Kinase Inhibitors KW - VEGFA protein, human KW - Vascular Endothelial Growth Factor A KW - Niacinamide KW - 25X51I8RD4 KW - sorafenib KW - 9ZOQ3TZI87 KW - KDR protein, human KW - EC 2.7.10.1 KW - Vascular Endothelial Growth Factor Receptor-2 KW - Index Medicus KW - pediatrics KW - solid tumors KW - Young Adult KW - Treatment Failure KW - Vascular Endothelial Growth Factor A -- blood KW - Humans KW - Neoplasm Proteins -- blood KW - Child KW - Adolescent KW - Vascular Endothelial Growth Factor Receptor-2 -- blood KW - Male KW - Female KW - Child, Preschool KW - Kidney Neoplasms -- drug therapy KW - Rhabdomyosarcoma -- blood KW - Wilms Tumor -- drug therapy KW - Antineoplastic Agents -- pharmacokinetics KW - Salvage Therapy KW - Protein Kinase Inhibitors -- pharmacokinetics KW - Wilms Tumor -- blood KW - Antineoplastic Agents -- adverse effects KW - Rhabdomyosarcoma -- enzymology KW - Kidney Neoplasms -- blood KW - Protein Kinase Inhibitors -- therapeutic use KW - Angiogenesis Inhibitors -- pharmacokinetics KW - Niacinamide -- adverse effects KW - Angiogenesis Inhibitors -- adverse effects KW - Phenylurea Compounds -- pharmacokinetics KW - Angiogenesis Inhibitors -- therapeutic use KW - Niacinamide -- pharmacokinetics KW - Kidney Neoplasms -- enzymology KW - Niacinamide -- analogs & derivatives KW - Wilms Tumor -- enzymology KW - Niacinamide -- therapeutic use KW - Protein Kinase Inhibitors -- adverse effects KW - Phenylurea Compounds -- therapeutic use KW - Phenylurea Compounds -- adverse effects KW - Antineoplastic Agents -- therapeutic use KW - Rhabdomyosarcoma -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698964631?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pediatric+blood+%26+cancer&rft.atitle=Phase+2+trial+of+sorafenib+in+children+and+young+adults+with+refractory+solid+tumors%3A+A+report+from+the+Children%27s+Oncology+Group.&rft.au=Kim%2C+AeRang%3BWidemann%2C+Brigitte+C%3BKrailo%2C+Mark%3BJayaprakash%2C+Nalini%3BFox%2C+Elizabeth%3BWeigel%2C+Brenda%3BBlaney%2C+Susan+M&rft.aulast=Kim&rft.aufirst=AeRang&rft.date=2015-09-01&rft.volume=62&rft.issue=9&rft.spage=1562&rft.isbn=&rft.btitle=&rft.title=Pediatric+blood+%26+cancer&rft.issn=1545-5017&rft_id=info:doi/10.1002%2Fpbc.25548 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-13 N1 - Date created - 2015-07-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Oncologist. 2007 Apr;12(4):426-37 [17470685] N Engl J Med. 2007 Jan 11;356(2):125-34 [17215530] J Pharm Biomed Anal. 2008 Jan 22;46(2):362-7 [18309574] N Engl J Med. 2008 Jul 24;359(4):378-90 [18650514] Clin Cancer Res. 2009 Feb 15;15(4):1411-6 [19228742] J Clin Oncol. 2008 Oct 10;26(29):4714-9 [18541894] Clin Cancer Res. 2008 Aug 1;14(15):4908-14 [18676765] J Clin Oncol. 2009 Apr 1;27(10):1675-84 [19255327] Thyroid. 2009 Apr;19(4):407-12 [19355831] Ann Oncol. 2009 May;20(5):807-15 [19150949] J Clin Oncol. 2009 Jul 1;27(19):3133-40 [19451436] Clin Cancer Res. 2010 Oct 1;16(19):4853-63 [20651059] Pediatr Blood Cancer. 2010 Dec 1;55(6):1126-33 [20672370] J Clin Oncol. 2010 Dec 10;28(35):5174-81 [21060028] Invest New Drugs. 2011 Jun;29(3):481-8 [20016927] J Clin Oncol. 2011 Aug 20;29(24):3293-300 [21768474] Cancer. 2012 Feb 1;118(3):770-6 [21751200] Pediatr Blood Cancer. 2012 Apr;58(4):539-44 [21922643] Clin Cancer Res. 2012 Nov 1;18(21):6011-22 [22962440] Ann Oncol. 2013 Apr;24(4):1093-8 [23230134] Cancer Discov. 2013 Jul;3(7):OF2 [23847363] J Clin Oncol. 2013 Aug 20;31(24):3034-43 [23857966] J Pediatr Surg. 2001 Feb;36(2):287-90 [11172417] J Pediatr Surg. 2001 Feb;36(2):357-61 [11172434] Stat Med. 2004 Mar 30;23(6):881-96 [15027078] Pediatrics. 2004 Aug;114(2 Suppl 4th Report):555-76 [15286277] Int J Oncol. 2004 Sep;25(3):549-53 [15289855] Thyroid. 2005 Apr;15(4):320-5 [15876153] Mod Pathol. 2005 Jul;18(7):898-902 [15968271] J Clin Oncol. 2006 Mar 20;24(9):1363-9 [16446323] Nat Rev Drug Discov. 2006 Oct;5(10):835-44 [17016424] Pediatr Blood Cancer. 2008 Mar;50(3):581-7 [17457854] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/pbc.25548 ER - TY - JOUR T1 - Postsynaptic gephyrin clustering controls the development of adult-born granule cells in the olfactory bulb. AN - 1697759516; 25772192 AB - In adult rodent olfactory bulb, GABAergic signaling regulates migration, differentiation, and synaptic integration of newborn granule cells (GCs), migrating from the subventricular zone. Here we show that these effects depend on the formation of a postsynaptic scaffold organized by gephyrin-the main scaffolding protein of GABAergic synapses, which anchors receptors and signaling molecules to the postsynaptic density-and are regulated by the phosphorylation status of gephyrin. Using lentiviral vectors to selectively transfect adult-born GCs, we observed that overexpression of the phospho-deficient gephyrin mutant eGFP-gephyrin(S270A), which facilitates the formation of supernumerary GABAergic synapses in vitro, favors dendritic branching and the formation of transient GABAergic synapses on spines, identified by the presence of α2-GABAA Rs. In contrast, overexpression of the dominant-negative eGFP-gephyrin(L2B) (a chimera that is enzymatically active but clustering defective), curtailed dendritic growth, spine formation, and long-term survival of GCs, pointing to the essential role of gephyrin cluster formation for its function. We could exclude any gephyrin overexpression artifacts, as GCs infected with eGFP-gephyrin were comparable to those infected with eGFP alone. The opposite effects induced by the two gephyrin mutant constructs indicate that the gephyrin scaffold at GABAergic synapses orchestrates signaling cascades acting on the cytoskeleton to regulate neuronal growth and synapse formation. Specifically, gephyrin phosphorylation emerges as a novel mechanism regulating morphological differentiation and long-term survival of adult-born olfactory bulb neurons. © 2015 Wiley Periodicals, Inc. JF - The Journal of comparative neurology AU - Deprez, Francine AU - Pallotto, Marta AU - Vogt, Fabia AU - Grabiec, Marta AU - Virtanen, Mari A AU - Tyagarajan, Shiva K AU - Panzanelli, Patrizia AU - Fritschy, Jean-Marc AD - University of Zurich, Institute of Pharmacology and Toxicology, 8057, Zurich, Switzerland. ; Circuit Dynamics and Connectivity Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA. ; Department of Neurosciences Fondamentales CMU, University of Geneva, 1211, Geneva, Switzerland. ; University of Turin, Department of Neuroscience Rita Levi Montalcini, Turin, Italy. Y1 - 2015/09/01/ PY - 2015 DA - 2015 Sep 01 SP - 1998 EP - 2016 VL - 523 IS - 13 KW - Carrier Proteins KW - 0 KW - Membrane Proteins KW - Receptors, GABA-A KW - Slc17a7 protein, mouse KW - Vesicular Glutamate Transport Protein 1 KW - Vesicular Inhibitory Amino Acid Transport Proteins KW - Viaat protein, mouse KW - enhanced green fluorescent protein KW - gephyrin KW - Green Fluorescent Proteins KW - 147336-22-9 KW - Index Medicus KW - RRID:AB_1586992 KW - GABA KW - lentiviruses KW - postsynaptic density KW - dendrites KW - spines KW - RRID:AB_887725 KW - RRID:AB_887717 KW - RRID:AB_10000240 KW - RRID:AB_1501344 KW - phosphorylation KW - RRID:AB_887869 KW - adult neurogenesis KW - RRID:AB_2315546 KW - Animals KW - Age Factors KW - Cell Survival -- genetics KW - Dendrites -- metabolism KW - HEK293 Cells KW - Humans KW - Vesicular Glutamate Transport Protein 1 -- metabolism KW - Transduction, Genetic KW - Mice KW - Cell Movement -- genetics KW - Vesicular Inhibitory Amino Acid Transport Proteins -- metabolism KW - Green Fluorescent Proteins -- genetics KW - Dendrites -- ultrastructure KW - Receptors, GABA-A -- metabolism KW - Mutation -- genetics KW - Green Fluorescent Proteins -- metabolism KW - Male KW - Neurogenesis -- physiology KW - Membrane Proteins -- ultrastructure KW - Carrier Proteins -- ultrastructure KW - Neurons -- metabolism KW - Carrier Proteins -- metabolism KW - Membrane Proteins -- metabolism KW - Carrier Proteins -- genetics KW - Neurons -- cytology KW - Post-Synaptic Density -- ultrastructure KW - Membrane Proteins -- genetics KW - Olfactory Bulb -- cytology KW - Post-Synaptic Density -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1697759516?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+comparative+neurology&rft.atitle=Postsynaptic+gephyrin+clustering+controls+the+development+of+adult-born+granule+cells+in+the+olfactory+bulb.&rft.au=Deprez%2C+Francine%3BPallotto%2C+Marta%3BVogt%2C+Fabia%3BGrabiec%2C+Marta%3BVirtanen%2C+Mari+A%3BTyagarajan%2C+Shiva+K%3BPanzanelli%2C+Patrizia%3BFritschy%2C+Jean-Marc&rft.aulast=Deprez&rft.aufirst=Francine&rft.date=2015-09-01&rft.volume=523&rft.issue=13&rft.spage=1998&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+comparative+neurology&rft.issn=1096-9861&rft_id=info:doi/10.1002%2Fcne.23776 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-18 N1 - Date created - 2015-07-20 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/cne.23776 ER - TY - JOUR T1 - Use of acetochlor and cancer incidence in the Agricultural Health Study AN - 1694976305; PQ0001664541 AB - Since its registration in 1994 acetochlor has become a commonly used herbicide in the US, yet no epidemiologic study has evaluated its carcinogenicity in humans. We evaluated the use of acetochlor and cancer incidence among licensed pesticide applicators in the Agricultural Health Study. In telephone interviews administered during 1999-2005, participants provided information on acetochlor use, use of other pesticides and additional potential confounders. We used Poisson regression to estimate relative risks (RR) and 95% confidence intervals (95% CI) for cancers that occurred from the time of interview through 2011 in Iowa and 2010 in North Carolina. Among 33,484 men, there were 4,026 applicators who used acetochlor and 3,234 incident cancers, with 304 acetochlor-exposed cases. Increased risk of lung cancer was observed among acetochlor users (RR=1.74; 95% CI: 1.07-2.84) compared to nonusers, and among individuals who reported using acetochlor/atrazine product mixtures (RR=2.33; 95% CI: 1.30-4.17), compared to nonusers of acetochlor. Colorectal cancer risk was significantly elevated among the highest category of acetochlor users (RR=1.75; 95% CI: 1.08-2.83) compared to never users. Additionally, borderline significantly increased risk of melanoma (RR=1.61; 95% CI: 0.98-2.66) and pancreatic cancer (RR=2.36; 95% CI: 0.98-5.65) were observed among acetochlor users. The associations between acetochlor use and lung cancer, colorectal cancer, melanoma and pancreatic cancer are suggestive, however the lack of exposure-response trends, small number of exposed cases and relatively short time between acetochlor use and cancer development prohibit definitive conclusions. What's new? Acetochlor is a commonly used herbicide in the U.S., yet no epidemiologic research has evaluated its carcinogenicity in humans. In this study, the authors examined the relationship between occupational exposure to acetochlor and human cancer risk in a large prospective cohort. Acetochlor use was associated with an increased risk of lung and colorectal cancer, and possibly pancreatic cancer and melanoma. Use of mixtures of acetochlor and atrazine, another widely used herbicide often applied concurrently with acetochlor, was also associated with an increased risk of lung cancer. JF - International Journal of Cancer AU - Lerro, Catherine C AU - Koutros, Stella AU - Andreotti, Gabriella AU - Hines, Cynthia J AU - Blair, Aaron AU - Lubin, Jay AU - Ma, Xiaomei AU - Zhang, Yawei AU - Beane Freeman, Laura E AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD. Y1 - 2015/09// PY - 2015 DA - Sep 2015 SP - 1167 EP - 1175 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 137 IS - 5 SN - 0020-7136, 0020-7136 KW - Risk Abstracts; Health & Safety Science Abstracts KW - ANW, USA, North Carolina KW - Pancreatic cancer KW - Herbicides KW - Cancer KW - Melanoma KW - Health risks KW - USA, Iowa KW - Carcinogenicity KW - Dose-response effects KW - Pesticides KW - Atrazine KW - Acetochlor KW - Colorectal carcinoma KW - Occupational exposure KW - Lung cancer KW - H 5000:Pesticides KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1694976305?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=Use+of+acetochlor+and+cancer+incidence+in+the+Agricultural+Health+Study&rft.au=Lerro%2C+Catherine+C%3BKoutros%2C+Stella%3BAndreotti%2C+Gabriella%3BHines%2C+Cynthia+J%3BBlair%2C+Aaron%3BLubin%2C+Jay%3BMa%2C+Xiaomei%3BZhang%2C+Yawei%3BBeane+Freeman%2C+Laura+E&rft.aulast=Lerro&rft.aufirst=Catherine&rft.date=2015-09-01&rft.volume=137&rft.issue=5&rft.spage=1167&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.29416 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-07-01 N1 - Last updated - 2015-08-05 N1 - SubjectsTermNotLitGenreText - Pancreatic cancer; Herbicides; Cancer; Melanoma; Health risks; Carcinogenicity; Dose-response effects; Acetochlor; Atrazine; Pesticides; Colorectal carcinoma; Occupational exposure; Lung cancer; ANW, USA, North Carolina; USA, Iowa DO - http://dx.doi.org/10.1002/ijc.29416 ER - TY - JOUR T1 - Can the observed association between serum perfluoroalkyl substances and delayed menarche be explained on the basis of puberty-related changes in physiology and pharmacokinetics? AN - 1689840951; 26043300 AB - An association between serum levels of two perfluoroalkyl substances (PFAS) and delayed age at menarche was reported in a cross-sectional study of adolescents. Because perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) have half-lives of years, growth dilution and the development of a new route of excretion (menstruation) could account for some or all of the reported association. To assess how much of the epidemiologic association between PFAS and delayed menarche can be explained by the correlation of growth and maturation with PFAS body burden. We developed a Monte Carlo (MC) physiologically-based pharmacokinetic (PBPK) model of PFAS to simulate plasma PFAS levels in a hypothetical female population aged 2 to 20years old. Realistic distributions of physiological parameters as well as timing of growth spurts and menarche were incorporated in the model. The association between PFAS level and delayed menarche in the simulated data was compared with the reported association. The prevalence of menarche, distributions of age-dependent physiological parameters, and quartiles of serum PFAS concentrations in the simulated subjects were comparable to those reported in the epidemiologic study. The delay of menarche in days per natural log increase in PFAS concentrations in the simulated data were about one third as large as the observed values. The reported relationship between PFAS and age at menarche appears to be at least partly explained by pharmacokinetics rather than a toxic effect of these substances. Copyright © 2015 Elsevier Ltd. All rights reserved. JF - Environment international AU - Wu, Huali AU - Yoon, Miyoung AU - Verner, Marc-André AU - Xue, Jianping AU - Luo, Man AU - Andersen, Melvin E AU - Longnecker, Matthew P AU - Clewell, Harvey J AD - The Hamner Institutes for Health Sciences, RTP, NC, USA. ; Department of Environmental Health, Harvard School of Public Health, Boston, USA. ; US Environmental Protection Agency, RTP, NC, USA. ; National Institute of Environmental Health Sciences, RTP, NC, USA. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 61 EP - 68 VL - 82 KW - Alkanesulfonic Acids KW - 0 KW - Caprylates KW - Fluorocarbons KW - perfluorooctanoic acid KW - 947VD76D3L KW - perfluorooctane sulfonic acid KW - 9H2MAI21CL KW - Index Medicus KW - PBPK KW - PFOA KW - Environmental exposure KW - PFOS KW - Menarche KW - Female KW - Cross-Sectional Studies KW - Humans KW - Adolescent KW - Male KW - Sexual Maturation KW - Prevalence KW - Fluorocarbons -- pharmacokinetics KW - Puberty -- physiology KW - Fluorocarbons -- blood KW - Menarche -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1689840951?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environment+international&rft.atitle=Can+the+observed+association+between+serum+perfluoroalkyl+substances+and+delayed+menarche+be+explained+on+the+basis+of+puberty-related+changes+in+physiology+and+pharmacokinetics%3F&rft.au=Wu%2C+Huali%3BYoon%2C+Miyoung%3BVerner%2C+Marc-Andr%C3%A9%3BXue%2C+Jianping%3BLuo%2C+Man%3BAndersen%2C+Melvin+E%3BLongnecker%2C+Matthew+P%3BClewell%2C+Harvey+J&rft.aulast=Wu&rft.aufirst=Huali&rft.date=2015-09-01&rft.volume=82&rft.issue=&rft.spage=61&rft.isbn=&rft.btitle=&rft.title=Environment+international&rft.issn=1873-6750&rft_id=info:doi/10.1016%2Fj.envint.2015.05.006 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-25 N1 - Date created - 2015-06-17 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.envint.2015.05.006 ER - TY - JOUR T1 - Epoxyeicosatrienoic acids regulate macrophage polarization and prevent LPS-induced cardiac dysfunction. AN - 1683754385; 25626689 AB - Macrophages, owning tremendous phenotypic plasticity and diverse functions, were becoming the target cells in various inflammatory, metabolic and immune diseases. Cytochrome P450 epoxygenase 2J2 (CYP2J2) metabolizes arachidonic acid to form epoxyeicosatrienoic acids (EETs), which possess various beneficial effects on cardiovascular system. In the present study, we evaluated the effects of EETs treatment on macrophage polarization and recombinant adeno-associated virus (rAAV)-mediated CYP2J2 expression on lipopolysaccharide (LPS)-induced cardiac dysfunction, and sought to investigate the underlying mechanisms. In vitro studies showed that EETs (1µmol/L) significantly inhibited LPS-induced M1 macrophage polarization and diminished the proinflammatory cytokines at transcriptional and post-transcriptional level; meanwhile it preserved M2 macrophage related molecules expression and upregulated anti-inflammatory cytokine IL-10. Furthermore, EETs down-regulated NF-κB activation and up-regulated peroxisome proliferator-activated receptors (PPARα/γ) and heme oxygenase 1 (HO-1) expression, which play important roles in regulating M1 and M2 polarization. In addition, LPS treatment in mice induced cardiac dysfunction, heart tissue damage and infiltration of M1 macrophages, as well as the increase of inflammatory cytokines in serum and heart tissue, but rAAV-mediated CYP2J2 expression increased EETs generation in heart and significantly attenuated the LPS-induced harmful effects, which mechanisms were similar as the in vitro study. Taken together, the results indicate that CYP2J2/EETs regulates macrophage polarization by attenuating NF-κB signaling pathway via PPARα/γ and HO-1 activation and its potential use in treatment of inflammatory diseases. © 2015 Wiley Periodicals, Inc. JF - Journal of cellular physiology AU - Dai, Meiyan AU - Wu, Lujin AU - He, Zuowen AU - Zhang, Shasha AU - Chen, Chen AU - Xu, Xizhen AU - Wang, Peihua AU - Gruzdev, Artiom AU - Zeldin, Darryl C AU - Wang, Dao Wen AD - Departments of Internal Medicine and Institute of Hypertension, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. ; Division of Intramural Research, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina. Y1 - 2015/09// PY - 2015 DA - September 2015 SP - 2108 EP - 2119 VL - 230 IS - 9 KW - Lipopolysaccharides KW - 0 KW - NF-kappa B KW - PPAR alpha KW - PPAR gamma KW - 8,11,14-Eicosatrienoic Acid KW - 7324-41-6 KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - arachidonate epoxygenase KW - EC 1.14.14.1 KW - Heme Oxygenase-1 KW - EC 1.14.14.18 KW - Index Medicus KW - Animals KW - Heme Oxygenase-1 -- genetics KW - Mice KW - Cell Polarity -- genetics KW - NF-kappa B -- genetics KW - PPAR alpha -- genetics KW - Gene Expression Regulation -- genetics KW - Macrophages -- pathology KW - Signal Transduction -- genetics KW - Lipopolysaccharides -- toxicity KW - PPAR alpha -- metabolism KW - PPAR gamma -- genetics KW - Macrophages -- metabolism KW - NF-kappa B -- metabolism KW - Inflammation -- therapy KW - Cytochrome P-450 Enzyme System -- therapeutic use KW - 8,11,14-Eicosatrienoic Acid -- analogs & derivatives KW - Myocardium -- pathology KW - Cytochrome P-450 Enzyme System -- genetics KW - 8,11,14-Eicosatrienoic Acid -- administration & dosage KW - Inflammation -- chemically induced KW - Inflammation -- genetics KW - Cytochrome P-450 Enzyme System -- metabolism KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Myocardium -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683754385?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+physiology&rft.atitle=Epoxyeicosatrienoic+acids+regulate+macrophage+polarization+and+prevent+LPS-induced+cardiac+dysfunction.&rft.au=Dai%2C+Meiyan%3BWu%2C+Lujin%3BHe%2C+Zuowen%3BZhang%2C+Shasha%3BChen%2C+Chen%3BXu%2C+Xizhen%3BWang%2C+Peihua%3BGruzdev%2C+Artiom%3BZeldin%2C+Darryl+C%3BWang%2C+Dao+Wen&rft.aulast=Dai&rft.aufirst=Meiyan&rft.date=2015-09-01&rft.volume=230&rft.issue=9&rft.spage=2108&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+physiology&rft.issn=1097-4652&rft_id=info:doi/10.1002%2Fjcp.24939 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-04 N1 - Date created - 2015-05-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Rev Immunol. 2008 Dec;8(12):958-69 [19029990] Life Sci. 2008 Aug 29;83(9-10):339-45 [18675280] Nat Rev Drug Discov. 2009 Oct;8(10):794-805 [19794443] PLoS One. 2009;4(10):e7421 [19823578] Circ J. 2009 Dec;73(12):2198-203 [19875896] Nat Rev Cardiol. 2010 Feb;7(2):77-86 [20065951] Cell. 2010 Mar 19;140(6):805-20 [20303872] Circ Res. 2010 May 28;106(10):1559-69 [20508200] J Pharmacol Exp Ther. 2010 Sep 1;334(3):784-94 [20501636] Annu Rev Pathol. 2011;6:19-48 [20887193] FASEB J. 2011 Feb;25(2):703-13 [21059750] Adv Drug Deliv Rev. 2011 Jul 18;63(8):597-609 [21477627] PLoS One. 2011;6(10):e26591 [22028915] J Lipid Res. 2012 Mar;53(3):456-66 [22223859] Immunobiology. 2012 May;217(5):468-75 [21820754] J Mol Cell Cardiol. 2012 Jun;52(6):1282-90 [22426029] Immunol Res. 2012 Sep;53(1-3):11-24 [22418728] Hum Gene Ther. 2012 Jul;23(7):688-99 [22260463] Prostaglandins Other Lipid Mediat. 2012 Aug;98(3-4):133-42 [22209722] Am J Physiol Cell Physiol. 2012 Aug 1;303(3):C278-90 [22621785] Biochem Biophys Res Commun. 2012 Sep 14;426(1):76-82 [22910418] Am J Physiol Renal Physiol. 2013 Apr 1;304(7):F948-57 [23408164] J Lipid Res. 2013 May;54(5):1448-56 [23446230] Clin Cancer Res. 2013 Apr 15;19(8):2014-24 [23493353] J Pharmacol Exp Ther. 2013 May;345(2):239-49 [23442249] Arterioscler Thromb Vasc Biol. 2013 Jun;33(6):1135-44 [23640482] Basic Res Cardiol. 2013 Jul;108(4):357 [23740215] Clin Sci (Lond). 2013 Oct;125(7):349-59 [23611540] Prostaglandins Other Lipid Mediat. 2013 Jul-Aug;104-105:8-17 [22922020] Mol Pharmacol. 2014 Jan;85(1):105-15 [24145329] Endocrinology. 2014 Mar;155(3):818-28 [24424052] Biochem Pharmacol. 2014 May 1;89(1):109-18 [24607272] Arterioscler Thromb Vasc Biol. 2014 May;34(5):1032-44 [24578383] Arch Biochem Biophys. 2014 Dec 15;564:83-8 [25241054] Curr Pharm Des. 2003;9(30):2541-51 [14529552] Science. 2003 Oct 17;302(5644):406-7 [14563997] Circulation. 2004 Jul 20;110(3):309-16 [15226216] Circulation. 2004 Aug 31;110(9):1128-33 [15313948] Science. 1999 Aug 20;285(5431):1276-9 [10455056] Trends Immunol. 2004 Dec;25(12):677-86 [15530839] Proc Natl Acad Sci U S A. 2005 Jul 12;102(28):9772-7 [15994227] J Pharmacol Exp Ther. 2005 Aug;314(2):522-32 [15840765] Proc Natl Acad Sci U S A. 2005 Nov 15;102(46):16747-52 [16267130] Nat Rev Immunol. 2005 Dec;5(12):953-64 [16322748] Cell Metab. 2006 Jul;4(1):13-24 [16814729] Prostaglandins Other Lipid Mediat. 2007 Jan;82(1-4):155-61 [17164143] PLoS One. 2007;2(2):e260 [17327920] Drug Metab Dispos. 2007 Jul;35(7):1126-34 [17431031] Cell Metab. 2007 Aug;6(2):137-43 [17681149] Am J Physiol Heart Circ Physiol. 2007 Nov;293(5):H2870-7 [17720769] Annu Rev Immunol. 2009;27:451-83 [19105661] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/jcp.24939 ER - TY - JOUR T1 - Synthesis and biological evaluation of 6-substituted indolizinoquinolinediones as catalytic DNA topoisomerase I inhibitors. AN - 1705474779; 26188908 AB - In our previous work, indolizinoquinolinedione derivative 1 was identified as a Top1 catalytic inhibitor. Herein, a series of 6-substituted indolizinoquinolinedione derivatives were synthesized through modification of the parent compound 1. Top1 cleavage and relaxation assays indicate that none of these novel compounds act as classical Top1 poison, and that the compounds with alkylamino terminus at C-6 side chain, including 8, 11-16, 18-21, 25, 26 and 28-30, are the most potent Top1 catalytic inhibitors. Top1-mediated unwinding assay demonstrated that 14, 22 and 26 were Top1 catalytic inhibitors without Top1-mediated unwinding effect. Moreover, MTT results showed that compounds 26, 28-30 exhibit significant cytotoxicity against human leukemia HL-60 cells, and that compound 26 exerts potent cytotoxicity against A549 lung cancer cells at nanomolar range. Copyright © 2015 Elsevier Masson SAS. All rights reserved. JF - European journal of medicinal chemistry AU - Yu, Le-Mao AU - Zhang, Xiao-Ru AU - Li, Xiao-Bing AU - Yang, Yuan AU - Wei, Hong-Yu AU - He, Xi-Xin AU - Gu, Lian-Quan AU - Huang, Zhi-Shu AU - Pommier, Yves AU - An, Lin-Kun AD - School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. ; College of Chinese Materia Medica, Guangzhou University of Chinese Medicine, Guangzhou 510006, China. ; Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892-4255, United States. ; School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China. Electronic address: lssalk@mail.sysu.edu.cn. Y1 - 2015/08/28/ PY - 2015 DA - 2015 Aug 28 SP - 525 EP - 533 VL - 101 KW - Antineoplastic Agents KW - 0 KW - Indolizines KW - N-(3-(4-methylpiperazin-1-yl)propyl)-5,12-dioxo-5,12-dihydroindolizino(2,3-g)quinoline-6-carboxamide KW - Quinolones KW - Topoisomerase I Inhibitors KW - DNA Topoisomerases, Type I KW - EC 5.99.1.2 KW - Index Medicus KW - Anticancer KW - DNA topoisomerase KW - Indolizinoquinolinedione KW - Inhibitor KW - Molecular Structure KW - Cell Proliferation -- drug effects KW - Drug Screening Assays, Antitumor KW - Tumor Cells, Cultured KW - Dose-Response Relationship, Drug KW - Humans KW - Biocatalysis -- drug effects KW - Structure-Activity Relationship KW - Topoisomerase I Inhibitors -- pharmacology KW - Topoisomerase I Inhibitors -- chemistry KW - Antineoplastic Agents -- administration & dosage KW - Indolizines -- chemical synthesis KW - Indolizines -- pharmacology KW - Quinolones -- chemistry KW - Quinolones -- chemical synthesis KW - Antineoplastic Agents -- chemistry KW - Antineoplastic Agents -- pharmacology KW - DNA Topoisomerases, Type I -- metabolism KW - Topoisomerase I Inhibitors -- chemical synthesis KW - Quinolones -- pharmacology KW - Indolizines -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1705474779?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+medicinal+chemistry&rft.atitle=Synthesis+and+biological+evaluation+of+6-substituted+indolizinoquinolinediones+as+catalytic+DNA+topoisomerase+I+inhibitors.&rft.au=Yu%2C+Le-Mao%3BZhang%2C+Xiao-Ru%3BLi%2C+Xiao-Bing%3BYang%2C+Yuan%3BWei%2C+Hong-Yu%3BHe%2C+Xi-Xin%3BGu%2C+Lian-Quan%3BHuang%2C+Zhi-Shu%3BPommier%2C+Yves%3BAn%2C+Lin-Kun&rft.aulast=Yu&rft.aufirst=Le-Mao&rft.date=2015-08-28&rft.volume=101&rft.issue=&rft.spage=525&rft.isbn=&rft.btitle=&rft.title=European+journal+of+medicinal+chemistry&rft.issn=1768-3254&rft_id=info:doi/10.1016%2Fj.ejmech.2015.07.007 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-24 N1 - Date created - 2015-08-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Chem Biol. 2010 May 28;17(5):421-33 [20534341] Eur J Med Chem. 2010 Sep;45(9):3938-42 [20638158] Biochemistry. 2010 Nov 30;49(47):10131-6 [21033700] Annu Rev Biochem. 2001;70:369-413 [11395412] J Med Chem. 2003 Nov 20;46(24):5129-38 [14613316] Annu Rev Biophys Bioeng. 1981;10:87-114 [7020585] Proc Natl Acad Sci U S A. 1981 Jun;78(6):3487-91 [6267594] Cancer Res. 1987 Feb 15;47(4):936-42 [3802100] Nucleic Acids Res. 1987 Aug 25;15(16):6713-31 [2819825] Annu Rev Biochem. 1996;65:635-92 [8811192] Science. 1998 Mar 6;279(5356):1534-41 [9488652] Nat Rev Cancer. 2006 Oct;6(10):789-802 [16990856] ACS Chem Biol. 2013 Jan 18;8(1):82-95 [23259582] Bioorg Med Chem. 2008 Apr 15;16(8):4617-25 [18296054] J Med Chem. 2006 Oct 19;49(21):6283-9 [17034134] Nat Protoc. 2008;3(11):1736-50 [18927559] J Med Chem. 2010 Mar 11;53(5):1979-89 [20155916] Chem Rev. 2009 Jul;109(7):2894-902 [19476377] Arch Pharm (Weinheim). 2009 Feb;342(2):80-6 [19173337] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ejmech.2015.07.007 ER - TY - JOUR T1 - Curcumin inhibits PhIP induced cytotoxicity in breast epithelial cells through multiple molecular targets. AN - 1689621438; 26004342 AB - Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), found in cooked meat, is a known food carcinogen that causes several types of cancer, including breast cancer, as PhIP metabolites produce DNA adduct and DNA strand breaks. Curcumin, obtained from the rhizome of Curcuma longa, has potent anticancer activity. To date, no study has examined the interaction of PhIP with curcumin in breast epithelial cells. The present study demonstrates the mechanisms by which curcumin inhibits PhIP-induced cytotoxicity in normal breast epithelial cells (MCF-10A). Curcumin significantly inhibited PhIP-induced DNA adduct formation and DNA double stand breaks with a concomitant decrease in reactive oxygen species (ROS) production. The expression of Nrf2, FOXO targets; DNA repair genes BRCA-1, H2AFX and PARP-1; and tumor suppressor P16 was studied to evaluate the influence on these core signaling pathways. PhIP induced the expression of various antioxidant and DNA repair genes. However, co-treatment with curcumin inhibited this expression. PhIP suppressed the expression of the tumor suppressor P16 gene, whereas curcumin co-treatment increased its expression. Caspase-3 and -9 were slightly suppressed by curcumin with a consequent inhibition of cell death. These results suggest that curcumin appears to be an effective anti-PhIP food additive likely acting through multiple molecular targets. Published by Elsevier Ireland Ltd. JF - Cancer letters AU - Jain, Ashok AU - Samykutty, Abhilash AU - Jackson, Carissa AU - Browning, Darren AU - Bollag, Wendy B AU - Thangaraju, Muthusamy AU - Takahashi, Satoru AU - Singh, Shree Ram AD - Department of Natural Sciences, Albany State University, Albany, Georgia 31705, USA. Electronic address: ashok.jain@asurams.edu. ; Department of Natural Sciences, Albany State University, Albany, Georgia 31705, USA. ; Cancer Center, Georgia Regents University, Augusta, Georgia 30912, USA. ; Department of Physiology, Georgia Regents University, Augusta, Georgia 30912, USA; Charlie Norwood VA Medical Center, Augusta, Georgia 30904, USA. ; Department of Experimental Pathology and Tumor Biology, Graduate School of Medical Sciences, Nagoya City University, Nagoya 467-8601, Japan. ; Basic Research Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, Maryland, USA. Electronic address: singhshr@mail.nih.gov. Y1 - 2015/08/28/ PY - 2015 DA - 2015 Aug 28 SP - 122 EP - 131 VL - 365 IS - 1 KW - Antioxidants KW - 0 KW - DNA Adducts KW - Imidazoles KW - Reactive Oxygen Species KW - 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine KW - 909C6UN66T KW - Curcumin KW - IT942ZTH98 KW - Index Medicus KW - Heterocyclic amines KW - DNA damage KW - Reactive oxygen species KW - Cancer prevention KW - DNA adduct KW - Phytochemicals KW - Reactive Oxygen Species -- metabolism KW - DNA Breaks, Double-Stranded -- drug effects KW - Cell Survival -- drug effects KW - Dose-Response Relationship, Drug KW - Humans KW - Apoptosis -- drug effects KW - Oxidative Stress -- drug effects KW - Cytoprotection KW - Gene Expression Regulation -- drug effects KW - DNA Adducts -- metabolism KW - Cell Line KW - Epithelial Cells -- metabolism KW - Imidazoles -- toxicity KW - Epithelial Cells -- drug effects KW - Antioxidants -- pharmacology KW - Epithelial Cells -- pathology KW - Signal Transduction -- drug effects KW - Mammary Glands, Human -- metabolism KW - Mammary Glands, Human -- pathology KW - Mammary Glands, Human -- drug effects KW - Curcumin -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1689621438?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+letters&rft.atitle=Curcumin+inhibits+PhIP+induced+cytotoxicity+in+breast+epithelial+cells+through+multiple+molecular+targets.&rft.au=Jain%2C+Ashok%3BSamykutty%2C+Abhilash%3BJackson%2C+Carissa%3BBrowning%2C+Darren%3BBollag%2C+Wendy+B%3BThangaraju%2C+Muthusamy%3BTakahashi%2C+Satoru%3BSingh%2C+Shree+Ram&rft.aulast=Jain&rft.aufirst=Ashok&rft.date=2015-08-28&rft.volume=365&rft.issue=1&rft.spage=122&rft.isbn=&rft.btitle=&rft.title=Cancer+letters&rft.issn=1872-7980&rft_id=info:doi/10.1016%2Fj.canlet.2015.05.017 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-24 N1 - Date created - 2015-06-16 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.canlet.2015.05.017 ER - TY - JOUR T1 - Near infrared photoimmunotherapy for lung metastases. AN - 1689620043; 26021765 AB - Lung metastases are a leading cause of cancer related deaths; nonetheless current treatments are limited. Near infrared photoimmunotherapy (NIR-PIT) is a new cancer treatment that combines the specificity of intravenously injected antibodies that target tumors with the toxicity induced by photosensitizers activated by NIR-light. Herein, we demonstrate the efficacy of NIR-PIT in a mouse model of lung metastases. Experiments were conducted with a HER2, luciferase and GFP expressing cell line (3T3/HER2-luc-GFP). An antibody-photosensitizer conjugate (APC) consisting of trastuzumab and a phthalocyanine dye, IRDye700DX, was synthesized. In vitro NIR-PIT-induced cytotoxicity was light dose dependent. With 3D culture, repeated NIR-PIT could eradicate entire spheroids. In vivo anti-tumor effects of NIR-PIT included significant reductions in both tumor volume (p = 0.0141 vs. APC) and bioluminescence image (BLI) (p = 0.0086 vs. APC) in the flank model, and prolonged survival (p < 0.0001). BLI demonstrated a significant reduction in lung metastases volume (p = 0.0117 vs. APC). Multiple NIR-PIT doses significantly prolonged survival in the lung metastasis model (p < 0.0001). These results suggested that NIR-PIT is a potential new therapy for the local control of lung metastases. Published by Elsevier Ireland Ltd. JF - Cancer letters AU - Sato, Kazuhide AU - Nagaya, Tadanobu AU - Mitsunaga, Makoto AU - Choyke, Peter L AU - Kobayashi, Hisataka AD - Molecular Imaging Program, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA. ; Molecular Imaging Program, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA. Electronic address: Kobayash@mail.nih.gov. Y1 - 2015/08/28/ PY - 2015 DA - 2015 Aug 28 SP - 112 EP - 121 VL - 365 IS - 1 KW - Antibodies, Monoclonal, Humanized KW - 0 KW - Antineoplastic Agents KW - Indoles KW - Luminescent Proteins KW - Photosensitizing Agents KW - Receptor, ErbB-2 KW - EC 2.7.10.1 KW - Trastuzumab KW - P188ANX8CK KW - phthalocyanine KW - V5PUF4VLGY KW - Index Medicus KW - Lung metastases KW - Near infrared photoimmunotherapy KW - HER2 receptor KW - Bioluminescence KW - Animals KW - Dose-Response Relationship, Drug KW - Tomography, X-Ray Computed KW - Tumor Burden KW - Luminescent Proteins -- metabolism KW - Mice KW - Mice, Nude KW - BALB 3T3 Cells KW - Transfection KW - Genes, Reporter KW - Xenograft Model Antitumor Assays KW - Luminescent Proteins -- genetics KW - Time Factors KW - Female KW - Receptor, ErbB-2 -- genetics KW - Receptor, ErbB-2 -- antagonists & inhibitors KW - Lung Neoplasms -- secondary KW - Lung Neoplasms -- immunology KW - Receptor, ErbB-2 -- immunology KW - Lung Neoplasms -- therapy KW - Indoles -- pharmacology KW - Antibodies, Monoclonal, Humanized -- pharmacology KW - Photosensitizing Agents -- pharmacology KW - Lung Neoplasms -- diagnostic imaging KW - Antineoplastic Agents -- pharmacology KW - Phototherapy -- methods KW - Immunotherapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1689620043?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+letters&rft.atitle=Near+infrared+photoimmunotherapy+for+lung+metastases.&rft.au=Sato%2C+Kazuhide%3BNagaya%2C+Tadanobu%3BMitsunaga%2C+Makoto%3BChoyke%2C+Peter+L%3BKobayashi%2C+Hisataka&rft.aulast=Sato&rft.aufirst=Kazuhide&rft.date=2015-08-28&rft.volume=365&rft.issue=1&rft.spage=112&rft.isbn=&rft.btitle=&rft.title=Cancer+letters&rft.issn=1872-7980&rft_id=info:doi/10.1016%2Fj.canlet.2015.05.018 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-24 N1 - Date created - 2015-06-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Cell Biochem. 2010 Jan 1;109(1):58-64 [19911396] Nat Rev Cancer. 2011 Feb;11(2):135-41 [21258397] Science. 2011 Mar 25;331(6024):1559-64 [21436443] Cancer Prev Res (Phila). 2011 May;4(5):767-73 [21430072] Nat Rev Clin Oncol. 2011 Jun;8(6):378-82 [21423255] Mol Biol Cell. 2011 Sep;22(17):3103-19 [21775625] Nat Rev Cancer. 2011 Oct;11(10):735-48 [21941285] Cancer Res. 2011 Dec 1;71(23):7216-25 [21987726] Nat Med. 2011 Dec;17(12):1685-91 [22057348] Cancer Res. 2012 Sep 15;72(18):4622-8 [22800710] Mol Cancer Ther. 2015 Jan;14(1):141-50 [25416790] Theranostics. 2015;5(7):698-709 [25897335] Neoplasia. 2000 Nov-Dec;2(6):491-5 [11228541] Nat Rev Cancer. 2002 Aug;2(8):563-72 [12154349] J Immunol. 1983 Mar;130(3):1473-7 [6185591] Proc Natl Acad Sci U S A. 1986 Nov;83(22):8744-8 [2877461] Nat Med. 1998 Feb;4(2):245-7 [9461201] Cancer Res. 1998 Oct 1;58(19):4217-21 [9766640] Nat Rev Cancer. 2005 Oct;5(10):796-806 [16195751] Nat Med. 2006 Aug;12(8):895-904 [16892035] Clin Cancer Res. 2007 May 15;13(10):2936-45 [17504994] BMC Cancer. 2012;12:345 [22873679] ACS Nano. 2013 Jan 22;7(1):717-24 [23214407] J Nucl Med. 2013 May;54(5):770-5 [23536226] Theranostics. 2013;3(6):357-65 [23781283] Semin Thorac Cardiovasc Surg. 2013 Winter;25(4):292-9 [24673958] Nat Rev Cancer. 2014 May;14(5):314-28 [24739578] Mol Oncol. 2014 May;8(3):620-32 [24508062] Nat Rev Cancer. 2014 Jul;14(7):481-93 [24943811] Thorax. 2014 Oct;69(10):946-9 [24415715] Int J Cancer. 2014 Dec 1;135(11):2697-710 [24740257] PLoS One. 2014;9(11):e113276 [25401794] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.canlet.2015.05.018 ER - TY - JOUR T1 - Mitochondrial uncoupling links lipid catabolism to Akt inhibition and resistance to tumorigenesis. AN - 1708894824; 26310111 AB - To support growth, tumour cells reprogramme their metabolism to simultaneously upregulate macromolecular biosynthesis while maintaining energy production. Uncoupling proteins (UCPs) oppose this phenotype by inducing futile mitochondrial respiration that is uncoupled from ATP synthesis, resulting in nutrient wasting. Here using a UCP3 transgene targeted to the basal epidermis, we show that forced mitochondrial uncoupling inhibits skin carcinogenesis by blocking Akt activation. Similarly, Akt activation is markedly inhibited in UCP3 overexpressing primary human keratinocytes. Mechanistic studies reveal that uncoupling increases fatty acid oxidation and membrane phospholipid catabolism, and impairs recruitment of Akt to the plasma membrane. Overexpression of Akt overcomes metabolic regulation by UCP3, rescuing carcinogenesis. These findings demonstrate that mitochondrial uncoupling is an effective strategy to limit proliferation and tumorigenesis through inhibition of Akt, and illuminate a novel mechanism of crosstalk between mitochondrial metabolism and growth signalling. JF - Nature communications AU - Nowinski, Sara M AU - Solmonson, Ashley AU - Rundhaug, Joyce E AU - Rho, Okkyung AU - Cho, Jiyoon AU - Lago, Cory U AU - Riley, Christopher L AU - Lee, Sunhee AU - Kohno, Shohei AU - Dao, Christine K AU - Nikawa, Takeshi AU - Bratton, Shawn B AU - Wright, Casey W AU - Fischer, Susan M AU - DiGiovanni, John AU - Mills, Edward M AD - Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, Texas 78712, USA. ; Center for Molecular and Cellular Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, Texas 78712, USA. ; Science Park Research Division, University of Texas MD Anderson Cancer Center, Smithville, Texas 78957, USA. ; Center for Molecular Medicine, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, Texas 78712, USA. ; Department of Nutritional Physiology, Institute of Health Biosciences, Tokushima University Graduate School, Tokushima 770-8503, Japan. Y1 - 2015/08/27/ PY - 2015 DA - 2015 Aug 27 SP - 8137 VL - 6 KW - Carcinogens KW - 0 KW - Ion Channels KW - Mitochondrial Proteins KW - Reactive Oxygen Species KW - UCP3 protein, human KW - Ucp3 protein, mouse KW - Uncoupling Protein 3 KW - Proto-Oncogene Proteins c-akt KW - EC 2.7.11.1 KW - Tetradecanoylphorbol Acetate KW - NI40JAQ945 KW - Index Medicus KW - Tetradecanoylphorbol Acetate -- toxicity KW - Reactive Oxygen Species -- metabolism KW - Animals KW - Immunoblotting KW - Humans KW - Carcinogens -- toxicity KW - Mitochondria KW - Mice KW - Mice, Transgenic KW - Metabolomics KW - Neoplasms, Experimental KW - Gene Ontology KW - Metabolome KW - Cell Proliferation -- genetics KW - Flow Cytometry KW - Skin Neoplasms -- genetics KW - Proto-Oncogene Proteins c-akt -- metabolism KW - Carcinogenesis -- genetics KW - Skin Neoplasms -- chemically induced KW - Mitochondrial Proteins -- genetics KW - Lipid Metabolism -- genetics KW - Keratinocytes -- metabolism KW - Mitochondrial Proteins -- metabolism KW - Ion Channels -- genetics KW - Skin Neoplasms -- metabolism KW - Ion Channels -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1708894824?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+communications&rft.atitle=Mitochondrial+uncoupling+links+lipid+catabolism+to+Akt+inhibition+and+resistance+to+tumorigenesis.&rft.au=Nowinski%2C+Sara+M%3BSolmonson%2C+Ashley%3BRundhaug%2C+Joyce+E%3BRho%2C+Okkyung%3BCho%2C+Jiyoon%3BLago%2C+Cory+U%3BRiley%2C+Christopher+L%3BLee%2C+Sunhee%3BKohno%2C+Shohei%3BDao%2C+Christine+K%3BNikawa%2C+Takeshi%3BBratton%2C+Shawn+B%3BWright%2C+Casey+W%3BFischer%2C+Susan+M%3BDiGiovanni%2C+John%3BMills%2C+Edward+M&rft.aulast=Nowinski&rft.aufirst=Sara&rft.date=2015-08-27&rft.volume=6&rft.issue=&rft.spage=8137&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms9137 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-26 N1 - Date created - 2015-08-28 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - GSE71038; GEO N1 - SuppNotes - Cited By: Nat Commun. 2014;5:3114 [24445449] Carcinogenesis. 2013 Sep;34(9):1968-75 [23633519] Cancer Prev Res (Phila). 2015 Jun;8(6):487-91 [25784177] Free Radic Biol Med. 2015 Sep;86:67-77 [25960046] Cancer Res. 2000 Mar 15;60(6):1561-70 [10749124] Carcinogenesis. 2001 Apr;22(4):651-9 [11285202] J Biol Chem. 2001 Dec 14;276(50):46722-8 [11592962] Nucleic Acids Res. 2002 Jan 1;30(1):207-10 [11752295] J Biol Chem. 2002 Jul 26;277(30):27385-92 [12011039] Mol Cell Biol. 2003 Oct;23(20):7315-28 [14517300] Mol Cell Biol. 2003 Dec;23(24):9389-404 [14645548] J Biol Chem. 2003 Dec 12;278(50):50226-33 [14522978] Cancer Res. 2004 Apr 1;64(7):2382-9 [15059889] Trends Biochem Sci. 2004 May;29(5):233-42 [15130559] Cancer Res. 2004 Jun 1;64(11):3892-9 [15172999] Clin Cancer Res. 2004 Sep 15;10(18 Pt 1):6203-7 [15448008] FEBS Lett. 1982 Dec 13;150(1):129-32 [6819159] Carcinogenesis. 1987 Dec;8(12):1807-15 [3119244] Exp Cell Res. 1989 Feb;180(2):341-52 [2492469] Proc Natl Acad Sci U S A. 1990 Dec;87(23):9178-82 [2251261] Cell Tissue Kinet. 1990 Nov;23(6):587-602 [2177380] J Biol Chem. 1995 May 26;270(21):12614-22 [7759510] Cell Growth Differ. 1995 Nov;6(11):1447-55 [8562483] Biochimie. 1996;78(3):155-64 [8831946] Mol Carcinog. 1997 Sep;20(1):125-36 [9328443] Cell Growth Differ. 1998 Jan;9(1):31-9 [9438386] Mol Carcinog. 1998 Jun;22(2):73-83 [9655251] Int J Obes Relat Metab Disord. 1999 Jun;23 Suppl 6:S4-11 [10454114] Science. 1956 Feb 24;123(3191):309-14 [13298683] Nat Rev Mol Cell Biol. 2005 Mar;6(3):248-61 [15738989] FASEB J. 2005 Jun;19(8):977-9 [15814607] Oncogene. 2005 Jun 16;24(26):4165-73 [15806154] Biochim Biophys Acta. 2005 Aug 15;1709(1):35-44 [16005426] Oncogene. 2005 Sep 15;24(41):6314-22 [16007201] Br J Dermatol. 2005 Nov;153(5):937-44 [16225603] J Invest Dermatol. 2008 Aug;128(8):1894-900 [18305572] FASEB J. 2008 Dec;22(12):4281-95 [18757500] Nat Protoc. 2009;4(1):44-57 [19131956] Nucleic Acids Res. 2009 Jan;37(1):1-13 [19033363] Mol Biol Cell. 2011 May 15;22(10):1791-805 [21460183] Cell Metab. 2011 Jul 6;14(1):21-32 [21723501] Carcinogenesis. 2006 May;27(5):956-61 [16401637] Science. 2006 Jun 16;312(5780):1650-3 [16728594] J Biol Chem. 2006 Dec 8;281(49):37372-80 [17030509] J Cell Biol. 2006 Dec 18;175(6):913-23 [17158952] Genetics. 2007 Jan;175(1):77-91 [17151231] Nat Protoc. 2006;1(4):1872-8 [17487171] Cell. 2007 Jun 29;129(7):1261-74 [17604717] Cancer Res. 2007 Nov 15;67(22):10879-88 [18006833] Cell Metab. 2007 Dec;6(6):497-505 [18054318] Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19345-50 [18032601] Cancer Res. 2008 Apr 15;68(8):2813-9 [18413749] Toxicon. 2008 Jun 15;51(8):1345-56 [18455213] J Invest Dermatol. 2008 Jul;128(7):1747-56 [18219276] Antioxid Redox Signal. 2011 Nov 15;15(10):2645-61 [21619484] J Cell Physiol. 2012 Apr;227(4):1709-20 [21688263] Cold Spring Harb Perspect Biol. 2012 Jul;4(7):a006783 [22687276] Eukaryot Cell. 2012 Aug;11(8):1055-66 [22707484] Carcinogenesis. 2012 Nov;33(11):2065-75 [22847181] Oncogene. 2012 Nov 1;31(44):4725-31 [22266853] Biochimie. 2013 Apr;95(4):667-79 [23089136] Cancer Res. 2014 Jul 15;74(14):3971-82 [24853548] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ncomms9137 ER - TY - JOUR T1 - Matriptase promotes inflammatory cell accumulation and progression of established epidermal tumors. AN - 1708157681; 25486433 AB - Deregulation of matriptase is a consistent feature of human epithelial cancers and correlates with poor disease outcome. We have previously shown that matriptase promotes multi-stage squamous cell carcinogenesis in transgenic mice through dual activation of pro-hepatocyte growth factor-cMet-Akt-mTor proliferation/survival signaling and PAR-2-Gαi-NFκB inflammatory signaling. Matriptase was congenitally and constitutively deregulated in our prior studies, and therefore it was unclear if aberrant matriptase signaling supports only initiation of tumor formation or if it is also critical for the progression of established tumors. To determine this, we here have generated triple-transgenic mice with constitutive deregulation of matriptase and simultaneous inducible expression of the cognate matriptase inhibitor, hepatocyte growth factor inhibitor (HAI)-2. As expected, constitutive expression of HAI-2 suppressed the formation of matriptase-dependent tumors in 7,12-Dimethylbenz(a)anthracene-treated mouse skin. Interestingly, however, the induction of HAI-2 expression in already established tumors markedly impaired malignant progression and caused regression of individual tumors. Tumor regression correlated with reduced accumulation of tumor-associated inflammatory cells, likely caused by diminished expression of pro-tumorigenic inflammatory cytokines. The data suggest that matriptase-dependent signaling may be a therapeutic target for both squamous cell carcinoma chemoprevention and for the treatment of established tumors. JF - Oncogene AU - Sales, K U AU - Friis, S AU - Abusleme, L AU - Moutsopoulos, N M AU - Bugge, T H AD - Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA. Y1 - 2015/08/27/ PY - 2015 DA - 2015 Aug 27 SP - 4664 EP - 4672 VL - 34 IS - 35 KW - Cytokines KW - 0 KW - HAI-2 protein, mouse KW - Inflammation Mediators KW - Membrane Proteins KW - Serine Endopeptidases KW - EC 3.4.21.- KW - matriptase KW - Index Medicus KW - Animals KW - Carcinogenesis -- metabolism KW - Macrophages -- immunology KW - Membrane Proteins -- metabolism KW - Carcinogenesis -- immunology KW - Disease Progression KW - Cytokines -- metabolism KW - Membrane Proteins -- genetics KW - Mice, Transgenic KW - Male KW - Female KW - Inflammation Mediators -- metabolism KW - Serine Endopeptidases -- physiology KW - Carcinoma, Squamous Cell -- enzymology KW - Skin Neoplasms -- enzymology KW - Carcinoma, Squamous Cell -- immunology KW - Skin Neoplasms -- immunology KW - Carcinoma, Squamous Cell -- pathology KW - Skin Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1708157681?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Matriptase+promotes+inflammatory+cell+accumulation+and+progression+of+established+epidermal+tumors.&rft.au=Sales%2C+K+U%3BFriis%2C+S%3BAbusleme%2C+L%3BMoutsopoulos%2C+N+M%3BBugge%2C+T+H&rft.aulast=Sales&rft.aufirst=K&rft.date=2015-08-27&rft.volume=34&rft.issue=35&rft.spage=4664&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2014.391 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-24 N1 - Date created - 2015-08-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2013 May 10;288(19):13885-96 [23548907] J Biol Chem. 2008 Nov 7;283(45):30433-7 [18650443] Virchows Arch. 2014 Jan;464(1):19-27 [24248283] Cancer Sci. 2014 Jan;105(1):44-51 [24147538] Histopathology. 2014 Jul;65(1):24-34 [24382204] Thromb Haemost. 2014 Aug;112(2):402-11 [24696092] Oncogene. 2014 Sep 18;33(38):4643-52 [24121274] Oncogene. 2015 Jan 15;34(3):346-56 [24469043] Cancer Res. 2003 Mar 1;63(5):1101-5 [12615728] Cancer. 2003 Nov 1;98(9):1898-904 [14584072] Chest. 2004 May;125(5):1843-52 [15136399] Prostate. 2004 Nov 1;61(3):228-35 [15368474] Nature. 1983 May 5-11;303(5912):72-4 [6843661] Br J Cancer. 1985 Jan;51(1):1-7 [3881118] Nature. 1986 Jul 3-9;322(6074):78-80 [3014349] Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5547-51 [1319065] EMBO J. 1995 Nov 1;14(21):5216-23 [7489711] J Dermatol Sci. 1998 May;17(1):1-7 [9651822] Cancer Res. 2004 Dec 15;64(24):8804-7 [15604235] Br J Cancer. 2005 Jan 31;92(2):278-83 [15611789] Oncogene. 2005 Aug 11;24(34):5333-43 [16007225] Genes Dev. 2005 Aug 15;19(16):1934-50 [16103220] Oncogene. 2000 Jun 15;19(26):2951-6 [10871846] J Biol Chem. 2000 Aug 25;275(34):26333-42 [10831593] J Biol Chem. 2000 Nov 24;275(47):36720-5 [10962009] J Med Chem. 2001 Apr 26;44(9):1349-55 [11311057] Bioorg Med Chem Lett. 2001 Sep 17;11(18):2515-9 [11549459] Clin Cancer Res. 2002 Apr;8(4):1101-7 [11948120] World J Gastroenterol. 2005 Oct 21;11(39):6202-7 [16273651] Ann Oncol. 2009 Jan;20(1):63-70 [18689863] Cancer Res. 2009 Mar 1;69(5):1828-35 [19223533] J Invest Dermatol. 2009 Jul;129(7):1816-23 [19242518] Development. 2009 Aug;136(15):2653-63 [19592578] Prostate. 2010 Sep 15;70(13):1422-8 [20687215] Am J Pathol. 2010 Dec;177(6):3145-58 [20971737] Cancer Res. 2010 Dec 1;70(23):9631-40 [21098708] Oncogene. 2011 Apr 28;30(17):2003-16 [21217780] J Pathol. 2012 Oct;228(2):181-92 [22262311] Int J Oncol. 2005 Oct;27(4):1061-70 [16142324] Biochemistry. 2003 Feb 4;42(4):892-900 [12549907] Mod Pathol. 2006 Mar;19(3):447-52 [16439987] Cancer Epidemiol Biomarkers Prev. 2006 Feb;15(2):217-27 [16492908] FEBS Lett. 2006 Apr 17;580(9):2227-32 [16566926] BMC Cancer. 2006;6:176 [16820046] Blood. 2006 Oct 15;108(8):2616-23 [16794252] Histol Histopathol. 2007 Mar;22(3):305-9 [17163404] Proc Natl Acad Sci U S A. 2007 Apr 3;104(14):5771-6 [17389401] J Biol Chem. 2008 Oct 24;283(43):29495-504 [18713750] Am J Pathol. 2013 Oct;183(4):1306-17 [24070417] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/onc.2014.391 ER - TY - JOUR T1 - Key bioactive reaction products of the NO/H2S interaction are S/N-hybrid species, polysulfides, and nitroxyl. AN - 1707557397; 26224837 AB - Experimental evidence suggests that nitric oxide (NO) and hydrogen sulfide (H2S) signaling pathways are intimately intertwined, with mutual attenuation or potentiation of biological responses in the cardiovascular system and elsewhere. The chemical basis of this interaction is elusive. Moreover, polysulfides recently emerged as potential mediators of H2S/sulfide signaling, but their biosynthesis and relationship to NO remain enigmatic. We sought to characterize the nature, chemical biology, and bioactivity of key reaction products formed in the NO/sulfide system. At physiological pH, we find that NO and sulfide form a network of cascading chemical reactions that generate radical intermediates as well as anionic and uncharged solutes, with accumulation of three major products: nitrosopersulfide (SSNO(-)), polysulfides, and dinitrososulfite [N-nitrosohydroxylamine-N-sulfonate (SULFI/NO)], each with a distinct chemical biology and in vitro and in vivo bioactivity. SSNO(-) is resistant to thiols and cyanolysis, efficiently donates both sulfane sulfur and NO, and potently lowers blood pressure. Polysulfides are both intermediates and products of SSNO(-) synthesis/decomposition, and they also decrease blood pressure and enhance arterial compliance. SULFI/NO is a weak combined NO/nitroxyl donor that releases mainly N2O on decomposition; although it affects blood pressure only mildly, it markedly increases cardiac contractility, and formation of its precursor sulfite likely contributes to NO scavenging. Our results unveil an unexpectedly rich network of coupled chemical reactions between NO and H2S/sulfide, suggesting that the bioactivity of either transmitter is governed by concomitant formation of polysulfides and anionic S/N-hybrid species. This conceptual framework would seem to offer ample opportunities for the modulation of fundamental biological processes governed by redox switching and sulfur trafficking. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Cortese-Krott, Miriam M AU - Kuhnle, Gunter G C AU - Dyson, Alex AU - Fernandez, Bernadette O AU - Grman, Marian AU - DuMond, Jenna F AU - Barrow, Mark P AU - McLeod, George AU - Nakagawa, Hidehiko AU - Ondrias, Karol AU - Nagy, Péter AU - King, S Bruce AU - Saavedra, Joseph E AU - Keefer, Larry K AU - Singer, Mervyn AU - Kelm, Malte AU - Butler, Anthony R AU - Feelisch, Martin AD - Cardiovascular Research Laboratory, Department of Cardiology, Pneumology and Angiology, Medical Faculty, Heinrich Heine University of Düsseldorf, 40225 Dusseldorf, Germany; ; Department of Nutrition, University of Reading, Whiteknights, Reading RG6 6AP, United Kingdom; ; Bloomsbury Institute of Intensive Care Medicine, University College London, London WC1E 6BT, United Kingdom; ; Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton General Hospital and Institute for Life Sciences, Southampton SO16 6YD, United Kingdom; ; Center for Molecular Medicine, Slovak Academy of Sciences, 83101 Bratislava, Slovak Republic; ; Department of Chemistry, Wake Forest University, Winston-Salem, NC 27109; ; Department of Chemistry, Warwick University, Coventry CV4 7AL, United Kingdom; ; Bruker UK Ltd., Coventry CV4 9GH, United Kingdom; ; Department of Organic and Medicinal Chemistry, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya-shi, Aichi 467-8603, Japan; ; Department of Molecular Immunology and Toxicology, National Institute of Oncology, 1122 Budapest, Hungary; ; Leidos Biomedical Research, Inc., National Cancer Institute-Frederick, Frederick, MD 21702; ; National Cancer Institute-Frederick, Frederick, MD 21702; ; Medical School, University of St. Andrews, St. Andrews, Fife KY16 9AJ, Scotland. ; Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton General Hospital and Institute for Life Sciences, Southampton SO16 6YD, United Kingdom; M.Feelisch@soton.ac.uk. Y1 - 2015/08/25/ PY - 2015 DA - 2015 Aug 25 SP - E4651 EP - E4660 VL - 112 IS - 34 KW - Nitrogen Oxides KW - 0 KW - Sulfides KW - Nitric Oxide KW - 31C4KY9ESH KW - Sulfur KW - 70FD1KFU70 KW - nitroxyl KW - GFQ4MMS07W KW - Nitrogen KW - N762921K75 KW - Hydrogen Sulfide KW - YY9FVM7NSN KW - Index Medicus KW - redox KW - gasotransmitter KW - nitric oxide KW - sulfide KW - Animals KW - Sulfur -- metabolism KW - Rats, Wistar KW - Nitrogen -- metabolism KW - Male KW - Biological Availability KW - Hydrogen Sulfide -- metabolism KW - Sulfides -- metabolism KW - Nitrogen Oxides -- metabolism KW - Nitric Oxide -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1707557397?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Key+bioactive+reaction+products+of+the+NO%2FH2S+interaction+are+S%2FN-hybrid+species%2C+polysulfides%2C+and+nitroxyl.&rft.au=Cortese-Krott%2C+Miriam+M%3BKuhnle%2C+Gunter+G+C%3BDyson%2C+Alex%3BFernandez%2C+Bernadette+O%3BGrman%2C+Marian%3BDuMond%2C+Jenna+F%3BBarrow%2C+Mark+P%3BMcLeod%2C+George%3BNakagawa%2C+Hidehiko%3BOndrias%2C+Karol%3BNagy%2C+P%C3%A9ter%3BKing%2C+S+Bruce%3BSaavedra%2C+Joseph+E%3BKeefer%2C+Larry+K%3BSinger%2C+Mervyn%3BKelm%2C+Malte%3BButler%2C+Anthony+R%3BFeelisch%2C+Martin&rft.aulast=Cortese-Krott&rft.aufirst=Miriam&rft.date=2015-08-25&rft.volume=112&rft.issue=34&rft.spage=E4651&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=1091-6490&rft_id=info:doi/10.1073%2Fpnas.1509277112 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-30 N1 - Date created - 2015-08-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Br J Pharmacol. 2006 Nov;149(6):625-34 [17016507] Biochem Biophys Res Commun. 2006 Apr 28;343(1):303-10 [16540095] Science. 2007 Sep 7;317(5843):1393-7 [17717153] Nat Rev Drug Discov. 2007 Nov;6(11):917-35 [17948022] Anesthesiology. 2008 Oct;109(4):675-82 [18813047] BMC Biol. 2010;8:30 [20370908] Arterioscler Thromb Vasc Biol. 2010 Oct;30(10):1998-2004 [20634473] Curr Opin Nephrol Hypertens. 2011 Mar;20(2):107-12 [21301337] Proc Natl Acad Sci U S A. 2011 Apr 5;108(14):5526-31 [21422282] Antioxid Redox Signal. 2011 Jun;14(11):2081-91 [21194352] J Am Chem Soc. 2011 Aug 3;133(30):11675-85 [21699183] Free Radic Biol Med. 2011 Sep 15;51(6):1137-45 [21718783] Science. 2011 Nov 18;334(6058):986-90 [22096201] Chem Res Toxicol. 2012 Apr 16;25(4):769-93 [22263838] Antioxid Redox Signal. 2012 Jul 1;17(1):22-31 [22229551] J Am Chem Soc. 2012 Jul 25;134(29):12016-27 [22741609] J Comp Physiol B. 2012 Oct;182(7):881-97 [22430869] PLoS One. 2012;7(12):e53319 [23285278] FASEB J. 2007 Jun;21(8):1699-706 [17314140] Clin Chem Lab Med. 2013 Mar 1;51(3):623-32 [23196804] FASEB J. 2013 Jun;27(6):2451-7 [23413359] J Am Chem Soc. 2013 Aug 28;135(34):12690-6 [23865676] Nitric Oxide. 2013 Nov 30;35:21-34 [23850631] Redox Biol. 2014;2:234-44 [24494198] Proc Natl Acad Sci U S A. 2014 Feb 25;111(8):3182-7 [24516168] Proc Natl Acad Sci U S A. 2014 May 27;111(21):7606-11 [24733942] Molecules. 2014;19(8):12789-813 [25153879] Nitric Oxide. 2014 Sep 15;41:4-10 [24491257] Free Radic Biol Med. 2014 Dec;77:82-94 [25229186] Methods Enzymol. 2015;554:3-29 [25725513] Nitric Oxide. 2015 Apr 30;46:123-30 [25529482] Nitric Oxide. 2015 Apr 30;46:14-24 [25541073] Nat Chem. 2015 Apr;7(4):301-7 [25803468] Free Radic Biol Med. 2013 Feb;55:1-7 [23165065] Eur J Pharmacol. 2001 Nov 2;430(2-3):311-5 [11711049] Chem Rev. 2002 Apr;102(4):1135-54 [11942789] FASEB J. 2002 Nov;16(13):1775-85 [12409320] Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10860-4 [1961756] Biochem J. 1995 Dec 1;312 ( Pt 2):333-9 [8526840] Methods Enzymol. 1996;268:281-93 [8782594] J Exp Zool. 1998 Oct 15;282(3):310-22 [9755482] Science. 2005 Apr 22;308(5721):518 [15845845] Comment In: Proc Natl Acad Sci U S A. 2015 Aug 25;112(34):10573-4 [26269567] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1073/pnas.1509277112 ER - TY - JOUR T1 - Gateway to deLiver: How malaria sporozoites cross the sinusoidal barrier AN - 1712569557; PQ0001960075 JF - Journal of Experimental Medicine AU - Sacks, David AD - National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health Y1 - 2015/08/24/ PY - 2015 DA - 2015 Aug 24 SP - 1340 PB - Rockefeller University Press, 1114 First Avenue New York NY 10021-8325 United States VL - 212 IS - 9 SN - 0022-1007, 0022-1007 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts KW - Human diseases KW - Barriers KW - Sporozoites KW - Malaria KW - K 03410:Animal Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1712569557?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Experimental+Medicine&rft.atitle=Gateway+to+deLiver%3A+How+malaria+sporozoites+cross+the+sinusoidal+barrier&rft.au=Sacks%2C+David&rft.aulast=Sacks&rft.aufirst=David&rft.date=2015-08-24&rft.volume=212&rft.issue=9&rft.spage=1340&rft.isbn=&rft.btitle=&rft.title=Journal+of+Experimental+Medicine&rft.issn=00221007&rft_id=info:doi/10.1084%2Fjem.2129insight1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Human diseases; Barriers; Malaria; Sporozoites DO - http://dx.doi.org/10.1084/jem.2129insight1 ER - TY - JOUR T1 - Pro-toxic dehydropyrrolizidine alkaloids in the traditional Andean herbal medicine "asmachilca". AN - 1701322834; 26087231 AB - Asmachilca is a Peruvian medicinal herb preparation ostensibly derived from Aristeguietia gayana (Wedd.) R.M. King & H. Rob. (Asteraceae: Eupatorieae). Decoctions of the plant have a reported bronchodilation effect that is purported to be useful in the treatment of respiratory allergies, common cold and bronchial asthma. However, its attractiveness to pyrrolizidine alkaloid-pharmacophagous insects indicated a potential for toxicity for human consumers. To determine if commercial asmachilca samples, including fully processed herbal teas, contain potentially toxic 1,2-dehydropyrrolizidine alkaloids. Two brands of "Asmachilca" herbal tea bags and four other commercial samples of botanical materials for preparing asmachilca medicine were extracted and analyzed using HPLC-esi(+)MS and MS/MS for the characteristic retention times and mass spectra of known dehydropyrrolizidine alkaloids. Other suspected dehydropyrrolizidine alkaloids were tentatively identified based on MS/MS profiles and high resolution molecular weight determinations. Further structure elucidation of isolated alkaloids was based on 1D and 2D NMR spectroscopy. Asmachilca attracted many species of moths which are known to pharmacophagously gather dehydropyrrolizidine alkaloids. Analysis of 5 of the asmachilca samples revealed the major presence of the dehydropyrrolizidine alkaloid monoesters rinderine and supinine, and their N-oxides. The 6th sample was very similar but did not contain supinine or its N-oxide. Small quantities of other dehydropyrrolizidine alkaloid monoesters, including echinatine and intermedine, were also detected. In addition, two major metabolites, previously undescribed, were isolated and identified as dehydropyrrolizidine alkaloid monoesters with two "head-to-tail" linked viridifloric and/or trachelanthic acids. Estimates of total pyrrolizidine alkaloid and N-oxide content in the botanical components of asmachilca varied from 0.4% to 0.9% (w/dw, dry weight) based on equivalents of lycopsamine. The mean pyrrolizidine alkaloid content of a hot water infusion of a commercial asmachilca herbal tea bag was 2.2±0.5mg lycopsamine equivalents. Morphological and chemical evidence showed that asmachilca is prepared from different plant species. All asmachilca samples and the herbal tea infusions contained toxicologically-relevant concentrations of pro-toxic 1,2-dehydropyrrolizidine alkaloid esters and, therefore, present a risk to the health of humans. This raises questions concerning the ongoing unrestricted availability of such products on the Peruvian and international market. In addition to medical surveys of consumers of asmachilca, in the context of chronic disease potentially associated with ingestion of the dehydropyrrolizidine alkaloids, the botanical origins of asmachilca preparations require detailed elucidation. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. JF - Journal of ethnopharmacology AU - Colegate, Steven M AU - Boppré, Michael AU - Monzón, Julio AU - Betz, Joseph M AD - USDA, ARS, Poisonous Plant Research Laboratory, Logan, UT 84341, USA; Department of Animal, Dairy and Veterinary Sciences, Utah State University, Logan, UT 84322, USA. Electronic address: steven.colegate@usu.edu. ; Forstzoologie und Entomologie, Albert-Ludwigs-Universität, D-79085 Freiburg, Germany. ; Office of Dietary Supplements, National Institutes of Health, 6100 Executive Blvd., Room 3B01, Bethesda, MD 20892, USA. Y1 - 2015/08/22/ PY - 2015 DA - 2015 Aug 22 SP - 179 EP - 194 VL - 172 KW - Pyrrolizidine Alkaloids KW - 0 KW - Tea KW - asmachilca KW - indicine KW - 480-82-0 KW - Index Medicus KW - Rinderine KW - Asmachilcadinine KW - Asmachilca KW - Aristeguietia gayana KW - 1,2-Dehydropyrrolizidine alkaloids KW - Asmachilcadine KW - Herbal tea KW - Eupatorium KW - Pyrrolizidine alkaloids KW - Intermedine KW - Supinine KW - Hepatotoxicity KW - Ethnobotany KW - Humans KW - Plants, Medicinal -- toxicity KW - Pyrrolizidine Alkaloids -- isolation & purification KW - Pyrrolizidine Alkaloids -- analysis KW - Tea -- chemistry KW - Asteraceae -- chemistry KW - Pyrrolizidine Alkaloids -- toxicity KW - Pyrrolizidine Alkaloids -- chemistry KW - Plants, Medicinal -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701322834?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+ethnopharmacology&rft.atitle=Pro-toxic+dehydropyrrolizidine+alkaloids+in+the+traditional+Andean+herbal+medicine+%22asmachilca%22.&rft.au=Colegate%2C+Steven+M%3BBoppr%C3%A9%2C+Michael%3BMonz%C3%B3n%2C+Julio%3BBetz%2C+Joseph+M&rft.aulast=Colegate&rft.aufirst=Steven&rft.date=2015-08-22&rft.volume=172&rft.issue=&rft.spage=179&rft.isbn=&rft.btitle=&rft.title=Journal+of+ethnopharmacology&rft.issn=1872-7573&rft_id=info:doi/10.1016%2Fj.jep.2015.06.012 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-03 N1 - Date created - 2015-08-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Asian Nat Prod Res. 2008 Mar-Apr;10(3-4):349-54 [18348059] Anal Bioanal Chem. 2007 Sep;389(1):13-7 [17572883] Phytochem Anal. 2005 Mar-Apr;16(2):108-19 [15881119] Headache. 2005 Mar;45(3):196-203 [15836592] J Agric Food Chem. 2005 Mar 23;53(6):1894-902 [15769110] Pharmazie. 1995 Feb;50(2):83-98 [7700976] J Pharm Sci. 1994 May;83(5):649-53 [8071814] Pharmazie. 2000 Oct;55(10):711-26 [11082830] Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2014;31(11):1886-95 [25222912] Anal Bioanal Chem. 2014 Nov;406(28):7345-54 [25286874] Phytochem Anal. 2014 Sep-Oct;25(5):429-38 [24816769] J Nat Prod. 2013 Oct 25;76(10):1829-35 [24107229] Anal Bioanal Chem. 2013 May;405(13):4419-28 [23224664] Phytochem Anal. 2013 May-Jun;24(3):201-12 [23070903] Pharmazie. 2013 Feb;68(2):83-92 [23469679] Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2011 Mar;28(3):260-81 [21360373] Pharmazie. 2009 Nov;64(11):699-716 [20099513] Pharmazie. 2011 Sep;66(9):637-47 [22026117] Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2011 Mar;28(3):308-24 [21360376] Mol Nutr Food Res. 2008 Oct;52(10):1193-200 [18792927] Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2011 Mar;28(3):293-307 [21360375] Chem Res Toxicol. 2015 Jan 20;28(1):4-20 [25483859] Phytochem Anal. 2015 May-Jun;26(3):215-25 [25645745] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jep.2015.06.012 ER - TY - JOUR T1 - The Interplay Between Host Genetic Variation, Viral Replication, and Microbial Translocation in Untreated HIV-Infected Individuals AN - 1773824945; PQ0002695522 AB - Systemic immune activation, a major determinant of human immunodeficiency virus (HIV) disease progression, is the result of a complex interplay between viral replication, dysregulation of the immune system, and microbial translocation due to gut mucosal damage. Although human genetic variants influencing HIV load have been identified, it is unknown how much the host genetic background contributes to interindividual differences in other determinants of HIV pathogenesis such as gut damage and microbial translocation. Using samples and data from 717 untreated participants in the Swiss HIV Cohort Study and a genome-wide association study design, we searched for human genetic determinants of plasma levels of intestinal fatty acid-binding protein (I-FABP/FABP2), a marker of gut damage, and of soluble CD14 (sCD14), a marker of lipopolysaccharide bioactivity and microbial translocation. We also assessed the correlations between HIV load, sCD14, and I-FABP. Although we found no genome-wide significant determinant of the tested plasma markers, we observed strong associations between sCD14 and both HIV load and I-FABP, shedding new light on the relationships between processes that drive progression of untreated HIV infection. JF - Journal of Infectious Diseases AU - Perkins, Molly R AU - Bartha, Istvan AU - Timmer, J Katherina AU - Liebner, Julia C AU - Wollinsky, David AU - Gunthard, Huldrych F AU - Hauser, Christoph AU - Bernasconi, Enos AU - Hoffmann, Matthias AU - Calmy, Alexandra AU - Battegay, Manuel AU - Telenti, Amalio AU - Douek, Daniel C AU - Fellay, Jacques AD - Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland Y1 - 2015/08/15/ PY - 2015 DA - 2015 Aug 15 SP - 578 EP - 584 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 212 IS - 4 SN - 0022-1899, 0022-1899 KW - Virology & AIDS Abstracts; Health & Safety Science Abstracts KW - HIV KW - host genomics KW - genome-wide association study KW - immune activation KW - microbial translocation KW - sCD14 KW - I-FABP KW - Protein transport KW - Data processing KW - Replication KW - Immune system KW - Mucosa KW - Genetic diversity KW - Fatty acid-binding protein KW - CD14 antigen KW - Infection KW - Plasma levels KW - Digestive tract KW - Infectious diseases KW - Human immunodeficiency virus KW - Intestine KW - Proteins KW - Lipopolysaccharides KW - Immune response KW - Translocation KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - V 22360:AIDS and HIV UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1773824945?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=The+Interplay+Between+Host+Genetic+Variation%2C+Viral+Replication%2C+and+Microbial+Translocation+in+Untreated+HIV-Infected+Individuals&rft.au=Perkins%2C+Molly+R%3BBartha%2C+Istvan%3BTimmer%2C+J+Katherina%3BLiebner%2C+Julia+C%3BWollinsky%2C+David%3BGunthard%2C+Huldrych+F%3BHauser%2C+Christoph%3BBernasconi%2C+Enos%3BHoffmann%2C+Matthias%3BCalmy%2C+Alexandra%3BBattegay%2C+Manuel%3BTelenti%2C+Amalio%3BDouek%2C+Daniel+C%3BFellay%2C+Jacques&rft.aulast=Perkins&rft.aufirst=Molly&rft.date=2015-08-15&rft.volume=212&rft.issue=4&rft.spage=578&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiv089 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Protein transport; Data processing; Replication; Immune system; Mucosa; Genetic diversity; Infection; CD14 antigen; Fatty acid-binding protein; Plasma levels; Digestive tract; Intestine; Lipopolysaccharides; Immune response; Translocation; Infectious diseases; Human immunodeficiency virus; Proteins DO - http://dx.doi.org/10.1093/infdis/jiv089 ER - TY - JOUR T1 - AVIA v2.0: annotation, visualization and impact analysis of genomic variants and genes AN - 1709191510; PQ0001896500 AB - Summary: As sequencing becomes cheaper and more widely available, there is a greater need to quickly and effectively analyze large-scale genomic data. While the functionality of AVIA v1.0, whose implementation was based on ANNOVAR, was comparable with other annotation web servers, AVIA v2.0 represents an enhanced web-based server that extends genomic annotations to cell-specific transcripts and protein-level functional annotations. With AVIA's improved interface, users can better visualize their data, perform comprehensive searches and categorize both coding and non-coding variants.Availability and implementation: AVIA is freely available through the web at http://avia.abcc.ncifcrf.gov. Supplementary information: Supplementary data are available at Bioinformatics online. JF - Bioinformatics AU - Vuong, Hue AU - Che, Anney AU - Ravichandran, Sarangan AU - Luke, Brian T AU - Collins, Jack R AU - Mudunuri, Uma S AD - *To whom correspondence should be addressed., Hue.Vuong@fnlcr.nih.gov Y1 - 2015/08/15/ PY - 2015 DA - 2015 Aug 15 SP - 2748 EP - 2750 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 31 IS - 16 SN - 1367-4803, 1367-4803 KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - Data processing KW - genomics KW - Bioinformatics KW - Internet KW - N 14810:Methods KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709191510?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioinformatics&rft.atitle=AVIA+v2.0%3A+annotation%2C+visualization+and+impact+analysis+of+genomic+variants+and+genes&rft.au=Vuong%2C+Hue%3BChe%2C+Anney%3BRavichandran%2C+Sarangan%3BLuke%2C+Brian+T%3BCollins%2C+Jack+R%3BMudunuri%2C+Uma+S&rft.aulast=Vuong&rft.aufirst=Hue&rft.date=2015-08-15&rft.volume=31&rft.issue=16&rft.spage=2748&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtv200 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2016-07-20 N1 - SubjectsTermNotLitGenreText - Data processing; Bioinformatics; genomics; Internet DO - http://dx.doi.org/10.1093/bioinformatics/btv200 ER - TY - JOUR T1 - Induced Pluripotent Stem Cell Models to Enable In Vitro Models for Screening in the Central Nervous System. AN - 1702657740; 25794298 AB - There is great need to develop more predictive drug discovery tools to identify new therapies to treat diseases of the central nervous system (CNS). Current nonpluripotent stem cell-based models often utilize non-CNS immortalized cell lines and do not enable the development of personalized models of disease. In this review, we discuss why in vitro models are necessary for translational research and outline the unique advantages of induced pluripotent stem cell (iPSC)-based models over those of current systems. We suggest that iPSC-based models can be patient specific and isogenic lines can be differentiated into many neural cell types for detailed comparisons. iPSC-derived cells can be combined to form small organoids, or large panels of lines can be developed that enable new forms of analysis. iPSC and embryonic stem cell-derived cells can be readily engineered to develop reporters for lineage studies or mechanism of action experiments further extending the utility of iPSC-based systems. We conclude by describing novel technologies that include strategies for the development of diversity panels, novel genomic engineering tools, new three-dimensional organoid systems, and modified high-content screens that may bring toxicology into the 21st century. The strategic integration of these technologies with the advantages of iPSC-derived cell technology, we believe, will be a paradigm shift for toxicology and drug discovery efforts. JF - Stem cells and development AU - Hunsberger, Joshua G AU - Efthymiou, Anastasia G AU - Malik, Nasir AU - Behl, Mamta AU - Mead, Ivy L AU - Zeng, Xianmin AU - Simeonov, Anton AU - Rao, Mahendra AD - 1 Wake Forest Institute for Regenerative Medicine , Winston-Salem, North Carolina. ; 2 Uniformed Services University of the Health Sciences , Bethesda, Maryland. ; 3 National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health (NIH) , Bethesda, Maryland. ; 4 National Toxicology Program, National Institute of Environmental Health Sciences , Research Triangle Park, North Carolina. ; 5 Buck Institute for Age Research , Novato, California. ; 6 National Center for Advancing Translational Sciences (NCATS), National Institutes of Health (NIH) , Rockville, Maryland. ; 7 New York Stem Cell Foundation , New York, New York. Y1 - 2015/08/15/ PY - 2015 DA - 2015 Aug 15 SP - 1852 EP - 1864 VL - 24 IS - 16 KW - Central Nervous System Agents KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Cell Culture Techniques -- methods KW - Central Nervous System Agents -- pharmacology KW - Induced Pluripotent Stem Cells -- drug effects KW - Neurons -- drug effects KW - Neurons -- cytology KW - Induced Pluripotent Stem Cells -- cytology KW - Drug Evaluation, Preclinical -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1702657740?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+cells+and+development&rft.atitle=Induced+Pluripotent+Stem+Cell+Models+to+Enable+In+Vitro+Models+for+Screening+in+the+Central+Nervous+System.&rft.au=Hunsberger%2C+Joshua+G%3BEfthymiou%2C+Anastasia+G%3BMalik%2C+Nasir%3BBehl%2C+Mamta%3BMead%2C+Ivy+L%3BZeng%2C+Xianmin%3BSimeonov%2C+Anton%3BRao%2C+Mahendra&rft.aulast=Hunsberger&rft.aufirst=Joshua&rft.date=2015-08-15&rft.volume=24&rft.issue=16&rft.spage=1852&rft.isbn=&rft.btitle=&rft.title=Stem+cells+and+development&rft.issn=1557-8534&rft_id=info:doi/10.1089%2Fscd.2014.0531 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-05 N1 - Date created - 2015-08-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Drug Discov Today. 2007 Sep;12(17-18):688-99 [17826681] Nat Rev Mol Cell Biol. 2007 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Ther. 2013 Oct;347(1):212-24 [23899905] Nat Rev Drug Discov. 2007 Jul;6(7):521-32 [17599084] Curr Opin Chem Biol. 2007 Aug;11(4):405-9 [17662644] Nature. 2014 Mar 27;507(7493):423-5 [24678540] PLoS One. 2014;9(4):e93608 [24695466] Nature. 2014 May 22;509(7501):487-91 [24717434] Nat Commun. 2014;5:4047 [24915161] Stem Cell Reports. 2014 Jun 3;2(6):866-80 [24936472] Cell Stem Cell. 2014 Jul 3;15(1):27-30 [24996167] Stem Cell Res Ther. 2014;5(2):46 [25022790] Stem Cell Res Ther. 2013;4(2):25 [23672848] Environ Sci Technol. 2014;48(15):8706-16 [24960280] Stem Cell Res Ther. 2014;5(4):87 [25157556] Hum Mol Genet. 2014 Oct 1;23(19):5123-32 [24838285] Neurotoxicology. 2014 Sep;44:204-17 [24997244] Nature. 2014 Nov 13;515(7526):274-8 [25307057] Cell Rep. 2014 Nov 20;9(4):1173-82 [25456120] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1089/scd.2014.0531 ER - TY - JOUR T1 - High Affinity Dopamine D3 Receptor (D3R)-Selective Antagonists Attenuate Heroin Self-Administration in Wild-Type but not D3R Knockout Mice. AN - 1704348113; 26203768 AB - The dopamine D3 receptor (D3R) is a promising target for the development of pharmacotherapeutics to treat substance use disorders. Several D3R-selective antagonists are effective in animal models of drug abuse, especially in models of relapse. Nevertheless, poor bioavailability, metabolic instability, and/or predicted toxicity have impeded success in translating these drug candidates to clinical use. Herein, we report a series of D3R-selective 4-phenylpiperazines with improved metabolic stability. A subset of these compounds was evaluated for D3R functional efficacy and off-target binding at selected 5-HT receptor subtypes, where significant overlap in SAR with D3R has been observed. Several high affinity D3R antagonists, including compounds 16 (Ki = 0.12 nM) and 32 (Ki = 0.35 nM), showed improved metabolic stability compared to the parent compound, PG648 (6). Notably, 16 and the classic D3R antagonist SB277011A (2) were effective in reducing self-administration of heroin in wild-type but not D3R knockout mice. JF - Journal of medicinal chemistry AU - Boateng, Comfort A AU - Bakare, Oluyomi M AU - Zhan, Jia AU - Banala, Ashwini K AU - Burzynski, Caitlin AU - Pommier, Elie AU - Keck, Thomas M AU - Donthamsetti, Prashant AU - Javitch, Jonathan A AU - Rais, Rana AU - Slusher, Barbara S AU - Xi, Zheng-Xiong AU - Newman, Amy Hauck AD - †Molecular Targets and Medications Discovery Branch, National Institute on Drug Abuse- Intramural Research Program, National Institutes of Health, 333 Cassell Drive, Baltimore, Maryland 21224, United States. ; ∥Departments of Psychiatry and Pharmacology, Columbia University College of Physicians and Surgeons, and Division of Molecular Therapeutics, New York State Psychiatric Institute, New York, New York 10032, United States. ; §Department of Neurology, Brain Science Institute, The Johns Hopkins University School of Medicine, 855 North Wolfe Street, Baltimore, Maryland 21205, United States. Y1 - 2015/08/13/ PY - 2015 DA - 2015 Aug 13 SP - 6195 EP - 6213 VL - 58 IS - 15 KW - Dopamine Antagonists KW - 0 KW - Receptors, Dopamine D3 KW - Heroin KW - 70D95007SX KW - Index Medicus KW - Animals KW - Mice, Inbred C57BL KW - Mice KW - Radioligand Assay KW - Male KW - Mice, Knockout KW - Dopamine Antagonists -- chemistry KW - Self Administration KW - Receptors, Dopamine D3 -- genetics KW - Dopamine Antagonists -- pharmacology KW - Receptors, Dopamine D3 -- antagonists & inhibitors KW - Heroin -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1704348113?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+medicinal+chemistry&rft.atitle=High+Affinity+Dopamine+D3+Receptor+%28D3R%29-Selective+Antagonists+Attenuate+Heroin+Self-Administration+in+Wild-Type+but+not+D3R+Knockout+Mice.&rft.au=Boateng%2C+Comfort+A%3BBakare%2C+Oluyomi+M%3BZhan%2C+Jia%3BBanala%2C+Ashwini+K%3BBurzynski%2C+Caitlin%3BPommier%2C+Elie%3BKeck%2C+Thomas+M%3BDonthamsetti%2C+Prashant%3BJavitch%2C+Jonathan+A%3BRais%2C+Rana%3BSlusher%2C+Barbara+S%3BXi%2C+Zheng-Xiong%3BNewman%2C+Amy+Hauck&rft.aulast=Boateng&rft.aufirst=Comfort&rft.date=2015-08-13&rft.volume=58&rft.issue=15&rft.spage=6195&rft.isbn=&rft.btitle=&rft.title=Journal+of+medicinal+chemistry&rft.issn=1520-4804&rft_id=info:doi/10.1021%2Facs.jmedchem.5b00776 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-08 N1 - Date created - 2015-08-13 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/acs.jmedchem.5b00776 ER - TY - JOUR T1 - Discovery of NCT-501, a Potent and Selective Theophylline-Based Inhibitor of Aldehyde Dehydrogenase 1A1 (ALDH1A1). AN - 1704344668; 26207746 AB - Aldehyde dehydrogenases (ALDHs) metabolize reactive aldehydes and possess important physiological and toxicological functions in areas such as CNS, metabolic disorders, and cancers. Increased ALDH (e.g., ALDH1A1) gene expression and catalytic activity are vital biomarkers in a number of malignancies and cancer stem cells, highlighting the need for the identification and development of small molecule ALDH inhibitors. A new series of theophylline-based analogs as potent ALDH1A1 inhibitors is described. The optimization of hits identified from a quantitative high throughput screening (qHTS) campaign led to analogs with improved potency and early ADME properties. This chemotype exhibits highly selective inhibition against ALDH1A1 over ALDH3A1, ALDH1B1, and ALDH2 isozymes as well as other dehydrogenases such as HPGD and HSD17β4. Moreover, the pharmacokinetic evaluation of selected analog 64 (NCT-501) is also highlighted. JF - Journal of medicinal chemistry AU - Yang, Shyh-Ming AU - Yasgar, Adam AU - Miller, Bettina AU - Lal-Nag, Madhu AU - Brimacombe, Kyle AU - Hu, Xin AU - Sun, Hongmao AU - Wang, Amy AU - Xu, Xin AU - Nguyen, Kimloan AU - Oppermann, Udo AU - Ferrer, Marc AU - Vasiliou, Vasilis AU - Simeonov, Anton AU - Jadhav, Ajit AU - Maloney, David J AD - †National Center for Advancing Translational Sciences, National Institutes of Health, 9800 Medical Center Drive, Rockville, Maryland 20850, United States. ; ‡Department of Pharmaceutical Sciences, Skaggs School of Pharmacy and Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, Colorado 80045, United States. ; §Botnar Research Center, NIHR Oxford Biomedical Research Unit, Oxford OX3 7LD, U.K. Y1 - 2015/08/13/ PY - 2015 DA - 2015 Aug 13 SP - 5967 EP - 5978 VL - 58 IS - 15 KW - Enzyme Inhibitors KW - 0 KW - NCT-501 KW - Piperazines KW - Theophylline KW - C137DTR5RG KW - ALDH1A1 protein, human KW - EC 1.2.1.3 KW - Aldehyde Dehydrogenase KW - Index Medicus KW - Drug Discovery KW - Structure-Activity Relationship KW - Piperazines -- chemistry KW - Theophylline -- pharmacology KW - Enzyme Inhibitors -- chemistry KW - Theophylline -- chemistry KW - Enzyme Inhibitors -- pharmacology KW - Enzyme Inhibitors -- pharmacokinetics KW - Aldehyde Dehydrogenase -- antagonists & inhibitors KW - Piperazines -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1704344668?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+medicinal+chemistry&rft.atitle=Discovery+of+NCT-501%2C+a+Potent+and+Selective+Theophylline-Based+Inhibitor+of+Aldehyde+Dehydrogenase+1A1+%28ALDH1A1%29.&rft.au=Yang%2C+Shyh-Ming%3BYasgar%2C+Adam%3BMiller%2C+Bettina%3BLal-Nag%2C+Madhu%3BBrimacombe%2C+Kyle%3BHu%2C+Xin%3BSun%2C+Hongmao%3BWang%2C+Amy%3BXu%2C+Xin%3BNguyen%2C+Kimloan%3BOppermann%2C+Udo%3BFerrer%2C+Marc%3BVasiliou%2C+Vasilis%3BSimeonov%2C+Anton%3BJadhav%2C+Ajit%3BMaloney%2C+David+J&rft.aulast=Yang&rft.aufirst=Shyh-Ming&rft.date=2015-08-13&rft.volume=58&rft.issue=15&rft.spage=5967&rft.isbn=&rft.btitle=&rft.title=Journal+of+medicinal+chemistry&rft.issn=1520-4804&rft_id=info:doi/10.1021%2Facs.jmedchem.5b00577 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-08 N1 - Date created - 2015-08-13 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/acs.jmedchem.5b00577 ER - TY - JOUR T1 - Cannabis smoke can be a major risk factor for early-age laryngeal cancer-a molecular signaling-based approach AN - 1859475655; PQ0001973904 AB - Epidermal growth factor receptor (EGFR) and its downstream elements are overexpressed in most cases of the head and neck squamous cell carcinoma. This study investigated the expression pattern of key proteins linked to the EGFR pathway in laryngeal carcinoma patients with a history of cannabis smoking. We selected 83 male glottic cancer patients, aged between 45 to 75 years with three distinct populations-nonsmoker, cigarette smoker, and cannabis smoker. Immunohistochemical staining was performed for EGFR, protein kinase B (PKB or Akt), nuclear factor kappa B p50 (NF- sub([ETH]s)B), and cyclooxygenase-2 (COX-2) followed by boolean scoring for statistical analysis. Experimental data showed upregulation of the selected EGFR cascade in tumor cells, stromal expression of EGFR, and nuclear localization of COX-2 in metaplastic gland cells of laryngeal cancer tissue sample. Statistical analyses indicated that overexpression of the EGFR cascade is significantly correlated to cannabis smoking. Cannabis smokers had higher expression (p1.5) as the lower age group had relatively higher number of cannabis smokers. This study provides evidence for a direct association between cannabis smoking and increased risk of laryngeal cancer. Higher expression of the EGFR cascade in cannabis smokers revealed that cannabis smoking may be a major cause for the early onset of aggressive laryngeal cancer. JF - Tumor Biology AU - Bhattacharyya, Sayantan AU - Mandal, Syamsundar AU - Banerjee, Samir AU - Mandal, Gautam Kumar AU - Bhowmick, Anup Kumar AU - Murmu, Nabendu AD - Department of Signal Transduction and Biogenic Amines, Chittaranjan National Cancer Institute, 37-S.P Mukherjee Road, Kolkata, 700026, India, nabendu.murmu@cnci.org.in Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 6029 EP - 6036 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 36 IS - 8 SN - 1010-4283, 1010-4283 KW - Toxicology Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1859475655?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Tumor+Biology&rft.atitle=Cannabis+smoke+can+be+a+major+risk+factor+for+early-age+laryngeal+cancer-a+molecular+signaling-based+approach&rft.au=Bhattacharyya%2C+Sayantan%3BMandal%2C+Syamsundar%3BBanerjee%2C+Samir%3BMandal%2C+Gautam+Kumar%3BBhowmick%2C+Anup+Kumar%3BMurmu%2C+Nabendu&rft.aulast=Bhattacharyya&rft.aufirst=Sayantan&rft.date=2015-08-01&rft.volume=36&rft.issue=8&rft.spage=6029&rft.isbn=&rft.btitle=&rft.title=Tumor+Biology&rft.issn=10104283&rft_id=info:doi/10.1007%2Fs13277-015-3279-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2017-01-01 N1 - Number of references - 51 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s13277-015-3279-4 ER - TY - JOUR T1 - Trials and tribulations of developing natural product drugs AN - 1808656551; PQ0003213517 AB - The development of natural product based drugs for antitumor therapy is fraught with problems of supply, unless the agent is ato provide enough for early preclinical studies. In this presentation I will give examples from three sources, one of which NCI worked on extensively, the others are examples of work by small companies from an Australian aboriginal usage of a plant, and some very clever work by an academic chemist at Yale University.The story of Picato(R) is the one from an Australian aboriginal lead and shows how compounds can come from odd places. The second, Kyprolis(R) is a tour-de-force from an academic laboratory, and the third, Eribulin(R) is the one that started from a very small amount of material from a Japanese sponge and ultimately led to the most complex totally synthesized drug for any disease. Highlights and "lessons learned" will be discussed for each of these as the overall problems, though similar, were addressed successfully in different ways. JF - Zhongguo Yaolixue yu Dulixue Zazhi - Chinese Journal of Pharmacology and Toxicology AU - Newman, David J AD - Natural Products Branch, National Cancer Institute, Frederick, MD, USA, djnewman664@verizon.net Y1 - 2015/08/01/ PY - 2015 DA - 2015 Aug 01 SP - 2 PB - Zhongguo Duli Xuehui VL - 29 SN - 1000-3002, 1000-3002 KW - Toxicology Abstracts KW - natural product drugs KW - antitumor KW - natural products KW - Drug development KW - Drugs KW - X 24360:Metals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808656551?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Zhongguo+Yaolixue+yu+Dulixue+Zazhi+-+Chinese+Journal+of+Pharmacology+and+Toxicology&rft.atitle=Trials+and+tribulations+of+developing+natural+product+drugs&rft.au=Newman%2C+David+J&rft.aulast=Newman&rft.aufirst=David&rft.date=2015-08-01&rft.volume=29&rft.issue=&rft.spage=2&rft.isbn=&rft.btitle=&rft.title=Zhongguo+Yaolixue+yu+Dulixue+Zazhi+-+Chinese+Journal+of+Pharmacology+and+Toxicology&rft.issn=10003002&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-04 N1 - SubjectsTermNotLitGenreText - Drug development; natural products; Drugs ER - TY - JOUR T1 - Clinical Scale Zinc Finger Nuclease-mediated Gene Editing of PD-1 in Tumor Infiltrating Lymphocytes for the Treatment of Metastatic Melanoma AN - 1776646147; PQ0002738129 AB - Programmed cell death-1 (PD-1) is expressed on activated T cells and represents an attractive target for gene-editing of tumor targeted T cells prior to adoptive cell transfer (ACT). We used zinc finger nucleases (ZFNs) directed against the gene encoding human PD-1 (PDCD-1) to gene-edit melanoma tumor infiltrating lymphocytes (TIL). We show that our clinical scale TIL production process yielded efficient modification of the PD-1 gene locus, with an average modification frequency of 74.8% (n= 3, range 69.9-84.1%) of the alleles in a bulk TIL population, which resulted in a 76% reduction in PD-1 surface-expression. Forty to 48% of PD-1 gene-edited cells had biallelic PD-1 modification. Importantly, the PD-1 gene-edited TIL product showed improved in vitro effector function and a significantly increased polyfunctional cytokine profile (TNF[alpha], GM-CSF, and IFN[gamma]) compared to unmodified TIL in two of the three donors tested. In addition, all donor cells displayed an effector memory phenotype and expanded approximately 500-2,000-fold in vitro. Thus, further study to determine the efficiency and safety of adoptive cell transfer using PD-1 gene-edited TIL for the treatment of metastatic melanoma is warranted. JF - Molecular Therapy AU - Beane, Joal D AU - Lee, Gary AU - Zheng, Zhili AU - Mendel, Matthew AU - Abate-Daga, Daniel AU - Bharathan, Mini AU - Black, Mary AU - Gandhi, Nimisha AU - Yu, Zhiya AU - Chandran, Smita AD - National Cancer Institute, Surgery Branch, Bethesda, Maryland, USA Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 1380 EP - 1390 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 23 IS - 8 SN - 1525-0016, 1525-0016 KW - Genetics Abstracts; Immunology Abstracts; Biotechnology and Bioengineering Abstracts KW - Granulocyte-macrophage colony-stimulating factor KW - Zinc finger proteins KW - Nuclease KW - Tumors KW - Melanoma KW - Effector cells KW - Metastases KW - PD-1 protein KW - Population genetics KW - Memory KW - Lymphocytes T KW - Cytokines KW - W 30940:Products KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1776646147?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Therapy&rft.atitle=Clinical+Scale+Zinc+Finger+Nuclease-mediated+Gene+Editing+of+PD-1+in+Tumor+Infiltrating+Lymphocytes+for+the+Treatment+of+Metastatic+Melanoma&rft.au=Beane%2C+Joal+D%3BLee%2C+Gary%3BZheng%2C+Zhili%3BMendel%2C+Matthew%3BAbate-Daga%2C+Daniel%3BBharathan%2C+Mini%3BBlack%2C+Mary%3BGandhi%2C+Nimisha%3BYu%2C+Zhiya%3BChandran%2C+Smita&rft.aulast=Beane&rft.aufirst=Joal&rft.date=2015-08-01&rft.volume=23&rft.issue=8&rft.spage=1380&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2015.71 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Metastases; Population genetics; PD-1 protein; Memory; Granulocyte-macrophage colony-stimulating factor; Lymphocytes T; Nuclease; Cytokines; Zinc finger proteins; Tumors; Effector cells; Melanoma DO - http://dx.doi.org/10.1038/mt.2015.71 ER - TY - JOUR T1 - Aging of the Human Vestibular System AN - 1735641958; 201514666 AB - Aging affects every sensory system in the body, including the vestibular system. Although its impact is often difficult to quantify, the deleterious impact of aging on the vestibular system is serious both medically and economically. Tests of vestibular function either fall short in their ability to quantify such anatomical deterioration, or they are insensitive to the associated physiologic decline and/or central compensatory mechanisms that accompany the vestibular aging process. When compared with healthy younger individuals, a paucity of subtle differences in test results has been reported in the healthy older population, and those differences are often observed only in response to nontraditional and/or more robust stimuli. With an estimated 115% increase in the geriatric population over 65 years of age by the year 2050, the number of balanced-disordered patients with a declining vestibular system is certain to reach near epidemic proportions. An understanding of the effects of age on the vestibular system is imperative if clinicians are to better manage elderly patients with balance disorders, dizziness, and vestibular, disease. Adapted from the source document JF - Seminars in Hearing AU - Zalewski, Christopher K AD - Otolaryngology Branch, Audiology Unit, National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health (NIH), Bethesda, Maryland Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 175 EP - 196 VL - 36 IS - 3 SN - 0734-0451, 0734-0451 KW - Elderly (21350) KW - Auditory System (06100) KW - Aging (01188) KW - Sensory Systems (77300) KW - article KW - 6310: hearing-pathological and normal; hearing-pathological and normal UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1735641958?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Allba&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+Hearing&rft.atitle=Aging+of+the+Human+Vestibular+System&rft.au=Zalewski%2C+Christopher+K&rft.aulast=Zalewski&rft.aufirst=Christopher&rft.date=2015-08-01&rft.volume=36&rft.issue=3&rft.spage=175&rft.isbn=&rft.btitle=&rft.title=Seminars+in+Hearing&rft.issn=07340451&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2015-12-01 N1 - Last updated - 2016-09-27 N1 - CODEN - SEMHE7 N1 - SubjectsTermNotLitGenreText - Aging (01188); Auditory System (06100); Elderly (21350); Sensory Systems (77300) ER - TY - JOUR T1 - Common genetic variants in epigenetic machinery genes and risk of upper gastrointestinal cancers AN - 1727681564; PQ0002142883 AB - Background: Populations in north central China are at high risk for oesophageal squamous cell carcinoma (ESCC) and gastric cancer (GC), and genetic variation in epigenetic machinery genes and pathways may contribute to this risk.Methods: We used the adaptive multilocus joint test to analyse 192 epigenetic genes involved in chromatin remodelling, DNA methylation and microRNA biosynthesis in 1942 ESCC and 1758 GC cases [1126 cardia (GCA) and 632 non-cardia adenocarcinoma (GNCA)] and 2111 controls with Chinese ancestry. We examined potential function of risk alleles using in silico and expression quantitative trait loci (eQTLs) analyses.Results: Suggestive pathway-based associations were observed for the overall epigenetic (P-value super(PATH)=0.034) and chromatin remodelling (P-value super(PATH)=0.039) pathways with risk of GCA, but not GC, GNCA or ESCC. Overall, 37 different epigenetic machinery genes were associated with risk of one or more upper gastrointestinal (UGI) cancer sites (P-value super(GENE)<0.0 5), including 14 chromatin remodelling genes whose products are involved in the regulation of HOX genes. We identified a gastric eQTL (rs12724079; rho=0.37; P=0.0006) which regulates mRNA expression of ASH1L. Several suggestive eQTLs were also found in oesophageal (rs10898459 in EED), gastric cardia (rs7157322 in DICER1; rs8179271 in ASH1L), and gastric non-cardia (rs1790733 in PPP1CA) tissues.Conclusions: Results of our analyses provide limited but suggestive evidence for a role of epigenetic gene variation in the aetiology of UGI cancer. JF - International Journal of Epidemiology AU - Sung, Hyuna AU - Yang, Howard H AU - Zhang, Han AU - Yang, Qi AU - Hu, Nan AU - Tang, Ze-Zhong AU - Su, Hua AU - Wang, Lemin AU - Wang, Chaoyu AU - Ding, Ti AU - Fan, Jin-Hu AU - Qiao, You-Lin AU - Wheeler, William AU - Giffen, Carol AU - Burdett, Laurie AU - Wang, Zhaoming AU - Lee, Maxwell P AU - Chanock, Stephen J AU - Dawsey, Sanford M AU - Freedman, Neal D AU - Abnet, Christian C AU - Goldstein, Alisa M AU - Yu, Kai AU - Taylor, Philip R AU - Hyland, Paula L AD - *Corresponding author. Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Institutes of Health, Bethesda, MD 20852, USA., hylandpl@mail.nih.gov Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 1341 EP - 1352 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 44 IS - 4 SN - 0300-5771, 0300-5771 KW - Genetics Abstracts; Health & Safety Science Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Risk Abstracts KW - Epigenetics KW - chromatin remodelling KW - DNA methylation KW - microRNA KW - oesophageal squamous cell carcinoma KW - gastric cancer KW - gastric cardia KW - gastric non-cardia KW - SNP KW - gene-based KW - pathway-based KW - Esophagus KW - Biosynthesis KW - Quantitative trait loci KW - Chromatin remodeling KW - miRNA KW - Transcription KW - Genetic diversity KW - squamous cell carcinoma KW - Cancer KW - Joints KW - Gene expression KW - Health risks KW - Guanylate cyclase KW - epigenetics KW - Machinery KW - Risk factors KW - Gene regulation KW - DNA KW - China, People's Rep. KW - Gastric cancer KW - Adenocarcinoma KW - H 11000:Diseases/Injuries/Trauma KW - N 14820:DNA Metabolism & Structure KW - R2 23060:Medical and environmental health KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727681564?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Epidemiology&rft.atitle=Common+genetic+variants+in+epigenetic+machinery+genes+and+risk+of+upper+gastrointestinal+cancers&rft.au=Sung%2C+Hyuna%3BYang%2C+Howard+H%3BZhang%2C+Han%3BYang%2C+Qi%3BHu%2C+Nan%3BTang%2C+Ze-Zhong%3BSu%2C+Hua%3BWang%2C+Lemin%3BWang%2C+Chaoyu%3BDing%2C+Ti%3BFan%2C+Jin-Hu%3BQiao%2C+You-Lin%3BWheeler%2C+William%3BGiffen%2C+Carol%3BBurdett%2C+Laurie%3BWang%2C+Zhaoming%3BLee%2C+Maxwell+P%3BChanock%2C+Stephen+J%3BDawsey%2C+Sanford+M%3BFreedman%2C+Neal+D%3BAbnet%2C+Christian+C%3BGoldstein%2C+Alisa+M%3BYu%2C+Kai%3BTaylor%2C+Philip+R%3BHyland%2C+Paula+L&rft.aulast=Sung&rft.aufirst=Hyuna&rft.date=2015-08-01&rft.volume=44&rft.issue=4&rft.spage=1341&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Epidemiology&rft.issn=03005771&rft_id=info:doi/10.1093%2Fije%2Fdyv050 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Esophagus; Quantitative trait loci; Chromatin remodeling; miRNA; Genetic diversity; Transcription; squamous cell carcinoma; Joints; Gene expression; Guanylate cyclase; epigenetics; Gene regulation; Risk factors; DNA methylation; Adenocarcinoma; Gastric cancer; Biosynthesis; Health risks; Machinery; DNA; Cancer; China, People's Rep. DO - http://dx.doi.org/10.1093/ije/dyv050 ER - TY - JOUR T1 - Novel antigens for RSV vaccines AN - 1727675580; PQ0002147321 AB - Respiratory syncytial virus (RSV) remains a leading global cause of infant mortality and adult morbidity. Infection, which recurs throughout life, elicits only short-lived immunity. The development of a safe and efficacious vaccine has, thus far, been elusive. Recent technological advances, however, have yielded promising RSV vaccine candidates that are based on solving atomic-level structures of surface glycoproteins interacting with neutralizing antibodies. The class I fusion glycoprotein, F, serves as the primary antigenic component of most vaccines, and is the target of the only licensed monoclonal antibody product used to reduce the frequency of severe disease in high-risk neonates. However, success of prior F-based vaccines has been limited by the lack of understanding how the conformational rearrangement between a metastable prefusion F (pre-F) and a stable postfusion F (post-F) affected the epitope content. Neutralizing epitopes reside on both conformations, but those specific to pre-F are far more potent than those previously identified and present on post-F. The solution of the pre-F structure and its subsequent characterization and stabilization illustrates the value of a structure-based approach to vaccine development, and provides hope that a safe and effective RSV vaccine is possible. JF - Current Opinion in Immunology AU - Graham, Barney S AU - Modjarrad, Kayvon AU - McLellan, Jason S AD - Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 30 EP - 38 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 35 SN - 0952-7915, 0952-7915 KW - Biotechnology and Bioengineering Abstracts; Immunology Abstracts KW - Mortality KW - Monoclonal antibodies KW - Immunity KW - Infection KW - Morbidity KW - Respiratory syncytial virus KW - Reviews KW - Risk groups KW - Neonates KW - Glycoproteins KW - Vaccines KW - Epitopes KW - Infants KW - Conformation KW - F 06905:Vaccines KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727675580?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+Opinion+in+Immunology&rft.atitle=Novel+antigens+for+RSV+vaccines&rft.au=Graham%2C+Barney+S%3BModjarrad%2C+Kayvon%3BMcLellan%2C+Jason+S&rft.aulast=Graham&rft.aufirst=Barney&rft.date=2015-08-01&rft.volume=35&rft.issue=&rft.spage=30&rft.isbn=&rft.btitle=&rft.title=Current+Opinion+in+Immunology&rft.issn=09527915&rft_id=info:doi/10.1016%2Fj.coi.2015.04.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Mortality; Monoclonal antibodies; Immunity; Infection; Morbidity; Reviews; Risk groups; Vaccines; Glycoproteins; Neonates; Epitopes; Conformation; Infants; Respiratory syncytial virus DO - http://dx.doi.org/10.1016/j.coi.2015.04.005 ER - TY - JOUR T1 - An in silico screen links gene expression signatures to drug response in glioblastoma stem cells AN - 1722176178; PQ0002101527 AB - Cancer stem cells (CSCs) are thought to promote resistance to chemotherapeutic drugs in glioblastoma, the most common and aggressive primary brain tumor. However, the use of high-throughput drug screens to discover novel small-molecule inhibitors for CSC has been hampered by their instability in long-term cell culture. We asked whether predictive models of drug response could be developed from gene expression signatures of established cell lines and applied to predict drug response in glioblastoma stem cells. Predictions for active compounds were confirmed both for 185 compounds in seven established glioma cell lines and 21 compounds in three glioblastoma stem cells. The use of established cell lines as a surrogate for drug response in CSC lines may enable the large-scale virtual screening of drug candidates that would otherwise be difficult or impossible to test directly in CSCs. JF - Pharmacogenomics Journal AU - Riddick, G AU - Song, H AU - Holbeck, S L AU - Kopp, W AU - Walling, J AU - Ahn, S AU - Zhang, W AU - Fine, H A AD - Neuro-Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA PY - 2015 SP - 347 EP - 353 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 15 IS - 4 SN - 1470-269X, 1470-269X KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts; CSA Neurosciences Abstracts KW - Gene expression KW - Brain tumors KW - Glioblastoma KW - Stem cells KW - Drug resistance KW - Glioma cells KW - Drug development KW - Cell culture KW - Drugs KW - G 07880:Human Genetics KW - N3 11028:Neuropharmacology & toxicology KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722176178?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacogenomics+Journal&rft.atitle=An+in+silico+screen+links+gene+expression+signatures+to+drug+response+in+glioblastoma+stem+cells&rft.au=Riddick%2C+G%3BSong%2C+H%3BHolbeck%2C+S+L%3BKopp%2C+W%3BWalling%2C+J%3BAhn%2C+S%3BZhang%2C+W%3BFine%2C+H+A&rft.aulast=Riddick&rft.aufirst=G&rft.date=2015-08-01&rft.volume=15&rft.issue=4&rft.spage=347&rft.isbn=&rft.btitle=&rft.title=Pharmacogenomics+Journal&rft.issn=1470269X&rft_id=info:doi/10.1038%2Ftpj.2014.61 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Brain tumors; Gene expression; Glioblastoma; Stem cells; Drug resistance; Glioma cells; Cell culture; Drug development; Drugs DO - http://dx.doi.org/10.1038/tpj.2014.61 ER - TY - JOUR T1 - Dietary factors and luteal phase deficiency in healthy eumenorrheic women AN - 1717490461; PQ0001944441 AB - STUDY QUESTION Are prospectively assessed dietary factors, including overall diet quality, macronutrients and micronutrients, associated with luteal phase deficiency (LPD) in healthy reproductive aged women with regular menstrual cycles? SUMMARY ANSWER Mediterranean Diet Score (MDS), fiber and isoflavone intake were positively associated with LPD while selenium was negatively associated with LPD after adjusting for age, percentage body fat and total energy intake. WHAT IS KNOWN ALREADY LPD may increase the risk of infertility and early miscarriage. Prior research has shown positive associations between LPD and low energy availability, either through high dietary restraint alone or in conjunction with high energy expenditure via exercise, but few studies with adequate sample sizes have been conducted investigating dietary factors and LPD among healthy, eumenorrheic women. STUDY DESIGN, SIZE, DURATION The BioCycle Study (2005-2007) prospectively enrolled 259 women from Western New York state, USA, and followed them for one (n = 9) or two (n = 250) menstrual cycles. PARTICIPANTS/MATERIALS, SETTING, METHODS Women aged 18-44 years, with self-reported BMI between 18 and 35 kg/m super(2) and cycle lengths between 21 and 35 days, were included in the study. Participants completed baseline questionnaires, four 24-h dietary recalls per cycle and daily diaries capturing vigorous exercise, perceived stress and sleep; they also provided up to eight fasting serum samples during clinic visits timed to specific phases of the menstrual cycle using a fertility monitor. Cycles were included for this analysis if the peak serum luteal progesterone was >1 ng/ml and a urine or serum LH surge was detected. Associations between prospectively assessed diet quality, macronutrients and micronutrients and LPD (defined as luteal duration <10 days) were evaluated using generalized linear models adjusting for age, percentage body fat and total energy intake. MAIN RESULTS AND THE ROLE OF CHANCE LPD occurred in 41 (8.9%) of the 463 cycles from 246 women in the final analysis. After adjusting for age, percentage body fat and total energy intake, LPD was positively associated with MDS, adjusted odds ratio (aOR): 1.70 (95% confidence interval [CI]: 1.17, 2.48), P = 0.01. In separate macro- and micronutrient adjusted models, increased fiber and isoflavone intake showed modest positive associations with LPD: fiber (per g), aOR: 1.10 (95% CI: 0.99, 1.23), P = 0.07; and isoflavones (per 10 mg), aOR: 1.38 (95% CI: 0.99, 1.92), P = 0.06. In contrast, selenium (per 10 mcg) was inversely associated with LPD, aOR: 0.80 (95% CI: 0.65, 0.97), P = 0.03. Additional adjustments for relevant lifestyle factors including vigorous exercise, perceived stress and sleep did not appreciably alter estimates. LIMITATIONS, REASONS FOR CAUTION The number of LPD cycles was limited, and thus these findings are exploratory. We relied on participant self-report of their medical history to apply exclusion criteria; it is possible that we admitted to the study women with a gynecologic or medical disease who were unaware of their diagnosis. WIDER IMPLICATIONS OF THE FINDINGS Our study suggests that diet quality may be associated with LPD among healthy eumenorrheic women. As LPD may contribute to infertility and early miscarriage, further research is warranted to elucidate how dietary factors, such as MDS, may influence LPD. The inverse association we found with selenium is supported by previous research and deserves further investigation to determine whether this finding has pathophysiologic and therapeutic implications. STUDY FUNDING/COMPETING INTEREST(S) This work was supported by the Intramural Research Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health. No competing interests declared. JF - Human Reproduction AU - Andrews, Mary A AU - Schliep, Karen C AU - Wactawski-Wende, Jean AU - Stanford, Joseph B AU - Zarek, Shvetha M AU - Radin, Rose G AU - Sjaarda, Lindsey A AU - Perkins, Neil J AU - Kalwerisky, Robyn A AU - Hammoud, Ahmad O AU - Mumford, Sunni L Y1 - 2015/08// PY - 2015 DA - Aug 2015 SP - 1942 EP - 1951 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 30 IS - 8 SN - 0268-1161, 0268-1161 KW - Risk Abstracts KW - luteal phase deficiency KW - menstrual cycle KW - Mediterranean diet KW - fiber KW - selenium KW - Diets KW - Infertility KW - Fertility KW - Age KW - Body mass KW - Abortion KW - Stress KW - ANW, USA, New York KW - Fibers KW - Selenium KW - Perception KW - MED KW - Energy KW - Reproduction KW - Micronutrients KW - Females KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1717490461?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+Reproduction&rft.atitle=Dietary+factors+and+luteal+phase+deficiency+in+healthy+eumenorrheic+women&rft.au=Andrews%2C+Mary+A%3BSchliep%2C+Karen+C%3BWactawski-Wende%2C+Jean%3BStanford%2C+Joseph+B%3BZarek%2C+Shvetha+M%3BRadin%2C+Rose+G%3BSjaarda%2C+Lindsey+A%3BPerkins%2C+Neil+J%3BKalwerisky%2C+Robyn+A%3BHammoud%2C+Ahmad+O%3BMumford%2C+Sunni+L&rft.aulast=Andrews&rft.aufirst=Mary&rft.date=2015-08-01&rft.volume=30&rft.issue=8&rft.spage=1942&rft.isbn=&rft.btitle=&rft.title=Human+Reproduction&rft.issn=02681161&rft_id=info:doi/10.1093%2Fhumrep%2Fdev133 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Diets; Infertility; Age; Fertility; Abortion; Body mass; Stress; Selenium; Fibers; Perception; Energy; Reproduction; Females; Micronutrients; ANW, USA, New York; MED DO - http://dx.doi.org/10.1093/humrep/dev133 ER - TY - JOUR T1 - Meconium Tenofovir Concentrations and Growth and Bone Outcomes in Prenatally Tenofovir Exposed HIV-Uninfected Children. AN - 1713941957; 25961889 AB - Maternal tenofovir disoproxil fumarate (TDF) treatment among HIV-infected pregnant women results in fetal tenofovir (TFV) exposure. Fetal TFV toxicity was demonstrated in animals, but most clinical investigations have not observed toxicity in humans. We evaluated HIV-exposed, uninfected infants in the Surveillance Monitoring for Antiretroviral Therapy Toxicities cohort of the Pediatric HIV/AIDS Cohort Study whose mothers were prescribed TDF for ≥ 8 third trimester weeks. Infant dual-energy X-ray absorptiometry scans were obtained at 0-4 weeks to measure whole body bone mineral content. Meconium TFV concentrations were quantified by liquid chromatography-tandem mass spectrometry. Fifty-eight TFV-exposed infants had meconium TFV quantified. Detectable concentrations were 11-48,100 ng/g; 3 infants had undetectable concentrations. Maternal TDF prescription duration ranged from 8 to 41 gestational weeks; infant gestational ages were 36-41 weeks. Meconium TFV concentrations were not correlated with TFV exposure duration or timing and did not vary by concomitant prescription of protease inhibitors. Increased meconium TFV concentrations were associated with greater gestational ages (ρ = 0.29, P = 0.03) and lower maternal plasma HIV RNA before delivery (ρ = -0.29, P = 0.04). Meconium TFV concentrations were not associated with infant weight, length (n = 58) or bone mineral content (n = 49). For the first time, we explored associations between meconium TFV concentrations and infant growth and bone measurements; we did not observe a meconium concentration-dependent relationship for these infant outcomes. These findings support other clinical research failing to show dose-response relationships for growth and bone outcomes among intrauterine TFV-exposed infants. High meconium TFV concentrations correlated with low maternal viral load, suggesting maternal TDF adherence significantly contributes to meconium TFV concentrations. JF - The Pediatric infectious disease journal AU - Himes, Sarah K AU - Wu, Julia W AU - Jacobson, Denise L AU - Tassiopoulos, Katherine AU - Hazra, Rohan AU - Kacanek, Deborah AU - Van Dyke, Russell B AU - Rich, Kenneth C AU - Siberry, George K AU - Huestis, Marilyn A AU - Pediatric HIVAIDS Cohort Study (PHACS) AD - From the *Chemistry and Drug Metabolism Section, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland; †Department of Epidemiology, ‡Center for Biostatistics in AIDS Research, Harvard School of Public Health, Boston, Massachusetts; §Maternal and Pediatric Infectious Disease Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland; ¶Department of Pediatrics, Tulane University School of Medicine, New Orleans, Louisiana; and ‖Pediatrics Department, University of Illinois at Chicago, Chicago, Illinois. ; Pediatric HIVAIDS Cohort Study (PHACS) Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 851 EP - 857 VL - 34 IS - 8 KW - Anti-HIV Agents KW - 0 KW - Tenofovir KW - 99YXE507IL KW - Index Medicus KW - Infectious Disease Transmission, Vertical KW - Young Adult KW - Humans KW - Gestational Age KW - Adult KW - Infant, Newborn KW - Middle Aged KW - Adolescent KW - Maternal Exposure KW - Male KW - Female KW - Pregnancy KW - Tenofovir -- analysis KW - Bone Density -- drug effects KW - Tenofovir -- therapeutic use KW - Tenofovir -- adverse effects KW - Anti-HIV Agents -- therapeutic use KW - Meconium -- chemistry KW - HIV Infections -- drug therapy KW - Anti-HIV Agents -- analysis KW - Anti-HIV Agents -- adverse effects KW - Anti-HIV Agents -- administration & dosage KW - Tenofovir -- administration & dosage KW - Pregnancy Complications, Infectious -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1713941957?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Pediatric+infectious+disease+journal&rft.atitle=Meconium+Tenofovir+Concentrations+and+Growth+and+Bone+Outcomes+in+Prenatally+Tenofovir+Exposed+HIV-Uninfected+Children.&rft.au=Himes%2C+Sarah+K%3BWu%2C+Julia+W%3BJacobson%2C+Denise+L%3BTassiopoulos%2C+Katherine%3BHazra%2C+Rohan%3BKacanek%2C+Deborah%3BVan+Dyke%2C+Russell+B%3BRich%2C+Kenneth+C%3BSiberry%2C+George+K%3BHuestis%2C+Marilyn+A%3BPediatric+HIVAIDS+Cohort+Study+%28PHACS%29&rft.aulast=Himes&rft.aufirst=Sarah&rft.date=2015-08-01&rft.volume=34&rft.issue=8&rft.spage=851&rft.isbn=&rft.btitle=&rft.title=The+Pediatric+infectious+disease+journal&rft.issn=1532-0987&rft_id=info:doi/10.1097%2FINF.0000000000000747 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-15 N1 - Date created - 2015-09-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Acquir Immune Defic Syndr. 2002 Mar 1;29(3):207-20 [11873070] J Pediatr. 1994 Mar;124(3):477-9 [8120725] J Anim Sci. 1995 Jun;73(6):1839-51 [7545661] J Acquir Immune Defic Syndr Hum Retrovirol. 1999 Apr 1;20(4):323-33 [10096575] Nat Med. 1999 Sep;5(9):1048-51 [10470083] J Physiol. 2006 Apr 1;572(Pt 1):51-8 [16469783] Antimicrob Agents Chemother. 2006 Jul;50(7):2471-7 [16801428] Acta Paediatr Suppl. 2006 Apr;450:76-85 [16817681] J Acquir Immune Defic Syndr. 2006 Aug 1;42(4):441-9 [16791115] Pediatrics. 2006 Sep;118(3):e711-8 [16923923] J Infect Dis. 2008 Jan 1;197(1):102-8 [18171292] J Pediatr. 2008 Apr;152(4):582-4 [18346519] Birth Defects Res A Clin Mol Teratol. 2008 Jul;82(7):487-93 [18435469] Antimicrob Agents Chemother. 2008 Sep;52(9):3144-60 [18573931] Clin Pharmacol Ther. 2008 Nov;84(5):604-12 [18701886] Clin Pharmacol Ther. 2009 Feb;85(2):182-9 [18987623] J Pharm Sci. 2009 Jul;98(7):2317-35 [19067393] HIV Med. 2009 Sep;10(8):482-7 [19459988] J Bone Miner Res. 2010 Apr;25(4):920-7 [20437610] Nicotine Tob Res. 2010 Jun;12(6):658-64 [20427459] J Pediatr. 2013 May;162(5):970-5 [23211926] Pediatr Nephrol. 2013 Jul;28(7):1011-23 [22878694] J Int AIDS Soc. 2013;16:18757 [23819908] Pediatr Infect Dis J. 2013 May;32(5):495-500 [23249917] J Acquir Immune Defic Syndr. 2013 Dec 1;64(4):374-81 [24169122] Clin Infect Dis. 2013 Dec;57(12):1773-81 [24046310] AIDS. 2014 Jan 2;28(1):9-17 [24413260] J Acquir Immune Defic Syndr. 2014 Jan 1;65(1):33-41 [23979002] J Acquir Immune Defic Syndr. 2006 Nov 1;43(3):278-83 [17079992] Mol Pharmacol. 2007 Feb;71(2):619-27 [17110501] Anal Bioanal Chem. 2007 Aug;388(7):1455-65 [17370066] AIDS Behav. 2010 Dec;14(6):1269-78 [20532607] Addiction. 2010 Dec;105(12):2151-9 [20854338] PLoS One. 2011;6(8):e23688 [21897852] Antimicrob Agents Chemother. 2011 Dec;55(12):5914-22 [21896911] Antivir Ther. 2011;16(8):1259-66 [22155907] PLoS One. 2012;7(3):e32445 [22479327] Am J Epidemiol. 2012 May 1;175(9):950-61 [22491086] AIDS. 2012 Jun 1;26(9):1151-9 [22382151] PLoS Med. 2012;9(5):e1001217 [22615543] PLoS One. 2012;7(6):e38377 [22719882] Biopharm Drug Dispos. 2012 Jul;33(5):265-77 [22610784] AIDS. 2013 Jan 14;27(2):211-20 [23032412] Anal Chem. 2013 Feb 5;85(3):1896-904 [23256731] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/INF.0000000000000747 ER - TY - JOUR T1 - Microbiota-Dependent Activation of an Autoreactive T Cell Receptor Provokes Autoimmunity in an Immunologically Privileged Site AN - 1712770150; PQ0001915545 AB - Activated retina-specific T cells that have acquired the ability to break through the blood-retinal barrier are thought to be causally involved in autoimmune uveitis, a major cause of human blindness. It is unclear where these autoreactive T cells first become activated, given that their cognate antigens are sequestered within the immune-privileged eye. We demonstrate in a novel mouse model of spontaneous uveitis that activation of retina-specific T cells is dependent on gut commensal microbiota. Retina-specific T cell activation involved signaling through the autoreactive T cell receptor (TCR) in response to non-cognate antigen in the intestine and was independent of the endogenous retinal autoantigen. Our findings not only have implications for the etiology of human uveitis, but also raise the possibility that activation of autoreactive TCRs by commensal microbes might be a more common trigger of autoimmune diseases than is currently appreciated. JF - Immunity AU - Horai, Reiko AU - Zarate-Blades, Carlos R AU - Dillenburg-Pilla, Patricia AU - Chen, Jun AU - Kielczewski, Jennifer L AU - Silver, Phyllis B AU - Jittayasothorn, Yingyos AU - Chan, Chi-Chao AU - Yamane, Hidehiro AU - Honda, Kenya AU - Caspi, Rachel R AD - Laboratory of Immunology, National Eye Institute, NIH, Bethesda, MD 20892, USA PY - 2015 SP - 343 EP - 353 PB - Elsevier Science Ltd., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 43 IS - 2 SN - 1074-7613, 1074-7613 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Immunology Abstracts KW - T-cell receptor KW - Etiology KW - Eye KW - Retina KW - Autoimmune diseases KW - Animal models KW - Commensals KW - Blindness KW - Autoantigens KW - Immune privilege KW - Cell activation KW - Digestive tract KW - Uveitis KW - Lymphocytes T KW - Intestine KW - A 01490:Miscellaneous KW - F 06930:Autoimmunity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1712770150?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Immunity&rft.atitle=Microbiota-Dependent+Activation+of+an+Autoreactive+T+Cell+Receptor+Provokes+Autoimmunity+in+an+Immunologically+Privileged+Site&rft.au=Horai%2C+Reiko%3BZarate-Blades%2C+Carlos+R%3BDillenburg-Pilla%2C+Patricia%3BChen%2C+Jun%3BKielczewski%2C+Jennifer+L%3BSilver%2C+Phyllis+B%3BJittayasothorn%2C+Yingyos%3BChan%2C+Chi-Chao%3BYamane%2C+Hidehiro%3BHonda%2C+Kenya%3BCaspi%2C+Rachel+R&rft.aulast=Horai&rft.aufirst=Reiko&rft.date=2015-08-01&rft.volume=43&rft.issue=2&rft.spage=343&rft.isbn=&rft.btitle=&rft.title=Immunity&rft.issn=10747613&rft_id=info:doi/10.1016%2Fj.immuni.2015.07.014 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Number of references - 39 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Etiology; T-cell receptor; Retina; Eye; Autoimmune diseases; Commensals; Animal models; Blindness; Autoantigens; Cell activation; Immune privilege; Digestive tract; Uveitis; Intestine; Lymphocytes T DO - http://dx.doi.org/10.1016/j.immuni.2015.07.014 ER - TY - JOUR T1 - Recent advances in image-guided targeted prostate biopsy AN - 1712769226; PQ0001938734 AB - Prostate cancer is a common malignancy in the United States that results in over 30,000 deaths per year. The current state of prostate cancer diagnosis, based on PSA screening and sextant biopsy, has been criticized for both overdiagnosis of low-grade tumors and underdiagnosis of clinically significant prostate cancers (Gleason score greater than or equal to 7). Recently, image guidance has been added to perform targeted biopsies of lesions detected on multi-parametric magnetic resonance imaging (mpMRI) scans. These methods have improved the ability to detect clinically significant cancer, while reducing the diagnosis of low-grade tumors. Several approaches have been explored to improve the accuracy of image-guided targeted prostate biopsy, including in-bore MRI-guided, cognitive fusion, and MRI/transrectal ultrasound fusion-guided biopsy. This review will examine recent advances in these image-guided targeted prostate biopsy techniques. JF - Abdominal Imaging AU - Brown, Anna M AU - Elbuluk, Osama AU - Mertan, Francesca AU - Sankineni, Sandeep AU - Margolis, Daniel J AU - Wood, Bradford J AU - Pinto, Peter A AU - Choyke, Peter L AU - Turkbey, Baris AD - Molecular Imaging Program, National Cancer Institute, NIH, Bethesda, MD, USA, turkbeyi@mail.nih.gov Y1 - 2015/08// PY - 2015 DA - Aug 2015 SP - 1788 EP - 1799 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 40 IS - 6 SN - 0942-8925, 0942-8925 KW - Biotechnology and Bioengineering Abstracts KW - Malignancy KW - Prostate cancer KW - Cognitive ability KW - Magnetic resonance imaging KW - Biopsy KW - Tumors KW - Ultrasound KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1712769226?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Abdominal+Imaging&rft.atitle=Recent+advances+in+image-guided+targeted+prostate+biopsy&rft.au=Brown%2C+Anna+M%3BElbuluk%2C+Osama%3BMertan%2C+Francesca%3BSankineni%2C+Sandeep%3BMargolis%2C+Daniel+J%3BWood%2C+Bradford+J%3BPinto%2C+Peter+A%3BChoyke%2C+Peter+L%3BTurkbey%2C+Baris&rft.aulast=Brown&rft.aufirst=Anna&rft.date=2015-08-01&rft.volume=40&rft.issue=6&rft.spage=1788&rft.isbn=&rft.btitle=&rft.title=Abdominal+Imaging&rft.issn=09428925&rft_id=info:doi/10.1007%2Fs00261-015-0353-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Number of references - 65 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Malignancy; Prostate cancer; Cognitive ability; Magnetic resonance imaging; Biopsy; Tumors; Ultrasound DO - http://dx.doi.org/10.1007/s00261-015-0353-8 ER - TY - JOUR T1 - Topical administration of a suppressor of cytokine signaling-1 (SOCS1) mimetic peptide inhibits ocular inflammation and mitigates ocular pathology during mouse uveitis AN - 1709178961; PQ0001871657 AB - Uveitis is a diverse group of potentially sight-threatening intraocular inflammatory diseases and pathology derives from sustained production of pro-inflammatory cytokines in the optical axis. Although topical or systemic steroids are effective therapies, their adverse effects preclude prolonged usage and are impetus for seeking alternative immunosuppressive agents, particularly for patients with refractory uveitis. In this study, we synthesized a 16 amino acid membrane-penetrating lipophilic suppressor of cytokine signaling 1 peptide (SOCS1-KIR) that inhibits JAK/STAT signaling pathways and show that it suppresses and ameliorates experimental autoimmune uveitis (EAU), the mouse model of human uveitis. Fundus images, histological and optical coherence tomography analysis of eyes showed significant suppression of clinical disease, with average clinical score of 0.5 compared to 2.0 observed in control mice treated with scrambled peptide. We further show that SOCS1-KIR conferred protection from ocular pathology by inhibiting the expansion of pathogenic Th17 cells and inhibiting trafficking of inflammatory cells into the neuroretina during EAU. Dark-adapted scotopic and photopic electroretinograms further reveal that SOCS1-KIR prevented decrement of retinal function, underscoring potential neuroprotective effects of SOCS1-KIR in uveitis. Importantly, SOCS1-KIR is non-toxic, suggesting that topical administration of SOCS1-Mimetics can be exploited as a non-invasive treatment for uveitis and for limiting cytokine-mediated pathology in other ocular inflammatory diseases including scleritis. JF - Journal of Autoimmunity AU - He, Chang AU - Yu, Cheng-Rong AU - Sun, Lin AU - Mahdi, Rashid M AU - Larkin, Joseph III AU - Egwuagu, Charles E AD - Molecular Immunology Section, National Eye Institute, National Institutes of Health, USA Y1 - 2015/08// PY - 2015 DA - Aug 2015 SP - 31 EP - 38 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 62 SN - 0896-8411, 0896-8411 KW - Toxicology Abstracts; Immunology Abstracts KW - Uveitis KW - Experimental autoimmune uveitis (EAU) KW - Suppressor of cytokine signaling KW - Ocular inflammation KW - SOCS1 KW - SOCS1 mimetic KW - Biologics KW - SOCS suppressor of cytokine signaling KW - SOCS1-KIR the kinase inhibitory region of SOCS1 KW - EAU experimental autoimmune uveitis KW - IRBP interphotoreceptor retinoid-binding protein KW - JAK janus kinase KW - STAT signal transducers and activators of transcription KW - Scleritis KW - Amino acids KW - Retina KW - Helper cells KW - Animal models KW - Neuroprotection KW - Steroid hormones KW - Immunosuppressive agents KW - Lipophilic KW - Inflammation KW - Inflammatory diseases KW - Electroretinograms KW - experimental autoimmune uveitis KW - Tomography KW - SOCS-1 protein KW - Experimental autoimmune uveoretinitis KW - Side effects KW - Signal transduction KW - X 24310:Pharmaceuticals KW - F 06930:Autoimmunity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709178961?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Autoimmunity&rft.atitle=Topical+administration+of+a+suppressor+of+cytokine+signaling-1+%28SOCS1%29+mimetic+peptide+inhibits+ocular+inflammation+and+mitigates+ocular+pathology+during+mouse+uveitis&rft.au=He%2C+Chang%3BYu%2C+Cheng-Rong%3BSun%2C+Lin%3BMahdi%2C+Rashid+M%3BLarkin%2C+Joseph+III%3BEgwuagu%2C+Charles+E&rft.aulast=He&rft.aufirst=Chang&rft.date=2015-08-01&rft.volume=62&rft.issue=&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Journal+of+Autoimmunity&rft.issn=08968411&rft_id=info:doi/10.1016%2Fj.jaut.2015.05.011 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Scleritis; Amino acids; Retina; Helper cells; Animal models; Neuroprotection; Steroid hormones; Immunosuppressive agents; Lipophilic; Inflammation; Inflammatory diseases; Uveitis; Electroretinograms; experimental autoimmune uveitis; Tomography; SOCS-1 protein; Experimental autoimmune uveoretinitis; Side effects; Signal transduction DO - http://dx.doi.org/10.1016/j.jaut.2015.05.011 ER - TY - JOUR T1 - Correlation between Choline Peak at MR Spectroscopy and Calcium-Sensing Receptor Expression Level in Breast Cancer: A Preliminary Clinical Study AN - 1709178804; PQ0001862577 AB - Purpose: The calcium-sensing receptor (CaSR) is overexpressed in many pathological states including breast cancer. Since choline kinase may be activated in breast cancer cells by CaSR resulting in increased phosphocholine production, we sought to correlate the total choline peak in breast lesions as measured by in vivo proton magnetic resonance spectroscopy ( super(1)H-MRS) with the CaSR expression levels in surgical specimens. Procedures: Thirty-six patients with breast lesions were MR scanned at 3T scanner. Tumour morphology and DCE-MR kinetics were evaluated. super(1)H-MRS was applied for Cho detection and compared with the CaSR immunohistochemistry analysis (score 0-5) on surgical breast specimens. Results: Thirty-four lesions demonstrated a DCE malignant kinetics curve (types 2 and 3), while two lesions showed a benign (type 1). Twenty of the 23 breast cancer lesions (87 %) with a consistent Cho peak expressed a CaSR score of 3-5, and ten of the 11 breast lesions negative for Cho (91 %) had a CaSR score of 1-2. The two benign lesions showed a non-uniform/weak intense expression of the CaSR (score 3) with a consistent Cho peak. Conclusions: The presence or absence of choline peak evaluated by super(1)H-MRS, well correlated with the expression of CaSR in patients with breast lesions (p<0.01), supports the hypothesis that CaSR may play an important role in the production of choline in breast cancer. JF - Molecular Imaging and Biology AU - Baio, Gabriella AU - Rescinito, Giuseppe AU - Rosa, Francesca AU - Pace, Daniele AU - Boccardo, Simona AU - Basso, Luca AU - Salvi, Sandra AU - Calabrese, Massimo AU - Truini, Mauro AU - Neumaier, Carlo Emanuele AD - Diagnostic Imaging and Senology Unit, IRCCS Azienda Ospedaliera Universitaria (AOU) San Martino-IST-National Cancer Institute, 16132, Genoa, Italy, gabriella.baio@abdn.ac.uk Y1 - 2015/08// PY - 2015 DA - Aug 2015 SP - 548 EP - 556 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 17 IS - 4 SN - 1536-1632, 1536-1632 KW - Biotechnology and Bioengineering Abstracts KW - Choline KW - Magnetic resonance spectroscopy KW - Kinetics KW - Calcium-sensing receptors KW - Breast cancer KW - Choline kinase KW - Immunohistochemistry KW - phosphocholine KW - Benign KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709178804?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Imaging+and+Biology&rft.atitle=Correlation+between+Choline+Peak+at+MR+Spectroscopy+and+Calcium-Sensing+Receptor+Expression+Level+in+Breast+Cancer%3A+A+Preliminary+Clinical+Study&rft.au=Baio%2C+Gabriella%3BRescinito%2C+Giuseppe%3BRosa%2C+Francesca%3BPace%2C+Daniele%3BBoccardo%2C+Simona%3BBasso%2C+Luca%3BSalvi%2C+Sandra%3BCalabrese%2C+Massimo%3BTruini%2C+Mauro%3BNeumaier%2C+Carlo+Emanuele&rft.aulast=Baio&rft.aufirst=Gabriella&rft.date=2015-08-01&rft.volume=17&rft.issue=4&rft.spage=548&rft.isbn=&rft.btitle=&rft.title=Molecular+Imaging+and+Biology&rft.issn=15361632&rft_id=info:doi/10.1007%2Fs11307-015-0823-y LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Number of references - 21 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Choline; Kinetics; Magnetic resonance spectroscopy; Calcium-sensing receptors; Breast cancer; Choline kinase; Immunohistochemistry; phosphocholine; Benign DO - http://dx.doi.org/10.1007/s11307-015-0823-y ER - TY - JOUR T1 - Comparison of multiple datasets with gridded precipitation observations over the Tibetan Plateau AN - 1709169743; PQ0001850660 AB - Precipitation is a critical component of the water balance, and hence its variability is critical for cryospheric and climate change in the Tibetan Plateau (TP). Mean annual and seasonal precipitation totals are compared between gridded observations interpolated to a high resolution (0.5 degree 0.5 degree ) and multiple reanalysis type-datasets during 1979-2001. The latter include two NCEP reanalyses (NCEP1 and NCEP2), two European Centre for Medium-Range Weather Forecasts (ECMWF) reanalyses (ERA-40 and ERA-Interim), three modern reanalyses [the twentieth century reanalysis (20century), MERRA and CFSR] and three merged analysis datasets (CMAP1, CMAP2 and GPCP). Observations show an increase in mean precipitation from the northwestern to the southeastern (SE) regions of the TP which are divided by an isohyet of 400 mm, and overall trends during the studied period are positive. Compared with observations, most of the datasets (NCEP1, NCEP2, CMAP1, CMAP2, ERA-Interim, ERA-40, GPCP, 20century, MERRA and CFSR) can both broadly capture the spatial distributions and identify temporal patterns and variabilities of mean precipitation. However, most multi-datasets overestimate precipitation especially in the SE where summer convection is dominant. There remain substantial disagreements and large discrepancies in precipitation trends due to differences in assimilation systems between datasets. Taylor diagrams are used to show the correlation coefficients, standard deviation, and root-mean-square difference of precipitation totals between interpolated observations and assimilated values on an annual and seasonal basis. Merged analysis data (CMAP1 and CMAP2) agree with observations more closely than reanalyses. Thus not all datasets are equally biased and choice of dataset is important. JF - Climate Dynamics AU - You, Qinglong AU - Min, Jinzhong AU - Zhang, Wei AU - Pepin, Nick AU - Kang, Shichang AD - Earth System Modelling Center (ESMC), Nanjing International Academy of Meteorological Sciences (NIAMS), Key Laboratory of Meteorological Disaster, Ministry of Education, Collaborative Innovation Center on Forecast and Evaluation of Meteorological Disasters, Nanjing University of Information Science and Technology, Nanjing, 210044, China, yqingl@126.com Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 791 EP - 806 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 45 IS - 3-4 SN - 0930-7575, 0930-7575 KW - Water Resources Abstracts; ASFA 2: Ocean Technology Policy & Non-Living Resources; Sustainability Science Abstracts; Meteorological & Geoastrophysical Abstracts KW - Convection KW - Variability KW - Spatial distribution KW - Rainfall KW - Climate change KW - Correlations KW - Hydrologic Budget KW - Summer KW - Convection development KW - Data assimilation KW - Data reanalysis KW - Seasonal precipitation KW - Plateaus KW - Sulfur dioxide KW - Standard Deviation KW - European Centre for Medium-Range Weather Forecasts KW - Seasonal variations KW - Weather forecasting KW - Atmospheric precipitations KW - Weather KW - Mean precipitation KW - Precipitation trends KW - Climates KW - Climate KW - Precipitation KW - Water balance KW - China, People's Rep., Xizang, Tibetan Plateau KW - Isohyets KW - Precipitation variability KW - SW 5010:Network design KW - M3 1010:Issues in Sustainable Development KW - Q2 09244:Air-sea coupling KW - M2 556.13:Evaporation/Evapotranspiration (556.13) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709169743?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Assamodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Climate+Dynamics&rft.atitle=Comparison+of+multiple+datasets+with+gridded+precipitation+observations+over+the+Tibetan+Plateau&rft.au=You%2C+Qinglong%3BMin%2C+Jinzhong%3BZhang%2C+Wei%3BPepin%2C+Nick%3BKang%2C+Shichang&rft.aulast=You&rft.aufirst=Qinglong&rft.date=2015-08-01&rft.volume=45&rft.issue=3-4&rft.spage=791&rft.isbn=&rft.btitle=&rft.title=Climate+Dynamics&rft.issn=09307575&rft_id=info:doi/10.1007%2Fs00382-014-2310-6 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Number of references - 44 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Convection; Water balance; Atmospheric precipitations; Climate change; Weather forecasting; Spatial distribution; Mean precipitation; Precipitation trends; Correlations; Convection development; Precipitation; Data reanalysis; Data assimilation; Seasonal precipitation; Precipitation variability; European Centre for Medium-Range Weather Forecasts; Weather; Plateaus; Sulfur dioxide; Rainfall; Climate; Summer; Seasonal variations; Variability; Standard Deviation; Isohyets; Climates; Hydrologic Budget; China, People's Rep., Xizang, Tibetan Plateau DO - http://dx.doi.org/10.1007/s00382-014-2310-6 ER - TY - JOUR T1 - A proposal for unified flow cytometer parameter naming AN - 1705090194; PQ0001826972 JF - Cytometry Part A AU - Roederer, Mario AD - Flow Cytometry Core and ImmunoTechnology Section, Vaccine Research Center, NIAID, NIH, Bethesda, Maryland. Y1 - 2015/08// PY - 2015 DA - Aug 2015 SP - 689 EP - 691 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 87 IS - 8 SN - 1552-4922, 1552-4922 KW - Biotechnology and Bioengineering Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1705090194?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cytometry+Part+A&rft.atitle=A+proposal+for+unified+flow+cytometer+parameter+naming&rft.au=Roederer%2C+Mario&rft.aulast=Roederer&rft.aufirst=Mario&rft.date=2015-08-01&rft.volume=87&rft.issue=8&rft.spage=689&rft.isbn=&rft.btitle=&rft.title=Cytometry+Part+A&rft.issn=15524922&rft_id=info:doi/10.1002%2Fcyto.a.22670 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2015-08-19 DO - http://dx.doi.org/10.1002/cyto.a.22670 ER - TY - JOUR T1 - Health effects of nuclear weapons testing AN - 1705071461; PQ0001839672 AB - Nuclear weapons were virtually unknown to the world before Aug 6, 1945, when the first atomic bomb was used against Japan in Hiroshima and the second 3 days later in Nagasaki. The 70th anniversary of this event is marked in the Lancet Series From Hiroshima and Nagasaki to Fukushima.13 The legacy of the atomic bomb extended far beyond Japan with atomic weapons testing programmes conducted worldwide for the next three and a half decades. Just 3 weeks before the atomic bomb attacks on Japan, the first nuclear explosion in history had taken place in secrecy in the desert of New Mexico, USA, when scientists working for the Manhattan Project tested the experimental nuclear bomb codenamed Trinity. JF - Lancet AU - Simon, Steven L AU - Bouville, Andre AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-9778, USA Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 407 EP - 409 PB - Elsevier B.V., Radarweg 29 Amsterdam 1043 NX Netherlands VL - 386 IS - 9992 SN - 0140-6736, 0140-6736 KW - Toxicology Abstracts; Health & Safety Science Abstracts KW - Historical account KW - USA, New Mexico KW - Weapons KW - Japan, Nagasaki KW - Deserts KW - Atomic bombs KW - Nuclear weapons KW - Explosions KW - X 24390:Radioactive Materials KW - H 7000:Fire Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1705071461?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lancet&rft.atitle=Health+effects+of+nuclear+weapons+testing&rft.au=Simon%2C+Steven+L%3BBouville%2C+Andre&rft.aulast=Simon&rft.aufirst=Steven&rft.date=2015-08-01&rft.volume=386&rft.issue=9992&rft.spage=407&rft.isbn=&rft.btitle=&rft.title=Lancet&rft.issn=01406736&rft_id=info:doi/10.1016%2FS0140-6736%2815%2961037-6 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Number of references - 17 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Deserts; Atomic bombs; Historical account; Weapons; Nuclear weapons; Explosions; USA, New Mexico; Japan, Nagasaki DO - http://dx.doi.org/10.1016/S0140-6736(15)61037-6 ER - TY - JOUR T1 - Modeling ligand recognition at the P2Y12 receptor in light of X-ray structural information. AN - 1704345698; 26194851 AB - The G protein-coupled P2Y12 receptor (P2Y12R) is an important antithrombotic target and of great interest for pharmaceutical discovery. Its recently solved, highly divergent crystallographic structures in complex either with nucleotides (full or partial agonist) or with a nonnucleotide antagonist raise the question of which structure is more useful to understand ligand recognition. Therefore, we performed extensive molecular modeling studies based on these structures and mutagenesis, to predict the binding modes of major classes of P2Y12R ligands previously reported. Various nucleotide derivatives docked readily to the agonist-bound P2Y12R, but uncharged nucleotide-like antagonist ticagrelor required a hybrid receptor resembling the agonist-bound P2Y12R except for the top portion of TM6. Supervised molecular dynamics (SuMD) of ticagrelor binding indicated interactions with the extracellular regions of P2Y12R, defining possible meta-binding sites. Ureas, sulfonylureas, sulfonamides, anthraquinones and glutamic acid piperazines docked readily to the antagonist-bound P2Y12R. Docking dinucleotides at both agonist- and antagonist-bound structures suggested interactions with two P2Y12R pockets. Thus, our structure-based approach consistently rationalized the main structure-activity relationships within each ligand class, giving useful information for designing improved ligands. JF - Journal of computer-aided molecular design AU - Paoletta, Silvia AU - Sabbadin, Davide AU - von Kügelgen, Ivar AU - Hinz, Sonja AU - Katritch, Vsevolod AU - Hoffmann, Kristina AU - Abdelrahman, Aliaa AU - Straßburger, Jens AU - Baqi, Younis AU - Zhao, Qiang AU - Stevens, Raymond C AU - Moro, Stefano AU - Müller, Christa E AU - Jacobson, Kenneth A AD - Molecular Recognition Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bldg. 8A, Rm. B1A-19, LBC, NIH, NIDDK, Bethesda, MD, 20892-0810, USA. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 737 EP - 756 VL - 29 IS - 8 KW - Anthraquinones KW - 0 KW - Ligands KW - Nucleotides KW - Purinergic P2Y Receptor Agonists KW - Purinergic P2Y Receptor Antagonists KW - Receptors, Purinergic P2Y12 KW - Sulfonamides KW - Index Medicus KW - Nucleotides -- metabolism KW - Models, Molecular KW - Humans KW - Anthraquinones -- metabolism KW - Nucleotides -- chemistry KW - Anthraquinones -- chemistry KW - Molecular Dynamics Simulation KW - Structure-Activity Relationship KW - Sulfonamides -- metabolism KW - Sulfonamides -- chemistry KW - Crystallography, X-Ray KW - Protein Conformation KW - Molecular Docking Simulation -- methods KW - Receptors, Purinergic P2Y12 -- metabolism KW - Purinergic P2Y Receptor Antagonists -- chemistry KW - Purinergic P2Y Receptor Agonists -- chemistry KW - Purinergic P2Y Receptor Antagonists -- metabolism KW - Purinergic P2Y Receptor Agonists -- metabolism KW - Receptors, Purinergic P2Y12 -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1704345698?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+computer-aided+molecular+design&rft.atitle=Modeling+ligand+recognition+at+the+P2Y12+receptor+in+light+of+X-ray+structural+information.&rft.au=Paoletta%2C+Silvia%3BSabbadin%2C+Davide%3Bvon+K%C3%BCgelgen%2C+Ivar%3BHinz%2C+Sonja%3BKatritch%2C+Vsevolod%3BHoffmann%2C+Kristina%3BAbdelrahman%2C+Aliaa%3BStra%C3%9Fburger%2C+Jens%3BBaqi%2C+Younis%3BZhao%2C+Qiang%3BStevens%2C+Raymond+C%3BMoro%2C+Stefano%3BM%C3%BCller%2C+Christa+E%3BJacobson%2C+Kenneth+A&rft.aulast=Paoletta&rft.aufirst=Silvia&rft.date=2015-08-01&rft.volume=29&rft.issue=8&rft.spage=737&rft.isbn=&rft.btitle=&rft.title=Journal+of+computer-aided+molecular+design&rft.issn=1573-4951&rft_id=info:doi/10.1007%2Fs10822-015-9858-z LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-13 N1 - Date created - 2015-08-13 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Med Chem. 2008 Feb 28;51(4):1007-25 [18232657] J Med Chem. 2014 Sep 11;57(17):7293-316 [25075638] ChemMedChem. 2008 May;3(5):732-6 [18224705] Thromb Res. 2008;122(4):533-40 [18539312] Biochem Pharmacol. 2008 Nov 15;76(10):1201-13 [18809389] J Med Chem. 2009 Jun 25;52(12):3784-93 [19463000] Bioorg Med Chem Lett. 2009 Aug 15;19(16):4657-63 [19604694] Bioorg Med Chem Lett. 2009 Oct 15;19(20):5919-23 [19748783] Bioorg Med Chem Lett. 2009 Nov 1;19(21):6148-56 [19796941] J Pharmacol Exp Ther. 2009 Nov;331(2):648-55 [19690189] Cardiovasc Ther. 2009 Winter;27(4):259-74 [19604248] Bioorg Med Chem Lett. 2010 Feb 15;20(4):1388-94 [20097563] Thromb Res. 2010 Feb;125(2):159-65 [19945153] J Med Chem. 2010 Mar 11;53(5):2010-37 [20141147] Drug News Perspect. 2010 Dec;23(10):670-84 [21180653] J Comput Chem. 2011 Apr 30;32(6):1183-94 [21387345] Bioorg Med Chem Lett. 2011 May 15;21(10):2877-81 [21507636] J Comput Aided Mol Des. 2011 Apr;25(4):329-38 [21461952] FEBS J. 2012 Jan;279(1):180-91 [22044483] J Med Chem. 2012 Oct 25;55(20):8615-29 [22984835] J Chem Inf Model. 2014 Oct 27;54(10):2846-55 [25245783] J Thromb Haemost. 2014 Nov;12(11):1898-905 [25186974] BMC Struct Biol. 2014;14:19 [25928393] Mol Pharmacol. 2015 Aug;88(2):220-30 [25837834] Nature. 2001 Jan 11;409(6817):202-7 [11196645] Bioorg Med Chem Lett. 2001 Jul 23;11(14):1805-8 [11459636] Biopolymers. 2000-2001;56(4):257-65 [11754339] J Med Chem. 2002 Dec 19;45(26):5694-709 [12477353] J Med Chem. 2004 Mar 25;47(7):1739-49 [15027865] Semin Vasc Med. 2003 May;3(2):113-22 [15199474] Pharmacol Rev. 1991 Sep;43(3):243-98 [1956953] Proc Natl Acad Sci U S A. 1992 Mar 15;89(6):2370-3 [1549600] J Mol Graph. 1996 Feb;14(1):33-8, 27-8 [8744570] J Med Chem. 1999 Jan 28;42(2):213-20 [9925726] Int Rev Cytol. 2004;240:31-304 [15548415] J Thromb Haemost. 2004 Nov;2(11):1980-8 [15550030] J Pharmacol Exp Ther. 2004 Dec;311(3):1038-43 [15345752] J Med Chem. 2005 Apr 21;48(8):2763-6 [15828813] J Comput Chem. 2005 Dec;26(16):1781-802 [16222654] J Med Chem. 2006 Jan 26;49(2):534-53 [16420040] Pharmacol Rev. 2006 Sep;58(3):281-341 [16968944] Bioorg Med Chem Lett. 2008 Mar 15;18(6):2167-71 [18276138] J Thromb Haemost. 2012 Dec;10(12):2573-80 [23083103] Mol Pharmacol. 2013 Jan;83(1):256-66 [23093496] Eur J Med Chem. 2013 Jul;65:360-75 [23747805] J Med Chem. 2013 Sep 12;56(17):7015-24 [23899349] Future Med Chem. 2013 Nov;5(17):2037-56 [24215345] Bioorg Med Chem Lett. 2014 Jan 1;24(1):141-6 [24332627] J Chem Inf Model. 2014 Feb 24;54(2):372-6 [24456045] PLoS One. 2014;9(4):e94780 [24722456] Nature. 2014 May 1;509(7498):119-22 [24784220] Nature. 2014 May 1;509(7498):115-8 [24670650] Neurobiol Dis. 2014 Oct;70:162-78 [24971933] Bioorg Med Chem Lett. 2007 Nov 1;17(21):6013-8 [17827008] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s10822-015-9858-z ER - TY - JOUR T1 - Informing tobacco cessation benefit use interventions for unionized blue-collar workers: a mixed-methods reasoned action approach AN - 1704344054; 4694800 AB - Blue-collar workers typically have high rates of tobacco use but low rates of using tobacco cessation resources available through their health benefits. Interventions to motivate blue-collar tobacco users to use effective cessation support are needed. Reasoned action theory is useful in this regard as it can identify the beliefs that shape tobacco cessation benefit use intentions. However, conventional reasoned action research cannot speak to how those beliefs can best be translated into intervention messages. In the present work, we expand the reasoned action approach by adding additional qualitative inquiry to better understand blue-collar smokers' beliefs about cessation benefit use. Across three samples of unionized blue-collar tobacco users, we identified (1) the 35 attitudinal, normative, and control beliefs that represented tobacco users' belief structure about cessation benefit use; (2) instrumental attitude as most important in explaining cessation intention; (3) attitudinal beliefs about treatment options' efficacy, health effects, and monetary implications of using benefits as candidates for message design; (4) multiple interpretations of cessation beliefs (e.g., short and long-term health effects); and (5) clear implications of these interpretations for creative message design. Taken together, the findings demonstrate how a mixed-method reasoned action approach can inform interventions that promote the use of tobacco cessation health benefits. Reprinted by permission of Springer JF - Prevention science AU - Yzer, Marco AU - Weisman, Susan AU - Mejia, Nicole AU - Hennrikus, Deborah AU - Choi, Kelvin AU - Simone, Susan De AD - University of Minnesota ; William Mitchell College of Law ; National Institute on Minority Health and Health Disparities Y1 - 2015/08// PY - 2015 DA - Aug 2015 SP - 811 EP - 821 VL - 16 IS - 6 SN - 1389-4986, 1389-4986 KW - Sociology KW - Smoking KW - Addicts KW - Blue collar workers KW - Tobacco KW - Health KW - Beliefs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1704344054?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Prevention+science&rft.atitle=Informing+tobacco+cessation+benefit+use+interventions+for+unionized+blue-collar+workers%3A+a+mixed-methods+reasoned+action+approach&rft.au=Yzer%2C+Marco%3BWeisman%2C+Susan%3BMejia%2C+Nicole%3BHennrikus%2C+Deborah%3BChoi%2C+Kelvin%3BSimone%2C+Susan+De&rft.aulast=Yzer&rft.aufirst=Marco&rft.date=2015-08-01&rft.volume=16&rft.issue=6&rft.spage=811&rft.isbn=&rft.btitle=&rft.title=Prevention+science&rft.issn=13894986&rft_id=info:doi/10.1007%2Fs11121-015-0566-7 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-08-17 N1 - Last updated - 2015-08-17 N1 - SubjectsTermNotLitGenreText - 1670 13682; 12766 3055 798 10286; 5772; 11755 5707 6071 1542 11325; 1547; 562 DO - http://dx.doi.org/10.1007/s11121-015-0566-7 ER - TY - JOUR T1 - Sexualized behaviors partially mediate the link between maltreatment and delinquent behaviors AN - 1704341468; 4694849 AB - The link between child maltreatment and juvenile delinquency has been well established, yet the underlying mechanisms through which the relationship may be explained are not very well understood. Although sexualized behaviors have been most studied in the context of sexual abuse, increasing evidence suggests that a broader conceptualization is warranted. Therefore, the current study tested sexualized behaviors as a mediator in the relation between child maltreatment of any type and delinquent behaviors using structural equation modeling. This study used a multi-site prospective sample of 804 children who were at high-risk for experiencing maltreatment and part of the Longitudinal Studies of Child Abuse and Neglect consortium. This study found that reported maltreatment was related to delinquency, and sexualized behaviors partially mediated the relationship between child maltreatment and juvenile delinquency. Specifically, children with more maltreatment reports before age 8 had increased sexualized behaviors at age 8, which in turn predicted greater delinquent behaviors at age 12. These results suggest that in addition to maltreatment experiences, early sexualized behaviors (i.e., at age 8) may also be markers for subsequent delinquent behaviors (i.e., at age 12). Researchers and clinicians should work to further clarify the connections among child maltreatment, sexualized behaviors, and delinquency. Reprinted by permission of Springer JF - Journal of child and family studies AU - Merrick, Melissa T AU - Litrownik, Alan J AU - Margolis, Benyamin AU - Wiley, Tisha R.A. AU - Everson, Mark D AU - Dubowitz, Howard AU - English, Diana AD - National Center for Injury Prevention and Control ; San Diego State University ; Health Resources and Services Administration ; National Institutes of Health ; University of North Carolina, Chapel Hill ; University of Maryland ; University of Washington Y1 - 2015/08// PY - 2015 DA - Aug 2015 SP - 2217 EP - 2228 VL - 24 IS - 8 SN - 1062-1024, 1062-1024 KW - Sociology KW - Sexuality KW - Sexual behaviour KW - Conceptualization KW - Juvenile delinquency KW - Mediation KW - Modelling UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1704341468?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+child+and+family+studies&rft.atitle=Sexualized+behaviors+partially+mediate+the+link+between+maltreatment+and+delinquent+behaviors&rft.au=Merrick%2C+Melissa+T%3BLitrownik%2C+Alan+J%3BMargolis%2C+Benyamin%3BWiley%2C+Tisha+R.A.%3BEverson%2C+Mark+D%3BDubowitz%2C+Howard%3BEnglish%2C+Diana&rft.aulast=Merrick&rft.aufirst=Melissa&rft.date=2015-08-01&rft.volume=24&rft.issue=8&rft.spage=2217&rft.isbn=&rft.btitle=&rft.title=Journal+of+child+and+family+studies&rft.issn=10621024&rft_id=info:doi/10.1007%2Fs10826-014-0024-3 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-08-17 N1 - Last updated - 2015-08-17 N1 - SubjectsTermNotLitGenreText - 7039 3364 11893 11979; 7869 2703 2698; 11563 1025 1542 11325 6071; 2688 2449 10404; 8162 8163; 11579 11538 DO - http://dx.doi.org/10.1007/s10826-014-0024-3 ER - TY - JOUR T1 - Sexualized Behaviors Partially Mediate the Link between Maltreatment and Delinquent Behaviors AN - 1703894193 AB - The link between child maltreatment and juvenile delinquency has been well established, yet the underlying mechanisms through which the relationship may be explained are not very well understood. Although sexualized behaviors have been most studied in the context of sexual abuse, increasing evidence suggests that a broader conceptualization is warranted. Therefore, the current study tested sexualized behaviors as a mediator in the relation between child maltreatment of any type and delinquent behaviors using structural equation modeling. This study used a multi-site prospective sample of 804 children who were at high-risk for experiencing maltreatment and part of the Longitudinal Studies of Child Abuse and Neglect consortium. This study found that reported maltreatment was related to delinquency, and sexualized behaviors partially mediated the relationship between child maltreatment and juvenile delinquency. Specifically, children with more maltreatment reports before age 8 had increased sexualized behaviors at age 8, which in turn predicted greater delinquent behaviors at age 12. These results suggest that in addition to maltreatment experiences, early sexualized behaviors (i.e., at age 8) may also be markers for subsequent delinquent behaviors (i.e., at age 12). Researchers and clinicians should work to further clarify the connections among child maltreatment, sexualized behaviors, and delinquency. JF - Journal of Child and Family Studies AU - Litrownik, Alan J AU - Margolis, Benyamin AU - Wiley, Tisha R A AU - Everson, Mark D AU - Dubowitz, Howard AU - English, Diana AD - Department of Psychology, San Diego State University, San Diego, CA, USA ; Division of Home Visiting and Early Childhood Systems, Maternal and Child Health Bureau, Health Resources and Services Administration, Rockville, MD, USA ; Office of Behavioral and Social Science Research, National Institutes of Health, Bethesda, MD, USA ; Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA ; Department of Pediatrics, University of Maryland, College Park, MD, USA ; School of Social Work, University of Washington, Seattle, WA, USA ; Merrick, Melissa T; Division of Violence Prevention, National Center for Injury Prevention and Control, Centers for Disease Control and Prevention, Atlanta, GA, USA Y1 - 2015/08// PY - 2015 DA - Aug 2015 SP - 2217 EP - 2228 CY - New York PB - Springer Science & Business Media VL - 24 IS - 8 SN - 1062-1024 KW - Psychology KW - Juvenile Delinquency KW - Child neglect KW - Maltreated children KW - Maltreatment KW - Sexual abuse KW - Children KW - Child Neglect KW - Child Sexual Abuse KW - Risk KW - Abused children KW - Age KW - Behaviour KW - Child abuse KW - Child maltreatment KW - Conceptualization KW - Delinquency KW - High risk KW - Juvenile offenders UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1703894193?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Child+and+Family+Studies&rft.atitle=Sexualized+Behaviors+Partially+Mediate+the+Link+between+Maltreatment+and+Delinquent+Behaviors&rft.au=Merrick%2C+Melissa+T%3BLitrownik%2C+Alan+J%3BMargolis%2C+Benyamin%3BWiley%2C+Tisha+R+A%3BEverson%2C+Mark+D%3BDubowitz%2C+Howard%3BEnglish%2C+Diana&rft.aulast=Merrick&rft.aufirst=Melissa&rft.date=2015-08-01&rft.volume=24&rft.issue=8&rft.spage=2217&rft.isbn=&rft.btitle=&rft.title=Journal+of+Child+and+Family+Studies&rft.issn=10621024&rft_id=info:doi/10.1007%2Fs10826-014-0024-3 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-08-13 N1 - Last updated - 2016-05-16 DO - http://dx.doi.org/10.1007/s10826-014-0024-3 ER - TY - JOUR T1 - Redox control of viral carcinogenesis: The human papillomavirus paradigm. AN - 1703698464; 25534611 AB - Cervical cancer is the second most common neoplastic disease among women worldwide. The initiating event of such cancer is the infection with certain types of human papillomavirus (HPV), a very common condition in the general population. However, the majority of HPV infections is subclinical and transitory and is resolved spontaneously. Intriguingly, viral oncogene expression, although necessary, is not per se sufficient to promote cervical cancer and other factors are involved in the progression of infected cells to the full neoplastic phenotype. In this perspective it has been suggested that the redox balance and the oxidative stress (OS) may represent interesting and under-explored candidates as promoting factors in HPV-initiated carcinogenesis. The current review discusses the possible interplay between the viral mechanisms modulating cell homeostasis and redox sensitive mechanisms. Experimental data and indirect evidences are presented on the activity of viral dependent functions on i) the regulation of enzymes and compounds involved in OS; ii) the protection from oxidation of detoxifying/antiapoptotic enzymes and redox-sensitive transcription factors; iii) the suppression of apoptosis; and iv) the modulation of host microRNAs regulating genes associated with antioxidant defense. The resulting tangled scenario suggests that viral hosting cells adapt their metabolisms in order to support their growth and survival in the increasingly oxidant micro-environment associated with HPV tumor initiation and progression. HPV can modulate the host cell redox homeostasis in order to favor infection and possibly tumor transformation. This article is part of a Special Issue entitled Redox regulation of differentiation and de-differentiation. Copyright © 2014 Elsevier B.V. All rights reserved. JF - Biochimica et biophysica acta AU - Foppoli, Cesira AU - De Marco, Federico AU - Cini, Chiara AU - Perluigi, M AD - Institute of Molecular Biology and Pathology, National Research Council, Rome, Italy. ; Laboratory of Virology, Regina Elena National Cancer Institute, Rome, Italy. ; Department of Biochemical Sciences, Sapienza University of Rome, Rome, Italy. ; Department of Biochemical Sciences, Sapienza University of Rome, Rome, Italy. Electronic address: marzia.perluigi@uniroma1.it. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 1622 EP - 1632 VL - 1850 IS - 8 SN - 0006-3002, 0006-3002 KW - MIRN34 microRNA, human KW - 0 KW - MicroRNAs KW - Oncogene Proteins, Viral KW - Reactive Oxygen Species KW - Index Medicus KW - Oxidative stress KW - Transcription factors KW - Cervical cancer KW - Human papillomavirus KW - Antioxidant systems KW - Oxidation-Reduction KW - Reactive Oxygen Species -- metabolism KW - MicroRNAs -- genetics KW - Humans KW - Models, Biological KW - Oncogene Proteins, Viral -- metabolism KW - Female KW - Uterine Cervical Neoplasms -- metabolism KW - Papillomaviridae -- physiology KW - Papillomavirus Infections -- virology KW - Papillomaviridae -- metabolism KW - Uterine Cervical Neoplasms -- genetics KW - Papillomavirus Infections -- genetics KW - Papillomavirus Infections -- metabolism KW - Uterine Cervical Neoplasms -- virology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1703698464?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Redox+control+of+viral+carcinogenesis%3A+The+human+papillomavirus+paradigm.&rft.au=Foppoli%2C+Cesira%3BDe+Marco%2C+Federico%3BCini%2C+Chiara%3BPerluigi%2C+M&rft.aulast=Foppoli&rft.aufirst=Cesira&rft.date=2015-08-01&rft.volume=1850&rft.issue=8&rft.spage=1622&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbagen.2014.12.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-30 N1 - Date created - 2015-05-21 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbagen.2014.12.016 ER - TY - JOUR T1 - MiRNA mimic screen for improved expression of functional neurotensin receptor from HEK 293 cells AN - 1701491795; PQ0001707806 AB - Obtaining adequate quantities of functional mammalian membrane proteins has been a bottleneck in their structural and functional studies because the expression of these proteins from mammalian cells is relatively low. To explore the possibility of enhancing expression of these proteins using miRNA, a stable T-REx-293 cell line expressing the neurotensin receptor type 1 (NTSR1), a hard-to-express G protein-coupled receptor (GPCR), was constructed. The cell line was then subjected to human miRNA mimic library screening. In parallel, an HEK293 cell line expressing luciferase was also screened with the same human miRNA mimic library. Five microRNA mimics: hsa-miR-22-5p, hsa-miR-18a-5p, hsa-miR-22-3p, hsa-miR-429, and hsa-miR-2110were identified from both screens. They led to 48% increase in the expression of functional NTSR1 and to 239% increase of luciferase expression. These miRNAs were also effective in enhancing the expression of secretedglypican-3 hFc-fusion protein from HEK293 cells.The results indicate that these molecules may have a wide role in enhancing the production of proteins with biomedical interest. Biotechnol. Bioeng. 2015; 112: 1632-1643. JF - Biotechnology and Bioengineering AU - Xiao, Su AU - Chen, Yu-Chi AU - Betenbaugh, Michael J AU - Martin, Scott E AU - Shiloach, Joseph AD - Biotechnology Core Laboratory, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, 20892. Y1 - 2015/08// PY - 2015 DA - Aug 2015 SP - 1632 EP - 1643 PB - Wiley Subscription Services VL - 112 IS - 8 SN - 0006-3592, 0006-3592 KW - Biotechnology and Bioengineering Abstracts KW - neurotensin receptors KW - G protein-coupled receptors KW - Mammalian cells KW - Structure-function relationships KW - miRNA KW - Membrane proteins KW - W 30940:Products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701491795?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biotechnology+and+Bioengineering&rft.atitle=MiRNA+mimic+screen+for+improved+expression+of+functional+neurotensin+receptor+from+HEK+293+cells&rft.au=Xiao%2C+Su%3BChen%2C+Yu-Chi%3BBetenbaugh%2C+Michael+J%3BMartin%2C+Scott+E%3BShiloach%2C+Joseph&rft.aulast=Xiao&rft.aufirst=Su&rft.date=2015-08-01&rft.volume=112&rft.issue=8&rft.spage=1632&rft.isbn=&rft.btitle=&rft.title=Biotechnology+and+Bioengineering&rft.issn=00063592&rft_id=info:doi/10.1002%2Fbit.25567 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - neurotensin receptors; Mammalian cells; G protein-coupled receptors; Structure-function relationships; miRNA; Membrane proteins DO - http://dx.doi.org/10.1002/bit.25567 ER - TY - JOUR T1 - Reproducibility and optimization of in vivo human diffusion-weighted MRS of the corpus callosum at 3T and 7T AN - 1701486088; PQ0001794770 AB - Diffusion-weighted MRS (DWS) of brain metabolites enables the study of cell-specific alterations in tissue microstructure by probing the diffusion of intracellular metabolites. In particular, the diffusion properties of neuronal N-acetylaspartate (NAA), typically co-measured with N-acetylaspartyl glutamate (NAAG) (NAA+NAAG=tNAA), have been shown to be sensitive to intraneuronal/axonal damage in pathologies such as stroke and multiple sclerosis. Lacking, so far, are empirical assessments of the reproducibility of DWS measures across time and subjects, as well as a systematic investigation of the optimal acquisition parameters for DWS experiments, both of which are sorely needed for clinical applications of the method. In this study, we acquired comprehensive single-volume DWS datasets of the human corpus callosum at 3T and 7T. We investigated the inter- and intra-subject variability of empirical and modeled diffusion properties of tNAA [D sub(avg)(tNAA) and D sub(model)(tNAA), respectively]. Subsequently, we used a jackknife-like resampling approach to explore the variance of these properties in partial data subsets reflecting different total scan durations. The coefficients of variation (C sub(V)) and repeatability coefficients (C sub(R)) for D sub(avg)(tNAA) and D sub(model)(tNAA) were calculated for both 3T and 7T, with overall lower variability in the 7T results. Although this work is limited to the estimation of the diffusion properties in the corpus callosum, we show that a careful choice of diffusion-weighting conditions at both field strengths allows the accurate measurement of tNAA diffusion properties in clinically relevant experimental time. Based on the resampling results, we suggest optimized acquisition schemes of 13-min duration at 3T and 10-min duration at 7T, whilst retaining low variability (C sub(V) approximately 8%) for the tNAA diffusion measures. Power calculations for the estimation of D sub(model)(tNAA) and D sub(avg)(tNAA) based on the suggested schemes show that less than 21 subjects per group are sufficient for the detection of a 10% effect between two groups in case-control studies. In this study, we show that the diffusion-weighted MRS (DWS) method is feasible for clinical studies. Our power calculations based on empirical and modeled total N-acetylaspartate (tNAA) diffusion measures show that a subtle difference of 10% can be detected when sample sizes of about 10 subjects per group are used in case-control studies. With the separate acquisition schemes suggested for 3T and 7T, robust DWS measures can be achieved within 10-13min of scan time. JF - NMR in Biomedicine AU - Wood, Emily T AU - Ercan, Ayse Ece AU - Branzoli, Francesca AU - Webb, Andrew AU - Sati, Pascal AU - Reich, Daniel S AU - Ronen, Itamar AD - Translational Neuroradiology Unit (NINDS), National Institutes of Health, Bethesda, MD, USA. Y1 - 2015/08// PY - 2015 DA - Aug 2015 SP - 976 EP - 987 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 28 IS - 8 SN - 0952-3480, 0952-3480 KW - Biotechnology and Bioengineering Abstracts KW - N-Acetylaspartylglutamic acid KW - Data processing KW - Multiple sclerosis KW - Stroke KW - Brain KW - Therapeutic applications KW - N-Acetylaspartate KW - Metabolites KW - Corpus callosum KW - Diffusion KW - N.M.R. KW - Glutamic acid KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701486088?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=NMR+in+Biomedicine&rft.atitle=Reproducibility+and+optimization+of+in+vivo+human+diffusion-weighted+MRS+of+the+corpus+callosum+at+3T+and+7T&rft.au=Wood%2C+Emily+T%3BErcan%2C+Ayse+Ece%3BBranzoli%2C+Francesca%3BWebb%2C+Andrew%3BSati%2C+Pascal%3BReich%2C+Daniel+S%3BRonen%2C+Itamar&rft.aulast=Wood&rft.aufirst=Emily&rft.date=2015-08-01&rft.volume=28&rft.issue=8&rft.spage=976&rft.isbn=&rft.btitle=&rft.title=NMR+in+Biomedicine&rft.issn=09523480&rft_id=info:doi/10.1002%2Fnbm.3340 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - N-Acetylaspartylglutamic acid; Data processing; Multiple sclerosis; Stroke; Brain; Therapeutic applications; N.M.R.; Metabolites; N-Acetylaspartate; Diffusion; Glutamic acid; Corpus callosum DO - http://dx.doi.org/10.1002/nbm.3340 ER - TY - JOUR T1 - Novel Roles for Notch3 and Notch4 Receptors in Gene Expression and Susceptibility to Ozone-Induced Lung Inflammation in Mice. AN - 1701311163; 25658374 AB - Ozone is a highly toxic air pollutant and global health concern. Mechanisms of genetic susceptibility to ozone-induced lung inflammation are not completely understood. We hypothesized that Notch3 and Notch4 are important determinants of susceptibility to ozone-induced lung inflammation. Wild-type (WT), Notch3 (Notch3-/-), and Notch4 (Notch4-/-) knockout mice were exposed to ozone (0.3 ppm) or filtered air for 6-72 hr. Relative to air-exposed controls, ozone increased bronchoalveolar lavage fluid (BALF) protein, a marker of lung permeability, in all genotypes, but significantly greater concentrations were found in Notch4-/- compared with WT and Notch3-/- mice. Significantly greater mean numbers of BALF neutrophils were found in Notch3-/- and Notch4-/- mice compared with WT mice after ozone exposure. Expression of whole lung Tnf was significantly increased after ozone in Notch3-/- and Notch4-/- mice, and was significantly greater in Notch3-/- compared with WT mice. Statistical analyses of the transcriptome identified differentially expressed gene networks between WT and knockout mice basally and after ozone, and included Trim30, a member of the inflammasome pathway, and Traf6, an inflammatory signaling member. These novel findings are consistent with Notch3 and Notch4 as susceptibility genes for ozone-induced lung injury, and suggest that Notch receptors protect against innate immune inflammation. JF - Environmental health perspectives AU - Verhein, Kirsten C AU - McCaw, Zachary AU - Gladwell, Wesley AU - Trivedi, Shweta AU - Bushel, Pierre R AU - Kleeberger, Steven R AD - Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH), Department of Health and Human Resources (DHHS), Research Triangle Park, North Carolina, USA. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 799 EP - 805 VL - 123 IS - 8 KW - Air Pollutants KW - 0 KW - Notch3 protein, mouse KW - Proto-Oncogene Proteins KW - Receptor, Notch3 KW - Receptors, Notch KW - Notch4 protein, mouse KW - 146991-60-8 KW - Ozone KW - 66H7ZZK23N KW - Index Medicus KW - Gene Expression -- drug effects KW - Animals KW - Bronchoalveolar Lavage Fluid KW - Mice KW - Disease Susceptibility -- immunology KW - Male KW - Mice, Knockout KW - Pneumonia -- chemically induced KW - Receptors, Notch -- genetics KW - Proto-Oncogene Proteins -- metabolism KW - Gene Expression Regulation -- drug effects KW - Proto-Oncogene Proteins -- genetics KW - Air Pollutants -- toxicity KW - Receptors, Notch -- metabolism KW - Ozone -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701311163?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Novel+Roles+for+Notch3+and+Notch4+Receptors+in+Gene+Expression+and+Susceptibility+to+Ozone-Induced+Lung+Inflammation+in+Mice.&rft.au=Verhein%2C+Kirsten+C%3BMcCaw%2C+Zachary%3BGladwell%2C+Wesley%3BTrivedi%2C+Shweta%3BBushel%2C+Pierre+R%3BKleeberger%2C+Steven+R&rft.aulast=Verhein&rft.aufirst=Kirsten&rft.date=2015-08-01&rft.volume=123&rft.issue=8&rft.spage=799&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1408852 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-17 N1 - Date created - 2015-08-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Pharmacogenetics. 1991 Nov;1(2):110-3 [1844868] Cell. 2004 May 14;117(4):515-26 [15137944] Nat Genet. 1997 Dec;17(4):475-8 [9398854] JAMA. 2004 Nov 17;292(19):2372-8 [15547165] Immunol Allergy Clin North Am. 2005 Feb;25(1):15-30 [15579362] Am J Physiol Lung Cell Mol Physiol. 2005 Oct;289(4):L627-35 [15923207] Nat Rev Immunol. 2007 Jan;7(1):64-75 [17170755] Am J Respir Crit Care Med. 2007 Apr 15;175(8):829-39 [17255564] J Immunol. 2007 Oct 1;179(7):4367-75 [17878331] Eur Respir J. 2007 Oct;30(4):677-83 [17652311] Am J Respir Cell Mol Biol. 2007 Nov;37(5):571-7 [17600316] BMC Bioinformatics. 2007;8:427 [17980031] Thorax. 2008 Jun;63(6):555-63 [18511640] Occup Environ Med. 2008 Nov;65(11):736-42 [18524839] Toxicol Sci. 2009 Feb;107(2):535-43 [19066396] Blood. 2009 Mar 26;113(13):3092-101 [19171875] Am J Respir Crit Care Med. 2009 May 15;179(10):875-82 [19234107] Allergy. 2009 Sep;64(9):1342-8 [19236316] Biochem Biophys Res Commun. 2010 May 28;396(2):407-12 [20417186] Eur Respir J. 2010 Aug;36(2):428-37 [20032013] Ann N Y Acad Sci. 2010 Aug;1203:113-9 [20716292] Cancer Cell. 2010 Sep 14;18(3):268-81 [20832754] Environ Health Perspect. 2010 Dec;118(12):1721-7 [20826374] J Immunol. 2010 Dec 15;185(12):7699-705 [21048113] Inhal Toxicol. 2010 Dec;22 Suppl 2:84-94 [20883109] PLoS One. 2011;6(4):e18525 [21494547] Br J Clin Pharmacol. 2011 Aug;72(2):282-93 [21426372] Environ Health Perspect. 2011 Aug;119(8):1091-7 [21543283] Int Arch Allergy Immunol. 2012;157(1):65-72 [21912175] J Biol Chem. 2012 Feb 24;287(9):6208-17 [22205705] J Immunol. 2012 May 1;188(9):4558-67 [22474022] Environ Health Perspect. 2012 Dec;120(12):1692-8 [23010656] Am J Respir Cell Mol Biol. 2013 Jan;48(1):27-34 [23002100] J Immunol. 2014 Sep 15;193(6):2873-80 [25092893] Immunol Res. 2011 Apr;49(1-3):173-91 [21132467] Mech Dev. 2000 Nov;98(1-2):95-8 [11044610] Cell. 2000 Oct 13;103(2):351-61 [11057907] Am J Physiol Lung Cell Mol Physiol. 2001 Mar;280(3):L537-46 [11159038] Am J Respir Crit Care Med. 2001 Aug 15;164(4):602-7 [11520723] Oncogene. 2003 Oct 30;22(49):7796-803 [14586405] Nat Genet. 1997 Dec;17(4):471-4 [9398853] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1289/ehp.1408852 ER - TY - CONF T1 - Current Research and Opportunities to Address Environmental Asbestos Exposures. AN - 1701300214; 26230287 AB - Asbestos-related diseases continue to result in approximately 120,000 deaths every year in the United States and worldwide. Although extensive research has been conducted on health effects of occupational exposures to asbestos, many issues related to environmental asbestos exposures remain unresolved. For example, environmental asbestos exposures associated with a former mine in Libby, Montana, have resulted in high rates of nonoccupational asbestos-related disease. Additionally, other areas with naturally occurring asbestos deposits near communities in the United States and overseas are undergoing investigations to assess exposures and potential health risks. Some of the latest public health, epidemiological, and basic research findings were presented at a workshop on asbestos at the 2014 annual meeting of the Society of Toxicology in Phoenix, Arizona. The following focus areas were discussed: a) mechanisms resulting in fibrosis and/or tumor development; b) relative toxicity of different forms of asbestos and other hazardous elongated mineral particles (EMPs); c) proper dose metrics (e.g., mass, fiber number, or surface area of fibers) when interpreting asbestos toxicity; d) asbestos exposure to susceptible populations; and e) using toxicological findings for risk assessment and remediation efforts. The workshop also featured asbestos research supported by the National Institute of Environmental Health Sciences, the Agency for Toxic Substances and Disease Registry, and the U.S. Environmental Protection Agency. Better protection of individuals from asbestos-related health effects will require stimulation of new multidisciplinary research to further our understanding of what constitutes hazardous exposures and risk factors associated with toxicity of asbestos and other hazardous EMPs (e.g., nanomaterials). JF - Environmental health perspectives AU - Carlin, Danielle J AU - Larson, Theodore C AU - Pfau, Jean C AU - Gavett, Stephen H AU - Shukla, Arti AU - Miller, Aubrey AU - Hines, Ronald Y1 - 2015/08// PY - 2015 DA - August 2015 SP - A194 EP - A197 VL - 123 IS - 8 KW - Environmental Pollutants KW - 0 KW - Asbestos KW - 1332-21-4 KW - Index Medicus KW - Humans KW - Environmental Restoration and Remediation KW - Risk Assessment KW - Environmental Pollutants -- toxicity KW - Environmental Exposure KW - Asbestos -- toxicity KW - Asbestosis -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701300214?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Environmental+health+perspectives&rft.atitle=Current+Research+and+Opportunities+to+Address+Environmental+Asbestos+Exposures.&rft.au=Carlin%2C+Danielle+J%3BLarson%2C+Theodore+C%3BPfau%2C+Jean+C%3BGavett%2C+Stephen+H%3BShukla%2C+Arti%3BMiller%2C+Aubrey%3BHines%2C+Ronald&rft.aulast=Carlin&rft.aufirst=Danielle&rft.date=2015-08-01&rft.volume=123&rft.issue=8&rft.spage=A194&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1409662 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-17 N1 - Date created - 2015-08-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Environ Health. 2014;13:59 [25043725] J Toxicol Environ Health A. 2015;78(3):151-65 [25506632] J Occup Environ Med. 2015 Jan;57(1):6-13 [25563535] Occup Environ Med. 2015 Mar;72(3):216-8 [25231672] Am J Ind Med. 2015 May;58(5):494-508 [25675894] J Thorac Oncol. 2015 May;10(5):731-7 [25668121] Curr Probl Diagn Radiol. 2015 Jul-Aug;44(4):371-82 [25444537] Arthritis Rheum. 2002 Jun;46(6):1602-13 [12115192] Mol Cell. 2002 Aug;10(2):417-26 [12191486] Environ Health Perspect. 2003 Nov;111(14):1753-9 [14594627] Am J Ind Med. 2014 Nov;57(11):1197-206 [24898907] Am J Respir Crit Care Med. 2004 Sep 15;170(6):691-715 [15355871] Am Rev Respir Dis. 1984 Jun;129(6):952-8 [6329050] Occup Environ Med. 1997 Sep;54(9):646-52 [9423577] Environ Health Perspect. 2005 Jan;113(1):25-30 [15626643] Environ Health Perspect. 2006 Aug;114(8):1243-7 [16882533] Am J Respir Crit Care Med. 2008 Mar 15;177(6):630-7 [18063841] Science. 2008 May 2;320(5876):674-7 [18403674] Am J Ind Med. 2008 Nov;51(11):877-80 [18651576] Radiology. 2010 Jun;255(3):924-33 [20501730] Environ Health Perspect. 2010 Jul;118(7):1033-28 [20332072] Environ Health Perspect. 2010 Jul;118(7):897-901 [20601329] Environ Health Perspect. 2010 Jul;118(7):A298-303 [20601321] Int J Occup Environ Health. 2010 Jul-Sep;16(3):279-90 [20662420] Toxicol Sci. 2010 Dec;118(2):420-34 [20855422] Inhal Toxicol. 2011 Feb;23(3):129-41 [21391781] J Immunotoxicol. 2011 Jun;8(2):159-69 [21457077] Inhal Toxicol. 2011 May;23(6):313-23 [21605006] J Toxicol Environ Health A. 2011;74(17):1111-32 [21797767] Proc Natl Acad Sci U S A. 2011 Aug 16;108(33):13618-23 [21788493] Environ Health Perspect. 2011 Dec;119(12):1806-10 [21807578] Toxicol Lett. 2012 Jan 25;208(2):168-73 [22085844] Environ Health Perspect. 2012 Jan;120(1):85-91 [21979745] J Toxicol Environ Health A. 2012;75(3):183-200 [22251266] Toxicol Sci. 2012 Dec;130(2):405-15 [22903825] Am J Ind Med. 2013 Feb;56(2):133-45 [22886909] Int J Cancer. 2013 Mar 15;132(6):1423-8 [22858896] Environ Geochem Health. 2013 Aug;35(4):419-30 [23315055] Part Fibre Toxicol. 2013;10:39 [23937860] Inhal Toxicol. 2013 Dec;25(14):774-84 [24304304] Part Fibre Toxicol. 2014;11:2 [24401117] Toxicol Appl Pharmacol. 2014 Mar 15;275(3):257-64 [24518925] Part Fibre Toxicol. 2014;11:24 [24885895] J Immunotoxicol. 2014 Jul-Sep;11(3):283-90 [24164284] J Expo Sci Environ Epidemiol. 2015 Jan;25(1):4-11 [23695492] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1289/ehp.1409662 ER - TY - JOUR T1 - Circulating immune/inflammation markers in Chinese workers occupationally exposed to formaldehyde. AN - 1700103823; 25908645 AB - Formaldehyde has been classified as a human myeloid leukemogen. However, the mechanistic basis for this association is still debated. We aimed to evaluate whether circulating immune/inflammation markers were altered in workers occupationally exposed to formaldehyde. Using a multiplexed bead-based assay, we measured serum levels of 38 immune/inflammation markers in a cross-sectional study of 43 formaldehyde-exposed and 51 unexposed factory workers in Guangdong, China. Linear regression models adjusting for potential confounders were used to compare marker levels in exposed and unexposed workers. We found significantly lower circulating levels of two markers among exposed factory workers compared with unexposed controls that remained significant after adjusting for potential confounders and multiple comparisons using a false discovery rate of 10%, including chemokine (C-X-C motif) ligand 11 (36.2 pg/ml in exposed versus 48.4 pg/ml in controls, P = 0.0008) and thymus and activation regulated chemokine (52.7 pg/ml in exposed versus 75.0 pg/ml in controls, P = 0.0028), suggesting immunosuppression among formaldehyde-exposed workers. Our findings are consistent with recently emerging understanding that immunosuppression might be associated with myeloid diseases. These findings, if replicated in a larger study, may provide insights into the mechanisms by which formaldehyde promotes leukemogenesis. Published by Oxford University Press 2015. JF - Carcinogenesis AU - Seow, Wei Jie AU - Zhang, Luoping AU - Vermeulen, Roel AU - Tang, Xiaojiang AU - Hu, Wei AU - Bassig, Bryan A AU - Ji, Zhiying AU - Shiels, Meredith S AU - Kemp, Troy J AU - Shen, Min AU - Qiu, Chuangyi AU - Reiss, Boris AU - Beane Freeman, Laura E AU - Blair, Aaron AU - Kim, Christopher AU - Guo, Weihong AU - Wen, Cuiju AU - Li, Laiyu AU - Pinto, Ligia A AU - Huang, Hanlin AU - Smith, Martyn T AU - Hildesheim, Allan AU - Rothman, Nathaniel AU - Lan, Qing AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA, Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA, USA, Division of Environmental Epidemiology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands, Guangdong Poison Control Center, Guangzhou, China, and HPV Immunology Laboratory, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA weijie.seow2@nih.gov. ; Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA, USA. ; Division of Environmental Epidemiology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands. ; Guangdong Poison Control Center, Guangzhou, China, and. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD 20850, USA, Division of Environmental Health Sciences, School of Public Health, University of California, Berkeley, CA, USA, Division of Environmental Epidemiology, Institute for Risk Assessment Sciences, Utrecht University, Utrecht, the Netherlands, Guangdong Poison Control Center, Guangzhou, China, and HPV Immunology Laboratory, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA. ; HPV Immunology Laboratory, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 852 EP - 857 VL - 36 IS - 8 KW - Biomarkers KW - 0 KW - CCL17 protein, human KW - CXCL11 protein, human KW - Chemokine CCL17 KW - Chemokine CXCL11 KW - Chemokines KW - Cytokines KW - Immunosuppressive Agents KW - TNF-Related Apoptosis-Inducing Ligand KW - TNFSF10 protein, human KW - Formaldehyde KW - 1HG84L3525 KW - Index Medicus KW - Cytokines -- blood KW - Chemokine CCL17 -- blood KW - Humans KW - Chemokine CXCL11 -- blood KW - TNF-Related Apoptosis-Inducing Ligand -- blood KW - Cross-Sectional Studies KW - Adult KW - Immunosuppressive Agents -- toxicity KW - Case-Control Studies KW - China KW - Female KW - Male KW - Chemokines -- blood KW - Inflammation -- chemically induced KW - Inflammation -- blood KW - Occupational Exposure -- adverse effects KW - Formaldehyde -- toxicity KW - Biomarkers -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1700103823?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Circulating+immune%2Finflammation+markers+in+Chinese+workers+occupationally+exposed+to+formaldehyde.&rft.au=Seow%2C+Wei+Jie%3BZhang%2C+Luoping%3BVermeulen%2C+Roel%3BTang%2C+Xiaojiang%3BHu%2C+Wei%3BBassig%2C+Bryan+A%3BJi%2C+Zhiying%3BShiels%2C+Meredith+S%3BKemp%2C+Troy+J%3BShen%2C+Min%3BQiu%2C+Chuangyi%3BReiss%2C+Boris%3BBeane+Freeman%2C+Laura+E%3BBlair%2C+Aaron%3BKim%2C+Christopher%3BGuo%2C+Weihong%3BWen%2C+Cuiju%3BLi%2C+Laiyu%3BPinto%2C+Ligia+A%3BHuang%2C+Hanlin%3BSmith%2C+Martyn+T%3BHildesheim%2C+Allan%3BRothman%2C+Nathaniel%3BLan%2C+Qing&rft.aulast=Seow&rft.aufirst=Wei&rft.date=2015-08-01&rft.volume=36&rft.issue=8&rft.spage=852&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgv055 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-19 N1 - Date created - 2015-07-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Toxicol Environ Health A. 2013;76(4-5):217-29 [23514064] Mol Cancer Ther. 2013 Sep;12(9):1728-37 [23699656] PLoS One. 2013;8(9):e74974 [24040369] Leukemia. 2013 Oct;27(10):2084-6 [23828261] Eur J Cancer. 2013 Jun;49(9):2152-60 [23571148] Toxicol Appl Pharmacol. 2014 Aug 1;278(3):266-74 [24844129] PLoS One. 2014;9(8):e104069 [25157974] Leukemia. 2014 Dec;28(12):2317-23 [24727673] Environ Health Perspect. 2013 Mar;121(3):339-44 [23322811] Blood. 2011 Nov 10;118(19):5201-10 [21911837] Leukemia. 2012 Mar;26(3):422-3 [21869837] Leukemia. 2012 Sep;26(9):2019-26 [22446501] Sci Total Environ. 2013 Jan 1;442:20-5 [23178760] Arch Toxicol. 2013 Jan;87(1):145-53 [23100157] Am J Ind Med. 2013 Feb;56(2):252-7 [22767408] Blood. 2001 Apr 1;97(7):2067-74 [11264173] Blood. 2001 Aug 1;98(3):533-40 [11468146] Hum Mol Genet. 2002 Apr 15;11(8):937-43 [11971875] QJM. 2003 Nov;96(11):793-807 [14566035] Toxicol Pathol. 1997 May-Jun;25(3):291-307 [9210261] J Exp Med. 1998 Jun 15;187(12):2009-21 [9625760] J Immunother. 2005 Jul-Aug;28(4):343-51 [16000952] Cancer Immunol Immunother. 2006 Jul;55(7):830-40 [16267679] J Proteome Res. 2006 Jun;5(6):1354-66 [16739987] J Leukoc Biol. 2006 Jun;79(6):1140-9 [16574768] Ann N Y Acad Sci. 2006 Sep;1076:635-48 [17119241] Arterioscler Thromb Vasc Biol. 2007 Feb;27(2):352-8 [17138933] IARC Monogr Eval Carcinog Risks Hum. 2006;88:1-478 [17366697] Mutat Res. 2009 Mar-Jun;681(2-3):150-68 [18674636] Adv Exp Med Biol. 2009;653:98-116 [19799114] Lancet Oncol. 2009 Dec;10(12):1143-4 [19998521] Cancer Epidemiol Biomarkers Prev. 2010 Jan;19(1):80-8 [20056626] Int J Cancer. 2010 May 15;126(10):2503-8 [19810095] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgv055 ER - TY - JOUR T1 - Hepatic stellate cell and monocyte interaction contributes to poor prognosis in hepatocellular carcinoma. AN - 1698956645; 25833323 AB - Hepatocellular carcinoma (HCC) patients suffer from a poor survival rate and a high incidence of postoperative recurrence. The hepatic microenvironment plays a significant role in the initiation, progression, and recurrence of HCC; however, the causal mechanisms of these phenomena are unclear. Given the predominant underlying fibrotic and cirrhotic conditions of the liver prone to HCC and its recurrence, alterations of components of the inflammatory milieu have been suggested as factors that promote HCC development. In particular, activated hepatic stellate cells (A-HSCs), which play a key role in liver fibrosis and cirrhosis, have been suggested as contributors to the HCC-prone microenvironment. Here, we have identified and validated an A-HSC-specific gene expression signature among nontumor tissues of 319 HCC patients that is significantly and independently associated with HCC recurrence and survival. Peritumoral, rather than tumor tissue-related, A-HSC-specific gene expression is associated with recurrence and poor survival. Analyses of A-HSC-specific gene signatures and further immunohistochemical validation in an additional 143 HCC patients have revealed that A-HSCs preferentially affect monocyte populations, shifting their gene expression from an inflammatory to an immunosuppressive signature. In addition, the interaction between A-HSCs and monocytes induces protumorigenic and progressive features of HCC cells by enhancing cell migration and tumor sphere formation. A-HSCs play a significant role in promoting HCC progression through interaction with and alteration of monocyte activities within the liver microenvironment; thus, disrupting the interactions and signaling events between the inflammatory milieu and components of the microenvironment may be useful therapeutic strategies for preventing HCC tumor relapse. © 2015 by the American Association for the Study of Liver Diseases. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA. JF - Hepatology (Baltimore, Md.) AU - Ji, Juling AU - Eggert, Tobias AU - Budhu, Anuradha AU - Forgues, Marshonna AU - Takai, Atsushi AU - Dang, Hien AU - Ye, Qinghai AU - Lee, Ju-Seog AU - Kim, Ji Hoon AU - Greten, Tim F AU - Wang, Xin Wei AD - Liver Carcinogenesis Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD. ; Gastrointestinal Malignancy Section, Center for Cancer Research, National Cancer Institute, Bethesda, MD. ; Liver Cancer Institute, Fudan University, Shanghai, China. ; Department of Systems Biology, University of Texas, M.D. Anderson Cancer Center, Houston, TX. ; Division of Gastroenterology and Hepatology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 481 EP - 495 VL - 62 IS - 2 KW - Biomarkers, Tumor KW - 0 KW - Index Medicus KW - Cell Movement KW - Analysis of Variance KW - Reproducibility of Results KW - Humans KW - Tumor Microenvironment KW - Prognosis KW - Aged KW - Predictive Value of Tests KW - Multivariate Analysis KW - Tumor Cells, Cultured KW - Middle Aged KW - Female KW - Male KW - Neoplasm Recurrence, Local -- genetics KW - Survival Analysis KW - Proportional Hazards Models KW - Neoplasm Recurrence, Local -- pathology KW - Hepatic Stellate Cells -- metabolism KW - Biomarkers, Tumor -- metabolism KW - Liver Neoplasms -- pathology KW - Liver Neoplasms -- metabolism KW - Hepatic Stellate Cells -- pathology KW - Carcinoma, Hepatocellular -- metabolism KW - Monocytes -- metabolism KW - Liver Neoplasms -- mortality KW - Monocytes -- pathology KW - Carcinoma, Hepatocellular -- pathology KW - Cell Communication KW - Carcinoma, Hepatocellular -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698956645?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hepatology+%28Baltimore%2C+Md.%29&rft.atitle=Hepatic+stellate+cell+and+monocyte+interaction+contributes+to+poor+prognosis+in+hepatocellular+carcinoma.&rft.au=Ji%2C+Juling%3BEggert%2C+Tobias%3BBudhu%2C+Anuradha%3BForgues%2C+Marshonna%3BTakai%2C+Atsushi%3BDang%2C+Hien%3BYe%2C+Qinghai%3BLee%2C+Ju-Seog%3BKim%2C+Ji+Hoon%3BGreten%2C+Tim+F%3BWang%2C+Xin+Wei&rft.aulast=Ji&rft.aufirst=Juling&rft.date=2015-08-01&rft.volume=62&rft.issue=2&rft.spage=481&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.27822 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-13 N1 - Date created - 2015-07-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Hepatology. 2011 Aug;54(2):707-13 [21520207] CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855] Cancer Res. 2012 May 15;72(10):2533-42 [22419664] Hepatology. 2012 Jul;56(1):332-49 [22331624] Gastroenterology. 2012 Oct;143(4):1073-83.e22 [22750464] Front Biosci (Schol Ed). 2013;5:217-30 [23277047] J Immunol. 2013 Jan 15;190(2):794-804 [23248262] Hepatology. 2013 Feb;57(2):829-39 [23081697] J Clin Invest. 2013 May;123(5):1902-10 [23635788] J Exp Clin Cancer Res. 2013;32:22 [23601182] J Hepatol. 2013 Sep;59(3):528-35 [23665041] Cancer Immunol Immunother. 2013 Sep;62(9):1439-51 [23760662] Nat Commun. 2013;4:2823 [24264436] Hepatology. 2014 Mar;59(3):1060-72 [24481979] J Immunol. 2014 Apr 15;192(8):3858-67 [24639350] Gastroenterology. 2014 Sep;147(3):577-594.e1 [25066692] Cell. 2013 Apr 11;153(2):449-60 [23562644] Ann Surg. 2000 Jul;232(1):10-24 [10862190] Cancer. 2001 Apr 15;91(8):1479-86 [11301395] Nat Rev Cancer. 2003 Apr;3(4):276-85 [12671666] Nat Med. 2003 Apr;9(4):416-23 [12640447] Gastroenterology. 2004 Apr;126(4):1005-14 [15057740] Nat Rev Cancer. 2004 Jul;4(7):540-50 [15229479] Hepatology. 2004 Sep;40(3):667-76 [15349906] J Clin Invest. 1993 Oct;92(4):1674-80 [8408620] Gut. 2005 Jan;54(1):142-51 [15591520] Genes Immun. 2005 Jun;6(4):319-31 [15789058] Cancer Res. 2005 Jun 1;65(11):4728-38 [15930291] Cancer Cell. 2006 Aug;10(2):99-111 [16904609] J Leukoc Biol. 2006 Dec;80(6):1197-213 [16946019] Gastroenterology. 2007 May;132(5):1937-46 [17484886] Cancer Res. 2008 Mar 1;68(5):1451-61 [18316609] Gastroenterology. 2008 Jul;135(1):234-43 [18485901] Cell. 2008 Aug 22;134(4):657-67 [18724938] N Engl J Med. 2008 Nov 6;359(19):1995-2004 [18923165] Gastroenterology. 2009 Mar;136(3):1012-24 [19150350] Am J Clin Pathol. 2009 Apr;131(4):498-510 [19289585] Cancer Sci. 2009 Apr;100(4):646-53 [19175606] Ann Surg Oncol. 2009 Sep;16(9):2555-64 [19548033] Hepatology. 2009 Sep;50(3):799-807 [19551844] Cancer Res. 2009 Sep 15;69(18):7385-92 [19723656] Cell. 2010 Mar 19;140(6):883-99 [20303878] Cancer Res. 2010 Dec 15;70(24):10202-12 [21159642] Hepatology. 2012 May;55(5):1443-52 [22105560] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/hep.27822 ER - TY - JOUR T1 - Drug-induced allergic hepatitis develops in mice when myeloid-derived suppressor cells are depleted prior to halothane treatment. AN - 1698956351; 25712247 AB - Clinical evidence suggests that many cases of serious idiosyncratic drug-induced liver injury are mediated by the adaptive immune system in response to hepatic drug-protein adducts, also referred to as "drug-induced allergic hepatitis"; but detailed mechanistic proof has remained elusive due to the lack of animal models. We have hypothesized that drug-induced allergic hepatitis is as rare in animals as it is in humans due at least in part to the tolerogenic nature of the liver. We provide evidence that immune tolerance can be overcome in a murine model of halothane-induced liver injury initiated by trifluoroacetylated protein adducts of halothane formed in the liver. Twenty-four hours after female Balb/cJ mice were initially treated with halothane, perivenous necrosis and an infiltration of CD11b(+) Gr-1(high) cells were observed in the liver. Further study revealed a subpopulation of myeloid-derived suppressor cells within the CD11b(+) Gr-1(high) cell fraction that inhibited the proliferation of both CD4(+) and CD8(+) T cells. When CD11b(+) Gr-1(high) cells were depleted from the liver with Gr-1 antibody treatment, enhanced liver injury was observed at 9 days after halothane rechallenge. Toxicity was associated with increased serum levels of interleukin-4 and immunoglobulins G1 and E directed against hepatic trifluoroacetylated protein adducts, as well as increased hepatic infiltration of eosinophils and CD4(+) T cells, all features of an allergic reaction. When hepatic CD4(+) T cells were depleted 5 days after halothane rechallenge, trifluoroacetylated protein adduct-specific serum immunoglobulin and hepatotoxicity were reduced. Our data provide a rational approach for developing animal models of drug-induced allergic hepatitis mediated by the adaptive immune system and suggest that impaired liver tolerance may predispose patients to this disease. © 2015 by the American Association for the Study of Liver Diseases. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA. JF - Hepatology (Baltimore, Md.) AU - Chakraborty, Mala AU - Fullerton, Aaron M AU - Semple, Kenrick AU - Chea, Lynette S AU - Proctor, William R AU - Bourdi, Mohammed AU - Kleiner, David E AU - Zeng, Xiangbin AU - Ryan, Pauline M AU - Dagur, Pradeep K AU - Berkson, Julia D AU - Reilly, Timothy P AU - Pohl, Lance R AD - Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD. ; Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD. ; Hematology Branch, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD. ; Exploratory Clinical & Translational Research, Bristol-Myers Squibb Company, Princeton, NJ. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 546 EP - 557 VL - 62 IS - 2 KW - Antigens, CD11b KW - 0 KW - Nitric Oxide KW - 31C4KY9ESH KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Halothane KW - UQT9G45D1P KW - Index Medicus KW - Animals KW - Analysis of Variance KW - Random Allocation KW - Alanine Transaminase -- metabolism KW - Nitric Oxide -- metabolism KW - Disease Models, Animal KW - Mice KW - Flow Cytometry KW - Mice, Inbred BALB C KW - Cell Proliferation KW - Immunohistochemistry KW - Female KW - Hepatitis -- immunology KW - Myeloid Cells -- metabolism KW - Chemical and Drug Induced Liver Injury -- pathology KW - CD8-Positive T-Lymphocytes -- metabolism KW - CD8-Positive T-Lymphocytes -- immunology KW - Antigens, CD11b -- metabolism KW - Halothane -- toxicity KW - Antigens, CD11b -- immunology KW - Myeloid Cells -- drug effects KW - Hepatitis -- pathology KW - Chemical and Drug Induced Liver Injury -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698956351?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hepatology+%28Baltimore%2C+Md.%29&rft.atitle=Drug-induced+allergic+hepatitis+develops+in+mice+when+myeloid-derived+suppressor+cells+are+depleted+prior+to+halothane+treatment.&rft.au=Chakraborty%2C+Mala%3BFullerton%2C+Aaron+M%3BSemple%2C+Kenrick%3BChea%2C+Lynette+S%3BProctor%2C+William+R%3BBourdi%2C+Mohammed%3BKleiner%2C+David+E%3BZeng%2C+Xiangbin%3BRyan%2C+Pauline+M%3BDagur%2C+Pradeep+K%3BBerkson%2C+Julia+D%3BReilly%2C+Timothy+P%3BPohl%2C+Lance+R&rft.aulast=Chakraborty&rft.aufirst=Mala&rft.date=2015-08-01&rft.volume=62&rft.issue=2&rft.spage=546&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.27764 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-13 N1 - Date created - 2015-07-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Comment In: Hepatology. 2015 Aug;62(2):346-8 [25833746] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/hep.27764 ER - TY - JOUR T1 - Perceived mother and father acceptance-rejection predict four unique aspects of child adjustment across nine countries AN - 1698868778 AB - Background It is generally believed that parental rejection of children leads to child maladaptation. However, the specific effects of perceived parental acceptance-rejection on diverse domains of child adjustment and development have been incompletely documented, and whether these effects hold across diverse populations and for mothers and fathers are still open questions. Methods This study assessed childrenʼs perceptions of mother and father acceptance-rejection in 1,247 families from China, Colombia, Italy, Jordan, Kenya, the Philippines, Sweden, Thailand, and the United States as antecedent predictors of later internalizing and externalizing behavior problems, school performance, prosocial behavior, and social competence. Results Higher perceived parental rejection predicted increases in internalizing and externalizing behavior problems and decreases in school performance and prosocial behavior across 3 years controlling for within-wave relations, stability across waves, and parental age, education, and social desirability bias. Patterns of relations were similar across mothers and fathers and, with a few exceptions, all nine countries. Conclusions Childrenʼs perceptions of maternal and paternal acceptance-rejection have small but nearly universal effects on multiple aspects of their adjustment and development regardless of the familyʼs country of origin. JF - Journal of Child Psychology and Psychiatry AU - Putnick, Diane L AU - Bornstein, Marc H AU - Lansford, Jennifer E AU - Malone, Patrick S AU - Pastorelli, Concetta AU - Skinner, Ann T AU - Sorbring, Emma AU - Tapanya, Sombat AU - Uribe Tirado, Liliana Maria AU - Zelli, Arnaldo AU - Alampay, Liane Peña AU - Al-Hassan, Suha M AU - Bacchini, Dario AU - Bombi, Anna Silvia AU - Chang, Lei AU - Deater-Deckard, Kirby AU - Di Giunta, Laura AU - Dodge, Kenneth A AU - Oburu, Paul AD - Child and Family Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA. ; Center for Child and Family Policy, Duke University, Durham, NC, USA. ; Department of Psychology, La Sapienza University of Rome, Rome, Italy. ; Department of Psychology, University West, Trollhättan, Sweden. ; Chiang Mai University, Chiang Mai, Thailand. ; Department of Psychology, La Sapienza University of Rome, Rome, Italy., Psychology Department, Universidad de San Buenaventura, Medellin, Colombia. ; Department of Sports Psychology, Foro Italico University of Rome, Rome, Italy. ; Ateneo de Manila University, Quezon City, Metro Manila, Philippines. ; Hashemite University, Zarqa, Jordan. ; Child and Family Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA., Second University of Naples, Naples, Italy. ; Child and Family Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA., Chinese University of Hong Kong, Hong Kong, China. ; Child and Family Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA., Virginia Polytechnic Institute and State University, Blacksburg, Virginia, USA. ; Child and Family Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA., Maseno University, Maseno, Kenya. ; Child and Family Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA. Y1 - 2015/08// PY - 2015 DA - Aug 2015 SP - 923 EP - 932 CY - Malden PB - Wiley Subscription Services, Inc. VL - 56 IS - 8 KW - Psychology KW - Academic achievement KW - Acceptance KW - Adjustment KW - Age differences KW - Behavioural problems KW - Bias KW - Children KW - Competence KW - Country of origin KW - Desirability KW - Philippines KW - Kenya KW - Jordan KW - Thailand KW - United States--US KW - Colombia KW - Italy KW - China KW - Sweden UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698868778?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Child+Psychology+and+Psychiatry&rft.atitle=Perceived+mother+and+father+acceptance-rejection+predict+four+unique+aspects+of+child+adjustment+across+nine+countries&rft.au=Putnick%2C+Diane+L%3BBornstein%2C+Marc+H%3BLansford%2C+Jennifer+E%3BMalone%2C+Patrick+S%3BPastorelli%2C+Concetta%3BSkinner%2C+Ann+T%3BSorbring%2C+Emma%3BTapanya%2C+Sombat%3BUribe+Tirado%2C+Liliana+Maria%3BZelli%2C+Arnaldo%3BAlampay%2C+Liane+Pe%C3%B1a%3BAl-Hassan%2C+Suha+M%3BBacchini%2C+Dario%3BBombi%2C+Anna+Silvia%3BChang%2C+Lei%3BDeater-Deckard%2C+Kirby%3BDi+Giunta%2C+Laura%3BDodge%2C+Kenneth+A%3BOburu%2C+Paul&rft.aulast=Putnick&rft.aufirst=Diane&rft.date=2015-08-01&rft.volume=56&rft.issue=8&rft.spage=923&rft.isbn=&rft.btitle=&rft.title=Journal+of+Child+Psychology+and+Psychiatry&rft.issn=&rft_id=info:doi/10.1111%2Fjcpp.12366 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-07-20 N1 - Last updated - 2015-12-14 N1 - SubjectsTermNotLitGenreText - China; Colombia; Italy; Jordan; Kenya; Philippines; Sweden; Thailand; United States--US DO - http://dx.doi.org/10.1111/jcpp.12366 ER - TY - JOUR T1 - Context-Dependent Cleavage of the Capsid Protein by the West Nile Virus Protease Modulates the Efficiency of Virus Assembly. AN - 1698391918; 26063422 AB - The molecular mechanisms that define the specificity of flavivirus RNA encapsulation are poorly understood. Virions composed of the structural proteins of one flavivirus and the genomic RNA of a heterologous strain can be assembled and have been developed as live attenuated vaccine candidates for several flaviviruses. In this study, we discovered that not all combinations of flavivirus components are possible. While a West Nile virus (WNV) subgenomic RNA could readily be packaged by structural proteins of the DENV2 strain 16681, production of infectious virions with DENV2 strain New Guinea C (NGC) structural proteins was not possible, despite the very high amino acid identity between these viruses. Mutagenesis studies identified a single residue (position 101) of the DENV capsid (C) protein as the determinant for heterologous virus production. C101 is located at the P1' position of the NS2B/3 protease cleavage site at the carboxy terminus of the C protein. WNV NS2B/3 cleavage of the DENV structural polyprotein was possible when a threonine (Thr101 in strain 16681) but not a serine (Ser101 in strain NGC) occupied the P1' position, a finding not predicted by in vitro protease specificity studies. Critically, both serine and threonine were tolerated at the P1' position of WNV capsid. More extensive mutagenesis revealed the importance of flanking residues within the polyprotein in defining the cleavage specificity of the WNV protease. A more detailed understanding of the context dependence of viral protease specificity may aid the development of new protease inhibitors and provide insight into associated patterns of drug resistance. West Nile virus (WNV) and dengue virus (DENV) are mosquito-borne flaviviruses that cause considerable morbidity and mortality in humans. No specific antiflavivirus therapeutics are available for treatment of infection. Proteolytic processing of the flavivirus polyprotein is an essential step in the replication cycle and is an attractive target for antiviral development. The design of protease inhibitors has been informed by insights into the molecular details of the interactions of proteases and their substrates. In this article, studies of the processing of WNV and DENV capsid proteins by the WNV protease identified an unexpected contribution of the sequence surrounding critical residues within the cleavage site on protease specificity. This demonstration of context-dependent protease cleavage has implications for the design of chimeric flaviviruses, new therapeutics, and the interpretation of flavivirus protease substrate specificity studies. Copyright © 2015, American Society for Microbiology. All Rights Reserved. JF - Journal of virology AU - VanBlargan, Laura A AU - Davis, Kaitlin A AU - Dowd, Kimberly A AU - Akey, David L AU - Smith, Janet L AU - Pierson, Theodore C AD - Viral Pathogenesis Section, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA Biological Sciences Graduate Program, University of Maryland, College Park, Maryland, USA. ; Viral Pathogenesis Section, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA Department of Biology, Johns Hopkins University, Baltimore, Maryland, USA. ; Viral Pathogenesis Section, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA. ; Life Sciences Institute, University of Michigan, Ann Arbor, Michigan, USA. ; Life Sciences Institute, University of Michigan, Ann Arbor, Michigan, USA Department of Biological Chemistry, University of Michigan, Ann Arbor, Michigan, USA. ; Viral Pathogenesis Section, Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA piersontc@mail.nih.gov. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 8632 EP - 8642 VL - 89 IS - 16 KW - Capsid Proteins KW - 0 KW - NS2B protein, flavivirus KW - Viral Nonstructural Proteins KW - Index Medicus KW - Static Electricity KW - Analysis of Variance KW - Plasmids -- genetics KW - Substrate Specificity KW - Species Specificity KW - Mutagenesis KW - Capsid Proteins -- metabolism KW - Virus Assembly -- physiology KW - West Nile virus -- enzymology KW - Viral Nonstructural Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698391918?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Context-Dependent+Cleavage+of+the+Capsid+Protein+by+the+West+Nile+Virus+Protease+Modulates+the+Efficiency+of+Virus+Assembly.&rft.au=VanBlargan%2C+Laura+A%3BDavis%2C+Kaitlin+A%3BDowd%2C+Kimberly+A%3BAkey%2C+David+L%3BSmith%2C+Janet+L%3BPierson%2C+Theodore+C&rft.aulast=VanBlargan&rft.aufirst=Laura&rft.date=2015-08-01&rft.volume=89&rft.issue=16&rft.spage=8632&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=1098-5514&rft_id=info:doi/10.1128%2FJVI.01253-15 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-22 N1 - Date created - 2015-07-22 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Virol. 1991 May;65(5):2467-75 [2016768] J Biol Chem. 1991 Aug 5;266(22):14539-47 [1860860] J Virol. 1991 Nov;65(11):6042-50 [1833562] Biochemistry. 1992 May 26;31(20):4793-800 [1591240] J Virol. 1992 Dec;66(12):7549-54 [1433530] J Virol. 1993 Apr;67(4):2327-35 [8445732] Proc Natl Acad Sci U S A. 1993 Jul 1;90(13):6218-22 [8392191] J Virol. 1994 Jun;68(6):3794-802 [8189517] J Biol Chem. 1996 Mar 1;271(9):4709-17 [8617736] J Biol Chem. 1997 Jul 4;272(27):16807-14 [9201986] J Biol Chem. 1997 Dec 5;272(49):30715-23 [9388208] J Virol. 1998 Mar;72(3):2141-9 [9499070] Virology. 2006 Mar 1;346(1):53-65 [16325883] J Virol. 1998 Jul;72(7):5967-77 [9621059] J Virol. 1999 Oct;73(10):8083-94 [10482557] J Biol Chem. 2004 Nov 19;279(47):48535-42 [15322074] J Virol. 2005 Jul;79(14):8698-706 [15994763] Virol J. 2005;2:53 [15985182] J Biol Chem. 2005 Aug 5;280(31):28766-74 [15932883] Biochem J. 2006 Jan 15;393(Pt 2):503-11 [16229682] J Virol. 2006 Feb;80(3):1290-301 [16415006] Nat Struct Mol Biol. 2006 Apr;13(4):372-3 [16532006] Biochem J. 2006 Jul 1;397(1):203-11 [16489931] J Biol Chem. 2006 Dec 1;281(48):37183-94 [17001080] J Biol Chem. 2006 Dec 15;281(50):38448-58 [17052977] Biochem J. 2007 Feb 1;401(3):743-52 [17067286] Int J Biochem Cell Biol. 2007;39(3):606-14 [17188926] J Virol. 2007 May;81(9):4501-9 [17301157] Protein Sci. 2007 May;16(5):795-806 [17400917] Nucleic Acids Res. 2007 Jul;35(Web Server issue):W522-5 [17488841] Cell Host Microbe. 2007 Apr 19;1(2):135-45 [18005691] Anal Biochem. 2008 May 1;376(1):151-3 [18312847] PLoS Pathog. 2008 May;4(5):e1000060 [18464894] Antimicrob Agents Chemother. 2008 Sep;52(9):3385-93 [18606844] J Med Chem. 2008 Sep 25;51(18):5714-21 [18729351] Virology. 2008 Nov 10;381(1):67-74 [18801552] J Mol Biol. 2009 Feb 6;385(5):1568-77 [19059417] Biol Chem. 2009 May-Jun;390(5-6):401-7 [19361286] J Virol. 2009 Dec;83(23):12631-5 [19776132] Virology. 2010 May 25;401(1):80-9 [20207389] Biol Chem. 2010 May;391(5):549-59 [20302513] Antimicrob Agents Chemother. 2011 Jan;55(1):229-38 [20937790] Biochem Biophys Res Commun. 2011 Apr 22;407(4):640-4 [21419753] PLoS One. 2011;6(11):e27252 [22096543] J Virol. 2012 Jan;86(1):438-46 [22031935] Antiviral Res. 2012 Feb;93(2):245-52 [22193283] J Virol. 2012 Jul;86(13):7072-83 [22532681] Nat Rev Microbiol. 2013 Feb;11(2):115-28 [23321534] J Virol. 2013 Jul;87(13):7367-81 [23616652] Proc Natl Acad Sci U S A. 2013 Nov 12;110(46):18662-7 [24158478] Viruses. 2013 Dec;5(12):2977-3006 [24300672] PLoS Pathog. 2013;9(12):e1003761 [24348242] Vaccine. 2014 Mar 10;32(12):1326-37 [24486372] Peptides. 2014 Feb;52:49-52 [24333681] Nat Commun. 2014;5:3877 [24846574] J Virol. 2014 Jul;88(13):7210-20 [24741083] Chem Rev. 2014 Nov 26;114(22):11348-81 [25268322] J Biol Chem. 2000 Apr 7;275(14):9963-9 [10744671] Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10037-41 [11517324] Cell. 2002 Mar 8;108(5):717-25 [11893341] Am J Trop Med Hyg. 2003 May;68(5):539-44 [12812340] Vaccine. 2003 Oct 1;21(27-30):4307-16 [14505913] J Virol. 2004 Jan;78(1):531-8 [14671135] Nucleic Acids Res. 2004 Jul 1;32(Web Server issue):W665-7 [15215472] Biochem Biophys Res Commun. 1967 Apr 20;27(2):157-62 [6035483] Proc Natl Acad Sci U S A. 1990 Nov;87(22):8898-902 [2147282] JAMA. 2014 Aug 13;312(6):631-40 [25117132] J Virol. 2014 Oct;88(19):11540-55 [25056895] J Biol Chem. 2014 Nov 28;289(48):33149-60 [25326389] Nat Rev Microbiol. 2015 Apr;13(4):230-9 [25730702] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/JVI.01253-15 ER - TY - JOUR T1 - A Data Analysis Pipeline Accounting for Artifacts in Tox21 Quantitative High-Throughput Screening Assays. AN - 1698037301; 25904095 AB - A main goal of the U.S. Tox21 program is to profile a 10K-compound library for activity against a panel of stress-related and nuclear receptor signaling pathway assays using a quantitative high-throughput screening (qHTS) approach. However, assay artifacts, including nonreproducible signals and assay interference (e.g., autofluorescence), complicate compound activity interpretation. To address these issues, we have developed a data analysis pipeline that includes an updated signal noise-filtering/curation protocol and an assay interference flagging system. To better characterize various types of signals, we adopted a weighted version of the area under the curve (wAUC) to quantify the amount of activity across the tested concentration range in combination with the assay-dependent point-of-departure (POD) concentration. Based on the 32 Tox21 qHTS assays analyzed, we demonstrate that signal profiling using wAUC affords the best reproducibility (Pearson's r = 0.91) in comparison with the POD (0.82) only or the AC(50) (i.e., half-maximal activity concentration, 0.81). Among the activity artifacts characterized, cytotoxicity is the major confounding factor; on average, about 8% of Tox21 compounds are affected, whereas autofluorescence affects less than 0.5%. To facilitate data evaluation, we implemented two graphical user interface applications, allowing users to rapidly evaluate the in vitro activity of Tox21 compounds. © 2015 Society for Laboratory Automation and Screening. JF - Journal of biomolecular screening AU - Hsieh, Jui-Hua AU - Sedykh, Alexander AU - Huang, Ruili AU - Xia, Menghang AU - Tice, Raymond R AD - Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA jui-hua.hsieh@nih.gov. ; MultiCASE Inc., Beachwood, OH, USA. ; National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, MD, USA. ; Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 887 EP - 897 VL - 20 IS - 7 KW - Small Molecule Libraries KW - 0 KW - Index Medicus KW - qHTS data analysis KW - in vitro activity profiling KW - Tox21 KW - concentration-response curve KW - United States KW - Reproducibility of Results KW - Humans KW - Data Interpretation, Statistical KW - Signal-To-Noise Ratio KW - Artifacts KW - High-Throughput Screening Assays -- standards KW - High-Throughput Screening Assays -- methods KW - Drug Discovery -- standards KW - Drug Discovery -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698037301?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+biomolecular+screening&rft.atitle=A+Data+Analysis+Pipeline+Accounting+for+Artifacts+in+Tox21+Quantitative+High-Throughput+Screening+Assays.&rft.au=Hsieh%2C+Jui-Hua%3BSedykh%2C+Alexander%3BHuang%2C+Ruili%3BXia%2C+Menghang%3BTice%2C+Raymond+R&rft.aulast=Hsieh&rft.aufirst=Jui-Hua&rft.date=2015-08-01&rft.volume=20&rft.issue=7&rft.spage=887&rft.isbn=&rft.btitle=&rft.title=Journal+of+biomolecular+screening&rft.issn=1552-454X&rft_id=info:doi/10.1177%2F1087057115581317 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-05 N1 - Date created - 2015-07-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biometrics. 2014 Mar;70(1):237-46 [24397816] J Biomol Screen. 2014 Mar;19(3):344-53 [24056003] J Biomol Screen. 2014 Mar;19(3):387-98 [23867716] Environ Health Perspect. 2013 Jul;121(7):756-65 [23603828] PLoS One. 2012;7(11):e49198 [23155465] Environ Health Perspect. 2012 Aug;120(8):1107-15 [22575717] Nature. 2012 Mar 29;483(7391):603-7 [22460905] Assay Drug Dev Technol. 2012 Feb;10(1):88-96 [22066911] Nat Rev Drug Discov. 2011 Sep;10(9):712 [21892149] Environ Health Perspect. 2011 Aug;119(8):1142-8 [21543282] PLoS Comput Biol. 2011 Apr;7(4):e1002037 [21552547] Environ Health Perspect. 2011 Mar;119(3):364-70 [20980217] Environ Toxicol Chem. 2010 Jan;29(1):220-9 [20821438] Curr Opin Chem Biol. 2010 Jun;14(3):315-24 [20417149] J Med Chem. 2010 Apr 8;53(7):2719-40 [20131845] Expert Opin Drug Metab Toxicol. 2010 Apr;6(4):505-18 [20074001] J Biomol Screen. 2009 Dec;14(10):1216-27 [19828774] Nat Rev Drug Discov. 2008 Aug;7(8):632-3 [18670425] BMC Bioinformatics. 2006;7:123 [16526949] Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11473-8 [16864780] J Biomol Screen. 2014 Jun;19(5):715-26 [24371213] Drug Discov Today. 2015 Mar;20(3):296-300 [25449657] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/1087057115581317 ER - TY - JOUR T1 - Human papillomavirus infection in oral squamous cell carcinomas from Chilean patients. AN - 1698036764; 26057833 AB - Human papillomavirus (HPV) is the causal agent of cervical, anogenital and a subset of oropharyngeal carcinomas. In addition, the role of HPV in oral carcinogenesis has been suggested, although the findings are inconclusive. In this study, using conventional polymerase chain reaction (PCR) and genotyping by specific PCR and DNA sequencing, we analyzed the HPV presence in 80 oral squamous cell carcinomas (OSCCs) from Chilean subjects. In addition, we determined the expression of p16, p53, pRb and Ki-67 using immunohistochemistry (IHC). The CDKN2A (p16) promoter methylation was evaluated using methylation-specific PCR (MSP). HPV sequences were found in 9/80 (11%) OSCCs. Non-statistically significant association with p53, pRb, Ki-67 and p16 levels were found (p=0.77; 0.29; 0.83; 0.21, respectively). HPV-16 and 18 were the most prevalent HPV genotypes in 8/9 (89%) OSCCs. In addition, CDKN2A (p16) was methylated in 39% of OSCCs. No association with HPV presence (p=0.917) was found. These results suggest that HPV positive OSCCs are entities that do not resemble the molecular alterations of HPV-associated tumors in a Chilean population. More studies are warranted to determine the role of HPV in OSCCs. Copyright © 2015 Elsevier Inc. All rights reserved. JF - Experimental and molecular pathology AU - Reyes, Montserrat AU - Rojas-Alcayaga, Gonzalo AU - Pennacchiotti, Gina AU - Carrillo, Diego AU - Muñoz, Juan P AU - Peña, Nelson AU - Montes, Rodrigo AU - Lobos, Nelson AU - Aguayo, Francisco AD - Oral Pathology and Medicine Department, Dental School, Universidad de Chile, Santiago 8380492, Chile. Electronic address: montserrat.reyes.r@gmail.com. ; Oral Pathology and Medicine Department, Dental School, Universidad de Chile, Santiago 8380492, Chile. Electronic address: grojasalcayaga@yahoo.es. ; Oral Pathology and Medicine Department, Dental School, Universidad de Chile, Santiago 8380492, Chile. Electronic address: pennacchiotti@gmail.com. ; Virology Program, Institute of Biomedical Sciences (ICBM), Faculty of Medicine, Universidad de Chile, Santiago 8389100, Chile. Electronic address: diegocarrillo@med.uchile.cl. ; Virology Program, Institute of Biomedical Sciences (ICBM), Faculty of Medicine, Universidad de Chile, Santiago 8389100, Chile. Electronic address: jp_182_mb@hotmail.com. ; Virology Program, Institute of Biomedical Sciences (ICBM), Faculty of Medicine, Universidad de Chile, Santiago 8389100, Chile. Electronic address: nelsonpena@med.uchile.cl. ; National Cancer Institute, Santiago 8380455, Chile. Electronic address: rmontesf@gmail.com. ; Oral Pathology and Medicine Department, Dental School, Universidad de Chile, Santiago 8380492, Chile. Electronic address: lobos.nelson@yahoo.cl. ; Virology Program, Institute of Biomedical Sciences (ICBM), Faculty of Medicine, Universidad de Chile, Santiago 8389100, Chile. Electronic address: faguayo@med.uchile.cl. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 95 EP - 99 VL - 99 IS - 1 KW - Biomarkers, Tumor KW - 0 KW - Cyclin-Dependent Kinase Inhibitor p16 KW - DNA, Viral KW - Ki-67 Antigen KW - TP53 protein, human KW - Tumor Suppressor Protein p53 KW - Index Medicus KW - p16 KW - p53 KW - Oral squamous cell carcinomas KW - pRb KW - HPV-16/18 KW - Human papillomavirus 16 -- isolation & purification KW - Humans KW - Ki-67 Antigen -- metabolism KW - Aged KW - Cyclin-Dependent Kinase Inhibitor p16 -- metabolism KW - Chile KW - Tumor Suppressor Protein p53 -- metabolism KW - Genotype KW - Human papillomavirus 18 -- genetics KW - Promoter Regions, Genetic KW - Ki-67 Antigen -- genetics KW - Aged, 80 and over KW - Human papillomavirus 18 -- isolation & purification KW - Middle Aged KW - Human papillomavirus 16 -- genetics KW - Tumor Suppressor Protein p53 -- genetics KW - Cyclin-Dependent Kinase Inhibitor p16 -- genetics KW - Immunohistochemistry KW - DNA, Viral -- genetics KW - Male KW - Female KW - Mouth -- virology KW - Carcinoma, Squamous Cell -- pathology KW - Papillomaviridae -- isolation & purification KW - Mouth Neoplasms -- virology KW - Papillomavirus Infections -- virology KW - Papillomaviridae -- genetics KW - Mouth Neoplasms -- pathology KW - Mouth -- pathology KW - Carcinoma, Squamous Cell -- virology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698036764?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Experimental+and+molecular+pathology&rft.atitle=Human+papillomavirus+infection+in+oral+squamous+cell+carcinomas+from+Chilean+patients.&rft.au=Reyes%2C+Montserrat%3BRojas-Alcayaga%2C+Gonzalo%3BPennacchiotti%2C+Gina%3BCarrillo%2C+Diego%3BMu%C3%B1oz%2C+Juan+P%3BPe%C3%B1a%2C+Nelson%3BMontes%2C+Rodrigo%3BLobos%2C+Nelson%3BAguayo%2C+Francisco&rft.aulast=Reyes&rft.aufirst=Montserrat&rft.date=2015-08-01&rft.volume=99&rft.issue=1&rft.spage=95&rft.isbn=&rft.btitle=&rft.title=Experimental+and+molecular+pathology&rft.issn=1096-0945&rft_id=info:doi/10.1016%2Fj.yexmp.2015.06.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-05 N1 - Date created - 2015-07-21 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.yexmp.2015.06.001 ER - TY - JOUR T1 - Targeting α-synuclein for treatment of Parkinson's disease: mechanistic and therapeutic considerations. AN - 1698028089; 26050140 AB - Progressive neuronal cell loss in a small subset of brainstem and mesencephalic nuclei and widespread aggregation of the α-synuclein protein in the form of Lewy bodies and Lewy neurites are neuropathological hallmarks of Parkinson's disease. Most cases occur sporadically, but mutations in several genes, including SNCA, which encodes α-synuclein, are associated with disease development. The discovery and development of therapeutic strategies to block cell death in Parkinson's disease has been limited by a lack of understanding of the mechanisms driving neurodegeneration. However, increasing evidence of multiple pivotal roles of α-synuclein in the pathogenesis of Parkinson's disease has led researchers to consider the therapeutic potential of several strategies aimed at reduction of α-synuclein toxicity. We critically assess the potential of experimental therapies targeting α-synuclein, and discuss steps that need to be taken for target validation and drug development. Copyright © 2015 Elsevier Ltd. All rights reserved. JF - The Lancet. Neurology AU - Dehay, Benjamin AU - Bourdenx, Mathieu AU - Gorry, Philippe AU - Przedborski, Serge AU - Vila, Miquel AU - Hunot, Stéphane AU - Singleton, Andrew AU - Olanow, C Warren AU - Merchant, Kalpana M AU - Bezard, Erwan AU - Petsko, Gregory A AU - Meissner, Wassilios G AD - Institute of Neurodegenerative Diseases, University of Bordeaux, Centre National de la Recherche Scientifique Unité Mixte de Recherche, Bordeaux, France. ; Research Unit of Theoretical & Applied Economics, University of Bordeaux, Centre National de la Recherche Scientifique Unité Mixte de Recherche, Pessac, France. ; Departments of Neurology, Pathology and Cell Biology, and the Center for Motor Neuron Biology and Disease, Columbia University, New York, NY, USA. ; Neurodegenerative Diseases Research Group, Vall d'Hebron Research Institute, Centro Investigación Biomédica en Red Enfermedades Neurodegenerativas, Barcelona, Spain; Department of Biochemistry and Molecular Biology, Autonomous University of Barcelona, Bellaterra, Barcelona, Spain; Catalan Institution for Research and Advanced Studies, Barcelona, Spain. ; Institut de la Communication et des Médias, Sorbonne Universités, Paris, France; University Pierre et Marie Curie, Université Paris, Institut de la Communication et des Médias, Paris, France; Centre National de la Recherche Scientifique, Institut de la Communication et des Médias, Paris, France; Inserm, Institut de la Communication et des Médias, Paris, France. ; Molecular Genetics Section and Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA. ; Departments of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, NY, USA. ; TransThera Consulting, Zionsville, IN, USA. ; Institute of Neurodegenerative Diseases, University of Bordeaux, Centre National de la Recherche Scientifique Unité Mixte de Recherche, Bordeaux, France. Electronic address: erwan.bezard@u-bordeaux.fr. ; Department of Neurology and Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY, USA. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 855 EP - 866 VL - 14 IS - 8 KW - alpha-Synuclein KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Drug Discovery KW - alpha-Synuclein -- metabolism KW - alpha-Synuclein -- chemistry KW - Parkinson Disease -- metabolism KW - alpha-Synuclein -- genetics KW - Parkinson Disease -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698028089?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Lancet.+Neurology&rft.atitle=Targeting+%CE%B1-synuclein+for+treatment+of+Parkinson%27s+disease%3A+mechanistic+and+therapeutic+considerations.&rft.au=Dehay%2C+Benjamin%3BBourdenx%2C+Mathieu%3BGorry%2C+Philippe%3BPrzedborski%2C+Serge%3BVila%2C+Miquel%3BHunot%2C+St%C3%A9phane%3BSingleton%2C+Andrew%3BOlanow%2C+C+Warren%3BMerchant%2C+Kalpana+M%3BBezard%2C+Erwan%3BPetsko%2C+Gregory+A%3BMeissner%2C+Wassilios+G&rft.aulast=Dehay&rft.aufirst=Benjamin&rft.date=2015-08-01&rft.volume=14&rft.issue=8&rft.spage=855&rft.isbn=&rft.btitle=&rft.title=The+Lancet.+Neurology&rft.issn=1474-4465&rft_id=info:doi/10.1016%2FS1474-4422%2815%2900006-X LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-15 N1 - Date created - 2015-07-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Comment In: Lancet Neurol. 2015 Aug;14(8):785-6 [26116313] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/S1474-4422(15)00006-X ER - TY - JOUR T1 - Spin trapping combined with quantitative mass spectrometry defines free radical redistribution within the oxidized hemoglobin:haptoglobin complex. AN - 1697757053; 25933590 AB - Extracellular or free hemoglobin (Hb) accumulates during hemolysis, tissue damage, and inflammation. Heme-triggered oxidative reactions can lead to diverse structural modifications of lipids and proteins, which contribute to the propagation of tissue damage. One important target of Hb׳s peroxidase reactivity is its own globin structure. Amino acid oxidation and crosslinking events destabilize the protein and ultimately cause accumulation of proinflammatory and cytotoxic Hb degradation products. The Hb scavenger haptoglobin (Hp) attenuates oxidation-induced Hb degradation. In this study we show that in the presence of hydrogen peroxide (H2O2), Hb and the Hb:Hp complex share comparable peroxidative reactivity and free radical generation. While oxidation of both free Hb and Hb:Hp complex generates a common tyrosine-based free radical, the spin-trapping reaction with 5,5-dimethyl-1-pyrroline N-oxide (DMPO) yields dissimilar paramagnetic products in Hb and Hb:Hp, suggesting that radicals are differently redistributed within the complex before reacting with the spin trap. With LC-MS(2) mass spectrometry we assigned multiple known and novel DMPO adduct sites. Quantification of these adducts suggested that the Hb:Hp complex formation causes extensive delocalization of accessible free radicals with drastic reduction of the major tryptophan and cysteine modifications in the β-globin chain of the Hb:Hp complex, including decreased βCys93 DMPO adduction. In contrast, the quantitative changes in DMPO adduct formation on Hb:Hp complex formation were less pronounced in the Hb α-globin chain. In contrast to earlier speculations, we found no evidence that free Hb radicals are delocalized to the Hp chain of the complex. The observation that Hb:Hp complex formation alters free radical distribution in Hb may help to better understand the structural basis for Hp as an antioxidant protein. Copyright © 2015 Elsevier Inc. All rights reserved. JF - Free radical biology & medicine AU - Vallelian, Florence AU - Garcia-Rubio, Ines AU - Puglia, Michele AU - Kahraman, Abdullah AU - Deuel, Jeremy W AU - Engelsberger, Wolfgang R AU - Mason, Ronald P AU - Buehler, Paul W AU - Schaer, Dominik J AD - Division of Internal Medicine, University Hospital, Zurich, Switzerland. ; Laboratory of Physical Chemistry, ETH Zürich, Switzerland; Centro Universitario de la Defensa, carretera de Huesca, Zaragoza, Spain. ; Division of Internal Medicine, University Hospital, Zurich, Switzerland; Functional Genomics Center, University of Zurich, Switzerland. ; Institute of Molecular Life Sciences, University of Zurich, Switzerland. ; Laboratory of Toxicology & Pharmacology, NIEHS/NIH, Research Triangle Park, NC, USA. ; Center of Biologics Evaluation and Research, Food and Drug Administration, Bethesda, MD, USA. ; Division of Internal Medicine, University Hospital, Zurich, Switzerland; Institute of Evolutionary Medicine, University of Zurich, Switzerland. Electronic address: dominik.schaer@usz.ch. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 259 EP - 268 VL - 85 KW - Amino Acids KW - 0 KW - Free Radicals KW - Haptoglobins KW - Hemoglobins KW - Hydrogen Peroxide KW - BBX060AN9V KW - Peroxidases KW - EC 1.11.1.- KW - Index Medicus KW - Hemoglobin KW - Haptoglobin KW - Oxidative stress KW - Radical KW - Oxidation KW - Spin trapping KW - Electron paramagnetic resonance (EPR) KW - Mass spectrometry KW - Oxidation-Reduction KW - Amino Acids -- chemistry KW - Humans KW - Electron Spin Resonance Spectroscopy KW - Hydrogen Peroxide -- pharmacology KW - Molecular Sequence Data KW - Chromatography, Liquid KW - Amino Acid Sequence KW - Peroxidases -- metabolism KW - Spin Trapping KW - Hemoglobins -- metabolism KW - Tandem Mass Spectrometry -- methods KW - Hemoglobins -- chemistry KW - Haptoglobins -- metabolism KW - Free Radicals -- metabolism KW - Haptoglobins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1697757053?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Free+radical+biology+%26+medicine&rft.atitle=Spin+trapping+combined+with+quantitative+mass+spectrometry+defines+free+radical+redistribution+within+the+oxidized+hemoglobin%3Ahaptoglobin+complex.&rft.au=Vallelian%2C+Florence%3BGarcia-Rubio%2C+Ines%3BPuglia%2C+Michele%3BKahraman%2C+Abdullah%3BDeuel%2C+Jeremy+W%3BEngelsberger%2C+Wolfgang+R%3BMason%2C+Ronald+P%3BBuehler%2C+Paul+W%3BSchaer%2C+Dominik+J&rft.aulast=Vallelian&rft.aufirst=Florence&rft.date=2015-08-01&rft.volume=85&rft.issue=&rft.spage=259&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2015.04.023 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-26 N1 - Date created - 2015-07-20 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.freeradbiomed.2015.04.023 ER - TY - JOUR T1 - (+)-Naltrexone is neuroprotective and promotes alternative activation in the mouse hippocampus after cardiac arrest/cardiopulmonary resuscitation. AN - 1697756863; 25774010 AB - Despite dramatic improvement in cardiopulmonary resuscitation (CPR) and other techniques for cardiac arrest (CA), the majority of survivors continue to show signs of decreased memory or executive cognitive function. Such memory impairment may be due to hippocampal CA1 neuronal death, which is delayed by several days after CA/CPR. Classical microgliosis in the CA1 region may contribute to neuronal death, yet the role of a key activation receptor Toll Like Receptor 4 (TLR4) has not been previously investigated for such neuronal death after CA/CPR. We show that (+)-naltrexone was neuroprotective after CA/CPR. TLR4 blockade was associated with decreased expression of markers for microglial/macrophage activation and T cell and B cell infiltration, as well as decreased pro-inflammatory cytokine levels. Notably, IL-10 expression was elevated in response to CA/CPR, but was not attenuated by (+)-naltrexone, suggesting that the local monocyte/microglial phenotype had shifted towards alternative activation. This was confirmed by elevated expression of Arginase-1, and decreased expression of NFκB p65 subunit. Thus, (+)-naltrexone and other TLR4 antagonists may represent a novel therapeutic strategy to alleviate the substantial burden of memory or executive cognitive function impairment after CA/CPR. Copyright © 2015 Elsevier Inc. All rights reserved. JF - Brain, behavior, and immunity AU - Grace, Peter M AU - Shimizu, Kaori AU - Strand, Keith A AU - Rice, Kenner C AU - Deng, Guiying AU - Watkins, Linda R AU - Herson, Paco S AD - Department of Psychology and The Center for Neuroscience, University of Colorado Boulder, Boulder, CO, USA. ; Department of Anesthesiology, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA. ; Chemical Biology Research Branch, National Institute on Drug Abuse and National Institute on Alcohol Abuse and Alcoholism, Rockville, MD, USA. ; Department of Pharmacology, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA. ; Department of Anesthesiology, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA; Department of Pharmacology, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA. Electronic address: paco.herson@ucdenver.edu. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 115 EP - 122 VL - 48 KW - Neuroprotective Agents KW - 0 KW - Interleukin-10 KW - 130068-27-8 KW - Naltrexone KW - 5S6W795CQM KW - Index Medicus KW - Neurotoxicity KW - TLR4 KW - M2 macrophages KW - Ischemia KW - M2 microglia KW - HIF1α KW - HIF2α KW - Animals KW - Neurons -- metabolism KW - Interleukin-10 -- metabolism KW - Neurons -- drug effects KW - Mice, Inbred C57BL KW - Mice KW - Microglia -- pathology KW - Microglia -- drug effects KW - Male KW - Cardiopulmonary Resuscitation KW - Neurons -- pathology KW - Microglia -- metabolism KW - Hippocampus -- metabolism KW - Naltrexone -- pharmacology KW - Heart Arrest -- metabolism KW - Hippocampus -- pathology KW - Heart Arrest -- pathology KW - Cell Death -- drug effects KW - Neuroprotective Agents -- pharmacology KW - Hippocampus -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1697756863?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain%2C+behavior%2C+and+immunity&rft.atitle=%28%2B%29-Naltrexone+is+neuroprotective+and+promotes+alternative+activation+in+the+mouse+hippocampus+after+cardiac+arrest%2Fcardiopulmonary+resuscitation.&rft.au=Grace%2C+Peter+M%3BShimizu%2C+Kaori%3BStrand%2C+Keith+A%3BRice%2C+Kenner+C%3BDeng%2C+Guiying%3BWatkins%2C+Linda+R%3BHerson%2C+Paco+S&rft.aulast=Grace&rft.aufirst=Peter&rft.date=2015-08-01&rft.volume=48&rft.issue=&rft.spage=115&rft.isbn=&rft.btitle=&rft.title=Brain%2C+behavior%2C+and+immunity&rft.issn=1090-2139&rft_id=info:doi/10.1016%2Fj.bbi.2015.03.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-13 N1 - Date created - 2015-07-20 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbi.2015.03.005 ER - TY - JOUR T1 - The role of microRNA in nutritional control. AN - 1697215342; 25832550 AB - MicroRNAs (miRNAs) are one of a growing class of noncoding RNAs that are involved in the regulation of a wide range of metabolic processes including cellular differentiation, cell proliferation and apoptosis. The generation of miRNA is regulated in complex ways, for example by small interfering RNAs (small nucleolar and nuclear RNAs) and various other metabolites. This complexity of control is likely to explain how a relatively small part of the DNA that codes for proteins has enabled the evolution of such complex organisms as mammals. Non-protein-coding DNA is therefore thought to carry the memory of early evolutionary steps that led to progressively complex metabolic controls. Clinically, miRNAs are becoming increasingly important following the recognition that some congenital abnormalities can be traced to defects in miRNA processing. The potential for manipulating metabolism and affecting disease processes by the pharmaceutical or biological targeting of specific miRNA pathways is now being tested. miRNAs are also released into the extracellular milieu after packaging by cells into nano-sized extracellular vesicles. Such vesicles can be taken up by adjacent and possibly more distant cells, thereby allowing coordinated intercellular communication in specific tissues. Extracellular miRNAs found in the blood stream may also serve as novel biomarkers for both diagnosing specific forms of cancer and assessing the likelihood of metastasis, and as powerful prognostic indices for various cancers. Here, we discuss the role of intracellular and extracellular miRNAs in nutritional control of various (patho)physiological processes. In this review, we provide an update of the presentations from the 25th Marabou Symposium (Stockholm, 14-16 June 2013) entitled 'Role of miRNA in health and nutrition', attended by 50 international experts © 2015 The Association for the Publication of the Journal of Internal Medicine. JF - Journal of internal medicine AU - Nolte-'t Hoen, E N M AU - Van Rooij, E AU - Bushell, M AU - Zhang, C-Y AU - Dashwood, R H AU - James, W P T AU - Harris, C AU - Baltimore, D AD - Department of Biochemistry and Cell Biology, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands. ; Hubrecht Institute, Koninklijke Nederlandse Academie van Wetenschappen (KNAW), University Medical Center Utrecht, Utrecht, The Netherlands. ; Medical Research Council (MRC) Toxicology Unit, University of Leicester, Leicester, UK. ; Jiangsu Engineering Research Center for microRNA Biology and Biotechnology, State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China. ; Center for Epigenetics and Disease Prevention, Institute of Biosciences & Technology, Texas A&M Health Science Center, Houston, TX, USA. ; London School of Hygiene and Tropical Medicine, London, UK. ; Laboratory of Human Carcinogenesis, National Cancer Institute, Center for Cancer Research, National Institutes of Health, Bethesda, MD, USA. ; Department of Biology, California Institute of Technology, Pasadena, CA, USA. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 99 EP - 109 VL - 278 IS - 2 KW - MicroRNAs KW - 0 KW - Index Medicus KW - nutrition KW - development KW - pathology KW - miRNA KW - metabolic control KW - signalling KW - Animals KW - Humans KW - Prognosis KW - Cell Communication KW - Nutrition Assessment KW - MicroRNAs -- genetics KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1697215342?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+internal+medicine&rft.atitle=The+role+of+microRNA+in+nutritional+control.&rft.au=Nolte-%27t+Hoen%2C+E+N+M%3BVan+Rooij%2C+E%3BBushell%2C+M%3BZhang%2C+C-Y%3BDashwood%2C+R+H%3BJames%2C+W+P+T%3BHarris%2C+C%3BBaltimore%2C+D&rft.aulast=Nolte-%27t+Hoen&rft.aufirst=E+N&rft.date=2015-08-01&rft.volume=278&rft.issue=2&rft.spage=99&rft.isbn=&rft.btitle=&rft.title=Journal+of+internal+medicine&rft.issn=1365-2796&rft_id=info:doi/10.1111%2Fjoim.12372 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-28 N1 - Date created - 2015-07-16 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/joim.12372 ER - TY - JOUR T1 - Maintenance pazopanib versus placebo in Non-Small Cell Lung Cancer patients non-progressive after first line chemotherapy: A double blind randomised phase III study of the lung cancer group, EORTC 08092 (EudraCT: 2010-018566-23, NCT01208064). AN - 1695757250; 26074395 AB - Switch maintenance is an effective strategy in the treatment of advanced Non-Small Cell Lung Cancer (NSCLC). Pazopanib is an oral, multi-targeted tyrosine kinase inhibitor (TKI). EORTC 08092 evaluated pazopanib given as maintenance treatment following standard first line platinum-based chemotherapy in patients with advanced NSCLC. Patients with non-progressive disease after 4-6 cycles of chemotherapy were randomised to receive either pazopanib 800mg/day or matched placebo until progression or unacceptable toxicity. The primary end-point was overall survival and secondary end-points were progression-free survival (PFS) and safety. A total of 600 patients were planned to be randomised. The trial was prematurely stopped following an early interim analysis, after 102 patients were randomised to pazopanib (n=50) or placebo (n=52). Median age was 64years in both arms. Median overall survival was 17.4 months for pazopanib and 12.3 months for placebo (adjusted hazard ratio (HR) 0.72 [95% confidence interval (CI) 0.40-1.28]; p=0.257). Median PFS was 4.3 months versus 3.2 months (HR 0.67, [95% CI 0.43-1.03], p=0.068). PFS rates at 4 months were 56% and 45% respectively. The majority of treatment-related adverse events (AEs) were grade 1-2. Grade 3-4 AEs (pazopanib versus placebo) were hypertension (38% versus 8%), neutropenia (8% versus 0%), and elevated SGPT (6% versus 0%). Of the patients randomised to pazopanib, 22% withdrew due to a treatment-related AE. Switch maintenance with pazopanib following platinum-based chemotherapy in advanced NSCLC patients had limited side-effects. This study was stopped due to lack of efficacy by stringent criteria for PFS at a futility interim analysis. Copyright © 2015 Elsevier Ltd. All rights reserved. JF - European journal of cancer (Oxford, England : 1990) AU - O'Brien, Mary E R AU - Gaafar, Rabab AU - Hasan, Baktiar AU - Menis, Jessica AU - Cufer, Tanja AU - Popat, Sanjay AU - Woll, Penella J AU - Surmont, Veerle AU - Georgoulias, Vassilis AU - Montes, Ana AU - Blackhall, Fiona AU - Hennig, Ivo AU - Schmid-Bindert, Gerald AU - Baas, Paul AU - EORTC-LCG AD - Royal Marsden Hospital, London and Sutton, United Kingdom. Electronic address: mary.obrien@rmh.nhs.uk. ; NCI, Cairo University, Egypt. Electronic address: rabab.gaafar@gmail.com. ; EORTC Headquarters, Brussels, Belgium. Electronic address: Baktiar.hasan@eortc.be. ; EORTC Headquarters, Brussels, Belgium. Electronic address: Jessica.menis@eortc.be. ; University Clinic Golnik, Golnik, Slovenia. Electronic address: tanja.cufer@klinika-golnik.si. ; Royal Marsden Hospital, London and Sutton, United Kingdom. Electronic address: sanjay.popat@rmh.nhs.uk. ; University of Sheffield, Sheffield, United Kingdom. Electronic address: p.j.woll@sheffield.ac.uk. ; Ghent University Hospital, Belgium. Electronic address: veerle.surmont@uzgent.be. ; University General Hospital Heraklion, Greece. Electronic address: georgsec@med.uoc.gr. ; Guy's and St. Thomas' NHS - Guy's Hospital, London, United Kingdom. Electronic address: ana.montes@gstt.nhs.uk. ; The Christie Hospital NHS Foundation, Manchester, United Kingdom. Electronic address: Fiona.Blackhall@christie.nhs.uk. ; Nottingham University Hospitals NHS Trust, Nottingham, United Kingdom. Electronic address: ivo.hennig@nuh.nhs.uk. ; Universitaetsmedizin Mannheim, Mannheim, Germany. Electronic address: gerald.schmid-bindert@umm.de. ; The Netherlands Cancer Institute - Antoni Van LeeuweenhoekZiekenhuis, Amsterdam, The Netherlands. Electronic address: p.baas@nki.nl. ; EORTC-LCG Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 1511 EP - 1528 VL - 51 IS - 12 KW - Protein Kinase Inhibitors KW - 0 KW - Pyrimidines KW - Sulfonamides KW - pazopanib KW - 7RN5DR86CK KW - Index Medicus KW - Pazopanib KW - Advanced KW - Phase III KW - NSCLC KW - Double blind KW - Maintenance KW - Kaplan-Meier Estimate KW - Disease-Free Survival KW - Double-Blind Method KW - Humans KW - Adult KW - Disease Progression KW - Aged KW - Middle Aged KW - Male KW - Female KW - Pyrimidines -- adverse effects KW - Sulfonamides -- adverse effects KW - Pyrimidines -- therapeutic use KW - Protein Kinase Inhibitors -- therapeutic use KW - Protein Kinase Inhibitors -- adverse effects KW - Lung Neoplasms -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Sulfonamides -- therapeutic use KW - Carcinoma, Non-Small-Cell Lung -- drug therapy KW - Maintenance Chemotherapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1695757250?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.atitle=Maintenance+pazopanib+versus+placebo+in+Non-Small+Cell+Lung+Cancer+patients+non-progressive+after+first+line+chemotherapy%3A+A+double+blind+randomised+phase+III+study+of+the+lung+cancer+group%2C+EORTC+08092+%28EudraCT%3A+2010-018566-23%2C+NCT01208064%29.&rft.au=O%27Brien%2C+Mary+E+R%3BGaafar%2C+Rabab%3BHasan%2C+Baktiar%3BMenis%2C+Jessica%3BCufer%2C+Tanja%3BPopat%2C+Sanjay%3BWoll%2C+Penella+J%3BSurmont%2C+Veerle%3BGeorgoulias%2C+Vassilis%3BMontes%2C+Ana%3BBlackhall%2C+Fiona%3BHennig%2C+Ivo%3BSchmid-Bindert%2C+Gerald%3BBaas%2C+Paul%3BEORTC-LCG&rft.aulast=O%27Brien&rft.aufirst=Mary+E&rft.date=2015-08-01&rft.volume=51&rft.issue=12&rft.spage=1511&rft.isbn=&rft.btitle=&rft.title=European+journal+of+cancer+%28Oxford%2C+England+%3A+1990%29&rft.issn=1879-0852&rft_id=info:doi/10.1016%2Fj.ejca.2015.04.026 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-21 N1 - Date created - 2015-07-11 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ejca.2015.04.026 ER - TY - JOUR T1 - Anthropometric, Metabolic and Molecular Determinants of Human Epidermal Growth Factor Receptor 2 Expression in Luminal B Breast Cancer AN - 1694984240; PQ0001499725 AB - Genomic and trascriptomic profiling has recently contributed details to the characterization of luminal B breast cancer. We explored the contribution of anthropometric, metabolic, and molecular determinants to the multifaceted heterogeneity of this breast cancer subtype, with a specific focus on the association between body mass index (BMI), pre-treatment fasting glucose, hormone receptors, and expression of human epidermal growth factor receptor 2 (HER2). Extensively annotated specimens were obtained from 154 women with luminal B breast cancer diagnosed at two Italian comprehensive cancer centres. Participants' characteristics were descriptively analyzed overall and by HER2 status (positive vs. negative). BMI (<25 vs greater than or equal to 25), pre-treatment fasting glucose ( 2 cycles with one patient remaining on study for 6 cycles. Target engagement was demonstrated by transcriptional upregulation of Hsp70 and Hsp27 in PBMCs. Statistically significant modulation of client proteins was not achieved in the 9 paired tumor biopsies evaluated; however, hierarchical clustering revealed two subgroups of patients with differential patterns of protein expression. Further combination studies are needed in order to target prospective driver oncoproteins. JF - Investigational new drugs AU - Do, Khanh AU - Speranza, Giovanna AU - Chang, Lun-Ching AU - Polley, Eric C AU - Bishop, Rachel AU - Zhu, Weimin AU - Trepel, Jane B AU - Lee, Sunmin AU - Lee, Min-Jung AU - Kinders, Robert J AU - Phillips, Larry AU - Collins, Jerry AU - Lyons, John AU - Jeong, Woondong AU - Antony, Ramya AU - Chen, Alice P AU - Neckers, Len AU - Doroshow, James H AU - Kummar, Shivaani AD - Division of Cancer Treatment and Diagnosis, National Cancer Institute, 31 Center Drive, Bldg 31, Rm 3A44, Bethesda, MD, 20892, USA. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 921 EP - 930 VL - 33 IS - 4 KW - (2,4-dihydroxy-5-isopropylphenyl)-(5-(4-methylpiperazin-1-ylmethyl)-1,3-dihydroisoindol-2-yl)methanone KW - 0 KW - Benzamides KW - HSP27 Heat-Shock Proteins KW - HSP70 Heat-Shock Proteins KW - HSP90 Heat-Shock Proteins KW - HSPB1 protein, human KW - Isoindoles KW - RNA, Messenger KW - Index Medicus KW - HSP70 Heat-Shock Proteins -- metabolism KW - HSP70 Heat-Shock Proteins -- genetics KW - Drug Administration Schedule KW - RNA, Messenger -- metabolism KW - Humans KW - HSP27 Heat-Shock Proteins -- genetics KW - Adult KW - Aged KW - Middle Aged KW - Maximum Tolerated Dose KW - Male KW - Female KW - Isoindoles -- administration & dosage KW - Neoplasms -- drug therapy KW - Benzamides -- adverse effects KW - Isoindoles -- pharmacology KW - Benzamides -- pharmacology KW - Isoindoles -- therapeutic use KW - HSP90 Heat-Shock Proteins -- antagonists & inhibitors KW - Isoindoles -- adverse effects KW - Benzamides -- administration & dosage KW - Neoplasms -- metabolism KW - Benzamides -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1694706120?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Investigational+new+drugs&rft.atitle=Phase+I+study+of+the+heat+shock+protein+90+%28Hsp90%29+inhibitor+onalespib+%28AT13387%29+administered+on+a+daily+for+2+consecutive+days+per+week+dosing+schedule+in+patients+with+advanced+solid+tumors.&rft.au=Do%2C+Khanh%3BSperanza%2C+Giovanna%3BChang%2C+Lun-Ching%3BPolley%2C+Eric+C%3BBishop%2C+Rachel%3BZhu%2C+Weimin%3BTrepel%2C+Jane+B%3BLee%2C+Sunmin%3BLee%2C+Min-Jung%3BKinders%2C+Robert+J%3BPhillips%2C+Larry%3BCollins%2C+Jerry%3BLyons%2C+John%3BJeong%2C+Woondong%3BAntony%2C+Ramya%3BChen%2C+Alice+P%3BNeckers%2C+Len%3BDoroshow%2C+James+H%3BKummar%2C+Shivaani&rft.aulast=Do&rft.aufirst=Khanh&rft.date=2015-08-01&rft.volume=33&rft.issue=4&rft.spage=921&rft.isbn=&rft.btitle=&rft.title=Investigational+new+drugs&rft.issn=1573-0646&rft_id=info:doi/10.1007%2Fs10637-015-0255-1 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-12 N1 - Date created - 2015-07-06 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT01246102; ClinicalTrials.gov N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s10637-015-0255-1 ER - TY - JOUR T1 - Nucleotides Acting at P2Y Receptors: Connecting Structure and Function. AN - 1690209322; 25837834 AB - Eight G protein-coupled P2Y receptor (P2YR) subtypes are important physiologic mediators. The human P2YRs are fully activated by ATP (P2Y2 and P2Y11), ADP (P2Y1, P2Y12, and P2Y13), UTP (P2Y2 and P2Y4), UDP (P2Y6 and P2Y14), and UDP glucose (P2Y14). Their structural elucidation is progressing rapidly. The X-ray structures of three ligand complexes of the Gi-coupled P2Y12R and two of the Gq-coupled P2Y1Rs were recently determined and will be especially useful in structure-based ligand design at two P2YR subfamilies. These high-resolution structures, which display unusual binding site features, complement mutagenesis studies for probing ligand recognition and activation. The structural requirements for nucleotide agonist recognition at P2YRs are relatively permissive with respect to the length of the phosphate moiety, but less so with respect to base recognition. Nucleotide-like antagonists and partial agonists are also known for P2Y1, P2Y2, P2Y4, and P2Y12Rs. Each P2YR subtype has the ability to be activated by structurally bifunctional agonists, such as dinucleotides, typically, dinucleoside triphosphates or tetraphosphates, and nucleoside polyphosphate sugars (e.g., UDP glucose) as well as the more conventional mononucleotide agonists. A range of dinucleoside polyphosphates, from triphosphates to higher homologs, occurs naturally. Earlier modeling predictions of the P2YRs were not very accurate, but recent findings have provided much detailed structural insight into this receptor family to aid in the rational design of new drugs. U.S. Government work not protected by U.S. copyright. JF - Molecular pharmacology AU - Jacobson, Kenneth A AU - Paoletta, Silvia AU - Katritch, Vsevolod AU - Wu, Beili AU - Gao, Zhan-Guo AU - Zhao, Qiang AU - Stevens, Raymond C AU - Kiselev, Evgeny AD - Molecular Recognition Section, Laboratory of Bioorganic Chemistry, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland (K.A.J., S.P., Z.-G.G., E.K.); The Bridge Institute, Dana and David Dornsife School of Letters, Arts, and Sciences, University of Southern California, Los Angeles, California (V.K., R.C.S.); and Chinese Academy of Sciences Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China (B.W., Q.Z.) kajacobs@helix.nih.gov. ; Molecular Recognition Section, Laboratory of Bioorganic Chemistry, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland (K.A.J., S.P., Z.-G.G., E.K.); The Bridge Institute, Dana and David Dornsife School of Letters, Arts, and Sciences, University of Southern California, Los Angeles, California (V.K., R.C.S.); and Chinese Academy of Sciences Key Laboratory of Receptor Research, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China (B.W., Q.Z.). Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 220 EP - 230 VL - 88 IS - 2 KW - Nucleotides KW - 0 KW - Purinergic P2Y Receptor Agonists KW - Receptors, Purinergic P2Y KW - Index Medicus KW - Models, Molecular KW - Humans KW - Structure-Activity Relationship KW - Protein Conformation KW - Binding Sites KW - Nucleotides -- metabolism KW - Purinergic P2Y Receptor Agonists -- chemistry KW - Receptors, Purinergic P2Y -- metabolism KW - Receptors, Purinergic P2Y -- chemistry KW - Purinergic P2Y Receptor Agonists -- metabolism KW - Nucleotides -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1690209322?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=Nucleotides+Acting+at+P2Y+Receptors%3A+Connecting+Structure+and+Function.&rft.au=Jacobson%2C+Kenneth+A%3BPaoletta%2C+Silvia%3BKatritch%2C+Vsevolod%3BWu%2C+Beili%3BGao%2C+Zhan-Guo%3BZhao%2C+Qiang%3BStevens%2C+Raymond+C%3BKiselev%2C+Evgeny&rft.aulast=Jacobson&rft.aufirst=Kenneth&rft.date=2015-08-01&rft.volume=88&rft.issue=2&rft.spage=220&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=1521-0111&rft_id=info:doi/10.1124%2Fmol.114.095711 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-10 N1 - Date created - 2015-06-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Curr Med Chem. 2006;13(3):289-312 [16475938] Pflugers Arch. 2006 Aug;452(5):563-72 [16688466] Pharmacol Rev. 2006 Sep;58(3):281-341 [16968944] J Biol Chem. 2006 Oct 20;281(42):31419-29 [16926152] Biochem J. 2007 Jul 15;405(2):277-86 [17338680] J Med Chem. 2007 Jul 12;50(14):3229-41 [17564423] Am J Respir Crit Care Med. 2007 Aug 15;176(4):362-9 [17446337] Bioorg Med Chem Lett. 2007 Nov 1;17(21):6013-8 [17827008] Proc Natl Acad Sci U S A. 2007 Oct 9;104(41):16359-64 [17913880] J Med Chem. 2008 Feb 28;51(4):1007-25 [18232657] Blood. 2012 Nov 22;120(22):4432-40 [22995898] J Thromb Haemost. 2012 Dec;10(12):2573-80 [23083103] Mol Pharmacol. 2013 Jan;83(1):256-66 [23093496] Purinergic Signal. 2013 Mar;9(1):59-66 [22892887] Biochem Pharmacol. 2013 Apr 1;85(7):991-8 [23333427] Mol Pharmacol. 2013 Apr;83(4):759-69 [23253448] J Med Chem. 2013 Jun 27;56(12):4938-52 [23751098] Biochem Biophys Res Commun. 2013 Jun 28;436(2):199-203 [23726915] J Med Chem. 2013 Feb 28;56(4):1704-14 [23368907] Cell Calcium. 2009 Oct;46(4):263-72 [19748117] Mol Pharmacol. 2009 Dec;76(6):1341-8 [19759354] J Med Chem. 2010 Jan 14;53(1):471-80 [19902968] Thromb Res. 2010 Feb;125(2):159-65 [19945153] J Bacteriol. 2010 Jun;192(12):3011-23 [20154123] J Med Chem. 2010 Jun 10;53(11):4488-501 [20446735] Drug Discov Today. 2010 Jul;15(13-14):570-8 [20594935] Eur J Pharmacol. 2010 Oct 10;644(1-3):10-6 [20599922] Exp Eye Res. 2011 Mar;92(3):221-6 [21147104] J Med Chem. 2011 Apr 28;54(8):2878-90 [21417463] Adv Pharmacol. 2011;61:263-99 [21586362] J Med Chem. 2011 Jun 23;54(12):4018-33 [21528910] FEBS J. 2012 Jan;279(1):180-91 [22044483] J Med Chem. 2012 Jan 12;55(1):437-48 [22107038] Biochem Biophys Res Commun. 2012 Jan 20;417(3):1035-40 [22214933] Purinergic Signal. 2012 Sep;8(3):437-502 [22555564] Exp Eye Res. 2012 Aug;101:49-55 [22677090] Chembiochem. 2012 Nov 5;13(16):2384-91 [22997138] Structure. 2012 Nov 7;20(11):1948-59 [23041369] Prog Brain Res. 1999;120:397-409 [10551014] J Biol Chem. 2000 Apr 14;275(15):10767-71 [10753868] Mol Pharmacol. 2000 May;57(5):926-31 [10779375] Pharmacol Ther. 2000 Aug-Sep;87(2-3):103-15 [11007994] J Biol Chem. 2001 Apr 13;276(15):11939-48 [11114308] Mol Pharmacol. 2001 Sep;60(3):432-9 [11502873] Eur J Pharmacol. 2001 Nov 2;430(2-3):203-10 [11711032] J Pharmacol Exp Ther. 2002 May;301(2):705-13 [11961076] J Pharmacol Exp Ther. 2002 Sep;302(3):871-80 [12183642] Mol Pharmacol. 2003 Oct;64(4):785-95 [14500734] J Med Chem. 2003 Nov 6;46(23):4974-87 [14584948] J Biol Chem. 2004 Mar 19;279(12):11456-64 [14670966] Biochem Pharmacol. 2004 Nov 15;68(10):2075-86 [15476678] J Med Chem. 2004 Oct 21;47(22):5393-404 [15481977] Proc Natl Acad Sci U S A. 1976 Nov;73(11):3984-8 [1069282] Drugs. 2013 Oct;73(15):1681-709 [24114622] Nature. 2013 Dec 5;504(7478):101-6 [24256733] PLoS One. 2014;9(4):e94780 [24722456] Nature. 2014 May 1;509(7498):119-22 [24784220] Nature. 2014 May 1;509(7498):115-8 [24670650] Trends Biochem Sci. 2014 May;39(5):233-44 [24767681] J Med Chem. 2014 May 8;57(9):3874-83 [24712832] J Med Chem. 2014 Jul 24;57(14):6150-64 [24931384] Neurosci Lett. 2014 Aug 22;578:80-4 [24970757] Proc Natl Acad Sci U S A. 2014 Nov 4;111(44):15821-6 [25341729] Nature. 2015 Apr 16;520(7547):317-21 [25822790] Bioorg Med Chem. 2015 Jul 15;23(14):4056-64 [25868749] Biochem Pharmacol. 2008 Mar 15;75(6):1341-7 [18199424] Bioorg Med Chem. 2008 Jun 15;16(12):6319-32 [18514530] Comb Chem High Throughput Screen. 2008 Jul;11(6):410-9 [18673269] Biochem Pharmacol. 2008 Nov 15;76(10):1201-13 [18809389] J Med Chem. 2009 May 14;52(9):2762-75 [19419204] Bioorg Med Chem Lett. 2009 Jun 1;19(11):3002-5 [19419868] Bioorg Med Chem. 2009 Jul 15;17(14):5298-311 [19502066] Br J Pharmacol. 2009 Aug;157(7):1142-53 [19563527] J Thromb Haemost. 2009 Sep;7(9):1556-65 [19552634] Proc Natl Acad Sci U S A. 1992 Mar 15;89(6):2370-3 [1549600] FEBS Lett. 1993 Jun 14;324(2):219-25 [8508924] Nature. 1994 Jan 13;367(6459):186-8 [8114917] J Biol Chem. 1995 Mar 3;270(9):4185-8 [7876172] Br J Pharmacol. 1995 Sep;116(1):1619-27 [8564228] Br J Pharmacol. 1996 Aug;118(8):1959-64 [8864529] Mol Pharmacol. 1996 Nov;50(5):1323-9 [8913364] Biochemistry. 1999 Mar 23;38(12):3498-507 [10090736] J Thromb Haemost. 2004 Nov;2(11):1980-8 [15550030] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/mol.114.095711 ER - TY - JOUR T1 - Differential DNA methylation profile of key genes in malignant prostate epithelial cells transformed by inorganic arsenic or cadmium. AN - 1686996451; 25922126 AB - Previous work shows altered methylation patterns in inorganic arsenic (iAs)- or cadmium (Cd)-transformed epithelial cells. Here, the methylation status near the transcriptional start site was assessed in the normal human prostate epithelial cell line (RWPE-1) that was malignantly transformed by 10μM Cd for 11weeks (CTPE) or 5μM iAs for 29weeks (CAsE-PE), at which time cells showed multiple markers of acquired cancer phenotype. Next generation sequencing of the transcriptome of CAsE-PE cells identified multiple dysregulated genes. Of the most highly dysregulated genes, five genes that can be relevant to the carcinogenic process (S100P, HYAL1, NTM, NES, ALDH1A1) were chosen for an in-depth analysis of the DNA methylation profile. DNA was isolated, bisulfite converted, and combined bisulfite restriction analysis was used to identify differentially methylated CpG sites, which was confirmed with bisulfite sequencing. Four of the five genes showed differential methylation in transformants relative to control cells that was inversely related to altered gene expression. Increased expression of HYAL1 (>25-fold) and S100P (>40-fold) in transformants was correlated with hypomethylation near the transcriptional start site. Decreased expression of NES (>15-fold) and NTM (>1000-fold) in transformants was correlated with hypermethylation near the transcriptional start site. ALDH1A1 expression was differentially expressed in transformed cells but was not differentially methylated relative to control. In conclusion, altered gene expression observed in Cd and iAs transformed cells may result from altered DNA methylation status. Published by Elsevier Inc. JF - Toxicology and applied pharmacology AU - Pelch, Katherine E AU - Tokar, Erik J AU - Merrick, B Alex AU - Waalkes, Michael P AD - National Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. ; Molecular Toxicology and Informatics Group, Biomolecular Screening Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Morrisville, NC 27560, USA. ; National Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. Electronic address: waalkes@niehs.nih.gov. Y1 - 2015/08/01/ PY - 2015 DA - 2015 Aug 01 SP - 159 EP - 167 VL - 286 IS - 3 KW - Cadmium KW - 00BH33GNGH KW - Arsenic KW - N712M78A8G KW - Index Medicus KW - Gene expression KW - Prostate cancer KW - DNA methylation KW - Inorganic arsenic KW - Humans KW - Cell Line, Transformed KW - Male KW - Cell Line KW - Prostate -- physiology KW - Prostate -- drug effects KW - Epithelial Cells -- physiology KW - Transcription, Genetic -- drug effects KW - Epithelial Cells -- drug effects KW - DNA Methylation -- physiology KW - Arsenic -- toxicity KW - Epithelial Cells -- pathology KW - DNA Methylation -- drug effects KW - Cadmium -- toxicity KW - Prostate -- pathology KW - Transcription, Genetic -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1686996451?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Differential+DNA+methylation+profile+of+key+genes+in+malignant+prostate+epithelial+cells+transformed+by+inorganic+arsenic+or+cadmium.&rft.au=Pelch%2C+Katherine+E%3BTokar%2C+Erik+J%3BMerrick%2C+B+Alex%3BWaalkes%2C+Michael+P&rft.aulast=Pelch&rft.aufirst=Katherine&rft.date=2015-08-01&rft.volume=286&rft.issue=3&rft.spage=159&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2015.04.011 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-17 N1 - Date created - 2015-06-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Prostate. 2001 Apr1;47(1):1-13 [11304724] Methods. 2001 Dec;25(4):402-8 [11846609] Bioinformatics. 2002 Nov;18(11):1427-31 [12424112] J Natl Cancer Inst. 2002 Dec 18;94(24):1888-91 [12488483] Mutat Res. 2003 Dec 10;533(1-2):107-20 [14643415] Toxicol Appl Pharmacol. 2005 Aug 15;206(3):288-98 [16039940] Cancer Res. 2007 Oct 1;67(19):9199-206 [17909025] Oncogene. 2007 Oct 4;26(45):6560-5 [17486081] Environ Health Perspect. 2007 Oct;115(10):1454-9 [17938735] Methods. 2008 Jan;44(1):47-54 [18158132] Int J Cancer. 2008 Jul 15;123(2):330-9 [18452169] J Biol Chem. 2008 Jul 11;283(28):19342-50 [18487201] Int J Cancer. 2004 Oct 20;112(1):121-9 [15305383] Sci China C Life Sci. 2004 Apr;47(2):158-64 [15379248] Proc Natl Acad Sci U S A. 1992 Mar 1;89(5):1827-31 [1542678] Nucleic Acids Res. 1997 Jun 15;25(12):2532-4 [9171110] Carcinogenesis. 1997 Jun;18(6):1215-23 [9214605] Toxicology. 1998 Mar 13;126(2):103-14 [9620542] Cell Mol Life Sci. 2004 Oct;61(19-20):2510-22 [15526158] Int J Cancer. 2005 Apr 10;114(3):346-55 [15551354] Epigenetics. 2012 Nov;7(11):1238-48 [22976526] Toxicol Appl Pharmacol. 2013 Dec 1;273(2):281-8 [23811327] Breast Cancer Res Treat. 2014 May;145(1):225-32 [24692081] J Cell Sci. 2014 May 15;127(Pt 10):2161-73 [24610946] Nucleic Acids Res. 2008 Jul 1;36(Web Server issue):W170-5 [18487274] Cancer Res. 2001 Jan 15;61(2):455-8 [11212230] Stem Cell Rev. 2008 Sep;4(3):193-201 [18563640] J Biol Chem. 2008 Oct 24;283(43):29215-27 [18718911] Stem Cells. 2009 May;27(5):1088-97 [19415779] Eur J Cancer. 2009 Nov;45(17):3104-18 [19818597] J Natl Cancer Inst. 2009 Dec 16;101(24):1670-81 [19933942] Fertil Steril. 2010 Mar 15;93(5):1615-1627.e18 [19473656] J Natl Cancer Inst. 2010 May 5;102(9):638-49 [20339138] BMC Bioinformatics. 2010;11:230 [20459626] Toxicol Sci. 2011 Jan;119(1):73-83 [20937726] Environ Health Perspect. 2011 Jan;119(1):11-9 [20682481] Stem Cell Rev. 2011 Jun;7(2):292-306 [21103958] Metallomics. 2011 Nov;3(11):1135-41 [21976018] J Cancer Res Clin Oncol. 2012 Jan;138(1):1-9 [21947242] Epigenomics. 2010 Feb;2(1):87-104 [20514360] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.taap.2015.04.011 ER - TY - JOUR T1 - Development, validation, and application of an ultra-performance liquid chromatography-sector field inductively coupled plasma mass spectrometry method for simultaneous determination of six organotin compounds in human serum. AN - 1686411147; 26048832 AB - Organotin compounds (OTCs) are heavily employed by industry for a wide variety of applications, including the production of plastics and as biocides. Reports of environmental prevalence, differential toxicity between OTCs, and poorly characterized human exposure have fueled the demand for sensitive, selective speciation methods. The objective of this investigation was to develop and validate a rapid, sensitive, and selective analytical method for the simultaneous determination of a suite of organotin compounds, including butyl (mono-, di-, and tri-substituted) and phenyl (mono-, di-, and tri-substituted) species in human serum. The analytical method utilized ultra-performance liquid chromatography (UPLC) coupled with sector field inductively coupled plasma mass spectrometry (SF-ICP-MS). The small (sub-2 µm) particle size of the UPLC column stationary phase and the sensitivity of the SF-ICP-MS enabled separation and sensitive determination of the analyte suite with a runtime of approximately 3 min. Validation activities included demonstration of method linearity over the concentration range of approximately 0.250-13.661 ng mL(-1), depending on the species; intraday precision of less than 21%, interday precision of less than 18%, intraday accuracy of -5.3% to 19%, and interday accuracy of -14% to 15% for all species; specificity, and matrix impact. In addition, sensitivity, and analyte stability under different storage scenarios were evaluated. Analyte stability was found to be limited for most species in freezer, refrigerator, and freeze-thaw conditions. The validated method was then applied for the determination of the OTCs in human serum samples from women participating in the Snart-Foraeldre/MiljØ (Soon-Parents/Environment) Study. The concentration of each OTC ranged from below the experimental limit of quantitation to 10.929 ng tin (Sn) mL(-1) serum. Speciation values were confirmed by a total Sn analysis. Copyright © 2015 Elsevier B.V. All rights reserved. JF - Talanta AU - Levine, Keith E AU - Young, Daniel J AU - Afton, Scott E AU - Harrington, James M AU - Essader, Amal S AU - Weber, Frank X AU - Fernando, Reshan A AU - Thayer, Kristina AU - Hatch, Elizabeth E AU - Robinson, Veronica G AU - Waidyanatha, Suramya AD - RTI International, Research Triangle Park, NC, United States. ; Division of National Toxicology Program, NIEHS, Research Triangle Park, NC, United States. ; Department of Epidemiology, Boston University School of Public Health, Boston, MA, United States. Y1 - 2015/08/01/ PY - 2015 DA - 2015 Aug 01 SP - 115 EP - 121 VL - 140 KW - Environmental Pollutants KW - 0 KW - Organotin Compounds KW - Index Medicus KW - Speciation KW - Metallomics KW - Serum KW - Biomonitoring KW - Ultra high pressure liquid chromatography KW - Inductively coupled plasma mass spectrometry KW - Organotin compounds KW - Humans KW - Linear Models KW - Limit of Detection KW - Chromatography, High Pressure Liquid -- methods KW - Mass Spectrometry -- methods KW - Environmental Pollutants -- blood KW - Organotin Compounds -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1686411147?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Talanta&rft.atitle=Development%2C+validation%2C+and+application+of+an+ultra-performance+liquid+chromatography-sector+field+inductively+coupled+plasma+mass+spectrometry+method+for+simultaneous+determination+of+six+organotin+compounds+in+human+serum.&rft.au=Levine%2C+Keith+E%3BYoung%2C+Daniel+J%3BAfton%2C+Scott+E%3BHarrington%2C+James+M%3BEssader%2C+Amal+S%3BWeber%2C+Frank+X%3BFernando%2C+Reshan+A%3BThayer%2C+Kristina%3BHatch%2C+Elizabeth+E%3BRobinson%2C+Veronica+G%3BWaidyanatha%2C+Suramya&rft.aulast=Levine&rft.aufirst=Keith&rft.date=2015-08-01&rft.volume=140&rft.issue=&rft.spage=115&rft.isbn=&rft.btitle=&rft.title=Talanta&rft.issn=1873-3573&rft_id=info:doi/10.1016%2Fj.talanta.2015.03.022 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-29 N1 - Date created - 2015-06-06 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.talanta.2015.03.022 ER - TY - JOUR T1 - Dopamine is a safe antiangiogenic drug which can also prevent 5-fluorouracil induced neutropenia. AN - 1681914712; 25556636 AB - The role of vascular endothelial growth factor A (VEGFA) in tumor angiogenesis is well established and accordingly, molecules targeting VEGFA or its receptors are being presently used in the clinics for treatment of several types of cancer. However, these antiangiogenic agents are expensive and have serious side effects. Thus identification of newer drugs with manageable systemic side effects or toxicities is of immense clinical importance. Since we have reported earlier that dopamine (DA) inhibits VEGFA induced angiogenesis in experimental tumor models, we therefore sought to investigate whether DA treatment results in similar toxicities like other antiangiogenic agents. Our results indicated that unlike sunitinib, another commonly used antiangiogenic agent in the clinics which targets VEGF receptors, DA [50 mg/kg/days × 7days intraperitoneally (i.p.)] not only could inhibit tumor angiogenesis and growth of HT29 human colon cancer and LLC (Lewis lung carcinoma) in mice, it also did not cause hypertension, hematological, renal and hepatic toxicities in normal, HT29 and LLC tumor bearing animals. Furthermore and interestingly, in contrast to the currently used antiangiogenic agents, DA also prevented 5-fluorouracil (5FU) induced neutropenia in HT29 colon cancer bearing mice. This action of DA was through inhibition of 5FU mediated suppression of colony forming unit-granulocyte macrophage colony forming units in the bone marrow. Thus our results indicate that DA may be safely used as an antiangiogenic drug for the treatment of malignant tumors. © 2014 UICC. JF - International journal of cancer AU - Sarkar, Chandrani AU - Chakroborty, Debanjan AU - Dasgupta, Partha Sarathi AU - Basu, Sujit AD - Department of Pathology, Ohio State University, Columbus, OH. ; Chittaranjan National Cancer Institute, Kolkata, 700026, India. Y1 - 2015/08/01/ PY - 2015 DA - 2015 Aug 01 SP - 744 EP - 749 VL - 137 IS - 3 KW - Angiogenesis Inhibitors KW - 0 KW - Antimetabolites, Antineoplastic KW - Fluorouracil KW - U3P01618RT KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - colon cancer KW - dopamine KW - lung cancer KW - toxicity KW - 5-FU KW - antiangiogenic drugs KW - Animals KW - Kidney -- metabolism KW - Humans KW - Kidney -- drug effects KW - Disease Models, Animal KW - Liver -- metabolism KW - Mice KW - Cell Line, Tumor KW - Liver Function Tests KW - Neovascularization, Pathologic -- drug therapy KW - Tumor Burden -- drug effects KW - Hematopoiesis -- drug effects KW - Liver -- drug effects KW - Xenograft Model Antitumor Assays KW - Blood Pressure -- drug effects KW - Colony-Forming Units Assay KW - Male KW - Fluorouracil -- adverse effects KW - Angiogenesis Inhibitors -- pharmacology KW - Dopamine -- pharmacology KW - Antimetabolites, Antineoplastic -- adverse effects KW - Neutropenia -- prevention & control KW - Neutropenia -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1681914712?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Dopamine+is+a+safe+antiangiogenic+drug+which+can+also+prevent+5-fluorouracil+induced+neutropenia.&rft.au=Sarkar%2C+Chandrani%3BChakroborty%2C+Debanjan%3BDasgupta%2C+Partha+Sarathi%3BBasu%2C+Sujit&rft.aulast=Sarkar&rft.aufirst=Chandrani&rft.date=2015-08-01&rft.volume=137&rft.issue=3&rft.spage=744&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.29414 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-05 N1 - Date created - 2015-05-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Curr Oncol Rep. 2012 Aug;14(4):285-94 [22544560] Clin J Oncol Nurs. 2013 Aug 1;17(4):425-33 [23899982] PLoS One. 2014;9(4):e93920 [24714590] Cell Metab. 2014 Aug 5;20(2):280-94 [25017943] Cancer Res. 1999 Oct 15;59(20):5209-18 [10537299] Nat Med. 2001 Nov;7(11):1194-201 [11689883] J Clin Invest. 2008 Apr;118(4):1380-9 [18340382] Clin Cancer Res. 2008 Apr 15;14(8):2502-10 [18413843] Curr Opin Investig Drugs. 2008 Dec;9(12):1324-35 [19037839] Ann Pharmacother. 2009 Mar;43(3):490-501 [19261963] Nat Rev Clin Oncol. 2009 Aug;6(8):465-77 [19581909] Hypertension. 2009 Sep;54(3):652-8 [19652084] MAbs. 2010 Mar-Apr;2(2):165-75 [20190566] Clin Cancer Res. 2011 Jun 1;17(11):3649-59 [21531818] Proc Natl Acad Sci U S A. 2011 Dec 20;108(51):20730-5 [22143796] AJR Am J Roentgenol. 2012 Jul;199(1):58-64 [22733894] Nat Med. 2001 May;7(5):569-74 [11329058] Anesthesiology. 2000 Feb;92(2):338-46 [10691218] Semin Oncol. 2002 Dec;29(6 Suppl 16):15-8 [12516034] Biotechniques. 2003 May;34(5):1048-50, 1052, 1054 passim [12765031] Clin Cancer Res. 2004 Jul 1;10(13):4349-56 [15240521] Am J Clin Oncol. 1986 Oct;9(5):403-10 [3776903] Nat Med. 1995 Jan;1(1):27-31 [7584949] J Thromb Haemost. 2005 Aug;3(8):1835-42 [16102050] Eur J Pharmacol. 2005 Oct 17;522(1-3):122-9 [16213483] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ijc.29414 ER - TY - JOUR T1 - Clinical predictive circulating peptides in rectal cancer patients treated with neoadjuvant chemoradiotherapy. AN - 1676612255; 25522009 AB - Preoperative chemoradiotherapy is worldwide accepted as a standard treatment for locally advanced rectal cancer. Current standard of treatment includes administration of ionizing radiation for 45-50.4 Gy in 25-28 fractions associated with 5-fluorouracil administration during radiation therapy. Unfortunately, 40% of patients have a poor or absent response and novel predictive biomarkers are demanding. For the first time, we apply a novel peptidomic methodology and analysis in rectal cancer patients treated with preoperative chemoradiotherapy. Circulating peptides (Molecular Weight <3 kDa) have been harvested from patients' plasma (n = 33) using nanoporous silica chip and analyzed by Matrix-Assisted Laser Desorption/Ionization-Time of Flight mass spectrometer. Peptides fingerprint has been compared between responders and non-responders. Random Forest classification selected three peptides at m/z 1082.552, 1098.537, and 1104.538 that were able to correctly discriminate between responders (n = 16) and non-responders (n = 17) before therapy (T0) providing an overall accuracy of 86% and an area under the receiver operating characteristic (ROC) curve of 0.92. In conclusion, the nanoporous silica chip coupled to mass spectrometry method was found to be a realistic method for plasma-based peptide analysis and we provide the first list of predictive circulating biomarker peptides in rectal cancer patients underwent preoperative chemoradiotherapy. © 2015 Wiley Periodicals, Inc. JF - Journal of cellular physiology AU - Crotti, Sara AU - Enzo, Maria Vittoria AU - Bedin, Chiara AU - Pucciarelli, Salvatore AU - Maretto, Isacco AU - Del Bianco, Paola AU - Traldi, Pietro AU - Tasciotti, Ennio AU - Ferrari, Mauro AU - Rizzolio, Flavio AU - Toffoli, Giuseppe AU - Giordano, Antonio AU - Nitti, Donato AU - Agostini, Marco AD - Experimental and Clinical Pharmacology Unit, Centro di Riferimento Oncologico, IRCCS National Cancer Institute, Aviano (PN), Italy; Istituto di Ricerca Pediatrica- Citt, à,, della Speranza, Corso Stati Uniti 4, Padova, Italy. Y1 - 2015/08// PY - 2015 DA - August 2015 SP - 1822 EP - 1828 VL - 230 IS - 8 KW - Biomarkers, Tumor KW - 0 KW - Peptides KW - Index Medicus KW - ROC Curve KW - Peptides -- blood KW - Area Under Curve KW - Aged, 80 and over KW - Humans KW - Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization KW - Enzyme-Linked Immunosorbent Assay KW - Aged KW - Middle Aged KW - Drug Resistance, Neoplasm KW - Male KW - Lab-On-A-Chip Devices KW - Female KW - Rectal Neoplasms -- therapy KW - Adenocarcinoma -- blood KW - Rectal Neoplasms -- blood KW - Neoadjuvant Therapy KW - Nanotechnology -- methods KW - Adenocarcinoma -- therapy KW - Chemoradiotherapy KW - Biomarkers, Tumor -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676612255?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+physiology&rft.atitle=Clinical+predictive+circulating+peptides+in+rectal+cancer+patients+treated+with+neoadjuvant+chemoradiotherapy.&rft.au=Crotti%2C+Sara%3BEnzo%2C+Maria+Vittoria%3BBedin%2C+Chiara%3BPucciarelli%2C+Salvatore%3BMaretto%2C+Isacco%3BDel+Bianco%2C+Paola%3BTraldi%2C+Pietro%3BTasciotti%2C+Ennio%3BFerrari%2C+Mauro%3BRizzolio%2C+Flavio%3BToffoli%2C+Giuseppe%3BGiordano%2C+Antonio%3BNitti%2C+Donato%3BAgostini%2C+Marco&rft.aulast=Crotti&rft.aufirst=Sara&rft.date=2015-08-01&rft.volume=230&rft.issue=8&rft.spage=1822&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+physiology&rft.issn=1097-4652&rft_id=info:doi/10.1002%2Fjcp.24894 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-15 N1 - Date created - 2015-04-28 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/jcp.24894 ER - TY - JOUR T1 - Proteomic Analysis of ABCA1-Null Macrophages Reveals a Role for Stomatin-Like Protein-2 in Raft Composition and Toll-Like Receptor Signaling AN - 1808642459; PQ0003436595 AB - Lipid raft membrane microdomains organize signaling by many prototypical receptors, including the Toll-like receptors (TLRs) of the innate immune system. Raft-localization of proteins is widely thought to be regulated by raft cholesterol levels, but this is largely on the basis of studies that have manipulated cell cholesterol using crude and poorly specific chemical tools, such as beta -cyclodextrins. To date, there has been no proteome-scale investigation of whether endogenous regulators of intracellular cholesterol trafficking, such as the ATP binding cassette (ABC)A1 lipid efflux transporter, regulate targeting of proteins to rafts. Abca1-/- macrophages have cholesterol-laden rafts that have been reported to contain increased levels of select proteins, including TLR4, the lipopolysaccharide receptor. Here, using quantitative proteomic profiling, we identified 383 proteins in raft isolates from Abca1+/+ and Abca1-/- macrophages. ABCA1 deletion induced wide-ranging changes to the raft proteome. Remarkably, many of these changes were similar to those seen in Abca1+/+ macrophages after lipopolysaccharide exposure. Stomatin-like protein (SLP)-2, a member of the stomatin-prohibitin-flotillin-HflK/C family of membrane scaffolding proteins, was robustly and specifically increased in Abca1-/- rafts. Pursuing SLP-2 function, we found that rafts of SLP-2-silenced macrophages had markedly abnormal composition. SLP-2 silencing did not compromise ABCA1-dependent cholesterol efflux but reduced macrophage responsiveness to multiple TLR ligands. This was associated with reduced raft levels of the TLR co-receptor, CD14, and defective lipopolysaccharide-induced recruitment of the common TLR adaptor, MyD88, to rafts. Taken together, we show that the lipid transporter ABCA1 regulates the protein repertoire of rafts and identify SLP-2 as an ABCA1-dependent regulator of raft composition and of the innate immune response. JF - Molecular and Cellular Proteomics AU - Chowdhury, Saiful M AU - Zhu, Xuewei AU - Aloor, Jim J AU - Azzam, Kathleen M AU - Gabor, Kristin A AU - Ge, William AU - Addo, Kezia A AU - Tomer, Kenneth B AU - Parks, John S AU - Fessler, Michael B AD - From the Laboratory of Respiratory Biology and, fesslerm@niehs.nih.gov Y1 - 2015/07/24/ PY - 2015 DA - 2015 Jul 24 SP - 1859 EP - 1870 PB - American Society for Biochemistry and Molecular Biology, 9650 Rockville Pike Bethesda MD 20814-3996 United States VL - 14 IS - 7 SN - 1535-9476, 1535-9476 KW - Biotechnology and Bioengineering Abstracts KW - Macrophages KW - MyD88 protein KW - ATP KW - ABCA1 protein KW - Cholesterol KW - CD14 antigen KW - Lipid rafts KW - adaptor proteins KW - ATP-binding protein KW - beta -Cyclodextrin KW - Lipopolysaccharides KW - Immune response KW - proteomics KW - TLR4 protein KW - Toll-like receptors KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808642459?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+Cellular+Proteomics&rft.atitle=Proteomic+Analysis+of+ABCA1-Null+Macrophages+Reveals+a+Role+for+Stomatin-Like+Protein-2+in+Raft+Composition+and+Toll-Like+Receptor+Signaling&rft.au=Chowdhury%2C+Saiful+M%3BZhu%2C+Xuewei%3BAloor%2C+Jim+J%3BAzzam%2C+Kathleen+M%3BGabor%2C+Kristin+A%3BGe%2C+William%3BAddo%2C+Kezia+A%3BTomer%2C+Kenneth+B%3BParks%2C+John+S%3BFessler%2C+Michael+B&rft.aulast=Chowdhury&rft.aufirst=Saiful&rft.date=2015-07-24&rft.volume=14&rft.issue=7&rft.spage=1859&rft.isbn=&rft.btitle=&rft.title=Molecular+and+Cellular+Proteomics&rft.issn=15359476&rft_id=info:doi/10.1074%2Fmcp.M114.045179 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Macrophages; MyD88 protein; ATP; ABCA1 protein; Cholesterol; CD14 antigen; Lipid rafts; adaptor proteins; beta -Cyclodextrin; ATP-binding protein; Lipopolysaccharides; proteomics; Immune response; TLR4 protein; Toll-like receptors DO - http://dx.doi.org/10.1074/mcp.M114.045179 ER - TY - JOUR T1 - α-Synuclein Shows High Affinity Interaction with Voltage-dependent Anion Channel, Suggesting Mechanisms of Mitochondrial Regulation and Toxicity in Parkinson Disease. AN - 1698964026; 26055708 AB - Participation of the small, intrinsically disordered protein α-synuclein (α-syn) in Parkinson disease (PD) pathogenesis has been well documented. Although recent research demonstrates the involvement of α-syn in mitochondrial dysfunction in neurodegeneration and suggests direct interaction of α-syn with mitochondria, the molecular mechanism(s) of α-syn toxicity and its effect on neuronal mitochondria remain vague. Here we report that at nanomolar concentrations, α-syn reversibly blocks the voltage-dependent anion channel (VDAC), the major channel of the mitochondrial outer membrane that controls most of the metabolite fluxes in and out of the mitochondria. Detailed analysis of the blockage kinetics of VDAC reconstituted into planar lipid membranes suggests that α-syn is able to translocate through the channel and thus target complexes of the mitochondrial respiratory chain in the inner mitochondrial membrane. Supporting our in vitro experiments, a yeast model of PD shows that α-syn toxicity in yeast depends on VDAC. The functional interactions between VDAC and α-syn, revealed by the present study, point toward the long sought after physiological and pathophysiological roles for monomeric α-syn in PD and in other α-synucleinopathies. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Rostovtseva, Tatiana K AU - Gurnev, Philip A AU - Protchenko, Olga AU - Hoogerheide, David P AU - Yap, Thai Leong AU - Philpott, Caroline C AU - Lee, Jennifer C AU - Bezrukov, Sergey M AD - From the Program in Physical Biology, Eunice Kennedy Shriver NICHD, National Institutes of Health, Bethesda, Maryland 20892, rostovtt@mail.nih.gov. ; From the Program in Physical Biology, Eunice Kennedy Shriver NICHD, National Institutes of Health, Bethesda, Maryland 20892, the Physics Department, University of Massachusetts, Amherst, Massachusetts 01003. ; the Liver Diseases Branch, NIDDK, National Institutes of Health, Bethesda, Maryland 20892. ; From the Program in Physical Biology, Eunice Kennedy Shriver NICHD, National Institutes of Health, Bethesda, Maryland 20892, the Center for Neutron Research, National Institute of Standards and Technology, Gaithersburg, Maryland 20899, and. ; the Laboratory of Molecular Biophysics, NHLBI, National Institutes of Health, Bethesda, Maryland 20892. ; From the Program in Physical Biology, Eunice Kennedy Shriver NICHD, National Institutes of Health, Bethesda, Maryland 20892. Y1 - 2015/07/24/ PY - 2015 DA - 2015 Jul 24 SP - 18467 EP - 18477 VL - 290 IS - 30 KW - Lipid Bilayers KW - 0 KW - alpha-Synuclein KW - Voltage-Dependent Anion Channel 1 KW - EC 1.6.- KW - Index Medicus KW - intrinsically disordered proteins KW - planar lipid bilayer KW - yeast KW - neurodegeneration KW - ion channel KW - alpha-synuclein KW - voltage-dependent anion channel (VDAC) KW - mitochondrial transport KW - Rats KW - Animals KW - Protein Interaction Maps KW - Nerve Degeneration -- metabolism KW - Humans KW - Nerve Degeneration -- pathology KW - Gene Expression Regulation KW - Protein Binding KW - Lipid Bilayers -- metabolism KW - Saccharomyces cerevisiae KW - Voltage-Dependent Anion Channel 1 -- genetics KW - alpha-Synuclein -- metabolism KW - Voltage-Dependent Anion Channel 1 -- metabolism KW - Parkinson Disease -- metabolism KW - Mitochondria -- pathology KW - Mitochondria -- metabolism KW - alpha-Synuclein -- genetics KW - Parkinson Disease -- pathology KW - Parkinson Disease -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698964026?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=%CE%B1-Synuclein+Shows+High+Affinity+Interaction+with+Voltage-dependent+Anion+Channel%2C+Suggesting+Mechanisms+of+Mitochondrial+Regulation+and+Toxicity+in+Parkinson+Disease.&rft.au=Rostovtseva%2C+Tatiana+K%3BGurnev%2C+Philip+A%3BProtchenko%2C+Olga%3BHoogerheide%2C+David+P%3BYap%2C+Thai+Leong%3BPhilpott%2C+Caroline+C%3BLee%2C+Jennifer+C%3BBezrukov%2C+Sergey+M&rft.aulast=Rostovtseva&rft.aufirst=Tatiana&rft.date=2015-07-24&rft.volume=290&rft.issue=30&rft.spage=18467&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M115.641746 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-19 N1 - Date created - 2015-07-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Pharmacol. 2015 Jan;87(1):1-8 [25332381] Chembiochem. 2014 Nov 24;15(17):2499-502 [25209675] Brain Res. 2014 Dec 3;1591:14-26 [25446002] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4897-902 [10781096] Neurosci Lett. 2002 Mar 8;320(3):146-50 [11852183] J Mol Neurosci. 2002 Jun;18(3):229-38 [12059041] Biochim Biophys Acta. 2003 Jun 10;1612(2):144-53 [12787932] Biochemistry. 2003 Jul 22;42(28):8530-40 [12859200] Science. 2003 Oct 31;302(5646):841 [14593171] Cell Biochem Biophys. 2003;39(3):279-92 [14716081] Nature. 2004 Jan 29;427(6973):461-5 [14749836] Mol Cell Biochem. 2004 Jan-Feb;256-257(1-2):107-15 [14977174] J Biol Chem. 2006 Dec 8;281(49):37496-506 [16990283] Neuroreport. 2007 Oct 8;18(15):1543-6 [17885598] J Am Chem Soc. 2007 Nov 14;129(45):14034-41 [17949000] Biochemistry. 2007 Dec 18;46(50):14369-79 [18031063] J Biol Chem. 2008 Mar 21;283(12):7554-60 [18192273] J Biol Chem. 2008 Apr 4;283(14):9089-100 [18245082] Exp Cell Res. 2008 Jun 10;314(10):2076-89 [18440504] J Neurochem. 2008 Oct;107(2):317-28 [18680555] Proc Natl Acad Sci U S A. 2008 Nov 18;105(46):17742-7 [18988731] J Neurosci. 2008 Nov 19;28(47):12305-17 [19020024] FEBS Lett. 2011 Jul 21;585(14):2363-6 [21722638] Biochim Biophys Acta. 2012 Feb;1818(2):162-71 [21819966] Biophys J. 2004 Nov;87(5):3162-71 [15507690] J Gen Physiol. 1973 Jun;61(6):687-708 [4541078] Biochim Biophys Acta. 1985 Jun 12;822(1):1-42 [2408671] Biophys J. 1987 Dec;52(6):1047-54 [2447968] J Membr Biol. 1989 Oct;111(2):103-11 [2482359] J Gen Physiol. 1990 Nov;96(5):921-42 [1704046] Methods Enzymol. 1991;194:3-21 [2005794] Neuron. 1995 Feb;14(2):467-75 [7857654] Biochemistry. 1996 Oct 29;35(43):13709-15 [8901511] J Biol Chem. 1996 Nov 8;271(45):28006-8 [8910409] Biophys J. 1997 May;72(5):1954-62 [9129800] Science. 1997 Jun 27;276(5321):2045-7 [9197268] Nature. 1997 Aug 28;388(6645):839-40 [9278044] Nat Genet. 1998 Feb;18(2):106-8 [9462735] J Biol Chem. 1998 Apr 17;273(16):9443-9 [9545270] FEBS Lett. 1998 Oct 9;436(3):309-12 [9801138] Nat Med. 1998 Nov;4(11):1318-20 [9809558] Biochem Biophys Res Commun. 2005 Jan 28;326(4):799-804 [15607740] Biophys J. 2005 Aug;89(2):1030-45 [15923222] J Bioenerg Biomembr. 2005 Jun;37(3):129-42 [16167170] Mol Cell Biol. 2005 Nov;25(22):10190-201 [16260631] Biochim Biophys Acta. 2006 Feb;1762(2):181-90 [16307870] Eur Biophys J. 2006 Dec;36(1):57-66 [17021806] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18746-51 [19033201] Proc Natl Acad Sci U S A. 2008 Dec 16;105(50):19720-5 [19060213] Neurosci Lett. 2009 May 1;454(3):187-92 [19429081] Dis Model Mech. 2010 Mar-Apr;3(3-4):194-208 [20038714] J Phys Chem B. 2010 Apr 8;114(13):4615-22 [20229987] FEBS Lett. 2010 Apr 16;584(8):1571-6 [20226185] Mol Aspects Med. 2010 Jun;31(3):227-85 [20346371] Biochim Biophys Acta. 2010 Jun-Jul;1797(6-7):1268-75 [20138821] Cancer Res. 2010 Dec 15;70(24):10192-201 [21159641] J Biol Chem. 2011 Jun 10;286(23):20710-26 [21489994] Mitochondrion. 2012 Jan;12(1):24-34 [21530686] Prog Mol Biol Transl Sci. 2012;107:125-88 [22482450] Biochim Biophys Acta. 2012 Jun;1818(6):1444-50 [22062421] Biochim Biophys Acta. 2012 Jun;1818(6):1526-35 [22100746] Cell. 2012 May 25;149(5):1048-59 [22632969] J Pharmacol Exp Ther. 2012 Sep;342(3):637-41 [22700429] J Neurol Sci. 2012 Nov 15;322(1-2):254-62 [22669122] PLoS One. 2013;8(2):e55848 [23393603] Cell Death Differ. 2013 Mar;20(3):465-77 [23154387] Acta Biochim Biophys Sin (Shanghai). 2013 Mar;45(3):170-8 [23291291] Neurology. 2013 Mar 12;80(11):1062-4 [23427326] Proc Natl Acad Sci U S A. 2013 Apr 9;110(15):5887-92 [23530243] Neurotherapeutics. 2013 Jul;10(3):391-9 [23512373] EMBO J. 2013 Nov 27;32(23):3041-54 [24129513] Biophys J. 2014 Feb 4;106(3):556-65 [24507596] Neurobiol Aging. 2014 May;35(5):1132-52 [24325796] Biochim Biophys Acta. 2014 May;1838(5):1362-71 [24412217] Science. 2014 May 30;344(6187):1023-8 [24876496] J Biol Chem. 2014 Aug 1;289(31):21490-507 [24942732] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M115.641746 ER - TY - JOUR T1 - Incidence of solid tumours among pesticide applicators exposed to the organophosphate insecticide diazinon in the Agricultural Health Study: an updated analysis AN - 1808632960; PQ0003435541 AB - ObjectiveDiazinon, a common organophosphate insecticide with genotoxic properties, was previously associated with lung cancer in the Agricultural Health Study (AHS) cohort, but few other epidemiological studies have examined diazinon-associated cancer risk. We used updated diazinon exposure and cancer incidence information to evaluate solid tumour risk in the AHS.MethodsMale pesticide applicators in Iowa and North Carolina reported lifetime diazinon use at enrolment (1993-1997) and follow-up (1998-2005); cancer incidence was assessed through 2010(North Carolina)/2011(Iowa). Among applicators with usage information sufficient to evaluate exposure-response patterns, we used Poisson regression to estimate adjusted rate ratios (RRs) and 95% CI for cancer sites with greater than or equal to 10 exposed cases for both lifetime (LT) exposure days and intensity-weighted (IW) lifetime exposure days (accounting for factors impacting exposure).ResultsWe observed elevated lung cancer risks (N=283) among applicators with the greatest number of LT (RR=1.60; 95% CI 1.11 to 2.31; Ptrend=0.02) and IW days of diazinon use (RR=1.41; 95% CI 0.98 to 2.04; Ptrend=0.08). Kidney cancer (N=94) risks were non-significantly elevated (RRLT days=1.77; 95% CI 0.90 to 3.51; Ptrend=0.09; RRIW days 1.37; 95% CI 0.64 to 2.92; Ptrend=0.50), as were risks for aggressive prostate cancer (N=656).ConclusionsOur updated evaluation of diazinon provides additional evidence of an association with lung cancer risk. Newly identified links to kidney cancer and associations with aggressive prostate cancer require further evaluation. JF - Occupational and Environmental Medicine AU - Jones, Rena R AU - Barone-Adesi, Francesco AU - Koutros, Stella AU - Lerro, Catherine C AU - Blair, Aaron AU - Lubin, Jay AU - Heltshe, Sonya L AU - Hoppin, Jane A AU - Alavanja, Michael C R AU - Beane Freeman, Laura E AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA Y1 - 2015/07/23/ PY - 2015 DA - 2015 Jul 23 SP - 496 EP - 503 PB - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom VL - 72 IS - 7 SN - 1351-0711, 1351-0711 KW - Health & Safety Science Abstracts KW - diazinon KW - insecticides KW - organophosphate KW - neoplasms KW - Risk assessment KW - ANW, USA, North Carolina KW - Organophosphates KW - Genotoxicity KW - Cancer KW - Health risks KW - Insecticides KW - Prostate cancer KW - USA, Iowa KW - Dose-response effects KW - Risk factors KW - Pesticides KW - Kidney KW - Diazinon KW - Lung cancer KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808632960?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+Environmental+Medicine&rft.atitle=Incidence+of+solid+tumours+among+pesticide+applicators+exposed+to+the+organophosphate+insecticide+diazinon+in+the+Agricultural+Health+Study%3A+an+updated+analysis&rft.au=Jones%2C+Rena+R%3BBarone-Adesi%2C+Francesco%3BKoutros%2C+Stella%3BLerro%2C+Catherine+C%3BBlair%2C+Aaron%3BLubin%2C+Jay%3BHeltshe%2C+Sonya+L%3BHoppin%2C+Jane+A%3BAlavanja%2C+Michael+C+R%3BBeane+Freeman%2C+Laura+E&rft.aulast=Jones&rft.aufirst=Rena&rft.date=2015-07-23&rft.volume=72&rft.issue=7&rft.spage=496&rft.isbn=&rft.btitle=&rft.title=Occupational+and+Environmental+Medicine&rft.issn=13510711&rft_id=info:doi/10.1136%2Foemed-2014-102728 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Risk assessment; Organophosphates; Genotoxicity; Cancer; Health risks; Prostate cancer; Insecticides; Risk factors; Dose-response effects; Pesticides; Kidney; Diazinon; Lung cancer; ANW, USA, North Carolina; USA, Iowa DO - http://dx.doi.org/10.1136/oemed-2014-102728 ER - TY - JOUR T1 - CLIP2 as radiation biomarker in papillary thyroid carcinoma. AN - 1698961279; 25284583 AB - A substantial increase in papillary thyroid carcinoma (PTC) among children exposed to the radioiodine fallout has been one of the main consequences of the Chernobyl reactor accident. Recently, the investigation of PTCs from a cohort of young patients exposed to the post-Chernobyl radioiodine fallout at very young age and a matched nonexposed control group revealed a radiation-specific DNA copy number gain on chromosomal band 7q11.23 and the radiation-associated mRNA overexpression of CLIP2. In this study, we investigated the potential role of CLIP2 as a radiation marker to be used for the individual classification of PTCs into CLIP2-positive and -negative cases-a prerequisite for the integration of CLIP2 into epidemiological modelling of the risk of radiation-induced PTC. We were able to validate the radiation-associated CLIP2 overexpression at the protein level by immunohistochemistry (IHC) followed by relative quantification using digital image analysis software (P=0.0149). Furthermore, we developed a standardized workflow for the determination of CLIP2-positive and -negative cases that combines visual CLIP2 IHC scoring and CLIP2 genomic copy number status. In addition to the discovery cohort (n=33), two independent validation cohorts of PTCs (n=115) were investigated. High sensitivity and specificity rates for all three investigated cohorts were obtained, demonstrating robustness of the developed workflow. To analyse the function of CLIP2 in radiation-associated PTC, the CLIP2 gene regulatory network was reconstructed using global mRNA expression data from PTC patient samples. The genes comprising the first neighbourhood of CLIP2 (BAG2, CHST3, KIF3C, NEURL1, PPIL3 and RGS4) suggest the involvement of CLIP2 in the fundamental carcinogenic processes including apoptosis, mitogen-activated protein kinase signalling and genomic instability. In our study, we successfully developed and independently validated a workflow for the typing of PTC clinical samples into CLIP2-positive and CLIP2-negative and provided first insights into the CLIP2 interactome in the context of radiation-associated PTC. JF - Oncogene AU - Selmansberger, M AU - Feuchtinger, A AU - Zurnadzhy, L AU - Michna, A AU - Kaiser, J C AU - Abend, M AU - Brenner, A AU - Bogdanova, T AU - Walch, A AU - Unger, K AU - Zitzelsberger, H AU - Hess, J AD - Research Unit Radiation Cytogenetics, Helmholtz Zentrum München, German Research Center for Environmental Health GmbH, Neuherberg, Germany. ; Research Unit Analytical Pathology, Helmholtz Zentrum München, German Research Center for Environmental Health GmbH, Neuherberg, Germany. ; Institute of Endocrinology and Metabolism, National Academy of Medical Sciences of the Ukraine, Kiev, Ukraine. ; Institute of Radiation Protection, Helmholtz Zentrum München, German Research Center for Environmental Health GmbH, Neuherberg, Germany. ; Bundeswehr Institute of Radiobiology, Munich, Germany. ; Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, NCI, Bethesda, MD, USA. Y1 - 2015/07/23/ PY - 2015 DA - 2015 Jul 23 SP - 3917 EP - 3925 VL - 34 IS - 30 KW - Biomarkers, Tumor KW - 0 KW - Iodine Radioisotopes KW - Microtubule-Associated Proteins KW - Radioactive Fallout KW - cytoplasmic linker protein 115 KW - Index Medicus KW - Infant KW - Chernobyl Nuclear Accident KW - Humans KW - Ukraine KW - Gene Regulatory Networks KW - Environmental Exposure KW - Case-Control Studies KW - Child KW - Adolescent KW - Iodine Radioisotopes -- toxicity KW - Child, Preschool KW - Biomarkers, Tumor -- metabolism KW - Microtubule-Associated Proteins -- metabolism KW - Thyroid Neoplasms -- metabolism KW - Neoplasms, Radiation-Induced -- metabolism KW - Carcinoma, Papillary -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698961279?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=CLIP2+as+radiation+biomarker+in+papillary+thyroid+carcinoma.&rft.au=Selmansberger%2C+M%3BFeuchtinger%2C+A%3BZurnadzhy%2C+L%3BMichna%2C+A%3BKaiser%2C+J+C%3BAbend%2C+M%3BBrenner%2C+A%3BBogdanova%2C+T%3BWalch%2C+A%3BUnger%2C+K%3BZitzelsberger%2C+H%3BHess%2C+J&rft.aulast=Selmansberger&rft.aufirst=M&rft.date=2015-07-23&rft.volume=34&rft.issue=30&rft.spage=3917&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2014.311 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-09 N1 - Date created - 2015-07-23 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/onc.2014.311 ER - TY - JOUR T1 - Metabolic Polymorphisms and Clinical Findings Related to Benzene Poisoning Detected in Exposed Brazilian Gas-Station Workers. AN - 1699490997; 26197327 AB - Benzene is a ubiquitous environmental pollutant and an important industrial chemical present in both gasoline and motor vehicle emissions. Occupational human exposure to benzene occurs in the petrochemical and petroleum refining industries as well as in gas-station workers, where it can lead to benzene poisoning (BP), but the mechanisms of BP are not completely understood. In Brazil, a significant number of gas-station service workers are employed. The aim of the present study was to evaluate alterations related to BP and metabolic polymorphisms in gas-station service workers exposed to benzene in the city of Rio de Janeiro, Brazil. Occupational exposure was based on clinical findings related to BP, and metabolic polymorphisms in 114 Brazilian gas-station attendants. These workers were divided into No Clinical Findings (NCF) and Clinical Findings (CF) groups. Neutrophil and Mean Corpuscular Volume (MCV) showed a significant difference between the two study groups, and neutrophil has the greatest impact on the alterations suggestive of BP. The clinical findings revealed higher frequencies of symptoms in the CF group, although not all members presented statistical significance. The frequencies of alleles related to risk were higher in the CF group for GSTM1, GSTT1, CYP2E1 7632T > A, but lower for NQO1 and CYP2E1 1053C > T genotypes. Moreover, an association was found between GSTM1 null and alterations related to BP, but we did not observe any effects of other polymorphisms. Variations in benzene metabolizing genes may modify benzene toxicity and should be taken into consideration during risk assessment evaluations. JF - International journal of environmental research and public health AU - Mitri, Simone AU - Fonseca, Antônio Sérgio Almeida AU - Otero, Ubirani Barros AU - Tabalipa, Marianne Medeiros AU - Moreira, Josino Costa AU - Sarcinelli, Paula de Novaes AD - Toxicology Laboratory, Center for Studies of Worker's Health and Human Ecology, Oswaldo Cruz Foundation, Rio de Janeiro 21041-210, Brazil. simitri@ensp.fiocruz.br. ; Medical Ambulatory, Center for Studies of Worker's Health and Human Ecology, Oswaldo Cruz Foundation, Rio de Janeiro 21041-210, Brazil. antoniosergio@ensp.fiocruz.br. ; Technical Unit of Occupational Exposure, Environmental and Cancer, Prevention and Surveillance Coordination, National Cancer Institute, Rio de Janeiro 20230-130, Brazil. uotero@inca.gov.br. ; Technical Unit of Occupational Exposure, Environmental and Cancer, Prevention and Surveillance Coordination, National Cancer Institute, Rio de Janeiro 20230-130, Brazil. mtabalipa@yahoo.com. ; Toxicology Laboratory, Center for Studies of Worker's Health and Human Ecology, Oswaldo Cruz Foundation, Rio de Janeiro 21041-210, Brazil. josinocm@fiocruz.br. ; Toxicology Laboratory, Center for Studies of Worker's Health and Human Ecology, Oswaldo Cruz Foundation, Rio de Janeiro 21041-210, Brazil. paula@ensp.fiocruz.br. Y1 - 2015/07/21/ PY - 2015 DA - 2015 Jul 21 SP - 8434 EP - 8447 VL - 12 IS - 7 KW - Air Pollutants, Occupational KW - 0 KW - Cytochrome P-450 CYP2E1 KW - EC 1.14.13.- KW - Glutathione Transferase KW - EC 2.5.1.18 KW - Benzene KW - J64922108F KW - Index Medicus KW - benzene metabolism KW - benzene poisoning KW - genetic polymorphisms KW - gas station worker KW - occupational health KW - Young Adult KW - Genetic Variation KW - Cross-Sectional Studies KW - Polymorphism, Genetic KW - Humans KW - Brazil KW - Adult KW - Middle Aged KW - Male KW - Female KW - Benzene -- metabolism KW - Glutathione Transferase -- metabolism KW - Air Pollutants, Occupational -- adverse effects KW - Oil and Gas Industry KW - Occupational Exposure -- adverse effects KW - Glutathione Transferase -- genetics KW - Cytochrome P-450 CYP2E1 -- metabolism KW - Cytochrome P-450 CYP2E1 -- genetics KW - Benzene -- poisoning UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1699490997?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+environmental+research+and+public+health&rft.atitle=Metabolic+Polymorphisms+and+Clinical+Findings+Related+to+Benzene+Poisoning+Detected+in+Exposed+Brazilian+Gas-Station+Workers.&rft.au=Mitri%2C+Simone%3BFonseca%2C+Ant%C3%B4nio+S%C3%A9rgio+Almeida%3BOtero%2C+Ubirani+Barros%3BTabalipa%2C+Marianne+Medeiros%3BMoreira%2C+Josino+Costa%3BSarcinelli%2C+Paula+de+Novaes&rft.aulast=Mitri&rft.aufirst=Simone&rft.date=2015-07-21&rft.volume=12&rft.issue=7&rft.spage=8434&rft.isbn=&rft.btitle=&rft.title=International+journal+of+environmental+research+and+public+health&rft.issn=1660-4601&rft_id=info:doi/10.3390%2Fijerph120708434 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-03 N1 - Date created - 2015-07-22 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Rev Saude Publica. 1993 Apr;27(2):145-51 [8278783] Chem Biol Interact. 2010 Mar 19;184(1-2):189-95 [20026321] Cancer Res. 1997 Jul 15;57(14):2839-42 [9230185] Cancer Epidemiol Biomarkers Prev. 2004 Nov;13(11 Pt 1):1729-35 [15533900] Drug Metab Rev. 2004 Oct;36(3-4):531-47 [15554234] Science. 2004 Dec 3;306(5702):1774-6 [15576619] Chem Biol Interact. 2005 May 30;153-154:75-83 [15935802] Braz J Med Biol Res. 2006 Feb;39(2):195-201 [16470306] Toxicol Lett. 2006 Apr 10;162(2-3):146-52 [16289653] Xenobiotica. 2007 Jan;37(1):103-12 [17178637] Sci Total Environ. 2007 Mar 15;374(2-3):183-98 [17261327] Mutat Res. 2011 Feb 3;719(1-2):7-13 [20951227] Mutat Res. 2012 Sep 18;747(2):218-27 [22617435] Toxicol Lett. 2012 Aug 13;213(1):57-62 [21300142] Toxicol Lett. 2012 Aug 13;213(1):63-8 [22173199] Int J Hyg Environ Health. 2013 Jun;216(3):324-32 [23088855] Carcinogenesis. 2008 Dec;29(12):2325-9 [18784359] Toxicol Lett. 2008 Nov 10;182(1-3):7-17 [18848868] Int Arch Occup Environ Health. 2009 Aug;82(8):985-95 [19009306] Environ Mol Mutagen. 2010 Jan;51(1):48-56 [19593802] Toxicol Lett. 2010 Jan 15;192(1):29-33 [19900514] J Toxicol Environ Health B Crit Rev. 2009;12(5-6):362-88 [20183527] Toxicol Lett. 2010 Apr 1;193(3):229-35 [20100551] Pharmacogenetics. 1999 Aug;9(4):445-51 [10780264] Mutat Res. 2000 Oct;463(3):285-308 [11018745] J Toxicol Environ Health A. 2000 Nov;61(5-6):339-46 [11086937] J Toxicol Environ Health A. 2000 Nov;61(5-6):357-72 [11086940] Occup Med (Lond). 2000 Sep;50(7):508-11 [11198676] Am J Ind Med. 2002 Oct;42(4):275-85 [12271475] Environ Health Perspect. 2002 Dec;110(12):1213-8 [12460800] Genet Mol Res. 2002;1(3):233-40 [14963830] Environ Mol Mutagen. 2004;43(2):100-9 [14991750] Environ Health Perspect. 2007 Jan;115(1):28-34 [17366815] Pharmacogenet Genomics. 2007 Oct;17(10):789-801 [17885617] J Toxicol Environ Health A. 2008;71(5):333-41 [18214807] Occup Environ Med. 2008 Jun;65(6):371-8 [18417556] Mutagenesis. 2008 Sep;23(5):415-22 [18550589] PLoS One. 2013;8(10):e76262 [24098457] Ann N Y Acad Sci. 2014 Mar;1310:74-83 [24571325] Int J Hyg Environ Health. 2014 Sep;217(7):726-32 [24698387] Br Med Bull. 2014 Sep;111(1):89-100 [25114269] Cien Saude Colet. 2014 Dec;19(12):4637-48 [25388172] Toxicol Lett. 2014 Dec 1;231(2):205-12 [24968062] Chem Biol Interact. 2010 Mar 19;184(1-2):58-66 [20056112] Toxicol Lett. 2014 Dec 1;231(2):194-204 [25447454] Annu Rev Public Health. 2010;31:133-48 2 p following 148 [20070208] Pathol Res Pract. 1994 Feb;190(2):151-4 [8058569] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3390/ijerph120708434 ER - TY - JOUR T1 - Activated platelet-T-cell conjugates in peripheral blood of patients with HIV infection: coupling coagulation/inflammation and T cells AN - 1808707439; PQ0003241778 AB - Background: Despite successfully suppressed viremia by treatment, patients with high levels of biomarkers of coagulation/inflammation are at an increased risk of developing non-AIDS defining serious illnesses such as cardiovascular diseases. Thus, there is a relationship between persistent immune activation and coagulation/inflammation, although the mechanisms are poorly understood. Platelets play an important role in this process. Although interactions between platelets and elements of the innate immune system, such as monocytes, are well described, little is known about the interaction between platelets and the adaptive immune system. Design: We investigated the interaction of a component of the coagulation system, platelets, and the adaptive immune system T cells. Methods: Healthy controls and combination antiretroviral therapy (cART)-treated HIV-infected patients with viral loads of less than 40copies/ml for more than 15 months were analysed for platelet-T-cell conjugate formation. Results: Platelets can form conjugates with T cells and were preferentially seen in CD4 super(+) and CD8 super(+) T-cell subsets with more differentiated phenotypes [memory, memory/effector and terminal effector memory (TEM)]. Compared with healthy controls, these conjugates in patients with HIV infection were more frequent, more often composed of activated platelets (CD42b super(+) CD62P super(+)), and were significantly associated with the D-dimer serum levels. Conclusion: These data support a model in which platelet-T-cell conjugates may play a critical role in the fast recruitment of antigen-experienced T cells to the place of injury. This mechanism can contribute in maintaining a state of coagulation/inflammation observed in these patients contributing to the pathology of the disease. JF - AIDS AU - Green, Samantha A AU - Smith, Mindy AU - Hasley, Rebecca B AU - Stephany, David AU - Harned, Adam AU - Nagashima, Kunio AU - Abdullah, Shahed AU - Pittaluga, Stefania AU - Imamichi, Tomozumi AU - Qin, Jing AU - Rupert, Adam AU - Ober, Alex AU - Lane, H Clifford AU - Catalfamo, Marta AD - CMRS/Laboratory of Immunoregulation, catalfam@mail.nih.gov Y1 - 2015/07/17/ PY - 2015 DA - 2015 Jul 17 SP - 1297 EP - 1308 PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 29 IS - 11 SN - 0269-9370, 0269-9370 KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - coagulation/inflammation and T cells KW - HIV infection KW - platelet-T-cell conjugates KW - Acquired immune deficiency syndrome KW - Pathology KW - Injuries KW - Immune system KW - Infection KW - CD4 antigen KW - Lymphocytes T KW - Monocytes KW - Bioindicators KW - Data processing KW - Coagulation KW - Recruitment KW - antiretroviral therapy KW - Memory cells KW - Peripheral blood KW - CD8 antigen KW - Antiretroviral agents KW - biomarkers KW - Inflammation KW - Serum levels KW - Human immunodeficiency virus KW - Platelets KW - Viremia KW - Cardiovascular diseases KW - V 22360:AIDS and HIV KW - H 11000:Diseases/Injuries/Trauma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808707439?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Activated+platelet-T-cell+conjugates+in+peripheral+blood+of+patients+with+HIV+infection%3A+coupling+coagulation%2Finflammation+and+T+cells&rft.au=Green%2C+Samantha+A%3BSmith%2C+Mindy%3BHasley%2C+Rebecca+B%3BStephany%2C+David%3BHarned%2C+Adam%3BNagashima%2C+Kunio%3BAbdullah%2C+Shahed%3BPittaluga%2C+Stefania%3BImamichi%2C+Tomozumi%3BQin%2C+Jing%3BRupert%2C+Adam%3BOber%2C+Alex%3BLane%2C+H+Clifford%3BCatalfamo%2C+Marta&rft.aulast=Green&rft.aufirst=Samantha&rft.date=2015-07-17&rft.volume=29&rft.issue=11&rft.spage=1297&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000701 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-04 N1 - SubjectsTermNotLitGenreText - Data processing; Coagulation; Injuries; Immune system; antiretroviral therapy; Memory cells; Peripheral blood; CD8 antigen; Infection; biomarkers; Inflammation; Serum levels; CD4 antigen; Platelets; Lymphocytes T; Monocytes; Cardiovascular diseases; Viremia; Bioindicators; Acquired immune deficiency syndrome; Pathology; Human immunodeficiency virus; Recruitment; Antiretroviral agents DO - http://dx.doi.org/10.1097/QAD.0000000000000701 ER - TY - JOUR T1 - Differences in Risk Factors for Recurrent Versus Incident Preterm Delivery AN - 1717491949; PQ0001938037 AB - Risk factors for preterm delivery have been described, but whether risk factors differ in the context of prior preterm delivery history is less understood. We assessed whether known risk factors were different in women with versus without prior preterm delivery using medical records of the first and second singleton deliveries in 25,820 Utah women (2002-2010). Longitudinal transition models with modified Poisson regression calculated adjusted relative risks and 95% confidence intervals, with multiplicative interactions between each preterm risk factor and prior preterm delivery status to explore whether risk factors varied between incident and recurrent preterm delivery at <37 weeks. Fewer second pregnancy factors were associated with recurrent preterm delivery, including alcohol, thyroid disease, and depression. Smoking was associated with increased risk for incident (relative risk (RR) = 1.95, 95% confidence interval (CI): 1.53, 2.49) but not recurrent (RR = 1.09, 95% CI: 0.71, 1.19) preterm delivery, whereas alcohol was associated with an increased risk for recurrent (RR = 2.38, 95% CI: 1.53, 3.71) but not incident (RR = 0.98, 95% CI: 0.67, 1.43; P sub(interaction) = 0.02 and <0.01) preterm delivery, respectively. Prior term delivery did not necessarily confer protection from known second pregnancy preterm delivery risk factors. In the setting of a prior preterm delivery, many risk factors did not persist. Prior preterm delivery history is important when assessing subsequent preterm delivery risk factors. JF - American Journal of Epidemiology AU - Grantz, Katherine L AU - Hinkle, Stefanie N AU - Mendola, Pauline AU - Sjaarda, Lindsey A AU - Leishear, Kira AU - Albert, Paul S AD - Correspondence to Dr. Katherine L. Grantz, Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6100 Executive Boulevard, Room 7B03, Rockville, MD 20852, katherine.grantz@nih.gov Y1 - 2015/07/15/ PY - 2015 DA - 2015 Jul 15 SP - 157 EP - 167 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 182 IS - 2 SN - 0002-9262, 0002-9262 KW - Risk Abstracts; Health & Safety Science Abstracts KW - birth intervals KW - premature birth KW - reproductive history KW - USA, Utah KW - Risk assessment KW - Alcohol KW - Historical account KW - Smoking KW - Depression KW - Risk factors KW - Thyroid KW - Pregnancy KW - H 12000:Epidemiology and Public Health KW - R2 23110:Psychological aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1717491949?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Differences+in+Risk+Factors+for+Recurrent+Versus+Incident+Preterm+Delivery&rft.au=Grantz%2C+Katherine+L%3BHinkle%2C+Stefanie+N%3BMendola%2C+Pauline%3BSjaarda%2C+Lindsey+A%3BLeishear%2C+Kira%3BAlbert%2C+Paul+S&rft.aulast=Grantz&rft.aufirst=Katherine&rft.date=2015-07-15&rft.volume=182&rft.issue=2&rft.spage=157&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwv032 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-10-28 N1 - SubjectsTermNotLitGenreText - Risk assessment; Smoking; Historical account; Alcohol; Depression; Risk factors; Thyroid; Pregnancy; USA, Utah DO - http://dx.doi.org/10.1093/aje/kwv032 ER - TY - JOUR T1 - A long-term efficacy study of gene replacement therapy for RPGR-associated retinal degeneration. AN - 1691017551; 25877300 AB - Mutations in the retinitis pigmentosa GTPase regulator (RPGR) gene account for >70% of X-linked retinitis pigmentosa (XLRP) and 15-20% of all inherited retinal degeneration. Gene replacement therapy for RPGR-XLRP was hampered by the relatively slow disease progression in mouse models and by difficulties in cloning the full-length RPGR-ORF15 cDNA that includes a purine-rich 3'-coding region; however, its effectiveness has recently been demonstrated in four dogs with RPGR mutations. To advance the therapy to clinical stage, we generated new stable vectors in AAV8 or AAV9 carrying mouse and human full-length RPGR-ORF15-coding sequence and conducted a comprehensive long-term dose-efficacy study in Rpgr-knockout mice. After validating their ability to produce full-length proteins that localize to photoreceptor connecting cilia, we evaluated various vector doses in mice during a 2-year study. We demonstrate that eyes treated with a single injection of mouse or human RPGR-ORF15 vector at an optimal dose maintained the expression of RPGR-ORF15 throughout the study duration and exhibited higher electroretinogram amplitude, thicker photoreceptor layer and better targeting of opsins to outer segments compared with sham-treated eyes. Furthermore, mice that received treatment at an advanced age also showed remarkable preservation of retinal structure and function. Retinal toxicity was observed at high vector doses, highlighting the importance of careful dose optimization in future clinical experiments. Our long-term dose-efficacy study should facilitate the design of human trials with human RPGR-ORF15 vector as a clinical candidate. Published by Oxford University Press 2015. This work is written by (a) US Government employee(s) and is in the public domain in the US. JF - Human molecular genetics AU - Wu, Zhijian AU - Hiriyanna, Suja AU - Qian, Haohua AU - Mookherjee, Suddhasil AU - Campos, Maria M AU - Gao, Chun AU - Fariss, Robert AU - Sieving, Paul A AU - Li, Tiansen AU - Colosi, Peter AU - Swaroop, Anand AD - National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA wuzh@mail.nih.gov swaroopa@nei.nih.gov. ; National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2015/07/15/ PY - 2015 DA - 2015 Jul 15 SP - 3956 EP - 3970 VL - 24 IS - 14 KW - Carrier Proteins KW - 0 KW - Eye Proteins KW - RPGR protein, human KW - RPGR protein, mouse KW - Index Medicus KW - Retina -- metabolism KW - Animals KW - Exons KW - Open Reading Frames KW - Humans KW - Dependovirus -- genetics KW - Disease Models, Animal KW - Mice KW - Mice, Knockout KW - Mice, Inbred C57BL KW - Genetic Vectors -- genetics KW - Mutation KW - Male KW - Electroretinography KW - Carrier Proteins -- metabolism KW - Eye Proteins -- metabolism KW - Eye Proteins -- genetics KW - Carrier Proteins -- genetics KW - Genetic Therapy KW - Retinitis Pigmentosa -- metabolism KW - Retinitis Pigmentosa -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1691017551?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+molecular+genetics&rft.atitle=A+long-term+efficacy+study+of+gene+replacement+therapy+for+RPGR-associated+retinal+degeneration.&rft.au=Wu%2C+Zhijian%3BHiriyanna%2C+Suja%3BQian%2C+Haohua%3BMookherjee%2C+Suddhasil%3BCampos%2C+Maria+M%3BGao%2C+Chun%3BFariss%2C+Robert%3BSieving%2C+Paul+A%3BLi%2C+Tiansen%3BColosi%2C+Peter%3BSwaroop%2C+Anand&rft.aulast=Wu&rft.aufirst=Zhijian&rft.date=2015-07-15&rft.volume=24&rft.issue=14&rft.spage=3956&rft.isbn=&rft.btitle=&rft.title=Human+molecular+genetics&rft.issn=1460-2083&rft_id=info:doi/10.1093%2Fhmg%2Fddv134 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-28 N1 - Date created - 2015-06-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Gene Ther. 2010 Jan;17(1):117-31 [19710705] J Virol. 2008 Aug;82(16):7875-85 [18524821] Mol Ther. 2010 Mar;18(3):643-50 [19953081] Invest Ophthalmol Vis Sci. 2011 Jan;52(1):494-503 [20861475] Ophthalmic Genet. 2011 Mar;32(1):1-11 [21174525] Sci Transl Med. 2011 Jun 22;3(88):88ra54 [21697530] Invest Ophthalmol Vis Sci. 2011 Jul;52(8):5189-201 [21546531] Arch Ophthalmol. 2012 Jan;130(1):9-24 [21911650] Proc Natl Acad Sci U S A. 2012 Feb 7;109(6):2132-7 [22308428] Sci Transl Med. 2012 Feb 8;4(120):120ra15 [22323828] PLoS One. 2012;7(5):e35865 [22563472] Invest Ophthalmol Vis Sci. 2012;53(9):5594-608 [22807293] Gene Ther. 2012 Oct;19(10):999-1009 [22071974] Invest Ophthalmol Vis Sci. 2012 Dec;53(13):8232-7 [23150612] PLoS One. 2013;8(1):e53463 [23382846] Proc Natl Acad Sci U S A. 2013 Feb 5;110(6):E517-25 [23341635] Invest Ophthalmol Vis Sci. 2013 Feb;54(2):1411-6 [23372056] Mol Ther. 2013 Mar;21(3):509-19 [23358189] Invest Ophthalmol Vis Sci. 2013 Jun;54(6):4061-71 [23620430] Invest Ophthalmol Vis Sci. 2013 Sep;54(9):6255-61 [23950152] Mol Ther. 2014 Feb;22(2):265-77 [24091916] Lancet. 2014 Mar 29;383(9923):1129-37 [24439297] JAMA Ophthalmol. 2014 Apr 1;132(4):428-36 [24525545] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3649-54 [10725384] Nat Genet. 2000 Aug;25(4):462-6 [10932196] Hum Mol Genet. 2002 May 1;11(9):993-1003 [11978759] Invest Ophthalmol Vis Sci. 2002 Nov;43(11):3373-82 [12407146] Invest Ophthalmol Vis Sci. 2003 Jun;44(6):2413-21 [12766038] Blood. 2003 Oct 1;102(7):2412-9 [12791653] Am J Hum Genet. 2003 Nov;73(5):1131-46 [14564670] J Biol Chem. 1998 Jul 31;273(31):19656-63 [9677393] Hum Mol Genet. 1999 Aug;8(8):1571-8 [10401007] Invest Ophthalmol Vis Sci. 2005 Feb;46(2):435-41 [15671266] J Virol. 2005 Dec;79(23):14793-803 [16282479] J Virol. 2006 Jan;80(1):426-39 [16352567] Am J Ophthalmol. 2006 Sep;142(3):515-8 [16935610] Proc Natl Acad Sci U S A. 2008 Sep 30;105(39):15112-7 [18809924] Hum Mol Genet. 2009 Jun 15;18(12):2099-114 [19299492] Gene Ther. 2009 Jul;16(7):916-26 [19458650] Hum Gene Ther. 2009 Sep;20(9):999-1004 [19583479] Lancet. 2009 Nov 7;374(9701):1597-605 [19854499] Lancet. 2006 Nov 18;368(9549):1795-809 [17113430] Hum Mutat. 2007 Jan;28(1):81-91 [16969763] Invest Ophthalmol Vis Sci. 2007 Sep;48(9):3954-61 [17724172] J Virol. 2007 Oct;81(20):11372-80 [17699581] Hum Mutat. 2008 May;29(5):605-8 [18361418] N Engl J Med. 2008 May 22;358(21):2240-8 [18441370] N Engl J Med. 2008 May 22;358(21):2231-9 [18441371] Invest Ophthalmol Vis Sci. 2010 Feb;51(2):1106-15 [20007830] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/hmg/ddv134 ER - TY - JOUR T1 - Genetic variants associated with longer telomere length are associated with increased lung cancer risk among never-smoking women in Asia: a report from the female lung cancer consortium in Asia. AN - 1680208917; 25516442 AB - Recent evidence from several relatively small nested case-control studies in prospective cohorts shows an association between longer telomere length measured phenotypically in peripheral white blood cell (WBC) DNA and increased lung cancer risk. We sought to further explore this relationship by examining a panel of seven telomere-length associated genetic variants in a large study of 5,457 never-smoking female Asian lung cancer cases and 4,493 never-smoking female Asian controls using data from a previously reported genome-wide association study. Using a group of 1,536 individuals with phenotypically measured telomere length in WBCs in the prospective Shanghai Women's Health study, we demonstrated the utility of a genetic risk score (GRS) of seven telomere-length associated variants to predict telomere length in an Asian population. We then found that GRSs used as instrumental variables to predict longer telomere length were associated with increased lung cancer risk (OR = 1.51 (95% CI = 1.34-1.69) for upper vs. lower quartile of the weighted GRS, p value = 4.54 × 10(-14) ) even after removing rs2736100 (p value = 4.81 × 10(-3) ), a SNP in the TERT locus robustly associated with lung cancer risk in prior association studies. Stratified analyses suggested the effect of the telomere-associated GRS is strongest among younger individuals. We found no difference in GRS effect between adenocarcinoma and squamous cell subtypes. Our results indicate that a genetic background that favors longer telomere length may increase lung cancer risk, which is consistent with earlier prospective studies relating longer telomere length with increased lung cancer risk. Published 2014. This article is a US Government work and, as such, is in the public domain of the United States of America. JF - International journal of cancer AU - Machiela, Mitchell J AU - Hsiung, Chao Agnes AU - Shu, Xiao-Ou AU - Seow, Wei Jie AU - Wang, Zhaoming AU - Matsuo, Keitaro AU - Hong, Yun-Chul AU - Seow, Adeline AU - Wu, Chen AU - Hosgood, H Dean AU - Chen, Kexin AU - Wang, Jiu-Cun AU - Wen, Wanqing AU - Cawthon, Richard AU - Chatterjee, Nilanjan AU - Hu, Wei AU - Caporaso, Neil E AU - Park, Jae Yong AU - Chen, Chien-Jen AU - Kim, Yeul Hong AU - Kim, Young Tae AU - Landi, Maria Teresa AU - Shen, Hongbing AU - Lawrence, Charles AU - Burdett, Laurie AU - Yeager, Meredith AU - Chang, I-Shou AU - Mitsudomi, Tetsuya AU - Kim, Hee Nam AU - Chang, Gee-Chen AU - Bassig, Bryan A AU - Tucker, Margaret AU - Wei, Fusheng AU - Yin, Zhihua AU - An, She-Juan AU - Qian, Biyun AU - Lee, Victor Ho Fun AU - Lu, Daru AU - Liu, Jianjun AU - Jeon, Hyo-Sung AU - Hsiao, Chin-Fu AU - Sung, Jae Sook AU - Kim, Jin Hee AU - Gao, Yu-Tang AU - Tsai, Ying-Huang AU - Jung, Yoo Jin AU - Guo, Huan AU - Hu, Zhibin AU - Hutchinson, Amy AU - Wang, Wen-Chang AU - Klein, Robert J AU - Chung, Charles C AU - Oh, In-Jae AU - Chen, Kuan-Yu AU - Berndt, Sonja I AU - Wu, Wei AU - Chang, Jiang AU - Zhang, Xu-Chao AU - Huang, Ming-Shyan AU - Zheng, Hong AU - Wang, Junwen AU - Zhao, Xueying AU - Li, Yuqing AU - Choi, Jin Eun AU - Su, Wu-Chou AU - Park, Kyong Hwa AU - Sung, Sook Whan AU - Chen, Yuh-Min AU - Liu, Li AU - Kang, Chang Hyun AU - Hu, Lingmin AU - Chen, Chung-Hsing AU - Pao, William AU - Kim, Young-Chul AU - Yang, Tsung-Ying AU - Xu, Jun AU - Guan, Peng AU - Tan, Wen AU - Su, Jian AU - Wang, Chih-Liang AU - Li, Haixin AU - Sihoe, Alan Dart Loon AU - Zhao, Zhenhong AU - Chen, Ying AU - Choi, Yi Young AU - Hung, Jen-Yu AU - Kim, Jun Suk AU - Yoon, Ho-Il AU - Cai, Qiuyin AU - Lin, Chien-Chung AU - Park, In Kyu AU - Xu, Ping AU - Dong, Jing AU - Kim, Christopher AU - He, Qincheng AU - Perng, Reury-Perng AU - Kohno, Takashi AU - Kweon, Sun-Seog AU - Chen, Chih-Yi AU - Vermeulen, Roel C H AU - Wu, Junjie AU - Lim, Wei-Yen AU - Chen, Kun-Chieh AU - Chow, Wong-Ho AU - Ji, Bu-Tian AU - Chan, John K C AU - Chu, Minjie AU - Li, Yao-Jen AU - Yokota, Jun AU - Li, Jihua AU - Chen, Hongyan AU - Xiang, Yong-Bing AU - Yu, Chong-Jen AU - Kunitoh, Hideo AU - Wu, Guoping AU - Jin, Li AU - Lo, Yen-Li AU - Shiraishi, Kouya AU - Chen, Ying-Hsiang AU - Lin, Hsien-Chih AU - Wu, Tangchun AU - Wong, Maria Pik AU - Wu, Yi-Long AU - Yang, Pan-Chyr AU - Zhou, Baosen AU - Shin, Min-Ho AU - Fraumeni, Joseph F AU - Zheng, Wei AU - Lin, Dongxin AU - Chanock, Stephen J AU - Rothman, Nathaniel AU - Lan, Qing AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD. ; Institute of Population Health Sciences, National Health Research Institutes, Zhunan, Taiwan. ; Department of Medicine, Vanderbilt University Medical Center, Nashville, TN. ; Cancer Genomics Research Laboratory, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD. ; Division of Epidemiology and Prevention, Aichi Cancer Center Research Institute, Nagoya, Japan. ; Department of Preventive Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea. ; Saw Swee Hock School of Public Health, National University of Singapore, Republic of Singapore. ; Department of Etiology and Carcinogenesis, Cancer Institute and Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China. ; Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY. ; Department of Epidemiology and Biostatistics, Key Laboratory of Cancer Prevention and Therapy, National Clinical Research Center of Cancer, Medical University Cancer Institute and Hospital, Tianjin, China. ; Ministry of Education Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University, Shanghai, China. ; Department of Human Genetics, University of Utah, Salt Lake City, UT. ; Lung Cancer Center, Kyungpook National University Medical Center, Daegu, Republic of Korea. ; Genomic Research Center, Taipei, Taiwan. ; Department of Internal Medicine, Division of Oncology/Hematology, College of Medicine, Korea University Anam Hospital, Seoul, Republic of Korea. ; Department of Thoracic and Cardiovascular Surgery, Cancer Research Institute, Seoul National University College of Medicine, Seoul, Republic of Korea. ; Jiangsu Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, Nanjing, China. ; Westat, Rockville, MD. ; National Institute of Cancer Research, National Health Research Institutes, Zhunan, Taiwan. ; Division of Thoracic Surgery, Kinki University School of Medicine, Sayama, Japan. ; Center for Creative Biomedical Scientists, Chonnam National University, Gwangju, Republic of Korea. ; Department of Medicine, School of Medicine, National Yang-Ming University, Taipei, Taiwan. ; China National Environmental Monitoring Center, Beijing, China. ; Department of Epidemiology, School of Public Health, China Medical University, Shenyang, China. ; Guangdong Lung Cancer Institute, Guangdong Provincial Key Laboratory of Translational Medicine in Lung Cancer, Guangdong General Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China. ; Department of Epidemiology and Biostatistics, School of Public Health, Shanghai Jiao Tong University, Shanghai, China. ; Department of Clinical Oncology, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Hong, Kong, China. ; Department of Human Genetics, Genome Institute of Singapore, Republic of Singapore. ; Molecular Diagnostics and Imaging Center, Kyungpook National University, Daegu, Republic of Korea. ; Cancer Research Institute, Korea University, Seoul, Republic of Korea. ; Department of Environmental Health, Graduate School of Public Health, Seoul National University, Seoul, Republic of Korea. ; Department of Epidemiology, Shanghai Cancer Institute, Shanghai, China. ; Department of Respiratory Thearpy, Chang Gung Memorial Hospital, Chiayi, Taiwan. ; Institute of Occupational Medicine and Ministry of Education Key Lab for Environment and Health, School of Public Health, Huazhong University of Science and Technology, Wuhan, China. ; Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, Icahn Institute for Genomics and Multiscale Biology, New York, NY. ; Lung and Esophageal Cancer Clinic, Chonnam National University Hwasun Hospital, Hwasun-Eup, Republic of Korea. ; Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan. ; Department of Internal Medicine, Kaohsiung Medical University Hospital, School of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan. ; Centre for Genomic Sciences, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Hong Kong, China. ; Cancer Prevention Institute of California, Fremont, CA. ; Cancer Research Center, Kyungpook National University Medical Center, Daegu, Republic of Korea. ; Department of Internal Medicine, Cancer Center, National Cheng Kung University Hospital, National College of Medicine, Cheng Kung University, Tainan, Taiwan. ; Department of Thoracic and Cardiovascular Surgery, Seoul St Mary's Hospital, Seoul, Republic of Korea. ; Department of Chest Medicine, Taipei Veterans General Hospital, Taipei, Taiwan. ; Cancer Center, Union Hospital, Huazhong University of Science and Technology, Wuhan, China. ; Division of Hematology and Oncology, Vanderbilt University Medical Center, Nashville, TN. ; Department of Internal Medicine, Division of Chest Medicine, Taichung Veterans General Hospital, Taichung, Taiwan. ; School of Public Health, the University of Hong Kong, Hong Kong. ; Department of Pulmonary and Critical Care, Chang Gung Memorial Hospital, Taoyuan, Taiwan. ; Department of Surgery, Division of Cardiothoracic Surgery, Queen Mary Hospital, Hong Kong, China. ; Department of Internal Medicine, Division of Medical Oncology, College of Medicine, Korea University Guro Hospital, Seoul, Republic of Korea. ; Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Republic of Korea. ; Department of Oncology, Wuhan Iron and Steel Corporation Staff Worker Hospital, Wuhan, China. ; Division of Genome Biology, National Cancer Center Research Institute, Tokyo, Japan. ; Jeonnam Regional Cancer Center, Chonnam National University Hwasun Hospital, Hwasun-Eup, Republic of Korea. ; Institute of Medicine, Division of Thoracic Surgery, Department of Surgery, Chung Shan Medical University, Chung Shan Medical University Hospital, Taichung, Taiwan. ; Division of Environmental Epidemiology, Institute for Risk Assessment Sciences (IRAS), Utrecht University, Utrecht, The Netherlands. ; Department of Pathology, Queen Elizabeth Hospital, Hong Kong, China. ; Qujing Center for Diseases Control and Prevention, Sanjiangdadao, Qujing, China. ; Department of Epidemiology, Shanghai Cancer Institute, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China. ; Department of Medical Oncology, Japanese Red Cross Medical Center, Tokyo, Japan. ; Department of Pathology, Li Ka Shing Faculty of Medicine, the University of Hong Kong, Hong Kong, China. ; Department of Internal Medicine, National Taiwan University College of Medicine, Taipei, Taiwan. ; Department of Preventive Medicine, Chonnam National University Medical School, Gwangju, Republic of Korea. Y1 - 2015/07/15/ PY - 2015 DA - 2015 Jul 15 SP - 311 EP - 319 VL - 137 IS - 2 KW - Index Medicus KW - genetics KW - genetic risk score KW - lung cancer KW - association study KW - telomere length KW - Republic of Korea KW - Taiwan KW - Hong Kong KW - Odds Ratio KW - Humans KW - Aged KW - Asian Continental Ancestry Group -- genetics KW - Genome-Wide Association Study -- statistics & numerical data KW - Telomere Homeostasis -- genetics KW - Smoking KW - Prospective Studies KW - Risk Factors KW - Singapore KW - Adult KW - Middle Aged KW - China KW - Female KW - Japan KW - Polymorphism, Single Nucleotide KW - Genetic Predisposition to Disease -- ethnology KW - Genetic Predisposition to Disease -- genetics KW - Telomere -- genetics KW - Lung Neoplasms -- genetics KW - Lung Neoplasms -- ethnology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680208917?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Genetic+variants+associated+with+longer+telomere+length+are+associated+with+increased+lung+cancer+risk+among+never-smoking+women+in+Asia%3A+a+report+from+the+female+lung+cancer+consortium+in+Asia.&rft.au=Machiela%2C+Mitchell+J%3BHsiung%2C+Chao+Agnes%3BShu%2C+Xiao-Ou%3BSeow%2C+Wei+Jie%3BWang%2C+Zhaoming%3BMatsuo%2C+Keitaro%3BHong%2C+Yun-Chul%3BSeow%2C+Adeline%3BWu%2C+Chen%3BHosgood%2C+H+Dean%3BChen%2C+Kexin%3BWang%2C+Jiu-Cun%3BWen%2C+Wanqing%3BCawthon%2C+Richard%3BChatterjee%2C+Nilanjan%3BHu%2C+Wei%3BCaporaso%2C+Neil+E%3BPark%2C+Jae+Yong%3BChen%2C+Chien-Jen%3BKim%2C+Yeul+Hong%3BKim%2C+Young+Tae%3BLandi%2C+Maria+Teresa%3BShen%2C+Hongbing%3BLawrence%2C+Charles%3BBurdett%2C+Laurie%3BYeager%2C+Meredith%3BChang%2C+I-Shou%3BMitsudomi%2C+Tetsuya%3BKim%2C+Hee+Nam%3BChang%2C+Gee-Chen%3BBassig%2C+Bryan+A%3BTucker%2C+Margaret%3BWei%2C+Fusheng%3BYin%2C+Zhihua%3BAn%2C+She-Juan%3BQian%2C+Biyun%3BLee%2C+Victor+Ho+Fun%3BLu%2C+Daru%3BLiu%2C+Jianjun%3BJeon%2C+Hyo-Sung%3BHsiao%2C+Chin-Fu%3BSung%2C+Jae+Sook%3BKim%2C+Jin+Hee%3BGao%2C+Yu-Tang%3BTsai%2C+Ying-Huang%3BJung%2C+Yoo+Jin%3BGuo%2C+Huan%3BHu%2C+Zhibin%3BHutchinson%2C+Amy%3BWang%2C+Wen-Chang%3BKlein%2C+Robert+J%3BChung%2C+Charles+C%3BOh%2C+In-Jae%3BChen%2C+Kuan-Yu%3BBerndt%2C+Sonja+I%3BWu%2C+Wei%3BChang%2C+Jiang%3BZhang%2C+Xu-Chao%3BHuang%2C+Ming-Shyan%3BZheng%2C+Hong%3BWang%2C+Junwen%3BZhao%2C+Xueying%3BLi%2C+Yuqing%3BChoi%2C+Jin+Eun%3BSu%2C+Wu-Chou%3BPark%2C+Kyong+Hwa%3BSung%2C+Sook+Whan%3BChen%2C+Yuh-Min%3BLiu%2C+Li%3BKang%2C+Chang+Hyun%3BHu%2C+Lingmin%3BChen%2C+Chung-Hsing%3BPao%2C+William%3BKim%2C+Young-Chul%3BYang%2C+Tsung-Ying%3BXu%2C+Jun%3BGuan%2C+Peng%3BTan%2C+Wen%3BSu%2C+Jian%3BWang%2C+Chih-Liang%3BLi%2C+Haixin%3BSihoe%2C+Alan+Dart+Loon%3BZhao%2C+Zhenhong%3BChen%2C+Ying%3BChoi%2C+Yi+Young%3BHung%2C+Jen-Yu%3BKim%2C+Jun+Suk%3BYoon%2C+Ho-Il%3BCai%2C+Qiuyin%3BLin%2C+Chien-Chung%3BPark%2C+In+Kyu%3BXu%2C+Ping%3BDong%2C+Jing%3BKim%2C+Christopher%3BHe%2C+Qincheng%3BPerng%2C+Reury-Perng%3BKohno%2C+Takashi%3BKweon%2C+Sun-Seog%3BChen%2C+Chih-Yi%3BVermeulen%2C+Roel+C+H%3BWu%2C+Junjie%3BLim%2C+Wei-Yen%3BChen%2C+Kun-Chieh%3BChow%2C+Wong-Ho%3BJi%2C+Bu-Tian%3BChan%2C+John+K+C%3BChu%2C+Minjie%3BLi%2C+Yao-Jen%3BYokota%2C+Jun%3BLi%2C+Jihua%3BChen%2C+Hongyan%3BXiang%2C+Yong-Bing%3BYu%2C+Chong-Jen%3BKunitoh%2C+Hideo%3BWu%2C+Guoping%3BJin%2C+Li%3BLo%2C+Yen-Li%3BShiraishi%2C+Kouya%3BChen%2C+Ying-Hsiang%3BLin%2C+Hsien-Chih%3BWu%2C+Tangchun%3BWong%2C+Maria+Pik%3BWu%2C+Yi-Long%3BYang%2C+Pan-Chyr%3BZhou%2C+Baosen%3BShin%2C+Min-Ho%3BFraumeni%2C+Joseph+F%3BZheng%2C+Wei%3BLin%2C+Dongxin%3BChanock%2C+Stephen+J%3BRothman%2C+Nathaniel%3BLan%2C+Qing&rft.aulast=Machiela&rft.aufirst=Mitchell&rft.date=2015-07-15&rft.volume=137&rft.issue=2&rft.spage=311&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.29393 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-31 N1 - Date created - 2015-05-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Carcinogenesis. 2000 Mar;21(3):477-84 [10688868] Cancer Sci. 2008 Jul;99(7):1385-9 [18452563] Nucleic Acids Res. 2009 Feb;37(3):e21 [19129229] Cancer Res. 2009 Apr 1;69(7):2896-901 [19318563] Clin Cancer Res. 2009 Dec 1;15(23):7429-33 [19934287] Cancer Epidemiol Biomarkers Prev. 2010 Feb;19(2):605-13 [20142254] Am J Hum Genet. 2010 Jun 11;86(6):929-42 [20560208] JAMA. 2010 Jul 7;304(1):69-75 [20606151] Nature. 2010 Oct 28;467(7319):1061-73 [20981092] Cancer Epidemiol Biomarkers Prev. 2011 Jun;20(6):1238-50 [21467229] PLoS One. 2011;6(6):e20466 [21695195] Lung Cancer. 2011 Aug;73(2):133-7 [21507503] Am J Hum Genet. 2011 Jul 15;89(1):82-93 [21737059] Cancer Res. 2011 Nov 1;71(21):6758-63 [22028319] Nat Genet. 2012 Jan;44(1):6-7 [22200770] Nat Genet. 2012 Dec;44(12):1330-5 [23143601] Nat Genet. 2013 Apr;45(4):422-7, 427e1-2 [23535734] Am J Epidemiol. 2013 Apr 1;177(7):617-24 [23444102] PLoS One. 2013;8(3):e59230 [23555636] Genes Chromosomes Cancer. 2013 Jul;52(7):595-609 [23629941] Int J Cancer. 2013 Dec 1;133(11):2672-80 [23674344] Cancer Prev Res (Phila). 2014 Jan;7(1):128-38 [24253316] Cancer Res. 2014 May 1;74(9):2476-86 [24618342] Cancer Res. 2014 Aug 1;74(15):4090-8 [24853549] Nat Genet. 2014 Jul;46(7):731-5 [24908248] Oncogene. 2002 Jan 21;21(4):619-26 [11850787] Science. 1994 Dec 23;266(5193):2011-5 [7605428] Nat Rev Genet. 2005 Aug;6(8):611-22 [16136653] N Engl J Med. 2006 Sep 7;355(10):1037-46 [16957149] Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):815-9 [17416776] Nat Genet. 2008 Dec;40(12):1404-6 [18978790] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ijc.29393 ER - TY - JOUR T1 - Cancer cell surface induced peptide folding allows intracellular translocation of drug. AN - 1686414892; 25979324 AB - Many lead molecules identified in drug discovery campaigns are eliminated from consideration due to poor solubility and low cell permeability. These orphaned molecules could have clinical value if solubilized and delivered properly. SVS-1 is a de novo designed peptide that preferentially folds at the surface of tumor cells, adopting a β-hairpin conformation that rapidly translocates into the cytoplasm, and ultimately nucleus, of cells. SVS-1 is stable in serum and small molecules attached to the peptide are effectively delivered to cancer cells via mechanisms involving physical translocation and, to a lesser extent, clathrin-dependent endocytosis. For example, ligating the model hydrophobic drug Paclitaxel (PTX) to SVS-1 improved its aqueous solubility by ~1000-fold and successfully delivered and released PTX to cancer cells in vitro and tumors in vivo without toxic adjuvants. These results suggest that SVS-1 can serve as a simple, effective delivery platform for molecules with poor solubility and permeability. Published by Elsevier B.V. JF - Journal of controlled release : official journal of the Controlled Release Society AU - Medina, Scott H AU - Schneider, Joel P AD - Chemical Biology Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD 21702, United States. ; Chemical Biology Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD 21702, United States. Electronic address: Joel.Schneider@nih.gov. Y1 - 2015/07/10/ PY - 2015 DA - 2015 Jul 10 SP - 317 EP - 326 VL - 209 KW - Antineoplastic Agents, Phytogenic KW - 0 KW - Peptides KW - SVS-1 peptide KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Biodistribution KW - Drug delivery KW - Cell-penetrating peptide KW - Translocation KW - In vivo efficacy KW - Paclitaxel -- administration & dosage KW - Animals KW - Neoplasms -- drug therapy KW - Solubility KW - Humans KW - Biological Transport KW - Paclitaxel -- therapeutic use KW - Cell Line, Tumor KW - Mice, Nude KW - Paclitaxel -- chemistry KW - Drug Liberation KW - Antineoplastic Agents, Phytogenic -- chemistry KW - Cell Survival -- drug effects KW - Antineoplastic Agents, Phytogenic -- therapeutic use KW - Serum -- chemistry KW - Protein Folding KW - Antineoplastic Agents, Phytogenic -- administration & dosage KW - Neoplasms -- metabolism KW - Drug Delivery Systems KW - Peptides -- administration & dosage KW - Peptides -- chemistry KW - Peptides -- therapeutic use KW - Peptides -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1686414892?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+controlled+release+%3A+official+journal+of+the+Controlled+Release+Society&rft.atitle=Cancer+cell+surface+induced+peptide+folding+allows+intracellular+translocation+of+drug.&rft.au=Medina%2C+Scott+H%3BSchneider%2C+Joel+P&rft.aulast=Medina&rft.aufirst=Scott&rft.date=2015-07-10&rft.volume=209&rft.issue=&rft.spage=317&rft.isbn=&rft.btitle=&rft.title=Journal+of+controlled+release+%3A+official+journal+of+the+Controlled+Release+Society&rft.issn=1873-4995&rft_id=info:doi/10.1016%2Fj.jconrel.2015.05.267 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-21 N1 - Date created - 2015-06-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1991 Mar 1;88(5):1864-8 [1672046] Cancer Chemother Pharmacol. 1992;30(6):444-50 [1356649] Br J Cancer. 1993 Dec;68(6):1104-9 [7903152] Biochem Biophys Res Commun. 1996 May 24;222(3):694-9 [8651907] J Biol Chem. 1997 Sep 26;272(39):24198-202 [9305871] FASEB J. 1998 Jan;12(1):67-77 [9438412] Cell Mol Life Sci. 2005 May;62(9):971-88 [15761668] Trends Cell Biol. 2001 Sep;11(9):385-91 [11514193] Exp Cell Res. 2001 Oct 1;269(2):237-44 [11570816] J Cell Biochem. 2001 Aug 1-9;83(2):259-70 [11573243] J Biol Chem. 2003 Jan 3;278(1):585-90 [12411431] Annu Rev Physiol. 2003;65:701-34 [12471163] Trends Biochem Sci. 2003 Apr;28(4):210-4 [12713905] J Am Chem Soc. 2005 Aug 24;127(33):11798-803 [16104758] J Control Release. 2005 Nov 28;108(2-3):396-408 [16157413] Cell Mol Life Sci. 2005 Dec;62(23):2739-49 [16231085] Proc Natl Acad Sci U S A. 2007 May 8;104(19):7893-8 [17483464] Biophys J. 2007 Oct 1;93(7):2363-72 [17557792] Expert Opin Drug Saf. 2007 Sep;6(5):609-21 [17877447] J Virol. 1989 Jan;63(1):1-8 [2535718] Acc Chem Res. 2008 Jan;41(1):108-19 [17663526] Chem Biol Drug Des. 2009 Jan;73(1):39-45 [19152633] Biopolymers. 2009;92(6):502-7 [19521977] Molecules. 2009;14(12):4892-914 [20032867] J Clin Pathol. 2010 Apr;63(4):322-9 [20354203] Bioconjug Chem. 2010 May 19;21(5):979-87 [20429547] Bioconjug Chem. 2009 Aug 19;20(8):1531-7 [19601640] J Am Chem Soc. 2012 Apr 11;134(14):6210-7 [22413859] J Control Release. 2012 Apr 30;159(2):181-8 [22285548] Trends Mol Med. 2012 Jul;18(7):385-93 [22682515] Drug Discov Today. 2012 Aug;17(15-16):850-60 [22465171] Biochemistry. 2012 Aug 14;51(32):6263-5 [22839778] Biopolymers. 2012;98(5):431-42 [23203688] Angew Chem Int Ed Engl. 2012 Dec 7;51(50):12454-8 [23129324] FEBS J. 2014 Jan;281(1):191-215 [24286593] PLoS One. 2014;9(6):e99653 [24937132] Nat Chem. 2014 Oct;6(10):855-7 [25242478] Biochem Pharmacol. 1999 Dec 1;58(11):1775-80 [10571252] J Biol Chem. 2003 Aug 15;278(33):31192-201 [12783857] Biochem Biophys Res Commun. 2003 Jul 18;307(1):100-7 [12849987] Eur J Biochem. 2001 Apr;268(7):2187-91 [11277943] J Cell Biol. 1970 Aug;46(2):396-402 [5449183] Exp Cell Res. 1984 Jan;150(1):29-35 [6198189] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jconrel.2015.05.267 ER - TY - JOUR T1 - Comparative toxicity and carcinogenicity of soluble and insoluble cobalt compounds. AN - 1687999675; 25896363 AB - Occupational exposure to cobalt is of widespread concern due to its use in a variety of industrial processes and the occurrence of occupational disease. Due to the lack of toxicity and carcinogenicity data following exposure to cobalt, and questions regarding bioavailability following exposure to different forms of cobalt, the NTP conducted two chronic inhalation exposure studies in rats and mice, one on soluble cobalt sulfate heptahydrate, and a more recent study on insoluble cobalt metal. Herein, we compare and contrast the toxicity profiles following whole-body inhalation exposures to these two forms of cobalt. In general, both forms were genotoxic in the Salmonella T98 strain in the absence of effects on micronuclei. The major sites of toxicity and carcinogenicity in both chronic inhalation studies were the respiratory tract in rats and mice, and the adrenal gland in rats. In addition, there were distinct sites of toxicity and carcinogenicity noted following exposure to cobalt metal. In rats, carcinogenicity was observed in the blood, and pancreas, and toxicity was observed in the testes of rats and mice. Taken together, these findings suggest that both forms of cobalt, soluble and insoluble, appear to be multi-site rodent carcinogens following inhalation exposure. Published by Elsevier Ireland Ltd. JF - Toxicology AU - Behl, Mamta AU - Stout, Matthew D AU - Herbert, Ronald A AU - Dill, Jeffrey A AU - Baker, Gregory L AU - Hayden, Barry K AU - Roycroft, Joseph H AU - Bucher, John R AU - Hooth, Michelle J AD - Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. Electronic address: behlmv@niehs.nih.gov. ; Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. ; Battelle Memorial Institute, Columbus, OH, USA. Y1 - 2015/07/03/ PY - 2015 DA - 2015 Jul 03 SP - 195 EP - 205 VL - 333 KW - Cobalt KW - 3G0H8C9362 KW - cobalt sulfate KW - H7965X29HX KW - Index Medicus KW - Rats KW - Mice KW - Toxicity KW - Cancer KW - Animals KW - Salmonella -- genetics KW - Adrenal Medulla -- pathology KW - Risk Assessment KW - Salmonella -- drug effects KW - Rats, Inbred F344 KW - Lung Neoplasms -- chemically induced KW - Time Factors KW - Male KW - Hematologic Neoplasms -- pathology KW - Hematologic Neoplasms -- chemically induced KW - Solubility KW - Adrenal Medulla -- drug effects KW - Pancreatic Neoplasms -- chemically induced KW - Testis -- pathology KW - Respiratory System -- pathology KW - Mutagenicity Tests KW - Pancreatic Neoplasms -- pathology KW - Testis -- drug effects KW - Inhalation Exposure KW - Toxicity Tests, Chronic KW - Carcinogenicity Tests KW - Adrenal Gland Neoplasms -- chemically induced KW - Adrenal Gland Neoplasms -- pathology KW - Species Specificity KW - Female KW - Lung Neoplasms -- pathology KW - Respiratory System -- drug effects KW - Cobalt -- toxicity KW - Cobalt -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687999675?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology&rft.atitle=Comparative+toxicity+and+carcinogenicity+of+soluble+and+insoluble+cobalt+compounds.&rft.au=Behl%2C+Mamta%3BStout%2C+Matthew+D%3BHerbert%2C+Ronald+A%3BDill%2C+Jeffrey+A%3BBaker%2C+Gregory+L%3BHayden%2C+Barry+K%3BRoycroft%2C+Joseph+H%3BBucher%2C+John+R%3BHooth%2C+Michelle+J&rft.aulast=Behl&rft.aufirst=Mamta&rft.date=2015-07-03&rft.volume=333&rft.issue=&rft.spage=195&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=1879-3185&rft_id=info:doi/10.1016%2Fj.tox.2015.04.008 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-17 N1 - Date created - 2015-06-13 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.tox.2015.04.008 ER - TY - JOUR T1 - Okazaki fragment maturation involves α-segment error editing by the mammalian FEN1/MutSα functional complex. AN - 1693710839; 25921062 AB - During nuclear DNA replication, proofreading-deficient DNA polymerase α (Pol α) initiates Okazaki fragment synthesis with lower fidelity than bulk replication by proofreading-proficient Pol δ or Pol ε. Here, we provide evidence that the exonuclease activity of mammalian flap endonuclease (FEN1) excises Pol α replication errors in a MutSα-dependent, MutLα-independent mismatch repair process we call Pol α-segment error editing (AEE). We show that MSH2 interacts with FEN1 and facilitates its nuclease activity to remove mismatches near the 5' ends of DNA substrates. Mouse cells and mice encoding FEN1 mutations display AEE deficiency, a strong mutator phenotype, enhanced cellular transformation, and increased cancer susceptibility. The results identify a novel role for FEN1 in a specialized mismatch repair pathway and a new cancer etiological mechanism. © 2015 The Authors. JF - The EMBO journal AU - Liu, Songbai AU - Lu, Guojun AU - Ali, Shafat AU - Liu, Wenpeng AU - Zheng, Li AU - Dai, Huifang AU - Li, Hongzhi AU - Xu, Hong AU - Hua, Yuejin AU - Zhou, Yajing AU - Ortega, Janice AU - Li, Guo-Min AU - Kunkel, Thomas A AU - Shen, Binghui AD - Colleges of Life Sciences and Agriculture and Biotechnology, Zhejiang University, Hangzhou Zhejiang, China Departments of Radiation Biology and Molecular Medicine, City of Hope National Medical Center and Beckman Research Institute, Duarte, CA, USA. ; Departments of Radiation Biology and Molecular Medicine, City of Hope National Medical Center and Beckman Research Institute, Duarte, CA, USA. ; Colleges of Life Sciences and Agriculture and Biotechnology, Zhejiang University, Hangzhou Zhejiang, China. ; Institute of Life Sciences, Jiangsu University, Zhen Jiang Jiangsu, China. ; Graduate Center for Toxicology, Markey Cancer Center, University of Kentucky College of Medicine, Lexington, KY, USA. ; Genome Integrity and Structural Biology Laboratory, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC, USA. ; Departments of Radiation Biology and Molecular Medicine, City of Hope National Medical Center and Beckman Research Institute, Duarte, CA, USA bshen@coh.org. Y1 - 2015/07/02/ PY - 2015 DA - 2015 Jul 02 SP - 1829 EP - 1843 VL - 34 IS - 13 KW - Okazaki fragments KW - 0 KW - DNA KW - 9007-49-2 KW - DNA Polymerase I KW - EC 2.7.7.- KW - Flap Endonucleases KW - EC 3.1.- KW - MutS DNA Mismatch-Binding Protein KW - EC 3.6.1.3 KW - Index Medicus KW - α‐segment error editing KW - MutSα KW - DNA mismatch repair KW - flap endonuclease 1 KW - Okazaki fragment maturation KW - Animals KW - DNA Replication -- genetics KW - HeLa Cells KW - Cells, Cultured KW - Humans KW - HEK293 Cells KW - Mice KW - Mice, Transgenic KW - Embryo, Mammalian KW - Male KW - Female KW - Saccharomyces cerevisiae KW - MutS DNA Mismatch-Binding Protein -- metabolism KW - MutS DNA Mismatch-Binding Protein -- genetics KW - Flap Endonucleases -- classification KW - DNA Mismatch Repair -- genetics KW - DNA -- metabolism KW - Flap Endonucleases -- genetics KW - Flap Endonucleases -- metabolism KW - DNA Polymerase I -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1693710839?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+EMBO+journal&rft.atitle=Okazaki+fragment+maturation+involves+%CE%B1-segment+error+editing+by+the+mammalian+FEN1%2FMutS%CE%B1+functional+complex.&rft.au=Liu%2C+Songbai%3BLu%2C+Guojun%3BAli%2C+Shafat%3BLiu%2C+Wenpeng%3BZheng%2C+Li%3BDai%2C+Huifang%3BLi%2C+Hongzhi%3BXu%2C+Hong%3BHua%2C+Yuejin%3BZhou%2C+Yajing%3BOrtega%2C+Janice%3BLi%2C+Guo-Min%3BKunkel%2C+Thomas+A%3BShen%2C+Binghui&rft.aulast=Liu&rft.aufirst=Songbai&rft.date=2015-07-02&rft.volume=34&rft.issue=13&rft.spage=1829&rft.isbn=&rft.btitle=&rft.title=The+EMBO+journal&rft.issn=1460-2075&rft_id=info:doi/10.15252%2Fembj.201489865 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-01 N1 - Date created - 2015-07-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cold Spring Harb Symp Quant Biol. 2009;74:91-101 [19903750] EMBO J. 2013 May 15;32(10):1425-39 [23604072] J Biol Chem. 2001 Sep 28;276(39):36295-302 [11477073] J Biol Chem. 2002 Apr 26;277(17):14379-89 [11825897] Genes Dev. 2003 Mar 1;17(5):603-14 [12629043] Mol Cell Biol. 2004 Apr;24(7):2734-46 [15024063] J Biol Chem. 2004 Apr 23;279(17):16895-8 [14988392] Nature. 1994 May 19;369(6477):207-12 [7910375] Proc Natl Acad Sci U S A. 1994 Oct 11;91(21):9803-7 [7524089] J Biol Chem. 2000 Dec 1;275(48):38022-31 [10984490] Proc Natl Acad Sci U S A. 2010 Dec 7;107(49):21070-5 [21041657] J Mol Cell Biol. 2011 Feb;3(1):23-30 [21278448] Cell. 2011 Apr 15;145(2):198-211 [21496641] Cell Res. 2011 Jul;21(7):1052-67 [21383776] Nat Struct Mol Biol. 2012 Jan;19(1):72-8 [22179786] Nat Commun. 2012;3:815 [22569363] PLoS One. 2012;7(6):e39156 [22723953] Annu Rev Biochem. 2013;82:119-38 [23451868] Bioinformatics. 2014 Jun 15;30(12):1771-3 [24532726] Nat Methods. 2015 Mar;12(3):251-7, 3 p following 257 [25622106] Nature. 2015 Feb 26;518(7540):502-6 [25624100] Nat Struct Mol Biol. 2015 Mar;22(3):185-91 [25622295] Nat Struct Mol Biol. 2015 Mar;22(3):192-8 [25664722] Nucleic Acids Res. 2001 Jul 15;29(14):3069-79 [11452032] Mol Cell Biol. 1999 Dec;19(12):8361-71 [10567561] Science. 1995 Jul 14;269(5221):238-40 [7618086] J Biol Chem. 1996 Apr 19;271(16):9173-6 [8621570] Cell. 1997 Jan 24;88(2):253-63 [9008166] Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7487-92 [9207118] J Biol Chem. 1999 Jun 18;274(25):17893-900 [10364235] EMBO Rep. 2005 Jan;6(1):83-9 [15592449] Cell. 2005 Sep 9;122(5):693-705 [16143102] Proc Natl Acad Sci U S A. 2005 Oct 4;102(40):14350-5 [16179390] Curr Biol. 2006 Jan 24;16(2):202-7 [16431373] Mol Cell Biol. 2007 Apr;27(8):3176-86 [17283043] Mol Cell. 2007 May 25;26(4):579-92 [17531815] Nat Med. 2007 Jul;13(7):812-9 [17589521] Cell Res. 2008 Jan;18(1):85-98 [18157157] J Mol Biol. 2008 Mar 28;377(3):679-90 [18291413] Mol Cell. 2008 Apr 25;30(2):137-44 [18439893] Mol Cell. 2008 Nov 7;32(3):325-36 [18995831] J Biol Chem. 2009 Feb 13;284(7):4041-5 [18835809] Proc Natl Acad Sci U S A. 2009 May 26;106(21):8495-500 [19420220] J Biol Chem. 2009 Aug 14;284(33):22184-94 [19525235] Nature. 2001 Jul 26;412(6845):456-61 [11473323] Mol Cell. 2012 Aug 10;47(3):444-56 [22749529] DNA Repair (Amst). 2013 Feb 1;12(2):92-6 [23245696] Am J Hum Genet. 2013 Feb 7;92(2):293-300 [23352259] Comment In: Cell Cycle. 2015;14(12):1767 [26039417] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.15252/embj.201489865 ER - TY - JOUR T1 - Metabolic Signatures of Human Breast Cancer. AN - 1826618701; 26005711 AB - Metabolomics has emerged as a new discovery tool with the promise of identifying therapeutic targets in cancer. Recent discoveries described essential metabolomic pathways in breast cancer and characterized oncometabolites that drive tumor growth and progression. Oncogenes like MYC and tumor suppressor genes like TP53 prominently affect breast cancer biology through regulation of cell metabolism and mitochondrial biogenesis. These findings indicate that tumors with dominant mutations could be susceptible to inhibitors of disease metabolism. Moreover, various pre-clinical and clinical studies have linked tumor metabolism to therapeutic response and patient survival. Thus, recent advances suggest that metabolic profiling provides new opportunities to improve outcomes in breast cancer. In this review, we have summarized some of the identified roles of oncometabolites in breast cancer biology and highlight their clinical utility. JF - Molecular & cellular oncology AU - Mishra, Prachi AU - Ambs, Stefan AD - Laboratory of Human Carcinogenesis, Center of Cancer Research, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD, USA. PY - 2015 VL - 2 IS - 3 KW - biomarker KW - metabolism KW - therapy KW - Cancer KW - prognosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826618701?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+%26+cellular+oncology&rft.atitle=Metabolic+Signatures+of+Human+Breast+Cancer.&rft.au=Mishra%2C+Prachi%3BAmbs%2C+Stefan&rft.aulast=Mishra&rft.aufirst=Prachi&rft.date=2015-07-01&rft.volume=2&rft.issue=3&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Molecular+%26+cellular+oncology&rft.issn=&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2015-05-25 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - Translational Genomics in Low- and Middle-Income Countries: Opportunities and Challenges AN - 1780517046; PQ0002840883 AB - Translation of genomic discoveries into patient care is slowly becoming a reality in developed economies around the world. In contrast, low- and middle-income countries (LMIC) have participated minimally in genomic research for several reasons including the lack of coherent national policies, the limited number of well-trained genomic scientists, poor research infrastructure, and local economic and cultural challenges. Recent initiatives such as the Human Heredity and Health in Africa (H3Africa), the Qatar Genome Project, and the Mexico National Institute of Genomic Medicine (INMEGEN) that aim to address these problems through capacity building and empowerment of local researchers have sparked a paradigm shift. In this short communication, we describe experiences of small-scale medical genetics and translational genomic research programs in LMIC. The lessons drawn from these programs drive home the importance of addressing resource, policy, and sociocultural dynamics to realize the promise of precision medicine driven by genomic science globally. By echoing lessons from a bench-to-community translational genomic research, we advocate that large-scale genomic research projects can be successfully linked with health care programs. To harness the benefits of genomics-led health care, LMIC governments should begin to develop national genomics policies that will address human and technology capacity development within the context of their national economic and sociocultural uniqueness. These policies should encourage international collaboration and promote the link between the public health program and genomics researchers. Finally, we highlight the potential catalytic roles of the global community to foster translational genomics in LMIC. copyright 2015 S. Karger AG, Basel JF - Public Health Genomics AU - Tekola-Ayele, Fasil AU - Rotimi, Charles N AD - Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, Md., USA Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 242 EP - 247 PB - S. Karger AG, P.O. Box Basel CH-4009 Switzerland VL - 18 IS - 4 SN - 1662-4246, 1662-4246 KW - Genetics Abstracts; Health & Safety Science Abstracts KW - Genomics KW - Translational research KW - Genomic medicine KW - Next-generation sequencing KW - Genetic testing KW - Family health history KW - Global health KW - Qatar KW - Translation KW - Culture KW - Heredity KW - Carrying capacity KW - International agreements KW - Public health KW - Infrastructure KW - Genetics KW - Mexico KW - Communications KW - Health care KW - Economics KW - Africa KW - Empowerment KW - genomics KW - Research programs KW - Technology KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780517046?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Public+Health+Genomics&rft.atitle=Translational+Genomics+in+Low-+and+Middle-Income+Countries%3A+Opportunities+and+Challenges&rft.au=Tekola-Ayele%2C+Fasil%3BRotimi%2C+Charles+N&rft.aulast=Tekola-Ayele&rft.aufirst=Fasil&rft.date=2015-07-01&rft.volume=18&rft.issue=4&rft.spage=242&rft.isbn=&rft.btitle=&rft.title=Public+Health+Genomics&rft.issn=16624246&rft_id=info:doi/10.1159%2F000433518 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-09-14 N1 - SubjectsTermNotLitGenreText - Translation; Heredity; Economics; genomics; Research programs; Public health; Infrastructure; Genetics; Culture; Communications; Health care; Carrying capacity; Empowerment; International agreements; Technology; Qatar; Mexico; Africa DO - http://dx.doi.org/10.1159/000433518 ER - TY - JOUR T1 - Racial Differences in Self-Reports of Short Sleep Duration in an Urban-Dwelling Environment AN - 1761675321; 201602190 AB - Objectives. To explore whether there are differences in sleep duration between blacks and whites residing in similar urban neighborhoods and examine whether the relationship between sleep durations and sociodemographic and/or health indices are consistent for blacks and whites. Methods. A total of 1,207 participants from the Healthy Aging in Neighborhoods of Disparities across the Life Span study (age: mean = 47, standard deviation = 8.74). Sleep duration was assessed by a self-report of hours of nightly sleep in the past month. Sociodemographic measures included age, sex, education, poverty status, and perceived neighborhood disorder. Health status was assessed using measures of vigilance, depression, perceived stress, coronary artery disease, diabetes, blood pressure, and inflammation. Results. There were no significant racial group differences in sleep duration. Whites, however, were more likely than blacks to report sleep durations of 7hr with increasing stress and education levels. Blacks were more likely than whites to report short sleep durations (i.e., 6-7hr vs. >7hr of sleep) with increasing inflammation levels. Discussion. Although racial disparities in sleep duration are minimized when the environment is equivalent between blacks and whites, the underlying demographic and health explanations for short sleep durations may vary between whites and blacks. Adapted from the source document. JF - Journals of Gerontology Series B: Psychological Sciences and Social Sciences AU - Gamaldo, Alyssa A AU - McNeely, Jessica M AU - Shah, Mauli T AU - Evans, Michele K AU - Zonderman, Alan B AD - National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, Maryland agamaldo@usf.edu Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 568 EP - 575 PB - Oxford University Press VL - 70 IS - 4 SN - 1079-5014, 1079-5014 KW - Aging Race Sleep duration KW - Blood Pressure KW - Sleep KW - Health Problems KW - Neighborhoods KW - Stress KW - Health KW - Blood Diseases KW - Racial Differences KW - Sociodemographic Factors KW - article KW - 0410: group interactions; social group identity & intergroup relations (groups based on race & ethnicity, age, & sexual orientation) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1761675321?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocabs&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journals+of+Gerontology+Series+B%3A+Psychological+Sciences+and+Social+Sciences&rft.atitle=Racial+Differences+in+Self-Reports+of+Short+Sleep+Duration+in+an+Urban-Dwelling+Environment&rft.au=Gamaldo%2C+Alyssa+A%3BMcNeely%2C+Jessica+M%3BShah%2C+Mauli+T%3BEvans%2C+Michele+K%3BZonderman%2C+Alan+B&rft.aulast=Gamaldo&rft.aufirst=Alyssa&rft.date=2015-07-01&rft.volume=70&rft.issue=4&rft.spage=568&rft.isbn=&rft.btitle=&rft.title=Journals+of+Gerontology+Series+B%3A+Psychological+Sciences+and+Social+Sciences&rft.issn=10795014&rft_id=info:doi/10.1093%2Fgeronb%2Fgbt117 LA - English DB - Sociological Abstracts N1 - Date revised - 2016-02-01 N1 - Last updated - 2016-09-28 N1 - CODEN - JGBSF3 N1 - SubjectsTermNotLitGenreText - Sleep; Racial Differences; Neighborhoods; Sociodemographic Factors; Stress; Health; Blood Pressure; Health Problems; Blood Diseases DO - http://dx.doi.org/10.1093/geronb/gbt117 ER - TY - JOUR T1 - Identification of known drugs targeting the endoplasmic reticulum stress response AN - 1746896328; PQ0001861723 AB - The endoplasmic reticulum (ER), a multifunctional organelle, plays a central role in cellular signaling, development, and stress response. Dysregulation of ER homeostasis has been associated with human diseases, such as cancer, inflammation, and diabetes. A broad spectrum of stressful stimuli including hypoxia as well as a variety of pharmacological agents can lead to the ER stress response. In this study, we have developed a stable ER stress reporter cell line that stably expresses a beta -lactamase reporter gene under the control of the ER stress response element (ESRE) present in the glucose-regulated protein, 78 kDa (GRP78) gene promoter. This assay has been optimized and miniaturized into a 1536-well plate format. In order to identify clinically used drugs that induce ER stress response, we screened approximately 2800 drugs from the NIH Chemical Genomics Center Pharmaceutical Collection (NPC library) using a quantitative high-throughput screening (qHTS) platform. From this study, we have identified several known ER stress inducers, such as 17-AAG (via HSP90 inhibition), as well as several novel ER stress inducers such as AMI-193 and spiperone. The confirmed drugs were further studied for their effects on the phosphorylation of eukaryotic initiation factor 2 alpha (eIF2 alpha ), the X-box-binding protein (XBP1) splicing, and GRP78 gene expression. These results suggest that the ER stress inducers identified from the NPC library using the qHTS approach could shed new lights on the potential therapeutic targets of these drugs. JF - Analytical and Bioanalytical Chemistry AU - Bi, Kun AU - Nishihara, Kana AU - Machleidt, Thomas AU - Hermanson, Spencer AU - Wang, Jun AU - Sakamuru, Srilatha AU - Huang, Ruili AU - Xia, Menghang AD - Life Science Solutions Group, Thermo Fisher Scientific, Rockford, IL, 61105, USA, mxia@mail.nih.gov PY - 2015 SP - 5343 EP - 5351 PB - Springer Science+Business Media, Berlin/Heidelberg Germany VL - 407 IS - 18 SN - 1618-2642, 1618-2642 KW - Aqualine Abstracts; Water Resources Abstracts KW - Stress KW - Inhibition KW - Libraries KW - Human Diseases KW - Assay KW - Proteins KW - Drugs KW - AQ 00001:Water Resources and Supplies KW - SW 5040:Data acquisition UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746896328?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+and+Bioanalytical+Chemistry&rft.atitle=Identification+of+known+drugs+targeting+the+endoplasmic+reticulum+stress+response&rft.au=Bi%2C+Kun%3BNishihara%2C+Kana%3BMachleidt%2C+Thomas%3BHermanson%2C+Spencer%3BWang%2C+Jun%3BSakamuru%2C+Srilatha%3BHuang%2C+Ruili%3BXia%2C+Menghang&rft.aulast=Bi&rft.aufirst=Kun&rft.date=2015-07-01&rft.volume=407&rft.issue=18&rft.spage=5343&rft.isbn=&rft.btitle=&rft.title=Analytical+and+Bioanalytical+Chemistry&rft.issn=16182642&rft_id=info:doi/10.1007%2Fs00216-015-8694-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 25 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Human Diseases; Libraries; Assay; Proteins; Stress; Inhibition; Drugs DO - http://dx.doi.org/10.1007/s00216-015-8694-2 ER - TY - JOUR T1 - Maternal ambient air pollution exposure preconception and during early gestation and offspring congenital orofacial defects AN - 1746889156; PQ0002312845 AB - Background Maternal air pollution exposure has been related to orofacial clefts but the literature is equivocal. Potential chronic preconception effects have not been studied. Objectives Criteria air pollutant exposure during three months preconception and gestational weeks 3-8 was studied in relation to orofacial defects. Methods Among 188,102 live births and fetal deaths from the Consortium on Safe Labor (2002-2008), 63 had isolated cleft palate (CP) and 159 had isolated cleft lip with or without cleft palate (CL plus or minus CP). Exposures were estimated using a modified Community Multiscale Air Quality model. Logistic regression with generalized estimating equations adjusted for site/region and maternal demographic, lifestyle and clinical factors calculated the odds ratio (OR) and 95% CI per interquartile increase in each pollutant. Results Preconception, carbon monoxide (CO; OR=2.24; CI: 1.21, 4.16) and particulate matter (PM) less than or equal to 10 mu m (OR=1.72; CI: 1.12, 2.66) were significantly associated with CP, while sulfur dioxide (SO2) was associated with CL plus or minus CP (OR=1.93; CI: 1.16, 3.21). During gestational weeks 3-8, CO remained a significant risk for CP (OR=2.74; CI: 1.62, 4.62) and nitrogen oxides (NO x ; OR=3.64; CI: 1.73, 7.66) and PM less than or equal to 2.5 mu m (PM2.5; OR=1.74; CI: 1.15, 2.64) were also related to the risk. Analyses by individual week revealed that positive associations of NO x and PM2.5 with CP were most prominent from weeks 3-6 and 3-5, respectively. Conclusions Exposure to several criteria air pollutants preconception and during early gestation was associated with elevated odds for CP, while CL plus or minus CP was only associated with preconception SO2 exposure. JF - Environmental Research AU - Zhu, Yeyi AU - Zhang, Cuilin AU - Liu, Danping AU - Grantz, Katherine L AU - Wallace, Maeve AU - Mendola, Pauline AD - Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Rockville, MD, USA Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 714 EP - 720 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 140 SN - 0013-9351, 0013-9351 KW - Toxicology Abstracts; Pollution Abstracts; Risk Abstracts; Health & Safety Science Abstracts; Environment Abstracts; Meteorological & Geoastrophysical Abstracts; Sustainability Science Abstracts KW - Air pollution KW - Preconception exposure KW - Organogenesis KW - Cleft palate KW - Cleft lip KW - Particulate matter KW - Statistical analysis KW - Air quality KW - Environmental research KW - Offspring KW - Particulates KW - orofacial clefts KW - Models KW - Demography KW - Carbon monoxide KW - Sulfur dioxide KW - Pollutants KW - Risk factors KW - Gestation KW - oxides KW - Particle size KW - Mortality KW - Atmospheric pollution KW - Mathematical models KW - Nitrogen oxides KW - Particulate atmospheric pollution KW - Fetuses KW - Air quality models KW - Cleft lip/palate KW - Photochemicals KW - Progeny KW - Nitric oxide KW - Nitrogen KW - M2 551.510.42:Air Pollution (551.510.42) KW - P 0000:AIR POLLUTION KW - M3 1010:Issues in Sustainable Development KW - X 24360:Metals KW - R2 23050:Environment KW - H 0500:General KW - ENA 01:Air Pollution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746889156?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Research&rft.atitle=Maternal+ambient+air+pollution+exposure+preconception+and+during+early+gestation+and+offspring+congenital+orofacial+defects&rft.au=Zhu%2C+Yeyi%3BZhang%2C+Cuilin%3BLiu%2C+Danping%3BGrantz%2C+Katherine+L%3BWallace%2C+Maeve%3BMendola%2C+Pauline&rft.aulast=Zhu&rft.aufirst=Yeyi&rft.date=2015-07-01&rft.volume=140&rft.issue=&rft.spage=714&rft.isbn=&rft.btitle=&rft.title=Environmental+Research&rft.issn=00139351&rft_id=info:doi/10.1016%2Fj.envres.2015.06.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Mathematical models; Particulate matter; orofacial clefts; Fetuses; Cleft lip/palate; Models; Air pollution; Carbon monoxide; Demography; Sulfur dioxide; Pollutants; Gestation; oxides; Nitric oxide; Progeny; Nitrogen; Atmospheric pollution; Statistical analysis; Environmental research; Particulate atmospheric pollution; Air quality models; Particle size; Mortality; Photochemicals; Risk factors; Air quality; Particulates; Offspring; Nitrogen oxides DO - http://dx.doi.org/10.1016/j.envres.2015.06.002 ER - TY - JOUR T1 - Dispositional Optimism and Perceived Risk Interact to Predict Intentions to Learn Genome Sequencing Results AN - 1732825358; PQ0002197799 AB - Objective: Dispositional optimism and risk perceptions are each associated with health-related behaviors and decisions and other outcomes, but little research has examined how these constructs interact, particularly in consequential health contexts. The predictive validity of risk perceptions for health-related information seeking and intentions may be improved by examining dispositional optimism as a moderator, and by testing alternate types of risk perceptions, such as comparative and experiential risk. Method: Participants (n = 496) had their genomes sequenced as part of a National Institutes of Health pilot cohort study (ClinSeq(R)). Participants completed a cross-sectional baseline survey of various types of risk perceptions and intentions to learn genome sequencing results for differing disease risks (e.g., medically actionable, nonmedically actionable, carrier status) and to use this information to change their lifestyle/health behaviors. Results: Risk perceptions (absolute, comparative, and experiential) were largely unassociated with intentions to learn sequencing results. Dispositional optimism and comparative risk perceptions interacted, however, such that individuals higher in optimism reported greater intentions to learn all 3 types of sequencing results when comparative risk was perceived to be higher than when it was perceived to be lower. This interaction was inconsistent for experiential risk and absent for absolute risk. Independent of perceived risk, participants high in dispositional optimism reported greater interest in learning risks for nonmedically actionable disease and carrier status, and greater intentions to use genome information to change their lifestyle/health behaviors. Conclusions: The relationship between risk perceptions and intentions may depend on how risk perceptions are assessed and on degree of optimism. JF - Health Psychology AU - Taber, Jennifer M AU - Klein, William M P AU - Ferrer, Rebecca A AU - Lewis, Katie L AU - Biesecker, Leslie G AU - Biesecker, Barbara B AD - National Institutes of Health, jennifer.taber@nih.gov PY - 2015 SP - 718 EP - 728 PB - American Psychological Association, 750 First St., N.E. Washington DC 20002-4242 United States VL - 34 IS - 7 SN - 0278-6133, 0278-6133 KW - Health & Safety Science Abstracts; Risk Abstracts KW - dispositional optimism KW - perceived risk KW - genetics KW - genomics KW - comparative risk KW - Risk assessment KW - Health risks KW - Behavior KW - Perception KW - Risk taking KW - H 0500:General KW - R2 23110:Psychological aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732825358?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Psychology&rft.atitle=Dispositional+Optimism+and+Perceived+Risk+Interact+to+Predict+Intentions+to+Learn+Genome+Sequencing+Results&rft.au=Taber%2C+Jennifer+M%3BKlein%2C+William+M+P%3BFerrer%2C+Rebecca+A%3BLewis%2C+Katie+L%3BBiesecker%2C+Leslie+G%3BBiesecker%2C+Barbara+B&rft.aulast=Taber&rft.aufirst=Jennifer&rft.date=2015-07-01&rft.volume=34&rft.issue=7&rft.spage=718&rft.isbn=&rft.btitle=&rft.title=Health+Psychology&rft.issn=02786133&rft_id=info:doi/10.1037%2Fhea0000159 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-01 N1 - Last updated - 2015-12-23 N1 - SubjectsTermNotLitGenreText - Risk assessment; Health risks; Behavior; Perception; Risk taking DO - http://dx.doi.org/10.1037/hea0000159 ER - TY - JOUR T1 - Covariation of Depressive Mood and Spontaneous Physical Activity in Major Depressive Disorder: Toward Continuous Monitoring of Depressive Mood AN - 1709177706; PQ0001856236 AB - The objective evaluation of depressive mood is considered to be useful for the diagnosis and treatment of depressive disorders. Thus, we investigated psychobehavioral correlates, particularly the statistical associations between momentary depressive mood and behavioral dynamics measured objectively, in patients with major depressive disorder (MDD) and healthy subjects. Patients with MDD ($n = 14$) and healthy subjects ($n = 43$) wore a watch-type computer device and rated their momentary symptoms using ecological momentary assessment. Spontaneous physical activity in daily life, referred to as locomotor activity, was also continuously measured by an activity monitor built into the device. A multilevel modeling approach was used to model the associations between changes in depressive mood scores and the local statistics of locomotor activity simultaneously measured. We further examined the cross validity of such associations across groups. The statistical model established indicated that worsening of the depressive mood was associated with the increased intermittency of locomotor activity, as characterized by a lower mean and higher skewness. The model was cross validated across groups, suggesting that the same psychobehavioral correlates are shared by both healthy subjects and patients, although the latter had significantly higher mean levels of depressive mood scores. Our findings suggest the presence of robust as well as common associations between momentary depressive mood and behavioral dynamics in healthy individuals and patients with depression, which may lead to the continuous monitoring of the pathogenic processes (from healthy states) and pathological states of MDD. JF - IEEE Journal of Biomedical and Health Informatics AU - Kim, Jinhyuk AU - Nakamura, Toru AU - Kikuchi, Hiroe AU - Yoshiuchi, Kazuhiro AU - Sasaki, Tsukasa AU - Yamamoto, Yoshiharu AD - Department of Psychosomatic Research, National Institute of Mental Health, Tokyo, Japan Y1 - 2015/07// PY - 2015 DA - Jul 2015 SP - 1347 EP - 1355 PB - Institute of Electrical and Electronics Engineers, Inc., 3 Park Avenue, 17th Fl New York NY 10016-5997 United States VL - 19 IS - 4 SN - 2168-2194, 2168-2194 KW - Biotechnology and Bioengineering Abstracts KW - Mood KW - Depression KW - Statistics KW - Mathematical models KW - Informatics KW - Locomotor activity KW - Physical activity KW - Computers KW - Statistical analysis KW - Models KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709177706?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IEEE+Journal+of+Biomedical+and+Health+Informatics&rft.atitle=Covariation+of+Depressive+Mood+and+Spontaneous+Physical+Activity+in+Major+Depressive+Disorder%3A+Toward+Continuous+Monitoring+of+Depressive+Mood&rft.au=Kim%2C+Jinhyuk%3BNakamura%2C+Toru%3BKikuchi%2C+Hiroe%3BYoshiuchi%2C+Kazuhiro%3BSasaki%2C+Tsukasa%3BYamamoto%2C+Yoshiharu&rft.aulast=Kim&rft.aufirst=Jinhyuk&rft.date=2015-07-01&rft.volume=19&rft.issue=4&rft.spage=1347&rft.isbn=&rft.btitle=&rft.title=IEEE+Journal+of+Biomedical+and+Health+Informatics&rft.issn=21682194&rft_id=info:doi/10.1109%2FJBHI.2015.2440764 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Mood; Mathematical models; Statistics; Depression; Informatics; Computers; Physical activity; Locomotor activity; Statistical analysis; Models DO - http://dx.doi.org/10.1109/JBHI.2015.2440764 ER - TY - JOUR T1 - SimConcept: A Hybrid Approach for Simplifying Composite Named Entities in Biomedical Text AN - 1709168728; PQ0001856251 AB - One particular challenge in biomedical named entity recognition (NER) and normalization is the identification and resolution of composite named entities, where a single span refers to more than one concept (e.g., BRCA1/2). Previous NER and normalization studies have either ignored composite mentions, used simple ad hoc rules, or only handled coordination ellipsis, making a robust approach for handling multitype composite mentions greatly needed. To this end, we propose a hybrid method integrating a machine-learning model with a pattern identification strategy to identify the individual components of each composite mention. Our method, which we have named SimConcept, is the first to systematically handle many types of composite mentions. The technique achieves high performance in identifying and resolving composite mentions for three key biological entities: genes (90.42% in F-measure), diseases (86.47% in F-measure), and chemicals (86.05% in F-measure). Furthermore, our results show that using our SimConcept method can subsequently improve the performance of gene and disease concept recognition and normalization. SimConcept is available for download at: http://www.ncbi.nlm.nih.gov/CBBresearch/Lu/Demo/SimConcept/ JF - IEEE Journal of Biomedical and Health Informatics AU - Wei, Chih-Hsuan AU - Leaman, Robert AU - Lu, Zhiyong AD - National Institutes of Health and National Center for Biotechnology Information (NCBI), National Library of Medicine, National Institutes of Health, Bethesda, MD, USA Y1 - 2015/07// PY - 2015 DA - Jul 2015 SP - 1385 EP - 1391 PB - Institute of Electrical and Electronics Engineers, Inc., 3 Park Avenue, 17th Fl New York NY 10016-5997 United States VL - 19 IS - 4 SN - 2168-2194, 2168-2194 KW - Biotechnology and Bioengineering Abstracts KW - Informatics KW - Hybrids KW - BRCA1 protein KW - Models KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709168728?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IEEE+Journal+of+Biomedical+and+Health+Informatics&rft.atitle=SimConcept%3A+A+Hybrid+Approach+for+Simplifying+Composite+Named+Entities+in+Biomedical+Text&rft.au=Wei%2C+Chih-Hsuan%3BLeaman%2C+Robert%3BLu%2C+Zhiyong&rft.aulast=Wei&rft.aufirst=Chih-Hsuan&rft.date=2015-07-01&rft.volume=19&rft.issue=4&rft.spage=1385&rft.isbn=&rft.btitle=&rft.title=IEEE+Journal+of+Biomedical+and+Health+Informatics&rft.issn=21682194&rft_id=info:doi/10.1109%2FJBHI.2015.2422651 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Informatics; Hybrids; BRCA1 protein; Models DO - http://dx.doi.org/10.1109/JBHI.2015.2422651 ER - TY - JOUR T1 - Optimal Drug Prediction From Personal Genomics Profiles AN - 1709167108; PQ0001856247 AB - Cancer patients often show heterogeneous drug responses such that only a small subset of patients is sensitive to a given anticancer drug. With the availability of large-scale genomic profiling via next-generation sequencing, it is now economically feasible to profile the whole transcriptome and genome of individual patients in order to identify their unique genetic mutations and differentially expressed genes, which are believed to be responsible for heterogeneous drug responses. Although subtyping analysis has identified patient subgroups sharing common biomarkers, there is no effective method to predict the drug response of individual patients precisely and reliably. Herein, we propose a novel computational algorithm to predict the drug response of individual patients based on personal genomic profiles, as well as pharmacogenomic and drug sensitivity data. Specifically, more than 600 cancer cell lines (viewed as individual patients) across over 50 types of cancers and their responses to 75 drugs were obtained from the genomics of drug sensitivity in cancer database. The drug-specific sensitivity signatures were determined from the changes in genomic profiles of individual cell lines in response to a specific drug. The optimal drugs for individual cell lines were predicted by integrating the votes from other cell lines. The experimental results show that the proposed drug prediction algorithm can be used to improve greatly the reliability of finding optimal drugs for individual patients and will, thus, form a key component in the precision medicine infrastructure for oncology care. JF - IEEE Journal of Biomedical and Health Informatics AU - Sheng, Jianting AU - Li, Fuhai AU - Wong, Stephen TC AD - NCI Center for Modeling Cancer Development, Department of Systems Medicine and Bioengineering, Houston Methodist Research Institute, Weill Cornell Medical College, Houston, TX, USA Y1 - 2015/07// PY - 2015 DA - Jul 2015 SP - 1264 EP - 1270 PB - Institute of Electrical and Electronics Engineers, Inc., 3 Park Avenue, 17th Fl New York NY 10016-5997 United States VL - 19 IS - 4 SN - 2168-2194, 2168-2194 KW - Biotechnology and Bioengineering Abstracts KW - Data processing KW - pharmacogenomics KW - Informatics KW - Algorithms KW - Oncology KW - Computer applications KW - Antitumor agents KW - biomarkers KW - Cancer KW - Gene expression KW - Databases KW - Tumor cell lines KW - genomics KW - Drugs KW - Mutation KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709167108?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IEEE+Journal+of+Biomedical+and+Health+Informatics&rft.atitle=Optimal+Drug+Prediction+From+Personal+Genomics+Profiles&rft.au=Sheng%2C+Jianting%3BLi%2C+Fuhai%3BWong%2C+Stephen+TC&rft.aulast=Sheng&rft.aufirst=Jianting&rft.date=2015-07-01&rft.volume=19&rft.issue=4&rft.spage=1264&rft.isbn=&rft.btitle=&rft.title=IEEE+Journal+of+Biomedical+and+Health+Informatics&rft.issn=21682194&rft_id=info:doi/10.1109%2FJBHI.2015.2412522 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Data processing; Informatics; pharmacogenomics; Algorithms; Oncology; Computer applications; biomarkers; Antitumor agents; Cancer; Gene expression; Databases; Tumor cell lines; genomics; Mutation; Drugs DO - http://dx.doi.org/10.1109/JBHI.2015.2412522 ER - TY - JOUR T1 - Critical role of evolutionarily conserved glycosylation at Asn211 in the intracellular trafficking and activity of sialyltransferase ST3Gal-II. AN - 1707558037; 25916169 AB - ST3Gal-II, a type II transmembrane protein, is the main mammalian sialyltransferase responsible for GD1a and GT1b ganglioside biosynthesis in brain. It contains two putative N-glycosylation sites (Asn(92) and Asn(211)). Whereas Asn(92) is only conserved in mammalian species, Asn(211) is highly conserved in mammals, birds and fish. The present study explores the occupancy and relevance for intracellular trafficking and enzyme activity of these potential N-glycosylations in human ST3Gal-II. We found that ST3Gal-II distributes along the Golgi complex, mainly in proximal compartments. By pharmacological, biochemical and site-directed mutagenesis, we observed that ST3Gal-II is mostly N-glycosylated at Asn(211) and that this co-translational modification is critical for its exit from the endoplasmic reticulum and proper Golgi localization. The individual N-glycosylation sites had different effects on ST3Gal-II enzymatic activity. Whereas the N-glycan at position Asn(211) seems to negatively influence the activity of the enzyme using both glycolipid and glycoprotein as acceptor substrates, the single N-glycan mutant at Asn(92) had only a moderate effect. Lastly, we demonstrated that the N-terminal ST3Gal-II domain containing the cytosolic, transmembrane and stem region (amino acids 1-51) is able to drive a protein reporter out of the endoplasmic reticulum and to retain it in the Golgi complex. This suggests that the C-terminal domain of ST3Gal-II depends on N-glycosylation to attain an optimum conformation for proper exit from the endoplasmic reticulum, but it does not represent an absolute requirement for Golgi complex retention of the enzyme. © 2015 Authors; published by Portland Press Limited. JF - The Biochemical journal AU - Ruggiero, Fernando M AU - Vilcaes, Aldo A AU - Iglesias-Bartolomé, Ramiro AU - Daniotti, José L AD - Centro de Investigaciones en Química Biológica de Córdoba (CIQUIBIC, UNC-CONICET), Departamento de Química Biológica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina. ; Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, U.S.A. ; Centro de Investigaciones en Química Biológica de Córdoba (CIQUIBIC, UNC-CONICET), Departamento de Química Biológica, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina daniotti@dqb.fcq.unc.edu.ar. Y1 - 2015/07/01/ PY - 2015 DA - 2015 Jul 01 SP - 83 EP - 95 VL - 469 IS - 1 KW - Asparagine KW - 7006-34-0 KW - Sialyltransferases KW - EC 2.4.99.- KW - beta-galactoside alpha-2,3-sialyltransferase KW - EC 2.4.99.4 KW - Index Medicus KW - sialyltransferase KW - N-glycan trimming KW - ganglioside KW - N-glycosylation KW - ST3Gal-II KW - glycolipid KW - Golgi complex KW - Animals KW - Cricetulus KW - Humans KW - Asparagine -- metabolism KW - Asparagine -- genetics KW - CHO Cells KW - Glycosylation KW - Protein Structure, Tertiary KW - Protein Transport -- physiology KW - Evolution, Molecular KW - Cricetinae KW - Endoplasmic Reticulum -- enzymology KW - Sialyltransferases -- genetics KW - Sialyltransferases -- metabolism KW - Golgi Apparatus -- enzymology KW - Golgi Apparatus -- genetics KW - Endoplasmic Reticulum -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1707558037?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Biochemical+journal&rft.atitle=Critical+role+of+evolutionarily+conserved+glycosylation+at+Asn211+in+the+intracellular+trafficking+and+activity+of+sialyltransferase+ST3Gal-II.&rft.au=Ruggiero%2C+Fernando+M%3BVilcaes%2C+Aldo+A%3BIglesias-Bartolom%C3%A9%2C+Ramiro%3BDaniotti%2C+Jos%C3%A9+L&rft.aulast=Ruggiero&rft.aufirst=Fernando&rft.date=2015-07-01&rft.volume=469&rft.issue=1&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=The+Biochemical+journal&rft.issn=1470-8728&rft_id=info:doi/10.1042%2FBJ20150072 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-25 N1 - Date created - 2015-08-26 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1042/BJ20150072 ER - TY - JOUR T1 - Nitrate and nitrite ingestion and risk of ovarian cancer among postmenopausal women in Iowa AN - 1705066347; PQ0001484979 AB - Nitrate and nitrite are precursors in the endogenous formation of N-nitroso compounds (NOC), potential human carcinogens. We evaluated the association of nitrate and nitrite ingestion with postmenopausal ovarian cancer risk in the Iowa Women's Health Study. Among 28,555 postmenopausal women, we identified 315 incident epithelial ovarian cancers from 1986 to 2010. Dietary nitrate and nitrite intakes were assessed at baseline using food frequency questionnaire data. Drinking water source at home was obtained in a 1989 follow-up survey. Nitrate-nitrogen (NO sub(3)-N) and total trihalomethane (TTHM) levels for Iowa public water utilities were linked to residences and average levels were computed based on each woman's duration at the residence. We computed multivariable-adjusted hazard ratios (HR) and 95% confidence intervals (CI) using Cox proportional hazards regression. We tested interactions of nitrate with TTHMs and dietary factors known to influence NOC formation. Ovarian cancer risk was 2.03 times higher (CI=1.22-3.38, p sub(trend)=0.003) in the highest quartile ( greater than or equal to 2.98 mg/L) compared with the lowest quartile ( less than or equal to 0.47 mg/L; reference) of NO sub(3)-N in public water, regardless of TTHM levels. Risk among private well users was also elevated (HR=1.53, CI=0.93-2.54) compared with the same reference group. Associations were stronger when vitamin C intake was 1 mm). We found that while specific S. aureus surface proteins are a prerequisite for agglomeration in synovial fluid, low activity of the Agr regulatory system and subsequent low production of the phenol-soluble modulin (PSM) surfactant peptides cause agglomerates to grow to exceptional dimensions. Our results indicate that PSMs function by disrupting interactions of biofilm matrix molecules, such as the polysaccharide intercellular adhesin (PIA), with the bacterial cell surface. Together, our findings support a two-step model of staphylococcal prosthetic joint infection: As we previously reported, interaction of S. aureus surface proteins with host matrix proteins such as fibrin initiates agglomeration; our present results show that, thereafter, the bacterial agglomerates grow to extremely large sizes owing to the lack of PSM expression under the specific conditions present in joints. Our findings provide a mechanistic explanation for the reported extreme resistance of joint infection to antibiotic treatment, lend support to the notions that Agr functionality and PSM production play a major role in defining different forms of S. aureus infection, and have important implications for antistaphylococcal therapeutic strategies. JF - Infection and Immunity AU - Dastgheyb, Sana S AU - Villaruz, Amer E AU - Le, Katherine Y AU - Tan, Vee Y AU - Duong, Anthony C AU - Chatterjee, Som S AU - Cheung, Gordon YC AU - Joo, Hwang-Soo AU - Hickok, Noreen J AU - Otto, Michael AD - Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, motto@niaid.nih.gov. Y1 - 2015/07// PY - 2015 DA - Jul 2015 SP - 2966 EP - 2975 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 83 IS - 7 SN - 0019-9567, 0019-9567 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Adhesins KW - Cell surface KW - fibrin KW - Joint diseases KW - Antibiotics KW - Polysaccharides KW - Infection KW - matrix protein KW - Synovial fluid KW - Biofilms KW - Staphylococcus aureus KW - Surfactants KW - Prosthetics KW - Agglomeration KW - J 02350:Immunology KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701494238?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Role+of+Phenol-Soluble+Modulins+in+Formation+of+Staphylococcus+aureus+Biofilms+in+Synovial+Fluid&rft.au=Dastgheyb%2C+Sana+S%3BVillaruz%2C+Amer+E%3BLe%2C+Katherine+Y%3BTan%2C+Vee+Y%3BDuong%2C+Anthony+C%3BChatterjee%2C+Som+S%3BCheung%2C+Gordon+YC%3BJoo%2C+Hwang-Soo%3BHickok%2C+Noreen+J%3BOtto%2C+Michael&rft.aulast=Dastgheyb&rft.aufirst=Sana&rft.date=2015-07-01&rft.volume=83&rft.issue=7&rft.spage=2966&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.00394-15 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Number of references - 44 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Cell surface; Adhesins; fibrin; Joint diseases; Antibiotics; Infection; Polysaccharides; matrix protein; Synovial fluid; Biofilms; Surfactants; Agglomeration; Prosthetics; Staphylococcus aureus DO - http://dx.doi.org/10.1128/IAI.00394-15 ER - TY - JOUR T1 - Novel CD4-Based Bispecific Chimeric Antigen Receptor Designed for Enhanced Anti-HIV Potency and Absence of HIV Entry Receptor Activity AN - 1701494209; PQ0001784911 AB - Adoptive transfer of CD8 T cells genetically engineered to express "chimeric antigen receptors" (CARs) represents a potential approach toward an HIV infection "functional cure" whereby durable virologic suppression is sustained after discontinuation of antiretroviral therapy. We describe a novel bispecific CAR in which a CD4 segment is linked to a single-chain variable fragment of the 17b human monoclonal antibody recognizing a highly conserved CD4-induced epitope on gp120 involved in coreceptor binding. We compared a standard CD4 CAR with CD4-17b CARs where the polypeptide linker between the CD4 and 17b moieties is sufficiently long (CD4-35-17b CAR) versus too short (CD4-10-17b) to permit simultaneous binding of the two moieties to a single gp120 subunit. When transduced into a peripheral blood mononuclear cell (PBMC) or T cells thereof, all three CD4-based CARs displayed specific functional activities against HIV-1 Env-expressing target cells, including stimulation of gamma interferon (IFN- gamma ) release, specific target cell killing, and suppression of HIV-1 pseudovirus production. In assays of spreading infection of PBMCs with genetically diverse HIV-1 primary isolates, the CD4-10-17b CAR displayed enhanced potency compared to the CD4 CAR whereas the CD4-35-17b CAR displayed diminished potency. Importantly, both CD4-17b CARs were devoid of a major undesired activity observed with the CD4 CAR, namely, rendering the transduced CD8+ T cells susceptible to HIV-1 infection. Likely mechanisms for the superior potency of the CD4-10-17b CAR over the CD4-35-17b CAR include the greater potential of the former to engage in the serial antigen binding required for efficient T cell activation and the ability of two CD4-10-17b molecules to simultaneously bind a single gp120 subunit. IMPORTANCE HIV research has been energized by prospects for a cure for HIV infection or, at least, for a "functional cure" whereby antiretroviral therapy can be discontinued without virus rebound. This report describes a novel CD4-based "chimeric antigen receptor" (CAR) which, when genetically engineered into T cells, gives them the capability to selectively respond to and kill HIV-infected cells. This CAR displays enhanced features compared to previously described CD4-based CARs, namely, increased potency and avoidance of the undesired rendering of the genetically modified CD8 T cells susceptible to HIV infection. When adoptively transferred back to the individual, the genetically modified T cells will hopefully provide durable killing of infected cells and sustained virus suppression without continued antiretroviral therapy, i.e., a functional cure. JF - Journal of Virology AU - Liu, Li AU - Patel, Bhavik AU - Ghanem, Mustafa H AU - Bundoc, Virgilio AU - Zheng, Zhili AU - Morgan, Richard A AU - Rosenberg, Steven A AU - Dey, Barna AU - Berger, Edward A AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, edward_berger@nih.gov. Y1 - 2015/07// PY - 2015 DA - Jul 2015 SP - 6685 EP - 6694 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 89 IS - 13 SN - 0022-538X, 0022-538X KW - Immunology Abstracts; Biotechnology and Bioengineering Abstracts; Virology & AIDS Abstracts KW - gamma -Interferon KW - Spreading KW - Monoclonal antibodies KW - antiretroviral therapy KW - CD8 antigen KW - Infection KW - Fv KW - Cell activation KW - Glycoprotein gp120 KW - Peripheral blood mononuclear cells KW - CD4 antigen KW - Human immunodeficiency virus KW - Genetic engineering KW - Human immunodeficiency virus 1 KW - Adoptive transfer KW - Lymphocytes T KW - Epitopes KW - W 30925:Genetic Engineering KW - V 22360:AIDS and HIV KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701494209?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Novel+CD4-Based+Bispecific+Chimeric+Antigen+Receptor+Designed+for+Enhanced+Anti-HIV+Potency+and+Absence+of+HIV+Entry+Receptor+Activity&rft.au=Liu%2C+Li%3BPatel%2C+Bhavik%3BGhanem%2C+Mustafa+H%3BBundoc%2C+Virgilio%3BZheng%2C+Zhili%3BMorgan%2C+Richard+A%3BRosenberg%2C+Steven+A%3BDey%2C+Barna%3BBerger%2C+Edward+A&rft.aulast=Liu&rft.aufirst=Li&rft.date=2015-07-01&rft.volume=89&rft.issue=13&rft.spage=6685&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.00474-15 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Number of references - 73 N1 - Last updated - 2015-11-25 N1 - SubjectsTermNotLitGenreText - gamma -Interferon; Spreading; Monoclonal antibodies; antiretroviral therapy; CD8 antigen; Infection; Fv; Cell activation; Glycoprotein gp120; CD4 antigen; Peripheral blood mononuclear cells; Genetic engineering; Lymphocytes T; Adoptive transfer; Epitopes; Human immunodeficiency virus; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1128/JVI.00474-15 ER - TY - JOUR T1 - Temperature and sheltering determine patterns of seedling establishment in an advancing subtropical treeline AN - 1701477275; PQ0001681166 AB - Questions An advance of high-altitude treelines has been reported in response to warming climate throughout the globe. Understanding local controls on the establishment of seedlings above the treeline is essential for predicting wider patterns of treeline response from a process-based perspective. Here we investigate patterns of seedling establishment in relation to microsite conditions in an advancing treeline ecotone in the subtropics, using climate data recorded at the plant-relevant scale. We sought to determine which temperature factors were of importance, if sheltering plays an important role in seedling establishment and if the response varied with seedling age. Location The Abies kawakamii treelines of the Central Mountain Range, Taiwan, 2800 to 3275 m a.s.l. Methods Seedlings were monitored in plots covering a range of treeline structural forms over a period of 2 yrs. Temperatures were recorded at plant-relevant height (5 cm) above ground and depth below ground with data loggers. Microtopographic sheltering (at a 10-m scale) and surrounding vegetation were measured. The influence of the above variables on seedling number and growth was investigated using generalized linear models and linear mixed effect models, respectively. Results Soil temperatures had more influence on seedling number than air temperature, whilst air temperature was positively associated with subsequent seedling growth. Establishment patterns were found to have a strong relationship with microtopographic sheltering, with more sheltered areas having elevated seedling numbers. Early growth may have significant implications for subsequent plant performance since smaller seedlings were more sensitive to both temperature and microtopography than larger seedlings. Conclusions Air and soil temperatures and microtopography determine spatial patterns of seedling establishment. Our results suggest that establishment above the treeline is likely to continue as the climate warms, although advance will not be spatially uniform due to the modifying influence of topography. This variability has important implications for the persistence and extinction of alpine plant communities occurring above treeline in topographically complex systems. What drives seedling establishment at altitudinal treeline? We recorded microclimate data across an advancing treeline ecotone and report an influence of soil temperature and micro-topographic shelter on establishment, and of air temperature on growth rates. If temperature increases continue it is likely that further establishment and advance will occur, although the influence of shelter suggests this will be spatially variable. JF - Journal of Vegetation Science AU - Greenwood, Sarah AU - Chen, Jan-Chang AU - Chen, Chaur-Tzuhn AU - Jump, Alistair S AD - Department of Forestry, National Pingtung University of Science and Technology, 1 Hseuh Fu Road, Nei Pu Hsiang, Pingtung, 912, Taiwan. Y1 - 2015/07// PY - 2015 DA - Jul 2015 SP - 711 EP - 721 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 26 IS - 4 SN - 1100-9233, 1100-9233 KW - Ecology Abstracts; Sustainability Science Abstracts KW - Treeline KW - Age KW - Body temperature KW - Abies KW - Soil temperature KW - Air temperature KW - Mountains KW - Microclimate KW - Topography KW - Temperature effects KW - Growth rate KW - Data processing KW - Extinction KW - Climate KW - Temperature KW - Vegetation KW - Shelter KW - Ecotones KW - ISEW, Taiwan KW - Plant communities KW - Seedlings KW - M3 1010:Issues in Sustainable Development KW - D 04040:Ecosystem and Ecology Studies UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701477275?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Vegetation+Science&rft.atitle=Temperature+and+sheltering+determine+patterns+of+seedling+establishment+in+an+advancing+subtropical+treeline&rft.au=Greenwood%2C+Sarah%3BChen%2C+Jan-Chang%3BChen%2C+Chaur-Tzuhn%3BJump%2C+Alistair+S&rft.aulast=Greenwood&rft.aufirst=Sarah&rft.date=2015-07-01&rft.volume=26&rft.issue=4&rft.spage=711&rft.isbn=&rft.btitle=&rft.title=Journal+of+Vegetation+Science&rft.issn=11009233&rft_id=info:doi/10.1111%2Fjvs.12269 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Growth rate; Treeline; Temperature effects; Age; Data processing; Extinction; Body temperature; Climate; Soil temperature; Vegetation; Shelter; Ecotones; Air temperature; Mountains; Plant communities; Microclimate; Seedlings; Topography; Temperature; Abies; ISEW, Taiwan DO - http://dx.doi.org/10.1111/jvs.12269 ER - TY - JOUR T1 - Racial Differences in Self-Reports of Short Sleep Duration in an Urban-Dwelling Environment AN - 1701262381 AB - Objectives. To explore whether there are differences in sleep duration between blacks and whites residing in similar urban neighborhoods and examine whether the relationship between sleep durations and sociodemographic and/or health indices are consistent for blacks and whites. Methods. A total of 1,207 participants from the Healthy Aging in Neighborhoods of Disparities across the Life Span study (age: mean = 47, standard deviation = 8.74). Sleep duration was assessed by a self-report of hours of nightly sleep in the past month. Sociodemographic measures included age, sex, education, poverty status, and perceived neighborhood disorder. Health status was assessed using measures of vigilance, depression, perceived stress, coronary artery disease, diabetes, blood pressure, and inflammation. Results. There were no significant racial group differences in sleep duration. Whites, however, were more likely than blacks to report sleep durations of <6/6-7hr compared with >7hr with increasing stress and education levels. Blacks were more likely than whites to report short sleep durations (i.e., 6-7hr vs. >7hr of sleep) with increasing inflammation levels. Discussion. Although racial disparities in sleep duration are minimized when the environment is equivalent between blacks and whites, the underlying demographic and health explanations for short sleep durations may vary between whites and blacks. JF - The Journals of Gerontology. Series B, Psychological Sciences and Social Sciences AU - McNeely, Jessica M AU - Shah, Mauli T AU - Evans, Michele K AU - Zonderman, Alan B AD - National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, Maryland ; Gamaldo, Alyssa A; National Institute on Aging Intramural Research Program, National Institutes of Health, Baltimore, Maryland Y1 - 2015/07// PY - 2015 DA - Jul 2015 SP - 568 EP - 575 CY - Washington PB - Oxford University Press, UK VL - 70 IS - 4 SN - 1079-5014 KW - Gerontology And Geriatrics KW - Aging KW - Race KW - Sleep duration KW - Neighbourhoods KW - Poverty KW - Racial differences KW - Racial inequalities KW - Selfreport KW - Sleep KW - Social disorganization KW - Sociodemographic aspects KW - Vigilance KW - Black White Differences KW - Racial Differences KW - Blood Pressure KW - Depression (Psychology) KW - Diabetes KW - Neighborhoods KW - Health KW - Health Problems KW - Ageing KW - Blood pressure KW - Coronary diseases KW - Depression KW - Deviation KW - Health inequalities KW - Health status KW - Inflammation KW - Life span UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701262381?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journals+of+Gerontology.+Series+B%2C+Psychological+Sciences+and+Social+Sciences&rft.atitle=Racial+Differences+in+Self-Reports+of+Short+Sleep+Duration+in+an+Urban-Dwelling+Environment&rft.au=Gamaldo%2C+Alyssa+A%3BMcNeely%2C+Jessica+M%3BShah%2C+Mauli+T%3BEvans%2C+Michele+K%3BZonderman%2C+Alan+B&rft.aulast=Gamaldo&rft.aufirst=Alyssa&rft.date=2015-07-01&rft.volume=70&rft.issue=4&rft.spage=568&rft.isbn=&rft.btitle=&rft.title=The+Journals+of+Gerontology.+Series+B%2C+Psychological+Sciences+and+Social+Sciences&rft.issn=10795014&rft_id=info:doi/10.1093%2Fgeronb%2Fgbt117 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-08-04 N1 - Last updated - 2016-05-24 DO - http://dx.doi.org/10.1093/geronb/gbt117 ER - TY - JOUR T1 - Temperament and Parenting Styles in Early Childhood Differentially Influence Neural Response to Peer Evaluation in Adolescence AN - 1698884163 AB - Behavioral inhibition (BI) is a temperament characterized by social reticence and withdrawal from unfamiliar or novel contexts and conveys risk for social anxiety disorder. Developmental outcomes associated with this temperament can be influenced by children’s caregiving context. The convergence of a child’s temperamental disposition and rearing environment is ultimately expressed at both the behavioral and neural levels in emotional and cognitive response patterns to social challenges. The present study used functional neuroimaging to assess the moderating effects of different parenting styles on neural response to peer rejection in two groups of adolescents characterized by their early childhood temperament ( M age=17.89 years, N=39, 17 males, 22 females; 18 with BI; 21 without BI). The moderating effects of authoritarian and authoritative parenting styles were examined in three brain regions linked with social anxiety: ventrolateral prefrontal cortex (vlPFC), striatum, and amygdala. In youth characterized with BI in childhood, but not in those without BI, diminished responses to peer rejection in vlPFC were associated with higher levels of authoritarian parenting. In contrast, all youth showed decreased caudate response to peer rejection at higher levels of authoritative parenting. These findings indicate that BI in early life relates to greater neurobiological sensitivity to variance in parenting styles, particularly harsh parenting, in late adolescence. These results are discussed in relation to biopsychosocial models of development. JF - Journal of Abnormal Child Psychology AU - Jarcho, Johanna M AU - Pérez-Edgar, Koraly AU - Degnan, Kathryn A AU - Pine, Daniel S AU - Fox, Nathan A AU - Nelson, Eric E AD - Section on Development and Affective Neuroscience, Intramural Program of Research, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA ; Department of Psychology, The Pennsylvania State University, University Park, PA, USA ; Department of Human Development and Quantitative Methodology, University of Maryland, College Park, MD, USA ; Guyer, Amanda E; Department of Human Ecology, Center for Mind and Brain, University of California Davis, 267 Cousteau Place, Davis, CA, 95618, USA Y1 - 2015/07// PY - 2015 DA - Jul 2015 SP - 863 EP - 874 CY - New York PB - Springer Science & Business Media VL - 43 IS - 5 SN - 0091-0627 KW - Medical Sciences--Physical Medicine And Rehabilitation KW - Adolescents KW - Biopsychosocial aspects KW - Cognitive responses KW - Cortex KW - Harsh KW - Inhibition KW - Neuroimaging KW - Parenting KW - Peer rejection KW - Rejection KW - Sensitivity KW - Social anxiety KW - Social influence KW - Temperament KW - Anxiety disorders KW - Authoritative parenting KW - Behaviour KW - Brain KW - Carers KW - Childhood KW - Children KW - Cognitive-Behavioural factors KW - Convergence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698884163?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Abnormal+Child+Psychology&rft.atitle=Temperament+and+Parenting+Styles+in+Early+Childhood+Differentially+Influence+Neural+Response+to+Peer+Evaluation+in+Adolescence&rft.au=Guyer%2C+Amanda+E%3BJarcho%2C+Johanna+M%3BP%C3%A9rez-Edgar%2C+Koraly%3BDegnan%2C+Kathryn+A%3BPine%2C+Daniel+S%3BFox%2C+Nathan+A%3BNelson%2C+Eric+E&rft.aulast=Guyer&rft.aufirst=Amanda&rft.date=2015-07-01&rft.volume=43&rft.issue=5&rft.spage=863&rft.isbn=&rft.btitle=&rft.title=Journal+of+Abnormal+Child+Psychology&rft.issn=00910627&rft_id=info:doi/10.1007%2Fs10802-015-9973-2 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-07-23 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1007/s10802-015-9973-2 ER - TY - JOUR T1 - Do School Resources Influence the Relationship Between Adolescent Financial Background and Their School Perceptions? AN - 1698882448 AB - BACKGROUND Socioeconomic status (SES) influences studentsʼ school perceptions and affects their performance, engagement, and personal beliefs. This study examined the effects of school population SES and school resources on the association between student SES and student perceptions. METHODS School liking, classmate social relationships, family affluence, and experience of hunger were assessed in a nationally representative sample of 12,642 students (grades 5-10) in the 2009-2010 Health Behavior in School-Aged Children study. School characteristics included school meal program, Title 1 dollars received per student, school resources, and urban/rural status. Multilevel analysis was used. RESULTS At the individual level, both school liking and social relationships were negatively associated with student grade level. Boys liked school less and had more positive perceptions of social relationships than girls. Students in rural schools and who experienced hunger liked schools less and had poorer perceptions of social relationships than their respective counterparts. School-level percentage of students eligible for free/reduced meals accounted for 33% of the between-school variance in social relationships. CONCLUSIONS Family and school economic characteristics and grade level influenced studentsʼ school perceptions. The associations between student SES, school population SES, and school perceptions suggests that school health professionals should recognize and address student economic issues at school. JF - The Journal of School Health AU - Summersett-Ringgold, Faith C AU - Li, Kaigang AU - Haynie, Denise L AU - Iannotti, Ronald J AD - Department of Psychiatry and Behavioral Sciences, Northwestern University, Feinberg School of Medicine, 710 N. Lake Shore Drive, Chicago, IL 60611. ; Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, 6100 Executive Blvd, Bethesda, MD 20852. ; Department of Exercise and Health Sciences, College of Nursing and Health Sciences, University of Massachusetts Boston, Boston, MA 02125. ; Department of Psychiatry and Behavioral Sciences, Northwestern University, Feinberg School of Medicine, 710 N. Lake Shore Drive, Chicago, IL 60611. Y1 - 2015/07// PY - 2015 DA - Jul 2015 SP - 413 EP - 422 CY - Kent PB - Wiley Subscription Services, Inc. VL - 85 IS - 7 SN - 0022-4391 KW - Physical Fitness And Hygiene KW - Adolescents KW - Rural communities KW - Social relationships KW - Socioeconomic status KW - Affluence KW - Girls KW - Health behaviour KW - Health professionals KW - Hunger KW - Liking KW - Meals KW - Multilevel analysis KW - Perceptions UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698882448?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+School+Health&rft.atitle=Do+School+Resources+Influence+the+Relationship+Between+Adolescent+Financial+Background+and+Their+School+Perceptions%3F&rft.au=Summersett-Ringgold%2C+Faith+C%3BLi%2C+Kaigang%3BHaynie%2C+Denise+L%3BIannotti%2C+Ronald+J&rft.aulast=Summersett-Ringgold&rft.aufirst=Faith&rft.date=2015-07-01&rft.volume=85&rft.issue=7&rft.spage=413&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+School+Health&rft.issn=00224391&rft_id=info:doi/10.1111%2Fjosh.12267 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-09-22 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1111/josh.12267 ER - TY - JOUR T1 - Epidemiologic studies of estrogen metabolism and breast cancer. AN - 1698390728; 25725255 AB - Early epidemiologic studies of estrogen metabolism measured only 2-hydroxyestrone and 16α-hydroxyestrone and relied on direct enzyme immunoassays without purification steps. Eight breast cancer studies have used these assays with prospectively collected blood or urine samples. Results were inconsistent, and generally not statistically significant; but the assays had limited specificity, especially at the low concentrations characteristic of postmenopausal women. To facilitate continued testing in population-based studies of the multiple laboratory-based hypotheses about the roles of estrogen metabolites, a novel liquid chromatography-tandem mass spectrometry (LC-MS/MS) assay was developed to measure concurrently all 15 estrogens and estrogen metabolites in human serum and urine, as unconjugated and total (glucuronidated+sulfated+unconjugated) concentrations. The assay has high sensitivity (lower limit of quantitation ∼1-2 pmol/L), reproducibility (coefficients of variation generally ⩽5%), and accuracy. Three prospective studies utilizing this comprehensive assay have demonstrated that enhanced 2-hydroxylation of parent estrogens (estrone+estradiol) is associated with reduced risk of postmenopausal breast cancer. In the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) cohort, the serum ratio of 2-hydroxylation pathway metabolites to parent estrogens was associated with a 28% reduction in breast cancer risk across extreme deciles (p-trend=.05), after adjusting for unconjugated estradiol and breast cancer risk factors. Incorporating this ratio into a risk prediction model already including unconjugated estradiol improved absolute risk estimates substantially (by ⩾14%) in 36% of the women, an encouraging result that needs replication. Additional epidemiologic studies of the role of estrogen metabolism in the etiology of hormone-related diseases and continued improvement of estrogen metabolism assays are justified. Published by Elsevier Inc. JF - Steroids AU - Ziegler, Regina G AU - Fuhrman, Barbara J AU - Moore, Steven C AU - Matthews, Charles E AD - Epidemiology and Biostatistics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892-9773, USA. Electronic address: Regina.Ziegler@nih.gov. ; Epidemiology and Biostatistics Program, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892-9773, USA. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 67 EP - 75 VL - 99 KW - Estrogens KW - 0 KW - Hydroxyestrones KW - 16-hydroxyestrone KW - 18186-49-7 KW - 2-hydroxyestrone KW - UQS3A06ILY KW - Index Medicus KW - 16α-hydroxyestrone KW - Breast cancer KW - Hormonal carcinogenesis KW - Estrogen metabolites KW - Estradiol KW - Prospective Studies KW - Postmenopause KW - Epidemiologic Studies KW - Risk Factors KW - Premenopause KW - Humans KW - Tandem Mass Spectrometry -- methods KW - Hydroxyestrones -- metabolism KW - Chromatography, Liquid KW - Female KW - Estrogens -- metabolism KW - Breast Neoplasms -- metabolism KW - Estrogens -- analysis KW - Breast Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698390728?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Steroids&rft.atitle=Epidemiologic+studies+of+estrogen+metabolism+and+breast+cancer.&rft.au=Ziegler%2C+Regina+G%3BFuhrman%2C+Barbara+J%3BMoore%2C+Steven+C%3BMatthews%2C+Charles+E&rft.aulast=Ziegler&rft.aufirst=Regina&rft.date=2015-07-01&rft.volume=99&rft.issue=&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=Steroids&rft.issn=1878-5867&rft_id=info:doi/10.1016%2Fj.steroids.2015.02.015 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-23 N1 - Date created - 2015-05-26 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.steroids.2015.02.015 ER - TY - JOUR T1 - Phase I trial of systemic intravenous infusion of interleukin-13-Pseudomonas exotoxin in patients with metastatic adrenocortical carcinoma. AN - 1696885993; 25767039 AB - Adrenocortical carcinoma (ACC) is a rare but lethal malignancy without effective current therapy for metastatic disease. IL-13-PE is a recombinant cytotoxin consisting of human interleukin-13 (IL-13) and a truncated form of Pseudomonas exotoxin A (PE). The main objectives of this Phase I dose-escalation trial were to assess the maximum-tolerated dose (MTD), safety, and pharmacokinetics (PK) of IL-13-PE in patients with metastatic ACC. Eligible patients had confirmed IL-13 receptor alpha 2 (IL-13Rα2) expressions in their tumors. IL-13-PE at dose of 1-2 μg/kg was administered intravenously (IV) on day 1, 3, and 5 in a 4-week cycle. Six patients received 1 μg/kg and two patients received 2 μg/kg of IL-13-PE. Dose-limiting toxicity was observed at 2 μg/kg, at which patients exhibited thrombocytopenia and renal insufficiency without requiring dialysis. PK analysis demonstrated that at MTD, the mean maximum serum concentration (Cmax ) of IL-13-PE was 21.0 ng/mL, and the terminal half-life of IL-13-PE was 30-39 min. Two (25%) of the eight patients had baseline neutralizing antibodies against PE. Three (75%) of the remaining four tested patients developed neutralizing antibodies against IL-13-PE within 14-28 days of initial treatment. Of the five patients treated at MTD and assessed for response, one patient had stable disease for 5.5 months before disease progression; the others progressed within 1-2 months. In conclusion, systemic IV administration of IL-13-PE is safe at 1 μg/kg. All tested patients developed high levels of neutralizing antibodies during IL-13-PE treatment. Use of strategies for immunodepletion before IL-13-PE treatment should be considered in future trials. © 2015 The Authors. Cancer Medicine published by John Wiley & Sons Ltd. JF - Cancer medicine AU - Liu-Chittenden, Yi AU - Jain, Meenu AU - Kumar, Parag AU - Patel, Dhaval AU - Aufforth, Rachel AU - Neychev, Vladimir AU - Sadowski, Samira AU - Gara, Sudheer K AU - Joshi, Bharat H AU - Cottle-Delisle, Candice AU - Merkel, Roxanne AU - Yang, Lily AU - Miettinen, Markku AU - Puri, Raj K AU - Kebebew, Electron AD - Endocrine Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. ; Clinical Pharmacokinetics Research Laboratory, Clinical Center Pharmacy Department, National Institutes of Health, Bethesda, Maryland. ; Tumor Vaccines and Biotechnology Branch, Division of Cellular and Gene Therapies, Center for Biologics Evaluation and Research, Food and Drug Administration, Silver Spring, Maryland. ; Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 1060 EP - 1068 VL - 4 IS - 7 KW - Antibodies, Neutralizing KW - 0 KW - Antineoplastic Agents KW - Bacterial Toxins KW - Exotoxins KW - Interleukin-13 KW - Recombinant Fusion Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Phase I KW - systemic administration KW - metastatic adrenocortical carcinoma KW - IL-13-PE KW - pharmacokinetics KW - maximum-tolerated dose KW - Young Adult KW - Infusions, Intravenous KW - Humans KW - Aged KW - Adult KW - Treatment Outcome KW - Neoplasm Metastasis KW - Middle Aged KW - Antibodies, Neutralizing -- blood KW - Maximum Tolerated Dose KW - Adolescent KW - Retreatment KW - Female KW - Male KW - Adrenocortical Carcinoma -- therapy KW - Recombinant Fusion Proteins -- pharmacokinetics KW - Recombinant Fusion Proteins -- adverse effects KW - Antineoplastic Agents -- administration & dosage KW - Antineoplastic Agents -- pharmacokinetics KW - Adrenal Cortex Neoplasms -- therapy KW - Recombinant Fusion Proteins -- administration & dosage KW - Adrenocortical Carcinoma -- drug therapy KW - Antineoplastic Agents -- adverse effects KW - Adrenocortical Carcinoma -- pathology KW - Adrenal Cortex Neoplasms -- pathology KW - Adrenal Cortex Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1696885993?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+medicine&rft.atitle=Phase+I+trial+of+systemic+intravenous+infusion+of+interleukin-13-Pseudomonas+exotoxin+in+patients+with+metastatic+adrenocortical+carcinoma.&rft.au=Liu-Chittenden%2C+Yi%3BJain%2C+Meenu%3BKumar%2C+Parag%3BPatel%2C+Dhaval%3BAufforth%2C+Rachel%3BNeychev%2C+Vladimir%3BSadowski%2C+Samira%3BGara%2C+Sudheer+K%3BJoshi%2C+Bharat+H%3BCottle-Delisle%2C+Candice%3BMerkel%2C+Roxanne%3BYang%2C+Lily%3BMiettinen%2C+Markku%3BPuri%2C+Raj+K%3BKebebew%2C+Electron&rft.aulast=Liu-Chittenden&rft.aufirst=Yi&rft.date=2015-07-01&rft.volume=4&rft.issue=7&rft.spage=1060&rft.isbn=&rft.btitle=&rft.title=Cancer+medicine&rft.issn=2045-7634&rft_id=info:doi/10.1002%2Fcam4.449 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-06 N1 - Date created - 2015-07-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Cancer Res Clin Oncol. 2010 Jun;136(6):839-46 [19916021] Neurosurgery. 2007 Nov;61(5):1031-7; discussion 1037-8 [18091279] Nat Rev Endocrinol. 2011 Jun;7(6):323-35 [21386792] Clin Cancer Res. 2011 Sep 15;17(18):5858-66 [21813634] Hum Gene Ther Methods. 2012 Apr;23(2):137-47 [22612657] J Clin Oncol. 2007 Mar 1;25(7):837-44 [17327604] Cancer. 2006 Sep 15;107(6):1407-18 [16902988] Mol Cancer Ther. 2008 Jun;7(6):1579-87 [18566228] Cancer. 2008 Dec 1;113(11):3130-6 [18973179] Best Pract Res Clin Endocrinol Metab. 2009 Apr;23(2):273-89 [19500769] Clin Cancer Res. 2010 Jan 15;16(2):577-86 [20068108] Cancer. 2012 Nov 15;118(22):5698-708 [22570059] Eur J Cancer. 2013 Jul;49(11):2579-86 [23561851] Cancer Res. 2000 Mar 1;60(5):1168-72 [10728667] Mol Med. 2000 May;6(5):440-9 [10952023] Clin Cancer Res. 2002 Jun;8(6):1948-56 [12060640] Clin Cancer Res. 2003 Dec 15;9(17):6381-8 [14695138] J Biol Chem. 1995 Jul 14;270(28):16775-80 [7622490] Blood. 1996 May 15;87(10):4333-9 [8639793] Clin Cancer Res. 1997 Feb;3(2):151-6 [9815666] Protein Expr Purif. 2005 Feb;39(2):189-98 [15642470] Nat Med. 2006 Jan;12(1):99-106 [16327802] World J Surg. 2006 May;30(5):872-8 [16680602] Technol Cancer Res Treat. 2006 Jun;5(3):239-50 [16700620] Neurosurg Focus. 2006;20(4):E15 [16709020] Neuro Oncol. 2010 Aug;12(8):871-81 [20511192] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/cam4.449 ER - TY - JOUR T1 - Dose-dependent expression of CLIP2 in post-Chernobyl papillary thyroid carcinomas. AN - 1695757874; 25957251 AB - A previous study on papillary thyroid carcinomas (PTC) in young patients who were exposed to (131)iodine from the Chernobyl fallout revealed an exclusive gain of chromosomal band 7q11.23 in exposed cases compared to an age-matched control cohort. CLIP2, a gene located within band 7q11.23 was shown to be differentially expressed between exposed and non-exposed cases at messenger RNA and protein level. Therefore, a standardized procedure for CLIP2 typing of PTCs has been developed in a follow-up study. Here we used CLIP2 typing data on 117 post-Chernobyl PTCs from two cohorts of exposed patients with individual dose estimates and 24 non-exposed controls to investigate a possible quantitative dose-response relationship of the CLIP2 marker. The 'Genrisk-T' cohort consisted of 45 PTCs and the 'UkrAm' cohort of 72 PTCs. Both cohorts differed in mean dose (0.59 Gy Genrisk-T, 1.2 Gy UkrAm) and mean age at exposure (AaE) (2 years Genrisk-T, 8 years UkrAm), whilst the median latency (16 years Genrisk-T, 18 years UkrAm) was comparable. We analyzed the association between the binary CLIP2 typing and continuous thyroid dose with logistic regression. A clear positive dose-response relationship was found for young PTC cases [age at operation (AaO) 20 years) with positivity for BRAF V600E mutation. © The Author 2015. Published by Oxford University Press. JF - Carcinogenesis AU - Selmansberger, Martin AU - Kaiser, Jan Christian AU - Hess, Julia AU - Güthlin, Denise AU - Likhtarev, I AU - Shpak, Victor AU - Tronko, Mykola AU - Brenner, Alina AU - Abend, Michael AU - Blettner, Maria AU - Unger, Kristian AU - Jacob, Peter AU - Zitzelsberger, Horst AD - Research Unit Radiation Cytogenetics and. ; Institute of Radiation Protection, Helmholtz Zentrum München, German Research Center for Environmental Health GmbH, 85674 Neuherberg, Germany, christian.kaiser@helmholtz-muenchen.de. ; Institute of Radiation Protection, Helmholtz Zentrum München, German Research Center for Environmental Health GmbH, 85674 Neuherberg, Germany. ; Radiation Protection Institute, Ukrainian Academy of Technological Sciences, 04050 Kyiv, Ukraine. ; Institute of Endocrinology and Metabolism, National Academy of Medical Sciences of the Ukraine, 254114 Kyiv, Ukraine. ; Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, NCI, Bethesda, MD 20892, USA. ; Bundeswehr Institute of Radiobiology, 80937 Munich, Germany and. ; Institut für Medizinische Biometrie, Epidemiologie und Informatik (IMBEI), Johannes Gutenberg Universität, 55131 Mainz, Germany. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 748 EP - 756 VL - 36 IS - 7 KW - Biomarkers, Tumor KW - 0 KW - Iodine Radioisotopes KW - Microtubule-Associated Proteins KW - cytoplasmic linker protein 115 KW - Index Medicus KW - Young Adult KW - Biomarkers, Tumor -- genetics KW - Chernobyl Nuclear Accident KW - Humans KW - Neoplasms, Radiation-Induced -- metabolism KW - Neoplasms, Radiation-Induced -- surgery KW - Iodine Radioisotopes -- administration & dosage KW - Child KW - Child, Preschool KW - Biomarkers, Tumor -- metabolism KW - Logistic Models KW - Adult KW - Cohort Studies KW - Adolescent KW - Microtubule-Associated Proteins -- metabolism KW - Microtubule-Associated Proteins -- genetics KW - Carcinoma -- surgery KW - Carcinoma -- etiology KW - Thyroid Neoplasms -- metabolism KW - Thyroid Neoplasms -- etiology KW - Dose-Response Relationship, Radiation KW - Thyroid Neoplasms -- surgery KW - Carcinoma -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1695757874?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Dose-dependent+expression+of+CLIP2+in+post-Chernobyl+papillary+thyroid+carcinomas.&rft.au=Selmansberger%2C+Martin%3BKaiser%2C+Jan+Christian%3BHess%2C+Julia%3BG%C3%BCthlin%2C+Denise%3BLikhtarev%2C+I%3BShpak%2C+Victor%3BTronko%2C+Mykola%3BBrenner%2C+Alina%3BAbend%2C+Michael%3BBlettner%2C+Maria%3BUnger%2C+Kristian%3BJacob%2C+Peter%3BZitzelsberger%2C+Horst&rft.aulast=Selmansberger&rft.aufirst=Martin&rft.date=2015-07-01&rft.volume=36&rft.issue=7&rft.spage=748&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgv043 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-24 N1 - Date created - 2015-07-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Br J Cancer. 2007 Sep 17;97(6):818-25 [17712314] Cancer. 2014 Mar 15;120(6):799-807 [24327398] Cancer Res. 2008 Sep 1;68(17):7176-82 [18757433] Oncogene. 2008 Dec;27 Suppl 2:S9-18 [19956182] Thyroid. 2010 May;20(5):475-87 [19725780] Radiat Prot Dosimetry. 2010 Jul;140(2):103-36 [20413418] Radiat Res. 2010 Dec;174(6):789-92 [21128804] Br J Cancer. 2011 Jan 4;104(1):181-7 [21102590] Clin Oncol (R Coll Radiol). 2011 May;23(4):276-81 [21345659] Proc Natl Acad Sci U S A. 2011 Jun 7;108(23):9595-600 [21606360] Environ Health Perspect. 2011 Jul;119(7):933-9 [21406336] Oncogene. 2015 Jul 23;34(30):3917-25 [25284583] Radiat Prot Dosimetry. 2003;105(1-4):601-8 [14527034] Radiat Res. 2004 Apr;161(4):481-92 [15038762] Radiat Res. 2004 Sep;162(3):241-8 [15332999] Genome Biol. 2004;5(10):R80 [15461798] Nature. 1998 Mar 5;392(6671):31-2 [9510245] Radiat Res. 2005 Feb;163(2):125-36 [15658887] J Pathol. 2005 Apr;205(5):558-64 [15714593] Br J Cancer. 2005 Apr 25;92(8):1545-52 [15812549] J Natl Cancer Inst. 2005 May 18;97(10):724-32 [15900042] Radiat Res. 2006 Jan;165(1):1-8 [16392956] J Radiol Prot. 2006 Jun;26(2):127-40 [16738412] Radiat Res. 2006 Jul;166(1 Pt 2):271-86 [16808613] J Natl Cancer Inst. 2006 Jul 5;98(13):897-903 [16818853] PLoS One. 2012;7(7):e39103 [22848350] Br J Cancer. 2012 Sep 4;107(6):994-1000 [22828612] Health Phys. 2013 Jan;104(1):78-86 [23192090] Int J Cancer. 2013 Mar 1;132(5):1222-6 [22847218] Cancer. 2013 May 15;119(10):1792-9 [23436219] Radiat Prot Dosimetry. 2013 Oct;156(4):407-23 [23595409] Br J Cancer. 2013 Oct 15;109(8):2286-94 [24045656] Radiat Res. 2007 Dec;168(6):639-49 [18088181] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgv043 ER - TY - JOUR T1 - Assessment of liver fibrosis using fast strain-encoded MRI driven by inherent cardiac motion AN - 1694972411; PQ0001665216 AB - Purpose An external driver-free MRI method for assessment of liver fibrosis offers a promising noninvasive tool for diagnosis and monitoring of liver disease. Lately, the heart's intrinsic motion and MR tagging have been utilized for the quantification of liver strain. However, MR tagging requires multiple breath-hold acquisitions and substantial postprocessing. In this study, we propose the use of a fast strain-encoded (FSENC) MRI method to measure the peak strain (Sp) in the liver's left lobe, which is in close proximity and caudal to the heart. Additionally, we introduce a new method of measuring heart-induced shear wave velocity (SWV) inside the liver. Methods Phantom and in vivo experiments (11 healthy subjects and 11 patients with liver fibrosis) were conducted. Reproducibility experiments were performed in seven healthy subjects. Results Peak liver strain, Sp, decreased significantly in fibrotic liver compared with healthy liver (6.46% plus or minus 2.27% vs 12.49% plus or minus 1.76%; P < 0.05). Heart-induced SWV increased significantly in patients compared with healthy subjects (0.15 plus or minus 0.04 m/s vs 0.63 plus or minus 0.32 m/s; P < 0.05). Reproducibility analysis yielded no significant difference in Sp (P = 0.47) or SWV (P = 0.56). Conclusion Accelerated external driver-free noninvasive assessment of left liver lobe strain and SWV is feasible using strain-encoded MRI. The two measures significantly separate healthy subjects from patients with fibrotic liver. Magn Reson Med 74:106-114, 2015. JF - Magnetic Resonance in Medicine AU - Harouni, Ahmed A AU - Gharib, Ahmed M AU - Osman, Nael F AU - Morse, Caryn AU - Heller, Theo AU - Abd-Elmoniem, Khaled Z AD - Imaging Sciences Training Program, The National Institute of Biomedical Imaging and Bioengineering, The National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/07// PY - 2015 DA - Jul 2015 SP - 106 EP - 114 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 74 IS - 1 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Heart KW - Liver diseases KW - Fibrosis KW - Magnetic resonance imaging KW - N.M.R. KW - Waves KW - Heart diseases KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1694972411?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Magnetic+Resonance+in+Medicine&rft.atitle=Assessment+of+liver+fibrosis+using+fast+strain-encoded+MRI+driven+by+inherent+cardiac+motion&rft.au=Harouni%2C+Ahmed+A%3BGharib%2C+Ahmed+M%3BOsman%2C+Nael+F%3BMorse%2C+Caryn%3BHeller%2C+Theo%3BAbd-Elmoniem%2C+Khaled+Z&rft.aulast=Harouni&rft.aufirst=Ahmed&rft.date=2015-07-01&rft.volume=74&rft.issue=1&rft.spage=106&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.25379 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-07-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Heart; Liver diseases; Fibrosis; Magnetic resonance imaging; Waves; N.M.R.; Heart diseases DO - http://dx.doi.org/10.1002/mrm.25379 ER - TY - JOUR T1 - Drug Dosing and Pharmacokinetics in Children With Obesity: A Systematic Review. AN - 1694961531; 25961828 AB - Obesity affects nearly one-sixth of US children and results in alterations to body composition and physiology that can affect drug disposition, possibly leading to therapeutic failure or toxic side effects. The depth of available literature regarding obesity's effect on drug safety, pharmacokinetics, and dosing in obese children is unknown. To perform a systematic literature review describing the current evidence of the effect of obesity on drug disposition in children. We searched the MEDLINE, Cochrane, and EMBASE databases (January 1, 1970-December 31, 2012) and included studies if they contained data on drug clearance, volume of distribution, or drug concentration in obese children (aged ≤18 years). We compared exposure and weight-normalized volume of distribution and clearance between obese and nonobese children. We explored the association between drug physicochemical properties and clearance and volume of distribution. Twenty studies met the inclusion criteria and contained pharmacokinetic data for 21 drugs. The median number of obese children studied per drug was 10 (range, 1-112) and ages ranged from newborn to 29 years (1 study described pharmacokinetics in children and adults together). Dosing schema varied and were either a fixed dose (6 [29%]) or based on body weight (10 [48%]) and body surface area (4 [19%]). Clinically significant pharmacokinetic alterations were observed in obese children for 65% (11 of 17) of the studied drugs. Pharmacokinetic alterations resulted in substantial differences in exposure between obese and nonobese children for 38% (5 of 13) of the drugs. We found no association between drug lipophilicity or Biopharmaceutical Drug Disposition Classification System class and changes in volume of distribution or clearance due to obesity. Consensus is lacking on the most appropriate weight-based dosing strategy for obese children. Prospective pharmacokinetic trials in obese children are needed to ensure therapeutic efficacy and enhance drug safety. JF - JAMA pediatrics AU - Harskamp-van Ginkel, Margreet W AU - Hill, Kevin D AU - Becker, Kristian C AU - Becker, Kristian AU - Testoni, Daniela AU - Cohen-Wolkowiez, Michael AU - Gonzalez, Daniel AU - Barrett, Jeffrey S AU - Benjamin, Daniel K AU - Siegel, David A AU - Banks, Patricia AU - Watt, Kevin M AU - Best Pharmaceuticals for Children Act–Pediatric Trials Network Administrative Core Committee AD - Department of Pediatrics, Duke University, Durham, North Carolina2Duke Clinical Research Institute, Duke University, Durham, North Carolina3Academic Medical Center, Department of Public Health, Amsterdam, the Netherlands. ; Department of Pediatrics, Duke University, Durham, North Carolina2Duke Clinical Research Institute, Duke University, Durham, North Carolina. ; Department of Pediatrics, Duke University, Durham, North Carolina2Duke Clinical Research Institute, Duke University, Durham, North Carolina4Division of Pharmacotherapy and Experimental Therapeutics, University of North Carolina Eshelman School of Pharmacy. ; Department of Clinical Pharmacology and Therapeutics, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania. ; Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, Maryland. ; Best Pharmaceuticals for Children Act–Pediatric Trials Network Administrative Core Committee Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 678 EP - 685 VL - 169 IS - 7 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Child KW - Body Composition KW - Drug Dosage Calculations KW - Pharmacokinetics KW - Child, Preschool KW - Obesity -- drug therapy KW - Metabolic Clearance Rate -- physiology KW - Body Weight -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1694961531?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA+pediatrics&rft.atitle=Drug+Dosing+and+Pharmacokinetics+in+Children+With+Obesity%3A+A+Systematic+Review.&rft.au=Harskamp-van+Ginkel%2C+Margreet+W%3BHill%2C+Kevin+D%3BBecker%2C+Kristian+C%3BBecker%2C+Kristian%3BTestoni%2C+Daniela%3BCohen-Wolkowiez%2C+Michael%3BGonzalez%2C+Daniel%3BBarrett%2C+Jeffrey+S%3BBenjamin%2C+Daniel+K%3BSiegel%2C+David+A%3BBanks%2C+Patricia%3BWatt%2C+Kevin+M%3BBest+Pharmaceuticals+for+Children+Act%E2%80%93Pediatric+Trials+Network+Administrative+Core+Committee&rft.aulast=Harskamp-van+Ginkel&rft.aufirst=Margreet&rft.date=2015-07-01&rft.volume=169&rft.issue=7&rft.spage=678&rft.isbn=&rft.btitle=&rft.title=JAMA+pediatrics&rft.issn=2168-6211&rft_id=info:doi/10.1001%2Fjamapediatrics.2015.132 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-22 N1 - Date created - 2015-07-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Arch Dis Child. 2012 Sep;97(9):842-7 [22833408] Curr Drug Saf. 2012 Nov 1;7(5):375-81 [23373553] JAMA Pediatr. 2013 May;167(5):476-82 [23478891] Pediatr Nephrol. 2013 Oct;28(10):1949-56 [23150030] JAMA. 2014 Feb 26;311(8):806-14 [24570244] Contraception. 2014 Nov;90(5):550-6 [25070547] Clin Pharmacokinet. 2000 Sep;39(3):215-31 [11020136] J Child Adolesc Psychopharmacol. 2001 Spring;11(1):53-7 [11322746] J Am Soc Nephrol. 2001 Jun;12(6):1211-7 [11373344] N Engl J Med. 2002 Apr 18;346(16):1221-31 [11961152] Drug Metab Rev. 1978;8(2):303-18 [720215] Pharm Res. 1989 Jun;6(6):486-91 [2762224] Ther Drug Monit. 1991 Jan;13(1):37-41 [2057989] Crit Care Med. 1993 Jan;21(1):111-7 [8420716] Clin Pharmacokinet. 1994 Nov;27(5):345-67 [7851053] Eur J Clin Pharmacol. 1995;47(6):525-30 [7768256] Int J Obes Relat Metab Disord. 1995 Apr;19(4):234-9 [7627246] Ann Pharmacother. 1995 Sep;29(9):843-7 [8547729] Br J Clin Pharmacol. 1997 Jun;43(6):563-70 [9205815] Acta Med Okayama. 1998 Jun;52(3):139-42 [9661740] Eur J Anaesthesiol. 1999 Aug;16(8):507-10 [10500937] Pharm Res. 2005 Jan;22(1):11-23 [15771225] Transplant Proc. 2006 Mar;38(2):463-5 [16549148] Blood. 2006 Dec 15;108(13):3997-4002 [16917005] Arch Pediatr Adolesc Med. 2007 Jan;161(1):11-4 [17199061] Pediatr Hematol Oncol. 2007 Sep;24(6):437-45 [17710661] Prev Chronic Dis. 2008 Jan;5(1):A04 [18081993] Cancer Chemother Pharmacol. 2009 Jul;64(2):243-51 [19020877] PLoS Med. 2009 Jul 21;6(7):e1000097 [19621072] Contraception. 2009 Aug;80(2):119-27 [19631786] Clin Pediatr (Phila). 2009 Oct;48(8):812-8 [19487762] Basic Clin Pharmacol Toxicol. 2010 Mar;106(3):162-7 [20002064] Contraception. 2010 Jun;81(6):474-80 [20472113] J Pediatr Gastroenterol Nutr. 2011 Feb;52(2):198-202 [21240014] Pediatr Infect Dis J. 2011 Apr;30(4):347-9 [20980932] Clin Pediatr (Phila). 2011 May;50(5):442-6 [21282257] Clin Pharmacol Ther. 2011 Jul;90(1):77-89 [21633345] Biol Blood Marrow Transplant. 2011 Sep;17(9):1383-8 [21288495] Contraception. 2011 Oct;84(4):363-7 [21920190] N Engl J Med. 2011 Oct 13;365(15):1365-7 [21995381] Am J Health Syst Pharm. 2011 Nov 1;68(21):2062-8 [22011985] BMC Health Serv Res. 2011;11:340 [22176689] Curr Hypertens Rep. 2012 Apr;14(2):152-9 [22318504] Clin Pharmacokinet. 2012 May 1;51(5):277-304 [22448619] Clin Pharmacokinet. 2012 Aug 1;51(8):543-51 [22690673] Comment In: JAMA Pediatr. 2015 Jul;169(7):626-8 [25961595] Erratum In: JAMA Pediatr. 2015 Dec;169(12):1179 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1001/jamapediatrics.2015.132 ER - TY - JOUR T1 - International Harmonization of Nomenclature and Diagnostic Criteria (INHAND): Progress to Date and Future Plans. AN - 1694509082; 25530274 AB - The International Harmonization of Nomenclature and Diagnostic Criteria for Lesions in Rats and Mice proposal (INHAND) has been operational since 2005. A Global Editorial Steering Committee manages the overall objectives of the project, and the development of harmonized terminology for each organ system is the responsibility of the Organ Working Groups, drawing upon experts from North America, Europe, and Japan. Great progress has been made with 9 systems published to date--respiratory, hepatobiliary, urinary, central/peripheral nervous systems, male reproductive and mammary, zymbals, clitoral, and preputial glands in Toxicologic Pathology and the integument and soft tissue and female reproductive in the Journal of Toxicologic Pathology as supplements and on a Web site--www.goReni.org. INHAND nomenclature guides offer diagnostic criteria and guidelines for recording lesions observed in rodent toxicity and carcinogenicity studies. The guides provide representative photomicrographs of morphologic changes, information regarding pathogenesis, and key references. The purpose of this brief communication is to provide an update on the progress of INHAND. © 2014 by The Author(s). JF - Toxicologic pathology AU - Keenan, C M AU - Baker, J AU - Bradley, A AU - Goodman, D G AU - Harada, T AU - Herbert, R AU - Kaufmann, W AU - Kellner, R AU - Mahler, B AU - Meseck, E AU - Nolte, T AU - Rittinghausen, S AU - Vahle, J AU - Yoshizawa, K AD - C. M. Keenan ToxPath Consulting, Doylestown, Pennsylvania, USA charlotte.keenan@msn.com. ; Charles River Pathology Associates, Frederick, Maryland, USA. ; Charles River Laboratories, Tranent, Scotland, UK. ; Independent Consultant, Potomac, Maryland, USA. ; The Institute of Environmental Toxicology, Joso-shi, Ibaraki, Japan. ; NIEHS, Research Triangle Park, North Carolina, USA. ; Merck KGaA, Darmstadt, Germany. ; Fraunhofer ITEM, Hannover, Germany. ; Novartis Institute for Biomedical Research, East Hanover, New Jersey, USA. ; Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach an der Riss, Germany. ; Eli Lilly & Company, Indianapolis, Indiana. ; Kansai Medical University, Hirakata, Osaka, Japan. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 730 EP - 732 VL - 43 IS - 5 KW - Index Medicus KW - rodent pathology KW - preclinical research and development KW - toxicologic pathology KW - Rats KW - Animals KW - Mice KW - Research Design KW - Toxicology -- standards KW - Pathology -- standards KW - Biomedical Research -- standards KW - Guidelines as Topic KW - Terminology as Topic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1694509082?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=International+Harmonization+of+Nomenclature+and+Diagnostic+Criteria+%28INHAND%29%3A+Progress+to+Date+and+Future+Plans.&rft.au=Keenan%2C+C+M%3BBaker%2C+J%3BBradley%2C+A%3BGoodman%2C+D+G%3BHarada%2C+T%3BHerbert%2C+R%3BKaufmann%2C+W%3BKellner%2C+R%3BMahler%2C+B%3BMeseck%2C+E%3BNolte%2C+T%3BRittinghausen%2C+S%3BVahle%2C+J%3BYoshizawa%2C+K&rft.aulast=Keenan&rft.aufirst=C&rft.date=2015-07-01&rft.volume=43&rft.issue=5&rft.spage=730&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623314560031 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-21 N1 - Date created - 2015-07-05 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/0192623314560031 ER - TY - JOUR T1 - Reliability of perfluoroalkyl substances in plasma of 100 women in two consecutive pregnancies. AN - 1693731945; 25957838 AB - The potential toxicity of background exposure to perfluoroalkyl substances (PFASs) is currently under active investigation. Such investigations typically rely on a single measure of PFAS concentration, yet the longer-term reliability of a single measure has not been well characterized, especially among reproductive-aged women. Our aim was to investigate the association between PFAS plasma concentrations of 100 women in two consecutive pregnancies and explore changes in plasma concentration related to reproductive factors. The women in our study were enrolled in the Norwegian Mother and Child Cohort Study (MoBa) from 2003 to 2009. About half of them breastfed exclusively for 6 months and the rest of the participants did not breastfeed between the two consecutive pregnancies (median time between pregnancies: 18 months). Maternal blood was collected at mid-pregnancy and plasma was analyzed for 10 PFASs. Statistical analyses were restricted to 6 PFASs that were quantifiable in more than 80% of the samples. We estimated the correlation between repeated PFAS measurements, the percentage change between pregnancies and the effect of several reproductive factors in multivariate linear regression models of PFAS concentrations in the second pregnancy. The Pearson correlation coefficient between repeated PFAS measurements was, for perfluorooctane sulfonate (PFOS), 0.80; perfluorooctanoate (PFOA), 0.50; perfluorohexane sulfonate (PFHxS), 0.74; perfluorononanoate (PFNA), 0.39; perfluoroundecanoate (PFUnDA), 0.71; and perfluorodecanoate (PFDA), 0.60. Adjustment for maternal age, delivery year, and time and breastfeeding between pregnancies did not substantially affect the observed correlations. We found 44-47% median reductions in the concentrations of PFOS, PFOA and PFHxS between pregnancies, while the change in concentrations between pregnancies was smaller and more variable for PFNA, PFUnDA and PFDA. The variation in plasma concentrations in the second pregnancy was mainly accounted for by the concentration in the first pregnancy; for PFOS, PFOA, and PFNA, breastfeeding also accounted for a substantial proportion. In conclusion, we found the reliability of PFAS measurements in maternal plasma to be moderate to high, and in these data, several factors, especially breastfeeding, were related to plasma concentrations. Copyright © 2015 Elsevier Inc. All rights reserved. JF - Environmental research AU - Papadopoulou, Eleni AU - Haug, Line S AU - Sabaredzovic, Azemira AU - Eggesbø, Merete AU - Longnecker, Matthew P AD - Division of Environmental Medicine, Norwegian Institute of Public Health, Lovisenberggata 8, 0456 Oslo, Norway. Electronic address: eleni.papadopoulou@fhi.no. ; Division of Environmental Medicine, Norwegian Institute of Public Health, Lovisenberggata 8, 0456 Oslo, Norway. ; Division of Epidemiology, Norwegian Institute of Public Health, Marcus Thranes gate 6, 0473 Oslo, Norway. ; Epidemiology Branch, National Institute of Environmental Health Sciences, NIH, DHHS, 111 T.W. Alexander Drive, Research Triangle Park, NC, USA. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 421 EP - 429 VL - 140 KW - Fluorocarbons KW - 0 KW - Index Medicus KW - MoBa KW - PFOS KW - Perfluoroalkyl substances KW - Correlations KW - Pregnancy KW - Reproducibility of Results KW - Humans KW - Cohort Studies KW - Adult KW - Norway KW - Female KW - Fluorocarbons -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1693731945?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+research&rft.atitle=Reliability+of+perfluoroalkyl+substances+in+plasma+of+100+women+in+two+consecutive+pregnancies.&rft.au=Papadopoulou%2C+Eleni%3BHaug%2C+Line+S%3BSabaredzovic%2C+Azemira%3BEggesb%C3%B8%2C+Merete%3BLongnecker%2C+Matthew+P&rft.aulast=Papadopoulou&rft.aufirst=Eleni&rft.date=2015-07-01&rft.volume=140&rft.issue=&rft.spage=421&rft.isbn=&rft.btitle=&rft.title=Environmental+research&rft.issn=1096-0953&rft_id=info:doi/10.1016%2Fj.envres.2015.04.022 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-25 N1 - Date created - 2015-07-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Int J Epidemiol. 2006 Oct;35(5):1146-50 [16926217] Chemosphere. 2014 Nov;114:337-9 [24938172] Environ Health Perspect. 2007 Sep;115(9):1298-305 [17805419] Environ Health Perspect. 2007 Nov;115(11):1596-602 [18007991] Environ Health Perspect. 2007 Nov;115(11):1677-82 [18008003] Environ Health Perspect. 2008 May;116(5):651-7 [18470314] J Chromatogr A. 2009 Jan 16;1216(3):385-93 [19026423] Environ Sci Technol. 2008 Dec 1;42(23):8971-7 [19192827] J Am Chem Soc. 2009 Feb 18;131(6):2290-6 [19170492] Int J Hyg Environ Health. 2009 May;212(3):239-70 [18565792] Environ Sci Technol. 2009 Mar 15;43(6):2131-6 [19368225] Environ Sci Technol. 2009 Aug 1;43(15):5565-75 [19731646] Paediatr Perinat Epidemiol. 2009 Nov;23(6):597-608 [19840297] Environ Sci Technol. 2013 Feb 5;47(3):1606-13 [23272997] Sci Total Environ. 2012 Nov 1;438:42-8 [22964400] Environ Int. 2010 Oct;36(7):772-8 [20579735] Chemosphere. 2013 Apr;91(2):115-7 [23232044] Sci Total Environ. 2013 Mar 1;447:430-7 [23410865] Environ Int. 2013 Apr;54:74-84 [23419425] Environ Health Perspect. 2013 Apr;121(4):447-52 [23410534] J Toxicol Environ Health A. 2013;76(7):409-21 [23611181] Environ Health Perspect. 2013 Aug;121(8):900-5 [23735465] Toxicol Lett. 2014 Oct 15;230(2):244-51 [24440341] Environ Pollut. 2015 Jan;196:462-72 [25467694] Kidney Int. 2004 Jan;65(1):259-65 [14675058] BMJ. 1996 Jul 6;313(7048):41-2 [8664775] Eur J Epidemiol. 2006;21(8):619-25 [17031521] Environ Sci Technol. 2013 Sep 17;47(18):10619-27 [23980546] Environ Int. 2014 Jan;62:104-12 [24189199] Environ Health Perspect. 2013 Nov-Dec;121(11-12):1313-8 [24007715] Chemosphere. 2014 Mar;98:78-83 [24238303] Rev Environ Contam Toxicol. 2010;208:161-77 [20811864] Environ Sci Technol. 2010 Sep 15;44(18):7123-9 [20722423] Environ Sci Technol. 2010 Dec 15;44(24):9550-6 [21090747] Environ Int. 2011 May;37(4):687-93 [21334069] Environ Health Perspect. 2011 Jun;119(6):878-85 [21233055] Environ Int. 2011 Oct;37(7):1206-12 [21620474] Integr Environ Assess Manag. 2011 Oct;7(4):513-41 [21793199] Environ Sci Technol. 2011 Oct 1;45(19):8137-43 [20939531] Environ Sci Technol. 2011 Oct 1;45(19):8037-45 [21469664] Environ Sci Technol. 2011 Oct 1;45(19):7954-61 [21866930] Environ Health Perspect. 2011 Nov;119(11):1659-64 [21757419] Epidemiology. 2012 Mar;23(2):257-63 [22081060] Int J Hyg Environ Health. 2012 Feb;215(2):216-9 [21937271] J Agric Food Chem. 2012 May 2;60(17):4408-15 [22494245] Environ Sci Technol. 2012 Aug 21;46(16):9071-9 [22770559] Epidemiology. 2014 Mar;25(2):255-64 [24407430] Environ Health Perspect. 2014 Feb;122(2):187-92 [24280536] Environ Pollut. 2014 May;188:102-8 [24583389] Am J Epidemiol. 2014 Apr 1;179(7):824-33 [24557813] Environ Int. 2014 Jun;67:43-53 [24657493] Environ Int. 2014 Aug;69:58-66 [24815340] Occup Environ Med. 2014 Jul;71(7):500-6 [24832944] Environ Int. 2014 Sep;70:62-75 [24932785] PLoS One. 2014;9(7):e101897 [25003331] Environ Sci Technol. 2014;48(15):8807-14 [24943117] Environ Res. 2007 Feb;103(2):176-84 [16893538] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.envres.2015.04.022 ER - TY - JOUR T1 - High-throughput gene targeting and phenotyping in zebrafish using CRISPR/Cas9. AN - 1693719485; 26048245 AB - The use of CRISPR/Cas9 as a genome-editing tool in various model organisms has radically changed targeted mutagenesis. Here, we present a high-throughput targeted mutagenesis pipeline using CRISPR/Cas9 technology in zebrafish that will make possible both saturation mutagenesis of the genome and large-scale phenotyping efforts. We describe a cloning-free single-guide RNA (sgRNA) synthesis, coupled with streamlined mutant identification methods utilizing fluorescent PCR and multiplexed, high-throughput sequencing. We report germline transmission data from 162 loci targeting 83 genes in the zebrafish genome, in which we obtained a 99% success rate for generating mutations and an average germline transmission rate of 28%. We verified 678 unique alleles from 58 genes by high-throughput sequencing. We demonstrate that our method can be used for efficient multiplexed gene targeting. We also demonstrate that phenotyping can be done in the F1 generation by inbreeding two injected founder fish, significantly reducing animal husbandry and time. This study compares germline transmission data from CRISPR/Cas9 with those of TALENs and ZFNs and shows that efficiency of CRISPR/Cas9 is sixfold more efficient than other techniques. We show that the majority of published "rules" for efficient sgRNA design do not effectively predict germline transmission rates in zebrafish, with the exception of a GG or GA dinucleotide genomic match at the 5' end of the sgRNA. Finally, we show that predicted off-target mutagenesis is of low concern for in vivo genetic studies. © 2015 Varshney et al.; Published by Cold Spring Harbor Laboratory Press. JF - Genome research AU - Varshney, Gaurav K AU - Pei, Wuhong AU - LaFave, Matthew C AU - Idol, Jennifer AU - Xu, Lisha AU - Gallardo, Viviana AU - Carrington, Blake AU - Bishop, Kevin AU - Jones, MaryPat AU - Li, Mingyu AU - Harper, Ursula AU - Huang, Sunny C AU - Prakash, Anupam AU - Chen, Wenbiao AU - Sood, Raman AU - Ledin, Johan AU - Burgess, Shawn M AD - Translational and Functional Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892, USA; ; Cancer Genetics and Comparative Genomics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland 20892, USA; ; Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA; ; Department of Organismal Biology, Science for Life Laboratory, Uppsala University, SE-752 36 Uppsala, Sweden. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 1030 EP - 1042 VL - 25 IS - 7 KW - RNA, Guide KW - 0 KW - Index Medicus KW - Gene Knockout Techniques KW - Animals KW - Alleles KW - Germ Cells -- immunology KW - Humans KW - Quantitative Trait Loci KW - Zebrafish KW - RNA, Guide -- genetics KW - Sequence Deletion KW - Mutagenesis KW - Genomics KW - Genome-Wide Association Study KW - Phenotype KW - High-Throughput Screening Assays KW - Gene Targeting -- methods KW - CRISPR-Cas Systems UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1693719485?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genome+research&rft.atitle=High-throughput+gene+targeting+and+phenotyping+in+zebrafish+using+CRISPR%2FCas9.&rft.au=Varshney%2C+Gaurav+K%3BPei%2C+Wuhong%3BLaFave%2C+Matthew+C%3BIdol%2C+Jennifer%3BXu%2C+Lisha%3BGallardo%2C+Viviana%3BCarrington%2C+Blake%3BBishop%2C+Kevin%3BJones%2C+MaryPat%3BLi%2C+Mingyu%3BHarper%2C+Ursula%3BHuang%2C+Sunny+C%3BPrakash%2C+Anupam%3BChen%2C+Wenbiao%3BSood%2C+Raman%3BLedin%2C+Johan%3BBurgess%2C+Shawn+M&rft.aulast=Varshney&rft.aufirst=Gaurav&rft.date=2015-07-01&rft.volume=25&rft.issue=7&rft.spage=1030&rft.isbn=&rft.btitle=&rft.title=Genome+research&rft.issn=1549-5469&rft_id=info:doi/10.1101%2Fgr.186379.114 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-24 N1 - Date created - 2015-07-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Methods. 2011 Jun;8(6):506-15 [21552255] Cell. 2014 Jun 5;157(6):1262-78 [24906146] Dis Model Mech. 2011 Nov;4(6):786-800 [21757509] Proc Natl Acad Sci U S A. 2012 Sep 25;109(39):E2579-86 [22949671] Nat Biotechnol. 2014 Dec;32(12):1262-7 [25184501] PLoS One. 2014;9(6):e100268 [24945275] Genome Biol. 2013;14(7):R69 [23815890] Genome Res. 2002 Jun;12(6):996-1006 [12045153] Development. 2003 Aug;130(15):3515-24 [12810598] Development. 2004 Feb;131(4):943-51 [14736743] Nucleic Acids Res. 2004;32(5):1792-7 [15034147] Nature. 2004 Apr 29;428(6986):955-9 [15057246] Nature. 2004 Oct 21;431(7011):931-45 [15496913] Biotechniques. 1996 Jun;20(6):1004-6, 1008-10 [8780871] Development. 1996 Dec;123:1-36 [9007226] Development. 1997 Aug;124(16):3157-65 [9272956] Neuron. 1998 Feb;20(2):271-83 [9491988] Biotechniques. 2007 Nov;43(5):610, 612, 614 [18072590] Nat Biotechnol. 2008 Jun;26(6):702-8 [18500334] Genome Biol. 2009;10(3):R25 [19261174] Bioinformatics. 2009 Aug 15;25(16):2078-9 [19505943] Genome Res. 2010 Oct;20(10):1420-31 [20810667] Genesis. 2010 Dec;48(12):707-16 [20960516] Genetics. 2014 Sep;198(1):167-70 [25009150] Nature. 2012 Nov 1;491(7422):114-8 [23000899] Dev Cell. 2015 Jan 12;32(1):97-108 [25533206] Nature. 2015 Mar 12;519(7542):223-8 [25533962] Science. 2012 Aug 17;337(6096):816-21 [22745249] Nucleic Acids Res. 2013 Jan;41(Database issue):D861-4 [23180778] Science. 2013 Feb 15;339(6121):819-23 [23287718] Science. 2013 Feb 15;339(6121):823-6 [23287722] Nat Methods. 2013 Mar;10(3):185 [23396284] PLoS One. 2013;8(2):e57239 [23451191] Nat Biotechnol. 2013 Mar;31(3):227-9 [23360964] Cell Res. 2013 Apr;23(4):465-72 [23528705] Genome Res. 2013 Apr;23(4):727-35 [23382537] Nature. 2013 Apr 25;496(7446):494-7 [23594742] Nature. 2013 Apr 25;496(7446):498-503 [23594743] Genome Res. 2013 Jun;23(6):1008-17 [23478401] PLoS One. 2013;8(7):e68708 [23874735] Nucleic Acids Res. 2013 Aug;41(14):e141 [23748566] Proc Natl Acad Sci U S A. 2013 Aug 20;110(34):13904-9 [23918387] Nat Biotechnol. 2013 Sep;31(9):822-6 [23792628] Nat Biotechnol. 2013 Sep;31(9):827-32 [23873081] Nat Biotechnol. 2013 Sep;31(9):839-43 [23934178] Nucleic Acids Res. 2014 Jan;42(Database issue):D749-55 [24316576] Nucleic Acids Res. 2014 Jan;42(Database issue):D1001-6 [24316577] J Hum Genet. 2014 Jan;59(1):5-15 [24196381] PLoS One. 2014;9(5):e98186 [24873830] Bioinformatics. 2011 Jun 15;27(12):1691-2 [21493652] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1101/gr.186379.114 ER - TY - JOUR T1 - Successive Stages of Amyloid-β Self-Assembly Characterized by Solid-State Nuclear Magnetic Resonance with Dynamic Nuclear Polarization. AN - 1693188147; 26068174 AB - Self-assembly of amyloid-β (Aβ) peptides in human brain tissue leads to neurodegeneration in Alzheimer's disease (AD). Amyloid fibrils, whose structures have been extensively characterized by solid state nuclear magnetic resonance (ssNMR) and other methods, are the thermodynamic end point of Aβ self-assembly. Oligomeric and protofibrillar assemblies, whose structures are less well-understood, are also observed as intermediates in the assembly process in vitro and have been implicated as important neurotoxic species in AD. We report experiments in which the structural evolution of 40-residue Aβ (Aβ40) is monitored by ssNMR measurements on frozen solutions prepared at four successive stages of the self-assembly process. Measurements on transient intermediates are enabled by ssNMR signal enhancements from dynamic nuclear polarization (DNP) at temperatures below 30 K. DNP-enhanced ssNMR data reveal a monotonic increase in conformational order from an initial state comprised primarily of monomers and small oligomers in solution at high pH, to larger oligomers near neutral pH, to metastable protofibrils, and finally to fibrils. Surprisingly, the predominant molecular conformation, indicated by (13)C NMR chemical shifts and by side chain contacts between F19 and L34 residues, is qualitatively similar at all stages. However, the in-register parallel β-sheet supramolecular structure, indicated by intermolecular (13)C spin polarization transfers, does not develop before the fibril stage. This work represents the first application of DNP-enhanced ssNMR to the characterization of peptide or protein self-assembly intermediates. JF - Journal of the American Chemical Society AU - Potapov, Alexey AU - Yau, Wai-Ming AU - Ghirlando, Rodolfo AU - Thurber, Kent R AU - Tycko, Robert AD - †Laboratory of Chemical Physics and ‡Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-0520, United States. Y1 - 2015/07/01/ PY - 2015 DA - 2015 Jul 01 SP - 8294 EP - 8307 VL - 137 IS - 25 KW - Amyloid beta-Peptides KW - 0 KW - Peptide Fragments KW - amyloid beta-protein (1-40) KW - Index Medicus KW - Protein Structure, Secondary KW - Models, Molecular KW - Nuclear Magnetic Resonance, Biomolecular KW - Hydrogen-Ion Concentration KW - Humans KW - Alzheimer Disease -- metabolism KW - Peptide Fragments -- metabolism KW - Peptide Fragments -- chemistry KW - Amyloid beta-Peptides -- metabolism KW - Amyloid beta-Peptides -- ultrastructure KW - Amyloid beta-Peptides -- chemistry KW - Peptide Fragments -- ultrastructure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1693188147?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+American+Chemical+Society&rft.atitle=Successive+Stages+of+Amyloid-%CE%B2+Self-Assembly+Characterized+by+Solid-State+Nuclear+Magnetic+Resonance+with+Dynamic+Nuclear+Polarization.&rft.au=Potapov%2C+Alexey%3BYau%2C+Wai-Ming%3BGhirlando%2C+Rodolfo%3BThurber%2C+Kent+R%3BTycko%2C+Robert&rft.aulast=Potapov&rft.aufirst=Alexey&rft.date=2015-07-01&rft.volume=137&rft.issue=25&rft.spage=8294&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Chemical+Society&rft.issn=1520-5126&rft_id=info:doi/10.1021%2Fjacs.5b04843 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-21 N1 - Date created - 2015-07-01 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/jacs.5b04843 ER - TY - JOUR T1 - Role of the store-operated calcium entry protein, STIM1, in neutrophil chemotaxis and infiltration into a murine model of psoriasis-inflamed skin. AN - 1693184156; 25837581 AB - Stromal interaction molecule 1 (STIM1) is a Ca(2+) sensor protein that initiates store-operated calcium entry (SOCE). STIM1 is known to be involved in the chemoattractant signaling pathway for FPR1 in cell lines, but its role in in vivo functioning of neutrophils is unclear. Plaque-type psoriasis is a chronic inflammatory skin disorder associated with chemoattractants driving neutrophils into the epidermis. We investigated the involvement of STIM1 in neutrophil chemotaxis in vitro, as well as during chronic psoriatic inflammation. To this end, we used conditional knockout (KO) mice lacking STIM1 in cells of myeloid lineage (STIM1(fl/fl) LysM-cre). We demonstrate that STIM1 is required for chemotaxis because of multiple chemoattractants in mouse neutrophils in vitro. Using an imiquimod-induced psoriasis-like skin model, we show that KO mice had less neutrophil infiltration in the epidermis than controls, whereas neither chemoattractant production in the epidermis nor macrophage migration was decreased. KO mice displayed a more rapid reversal of the outward signs of psoriasis (plaques). Thus, KO of STIM1 impairs neutrophil contribution to psoriatic inflammation. Our data provide new insights to our understanding of how STIM1 orchestrates the cellular behavior underlying chemotaxis and illustrate the important role of SOCE in a disease-related pathologic model. © FASEB. JF - FASEB journal : official publication of the Federation of American Societies for Experimental Biology AU - Steinckwich, Natacha AU - Myers, Page AU - Janardhan, Kyathanahalli S AU - Flagler, Norris D AU - King, Debra AU - Petranka, John G AU - Putney, James W AD - *Signal Transduction Laboratory, Comparative Medicine Branch, Integrated Laboratory Systems, Incorporated, Cellular and Molecular Pathology Branch,National Toxicology Program, and Special Techniques Group, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA. ; *Signal Transduction Laboratory, Comparative Medicine Branch, Integrated Laboratory Systems, Incorporated, Cellular and Molecular Pathology Branch,National Toxicology Program, and Special Techniques Group, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA putney@niehs.nih.gov. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 3003 EP - 3013 VL - 29 IS - 7 KW - Aminoquinolines KW - 0 KW - Calcium Channels KW - Membrane Proteins KW - Neoplasm Proteins KW - RNA, Small Interfering KW - STIM1 protein, human KW - Stim1 protein, mouse KW - Stromal Interaction Molecule 1 KW - imiquimod KW - P1QW714R7M KW - Index Medicus KW - calcium signaling KW - leukocyte migration KW - chronic inflammatory disease KW - Animals KW - Skin -- physiopathology KW - Neoplasm Proteins -- antagonists & inhibitors KW - HL-60 Cells KW - Humans KW - Skin -- pathology KW - Disease Models, Animal KW - RNA, Small Interfering -- genetics KW - Neutrophil Infiltration -- physiology KW - Mice KW - Membrane Proteins -- genetics KW - Chemotaxis, Leukocyte -- physiology KW - Mice, Knockout KW - Aminoquinolines -- toxicity KW - Neoplasm Proteins -- physiology KW - Neoplasm Proteins -- genetics KW - In Vitro Techniques KW - Membrane Proteins -- antagonists & inhibitors KW - Signal Transduction KW - Membrane Proteins -- physiology KW - Calcium Channels -- deficiency KW - Neutrophils -- pathology KW - Calcium Channels -- physiology KW - Psoriasis -- physiopathology KW - Psoriasis -- pathology KW - Neutrophils -- physiology KW - Calcium Channels -- genetics KW - Psoriasis -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1693184156?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.atitle=Role+of+the+store-operated+calcium+entry+protein%2C+STIM1%2C+in+neutrophil+chemotaxis+and+infiltration+into+a+murine+model+of+psoriasis-inflamed+skin.&rft.au=Steinckwich%2C+Natacha%3BMyers%2C+Page%3BJanardhan%2C+Kyathanahalli+S%3BFlagler%2C+Norris+D%3BKing%2C+Debra%3BPetranka%2C+John+G%3BPutney%2C+James+W&rft.aulast=Steinckwich&rft.aufirst=Natacha&rft.date=2015-07-01&rft.volume=29&rft.issue=7&rft.spage=3003&rft.isbn=&rft.btitle=&rft.title=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.issn=1530-6860&rft_id=info:doi/10.1096%2Ffj.14-265215 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-14 N1 - Date created - 2015-07-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1978 May;75(5):2458-62 [276884] J Invest Dermatol. 2002 Jan;118(1):49-54 [11851875] J Immunol. 2011 Feb 15;186(4):2182-91 [21239714] Toxicol Pathol. 2011 Feb;39(2):435-48 [21300792] J Immunol. 2011 Jul 1;187(1):472-81 [21632714] J Immunol. 2012 Jan 1;188(1):462-9 [22131335] Cell Physiol Biochem. 2012;30(1):221-37 [22759969] Am J Physiol Cell Physiol. 2012 Sep 1;303(5):C490-8 [22673622] Blood. 2014 Apr 3;123(14):2238-49 [24493668] Oncogene. 2014 May 1;33(18):2307-16 [23686305] J Cell Biol. 1990 Jan;110(1):43-52 [2295684] J Cell Biol. 1991 Mar;112(6):1249-57 [1900302] Cell. 1996 Feb 9;84(3):359-69 [8608589] Cell. 1996 Feb 9;84(3):371-9 [8608590] Biochem J. 1996 Jul 15;317 ( Pt 2):403-9 [8713065] Cell. 1996 Nov 15;87(4):601-6 [8929529] Biochem Biophys Res Commun. 1997 Jan 13;230(2):258-61 [9016761] Nature. 2006 May 11;441(7090):179-85 [16582901] Science. 2006 May 26;312(5777):1220-3 [16645049] Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9357-62 [16751269] Curr Med Chem. 2007;14(6):681-7 [17346155] Ann Biomed Eng. 2008 Apr;36(4):632-46 [18278555] Nat Immunol. 2008 Apr;9(4):432-43 [18327260] Methods. 2008 Nov;46(3):204-12 [18929662] J Immunol. 2009 May 1;182(9):5836-45 [19380832] Biochem Pharmacol. 2009 Sep 1;78(5):504-13 [19433064] N Engl J Med. 2009 Jul 30;361(5):496-509 [19641206] Blood. 2010 Jan 21;115(3):657-66 [19965684] J Leukoc Biol. 2010 Jul;88(1):57-68 [20400677] Transgenic Res. 1999 Aug;8(4):265-77 [10621974] Pharmacol Rev. 2000 Mar;52(1):145-76 [10699158] J Invest Dermatol. 2000 May;114(5):976-83 [10771480] J Am Acad Dermatol. 2000 Aug;43(2 Pt 2):391-5 [10901732] Blood. 2000 Dec 1;96(12):3816-22 [11090065] Nat Rev Rheumatol. 2010 Dec;6(12):704-14 [20877306] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1096/fj.14-265215 ER - TY - JOUR T1 - Endometrial cancer: redefining the molecular-targeted approach. AN - 1692752988; 25935126 AB - Endometrial cancer (EC) is the most frequent gynecologic malignancy in the world. Metastatic and recurrent disease confers a worse prognosis, and the side effects of the current cytotoxic agents are the main cause of treatment disruption. Recently, the genetic alterations that facilitate the start, development and progression of EC have been elucidated, reclassifying the disease in distinct subtypes with different mechanisms of carcinogenesis. Targeted therapy aims to interfere specifically these mechanisms causing less toxicity, therefore opening new perspectives for a tailored treatment and improvement of response and survival rates for heavily treated recurrent disease. Treatment with hormone therapy was not addressed in this review because it is an extensively discussed issue and would divert the discussion about molecular-targeted therapy. The purpose of this paper was to review the available literature data regarding the main genetic abnormalities related to the carcinogenesis and evaluate the safety and efficacy of the molecular-targeted agents in the treatment of metastatic and recurrent EC. JF - Cancer chemotherapy and pharmacology AU - Silva, Jesse Lopes da AU - Paulino, Eduardo AU - Dias, Mariane Fontes AU - Melo, Andréia Cristina de AD - Hospital do Cancer II, National Cancer Institute (INCA), Rio De Janeiro, Brazil, jessejeu@yahoo.com.br. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 1 EP - 11 VL - 76 IS - 1 KW - Index Medicus KW - Carcinoma, Endometrioid -- genetics KW - Survival Rate KW - Humans KW - Female KW - Carcinoma, Endometrioid -- drug therapy KW - Endometrial Neoplasms -- drug therapy KW - Molecular Targeted Therapy -- methods KW - Endometrial Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1692752988?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+chemotherapy+and+pharmacology&rft.atitle=Endometrial+cancer%3A+redefining+the+molecular-targeted+approach.&rft.au=Silva%2C+Jesse+Lopes+da%3BPaulino%2C+Eduardo%3BDias%2C+Mariane+Fontes%3BMelo%2C+Andr%C3%A9ia+Cristina+de&rft.aulast=Silva&rft.aufirst=Jesse+Lopes&rft.date=2015-07-01&rft.volume=76&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Cancer+chemotherapy+and+pharmacology&rft.issn=1432-0843&rft_id=info:doi/10.1007%2Fs00280-015-2758-z LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-08 N1 - Date created - 2015-06-30 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00280-015-2758-z ER - TY - JOUR T1 - A typical case of myoclonic epilepsy with ragged red fibers (MERRF) and the lessons learned. AN - 1692292262; 26119441 AB - Mitochondrial diseases have a special predilection to involve the brain in view of its high metabolic demand and the tendency for the formation of excitatory neurotransmitters when there is deficiency of intracellular ATP. These diseases have a great phenotypic variation and need a high degree of suspicion. However, some specific syndromes are well defined, both genotypically and phenotypically. Some of the drugs are potentially fatal mitochondrial poisons and an insight into that may be lifesaving as well as prevent serious morbidities.We report a typical case of myoclonic epilepsy with ragged red fibers (MERRF) with classical phenotype and genotype. There was rapid multiaxial deterioration with the introduction of sodium valproate which partly reversed on introducing mitochondrial cocktail and withdrawal of the offending drug.Sodium valproate, phenobarbitone, chloramphenicol and many anti-viral agents are mitochondrial poisons that increase the morbidity and mortality in patients with mitochondrial disease. More harm to the patient can be avoided with insight into this information. JF - Journal of postgraduate medicine AU - Chandra, S R AU - Issac, T G AU - Gayathri, N AU - Gupta, N AU - Abbas, M M AD - Department of Neurology, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka, India. PY - 2015 SP - 200 EP - 202 VL - 61 IS - 3 KW - Index Medicus KW - Drug Therapy, Combination KW - Humans KW - Adolescent KW - Female KW - Epilepsies, Myoclonic -- blood KW - Mitochondrial Diseases -- pathology KW - MERRF Syndrome -- diagnosis KW - Mitochondrial Diseases -- therapy KW - Epilepsies, Myoclonic -- pathology KW - Mitochondria -- pathology KW - Epilepsies, Myoclonic -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1692292262?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+postgraduate+medicine&rft.atitle=A+typical+case+of+myoclonic+epilepsy+with+ragged+red+fibers+%28MERRF%29+and+the+lessons+learned.&rft.au=Chandra%2C+S+R%3BIssac%2C+T+G%3BGayathri%2C+N%3BGupta%2C+N%3BAbbas%2C+M+M&rft.aulast=Chandra&rft.aufirst=S&rft.date=2015-07-01&rft.volume=61&rft.issue=3&rft.spage=200&rft.isbn=&rft.btitle=&rft.title=Journal+of+postgraduate+medicine&rft.issn=0972-2823&rft_id=info:doi/10.4103%2F0022-3859.150905 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-11 N1 - Date created - 2015-06-29 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.4103/0022-3859.150905 ER - TY - JOUR T1 - Birthweight and Childhood Cancer: Preliminary Findings from the International Childhood Cancer Cohort Consortium (I4C). AN - 1691601292; 25989709 AB - Evidence relating childhood cancer to high birthweight is derived primarily from registry and case-control studies. We aimed to investigate this association, exploring the potential modifying roles of age at diagnosis and maternal anthropometrics, using prospectively collected data from the International Childhood Cancer Cohort Consortium. We pooled data on infant and parental characteristics and cancer incidence from six geographically and temporally diverse member cohorts [the Avon Longitudinal Study of Parents and Children (UK), the Collaborative Perinatal Project (USA), the Danish National Birth Cohort (Denmark), the Jerusalem Perinatal Study (Israel), the Norwegian Mother and Child Cohort Study (Norway), and the Tasmanian Infant Health Survey (Australia)]. Birthweight metrics included a continuous measure, deciles, and categories (≥ 4.0 vs. < 4.0 kilogram). Childhood cancer (377 cases diagnosed prior to age 15 years) risk was analysed by type (all sites, leukaemia, acute lymphoblastic leukaemia, and non-leukaemia) and age at diagnosis. We estimated hazard ratios (HR) and 95% confidence intervals (CI) from Cox proportional hazards models stratified by cohort. A linear relationship was noted for each kilogram increment in birthweight adjusted for gender and gestational age for all cancers [HR = 1.26; 95% CI 1.02, 1.54]. Similar trends were observed for leukaemia. There were no significant interactions with maternal pre-pregnancy overweight or pregnancy weight gain. Birthweight ≥ 4.0 kg was associated with non-leukaemia cancer among children diagnosed at age ≥ 3 years [HR = 1.62; 95% CI 1.06, 2.46], but not at younger ages [HR = 0.7; 95% CI 0.45, 1.24, P for difference = 0.02]. Childhood cancer incidence rises with increasing birthweight. In older children, cancers other than leukaemia are particularly related to high birthweight. Maternal adiposity, currently widespread, was not demonstrated to substantially modify these associations. Common factors underlying foetal growth and carcinogenesis need to be further explored. © 2015 The Authors. Paediatric and Perinatal Epidemiology published by John Wiley & Sons Ltd. JF - Paediatric and perinatal epidemiology AU - Paltiel, Ora AU - Tikellis, Gabriella AU - Linet, Martha AU - Golding, Jean AU - Lemeshow, Stanley AU - Phillips, Gary AU - Lamb, Karen AU - Stoltenberg, Camilla AU - Håberg, Siri E AU - Strøm, Marin AU - Granstrøm, Charlotta AU - Northstone, Kate AU - Klebanoff, Mark AU - Ponsonby, Anne-Louise AU - Milne, Elizabeth AU - Pedersen, Marie AU - Kogevinas, Manolis AU - Ha, Eunhee AU - Dwyer, Terence AU - International Childhood Cancer Cohort Consortium AD - Department of Hematology, Braun School of Public Health, Hadassah-Hebrew University, Jerusalem, Israel. ; Department of Environmental and Genetic Epidemiology, Murdoch Children's Research Institute, Royal Childrens Hospital, University of Melbourne, Melbourne, Australia. ; Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, UK. ; Centre for Child & Adolescent Health, School of Social & Community Medicine, University of Bristol, Bristol, UK. ; Division of Biostatistics, College of Public Health, The Ohio State University, Columbus, Ohio, UK. ; Division of Biostatistics, The Ohio State University Center for Biostatistics, Columbus, Ohio, UK. ; Centre for Physical Activity and Nutrition, Deakin University, Burwood, Australia. ; Norwegian Institute of Public Health, Oslo, Norway. ; Department of Epidemiology Research, Center for Fetal Programming, Statenserum Institute, Copenhagen, Denmark. ; ALSPAC (Children of the 90s), School of Social and Community Medicine, University of Bristol, Bristol, UK. ; Telethon Kids Institute, University of Western Australia, Perth, Western Australia, Australia. ; Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain. ; School of Medicine, Ewha Medical Research Center, Department of Preventive Medicine, Ewha Womans University, Seoul, Korea. ; Department of Environmental and Genetic Epidemiology, Murdoch Children's Research Institute, Royal Childrens Hospital, University of Melbourne, Melbourne, Australia; The George Institute for Global Health, University of Oxford, Oxford, UK. ; International Childhood Cancer Cohort Consortium Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 335 EP - 345 VL - 29 IS - 4 KW - Index Medicus KW - leukemia KW - pooled analysis. KW - cohort studies KW - Childhood cancer KW - Odds Ratio KW - Israel -- epidemiology KW - Norway -- epidemiology KW - Age of Onset KW - Australia -- epidemiology KW - Humans KW - Infant, Newborn KW - Child KW - Child, Preschool KW - Infant KW - United Kingdom -- epidemiology KW - Risk Factors KW - Denmark -- epidemiology KW - Adolescent KW - United States -- epidemiology KW - Female KW - Male KW - Birth Weight KW - Neoplasms -- epidemiology KW - Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1691601292?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Paediatric+and+perinatal+epidemiology&rft.atitle=Birthweight+and+Childhood+Cancer%3A+Preliminary+Findings+from+the+International+Childhood+Cancer+Cohort+Consortium+%28I4C%29.&rft.au=Paltiel%2C+Ora%3BTikellis%2C+Gabriella%3BLinet%2C+Martha%3BGolding%2C+Jean%3BLemeshow%2C+Stanley%3BPhillips%2C+Gary%3BLamb%2C+Karen%3BStoltenberg%2C+Camilla%3BH%C3%A5berg%2C+Siri+E%3BStr%C3%B8m%2C+Marin%3BGranstr%C3%B8m%2C+Charlotta%3BNorthstone%2C+Kate%3BKlebanoff%2C+Mark%3BPonsonby%2C+Anne-Louise%3BMilne%2C+Elizabeth%3BPedersen%2C+Marie%3BKogevinas%2C+Manolis%3BHa%2C+Eunhee%3BDwyer%2C+Terence%3BInternational+Childhood+Cancer+Cohort+Consortium&rft.aulast=Paltiel&rft.aufirst=Ora&rft.date=2015-07-01&rft.volume=29&rft.issue=4&rft.spage=335&rft.isbn=&rft.btitle=&rft.title=Paediatric+and+perinatal+epidemiology&rft.issn=1365-3016&rft_id=info:doi/10.1111%2Fppe.12193 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-16 N1 - Date created - 2015-06-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Int J Cancer. 2013 Dec 15;133(12):2968-79 [23754574] Paediatr Perinat Epidemiol. 2010 Sep;24(5):449-69 [20670226] Int J Epidemiol. 2015 Feb;44(1):153-68 [25626438] PLoS One. 2013;8(8):e70549 [23936446] Am J Obstet Gynecol. 2001 Oct;185(4):845-9 [11641663] Arch Dis Child Fetal Neonatal Ed. 2002 Jan;86(1):F2-3 [11815536] Int J Cancer. 2004 Jun 20;110(3):465-7 [15095317] J Natl Cancer Inst. 2004 Oct 20;96(20):1549-56 [15494605] Acta Paediatr Scand. 1966;:Suppl 167:1+ [5940749] Int J Epidemiol. 2007 Aug;36(4):724-30 [17255350] Am J Clin Nutr. 2008 Jun;87(6):1750-9 [18541565] Int J Cancer. 2009 Jun 1;124(11):2658-70 [19173295] Epidemiology. 2009 Jul;20(4):484-7 [19525684] Am J Epidemiol. 2009 Aug 1;170(3):379-87 [19498073] Pediatr Blood Cancer. 2010 Feb;54(2):242-9 [19813253] Curr Opin Obstet Gynecol. 2009 Dec;21(6):521-6 [19809317] Cancer Epidemiol Biomarkers Prev. 2010 Apr;19(4):1042-52 [20332267] Eur J Pediatr. 2010 Jul;169(7):875-81 [20101509] BMC Public Health. 2007;7:168 [17650297] Stat Med. 2011 Feb 20;30(4):377-99 [21225900] Leuk Lymphoma. 2011 Apr;52(4):709-12 [21438834] Circulation. 2012 Mar 20;125(11):1381-9 [22344037] Cancer Causes Control. 2012 Sep;23(9):1577-85 [22878902] Mol Genet Metab. 2012 Sep;107(1-2):25-30 [22867885] Eur J Cancer. 2013 Apr;49(6):1437-47 [23266048] Pediatrics. 2013 Nov;132(5):e1265-75 [24167169] Cancer. 1969 Apr;23(4):913-9 [5775981] Am J Epidemiol. 1984 May;119(5):788-95 [6720675] Arch Dis Child. 1987 Mar;62(3):279-87 [3646026] Obstet Gynecol. 1994 Mar;83(3):342-52 [8127523] J Natl Cancer Inst. 1997 Jul 2;89(13):939-47 [9214673] J Natl Cancer Inst. 1962 Jan;28:231-44 [14468028] Br J Cancer. 2006 Jun 5;94(11):1738-44 [16736025] Pediatr Int. 2006 Oct;48(5):470-8 [16970785] Cancer Causes Control. 2007 Aug;18(6):655-63 [17503007] Am J Epidemiol. 2007 Jul 15;166(2):151-9 [17443021] Erratum In: Paediatr Perinat Epidemiol. 2015 Nov;29(6):589 [26443988] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/ppe.12193 ER - TY - JOUR T1 - Alternative Donor Allogeneic Hematopoietic Cell Transplantation for Acute Myeloid Leukemia. AN - 1691599608; 26111471 AB - Allogeneic hematopoietic cell transplantation (alloHCT) provides a potentially curative therapy for patients with high-risk or chemorefractory acute myeloid leukemia (AML). Historically, the applicability of alloHCT has been limited as only 30%-35% of patients have human leukocyte antigen (HLA)-matched siblings and outcomes using other donor types have been markedly inferior due to excess toxicity, graft failure, graft-versus-host disease (GVHD), and consequently non-relapse mortality. Advances in HLA typing, GVHD prophylactic approaches, and other transplantation techniques have successfully addressed these historical challenges. Herein, we review recent alloHCT studies using volunteer unrelated donors, umbilical cord blood units, or HLA-haploidentical donors, specifically focusing on studies that compared outcomes between donor sources. Although none are randomized and most are retrospective, these analyses suggest that current outcomes for AML patients using most alternative donor types are comparable to those seen using HLA-matched siblings. Published by Elsevier Inc. JF - Seminars in hematology AU - Kanakry, Christopher G AU - de Lima, Marcos J AU - Luznik, Leo AD - Experimental Transplantation and Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. Electronic address: christopher.kanakry@nih.gov. ; University Hospitals Case Medical Center, Case Western Reserve University School of Medicine, Cleveland, OH. ; Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 232 EP - 242 VL - 52 IS - 3 KW - Index Medicus KW - Histocompatibility Testing KW - Haploidy KW - Humans KW - Transplantation, Homologous KW - Graft vs Host Disease -- etiology KW - Tissue Donors KW - Leukemia, Myeloid, Acute -- therapy KW - Hematopoietic Stem Cell Transplantation -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1691599608?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+hematology&rft.atitle=Alternative+Donor+Allogeneic+Hematopoietic+Cell+Transplantation+for+Acute+Myeloid+Leukemia.&rft.au=Kanakry%2C+Christopher+G%3Bde+Lima%2C+Marcos+J%3BLuznik%2C+Leo&rft.aulast=Kanakry&rft.aufirst=Christopher&rft.date=2015-07-01&rft.volume=52&rft.issue=3&rft.spage=232&rft.isbn=&rft.btitle=&rft.title=Seminars+in+hematology&rft.issn=1532-8686&rft_id=info:doi/10.1053%2Fj.seminhematol.2015.03.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-22 N1 - Date created - 2015-06-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: N Engl J Med. 1995 Jan 26;332(4):217-23 [7808487] Blood. 1995 Aug 15;86(4):1606-13 [7632970] J Clin Oncol. 1997 May;15(5):1767-77 [9164184] N Engl J Med. 1998 Oct 22;339(17):1177-85 [9780337] N Engl J Med. 1998 Oct 22;339(17):1186-93 [9780338] Blood. 1998 Nov 15;92(10):3515-20 [9808542] N Engl J Med. 1998 Nov 26;339(22):1565-77 [9828244] J Clin Oncol. 2005 May 20;23(15):3447-54 [15753458] Blood. 2006 Apr 15;107(8):3065-73 [16380454] Bone Marrow Transplant. 2006 Aug;38(4):291-7 [16883312] Bone Marrow Transplant. 2006 Dec;38(12):799-805 [17075568] J Clin Oncol. 2006 Dec 20;24(36):5695-702 [17116940] Lancet. 2007 Jun 9;369(9577):1947-54 [17560447] Blood. 2007 Dec 15;110(13):4576-83 [17785583] Blood Cells Mol Dis. 2008 Jan-Feb;40(1):13-9 [17869547] Biol Blood Marrow Transplant. 2008 Mar;14(3):282-9 [18275894] Biol Blood Marrow Transplant. 2008 Jun;14(6):641-50 [18489989] Blood. 2008 Nov 1;112(9):3574-81 [18606875] J Clin Oncol. 2008 Nov 10;26(32):5183-91 [18768435] Biol Blood Marrow Transplant. 2009 Feb;15(2):257-65 [19167686] Blood. 2009 Feb 19;113(8):1631-8 [19104080] Blood. 2009 Mar 26;113(13):3110-8 [19059878] Blood Cells Mol Dis. 2009 Jul-Aug;43(1):98-104 [19356956] Blood. 2009 Nov 5;114(19):4293-9 [19706886] Blood. 2010 Apr 22;115(16):3224-30 [20124511] Lancet Oncol. 2010 Jul;11(7):653-60 [20558104] Leukemia. 2010 Jul;24(7):1276-82 [20485378] Biol Blood Marrow Transplant. 2010 Oct;16(10):1382-7 [20447462] Blood. 2010 Sep 16;116(11):1839-48 [20538804] J Clin Oncol. 2010 Oct 20;28(30):4642-8 [20805454] Blood. 2010 Nov 25;116(22):4693-9 [20686119] Blood. 2010 Nov 25;116(22):4439-43 [20716774] Biol Blood Marrow Transplant. 2011 Jun;17(6):821-30 [20831895] Blood. 2011 Jun 9;117(23):6375-82 [21467544] Blood. 2011 Jul 14;118(2):282-8 [21527516] Biol Blood Marrow Transplant. 2011 Sep;17(9):1327-34 [21232621] Blood. 2011 Dec 8;118(24):6438-45 [21976674] Bone Marrow Transplant. 2012 Apr;47(4):494-8 [21602900] Biol Blood Marrow Transplant. 2012 May;18(5):805-12 [22015993] Blood. 2012 Jun 7;119(23):5591-8 [22496153] Bone Marrow Transplant. 2012 Jul;47(7):924-33 [22002488] Semin Oncol. 2012 Dec;39(6):683-93 [23206845] N Engl J Med. 2012 Dec 13;367(24):2305-15 [23234514] Blood. 2013 Jan 31;121(5):849-57 [23165479] Blood. 2013 Jan 31;121(5):752-8 [23223509] J Clin Oncol. 2013 Apr 1;31(10):1310-6 [23423745] Biol Blood Marrow Transplant. 2013 Jun;19(6):898-903 [23467126] Biol Blood Marrow Transplant. 2013 Jun;19(6):934-9 [23523970] Blood. 2013 May 30;121(22):4603-10 [23596045] Biol Blood Marrow Transplant. 2013 Sep;19(9):1355-60 [23791622] Sci Transl Med. 2013 Nov 13;5(211):211ra157 [24225944] Bone Marrow Transplant. 2014 Feb;49(2):206-11 [24141650] Blood. 2014 Feb 20;123(8):1270-8 [24408320] Haematologica. 2014 Mar;99(3):535-40 [24143000] Leukemia. 2014 Apr;28(4):779-86 [24005245] Biol Blood Marrow Transplant. 2014 Jun;20(6):816-22 [24582782] N Engl J Med. 2014 Jul 24;371(4):339-48 [25054717] Blood. 2014 Jul 24;124(4):638-44 [24923299] Transplantation. 2014 Sep 15;98(5):569-77 [24798307] Biol Blood Marrow Transplant. 2014 Oct;20(10):1573-9 [24910379] Biol Blood Marrow Transplant. 2014 Oct;20(10):1560-5 [24933658] Blood. 2014 Oct 16;124(16):2596-606 [25161269] Blood. 2014 Oct 23;124(17):2735-43 [25214441] Biol Blood Marrow Transplant. 2014 Dec;20(12):2015-22 [25255162] Biol Blood Marrow Transplant. 2014 Dec;20(12):1975-81 [25263628] Blood. 2014 Dec 11;124(25):3817-27 [25316679] Blood. 2000 Dec 15;96(13):4075-83 [11110676] Bone Marrow Transplant. 2002 Nov;30(10):681-6 [12420207] Blood. 2004 Oct 1;104(7):1923-30 [15191952] Blood. 1977 Apr;49(4):511-33 [14751] N Engl J Med. 1980 May 8;302(19):1041-6 [6245359] N Engl J Med. 1980 Sep 4;303(10):565-7 [6995837] Lancet. 1983 Mar 19;1(8325):612-5 [6131300] Ann Intern Med. 1985 Mar;102(3):285-91 [3882039] N Engl J Med. 1989 Jan 26;320(4):197-204 [2643045] Proc Natl Acad Sci U S A. 1989 May;86(10):3828-32 [2566997] Hum Immunol. 1990 Oct;29(2):79-91 [2249952] Transplantation. 1991 Feb;51(2):443-7 [1994541] Blood. 1994 Jan 1;83(1):280-7 [8274743] Bone Marrow Transplant. 1993 Oct;12(4):371-80 [8275037] Blood. 1994 Dec 1;84(11):3948-55 [7524753] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1053/j.seminhematol.2015.03.005 ER - TY - JOUR T1 - Durable fear memories require PSD-95. AN - 1691015002; 25510511 AB - Traumatic fear memories are highly durable but also dynamic, undergoing repeated reactivation and rehearsal over time. Although overly persistent fear memories underlie anxiety disorders, such as posttraumatic stress disorder, the key neural and molecular mechanisms underlying fear memory durability remain unclear. Postsynaptic density 95 (PSD-95) is a synaptic protein regulating glutamate receptor anchoring, synaptic stability and certain types of memory. Using a loss-of-function mutant mouse lacking the guanylate kinase domain of PSD-95 (PSD-95(GK)), we analyzed the contribution of PSD-95 to fear memory formation and retrieval, and sought to identify the neural basis of PSD-95-mediated memory maintenance using ex vivo immediate-early gene mapping, in vivo neuronal recordings and viral-mediated knockdown (KD) approaches. We show that PSD-95 is dispensable for the formation and expression of recent fear memories, but essential for the formation of precise and flexible fear memories and for the maintenance of memories at remote time points. The failure of PSD-95(GK) mice to retrieve remote cued fear memory was associated with hypoactivation of the infralimbic (IL) cortex (but not the anterior cingulate cortex (ACC) or prelimbic cortex), reduced IL single-unit firing and bursting, and attenuated IL gamma and theta oscillations. Adeno-associated virus-mediated PSD-95 KD in the IL, but not the ACC, was sufficient to impair recent fear extinction and remote fear memory, and remodel IL dendritic spines. Collectively, these data identify PSD-95 in the IL as a critical mechanism supporting the durability of fear memories over time. These preclinical findings have implications for developing novel approaches to treating trauma-based anxiety disorders that target the weakening of overly persistent fear memories. JF - Molecular psychiatry AU - Fitzgerald, P J AU - Pinard, C R AU - Camp, M C AU - Feyder, M AU - Sah, A AU - Bergstrom, H C AU - Graybeal, C AU - Liu, Y AU - Schlüter, O M AU - Grant, S G AU - Singewald, N AU - Xu, W AU - Holmes, A AD - Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA. ; Department of Pharmacology and Toxicology, Institute of Pharmacy and CMBI, University of Innsbruck, Innsbruck, Austria. ; Picower Institute for Learning and Memory, Department of Brain and Cognitive Science, Massachusetts Institute of Technology, Cambridge, MA, USA. ; European Neuroscience Institute, Gottingen, Germany. ; Centre for Clinical Brain Sciences and Centre for Neuroregeneration, The University of Edinburgh, Edinburgh, UK. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 901 EP - 912 VL - 20 IS - 7 KW - Membrane Proteins KW - 0 KW - Dlgh4 protein, mouse KW - EC 2.7.4.8 KW - Guanylate Kinases KW - Index Medicus KW - Action Potentials -- physiology KW - Animals KW - Freezing Reaction, Cataleptic -- physiology KW - Theta Rhythm -- physiology KW - Conditioning, Classical -- physiology KW - Electrodes, Implanted KW - Extinction, Psychological -- physiology KW - Pyramidal Cells -- physiology KW - Mice, Mutant Strains KW - Gene Knockdown Techniques KW - Gamma Rhythm -- physiology KW - Cues KW - Dendritic Spines -- metabolism KW - Pyramidal Cells -- cytology KW - Olfactory Perception -- physiology KW - Electroshock KW - Male KW - Female KW - Cerebral Cortex -- cytology KW - Guanylate Kinases -- genetics KW - Cerebral Cortex -- physiology KW - Membrane Proteins -- metabolism KW - Guanylate Kinases -- metabolism KW - Memory -- physiology KW - Membrane Proteins -- genetics KW - Fear -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1691015002?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+psychiatry&rft.atitle=Durable+fear+memories+require+PSD-95.&rft.au=Fitzgerald%2C+P+J%3BPinard%2C+C+R%3BCamp%2C+M+C%3BFeyder%2C+M%3BSah%2C+A%3BBergstrom%2C+H+C%3BGraybeal%2C+C%3BLiu%2C+Y%3BSchl%C3%BCter%2C+O+M%3BGrant%2C+S+G%3BSingewald%2C+N%3BXu%2C+W%3BHolmes%2C+A&rft.aulast=Fitzgerald&rft.aufirst=P&rft.date=2015-07-01&rft.volume=20&rft.issue=7&rft.spage=901&rft.isbn=&rft.btitle=&rft.title=Molecular+psychiatry&rft.issn=1476-5578&rft_id=info:doi/10.1038%2Fmp.2014.161 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-24 N1 - Date created - 2015-06-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Rev Neurosci. 2005 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[12437938] Methods Mol Med. 2003;76:221-36 [12526166] J Physiol. 2003 Feb 1;546(Pt 3):859-67 [12563010] J Neurosci. 2003 Oct 29;23(30):9897-905 [14586019] J Neurosci. 2003 Nov 26;23(34):10809-14 [14645473] Neuron. 2003 Oct 30;40(3):595-607 [14642282] Proc Natl Acad Sci U S A. 2004 Feb 17;101(7):2185-90 [14766964] Neuron. 2004 Feb 19;41(4):625-38 [14980210] J Neurosci. 2004 Apr 14;24(15):3810-5 [15084662] Science. 2004 May 7;304(5672):881-3 [15131309] Science. 2004 Jul 2;305(5680):96-9 [15232109] Nat Rev Neurosci. 2004 Oct;5(10):771-81 [15378037] Erratum In: Mol Psychiatry. 2015 Jul;20(7):913 [25824301] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/mp.2014.161 ER - TY - JOUR T1 - Romidepsin in peripheral and cutaneous T-cell lymphoma: mechanistic implications from clinical and correlative data. AN - 1690652110; 25891346 AB - Romidepsin is an epigenetic agent approved for the treatment of patients with cutaneous or peripheral T-cell lymphoma (CTCL and PTCL). Here we report data in all patients treated on the National Cancer Institute 1312 trial, demonstrating long-term disease control and the ability to retreat patients relapsing off-therapy. In all, 84 patients with CTCL and 47 with PTCL were enrolled. Responses occurred early, were clinically meaningful and of very long duration in some cases. Notably, patients with PTCL receiving romidepsin as third-line therapy or later had a comparable response rate (32%) of similar duration as the total population (38%). Eight patients had treatment breaks of 3.5 months to 10 years; in four of six patients, re-initiation of treatment led to clear benefit. Safety data show slightly greater haematological and constitutional toxicity in PTCL. cDNA microarray studies show unique individual gene expression profiles, minimal overlap between patients, and both induction and repression of gene expression that reversed within 24 h. These data argue against cell death occurring as a result of an epigenetics-mediated gene induction programme. Together this work supports the safety and activity of romidepsin in T-cell lymphoma, but suggests a complex mechanism of action. © 2015 John Wiley & Sons Ltd. JF - British journal of haematology AU - Bates, Susan E AU - Eisch, Robin AU - Ling, Alexander AU - Rosing, Douglas AU - Turner, Maria AU - Pittaluga, Stefania AU - Prince, H Miles AU - Kirschbaum, Mark H AU - Allen, Steven L AU - Zain, Jasmine AU - Geskin, Larisa J AU - Joske, David AU - Popplewell, Leslie AU - Cowen, Edward W AU - Jaffe, Elaine S AU - Nichols, Jean AU - Kennedy, Sally AU - Steinberg, Seth M AU - Liewehr, David J AU - Showe, Louise C AU - Steakley, Caryn AU - Wright, John AU - Fojo, Tito AU - Litman, Thomas AU - Piekarz, Richard L AD - Developmental Therapeutics Branch, NCI, NIH, Bethesda, MD, USA. ; Department of Radiology, Warren G Magnuson Clinical Center, NIH, Bethesda, MD, USA. ; Consultative Cardiology, NHLBI, NIH, Bethesda, MD, USA. ; Dermatology Branch, NCI, Bethesda, MD, USA. ; Laboratory of Pathology, CCR, NCI, Bethesda, MD, USA. ; Peter MacCallum Cancer Centre, East Melbourne, Vic., Australia. ; Hematological Malignancies, Penn State Hershey Medical Center, Hershey, PA, USA. ; Hofstra North Shore-LIJ School of Medicine and Monter Cancer Center, Lake Success, NY, USA. ; Columbia University, New York, NY, USA. ; Department of Dermatology, University of Pittsburgh Medical Center, Pittsburgh, PA, USA. ; Sir Charles Gairdner Hospital, Nedlands, WA, Australia. ; City of Hope National Cancer Center, Duarte, CA, USA. ; Celgene Corporation, Cambridge, MA, USA. ; Independent Pharmaceutical Consultant, Boston, MA, USA. ; Biostatistics and Data Management, NCI, Bethesda, MD, USA. ; The Wistar Institute, Philadelphia, PA, USA. ; Center for Cancer Research, NCI, Bethesda, MD, USA. ; Cancer Therapy Evaluation Program, DCTDC, NCI, Bethesda, MD, USA. ; LEO Pharma A/S, Ballerup, Denmark. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 96 EP - 109 VL - 170 IS - 1 KW - Antibiotics, Antineoplastic KW - 0 KW - Depsipeptides KW - Histone Deacetylase Inhibitors KW - romidepsin KW - CX3T89XQBK KW - Index Medicus KW - epigenetic therapy KW - histone deacetylase inhibitor KW - T-cell lymphoma KW - chromatin KW - Prospective Studies KW - Aged, 80 and over KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Epigenomics KW - Skin Neoplasms -- drug therapy KW - Histone Deacetylase Inhibitors -- adverse effects KW - Depsipeptides -- adverse effects KW - Histone Deacetylase Inhibitors -- therapeutic use KW - Skin Neoplasms -- pathology KW - Lymphoma, T-Cell, Cutaneous -- pathology KW - Depsipeptides -- therapeutic use KW - Lymphoma, T-Cell, Cutaneous -- drug therapy KW - Antibiotics, Antineoplastic -- adverse effects KW - Antibiotics, Antineoplastic -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1690652110?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+haematology&rft.atitle=Romidepsin+in+peripheral+and+cutaneous+T-cell+lymphoma%3A+mechanistic+implications+from+clinical+and+correlative+data.&rft.au=Bates%2C+Susan+E%3BEisch%2C+Robin%3BLing%2C+Alexander%3BRosing%2C+Douglas%3BTurner%2C+Maria%3BPittaluga%2C+Stefania%3BPrince%2C+H+Miles%3BKirschbaum%2C+Mark+H%3BAllen%2C+Steven+L%3BZain%2C+Jasmine%3BGeskin%2C+Larisa+J%3BJoske%2C+David%3BPopplewell%2C+Leslie%3BCowen%2C+Edward+W%3BJaffe%2C+Elaine+S%3BNichols%2C+Jean%3BKennedy%2C+Sally%3BSteinberg%2C+Seth+M%3BLiewehr%2C+David+J%3BShowe%2C+Louise+C%3BSteakley%2C+Caryn%3BWright%2C+John%3BFojo%2C+Tito%3BLitman%2C+Thomas%3BPiekarz%2C+Richard+L&rft.aulast=Bates&rft.aufirst=Susan&rft.date=2015-07-01&rft.volume=170&rft.issue=1&rft.spage=96&rft.isbn=&rft.btitle=&rft.title=British+journal+of+haematology&rft.issn=1365-2141&rft_id=info:doi/10.1111%2Fbjh.13400 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-21 N1 - Date created - 2015-06-22 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00007345; ClinicalTrials.gov N1 - SuppNotes - Cited By: Clin Cancer Res. 2002 Mar;8(3):718-28 [11895901] Int J Cancer. 2010 Nov 1;127(9):2199-208 [20127862] Blood. 2004 Jun 15;103(12):4636-43 [14996704] Biol Pharm Bull. 2005 Jan;28(1):124-9 [15635176] Cell Cycle. 2005 May;4(5):717-26 [15846093] J Invest Dermatol. 2005 Nov;125(5):1045-52 [16297208] J Biol Chem. 2006 Mar 3;281(9):5612-22 [16377638] Clin Cancer Res. 2006 Jun 15;12(12):3762-73 [16778104] J Clin Oncol. 2012 Feb 20;30(6):631-6 [22271479] Clin J Oncol Nurs. 2012 Apr;16(2):195-204 [22459529] Blood. 2012 Aug 16;120(7):1466-9 [22760778] Adv Cancer Res. 2012;116:87-129 [23088869] Cell Death Dis. 2013;4:e519 [23449455] Blood Purif. 2012;34(3-4):349-53 [23344085] Blood. 2013 May 16;121(20):4115-25 [23532732] J Clin Oncol. 2013 Jun 1;31(16):1970-6 [23610113] Clin Cancer Res. 2013 Jun 1;19(11):3095-104 [23589175] Br J Haematol. 2013 Jul;162(1):138-41 [23590726] Blood. 2013 Jun 27;121(26):5154-7 [23678006] Mol Cancer Ther. 2013 Aug;12(8):1545-55 [23686769] J Clin Oncol. 2013 Aug 20;31(24):3019-25 [23857971] Cell Cycle. 2013 Sep 1;12(17):2829-38 [23966164] Nat Genet. 2014 Feb;46(2):166-70 [24413734] J Hematol Oncol. 2014;7:11 [24456586] Br J Dermatol. 2014 Jun;170(6):1266-75 [24641245] Mol Carcinog. 2014 Sep;53(9):722-35 [23475695] Clin Cancer Res. 2014 Oct 15;20(20):5240-54 [25320373] J Clin Oncol. 1999 Apr;17(4):1244 [10561185] J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437] Anticancer Drugs. 2000 Jul;11(6):445-54 [11001385] Blood. 2001 Nov 1;98(9):2865-8 [11675364] Mol Cancer Res. 2006 Aug;4(8):563-73 [16877702] Blood. 2007 Jan 1;109(1):31-9 [16960145] Clin Cancer Res. 2007 Feb 15;13(4):1076-82 [17317814] Proc Natl Acad Sci U S A. 2007 May 8;104(19):8071-6 [17470784] J Clin Oncol. 2007 Jul 20;25(21):3109-15 [17577020] Blood. 2007 Oct 15;110(8):3015-27 [17638852] Clin Cancer Res. 2008 Jan 1;14(1):188-98 [18172270] Mol Cancer Ther. 2008 May;7(5):1066-79 [18483296] J Am Acad Dermatol. 2008 May;58(5 Suppl 1):S88-91 [18489056] Clin Cancer Res. 2008 Jul 15;14(14):4500-10 [18628465] Cell Cycle. 2008 Jul 15;7(14):2139-45 [18641459] Clin Cancer Res. 2009 May 15;15(10):3354-65 [19417023] Blood. 2009 Jul 9;114(2):380-93 [19383971] Haematologica. 2009 Nov;94(11):1618-22 [19608677] J Clin Oncol. 2009 Nov 10;27(32):5410-7 [19826128] Mol Cell Biol. 2009 Dec;29(23):6149-69 [19805519] BMC Med Genomics. 2009;2:67 [19948057] Br J Haematol. 2010 Jan;148(2):256-67 [19874311] Blood. 2010 Aug 5;116(5):767-71 [20484084] Haematologica. 2010 Apr;95(4):613-21 [20133897] Adv Exp Med Biol. 2010;687:79-96 [20919639] J Clin Oncol. 2010 Oct 10;28(29):4485-91 [20697094] Cancer Res. 2011 May 15;71(10):3603-15 [21398407] Cancer Res. 2010 Jun 1;70(11):4470-80 [20460513] Expert Rev Anticancer Ther. 2010 Jul;10(7):997-1008 [20645688] Br J Pharmacol. 2011 Apr;162(7):1590-602 [21198545] Blood. 2011 Jun 2;117(22):5827-34 [21355097] Anticancer Res. 2011 Sep;31(9):2723-32 [21868513] Exp Hematol. 2011 Oct;39(10):1007-1017.e1 [21767511] Leukemia. 2012 Feb;26(2):323-31 [21818116] J Exp Ther Oncol. 2002 Nov-Dec;2(6):325-32 [12440223] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/bjh.13400 ER - TY - JOUR T1 - Strategy for selecting nanotechnology carriers to overcome immunological and hematological toxicities challenging clinical translation of nucleic acid-based therapeutics. AN - 1690215451; 25994601 AB - Clinical translation of nucleic acid-based therapeutics (NATs) is hampered by assorted challenges in immunotoxicity, hematotoxicity, pharmacokinetics, toxicology and formulation. Nanotechnology-based platforms are being considered to help address some of these challenges due to the nanoparticles' ability to change drug biodistribution, stability, circulation half-life, route of administration and dosage. Addressing toxicology and pharmacology concerns by various means including NATs reformulation using nanotechnology-based carriers has been reviewed before. However, little attention was given to the immunological and hematological issues associated with nanotechnology reformulation. This review focuses on application of nanotechnology carriers for delivery of various types of NATs, and how reformulation using nanoparticles affects immunological and hematological toxicities of this promising class of therapeutic agents. NATs share several immunological and hematological toxicities with common nanotechnology carriers. In order to avoid synergy or exaggeration of undesirable immunological and hematological effects of NATs by a nanocarrier, it is critical to consider the immunological compatibility of the nanotechnology platform and its components. Since receptors sensing nucleic acids are located essentially in all cellular compartments, a strategy for developing a nanoformulation with reduced immunotoxicity should first focus on precise delivery to the target site/cells and then on optimizing intracellular distribution. JF - Expert opinion on drug delivery AU - Dobrovolskaia, Marina A AU - McNeil, Scott E AD - Principal Scientist, Immunology Section Head,Nanotechnology Characterization Laboratory, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research , P .O. Box B, Frederick, MD 21702 , USA +1 301 8466939 ; +1 301 846 6399 ; marina@mail.nih.gov. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 1163 EP - 1175 VL - 12 IS - 7 KW - Nucleic Acids KW - 0 KW - Pharmaceutical Preparations KW - Index Medicus KW - drug delivery KW - immunotoxicity KW - nanoparticles KW - nucleic acid therapeutics KW - Pharmaceutical Preparations -- administration & dosage KW - Animals KW - Half-Life KW - Chemistry, Pharmaceutical KW - Humans KW - Tissue Distribution KW - Nanotechnology KW - Drug Delivery Systems KW - Nucleic Acids -- adverse effects KW - Nucleic Acids -- pharmacokinetics KW - Nanoparticles KW - Nucleic Acids -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1690215451?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Expert+opinion+on+drug+delivery&rft.atitle=Strategy+for+selecting+nanotechnology+carriers+to+overcome+immunological+and+hematological+toxicities+challenging+clinical+translation+of+nucleic+acid-based+therapeutics.&rft.au=Dobrovolskaia%2C+Marina+A%3BMcNeil%2C+Scott+E&rft.aulast=Dobrovolskaia&rft.aufirst=Marina&rft.date=2015-07-01&rft.volume=12&rft.issue=7&rft.spage=1163&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+drug+delivery&rft.issn=1744-7593&rft_id=info:doi/10.1517%2F17425247.2015.1042857 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-22 N1 - Date created - 2015-06-20 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1517/17425247.2015.1042857 ER - TY - JOUR T1 - Identification and Characterization of Cefazolin-Induced Liver Injury. AN - 1690214409; 25528012 AB - Cephalosporin antibiotics are popular because they have a broad spectrum of activity and are generally well tolerated; however, cephalosporin-induced liver injury is considered rare. We describe a new syndrome associated with a single intravenous dose of cefazolin and the clinical features of cephalosporin-induced liver injury. The Drug-Induced Liver Injury (DILI) Network collected detailed clinical data on 1212 patients with DILI between 2004 and 2012. We analyzed data from 41 patients in whom cephalosporins were implicated as primary agents of liver disease; 33 formally were adjudicated as having cephalosporin-induced DILI. Nineteen patients developed clinically apparent DILI after a single intravenous dose of cefazolin. All patients developed self-limited liver injury 3 to 23 days after receiving cefazolin during surgery-often during a minor outpatient procedure. The latency period was 20 days. Clinical features included itching, jaundice, nausea, fever, and rash. Laboratory abnormalities included a mixed or cholestatic pattern of serum enzyme increases. We identified 14 more patients with DILI attributed to other cephalosporins (5 first-generation, 2 second-generation, 6 third-generation, and 1 fourth-generation agent). Although latency and injury patterns were similar for cefazolin and other cephalosporins, the other cephalosporins were associated with more severe courses of injury, including 2 deaths from liver failure. DILI can develop after a single dose of cefazolin. It is characterized by a latency period of 1 to 3 weeks after exposure, a cholestatic biochemical pattern, and a self-limited moderate to severe clinical course. Other cephalosporins can cause a similar but more severe injury. Copyright © 2015 AGA Institute. Published by Elsevier Inc. All rights reserved. JF - Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association AU - Alqahtani, Saleh A AU - Kleiner, David E AU - Ghabril, Marwan AU - Gu, Jiezhun AU - Hoofnagle, Jay H AU - Rockey, Don C AU - Drug-Induced Liver Injury Network (DILIN) Study Investigators AD - Division of Digestive and Liver Diseases, The University of Texas Southwestern, Dallas, Texas. ; Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. ; Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana. ; Duke Clinical Research Institute, Duke University Medical Center, Durham, North Carolina. ; Liver Disease Research Branch, Division of Digestive Diseases and Nutrition, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland. ; Division of Digestive and Liver Diseases, The University of Texas Southwestern, Dallas, Texas. Electronic address: rockey@musc.edu. ; Drug-Induced Liver Injury Network (DILIN) Study Investigators Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 1328 EP - 1336.e2 VL - 13 IS - 7 KW - Anti-Bacterial Agents KW - 0 KW - Cefazolin KW - IHS69L0Y4T KW - Index Medicus KW - Cephalosporin KW - Antibiotic KW - Hepatotoxicity KW - DILIN KW - Prospective Studies KW - Aged, 80 and over KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Administration, Intravenous KW - Male KW - Female KW - Cefazolin -- administration & dosage KW - Chemical and Drug Induced Liver Injury -- pathology KW - Chemical and Drug Induced Liver Injury -- diagnosis KW - Anti-Bacterial Agents -- adverse effects KW - Anti-Bacterial Agents -- administration & dosage KW - Cefazolin -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1690214409?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+gastroenterology+and+hepatology+%3A+the+official+clinical+practice+journal+of+the+American+Gastroenterological+Association&rft.atitle=Identification+and+Characterization+of+Cefazolin-Induced+Liver+Injury.&rft.au=Alqahtani%2C+Saleh+A%3BKleiner%2C+David+E%3BGhabril%2C+Marwan%3BGu%2C+Jiezhun%3BHoofnagle%2C+Jay+H%3BRockey%2C+Don+C%3BDrug-Induced+Liver+Injury+Network+%28DILIN%29+Study+Investigators&rft.aulast=Alqahtani&rft.aufirst=Saleh&rft.date=2015-07-01&rft.volume=13&rft.issue=7&rft.spage=1328&rft.isbn=&rft.btitle=&rft.title=Clinical+gastroenterology+and+hepatology+%3A+the+official+clinical+practice+journal+of+the+American+Gastroenterological+Association&rft.issn=1542-7714&rft_id=info:doi/10.1016%2Fj.cgh.2014.11.036 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-11 N1 - Date created - 2015-06-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: JAMA. 1974 Jul 15;229(3):318-9 [4406795] Lancet. 1982 Aug 7;2(8293):336-7 [6124751] Drug Intell Clin Pharm. 1985 Jul-Aug;19(7-8):553-5 [4028960] Infect Dis Clin North Am. 1989 Sep;3(3):595-612 [2671141] N Engl J Med. 1990 Jan 18;322(3):141-7 [2403654] Am Fam Physician. 1991 Mar;43(3):937-48 [2000736] N Engl J Med. 1992 Jan 30;326(5):281-6 [1728731] Arch Surg. 1992 Jan;127(1):83-9; discussion 89 [1734854] Adv Ther. 1995 Mar-Apr;12(2):83-101 [10150326] Med Clin North Am. 1995 Jul;79(4):705-19 [7791418] Am J Gastroenterol. 1998 May;93(5):836-7 [9625142] Gastroenterology. 2005 Aug;129(2):512-21 [16083708] Dig Liver Dis. 2006 Jan;38(1):33-8 [16054882] Trans R Soc Trop Med Hyg. 2006 Aug;100(8):795-7 [16682062] Clin Infect Dis. 2006 Aug 1;43(3):322-30 [16804848] Aliment Pharmacol Ther. 2006 Oct 15;24(8):1187-95 [17014577] Hepatology. 2006 Oct;44(4):850-6 [17006920] Plast Reconstr Surg. 2007 Mar;119(3):1136-7 [17312549] Scand J Infect Dis. 2007;39(2):190-2 [17366046] Toxicol Pathol. 2007 Oct;35(6):840-5 [17943651] J Gen Intern Med. 2008 Nov;23(11):1914-6 [18752027] Gastroenterology. 2008 Dec;135(6):1924-34, 1934.e1-4 [18955056] Drug Saf. 2009;32(1):55-68 [19132805] World J Gastroenterol. 2009 Jun 7;15(21):2669-71 [19496200] Hepatology. 2010 Jun;51(6):2117-26 [20512999] Clin Exp Dermatol. 2011 Jan;36(1):6-11 [21143513] Turk J Gastroenterol. 2011 Aug;22(4):445 [21948584] Liver Transpl. 2004 Aug;10(8):1018-23 [15390328] J Clin Gastroenterol. 2004 Oct;38(9):833 [15365421] Gastroenterology. 2013 Jun;144(7):1419-25, 1425.e1-3; quiz e19-20 [23419359] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.cgh.2014.11.036 ER - TY - JOUR T1 - Prevention of myelosuppression and genotoxicity induced by cisplatin in murine bone marrow cells: effect of an organovanadium compound vanadium(III)-l-cysteine. AN - 1689843341; 25778689 AB - Cisplatin (CDDP) is one of the first-line anticancer drugs indicated for use against various form of human malignancies; but, the therapeutic outcome of CDDP chemotherapy is limited due to the development of myelosuppression and genotoxicity which may lead to secondary cancer. Induction of oxidative stress in normal host cells is thought to be responsible for these adverse effects. Therefore, in search of a potential chemoprotectant, an oraganovanadium compound, viz., vanadium(III)-l-cysteine (VC-III) was evaluated against CDDP-induced clastogenicity and cytotoxicity in bone marrow cells of Swiss albino mice. CDDP was administered intraperitoneally (5mg/kg body weight [b.w.]) and VC-III was given by oral gavage (1mg/kg b.w.) in concomitant and pretreatment schedule. The results showed that VC-III administration significantly (P < 0.001) enhanced cell proliferation and inhibited apoptosis in the bone marrow niche indicating recovery of CDDP-induced myelosuppression. VC-III also significantly (P < 0.001) decreased the percentage of chromosomal aberrations, the frequency of micronuclei formation and the extent of DNA damage. The observed antigenotoxic and cytoprotective effect of VC-III was attributed to its attenuation of free radicals status and restoration of oxidised and reduced glutathione levels. These results suggest that VC-III is a potential candidate for future development as a chemoprotective agent against chemotherapy-associated primary and secondary complications. © The Author 2015. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. JF - Mutagenesis AU - Basu, Abhishek AU - Ghosh, Prosenjit AU - Bhattacharjee, Arin AU - Patra, Arup Ranjan AU - Bhattacharya, Sudin AD - Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, 37, S. P. Mukherjee Road, Kolkata 700026, West Bengal, India. ; Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, 37, S. P. Mukherjee Road, Kolkata 700026, West Bengal, India sudinb19572004@yahoo.co.in. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 509 EP - 517 VL - 30 IS - 4 KW - Antineoplastic Agents KW - 0 KW - Organometallic Compounds KW - Vanadates KW - 3WHH0066W5 KW - Cysteine KW - K848JZ4886 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Animals KW - Humans KW - Oxidative Stress -- drug effects KW - Antineoplastic Agents -- toxicity KW - Mice KW - Female KW - DNA Damage -- drug effects KW - Bone Marrow Cells -- drug effects KW - Chromosome Aberrations -- drug effects KW - Chromosome Aberrations -- chemically induced KW - Vanadates -- chemistry KW - Cysteine -- chemistry KW - Bone Marrow Diseases -- prevention & control KW - Bone Marrow Diseases -- chemically induced KW - Cisplatin -- toxicity KW - Bone Marrow Cells -- pathology KW - Organometallic Compounds -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1689843341?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mutagenesis&rft.atitle=Prevention+of+myelosuppression+and+genotoxicity+induced+by+cisplatin+in+murine+bone+marrow+cells%3A+effect+of+an+organovanadium+compound+vanadium%28III%29-l-cysteine.&rft.au=Basu%2C+Abhishek%3BGhosh%2C+Prosenjit%3BBhattacharjee%2C+Arin%3BPatra%2C+Arup+Ranjan%3BBhattacharya%2C+Sudin&rft.aulast=Basu&rft.aufirst=Abhishek&rft.date=2015-07-01&rft.volume=30&rft.issue=4&rft.spage=509&rft.isbn=&rft.btitle=&rft.title=Mutagenesis&rft.issn=1464-3804&rft_id=info:doi/10.1093%2Fmutage%2Fgev011 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-08 N1 - Date created - 2015-06-17 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/mutage/gev011 ER - TY - JOUR T1 - Individual Differences in Impulsive Action Reflect Variation in the Cortical Serotonin 5-HT2A Receptor System. AN - 1688007281; 25666313 AB - Impulsivity is an important feature of multiple neuropsychiatric disorders, and individual variation in the degree of inherent impulsivity could play a role in the generation or exacerbation of problematic behaviors. Serotonin (5-HT) actions at the 5-HT2AR receptor (5-HT2AR) promote and 5-HT2AR antagonists suppress impulsive action (the inability to withhold premature responses; motor impulsivity) upon systemic administration or microinfusion directly into the medial prefrontal cortex (mPFC), a node in the corticostriatal circuit that is thought to play a role in the regulation of impulsive action. We hypothesized that the functional capacity of the 5-HT2AR, which is governed by its expression, localization, and protein/protein interactions (eg, postsynaptic density 95 (PSD95)), may drive the predisposition to inherent impulsive action. Stable high-impulsive (HI) and low-impulsive (LI) phenotypes were identified from an outbred rodent population with the 1-choice serial reaction time (1-CSRT) task. HI rats exhibited a greater head-twitch response following administration of the preferential 5-HT2AR agonist 2,5-dimethoxy-4-iodoamphetamine (DOI) and were more sensitive to the effects of the selective 5-HT2AR antagonist M100907 to suppress impulsive action relative to LI rats. A positive correlation was observed between levels of premature responses and 5-HT2AR binding density in frontal cortex ([(3)H]-ketanserin radioligand binding). Elevated mPFC 5-HT2AR protein expression concomitant with augmented association of the 5-HT2AR with PSD95 differentiated HI from LI rats. The observed differential sensitivity of HI and LI rats to 5-HT2AR ligands and associated distinct 5-HT2AR protein profiles provide evidence that spontaneously occurring individual differences in impulsive action reflect variation in the cortical 5-HT2AR system. JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology AU - Fink, Latham H L AU - Anastasio, Noelle C AU - Fox, Robert G AU - Rice, Kenner C AU - Moeller, F Gerard AU - Cunningham, Kathryn A AD - 1] Center for Addiction Research, University of Texas Medical Branch, Galveston, TX, USA [2] Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, TX, USA. ; Chemical Biology Research Branch, National Institute on Drug Abuse and National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD, USA. ; Department of Psychiatry, Virginia Commonwealth University School of Medicine, Richmond, VA, USA. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 1957 EP - 1968 VL - 40 IS - 8 KW - 4-iodo-2,5-dimethoxy-beta-phenethylamine KW - 0 KW - Dimethoxyphenylethylamine KW - Fluorobenzenes KW - Piperidines KW - Receptor, Serotonin, 5-HT2A KW - Serotonin Agents KW - Tritium KW - 10028-17-8 KW - Ketanserin KW - 97F9DE4CT4 KW - volinanserin KW - EW71EE171J KW - Index Medicus KW - Tritium -- pharmacokinetics KW - Reaction Time -- drug effects KW - Animals KW - Immunoprecipitation KW - Ketanserin -- pharmacokinetics KW - Dimethoxyphenylethylamine -- analogs & derivatives KW - Piperidines -- pharmacology KW - Rats KW - Rats, Sprague-Dawley KW - Serotonin Agents -- pharmacology KW - Fluorobenzenes -- pharmacology KW - Protein Binding -- drug effects KW - Choice Behavior -- physiology KW - Dimethoxyphenylethylamine -- pharmacology KW - Head Movements -- drug effects KW - Male KW - Receptor, Serotonin, 5-HT2A -- metabolism KW - Impulsive Behavior -- drug effects KW - Prefrontal Cortex -- metabolism KW - Impulsive Behavior -- physiology KW - Prefrontal Cortex -- drug effects KW - Individuality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1688007281?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.atitle=Individual+Differences+in+Impulsive+Action+Reflect+Variation+in+the+Cortical+Serotonin+5-HT2A+Receptor+System.&rft.au=Fink%2C+Latham+H+L%3BAnastasio%2C+Noelle+C%3BFox%2C+Robert+G%3BRice%2C+Kenner+C%3BMoeller%2C+F+Gerard%3BCunningham%2C+Kathryn+A&rft.aulast=Fink&rft.aufirst=Latham+H&rft.date=2015-07-01&rft.volume=40&rft.issue=8&rft.spage=1957&rft.isbn=&rft.btitle=&rft.title=Neuropsychopharmacology+%3A+official+publication+of+the+American+College+of+Neuropsychopharmacology&rft.issn=1740-634X&rft_id=info:doi/10.1038%2Fnpp.2015.46 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-08 N1 - Date created - 2015-06-13 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: ACS Chem Neurosci. 2013 Jan 16;4(1):110-21 [23336050] ACS Chem Neurosci. 2015 Jul 15;6(7):1165-75 [25547199] Neuropharmacology. 2000 Jan 28;39(3):471-81 [10698013] J Neurosci Res. 2000 Jul 15;61(2):186-92 [10878591] Pharmacol Biochem Behav. 2000 Aug;66(4):729-38 [10973510] Brain Res Bull. 2001 Jan 1;54(1):65-75 [11226715] Am J Psychiatry. 2001 Nov;158(11):1783-93 [11691682] EMBO J. 2002 May 15;21(10):2332-42 [12006486] Neuropsychopharmacology. 2002 Jun;26(6):716-28 [12007742] Neuroscience. 2002;113(1):23-35 [12123681] Psychopharmacology (Berl). 2002 Oct;163(3-4):362-80 [12373437] Behav Res Methods Instrum Comput. 2002 Aug;34(3):391-8 [12395555] Psychopharmacology (Berl). 2003 Jan;165(2):136-45 [12420150] Neuroscience. 2003;116(1):107-17 [12535944] Psychopharmacology (Berl). 2003 May;167(3):304-14 [12677356] Pharmacol Toxicol. 2003 May;92(5):214-25 [12753409] J Biol Chem. 2003 Jun 13;278(24):21901-8 [12682061] J Biol Chem. 2004 May 7;279(19):20257-66 [14988405] Neuropsychopharmacology. 2004 Jul;29(7):1331-43 [15054475] Mol Pharmacol. 1982 Mar;21(2):301-14 [7099138] J Neurosci. 2013 Jan 23;33(4):1615-30 [23345234] Dis Model Mech. 2013 Mar;6(2):302-11 [23355644] Neuropharmacology. 2013 Jul;70:112-21 [23353901] Eur J Neurosci. 2013 Jun;37(11):1779-88 [23510331] Neuropsychopharmacology. 2013 Sep;38(10):1963-73 [23632436] Eur Neuropsychopharmacol. 2013 Aug;23(8):852-64 [23176747] Neuropharmacology. 2014 Jan;76 Pt B:460-78 [23850573] Biol Psychiatry. 2014 Jan 15;75(2):115-23 [23973096] Neuropsychopharmacology. 2014 Jan;39(2):370-82 [23939424] Behav Brain Res. 2003 Nov 30;146(1-2):105-19 [14643464] Behav Pharmacol. 2014 Feb;25(1):44-52 [24346289] Neuroscience. 2014 Mar 28;263:36-45 [24412375] Brain Res. 1985 Nov 4;346(2):231-49 [4052777] Neuropharmacology. 1985 Dec;24(12):1201-5 [4094656] Biol Psychiatry. 1989 Jul;26(3):297-302 [2742945] Ann N Y Acad Sci. 1990;600:183-91; discussion 192-3 [2252309] Brain Res Mol Brain Res. 1994 Apr;23(1-2):163-78 [8028479] Cereb Cortex. 1996 May-Jun;6(3):470-81 [8670672] Behav Brain Res. 1997 Feb;83(1-2):15-23 [9062655] J Pharmacol Exp Ther. 1997 Aug;282(2):699-706 [9262333] Naunyn Schmiedebergs Arch Pharmacol. 1997 Oct;356(4):446-54 [9349630] Psychopharmacology (Berl). 1997 Oct;133(4):329-42 [9372531] Pharmacol Biochem Behav. 1998 Nov;61(3):323-30 [9768567] J Comp Neurol. 1999 Jun 28;409(2):187-209 [10379914] J Psychopharmacol. 1999;13(2):180-92 [10475725] Br J Pharmacol. 1999 Sep;128(1):13-20 [10498829] Psychopharmacology (Berl). 2004 Nov;176(3-4):376-85 [15232674] Neurosci Biobehav Rev. 2004 Nov;28(7):771-84 [15555683] Neuroscience. 2006;139(3):865-76 [16500029] Behav Pharmacol. 2011 Dec;22(8):805-13 [22015807] Psychopharmacology (Berl). 2012 Jan;219(2):387-400 [21863235] Neuropsychopharmacology. 2012 Aug;37(9):2057-66 [22510726] Biol Lett. 2005 Jun 22;1(2):223-6 [17148172] Science. 2007 Mar 2;315(5816):1267-70 [17332411] Proc Natl Acad Sci U S A. 2007 Jun 5;104(23):9870-5 [17535909] Psychopharmacology (Berl). 2007 Dec;195(2):223-34 [17673981] Neuropsychopharmacology. 2008 Sep;33(10):2398-406 [18046307] J Neurosci. 2009 Jun 3;29(22):7124-36 [19494135] Cereb Cortex. 2009 Jul;19(7):1678-86 [19029064] Neurosci Biobehav Rev. 2010 Jan;34(1):50-72 [19615404] Neuropsychopharmacology. 2010 Feb;35(3):591-604 [19940844] J Neurochem. 2010 Jun;113(6):1504-15 [20345755] Behav Pharmacol. 2011 Jun;22(3):248-61 [21499079] Br J Pharmacol. 2011 Oct;164(4):1301-21 [21410459] Curr Protoc Pharmacol. 2001 May;Chapter 1:Unit1.23 [21959751] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/npp.2015.46 ER - TY - JOUR T1 - Immunological and hematological toxicities challenging clinical translation of nucleic acid-based therapeutics. AN - 1687998186; 26017628 AB - Nucleic acid-based therapeutics (NATs) are proven agents in correcting disorders caused by gene mutations, as treatments against cancer, microbes and viruses, and as vaccine adjuvants. Although many traditional small molecule NATs have been approved for clinical use, commercialization of macromolecular NATs has been considerably slower, and only a few have successfully reached the market. Preclinical and clinical evaluation of macromolecular NATs has revealed many assorted challenges in immunotoxicity, hematotoxicity, pharmacokinetics (PKs), toxicology and formulation. Extensive review has been given to the PK and toxicological concerns of NATs including approaches designed to overcome these issues. Immunological and hematological issues are a commonly reported side effect of NAT treatment; however, literature exploring the mechanistic background of these effects is sparse. This review focuses on the immunomodulatory properties of various types of therapeutic nucleic acid concepts. The most commonly observed immunological and hematological toxicities are described for various NAT classes, with citations of how to circumvent these toxicities. Although some success with overcoming immunological and hematological toxicities of NATs has been achieved in recent years, immunostimulation remains the main dose-limiting factor challenging clinical translation of these promising therapies. Novel delivery vehicles should be considered to overcome this challenge. JF - Expert opinion on biological therapy AU - Dobrovolskaia, Marina A AU - McNeil, Scott E AD - Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Nanotechnology Characterization Laboratory, Cancer Research Technology Program , P.O. Box B, Frederick, MD 21702 , USA +1 301 846 6939 ; +1 301 846 6399 ; marina@mail.nih.gov. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 1023 EP - 1048 VL - 15 IS - 7 KW - Antineoplastic Agents KW - 0 KW - DNA, Catalytic KW - Nucleic Acids KW - Nucleosides KW - Nucleotides KW - Oligonucleotides, Antisense KW - RNA, Catalytic KW - Index Medicus KW - nucleic acid-based therapeutics KW - hematotoxicity KW - immunotoxicity KW - drug safety KW - RNA, Catalytic -- chemistry KW - Animals KW - Neoplasms -- drug therapy KW - Nucleosides -- therapeutic use KW - Oligonucleotides, Antisense -- chemistry KW - Humans KW - Nucleosides -- pharmacology KW - Oligonucleotides, Antisense -- pharmacology KW - Nucleotides -- chemistry KW - RNA, Catalytic -- pharmacology KW - Nucleosides -- chemistry KW - DNA, Catalytic -- pharmacology KW - Oligonucleotides, Antisense -- therapeutic use KW - Nucleotides -- therapeutic use KW - Immune System -- drug effects KW - RNA, Catalytic -- therapeutic use KW - DNA, Catalytic -- therapeutic use KW - DNA, Catalytic -- chemistry KW - RNA Interference KW - Nucleotides -- pharmacology KW - Neoplasms -- immunology KW - Antineoplastic Agents -- toxicity KW - Nucleic Acids -- chemistry KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- chemistry KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687998186?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Expert+opinion+on+biological+therapy&rft.atitle=Immunological+and+hematological+toxicities+challenging+clinical+translation+of+nucleic+acid-based+therapeutics.&rft.au=Dobrovolskaia%2C+Marina+A%3BMcNeil%2C+Scott+E&rft.aulast=Dobrovolskaia&rft.aufirst=Marina&rft.date=2015-07-01&rft.volume=15&rft.issue=7&rft.spage=1023&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+biological+therapy&rft.issn=1744-7682&rft_id=info:doi/10.1517%2F14712598.2015.1014794 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-19 N1 - Date created - 2015-06-11 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1517/14712598.2015.1014794 ER - TY - JOUR T1 - Endocrine disruptors and female cancer: Informing the patients (Review). AN - 1687996308; 25998096 AB - Pollutants altering the endocrine system, known as endocrine disruptors (ED), may modify the risk of female cancers. The carcinogenic effect of ED on humans has been confirmed by experimental studies for various substances including pesticides, DDT, dioxins, phthalates, bisphenol A, diethylstilbestrol, as well as heavy metals, but it is difficult to quantify precisely for several reasons hereby reviewed. Carcinogenesis is a complex and multifactorial mechanism that manifests itself over a long period of time, making difficult the detection of the specific contribution of the pollutants, whose absorbed dose is often unknown. The combined effect of various substances leads to complex interactions whose outcome is difficult to predict. These substances may accumulate and carry out their harmful effect on critical periods of life, probably also at doses considered harmless to an adult. ED can also have epigenetic adverse effects on the health of future generations. In conclusion, the carcinogenic effects of endocrine disruptors on female cancer types is plausible although additional studies are needed to clarify their mechanisms and entities. In the last part of the review we suggest ways to reduce ED exposure as it is mandatory to implement necessary measures to limit exposure, particularly during those periods of life most vulnerable to the impact of oncogenic environmental causes, such as the embryonic period and puberty. JF - Oncology reports AU - Del Pup, Lino AU - Mantovani, Alberto AU - Luce, Amalia AU - Cavaliere, Carla AU - Facchini, Gaetano AU - Di Francia, Raffaele AU - Caraglia, Michele AU - Berretta, Massimiliano AD - Division of Gynecological Oncology, CRO Aviano, National Cancer Institute, I-33081 Aviano, Italy. ; National Institute of Health, I-00161 Rome, Italy. ; Department of Biochemistry, Biophysics and General Pathology, Second University of Naples, I-80138 Naples, Italy. ; Division of Medical Oncology, Department of Uro-Gynaecological Oncology, Istituto Nazionale Tumori ̔Fondazione Giovanni Pascale', IRCCS, I-80131 Naples, Italy. ; Hematology-Oncology and Stem Cell Transplantation Unit, Istituto Nazionale Tumori ̔Fondazione Giovanni Pascale', IRCCS, I-80131 Naples, Italy. ; Department of Medical Oncology, CRO Aviano, National Cancer Institute, I-33081 Aviano, Italy. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 3 EP - 11 VL - 34 IS - 1 KW - Endocrine Disruptors KW - 0 KW - Index Medicus KW - Risk Factors KW - Humans KW - Female KW - Endocrine Disruptors -- toxicity KW - Neoplasms -- pathology KW - Neoplasms -- chemically induced KW - Endocrine Disruptors -- classification KW - Carcinogenesis KW - Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687996308?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncology+reports&rft.atitle=Endocrine+disruptors+and+female+cancer%3A+Informing+the+patients+%28Review%29.&rft.au=Del+Pup%2C+Lino%3BMantovani%2C+Alberto%3BLuce%2C+Amalia%3BCavaliere%2C+Carla%3BFacchini%2C+Gaetano%3BDi+Francia%2C+Raffaele%3BCaraglia%2C+Michele%3BBerretta%2C+Massimiliano&rft.aulast=Del+Pup&rft.aufirst=Lino&rft.date=2015-07-01&rft.volume=34&rft.issue=1&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=Oncology+reports&rft.issn=1791-2431&rft_id=info:doi/10.3892%2For.2015.3997 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-15 N1 - Date created - 2015-06-11 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3892/or.2015.3997 ER - TY - JOUR T1 - Advancing research on endocrine disrupting chemicals in breast cancer: Expert panel recommendations. AN - 1687361575; 25549947 AB - Breast cancer incidence continues to increase in the US and Europe, a reflection of the growing influence of environment factors that interact with personal genetics. The US Environmental Protection Agency estimates that there are approximately 10,000 endocrine disrupting chemicals among the common daily exposures that could affect the risk of disease. The daunting tasks of identifying, characterizing, and elucidating the mechanisms of endocrine disrupting chemicals in breast cancer need to be addressed to produce a comprehensive model that will facilitate preventive strategies and public policy. An expert panel met to describe and bring attention to needs linking common environmental exposures, critical windows of exposure, and optimal times of assessment in investigating breast cancer risk. The group included investigators with extensive experience in the use of rodent models and in leading population studies and produced a set of recommendations for effective approaches to gaining insights into the environmental origins of breast cancer across the lifespan. Published by Elsevier Inc. JF - Reproductive toxicology (Elmsford, N.Y.) AU - Teitelbaum, Susan L AU - Belpoggi, Fiorella AU - Reinlib, Les AD - Department of Preventive Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA. ; Cesare Maltoni Cancer Research Center, Ramazzini Institute, Bentivoglio, Bologna, Italy. ; National Institute of Environmental Health Sciences, National Institutes of Health, US Department of Health and Human Services, Research Triangle Park, NC, USA. Electronic address: reinlib@niehs.nih.gov. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 141 EP - 147 VL - 54 KW - Carcinogens, Environmental KW - 0 KW - Endocrine Disruptors KW - Index Medicus KW - Endocrine disrupting chemicals KW - Windows of susceptibility KW - Mammary gland biology KW - Breast cancer KW - Sexual Development KW - Animals KW - Age Factors KW - Cell Transformation, Neoplastic -- pathology KW - Disease Susceptibility KW - Risk Factors KW - Humans KW - Cell Transformation, Neoplastic -- metabolism KW - Cell Transformation, Neoplastic -- chemically induced KW - Environmental Exposure -- adverse effects KW - Time Factors KW - Female KW - Risk Assessment KW - Mammary Glands, Animal -- drug effects KW - Mammary Glands, Human -- metabolism KW - Breast Neoplasms -- metabolism KW - Mammary Glands, Animal -- growth & development KW - Carcinogens, Environmental -- toxicity KW - Research Design KW - Endocrine Disruptors -- toxicity KW - Breast Neoplasms -- pathology KW - Biomedical Research -- methods KW - Mammary Glands, Animal -- metabolism KW - Mammary Glands, Animal -- pathology KW - Mammary Glands, Human -- pathology KW - Mammary Glands, Human -- growth & development KW - Breast Neoplasms -- chemically induced KW - Mammary Glands, Human -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687361575?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.atitle=Advancing+research+on+endocrine+disrupting+chemicals+in+breast+cancer%3A+Expert+panel+recommendations.&rft.au=Teitelbaum%2C+Susan+L%3BBelpoggi%2C+Fiorella%3BReinlib%2C+Les&rft.aulast=Teitelbaum&rft.aufirst=Susan&rft.date=2015-07-01&rft.volume=54&rft.issue=&rft.spage=141&rft.isbn=&rft.btitle=&rft.title=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.issn=1873-1708&rft_id=info:doi/10.1016%2Fj.reprotox.2014.12.015 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-04 N1 - Date created - 2015-06-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Hum Reprod. 2014 Jul;29(7):1558-66 [24781428] Environ Health Perspect. 2013 Sep;121(9):1040-6 [23876597] Int J Circumpolar Health. 2014;73:25760 [25442219] Reprod Toxicol. 2015 Jul;54:129-35 [25463529] J Epidemiol Biostat. 1999;4(3):191-210; discussion 210-5 [10695959] Environ Health Perspect. 2000 Jun;108 Suppl 3:451-5 [10852844] Environ Health Perspect. 2000 Jun;108 Suppl 3:573-94 [10852857] J Natl Cancer Inst. 2001 Jan 3;93(1):60-2 [11136844] Cancer Epidemiol Biomarkers Prev. 2006 Aug;15(8):1509-14 [16896041] BMC Genomics. 2007;8:453 [18062813] J Toxicol Environ Health B Crit Rev. 2008 Mar;11(3-4):276-300 [18368557] Br J Cancer. 2008 May 6;98(9):1485-93 [18392054] Curr Stem Cell Res Ther. 2009 Jan;4(1):50-60 [19149630] Cancer Epidemiol Biomarkers Prev. 2009 Sep;18(9):2447-52 [19690178] Environ Health Perspect. 2010 Apr;118(4):539-44 [20368132] Environ Health Perspect. 2010 May;118(5):596-601 [20435547] Cancer Causes Control. 2010 Jul;21(7):999-1007 [20204493] Nat Rev Endocrinol. 2010 Jul;6(7):363-70 [20498677] Environ Health. 2011;10(1):5 [21241498] Environ Health Perspect. 2010 Nov;118(11):1614-9 [20675265] Toxicol Appl Pharmacol. 2011 Jul 15;254(2):181-91 [21034758] Toxicol Sci. 2011 Jul;122(1):134-45 [21482639] Br J Cancer. 2011 Aug 23;105(5):709-22 [21772329] Nat Med. 2011 Sep;17(9):1109-15 [21822285] J Steroid Biochem Mol Biol. 2011 Oct;127(1-2):16-26 [21397692] Chemosphere. 2011 Dec;85(11):1701-6 [22014662] Environ Health Perspect. 2011 Dec;119(12):1700-5 [21810551] Endocrinology. 2012 Jan;153(1):42-55 [22109888] FASEB J. 2012 Feb;26(2):778-87 [22049059] Eur J Epidemiol. 2012 Jan;27(1):1-3 [22286719] Int J Androl. 2012 Jun;35(3):216-26 [22428786] Reprod Toxicol. 2012 Jul;33(4):563-76 [22414604] Int J Mol Sci. 2012;13(8):10143-53 [22949852] Environ Health Perspect. 2012 Oct;120(10):1432-7 [22935244] Environ Health Perspect. 2012 Nov;120(11):1613-8 [23124194] J Mammary Gland Biol Neoplasia. 2013 Mar;18(1):25-42 [23392570] J Adolesc Health. 2013 May;52(5 Suppl):S15-20 [23601607] ILAR J. 2012;53(3-4):289-305 [23744968] Breast J. 2001 Sep-Oct;7(5):278-91 [11906437] Environ Health Perspect. 2002 Jul;110(7):625-8 [12117637] Nature. 2003 May 29;423(6939):545-50 [12774124] Radiat Res. 2003 Dec;160(6):707-17 [14640793] Trends Endocrinol Metab. 2004 Jul;15(5):193-7 [15223047] Lancet. 1989 Sep 9;2(8663):577-80 [2570282] IARC Sci Publ. 1991;(112):3-23 [1855946] J Endocrinol. 1997 Mar;152(3):477-87 [9071969] J Anat. 1953 Oct;87(4):387-406 [13117757] J Mammary Gland Biol Neoplasia. 2013 Jun;18(2):199-208 [23702822] Toxicol Sci. 2014 Jan;137(1):1-2 [24213143] Sci Rep. 2014;4:5664 [25012808] Climacteric. 2014 Aug;17(4):377-84 [24228746] J Expo Sci Environ Epidemiol. 2013 Jul;23(4):343-9 [22781437] Nutrition. 2005 Jun;21(6):775-7 [15925305] Birth Defects Res C Embryo Today. 2013 Jun;99(2):134-46 [23897597] J Clin Endocrinol Metab. 2014 Oct;99(10):3829-35 [25029416] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.reprotox.2014.12.015 ER - TY - JOUR T1 - The mammary gland is a sensitive pubertal target in CD-1 and C57Bl/6 mice following perinatal perfluorooctanoic acid (PFOA) exposure. AN - 1687361564; 25499722 AB - Perfluorooctanoic acid (PFOA) is a developmental toxicant in mice, with varied strain outcomes depending on dose and period of exposure. The impact of PFOA on female mouse pubertal development at low doses (≤1mg/kg) has yet to be determined. Therefore, female offspring from CD-1 and C57Bl/6 dams exposed to PFOA, creating serum concentrations similar to humans, were examined for pubertal onset, including mammary gland development. Pups demonstrated a shorter PFOA elimination half-life than that reported for adult mice. Prenatal exposure to PFOA caused significant mammary developmental delays in female offspring in both strains. Delays started during puberty and persisted into young adulthood; severity was dose-dependent. Also an evaluation of female serum hormone levels and pubertal timing onset revealed no effects of PFOA compared to controls in either strain. These data suggest that the mammary gland is more sensitive to early low level PFOA exposures compared to other pubertal endpoints, regardless of strain. Published by Elsevier Inc. JF - Reproductive toxicology (Elmsford, N.Y.) AU - Tucker, Deirdre K AU - Macon, Madisa B AU - Strynar, Mark J AU - Dagnino, Sonia AU - Andersen, Erik AU - Fenton, Suzanne E AD - Curriculum in Toxicology, University of North Carolina at Chapel Hill, School of Medicine, Chapel Hill, NC 27599, United States; National Toxicology Program Laboratory, Division of the NTP, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, United States. ; Methods Development and Application Branch, Human Exposure and Atmospheric Sciences Division, National Exposure Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, United States. ; ORISE fellow at the National Exposure Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, United States. ; Exposure Measurements and Analysis Branch, Human Exposure and Atmospheric Sciences Division, National Exposure Research Laboratory, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, NC 27711, United States. ; National Toxicology Program Laboratory, Division of the NTP, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, United States. Electronic address: fentonse@niehs.nih.gov. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 26 EP - 36 VL - 54 KW - Caprylates KW - 0 KW - Environmental Pollutants KW - Fluorocarbons KW - perfluorooctanoic acid KW - 947VD76D3L KW - Index Medicus KW - CD-1 KW - Mammary gland KW - Vaginal opening KW - Perfluorooctanoic acid KW - Estrous cycle KW - C57Bl/6 KW - Puberty KW - Animals KW - Age Factors KW - Liver -- pathology KW - Dose-Response Relationship, Drug KW - Body Burden KW - Gestational Age KW - Pregnancy KW - Risk Assessment KW - Sexual Development -- drug effects KW - Liver -- drug effects KW - Risk Factors KW - Mice, Inbred C57BL KW - Female KW - Maternal Exposure -- adverse effects KW - Mammary Glands, Animal -- drug effects KW - Environmental Pollutants -- toxicity KW - Fluorocarbons -- toxicity KW - Mammary Glands, Animal -- growth & development KW - Caprylates -- toxicity KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687361564?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.atitle=The+mammary+gland+is+a+sensitive+pubertal+target+in+CD-1+and+C57Bl%2F6+mice+following+perinatal+perfluorooctanoic+acid+%28PFOA%29+exposure.&rft.au=Tucker%2C+Deirdre+K%3BMacon%2C+Madisa+B%3BStrynar%2C+Mark+J%3BDagnino%2C+Sonia%3BAndersen%2C+Erik%3BFenton%2C+Suzanne+E&rft.aulast=Tucker&rft.aufirst=Deirdre&rft.date=2015-07-01&rft.volume=54&rft.issue=&rft.spage=26&rft.isbn=&rft.btitle=&rft.title=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.issn=1873-1708&rft_id=info:doi/10.1016%2Fj.reprotox.2014.12.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-04 N1 - Date created - 2015-06-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Environ Pollut. 2014 Jan;184:327-34 [24095703] Endocr Rev. 2012 Jun;33(3):378-455 [22419778] Environ Health Perspect. 2014 Feb;122(2):187-92 [24280536] J Steroid Biochem Mol Biol. 2011 Oct;127(1-2):16-26 [21397692] Environ Health. 2011;10:88 [21978366] Endocr Relat Cancer. 2014 Apr;21(2):T33-55 [24532474] Cancer Causes Control. 2014 Nov;25(11):1439-48 [25148915] Reprod Toxicol. 2012 Jul;33(4):563-76 [22414604] Cold Spring Harb Perspect Biol. 2010 Dec;2(12):a003178 [20739412] J Mammary Gland Biol Neoplasia. 2013 Mar;18(1):43-61 [23417729] Toxicol Sci. 2009 Feb;107(2):331-41 [19005225] Reprod Toxicol. 2009 Jun;27(3-4):299-306 [19013232] Reprod Toxicol. 2009 Jun;27(3-4):360-4 [19028561] Reprod Toxicol. 2009 Jun;27(3-4):289-98 [19095057] Reprod Toxicol. 2009 Jun;27(3-4):365-72 [19429407] Curr Protoc Neurosci. 2009 Jul;Appendix 4:Appendix 4I [19575469] Environ Health Perspect. 2009 Dec;117(12):1873-82 [20049206] Toxicol Sci. 2010 May;115(1):214-24 [20118188] Cell Res. 2011 Feb;21(2):245-57 [21243011] Neurotox Res. 2011 Apr;19(3):452-61 [20512442] Epigenetics. 2010 Aug 16;5(6):539-46 [20523118] Pediatr Rev. 2011 Jun;32(6):223-9 [21632873] Toxicol Sci. 2011 Jul;122(1):134-45 [21482639] Nat Rev Mol Cell Biol. 2011 Sep;12(9):581-93 [21829222] Environ Sci Technol. 2011 Oct 1;45(19):8160-6 [21534542] Matern Child Health J. 2015 Mar;19(3):519-27 [24916206] Microsc Res Tech. 2001 Jan 15;52(2):155-62 [11169863] Toxicol Sci. 2001 Mar;60(1):44-55 [11222872] Biol Reprod. 2001 Oct;65(4):1215-23 [11566746] Toxicol Sci. 2002 May;67(1):63-74 [11961217] Crit Rev Toxicol. 2004 Jul-Aug;34(4):351-84 [15328768] Science. 1968 Aug 9;161(3841):584-5 [5690897] Biol Reprod. 1990 Apr;42(4):649-55 [2346773] J Endocrinol. 1956 Jul;13(4):399-404 [13345955] Endocrinology. 2005 Sep;146(9):4138-47 [15919749] Toxicol Sci. 2006 Apr;90(2):510-8 [16415327] Endocrinology. 2006 Jun;147(6 Suppl):S18-24 [16690811] J Occup Environ Med. 2006 Aug;48(8):771-9 [16902369] Int Arch Occup Environ Health. 2007 Feb;80(4):313-9 [16915390] Toxicol Sci. 2007 Mar;96(1):133-44 [17132714] Environ Health Perspect. 2007 Apr;115(4):592-8 [17450229] Environ Health Perspect. 2007 Nov;115(11):1670-6 [18008002] Pediatrics. 2008 Feb;121 Suppl 3:S192-207 [18245512] Toxicol Sci. 2015 May;145(1):211 [25490953] Reprod Toxicol. 2015 Jul;54:148-55 [25091782] Pediatrics. 2013 Dec;132(6):1019-27 [24190685] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.reprotox.2014.12.002 ER - TY - JOUR T1 - Environmental exposures, breast development and cancer risk: Through the looking glass of breast cancer prevention. AN - 1687361558; 25499721 AB - This review summarizes the report entitled: Breast Cancer and the Environment: Prioritizing Prevention, highlights research gaps and the importance of focusing on early life exposures for breast development and breast cancer risk. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Reproductive toxicology (Elmsford, N.Y.) AU - Forman, Michele R AU - Winn, Deborah M AU - Collman, Gwen W AU - Rizzo, Jeanne AU - Birnbaum, Linda S AD - University of Texas at Austin, Austin, TX 78712, United States. Electronic address: mforman@austin.utexas.edu. ; National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, United States. ; National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, United States. ; Breast Cancer Fund, San Francisco, CA 94109, United States. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 6 EP - 10 VL - 54 KW - Carcinogens, Environmental KW - 0 KW - Index Medicus KW - Life course KW - Environment KW - Prevention KW - Breast development KW - Breast cancer KW - Maternal Exposure -- adverse effects KW - Life Style KW - Animals KW - Age Factors KW - Risk Factors KW - Humans KW - Signal Transduction -- drug effects KW - Male KW - Female KW - Risk Assessment KW - Prenatal Exposure Delayed Effects KW - Pregnancy KW - Cell Transformation, Neoplastic -- pathology KW - Mammary Glands, Animal -- drug effects KW - Cell Transformation, Neoplastic -- metabolism KW - Mammary Glands, Human -- metabolism KW - Breast Neoplasms -- metabolism KW - Carcinogens, Environmental -- toxicity KW - Breast Neoplasms -- pathology KW - Mammary Glands, Animal -- metabolism KW - Mammary Glands, Animal -- pathology KW - Breast Neoplasms -- prevention & control KW - Cell Transformation, Neoplastic -- chemically induced KW - Mammary Glands, Human -- pathology KW - Breast Neoplasms -- chemically induced KW - Environmental Exposure -- adverse effects KW - Mammary Glands, Human -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687361558?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.atitle=Environmental+exposures%2C+breast+development+and+cancer+risk%3A+Through+the+looking+glass+of+breast+cancer+prevention.&rft.au=Forman%2C+Michele+R%3BWinn%2C+Deborah+M%3BCollman%2C+Gwen+W%3BRizzo%2C+Jeanne%3BBirnbaum%2C+Linda+S&rft.aulast=Forman&rft.aufirst=Michele&rft.date=2015-07-01&rft.volume=54&rft.issue=&rft.spage=6&rft.isbn=&rft.btitle=&rft.title=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.issn=1873-1708&rft_id=info:doi/10.1016%2Fj.reprotox.2014.10.019 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-04 N1 - Date created - 2015-06-09 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.reprotox.2014.10.019 ER - TY - JOUR T1 - Concentrations of environmental phenols and parabens in milk, urine and serum of lactating North Carolina women. AN - 1687361326; 25463527 AB - Phenols and parabens show some evidence for endocrine disruption in laboratory animals. The goal of the Methods Advancement for Milk Analysis (MAMA) Study was to develop or adapt methods to measure parabens (methyl, ethyl, butyl, propyl) and phenols (bisphenol A (BPA), 2,4- and 2,5-dichlorophenol, benzophenone-3, triclosan) in urine, milk and serum twice during lactation, to compare concentrations across matrices and with endogenous biomarkers among 34 North Carolina women. These non-persistent chemicals were detected in most urine samples (53-100%) and less frequently in milk or serum; concentrations differed by matrix. Although urinary parabens, triclosan and dichlorophenols concentrations correlated significantly at two time points, those of BPA and benzophenone-3 did not, suggesting considerable variability in those exposures. These pilot data suggest that nursing mothers are exposed to phenols and parabens; urine is the best measurement matrix; and correlations between chemical and endogenous immune-related biomarkers merit further investigation. Published by Elsevier Inc. JF - Reproductive toxicology (Elmsford, N.Y.) AU - Hines, Erin P AU - Mendola, Pauline AU - von Ehrenstein, Ondine S AU - Ye, Xiaoyun AU - Calafat, Antonia M AU - Fenton, Suzanne E AD - Office of Research and Development, National Center for Environmental Assessment, U.S. Environmental Protection Agency, RTP, NC. Electronic address: hines.erin@epa.gov. ; Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Rockville, MD. Electronic address: pauline.mendola@nih.gov. ; Department of Community Health Sciences, Fielding School of Public Health, University of California Los Angeles, Los Angeles, CA. Electronic address: ovehren@ucla.edu. ; Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA. Electronic address: xay5@cdc.gov. ; Division of Laboratory Sciences, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, GA. Electronic address: aic7@cdc.gov. ; Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, RTP, NC. Electronic address: fentonse@niehs.nih.gov. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 120 EP - 128 VL - 54 KW - Biomarkers KW - 0 KW - Environmental Pollutants KW - Parabens KW - Phenols KW - Index Medicus KW - Urine KW - Serum KW - MAMA Study KW - Biomonitoring KW - Breast milk KW - BPA KW - Parabens phenols KW - Lactation KW - Maternal Exposure -- adverse effects KW - Young Adult KW - Risk Factors KW - Humans KW - Body Burden KW - North Carolina KW - Adult KW - Biomarkers -- metabolism KW - Pilot Projects KW - Adolescent KW - Female KW - Environmental Monitoring -- methods KW - Risk Assessment KW - Environmental Pollutants -- metabolism KW - Parabens -- metabolism KW - Phenols -- blood KW - Phenols -- metabolism KW - Lactation -- blood KW - Parabens -- adverse effects KW - Environmental Pollutants -- urine KW - Phenols -- adverse effects KW - Milk, Human -- metabolism KW - Lactation -- metabolism KW - Lactation -- urine KW - Phenols -- urine KW - Environmental Pollutants -- blood KW - Environmental Pollutants -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687361326?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.atitle=Concentrations+of+environmental+phenols+and+parabens+in+milk%2C+urine+and+serum+of+lactating+North+Carolina+women.&rft.au=Hines%2C+Erin+P%3BMendola%2C+Pauline%3Bvon+Ehrenstein%2C+Ondine+S%3BYe%2C+Xiaoyun%3BCalafat%2C+Antonia+M%3BFenton%2C+Suzanne+E&rft.aulast=Hines&rft.aufirst=Erin&rft.date=2015-07-01&rft.volume=54&rft.issue=&rft.spage=120&rft.isbn=&rft.btitle=&rft.title=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.issn=1873-1708&rft_id=info:doi/10.1016%2Fj.reprotox.2014.11.006 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-04 N1 - Date created - 2015-06-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Chromatogr B Analyt Technol Biomed Life Sci. 2006 Nov 21;844(1):53-9 [16893688] Sci Total Environ. 2006 Dec 15;372(1):87-93 [17007908] Chemosphere. 2007 Jan;66(6):1160-4 [16904728] Anticancer Res. 2010 Mar;30(3):815-27 [20393002] Environ Health Perspect. 2010 Jun;118(6):856-63 [20129873] J Anal Toxicol. 2010 Jul-Aug;34(6):293-303 [20663281] Toxicol Sci. 2010 Sep;117(1):45-53 [20562219] Food Chem Toxicol. 2000 Apr;38(4):319-23 [10722885] Environ Health Perspect. 2001 Mar;109(3):239-44 [11333184] Chemosphere. 2002 Mar;46(9-10):1485-9 [12002480] Toxicol Ind Health. 2001 Feb;17(1):31-9 [12004923] Food Chem Toxicol. 2002 Dec;40(12):1807-13 [12419695] Environ Health Perspect. 2003 Apr;111(4):642-6 [12676629] Environ Health Perspect. 2003 Nov;111(14):1723-9 [14594622] Biol Reprod. 2011 Sep;85(3):490-7 [21636739] PLoS One. 2012;7(2):e31109 [22347437] Environ Health Perspect. 2012 May;120(5):752-7 [22271837] Andrologia. 2012 May;44 Suppl 1:187-93 [21592178] J Med Toxicol. 2012 Jun;8(2):160-5 [22108840] J Expo Sci Environ Epidemiol. 2012 Nov;22(6):610-6 [22617719] Environ Health Perspect. 2012 Nov;120(11):1538-43 [22721761] Environ Sci Technol. 2012 Nov 20;46(22):12664-71 [23102149] Environ Health Perspect. 2013 Mar;121(3):283-6 [23458838] Int Arch Occup Environ Health. 2014 Jan;87(1):13-20 [23212895] Crit Rev Toxicol. 2014 Aug;44(7):600-17 [25068490] Int J Methods Psychiatr Res. 2014 Sep;23(3):320-30 [24912670] Int J Epidemiol. 2015 Jun;44(3):789-800 [25011454] Anal Chim Acta. 2008 Aug 1;622(1-2):150-6 [18602546] Biomed Chromatogr. 2004 Oct;18(8):501-7 [15386523] J Toxicol Environ Health. 1984;14(5-6):723-30 [6520883] Contact Dermatitis. 1995 Jan;32(1):28-30 [7720367] Toxicol Appl Pharmacol. 2005 Feb 15;203(1):9-17 [15694459] Chemosphere. 2005 Aug;60(7):898-906 [15992596] Anal Chem. 2005 Aug 15;77(16):5407-13 [16097788] Anal Bioanal Chem. 2005 Oct;383(4):638-44 [16132150] J Chromatogr B Analyt Technol Biomed Life Sci. 2006 Feb 2;831(1-2):110-5 [16377264] Environ Sci Technol. 2006 Feb 1;40(3):687-95 [16509304] Environ Health Perspect. 2006 Oct;114(10):1581-4 [17035146] Food Chem Toxicol. 2007 Jan;45(1):125-9 [17011099] Environ Health Perspect. 2007 Jan;115(1):116-21 [17366830] Reprod Toxicol. 2007 Apr-May;23(3):383-90 [17123778] J Hum Lact. 2007 May;23(2):144-56 [17478867] Environ Health Perspect. 2008 Jan;116(1):39-44 [18197297] Environ Health Perspect. 2008 Mar;116(3):303-7 [18335095] Environ Health Perspect. 2008 Jul;116(7):893-7 [18629311] Talanta. 2008 Aug 15;76(4):865-71 [18656671] Toxicol Sci. 2009 Jan;107(1):56-64 [18940961] Environ Health Perspect. 2009 Jan;117(1):86-92 [19165392] Reprod Toxicol. 2009 Jun;27(3-4):239-45 [19429402] Endocr Rev. 2009 Jun;30(4):293-342 [19502515] Environ Int. 2009 Nov;35(8):1160-3 [19665798] Environ Health Perspect. 2009 Oct;117(10):1481-5 [20019895] Toxicol Mech Methods. 2010 Mar;20(3):133-6 [20163291] J Chromatogr B Analyt Technol Biomed Life Sci. 2010 Oct 1;878(27):2606-10 [20202916] Chemosphere. 2010 Nov;81(10):1171-83 [21030064] Toxicol Lett. 2010 Dec 15;199(3):372-6 [20933065] Environ Health Perspect. 2011 Feb;119(2):252-7 [20876036] Environ Int. 2011 Jul;37(5):858-66 [21440302] Scand J Public Health. 2011 Jul;39(7 Suppl):115-20 [21775368] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.reprotox.2014.11.006 ER - TY - JOUR T1 - Cancer survivorship: long-term side-effects of anticancer treatments of gastrointestinal cancer. AN - 1686994809; 26049277 AB - Surveillance of patients with a history of cancer is a frequent practice in oncology. However, it is often aimed at the early diagnosis of relapse and tends to underestimate the evaluation and care of factors impairing quality of life (QoL). Among these, long-term toxicities of anticancer treatments are one of the major threats to a complete physical and psychosocial recovery. We aimed to review the relevant literature on long-term side-effects of treatment in gastrointestinal cancers. We focused on esophageal, gastric, pancreatic, liver and colorectal cancers. A significant fraction of patients treated for these cancers suffer with some form of late toxicity from surgery, radiotherapy or chemotherapy. Prompt evaluation and management is of the utmost importance in reducing the impact of these symptoms on QoL. The knowledge of the reviewed data should encourage a multidisciplinary approach to surveillance and convince clinicians of the comprehensive role of survivorship care. JF - Current opinion in oncology AU - Numico, Gianmauro AU - Longo, Vito AU - Courthod, Giulia AU - Silvestris, Nicola AD - aMedical Oncology and Hematology, Ospedale U.Parini, Aosta bMedical Oncology Unit, 'Mons R Dimiccoli' Hospital, Barletta cMedical Oncology Unit, National Cancer Institute 'Giovanni Paolo II', Bari, Italy. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 351 EP - 357 VL - 27 IS - 4 KW - Antinematodal Agents KW - 0 KW - Index Medicus KW - Humans KW - Antinematodal Agents -- adverse effects KW - Radiotherapy -- adverse effects KW - Gastrointestinal Neoplasms -- epidemiology KW - Drug-Related Side Effects and Adverse Reactions -- pathology KW - Drug-Related Side Effects and Adverse Reactions -- psychology KW - Drug-Related Side Effects and Adverse Reactions -- epidemiology KW - Gastrointestinal Neoplasms -- therapy KW - Survivors -- psychology KW - Gastrointestinal Neoplasms -- pathology KW - Gastrointestinal Neoplasms -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1686994809?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+oncology&rft.atitle=Cancer+survivorship%3A+long-term+side-effects+of+anticancer+treatments+of+gastrointestinal+cancer.&rft.au=Numico%2C+Gianmauro%3BLongo%2C+Vito%3BCourthod%2C+Giulia%3BSilvestris%2C+Nicola&rft.aulast=Numico&rft.aufirst=Gianmauro&rft.date=2015-07-01&rft.volume=27&rft.issue=4&rft.spage=351&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+oncology&rft.issn=1531-703X&rft_id=info:doi/10.1097%2FCCO.0000000000000203 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-25 N1 - Date created - 2015-06-08 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/CCO.0000000000000203 ER - TY - JOUR T1 - The NADPH oxidase NOX5 protects against apoptosis in ALK-positive anaplastic large-cell lymphoma cell lines. AN - 1686420391; 25797883 AB - Reactive oxygen species (ROS) are key modulators of apoptosis and carcinogenesis. One of the important sources of ROS is NADPH oxidases (NOXs). The isoform NOX5 is highly expressed in lymphoid tissues, but it has not been detected in any common Hodgkin or non-Hodgkin lymphoma cell lines. In diverse, nonlymphoid malignant cells NOX5 exerts an antiapoptotic effect. Apoptosis suppression is the hallmark feature of a rare type of lymphoma, termed anaplastic lymphoma kinase-positive (ALK(+)) anaplastic large-cell lymphoma (ALCL), and a major factor in the therapy resistance and relapse of ALK(+) ALCL tumors. We applied RT-PCR and Western blot analysis to detect NOX5 expression in three ALK(+) ALCL cell lines (Karpas-299, SR-786, SUP-M2). We investigated the role of NOX5 in apoptosis by small-interfering RNA (siRNA)-mediated gene silencing and chemical inhibition of NOX5 using FACS analysis and examining caspase 3 cleavage in Karpas-299 cells. We used immunohistochemistry to detect NOX5 in ALK(+) ALCL pediatric tumors. NOX5 mRNA was uniquely detected in ALK(+) ALCL cells, whereas cell lines of other lymphoma classes were devoid of NOX5. Transfection of NOX5-specific siRNA and chemical inhibition of NOX5 abrogated calcium-induced superoxide production and increased caspase 3-mediated apoptosis in Karpas-299 cells. Immunohistochemistry revealed focal NOX5 reactivity in pediatric ALK(+) ALCL tumor cells. These results indicate that NOX5-derived ROS contribute to apoptosis blockage in ALK(+) ALCL cell lines and suggest NOX5 as a potential pharmaceutical target to enhance apoptosis and thus to suppress tumor progression and prevent relapse in pediatric ALK(+) ALCL patients that resist classical therapeutic approaches. Copyright © 2015 Elsevier Inc. All rights reserved. JF - Free radical biology & medicine AU - Carnesecchi, S AU - Rougemont, A-L AU - Doroshow, J H AU - Nagy, M AU - Mouche, S AU - Gumy-Pause, F AU - Szanto, I AD - Department of Cellular Physiology and Metabolism and; Department of Pathology and Immunology, University of Geneva, CH-1211 Geneva 4, Switzerland. ; Division of Clinical Pathology and. ; Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Department of Pathology and Immunology, University of Geneva, CH-1211 Geneva 4, Switzerland. ; Department of Cellular Physiology and Metabolism and. ; Department of Pediatrics, Hematology/Oncology Unit, CANSEARCH Research Laboratory, Geneva, Switzerland. ; Department of Cellular Physiology and Metabolism and; Department of Internal Medicine Specialties, University Hospitals of Geneva, Geneva, Switzerland. Electronic address: ildiko.szanto@unige.ch. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 22 EP - 29 VL - 84 KW - Membrane Proteins KW - 0 KW - NOX5 protein, human KW - EC 1.6.- KW - NADPH Oxidase KW - EC 1.6.3.1 KW - Receptor Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - anaplastic lymphoma kinase KW - Index Medicus KW - Karpas-299 KW - NOX5 KW - Apoptosis KW - Reactive oxygen species KW - Free radicals KW - Anaplastic large-cell lymphoma KW - Infant KW - Humans KW - Gene Expression KW - Cell Line, Tumor KW - Adolescent KW - Male KW - Female KW - Child, Preschool KW - Lymphoma, Large-Cell, Anaplastic -- pathology KW - NADPH Oxidase -- physiology KW - Receptor Protein-Tyrosine Kinases -- metabolism KW - Lymphoma, Large-Cell, Anaplastic -- enzymology KW - Membrane Proteins -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1686420391?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Free+radical+biology+%26+medicine&rft.atitle=The+NADPH+oxidase+NOX5+protects+against+apoptosis+in+ALK-positive+anaplastic+large-cell+lymphoma+cell+lines.&rft.au=Carnesecchi%2C+S%3BRougemont%2C+A-L%3BDoroshow%2C+J+H%3BNagy%2C+M%3BMouche%2C+S%3BGumy-Pause%2C+F%3BSzanto%2C+I&rft.aulast=Carnesecchi&rft.aufirst=S&rft.date=2015-07-01&rft.volume=84&rft.issue=&rft.spage=22&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2015.02.027 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-04 N1 - Date created - 2015-06-05 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.freeradbiomed.2015.02.027 ER - TY - JOUR T1 - Cardiomyocytes are Protected from Antiretroviral Nucleoside Analog-Induced Mitochondrial Toxicity by Overexpression of PGC-1α. AN - 1686419056; 25377427 AB - The nucleoside reverse transcriptase inhibitors (NRTIs), used for treatment of the human immunodeficiency virus-1, compromise mitochondria in cardiomyocytes and other host cells, limiting the clinical use of these drugs. To explore underlying mechanisms, we overexpressed PGC-1α, a master regulator of mitochondrial biogenesis, twofold in H9c2 rat cardiomyocyte cultures, hypothesizing that this might protect the mitochondria from damage induced by the NRTI combination zidovudine (AZT) and didanosine (ddI). The experimental groups, evaluated during 16 passages (P) of drug exposure, included: PGC-1α-overexpressing cells with no exposure, or exposure to 50 µM AZT plus 50 µM ddI; and control cells with no exposure or exposure to the same doses of AZT and ddI. The AZT/ddI combination caused a growth inhibition of 15-20% in control cells, but none in PGC-1α cells. Apoptosis was highest in AZT/ddI-exposed control cells, and PGC-1α overexpression protected cells from AZT/ddI-induced apoptosis. At P3, P6, P8, and P12, uncoupled mitochondrial oxygen consumption rate, determined by Seahorse 24 XF Analyzer, as higher in AZT/ddI-exposed PGC-1α cells, compared to AZT/ddI-exposed control cells (p < 0.05 at all P). Complex I activity was higher in AZT/ddI-exposed PGC-1α overexpressing cells than that in AZT/ddI-exposed control cells (p < 0.05), and reactive oxygen species levels were lower in PGC-1α overexpressing cells than that in control cells (p < 0.05) when both were exposed to AZT/ddI. Taken together, these experiments show proof of concept that overexpression of PGC-1α protects cardiomyocytes from NRTI-induced toxicity, and suggest that a pharmaceutical agent with similar activity may protect against NRTI-induced mitochondrial toxicity. JF - Cardiovascular toxicology AU - Liu, Yongmin AU - Shim, Eunwoo AU - Crespo-Mejias, Yasmin AU - Nguyen, PhuongGiang AU - Gibbons, Alexander AU - Liu, Daniel AU - Shide, Eric AU - Poirier, Miriam C AD - Carcinogen-DNA Interactions Section, Laboratory of Cancer Biology and Genetics, CCR, National Cancer Institute, NIH, Bldg. 37, Rm 4032, 37 Convent Drive, MSC-4255, Bethesda, MD, 20892-4255, USA, yongminl@mail.nih.gov. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 224 EP - 231 VL - 15 IS - 3 KW - Anti-Retroviral Agents KW - 0 KW - Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha KW - Ppargc1a protein, rat KW - Reverse Transcriptase Inhibitors KW - Transcription Factors KW - Index Medicus KW - Rats KW - Animals KW - Cell Survival -- drug effects KW - Gene Expression Regulation KW - Cell Survival -- physiology KW - Cell Line KW - Myocytes, Cardiac -- drug effects KW - Anti-Retroviral Agents -- toxicity KW - Mitochondria -- pathology KW - Mitochondria -- drug effects KW - Mitochondria -- metabolism KW - Reverse Transcriptase Inhibitors -- toxicity KW - Myocytes, Cardiac -- pathology KW - Transcription Factors -- biosynthesis KW - Myocytes, Cardiac -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1686419056?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cardiovascular+toxicology&rft.atitle=Cardiomyocytes+are+Protected+from+Antiretroviral+Nucleoside+Analog-Induced+Mitochondrial+Toxicity+by+Overexpression+of+PGC-1%CE%B1.&rft.au=Liu%2C+Yongmin%3BShim%2C+Eunwoo%3BCrespo-Mejias%2C+Yasmin%3BNguyen%2C+PhuongGiang%3BGibbons%2C+Alexander%3BLiu%2C+Daniel%3BShide%2C+Eric%3BPoirier%2C+Miriam+C&rft.aulast=Liu&rft.aufirst=Yongmin&rft.date=2015-07-01&rft.volume=15&rft.issue=3&rft.spage=224&rft.isbn=&rft.btitle=&rft.title=Cardiovascular+toxicology&rft.issn=1559-0259&rft_id=info:doi/10.1007%2Fs12012-014-9288-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-29 N1 - Date created - 2015-06-05 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s12012-014-9288-5 ER - TY - JOUR T1 - Photoimmunotherapy lowers recurrence after pancreatic cancer surgery in orthotopic nude mouse models. AN - 1686413146; 25799527 AB - Photoimmunotherapy (PIT) is based on the use of a monoclonal antibody specific to cancer epitopes conjugated to a photosensitizer near-infrared phthalocyanine dye (IR700). In this study, PIT with IR700 conjugated to anti-carcinoembryonic antigen (CEA) was used as an adjunct to surgery in orthotopically-implanted human pancreatic cancer in a nude mouse model to eliminate microscopic disease in the post-surgical tumor bed and prevent local as well as metastatic recurrence. Athymic nude mice were orthotopically implanted with the human pancreatic cancer cell line BxPC3 expressing green fluorescent protein. After tumor engraftment, the mice were divided into two groups as follows: bright light surgery (BLS) + anti-CEA-IR700 + 690 nm laser (PIT); and BLS only. Anti-CEA-IR700 (100 μg) was administered to the treatment group via tail-vein injection 24 h before therapy. Tumors were resected, and the surgical bed was treated with intraoperative phototherapy at an intensity of 150 mW/cm(2) for 30 min. Mice were imaged noninvasively for 8 wk using an OV-100 small animal fluorescence imager. BLS + PIT reduced local recurrence to 1/7 mice from 7/7 mice with BLS-only (P = 0.001) and metastatic recurrence to 2/7 mice compared with 6/7 mice with BLS-only (P = 0.03). Local tumor growth continued at a rapid rate after BLS-only compared with BLS + PIT where almost no local growth occurred. There was a significant difference in tumor size between mice in the BLS + PIT (2.14 mm(2), 95% confidence interval [CI] [-2.06 to 6.34] and BLS-only groups (115.2 mm(2), 95% CI [88.8-141.6]) at 6 wk after surgery (P < 0.001). There was also a significant difference in tumor weight between the BLS + PIT group (6.65 mg, 95% CI [-6.35 to 19.65] and BLS-only group (1100 mg, 95% CI [794-1406] at 8 wk after surgery (P < 0.001). PIT holds promise in the treatment of pancreatic cancer and may serve as a useful adjunct to surgery in the eradication of microscopic residual disease that can lead to both local and metastatic recurrence. Further studies are warranted to investigate the potential toxicities of PIT, especially with regard to anastomoses, such as those involved in pancreaticoduodenectomy. Copyright © 2015 Elsevier Inc. All rights reserved. JF - The Journal of surgical research AU - Maawy, Ali A AU - Hiroshima, Yukihiko AU - Zhang, Yong AU - Garcia-Guzman, Miguel AU - Luiken, George A AU - Kobayashi, Hisataka AU - Hoffman, Robert M AU - Bouvet, Michael AD - Department of Surgery, University of California San Diego, San Diego, California. ; Department of Surgery, University of California San Diego, San Diego, California; AntiCancer, Inc, San Diego, California; Department of Surgery, Yokohama City University, Yokohama City, Japan. ; AntiCancer, Inc, San Diego, California. ; Aspyrian Therapeutics, San Diego, California. ; OncoFluor, Inc, San Diego, California. ; National Institutes of Health, Bethesda, Maryland. ; Department of Surgery, University of California San Diego, San Diego, California; AntiCancer, Inc, San Diego, California. ; Department of Surgery, University of California San Diego, San Diego, California; Department of Surgery, VA Healthcare System, San Diego, California. Electronic address: mbouvet@ucsd.edu. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 5 EP - 11 VL - 197 IS - 1 KW - Antibodies, Monoclonal KW - 0 KW - Carcinoembryonic Antigen KW - Indoles KW - Photosensitizing Agents KW - phthalocyanine KW - V5PUF4VLGY KW - Index Medicus KW - Orthotopic mouse models KW - Surgery KW - CEA KW - Pancreatic cancer KW - Photoimmunotherapy KW - Neoplasm Transplantation KW - Animals KW - Carcinoembryonic Antigen -- immunology KW - Humans KW - Treatment Outcome KW - Mice, Nude KW - Mice KW - Cell Line, Tumor KW - Chemotherapy, Adjuvant KW - Pancreatectomy KW - Photosensitizing Agents -- therapeutic use KW - Indoles -- therapeutic use KW - Pancreatic Neoplasms -- drug therapy KW - Photochemotherapy -- methods KW - Pancreatic Neoplasms -- surgery KW - Neoplasm Recurrence, Local -- prevention & control KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1686413146?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+surgical+research&rft.atitle=Photoimmunotherapy+lowers+recurrence+after+pancreatic+cancer+surgery+in+orthotopic+nude+mouse+models.&rft.au=Maawy%2C+Ali+A%3BHiroshima%2C+Yukihiko%3BZhang%2C+Yong%3BGarcia-Guzman%2C+Miguel%3BLuiken%2C+George+A%3BKobayashi%2C+Hisataka%3BHoffman%2C+Robert+M%3BBouvet%2C+Michael&rft.aulast=Maawy&rft.aufirst=Ali&rft.date=2015-07-01&rft.volume=197&rft.issue=1&rft.spage=5&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+surgical+research&rft.issn=1095-8673&rft_id=info:doi/10.1016%2Fj.jss.2015.02.037 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-17 N1 - Date created - 2015-06-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: PLoS One. 2014;9(5):e97965 [24859320] Hepatogastroenterology. 2012 Sep;59(118):1994-9 [22369743] J Laparoendosc Adv Surg Tech A. 2014 Apr;24(4):241-7 [24494971] J Surg Oncol. 2014 Apr;109(5):451-8 [24249594] Cancer Res. 2002 Mar 1;62(5):1534-40 [11888932] J Am Coll Surg. 2012 Jun;214(6):997-1007.e2 [22542065] Bioconjug Chem. 2012 Mar 21;23(3):604-9 [22369484] Nat Med. 2011 Dec;17(12):1685-91 [22057348] J Gastrointest Surg. 2008 Nov;12(11):1938-50 [18665430] Cancer Res. 2006 Apr 15;66(8):4208-14 [16618743] Clin Transl Oncol. 2005 Jun;7(5):189-97 [15960930] Ann Oncol. 1999;10 Suppl 4:82-4 [10436792] Cancer Res. 1993 Jul 1;53(13):3070-2 [8319214] Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5645-9 [1608975] J Surg Res. 2003 Jul;113(1):151-60 [12943825] Clin Exp Metastasis. 2000;18(3):213-8 [11315094] Am J Surg. 2000 Jul;180(1):13-7 [11036132] Mol Oncol. 2014 May;8(3):620-32 [24508062] BMC Cancer. 2012;12:345 [22873679] J Biomed Opt. 2013 Dec;18(12):126016 [24356647] Ann Surg Oncol. 2014 Apr;21(4):1405-11 [24499827] J Surg Res. 2014 Apr;187(2):510-7 [24373959] BMC Cancer. 2014;14:389 [24885589] J Am Coll Surg. 2014 Jul;219(1):132-41 [24768506] PLoS One. 2015;10(3):e0121989 [25799218] N Engl J Med. 2014 Sep 11;371(11):1039-49 [25207767] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jss.2015.02.037 ER - TY - JOUR T1 - Ambient temperature and risk of first primary basal cell carcinoma: A nationwide United States cohort study. AN - 1686065532; 25996074 AB - The Earth's surface is warming and animal studies have shown higher temperatures promote ultraviolet radiation (UVR) skin carcinogenesis. There are, however, no population studies of long-term temperature exposure and basal cell carcinoma (BCC) risk. We linked average lifetime summer ambient temperatures (based on weather station data) and satellite-based UVR estimates to self-reported lifetime residences in the U.S. Radiologic Technologists' cohort. We assessed the relationship between time-dependent average lifetime summer ambient temperature (20-year lag) in quintiles and BCC in whites, using Cox proportional hazards regression. Risks were adjusted for time-dependent lagged average lifetime UVR and time outdoors, body mass index, eye color, and sex (baseline hazard stratified on birth cohort). During a median 19.4 years follow-up, we identified 3556 BCC cases. There was no significant trend in risk between temperature and BCC. However, BCC risk was highest in the fourth quintile of temperature (Q4 vs. Q1; hazards ratio (HR)=1.18; 95% confidence interval (CI)=1.06-1.31, p-trend=0.09). BCC risk was strongly related to average lifetime ambient UVR exposure (Q5 vs. Q1; HR=1.54 (95% CI=1.35-1.75, p-trend=<0.001)). Future studies of temperature and BCC risk should include a broad range of UVR and temperature values, along with improved indicators of exposure to temperatures and UVR. Published by Elsevier B.V. JF - Journal of photochemistry and photobiology. B, Biology AU - Michal Freedman, D AU - Kitahara, Cari M AU - Linet, Martha S AU - Alexander, Bruce H AU - Neta, Gila AU - Little, Mark P AU - Cahoon, Elizabeth K AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Rockville, MD, USA. Electronic address: freedmam@mail.nih.gov. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Rockville, MD, USA. ; Division of Environmental Health Sciences, School of Public Health, University of Minnesota, Minneapolis, MN, USA. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 284 EP - 289 VL - 148 KW - Index Medicus KW - Ultraviolet Rays KW - Sex Factors KW - Risk Factors KW - Humans KW - Cohort Studies KW - Adult KW - Temperature KW - Follow-Up Studies KW - Eye Color KW - Body Mass Index KW - Male KW - Female KW - Proportional Hazards Models KW - Carcinoma, Basal Cell -- etiology KW - Skin Neoplasms -- etiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1686065532?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+photochemistry+and+photobiology.+B%2C+Biology&rft.atitle=Ambient+temperature+and+risk+of+first+primary+basal+cell+carcinoma%3A+A+nationwide+United+States+cohort+study.&rft.au=Michal+Freedman%2C+D%3BKitahara%2C+Cari+M%3BLinet%2C+Martha+S%3BAlexander%2C+Bruce+H%3BNeta%2C+Gila%3BLittle%2C+Mark+P%3BCahoon%2C+Elizabeth+K&rft.aulast=Michal+Freedman&rft.aufirst=D&rft.date=2015-07-01&rft.volume=148&rft.issue=&rft.spage=284&rft.isbn=&rft.btitle=&rft.title=Journal+of+photochemistry+and+photobiology.+B%2C+Biology&rft.issn=1873-2682&rft_id=info:doi/10.1016%2Fj.jphotobiol.2015.04.025 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-05 N1 - Date created - 2015-06-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Photochem Photobiol B. 2001 Oct;63(1-3):8-18 [11684447] Photochem Photobiol Sci. 2002 May;1(5):324-6 [12653470] Cancer Radiother. 2004 Apr;8(2):81-7 [15063875] Int J Cancer. 1976 Mar 15;17(3):296-303 [1254353] Radiat Res. 1984 Oct;100(1):192-204 [6494429] Cancer. 1992 Jan 15;69(2):586-98 [1728391] J Natl Cancer Inst. 1996 Dec 18;88(24):1848-53 [8961975] Am J Epidemiol. 1997 Jan 1;145(1):72-80 [8982025] Oncogene. 1999 Oct 7;18(41):5638-45 [10523843] Cancer Lett. 2013 Aug 28;337(1):35-40 [23748013] Arch Dermatol. 1964 Jun;89:858-64 [14164974] Photochem Photobiol Sci. 2008 Jun;7(6):730-3 [18528559] Coll Antropol. 2008 Oct;32 Suppl 2:167-70 [19138022] Lancet. 2010 Feb 20;375(9715):673-85 [20171403] Photochem Photobiol. 2010 May-Jun;86(3):481-91 [20550646] Int J Cancer. 2012 Jul 15;131(2):E149-55 [21989791] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jphotobiol.2015.04.025 ER - TY - JOUR T1 - Nano-Se attenuates cyclophosphamide-induced pulmonary injury through modulation of oxidative stress and DNA damage in Swiss albino mice. AN - 1684430953; 25920447 AB - Chemotherapy is an integral part of modern day treatment regimen but anticancer drugs fail to demarcate between cancerous and normal cells thereby causing severe form of systemic toxicity. Among which pulmonary toxicity is a dreadful complication developed in cancer patients upon cyclophosphamide (CP) therapy. Oxidative stress, fibrosis, and apoptosis are the major patho-mechanisms involved in CP-induced pulmonary toxicity. In the present study, we have synthesized Nano-Se, nanotechnology-based new form of elemental selenium which has significantly lower toxicity and acceptable bioavailability. In order to meet the need of effective drugs against CP-induced adverse effects, nano selenium (Nano-Se) was tested for its possible protective efficacy on CP-induced pulmonary toxicity and bone marrow toxicity. CP intoxication resulted in structural and functional lung impairment which was revealed by massive histopathological changes. Lung injury was associated with oxidative stress/lipid peroxidation as evident by increased in reactive oxygen species, nitric oxide level, and malondialdehyde (MDA) formation with decreased in level of antioxidants such as reduced glutathione, glutathione-S-transferase, glutathione peroxidase, superoxide dismutase, and catalase. Furthermore, CP at a dose of 25 mg/kg b.w. increased pulmonary DNA damage ('comet tail') and triggered DNA fragmentation and apoptosis in mouse bone marrow cells. On the other hand, Nano-Se at a dose of 2 mg Se/kg b.w., significantly inhibited CP-induced DNA damage in bronchoalveolar lavage cells, and decreased the apoptosis and percentage of DNA fragmentation in bone marrow cells and also antagonized the reduction of the activities of antioxidant enzymes and the increase level of MDA. Thus, our results suggest that Nano-Se in pre- and co-administration may serve as a promising preventive strategy against CP-induced pulmonary toxicity. JF - Molecular and cellular biochemistry AU - Bhattacharjee, Arin AU - Basu, Abhishek AU - Biswas, Jaydip AU - Bhattacharya, Sudin AD - Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata, 700026, West Bengal, India. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 243 EP - 256 VL - 405 IS - 1-2 KW - Antioxidants KW - 0 KW - Reactive Oxygen Species KW - Nitric Oxide KW - 31C4KY9ESH KW - Malondialdehyde KW - 4Y8F71G49Q KW - Cyclophosphamide KW - 8N3DW7272P KW - Selenium KW - H6241UJ22B KW - Index Medicus KW - Bone Marrow Cells -- drug effects KW - Reactive Oxygen Species -- metabolism KW - Animals KW - Lipid Peroxidation -- drug effects KW - Nanotechnology -- methods KW - Nitric Oxide -- metabolism KW - Mice KW - Malondialdehyde -- metabolism KW - Bone Marrow Cells -- metabolism KW - Bronchoalveolar Lavage -- methods KW - Antioxidants -- metabolism KW - Apoptosis -- drug effects KW - Female KW - Lung Injury -- metabolism KW - Lung Injury -- chemically induced KW - Selenium -- pharmacology KW - Oxidative Stress -- drug effects KW - Lung Injury -- drug therapy KW - Nanoparticles -- administration & dosage KW - DNA Damage -- drug effects KW - Cyclophosphamide -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1684430953?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biochemistry&rft.atitle=Nano-Se+attenuates+cyclophosphamide-induced+pulmonary+injury+through+modulation+of+oxidative+stress+and+DNA+damage+in+Swiss+albino+mice.&rft.au=Bhattacharjee%2C+Arin%3BBasu%2C+Abhishek%3BBiswas%2C+Jaydip%3BBhattacharya%2C+Sudin&rft.aulast=Bhattacharjee&rft.aufirst=Arin&rft.date=2015-07-01&rft.volume=405&rft.issue=1-2&rft.spage=243&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biochemistry&rft.issn=1573-4919&rft_id=info:doi/10.1007%2Fs11010-015-2415-1 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-16 N1 - Date created - 2015-05-28 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s11010-015-2415-1 ER - TY - JOUR T1 - RNA-Seq-based toxicogenomic assessment of fresh frozen and formalin-fixed tissues yields similar mechanistic insights. AN - 1683754470; 25378103 AB - Formalin-fixed, paraffin-embedded (FFPE) pathology specimens represent a potentially vast resource for transcriptomic-based biomarker discovery. We present here a comparison of results from a whole transcriptome RNA-Seq analysis of RNA extracted from fresh frozen and FFPE livers. The samples were derived from rats exposed to aflatoxin B1 (AFB1 ) and a corresponding set of control animals. Principal components analysis indicated that samples were separated in the two groups representing presence or absence of chemical exposure, both in fresh frozen and FFPE sample types. Sixty-five percent of the differentially expressed transcripts (AFB1 vs. controls) in fresh frozen samples were also differentially expressed in FFPE samples (overlap significance: P < 0.0001). Genomic signature and gene set analysis of AFB1 differentially expressed transcript lists indicated highly similar results between fresh frozen and FFPE at the level of chemogenomic signatures (i.e., single chemical/dose/duration elicited transcriptomic signatures), mechanistic and pathology signatures, biological processes, canonical pathways and transcription factor networks. Overall, our results suggest that similar hypotheses about the biological mechanism of toxicity would be formulated from fresh frozen and FFPE samples. These results indicate that phenotypically anchored archival specimens represent a potentially informative resource for signature-based biomarker discovery and mechanistic characterization of toxicity. Copyright © 2014 John Wiley & Sons, Ltd. JF - Journal of applied toxicology : JAT AU - Auerbach, Scott S AU - Phadke, Dhiral P AU - Mav, Deepak AU - Holmgren, Stephanie AU - Gao, Yuan AU - Xie, Bin AU - Shin, Joo Heon AU - Shah, Ruchir R AU - Merrick, B Alex AU - Tice, Raymond R AD - Biomolecular Screening Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, 27709, USA. ; SRA International, Durham, NC, USA. ; Library & Information Services Branch, Office of the Deputy Director, National Institute of Environmental Health Sciences, Research Triangle Park, NC, 27709, USA. ; Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD, 21205, USA. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 766 EP - 780 VL - 35 IS - 7 KW - Biomarkers, Pharmacological KW - 0 KW - Formaldehyde KW - 1HG84L3525 KW - Aflatoxin B1 KW - 9N2N2Y55MH KW - Index Medicus KW - Mechanism KW - FFPE KW - RNA-Seq KW - Toxicogenomics KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Biomarkers, Pharmacological -- analysis KW - Freezing KW - Gene Expression Regulation -- drug effects KW - Aflatoxin B1 -- toxicity KW - Male KW - Liver -- pathology KW - Liver -- drug effects KW - Toxicogenetics -- methods KW - Sequence Analysis, RNA -- methods KW - Gene Expression Profiling -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683754470?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+applied+toxicology+%3A+JAT&rft.atitle=RNA-Seq-based+toxicogenomic+assessment+of+fresh+frozen+and+formalin-fixed+tissues+yields+similar+mechanistic+insights.&rft.au=Auerbach%2C+Scott+S%3BPhadke%2C+Dhiral+P%3BMav%2C+Deepak%3BHolmgren%2C+Stephanie%3BGao%2C+Yuan%3BXie%2C+Bin%3BShin%2C+Joo+Heon%3BShah%2C+Ruchir+R%3BMerrick%2C+B+Alex%3BTice%2C+Raymond+R&rft.aulast=Auerbach&rft.aufirst=Scott&rft.date=2015-07-01&rft.volume=35&rft.issue=7&rft.spage=766&rft.isbn=&rft.btitle=&rft.title=Journal+of+applied+toxicology+%3A+JAT&rft.issn=1099-1263&rft_id=info:doi/10.1002%2Fjat.3068 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-18 N1 - Date created - 2015-05-27 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/jat.3068 ER - TY - JOUR T1 - Chronic inorganic arsenic exposure in vitro induces a cancer cell phenotype in human peripheral lung epithelial cells. AN - 1683353761; 25804888 AB - Inorganic arsenic is a human lung carcinogen. We studied the ability of chronic inorganic arsenic (2 μM; as sodium arsenite) exposure to induce a cancer phenotype in the immortalized, non-tumorigenic human lung peripheral epithelial cell line, HPL-1D. After 38 weeks of continuous arsenic exposure, secreted matrix metalloproteinase-2 (MMP2) activity increased to over 200% of control, levels linked to arsenic-induced cancer phenotypes in other cell lines. The invasive capacity of these chronic arsenic-treated lung epithelial (CATLE) cells increased to 320% of control and colony formation increased to 280% of control. CATLE cells showed enhanced proliferation in serum-free media indicative of autonomous growth. Compared to control cells, CATLE cells showed reduced protein expression of the tumor suppressor gene PTEN (decreased to 26% of control) and the putative tumor suppressor gene SLC38A3 (14% of control). Morphological evidence of epithelial-to-mesenchymal transition (EMT) occurred in CATLE cells together with appropriate changes in expression of the EMT markers vimentin (VIM; increased to 300% of control) and e-cadherin (CDH1; decreased to 16% of control). EMT is common in carcinogenic transformation of epithelial cells. CATLE cells showed increased KRAS (291%), ERK1/2 (274%), phosphorylated ERK (p-ERK; 152%), and phosphorylated AKT1 (p-AKT1; 170%) protein expression. Increased transcript expression of metallothioneins, MT1A and MT2A and the stress response genes HMOX1 (690%) and HIF1A (247%) occurred in CATLE cells possibly in adaptation to chronic arsenic exposure. Thus, arsenic induced multiple cancer cell characteristics in human peripheral lung epithelial cells. This model may be useful to assess mechanisms of arsenic-induced lung cancer. Published by Elsevier Inc. JF - Toxicology and applied pharmacology AU - Person, Rachel J AU - Ngalame, Ntube N Olive AU - Makia, Ngome L AU - Bell, Matthew W AU - Waalkes, Michael P AU - Tokar, Erik J AD - Stem Cell Toxicology Group, National Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. ; Stem Cell Toxicology Group, National Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. Electronic address: tokare@niehs.nih.gov. Y1 - 2015/07/01/ PY - 2015 DA - 2015 Jul 01 SP - 36 EP - 43 VL - 286 IS - 1 KW - Carcinogens KW - 0 KW - KRAS protein, human KW - MT1A protein, human KW - MT2A protein, human KW - Proto-Oncogene Proteins KW - Metallothionein KW - 9038-94-2 KW - MAPK1 protein, human KW - EC 2.7.11.24 KW - Mitogen-Activated Protein Kinase 1 KW - Mitogen-Activated Protein Kinase 3 KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - ras Proteins KW - Arsenic KW - N712M78A8G KW - Index Medicus KW - Transformation KW - KRAS KW - Human lung cells KW - Adaptation KW - Inorganic arsenic KW - Lung cancer KW - Phenotype KW - Mitogen-Activated Protein Kinase 3 -- metabolism KW - Lung Neoplasms KW - Cells, Cultured KW - Mitogen-Activated Protein Kinase 1 -- metabolism KW - Humans KW - Proto-Oncogene Proteins -- metabolism KW - Epithelial-Mesenchymal Transition -- drug effects KW - Cell Line, Tumor KW - ras Proteins -- metabolism KW - Adenocarcinoma KW - Metallothionein -- metabolism KW - Epithelial Cells -- physiology KW - Epithelial Cells -- drug effects KW - Arsenic -- toxicity KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683353761?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Chronic+inorganic+arsenic+exposure+in+vitro+induces+a+cancer+cell+phenotype+in+human+peripheral+lung+epithelial+cells.&rft.au=Person%2C+Rachel+J%3BNgalame%2C+Ntube+N+Olive%3BMakia%2C+Ngome+L%3BBell%2C+Matthew+W%3BWaalkes%2C+Michael+P%3BTokar%2C+Erik+J&rft.aulast=Person&rft.aufirst=Rachel&rft.date=2015-07-01&rft.volume=286&rft.issue=1&rft.spage=36&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2015.03.014 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-05 N1 - Date created - 2015-05-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Chembiochem. 2009 Jan 5;10(1):55-62 [19089881] J Biol Chem. 2009 May 8;284(19):12609-21 [19276070] Curr Protein Pept Sci. 2009 Aug;10(4):360-75 [19689357] J Natl Cancer Inst. 2009 Dec 16;101(24):1670-81 [19933942] Environ Health Perspect. 2010 Jan;118(1):108-15 [20056578] J Natl Cancer Inst. 2010 May 5;102(9):638-49 [20339138] Cancer Invest. 2010 Jul;28(6):661-9 [20394501] Environ Res. 2010 Jul;110(5):455-62 [19735913] Toxicol Sci. 2010 Jul;116(1):44-57 [20375083] Mol Oncol. 2010 Oct;4(5):397-403 [20594926] Toxicol Sci. 2011 Jan;119(1):73-83 [20937726] Cancer Res. 2011 Feb 1;71(3):629-33 [21266353] Toxicol Appl Pharmacol. 2011 Sep 15;255(3):242-50 [21820459] Cell Mol Life Sci. 2011 Dec;68(23):3853-68 [21744247] Respirology. 2012 Jan;17(1):50-65 [22040022] Environ Health Perspect. 2012 Jan;120(1):92-7 [21954225] Toxicol Appl Pharmacol. 2012 Jan 1;258(1):10-8 [22015448] Toxicol Appl Pharmacol. 2012 Jun 1;261(2):204-16 [22521957] Environ Health Perspect. 2012 Jun;120(6):865-71 [22472196] Anticancer Agents Med Chem. 2012 Sep;12(7):744-52 [22292754] Environ Health Perspect. 2012 Nov;120(11):1527-31 [22949133] Tumour Biol. 2012 Dec;33(6):1819-28 [22718017] Exp Mol Pathol. 2013 Feb;94(1):301-8 [23064051] Pathology. 2013 Apr;45(3):305-15 [23448809] Biochem Biophys Res Commun. 2013 Apr 19;433(4):477-83 [23523794] Cancer Metastasis Rev. 2013 Jun;32(1-2):147-62 [23085856] Toxicol Lett. 2013 Jul 18;220(3):277-85 [23664956] Toxicol Appl Pharmacol. 2013 Oct 15;272(2):542-50 [23811328] Toxicol Appl Pharmacol. 2013 Dec 1;273(2):281-8 [23811327] PLoS One. 2014;9(1):e85614 [24465620] Arch Toxicol. 2014 Feb;88(2):263-74 [24068038] Arch Toxicol. 2014 Feb;88(2):249-61 [24091636] Chem Res Toxicol. 2013 Jan 18;26(1):96-105 [23137061] Toxicol Sci. 2014 Apr;138(2):268-77 [24431212] Arch Toxicol. 2014 Aug;88(8):1619-29 [25005685] Pharmacogenomics. 2014 Aug;15(11):1507-18 [25303301] Nat Rev Drug Discov. 2014 Dec;13(12):928-42 [25435214] Toxicol Sci. 2014 Dec;142(2):489-96 [25273566] Toxicol Appl Pharmacol. 2015 Feb 1;282(3):267-74 [25485709] Toxicol Sci. 2000 Jun;55(2):460-7 [10828279] J Biol Chem. 2001 Aug 24;276(34):31858-62 [11445557] Histopathology. 2002 Feb;40(2):143-51 [11952858] Cell Mol Life Sci. 2002 Apr;59(4):627-47 [12022471] Nat Rev Cancer. 2002 Jul;2(7):489-501 [12094235] J Natl Cancer Inst. 2002 Dec 18;94(24):1888-91 [12488483] Cancer Epidemiol Biomarkers Prev. 2004 Apr;13(4):638-43 [15066930] IARC Monogr Eval Carcinog Risks Hum Suppl. 1987;7:1-440 [3482203] Cancer Res. 1997 Nov 1;57(21):4898-904 [9354455] Curr Med Chem. 2005;12(10):1161-208 [15892631] Toxicol Appl Pharmacol. 2005 Aug 15;206(3):288-98 [16039940] Int J Cancer. 2006 Jul 1;119(1):99-107 [16432833] J Am Chem Soc. 2006 Sep 27;128(38):12473-83 [16984198] Annu Rev Pharmacol Toxicol. 2007;47:243-62 [17002598] Toxicol Sci. 2007 Feb;95(2):313-20 [17077188] Toxicol Sci. 2007 Feb;95(2):321-30 [17093206] Yakugaku Zasshi. 2007 Apr;127(4):665-73 [17409696] Mol Diagn Ther. 2007;11(3):183-92 [17570740] Nature. 2007 Jul 26;448(7152):439-44 [17611497] Free Radic Biol Med. 2008 Sep 1;45(5):651-8 [18572023] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.taap.2015.03.014 ER - TY - JOUR T1 - Role of fibroblast growth factor 21 in the early stage of NASH induced by methionine- and choline-deficient diet. AN - 1681910795; 25736301 AB - Fibroblast growth factor 21 (FGF21) is a modulator of energy homeostasis and is increased in human nonalcoholic liver disease (NAFLD) and after feeding of methionine- and choline-deficient diet (MCD), a conventional inducer of murine nonalcoholic steatohepatitis (NASH). However, the significance of FGF21 induction in the occurrence of MCD-induced NASH remains undetermined. C57BL/6J Fgf21-null and wild-type mice were treated with MCD for 1 week. Hepatic Fgf21 mRNA was increased early after commencing MCD treatment independent of peroxisome proliferator-activated receptor (PPAR) α and farnesoid X receptor. While no significant differences in white adipose lipolysis were seen in both genotypes, hepatic triglyceride (TG) contents were increased in Fgf21-null mice, likely due to the up-regulation of genes encoding CD36 and phosphatidic acid phosphatase 2a/2c, involved in fatty acid (FA) uptake and diacylglycerol synthesis, respectively, and suppression of increased mRNAs encoding carnitine palmitoyl-CoA transferase 1α, PPARγ coactivator 1α, and adipose TG lipase, which are associated with lipid clearance in the liver. The MCD-treated Fgf21-null mice showed increased hepatic endoplasmic reticulum (ER) stress. Exposure of primary hepatocytes to palmitic acid elevated the mRNA levels encoding DNA damage-inducible transcript 3, an indicator of ER stress, and FGF21 in a PPARα-independent manner, suggesting that lipid-induced ER stress can enhance hepatic FGF21 expression. Collectively, FGF21 is elevated in the early stage of MCD-induced NASH likely to minimize hepatic lipid accumulation and ensuing ER stress. These results provide a possible mechanism on how FGF21 is increased in NAFLD/NASH. Published by Elsevier B.V. JF - Biochimica et biophysica acta AU - Tanaka, Naoki AU - Takahashi, Shogo AU - Zhang, Yuan AU - Krausz, Kristopher W AU - Smith, Philip B AU - Patterson, Andrew D AU - Gonzalez, Frank J AD - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States; Department of Metabolic Regulation, Shinshu University Graduate School of Medicine, Matsumoto, Japan. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States. ; Department of Pharmacology, UT Southwestern Medical Center, Dallas, TX, United States. ; Department of Veterinary and Biomedical Sciences and the Center for Molecular Toxicology and Carcinogenesis, The Pennsylvania State University, University Park, PA, United States. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States. Electronic address: gonzalef@mail.nih.gov. Y1 - 2015/07// PY - 2015 DA - July 2015 SP - 1242 EP - 1252 VL - 1852 IS - 7 SN - 0006-3002, 0006-3002 KW - Antigens, CD36 KW - 0 KW - PPAR alpha KW - Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha KW - Ppargc1a protein, mouse KW - RNA, Messenger KW - Receptors, Cytoplasmic and Nuclear KW - Transcription Factors KW - Triglycerides KW - farnesoid X-activated receptor KW - fibroblast growth factor 21 KW - Fibroblast Growth Factors KW - 62031-54-3 KW - Methionine KW - AE28F7PNPL KW - Lipase KW - EC 3.1.1.3 KW - PNPLA2 protein, mouse KW - Phosphatidate Phosphatase KW - EC 3.1.3.4 KW - Index Medicus KW - PGC1α KW - Lipotoxicity KW - ATGL KW - ER stress KW - PPARα KW - Animals KW - Transcription Factors -- metabolism KW - Endoplasmic Reticulum Stress KW - RNA, Messenger -- genetics KW - Adipocytes, White -- metabolism KW - PPAR alpha -- genetics KW - Phosphatidate Phosphatase -- genetics KW - Triglycerides -- metabolism KW - Male KW - Lipase -- metabolism KW - Antigens, CD36 -- metabolism KW - Antigens, CD36 -- genetics KW - Mice KW - Transcription Factors -- genetics KW - Diet -- adverse effects KW - RNA, Messenger -- metabolism KW - Cells, Cultured KW - Receptors, Cytoplasmic and Nuclear -- metabolism KW - Mice, Inbred C57BL KW - Lipase -- genetics KW - PPAR alpha -- metabolism KW - Phosphatidate Phosphatase -- metabolism KW - Lipolysis KW - Hepatocytes -- metabolism KW - Non-alcoholic Fatty Liver Disease -- metabolism KW - Choline Deficiency -- complications KW - Non-alcoholic Fatty Liver Disease -- etiology KW - Methionine -- deficiency KW - Fibroblast Growth Factors -- metabolism KW - Fibroblast Growth Factors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1681910795?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Role+of+fibroblast+growth+factor+21+in+the+early+stage+of+NASH+induced+by+methionine-+and+choline-deficient+diet.&rft.au=Tanaka%2C+Naoki%3BTakahashi%2C+Shogo%3BZhang%2C+Yuan%3BKrausz%2C+Kristopher+W%3BSmith%2C+Philip+B%3BPatterson%2C+Andrew+D%3BGonzalez%2C+Frank+J&rft.aulast=Tanaka&rft.aufirst=Naoki&rft.date=2015-07-01&rft.volume=1852&rft.issue=7&rft.spage=1242&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbadis.2015.02.012 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-27 N1 - Date created - 2015-05-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Invest. 2015 Jan;125(1):386-402 [25500885] Cell Metab. 2012 Nov 7;16(5):634-44 [23140643] Biochim Biophys Acta. 2000 Jun 21;1492(1):203-6 [10858549] J Biol Chem. 1998 Mar 6;273(10):5678-84 [9488698] J Clin Invest. 2005 May;115(5):1343-51 [15864352] J Clin Invest. 2005 Jun;115(6):1627-35 [15902306] Endocrinology. 2006 Jul;147(7):3398-407 [16601139] Endocrinology. 2007 Feb;148(2):774-81 [17068132] Cell Metab. 2007 Jun;5(6):415-25 [17550777] Cell Metab. 2007 Jun;5(6):426-37 [17550778] FEBS Lett. 2008 May 28;582(12):1725-30 [18460341] Endocrinology. 2008 Dec;149(12):6018-27 [18687777] FEBS Lett. 2009 Oct 6;583(19):3230-4 [19751733] Gastroenterology. 2009 Nov;137(5):1795-804 [19664632] Am J Clin Nutr. 2010 Jan;91(1):254S-257S [19906798] J Biol Chem. 2010 Mar 5;285(10):7670-85 [20032461] J Hepatol. 2013 Mar;58(3):557-63 [23142063] Biochimie. 2013 Apr;95(4):692-9 [23123503] Cell Metab. 2013 Sep 3;18(3):333-40 [24011069] J Clin Invest. 2014 Feb;124(2):515-27 [24401271] PLoS One. 2014;9(4):e94996 [24733293] Hepatology. 2014 Sep;60(3):977-89 [24590984] Biochem J. 2014 Oct 15;463(2):191-9 [25055037] Biochim Biophys Acta. 2014 Nov;1841(11):1596-607 [25178843] J Biol Chem. 2014 Oct 24;289(43):29751-65 [25170079] Gastroenterology. 2014 Nov;147(5):1073-83.e6 [25083607] J Biol Chem. 2015 Jan 30;290(5):3092-105 [25477509] Am J Physiol Gastrointest Liver Physiol. 2010 Jul;299(1):G236-43 [20430872] Hepatology. 2010 Aug;52(2):774-88 [20683968] Eur J Clin Invest. 2010 Oct;40(10):887-92 [20624171] J Hepatol. 2010 Nov;53(5):934-40 [20675007] Hepatology. 2010 Nov;52(5):1836-46 [21038418] Hepatology. 2011 Jan;53(1):116-26 [20967758] J Biol Chem. 2011 Apr 15;286(15):12983-90 [21317437] Science. 2011 Jun 24;332(6037):1519-23 [21700865] Mol Med. 2011;17(7-8):736-40 [21373720] J Biol Chem. 2011 Nov 11;286(45):39336-48 [21941003] Genes Dev. 2012 Feb 1;26(3):271-81 [22302939] Cell. 2012 Feb 3;148(3):556-67 [22304921] Endocrinology. 2012 Jun;153(6):2689-700 [22474187] Hepatology. 2012 Jul;56(1):118-29 [22290395] J Biol Chem. 2012 Jul 20;287(30):25123-38 [22661717] Gastroenterology. 2010 Aug;139(2):456-63 [20451522] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbadis.2015.02.012 ER - TY - JOUR T1 - The Emergence of Environmental Health Literacy-From Its Roots to Its Future Potential. AN - 1826624031; 26126293 AB - Environmental health literacy (EHL) is coalescing into a new sub-discipline that combines key principles and procedural elements from the fields of risk communication, health literacy, environmental health sciences (EHS), communications research and safety culture. These disciplines have contributed unique expertise and perspectives to the development of EHL. Since 1992, National Institute of Environmental Health Sciences (NIEHS) has contributed to the evolution of EHL and now seeks to stimulate its scientific advancement and rigor. The principal objective of this article is to stimulate a conversation on, and advance research in, EHL. In this article we propose a definition of and conceptual framework for EHL, describe EHL in its social and historical context, identify the complementary fields and domains where EHL is being defined and implemented, and outline a research agenda. Through extensive reviews of web and literature searches we see that the concept of EHL is evolving rapidly, as are the definitions of its scope and inquiry. While several authors outline different frameworks, we believe that a more nuanced model based on Bloom's Taxonomy is better suited to EHL and future research in this area. We posit that EHL can potentially benefit the conduct and outcomes of community-engaged and health disparities EHS research and ensure that the translation of research findings lead to greater understanding of specific risks, the reduction of exposures, and the improvement of health outcomes for individuals and communities. We provide four recommendations to advance work in EHL. JF - Environmental health perspectives AU - Finn, Symma AU - O'Fallon, Liam AD - National Institute of Environmental Health Sciences, Division of Extramural Research and Training, Research Triangle Park, North Carolina, USA. Y1 - 2015/06/30/ PY - 2015 DA - 2015 Jun 30 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826624031?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=The+Emergence+of+Environmental+Health+Literacy-From+Its+Roots+to+Its+Future+Potential.&rft.au=Finn%2C+Symma%3BO%27Fallon%2C+Liam&rft.aulast=Finn&rft.aufirst=Symma&rft.date=2015-06-30&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2015-06-30 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - Quantification of recombinant immunotoxin delivery to solid tumors allows for direct comparison of in vivo and in vitro results. AN - 1691602206; 26111884 AB - Solid tumors present challenges for delivery of protein therapeutics; current methods cannot quantify the functional effects of these agents. RG7787 (anti-mesothelin recombinant immunotoxin) is highly cytotoxic to pancreatic cancer cell lines, but with limited activity in vivo. To investigate this discrepancy, we developed a flow cytometry method to quantify the amount of RG7787 internalized per cell in tumors and used it to analyze tumor responses by determining the number of molecules of RG7787 internalized per cell in vivo and comparing it to that needed to kill cells in vitro. At a maximum tolerated dose of 7.5 mg/kg, tumor cells in vivo internalized a wide range of RG7787 with the average amount equivalent to the amount that induced growth arrest in vitro. However, 20% of cells accumulated 20,300 ITs per cell, sufficient to kill cells in vitro. At 2.5 mg/kg the top 20% of cells internalized enough RG7787 to only induce growth arrest. These data are in agreement with tumor responses; 22% regression following a 7.5 mg/kg dose and growth stabilization following 2.5 mg/kg. Comparing amounts of RIT delivered in vivo and in vitro can explain tumor responses and should facilitate the development of more active immunotoxins and other antibody based agents. JF - Scientific reports AU - Mason-Osann, Emily AU - Hollevoet, Kevin AU - Niederfellner, Gerhard AU - Pastan, Ira AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. ; Roche Pharmaceutical Research &Early Development, Discovery Oncology, Innovation Center Penzberg, Roche Diagnostics GmbH, Nonnenwald 2, 82377 Penzberg, Germany. Y1 - 2015/06/26/ PY - 2015 DA - 2015 Jun 26 SP - 10832 VL - 5 KW - Alexa Fluor 647 KW - 0 KW - Carbocyanines KW - Immunoconjugates KW - RG7787 KW - Index Medicus KW - Microscopy, Fluorescence KW - Animals KW - Pancreatic Neoplasms -- pathology KW - Pancreatic Neoplasms -- metabolism KW - Carbocyanines -- chemistry KW - Humans KW - Apoptosis -- drug effects KW - Transplantation, Heterologous KW - Mice, Nude KW - Mice KW - Cell Line, Tumor KW - Pancreatic Neoplasms -- drug therapy KW - Drug Dosage Calculations KW - Female KW - Immunoconjugates -- metabolism KW - Immunoconjugates -- toxicity KW - Immunoconjugates -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1691602206?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scientific+reports&rft.atitle=Quantification+of+recombinant+immunotoxin+delivery+to+solid+tumors+allows+for+direct+comparison+of+in+vivo+and+in+vitro+results.&rft.au=Mason-Osann%2C+Emily%3BHollevoet%2C+Kevin%3BNiederfellner%2C+Gerhard%3BPastan%2C+Ira&rft.aulast=Mason-Osann&rft.aufirst=Emily&rft.date=2015-06-26&rft.volume=5&rft.issue=&rft.spage=10832&rft.isbn=&rft.btitle=&rft.title=Scientific+reports&rft.issn=2045-2322&rft_id=info:doi/10.1038%2Fsrep10832 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-06 N1 - Date created - 2015-06-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Eur J Cancer. 2004 Jun;40(9):1418-22 [15177502] FEBS J. 2011 Dec;278(23):4683-700 [21585657] Mol Cancer Ther. 2014 Aug;13(8):2040-9 [24928849] J Clin Pathol. 1983 May;36(5):539-45 [6302135] J Clin Pathol. 1984 Feb;37(2):131-5 [6198338] Cancer Res. 1992 Oct 1;52(19):5144-53 [1327501] Int J Oncol. 1998 Oct;13(4):871-5 [9735419] Int J Cancer. 1999 Feb 9;80(4):559-63 [9935157] Mol Cancer Ther. 2004 Nov;3(11):1493-501 [15542788] Mol Cancer Ther. 2012 Mar;11(3):752-62 [22222630] Cancer Cell. 2012 Mar 20;21(3):418-29 [22439937] PLoS One. 2012;7(5):e36258 [22590529] Nat Nanotechnol. 2012 Jun;7(6):383-8 [22484912] Cancer Res. 2012 Jul 1;72(13):3143-52 [22562466] Proc Natl Acad Sci U S A. 2012 Jul 17;109(29):11782-7 [22753489] J Control Release. 2012 Aug 20;162(1):218-24 [22732476] Mol Cancer Ther. 2013 Jan;12(1):48-57 [23136186] Expert Opin Drug Deliv. 2013 Oct;10(10):1429-48 [23789923] Sci Transl Med. 2013 Oct 23;5(208):208ra147 [24154601] Oncol Rep. 2014 Mar;31(3):1296-304 [24435655] Small. 2014 Feb 12;10(3):524-35 [24106138] Mol Cancer Ther. 2014 Mar;13(3):651-61 [24435448] Cancer Res. 2014 Jun 1;74(11):2907-12 [24824231] Carcinogenesis. 2014 Jul;35(7):1451-60 [24908682] Nat Rev Cancer. 2006 Aug;6(8):583-92 [16862189] Clin Immunol. 2006 Nov;121(2):144-58 [16904380] Clin Cancer Res. 2007 Mar 1;13(5):1571-5 [17332303] Cancer Res. 2010 Feb 1;70(3):1082-9 [20103626] Thyroid. 2011 Mar;21(3):267-77 [21323588] Cancer Res. 2011 Mar 15;71(6):2250-9 [21406401] Drug Discov Ther. 2013 Oct;7(5):178-84 [24270381] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/srep10832 ER - TY - JOUR T1 - Structure-Activity Relationships of (+)-Naltrexone-Inspired Toll-like Receptor 4 (TLR4) Antagonists. AN - 1691596897; 26010811 AB - Activation of Toll-like receptors has been linked to neuropathic pain and opioid dependence. (+)-Naltrexone acts as a Toll-like receptor 4 (TLR4) antagonist and has been shown to reverse neuropathic pain in rat studies. We designed and synthesized compounds based on (+)-naltrexone and (+)-noroxymorphone and evaluated their TLR4 antagonist activities by their effects on inhibiting lipopolysaccharide (LPS) induced TLR4 downstream nitric oxide (NO) production in microglia BV-2 cells. Alteration of the N-substituent in (+)-noroxymorphone gave us a potent TLR4 antagonist. The most promising analog, (+)-N-phenethylnoroxymorphone ((4S,4aR,7aS,12bR)-4a,9-dihydroxy-3-phenethyl-2,3,4,4a,5,6-hexahydro-1H-4,12-methanobenzofuro[3,2-e]isoquinolin-7(7aH)-one, 1j) showed ∼75 times better TLR-4 antagonist activity than (+)-naltrexone, and the ratio of its cell viability IC50, a measure of its toxicity, to TLR-4 antagonist activity (140 μM/1.4 μM) was among the best of the new analogs. This compound (1j) was active in vivo; it significantly increased and prolonged morphine analgesia. JF - Journal of medicinal chemistry AU - Selfridge, Brandon R AU - Wang, Xiaohui AU - Zhang, Yingning AU - Yin, Hang AU - Grace, Peter M AU - Watkins, Linda R AU - Jacobson, Arthur E AU - Rice, Kenner C AD - †Drug Design and Synthesis Section, Molecular Targets and Medications Discovery Branch, Intramural Research Program, National Institute on Drug Abuse and the National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Department of Health and Human Services, 9800 Medical Center Drive, Bethesda, Maryland 20892-3373, United States. ; ‡Department of Psychology and Neuroscience, University of Colorado at Boulder, Boulder, Colorado 80309, United States. ; §Department of Chemistry and Biochemistry the BioFrontiers Institute, University of Colorado at Boulder, Boulder, Colorado 80309, United States. Y1 - 2015/06/25/ PY - 2015 DA - 2015 Jun 25 SP - 5038 EP - 5052 VL - 58 IS - 12 KW - Analgesics, Opioid KW - 0 KW - Lipopolysaccharides KW - Morphinans KW - Toll-Like Receptor 4 KW - Nitric Oxide KW - 31C4KY9ESH KW - Naltrexone KW - 5S6W795CQM KW - Morphine KW - 76I7G6D29C KW - noroxymorphone KW - 9NZ7111A9O KW - Index Medicus KW - Animals KW - Humans KW - Structure-Activity Relationship KW - Morphine -- pharmacology KW - Rats KW - Rats, Sprague-Dawley KW - Lipopolysaccharides -- immunology KW - Analgesics, Opioid -- pharmacology KW - Microglia -- cytology KW - Microglia -- immunology KW - Nitric Oxide -- immunology KW - Drug Synergism KW - Microglia -- drug effects KW - Cell Line KW - Male KW - Toll-Like Receptor 4 -- immunology KW - Toll-Like Receptor 4 -- antagonists & inhibitors KW - Morphinans -- chemistry KW - Naltrexone -- analogs & derivatives KW - Naltrexone -- pharmacology KW - Morphinans -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1691596897?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+medicinal+chemistry&rft.atitle=Structure-Activity+Relationships+of+%28%2B%29-Naltrexone-Inspired+Toll-like+Receptor+4+%28TLR4%29+Antagonists.&rft.au=Selfridge%2C+Brandon+R%3BWang%2C+Xiaohui%3BZhang%2C+Yingning%3BYin%2C+Hang%3BGrace%2C+Peter+M%3BWatkins%2C+Linda+R%3BJacobson%2C+Arthur+E%3BRice%2C+Kenner+C&rft.aulast=Selfridge&rft.aufirst=Brandon&rft.date=2015-06-25&rft.volume=58&rft.issue=12&rft.spage=5038&rft.isbn=&rft.btitle=&rft.title=Journal+of+medicinal+chemistry&rft.issn=1520-4804&rft_id=info:doi/10.1021%2Facs.jmedchem.5b00426 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-14 N1 - Date created - 2015-06-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Br J Pharmacol. 2016 Mar;173(5):856-69 [26603732] J Am Chem Soc. 1967 Apr 12;89(8):1942-7 [6040525] Mol Psychiatry. 2015 Dec;20(12):1525-37 [25644383] CNS Neurol Disord Drug Targets. 2015;14(6):692-9 [26022268] Trends Pharmacol Sci. 2014 Sep;35(9):432-3 [25109571] Trends Pharmacol Sci. 2014 Sep;35(9):431-2 [25109569] Nat Rev Drug Discov. 2014 Jul;13(7):533-48 [24948120] J Org Chem. 2014 Jun 6;79(11):5007-18 [24773391] Neuropharmacology. 2014 Jan;76 Pt B:218-27 [23764149] FASEB J. 2013 Jul;27(7):2713-22 [23568774] Chem Soc Rev. 2013 Jun 21;42(12):4859-66 [23503527] Biol Psychiatry. 2013 Apr 15;73(8):729-37 [23384483] Nat Neurosci. 2013 Mar;16(3):253-5 [23434975] J Neurosci. 2012 Aug 15;32(33):11187-200 [22895704] Proc Natl Acad Sci U S A. 2012 Apr 17;109(16):6325-30 [22474354] Pharmacol Ther. 2012 May;134(2):219-45 [22316499] Pharmacol Rev. 2011 Sep;63(3):772-810 [21752874] Proc Natl Acad Sci U S A. 2010 Jun 29;107(26):11942-7 [20547845] Cell. 2010 Mar 19;140(6):805-20 [20303872] Brain Behav Immun. 2010 Jan;24(1):83-95 [19679181] ALTEX. 2009;26(2):83-94 [19565166] Trends Neurosci. 2009 Jun;32(6):339-46 [19414201] Nature. 2009 Apr 30;458(7242):1191-5 [19252480] Org Lett. 2009 Feb 5;11(3):539-42 [19115979] Anesthesiology. 2009 Jan;110(1):166-81 [19104184] J Org Chem. 2008 Oct 17;73(20):8093-6 [18811203] Eur J Neurosci. 2008 Jul;28(1):20-9 [18662331] Neurosci Biobehav Rev. 2001 Jan;25(1):43-52 [11166077] Nat Rev Immunol. 2014 Apr;14(4):217-31 [24577438] J Med Chem. 1978 Apr;21(4):398-400 [206698] J Med Chem. 1978 Dec;21(12):1320-2 [722742] Pain. 1988 Jan;32(1):77-88 [3340425] J Med Chem. 1992 Jul 24;35(15):2826-35 [1322988] Anal Biochem. 1993 Oct;214(1):11-6 [7504409] J Neurosci Methods. 1999 Aug 1;90(1):81-6 [10517276] J Org Chem. 2005 Mar 4;70(5):1907-10 [15730320] Org Lett. 2005 Jun 23;7(13):2531-4 [15957883] ScientificWorldJournal. 2007;7:98-111 [17982582] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/acs.jmedchem.5b00426 ER - TY - JOUR T1 - Coupling of Zinc-Binding and Secondary Structure in Nonfibrillar Aβ40 Peptide Oligomerization. AN - 1690651499; 26017140 AB - Nonfibrillar neurotoxic amyloid β (Aβ) oligomer structures are typically rich in β-sheets, which could be promoted by metal ions like Zn(2+). Here, using molecular dynamics (MD) simulations, we systematically examined combinations of Aβ40 peptide conformations and Zn(2+) binding modes to probe the effects of secondary structure on Aβ dimerization energies and kinetics. We found that random conformations do not contribute to dimerization either thermodynamically or kinetically. Zn(2+) couples with preformed secondary structures (α-helix and β-hairpin) to speed dimerization and stabilize the resulting dimer. Partial α-helices increase the dimerization speed, and dimers with α-helix rich conformations have the lowest energy. When Zn(2+) coordinates with residues D1, H6, H13, and H14, Aβ40 β-hairpin monomers have the fastest dimerization speed. Dimers with experimentally observed zinc coordination (E11, H6, H13, and H14) form with slower rate but have lower energy. Zn(2+) cannot stabilize fibril-like β-arch dimers. However, Zn(2+)-bound β-arch tetramers have the lowest energy. Collectively, zinc-stabilized β-hairpin oligomers could be important in the nucleation-polymerization of cross-β structures. Our results are consistent with experimental findings that α-helix to β-structural transition should accompany Aβ aggregation in the presence of zinc ions and that Zn(2+) stabilizes nonfibrillar Aβ oligomers and, thus, inhibits formation of less toxic Aβ fibrils. JF - Journal of chemical information and modeling AU - Xu, Liang AU - Shan, Shengsheng AU - Chen, Yonggang AU - Wang, Xiaojuan AU - Nussinov, Ruth AU - Ma, Buyong AD - ∥Sackler Institute of Molecular Medicine, Department of Human Genetics and Molecular Medicine, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel. ; ⊥Basic Science Program, Leidos Biomedical Research, Inc., Cancer and Inflammation Program, National Cancer Institute, Frederick, Maryland 21702, United States. Y1 - 2015/06/22/ PY - 2015 DA - 2015 Jun 22 SP - 1218 EP - 1230 VL - 55 IS - 6 KW - Amyloid beta-Peptides KW - 0 KW - Peptide Fragments KW - Protein Aggregates KW - amyloid beta-protein (1-40) KW - Zinc KW - J41CSQ7QDS KW - Index Medicus KW - Protein Structure, Secondary KW - Thermodynamics KW - Protein Stability KW - Kinetics KW - Protein Binding KW - Peptide Fragments -- metabolism KW - Peptide Fragments -- chemistry KW - Amyloid beta-Peptides -- metabolism KW - Amyloid beta-Peptides -- chemistry KW - Zinc -- metabolism KW - Molecular Dynamics Simulation KW - Protein Multimerization UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1690651499?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+chemical+information+and+modeling&rft.atitle=Coupling+of+Zinc-Binding+and+Secondary+Structure+in+Nonfibrillar+A%CE%B240+Peptide+Oligomerization.&rft.au=Xu%2C+Liang%3BShan%2C+Shengsheng%3BChen%2C+Yonggang%3BWang%2C+Xiaojuan%3BNussinov%2C+Ruth%3BMa%2C+Buyong&rft.aulast=Xu&rft.aufirst=Liang&rft.date=2015-06-22&rft.volume=55&rft.issue=6&rft.spage=1218&rft.isbn=&rft.btitle=&rft.title=Journal+of+chemical+information+and+modeling&rft.issn=1549-960X&rft_id=info:doi/10.1021%2Facs.jcim.5b00063 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-22 N1 - Date created - 2015-06-22 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/acs.jcim.5b00063 ER - TY - JOUR T1 - Parma consensus statement on metabolic disruptors. AN - 1690649338; 26092037 AB - A multidisciplinary group of experts gathered in Parma Italy for a workshop hosted by the University of Parma, May 16-18, 2014 to address concerns about the potential relationship between environmental metabolic disrupting chemicals, obesity and related metabolic disorders. The objectives of the workshop were to: 1. Review findings related to the role of environmental chemicals, referred to as "metabolic disruptors", in obesity and metabolic syndrome with special attention to recent discoveries from animal model and epidemiology studies; 2. Identify conclusions that could be drawn with confidence from existing animal and human data; 3. Develop predictions based on current data; and 4. Identify critical knowledge gaps and areas of uncertainty. The consensus statements are intended to aid in expanding understanding of the role of metabolic disruptors in the obesity and metabolic disease epidemics, to move the field forward by assessing the current state of the science and to identify research needs on the role of environmental chemical exposures in these diseases. We propose broadening the definition of obesogens to that of metabolic disruptors, to encompass chemicals that play a role in altered susceptibility to obesity, diabetes and related metabolic disorders including metabolic syndrome. JF - Environmental health : a global access science source AU - Heindel, Jerrold J AU - vom Saal, Frederick S AU - Blumberg, Bruce AU - Bovolin, Patrizia AU - Calamandrei, Gemma AU - Ceresini, Graziano AU - Cohn, Barbara A AU - Fabbri, Elena AU - Gioiosa, Laura AU - Kassotis, Christopher AU - Legler, Juliette AU - La Merrill, Michele AU - Rizzir, Laura AU - Machtinger, Ronit AU - Mantovani, Alberto AU - Mendez, Michelle A AU - Montanini, Luisa AU - Molteni, Laura AU - Nagel, Susan C AU - Parmigiani, Stefano AU - Panzica, Giancarlo AU - Paterlini, Silvia AU - Pomatto, Valentina AU - Ruzzin, Jérôme AU - Sartor, Giorgio AU - Schug, Thaddeus T AU - Street, Maria E AU - Suvorov, Alexander AU - Volpi, Riccardo AU - Zoeller, R Thomas AU - Palanza, Paola AD - Division of Extramural Research and Training, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. heindelj@niehs.nih.gov. ; Division of Biological Sciences, University of Missouri, Columbia, MO, USA. vomsaalf@umissouri.edu. ; Department of Developmental and Cell Biology, University of California, Irvine, CA, USA. Blumberg@uci.edu. ; Department of Life Sciences and Systems Biology, University of Turin, Turin, Italy. patrizia.bovolin@unito.it. ; Department of Cell Biology and Neurosciences, Insituto Superiore di Sanita, Rome, Italy. gemma.calamandrei@iss.it. ; Department of Clinical and Experimental Medicine, University of Parma, Parma, Italy. graziano.ceresini@unipr.it. ; Public Health Institute, Berkeley, CA, USA. bcohn@chdstudies.org. ; Interdepartment Center for Environmental Science Research, University of Bologna, Ravenna, Italy. elena.fabbri@unibo.it. ; Department of Neuroscience, University of Parma, Parma, Italy. laura.gioiosa@unipr.it. ; Division of Biological Sciences, University of Missouri, Columbia, MO, USA. cdkassotis@mail.missouri.edu. ; Department of Toxicology and Environmental Health, VU University Amsterdam, Amsterdam, Netherlands. juliette.legler@vu.nl. ; Department of Environmental Toxicology, University of California, Davis, CA, USA. mlamerrill@ucdavis.edu. ; Department of Health Sciences, University of Milano-Bicocca, Monza, Italy. l.rizzi3@campus.unimib.it. ; Sheba Medical Center and Tel-Aviv University, Tel -Aviv, Israel. mmachtin@gmail.com. ; Instituto Superiore di Sanita, Rome, Italy. alberto.mantovani@iss.it. ; School of Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. mmendez@email.unc.edu. ; Department of Pediatrics, University of Parma, Parma, Italy. luisa.montanini@unipr.it. ; University of Milano-Bicocca, Monza, Italy. l.molteni3@campus.unimib.it. ; Department of Obstetrics, Gynecology and Women's Health, University of Missouri, Columbia, MO, USA. nagels@health.missouri.edu. ; Faculty of Medicine, University of Parma, Parma, Italy. stefano.parmigiani@unipr.it. ; Department of Neuroscience and Neuroscience Institute Cavalieri Ottolenghi (NICO), University of Turin, Turin, Italy. giancarlo.panzica@unito.it. ; Department of Neuroscience and Neuroscience Institute Cavalieri Ottolenghi (NICO), University of Turin, Turin, Italy. silvia.paterlini@studenti.unipr.it. ; Department of Life Sciences and Systems Biology, University of Turin, Turin, Italy. valentina.pomatto@unito.it. ; Department of Biology, University of Bergen, Bergen, Norway. jerome.ruzzin@bio.uib.no. ; Department of Pharmacy and Biotechnology, University of Bologna, Bologna, Italy. giorgio.sartor@unibo.it. ; Division of Extramural Research and Training, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. schugt2@niehs.nih.gov. ; Department of Pediatrics, University Hospital, Parma, Italy. mariaelisabeth.street@unipr.it. ; Division of Biological Sciences, University of Missouri, Columbia, MO, USA. asuvorov@schoolph.umass.edu. ; Department of Internal Medicine, University of Parma, Parma, Italy. Riccardo.volpi@unipr.it. ; Department of Biology, University of Massachusetts, Amherst, MA, USA. tzoeller@bio.umass.edu. ; Department of Neuroscience, University of Parma, Parma, Italy. paola.palanza@unipr.it. Y1 - 2015/06/20/ PY - 2015 DA - 2015 Jun 20 SP - 54 VL - 14 KW - Environmental Pollutants KW - 0 KW - Hazardous Substances KW - Index Medicus KW - Metabolic Syndrome X -- chemically induced KW - Humans KW - Diabetes Mellitus -- chemically induced KW - Congresses as Topic KW - Obesity -- chemically induced KW - Italy KW - Hazardous Substances -- adverse effects KW - Consensus Development Conferences as Topic KW - Environmental Exposure -- adverse effects KW - Environmental Pollutants -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1690649338?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+%3A+a+global+access+science+source&rft.atitle=Parma+consensus+statement+on+metabolic+disruptors.&rft.au=Heindel%2C+Jerrold+J%3Bvom+Saal%2C+Frederick+S%3BBlumberg%2C+Bruce%3BBovolin%2C+Patrizia%3BCalamandrei%2C+Gemma%3BCeresini%2C+Graziano%3BCohn%2C+Barbara+A%3BFabbri%2C+Elena%3BGioiosa%2C+Laura%3BKassotis%2C+Christopher%3BLegler%2C+Juliette%3BLa+Merrill%2C+Michele%3BRizzir%2C+Laura%3BMachtinger%2C+Ronit%3BMantovani%2C+Alberto%3BMendez%2C+Michelle+A%3BMontanini%2C+Luisa%3BMolteni%2C+Laura%3BNagel%2C+Susan+C%3BParmigiani%2C+Stefano%3BPanzica%2C+Giancarlo%3BPaterlini%2C+Silvia%3BPomatto%2C+Valentina%3BRuzzin%2C+J%C3%A9r%C3%B4me%3BSartor%2C+Giorgio%3BSchug%2C+Thaddeus+T%3BStreet%2C+Maria+E%3BSuvorov%2C+Alexander%3BVolpi%2C+Riccardo%3BZoeller%2C+R+Thomas%3BPalanza%2C+Paola&rft.aulast=Heindel&rft.aufirst=Jerrold&rft.date=2015-06-20&rft.volume=14&rft.issue=&rft.spage=54&rft.isbn=&rft.btitle=&rft.title=Environmental+health+%3A+a+global+access+science+source&rft.issn=1476-069X&rft_id=info:doi/10.1186%2Fs12940-015-0042-7 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-04 N1 - Date created - 2015-06-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: JAMA. 2012 Sep 19;308(11):1113-21 [22990270] Endocr Rev. 2012 Jun;33(3):378-455 [22419778] Can J Cardiol. 2012 Nov-Dec;28(6):642-52 [22889821] Nat Rev Endocrinol. 2013 Jan;9(1):9-10 [23147575] Front Biosci (Elite Ed). 2013;5:725-33 [23277027] Arch Intern Med. 1999 Jul 12;159(13):1450-6 [10399896] Mol Endocrinol. 2006 Sep;20(9):2141-55 [16613991] Environ Health Perspect. 2007 Jun;115(6):876-82 [17589594] Reprod Toxicol. 2008 Jan;25(1):2-6 [17949945] Proc Nutr Soc. 2008 Feb;67(1):82-90 [18234135] Environ Health. 2008;7:27 [18522739] JAMA. 2008 Sep 17;300(11):1303-10 [18799442] Mol Cell Endocrinol. 2009 May 25;304(1-2):84-9 [19433252] Mol Cell Endocrinol. 2009 May 25;304(1-2):90-6 [19433253] Mol Cell Endocrinol. 2009 May 25;304(1-2):97-105 [19433254] Environ Health Perspect. 2009 Oct;117(10):1549-55 [20019905] Int J Androl. 2012 Jun;35(3):437-48 [22372658] J Dev Orig Health Dis. 2015 Jun;6(3):242-9 [25665487] Mt Sinai J Med. 2011 Jan-Feb;78(1):22-48 [21259261] Annu Rev Physiol. 2011;73:135-62 [21054169] Birth Defects Res C Embryo Today. 2011 Mar;93(1):34-50 [21425440] Proc Biol Sci. 2011 Jun 7;278(1712):1626-32 [21106594] Obes Rev. 2011 Aug;12(8):622-36 [21457182] Int J Gynaecol Obstet. 2011 Nov;115 Suppl 1:S3-5 [22099437] Am J Clin Nutr. 2011 Dec;94(6 Suppl):1939S-1942S [22089436] Endocrinology. 2012 Feb;153(2):712-20 [22166976] Environ Health Perspect. 2012 Mar;120(3):332-9 [22042266] PLoS One. 2013;8(1):e55387 [23359474] Environ Health Perspect. 2013 Mar;121(3):359-66 [23322813] Reprod Toxicol. 2013 Apr;36:104-16 [23453003] Endocrinology. 2013 Apr;154(4):1465-75 [23493373] Environ Health Perspect. 2013 May;121(5):594-9 [23591545] Pediatrics. 2013 Sep;132(3):e646-55 [23958772] BMC Med. 2013;11:228 [24228800] Reprod Toxicol. 2013 Dec;42:256-68 [23892310] Obesity (Silver Spring). 2014 Feb;22(2):488-96 [23963708] Brain Behav Immun. 2014 Mar;37:30-44 [24184474] Reprod Toxicol. 2014 Apr;44:15-22 [23791931] JAMA. 2014 May 7;311(17):1778-86 [24794371] JAMA. 2014 Jul;312(2):189-90 [25005661] PLoS One. 2014;9(7):e103337 [25076055] J Endocrinol. 2014 Sep;222(3):313-25 [25112833] Dialogues Clin Neurosci. 2014 Sep;16(3):321-33 [25364283] Mol Cell Endocrinol. 2014 Dec;398(1-2):13-23 [25079508] Mol Cell Endocrinol. 2014 Dec;398(1-2):4-12 [25088466] Obes Rev. 2015 Jan;16(1):1-12 [25407540] Environ Health. 2015;14:118 [25533907] Biosci Rep. 2012 Dec;32(6):619-29 [22953781] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/s12940-015-0042-7 ER - TY - JOUR T1 - Toxicities of Immunotherapy for the Practitioner. AN - 1690217346; 25918278 AB - The toxicities of immunotherapy for cancer are as diverse as the type of treatments that have been devised. These range from cytokine therapies that induce capillary leakage to vaccines associated with low levels of autoimmunity to cell therapies that can induce damaging cross-reactivity with normal tissue to checkpoint protein inhibitors that induce immune-related adverse events that are autoinflammatory in nature. The thread that ties these toxicities together is their mechanism-based immune nature and the T-cell-mediated adverse events seen. The basis for the majority of these adverse events is a hyperactivated T-cell response with reactivity directed against normal tissue, resulting in the generation of high levels of CD4 T-helper cell cytokines or increased migration of cytolytic CD8 T cells within normal tissues. The T-cell immune response is not tissue specific and may reflect a diffuse expansion of the T-cell repertoire that induces cross-reactivity with normal tissue, effectively breaking tolerance that is active with cytokines, vaccines, and checkpoint protein inhibitors and passive in the case of adoptive cell therapy. Cytokines seem to generate diffuse and nonspecific T-cell reactivity, whereas checkpoint protein inhibition, vaccines, and adoptive cell therapy seem to activate more specific T cells that interact directly with normal tissues, potentially causing specific organ damage. In this review, we summarize the toxicities that are unique to immunotherapies, emphasizing the need to familiarize the oncology practitioner with the spectrum of adverse events seen with newly approved and emerging modalities. © 2015 by American Society of Clinical Oncology. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Weber, Jeffrey S AU - Yang, James C AU - Atkins, Michael B AU - Disis, Mary L AD - Jeffrey S. Weber, Moffitt Cancer Center, Tampa, FL; James C. Yang, National Cancer Institute, Bethesda, MD; Michael B. Atkins, Lombardi Cancer Center, Georgetown University, Washington, DC; and Mary L. Disis, The Fred Hutchinson Cancer Center, University of Washington, Seattle, WA. jeffrey.weber@moffitt.org. ; Jeffrey S. Weber, Moffitt Cancer Center, Tampa, FL; James C. Yang, National Cancer Institute, Bethesda, MD; Michael B. Atkins, Lombardi Cancer Center, Georgetown University, Washington, DC; and Mary L. Disis, The Fred Hutchinson Cancer Center, University of Washington, Seattle, WA. Y1 - 2015/06/20/ PY - 2015 DA - 2015 Jun 20 SP - 2092 EP - 2099 VL - 33 IS - 18 KW - Cancer Vaccines KW - 0 KW - Cytokines KW - Interferon-alpha KW - Index Medicus KW - CD8-Positive T-Lymphocytes -- cytology KW - CD4-Positive T-Lymphocytes -- cytology KW - Autoimmunity -- immunology KW - Cancer Vaccines -- chemistry KW - Interferon-alpha -- chemistry KW - Humans KW - Immunotherapy, Adoptive KW - Cytokines -- metabolism KW - Cell- and Tissue-Based Therapy KW - Immunotherapy -- adverse effects KW - Neoplasms -- therapy KW - Neoplasms -- immunology KW - Immunotherapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1690217346?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Toxicities+of+Immunotherapy+for+the+Practitioner.&rft.au=Weber%2C+Jeffrey+S%3BYang%2C+James+C%3BAtkins%2C+Michael+B%3BDisis%2C+Mary+L&rft.aulast=Weber&rft.aufirst=Jeffrey&rft.date=2015-06-20&rft.volume=33&rft.issue=18&rft.spage=2092&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=1527-7755&rft_id=info:doi/10.1200%2FJCO.2014.60.0379 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-31 N1 - Date created - 2015-06-19 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1200/JCO.2014.60.0379 ER - TY - JOUR T1 - Identification of a functional nuclear translocation sequence in hPPIP5K2. AN - 1690213459; 26084399 AB - Cells contain several inositol pyrophosphates (PP-InsPs; also known as diphosphoinositol polyphosphates), which play pivotal roles in cellular and organismic homeostasis. It has been proposed that determining mechanisms of compartmentation of the synthesis of a particular PP-InsP is key to understanding how each of them may exert a specific function. Human PPIP5K2 (hPPIP5K2), one of the key enzymes that synthesizes PP-InsPs, contains a putative consensus sequence for a nuclear localization signal (NLS). However, such in silico analysis has limited predictive power, and may be complicated by phosphorylation events that can dynamically modulate NLS function. We investigated if this candidate NLS is functional and regulated, using the techniques of cell biology, mutagenesis and mass spectrometry. Multiple sequence alignments revealed that the metazoan PPIP5K2 family contains a candidate NLS within a strikingly well-conserved 63 amino-acid domain. By analyzing the distribution of hPPIP5K2-GFP in HEK293T cells with the techniques of confocal microscopy and imaging flow cytometry, we found that a distinct pool of hPPIP5K2 is present in the nucleus. Imaging flow cytometry yielded particular insight into the characteristics of the nuclear hPPIP5K2 sub-pool, through a high-throughput, statistically-robust analysis of many hundreds of cells. Mutagenic disruption of the candidate NLS in hPPIP5K2 reduced its degree of nuclear localization. Proximal to the NLS is a Ser residue (S1006) that mass spectrometry data indicate is phosphorylated inside cells. The degree of nuclear localization of hPPIP5K2 was increased when S1006 was rendered non-phosphorylatable by its mutation to Ala. Conversely, a S1006D phosphomimetic mutant of hPPIP5K2 exhibited a lower degree of nuclear localization. The current study describes for the first time the functional significance of an NLS in the conserved PPIP5K2 family. We have further demonstrated that there is phosphorylation of a Ser residue that is proximal to the NLS of hPPIP5K2. These conclusions draw attention to nuclear compartmentation of PPIP5K2 as being a physiologically relevant and covalently-regulated event. Our study also increases general insight into the consensus sequences of other NLSs, the functions of which might be similarly regulated. JF - BMC cell biology AU - Yong, Sheila T AU - Nguyen, Hoai-Nghia AU - Choi, Jae H AU - Bortner, Carl D AU - Williams, Jason AU - Pulloor, Niyas K AU - Krishnan, Manoj N AU - Shears, Stephen B AD - Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, 101 T.W. Alexander Drive, Research Triangle Park, NC, 27709, USA. yongst.work@gmail.com. ; Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, 101 T.W. Alexander Drive, Research Triangle Park, NC, 27709, USA. hoainghia.nguyen@nih.gov. ; Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, 101 T.W. Alexander Drive, Research Triangle Park, NC, 27709, USA. jae.choi@thermofisher.com. ; Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, 101 T.W. Alexander Drive, Research Triangle Park, NC, 27709, USA. bortner@niehs.nih.gov. ; Protein Microcharacterization Core Facility, Mass Spectrometry Group, National Institute of Environmental Health Sciences, National Institutes of Health, 101 T.W. Alexander Drive, Research Triangle Park, NC, 27709, USA. willia56@niehs.nih.gov. ; Program on Emerging Infectious Diseases, DUKE-NUS Graduate Medical School, 8 College Road, Singapore, 169857, Republic of Singapore. niyas@duke-nus.edu.sg. ; Program on Emerging Infectious Diseases, DUKE-NUS Graduate Medical School, 8 College Road, Singapore, 169857, Republic of Singapore. manoj.krishnan@duke-nus.edu.sg. ; Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, National Institutes of Health, 101 T.W. Alexander Drive, Research Triangle Park, NC, 27709, USA. shears@niehs.nih.gov. Y1 - 2015/06/18/ PY - 2015 DA - 2015 Jun 18 SP - 17 VL - 16 KW - Phosphopeptides KW - 0 KW - Recombinant Fusion Proteins KW - Green Fluorescent Proteins KW - 147336-22-9 KW - Phosphotransferases (Phosphate Group Acceptor) KW - EC 2.7.4.- KW - PPIP5K2 protein, human KW - EC 2.7.4.24 KW - Index Medicus KW - Recombinant Fusion Proteins -- biosynthesis KW - Animals KW - Phosphopeptides -- analysis KW - HEK293 Cells KW - Humans KW - Amino Acid Sequence KW - Tandem Mass Spectrometry KW - Recombinant Fusion Proteins -- chemistry KW - Green Fluorescent Proteins -- genetics KW - Microscopy, Fluorescence KW - Sequence Alignment KW - Phosphorylation KW - Recombinant Fusion Proteins -- genetics KW - Molecular Sequence Data KW - Flow Cytometry KW - Green Fluorescent Proteins -- metabolism KW - Amino Acid Substitution KW - Protein Transport KW - Phosphotransferases (Phosphate Group Acceptor) -- chemistry KW - Cell Nucleus -- metabolism KW - Phosphotransferases (Phosphate Group Acceptor) -- metabolism KW - Phosphotransferases (Phosphate Group Acceptor) -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1690213459?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+cell+biology&rft.atitle=Identification+of+a+functional+nuclear+translocation+sequence+in+hPPIP5K2.&rft.au=Yong%2C+Sheila+T%3BNguyen%2C+Hoai-Nghia%3BChoi%2C+Jae+H%3BBortner%2C+Carl+D%3BWilliams%2C+Jason%3BPulloor%2C+Niyas+K%3BKrishnan%2C+Manoj+N%3BShears%2C+Stephen+B&rft.aulast=Yong&rft.aufirst=Sheila&rft.date=2015-06-18&rft.volume=16&rft.issue=&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=BMC+cell+biology&rft.issn=1471-2121&rft_id=info:doi/10.1186%2Fs12860-015-0063-7 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-13 N1 - Date created - 2015-06-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Cell Sci. 1992 Nov;103 ( Pt 3):857-62 [1478975] J Biol Chem. 2004 May 14;279(20):20613-21 [14998990] Science. 2004 Dec 17;306(5704):2101-5 [15604408] J Immunol Methods. 2006 Apr 20;311(1-2):117-29 [16563425] Nat Biotechnol. 2007 Mar;25(3):285-6 [17344875] Science. 2007 Apr 6;316(5821):106-9 [17412958] Science. 2007 Apr 6;316(5821):109-12 [17412959] Proc Natl Acad Sci U S A. 2007 Sep 25;104(39):15305-10 [17873058] J Biol Chem. 2007 Oct 19;282(42):30754-62 [17690096] J Biol Chem. 2007 Oct 19;282(42):30763-75 [17702752] Nat Chem Biol. 2008 Jan;4(1):25-32 [18059263] Chem Biol. 2008 Mar;15(3):274-86 [18355727] J Biol Chem. 2009 Jan 16;284(3):1863-72 [18981179] J Biol Chem. 2009 Apr 17;284(16):10571-82 [19208622] J Cell Physiol. 2009 Jul;220(1):8-15 [19326391] Proc Natl Acad Sci U S A. 2009 Jun 23;106(25):10171-6 [19520826] Mol Pharmacol. 2009 Aug;76(2):236-52 [19439500] Virus Genes. 2010 Jun;40(3):423-31 [20155311] J Biomol Screen. 2010 Aug;15(7):726-34 [20488979] Cell. 2010 Dec 10;143(6):897-910 [21145457] Biochem J. 2011 Mar 15;434(3):415-26 [21222653] Cytometry A. 2011 Jun;79(6):461-9 [21520400] Methods Cell Biol. 2011;102:207-30 [21704840] Biochim Biophys Acta. 2011 Sep;1813(9):1562-77 [20977914] Science. 2011 Nov 11;334(6057):802-5 [22076377] Nat Chem Biol. 2012 Jan;8(1):111-6 [22119861] Science. 2012 Jun 1;336(6085):1178-81 [22555432] RNA. 2012 Aug;18(8):1573-9 [22745225] Cell Rep. 2013 May 30;3(5):1476-82 [23643537] Biochem J. 2013 Aug 1;453(3):413-26 [23682967] Acta Crystallogr D Biol Crystallogr. 2013 Dec;69(Pt 12):2495-505 [24311590] Methods Cell Biol. 2014;122:353-78 [24857738] Traffic. 2014 Jul;15(7):727-48 [24766099] Adv Biol Regul. 2015 Jan;57:203-16 [25453220] Curr Biol. 1999 Nov 18;9(22):1323-6 [10574768] Proc Natl Acad Sci U S A. 2000 Nov 7;97(23):12577-82 [11050185] J Biol Chem. 2001 Oct 19;276(42):39179-85 [11502751] FEBS Lett. 2002 Feb 20;513(1):71-6 [11911883] Cell. 2003 Sep 5;114(5):559-72 [13678580] Mol Cell Biol. 1999 Feb;19(2):1210-7 [9891055] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/s12860-015-0063-7 ER - TY - JOUR T1 - Selectivity and anti-Parkinson's potential of thiadiazolidinone RGS4 inhibitors. AN - 1689843528; 25844489 AB - Many current therapies target G protein coupled receptors (GPCR), transporters, or ion channels. In addition to directly targeting these proteins, disrupting the protein-protein interactions that localize or regulate their function could enhance selectivity and provide unique pharmacologic actions. Regulators of G protein signaling (RGS) proteins, especially RGS4, play significant roles in epilepsy and Parkinson's disease. Thiadiazolidinone (TDZD) inhibitors of RGS4 are nanomolar potency blockers of the biochemical actions of RGS4 in vitro. Here, we demonstrate the substantial selectivity (8- to >5000-fold) of CCG-203769 for RGS4 over other RGS proteins. It is also 300-fold selective for RGS4 over GSK-3β, another target of this class of chemical scaffolds. It does not inhibit the cysteine protease papain at 100 μM. CCG-203769 enhances Gαq-dependent cellular Ca(2+) signaling in an RGS4-dependent manner. TDZD inhibitors also enhance Gαi-dependent δ-OR inhibition of cAMP production in SH-SY-5Y cells, which express endogenous receptors and RGS4. Importantly, CCG-203769 potentiates the known RGS4 mechanism of Gαi-dependent muscarinic bradycardia in vivo. Furthermore, it reverses raclopride-induced akinesia and bradykinesia in mice, a model of some aspects of the movement disorder in Parkinson's disease. A broad assessment of compound effects revealed minimal off-target effects at concentrations necessary for cellular RGS4 inhibition. These results expand our understanding of the mechanism and specificity of TDZD RGS inhibitors and support the potential for therapeutic targeting of RGS proteins in Parkinson's disease and other neural disorders. JF - ACS chemical neuroscience AU - Blazer, Levi L AU - Storaska, Andrew J AU - Jutkiewicz, Emily M AU - Turner, Emma M AU - Calcagno, Mariangela AU - Wade, Susan M AU - Wang, Qin AU - Huang, Xi-Ping AU - Traynor, John R AU - Husbands, Stephen M AU - Morari, Michele AU - Neubig, Richard R AD - †Department of Pharmacology, University of Michigan Medical School, Ann Arbor, Michigan 48109, United States. ; §Department of Pharmacy and Pharmacology, University of Bath, Bath, U.K. ; ∥Section of Pharmacology, Department of Medical Science, University of Ferrara, Ferrara, Italy 44121. ; ⊥National Institute of Mental Health Psychoactive Drug Screening Program (NIMH PDSP), Department of Pharmacology, University of North Carolina, Chapel Hill, North Carolina 27599, United States. ; ‡Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan 48824, United States. Y1 - 2015/06/17/ PY - 2015 DA - 2015 Jun 17 SP - 911 EP - 919 VL - 6 IS - 6 KW - Antiparkinson Agents KW - 0 KW - Cholinergic Agonists KW - RGS Proteins KW - RGS4 protein KW - 175335-35-0 KW - Raclopride KW - 430K3SOZ7G KW - Carbachol KW - 8Y164V895Y KW - Cyclic AMP KW - E0399OZS9N KW - GSK3B protein, human KW - EC 2.7.11.1 KW - Glycogen Synthase Kinase 3 beta KW - Gsk3b protein, mouse KW - Gsk3b protein, rat KW - Glycogen Synthase Kinase 3 KW - EC 2.7.11.26 KW - Papain KW - EC 3.4.22.2 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - protein−protein interaction KW - Regulator of G-protein signaling KW - Parkinson’s disease KW - PPI KW - thiadiazolidinone KW - RGS KW - Animals KW - Bradycardia -- drug therapy KW - Parkinsonian Disorders -- physiopathology KW - Dose-Response Relationship, Drug KW - Humans KW - HEK293 Cells KW - Cholinergic Agonists -- pharmacology KW - Motor Activity -- physiology KW - Cell Line, Tumor KW - Parkinsonian Disorders -- drug therapy KW - Calcium -- metabolism KW - Rats, Sprague-Dawley KW - Papain -- metabolism KW - Bradycardia -- physiopathology KW - Mice, Inbred C57BL KW - Cyclic AMP -- metabolism KW - Motor Activity -- drug effects KW - Glycogen Synthase Kinase 3 -- metabolism KW - Carbachol -- pharmacology KW - Male KW - RGS Proteins -- metabolism KW - Antiparkinson Agents -- pharmacology KW - RGS Proteins -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1689843528?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=ACS+chemical+neuroscience&rft.atitle=Selectivity+and+anti-Parkinson%27s+potential+of+thiadiazolidinone+RGS4+inhibitors.&rft.au=Blazer%2C+Levi+L%3BStoraska%2C+Andrew+J%3BJutkiewicz%2C+Emily+M%3BTurner%2C+Emma+M%3BCalcagno%2C+Mariangela%3BWade%2C+Susan+M%3BWang%2C+Qin%3BHuang%2C+Xi-Ping%3BTraynor%2C+John+R%3BHusbands%2C+Stephen+M%3BMorari%2C+Michele%3BNeubig%2C+Richard+R&rft.aulast=Blazer&rft.aufirst=Levi&rft.date=2015-06-17&rft.volume=6&rft.issue=6&rft.spage=911&rft.isbn=&rft.btitle=&rft.title=ACS+chemical+neuroscience&rft.issn=1948-7193&rft_id=info:doi/10.1021%2Facschemneuro.5b00063 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-15 N1 - Date created - 2015-06-17 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/acschemneuro.5b00063 ER - TY - JOUR T1 - Designing the furin-cleavable linker in recombinant immunotoxins based on Pseudomonas exotoxin A. AN - 1689841205; 25997032 AB - Recombinant immunotoxins (RITs) are fusion proteins that join antibodies to protein toxins for targeted cell killing. RITs armed with Pseudomonas exotoxin A (PE) are undergoing clinical trials for the treatment of cancer. The current design of PE-based RITs joins an antibody fragment to the catalytic domain of PE using a polypeptide linker that is cleaved by the protease furin. Intracellular cleavage of native PE by furin is required for cytotoxicity, yet the PE cleavage site has been shown to be a poor furin substrate. Here we describe the rational design of more efficiently cleaved furin linkers in PE-based RITs, and experiments evaluating their effects on cleavage and cytotoxicity. We found that changes to the furin site could greatly influence both cleavage and cytotoxicity, but the two parameters were not directly correlated. Furthermore, the effects of alterations to the furin linker were not universal. Identical mutations in the anti-CD22 RIT HA22-LR often displayed different cytotoxicity from mutations in the anti-mesothelin RIT SS1-LR/GGS, underscoring the prominent role of the target site in their intoxication pathways. Combining several beneficial mutations in HA22-LR resulted in a variant (HA22-LR/FUR) with a remarkably enhanced cleavage rate and improved cytotoxicity against five B cell lines and similar or enhanced cytotoxicity in five out of six hairy cell leukemia patient samples. This result informs the design of protease-sensitive linkers and suggests that HA22-LR/FUR may be a candidate for further preclinical development. JF - Bioconjugate chemistry AU - Weldon, John E AU - Skarzynski, Martin AU - Therres, Jamy A AU - Ostovitz, Joshua R AU - Zhou, Hong AU - Kreitman, Robert J AU - Pastan, Ira AD - †Department of Biological Sciences, Jess and Mildred Fisher College of Science and Mathematics, Towson University, Towson, Maryland 21252, United States. ; ‡Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, United States. Y1 - 2015/06/17/ PY - 2015 DA - 2015 Jun 17 SP - 1120 EP - 1128 VL - 26 IS - 6 KW - Antineoplastic Agents KW - 0 KW - Bacterial Toxins KW - Exotoxins KW - Immunotoxins KW - Recombinant Fusion Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Furin KW - EC 3.4.21.75 KW - Index Medicus KW - Recombinant Fusion Proteins -- metabolism KW - Leukemia -- drug therapy KW - Cell Survival -- drug effects KW - Models, Molecular KW - Humans KW - Recombinant Fusion Proteins -- pharmacology KW - Cell Line, Tumor KW - Amino Acid Sequence KW - Recombinant Fusion Proteins -- chemistry KW - Exotoxins -- pharmacology KW - Virulence Factors -- chemistry KW - Antineoplastic Agents -- metabolism KW - Bacterial Toxins -- pharmacology KW - Exotoxins -- chemistry KW - Immunotoxins -- metabolism KW - ADP Ribose Transferases -- pharmacology KW - Virulence Factors -- pharmacology KW - Immunotoxins -- chemistry KW - ADP Ribose Transferases -- chemistry KW - Bacterial Toxins -- metabolism KW - Virulence Factors -- metabolism KW - Furin -- metabolism KW - ADP Ribose Transferases -- metabolism KW - Exotoxins -- metabolism KW - Bacterial Toxins -- chemistry KW - Immunotoxins -- pharmacology KW - Antineoplastic Agents -- chemistry KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1689841205?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioconjugate+chemistry&rft.atitle=Designing+the+furin-cleavable+linker+in+recombinant+immunotoxins+based+on+Pseudomonas+exotoxin+A.&rft.au=Weldon%2C+John+E%3BSkarzynski%2C+Martin%3BTherres%2C+Jamy+A%3BOstovitz%2C+Joshua+R%3BZhou%2C+Hong%3BKreitman%2C+Robert+J%3BPastan%2C+Ira&rft.aulast=Weldon&rft.aufirst=John&rft.date=2015-06-17&rft.volume=26&rft.issue=6&rft.spage=1120&rft.isbn=&rft.btitle=&rft.title=Bioconjugate+chemistry&rft.issn=1520-4812&rft_id=info:doi/10.1021%2Facs.bioconjchem.5b00190 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-14 N1 - Date created - 2015-06-17 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/acs.bioconjchem.5b00190 ER - TY - JOUR T1 - Generation and characterization of a SIVmac239 clone corrected at four suboptimal nucleotides. AN - 1689622509; 26076651 AB - SIVmac239 is a commonly used virus in non-human primate models of HIV transmission and pathogenesis. Previous studies identified four suboptimal nucleotides in the SIVmac239 genome, which putatively inhibit its replicative capacity. Since all four suboptimal changes revert to the optimal nucleotide consensus sequence during viral replication in vitro and in vivo, we sought to eliminate the variability of generating these mutations de novo and increase the overall consistency of viral replication by introducing the optimal nucleotides directly to the infectious molecular clone. Using site directed mutagenesis of the full-length/nef-open SIVmac239 clone, we reverted all four nucleotides to the consensus/optimal base to generate SIVmac239Opt and subsequently tested its infectivity and replicative capacity in vitro and in vivo. In primary and cell line cultures, we observed that the optimized virus displayed consistent modest but not statistically significant increases in replicative kinetics compared to wild type. In vivo, SIVmac239Opt replicated to high peak titers with an average of 1.2 × 10(8) viral RNA copies/ml at day 12 following intrarectal challenge, reaching set-point viremia of 1.2 × 10(6) viral RNA copies/ml by day 28. Although the peak and set point viremia means were not statistically different from the original "wild type" SIVmac239, viral load variation at set point was greater for SIVmac239WT compared to SIVmac239Opt (p = 0.0015) demonstrating a greater consistency of the optimized virus. Synonymous mutations were added to the integrase gene of SIVmac239Opt to generate a molecular tag consisting of ten genetically distinguishable viral variants referred to as SIVmac239OptX (Del Prete et al., J Virol. doi: 10.1128/JVI.01026-14 , 2014). Replication dynamics in vitro of these optimized clones were not statistically different from the parental clones. Interestingly, the consistently observed rapid reversion of the primer binding site suboptimal nucleotide is not due to viral RT error but is changed post-integration of a mismatched base via host proofreading mechanisms. Overall, our results demonstrate that SIVmac239Opt is a functional alternative to parental SIVmac239 with marginally faster replication dynamics and with increased replication uniformity providing a more consistent and reproducible infection model in nonhuman primates. JF - Retrovirology AU - Fennessey, Christine M AU - Reid, Carolyn AU - Lipkey, Leslie AU - Newman, Laura AU - Oswald, Kelli AU - Piatak, Michael AU - Roser, James D AU - Chertova, Elena AU - Smedley, Jeremy AU - Gregory Alvord, W AU - Del Prete, Gregory Q AU - Estes, Jacob D AU - Lifson, Jeffrey D AU - Keele, Brandon F AD - Retroviral Evolution Section, AIDS and Cancer Virus Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Building 535, Rm. 408, Frederick, MD, 21702-1201, USA. cmfennessey@gmail.com. ; Retroviral Evolution Section, AIDS and Cancer Virus Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Building 535, Rm. 408, Frederick, MD, 21702-1201, USA. reidcm@mail.nih.gov. ; Retroviral Evolution Section, AIDS and Cancer Virus Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Building 535, Rm. 408, Frederick, MD, 21702-1201, USA. leslie.lipkey@nih.gov. ; Retroviral Evolution Section, AIDS and Cancer Virus Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Building 535, Rm. 408, Frederick, MD, 21702-1201, USA. laura.newman@nih.gov. ; Retroviral Evolution Section, AIDS and Cancer Virus Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Building 535, Rm. 408, Frederick, MD, 21702-1201, USA. oswaldk@mail.nih.gov. ; Retroviral Evolution Section, AIDS and Cancer Virus Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Building 535, Rm. 408, Frederick, MD, 21702-1201, USA. michael.piatak@nih.gov. ; Retroviral Evolution Section, AIDS and Cancer Virus Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Building 535, Rm. 408, Frederick, MD, 21702-1201, USA. roserj@mail.nih.gov. ; Retroviral Evolution Section, AIDS and Cancer Virus Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Building 535, Rm. 408, Frederick, MD, 21702-1201, USA. Elena.Chertova@nih.gov. ; Laboratory Animal Sciences Program, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA. jeremy.smedley@wanprc.org. ; Statistical Consulting, Data Management Services, Leidos Biomedical Research Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA. Greg.Alvord@nih.gov. ; Retroviral Evolution Section, AIDS and Cancer Virus Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Building 535, Rm. 408, Frederick, MD, 21702-1201, USA. gregory.delprete@nih.gov. ; Retroviral Evolution Section, AIDS and Cancer Virus Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Building 535, Rm. 408, Frederick, MD, 21702-1201, USA. estesj@mail.nih.gov. ; Retroviral Evolution Section, AIDS and Cancer Virus Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Building 535, Rm. 408, Frederick, MD, 21702-1201, USA. lifsonj@mail.nih.gov. ; Retroviral Evolution Section, AIDS and Cancer Virus Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Building 535, Rm. 408, Frederick, MD, 21702-1201, USA. keelebf@mail.nih.gov. Y1 - 2015/06/16/ PY - 2015 DA - 2015 Jun 16 SP - 49 VL - 12 KW - Nucleotides KW - 0 KW - Index Medicus KW - Virulence KW - Viral Load KW - Mutagenesis, Site-Directed KW - Animals KW - Cells, Cultured KW - Disease Models, Animal KW - Simian Acquired Immunodeficiency Syndrome -- virology KW - Macaca mulatta KW - Viremia KW - Virus Replication KW - Simian Immunodeficiency Virus -- genetics KW - Simian Immunodeficiency Virus -- physiology KW - Nucleotides -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1689622509?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Retrovirology&rft.atitle=Generation+and+characterization+of+a+SIVmac239+clone+corrected+at+four+suboptimal+nucleotides.&rft.au=Fennessey%2C+Christine+M%3BReid%2C+Carolyn%3BLipkey%2C+Leslie%3BNewman%2C+Laura%3BOswald%2C+Kelli%3BPiatak%2C+Michael%3BRoser%2C+James+D%3BChertova%2C+Elena%3BSmedley%2C+Jeremy%3BGregory+Alvord%2C+W%3BDel+Prete%2C+Gregory+Q%3BEstes%2C+Jacob+D%3BLifson%2C+Jeffrey+D%3BKeele%2C+Brandon+F&rft.aulast=Fennessey&rft.aufirst=Christine&rft.date=2015-06-16&rft.volume=12&rft.issue=&rft.spage=49&rft.isbn=&rft.btitle=&rft.title=Retrovirology&rft.issn=1742-4690&rft_id=info:doi/10.1186%2Fs12977-015-0175-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-24 N1 - Date created - 2015-06-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Adv Pharmacol. 2000;49:437-77 [11013771] J Virol. 2010 Oct;84(19):10406-12 [20686016] J Virol. 2002 Jun;76(11):5803-6 [11992009] Eur J Biochem. 1979 Jun;97(1):305-18 [225173] Nucleic Acids Res. 1983 Apr 11;11(7):2053-64 [6300790] Science. 1988 Nov 25;242(4882):1168-71 [2460924] Cell. 1991 May 17;65(4):651-62 [2032289] J Biol Chem. 1992 Dec 25;267(36):25988-97 [1281479] J Virol. 1993 Jun;67(6):3246-53 [8497049] J Virol. 1995 May;69(5):3090-7 [7707537] J Gen Virol. 1997 Apr;78 ( Pt 4):837-40 [9129656] J Med Primatol. 2005 Oct;34(5-6):303-12 [16128925] J Virol. 2007 Aug;81(16):8827-32 [17537848] Virology. 2008 May 25;375(1):148-58 [18304600] PLoS One. 2011;6(2):e16714 [21415914] J Virol. 2001 Apr;75(8):4019-22 [11264395] Proc Natl Acad Sci U S A. 2008 May 27;105(21):7552-7 [18490657] Virology. 2013 Feb 5;436(1):33-48 [23123038] J Virol. 2013 Mar;87(6):3538-48 [23325681] Curr Opin HIV AIDS. 2013 Jul;8(4):280-7 [23666391] J Virol. 2014 Jul;88(14):8077-90 [24807714] PLoS Pathog. 2009 Jan;5(1):e1000274 [19165325] J Virol. 2009 Apr;83(8):3556-67 [19193811] J Exp Med. 2009 May 11;206(5):1117-34 [19414559] J Exp Med. 2009 Jun 8;206(6):1273-89 [19487424] PLoS Pathog. 2010 May;6(5):e1000890 [20485520] J Virol. 2010 Jul;84(14):7083-95 [20463069] AIDS Res Hum Retroviruses. 2011 Dec;27(12):1259-69 [21732792] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/s12977-015-0175-3 ER - TY - JOUR T1 - Radiation Enhancement of Head and Neck Squamous Cell Carcinoma by the Dual PI3K/mTOR Inhibitor PF-05212384 AN - 1808631114; PQ0003441821 AB - Purpose: Radiation remains a mainstay for the treatment of nonmetastatic head and neck squamous cell carcinoma (HNSCC), a malignancy characterized by a high rate of PI3K/mTOR signaling axis activation. We investigated the ATP-competitive dual PI3K/mTOR inhibitor, PF-05212384, as a radiosensitizer in preclinical HNSCC models.Experimental Design: Extent of radiation enhancement of two HNSCC cell lines (UMSCC1-wtP53 and UMSCC46-mtP53) and normal human fibroblast (1522) was assessed by in vitro clonogenic assay with appropriate target inhibition verified by immunoblotting. Radiation-induced DNA damage repair was evaluated by gamma H2AX Western blots with the mechanism of DNA double-strand break repair abrogation investigated by cell cycle analysis, immunoblotting, and RT-PCR. PF-05212384 efficacy in vivo was assessed by UMSCC1 xenograft tumor regrowth delay, xenograft lysate immunoblotting, and tissue section immunohistochemistry.Results: PF-05212384 effectively inhibited PI3K and mTOR, resulting in significant radiosensitization of exponentially growing and plateau-phase cells with 24-hour treatment following irradiation, and variable radiation enhancement with 24-hour treatment before irradiation. Tumor cells radiosensitized to a greater extent than normal human fibroblasts. Postirradiation PF-05212384 treatment delays gamma H2AX foci resolution. PF-05212384 24-hour exposure resulted in an evident G1-S phase block in p53-competent cells. Fractionated radiation plus i.v. PF-05212384 synergistically delayed nude mice bearing UMSCC1 xenograft regrowth, with potential drug efficacy biomarkers identified, including pS6, pAkt, p4EBP1, and Ki67.Conclusions: Taken together, our results of significant radiosensitization both in vitro and in vivo validate the PI3K/mTOR axis as a radiation modification target and PF-05212384 as a potential clinical radiation modifier of nonmetastatic HNSCC. Clin Cancer Res; 21(12); 2792-801. copyright 2015 AACR. JF - Clinical Cancer Research AU - Leiker, Andrew J AU - DeGraff, William AU - Choudhuri, Rajani AU - Sowers, Anastasia L AU - Thetford, Angela AU - Cook, John A AU - Van Waes, Carter AU - Mitchell, James B AD - Medical Research Scholars Program, NIH, Bethesda, Maryland, jbm@helix.nih.gov Y1 - 2015/06/15/ PY - 2015 DA - 2015 Jun 15 SP - 2792 EP - 2801 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 12 SN - 1078-0432, 1078-0432 KW - Biotechnology and Bioengineering Abstracts KW - Western blotting KW - Immunoblotting KW - alpha Radiation KW - Cell cycle KW - Radiosensitization KW - squamous cell carcinoma KW - Tumors KW - DNA repair KW - Tumor cells KW - biomarkers KW - Fibroblasts KW - DNA damage KW - 1-Phosphatidylinositol 3-kinase KW - Radiosensitizers KW - Radiation KW - Head and neck cancer KW - Polymerase chain reaction KW - Xenografts KW - TOR protein KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808631114?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Cancer+Research&rft.atitle=Radiation+Enhancement+of+Head+and+Neck+Squamous+Cell+Carcinoma+by+the+Dual+PI3K%2FmTOR+Inhibitor+PF-05212384&rft.au=Leiker%2C+Andrew+J%3BDeGraff%2C+William%3BChoudhuri%2C+Rajani%3BSowers%2C+Anastasia+L%3BThetford%2C+Angela%3BCook%2C+John+A%3BVan+Waes%2C+Carter%3BMitchell%2C+James+B&rft.aulast=Leiker&rft.aufirst=Andrew&rft.date=2015-06-15&rft.volume=21&rft.issue=12&rft.spage=2792&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-3279 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Immunoblotting; Western blotting; alpha Radiation; Cell cycle; squamous cell carcinoma; Radiosensitization; Tumors; DNA repair; biomarkers; Tumor cells; Fibroblasts; DNA damage; Radiosensitizers; 1-Phosphatidylinositol 3-kinase; Radiation; Polymerase chain reaction; Head and neck cancer; Xenografts; TOR protein DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-3279 ER - TY - JOUR T1 - Comparison of Interviewer-Administered and Automated Self-Administered 24-Hour Dietary Recalls in 3 Diverse Integrated Health Systems AN - 1701474576; PQ0001732756 AB - Twenty-four-hour dietary recalls provide high-quality intake data but have been prohibitively expensive for large epidemiologic studies. This study's goal was to assess whether the web-based Automated Self-Administered 24-Hour Recall (ASA24) performs similarly enough to the standard interviewer-administered, Automated Multiple-Pass Method (AMPM) 24-hour dietary recall to be considered a viable alternative. In 2010-2011, 1,081 adults from 3 integrated health systems in Detroit, Michigan; Marshfield, Wisconsin; and Kaiser-Permanente Northern California participated in a field trial. A quota design ensured a diverse sample by sex, age, and race/ethnicity. Each participant was asked to complete 2 recalls and was randomly assigned to 1 of 4 protocols differing by type of recall and administration order. For energy, the mean intakes were 2,425 versus 2,374 kcal for men and 1,876 versus 1,906 kcal for women by AMPM and ASA24, respectively. Of 20 nutrients/food groups analyzed and controlling for false discovery rate, 87% were judged equivalent at the 20% bound. ASA24 was preferred over AMPM by 70% of the respondents. Attrition was lower in the ASA24/AMPM study group than in the AMPM/ASA24 group, and it was lower in the ASA24/ASA24 group than in the AMPM/AMPM group. ASA24 offers the potential to collect high-quality dietary intake information at low cost with less attrition. JF - American Journal of Epidemiology AU - Thompson, Frances E AU - Dixit-Joshi, Sujata AU - Potischman, Nancy AU - Dodd, Kevin W AU - Kirkpatrick, Sharon I AU - Kushi, Lawrence H AU - Alexander, Gwen L AU - Coleman, Laura A AU - Zimmerman, Thea P AU - Sundaram, Maria E AU - Clancy, Heather A AU - Groesbeck, Michelle AU - Douglass, Deirdre AU - George, Stephanie M AU - Schap, TusaRebecca E AU - Subar, Amy F AD - Correspondence to Dr. Frances E. Thompson, Division of Cancer Control and Population Sciences, National Cancer Institute, Room 4E120, 9609 Medical Center Drive, MSC 9762, Bethesda, MD 20892-9762, thompsof@mail.nih.gov Y1 - 2015/06/15/ PY - 2015 DA - 2015 Jun 15 SP - 970 EP - 978 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 181 IS - 12 SN - 0002-9262, 0002-9262 KW - Health & Safety Science Abstracts KW - comparative study KW - diet survey KW - experimental design KW - nutritional assessment KW - population KW - Diets KW - Age KW - USA, Michigan, Detroit KW - Attrition KW - INE, USA, California KW - Energy KW - USA, Wisconsin KW - Ingestion KW - Ethnic groups KW - H 12000:Epidemiology and Public Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701474576?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Comparison+of+Interviewer-Administered+and+Automated+Self-Administered+24-Hour+Dietary+Recalls+in+3+Diverse+Integrated+Health+Systems&rft.au=Thompson%2C+Frances+E%3BDixit-Joshi%2C+Sujata%3BPotischman%2C+Nancy%3BDodd%2C+Kevin+W%3BKirkpatrick%2C+Sharon+I%3BKushi%2C+Lawrence+H%3BAlexander%2C+Gwen+L%3BColeman%2C+Laura+A%3BZimmerman%2C+Thea+P%3BSundaram%2C+Maria+E%3BClancy%2C+Heather+A%3BGroesbeck%2C+Michelle%3BDouglass%2C+Deirdre%3BGeorge%2C+Stephanie+M%3BSchap%2C+TusaRebecca+E%3BSubar%2C+Amy+F&rft.aulast=Thompson&rft.aufirst=Frances&rft.date=2015-06-15&rft.volume=181&rft.issue=12&rft.spage=970&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwu467 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2015-09-03 N1 - SubjectsTermNotLitGenreText - Diets; Age; Attrition; Energy; Ingestion; Ethnic groups; USA, Michigan, Detroit; INE, USA, California; USA, Wisconsin DO - http://dx.doi.org/10.1093/aje/kwu467 ER - TY - JOUR T1 - An indoxyl compound 5-bromo-4-chloro-3-indolyl 1,3-diacetate, CAC-0982, suppresses activation of Fyn kinase in mast cells and IgE-mediated allergic responses in mice. AN - 1681916004; 25902337 AB - Mast cells, constituents of virtually all organs and tissues, are critical cells in IgE-mediated allergic responses. The aim of this study was to investigate the effect and mechanism of an indoxyl chromogenic compound, 5-bromo-4-chloro-3-indolyl 1,3-diacetate, CAC-0982, on IgE-mediated mast cell activation and allergic responses in mice. CAC-0982 reversibly suppressed antigen-stimulated degranulation in murine mast cells (IC50, ~3.8μM) and human mast cells (IC50, ~3.0μM). CAC-0982 also inhibited the expression and secretion of IL-4 and TNF-α in mast cells. Furthermore, CAC-0982 suppressed the mast cell-mediated allergic responses in mice in a dose-dependent manner (ED50 27.9mg/kg). As for the mechanism, CAC-0982 largely suppressed the phosphorylation of Syk and its downstream signaling molecules, including LAT, Akt, Erk1/2, p38, and JNK. Notably, the tyrosine kinase assay of antigen-stimulated mast cells showed that CAC-0982 inhibited Fyn kinase, one of the upstream tyrosine kinases for Syk activation in mast cells. Taken together, these results suggest that CAC-0982 may be used as a new treatment for regulating IgE-mediated allergic diseases through the inhibition of the Fyn/Syk pathway in mast cells. Copyright © 2015 Elsevier Inc. All rights reserved. JF - Toxicology and applied pharmacology AU - Lee, Jun Ho AU - Kim, Tae Hyung AU - Kim, Hyuk Soon AU - Kim, A-Ram AU - Kim, Do-Kyun AU - Nam, Seung Taek AU - Kim, Hyun Woo AU - Park, Young Hwan AU - Her, Erk AU - Park, Yeong Min AU - Kim, Hyung Sik AU - Kim, Young Mi AU - Choi, Wahn Soo AD - Department of Immunology, School of Medicine, Konkuk University, Chungju 380-701, Republic of Korea; College of Medicine, Korea University, Seoul 136-701, Republic of Korea. ; College of Pharmacy, Sungkyunkwan University, Suwon 440-746, Republic of Korea. ; Department of Immunology, School of Medicine, Konkuk University, Chungju 380-701, Republic of Korea. ; Department of Immunology, School of Medicine, Konkuk University, Chungju 380-701, Republic of Korea; Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. ; College of Pharmacy, Duksung Women's University, Seoul 132-714, Republic of Korea. ; Department of Immunology, School of Medicine, Konkuk University, Chungju 380-701, Republic of Korea. Electronic address: wahnchoi@kku.ac.kr. Y1 - 2015/06/15/ PY - 2015 DA - 2015 Jun 15 SP - 179 EP - 186 VL - 285 IS - 3 KW - CAC-0982 KW - 0 KW - Indoles KW - Intracellular Signaling Peptides and Proteins KW - Tumor Necrosis Factor-alpha KW - Interleukin-4 KW - 207137-56-2 KW - Immunoglobulin E KW - 37341-29-0 KW - indoxyl KW - 480-93-3 KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Proto-Oncogene Proteins c-fyn KW - EC 2.7.10.2 KW - SYK protein, human KW - Syk Kinase KW - Syk protein, mouse KW - Index Medicus KW - Syk kinase KW - Allergy KW - 5-Bromo-4-chloro-3-indolyl 1,3-diacetate CAC-0982 KW - Mast cells KW - Fyn kinase KW - Hypersensitivity -- drug therapy KW - Hypersensitivity -- immunology KW - Animals KW - Interleukin-4 -- metabolism KW - Intracellular Signaling Peptides and Proteins -- metabolism KW - Phosphorylation KW - Humans KW - Mice KW - Protein-Tyrosine Kinases -- metabolism KW - Tumor Necrosis Factor-alpha -- metabolism KW - Signal Transduction KW - Proto-Oncogene Proteins c-fyn -- metabolism KW - Immunoglobulin E -- immunology KW - Indoles -- pharmacology KW - Mast Cells -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1681916004?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=An+indoxyl+compound+5-bromo-4-chloro-3-indolyl+1%2C3-diacetate%2C+CAC-0982%2C+suppresses+activation+of+Fyn+kinase+in+mast+cells+and+IgE-mediated+allergic+responses+in+mice.&rft.au=Lee%2C+Jun+Ho%3BKim%2C+Tae+Hyung%3BKim%2C+Hyuk+Soon%3BKim%2C+A-Ram%3BKim%2C+Do-Kyun%3BNam%2C+Seung+Taek%3BKim%2C+Hyun+Woo%3BPark%2C+Young+Hwan%3BHer%2C+Erk%3BPark%2C+Yeong+Min%3BKim%2C+Hyung+Sik%3BKim%2C+Young+Mi%3BChoi%2C+Wahn+Soo&rft.aulast=Lee&rft.aufirst=Jun&rft.date=2015-06-15&rft.volume=285&rft.issue=3&rft.spage=179&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2015.04.009 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-28 N1 - Date created - 2015-05-18 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.taap.2015.04.009 ER - TY - JOUR T1 - Sensitive detection of active Shiga toxin using low cost CCD based optical detector. AN - 1660413065; 25677808 AB - To reduce the sources and incidence of food-borne illness there is a need to develop affordable, sensitive devices for detection of active toxins, such as Shiga toxin type 2 (Stx2). Currently the widely used methods for measuring Shiga toxin are immunoassay that cannot distinguish between the active form of the toxin, which poses a threat to life, to the inactive form which can bind to antibodies but show no toxicity. In this work, we determine toxin activity based on Shiga toxin inhibition of green fluorescent protein (GFP) combined with low cost charge-coupled device (CCD) fluorescence detection, which is more clinically relevant than immunoassay. For assay detection, a simple low cost fluorescence detection system was constructed using a CCD camera and light emitting diode (LED) excitation source, to measure GFP expression. The system was evaluated and compared to a commercial fluorometer using photomultiplier detection for detecting active Stx2 in the range 100 ng/mL-0.01 pg/mL. The result shows that there is a negative linear relationship between Stx2 concentrations and luminous intensity of GFP, imaged by the CCD camera (R(2)=0.85) or fluorometer (R(2)=0.86). The low cost (∼$300) CCD camera is capable of detecting Shiga toxin activity at comparable levels as a more expensive (∼$30,000) fluorometer. These results demonstrate the utility and the potential of low cost detectors for toxin activity; this approach may increase the availability of foodborne bacterial toxin diagnostics in regions where there are limited resources and could be readily adapted to the detection of other food-borne toxins. Published by Elsevier B.V. JF - Biosensors & bioelectronics AU - Rasooly, Reuven AU - Balsam, Josh AU - Hernlem, Bradley J AU - Rasooly, Avraham AD - Western Regional Research Center, Agricultural Research Service, U.S. Department of Agriculture, Albany, CA, United States. Electronic address: reuven.rasooly@ars.usda.gov. ; Division of Biology, Office of Science and Engineering, FDA, Silver Spring, MD 20993, United States; University of Maryland, College Park, MD 20742, United States. ; Western Regional Research Center, Agricultural Research Service, U.S. Department of Agriculture, Albany, CA, United States. ; Division of Biology, Office of Science and Engineering, FDA, Silver Spring, MD 20993, United States; Office of Cancer Complementary and Alternative Medicine, National Cancer Institute, Rockville, MD 20850, United States. Y1 - 2015/06/15/ PY - 2015 DA - 2015 Jun 15 SP - 705 EP - 711 VL - 68 KW - Shiga Toxin 2 KW - 0 KW - Green Fluorescent Proteins KW - 147336-22-9 KW - Index Medicus KW - Food KW - Adenovirus KW - CCD camera KW - Shiga toxin KW - Humans KW - Food Analysis KW - Shiga Toxin 2 -- isolation & purification KW - Biosensing Techniques UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660413065?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biosensors+%26+bioelectronics&rft.atitle=Sensitive+detection+of+active+Shiga+toxin+using+low+cost+CCD+based+optical+detector.&rft.au=Rasooly%2C+Reuven%3BBalsam%2C+Josh%3BHernlem%2C+Bradley+J%3BRasooly%2C+Avraham&rft.aulast=Rasooly&rft.aufirst=Reuven&rft.date=2015-06-15&rft.volume=68&rft.issue=&rft.spage=705&rft.isbn=&rft.btitle=&rft.title=Biosensors+%26+bioelectronics&rft.issn=1873-4235&rft_id=info:doi/10.1016%2Fj.bios.2015.01.065 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-25 N1 - Date created - 2015-03-02 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bios.2015.01.065 ER - TY - JOUR T1 - Quantitative mass spectrometry measurements reveal stoichiometry of principal postsynaptic density proteins. AN - 1686421294; 25874902 AB - Quantitative studies are presented of postsynaptic density (PSD) fractions from rat cerebral cortex with the ultimate goal of defining the average copy numbers of proteins in the PSD complex. Highly specific and selective isotope dilution mass spectrometry assays were developed using isotopically labeled polypeptide concatemer internal standards. Interpretation of PSD protein stoichiometry was achieved as a molar ratio with respect to PSD-95 (SAP-90, DLG4), and subsequently, copy numbers were estimated using a consensus literature value for PSD-95. Average copy numbers for several proteins at the PSD were estimated for the first time, including those for AIDA-1, BRAGs, and densin. Major findings include evidence for the high copy number of AIDA-1 in the PSD (144 ± 30)-equivalent to that of the total GKAP family of proteins (150 ± 27)-suggesting that AIDA-1 is an element of the PSD scaffold. The average copy numbers for NMDA receptor sub-units were estimated to be 66 ± 18, 27 ± 9, and 45 ± 15, respectively, for GluN1, GluN2A, and GluN2B, yielding a total of 34 ± 10 NMDA channels. Estimated average copy numbers for AMPA channels and their auxiliary sub-units TARPs were 68 ± 36 and 144 ± 38, respectively, with a stoichiometry of ∼1:2, supporting the assertion that most AMPA receptors anchor to the PSD via TARP sub-units. This robust, quantitative analysis of PSD proteins improves upon and extends the list of major PSD components with assigned average copy numbers in the ongoing effort to unravel the complex molecular architecture of the PSD. JF - Journal of proteome research AU - Lowenthal, Mark S AU - Markey, Sanford P AU - Dosemeci, Ayse AD - †Biomolecular Measurement Division, National Institute of Standards and Technology, Gaithersburg, Maryland 20899, United States. ; §Laboratory of Neurobiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892, United States. Y1 - 2015/06/05/ PY - 2015 DA - 2015 Jun 05 SP - 2528 EP - 2538 VL - 14 IS - 6 KW - Nerve Tissue Proteins KW - 0 KW - Index Medicus KW - protein stoichiometry KW - postsynaptic density KW - multiple reaction monitoring KW - copy numbers KW - Rats KW - Animals KW - Nerve Tissue Proteins -- metabolism KW - Mass Spectrometry -- methods KW - Synapses -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1686421294?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+proteome+research&rft.atitle=Quantitative+mass+spectrometry+measurements+reveal+stoichiometry+of+principal+postsynaptic+density+proteins.&rft.au=Lowenthal%2C+Mark+S%3BMarkey%2C+Sanford+P%3BDosemeci%2C+Ayse&rft.aulast=Lowenthal&rft.aufirst=Mark&rft.date=2015-06-05&rft.volume=14&rft.issue=6&rft.spage=2528&rft.isbn=&rft.btitle=&rft.title=Journal+of+proteome+research&rft.issn=1535-3907&rft_id=info:doi/10.1021%2Facs.jproteome.5b00109 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-15 N1 - Date created - 2015-06-05 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/acs.jproteome.5b00109 ER - TY - JOUR T1 - Simultaneous determination of 40 novel psychoactive stimulants in urine by liquid chromatography-high resolution mass spectrometry and library matching. AN - 1680189431; 25931378 AB - The emergence of novel psychoactive substances is an ongoing challenge for analytical toxicologists. Different analogs are continuously introduced in the market to circumvent legislation and to enhance their pharmacological activity. Although detection of drugs in blood indicates recent exposure and link intoxication to the causative agent, urine is still the most preferred testing matrix in clinical and forensic settings. We developed a method for the simultaneous quantification of 8 piperazines, 4 designer amphetamines and 28 synthetic cathinones and 4 metabolites, in urine by liquid chromatography coupled to high-resolution mass spectrometry (LC-HRMS). Data were acquired in full scan and data dependent MS(2) mode. Compounds were quantified by precursor ion exact mass, and confirmed by product ion spectra library matching, taking into account product ions' exact mass and intensities. One-hundred μL urine was subjected to solid phase cation exchange extraction (SOLA SCX). The chromatographic reverse-phase separation was achieved with gradient mobile phase of 0.1% formic acid in water and in acetonitrile in 20 min. The assay was linear from 2.5 or 5 to 500 μg/L. Imprecision (n=15) was <15.4%, and accuracy (n=15) 84.2-118.5%. Extraction efficiency was 51.2-111.2%, process efficiency 57.7-104.9% and matrix effect ranged from -41.9% to 238.5% (CV<23.3%, except MDBZP CV<34%). Authentic urine specimens (n=62) were analyzed with the method that provides a comprehensive confirmation for 40 new stimulant drugs with specificity and sensitivity. Published by Elsevier B.V. JF - Journal of chromatography. A AU - Concheiro, Marta AU - Castaneto, Marisol AU - Kronstrand, Robert AU - Huestis, Marilyn A AD - Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA; Currently Department of Sciences, John Jay College of Criminal Justice, City University of New York, New York, NY, USA. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA; Program in Toxicology, University of Maryland Baltimore, Baltimore, MD, USA. ; Department of Forensic Genetics and Forensic Toxicology, National Board of Forensic Medicine, Linköping, Sweden; Division of Drug Research, Department of Medical and Health Sciences, Linköping University, Linköping, Sweden. ; Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA. Electronic address: mhuestis@intra.nida.nih.gov. Y1 - 2015/06/05/ PY - 2015 DA - 2015 Jun 05 SP - 32 EP - 42 VL - 1397 KW - Amphetamines KW - 0 KW - Central Nervous System Stimulants KW - Index Medicus KW - Synthetic cathinones KW - Piperazines KW - Urine KW - LC–HRMS KW - Novel psychoactive substance KW - Reproducibility of Results KW - Humans KW - Central Nervous System Stimulants -- urine KW - Amphetamines -- urine KW - Limit of Detection KW - Urinalysis -- methods KW - Mass Spectrometry KW - Chromatography, Liquid KW - Substance Abuse Detection -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680189431?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+chromatography.+A&rft.atitle=Simultaneous+determination+of+40+novel+psychoactive+stimulants+in+urine+by+liquid+chromatography-high+resolution+mass+spectrometry+and+library+matching.&rft.au=Concheiro%2C+Marta%3BCastaneto%2C+Marisol%3BKronstrand%2C+Robert%3BHuestis%2C+Marilyn+A&rft.aulast=Concheiro&rft.aufirst=Marta&rft.date=2015-06-05&rft.volume=1397&rft.issue=&rft.spage=32&rft.isbn=&rft.btitle=&rft.title=Journal+of+chromatography.+A&rft.issn=1873-3778&rft_id=info:doi/10.1016%2Fj.chroma.2015.04.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-30 N1 - Date created - 2015-05-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Anal Toxicol. 2013 Sep;37(7):452-74 [23934984] Drug Test Anal. 2011 Jul-Aug;3(7-8):496-504 [21744513] J Chromatogr B Analyt Technol Biomed Life Sci. 2013 Jul 1;930:112-20 [23727875] J Addict Med. 2013 May-Jun;7(3):153-62 [23732954] J Anal Toxicol. 2013 Mar;37(2):64-73 [23316030] J Anal Toxicol. 2013 Jan-Feb;37(1):43-6 [23111916] J Med Toxicol. 2012 Mar;8(1):33-42 [22108839] J Chromatogr A. 2012 Jan 27;1222:116-20 [22209305] Drug Metab Dispos. 1998 Jun;26(6):572-5 [9616194] J Anal Toxicol. 2010 Nov;34(9):594-8 [21073814] J Anal Toxicol. 2008 Mar;32(2):172-7 [18334102] Anal Bioanal Chem. 2010 Apr;396(7):2403-14 [20069283] Anal Bioanal Chem. 2015 Jan;407(3):883-97 [25224637] J Chromatogr B Analyt Technol Biomed Life Sci. 2014 Oct 15;969:272-84 [25203724] J Chromatogr A. 2014 Sep 19;1360:119-27 [25108769] J Med Toxicol. 2014 Sep;10(3):299-302 [24706157] Anal Bioanal Chem. 2014 Jul;406(18):4425-41 [24828977] Anal Bioanal Chem. 2013 Nov;405(29):9437-48 [24196122] J Anal Toxicol. 2013 Oct;37(8):542-6 [23839071] J Chromatogr A. 2013 Aug 9;1302:95-104 [23838299] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.chroma.2015.04.002 ER - TY - JOUR T1 - WEE1 murine deficiency induces hyper-activation of APC/C and results in genomic instability and carcinogenesis. AN - 1686410801; 25088202 AB - The tyrosine kinase WEE1 controls the timing of entry into mitosis in eukaryotes and its genetic deletion leads to pre-implantation lethality in mice. Here, we show that besides the premature mitotic entry phenotype, Wee1 mutant murine cells fail to complete mitosis properly and exhibit several additional defects that contribute to the deregulation of mitosis, allowing mutant cells to progress through mitosis at the expense of genomic integrity. WEE1 interacts with the anaphase promoting complex, functioning as a negative regulator, and the deletion of Wee1 results in hyper-activation of this complex. Mammary specific knockout mice overcome the DNA damage response pathway triggered by the mis-coordination of the cell cycle in mammary epithelial cells and heterozygote mice spontaneously develop mammary tumors. Thus, WEE1 functions as a haploinsufficient tumor suppressor that coordinates distinct cell division events to allow correct segregation of genetic information into daughter cells and maintain genome integrity. JF - Oncogene AU - Vassilopoulos, A AU - Tominaga, Y AU - Kim, H-Seok AU - Lahusen, T AU - Li, B AU - Yu, H AU - Gius, D AU - Deng, C-X AD - 1] Genetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA [2] Department of Radiation Oncology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. ; Genetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA. ; 1] Genetics of Development and Disease Branch, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA [2] Department of Life Science, Ewha Womans University, Seoul, South Korea. ; Department of Pharmacology, Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA. ; Department of Radiation Oncology, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. Y1 - 2015/06/04/ PY - 2015 DA - 2015 Jun 04 SP - 3023 EP - 3035 VL - 34 IS - 23 KW - Cell Cycle Proteins KW - 0 KW - Nuclear Proteins KW - Tamoxifen KW - 094ZI81Y45 KW - Anaphase-Promoting Complex-Cyclosome KW - EC 2.3.2.27 KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Wee1 protein, mouse KW - EC 2.7.10.2 KW - Index Medicus KW - Animals KW - Genomic Instability KW - Epithelial Cells -- pathology KW - Mitosis KW - Mice KW - Female KW - Mice, Knockout KW - Gene Deletion KW - Protein-Tyrosine Kinases -- genetics KW - Nuclear Proteins -- genetics KW - Mammary Glands, Animal -- cytology KW - Cell Cycle Proteins -- genetics KW - Mammary Glands, Animal -- pathology KW - Anaphase-Promoting Complex-Cyclosome -- metabolism KW - Protein-Tyrosine Kinases -- metabolism KW - Nuclear Proteins -- metabolism KW - Cell Transformation, Neoplastic -- genetics KW - Cell Cycle Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1686410801?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=WEE1+murine+deficiency+induces+hyper-activation+of+APC%2FC+and+results+in+genomic+instability+and+carcinogenesis.&rft.au=Vassilopoulos%2C+A%3BTominaga%2C+Y%3BKim%2C+H-Seok%3BLahusen%2C+T%3BLi%2C+B%3BYu%2C+H%3BGius%2C+D%3BDeng%2C+C-X&rft.aulast=Vassilopoulos&rft.aufirst=A&rft.date=2015-06-04&rft.volume=34&rft.issue=23&rft.spage=3023&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2014.239 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-07 N1 - Date created - 2015-06-04 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/onc.2014.239 ER - TY - JOUR T1 - Carfilzomib is an effective anticancer agent in anaplastic thyroid cancer AN - 1859483987; PQ0002561304 AB - Anaplastic thyroid cancer (ATC) is one of the most aggressive human malignancies. Currently, there is no standard or effective therapy for ATC. Drug repurposing for cancer treatment is an emerging approach for identifying compounds that may have antineoplastic effects. The aim of this study was to use high-throughput drug library screening to identify and subsequently validate novel therapeutic agents with anticancer effects in ATC. We performed quantitative high-throughput screening (qHTS) in ATC cell lines (SW-1736, 8505C, and C-643), using a compound library of 3282 drugs. qHTS identified 100 compounds that were active in all three ATC cell lines. Proteasome inhibitors were one of the most active drug categories according to enrichment analysis. Of the three proteasome inhibitors screened, a second-generation proteasome inhibitor, carfilzomib, was the most active. Treatment of ATC cells with carfilzomib significantly inhibited cellular proliferation and induced G2/M cell cycle arrest and caspase-dependent apoptosis. Mechanistically, carfilzomib increased expression of p27 (CDKN1 B) and decreased expression of the anti-apoptotic protein ATF4. Pretreatment with carfilzomib reduced in vivo metastases (lung, bone, liver, and kidney) and disease progression, and decreased N-cadherin expression. Carfilzomib treatment of mice with established, widely metastatic disease significantly increased their survival, without significant toxicity. Our findings support the use or clinical study of carfilzomib as a therapeutic option in patients with advanced and metastatic ATC. JF - Endocrine-Related Cancer AU - Mehta, Amit AU - Zhang, Lisa AU - Boufraqech, Myriem AU - Zhang, Yaqin AU - Patel, Dhaval AU - Shen, Min AU - Kebebew, Electron AD - Endocrine Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA, kebebewe@mail.nih.gov Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 319 EP - 329 PB - BioScientifica Ltd., Euro House, 22 Apex Ct, Woodlands Bristol, BS32 4JT United Kingdom VL - 22 IS - 3 SN - 1351-0088, 1351-0088 KW - Biotechnology and Bioengineering Abstracts KW - anaplastic thyroid cancer KW - high-throughput screening KW - carfilzomib KW - proteasome inhibitor UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1859483987?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrine-Related+Cancer&rft.atitle=Carfilzomib+is+an+effective+anticancer+agent+in+anaplastic+thyroid+cancer&rft.au=Mehta%2C+Amit%3BZhang%2C+Lisa%3BBoufraqech%2C+Myriem%3BZhang%2C+Yaqin%3BPatel%2C+Dhaval%3BShen%2C+Min%3BKebebew%2C+Electron&rft.aulast=Mehta&rft.aufirst=Amit&rft.date=2015-06-01&rft.volume=22&rft.issue=3&rft.spage=319&rft.isbn=&rft.btitle=&rft.title=Endocrine-Related+Cancer&rft.issn=13510088&rft_id=info:doi/10.1530%2FERC-14-0510 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2017-01-01 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1530/ERC-14-0510 ER - TY - JOUR T1 - Evidence for changes in beta- and gamma-actin proportions during inner ear hair cell life AN - 1827923398; PQ0001865411 AB - Cytoplasmic actin isoforms beta ( beta -) and gamma ( gamma -) perform crucial physiological roles in inner ear hair cells (HC). The stereocilium, which is structured by parallel actin filaments composed of both isoforms, is the responsive organelle to mechanical stimuli such as sound, gravity and head movements. Modifications in isoform proportions affect the function of the stereocilia as previously shown in genetic studies of mutant mice. Here, immunogold labeling TEM studies in mice showed that both beta - and gamma -actin isoforms colocalize throughout stereocilia actin filaments, adherens junctions and cuticular plates as early as embryonic stage 16.5. Gold-particle quantification indicated that there was 40% more gamma - actin than beta -actin at E16.5. In contrast, beta - and gamma -actin were equally concentrated in adult stereocilia of cochlear and vestibular HC. Interestingly, all actin-based structures presented almost five-fold more beta -actin than gamma -actin in 22 month- old mice, suggesting that gamma -actin is probably under-expressed during the aging process. These data provide evidence of dynamic modifications of the actin isoforms in stereocilia, cuticular plates and cell junctions during the whole HC life. JF - Cytoskeleton AU - Andrade, Leonardo R AD - Laboratory of Cell Structure and Dynamics, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 282 EP - 291 PB - Wiley-Blackwell, Baffins Lane Chichester W. Sussex PO19 1UD United Kingdom VL - 72 IS - 6 SN - 1949-3584, 1949-3584 KW - Biotechnology and Bioengineering Abstracts KW - Cochlea KW - Data processing KW - adherens junctions KW - Head KW - Gravity KW - Aging KW - Mechanical stimuli KW - Cytoskeleton KW - Hair cells KW - Vestibular system KW - Sound KW - Cell junctions KW - Embryos KW - Actin KW - Organelles KW - Filaments KW - Inner ear KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1827923398?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cytoskeleton&rft.atitle=Evidence+for+changes+in+beta-+and+gamma-actin+proportions+during+inner+ear+hair+cell+life&rft.au=Andrade%2C+Leonardo+R&rft.aulast=Andrade&rft.aufirst=Leonardo&rft.date=2015-06-01&rft.volume=72&rft.issue=6&rft.spage=282&rft.isbn=&rft.btitle=&rft.title=Cytoskeleton&rft.issn=19493584&rft_id=info:doi/10.1002%2Fcm.21227 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-10-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Cochlea; Data processing; Head; adherens junctions; Gravity; Aging; Mechanical stimuli; Cytoskeleton; Hair cells; Vestibular system; Sound; Cell junctions; Actin; Embryos; Organelles; Inner ear; Filaments DO - http://dx.doi.org/10.1002/cm.21227 ER - TY - JOUR T1 - Controlled Cannabis Vaporizer Administration: Blood and Plasma Cannabinoids with and without Alcohol AN - 1811909780; PQ0003434285 AB - BACKGROUND:Increased medical and legal cannabis intake is accompanied by greater use of cannabis vaporization and more cases of driving under the influence of cannabis. Although simultaneous Delta 9-tetrahydrocannabinol (THC) and alcohol use is frequent, potential pharmacokinetic interactions are poorly understood. Here we studied blood and plasma vaporized cannabinoid disposition, with and without simultaneous oral low-dose alcohol.METHODS:Thirty-two adult cannabis smokers ( greater than or equal to 1 time/3 months, less than or equal to 3 days/week) drank placebo or low-dose alcohol (target approximately 0.065% peak breath-alcohol concentration) 10 min before inhaling 500 mg placebo, low-dose (2.9%) THC, or high-dose (6.7%) THC vaporized cannabis (6 within-individual alcohol-cannabis combinations). Blood and plasma were obtained before and up to 8.3 h after ingestion.RESULTS:Nineteen participants completed all sessions. Median (range) maximum blood concentrations (Cmax) for low and high THC doses (no alcohol) were 32.7 (11.4-66.2) and 42.2 (15.2-137) mu g/L THC, respectively, and 2.8 (0-9.1) and 5.0 (0-14.2) mu g/L 11-OH-THC. With alcohol, low and high dose Cmax values were 35.3 (13.0-71.4) and 67.5 (18.1-210) mu g/L THC and 3.7 (1.4-6.0) and 6.0 (0-23.3) mu g/L 11-OH-THC, significantly higher than without alcohol. With a THC detection cutoff of greater than or equal to 1 mu g/L, greater than or equal to 16.7% of participants remained positive 8.3 h postdose, whereas less than or equal to 21.1% were positive by 2.3 h with a cutoff of greater than or equal to 5 mu g/L.CONCLUSIONS:Vaporization is an effective THC delivery route. The significantly higher blood THC and 11-OH-THC Cmax values with alcohol possibly explain increased performance impairment observed from cannabis-alcohol combinations. Chosen driving-related THC cutoffs should be considered carefully to best reflect performance impairment windows. Our results will help facilitate forensic interpretation and inform the debate on drugged driving legislation. JF - Clinical Chemistry AU - Hartman, Rebecca L AU - Brown, Timothy L AU - Milavetz, Gary AU - Spurgin, Andrew AU - Gorelick, David A AU - Gaffney, Gary AU - Huestis, Marilyn A AD - Program in Toxicology, University of Maryland, Baltimore, MD; , mhuestis@intra.nida.nih.gov Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 850 EP - 869 PB - American Association for Clinical Chemistry, Inc. VL - 61 IS - 6 SN - 0009-9147, 0009-9147 KW - Toxicology Abstracts KW - Tetrahydrocannabinol KW - Blood KW - Cannabinoids KW - alcohols KW - Cannabis KW - Forensic science KW - Disposition KW - Legislation KW - Pharmacokinetics KW - X 24380:Social Poisons & Drug Abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1811909780?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+Chemistry&rft.atitle=Controlled+Cannabis+Vaporizer+Administration%3A+Blood+and+Plasma+Cannabinoids+with+and+without+Alcohol&rft.au=Hartman%2C+Rebecca+L%3BBrown%2C+Timothy+L%3BMilavetz%2C+Gary%3BSpurgin%2C+Andrew%3BGorelick%2C+David+A%3BGaffney%2C+Gary%3BHuestis%2C+Marilyn+A&rft.aulast=Hartman&rft.aufirst=Rebecca&rft.date=2015-06-01&rft.volume=61&rft.issue=6&rft.spage=850&rft.isbn=&rft.btitle=&rft.title=Clinical+Chemistry&rft.issn=00099147&rft_id=info:doi/10.1373%2Fclinchem.2015.238287 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-08-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Tetrahydrocannabinol; Blood; Cannabinoids; Forensic science; Cannabis; alcohols; Disposition; Pharmacokinetics; Legislation DO - http://dx.doi.org/10.1373/clinchem.2015.238287 ER - TY - JOUR T1 - Synthesis and characterization of image-able polyvinyl alcohol microspheres for image-guided chemoembolization AN - 1780527902; PQ0002881748 AB - Therapeutic embolization of blood vessels is a minimally invasive, catheter-based procedure performed with solid or liquid emboli to treat bleeding, vascular malformations, and vascular tumors. Hepatocellular carcinoma (HCC) affects about half a million people per year. When unresectable, HCC is treated with embolization and local drug therapy by transarterial chemoembolization (TACE). For TACE, drug eluting beads (DC Bead super( registered )) may be used to occlude or reduce arterial blood supply and deliver chemotherapeutics locally to the tumor. Although this treatment has been shown to be safe and to improve patient survival, the procedure lacks imaging feedback regarding the location of embolic agent and drug coverage. To address this shortcoming, herein we report the synthesis and characterization of image-able drug eluting beads (iBeads) from the commercial DC Bead super( registered ) product. Two different radiopaque beads were synthesized. In one approach, embolic beads were conjugated with 2,3,5-triiodobenzyl alcohol in the presence of 1,1'-carbonyldiimidazol to give iBead I. iBead II was synthesized with a similar approach but instead using a trimethylenediamine spacer and 2,3,5-triiodobenzoic acid. Doxorubicin was loaded into the iBeads II using a previously reported method. Size and shape of iBeads were evaluated using an upright microscope and their conspicuity assessed using a clinical CT and micro-CT. Bland and Dox-loaded iBeads II visualized with both clinical CT and microCT. Under microCT, individual bland and Dox loaded beads had a mean attenuation of 7904 plus or minus 804 and 11,873.96 plus or minus 706.12 HU, respectively. These iBeads have the potential to enhance image-guided TACE procedures by providing localization of embolic-particle and drug. JF - Journal of Materials Science: Materials in Medicine AU - Negussie, Ayele H AU - Dreher, Matthew R AU - Johnson, Carmen Gacchina AU - Tang, Yiqing AU - Lewis, Andrew L AU - Storm, Gert AU - Sharma, Karun V AU - Wood, Bradford J AD - Center for Interventional Oncology, Radiology and Imaging Sciences, Clinical Center, National Institutes of Health, Bethesda, MD, 20814, USA, bwood@cc.nih.gov Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 1 EP - 10 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 26 IS - 6 SN - 0957-4530, 0957-4530 KW - Biotechnology and Bioengineering Abstracts KW - Drug delivery KW - Invasiveness KW - Microscopes KW - Spacer KW - Tumors KW - Doxorubicin KW - Polyvinyl alcohol KW - Blood vessels KW - Computed tomography KW - alcohols KW - Bleeding KW - microspheres KW - Feedback KW - Embolization KW - Drugs KW - Hepatocellular carcinoma KW - W 30920:Tissue Engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780527902?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Materials+Science%3A+Materials+in+Medicine&rft.atitle=Synthesis+and+characterization+of+image-able+polyvinyl+alcohol+microspheres+for+image-guided+chemoembolization&rft.au=Negussie%2C+Ayele+H%3BDreher%2C+Matthew+R%3BJohnson%2C+Carmen+Gacchina%3BTang%2C+Yiqing%3BLewis%2C+Andrew+L%3BStorm%2C+Gert%3BSharma%2C+Karun+V%3BWood%2C+Bradford+J&rft.aulast=Negussie&rft.aufirst=Ayele&rft.date=2015-06-01&rft.volume=26&rft.issue=6&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+Materials+Science%3A+Materials+in+Medicine&rft.issn=09574530&rft_id=info:doi/10.1007%2Fs10856-015-5530-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Number of references - 88 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Drug delivery; Invasiveness; Microscopes; Spacer; Tumors; Doxorubicin; Polyvinyl alcohol; Blood vessels; Computed tomography; microspheres; Bleeding; alcohols; Feedback; Drugs; Embolization; Hepatocellular carcinoma DO - http://dx.doi.org/10.1007/s10856-015-5530-3 ER - TY - JOUR T1 - Biochip array technology immunoassay performance and quantitative confirmation of designer piperazines for urine workplace drug testing AN - 1746890717; PQ0001805635 AB - Designer piperazines are emerging novel psychoactive substances (NPS) with few high-throughput screening methods for their identification. We evaluated a biochip array technology (BAT) immunoassay for phenylpiperazines (PNP) and benzylpiperazines (BZP) and analyzed 20,017 randomly collected urine workplace specimens. Immunoassay performance at recommended cutoffs was evaluated for PNPI (5 mu g/L), PNPII (7.5 mu g/L), and BZP (5 mu g/L) antibodies. Eight hundred forty positive and 206 randomly selected presumptive negative specimens were confirmed by liquid chromatography high-resolution mass spectrometry (LC-HRMS). Assay limits of detection for PNPI, PNPII, and BZP were 2.9, 6.3, and 2.1 mu g/L, respectively. Calibration curves were linear (R super(2)>0.99) with upper limits of 42 mu g/L for PNPI/PNII and 100 mu g/L for BZP. Quality control samples demonstrated imprecision <19.3 %CV and accuracies 86.0-94.5 % of target. There were no interferences from 106 non-piperazine substances. Seventy-eight of 840 presumptive positive specimens (9.3 %) were LC-HRMS positive, with 72 positive for 1-(3-chlorophenyl)piperazine (mCPP), a designer piperazine and antidepressant trazodone metabolite. Of 206 presumptive negative specimens, one confirmed positive for mCPP (3.3 mu g/L) and one for BZP (3.6 mu g/L). BAT specificity (21.1 to 91.4 %) and efficiency (27.0 to 91.6 %) increased, and sensitivity slightly decreased (97.5 to 93.8 %) with optimized cutoffs of 25 mu g/L PNPI, 42 mu g/L PNPI, and 100 mu g/L BZP. A high-throughput screening method is needed to identify piperazine NPS. We evaluated performance of the Randox BAT immunoassay to identify urinary piperazines and documented improved performance when antibody cutoffs were raised. In addition, in randomized workplace urine specimens, all but two positive specimens contained mCPP and/or trazodone, most likely from legitimate medical prescriptions. [Figure not available: see fulltext.] JF - Analytical and Bioanalytical Chemistry AU - Castaneto, Marisol S AU - Barnes, Allan J AU - Concheiro, Marta AU - Klette, Kevin L AU - Martin, Thomas A AU - Huestis, Marilyn A AD - Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, 251 Bayview Blvd., Baltimore, MD, 21224, USA, mhuestis@intra.nida.nih.gov PY - 2015 SP - 4639 EP - 4648 PB - Springer Science+Business Media, Berlin/Heidelberg Germany VL - 407 IS - 16 SN - 1618-2642, 1618-2642 KW - Aqualine Abstracts; Water Resources Abstracts KW - Mass Spectrometry KW - Cutoffs KW - Metabolites KW - Performance Evaluation KW - Calibrations KW - Urine KW - Assay KW - Liquid Chromatography KW - Quality Control KW - AQ 00001:Water Resources and Supplies KW - SW 5040:Data acquisition UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746890717?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+and+Bioanalytical+Chemistry&rft.atitle=Biochip+array+technology+immunoassay+performance+and+quantitative+confirmation+of+designer+piperazines+for+urine+workplace+drug+testing&rft.au=Castaneto%2C+Marisol+S%3BBarnes%2C+Allan+J%3BConcheiro%2C+Marta%3BKlette%2C+Kevin+L%3BMartin%2C+Thomas+A%3BHuestis%2C+Marilyn+A&rft.aulast=Castaneto&rft.aufirst=Marisol&rft.date=2015-06-01&rft.volume=407&rft.issue=16&rft.spage=4639&rft.isbn=&rft.btitle=&rft.title=Analytical+and+Bioanalytical+Chemistry&rft.issn=16182642&rft_id=info:doi/10.1007%2Fs00216-015-8660-z LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 26 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Mass Spectrometry; Performance Evaluation; Calibrations; Cutoffs; Urine; Assay; Liquid Chromatography; Metabolites; Quality Control DO - http://dx.doi.org/10.1007/s00216-015-8660-z ER - TY - JOUR T1 - Prevention of irinotecan induced diarrhea by probiotics: A randomized double blind, placebo controlled pilot study AN - 1746884764; PQ0002261209 AB - Purpose Diarrhea is one of the dose limiting toxicity of irinotecan. SN-38 is main irinotecan metabolite responsible for diarrhea development, which is excreted in glucuronidated form into the intestine. This study aimed to determine the effectiveness of the probiotics in the prevention of irinotecan induced diarrhea due to reduction of intestinal beta-d-glucuronidase activity. Methods Between January 2011 and December 2013, 46 patients with colorectal cancer starting a new line of irinotecan based therapy were included. Patients were randomized 1:1 to probiotics (PRO) or placebo (PLA). Probiotic formula Colon Dophilus(TM), was administered at a dose of 10109CFU of bacteria tid, orally for 12 weeks of chemotherapy. The study was prematurely terminated due to slow accrual, when 46 of 220 planned patients were accrued. Results Twenty-three patients were randomized to PRO and 23 patients to PLA. Administration of probiotics compared to placebo led to a reduction in the incidence of severe diarrhea of grade 3 or 4 (0% for PRO vs. 17.4% for PLA, p=0.11), as well as reduction of the overall incidence of diarrhea (39.1% for PRO vs. 60.9% for PLA, p=0.24) and incidence of enterocolitis (0% for PRO vs. 8.7% for PLA). Patients on PRO used less antidiarrheal drugs compared to PLA. There was no infection caused by probiotic strains recorded. Conclusions Administration of probiotics in patients with colorectal cancer treated with irinotecan-based chemotherapy is safe and could lead to a reduction in the incidence and severity of gastrointestinal toxicity. JF - Complementary Therapies in Medicine AU - Mego, Michal AU - Chovanec, Jozef AU - Vochyanova-Andrezalova, Iveta AU - Konkolovsky, Peter AU - Mikulova, Milada AU - Reckova, Maria AU - Miskovska, Vera AU - Bystricky, Branislav AU - Beniak, Juraj AU - Medvecova, Lenka AU - Lagin, Adela AU - Svetlovska, Daniela AU - Spanik, Stanislav AU - Zajac, Vladimir AU - Mardiak, Jozef AU - Drgona, Lubos AD - 2nd Department of Oncology and National Cancer Institute, Comenius University, Faculty of Medicine, Klenova 1, 833 10 Bratislava, Slovakia PY - 2015 SP - 356 EP - 362 PB - Elsevier VL - 23 IS - 3 SN - 0965-2299, 0965-2299 KW - Microbiology Abstracts B: Bacteriology KW - Irinotecan KW - Probiotics KW - Diarrhea KW - Prevention UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746884764?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Complementary+Therapies+in+Medicine&rft.atitle=Prevention+of+irinotecan+induced+diarrhea+by+probiotics%3A+A+randomized+double+blind%2C+placebo+controlled+pilot+study&rft.au=Mego%2C+Michal%3BChovanec%2C+Jozef%3BVochyanova-Andrezalova%2C+Iveta%3BKonkolovsky%2C+Peter%3BMikulova%2C+Milada%3BReckova%2C+Maria%3BMiskovska%2C+Vera%3BBystricky%2C+Branislav%3BBeniak%2C+Juraj%3BMedvecova%2C+Lenka%3BLagin%2C+Adela%3BSvetlovska%2C+Daniela%3BSpanik%2C+Stanislav%3BZajac%2C+Vladimir%3BMardiak%2C+Jozef%3BDrgona%2C+Lubos&rft.aulast=Mego&rft.aufirst=Michal&rft.date=2015-06-01&rft.volume=23&rft.issue=3&rft.spage=356&rft.isbn=&rft.btitle=&rft.title=Complementary+Therapies+in+Medicine&rft.issn=09652299&rft_id=info:doi/10.1016%2Fj.ctim.2015.03.008 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 37 N1 - Last updated - 2015-12-09 DO - http://dx.doi.org/10.1016/j.ctim.2015.03.008 ER - TY - JOUR T1 - Chlamydia trachomatis inclusion membrane protein CT850 interacts with the dynein light chain DYNLT1 (Tctex1) AN - 1746876808; PQ0002261178 AB - Chlamydia trachomatis actively subverts the minus-end directed microtubule motor, dynein, to traffic along microtubule tracks to the Microtubule Organizing Center (MTOC) where it remains within a membrane bound replicative vacuole for the duration of its intracellular development. Unlike most substrates of the dynein motor, disruption of the dynactin cargo-linking complex by over-expression of the p50 dynamitin subunit does not inhibit C. trachomatis transport. A requirement for chlamydial protein synthesis to initiate this process suggests that a chlamydial product supersedes a requirement for p50 dynamitin. A yeast 2-hybrid system was used to screen the chlamydia inclusion membrane protein CT850 against a HeLa cell cDNA library and identified an interaction with the dynein light chain DYNLT1 (Tctex1). This interaction was at least partially dependent upon an (R/K-R/K-X-X-R/K) motif that is characteristic of DYNLT1 binding domains. CT850 expressed ectopically in HeLa cells localized at the MTOC and this localization is similarly dependent upon the predicted DYNLT1 binding domain. Furthermore, DYNLT1 is enriched at focal concentrations of CT850 on the chlamydial inclusion membrane that are known to interact with dynein and microtubules. Depletion of DYNLT1 disrupts the characteristic association of the inclusion membrane with centrosomes. Collectively, the results suggest that CT850 interacts with DYNLT1 to promote appropriate positioning of the inclusion at the MTOC. JF - Biochemical and Biophysical Research Communications AU - Mital, Jeffrey AU - Lutter, Erika I AU - Barger, Alexandra C AU - Dooley, Cheryl A AU - Hackstadt, Ted AD - Host-Parasite Interactions Section, Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840, USA Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 165 EP - 170 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 462 IS - 2 SN - 0006-291X, 0006-291X KW - Microbiology Abstracts B: Bacteriology KW - Chlamydia KW - Microtubules KW - Dynein KW - Vesicle trafficking KW - Light chains KW - Protein biosynthesis KW - Centrosomes KW - Overexpression KW - Vacuoles KW - Chlamydia trachomatis KW - Membrane proteins KW - dynactin KW - Traffic KW - J 02330:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746876808?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemical+and+Biophysical+Research+Communications&rft.atitle=Chlamydia+trachomatis+inclusion+membrane+protein+CT850+interacts+with+the+dynein+light+chain+DYNLT1+%28Tctex1%29&rft.au=Mital%2C+Jeffrey%3BLutter%2C+Erika+I%3BBarger%2C+Alexandra+C%3BDooley%2C+Cheryl+A%3BHackstadt%2C+Ted&rft.aulast=Mital&rft.aufirst=Jeffrey&rft.date=2015-06-01&rft.volume=462&rft.issue=2&rft.spage=165&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+Biophysical+Research+Communications&rft.issn=0006291X&rft_id=info:doi/10.1016%2Fj.bbrc.2015.04.116 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Light chains; Microtubules; Protein biosynthesis; Overexpression; Centrosomes; Vacuoles; Dynein; Membrane proteins; dynactin; Traffic; Chlamydia trachomatis DO - http://dx.doi.org/10.1016/j.bbrc.2015.04.116 ER - TY - JOUR T1 - Non-thyroid cancer in Northern Ukraine in the post-Chernobyl period: Short report AN - 1732824262; PQ0002247946 AB - The Chernobyl nuclear power plant accident in Ukraine in 1986 led to widespread radioactive releases into the environment - primarily of radioiodines and cesium - heavily affecting the northern portions of the country, with settlement-averaged thyroid doses estimated to range from 10mGy to more than 10Gy. The increased risk of thyroid cancer among exposed children and adolescents is well established but the impact of radioactive contamination on the risk of other types of cancer is much less certain. To provide data on a public health issue of major importance, we have analyzed the incidence of non-thyroid cancers during the post-Chernobyl period in a well-defined cohort of 13,203 individuals who were <18 years of age at the time of the accident. The report is based on standardized incidence ratio (SIR) analysis of 43 non-thyroid cancers identified through linkage with the National Cancer Registry of Ukraine for the period 1998 through 2009. We compared the observed and expected number of cases in three cancer groupings: all solid cancers excluding thyroid, leukemia, and lymphoma. Our analyses found no evidence of a statistically significant elevation in cancer risks in this cohort exposed at radiosensitive ages, although the cancer trends, particularly for leukemia (SIR=1.92, 95% confidence interval: 0.69; 4.13), should continue to be monitored. JF - Cancer Epidemiology AU - Hatch, M AU - Ostroumova, E AU - Brenner, A AU - Federenko, Z AU - Gorokh, Y AU - Zvinchuk, O AU - Shpak, V AU - Tereschenko, V AU - Tronko, M AU - Mabuchi, K AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 279 EP - 283 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 39 IS - 3 SN - 1877-7821, 1877-7821 KW - Pollution Abstracts; Risk Abstracts; Toxicology Abstracts; Health & Safety Science Abstracts KW - I-131 Iodine-131 KW - NCRU National Cancer Institute of Ukraine KW - Cs cesium KW - SIR standardized incidence ratio KW - CI confidence interval KW - mSv milliSievert KW - Ionizing radiation KW - Chernobyl accident KW - Cancer incidence KW - Standardized incidence ratio KW - Ecological study KW - Ukraine, Chernobyl KW - Age KW - Cesium KW - Contamination KW - Ukraine KW - Statistical analysis KW - Public health KW - Leukemia KW - Accidents KW - thyroid cancer KW - Lymphoma KW - Adolescents KW - Data processing KW - Adolescence KW - MED, Ukraine KW - Thyroid KW - Radioactive pollution KW - Children KW - Cancer KW - Health risks KW - Nuclear power plants KW - Standards KW - X 24390:Radioactive Materials KW - H 8000:Radiation Safety/Electrical Safety KW - R2 23060:Medical and environmental health KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732824262?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Epidemiology&rft.atitle=Non-thyroid+cancer+in+Northern+Ukraine+in+the+post-Chernobyl+period%3A+Short+report&rft.au=Hatch%2C+M%3BOstroumova%2C+E%3BBrenner%2C+A%3BFederenko%2C+Z%3BGorokh%2C+Y%3BZvinchuk%2C+O%3BShpak%2C+V%3BTereschenko%2C+V%3BTronko%2C+M%3BMabuchi%2C+K&rft.aulast=Hatch&rft.aufirst=M&rft.date=2015-06-01&rft.volume=39&rft.issue=3&rft.spage=279&rft.isbn=&rft.btitle=&rft.title=Cancer+Epidemiology&rft.issn=18777821&rft_id=info:doi/10.1016%2Fj.canep.2015.02.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Age; Data processing; Cesium; Contamination; Adolescence; Statistical analysis; Children; Public health; Leukemia; Nuclear power plants; Accidents; thyroid cancer; Lymphoma; Thyroid; Radioactive pollution; Cancer; Health risks; Standards; Adolescents; Ukraine, Chernobyl; Ukraine; MED, Ukraine DO - http://dx.doi.org/10.1016/j.canep.2015.02.002 ER - TY - JOUR T1 - Enhanced immunostimulatory effects of DNA-encapsulated peptide hydrogels AN - 1732808187; PQ0002215177 AB - DNA that encodes tumor-specific antigens represents potential immunostimulatory agents. However, rapid enzymatic degradation and fragmentation of DNA during administration can result in limited vector expression and, consequently, poor efficacy. These challenges have necessitated the use of novel strategies for DNA delivery. Herein, we study the ability of cationic self-assembling peptide hydrogels to encapsulate plasmid DNA, and enhance its immunostimulatory potential in vivo. The effect of network charge on the gel's ability to retain the DNA was assessed employing three gel-forming peptides that vary systematically in formal charge. The peptide HLT2, having a formal charge of +5 at neutral pH, was optimal in encapsulating microgram quantities of DNA with little effect on its rheological properties, allowing its effective syringe delivery in vivo. The plasmid, DNA(TA), encapsulated within these gels encodes for a melanoma-specific gp100 antigen fused to the alarmin protein adjuvant HMGN1. Implantation of DNA(TA)-loaded HLT2 gels into mice resulted in an acute inflammatory response with the presence of polymorphonuclear cells, which was followed by infiltrating macrophages. These cellular infiltrates aid in the processing of encapsulated DNA, promoting increased lymphoproliferation and producing an enhanced immune response mediated by CD4+/IFN gamma + expressing Th1 cells, and complemented by the formation of gp100-specific antibodies. JF - Biomaterials AU - Medina, Scott H AU - Li, Sandra AU - Howard, OMZack AU - Dunlap, Micah AU - Trivett, Anna AU - Schneider, Joel P AU - Oppenheim, Joost J AD - Chemical Biology Laboratory, National Cancer Institute, National Institutes of Health, Frederick, MD 21702, USA Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 545 EP - 553 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 53 SN - 0142-9612, 0142-9612 KW - Immunology Abstracts; Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - DNA KW - Peptide KW - Drug delivery KW - Self assembly KW - Gene expression KW - Macrophages KW - Helper cells KW - Leukocytes (polymorphonuclear) KW - Adjuvants KW - Plasmids KW - Inflammation KW - Expression vectors KW - DNA fragmentation KW - Antibodies KW - CD4 antigen KW - hydrogels KW - Immunostimulation KW - Glycoprotein gp100 KW - Lymphocytes T KW - Syringes KW - Immune response KW - pH effects KW - W 30920:Tissue Engineering KW - N 14810:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732808187?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biomaterials&rft.atitle=Enhanced+immunostimulatory+effects+of+DNA-encapsulated+peptide+hydrogels&rft.au=Medina%2C+Scott+H%3BLi%2C+Sandra%3BHoward%2C+OMZack%3BDunlap%2C+Micah%3BTrivett%2C+Anna%3BSchneider%2C+Joel+P%3BOppenheim%2C+Joost+J&rft.aulast=Medina&rft.aufirst=Scott&rft.date=2015-06-01&rft.volume=53&rft.issue=&rft.spage=545&rft.isbn=&rft.btitle=&rft.title=Biomaterials&rft.issn=01429612&rft_id=info:doi/10.1016%2Fj.biomaterials.2015.02.125 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-01 N1 - Last updated - 2016-02-29 N1 - SubjectsTermNotLitGenreText - Macrophages; Leukocytes (polymorphonuclear); Helper cells; Adjuvants; Plasmids; Inflammation; Expression vectors; DNA fragmentation; CD4 antigen; Antibodies; hydrogels; Immunostimulation; Glycoprotein gp100; DNA; Lymphocytes T; Syringes; Immune response; pH effects DO - http://dx.doi.org/10.1016/j.biomaterials.2015.02.125 ER - TY - JOUR T1 - The Post-2015 Development Agenda: Keeping Our Focus on the Worst Off AN - 1727695427; PQ0002136514 AB - Non-communicable diseases now account for the majority of the global burden of disease and an International campaign has emerged to raise their priority on the post-2015 development agenda. We argue, to the contrary, that there remain strong reasons to prioritize maternal and child health. Policy-makers ought to assign highest priority to the health conditions that afflict the worst off. In virtue of how little healthy life they have had, children who die young are among the globally worst off. Moreover, many interventions to deal with the conditions that cause mortality In the young are low-cost and provide great benefits to their recipients. Consistent with the original Millennium Development Goals, the international community should continue to prioritize reductions in communicable diseases, neonatal conditions, and maternal health despite the shifts in the global burden of disease. JF - American Journal of Tropical Medicine and Hygiene AU - Sharp, Daniel AU - Millum, Joseph AD - Clinical Center Department of Bioethics, National Institutes of Health, Bethesda, Maryland, joseph.millum@nih.gov Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 1087 EP - 1089 PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States VL - 92 IS - 6 SN - 0002-9637, 0002-9637 KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Health & Safety Science Abstracts KW - Mortality KW - Priorities KW - Intervention KW - Development KW - Neonates KW - Children KW - Hygiene KW - Mortality causes KW - K 03400:Human Diseases KW - J 02400:Human Diseases KW - Q1 08121:Law, policy, economics and social sciences KW - H 0500:General KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727695427?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=The+Post-2015+Development+Agenda%3A+Keeping+Our+Focus+on+the+Worst+Off&rft.au=Sharp%2C+Daniel%3BMillum%2C+Joseph&rft.aulast=Sharp&rft.aufirst=Daniel&rft.date=2015-06-01&rft.volume=92&rft.issue=6&rft.spage=1087&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.15-0087 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Hygiene; Mortality causes; Mortality; Neonates; Development; Children; Intervention; Priorities DO - http://dx.doi.org/10.4269/ajtmh.15-0087 ER - TY - JOUR T1 - Responding to the Pandemic of Falsified Medicines AN - 1727680927; PQ0002197821 AB - Over the past decade, the number of countries reporting falsified (fake, spurious/falsely labeled/counterfeit) medicines and the types and quantities of fraudulent drugs being distributed have increased greatly. The obstacles in combating falsified pharmaceuticals include 1) lack of consensus on definitions, 2) paucity of reliable and scalable technology to detect fakes before they reach patients, 3) poor global and national leadership and accountability systems for combating this scourge, and 4) deficient manufacturing and regulatory challenges, especially in China and India where fake products often originate. The major needs to improve the quality of the world's medicines fall into three main areas: 1) research to develop and compare accurate and affordable tools to identify high-quality drugs at all levels of distribution; 2) an international convention and national legislation to facilitate production and utilization of high-quality drugs and protect all countries from the criminal and the negligent who make, distribute, and sell life-threatening products; and 3) a highly qualified, well-supported international science and public health organization that will establish standards, drug-quality surveillance, and training programs like the U.S. Food and Drug Administration. Such leadership would give authoritative guidance for countries in cooperation with national medical regulatory agencies, pharmaceutical companies, and international agencies, all of which have an urgent interest and investment in ensuring that patients throughout the world have access to good quality medicines. The organization would also advocate strongly for including targets for achieving good quality medicines in the United Nations Millennium Development Goals and Sustainable Development Goals. JF - American Journal of Tropical Medicine and Hygiene AU - Nayyar, Gaurvika M L AU - Altaran, Amir AU - Clark, John P AU - Culzoni, M Julia AU - Fernandez, Facundo M AU - Herrington, James E AU - Kendall, Megan AU - Newton, Paul N AU - Breman, Joel G AD - Johns Hopkins Bloomberg School of Public Health and Johns Hopkins Carey Business School, Baltimore, Maryland, jbreman@nih.gov Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 113 EP - 118 PB - American Society of Tropical Medicine and Hygiene, 60 Revere Drive, Suite 500 Northbrook IL 60062 United States VL - 92 SN - 0002-9637, 0002-9637 KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Health & Safety Science Abstracts; ASFA 1: Biological Sciences & Living Resources; Sustainability Science Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality KW - Cooperation KW - Sustainable development KW - Accountability KW - Lead KW - India KW - Public health KW - pandemics KW - International organizations KW - United Nations KW - Drugs KW - International standardization KW - Training KW - Surveillance and enforcement KW - Sustainable Development KW - Pharmaceuticals KW - Governments KW - Medicine KW - China, People's Rep. KW - Hygiene KW - Legislation KW - Technology KW - M3 1010:Issues in Sustainable Development KW - K 03400:Human Diseases KW - J 02400:Human Diseases KW - Q1 08604:Stock assessment and management KW - Q5 08524:Public health, medicines, dangerous organisms KW - H 4000:Food and Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727680927?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=Responding+to+the+Pandemic+of+Falsified+Medicines&rft.au=Nayyar%2C+Gaurvika+M+L%3BAltaran%2C+Amir%3BClark%2C+John+P%3BCulzoni%2C+M+Julia%3BFernandez%2C+Facundo+M%3BHerrington%2C+James+E%3BKendall%2C+Megan%3BNewton%2C+Paul+N%3BBreman%2C+Joel+G&rft.aulast=Nayyar&rft.aufirst=Gaurvika+M&rft.date=2015-06-01&rft.volume=92&rft.issue=&rft.spage=113&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.14-0393 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Sustainable Development; International organizations; Surveillance and enforcement; Medicine; Governments; Hygiene; Drugs; Legislation; Public health; pandemics; Cooperation; Sustainable development; Pharmaceuticals; Lead; Training; United Nations; Accountability; Technology; International standardization; China, People's Rep.; India DO - http://dx.doi.org/10.4269/ajtmh.14-0393 ER - TY - JOUR T1 - Season and preterm birth in Norway: A cautionary tale AN - 1717489666; PQ0001944520 AB - Background: Preterm birth is a common, costly and dangerous pregnancy complication. Seasonality of risk would suggest modifiable causes.Methods: We examine seasonal effects on preterm birth, using data from the Medical Birth Registry of Norway (2321652 births), and show that results based on births are misleading and a fetuses-at-risk approach is essential. In our harmonic-regression Cox proportional hazards model we consider fetal risk of birth between 22 and 37 completed weeks of gestation. We examine effects of both day of year of conception (for early effects) and day of ongoing gestation (for seasonal effects on labour onset) as modifiers of gestational-age-based risk.Results: Naive analysis of preterm rates across days of birth shows compelling evidence for seasonality (P<10 super(-152)). However, the reconstructed numbers of conceptions also vary with season (P<10 super(-307)), confounding results by inducing seasonal variation in the age distribution of the fetal population at risk. When we instead properly treat fetuses as the individuals at risk, restrict analysis to pregnancies with relatively accurate ultrasound-based assessment of gestational age (available since 1998) and adjust for socio-demographic factors and maternal smoking, we find modest effects of both time of year of conception and time of year at risk, with peaks for early preterm near early January and early July.Conclusions: Analyses of seasonal effects on preterm birth are demonstrably vulnerable to confounding by seasonality of conception, measurement error in conception dating, and socio-demographic factors. The seasonal variation based on fetuses reveals two peaks for early preterm, coinciding with New Year's Day and the early July beginning of Norway's summer break, and may simply reflect a holiday-related pattern of unintended conception. JF - International Journal of Epidemiology AU - Weinberg, Clarice R AU - Shi, Min AU - DeRoo, Lisa A AU - Basso, Olga AU - Skjaerven, Rolv AD - *Corresponding author. MD A3-03, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709. E-mail:, weinber2@niehs.nih.gov Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 1068 EP - 1078 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 44 IS - 3 SN - 0300-5771, 0300-5771 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Preterm birth KW - seasonality KW - harmonic analysis KW - Risk assessment KW - Smoking KW - Age KW - ANE, Norway KW - Complications KW - Risk factors KW - Summer KW - Vulnerability KW - Seasonal variations KW - Fetuses KW - Pregnancy KW - R2 23060:Medical and environmental health KW - H 12000:Epidemiology and Public Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1717489666?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Epidemiology&rft.atitle=Season+and+preterm+birth+in+Norway%3A+A+cautionary+tale&rft.au=Weinberg%2C+Clarice+R%3BShi%2C+Min%3BDeRoo%2C+Lisa+A%3BBasso%2C+Olga%3BSkjaerven%2C+Rolv&rft.aulast=Weinberg&rft.aufirst=Clarice&rft.date=2015-06-01&rft.volume=44&rft.issue=3&rft.spage=1068&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Epidemiology&rft.issn=03005771&rft_id=info:doi/10.1093%2Fije%2Fdyv100 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2016-03-30 N1 - SubjectsTermNotLitGenreText - Risk assessment; Smoking; Age; Complications; Risk factors; Summer; Vulnerability; Seasonal variations; Fetuses; Pregnancy; ANE, Norway DO - http://dx.doi.org/10.1093/ije/dyv100 ER - TY - JOUR T1 - The Curvature Induction of Surface-Bound Antimicrobial Peptides Piscidin 1 and Piscidin 3 Varies with Lipid Chain Length AN - 1709186787; PQ0001896914 AB - The initial steps of membrane disruption by antimicrobial peptides (AMPs) involve binding to bacterial membranes in a surface-bound (S) orientation. To evaluate the effects of lipid composition on the S state, molecular dynamics simulations of the AMPs piscidin 1 (p1) and piscidin 3 (p3) were carried out in four different bilayers: 3:1 DMPC/DMPG, 3:1 POPC/POPG, 1:1 POPE/POPG, and 4:1 POPC/cholesterol. In all cases, the addition of 1:40 piscidin caused thinning of the bilayer, though thinning was least for DMPC/DMPG. The peptides also insert most deeply into DMPC/DMPG, spanning the region from the bilayer midplane to the headgroups, and thereby only mildly disrupting the acyl chains. In contrast, the peptides insert less deeply in the palmitoyl-oleoyl containing membranes, do not reach the midplane, and substantially disrupt the chains, i.e., the neighboring acyl chains bend under the peptide, forming a basket-like conformation. Curvature free energy derivatives calculated from the simulation pressure profiles reveal that the peptides generate positive curvature in membranes with palmitoyl and oleoyl chains but negative curvature in those with myristoyl chains. Curvature inductions predicted with a continuum elastic model follow the same trends, though the effect is weaker, and a small negative curvature induction is obtained in POPC/POPG. These results do not directly speak to the relative stability of the inserted (I) states or ease of pore formation, which requires the free energy pathway between the S and I states. Nevertheless, they do highlight the importance of lipid composition and acyl chain packing. JF - Journal of Membrane Biology AU - Perrin, BScott AU - Sodt, Alexander J AU - Cotten, Myriam L AU - Pastor, Richard W AD - Laboratory of Computational Biology, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, 20892, USA, pastorr@nhlbi.nih.gov Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 455 EP - 467 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 248 IS - 3 SN - 0022-2631, 0022-2631 KW - Microbiology Abstracts B: Bacteriology KW - Thinning KW - Pores KW - Lipid composition KW - Packing KW - Cholesterol KW - Pressure KW - Antimicrobial peptides KW - Free energy KW - Models KW - Conformation KW - J 02330:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709186787?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Membrane+Biology&rft.atitle=The+Curvature+Induction+of+Surface-Bound+Antimicrobial+Peptides+Piscidin+1+and+Piscidin+3+Varies+with+Lipid+Chain+Length&rft.au=Perrin%2C+BScott%3BSodt%2C+Alexander+J%3BCotten%2C+Myriam+L%3BPastor%2C+Richard+W&rft.aulast=Perrin&rft.aufirst=BScott&rft.date=2015-06-01&rft.volume=248&rft.issue=3&rft.spage=455&rft.isbn=&rft.btitle=&rft.title=Journal+of+Membrane+Biology&rft.issn=00222631&rft_id=info:doi/10.1007%2Fs00232-014-9733-1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Number of references - 44 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Thinning; Pores; Lipid composition; Cholesterol; Packing; Pressure; Antimicrobial peptides; Free energy; Conformation; Models DO - http://dx.doi.org/10.1007/s00232-014-9733-1 ER - TY - JOUR T1 - The Turbulent Network Dynamics of Microbial Evolution and the Statistical Tree of Life AN - 1709186134; PQ0001862221 AB - The wide spread and high rate of gene exchange and loss in the prokaryotic world translate into "network genomics". The rates of gene gain and loss are comparable with the rate of point mutations but are substantially greater than the duplication rate. Thus, evolution of prokaryotes is primarily shaped by gene gain and loss. These processes are essential to prevent mutational meltdown of microbial populations by stopping Muller's ratchet and appear to trigger emergence of major novel clades by opening up new ecological niches. At least some bacteria and archaea seem to have evolved dedicated devices for gene transfer. Despite the dominance of gene gain and loss, evolution of genes is intrinsically tree-like. The significant coherence between the topologies of numerous gene trees, particularly those for (nearly) universal genes, is compatible with the concept of a statistical tree of life, which forms the framework for reconstruction of the evolutionary processes in the prokaryotic world. JF - Journal of Molecular Evolution AU - Koonin, Eugene V AD - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD, 20894, USA, koonin@ncbi.nlm.nih.gov Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 244 EP - 250 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 80 IS - 5-6 SN - 0022-2844, 0022-2844 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Genetics Abstracts KW - Statistics KW - molecular evolution KW - Archaea KW - Gene transfer KW - Niches KW - Point mutation KW - Evolutionary genetics KW - genomics KW - Prokaryotes KW - Dominance KW - A 01490:Miscellaneous KW - G 07770:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709186134?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Molecular+Evolution&rft.atitle=The+Turbulent+Network+Dynamics+of+Microbial+Evolution+and+the+Statistical+Tree+of+Life&rft.au=Koonin%2C+Eugene+V&rft.aulast=Koonin&rft.aufirst=Eugene&rft.date=2015-06-01&rft.volume=80&rft.issue=5-6&rft.spage=244&rft.isbn=&rft.btitle=&rft.title=Journal+of+Molecular+Evolution&rft.issn=00222844&rft_id=info:doi/10.1007%2Fs00239-015-9679-7 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Number of references - 57 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - molecular evolution; Statistics; Gene transfer; Niches; Point mutation; Prokaryotes; genomics; Evolutionary genetics; Dominance; Archaea DO - http://dx.doi.org/10.1007/s00239-015-9679-7 ER - TY - JOUR T1 - SUSPECTED LYME BORRELIOSIS IN A CAPTIVE ADULT CHIMPANZEE (PAN TROGLODYTES) AN - 1709172918; PQ0001667191 AB - An 18-yr-old female captive-born chimpanzee (Pan troglodytes) presented with an intermittent history of inappetence, lethargy, and lower limb stiffness. No notable abnormalities were found on exam or complete blood cell count and serum biochemistry analysis. Serologic testing was strongly positive via indirect fluorescent antibody testing and Western blot for Borrelia burgdorferi. Treatment with doxycycline was initiated, and a clinical response was seen within 1 wk. Convalescent serum exhibited an eightfold increase in titer. Serologic testing was performed on several conspecifics with banked serum; while some low positive titers were present and presumed indicative of past exposure, no titer was elevated to the extent of the affected chimpanzee during its course of disease. To the authors' knowledge, this is the first report of suspected Lyme borreliosis in a great ape species, and the case originates from an area of the United States with a high incidence of human borreliosis. JF - Journal of Zoo and Wildlife Medicine AU - Wack, Allison N AU - Holland, Cynthia J AU - Lopez, Job E AU - Schwan, Tom G AU - Bronson, Ellen AD - From The Maryland Zoo in Baltimore, 1876 Mansion House Drive, Baltimore, Maryland 21217, USA (Wack, Bronson); Protatek Reference Laboratory, 540 West Iron Avenue, Suite 106, Mesa, Arizona 85210, USA (Holland); and the Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, NIAID, NIH, 903 South 4th Street, Hamilton, Montana 59840, USA (Lopez, Schwan). Present address (Lopez): Department of Pediatrics, National School of Tropical Medicine, Baylor College of Medicine, 1102 Bates Street, Feigin Center, Suite 550, Houston, Texas 77030, USA., allisonwack@gmail.com Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 423 EP - 426 PB - American Association of Zoo Veterinarians VL - 46 IS - 2 SN - 1042-7260, 1042-7260 KW - Microbiology Abstracts B: Bacteriology KW - Borrelia burgdorferi KW - Borreliosis KW - Chimpanzee KW - Lyme disease KW - Pan troglodytes KW - Western blotting KW - Antibodies KW - Limbs KW - Conspecifics KW - Blood cells KW - Doxycycline KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709172918?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Zoo+and+Wildlife+Medicine&rft.atitle=SUSPECTED+LYME+BORRELIOSIS+IN+A+CAPTIVE+ADULT+CHIMPANZEE+%28PAN+TROGLODYTES%29&rft.au=Wack%2C+Allison+N%3BHolland%2C+Cynthia+J%3BLopez%2C+Job+E%3BSchwan%2C+Tom+G%3BBronson%2C+Ellen&rft.aulast=Wack&rft.aufirst=Allison&rft.date=2015-06-01&rft.volume=46&rft.issue=2&rft.spage=423&rft.isbn=&rft.btitle=&rft.title=Journal+of+Zoo+and+Wildlife+Medicine&rft.issn=10427260&rft_id=info:doi/10.1638%2F2014-0231R.1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Number of references - 10 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Western blotting; Antibodies; Limbs; Conspecifics; Borreliosis; Blood cells; Doxycycline; Borrelia burgdorferi; Pan troglodytes DO - http://dx.doi.org/10.1638/2014-0231R.1 ER - TY - JOUR T1 - Microparticles: markers and mediators of sepsis-induced microvascular dysfunction, immunosuppression, and AKI AN - 1709171259; PQ0001721010 AB - Sepsis is a severe and complex syndrome that lacks effective prevention or therapeutics. The effects of sepsis on the microvasculature have become an attractive area for possible new targets and therapeutics. Microparticles (MPs) are cell membrane-derived particles that can promote coagulation, inflammation, and angiogenesis, and they can participate in cell-to-cell communication. MPs retain cell membrane and cytoplasmic constituents of their parental cells, including two procoagulants: phosphatidylserine and tissue factor. We highlight the role of microparticles released by endothelial and circulating cells after sepsis-induced microvascular injury, and we discuss possible mechanisms by which microparticles can contribute to endothelial dysfunction, immunosuppression, and multiorgan dysfunction-including sepsis-AKI. Once viewed as cellular byproducts, microparticles are emerging as a new class of markers and mediators in the pathogenesis of sepsis. JF - Kidney International AU - Souza, Ana Carolina P AU - Yuen, Peter S T AU - Star, Robert A AD - Renal Diagnostics and Therapeutics Unit, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA Y1 - 2015/06// PY - 2015 DA - Jun 2015 SP - 1100 EP - 1108 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 87 IS - 6 SN - 0085-2538, 0085-2538 KW - Immunology Abstracts; Microbiology Abstracts B: Bacteriology KW - Microvasculature KW - Injuries KW - Coagulation KW - Tissue factor KW - microparticles KW - Angiogenesis KW - Inflammation KW - Sepsis KW - Cell membranes KW - phosphatidylserine KW - Kidney KW - Cell interactions KW - Immunosuppression KW - J 02350:Immunology KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709171259?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Kidney+International&rft.atitle=Microparticles%3A+markers+and+mediators+of+sepsis-induced+microvascular+dysfunction%2C+immunosuppression%2C+and+AKI&rft.au=Souza%2C+Ana+Carolina+P%3BYuen%2C+Peter+S+T%3BStar%2C+Robert+A&rft.aulast=Souza&rft.aufirst=Ana+Carolina&rft.date=2015-06-01&rft.volume=87&rft.issue=6&rft.spage=1100&rft.isbn=&rft.btitle=&rft.title=Kidney+International&rft.issn=00852538&rft_id=info:doi/10.1038%2Fki.2015.26 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Microvasculature; microparticles; Tissue factor; Coagulation; Injuries; Angiogenesis; Inflammation; Sepsis; Cell membranes; phosphatidylserine; Kidney; Cell interactions; Immunosuppression DO - http://dx.doi.org/10.1038/ki.2015.26 ER - TY - JOUR T1 - Increased Infectivity of Anchorless Mouse Scrapie Prions in Transgenic Mice Overexpressing Human Prion Protein AN - 1701480718; PQ0001679751 AB - Prion protein (PrP) is found in all mammals, mostly as a glycoprotein anchored to the plasma membrane by a C-terminal glycosylphosphatidylinositol (GPI) linkage. Following prion infection, host protease-sensitive prion protein (PrPsen or PrPC) is converted into an abnormal, disease-associated, protease-resistant form (PrPres). Biochemical characteristics, such as the PrP amino acid sequence, and posttranslational modifications, such as glycosylation and GPI anchoring, can affect the transmissibility of prions as well as the biochemical properties of the PrPres generated. Previous in vivo studies on the effects of GPI anchoring on prion infectivity have not examined cross-species transmission. In this study, we tested the effect of lack of GPI anchoring on a species barrier model using mice expressing human PrP. In this model, anchorless 22L prions derived from tg44 mice were more infectious than 22L prions derived from C57BL/10 mice when tested in tg66 transgenic mice, which expressed wild-type anchored human PrP at 8- to 16-fold above normal. Thus, the lack of the GPI anchor on the PrPres from tg44 mice appeared to reduce the effect of the mouse-human PrP species barrier. In contrast, neither source of prions induced disease in tgRM transgenic mice, which expressed human PrP at 2- to 4-fold above normal. IMPORTANCE Prion protein (PrP) is found in all mammals, usually attached to cells by an anchor molecule called GPI. Following prion infection, PrP is converted into a disease-associated form (PrPres). While most prion diseases are species specific, this finding is not consistent, and species barriers differ in strength. The amino acid sequence of PrP varies among species, and this variability affects prion species barriers. However, other PrP modifications, including glycosylation and GPI anchoring, may also influence cross-species infectivity. We studied the effect of PrP GPI anchoring using a mouse-to-human species barrier model. Experiments showed that prions produced by mice expressing only anchorless PrP were more infectious than prions produced in mice expressing anchored PrP. Thus, the lack of the GPI anchor on prions reduced the effect of the mouse-human species barrier. Our results suggest that prion diseases that produce higher levels of anchorless PrP may pose an increased risk for cross-species infection. JF - Journal of Virology AU - Race, Brent AU - Phillips, Katie AU - Meade-White, Kimberly AU - Striebel, James AU - Chesebro, Bruce AD - Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA, raceb@niaid.nih.gov. PY - 2015 SP - 6022 EP - 6032 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 89 IS - 11 SN - 0022-538X, 0022-538X KW - Biotechnology and Bioengineering Abstracts; Genetics Abstracts; Virology & AIDS Abstracts KW - Animal models KW - Glycosylation KW - Scrapie KW - Transgenic mice KW - Infection KW - Infectivity KW - Plasma membranes KW - Biochemical characteristics KW - Prion protein KW - Glycosylphosphatidylinositol KW - Glycoproteins KW - Amino acid sequence KW - W 30925:Genetic Engineering KW - G 07870:Mammals KW - V 22380:Prions UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701480718?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Increased+Infectivity+of+Anchorless+Mouse+Scrapie+Prions+in+Transgenic+Mice+Overexpressing+Human+Prion+Protein&rft.au=Race%2C+Brent%3BPhillips%2C+Katie%3BMeade-White%2C+Kimberly%3BStriebel%2C+James%3BChesebro%2C+Bruce&rft.aulast=Race&rft.aufirst=Brent&rft.date=2015-06-01&rft.volume=89&rft.issue=11&rft.spage=6022&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.00362-15 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Number of references - 76 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Infectivity; Plasma membranes; Biochemical characteristics; Animal models; Prion protein; Glycosylphosphatidylinositol; Glycoproteins; Scrapie; Glycosylation; Infection; Transgenic mice; Amino acid sequence DO - http://dx.doi.org/10.1128/JVI.00362-15 ER - TY - JOUR T1 - Polybrominated Diphenyl Ethers and Thyroid Cancer Risk in the Prostate, Colorectal, Lung, and Ovarian Cancer Screening Trial Cohort AN - 1701480198; PQ0001732751 AB - Polybrominated diphenyl ethers (PBDEs) alter thyroid hormone homeostasis, but their relationship with thyroid cancer is unknown. To investigate whether serum concentrations of PBDE were associated with thyroid cancer, we conducted a nested, case-control study in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, a large multicenter clinical trial in the United States. Cases with thyroid cancer (n = 104) were recruited from 1992 to 2001 and diagnosed through 2009, and controls (n = 208) were individually matched (2:1) to cases by race, sex, birth date (within 1 year), center, and blood collection date (within 15 days). We used gas chromatography isotope dilution high-resolution mass spectrometry to measure 10 tri- to heptabrominated diphenyl eithers in serum samples. Odds ratios and 95% confidence intervals were calculated using conditional logistic regression for lipid-adjusted PBDE levels detected in more than 50% of controls and for the sum of these BDEs ( capital sigma PBDEs). We observed no significant differences between cases and controls in lipid-adjusted concentrations of capital sigma PBDEs (for cases, median = 12.8 ng/g lipid (interquartile range, 6.2-42.1); for controls, median = 19.4 ng/g lipid (interquartile range, 7.6-50.2)) or for individual congeners. Increasing quartiles of capital sigma PBDEs and 4 BDE congeners were not associated with risk of thyroid cancer (for the fourth vs. first quartile of capital sigma PBDEs, adjusted odd ratio = 0.62, 95% confidence interval: 0.29, 1.30; P for trend = 0.56). Our study does not support an association between exposure to PBDEs and thyroid cancer. JF - American Journal of Epidemiology AU - Aschebrook-Kilfoy, Briseis AU - DellaValle, Curt T AU - Purdue, Mark AU - Kim, Christopher AU - Zhang, Yawei AU - Sjodin, Andreas AU - Ward, Mary H AD - Correspondence to Dr. Mary H. Ward, Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH/DHHS, 9609 Medical Center Drive, 6E-138, Rockville, MD 20850 MSC 9771, wardm@mail.nih.gov Y1 - 2015/06/01/ PY - 2015 DA - 2015 Jun 01 SP - 883 EP - 888 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 181 IS - 11 SN - 0002-9262, 0002-9262 KW - Toxicology Abstracts; Risk Abstracts; Health & Safety Science Abstracts KW - brominated diphenyl ethers KW - flame retardants KW - thyroid cancer risk KW - Isotopes KW - Mass spectrometry KW - Homeostasis KW - Hormones KW - Clinical trials KW - Mass spectroscopy KW - Polybrominated diphenyl ethers KW - Thyroid hormones KW - Gas chromatography KW - thyroid cancer KW - Congeners KW - Ovarian carcinoma KW - Races KW - Sex KW - Lung cancer KW - Ovarian cancer KW - Thyroid KW - Cancer KW - Birth KW - Health risks KW - Blood KW - USA KW - polybrominated diphenyl ethers KW - Lung KW - Prostate KW - R2 23060:Medical and environmental health KW - X 24350:Industrial Chemicals KW - H 4000:Food and Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701480198?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Polybrominated+Diphenyl+Ethers+and+Thyroid+Cancer+Risk+in+the+Prostate%2C+Colorectal%2C+Lung%2C+and+Ovarian+Cancer+Screening+Trial+Cohort&rft.au=Aschebrook-Kilfoy%2C+Briseis%3BDellaValle%2C+Curt+T%3BPurdue%2C+Mark%3BKim%2C+Christopher%3BZhang%2C+Yawei%3BSjodin%2C+Andreas%3BWard%2C+Mary+H&rft.aulast=Aschebrook-Kilfoy&rft.aufirst=Briseis&rft.date=2015-06-01&rft.volume=181&rft.issue=11&rft.spage=883&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwu358 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2015-09-03 N1 - SubjectsTermNotLitGenreText - Ovarian cancer; Isotopes; Homeostasis; Clinical trials; Mass spectroscopy; Birth; Thyroid hormones; Blood; polybrominated diphenyl ethers; Gas chromatography; thyroid cancer; Congeners; Prostate; Races; Lung cancer; Sex; Polybrominated diphenyl ethers; Health risks; Lung; Thyroid; Mass spectrometry; Ovarian carcinoma; Hormones; Cancer; USA DO - http://dx.doi.org/10.1093/aje/kwu358 ER - TY - JOUR T1 - Continual Reintroduction of Human Pandemic H1N1 Influenza A Viruses into Swine in the United States, 2009 to 2014 AN - 1701480110; PQ0001679793 AB - The diversity of influenza A viruses in swine (swIAVs) presents an important pandemic threat. Knowledge of the human-swine interface is particularly important for understanding how viruses with pandemic potential evolve in swine hosts. Through phylogenetic analysis of contemporary swIAVs in the United States, we demonstrate that human-to-swine transmission of pandemic H1N1 (pH1N1) viruses has occurred continuously in the years following the 2009 H1N1 pandemic and has been an important contributor to the genetic diversity of U.S. swIAVs. Although pandemic H1 and N1 segments had been largely removed from the U.S. swine population by 2013 via reassortment with other swIAVs, these antigens reemerged following multiple human-to-swine transmission events during the 2013-2014 seasonal epidemic. These findings indicate that the six internal gene segments from pH1N1 viruses are likely to be sustained long term in the U.S. swine population, with periodic reemergence of pandemic hemagglutinin (HA) and neuraminidase (NA) segments in association with seasonal pH1N1 epidemics in humans. Vaccinating U.S. swine workers may reduce infection of both humans and swine and in turn limit the role of humans as sources of influenza virus diversity in pigs. IMPORTANCE Swine are important hosts in the evolution of influenza A viruses with pandemic potential. Here, we analyze influenza virus sequence data generated by the U.S. Department of Agriculture's national surveillance system to identify the central role of humans in the reemergence of pandemic H1N1 (pH1N1) influenza viruses in U.S. swine herds in 2014. These findings emphasize the important role of humans as continuous sources of influenza virus diversity in swine and indicate that influenza viruses with pandemic HA and NA segments are likely to continue to reemerge in U.S. swine in association with seasonal pH1N1 epidemics in humans. JF - Journal of Virology AU - Nelson, Martha I AU - Stratton, Jered AU - Killian, Mary Lea AU - Janas-Martindale, Alicia AU - Vincent, Amy L AD - Fogarty International Center, National Institutes of Health, Bethesda, Maryland, USA, nelsonma@mail.nih.gov. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 6218 EP - 6226 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 89 IS - 12 SN - 0022-538X, 0022-538X KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Agriculture KW - Reintroduction KW - Phylogeny KW - Data processing KW - Epidemics KW - Hemagglutinins KW - Influenza A KW - Viruses KW - Genetic diversity KW - Infection KW - Influenza KW - Workers KW - USA KW - pandemics KW - Influenza virus KW - Sulfur dioxide KW - Exo- alpha -sialidase KW - Seasonal variations KW - Evolution KW - H 1000:Occupational Safety and Health KW - V 22310:Genetics, Taxonomy & Structure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701480110?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Continual+Reintroduction+of+Human+Pandemic+H1N1+Influenza+A+Viruses+into+Swine+in+the+United+States%2C+2009+to+2014&rft.au=Nelson%2C+Martha+I%3BStratton%2C+Jered%3BKillian%2C+Mary+Lea%3BJanas-Martindale%2C+Alicia%3BVincent%2C+Amy+L&rft.aulast=Nelson&rft.aufirst=Martha&rft.date=2015-06-01&rft.volume=89&rft.issue=12&rft.spage=6218&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.00459-15 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Number of references - 36 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Phylogeny; Reintroduction; Agriculture; Epidemics; Data processing; Influenza A; Hemagglutinins; Genetic diversity; Infection; Workers; pandemics; Exo- alpha -sialidase; Evolution; Influenza; Sulfur dioxide; Viruses; Seasonal variations; Influenza virus; USA DO - http://dx.doi.org/10.1128/JVI.00459-15 ER - TY - JOUR T1 - Cartilage Regeneration of Adipose-Derived Stem Cells in the TGF- beta 1-Immobilized PLGA-Gelatin Scaffold AN - 1701477712; PQ0001806208 AB - Articular cartilage has restricted self-regenerative capacity; therefore, treatment of cartilage lesions is a great challenge in the field of orthopedics. In the present study, we evaluate the enhancing effect of a transforming growth factor-beta 1 (TGF- beta 1)-immobilized scaffold, fabricated by incorporating TGF- beta 1-loaded gelatin microspheres into PLGA framework, on the differentiation of adipose-derived stem cells (ASCs) into chondrocytes. Significant increase in cell proliferation was observed in the TGF- beta 1-immobilized PLGA-gelatin scaffold, as compared with the ASC-seeded non-TGF- beta 1-immobilized PLGA-gelatin scaffold. When chondrogenic differentiation of ASCs was evaluated for both constructs, sulfated glycosaminoglycan (sGAG) content was significantly higher in the TGF- beta 1-immobilized scaffold. This study showed that ASCs containing the TGF- beta 1-immobilized scaffold better promoted cartilage regeneration in defective articular cartilage, which is assessed by histological observation. Based on the above results, we conclude that TGF- beta 1-immobilized PLGA-gelatin scaffold seeded with ASCs considerably enhances the quality of the tissue-engineered cartilage, therefore, advancing the field of cartilage tissue engineering. JF - Stem Cell Reviews AU - Yin, Feng AU - Cai, Junfeng AU - Zen, Wen AU - Wei, Yanhui AU - Zhou, Wei AU - Yuan, Feng AU - Singh, Shree Ram AU - Wei, Yiyong AD - Department of Joint and Bone Disease Shanghai East Hospital, Tongji University School of Medicine, Shanghai, 200120, People's Republic of China, singhshr@mail.nih.gov Y1 - 2015/06// PY - 2015 DA - Jun 2015 SP - 453 EP - 459 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 11 IS - 3 SN - 1550-8943, 1550-8943 KW - Biotechnology and Bioengineering Abstracts KW - Transforming growth factor- beta 1 KW - polylactide-co-glycolide KW - Orthopedics KW - Gelatin KW - Chondrocytes KW - Tissue engineering KW - scaffolds KW - Differentiation KW - Stem cells KW - Glycosaminoglycans KW - microspheres KW - Cell proliferation KW - Cartilage (articular) KW - Chondrogenesis KW - W 30920:Tissue Engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701477712?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+Cell+Reviews&rft.atitle=Cartilage+Regeneration+of+Adipose-Derived+Stem+Cells+in+the+TGF-+beta+1-Immobilized+PLGA-Gelatin+Scaffold&rft.au=Yin%2C+Feng%3BCai%2C+Junfeng%3BZen%2C+Wen%3BWei%2C+Yanhui%3BZhou%2C+Wei%3BYuan%2C+Feng%3BSingh%2C+Shree+Ram%3BWei%2C+Yiyong&rft.aulast=Yin&rft.aufirst=Feng&rft.date=2015-06-01&rft.volume=11&rft.issue=3&rft.spage=453&rft.isbn=&rft.btitle=&rft.title=Stem+Cell+Reviews&rft.issn=15508943&rft_id=info:doi/10.1007%2Fs12015-014-9561-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Number of references - 28 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Transforming growth factor- beta 1; polylactide-co-glycolide; Orthopedics; Gelatin; Chondrocytes; Tissue engineering; scaffolds; Differentiation; Stem cells; Glycosaminoglycans; microspheres; Cartilage (articular); Cell proliferation; Chondrogenesis DO - http://dx.doi.org/10.1007/s12015-014-9561-9 ER - TY - JOUR T1 - Biomarker development in the context of urologic cancers. AN - 1700106972; 25746942 AB - The Food and Drug Administration (FDA) has called for the use of analytically validated biomarkers that have strong evidence of being fit for purpose to identify patients likely to respond and to evaluate the patient response to a therapy, potential toxicity, and drug resistance. This article discusses development and application of these biomarkers in the context of urologic cancers-specifically in cancers of the prostate and urinary bladder. The FDA has defined four specific categories for contexts of biomarker use: prognostic, predictive, response-indicator, and efficacy-response (surrogate endpoints). Prognostic and predictive biomarkers include pretreatment characteristics of the patient and the tumor. Response-indicator and efficacy response biomarkers occur after treatment and show the effects of treatment on biomarkers. Efficacy response biomarkers show changes associated with clinical benefit and can be surrogates for clinical endpoints leading to drug approvals. Well-structured development plans are required to satisfy rigorous criteria that must be met to qualify biomarkers for specific contexts of use in drug development and patient management. A description of the extensive effort applied to the validation and qualification of circulating tumor cells in castration resistant prostate cancer is described as an example of the potential utility of biomarkers in urological cancers. Many potential biomarkers have been identified in prostate and urinary bladder cancers, but few have sufficient demonstration of analytical and clinical validity to meet FDA standards for use in clinical settings. Circulating tumor cell (CTC) assays are particularly promising candidates for informative new biomarkers to measure disease before and after treatment. New technologies are providing opportunities for high definition, more informative analysis. Statistical and computational methodologies to describe assay results are also rapidly evolving. These advances will lead to better diagnosis, earlier indications of treatment response and failure, and better definition of patient cohorts that will respond to a specific treatment. Copyright © 2015 Elsevier Inc. All rights reserved. JF - Urologic oncology AU - Kelloff, Gary J AU - Sigman, Caroline C AU - Scher, Howard I AD - Division of Cancer Treatment and Diagnosis, National Cancer Institute, National Institutes of Health, Rockville, MD. ; CCS Associates, Mountain View, CA. Electronic address: csigman@ccsainc.com. ; Genitourinary Oncology Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY; Department of Medicine, Weill Cornell Medical College, New York, NY. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 295 EP - 301 VL - 33 IS - 6 KW - Biomarkers, Tumor KW - 0 KW - Index Medicus KW - Biomarker qualification KW - Analytical validation KW - Prostate cancer biomarkers KW - Bladder cancer biomarkers KW - Biomarker KW - Clinical utility KW - Circulating tumor cells (CTCs) KW - Humans KW - Prognosis KW - Biomarkers, Tumor -- metabolism KW - Urologic Neoplasms -- genetics KW - Urologic Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1700106972?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Urologic+oncology&rft.atitle=Biomarker+development+in+the+context+of+urologic+cancers.&rft.au=Kelloff%2C+Gary+J%3BSigman%2C+Caroline+C%3BScher%2C+Howard+I&rft.aulast=Kelloff&rft.aufirst=Gary&rft.date=2015-06-01&rft.volume=33&rft.issue=6&rft.spage=295&rft.isbn=&rft.btitle=&rft.title=Urologic+oncology&rft.issn=1873-2496&rft_id=info:doi/10.1016%2Fj.urolonc.2015.01.007 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-24 N1 - Date created - 2015-05-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Rev Clin Oncol. 2013 Apr;10(4):225-34 [23459624] Clin Pharmacol Ther. 2007 Jan;81(1):104-7 [17186007] N Engl J Med. 2013 Jan 10;368(2):138-48 [23228172] J Nucl Med. 2010 Sep;51(9):1344-8 [20720059] Neoplasia. 2010 Aug;12(8):628-36 [20689757] Clin Cancer Res. 2010 Jul 1;16(13):3299-318 [20501613] Nat Rev Clin Oncol. 2010 Jun;7(6):309-17 [20368727] Pain Med. 2010 Mar;11(3):337-46 [20030743] J Clin Oncol. 2009 Nov 10;27(32):5431-8 [19805692] Cell. 2009 Mar 6;136(5):823-37 [19269363] Clin Cancer Res. 2008 May 1;14(9):2763-7 [18451243] Nat Rev Cancer. 2008 May;8(5):329-40 [18404148] J Clin Oncol. 2008 Mar 1;26(7):1148-59 [18309951] Ann Oncol. 2007 Mar;18(3):522-8 [17229776] Arch Esp Urol. 2013 Jun;66(5):495-504 [23793767] Clin Cancer Res. 2014 Mar 15;20(6):1428-44 [24634466] Oncology (Williston Park). 2014 Feb;28(2):135-42 [24701701] Cancer Discov. 2014 Jun;4(6):650-61 [24801577] Nat Rev Drug Discov. 2014 Nov;13(11):783-4 [25359359] Clin Cancer Res. 2007 Apr 1;13(7):2023-9 [17404082] J Clin Oncol. 2013 Feb 1;31(4):412-9 [23169517] N Engl J Med. 2012 Sep 27;367(13):1187-97 [22894553] Clin Cancer Res. 2012 Mar 15;18(6):1540-6 [22422406] Nat Rev Drug Discov. 2012 Mar;11(3):201-14 [22322254] Cancer J. 2011 Nov-Dec;17(6):438-50 [22157288] Curr Opin Urol. 2011 Sep;21(5):420-7 [21814055] N Engl J Med. 2011 Jun 30;364(26):2507-16 [21639808] Clin Cancer Res. 2011 Jun 15;17(12):3903-12 [21680546] Clin Cancer Res. 2011 Apr 15;17(8):2561-9 [21177407] Breast Cancer Res Treat. 2011 May;127(1):133-42 [21221771] Cell. 2011 Mar 4;144(5):646-74 [21376230] Cold Spring Harb Perspect Biol. 2010 Nov;2(11):a003244 [20591988] Br J Cancer. 2010 Oct 26;103(9):1313-7 [20924371] Cancer Res. 2010 Sep 15;70(18):7017-26 [20843819] Sci Transl Med. 2010 Sep 1;2(47):47ps44 [20811041] J Clin Oncol. 1996 Jun;14(6):1756-64 [8656243] J Clin Oncol. 1999 Jun;17(6):1654-63 [10561201] Cell. 2000 Jan 7;100(1):57-70 [10647931] Urology. 2004 May;63(5):940-5 [15134985] Clin Cancer Res. 2004 Jun 1;10(11):3885-96 [15173098] Science. 2005 Oct 28;310(5748):644-8 [16254181] Nat Rev Cancer. 2006 Jul;6(7):565-71 [16794639] J Transl Med. 2012;10:138 [22747748] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.urolonc.2015.01.007 ER - TY - JOUR T1 - Prevalence, associated factors and source of support concerning supportive care needs among Japanese cancer survivors AN - 1695153495 AB - Background The current study aimed to describe cancer survivorsʼ supportive care needs in Japan, to identify associated factors of unmet needs, and to describe the source of support that are preferred and actually used by cancer survivors. Methods Using a web-based questionnaire, we examined unmet supportive needs and its associated factors among 628 adult Japanese cancer survivors. The questionnaire comprised 16 items representing five domains (medical-psychological, financial, social-spiritual, sexual, and physical needs). Results Prevalence of unmet need ranged from 5 to 18%, depending on different domains. The prevalence was high in medical-psychological and financial domains and relatively low in physical and sexual domains. Poor performance status, psychiatric morbidity and low income status were associated with unmet needs of most domains. Most cancer survivors preferred and actually sought support from their family and friends. Financial needs were preferred to be provided by non-medical professionals. Call for peer support was intense, especially for medical-psychological, social-spiritual, and sexual needs; however, peer support was not well-provided. Conclusions This study illustrated characteristics of Japanese cancer survivors who are likely to have unmet needs. The study demonstrated need for expanded involvement of non-medical professionals and peer support, especially in the domains of medical-psychological, social-spiritual, financial and sexual needs. JF - Psycho-Oncology AU - Umezawa, Shino AU - Fujisawa, Daisuke AU - Fujimori, Maiko AU - Ogawa, Asao AU - Matsushima, Eisuke AU - Miyashita, Mitsunori AD - Psycho-Oncology Division, National Cancer Center Hospital East, Kashiwa, Chiba, Japan., Section of Liaison Psychiatry and Palliative Medicine, Division of Comprehensive Patient Care, Tokyo Medical and Dental University Graduate School of Medical and Dental Sciences, Tokyo, Japan. ; Psycho-Oncology Division, National Cancer Center Hospital East, Kashiwa, Chiba, Japan., Center for Psychiatric Oncology and Behavioral Sciences, Massachusetts General Hospital, Boston, MA, USA., Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan. ; Psycho-Oncology Division, National Cancer Center Hospital East, Kashiwa, Chiba, Japan., Center for Suicide Prevention, National Institute of Mental Health, National Center for Neurology Psychiatry, Tokyo, Japan. ; Psycho-Oncology Division, National Cancer Center Hospital East, Kashiwa, Chiba, Japan. ; Section of Liaison Psychiatry and Palliative Medicine, Division of Comprehensive Patient Care, Tokyo Medical and Dental University Graduate School of Medical and Dental Sciences, Tokyo, Japan. ; Division of Palliative Nursing, Health Sciences, Tohoku University Graduate School of Medicine, Sendai, Japan. ; Psycho-Oncology Division, National Cancer Center Hospital East, Kashiwa, Chiba, Japan.; Section of Liaison Psychiatry and Palliative Medicine, Division of Comprehensive Patient Care, Tokyo Medical and Dental University Graduate School of Medical and Dental Sciences, Tokyo, Japan. Y1 - 2015/06// PY - 2015 DA - Jun 2015 SP - 635 EP - 642 CY - Chichester PB - Wiley Subscription Services, Inc. VL - 24 IS - 6 SN - 1057-9249 KW - Medical Sciences--Psychiatry And Neurology KW - Cancer KW - Computer based KW - Friends KW - Internet KW - Medical professionals KW - Morbidity KW - Psychiatric morbidity KW - Survivors KW - Unmet needs KW - Japan UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1695153495?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psycho-Oncology&rft.atitle=Prevalence%2C+associated+factors+and+source+of+support+concerning+supportive+care+needs+among+Japanese+cancer+survivors&rft.au=Umezawa%2C+Shino%3BFujisawa%2C+Daisuke%3BFujimori%2C+Maiko%3BOgawa%2C+Asao%3BMatsushima%2C+Eisuke%3BMiyashita%2C+Mitsunori&rft.aulast=Umezawa&rft.aufirst=Shino&rft.date=2015-06-01&rft.volume=24&rft.issue=6&rft.spage=635&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.3702 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-09-22 N1 - Last updated - 2016-05-12 N1 - SubjectsTermNotLitGenreText - Japan DO - http://dx.doi.org/10.1002/pon.3702 ER - TY - JOUR T1 - A proteomic approach to discover and compare interacting partners of papillomavirus E2 proteins from diverse phylogenetic groups AN - 1694977920; PQ0001665427 AB - Papillomaviruses are a very successful group of viruses that replicate persistently in localized regions of the stratified epithelium of their specific host. Infection results in pathologies ranging from asymptomatic infection, benign warts, to malignant carcinomas. Despite this diversity, papillomavirus genomes are small (7-8 kbp) and contain at most eight genes. To sustain the complex papillomaviral life cycle, each viral protein has multiple functions and interacts with and manipulates a plethora of cellular proteins. In this study, we use tandem affinity purification and MS to identify host factors that interact with 11 different papillomavirus E2 proteins from diverse phylogenetic groups. The E2 proteins function in viral transcription and replication and correspondingly interact with host proteins involved in transcription, chromatin remodeling and modification, replication, and RNA processing. JF - Proteomics AU - Jang, Moon Kyoo AU - Anderson, DEric AU - Doorslaer, Koenraad AU - McBride, Alison A AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD, USA. Y1 - 2015/06// PY - 2015 DA - Jun 2015 SP - 2038 EP - 2050 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 15 IS - 12 SN - 1615-9853, 1615-9853 KW - Virology & AIDS Abstracts; Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Genomes KW - Phylogeny KW - Chromatin remodeling KW - Replication KW - Life cycle KW - Transcription KW - Asymptomatic infection KW - E2 protein KW - protein purification KW - Carcinoma KW - RNA processing KW - Warts KW - RNA modification KW - Epithelium KW - proteomics KW - Papillomavirus KW - Benign KW - G 07880:Human Genetics KW - W 30960:Bioinformatics & Computer Applications KW - V 22370:Oncology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1694977920?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proteomics&rft.atitle=A+proteomic+approach+to+discover+and+compare+interacting+partners+of+papillomavirus+E2+proteins+from+diverse+phylogenetic+groups&rft.au=Jang%2C+Moon+Kyoo%3BAnderson%2C+DEric%3BDoorslaer%2C+Koenraad%3BMcBride%2C+Alison+A&rft.aulast=Jang&rft.aufirst=Moon&rft.date=2015-06-01&rft.volume=15&rft.issue=12&rft.spage=2038&rft.isbn=&rft.btitle=&rft.title=Proteomics&rft.issn=16159853&rft_id=info:doi/10.1002%2Fpmic.201400613 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-07-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Phylogeny; Genomes; Chromatin remodeling; Replication; Transcription; Life cycle; E2 protein; Asymptomatic infection; protein purification; Carcinoma; RNA processing; Warts; RNA modification; Epithelium; proteomics; Benign; Papillomavirus DO - http://dx.doi.org/10.1002/pmic.201400613 ER - TY - JOUR T1 - Re: Assessment by three-dimensional power Doppler ultrasound of cerebral blood flow perfusion in fetuses with congenital heart disease. S. Zeng, J. Zhou, Q. Peng, L. Tian, G. Xu, Y. Zhao, T. Wang and Q. Zhou. Ultrasound Obstet Gynecol 2015; 45: 649-656 AN - 1694969991; PQ0001665840 AB - Linked Comment: Ultrasound Obstet Gynecol 2015; 45: 649-656 JF - Ultrasound in Obstetrics and Gynecology AU - Hernandez-Andrade, E AD - Department of Obstetrics and Gynecology, Division of Maternal Fetal Medicine, Wayne State University, School of Medicine, Perinatology Research Branch, NICHD/NIH/DHHS, Detroit, MI, USA. Y1 - 2015/06// PY - 2015 DA - Jun 2015 SP - 629 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 45 IS - 6 SN - 0960-7692, 0960-7692 KW - Biotechnology and Bioengineering Abstracts KW - Perfusion KW - Gynecology KW - Doppler effect KW - Ultrasound KW - Obstetrics KW - Cerebral blood flow KW - Fetuses KW - Heart diseases KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1694969991?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Ultrasound+in+Obstetrics+and+Gynecology&rft.atitle=Re%3A+Assessment+by+three-dimensional+power+Doppler+ultrasound+of+cerebral+blood+flow+perfusion+in+fetuses+with+congenital+heart+disease.+S.+Zeng%2C+J.+Zhou%2C+Q.+Peng%2C+L.+Tian%2C+G.+Xu%2C+Y.+Zhao%2C+T.+Wang+and+Q.+Zhou.+Ultrasound+Obstet+Gynecol+2015%3B+45%3A+649-656&rft.au=Hernandez-Andrade%2C+E&rft.aulast=Hernandez-Andrade&rft.aufirst=E&rft.date=2015-06-01&rft.volume=45&rft.issue=6&rft.spage=629&rft.isbn=&rft.btitle=&rft.title=Ultrasound+in+Obstetrics+and+Gynecology&rft.issn=09607692&rft_id=info:doi/10.1002%2Fuog.14887 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-07-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Perfusion; Gynecology; Doppler effect; Obstetrics; Ultrasound; Fetuses; Cerebral blood flow; Heart diseases DO - http://dx.doi.org/10.1002/uog.14887 ER - TY - JOUR T1 - Association between arterial stiffness, cerebral small vessel disease and cognitive impairment: A systematic review and meta-analysis. AN - 1694705267; 25827412 AB - Arterial stiffness may be a cause of cerebral small vessel disease and cognitive impairment. We therefore performed a systematic review and meta-analysis of studies on the association between stiffness, cerebral small vessel disease and cognitive impairment. For the associations between stiffness (i.e. carotid-femoral pulse wave velocity (cfPWV), brachial-ankle PWV (baPWV), carotid stiffness and pulse pressure) on the one hand and cerebral small vessel disease and cognitive impairment on the other, we identified 23 (n=15,666/20 cross-sectional; 1 longitudinal; 2 combined cross-sectional/longitudinal) and 41 studies (n=57,671/26 cross-sectional; 11 longitudinal; 4 combined cross-sectional/longitudinal), respectively. Pooled analyses of cross-sectional studies showed that greater stiffness was associated with markers of cerebral small vessel disease with odds ratios, per +1 SD, of 1.29-1.32 (P<.001). Studies on cognitive impairment could not be pooled due to large heterogeneity. Some (but not all) studies showed an association between greater stiffness and cognitive impairment, and the strength of this association was relatively weak. The present study supports the hypothesis that greater arterial stiffness is a contributor to microvascular brain disease. Copyright © 2015 Elsevier Ltd. All rights reserved. JF - Neuroscience and biobehavioral reviews AU - van Sloten, Thomas T AU - Protogerou, Athanase D AU - Henry, Ronald M A AU - Schram, Miranda T AU - Launer, Lenore J AU - Stehouwer, Coen D A AD - Department of Medicine, Cardiovascular Research Institute Maastricht and School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Centre, Prof. Debyelaan 25, Maastricht, The Netherlands. ; Department of Medicine, Cardiovascular Research Institute Maastricht, Maastricht University Medical Centre, Prof. Debyelaan 25, Maastricht, The Netherlands. ; Intramural Research Program, Laboratory of Epidemiology and Population Sciences, National Institute on Aging, National Institutes of Health, 7201 Wisconsin Avenue, Bethesda, MD, USA. ; Department of Medicine, Cardiovascular Research Institute Maastricht, Maastricht University Medical Centre, Prof. Debyelaan 25, Maastricht, The Netherlands. Electronic address: cda.stehouwer@mumc.nl. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 121 EP - 130 VL - 53 KW - Index Medicus KW - Cerebral small vessel disease KW - Arterial stiffness KW - Cerebral infarcts KW - Meta-analysis KW - Cerebral microbleeds KW - Systematic review KW - Dementia KW - Cognitive impairment KW - White matter hyperintensities KW - Blood Pressure KW - Risk Factors KW - Humans KW - Cerebral Small Vessel Diseases -- psychology KW - Cognition Disorders -- epidemiology KW - Cognition Disorders -- physiopathology KW - Cerebral Small Vessel Diseases -- physiopathology KW - Vascular Stiffness KW - Cerebral Small Vessel Diseases -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1694705267?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuroscience+and+biobehavioral+reviews&rft.atitle=Association+between+arterial+stiffness%2C+cerebral+small+vessel+disease+and+cognitive+impairment%3A+A+systematic+review+and+meta-analysis.&rft.au=van+Sloten%2C+Thomas+T%3BProtogerou%2C+Athanase+D%3BHenry%2C+Ronald+M+A%3BSchram%2C+Miranda+T%3BLauner%2C+Lenore+J%3BStehouwer%2C+Coen+D+A&rft.aulast=van+Sloten&rft.aufirst=Thomas&rft.date=2015-06-01&rft.volume=53&rft.issue=&rft.spage=121&rft.isbn=&rft.btitle=&rft.title=Neuroscience+and+biobehavioral+reviews&rft.issn=1873-7528&rft_id=info:doi/10.1016%2Fj.neubiorev.2015.03.011 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-28 N1 - Date created - 2015-05-08 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.neubiorev.2015.03.011 ER - TY - JOUR T1 - Whole pelvic intensity-modulated radiotherapy for gynecological malignancies: A review of the literature. AN - 1693184188; 25600840 AB - Radiation therapy has long played a major role in the treatment of gynecological malignancies. There is increasing interest in the utility of intensity-modulated radiotherapy (IMRT) and its application to treat gynecological malignancies. Herein, we review the state-of-the-art use of IMRT for gynecological malignancies and report how it is being used alone as well as in combination with chemotherapy in both the adjuvant and definitive settings. Based on dosimetric and clinical evidence, IMRT can reduce gastrointestinal, genitourinary, and hematological toxicities compared with 3D-conformal radiotherapy for gynecologic malignancies. We discuss how these attributes of IMRT may lead to improvements in disease outcomes by allowing for dose escalation of radiation therapy, intensification of chemotherapy, and limiting toxicity-related treatment breaks. Currently accruing trials investigating pelvic IMRT for cervical and endometrial cancers are discussed. Published by Elsevier Ireland Ltd. JF - Critical reviews in oncology/hematology AU - Hymel, Rockne AU - Jones, Guy C AU - Simone, Charles B AD - Louisiana State University Health Sciences Center, School of Medicine, 1901 Perdido Street, New Orleans, LA 70112, United States. Electronic address: rhyme1@lsuhsc.edu. ; Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, United States. Electronic address: guy.jones@nih.gov. ; Department of Radiation Oncology, University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA 19104, United States. Electronic address: charles.simone@uphs.upenn.edu. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 371 EP - 379 VL - 94 IS - 3 KW - Index Medicus KW - Radiation therapy KW - IMRT KW - Endometrial KW - Cervical KW - Gynecologic KW - Radiometry KW - Radiotherapy, Image-Guided KW - Radiotherapy Dosage KW - Humans KW - Treatment Outcome KW - Female KW - Radiotherapy, Intensity-Modulated -- methods KW - Pelvis -- radiation effects KW - Genital Neoplasms, Female -- radiotherapy KW - Genital Neoplasms, Female -- mortality KW - Radiotherapy, Intensity-Modulated -- adverse effects KW - Pelvis -- pathology KW - Genital Neoplasms, Female -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1693184188?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Critical+reviews+in+oncology%2Fhematology&rft.atitle=Whole+pelvic+intensity-modulated+radiotherapy+for+gynecological+malignancies%3A+A+review+of+the+literature.&rft.au=Hymel%2C+Rockne%3BJones%2C+Guy+C%3BSimone%2C+Charles+B&rft.aulast=Hymel&rft.aufirst=Rockne&rft.date=2015-06-01&rft.volume=94&rft.issue=3&rft.spage=371&rft.isbn=&rft.btitle=&rft.title=Critical+reviews+in+oncology%2Fhematology&rft.issn=1879-0461&rft_id=info:doi/10.1016%2Fj.critrevonc.2014.12.015 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-07 N1 - Date created - 2015-05-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Int J Radiat Oncol Biol Phys. 2010 Aug 1;77(5):1590-5 [20378265] Radiother Oncol. 2011 Mar;98(3):340-6 [21295877] Radiother Oncol. 1999 Jul;52(1):29-34 [10577683] Gynecol Oncol. 2001 Sep;82(3):456-63 [11520140] Int J Radiat Oncol Biol Phys. 2002 Apr 1;52(5):1330-7 [11955746] Int J Radiat Oncol Biol Phys. 2002 Dec 1;54(5):1388-96 [12459361] Int J Radiat Oncol Biol Phys. 2003 Aug 1;56(5):1354-60 [12873680] Int J Radiat Oncol Biol Phys. 2003 Oct 1;57(2):516-21 [12957265] Br J Radiol. 2003 Oct;76(910):678-89 [14512327] Gynecol Oncol. 2003 Oct;91(1):39-45 [14529660] Semin Oncol. 2003 Oct;30(5):596-615 [14571409] Gynecol Oncol. 2004 Mar;92(3):744-51 [14984936] Int J Radiat Oncol Biol Phys. 2004 Oct 1;60(2):505-12 [15380585] Int J Radiat Oncol Biol Phys. 1995 Jul 30;32(5):1275-88 [7635767] Int J Radiat Oncol Biol Phys. 1997 Jan 15;37(2):351-8 [9069307] Int J Radiat Oncol Biol Phys. 1999 Jul 1;44(4):855-66 [10386643] Cancer. 2005 Sep 15;104(6):1296-303 [16078260] Gynecol Oncol. 2006 Aug;102(2):195-9 [16647748] Radiother Oncol. 2006 Jul;80(1):19-26 [16766068] Int J Radiat Oncol Biol Phys. 2008 Apr 1;70(5):1507-15 [18164850] Radiother Oncol. 2008 Aug;88(2):250-7 [18538873] Int J Radiat Oncol Biol Phys. 2009 May 1;74(1):304-12 [19362250] Int J Radiat Oncol Biol Phys. 2009 Aug 1;74(5):1405-18 [19616743] Lancet. 2010 Mar 6;375(9717):816-23 [20206777] Int J Radiat Oncol Biol Phys. 2011 May 1;80(1):273-80 [21109360] Int J Radiat Oncol Biol Phys. 2011 Nov 15;81(4):e645-50 [21640508] Int J Radiat Oncol Biol Phys. 2012 Apr 1;82(5):1949-56 [21763081] Int J Radiat Oncol Biol Phys. 2012 Sep 1;84(1):e23-8 [22543211] Int J Radiat Oncol Biol Phys. 2013 Mar 1;85(3):686-92 [22795805] Gynecol Oncol. 2013 Mar;128(3):535-9 [23174538] Int J Radiat Oncol Biol Phys. 2013 May 1;86(1):27-33 [23154075] Acta Oncol. 2013 Oct;52(7):1430-6 [23902275] Int J Radiat Oncol Biol Phys. 2013 Nov 1;87(3):542-8 [24074927] Radiother Oncol. 2014 Jun;111(3):442-5 [25034933] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.critrevonc.2014.12.015 ER - TY - JOUR T1 - Consumer attitudes and perceptions on mHealth privacy and security: findings from a mixed-methods study AN - 1690394715; 4684053 AB - This study examined consumers' attitudes and perceptions regarding mobile health (mHealth) technology use in health care. Twenty-four focus groups with 256 participants were conducted in 5 geographically diverse locations. Participants were also diverse in age, education, race/ethnicity, gender, and rural versus urban settings. Several key themes emerged from the focus groups. Findings suggest that consumer attitudes regarding mHealth privacy/security are highly contextualized, with concerns depending on the type of information being communicated, where and when the information is being accessed, who is accessing or seeing the information, and for what reasons. Consumers frequently considered the tradeoffs between the privacy/security of using mHealth technologies and the potential benefits. Having control over mHealth privacy/security features and trust in providers were important issues for consumers. Overall, this study found significant diversity in attitudes regarding mHealth privacy/security both within and between traditional demographic groups. Thus, to address consumers' concerns regarding mHealth privacy and security, a one-size-fits-all approach may not be adequate. Health care providers and technology developers should consider tailoring mHealth technology according to how various types of information are communicated in the health care setting, as well as according to the comfort, skills, and concerns individuals may have with mHealth technology. Reprinted by permission of Taylor & Francis Ltd. JF - Journal of health communication AU - Atienza, Audie A AU - Zarcadoolas, Christina AU - Vaughon, Wendy AU - Hughes, Penelope AU - Patel, Vaishali AU - Chou, Wen-ying Sylvia AU - Pritts, Joy AD - National Institutes of Health ; City University of New York Y1 - 2015/06// PY - 2015 DA - Jun 2015 SP - 673 EP - 679 VL - 20 IS - 6 SN - 1081-0730, 1081-0730 KW - Sociology KW - Attitudes KW - Privacy protection KW - Health care KW - Perception KW - Privacy KW - Consumers UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1690394715?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+health+communication&rft.atitle=Consumer+attitudes+and+perceptions+on+mHealth+privacy+and+security%3A+findings+from+a+mixed-methods+study&rft.au=Atienza%2C+Audie+A%3BZarcadoolas%2C+Christina%3BVaughon%2C+Wendy%3BHughes%2C+Penelope%3BPatel%2C+Vaishali%3BChou%2C+Wen-ying+Sylvia%3BPritts%2C+Joy&rft.aulast=Atienza&rft.aufirst=Audie&rft.date=2015-06-01&rft.volume=20&rft.issue=6&rft.spage=673&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2015.1018560 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-06-23 N1 - Last updated - 2015-06-23 N1 - SubjectsTermNotLitGenreText - 2803 3874 556; 1378 10404; 9382; 5775 13521; 10183; 10184 10183 DO - http://dx.doi.org/10.1080/10810730.2015.1018560 ER - TY - JOUR T1 - Clinical activity and safety of the dual pathway inhibitor rigosertib for higher risk myelodysplastic syndromes following DNA methyltransferase inhibitor therapy. AN - 1689844241; 24777753 AB - Rigosertib (ON 01910.Na) is an inhibitor of the phosphoinositide 3-kinase and polo-like kinase pathways that induces mitotic arrest and apoptosis in neoplastic cells, while sparing normal cells. Our purpose is to summarize the clinical activity and safety of intravenous (IV) rigosertib delivered by an external ambulatory infusion pump in patients with refractory anemia with excess blasts-1, -2, or, -t myelodysplastic syndromes (MDS) following prior treatment with DNA methyltransferase (DNMT) inhibitors. A total of 39 patients with MDS who fulfilled these criteria were enrolled in four phase 1-2 clinical trials of IV rigosertib. Thirty five (88%) had higher risk disease according to the Revised International Prognostic Scoring System. Median overall survival for this group of 39 patients was 35 weeks. Of 30 evaluable patients with follow-up bone marrow biopsies, 12 (40%) achieved complete (n = 5) or partial (n = 7) bone marrow blast responses. In addition, 15 patients achieved stabilization of bone marrow blasts. One patient with a complete bone marrow response also achieved a complete cytogenetic response. A second patient with stable bone marrow blasts achieved a partial cytogenetic response. Two of the responding patients and three patients with stable disease had hematological improvements. Rigosertib-induced bone marrow blast decreases and stability appeared to be predictive of prolonged survival. IV rigosertib had a favorable safety profile without significant myelosuppression. Most common drug-related toxicities included fatigue, diarrhea, nausea, dysuria, and hematuria. In summary, IV rigosertib is well tolerated and has clinical activity in patients with higher risk MDS following DNMT inhibitor treatment. A multinational pivotal phase 3 randomized clinical trial of rigosertib versus best supportive care for patients with MDS with excess blasts following prior treatment with DNMT inhibitors (ONTIME: ON 01910.Na Trial In Myelodysplastic SyndromE) has recently completed enrollment. © 2014 The Authors. Hematological Oncology published by John Wiley & Sons, Ltd. JF - Hematological oncology AU - Silverman, Lewis R AU - Greenberg, Peter AU - Raza, Azra AU - Olnes, Matthew J AU - Holland, James F AU - Reddy, Premkumar AU - Maniar, Manoj AU - Wilhelm, Francois AD - Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. ; Dept. of Medicine (Hematology), Stanford University Cancer Center, Stanford, CA, USA. ; Columbia University Medical Center, New York, NY, USA. ; Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda, MD, USA. ; Onconova Therapeutics Inc, Newtown, PA, USA. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 57 EP - 66 VL - 33 IS - 2 KW - Cell Cycle Proteins KW - 0 KW - Enzyme Inhibitors KW - ON 01910 KW - Protein Kinase Inhibitors KW - Proto-Oncogene Proteins KW - Sulfones KW - DNA (Cytosine-5-)-Methyltransferase KW - EC 2.1.1.37 KW - Phosphatidylinositol 3-Kinases KW - EC 2.7.1.- KW - Protein-Serine-Threonine Kinases KW - EC 2.7.11.1 KW - polo-like kinase 1 KW - Glycine KW - TE7660XO1C KW - Index Medicus KW - myelodysplastic syndromes KW - ON 01910.Na KW - phosphatidylinositol 3-kinase KW - rigosertib KW - DNA methyl transferase inhibitors KW - polo-like kinase KW - Cell Cycle Proteins -- antagonists & inhibitors KW - Humans KW - Aged KW - Protein-Serine-Threonine Kinases -- antagonists & inhibitors KW - Proto-Oncogene Proteins -- antagonists & inhibitors KW - Anemia, Refractory, with Excess of Blasts -- enzymology KW - Protein Kinase Inhibitors -- therapeutic use KW - Aged, 80 and over KW - Anemia, Refractory, with Excess of Blasts -- pathology KW - Leukemia, Myeloid, Acute -- drug therapy KW - Male KW - Bone Marrow -- pathology KW - Drug Administration Schedule KW - Infusions, Intravenous KW - Protein Kinase Inhibitors -- pharmacology KW - Dose-Response Relationship, Drug KW - Anemia, Refractory, with Excess of Blasts -- drug therapy KW - Kaplan-Meier Estimate KW - Risk KW - Signal Transduction -- drug effects KW - DNA Methylation -- drug effects KW - Leukemia, Myeloid, Acute -- enzymology KW - Middle Aged KW - Leukemia, Myeloid, Acute -- pathology KW - Female KW - Phosphatidylinositol 3-Kinases -- antagonists & inhibitors KW - Enzyme Inhibitors -- therapeutic use KW - Clinical Trials, Phase I as Topic -- statistics & numerical data KW - Clinical Trials, Phase II as Topic -- statistics & numerical data KW - Glycine -- analogs & derivatives KW - Myelodysplastic Syndromes -- pathology KW - Glycine -- administration & dosage KW - Sulfones -- administration & dosage KW - Sulfones -- adverse effects KW - Sulfones -- pharmacology KW - Glycine -- pharmacology KW - Sulfones -- therapeutic use KW - Glycine -- therapeutic use KW - DNA (Cytosine-5-)-Methyltransferase -- antagonists & inhibitors KW - Myelodysplastic Syndromes -- drug therapy KW - Myelodysplastic Syndromes -- enzymology KW - Enzyme Inhibitors -- pharmacology KW - Glycine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1689844241?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hematological+oncology&rft.atitle=Clinical+activity+and+safety+of+the+dual+pathway+inhibitor+rigosertib+for+higher+risk+myelodysplastic+syndromes+following+DNA+methyltransferase+inhibitor+therapy.&rft.au=Silverman%2C+Lewis+R%3BGreenberg%2C+Peter%3BRaza%2C+Azra%3BOlnes%2C+Matthew+J%3BHolland%2C+James+F%3BReddy%2C+Premkumar%3BManiar%2C+Manoj%3BWilhelm%2C+Francois&rft.aulast=Silverman&rft.aufirst=Lewis&rft.date=2015-06-01&rft.volume=33&rft.issue=2&rft.spage=57&rft.isbn=&rft.btitle=&rft.title=Hematological+oncology&rft.issn=1099-1069&rft_id=info:doi/10.1002%2Fhon.2137 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-19 N1 - Date created - 2015-06-17 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/hon.2137 ER - TY - JOUR T1 - Expression and clinical significance of genes frequently mutated in small cell lung cancers defined by whole exome/RNA sequencing. AN - 1686421030; 25863124 AB - Small cell lung cancer (SCLC) is the most aggressive type of lung cancer. Only 15% of SCLC patients survive beyond 2 years after diagnosis. Therefore, for the improvement of patients' outcome in this disease, it is necessary to identify genetic alterations applicable as therapeutic targets in SCLC cells. The purpose of this study is the identification of genes frequently mutated and expressed in SCLCs that will be targetable for therapy of SCLC patients. Exome sequencing was performed in 28 primary tumors and 16 metastatic tumors from 38 patients with SCLCs. Expression of mutant alleles was verified in 19 cases by RNA sequencing. TP53, RB1 and PTEN were identified as being significantly mutated genes. Additional 36 genes were identified as being frequently (≥10%) mutated in SCLCs by combining the results of this study and two recent studies. Mutated alleles were expressed in 8 of the 36 genes, TMEM132D, SPTA1, VPS13B, CSMD2, ANK2, ASTN1, ASPM and FBN3. In particular, the TMEM132D, SPTA1 and VPS13B genes were commonly mutated in both early and late stage tumors, primary tumors and metastases, and tumors before and after chemotherapy, as in the case of the TP53 and RB1 genes. Therefore, in addition to TP53, RB1 and PTEN, TMEM132D, SPTA1 and VPS13B could be also involved in SCLC development, with the products from their mutated alleles being potential therapeutic targets in SCLC patients. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Carcinogenesis AU - Iwakawa, Reika AU - Kohno, Takashi AU - Totoki, Yasushi AU - Shibata, Tatsuhiro AU - Tsuchihara, Katsuya AU - Mimaki, Sachiyo AU - Tsuta, Koji AU - Narita, Yoshitaka AU - Nishikawa, Ryo AU - Noguchi, Masayuki AU - Harris, Curtis C AU - Robles, Ana I AU - Yamaguchi, Rui AU - Imoto, Seiya AU - Miyano, Satoru AU - Totsuka, Hirohiko AU - Yoshida, Teruhiko AU - Yokota, Jun AD - Division of Genome Biology, National Cancer Center Research Institute, Tokyo 104-0045, Japan. ; Division of Genome Biology, National Cancer Center Research Institute, Tokyo 104-0045, Japan, Division of Translational Research, Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Tokyo 104-0045, Japan. ; Division of Cancer Genomics, National Cancer Center Research Institute, Tokyo 104-0045, Japan. ; Division of Translational Research, Exploratory Oncology Research and Clinical Trial Center, National Cancer Center, Tokyo 104-0045, Japan. ; Pathology Division and. ; Department of Neurosurgery and Neuro-Oncology, National Cancer Center Hospital, Tokyo 104-0045, Japan. ; Department of Neuro-Oncology/Neurosurgery, International Medical Center, Saitama Medical University, Saitama 350-1298, Japan. ; Department of Pathology, Faculty of Medicine, University of Tsukuba, Ibaraki 305-8575, Japan. ; Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4258, USA. ; Human Genome Center, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan. ; Bioinfomatics Group, Research and Development Center, Solution Division 4, Hitachi Government and Public Corporation System Engineering Ltd, Tokyo 135-8633, Japan. ; Division of Genetics, National Cancer Center Research Institute, Tokyo 104-0045, Japan and. ; Division of Genome Biology, National Cancer Center Research Institute, Tokyo 104-0045, Japan, Cancer Genome Biology Group, Institute of Predictive and Personalized Medicine of Cancer, 08916 Barcelona, Spain jyokota@ncc.go.jp. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 616 EP - 621 VL - 36 IS - 6 KW - Membrane Proteins KW - 0 KW - Retinoblastoma Protein KW - TMEM132D protein, human KW - TP53 protein, human KW - Tumor Suppressor Protein p53 KW - VPS13B protein, human KW - Vesicular Transport Proteins KW - Spectrin KW - 12634-43-4 KW - PTEN Phosphohydrolase KW - EC 3.1.3.67 KW - PTEN protein, human KW - Index Medicus KW - Vesicular Transport Proteins -- genetics KW - Gene Frequency KW - Humans KW - Aged KW - Spectrin -- genetics KW - Membrane Proteins -- genetics KW - PTEN Phosphohydrolase -- genetics KW - Base Sequence KW - Aged, 80 and over KW - Sequence Analysis, RNA KW - Middle Aged KW - Tumor Suppressor Protein p53 -- genetics KW - Exome -- genetics KW - Female KW - Male KW - Retinoblastoma Protein -- genetics KW - Small Cell Lung Carcinoma -- genetics KW - Mutation -- genetics KW - Lung Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1686421030?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Carcinogenesis&rft.atitle=Expression+and+clinical+significance+of+genes+frequently+mutated+in+small+cell+lung+cancers+defined+by+whole+exome%2FRNA+sequencing.&rft.au=Iwakawa%2C+Reika%3BKohno%2C+Takashi%3BTotoki%2C+Yasushi%3BShibata%2C+Tatsuhiro%3BTsuchihara%2C+Katsuya%3BMimaki%2C+Sachiyo%3BTsuta%2C+Koji%3BNarita%2C+Yoshitaka%3BNishikawa%2C+Ryo%3BNoguchi%2C+Masayuki%3BHarris%2C+Curtis+C%3BRobles%2C+Ana+I%3BYamaguchi%2C+Rui%3BImoto%2C+Seiya%3BMiyano%2C+Satoru%3BTotsuka%2C+Hirohiko%3BYoshida%2C+Teruhiko%3BYokota%2C+Jun&rft.aulast=Iwakawa&rft.aufirst=Reika&rft.date=2015-06-01&rft.volume=36&rft.issue=6&rft.spage=616&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgv026 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-24 N1 - Date created - 2015-06-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Lancet. 2011 Nov 12;378(9804):1741-55 [21565397] Bioinformatics. 2011 Nov 1;27(21):2987-93 [21903627] Clin Cancer Res. 2011 Mar 15;17(6):1481-9 [21148746] CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855] Nature. 2010 Jan 14;463(7278):184-90 [20016488] Bioinformatics. 2009 Aug 15;25(16):2078-9 [19505943] Clin Cancer Res. 2007 Jan 1;13(1):111-20 [17200345] J Cell Biochem Suppl. 1996;24:32-91 [8806092] Carcinogenesis. 2000 Mar;21(3):497-503 [10688870] J Thorac Oncol. 2015 Sep;10(9):1240-2 [26291007] Nature. 2013 Sep 19;501(7467):338-45 [24048066] Genes Chromosomes Cancer. 2013 Sep;52(9):802-16 [23716474] Nature. 2013 Jul 11;499(7457):214-8 [23770567] J Clin Oncol. 2013 Jun 10;31(17):2167-72 [23630207] Nucleic Acids Res. 2013 Apr;41(7):e89 [23471004] J Natl Compr Canc Netw. 2013 Jan 1;11(1):78-98 [23307984] Proc Natl Acad Sci U S A. 2012 Oct 16;109(42):17034-9 [23035247] Nat Genet. 2012 Oct;44(10):1111-6 [22941189] Nat Genet. 2012 Oct;44(10):1104-10 [22941188] J Clin Oncol. 2012 Aug 20;30(24):2956-62 [22665543] Nat Med. 2012 Mar;18(3):375-7 [22327624] Cancer Res. 2012 Jan 1;72(1):100-11 [22080568] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/carcin/bgv026 ER - TY - JOUR T1 - Molecular pathway of near-infrared laser phototoxicity involves ATF-4 orchestrated ER stress. AN - 1685763253; 26030745 AB - High power lasers are used extensively in medicine while lower power applications are popular for optical imaging, optogenetics, skin rejuvenation and a therapeutic modality termed photobiomodulation (PBM). This study addresses the therapeutic dose limits, biological safety and molecular pathway of near-infrared (NIR) laser phototoxicity. Increased erythema and tissue damage were noted in mice skin and cytotoxicity in cell cultures at phototoxic laser doses involving generation of reactive oxygen species (ROS) coupled with a rise in surface temperature (>45 °C). NIR laser phototoxicity results from Activating Transcription Factor-4 (ATF-4) mediated endoplasmic reticulum stress and autophagy. Neutralizations of heat or ROS and overexpressing ATF-4 were noted to rescue NIR laser phototoxicity. Further, NIR laser mediated phototoxicity was noted to be non-genotoxic and non-mutagenic. This study outlines the mechanism of NIR laser phototoxicity and the utility of monitoring surface temperature and ATF4 expression as potential biomarkers to develop safe and effective clinical applications. JF - Scientific reports AU - Khan, Imran AU - Tang, Elieza AU - Arany, Praveen AD - Cell Regulation and Control Unit, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda MD. Y1 - 2015/06/01/ PY - 2015 DA - 2015 Jun 01 SP - 10581 VL - 5 KW - Reactive Oxygen Species KW - 0 KW - Activating Transcription Factor 4 KW - 145891-90-3 KW - Index Medicus KW - Reactive Oxygen Species -- metabolism KW - Hot Temperature KW - Animals KW - Skin -- radiation effects KW - Apoptosis KW - Reproducibility of Results KW - Skin -- metabolism KW - Humans KW - Mice KW - DNA Damage -- radiation effects KW - Skin Temperature -- radiation effects KW - Cell Line KW - Activating Transcription Factor 4 -- metabolism KW - Endoplasmic Reticulum Stress KW - Signal Transduction -- radiation effects KW - Lasers -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1685763253?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scientific+reports&rft.atitle=Molecular+pathway+of+near-infrared+laser+phototoxicity+involves+ATF-4+orchestrated+ER+stress.&rft.au=Khan%2C+Imran%3BTang%2C+Elieza%3BArany%2C+Praveen&rft.aulast=Khan&rft.aufirst=Imran&rft.date=2015-06-01&rft.volume=5&rft.issue=&rft.spage=10581&rft.isbn=&rft.btitle=&rft.title=Scientific+reports&rft.issn=2045-2322&rft_id=info:doi/10.1038%2Fsrep10581 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-24 N1 - Date created - 2015-06-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Lasers Surg Med. 2005 Mar;36(3):171-85 [15704098] J Biol Chem. 2005 Feb 11;280(6):4761-71 [15557336] Photomed Laser Surg. 2005 Aug;23(4):355-61 [16144476] Photomed Laser Surg. 2006 Apr;24(2):179-85 [16706696] Nat Rev Mol Cell Biol. 2007 Jul;8(7):519-29 [17565364] Lasers Surg Med. 2007 Jul;39(6):534-42 [17659591] Exp Cell Res. 2007 Oct 1;313(16):3556-67 [17707795] Trends Biochem Sci. 2007 Oct;32(10):469-76 [17920280] Lasers Surg Med. 2007 Oct;39(9):706-15 [17960752] Wound Repair Regen. 2007 Nov-Dec;15(6):866-74 [18028135] Arch Physiol Biochem. 2007 Oct-Dec;113(4-5):234-58 [18158646] Ageing Res Rev. 2008 Jan;7(1):1-7 [18162444] J Exp Med. 2008 May 12;205(5):1227-42 [18458112] Free Radic Res. 2008 Aug;42(8):689-706 [18671159] Arch Facial Plast Surg. 2008 Nov-Dec;10(6):381-90 [19018058] J Clin Invest. 2009 Sep;119(9):2807-17 [19726872] Mutat Res. 2009 Sep-Oct;679(1-2):50-8 [19628053] Lancet. 2009 Dec 5;374(9705):1897-908 [19913903] J Biol Chem. 2010 Oct 22;285(43):33165-74 [20732869] Photochem Photobiol. 2010 Nov-Dec;86(6):1364-72 [20735808] Toxicol In Vitro. 2011 Feb;25(1):231-41 [21092754] PLoS One. 2011;6(7):e22453 [21814580] Science. 2011 Nov 25;334(6059):1081-6 [22116877] J Biophotonics. 2012 Nov;5(11-12):827-37 [22807422] Hum Exp Toxicol. 2013 Feb;32(2):120-52 [23060412] J Neurosci. 2013 Feb 6;33(6):2398-407 [23392669] Anticancer Res. 2013 Jul;33(7):2823-31 [23780966] J Invest Dermatol. 2013 Jun;133(E1):E21-3 [23820722] Biochim Biophys Acta. 2013 Oct;1833(10):2165-75 [23665047] Sci Rep. 2013;3:2346 [23907635] Nat Nanotechnol. 2013 Nov;8(11):807-19 [24202536] Sci Transl Med. 2014 May 28;6(238):238ra69 [24871130] Toxicol Sci. 2014 Jul;140(1):103-17 [24743697] J Toxicol Sci. 2013;38(3):503-11 [23719928] Br J Radiol. 2000 May;73(869):514-6 [10884748] Mol Biol Cell. 2000 Sep;11(9):2833-43 [10982384] J Dermatol. 2000 Nov;27(11):700-5 [11138535] Semin Cutan Med Surg. 2000 Dec;19(4):253-66 [11149606] Lasers Surg Med. 2001;28(3):204-11 [11295753] J Clin Laser Med Surg. 2001 Dec;19(6):305-14 [11776448] Neuron. 2002 Jan 3;33(1):15-22 [11779476] Blood. 2002 Feb 1;99(3):736-45 [11806972] Dermatol Clin. 2002 Jan;20(1):135-46 [11859588] Proc Natl Acad Sci U S A. 2003 Mar 18;100(6):3439-44 [12626762] Mol Cell. 2003 Mar;11(3):619-33 [12667446] J Invest Dermatol. 2003 May;120(5):849-57 [12713592] Cell. 2004 Apr 30;117(3):387-98 [15109498] Mol Cell Biol. 2004 Sep;24(17):7469-82 [15314157] Acta Chir Acad Sci Hung. 1973;14(4):347-56 [4787498] Lasers Surg Med. 1989;9(5):497-505 [2811573] J Cell Biol. 1992 Nov;119(3):493-501 [1400587] J Immunol Methods. 1992 Nov 25;156(1):39-45 [1431161] Am Biotechnol Lab. 1993 Mar;11(4):48-50 [7763491] Lasers Surg Med. 1995;17(2):102-59 [8569410] Photomed Laser Surg. 2005 Jun;23(3):251-9 [15954811] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/srep10581 ER - TY - JOUR T1 - Cerebral Small Vessel Disease and Association With Higher Incidence of Depressive Symptoms in a General Elderly Population: The AGES-Reykjavik Study. AN - 1685755314; 25734354 AB - The vascular depression hypothesis postulates that cerebral small vessel disease (CSVD) leads to depressive symptoms by disruption of brain structures involved in mood regulation. However, longitudinal data on the association between CSVD and depressive symptoms are scarce. The authors investigated the association between CSVD and incident depressive symptoms. Longitudinal data were taken from the Age, Gene/Environment Susceptibility-Reykjavik Study of 1,949 participants free of dementia and without baseline depressive symptoms (mean age: 74.6 years [SD=4.6]; women, 56.6%). MRI markers of CSVD, detected at baseline (2002-2006) and follow-up (2007-2011), included white matter hyperintensity volume, subcortical infarcts, cerebral microbleeds, Virchow-Robin spaces, and total brain parenchyma volume. Incident depressive symptoms were defined by a score ≥6 on the 15-item Geriatric Depression Scale and/or use of antidepressant medication. Depressive symptoms occurred in 10.1% of the participants. The association for a greater onset of depressive symptoms was significant for participants with 1 standard deviation increase in white matter hyperintensity volume over time, new subcortical infarcts, new Virchow-Robin spaces, 1 standard deviation lower total brain volume at baseline, and 1 standard deviation decreased total brain volume over time, after adjustments for cognitive function and sociodemographic and cardiovascular factors. Results were qualitatively similar when change in the Geriatric Depression Scale score over time was used as the outcome instead of incident depressive symptoms. Most markers of progression of CSVD over time and some markers of baseline CSVD are associated with concurrently developing new depressive symptoms. These findings support the vascular depression hypothesis. JF - The American journal of psychiatry AU - van Sloten, Thomas T AU - Sigurdsson, Sigurdur AU - van Buchem, Mark A AU - Phillips, Caroline L AU - Jonsson, Palmi V AU - Ding, Jie AU - Schram, Miranda T AU - Harris, Tamara B AU - Gudnason, Vilmundur AU - Launer, Lenore J AD - From the Department of Medicine, the Cardiovascular Research Institute Maastricht, and the School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Centre, Maastricht, the Netherlands; Icelandic Heart Association, Kopavogur, Iceland; the Department of Radiology, Leiden University Medical Center, Leiden, the Netherlands; Intramural Research Program, Laboratory of Epidemiology and Population Sciences, National Institute on Aging, National Institutes of Health, Bethesda, Md.; the Department of Geriatrics, Landspitali University Hospital, Reykjavik, Iceland; and the Faculty of Medicine, University of Iceland, Reykjavik, Iceland. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 570 EP - 578 VL - 172 IS - 6 KW - Abridged Index Medicus KW - Index Medicus KW - Magnetic Resonance Imaging KW - Humans KW - Aged KW - Cerebral Infarction -- diagnosis KW - Longitudinal Studies KW - Aged, 80 and over KW - Brain -- pathology KW - Cohort Studies KW - Incidence KW - Statistics as Topic KW - Gene-Environment Interaction KW - Genetic Predisposition to Disease KW - Netherlands KW - Cerebral Infarction -- epidemiology KW - Male KW - Cerebral Infarction -- psychology KW - Female KW - Depressive Disorder -- epidemiology KW - Cerebral Small Vessel Diseases -- psychology KW - Depressive Disorder -- psychology KW - Cerebral Small Vessel Diseases -- genetics KW - Depressive Disorder -- diagnosis KW - Cerebral Small Vessel Diseases -- diagnosis KW - Depressive Disorder -- genetics KW - Cerebral Small Vessel Diseases -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1685755314?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+psychiatry&rft.atitle=Cerebral+Small+Vessel+Disease+and+Association+With+Higher+Incidence+of+Depressive+Symptoms+in+a+General+Elderly+Population%3A+The+AGES-Reykjavik+Study.&rft.au=van+Sloten%2C+Thomas+T%3BSigurdsson%2C+Sigurdur%3Bvan+Buchem%2C+Mark+A%3BPhillips%2C+Caroline+L%3BJonsson%2C+Palmi+V%3BDing%2C+Jie%3BSchram%2C+Miranda+T%3BHarris%2C+Tamara+B%3BGudnason%2C+Vilmundur%3BLauner%2C+Lenore+J&rft.aulast=van+Sloten&rft.aufirst=Thomas&rft.date=2015-06-01&rft.volume=172&rft.issue=6&rft.spage=570&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+psychiatry&rft.issn=1535-7228&rft_id=info:doi/10.1176%2Fappi.ajp.2014.14050578 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-24 N1 - Date created - 2015-06-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Circulation. 1996 Jun 1;93(11):1976-80 [8640971] Psychiatry Res. 2013 Feb 28;211(2):180-2 [23154097] Arch Gen Psychiatry. 1997 Oct;54(10):915-22 [9337771] Int J Geriatr Psychiatry. 1999 Oct;14(10):858-65 [10521885] Arch Gen Psychiatry. 1999 Oct;56(10):889-95 [10530630] Int J Geriatr Psychiatry. 2006 Apr;21(4):375-81 [16534770] Am J Epidemiol. 2007 May 1;165(9):1076-87 [17351290] Biol Psychiatry. 2008 Apr 1;63(7):663-9 [17977521] J Neurol Neurosurg Psychiatry. 2008 Sep;79(9):1002-6 [18270235] Arch Gen Psychiatry. 2008 Dec;65(12):1394-401 [19047526] Epidemiology. 2009 Jul;20(4):488-95 [19525685] JAMA. 2009 Jun 24;301(24):2563-70 [19549973] Epidemiology. 2010 Jan;21(1):78-81 [20010211] Stroke. 2010 May;41(5):891-7 [20360538] Lancet Neurol. 2013 May;12(5):483-97 [23602162] JAMA Psychiatry. 2013 Aug;70(8):803-11 [23760442] Int J Geriatr Psychiatry. 2013 Oct;28(10):1069-76 [23348834] Psychol Med. 2012 Feb;42(2):359-70 [21835088] Stroke. 2014 Feb;45(2):438-43 [24357656] Am J Geriatr Psychiatry. 2014 Dec;22(12):1469-77 [24211028] J Gerontol A Biol Sci Med Sci. 2000 Apr;55(4):M221-31 [10811152] Arch Gen Psychiatry. 2000 Nov;57(11):1071-6 [11074873] Stroke. 2002 Jun;33(6):1636-44 [12053004] Biol Psychiatry. 2003 Aug 1;54(3):248-61 [12893101] J Psychiatr Res. 1982-1983;17(1):37-49 [7183759] J Neuropsychiatry Clin Neurosci. 1991 Summer;3(3):243-54 [1821241] Arch Gen Psychiatry. 2010 May;67(5):489-96 [20439830] Nat Rev Neurol. 2011 Jun;7(6):323-31 [21537355] JAMA. 2011 Sep 21;306(11):1241-9 [21934057] Ann Neurol. 2011 Nov;70(5):774-80 [22162060] Neuroimage. 2012 Feb 15;59(4):3862-70 [22119006] Arch Gen Psychiatry. 2012 Jun;69(6):636-42 [22664551] Br J Psychiatry. 2012 Jul;201(1):40-5 [22626634] Arch Gen Psychiatry. 2012 Oct;69(10):1073-9 [23026957] Neurology. 2012 Nov 13;79(20):2029-36 [23115210] Int J Geriatr Psychiatry. 2013 Jan;28(1):66-74 [22415749] Biol Psychiatry. 2013 Jan 15;73(2):169-76 [23079234] Am J Psychiatry. 1997 Apr;154(4):497-501 [9090336] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1176/appi.ajp.2014.14050578 ER - TY - JOUR T1 - A review of nonoccupational pathways for pesticide exposure in women living in agricultural areas. AN - 1685752215; 25636067 AB - Women living in agricultural areas may experience high pesticide exposures compared with women in urban or suburban areas because of their proximity to farm activities. Our objective was to review the evidence in the published literature for the contribution of nonoccupational pathways of pesticide exposure in women living in North American agricultural areas. We evaluated the following nonoccupational exposure pathways: paraoccupational (i.e., take-home or bystander exposure), agricultural drift, residential pesticide use, and dietary ingestion. We also evaluated the role of hygiene factors (e.g., house cleaning, shoe removal). Among 35 publications identified (published 1995-2013), several reported significant or suggestive (p < 0.1) associations between paraoccupational (n = 19) and agricultural drift (n = 10) pathways and pesticide dust or biomarker levels, and 3 observed that residential use was associated with pesticide concentrations in dust. The 4 studies related to ingestion reported low detection rates of most pesticides in water; additional studies are needed to draw conclusions about the importance of this pathway. Hygiene factors were not consistently linked to exposure among the 18 relevant publications identified. Evidence supported the importance of paraoccupational, drift, and residential use pathways. Disentangling exposure pathways was difficult because agricultural populations are concurrently exposed to pesticides via multiple pathways. Most evidence was based on measurements of pesticides in residential dust, which are applicable to any household member and are not specific to women. An improved understanding of nonoccupational pesticide exposure pathways in women living in agricultural areas is critical for studying health effects in women and for designing effective exposure-reduction strategies. JF - Environmental health perspectives AU - Deziel, Nicole C AU - Friesen, Melissa C AU - Hoppin, Jane A AU - Hines, Cynthia J AU - Thomas, Kent AU - Freeman, Laura E Beane AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 515 EP - 524 VL - 123 IS - 6 KW - Environmental Pollutants KW - 0 KW - Pesticides KW - Index Medicus KW - Agriculture KW - North America KW - Humans KW - Female KW - Pesticides -- metabolism KW - Environmental Pollutants -- metabolism KW - Environmental Exposure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1685752215?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=A+review+of+nonoccupational+pathways+for+pesticide+exposure+in+women+living+in+agricultural+areas.&rft.au=Deziel%2C+Nicole+C%3BFriesen%2C+Melissa+C%3BHoppin%2C+Jane+A%3BHines%2C+Cynthia+J%3BThomas%2C+Kent%3BFreeman%2C+Laura+E+Beane&rft.aulast=Deziel&rft.aufirst=Nicole&rft.date=2015-06-01&rft.volume=123&rft.issue=6&rft.spage=515&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1408273 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-24 N1 - Date created - 2015-06-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Environ Health Perspect. 2010 Oct;118(10):1355-62 [20562050] Environ Health Perspect. 2011 Jul;119(7):970-6 [21330232] J Toxicol Environ Health A. 2005 Aug 13;68(15):1359-70 [16020195] Rev Environ Health. 2005 Apr-Jun;20(2):77-101 [16121832] Environ Health Perspect. 2005 Dec;113(12):1802-7 [16330368] J Occup Environ Med. 2011 Aug;53(8):884-91 [21775902] J Environ Qual. 2012 Mar-Apr;41(2):479-94 [22370411] J Occup Environ Hyg. 2012;9(5):289-97 [22506545] Environ Res. 2012 Aug;117:8-16 [22683313] J Occup Environ Med. 2012 Sep;54(9):1163-9 [22772953] Arch Environ Contam Toxicol. 2001 Jul;41(1):112-6 [11385597] Environ Res. 2000 Nov;84(3):290-302 [11097803] Environ Health Perspect. 2013 May;121(5):565-71 [23462689] Environ Health Perspect. 2001 May;109(5):533-8 [11401767] Environ Health Perspect. 2002 May;110(5):549-53 [12003762] J Chromatogr B Analyt Technol Biomed Life Sci. 2002 Oct 5;778(1-2):5-29 [12376114] Environ Health Perspect. 2002 Dec;110(12):A787-92 [12460819] J Toxicol Environ Health A. 2003 Jan 24;66(2):103-32 [12653018] AAOHN J. 2003 Mar;51(3):113-9 [12670098] Environ Health Perspect. 2004 Feb;112(2):142-7 [14754567] Environ Health Perspect. 2004 Mar;112(3):321-6 [14998747] Environ Health Perspect. 2004 Mar;112(3):382-7 [14998757] Am J Ind Med. 2004 Jun;45(6):491-9 [15164393] Environ Res. 2004 Nov;96(3):283-9 [15364595] Arch Environ Contam Toxicol. 1994 Jan;26(1):37-46 [8110022] J Occup Med. 1994 Nov;36(11):1240-6 [7861269] Environ Health Perspect. 1995 Dec;103(12):1126-34 [8747019] J Expo Anal Environ Epidemiol. 1997 Jan-Mar;7(1):61-80 [9076610] J Expo Anal Environ Epidemiol. 1997 Apr-Jun;7(2):217-34 [9185013] Am J Ind Med. 1998 Dec;34(6):581-7 [9816416] J Expo Anal Environ Epidemiol. 2004 Nov;14(6):473-8 [15026777] J Occup Environ Hyg. 2005 Jul;2(7):357-67 [16020099] J Expo Sci Environ Epidemiol. 2006 Jan;16(1):98-104 [16015277] Environ Health Perspect. 2006 Jun;114(6):893-7 [16759991] Environ Health Perspect. 2006 Jul;114(7):999-1006 [16835050] J Expo Sci Environ Epidemiol. 2006 Sep;16(5):447-56 [16570094] J Expo Sci Environ Epidemiol. 2006 Sep;16(5):387-96 [16249796] J Agromedicine. 2006;11(2):81-8 [17135145] Ann Occup Hyg. 2007 Jan;51(1):53-65 [16984946] Environ Health Perspect. 2007 Mar;115(3):370-6 [17431485] Environ Sci Technol. 2007 May 15;41(10):3408-14 [17547156] J Expo Sci Environ Epidemiol. 2007 Jul;17(4):388-99 [17033681] Hum Reprod Update. 2008 Jan-Feb;14(1):59-72 [18070835] Environ Health Perspect. 2008 May;116(5):687-94 [18470300] Radiat Prot Dosimetry. 2008;132(2):148-55 [18930927] Environ Sci Technol. 2009 Dec 1;43(23):8767-74 [19943644] Environ Health Perspect. 2010 Jun;118(6):856-63 [20129873] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1289/ehp.1408273 ER - TY - JOUR T1 - Inactivation of a Gα(s)-PKA tumour suppressor pathway in skin stem cells initiates basal-cell carcinogenesis. AN - 1684436289; 25961504 AB - Genomic alterations in GNAS, the gene coding for the Gαs heterotrimeric G protein, are associated with a large number of human diseases. Here, we explored the role of Gαs on stem cell fate decisions by using the mouse epidermis as a model system. Conditional epidermal deletion of Gnas or repression of PKA signalling caused a remarkable expansion of the stem cell compartment, resulting in rapid basal-cell carcinoma formation. In contrast, inducible expression of active Gαs in the epidermis caused hair follicle stem cell exhaustion and hair loss. Mechanistically, we found that Gαs-PKA disruption promotes the cell autonomous Sonic Hedgehog pathway stimulation and Hippo signalling inhibition, resulting in the non-canonical activation of GLI and YAP1. Our study highlights an important tumour suppressive function of Gαs-PKA, limiting the proliferation of epithelial stem cells and maintaining proper hair follicle homeostasis. These findings could have broad implications in multiple pathophysiological conditions, including cancer. JF - Nature cell biology AU - Iglesias-Bartolome, Ramiro AU - Torres, Daniela AU - Marone, Romina AU - Feng, Xiaodong AU - Martin, Daniel AU - Simaan, May AU - Chen, Min AU - Weinstein, Lee S AU - Taylor, Susan S AU - Molinolo, Alfredo A AU - Gutkind, J Silvio AD - Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, Maryland 20892, USA. ; National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. ; 1] Department of Pharmacology, University of California San Diego, La Jolla, California 92093, USA [2] Department of Chemistry and Biochemistry, University of California San Diego, La Jolla, California 92093, USA. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 793 EP - 803 VL - 17 IS - 6 KW - Adaptor Proteins, Signal Transducing KW - 0 KW - Chromogranins KW - Gli protein, mouse KW - Hedgehog Proteins KW - Kruppel-Like Transcription Factors KW - Phosphoproteins KW - RNA, Small Interfering KW - Shh protein, mouse KW - Tumor Suppressor Proteins KW - Yap protein, mouse KW - Zinc Finger Protein GLI1 KW - Lats1 protein, mouse KW - EC 2.7.1.- KW - Hippo protein, mouse KW - EC 2.7.11.1 KW - LATS2 protein, mouse KW - Protein-Serine-Threonine Kinases KW - Gnas protein, mouse KW - EC 3.6.1.- KW - GTP-Binding Protein alpha Subunits, Gs KW - EC 3.6.5.1 KW - Index Medicus KW - Animals KW - Protein-Serine-Threonine Kinases -- metabolism KW - Humans KW - HEK293 Cells KW - Tumor Suppressor Proteins -- genetics KW - Cell Differentiation -- genetics KW - Protein-Serine-Threonine Kinases -- antagonists & inhibitors KW - Mice, Knockout KW - Adaptor Proteins, Signal Transducing -- metabolism KW - Tumor Suppressor Proteins -- metabolism KW - Cell Proliferation -- genetics KW - RNA Interference KW - Phosphoproteins -- metabolism KW - 3T3 Cells KW - Phosphoproteins -- genetics KW - Mice KW - Protein-Serine-Threonine Kinases -- genetics KW - Hedgehog Proteins -- metabolism KW - Adaptor Proteins, Signal Transducing -- genetics KW - Kruppel-Like Transcription Factors -- metabolism KW - Gene Expression Regulation, Developmental KW - Cell Line KW - Stem Cells -- cytology KW - GTP-Binding Protein alpha Subunits, Gs -- genetics KW - Hair Follicle -- cytology KW - GTP-Binding Protein alpha Subunits, Gs -- metabolism KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1684436289?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+cell+biology&rft.atitle=Inactivation+of+a+G%CE%B1%28s%29-PKA+tumour+suppressor+pathway+in+skin+stem+cells+initiates+basal-cell+carcinogenesis.&rft.au=Iglesias-Bartolome%2C+Ramiro%3BTorres%2C+Daniela%3BMarone%2C+Romina%3BFeng%2C+Xiaodong%3BMartin%2C+Daniel%3BSimaan%2C+May%3BChen%2C+Min%3BWeinstein%2C+Lee+S%3BTaylor%2C+Susan+S%3BMolinolo%2C+Alfredo+A%3BGutkind%2C+J+Silvio&rft.aulast=Iglesias-Bartolome&rft.aufirst=Ramiro&rft.date=2015-06-01&rft.volume=17&rft.issue=6&rft.spage=793&rft.isbn=&rft.btitle=&rft.title=Nature+cell+biology&rft.issn=1476-4679&rft_id=info:doi/10.1038%2Fncb3164 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-31 N1 - Date created - 2015-05-29 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - GSE58894; GEO N1 - SuppNotes - Cited By: Science. 2002 May 31;296(5573):1636-9 [12040175] Nat Rev Mol Cell Biol. 2002 Sep;3(9):639-50 [12209124] Development. 2002 Oct;129(20):4753-61 [12361967] Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14071-6 [12391318] Genes Dev. 2003 Feb 15;17(4):488-501 [12600942] Mod Pathol. 2006 Feb;19 Suppl 2:S127-47 [16446711] Am J Physiol Renal Physiol. 2007 Jan;292(1):F27-37 [16822937] Nat Rev Cancer. 2007 Feb;7(2):79-94 [17251915] Nat Protoc. 2006;1(5):2315-9 [17406473] Biochim Biophys Acta. 2008 Jan;1785(1):32-54 [17980164] Oncogene. 2008 Mar 20;27(13):1844-52 [17934524] EMBO J. 2008 Apr 23;27(8):1231-42 [18369314] Oncogene. 2008 May 22;27(23):3233-43 [18071304] Genes Dev. 2008 Jul 15;22(14):1962-71 [18579750] Nat Rev Cancer. 2008 Oct;8(10):743-54 [18813320] Nat Rev Mol Cell Biol. 2009 Mar;10(3):207-17 [19209183] Genes Dev. 2009 Dec 1;23(23):2729-41 [19952108] Nat Cell Biol. 2010 Mar;12(3):299-305 [20154679] Sci Signal. 2010;3(117):pe14 [20388915] Nat Protoc. 2010 May;5(5):898-911 [20431535] Dev Cell. 2010 Oct 19;19(4):491-505 [20951342] Dev Cell. 2010 Nov 16;19(5):727-39 [21074722] Cell Stem Cell. 2010 Dec 3;7(6):656-70 [21112561] Cancer Cell. 2011 Jan 18;19(1):114-24 [21215705] Proc Natl Acad Sci U S A. 2011 Feb 8;108(6):2270-5 [21262812] Cell. 2011 Mar 4;144(5):782-95 [21376238] Nat Rev Cancer. 2012 Mar;12(3):170-80 [22362215] Clin Cancer Res. 2012 May 1;18(9):2558-68 [22409888] Cell. 2012 Aug 17;150(4):780-91 [22863277] Cell Stem Cell. 2012 Sep 7;11(3):401-14 [22958932] Nat Rev Mol Cell Biol. 2012 Oct;13(10):646-58 [22992589] Sci Signal. 2012 Oct 16;5(246):re6 [23074268] J Clin Invest. 2012 Dec;122(12):4505-18 [23143302] Semin Cell Dev Biol. 2012 Dec;23(9):946-53 [23085626] EMBO Rep. 2013 Jan;14(1):39-48 [23229591] Mol Cell. 2013 Jan 10;49(1):94-108 [23177739] Methods Mol Biol. 2013;989:45-60 [23483386] Nat Rev Cancer. 2013 Jun;13(6):412-24 [23640210] EMBO J. 2013 May 29;32(11):1543-55 [23644383] Genes Dev. 2013 Jun 1;27(11):1223-32 [23752589] Cell. 2013 Sep 12;154(6):1342-55 [24012335] Sci Rep. 2013;3:2937 [24121824] Nat Med. 2013 Nov;19(11):1505-12 [24076664] Nat Cell Biol. 2014 Jan;16(1):108-17 [24362629] Cell Rep. 2014 Jan 16;6(1):168-81 [24373970] Cancer Cell. 2014 Mar 17;25(3):393-405 [24651015] Cell. 2014 May 8;157(4):935-49 [24813615] J Cell Biol. 2014 May 12;205(3):325-38 [24798736] EMBO Rep. 2014 Jun;15(6):642-56 [24825474] Nat Med. 2014 Sep;20(9):1035-42 [25150496] Cell Stem Cell. 2011 May 6;8(5):552-65 [21549329] J Invest Dermatol. 2000 May;114(5):901-8 [10771469] Cell. 2000 Nov 10;103(4):609-20 [11106731] Cell. 2001 May 18;105(4):533-45 [11371349] Development. 2002 Jan;129(1):95-109 [11782404] Nat Rev Cancer. 2003 Dec;3(12):903-11 [14737121] J Biol Chem. 2004 Apr 30;279(18):18559-66 [14981079] Nature. 1989 Aug 31;340(6236):692-6 [2549426] Science. 1991 Jul 26;253(5018):414-20 [1862343] N Engl J Med. 1991 Dec 12;325(24):1688-95 [1944469] Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8551-6 [10411913] Cancer Res. 2004 Dec 15;64(24):8804-7 [15604235] J Clin Invest. 2005 Nov;115(11):3217-27 [16239968] Science. 2005 Dec 2;310(5753):1504-10 [16293724] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ncb3164 ER - TY - JOUR T1 - The minimal promoter region of the dense-core vesicle protein IA-2: transcriptional regulation by CREB. AN - 1684431489; 25528004 AB - IA-2 is a transmembrane protein found in the dense-core vesicles (DCV) of neuroendocrine cells and one of the major autoantigens in type 1 diabetes. DCV are involved in the secretion of hormones (e.g., insulin) and neurotransmitters. Stimulation of pancreatic β cells with glucose upregulates the expression of IA-2 and an increase in IA-2 results in an increase in the number of DCV. Little is known, however, about the promoter region of IA-2 or the transcriptional factors that regulate the expression of this gene. In the present study, we constructed eight deletion fragments from the upstream region of the IA-2 transcription start site and linked them to a luciferase reporter. By this approach, we have identified a short bp region (-216 to +115) that has strong promoter activity. We also identified a transcription factor, cAMP responsive element-binding protein (CREB), which binds to two CREB-related binding sites located in this region. The binding of CREB to these sites enhanced IA-2 transcription by more than fivefold. We confirmed these findings by site-directed mutagenesis, chromatin immunoprecipitation assays and RNAi inhibition. Based on these findings, we conclude that the PKA pathway is a critical, but not the exclusive signaling pathway involved in IA-2 gene expression. JF - Acta diabetologica AU - Cai, Tao AU - Hirai, Hiroki AU - Xu, Huanyu AU - Notkins, Abner L AD - Experimental Medicine Section, Laboratory of Sensory Biology, National Institute of Dental and Craniofacial Research (NIDCR), National Institutes of Health (NIH), B30/Rm106, Bethesda, MD, 20892, USA, tcai@mail.nih.gov. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 573 EP - 580 VL - 52 IS - 3 KW - CREB-Binding Protein KW - EC 2.3.1.48 KW - PTPRN protein, human KW - EC 3.1.3.48 KW - Receptor-Like Protein Tyrosine Phosphatases, Class 8 KW - Index Medicus KW - Base Sequence KW - Humans KW - Molecular Sequence Data KW - Transcription, Genetic KW - Protein Binding KW - Binding Sites KW - Promoter Regions, Genetic KW - CREB-Binding Protein -- metabolism KW - Receptor-Like Protein Tyrosine Phosphatases, Class 8 -- genetics KW - Gene Expression Regulation KW - Receptor-Like Protein Tyrosine Phosphatases, Class 8 -- metabolism KW - CREB-Binding Protein -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1684431489?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Acta+diabetologica&rft.atitle=The+minimal+promoter+region+of+the+dense-core+vesicle+protein+IA-2%3A+transcriptional+regulation+by+CREB.&rft.au=Cai%2C+Tao%3BHirai%2C+Hiroki%3BXu%2C+Huanyu%3BNotkins%2C+Abner+L&rft.aulast=Cai&rft.aufirst=Tao&rft.date=2015-06-01&rft.volume=52&rft.issue=3&rft.spage=573&rft.isbn=&rft.btitle=&rft.title=Acta+diabetologica&rft.issn=1432-5233&rft_id=info:doi/10.1007%2Fs00592-014-0689-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-15 N1 - Date created - 2015-05-29 N1 - Date revised - 2017-01-31 N1 - Last updated - 2017-01-31 DO - http://dx.doi.org/10.1007/s00592-014-0689-5 ER - TY - JOUR T1 - Meconium Atazanavir Concentrations and Early Language Outcomes in HIV-Exposed Uninfected Infants With Prenatal Atazanavir Exposure. AN - 1683754436; 26009830 AB - To investigate whether prenatal atazanavir (ATV) exposure, assessed by meconium antiretroviral (ARV) quantification, predicts early child language outcomes. Prenatal ATV exposure previously was associated with poorer language development in 1-year olds. Pregnant women with HIV and their uninfected infants enrolled in the Surveillance Monitoring of Antiretroviral Therapy Toxicities study. Meconium ARV concentrations were quantified by liquid chromatography-tandem mass spectrometry. Language development at 1 year was assessed with MacArthur-Bates Communicative Development Inventory (CDI) and Bayley Scales of Infant and Toddler Development-Third Edition (Bayley-III). Late language emergence was defined as ≥ 1 of 4 CDI scores ≤ 10th percentile for age. Associations between fetal ATV exposure timing and duration, meconium ATV concentration, and language outcomes were evaluated, adjusting for potential confounders. Through 2013, meconium samples were available from 175 of 432 infants with prenatal ATV exposure. Valid Bayley-III (n = 93) and CDI (n = 106) assessments also were available. After adjustment for potential confounders, higher ATV meconium concentrations were associated with lower late language emergence risk (P = 0.04) and cumulative ATV exposure duration also was associated with higher Bayley-III Language scores (P = 0.03). Maternal ATV duration and initiation week correlated with ATV meconium concentrations (positively and negatively, respectively). Higher meconium ATV concentrations were protective against developmental language delays at 1 year, suggesting the importance of fetal ATV detoxification into meconium. This information supports ATV exposure safety for infant language development. ATV is a preferred ARV for pregnant women with HIV, suggesting the importance of ATV safety investigations. Additionally, further pursuit of the influences on language development in HIV-exposed uninfected infants is required. JF - Journal of acquired immune deficiency syndromes (1999) AU - Himes, Sarah K AU - Huo, Yanling AU - Siberry, George K AU - Williams, Paige L AU - Rice, Mabel L AU - Sirois, Patricia A AU - Frederick, Toni AU - Hazra, Rohan AU - Huestis, Marilyn A AU - Pediatric HIVAIDS Cohort Study AD - *Chemistry and Drug Metabolism Section, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD; †Center for Biostatistics in AIDS Research, Harvard School of Public Health, Boston, MA; ‡Maternal and Pediatric Infectious Disease Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD; §Speech, Language, Hearing Department, University of Kansas, Lawrence, KS; ‖Department of Pediatrics, Tulane University School of Medicine, New Orleans, LA; and ¶Department of Research Pediatrics, Maternal, Child, and Adolescent Program for Infectious Diseases and Virology, Keck School of Medicine of USC, Los Angeles, CA. ; Pediatric HIVAIDS Cohort Study Y1 - 2015/06/01/ PY - 2015 DA - 2015 Jun 01 SP - 178 EP - 186 VL - 69 IS - 2 KW - Anti-HIV Agents KW - 0 KW - Oligopeptides KW - Pyridines KW - Atazanavir Sulfate KW - 4MT4VIE29P KW - Index Medicus KW - AIDS/HIV KW - Infant KW - Humans KW - HIV Infections -- drug therapy KW - Adult KW - Infant, Newborn KW - Chromatography, Liquid KW - Tandem Mass Spectrometry KW - Pregnancy Complications, Infectious -- drug therapy KW - Male KW - Female KW - Pregnancy KW - Maternal-Fetal Exchange KW - Pyridines -- analysis KW - Language Development KW - Oligopeptides -- analysis KW - Meconium -- chemistry KW - Anti-HIV Agents -- analysis KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683754436?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+acquired+immune+deficiency+syndromes+%281999%29&rft.atitle=Meconium+Atazanavir+Concentrations+and+Early+Language+Outcomes+in+HIV-Exposed+Uninfected+Infants+With+Prenatal+Atazanavir+Exposure.&rft.au=Himes%2C+Sarah+K%3BHuo%2C+Yanling%3BSiberry%2C+George+K%3BWilliams%2C+Paige+L%3BRice%2C+Mabel+L%3BSirois%2C+Patricia+A%3BFrederick%2C+Toni%3BHazra%2C+Rohan%3BHuestis%2C+Marilyn+A%3BPediatric+HIVAIDS+Cohort+Study&rft.aulast=Himes&rft.aufirst=Sarah&rft.date=2015-06-01&rft.volume=69&rft.issue=2&rft.spage=178&rft.isbn=&rft.btitle=&rft.title=Journal+of+acquired+immune+deficiency+syndromes+%281999%29&rft.issn=1944-7884&rft_id=info:doi/10.1097%2FQAI.0000000000000558 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-10 N1 - Date created - 2015-05-27 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/QAI.0000000000000558 ER - TY - JOUR T1 - Features and Outcomes of 899 Patients With Drug-Induced Liver Injury: The DILIN Prospective Study. AN - 1683575336; 25754159 AB - The Drug-Induced Liver Injury Network is conducting a prospective study of patients with DILI in the United States. We present characteristics and subgroup analyses from the first 1257 patients enrolled in the study. In an observational longitudinal study, we began collecting data on eligible individuals with suspected DILI in 2004, following them for 6 months or longer. Subjects were evaluated systematically for other etiologies, causes, and severity of DILI. Among 1257 enrolled subjects with suspected DILI, the causality was assessed in 1091 patients, and 899 were considered to have definite, highly likely, or probable DILI. Ten percent of patients died or underwent liver transplantation, and 17% had chronic liver injury. In the 89 patients (10%) with pre-existing liver disease, DILI appeared to be more severe than in those without (difference not statistically significant; P = .09) and mortality was significantly higher (16% vs 5.2%; P 365 days were nitrofurantoin (25%) or minocycline (17%). There were no differences in outcomes of patients with short vs long latency of DILI. Compared with individuals younger than 65 years, individuals 65 years or older (n = 149) were more likely to have cholestatic injury, although mortality and rate of liver transplantation did not differ. Nine patients (1%) had concomitant severe skin reactions; implicated agents were lamotrigine, azithromycin, carbamazepine, moxifloxacin, cephalexin, diclofenac, and nitrofurantoin. Four of these patients died. Mortality from DILI is significantly higher in individuals with pre-existing liver disease or concomitant severe skin reactions compared with patients without. Additional studies are needed to confirm the association between azithromycin and increased DILI in patients with chronic liver disease. Older age and short or long latencies are not associated with DILI mortality. Copyright © 2015 AGA Institute. Published by Elsevier Inc. All rights reserved. JF - Gastroenterology AU - Chalasani, Naga AU - Bonkovsky, Herbert L AU - Fontana, Robert AU - Lee, William AU - Stolz, Andrew AU - Talwalkar, Jayant AU - Reddy, K Rajendar AU - Watkins, Paul B AU - Navarro, Victor AU - Barnhart, Huiman AU - Gu, Jiezhun AU - Serrano, Jose AU - United States Drug Induced Liver Injury Network AD - Indiana University School of Medicine, Indianapolis, Indianapolis. ; Carolinas Health Care System, Charlotte, North Carolina. ; University of Michigan, Ann Arbor, Michigan. ; University of Texas at Southwestern, Dallas, Texas. ; University of Southern California, Los Angeles, California. ; Mayo Clinic, Rochester, Minnesota. ; University of Pennsylvania, Philadelphia, Pennsylvania. ; University of North Carolina, Chapel Hill, North Carolina. ; Einstein Medical Center, Philadelphia, Pennsylvania. ; Duke Clinical Research Institute, Raleigh, North Carolina. ; National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland. ; United States Drug Induced Liver Injury Network Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 1340 EP - 52.e7 VL - 148 IS - 7 KW - Abridged Index Medicus KW - Index Medicus KW - Medication KW - DILI KW - Idiosyncratic KW - Toxicity KW - DILIN KW - Severity of Illness Index KW - Age Factors KW - Humans KW - Prognosis KW - Aged KW - Drug-Induced Liver Injury, Chronic -- epidemiology KW - Longitudinal Studies KW - Comorbidity KW - Prospective Studies KW - Risk Factors KW - Adult KW - Middle Aged KW - United States -- epidemiology KW - Time Factors KW - Drug Eruptions -- epidemiology KW - Female KW - Male KW - Chemical and Drug Induced Liver Injury -- mortality KW - Chemical and Drug Induced Liver Injury -- epidemiology KW - Chemical and Drug Induced Liver Injury -- diagnosis KW - Chemical and Drug Induced Liver Injury -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683575336?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastroenterology&rft.atitle=Features+and+Outcomes+of+899+Patients+With+Drug-Induced+Liver+Injury%3A+The+DILIN+Prospective+Study.&rft.au=Chalasani%2C+Naga%3BBonkovsky%2C+Herbert+L%3BFontana%2C+Robert%3BLee%2C+William%3BStolz%2C+Andrew%3BTalwalkar%2C+Jayant%3BReddy%2C+K+Rajendar%3BWatkins%2C+Paul+B%3BNavarro%2C+Victor%3BBarnhart%2C+Huiman%3BGu%2C+Jiezhun%3BSerrano%2C+Jose%3BUnited+States+Drug+Induced+Liver+Injury+Network&rft.aulast=Chalasani&rft.aufirst=Naga&rft.date=2015-06-01&rft.volume=148&rft.issue=7&rft.spage=1340&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=1528-0012&rft_id=info:doi/10.1053%2Fj.gastro.2015.03.006 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-04 N1 - Date created - 2015-05-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Hepatology. 2010 Dec;52(6):2065-76 [20949552] Clin Gastroenterol Hepatol. 2011 Jun;9(6):517-523.e3 [21356330] Hepatology. 2009 Jun;49(6):2001-9 [19475693] Drug Saf. 2009;32(1):55-68 [19132805] Aliment Pharmacol Ther. 2010 Nov;32(9):1174-83 [20815829] Gastroenterology. 2008 Dec;135(6):1924-34, 1934.e1-4 [18955056] J Clin Gastroenterol. 2013 Jul;47(6):553-8 [23388845] Hepatology. 2014 Oct;60(4):1399-408 [25043597] Am J Gastroenterol. 2014 Jul;109(7):950-66; quiz 967 [24935270] Gastroenterology. 2014 Jul;147(1):96-108.e4 [24681128] Hepatology. 2014 Feb;59(2):661-70 [24037963] Clin Liver Dis. 2013 Nov;17(4):749-67, xi [24099029] Clin Liver Dis. 2013 Nov;17(4):575-86, viii [24099019] J Am Acad Dermatol. 2013 Aug;69(2):187.e1-16; quiz 203-4 [23866879] J Am Acad Dermatol. 2013 Aug;69(2):173.e1-13; quiz 185-6 [23866878] Dig Dis Sci. 2013 Jun;58(6):1766-75 [23377559] Hepatology. 2006 Oct;44(4):850-6 [17006920] Gastroenterology. 2005 Aug;129(2):512-21 [16083708] Arthritis Rheum. 1997 Sep;40(9):1601-11 [9324014] J Clin Epidemiol. 1993 Nov;46(11):1331-6 [8229111] J Clin Epidemiol. 1993 Nov;46(11):1323-30 [8229110] Hepatology. 1988 May-Jun;8(3):599-606 [3371877] Gastroenterology. 1975 Aug;69(2):289-302 [1150039] Am J Respir Crit Care Med. 2002 Oct 1;166(7):916-9 [12359646] Hepatology. 2002 Aug;36(2):451-5 [12143055] Gastroenterology. 2013 Jun;144(7):1419-25, 1425.e1-3; quiz e19-20 [23419359] Ann Intern Med. 2012 Jun 19;156(12):857-60, W297-300 [22711078] Gastroenterology. 2011 Nov;141(5):1665-72.e1-9 [21855518] Hepatology. 2011 Oct;54(4):1344-50 [21735470] J Pediatr Gastroenterol Nutr. 2011 Aug;53(2):182-9 [21788760] Comment In: Gastroenterology. 2015 Jun;148(7):1271-3 [25921378] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1053/j.gastro.2015.03.006 ER - TY - JOUR T1 - No evidence for reduction of opioid-withdrawal symptoms by cannabis smoking during a methadone dose taper AN - 1683502812 AB - Background and Objectives To support medication development with cannabinoids, smoked cannabis has been said to alleviate symptoms of opioid withdrawal. We evaluated that hypothesis. Methods We analyzed data from the methadone-taper phase of a clinical trial we had conducted. Participants were 116 outpatient heroin and cocaine users (of whom 46 were also cannabis users) who stayed for the 10-week taper. Main outcome measures were weekly urine screens for cannabinoids, plus every-two-week assessments of opioid-withdrawal symptoms. Results Opioid-withdrawal scores did not differ overall between users and nonusers of cannabis. In a lagged analysis in the 46 users, there was a slight (not statistically significant) indication that weeks of higher opiate-withdrawal symptoms preceded weeks of cannabis use (effect-size r=.20, 95% CI −.10 to .46, p=.52). Even if this finding is taken to suggest self-medication with cannabis, a lagged analysis in the other temporal direction showed no indication that cannabis use predicted lower opiate-withdrawal symptoms the next week (effect-size r=.01, 95% CI −.28 to .30, p=.69). These findings persisted in sensitivity analyses controlling for each of 17 potential confounds. Discussion and Conclusion With our findings, the clinical evidence for smoked cannabis as a reducer of opioid-withdrawal symptoms moves slightly further from “inconclusive” or “mixed” and closer to negative, at least in the context of a methadone dose taper like the one used here. Scientific Significance This finding may remove one rationale for medication development using cannabinoids to treat opioid withdrawal, but leaves other rationales intact. (Am J Addict 2015;XX: XX–XX) JF - The American Journal on Addictions AU - Epstein, David H AU - Preston, Kenzie L AD - Treatment Section, Clinical Pharmacology & Therapeutics Branch, Intramural Research Branch of the National Institute on Drug Abuse, Baltimore, Maryland. ; Treatment Section, Clinical Pharmacology & Therapeutics Branch, Intramural Research Branch of the National Institute on Drug Abuse, Baltimore, Maryland. Y1 - 2015/06// PY - 2015 DA - Jun 2015 SP - 323 EP - 328 CY - Hoboken PB - Wiley Subscription Services, Inc. VL - 24 IS - 4 SN - 1055-0496 KW - Medical Sciences--Psychiatry And Neurology KW - Cannabis KW - Addicts KW - Analysis KW - Canabis KW - Clinical research KW - Withdrawal symptoms KW - Clinical trials KW - Cocaine KW - Drugs KW - Heroin KW - Methadone KW - Sensitivity KW - Smoking KW - Symptoms KW - Urine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683502812?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+Journal+on+Addictions&rft.atitle=No+evidence+for+reduction+of+opioid-withdrawal+symptoms+by+cannabis+smoking+during+a+methadone+dose+taper&rft.au=Epstein%2C+David+H%3BPreston%2C+Kenzie+L&rft.aulast=Epstein&rft.aufirst=David&rft.date=2015-06-01&rft.volume=24&rft.issue=4&rft.spage=323&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+on+Addictions&rft.issn=10550496&rft_id=info:doi/10.1111%2Fajad.12183 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-05-12 N1 - Last updated - 2016-05-12 DO - http://dx.doi.org/10.1111/ajad.12183 ER - TY - JOUR T1 - Aprepitant versus metoclopramide, both combined with dexamethasone, for the prevention of cisplatin-induced delayed emesis: a randomized, double-blind study. AN - 1683357293; 25743855 AB - A combination of aprepitant, a 5-HT3 receptor antagonist (r.a.), and dexamethasone is recommended for the prophylaxis of cisplatin-induced nausea and vomiting in the acute phase, and aprepitant + dexamethasone (A + D) in the delayed phase. The aim of this study was to verify if A + D is superior to metoclopramide plus dexamethasone (M + D) in preventing delayed emesis in cancer patients receiving the same prophylaxis for acute emesis. A randomized double-blind study comparing A + D versus M + D was completed in previously untreated cancer patients. Before chemotherapy, all patients were treated with intravenous palonosetron 0.25 mg and dexamethasone 12 mg, and oral aprepitant 125 mg. On day 2-4, patients randomly received oral dexamethasone 8 mg plus aprepitant 80 mg once daily (days 2-3) or metoclopramide 20 mg four times daily plus dexamethasone 8 mg bid. Primary endpoint was rate of complete response (no vomiting, no rescue treatment) in day 2-5 after chemotherapy. Due to difficulty in the accrual of patients, 303 of the 480 planned patients were enrolled, 284 were fully evaluable, 147 receiving A + D, 137 M + D. Day 1 results were similar in both arms. On day 2-5, complete response rate was not significantly different (80.3% with A + D versus 82.5% with M + D, P < 0.38, respectively), and all secondary endpoints were also similar (complete protection, total control, no vomiting, no nausea, and score of Functional Living Index-Emesis; P < 0.24). Adverse events incidence was not significantly different between the two treatments. In cancer patients submitted to cisplatin-based chemotherapy, receiving the same antiemetic prophylaxis for acute emesis, A + D is not superior to M + D in preventing delayed emesis, and both treatments present similar toxicity. NCT00869310. © The Author 2015. Published by Oxford University Press on behalf of the European Society for Medical Oncology. All rights reserved. For permissions, please email: journals.permissions@oup.com. JF - Annals of oncology : official journal of the European Society for Medical Oncology AU - Roila, F AU - Ruggeri, B AU - Ballatori, E AU - Fatigoni, S AU - Caserta, C AU - Licitra, L AU - Mirabile, A AU - Ionta, M T AU - Massidda, B AU - Cavanna, L AU - Palladino, M A AU - Tocci, A AU - Fava, S AU - Colantonio, I AU - Angelelli, L AU - Ciuffreda, L AU - Fasola, G AU - Zerilli, F AU - Italian Group for Antiemetic Research AD - Medical Oncology Division, 'S. Maria' Hospital, Terni roila.fausto@libero.it. ; Clinical Governance, ASUR Marche, Ascoli Piceno. ; Internal Medicine and Public Health, University of L'Aquila, Spinetoli. ; Medical Oncology Division, 'S. Maria' Hospital, Terni. ; Medical Oncology, National Cancer Institute, Milano. ; Medical Oncology II, University Hospital, Cagliari. ; Medical Oncology, Piacenza Hospital, Piacenza. ; Medical Oncology, Azienda Ospedaliera di Legnano, Legnano. ; Medical Oncology, Santa Croce e Carle Hospital, Cuneo. ; Medical Oncology, ASUR Marche, Ascoli Piceno. ; Medical Oncology, Molinette Hospital, Torino. ; Medical Oncology, University Hospital S. Maria della Misericordia, Udine. ; Medical Oncology, S. Antonio Abate Hospital, Trapani, Italy. ; Italian Group for Antiemetic Research Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 1248 EP - 1253 VL - 26 IS - 6 KW - Antiemetics KW - 0 KW - Antineoplastic Agents KW - Drug Combinations KW - Isoquinolines KW - Morpholines KW - Quinuclidines KW - aprepitant KW - 1NF15YR6UY KW - palonosetron KW - 5D06587D6R KW - Dexamethasone KW - 7S5I7G3JQL KW - Metoclopramide KW - L4YEB44I46 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - metoclopramide KW - delayed emesis KW - cisplatin KW - Administration, Oral KW - Young Adult KW - Drug Administration Schedule KW - Double-Blind Method KW - Humans KW - Quality of Life KW - Activities of Daily Living KW - Aged KW - Administration, Intravenous KW - Italy KW - Risk Factors KW - Adult KW - Treatment Outcome KW - Middle Aged KW - Adolescent KW - Time Factors KW - Quinuclidines -- administration & dosage KW - Isoquinolines -- administration & dosage KW - Male KW - Female KW - Nausea -- chemically induced KW - Nausea -- psychology KW - Antiemetics -- administration & dosage KW - Vomiting -- prevention & control KW - Nausea -- prevention & control KW - Dexamethasone -- adverse effects KW - Vomiting -- psychology KW - Vomiting -- chemically induced KW - Morpholines -- administration & dosage KW - Metoclopramide -- administration & dosage KW - Dexamethasone -- administration & dosage KW - Cisplatin -- adverse effects KW - Morpholines -- adverse effects KW - Antiemetics -- adverse effects KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683357293?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+oncology+%3A+official+journal+of+the+European+Society+for+Medical+Oncology&rft.atitle=Aprepitant+versus+metoclopramide%2C+both+combined+with+dexamethasone%2C+for+the+prevention+of+cisplatin-induced+delayed+emesis%3A+a+randomized%2C+double-blind+study.&rft.au=Roila%2C+F%3BRuggeri%2C+B%3BBallatori%2C+E%3BFatigoni%2C+S%3BCaserta%2C+C%3BLicitra%2C+L%3BMirabile%2C+A%3BIonta%2C+M+T%3BMassidda%2C+B%3BCavanna%2C+L%3BPalladino%2C+M+A%3BTocci%2C+A%3BFava%2C+S%3BColantonio%2C+I%3BAngelelli%2C+L%3BCiuffreda%2C+L%3BFasola%2C+G%3BZerilli%2C+F%3BItalian+Group+for+Antiemetic+Research&rft.aulast=Roila&rft.aufirst=F&rft.date=2015-06-01&rft.volume=26&rft.issue=6&rft.spage=1248&rft.isbn=&rft.btitle=&rft.title=Annals+of+oncology+%3A+official+journal+of+the+European+Society+for+Medical+Oncology&rft.issn=1569-8041&rft_id=info:doi/10.1093%2Fannonc%2Fmdv132 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-13 N1 - Date created - 2015-05-25 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00869310; ClinicalTrials.gov N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/annonc/mdv132 ER - TY - JOUR T1 - Lead exposure in US worksites: A literature review and development of an occupational lead exposure database from the published literature AN - 1683354188; PQ0001587016 AB - Background Retrospective exposure assessment of occupational lead exposure in population-based studies requires historical exposure information from many occupations and industries. Methods We reviewed published US exposure monitoring studies to identify lead measurement data. We developed an occupational lead exposure database from the 175 identified papers containing 1,111 sets of lead concentration summary statistics (21% area air, 47% personal air, 32% blood). We also extracted ancillary exposure-related information, including job, industry, task/location, year collected, sampling strategy, control measures in place, and sampling and analytical methods. Results The measurements were published between 1940 and 2010 and represented 27 2-digit standardized industry classification codes. The majority of the measurements were related to lead-based paint work, joining or cutting metal using heat, primary and secondary metal manufacturing, and lead acid battery manufacturing. Conclusions This database can be used in future statistical analyses to characterize differences in lead exposure across time, jobs, and industries. Am. J. Ind. Med. 58:605-616, 2015. JF - American Journal of Industrial Medicine AU - Koh, Dong-Hee AU - Locke, Sarah J AU - Chen, Yu-Cheng AU - Purdue, Mark P AU - Friesen, Melissa C AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland. Y1 - 2015/06// PY - 2015 DA - Jun 2015 SP - 605 EP - 616 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 58 IS - 6 SN - 0271-3586, 0271-3586 KW - Toxicology Abstracts; Health & Safety Science Abstracts KW - Historical account KW - Statistics KW - Heavy metals KW - Statistical analysis KW - Lead KW - Batteries KW - Classification KW - Sampling KW - Occupational exposure KW - Metals KW - Data processing KW - Population studies KW - Working conditions KW - Blood KW - Databases KW - Literature reviews KW - Heat KW - Reviews KW - Standards KW - Paints KW - X 24360:Metals KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683354188?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Industrial+Medicine&rft.atitle=Lead+exposure+in+US+worksites%3A+A+literature+review+and+development+of+an+occupational+lead+exposure+database+from+the+published+literature&rft.au=Koh%2C+Dong-Hee%3BLocke%2C+Sarah+J%3BChen%2C+Yu-Cheng%3BPurdue%2C+Mark+P%3BFriesen%2C+Melissa+C&rft.aulast=Koh&rft.aufirst=Dong-Hee&rft.date=2015-06-01&rft.volume=58&rft.issue=6&rft.spage=605&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Industrial+Medicine&rft.issn=02713586&rft_id=info:doi/10.1002%2Fajim.22448 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Last updated - 2015-08-05 N1 - SubjectsTermNotLitGenreText - Statistics; Data processing; Heavy metals; Statistical analysis; Population studies; Lead; Databases; Blood; Classification; Literature reviews; Heat; Reviews; Sampling; Occupational exposure; Paints; Historical account; Metals; Batteries; Standards; Working conditions DO - http://dx.doi.org/10.1002/ajim.22448 ER - TY - JOUR T1 - Decreased vesicular storage and aldehyde dehydrogenase activity in multiple system atrophy. AN - 1682890643; 25829070 AB - Parkinson disease (PD) and multiple system atrophy (MSA) share some neuropathologic features (nigrostriatal dopaminergic lesion, alpha-synuclein deposition) but not others (Lewy bodies in PD, glial cytoplasmic inclusions in MSA). In PD evidence has accrued for a vesicular storage defect and decreased aldehyde dehydrogenase (ALDH) activity in residual dopaminergic terminals, resulting in accumulation of the toxic dopamine (DA) metabolite 3,4-dihydroxyphenylacetaldehyde (DOPAL). In this study we asked whether MSA entails a similar abnormal neurochemical pattern. DA and its main neuronal metabolite 3,4-dihydroxyphenylacetic acid (DOPAC), norepinephrine (NE) and its main neuronal metabolite 3,4-dihydroxyphenylglycol (DHPG), the catecholamine precursor DOPA, and DOPAL were measured in striatal and frontal cortical tissue from patients with pathologically proven end-stage MSA (N = 15), sporadic PD (N = 17), and control subjects (N = 18). Compared to the control group, the MSA and PD groups had similarly decreased putamen DA (by 96% and 93%, p < 0.0001), DOPAC (97% and 95%, p < 0.0001), NE (91% and 74%, p < 0.0001), and DHPG (81% and 74%, p < 0.0001). In the MSA and PD groups, ratios of DOPAL:DA were 2.3 and 3.5 times control and DHPG:NE 3.1 and 2.6 times control, while DOPAC:DOPAL ratios were decreased by 61% and 74%. In both diseases cortical NE and DHPG were decreased, while DA and DOPAC were not. MSA and PD entail a catecholamine metabolic profile indicating impaired vesicular storage, decreased ALDH activity, and DOPAL buildup, which might be part of a common pathway in catecholamine neuronal death. Targeting this pathway by interfering with catecholaldehyde production or effects constitutes a novel treatment approach. Published by Elsevier Ltd. JF - Parkinsonism & related disorders AU - Goldstein, David S AU - Sullivan, Patricia AU - Holmes, Courtney AU - Kopin, Irwin J AU - Sharabi, Yehonatan AU - Mash, Deborah C AD - Clinical Neurocardiology Section, Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA. Electronic address: goldsteind@ninds.nih.gov. ; Clinical Neurocardiology Section, Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, Bethesda, MD, USA. ; Department of Internal Medicine, Chaim Sheba Medical Center, Tel-HaShomer, and Sackler Faculty of Medicine, Tel-Aviv University, Israel. ; Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 567 EP - 572 VL - 21 IS - 6 KW - 3,4-Dihydroxyphenylacetic Acid KW - 102-32-9 KW - Methoxyhydroxyphenylglycol KW - 534-82-7 KW - 3,4-dihydroxyphenylacetaldehyde KW - 5707-55-1 KW - Dihydroxyphenylalanine KW - 63-84-3 KW - dihydroxyphenylethylene glycol KW - CF5G2G268A KW - Aldehyde Dehydrogenase KW - EC 1.2.1.3 KW - Dopamine KW - VTD58H1Z2X KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - Multiple system atrophy KW - Parkinson disease KW - Putamen KW - DOPAL KW - Methoxyhydroxyphenylglycol -- metabolism KW - Neurons -- metabolism KW - Aged, 80 and over KW - 3,4-Dihydroxyphenylacetic Acid -- metabolism KW - Norepinephrine -- metabolism KW - Humans KW - Dihydroxyphenylalanine -- metabolism KW - Aged KW - Methoxyhydroxyphenylglycol -- analogs & derivatives KW - Male KW - Female KW - 3,4-Dihydroxyphenylacetic Acid -- analogs & derivatives KW - Corpus Striatum -- metabolism KW - Parkinson Disease -- metabolism KW - Frontal Lobe -- metabolism KW - Dopamine -- metabolism KW - Multiple System Atrophy -- metabolism KW - Aldehyde Dehydrogenase -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1682890643?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Parkinsonism+%26+related+disorders&rft.atitle=Decreased+vesicular+storage+and+aldehyde+dehydrogenase+activity+in+multiple+system+atrophy.&rft.au=Goldstein%2C+David+S%3BSullivan%2C+Patricia%3BHolmes%2C+Courtney%3BKopin%2C+Irwin+J%3BSharabi%2C+Yehonatan%3BMash%2C+Deborah+C&rft.aulast=Goldstein&rft.aufirst=David&rft.date=2015-06-01&rft.volume=21&rft.issue=6&rft.spage=567&rft.isbn=&rft.btitle=&rft.title=Parkinsonism+%26+related+disorders&rft.issn=1873-5126&rft_id=info:doi/10.1016%2Fj.parkreldis.2015.03.006 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-02 N1 - Date created - 2015-05-22 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Can J Neurol Sci. 1991 Aug;18(3):275-8 [1913360] J Chromatogr B Biomed Appl. 1994 Mar 4;653(2):131-8 [8205240] Acta Neurol Scand. 1995 Aug;92(2):116-21 [7484057] Arch Neurol. 1997 Aug;54(8):937-44 [9267967] N Engl J Med. 1988 Apr 7;318(14):876-80 [3352672] Psychopharmacology (Berl). 1978 Apr 14;57(1):77-81 [96472] Synapse. 2003 Dec 1;50(3):200-5 [14515337] J Neurochem. 2014 Oct;131(2):219-28 [24848581] Pharmacol Ther. 2014 Dec;144(3):268-82 [24945828] Parkinsonism Relat Disord. 2014 Aug;20(8):840-4 [24816002] Neurobiol Aging. 2014 Sep;35(9):2180.e1-5 [24746362] Neurosci Lett. 2014 May 21;569:27-32 [24670480] J Neurochem. 2013 Sep;126(5):591-603 [23786406] Brain. 2013 Aug;136(Pt 8):2419-31 [23884810] Brain. 2012 Jun;135(Pt 6):1900-13 [22451506] J Clin Invest. 2011 Aug;121(8):3320-30 [21785221] J Biol Chem. 2011 Jul 29;286(30):26978-86 [21642436] Proc Natl Acad Sci U S A. 2011 Mar 8;108(10):4194-9 [21325059] Brain. 2010 Jan;133(Pt 1):172-88 [19903734] Chem Res Toxicol. 2009 Jul;22(7):1256-63 [19537779] Parkinsonism Relat Disord. 2008 Dec;14(8):600-7 [18325818] Neurology. 2008 Aug 26;71(9):670-6 [18725592] Arch Neurol. 2008 Aug;65(8):1074-80 [18695057] Nat Neurosci. 2008 Jul;11(7):755-61 [18536709] Acta Neuropathol. 2008 Feb;115(2):193-203 [17965867] Ann Neurol. 1998 Sep;44(3):415-22 [9749615] Nature. 1997 Aug 28;388(6645):839-40 [9278044] Cereb Cortex. 1998 Jun;8(4):321-45 [9651129] Neurosci Lett. 1998 Jun 19;249(2-3):180-2 [9682846] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.parkreldis.2015.03.006 ER - TY - JOUR T1 - Transgenic mice and metabolomics for study of hepatic xenobiotic metabolism and toxicity. AN - 1682425064; 25836352 AB - The study of xenobiotic metabolism and toxicity has been greatly aided by the use of genetically modified mouse models and metabolomics. Gene knockout mice can be used to determine the enzymes responsible for the metabolism of xenobiotics in vivo and to examine the mechanisms of xenobiotic-induced toxicity. Humanized mouse models are especially important because there exist marked species differences in the xenobiotic-metabolizing enzymes and the nuclear receptors that regulate these enzymes. Humanized mice expressing CYPs and nuclear receptors including the pregnane X receptor, the major regulator of xenobiotic metabolism and transport were produced. With genetically modified mouse models, metabolomics can determine the metabolic map of many xenobiotics with a level of sensitivity that allows the discovery of even minor metabolites. This technology can be used for determining the mechanism of xenobiotic toxicity and to find early biomarkers for toxicity. Metabolomics and genetically modified mouse models can be used for the study of xenobiotic metabolism and toxicity by: i) comparison of the metabolomics profiles between wild-type and genetically modified mice, and searching for genotype-dependent endogenous metabolites; ii) searching for and elucidating metabolites derived from xenobiotics; and iii) discovery of specific alterations of endogenous compounds induced by xenobiotics-induced toxicity. JF - Expert opinion on drug metabolism & toxicology AU - Gonzalez, Frank J AU - Fang, Zhong-Ze AU - Ma, Xiaochao AD - National Institutes of Health, National Cancer Institute, Center for Cancer Research, Laboratory of Metabolism , Bethesda, MD 20892 , USA +1 301 496 9067 ; +1 301 496 8419 ; gonzalef@mail.nih.gov. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 869 EP - 881 VL - 11 IS - 6 KW - Xenobiotics KW - 0 KW - Index Medicus KW - UPLC-ESI-QTOFMS KW - CYP3A4 KW - genetically modified mice KW - pregnane X receptor KW - xenobiotics KW - metabolomics KW - CYP KW - Animals KW - Humans KW - Mice KW - Mice, Transgenic KW - Species Specificity KW - Mice, Knockout KW - Metabolomics -- methods KW - Xenobiotics -- metabolism KW - Liver -- metabolism KW - Xenobiotics -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1682425064?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Expert+opinion+on+drug+metabolism+%26+toxicology&rft.atitle=Transgenic+mice+and+metabolomics+for+study+of+hepatic+xenobiotic+metabolism+and+toxicity.&rft.au=Gonzalez%2C+Frank+J%3BFang%2C+Zhong-Ze%3BMa%2C+Xiaochao&rft.aulast=Gonzalez&rft.aufirst=Frank&rft.date=2015-06-01&rft.volume=11&rft.issue=6&rft.spage=869&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+drug+metabolism+%26+toxicology&rft.issn=1744-7607&rft_id=info:doi/10.1517%2F17425255.2015.1032245 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-15 N1 - Date created - 2015-05-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nutr Rev. 2007 Jun;65(6 Pt 2):S2-6 [17605307] Drug Metab Rev. 2007;39(2-3):581-97 [17786640] Chem Res Toxicol. 2008 Jan;21(1):9-27 [18171018] J Biol Chem. 2008 Feb 22;283(8):4543-59 [18093979] J Biol Chem. 2008 Mar 21;283(12):7901-11 [18180294] AIDS. 2008 May 11;22(8):931-5 [18453852] J Clin Invest. 2008 Sep;118(9):3228-39 [18677425] Drug Metab Dispos. 2008 Oct;36(10):2058-63 [18645036] Arch Toxicol. 2014 Aug;88(8):1491-502 [24710571] Hepatology. 2014 Oct;60(4):1336-45 [24923598] Exp Mol Pathol. 2014 Dec;97(3):492-510 [25217800] J Appl Toxicol. 2015 Feb;35(2):142-51 [24652713] Nat Rev Cancer. 2014 Dec;14(12):801-14 [25568920] J Lab Autom. 2015 Jun;20(3):216-50 [25617027] Nature. 2000 Oct 19;407(6806):920-3 [11057673] Proc Natl Acad Sci U S A. 2001 Mar 13;98(6):3369-74 [11248085] Nat Rev Drug Discov. 2002 Feb;1(2):153-61 [12120097] J Biol Chem. 2003 Apr 11;278(15):13480-6 [12566435] Drug Metab Dispos. 2003 May;31(5):548-58 [12695342] Semin Liver Dis. 2003 May;23(2):183-94 [12800071] Genesis. 2003 Aug;36(4):177-81 [12929087] J Immunol. 2004 Mar 1;172(5):2731-8 [14978070] Am J Pathol. 2004 Sep;165(3):901-12 [15331414] Hepatology. 2004 Oct;40(4):972-80 [15382117] J Clin Pharmacol. 2004 Nov;44(11):1273-81 [15496645] J Biol Chem. 1985 Nov 5;260(25):13607-12 [4055750] Toxicology. 1988 Nov 14;52(1-2):1-53 [3055427] J Biol Chem. 1989 Feb 25;264(6):3568-72 [2914964] Chem Res Toxicol. 2011 Dec 19;24(12):2109-14 [22040299] Annu Rev Pharmacol Toxicol. 2012;52:37-56 [21819238] Toxicol Lett. 2012 Oct 2;214(1):9-18 [22902350] Bioanalysis. 2012 Sep;4(18):2291-301 [23046269] Cell Metab. 2012 Nov 7;16(5):634-44 [23140643] J Proteome Res. 2013 Mar 1;12(3):1369-76 [23301521] Mol Cell Endocrinol. 2013 Apr 10;368(1-2):17-29 [22609541] Nat Med. 2013 Apr;19(4):418-20 [23475203] Compr Physiol. 2012 Oct;2(4):2811-28 [23720266] Compr Physiol. 2013 Jul;3(3):1191-212 [23897684] Mol Pharmacol. 2013 Sep;84(3):304-13 [23761301] Stem Cell Rev. 2013 Aug;9(4):493-504 [22076752] J Appl Toxicol. 2013 Dec;33(12):1365-83 [23722930] Drug Discov Today. 2013 Dec;18(23-24):1200-11 [23872278] Curr Top Med Chem. 2014;14(1):110-29 [24236723] Xenobiotica. 2014 Jan;44(2):96-108 [23845026] Xenobiotica. 2014 Jan;44(2):123-34 [24329499] J Lipid Res. 2014 Mar;55(3):455-65 [24343899] Biotechnol Adv. 2014 Mar-Apr;32(2):504-13 [24440487] Cell Mol Life Sci. 2014 Apr;71(7):1171-90 [23807210] Future Med Chem. 2014 Apr;6(5):481-3 [24649949] Drug Metab Dispos. 2014 Jun;42(6):1022-30 [24671958] Toxicol Sci. 2014 Jun;139(2):501-11 [24690595] Curr Top Med Chem. 2014;14(11):1325-38 [24805059] Gut. 1995 Feb;36(2):259-67 [7883227] Science. 1995 May 5;268(5211):722-6 [7732381] J Pharmacol Exp Ther. 1996 Apr;277(1):423-31 [8613951] Proc Natl Acad Sci U S A. 1996 Jun 25;93(13):6731-6 [8692887] Crit Rev Toxicol. 1996 Sep;26(5):551-83 [8891430] AIDS. 1997 Mar 15;11(4):F29-33 [9084785] Drug Metab Dispos. 1997 Apr;25(4):489-501 [9107549] J Pharmacokinet Biopharm. 1996 Oct;24(5):475-90 [9131486] Proc Natl Acad Sci U S A. 1998 Apr 28;95(9):5275-80 [9560266] Toxicol Appl Pharmacol. 1998 Sep;152(1):193-9 [9772215] Am J Med. 1997 May 19;102(5B):65-7; discussion 68-9 [9845500] Annu Rev Pharmacol Toxicol. 1999;39:1-17 [10331074] Ann N Y Acad Sci. 2004 Nov;1033:17-29 [15591000] Pharmacogenomics. 2005 Oct;6(7):691-9 [16207146] Curr Drug Metab. 2006 Feb;7(2):165-82 [16472106] Dig Liver Dis. 2006 Jun;38(6):363-73 [16631422] Am J Respir Crit Care Med. 2006 Oct 15;174(8):935-52 [17021358] Drug Metab Dispos. 2007 Jan;35(1):1-8 [17020953] Chem Res Toxicol. 2007 Mar;20(3):531-42 [17279779] Chem Res Toxicol. 2007 Mar;20(3):344-69 [17302443] J Biol Chem. 2012 Feb 24;287(9):6336-49 [22228769] Hepatology. 2012 Jul;56(1):281-90 [22318764] Arch Toxicol. 2012 Aug;86(8):1251-71 [22569772] Mol Endocrinol. 2000 Jan;14(1):27-39 [10628745] Cancer Res. 2000 Jul 1;60(13):3454-60 [10910056] Nature. 2000 Jul 27;406(6794):435-9 [10935643] J Pharmacol Exp Ther. 2008 Nov;327(2):288-99 [18682571] AIDS. 2009 Jan 28;23(3):279-91 [19114854] J Acquir Immune Defic Syndr. 2009 Mar 1;50(3):290-3 [19194314] Chem Res Toxicol. 2009 Apr;22(4):699-707 [19256530] Hepatology. 2009 May;49(5):1403-18 [19296471] Drug Metab Dispos. 2009 Sep;37(9):1938-47 [19487251] Proc Natl Acad Sci U S A. 2009 Aug 25;106(34):14728-33 [19667173] Clin Pharmacol Ther. 2010 Jan;87(1):109-16 [19940846] Toxicol Appl Pharmacol. 2010 Mar 1;243(2):154-66 [19932708] Toxicology. 2010 Feb 9;268(3):125-31 [19683031] Rapid Commun Mass Spectrom. 2010 May 15;24(9):1241-50 [20391594] Methods Mol Biol. 2010;637:1-21 [20419427] J Proteome Res. 2010 Aug 6;9(8):4176-88 [20540569] Bioanalysis. 2009 Dec;1(9):1645-63 [21083109] Drug Metab Rev. 2011 May;43(2):152-64 [21425933] Br J Pharmacol. 2011 Jun;163(3):461-8 [21091656] Chem Res Toxicol. 2011 May 16;24(5):744-51 [21469730] Toxicol Sci. 2011 Jun;121(2):207-33 [21447610] J Proteome Res. 2011 Sep 2;10(9):4120-33 [21749142] Curr Drug Metab. 2011 Dec;12(10):997-1006 [22023319] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1517/17425255.2015.1032245 ER - TY - JOUR T1 - Environmental chemical exposure may contribute to uterine cancer development: studies with tetrabromobisphenol A. AN - 1682424603; 25476797 AB - Tetrabromobisphenol A (TBBPA), a widely used flame retardant, caused uterine tumors in rats. In this study, TBBPA was administered to male and female Wistar Han rats and B6C3F1/N mice by oral gavage in corn oil for 2 years at doses up to 1,000 mg/kg. TBBPA induced uterine epithelial tumors including adenomas, adenocarcinomas, and malignant mixed Müllerian tumors (MMMTs). In addition, endometrial epithelial atypical hyperplasia occurred in TBBPA-treated rats. Also found to be related to TBBPA treatment, but at lower incidence and at a lower statistical significance, were testicular tumors in rats, and hepatic tumors, hemangiosarcomas (all organs), and intestinal tumors in male mice. It is hypothesized that the TBBPA uterine tumor carcinogenic mechanisms involve altered estrogen levels and/or oxidative damage. TBBPA treatment may affect hydroxysteroid-dehydrogenase-17β (HSD17β) and/or sulfotransferases, enzymes involved in estrogen homeostasis. Metabolism of TBBPA may also result in the formation of free radicals. The finding of TBBPA-mediated uterine cancer in rats is of concern because TBBPA exposure is widespread and endometrial tumors are a common malignancy in women. Further work is needed to understand TBBPA cancer mechanisms. © 2014 by The Author(s). JF - Toxicologic pathology AU - Dunnick, J K AU - Sanders, J M AU - Kissling, G E AU - Johnson, C L AU - Boyle, M H AU - Elmore, S A AD - National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, North Carolina, USA dunnickj@niehs.nih.gov. ; National Cancer Institute, National Institutes of Health, Research Triangle Park, North Carolina, USA. ; National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, North Carolina, USA. ; Charles River Laboratories, Pathology Associates, Research Triangle Park, North Carolina, USA. ; Integrated Laboratory Systems, Research Triangle Park, North Carolina, USA. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 464 EP - 473 VL - 43 IS - 4 KW - Carcinogens KW - 0 KW - Environmental Pollutants KW - Polybrominated Biphenyls KW - tetrabromobisphenol A KW - FQI02RFC3A KW - Index Medicus KW - malignant mixed Müllerian tumors (MMMT) KW - flame retardants KW - uterine tumors KW - Animals KW - Body Weight -- drug effects KW - Carcinogenicity Tests KW - Uterus -- pathology KW - Uterus -- drug effects KW - Female KW - Environmental Pollutants -- toxicity KW - Uterine Neoplasms -- chemically induced KW - Carcinogens -- toxicity KW - Polybrominated Biphenyls -- toxicity KW - Uterine Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1682424603?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Environmental+chemical+exposure+may+contribute+to+uterine+cancer+development%3A+studies+with+tetrabromobisphenol+A.&rft.au=Dunnick%2C+J+K%3BSanders%2C+J+M%3BKissling%2C+G+E%3BJohnson%2C+C+L%3BBoyle%2C+M+H%3BElmore%2C+S+A&rft.aulast=Dunnick&rft.aufirst=J&rft.date=2015-06-01&rft.volume=43&rft.issue=4&rft.spage=464&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623314557335 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-16 N1 - Date created - 2015-05-20 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/0192623314557335 ER - TY - JOUR T1 - Characterization of Batracylin-induced Renal and Bladder Toxicity in Rats. AN - 1682424491; 25274659 AB - Batracylin (NSC-320846) is a dual inhibitor of DNA topoisomerases I and II. Batracylin advanced as an anticancer agent to Phase I clinical trials where dose limiting hemorrhagic cystitis (bladder inflammation and bleeding) was observed. To further investigate batracylin's mechanism of toxicity, studies were conducted in Fischer 344 rats. Once daily oral administration of 16 or 32 mg/kg batracylin to rats for 4 days caused overt toxicity. Abnormal clinical observations and adverse effects on clinical pathology, urinalysis, and histology indicated acute renal damage and urothelial damage and bone marrow dysfunction. Scanning electron microscopy revealed sloughing of the superficial and intermediate urothelial layers. DNA damage was evident in kidney and bone marrow as indicated by histone γ-H2AX immunofluorescence. After a single oral administration of 16 or 32 mg/kg, the majority of batracylin was converted to N-acetylbatracylin (NAB) with a half-life of 4 hr to 11 hr. Mesna (Mesnex™), a drug known to reduce the incidence of hemorrhagic cystitis induced by ifosfamide or cyclophosphamide, was administered to rats prior to batracylin, but did not alleviate batracylin-induced bladder and renal toxicity. These findings suggest that batracylin results in DNA damage-based mechanisms of toxicity and not an acrolein-based mechanism of toxicity as occurs after ifosfamide or cyclophosphamide administration. © 2014 by The Author(s). JF - Toxicologic pathology AU - Davis, Myrtle AU - Bunin, Deborah I AU - Samuelsson, Steven J AU - Altera, Kenneth P AU - Kinders, Robert J AU - Lawrence, Scott M AU - Ji, Jiuping AU - Ames, Matthew M AU - Buhrow, Sarah A AU - Walden, Chad AU - Reid, Joel M AU - Rausch, Linda L AU - Parman, Toufan AD - Toxicology and Pharmacology Branch, Division of Cancer Treatment and Diagnosis, The National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA davismillinm@mail.nih.gov. ; SRI International, Menlo Park, California, USA. ; Pharmacodynamics Assay Development and Implementation Section, Laboratory of Human Toxicology and Pharmacology, Applied/Developmental Research Directorate, Frederick National Laboratory for Cancer Research, Frederick, Maryland, USA. ; Department of Oncology, Division of Oncology Research, Mayo Clinic, Rochester, Minnesota. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 519 EP - 529 VL - 43 IS - 4 KW - Biomarkers, Tumor KW - 0 KW - Histones KW - Phosphoproteins KW - Quinazolines KW - gamma-H2AX protein, rat KW - batracylin KW - 67199-66-0 KW - Mesna KW - NR7O1405Q9 KW - Index Medicus KW - DNA damage KW - renal toxicity KW - γH2AX KW - bladder toxicity KW - Rats KW - Mesna -- pharmacology KW - Animals KW - Random Allocation KW - Histones -- metabolism KW - Body Weight -- drug effects KW - Biomarkers, Tumor -- analysis KW - Glycosuria -- chemically induced KW - Male KW - Female KW - Phosphoproteins -- metabolism KW - Quinazolines -- pharmacokinetics KW - Kidney Neoplasms -- pathology KW - Urinary Bladder Neoplasms -- pathology KW - Kidney Neoplasms -- chemically induced KW - Kidney Neoplasms -- metabolism KW - Urinary Bladder Neoplasms -- metabolism KW - Quinazolines -- toxicity KW - Urinary Bladder Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1682424491?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Characterization+of+Batracylin-induced+Renal+and+Bladder+Toxicity+in+Rats.&rft.au=Davis%2C+Myrtle%3BBunin%2C+Deborah+I%3BSamuelsson%2C+Steven+J%3BAltera%2C+Kenneth+P%3BKinders%2C+Robert+J%3BLawrence%2C+Scott+M%3BJi%2C+Jiuping%3BAmes%2C+Matthew+M%3BBuhrow%2C+Sarah+A%3BWalden%2C+Chad%3BReid%2C+Joel+M%3BRausch%2C+Linda+L%3BParman%2C+Toufan&rft.aulast=Davis&rft.aufirst=Myrtle&rft.date=2015-06-01&rft.volume=43&rft.issue=4&rft.spage=519&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623314548766 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-16 N1 - Date created - 2015-05-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Int J Oncol. 2009 Jul;35(1):41-7 [19513550] Curr Med Chem. 2012;19(26):4475-87 [22830346] J Clin Oncol. 1990 Jan;8(1):170-8 [2104923] Invest New Drugs. 1989 Nov;7(4):295-306 [2557298] Invest New Drugs. 1988 Sep;6(3):147-53 [3192381] Methods Mol Biol. 2011;682:249-70 [21057933] Cancer Res. 2007 Oct 15;67(20):9971-9 [17942930] Toxicol Pathol. 2007 Apr;35(3):337-47 [17455081] J Med Chem. 1994 Sep 30;37(20):3434-9 [7932571] Pharm Res. 1993 Jun;10(6):918-23 [8391697] J Cancer Res Clin Oncol. 1981;100(3):311-20 [6792207] Cell Biol Toxicol. 2000;16(1):31-9 [10890504] J Biol Chem. 2000 Mar 31;275(13):9390-5 [10734083] Cancer Chemother Pharmacol. 2013 Oct;72(4):917-23 [23912694] Nature. 2009 Apr 2;458(7238):591-6 [19234442] Cancer Res. 2011 Sep 1;71(17):5626-34 [21795476] Invest New Drugs. 1991 Aug;9(3):219-25 [1783521] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/0192623314548766 ER - TY - JOUR T1 - Hepatic Mitochondrial Alteration in CD-1 Mice Associated with Prenatal Exposures to Low Doses of Perfluorooctanoic Acid (PFOA). AN - 1682424468; 25326589 AB - Perfluorooctanoic acid (PFOA) is a perfluoroalkyl acid primarily used as an industrial surfactant. It persists in the environment and has been linked to potentially toxic and/or carcinogenic effects in animals and people. As a known activator of peroxisome proliferator-activated receptors (PPARs), PFOA exposure can induce defects in fatty acid oxidation, lipid transport, and inflammation. Here, pregnant CD-1 mice were orally gavaged with 0, 0.01, 0.1, 0.3, and 1 mg/kg of PFOA from gestation days (GD) 1 through 17. On postnatal day (PND) 21, histopathologic changes in the livers of offspring included hepatocellular hypertrophy and periportal inflammation that increased in severity by PND 91 in an apparent dose-dependent response. Transmission electron microscopy (TEM) of selected liver sections from PND 91 mice revealed PFOA-induced cellular damage and mitochondrial abnormalities with no evidence of peroxisome proliferation. Within hypertrophied hepatocytes, mitochondria were not only increased in number but also exhibited altered morphologies suggestive of increased and/or uncontrolled fission and fusion reactions. These findings suggest that peroxisome proliferation is not a component of PFOA-induced hepatic toxicity in animals that are prenatally exposed to low doses of PFOA. © 2014 by The Author(s). JF - Toxicologic pathology AU - Quist, Erin M AU - Filgo, Adam J AU - Cummings, Connie A AU - Kissling, Grace E AU - Hoenerhoff, Mark J AU - Fenton, Suzanne E AD - NTP Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA Cellular and Molecular Pathology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA Comparative Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USA. ; NTP Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA Curriculum in Toxicology, University of North Carolina, Chapel Hill, North Carolina, USA. ; UltraPath Imaging, Durham, North Carolina, USA. ; Biostatistics Branch, Division of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA. ; Cellular and Molecular Pathology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA. ; NTP Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA fentonse@niehs.nih.gov. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 546 EP - 557 VL - 43 IS - 4 KW - Caprylates KW - 0 KW - Fluorocarbons KW - PPAR alpha KW - perfluorooctanoic acid KW - 947VD76D3L KW - Index Medicus KW - peroxisome proliferation KW - mouse KW - mitochondrial damage KW - PFOA KW - liver KW - hepatocellular hypertrophy KW - PPARα KW - Animals KW - Hepatocytes -- drug effects KW - Liver -- cytology KW - Liver -- pathology KW - Dose-Response Relationship, Drug KW - Liver -- metabolism KW - Mice KW - Hepatocytes -- pathology KW - Pregnancy KW - Liver -- drug effects KW - Body Weight -- drug effects KW - PPAR alpha -- metabolism KW - Female KW - Hepatocytes -- metabolism KW - Prenatal Exposure Delayed Effects -- pathology KW - Prenatal Exposure Delayed Effects -- metabolism KW - Prenatal Exposure Delayed Effects -- chemically induced KW - Mitochondria, Liver -- metabolism KW - Mitochondria, Liver -- pathology KW - Fluorocarbons -- toxicity KW - Caprylates -- toxicity KW - Mitochondria, Liver -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1682424468?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Hepatic+Mitochondrial+Alteration+in+CD-1+Mice+Associated+with+Prenatal+Exposures+to+Low+Doses+of+Perfluorooctanoic+Acid+%28PFOA%29.&rft.au=Quist%2C+Erin+M%3BFilgo%2C+Adam+J%3BCummings%2C+Connie+A%3BKissling%2C+Grace+E%3BHoenerhoff%2C+Mark+J%3BFenton%2C+Suzanne+E&rft.aulast=Quist&rft.aufirst=Erin&rft.date=2015-06-01&rft.volume=43&rft.issue=4&rft.spage=546&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623314551841 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-16 N1 - Date created - 2015-05-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Environ Health Perspect. 2012 May;120(5):655-60 [22289616] Environ Sci Technol. 2011 Oct 1;45(19):7954-61 [21866930] Toxicol Sci. 2011 Jul;122(1):134-45 [21482639] Environ Res. 2012 Jul;116:93-117 [22560884] EXS. 2012;101:47-86 [22945566] Toxicol Pathol. 2012 Oct;40(7):971-94 [22723046] Toxicol Pathol. 2013 Feb;41(2):210-26 [23344891] Toxicol Lett. 2013 Nov 25;223(2):211-20 [24035753] Toxicol Pathol. 2015 Jun;43(4):558-68 [25398757] Int Immunopharmacol. 2002 Feb;2(2-3):389-97 [11811941] Toxicol Lett. 2002 Mar 24;129(1-2):23-32 [11879971] Toxicol Sci. 2002 Apr;66(2):244-52 [11896291] Toxicol Sci. 2006 Apr;90(2):510-8 [16415327] J Occup Environ Med. 2006 Aug;48(8):759-70 [16902368] Toxicology. 2007 Sep 24;239(1-2):15-33 [17681415] Toxicol Pathol. 2008 Jun;36(4):632-9 [18467680] Mol Cell Endocrinol. 2009 May 25;304(1-2):97-105 [19433254] Reprod Toxicol. 2012 Jul;33(4):491-505 [22154759] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/0192623314551841 ER - TY - JOUR T1 - Perfluorooctanoic Acid (PFOA)-induced Liver Lesions in Two Strains of Mice Following Developmental Exposures: PPARα Is Not Required. AN - 1682424452; 25398757 AB - Perfluorooctanoic acid (PFOA) is a ubiquitous pollutant that causes liver toxicity in rodents, a process believed to be dependent on peroxisome proliferator-activated receptor-alpha (PPARα) activation. Differences between humans and rodents have made the human relevance of some health effects caused by PFOA controversial. We analyzed liver toxicity at 18 months following gestational PFOA exposure in CD-1 and 129/Sv strains of mice and compared PFOA-induced effects between strains and in wild type (WT) and PPARα-knockout (KO) 129/Sv mice. Pregnant mice were exposed daily to doses (0.01-5 mg/kg/BW) of PFOA from gestation days 1 to 17. The female offspring were necropsied at 18 months, and liver sections underwent a full pathology review. Hepatocellular adenomas formed in PFOA-exposed PPARα-KO 129/Sv and CD-1 mice and were absent in untreated controls from those groups and WT 129/Sv. Hepatocellular hypertrophy was significantly increased by PFOA exposure in CD-1, and an increased severity was found in WT 129/Sv mice. PFOA significantly increased nonneoplastic liver lesions in PPARα-KO mice (hepatocyte hypertrophy, bile duct hyperplasia, and hematopoietic cell proliferation). Low-dose gestational exposures to PFOA induced latent PPARα-independent liver toxicity that was observed in aged mice. Evidence of liver toxicity in PPARα-KO mice warrants further investigation into PPARα-independent pathways. © 2014 by The Author(s). JF - Toxicologic pathology AU - Filgo, Adam J AU - Quist, Erin M AU - Hoenerhoff, Mark J AU - Brix, Amy E AU - Kissling, Grace E AU - Fenton, Suzanne E AD - Curriculum in Toxicology, University of North Carolina, School of Medicine, Chapel Hill, North Carolina, USA NTP Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA. ; NTP Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA Comparative Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina, USA Cellular and Molecular Pathology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA. ; Cellular and Molecular Pathology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA. ; Experimental Pathology Laboratories, Inc., Research Triangle Park, North Carolina, USA. ; Biostatistics Branch, Division of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA. ; NTP Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA fentonse@niehs.nih.gov. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 558 EP - 568 VL - 43 IS - 4 KW - Caprylates KW - 0 KW - Fluorocarbons KW - PPAR alpha KW - perfluorooctanoic acid KW - 947VD76D3L KW - Index Medicus KW - developmental exposure KW - PFOA KW - pathology KW - liver KW - tumor KW - PPARα KW - Animals KW - Mice KW - Male KW - Female KW - Pregnancy KW - Mice, Knockout KW - Prenatal Exposure Delayed Effects -- pathology KW - Prenatal Exposure Delayed Effects -- metabolism KW - Liver Neoplasms, Experimental -- pathology KW - Liver Neoplasms, Experimental -- metabolism KW - Liver -- drug effects KW - Prenatal Exposure Delayed Effects -- chemically induced KW - Fluorocarbons -- toxicity KW - Liver Neoplasms, Experimental -- chemically induced KW - Caprylates -- toxicity KW - PPAR alpha -- metabolism KW - PPAR alpha -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1682424452?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Perfluorooctanoic+Acid+%28PFOA%29-induced+Liver+Lesions+in+Two+Strains+of+Mice+Following+Developmental+Exposures%3A+PPAR%CE%B1+Is+Not+Required.&rft.au=Filgo%2C+Adam+J%3BQuist%2C+Erin+M%3BHoenerhoff%2C+Mark+J%3BBrix%2C+Amy+E%3BKissling%2C+Grace+E%3BFenton%2C+Suzanne+E&rft.aulast=Filgo&rft.aufirst=Adam&rft.date=2015-06-01&rft.volume=43&rft.issue=4&rft.spage=558&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623314558463 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-16 N1 - Date created - 2015-05-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Toxicol Sci. 2007 Mar;96(1):133-44 [17132714] Toxicol Sci. 2007 Feb;95(2):462-73 [17098816] Toxicol Sci. 2007 Jan;95(1):108-17 [17047030] Reprod Toxicol. 2009 Jun;27(3-4):239-45 [19429402] Mol Pharmacol. 1998 Jan;53(1):14-22 [9443928] Carcinogenesis. 2005 Jan;26(1):219-27 [15447978] Toxicol Sci. 2006 Apr;90(2):510-8 [16415327] Reprod Toxicol. 2012 Jul;33(4):405-9 [22429996] Reprod Toxicol. 2012 Jul;33(4):563-76 [22414604] Reprod Toxicol. 2012 Jul;33(4):410-8 [22120428] Environ Health Perspect. 2012 Apr;120(4):590-4 [22182702] Arch Toxicol. 2012 Jan;86(1):63-74 [21499893] Environ Sci Technol. 2011 Oct 1;45(19):8037-45 [21469664] Toxicol Sci. 2011 Jul;122(1):134-45 [21482639] Toxicol Pathol. 2010 Dec;38(7 Suppl):5S-81S [21191096] Environ Sci Technol. 2010 Sep 15;44(18):7123-9 [20722423] Ind Health. 2010;48(1):96-107 [20160413] Toxicol Sci. 2013 Feb;131(2):568-82 [23143925] Environ Sci Pollut Res Int. 2013 Nov;20(11):7970-8 [23436123] Toxicol Appl Pharmacol. 1999 Dec 1;161(2):209-18 [10581215] Toxicol Sci. 2001 Mar;60(1):44-55 [11222872] Toxicol Lett. 2002 Mar 24;129(1-2):23-32 [11879971] Toxicol Sci. 2002 Sep;69(1):244-57 [12215680] Cancer Res. 2004 Jun 1;64(11):3849-54 [15172993] Carcinogenesis. 1997 Nov;18(11):2029-33 [9395198] Environ Sci Technol. 2009 Apr 1;43(7):2641-7 [19452929] Mol Cell Endocrinol. 2009 May 25;304(1-2):97-105 [19433254] J Occup Environ Med. 2006 Aug;48(8):759-70 [16902368] Toxicol Sci. 2007 Aug;98(2):571-81 [17488742] J Occup Health. 2007 May;49(3):172-82 [17575397] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/0192623314558463 ER - TY - JOUR T1 - In vivo antibacterial activity and pharmacological properties of the membrane-active glycopeptide antibiotic YV11455. AN - 1682208429; 25900818 AB - The membrane-active glycopeptide antibiotic YV11455 is a lipophilic cationic vancomycin analogue that demonstrates rapid and concentration-dependent killing of clinically relevant multidrug-resistant (MDR) Gram-positive bacteria in vitro. YV11455 was 2-fold and 54-270-fold more effective than vancomycin against clinical isolates of vancomycin-sensitive and vancomycin-resistant bacteria, respectively. In this study, the in vivo efficacy, pharmacodynamics, pharmacokinetics and acute toxicology of YV11455 were investigated. In vivo activity and pharmacodynamics were determined in the neutropenic mouse thigh infection model against meticillin-resistant Staphylococcus aureus (MRSA). YV11455 produced dose-dependent reductions in MRSA titres in thigh muscle. When administered intravenously, the 50% effective dose (ED(50)) for YV11455 against MRSA was found to be 3.3 mg/kg body weight, and titres were reduced by up to ca. 3log(10)CFU/g from pre-treatment values at a dosage of 12 mg/kg with single treatment. Single-dose pharmacokinetic studies demonstrated linear kinetics and a prolonged half-life, with an increase in drug exposure (area under the concentration-time curve) compared with vancomycin. The peak plasma concentration following an intravenous dose of 12 mg/kg was 543.5 μg/mL. Acute toxicology studies revealed that YV11455 did not cause any significant alterations in biochemical parameters or histological pictures related to major organs such as the liver and kidney at its pharmacodynamic endpoint (ED(3-log kill)). These findings collectively suggest that YV11455 could be used clinically for the treatment of infections caused by MDR Gram-positive bacteria. Copyright © 2015 Elsevier B.V. and the International Society of Chemotherapy. All rights reserved. JF - International journal of antimicrobial agents AU - Yarlagadda, Venkateswarlu AU - Konai, Mohini M AU - Manjunath, Goutham B AU - Prakash, Relekar G AU - Mani, Bhuvana AU - Paramanandham, Krishnamoorthy AU - Ranjan, Shome B AU - Ravikumar, Raju AU - Chakraborty, Subhankari P AU - Roy, Somenath AU - Haldar, Jayanta AD - Chemical Biology and Medicinal Chemistry Laboratory, New Chemistry Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Jakkur, Bangalore 560064, Karnataka, India. ; National Institute of Veterinary Epidemiology and Disease Informatics (NIVEDI), Hebbal, Bangalore 560024, Karnataka, India. ; Department of Neuromicrobiology, National Institute of Mental Health and Neurosciences, Hosur Road, Bangalore 560029, Karnataka, India. ; Immunology and Microbiology Laboratory, Department of Human Physiology with Community Health, Vidyasagar University, Midnapore 721102, West Bengal, India. ; Chemical Biology and Medicinal Chemistry Laboratory, New Chemistry Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Jakkur, Bangalore 560064, Karnataka, India. Electronic address: jayanta@jncasr.ac.in. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 627 EP - 634 VL - 45 IS - 6 KW - Anti-Bacterial Agents KW - 0 KW - Glycopeptides KW - Vancomycin KW - 6Q205EH1VU KW - Index Medicus KW - Vancomycin-resistant bacteria KW - Pharmacological properties KW - Membrane-active antibiotic KW - In vivo efficacy KW - Glycopeptide antibiotics KW - Antibiotic resistance KW - Kidney Function Tests KW - Animals KW - Muscles -- microbiology KW - Methicillin-Resistant Staphylococcus aureus -- drug effects KW - Drug-Related Side Effects and Adverse Reactions -- pathology KW - Disease Models, Animal KW - Mice KW - Bacterial Load KW - Liver Function Tests KW - Female KW - Vancomycin -- pharmacology KW - Glycopeptides -- administration & dosage KW - Anti-Bacterial Agents -- adverse effects KW - Vancomycin -- pharmacokinetics KW - Anti-Bacterial Agents -- pharmacology KW - Glycopeptides -- pharmacokinetics KW - Staphylococcal Infections -- microbiology KW - Anti-Bacterial Agents -- pharmacokinetics KW - Glycopeptides -- pharmacology KW - Staphylococcal Infections -- drug therapy KW - Vancomycin -- adverse effects KW - Vancomycin -- administration & dosage KW - Anti-Bacterial Agents -- administration & dosage KW - Glycopeptides -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1682208429?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+antimicrobial+agents&rft.atitle=In+vivo+antibacterial+activity+and+pharmacological+properties+of+the+membrane-active+glycopeptide+antibiotic+YV11455.&rft.au=Yarlagadda%2C+Venkateswarlu%3BKonai%2C+Mohini+M%3BManjunath%2C+Goutham+B%3BPrakash%2C+Relekar+G%3BMani%2C+Bhuvana%3BParamanandham%2C+Krishnamoorthy%3BRanjan%2C+Shome+B%3BRavikumar%2C+Raju%3BChakraborty%2C+Subhankari+P%3BRoy%2C+Somenath%3BHaldar%2C+Jayanta&rft.aulast=Yarlagadda&rft.aufirst=Venkateswarlu&rft.date=2015-06-01&rft.volume=45&rft.issue=6&rft.spage=627&rft.isbn=&rft.btitle=&rft.title=International+journal+of+antimicrobial+agents&rft.issn=1872-7913&rft_id=info:doi/10.1016%2Fj.ijantimicag.2015.02.013 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-02 N1 - Date created - 2015-05-19 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ijantimicag.2015.02.013 ER - TY - JOUR T1 - Biomarker-driven phase 2 study of MK-2206 and selumetinib (AZD6244, ARRY-142886) in patients with colorectal cancer. AN - 1681913755; 25637165 AB - PI3K/AKT/mTOR and RAS/RAF/MEK pathways are frequently dysregulated in colorectal cancer (CRC). We conducted a biomarker-driven trial of the combination of MK-2206, an allosteric AKT 1/2/3 inhibitor, and selumetinib, a MEK 1/2 inhibitor, in patients with CRC to evaluate inhibition of phosphorylated ERK (pERK) and AKT (pAKT) in paired tumor biopsies. Adult patients with advanced CRC were enrolled in successive cohorts stratified by KRAS mutation status. Initially, 12 patients received oral MK-2206 90 mg weekly with oral selumetinib 75 mg daily in 28-day cycles. Following an interim analysis, the doses of MK-2206 and selumetinib were increased to 135 mg weekly and 100 mg daily, respectively. Paired tumor biopsies were evaluated for target modulation. Common toxicities were gastrointestinal, hepatic, dermatologic, and hematologic. Of 21 patients enrolled, there were no objective responses. Target modulation did not achieve the pre-specified criteria of dual 70 % inhibition of pERK and pAKT levels in paired tumor biopsies. Despite strong scientific rationale and preclinical data, clinical activity was not observed. The desired level of target inhibition was not achieved. Overlapping toxicities limited the ability to dose escalate to achieve exposures likely needed for clinical activity, highlighting the challenges in developing optimal combinations of targeted agents. JF - Investigational new drugs AU - Do, Khanh AU - Speranza, Giovanna AU - Bishop, Rachel AU - Khin, Sonny AU - Rubinstein, Larry AU - Kinders, Robert J AU - Datiles, Manuel AU - Eugeni, Michelle AU - Lam, Michael H AU - Doyle, L Austin AU - Doroshow, James H AU - Kummar, Shivaani AD - Division of Cancer Treatment and Diagnosis, National Cancer Institute, 31 Center Drive, Bldg 31, Rm 3A44, Bethesda, MD, 20892, USA. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 720 EP - 728 VL - 33 IS - 3 KW - AZD 6244 KW - 0 KW - Antineoplastic Agents KW - Benzimidazoles KW - Biomarkers, Tumor KW - Heterocyclic Compounds, 3-Ring KW - MK 2206 KW - Index Medicus KW - Young Adult KW - Humans KW - Adult KW - Treatment Outcome KW - Xenograft Model Antitumor Assays KW - Tomography KW - Aged KW - Middle Aged KW - HCT116 Cells KW - Adolescent KW - Male KW - Female KW - Benzimidazoles -- adverse effects KW - Benzimidazoles -- pharmacology KW - Antineoplastic Combined Chemotherapy Protocols -- pharmacology KW - Benzimidazoles -- therapeutic use KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Colorectal Neoplasms -- drug therapy KW - Antineoplastic Agents -- adverse effects KW - Heterocyclic Compounds, 3-Ring -- pharmacology KW - Biomarkers, Tumor -- metabolism KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Heterocyclic Compounds, 3-Ring -- adverse effects KW - Heterocyclic Compounds, 3-Ring -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1681913755?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Investigational+new+drugs&rft.atitle=Biomarker-driven+phase+2+study+of+MK-2206+and+selumetinib+%28AZD6244%2C+ARRY-142886%29+in+patients+with+colorectal+cancer.&rft.au=Do%2C+Khanh%3BSperanza%2C+Giovanna%3BBishop%2C+Rachel%3BKhin%2C+Sonny%3BRubinstein%2C+Larry%3BKinders%2C+Robert+J%3BDatiles%2C+Manuel%3BEugeni%2C+Michelle%3BLam%2C+Michael+H%3BDoyle%2C+L+Austin%3BDoroshow%2C+James+H%3BKummar%2C+Shivaani&rft.aulast=Do&rft.aufirst=Khanh&rft.date=2015-06-01&rft.volume=33&rft.issue=3&rft.spage=720&rft.isbn=&rft.btitle=&rft.title=Investigational+new+drugs&rft.issn=1573-0646&rft_id=info:doi/10.1007%2Fs10637-015-0212-z LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-16 N1 - Date created - 2015-05-18 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s10637-015-0212-z ER - TY - JOUR T1 - Elucidating the links between endocrine disruptors and neurodevelopment. AN - 1681912233; 25714811 AB - Recent data indicate that approximately 12% of children in the United States are affected by neurodevelopmental disorders, including attention deficit hyperactivity disorder, learning disorders, intellectual disabilities, and autism spectrum disorders. Accumulating evidence indicates a multifactorial etiology for these disorders, with social, physical, genetic susceptibility, nutritional factors, and chemical toxicants acting together to influence risk. Exposure to endocrine-disrupting chemicals during the early stages of life can disrupt normal patterns of development and thus alter brain function and disease susceptibility later in life. This article highlights research efforts and pinpoints approaches that could shed light on the possible associations between environmental chemicals that act on the endocrine system and compromised neurodevelopmental outcomes. JF - Endocrinology AU - Schug, Thaddeus T AU - Blawas, Ashley M AU - Gray, Kimberly AU - Heindel, Jerrold J AU - Lawler, Cindy P AD - Division of Extramural Research and Training (T.T.S., K.G., J.J.H., C.P.L.), National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina 27709; and Duke University (A.M.B.), Durham, North Carolina 27708. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 1941 EP - 1951 VL - 156 IS - 6 KW - Benzhydryl Compounds KW - 0 KW - Endocrine Disruptors KW - Metals, Heavy KW - Pesticides KW - Phenols KW - DDT KW - CIW5S16655 KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - bisphenol A KW - MLT3645I99 KW - Abridged Index Medicus KW - Index Medicus KW - Benzhydryl Compounds -- toxicity KW - Disease Susceptibility KW - Polychlorinated Biphenyls -- toxicity KW - Humans KW - DDT -- toxicity KW - Phenols -- toxicity KW - Endocrine System -- drug effects KW - Metals, Heavy -- toxicity KW - Pesticides -- toxicity KW - Endocrine Disruptors -- toxicity KW - Nervous System -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1681912233?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrinology&rft.atitle=Elucidating+the+links+between+endocrine+disruptors+and+neurodevelopment.&rft.au=Schug%2C+Thaddeus+T%3BBlawas%2C+Ashley+M%3BGray%2C+Kimberly%3BHeindel%2C+Jerrold+J%3BLawler%2C+Cindy+P&rft.aulast=Schug&rft.aufirst=Thaddeus&rft.date=2015-06-01&rft.volume=156&rft.issue=6&rft.spage=1941&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=1945-7170&rft_id=info:doi/10.1210%2Fen.2014-1734 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-19 N1 - Date created - 2015-05-18 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1210/en.2014-1734 ER - TY - JOUR T1 - Expression of KRASG12V in Zebrafish Gills Induces Hyperplasia and CXCL8-Associated Inflammation. AN - 1681909151; 25798815 AB - The zebrafish (Danio rerio) represents an important animal model for analyzing genetic contributors to carcinogenesis. To assess the role for mutationally activated Ras in ovarian cancer, we developed a transgenic zebrafish model using the putative promoter for zebrafish insulin-like growth factor 3 (igf3) to drive expression of the human oncogene KRAS(G12V) fused to EGFP. A member of the IGF family, igf3 is unique to teleosts and reportedly exhibits gonad-specific expression in fish species. In contrast to previous studies, we observed igf3 expression in wild-type zebrafish gills in addition to gonads, indicating that igf3 expression is not necessarily gonad specific. In transgenic zebrafish, expression of EGFP-KRAS(G12V) driven by the igf3 promoter occurred only in the gills and resulted in proliferation of a putative progenitor cell population, chondroid hyperplasia, and localized inflammation. KRAS(G12V)-transformed cells in transgenic zebrafish showed activation of the ERK-MAP kinase pathway and expressed the zebrafish homologue for human CXCL8, a cytokine produced by mammalian Ras-transformed cells in tumor-associated inflammatory lesions. These findings indicate that KRAS(G12V)-transformed cells in zebrafish recruit inflammatory cells, but may require additional mutational events for neoplastic transformation. The conserved role for mutationally activated KRAS in leukocyte recruitment indicates that zebrafish can provide a valuable comparative model for Ras-associated inflammation. JF - Zebrafish AU - Shive, Heather R AU - West, Robert R AU - Embree, Lisa J AU - Sexton, Jamie M AU - Hickstein, Dennis D AD - Experimental Transplantation and Immunology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health , Bethesda, Maryland. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 221 EP - 229 VL - 12 IS - 3 KW - Cxcl8-l1, zebrafish KW - 0 KW - Interleukin-8 KW - KRAS protein, human KW - SOX9 Transcription Factor KW - Somatomedins KW - Zebrafish Proteins KW - enhanced green fluorescent protein KW - insulin-like growth factor 3, zebrafish KW - Green Fluorescent Proteins KW - 147336-22-9 KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - Index Medicus KW - Animals KW - Gills -- pathology KW - Animals, Genetically Modified KW - Zebrafish KW - Gills -- metabolism KW - Hyperplasia KW - MAP Kinase Signaling System KW - Promoter Regions, Genetic KW - Oncogenes KW - SOX9 Transcription Factor -- metabolism KW - Female KW - Male KW - Proto-Oncogene Proteins p21(ras) -- metabolism KW - Neoplasms, Experimental -- etiology KW - Inflammation -- etiology KW - Neoplasms, Experimental -- metabolism KW - Inflammation -- metabolism KW - Interleukin-8 -- metabolism KW - Zebrafish Proteins -- metabolism KW - Somatomedins -- metabolism KW - Proto-Oncogene Proteins p21(ras) -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1681909151?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Zebrafish&rft.atitle=Expression+of+KRASG12V+in+Zebrafish+Gills+Induces+Hyperplasia+and+CXCL8-Associated+Inflammation.&rft.au=Shive%2C+Heather+R%3BWest%2C+Robert+R%3BEmbree%2C+Lisa+J%3BSexton%2C+Jamie+M%3BHickstein%2C+Dennis+D&rft.aulast=Shive&rft.aufirst=Heather&rft.date=2015-06-01&rft.volume=12&rft.issue=3&rft.spage=221&rft.isbn=&rft.btitle=&rft.title=Zebrafish&rft.issn=1557-8542&rft_id=info:doi/10.1089%2Fzeb.2014.1038 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-14 N1 - Date created - 2015-05-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Res. 2010 Nov 1;70(21):8435-45 [20959488] Proc Natl Acad Sci U S A. 2010 Nov 9;107(45):19350-5 [20974951] Biol Reprod. 2011 Mar;84(3):476-86 [21084715] Blood. 2011 Mar 10;117(10):2887-90 [21063026] Biol Reprod. 2012 May;86(5):163, 1-10 [22337331] PLoS One. 2014;9(1):e87177 [24489863] Development. 2002 Nov;129(21):5065-79 [12397114] J Natl Cancer Inst. 2003 Mar 19;95(6):484-6 [12644542] Dev Comp Immunol. 2010 Mar;34(3):352-9 [19941893] Gen Comp Endocrinol. 2010 May 15;167(1):128-34 [20138177] Semin Cancer Biol. 2004 Apr;14(2):105-14 [15018894] Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9360-5 [12878728] Cancer Res. 1989 Sep 1;49(17):4682-9 [2547513] Annu Rev Cell Biol. 1990;6:679-714 [2275824] Proc Natl Acad Sci U S A. 1995 Jun 6;92(12):5371-5 [7777514] Nature. 1997 Feb 6;385(6616):544-8 [9020362] Curr Biol. 1997 Apr 1;7(4):R258-60 [9162506] J Biol Chem. 1998 Aug 7;273(32):19925-8 [9685325] Oncogene. 1998 Sep 17;17(11 Reviews):1395-413 [9779987] Cancer Cell. 2004 Nov;6(5):447-58 [15542429] Development. 2005 Mar;132(5):1069-83 [15689370] Biochem Biophys Res Commun. 2008 Mar 7;367(2):336-41 [18166148] Oncogene. 2006 Mar 30;25(14):2105-12 [16288213] Proc Natl Acad Sci U S A. 2005 Oct 11;102(41):14665-70 [16203988] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1089/zeb.2014.1038 ER - TY - JOUR T1 - X-linked acrogigantism syndrome: clinical profile and therapeutic responses. AN - 1681262869; 25712922 AB - X-linked acrogigantism (X-LAG) is a new syndrome of pituitary gigantism, caused by microduplications on chromosome Xq26.3, encompassing the gene GPR101, which is highly upregulated in pituitary tumors. We conducted this study to explore the clinical, radiological, and hormonal phenotype and responses to therapy in patients with X-LAG syndrome. The study included 18 patients (13 sporadic) with X-LAG and microduplication of chromosome Xq26.3. All sporadic cases had unique duplications and the inheritance pattern in two families was dominant, with all Xq26.3 duplication carriers being affected. Patients began to grow rapidly as early as 2-3 months of age (median 12 months). At diagnosis (median delay 27 months), patients had a median height and weight standard deviation scores (SDS) of >+3.9 SDS. Apart from the increased overall body size, the children had acromegalic symptoms including acral enlargement and facial coarsening. More than a third of cases had increased appetite. Patients had marked hypersecretion of GH/IGF1 and usually prolactin, due to a pituitary macroadenoma or hyperplasia. Primary neurosurgical control was achieved with extensive anterior pituitary resection, but postoperative hypopituitarism was frequent. Control with somatostatin analogs was not readily achieved despite moderate to high levels of expression of somatostatin receptor subtype-2 in tumor tissue. Postoperative use of adjuvant pegvisomant resulted in control of IGF1 in all five cases where it was employed. X-LAG is a new infant-onset gigantism syndrome that has a severe clinical phenotype leading to challenging disease management. © 2015 Society for Endocrinology. JF - Endocrine-related cancer AU - Beckers, Albert AU - Lodish, Maya Beth AU - Trivellin, Giampaolo AU - Rostomyan, Liliya AU - Lee, Misu AU - Faucz, Fabio R AU - Yuan, Bo AU - Choong, Catherine S AU - Caberg, Jean-Hubert AU - Verrua, Elisa AU - Naves, Luciana Ansaneli AU - Cheetham, Tim D AU - Young, Jacques AU - Lysy, Philippe A AU - Petrossians, Patrick AU - Cotterill, Andrew AU - Shah, Nalini Samir AU - Metzger, Daniel AU - Castermans, Emilie AU - Ambrosio, Maria Rosaria AU - Villa, Chiara AU - Strebkova, Natalia AU - Mazerkina, Nadia AU - Gaillard, Stéphan AU - Barra, Gustavo Barcelos AU - Casulari, Luis Augusto AU - Neggers, Sebastian J AU - Salvatori, Roberto AU - Jaffrain-Rea, Marie-Lise AU - Zacharin, Margaret AU - Santamaria, Beatriz Lecumberri AU - Zacharieva, Sabina AU - Lim, Ee Mun AU - Mantovani, Giovanna AU - Zatelli, Maria Chaira AU - Collins, Michael T AU - Bonneville, Jean-François AU - Quezado, Martha AU - Chittiboina, Prashant AU - Oldfield, Edward H AU - Bours, Vincent AU - Liu, Pengfei AU - W de Herder, Wouter AU - Pellegata, Natalia AU - Lupski, James R AU - Daly, Adrian F AU - Stratakis, Constantine A AD - Department of EndocrinologyCentre Hospitalier Universitaire de Liège, University of Liège, Domaine Universitaire du Sart-Tilman, 4000 Liège, BelgiumProgram on Developmental Endocrinology and GeneticsSection on Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), NIH-Clinical Research Center, 10 Center Drive, Building 10, Room 1-3330, MSC1103, Bethesda, Maryland 20892-1862, USAHelmholtz Zentrum MünchenInstitute of Pathology, Neuherberg, GermanyDepartment of Molecular and Human GeneticsBaylor College of Medicine, Houston, Texas, USADepartment of Pediatric Endocrinology and DiabetesPrincess Margaret Hospital for Children, Subiaco, Western Australia, AustraliaDepartment of Clinical GeneticsCentre Hospitalier Universitaire de Liège, University of Liège, Liège, BelgiumEndocrinology and Diabetology UnitFondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Department of Clinical Sciences and Community Health, University of Milan, Milan, ItalyDepartment of EndocrinologyUniversity of Brasilia, Brasilia, BrazilDepartment of Paediatric EndocrinologyRoyal Victoria Infirmary, Newcastle University, Newcastle upon Tyne, UKINSERM U 693GHU Paris-Sud - Hôpital de Bicêtre, 78 rue du Général Leclerc, 94270 Le Kremlin-Bicêtre, FrancePediatric Endocrinology UnitUniversité Catholique de Louvain, Bruxelles, BelgiumMater Medical Research InstituteUniversity of Queensland, Brisbane, Queensland, AustraliaDepartment of EndocrinologyKEM Hospital, Mumbai, IndiaEndocrinology and Diabetes UnitBC Children's Hospital, Vancouver, British Columbia, CanadaSection of EndocrinologyDepartment of Medical Sciences, University of Ferrara, Ferrara, ItalyService d'Anatomie et Cytologie PathologiquesHopital Foch, Suresnes, FranceINSERM Unité 1016Institut Cochin, Hopital Cochin, Université Paris Descartes, Paris, FranceInstitute of Pediatric EndocrinologyEndocrinological Research Centre, Moscow Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 353 EP - 367 VL - 22 IS - 3 KW - Index Medicus KW - pediatric KW - duplication KW - pituitary adenoma KW - X chromosome KW - FIPA KW - GPR101 KW - X-LAG syndrome KW - gigantism KW - Young Adult KW - Humans KW - Chromosomes, Human, X KW - Child KW - Adenoma -- therapy KW - Child, Preschool KW - Infant KW - Pituitary Neoplasms -- pathology KW - Pituitary Neoplasms -- genetics KW - Adenoma -- genetics KW - Adenoma -- pathology KW - Adolescent KW - Female KW - Male KW - Pituitary Neoplasms -- therapy KW - Gigantism -- therapy KW - Gigantism -- pathology KW - Acromegaly -- pathology KW - Acromegaly -- therapy KW - Gigantism -- genetics KW - Acromegaly -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1681262869?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Endocrine-related+cancer&rft.atitle=X-linked+acrogigantism+syndrome%3A+clinical+profile+and+therapeutic+responses.&rft.au=Beckers%2C+Albert%3BLodish%2C+Maya+Beth%3BTrivellin%2C+Giampaolo%3BRostomyan%2C+Liliya%3BLee%2C+Misu%3BFaucz%2C+Fabio+R%3BYuan%2C+Bo%3BChoong%2C+Catherine+S%3BCaberg%2C+Jean-Hubert%3BVerrua%2C+Elisa%3BNaves%2C+Luciana+Ansaneli%3BCheetham%2C+Tim+D%3BYoung%2C+Jacques%3BLysy%2C+Philippe+A%3BPetrossians%2C+Patrick%3BCotterill%2C+Andrew%3BShah%2C+Nalini+Samir%3BMetzger%2C+Daniel%3BCastermans%2C+Emilie%3BAmbrosio%2C+Maria+Rosaria%3BVilla%2C+Chiara%3BStrebkova%2C+Natalia%3BMazerkina%2C+Nadia%3BGaillard%2C+St%C3%A9phan%3BBarra%2C+Gustavo+Barcelos%3BCasulari%2C+Luis+Augusto%3BNeggers%2C+Sebastian+J%3BSalvatori%2C+Roberto%3BJaffrain-Rea%2C+Marie-Lise%3BZacharin%2C+Margaret%3BSantamaria%2C+Beatriz+Lecumberri%3BZacharieva%2C+Sabina%3BLim%2C+Ee+Mun%3BMantovani%2C+Giovanna%3BZatelli%2C+Maria+Chaira%3BCollins%2C+Michael+T%3BBonneville%2C+Jean-Fran%C3%A7ois%3BQuezado%2C+Martha%3BChittiboina%2C+Prashant%3BOldfield%2C+Edward+H%3BBours%2C+Vincent%3BLiu%2C+Pengfei%3BW+de+Herder%2C+Wouter%3BPellegata%2C+Natalia%3BLupski%2C+James+R%3BDaly%2C+Adrian+F%3BStratakis%2C+Constantine+A&rft.aulast=Beckers&rft.aufirst=Albert&rft.date=2015-06-01&rft.volume=22&rft.issue=3&rft.spage=353&rft.isbn=&rft.btitle=&rft.title=Endocrine-related+cancer&rft.issn=1479-6821&rft_id=info:doi/10.1530%2FERC-15-0038 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-08 N1 - Date created - 2015-05-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Neuroendocrinology. 2012;95(3):257-66 [22327438] Tokai J Exp Clin Med. 1995 Jul;20(2):71-9 [8797263] J Clin Endocrinol Metab. 2012 Jun;97(6):2093-104 [22442262] J Neuroendocrinol. 1996 Dec;8(12):891-900 [8953466] Arch Dis Child. 1958 Feb;33(167):49-54 [13509743] J Clin Endocrinol Metab. 1961 Mar;21:343-53 [13716991] J Clin Endocrinol Metab. 2005 Apr;90(4):2104-9 [15671091] Eur J Endocrinol. 2005 Aug;153(2):195-201 [16061823] Exp Clin Endocrinol Diabetes. 2007 Mar;115(3):198-202 [17427111] Cell. 2007 Dec 28;131(7):1235-47 [18160035] Pediatr Endocrinol Rev. 2008 Feb;5 Suppl 2:720-6 [18317443] J Clin Endocrinol Metab. 2008 Aug;93(8):2953-6 [18492755] Nat Genet. 2009 Jul;41(7):849-53 [19543269] Endocr Relat Cancer. 2009 Sep;16(3):1029-43 [19556287] Int J Cancer. 2009 Nov 1;125(9):2122-6 [19637311] J Endocrinol Invest. 2010 May;33(5):325-31 [19955848] J Clin Endocrinol Metab. 2010 Nov;95(11):E373-83 [20685857] Endocr Relat Cancer. 2011 Jun;18(3):347-56 [21450940] J Clin Endocrinol Metab. 2012 Aug;97(8):E1411-20 [22659247] Ann Endocrinol (Paris). 2012 Dec;73(6):497-502 [23122576] Intern Med J. 2013 Mar;43(3):345-7 [23441666] Endocr Rev. 2013 Apr;34(2):239-77 [23371967] Acta Neuropathol. 2013 Jul;126(1):137-50 [23756599] Endocr Relat Cancer. 2013 Oct;20(5):753-66 [23940012] Mol Cell Endocrinol. 2014 Apr 5;386(1-2):85-91 [24012779] Mol Endocrinol. 2014 Apr;28(4):554-64 [24606125] J Clin Endocrinol Metab. 1999 Dec;84(12):4379-84 [10599691] J Clin Endocrinol Metab. 2000 Dec;85(12):4776-80 [11134142] J Mol Endocrinol. 2014 Jun;52(3):R223-40 [24647046] J Clin Endocrinol Metab. 2014 Jun;99(6):1955-69 [24517150] Arch Dis Child. 2014 Aug;99(8):772-7 [24833789] N Engl J Med. 2014 Dec 18;371(25):2363-74 [25470569] Endocr Relat Cancer. 2015 Feb;22(1):111-9 [25515731] Neuroendocrinology. 2016;103(1):7-17 [25572320] Neuroendocrinology. 1997 Feb;65(2):117-28 [9067989] Am J Dis Child. 1972 May;123(5):504-6 [4337298] J Clin Endocrinol Metab. 1973 Sep;37(3):380-8 [4206490] Nature. 1985 May 30-Jun 5;315(6018):413-6 [3923368] Mol Endocrinol. 1988 Jul;2(7):606-12 [3137455] Endocrinology. 1989 Aug;125(2):801-9 [2502376] Endocrinology. 1989 Nov;125(5):2710-8 [2507296] Proc Soc Exp Biol Med. 1990 Mar;193(3):232-5 [2106141] N Engl J Med. 1990 Aug 2;323(5):322-7 [2164153] Am J Pathol. 1992 Oct;141(4):895-906 [1415483] Endocrinology. 1992 Nov;131(5):2083-9 [1425411] J Clin Endocrinol Metab. 1993 Jan;76(1):216-22 [8421089] Endocr Res. 1993 Mar;19(1):33-46 [7681768] J Endocrinol. 1995 May;145(2):307-14 [7616164] Clin Endocrinol (Oxf). 1995 May;42(5):539-49 [7621575] Mol Cell Endocrinol. 1996 Mar 1;117(1):75-81 [8734475] Endocr Relat Cancer. 2012 Jun;19(3):L25-9 [22420004] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1530/ERC-15-0038 ER - TY - JOUR T1 - A CLAG3 mutation in an amphipathic transmembrane domain alters malaria parasite nutrient channels and confers leupeptin resistance. AN - 1680959899; 25870226 AB - Erythrocytes infected with malaria parasites have increased permeability to ions and nutrients, as mediated by the plasmodial surface anion channel (PSAC) and recently linked to parasite clag3 genes. Although the encoded protein is integral to the host membrane, its precise contribution to solute transport remains unclear because it lacks conventional transmembrane domains and does not have homology to ion channel proteins in other organisms. Here, we identified a probable CLAG3 transmembrane domain adjacent to a variant extracellular motif. Helical-wheel analysis revealed strict segregation of polar and hydrophobic residues to opposite faces of a predicted α-helical transmembrane domain, suggesting that the domain lines a water-filled pore. A single CLAG3 mutation (A1210T) in a leupeptin-resistant PSAC mutant falls within this transmembrane domain and may affect pore structure. Allelic-exchange transfection and site-directed mutagenesis revealed that this mutation alters solute selectivity in the channel. The A1210T mutation also reduces the blocking affinity of PSAC inhibitors that bind on opposite channel faces, consistent with global changes in channel structure. Transfected parasites carrying this mutation survived a leupeptin challenge significantly better than a transfection control did. Thus, the A1210T mutation contributes directly to both altered PSAC activity and leupeptin resistance. These findings reveal the molecular basis of a novel antimalarial drug resistance mechanism, provide a framework for determining the channel's composition and structure, and should guide the development of therapies targeting the PSAC. Copyright © 2015, American Society for Microbiology. All Rights Reserved. JF - Infection and immunity AU - Sharma, Paresh AU - Rayavara, Kempaiah AU - Ito, Daisuke AU - Basore, Katherine AU - Desai, Sanjay A AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, USA. ; Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, USA sdesai@niaid.nih.gov. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 2566 EP - 2574 VL - 83 IS - 6 KW - Cysteine Proteinase Inhibitors KW - 0 KW - Leupeptins KW - Protozoan Proteins KW - leupeptin KW - J97339NR3V KW - Index Medicus KW - Drug Resistance -- physiology KW - Animals KW - Drug Resistance -- genetics KW - Gene Expression Regulation -- physiology KW - Computer Simulation KW - Molecular Sequence Data KW - Biological Transport KW - Amino Acid Sequence KW - Protein Structure, Tertiary KW - Mutation KW - Models, Biological KW - Genome, Protozoan KW - Cysteine Proteinase Inhibitors -- pharmacology KW - Protozoan Proteins -- metabolism KW - Leupeptins -- pharmacology KW - Plasmodium falciparum -- genetics KW - Protozoan Proteins -- genetics KW - Cell Membrane -- physiology KW - Plasmodium falciparum -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680959899?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+immunity&rft.atitle=A+CLAG3+mutation+in+an+amphipathic+transmembrane+domain+alters+malaria+parasite+nutrient+channels+and+confers+leupeptin+resistance.&rft.au=Sharma%2C+Paresh%3BRayavara%2C+Kempaiah%3BIto%2C+Daisuke%3BBasore%2C+Katherine%3BDesai%2C+Sanjay+A&rft.aulast=Sharma&rft.aufirst=Paresh&rft.date=2015-06-01&rft.volume=83&rft.issue=6&rft.spage=2566&rft.isbn=&rft.btitle=&rft.title=Infection+and+immunity&rft.issn=1098-5522&rft_id=info:doi/10.1128%2FIAI.02966-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-28 N1 - Date created - 2015-05-13 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Exp Parasitol. 2007 Mar;115(3):296-300 [17087929] Eukaryot Cell. 2005 Dec;4(12):2153-9 [16339732] Proc Natl Acad Sci U S A. 2007 Jan 16;104(3):1063-8 [17213308] Int J Parasitol. 2007 Apr;37(5):475-82 [17292372] Cell Microbiol. 2007 Apr;9(4):851-60 [17087736] PLoS Pathog. 2007 Aug 3;3(8):e107 [17676953] Parasitol Int. 2007 Dec;56(4):255-62 [17596999] Mol Biochem Parasitol. 2008 Mar;158(1):11-21 [18155305] Mol Biochem Parasitol. 2008 Aug;160(2):81-9 [18508137] Antimicrob Agents Chemother. 2008 Jul;52(7):2346-54 [18443109] J Membr Biol. 2008 Nov-Dec;226(1-3):27-34 [19050955] Trends Parasitol. 2009 Mar;25(3):139-44 [19200784] Mol Pharmacol. 2010 May;77(5):724-33 [20101003] PLoS One. 2011;6(5):e19334 [21573242] Mol Microbiol. 2011 Apr;80(2):391-406 [21306446] Biochim Biophys Acta. 2010 Sep;1798(9):1679-88 [20451492] Cell. 2011 May 27;145(5):665-77 [21620134] Biochim Biophys Acta. 2012 Mar;1818(3):367-74 [22115742] Malar J. 2012;11:124 [22531353] Cell Microbiol. 2012 Jul;14(7):1003-9 [22432505] Mol Pharmacol. 2012 Dec;82(6):1104-14 [22949525] Malar J. 2013;12:187 [23742293] J Biol Chem. 2013 Jul 5;288(27):19429-40 [23720749] Cell Microbiol. 2013 Nov;15(11):1913-23 [23819786] Trends Parasitol. 2014 Mar;30(3):151-9 [24507014] PLoS One. 2014;9(4):e93759 [24699906] Nature. 2014 Jul 31;511(7511):592-5 [25043010] ACS Chem Biol. 2014 Oct 17;9(10):2366-73 [25089658] Nature. 2000 Aug 31;406(6799):1001-5 [10984055] Biochim Biophys Acta. 2000 Jan 15;1463(1):88-98 [10631297] J Mol Biol. 2001 Jan 19;305(3):567-80 [11152613] Methods. 2001 Dec;25(4):402-8 [11846609] Biophys J. 2003 Jan;84(1):116-23 [12524269] Trends Parasitol. 2003 May;19(5):232-9 [12763430] Nature. 1982 Sep 23;299(5881):371-4 [7110359] Mol Biochem Parasitol. 1985 Mar;14(3):313-22 [3887158] Biochim Biophys Acta. 1986 Sep 25;861(1):194-6 [3530325] Biochem Pharmacol. 1987 Jan 1;36(1):123-9 [3099799] Comput Appl Biosci. 1994 Dec;10(6):685-6 [7704669] J Gen Physiol. 1996 Feb;107(2):195-205 [8833341] J Gen Physiol. 1999 Mar;113(3):415-23 [10051517] Blood. 2004 Dec 15;104(13):4279-86 [15319279] Diabetes Metab Res Rev. 2005 Jan-Feb;21(1):31-8 [15624123] J Biol Chem. 2005 Apr 29;280(17):16861-7 [15701633] Bioinformatics. 2005 Jun;21 Suppl 1:i251-7 [15961464] Mol Biochem Parasitol. 2005 Sep;143(1):20-8 [15953647] Mol Biochem Parasitol. 2007 Feb;151(2):229-32 [17166605] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/IAI.02966-14 ER - TY - JOUR T1 - Telomere length variation: A potential new telomere biomarker for lung cancer risk. AN - 1680209636; 25840848 AB - In this report the associations between telomere length variation (TLV), mean telomere length in blood lymphocytes and lung cancer risk were examined. The study design is case-control. Cases (N=191) were patients newly diagnosed with histologically confirmed non-small cell lung cancer. Controls (N=207) were healthy individuals recruited from the same counties as cases and matched to cases on age and gender. Telomere fluorescent in situ hybridization was used to measure telomere features using short-term cultured blood lymphocytes. Logistic regression was used to estimate the strength of association between telomere features and lung cancer risk. Telomere length variation across all chromosomal ends was significantly associated with lung cancer risk; adjusted odds ratios 4.67 [95% confidence interval (CI): 1.46-14.9] and 0.46 (95% CI: 0.25-0.84) for younger (age≤60) and older (age>60) individuals, respectively. TLV and mean telomere length jointly affected lung cancer risk: when comparing individuals with short telomere length and high TLV to those with long telomere length and low TLV, adjusted odd ratios were 8.21 (95% CI: 1.71-39.5) and 0.33 (95% CI: 0.15-0.72) for younger and older individuals, respectively. TLV in blood lymphocytes is significantly associated with lung cancer risk and the associations were modulated by age. TLV in combination with mean telomere length might be useful in identifying high risk population for lung cancer computerized tomography screening. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. JF - Lung cancer (Amsterdam, Netherlands) AU - Sun, Bing AU - Wang, Ying AU - Kota, Krishna AU - Shi, Yaru AU - Motlak, Salaam AU - Makambi, Kepher AU - Loffredo, Christopher A AU - Shields, Peter G AU - Yang, Qin AU - Harris, Curtis C AU - Zheng, Yun-Ling AD - Cancer Prevention and Control Program, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, United States. ; Cancer Prevention and Control Program, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, United States; Department of Biostatistics, Bioinformatics, and Biomathematics, Georgetown University Medical Center, Washington, DC, United States. ; James Cancer Hospital, The Ohio State University Wexner Medical Center, Columbus, OH 43220, United States. ; Cancer Biology Division, Department of Radiation Oncology, Washington University School of Medicine, Saint Louis, MO, United States. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD, United States. ; Cancer Prevention and Control Program, Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Washington, DC, United States. Electronic address: yz37@georgetown.edu. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 297 EP - 303 VL - 88 IS - 3 KW - Biomarkers, Tumor KW - 0 KW - Index Medicus KW - Telomere length KW - Telomere length variation KW - Blood-based biomarker KW - Risk prediction KW - Telomere dysfunction KW - Lung cancer KW - Odds Ratio KW - Telomere Shortening KW - Humans KW - Aged KW - Lymphocytes -- metabolism KW - Aged, 80 and over KW - Risk Factors KW - Chromosomes, Human KW - Adult KW - Case-Control Studies KW - Middle Aged KW - Female KW - Male KW - Telomere Homeostasis KW - Telomere -- genetics KW - Lung Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680209636?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Lung+cancer+%28Amsterdam%2C+Netherlands%29&rft.atitle=Telomere+length+variation%3A+A+potential+new+telomere+biomarker+for+lung+cancer+risk.&rft.au=Sun%2C+Bing%3BWang%2C+Ying%3BKota%2C+Krishna%3BShi%2C+Yaru%3BMotlak%2C+Salaam%3BMakambi%2C+Kepher%3BLoffredo%2C+Christopher+A%3BShields%2C+Peter+G%3BYang%2C+Qin%3BHarris%2C+Curtis+C%3BZheng%2C+Yun-Ling&rft.aulast=Sun&rft.aufirst=Bing&rft.date=2015-06-01&rft.volume=88&rft.issue=3&rft.spage=297&rft.isbn=&rft.btitle=&rft.title=Lung+cancer+%28Amsterdam%2C+Netherlands%29&rft.issn=1872-8332&rft_id=info:doi/10.1016%2Fj.lungcan.2015.03.011 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-03 N1 - Date created - 2015-05-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Am J Pathol. 2011 Oct;179(4):1608-15 [21888887] Lung Cancer. 2011 Aug;73(2):133-7 [21507503] PLoS One. 2013;8(3):e59230 [23555636] Ageing Res Rev. 2013 Mar;12(2):642-52 [23541441] Mod Pathol. 2013 Nov;26(11):1425-32 [23765250] Transl Res. 2013 Dec;162(6):353-63 [23732052] Neoplasia. 2013 Nov;15(11):1301-13 [24339742] Nucleic Acids Res. 2014 Apr;42(7):4391-405 [24500201] Cell Cycle. 2014;13(11):1765-76 [24721976] Cancer Res. 2014 Aug 1;74(15):4090-8 [24853549] FASEB J. 2000 Jul;14(10):1325-34 [10877825] Nature. 2000 Aug 10;406(6796):641-5 [10949306] Free Radic Biol Med. 2000 Jul 15;29(2):156-69 [10980404] Cell. 2001 Sep 21;106(6):661-73 [11572773] Cell. 2001 Oct 5;107(1):67-77 [11595186] Ann N Y Acad Sci. 2002 Apr;959:24-9 [11976182] Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8191-6 [12034875] Trends Biochem Sci. 2002 Jul;27(7):339-44 [12114022] Science. 2002 Jul 26;297(5581):565-9 [12142527] Carcinogenesis. 2003 Feb;24(2):269-74 [12584177] J Natl Cancer Inst. 2003 Aug 20;95(16):1211-8 [12928346] Oncogene. 2004 Feb 12;23(6):1221-8 [14716292] J Cell Sci. 2004 May 1;117(Pt 11):2417-26 [15126641] Mech Ageing Dev. 2004 Jun;125(6):405-16 [15272504] Mutat Res. 2004 Sep;567(1):85-104 [15341904] Mol Cell Biol. 2004 Nov;24(22):9948-57 [15509797] Nat Med. 1997 Nov;3(11):1271-4 [9359704] Science. 1998 Jan 16;279(5349):334-5 [9454329] Clin Cancer Res. 2005 Jan 1;11(1):217-25 [15671549] Genes Dev. 2005 Sep 15;19(18):2100-10 [16166375] Genes Chromosomes Cancer. 2005 Dec;44(4):339-50 [16052508] Cancer Res. 2005 Oct 15;65(20):9566-73 [16230422] Nature. 2007 Jun 7;447(7145):725-9 [17554309] PLoS Genet. 2008 Jan;4(1):e10 [18208333] Cancer Sci. 2008 Jul;99(7):1385-9 [18452563] Nature. 2009 Jul 2;460(7251):66-72 [19571879] Genes Dev. 2009 Sep 1;23(17):2060-75 [19679647] Lung Cancer. 2009 Nov;66(2):157-61 [19285750] N Engl J Med. 2009 Dec 10;361(24):2353-65 [20007561] Nat New Biol. 1972 Oct 18;239(94):197-201 [4507727] J Theor Biol. 1973 Sep 14;41(1):181-90 [4754905] Cell. 1985 Dec;43(2 Pt 1):405-13 [3907856] Nature. 1990 May 31;345(6274):458-60 [2342578] Proc Natl Acad Sci U S A. 1994 Oct 11;91(21):9857-60 [7937905] EMBO J. 1995 Sep 1;14(17):4240-8 [7556065] Annu Rev Biochem. 1996;65:337-65 [8811183] Nat Rev Cancer. 2011 Mar;11(3):161-76 [21346783] Hum Mol Genet. 2011 Jan 15;20(2):378-86 [20956286] Cell. 1997 Oct 3;91(1):25-34 [9335332] Mutat Res. 2012 Feb 1;730(1-2):43-51 [21745483] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.lungcan.2015.03.011 ER - TY - JOUR T1 - Methylone-induced hyperthermia and lethal toxicity: role of the dopamine and serotonin transporters. AN - 1676338636; 25794333 AB - Methylone (2-methylamino-1-[3,4-methylenedioxy-phenyl]propan-1-one), an amphetamine analog, has emerged as a popular drug of abuse worldwide. Methylone induces hyperthermia, which is thought to contribute toward the lethal consequences of methylone overdose. Methylone has been assumed to induce hyperthermic effects through inhibition of serotonin and/or dopamine transporters (SERT and DAT, respectively). To examine the roles of each of these proteins in methylone-induced toxic effects, we used SERT and DAT knockout (KO) mice and assessed the hyperthermic and lethal effects caused by a single administration of methylone. Methylone produced higher rates of lethal toxicity compared with other amphetamine analogs in wild-type mice. Compared with wild-type mice, lethality was significantly lower in DAT KO mice, but not in SERT KO mice. By contrast, only a slight diminution in the hyperthermic effects of methylone was observed in DAT KO mice, whereas a slight enhancement of these effects was observed in SERT KO mice. Administration of the selective D1 receptor antagonist SCH 23390 and the D2 receptor antagonist raclopride reduced methylone-induced hyperthermia, but these drugs also had hypothermic effects in saline-treated mice, albeit to a smaller extent than the effects observed in methylone-treated mice. In contradistinction to 3,4-methylenedioxymethamphetamine, which induces its toxicity through SERT and DAT, these data indicate that DAT, but not SERT, is strongly associated with the lethal toxicity produced by methylone, which did not seem to be dependent on the hyperthermic effects of methylone. DAT is therefore a strong candidate molecule for interventions aimed at preventing acute neurotoxic and lethal effects of methylone. JF - Behavioural pharmacology AU - Piao, Ying-Shan AU - Hall, Frank Scott AU - Moriya, Yuki AU - Ito, Miki AU - Ohara, Arihisa AU - Kikura-Hanajiri, Ruri AU - Goda, Yukihiro AU - Lesch, Klaus-Peter AU - Murphy, Dennis L AU - Uhl, George R AU - Sora, Ichiro AD - aDepartment of Biological Psychiatry, Tohoku University Graduate School of Medicine, Sendai bDivision of Pharmacognosy, Phytochemistry, and Narcotics, National Institute of Health Sciences, Tokyo cDepartment of Psychiatry, Kobe University Graduate School of Medicine, Kobe, Japan dDepartment of Pharmacology, College of Pharmacy and Pharmaceutical Sciences, University of Toledo, Toledo, Ohio eLaboratory of Clinical Science, National Institute of Mental Health, Bethesda fMolecular Neurobiology Branch, National Institute on Drug Abuse, Intramural Research Program, Baltimore, Maryland, USA gDepartment of Psychiatry, University of Wurzburg, Wurzburg, Germany hDepartment of Geriatrics, Beijing Tiantan Hospital, Capital Medical University, Beijing, China. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 345 EP - 352 VL - 26 IS - 4 KW - Benzazepines KW - 0 KW - Central Nervous System Stimulants KW - Dopamine Antagonists KW - Dopamine Plasma Membrane Transport Proteins KW - Receptors, Dopamine D1 KW - Receptors, Dopamine D2 KW - SCH 23390 KW - Serotonin Plasma Membrane Transport Proteins KW - Slc6a4 protein, mouse KW - Raclopride KW - 430K3SOZ7G KW - Methamphetamine KW - 44RAL3456C KW - methylone KW - L4I4B1R01F KW - Index Medicus KW - Models, Animal KW - Animals KW - Benzazepines -- pharmacology KW - Body Temperature -- drug effects KW - Dopamine Antagonists -- pharmacology KW - Raclopride -- pharmacology KW - Receptors, Dopamine D1 -- metabolism KW - Receptors, Dopamine D2 -- metabolism KW - Mice, Knockout KW - Receptors, Dopamine D1 -- antagonists & inhibitors KW - Body Temperature -- physiology KW - Female KW - Male KW - Fever -- chemically induced KW - Serotonin Plasma Membrane Transport Proteins -- metabolism KW - Dopamine Plasma Membrane Transport Proteins -- genetics KW - Central Nervous System Stimulants -- toxicity KW - Fever -- mortality KW - Dopamine Plasma Membrane Transport Proteins -- metabolism KW - Methamphetamine -- analogs & derivatives KW - Fever -- drug therapy KW - Fever -- metabolism KW - Serotonin Plasma Membrane Transport Proteins -- genetics KW - Methamphetamine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676338636?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Behavioural+pharmacology&rft.atitle=Methylone-induced+hyperthermia+and+lethal+toxicity%3A+role+of+the+dopamine+and+serotonin+transporters.&rft.au=Piao%2C+Ying-Shan%3BHall%2C+Frank+Scott%3BMoriya%2C+Yuki%3BIto%2C+Miki%3BOhara%2C+Arihisa%3BKikura-Hanajiri%2C+Ruri%3BGoda%2C+Yukihiro%3BLesch%2C+Klaus-Peter%3BMurphy%2C+Dennis+L%3BUhl%2C+George+R%3BSora%2C+Ichiro&rft.aulast=Piao&rft.aufirst=Ying-Shan&rft.date=2015-06-01&rft.volume=26&rft.issue=4&rft.spage=345&rft.isbn=&rft.btitle=&rft.title=Behavioural+pharmacology&rft.issn=1473-5849&rft_id=info:doi/10.1097%2FFBP.0000000000000135 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-13 N1 - Date created - 2015-04-27 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/FBP.0000000000000135 ER - TY - JOUR T1 - Food and Beverage Policies and Public Health Ethics AN - 1676061185 AB - Government food and beverage policies can play an important role in promoting public health. Few people would question this assumption. Difficult questions can arise, however, when policymakers, public health officials, citizens, and businesses deliberate about food and beverage policies, because competing values may be at stake, such as public health, individual autonomy, personal responsibility, economic prosperity, and fairness. An ethically justified policy strikes a reasonable among competing values by meeting the following criteria: (1) the policy serves important social goal(s); (2) the policy is likely to be effective at achieving those goal(s); (3) less burdensome options are not likely to be effective at achieving the goals; (4) the policy is fair. JF - Health Care Analysis : HCA AD - Resnik, David B; National Institute of Environmental Health Sciences, National Institutes of Health, 111 Alexander Drive, Mail Drop CU 03, Box 12233, Research Triangle Park, NC, 27709, USA Y1 - 2015/06// PY - 2015 DA - Jun 2015 SP - 122 EP - 133 CY - Chichester PB - Springer Science & Business Media VL - 23 IS - 2 SN - 1065-3058 KW - Medical Sciences KW - Autonomy KW - Businesses KW - Ethics KW - Fairness KW - Food KW - Health promotion KW - Healthy food KW - Policy making KW - Public health KW - Strikes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676061185?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Care+Analysis+%3A+HCA&rft.atitle=Food+and+Beverage+Policies+and+Public+Health+Ethics&rft.au=Resnik%2C+David+B&rft.aulast=Resnik&rft.aufirst=David&rft.date=2015-06-01&rft.volume=23&rft.issue=2&rft.spage=122&rft.isbn=&rft.btitle=&rft.title=Health+Care+Analysis+%3A+HCA&rft.issn=10653058&rft_id=info:doi/10.1007%2Fs10728-013-0266-z LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-04-27 N1 - Last updated - 2016-05-12 DO - http://dx.doi.org/10.1007/s10728-013-0266-z ER - TY - JOUR T1 - A novel role of microglial NADPH oxidase in mediating extra-synaptic function of norepinephrine in regulating brain immune homeostasis. AN - 1674693268; 25740080 AB - Although the peripheral anti-inflammatory effect of norepinephrine (NE) is well documented, the mechanism by which this neurotransmitter functions as an anti-inflammatory/neuroprotective agent in the central nervous system (CNS) is unclear. This article aimed to determine the anti-inflammatory/neuroprotective effects and underlying mechanisms of NE in inflammation-based dopaminergic neurotoxicity models. In mice, NE-depleting toxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) was injected at 6 months of lipopolysaccharide (LPS)-induced neuroinflammation. It was found that NE depletion enhanced LPS-induced dopaminergic neuron loss in the substantia nigra. This piece of in vivo data prompted us to conduct a series of studies in an effort to elucidate the mechanism as to how NE affects dopamine neuron survival by using primary midbrain neuron/glia cultures. Results showed that submicromolar concentrations of NE dose-dependently protected dopaminergic neurons from LPS-induced neurotoxicity by inhibiting microglia activation and subsequent release of pro-inflammatory factors. However, NE-elicited neuroprotection was not totally abolished in cultures from β2-adrenergic receptor (β2-AR)-deficient mice, suggesting that novel pathways other than β2-AR are involved. To this end, It was found that submicromolar NE dose-dependently inhibited NADPH oxidase (NOX2)-generated superoxide, which contributes to the anti-inflammatory and neuroprotective effects of NE. This novel mechanism was indeed adrenergic receptors independent since both (+) and (-) optic isomers of NE displayed the same potency. We further demonstrated that NE inhibited LPS-induced NOX2 activation by blocking the translocation of its cytosolic subunit to plasma membranes. In summary, we revealed a potential physiological role of NE in maintaining brain immune homeostasis and protecting neurons via a novel mechanism. © 2015 Wiley Periodicals, Inc. JF - Glia AU - Jiang, Lulu AU - Chen, Shih-Heng AU - Chu, Chun-Hsien AU - Wang, Shi-Jun AU - Oyarzabal, Esteban AU - Wilson, Belinda AU - Sanders, Virginia AU - Xie, Keqin AU - Wang, Qingshan AU - Hong, Jau-Shyong AD - Institute of Toxicology, School of Public Health, Shandong University, Jinan, Shandong, 250012, China; Neuropharmacology Section, Laboratory of Neurobiology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, 27709. Y1 - 2015/06// PY - 2015 DA - June 2015 SP - 1057 EP - 1072 VL - 63 IS - 6 KW - Benzylamines KW - 0 KW - Lipopolysaccharides KW - Neurotransmitter Uptake Inhibitors KW - Receptors, Adrenergic, beta-2 KW - NADPH Oxidase KW - EC 1.6.3.1 KW - DSP 4 KW - PQ1P7JP5C1 KW - Norepinephrine KW - X4W3ENH1CV KW - Index Medicus KW - neurotransmitter KW - extra-synaptic KW - DSP-4 KW - neurodegeneration KW - volume transmission KW - Benzylamines -- pharmacology KW - Animals KW - Coculture Techniques KW - COS Cells KW - Receptors, Adrenergic, beta-2 -- genetics KW - Homeostasis -- physiology KW - Mice, Inbred BALB C KW - Mice, Knockout KW - Rats, Inbred F344 KW - Cell Survival -- drug effects KW - Neurotransmitter Uptake Inhibitors -- pharmacology KW - Cercopithecus aethiops KW - Lipopolysaccharides -- toxicity KW - Cell Line KW - Cell Survival -- physiology KW - Male KW - Receptors, Adrenergic, beta-2 -- metabolism KW - NADPH Oxidase -- metabolism KW - Microglia -- enzymology KW - Dopaminergic Neurons -- drug effects KW - Norepinephrine -- metabolism KW - Brain -- pathology KW - Brain -- drug effects KW - Dopaminergic Neurons -- immunology KW - Brain -- immunology KW - Dopaminergic Neurons -- pathology KW - Microglia -- pathology KW - Microglia -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1674693268?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Glia&rft.atitle=A+novel+role+of+microglial+NADPH+oxidase+in+mediating+extra-synaptic+function+of+norepinephrine+in+regulating+brain+immune+homeostasis.&rft.au=Jiang%2C+Lulu%3BChen%2C+Shih-Heng%3BChu%2C+Chun-Hsien%3BWang%2C+Shi-Jun%3BOyarzabal%2C+Esteban%3BWilson%2C+Belinda%3BSanders%2C+Virginia%3BXie%2C+Keqin%3BWang%2C+Qingshan%3BHong%2C+Jau-Shyong&rft.aulast=Jiang&rft.aufirst=Lulu&rft.date=2015-06-01&rft.volume=63&rft.issue=6&rft.spage=1057&rft.isbn=&rft.btitle=&rft.title=Glia&rft.issn=1098-1136&rft_id=info:doi/10.1002%2Fglia.22801 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-08 N1 - Date created - 2015-04-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Neurochem. 1995 Jul;65(1):111-6 [7790854] Neurodegeneration. 1996 Sep;5(3):241-9 [8910902] J Biol Chem. 1996 Nov 29;271(48):30326-9 [8939991] Brain Res Mol Brain Res. 1998 Jun 1;57(1):1-9 [9630473] Adv Exp Med Biol. 1998;437:269-78 [9666280] Rev Neurol (Paris). 1997;153 Suppl 1:S39-45 [9686247] Prog Neurobiol. 2005 Jun;76(2):77-98 [16081203] J Leukoc Biol. 2006 May;79(5):881-95 [16641134] J Leukoc Biol. 2006 Jun;79(6):1093-104 [16531560] J Exp Med. 2006 Aug 7;203(8):1915-25 [16880255] J Pharmacol Exp Ther. 2006 Oct;319(1):44-52 [16807359] J Neurol Sci. 2006 Oct 25;248(1-2):35-41 [16753180] Nat Rev Neurosci. 2007 Jan;8(1):57-69 [17180163] Glia. 2007 Apr 1;55(5):453-62 [17203472] Biomed Environ Sci. 2007 Aug;20(4):317-20 [17948767] J Pharmacol Exp Ther. 2000 May;293(2):607-17 [10773035] J Immunol. 2008 Jul 1;181(1):660-8 [18566433] Neurotoxicology. 2008 Sep;29(5):864-70 [18471886] J Immunol. 2008 Nov 15;181(10):7194-204 [18981141] Physiol Res. 2008;57 Suppl 3:S89-99 [18481911] PLoS One. 2009;4(2):e4414 [19212441] Nat Rev Neurosci. 2009 Mar;10(3):211-23 [19190638] Proc Natl Acad Sci U S A. 2010 Mar 30;107(13):6058-63 [20231476] J Neurosci. 2011 Jan 19;31(3):1081-92 [21248133] J Immunol. 2011 Apr 1;186(7):4443-54 [21335487] Environ Health Perspect. 2011 Jun;119(6):807-14 [21245015] Parkinsonism Relat Disord. 2012 Jan;18 Suppl 1:S207-9 [22166436] Cold Spring Harb Perspect Med. 2012 Jan;2(1):a009381 [22315722] J Neuroinflammation. 2012;9:32 [22340895] J Neuroinflammation. 2012;9:124 [22695044] Glia. 2013 Jan;61(1):71-90 [22674585] Glia. 2013 Jun;61(6):855-68 [23536230] Methods Mol Biol. 2013;1041:231-40 [23813383] Nat Neurosci. 2013 Aug;16(8):1016-23 [23852112] Science. 2013 Oct 18;342(6156):373-7 [24136970] J Neurosci. 2014 Sep 10;34(37):12490-503 [25209287] Glia. 2014 Dec;62(12):2034-43 [25043383] Am J Physiol Lung Cell Mol Physiol. 2000 Oct;279(4):L675-82 [11000127] Glia. 2001 Jul;35(1):53-62 [11424192] Biochim Biophys Acta. 1979 Feb 1;582(3):470-85 [570425] J Neurochem. 2001 Oct;79(1):200-10 [11595772] Pharmacol Rev. 2001 Dec;53(4):487-525 [11734616] J Comp Neurol. 2002 Feb 11;443(3):250-8 [11807835] J Neurosci. 2002 Feb 1;22(3):782-90 [11826108] FASEB J. 2002 Jul;16(9):993-1000 [12087060] Brain Behav Immun. 2002 Aug;16(4):290-332 [12096881] J Biol Chem. 2002 Aug 23;277(34):31249-56 [12063255] Mol Pharmacol. 2002 Nov;62(5):1043-52 [12391266] J Neurochem. 2002 Nov;83(4):973-83 [12421370] Neuropharmacology. 2002 Nov;43(6):1026-34 [12423672] J Neurovirol. 2002 Dec;8(6):474-9 [12476342] Neurobiol Aging. 2003 Mar-Apr;24(2):197-211 [12498954] Methods Mol Med. 2003;79:387-95 [12506711] Arch Neurol. 2003 Mar;60(3):337-41 [12633144] ScientificWorldJournal. 2003 Aug 2;3:677-83 [12920309] J Biol Chem. 2004 Jan 9;279(2):1415-21 [14578353] J Neurochem. 2004 Feb;88(4):939-47 [14756815] Proc Natl Acad Sci U S A. 1975 Apr;72(4):1564-8 [1055427] Mol Pharmacol. 1976 Jul;12(4):568-80 [8699] Br J Pharmacol. 1976 Dec;58(4):521-7 [1000130] Brain Res. 1977 May 20;127(1):25-53 [301051] J Physiol. 1979 May;290(2):44P [469786] Brain Res. 1980 Apr 28;188(2):513-23 [7370771] Eur J Pharmacol. 1981 Jun 19;72(2-3):173-88 [6265244] J Neurosci. 1985 Jul;5(7):1925-33 [3926960] Proc Natl Acad Sci U S A. 1987 Jul;84(13):4384-8 [2885836] Proc Natl Acad Sci U S A. 1988 Sep;85(17):6301-5 [2842764] Neuroscience. 1989;30(1):181-97 [2747911] J Neurosci. 1989 Nov;9(11):4062-7 [2511282] J Biol Chem. 1990 May 15;265(14):8183-9 [1970822] J Immunol. 1992 Jun 1;148(11):3441-5 [1350291] Arch Biochem Biophys. 1993 Apr;302(1):118-27 [7682389] Brain Res. 1993 Jun 18;614(1-2):21-8 [7688646] Infect Immun. 1994 May;62(5):2046-50 [8168970] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/glia.22801 ER - TY - CPAPER T1 - A Vaccine against Ebola Virus T2 - 115th General Meeting of the American Society for Microbiology (ASM 2015) AN - 1658699050; 6336158 JF - 115th General Meeting of the American Society for Microbiology (ASM 2015) AU - Sullivan, Nancy Y1 - 2015/05/30/ PY - 2015 DA - 2015 May 30 KW - Disease control KW - Vaccines KW - Ebola virus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658699050?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=115th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2015%29&rft.atitle=A+Vaccine+against+Ebola+Virus&rft.au=Sullivan%2C+Nancy&rft.aulast=Sullivan&rft.aufirst=Nancy&rft.date=2015-05-30&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=115th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={224BAD71-94EA-4FA5-8DF3-F4087BDC3625} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-28 N1 - Last updated - 2015-02-27 ER - TY - JOUR T1 - Topoisomerase I alone is sufficient to produce short DNA deletions and can also reverse nicks at ribonucleotide sites. AN - 1684432793; 25887397 AB - Ribonucleotide monophosphates (rNMPs) are among the most frequent form of DNA aberration, as high ratios of ribonucleotide triphosphate:deoxyribonucleotide triphosphate pools result in approximately two misincorporated rNMPs/kb of DNA. The main pathway for the removal of rNMPs is by RNase H2. However, in a RNase H2 knock-out yeast strain, a topoisomerase I (Top1)-dependent mutator effect develops with accumulation of short deletions within tandem repeats. Proposed models for these deletions implicated processing of Top1-generated nicks at rNMP sites and/or sequential Top1 binding, but experimental support has been lacking thus far. Here, we investigated the biochemical mechanism of the Top1-induced short deletions at the rNMP sites by generating nicked DNA substrates bearing 2',3'-cyclic phosphates at the nick sites, mimicking the Top1-induced nicks. We demonstrate that a second Top1 cleavage complex adjacent to the nick and subsequent faulty Top1 religation led to the short deletions. Moreover, when acting on the nicked DNA substrates containing 2',3'-cyclic phosphates, Top1 generated not only the short deletion, but also a full-length religated DNA product. A catalytically inactive Top1 mutant (Top1-Y723F) also induced the full-length products, indicating that Top1 binding independent of its enzymatic activity promotes the sealing of DNA backbones via nucleophilic attacks by the 5'-hydroxyl on the 2',3'-cyclic phosphate. The resealed DNA would allow renewed attempt for repair by the error-free RNase H2-dependent pathway in vivo. Our results provide direct evidence for the generation of short deletions by sequential Top1 cleavage events and for the promotion of nick religation at rNMP sites by Top1. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Huang, Shar-Yin Naomi AU - Ghosh, Sanchari AU - Pommier, Yves AD - From the Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892. ; From the Developmental Therapeutics Branch and Laboratory of Molecular Pharmacology, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892 pommier@nih.gov. Y1 - 2015/05/29/ PY - 2015 DA - 2015 May 29 SP - 14068 EP - 14076 VL - 290 IS - 22 KW - Phosphates KW - 0 KW - Recombinant Proteins KW - Ribonucleotides KW - DNA KW - 9007-49-2 KW - ribonuclease HII KW - EC 3.1.26.- KW - Ribonuclease H KW - EC 3.1.26.4 KW - DNA Topoisomerases, Type I KW - EC 5.99.1.2 KW - TOP1 protein, human KW - Index Medicus KW - DNA damage KW - DNA topoisomerase KW - mutagenesis mechanism KW - genomic instability KW - DNA repair KW - DNA Repair KW - Sequence Homology, Nucleic Acid KW - Humans KW - Phosphates -- chemistry KW - Ribonuclease H -- metabolism KW - Binding Sites KW - Gene Deletion KW - Mutagenesis KW - Base Sequence KW - Recombinant Proteins -- metabolism KW - Ribonucleotides -- chemistry KW - Molecular Sequence Data KW - Mutation KW - Catalysis KW - DNA -- chemistry KW - DNA Topoisomerases, Type I -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1684432793?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Topoisomerase+I+alone+is+sufficient+to+produce+short+DNA+deletions+and+can+also+reverse+nicks+at+ribonucleotide+sites.&rft.au=Huang%2C+Shar-Yin+Naomi%3BGhosh%2C+Sanchari%3BPommier%2C+Yves&rft.aulast=Huang&rft.aufirst=Shar-Yin&rft.date=2015-05-29&rft.volume=290&rft.issue=22&rft.spage=14068&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M115.653345 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-18 N1 - Date created - 2015-05-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nature. 2005 Mar 31;434(7033):671-4 [15800630] Nat Chem Biol. 2010 Oct;6(10):774-81 [20729855] J Biol Chem. 2005 Oct 28;280(43):36518-28 [16141202] Nucleic Acids Res. 2007;35(13):4474-84 [17576665] Nat Protoc. 2008;3(11):1736-50 [18927559] Proc Natl Acad Sci U S A. 2010 Mar 16;107(11):4949-54 [20194773] Mol Cell. 2012 Jan 13;45(1):99-110 [22244334] Cell. 2012 May 25;149(5):1008-22 [22579044] Mol Cell. 2012 Sep 28;47(6):980-6 [22864116] Proc Natl Acad Sci U S A. 2012 Oct 2;109(40):16125-30 [22991469] DNA Repair (Amst). 2013 Feb 1;12(2):121-7 [23245697] Nat Genet. 2013 Feb;45(2):136-44 [23263490] DNA Repair (Amst). 2013 Mar 1;12(3):205-11 [23305949] Mol Cell. 2013 Mar 7;49(5):1010-5 [23375499] Cancer Res. 2013 Jul 15;73(14):4372-82 [23856246] PLoS Genet. 2013 Nov;9(11):e1003878 [24244177] PLoS Genet. 2013 Nov;9(11):e1003924 [24244191] Nature. 2014 Feb 6;506(7486):111-5 [24362567] Mutat Res. 2014 Mar;761:21-33 [24495324] DNA Repair (Amst). 2014 Jul;19:27-37 [24794402] Gynecol Oncol. 2014 Jul;134(1):15-9 [24844595] Nature. 2014 Jul 10;511(7508):251-4 [24896181] Nucleic Acids Res. 2014;42(16):10226-34 [25159610] Nat Struct Mol Biol. 2015 Mar;22(3):185-91 [25622295] DNA Repair (Amst). 2015 Apr;28:107-15 [25758781] EMBO J. 2015 May 5;34(9):1259-69 [25777529] Mol Cell Biol. 2000 Jun;20(11):3977-87 [10805740] Nucleic Acids Res. 2000 Sep 1;28(17):3323-31 [10954601] Annu Rev Biochem. 2001;70:369-413 [11395412] Nat Rev Mol Cell Biol. 2002 Jun;3(6):430-40 [12042765] J Biol Chem. 1985 Nov 25;260(27):14873-8 [2997227] J Biol Chem. 1992 Apr 25;267(12):8620-7 [1314832] J Biol Chem. 1993 Sep 5;268(25):18943-50 [7689562] Biochem Biophys Res Commun. 1994 Dec 30;205(3):1601-9 [7811242] Biochemistry. 1995 May 9;34(18):6120-9 [7742316] Proc Natl Acad Sci U S A. 1996 Oct 15;93(21):11534-9 [8876170] J Biol Chem. 1997 Oct 17;272(42):26441-7 [9334220] Science. 1998 Mar 6;279(5356):1504-13 [9488644] Mol Cell. 1997 Dec;1(1):89-97 [9659906] Mol Cell. 1998 Apr;1(5):741-8 [9660957] Proc Natl Acad Sci U S A. 2011 Jan 11;108(2):692-7 [21177431] J Biol Chem. 2011 Feb 11;286(6):4117-22 [21098490] Biochem J. 2011 Jun 15;436(3):559-66 [21463258] Science. 2011 Jun 24;332(6037):1561-4 [21700875] Nat Struct Mol Biol. 2012 Jan;19(1):98-104 [22139012] Biochim Biophys Acta. 1998 Oct 1;1400(1-3):83-105 [9748515] J Biol Chem. 1999 Mar 26;274(13):8516-23 [10085084] Structure. 2010 Mar 14;18(4):449-57 [20399182] Chem Biol. 2010 May 28;17(5):421-33 [20534341] Chromosoma. 2005 Jul;114(2):75-85 [15830206] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M115.653345 ER - TY - JOUR T1 - Targeting of folate receptor β on acute myeloid leukemia blasts with chimeric antigen receptor-expressing T cells. AN - 1684431447; 25887778 AB - T cells expressing a chimeric antigen receptor (CAR) can produce dramatic results in lymphocytic leukemia patients; however, therapeutic strategies for myeloid leukemia remain limited. Folate receptor β (FRβ) is a myeloid-lineage antigen expressed on 70% of acute myeloid leukemia (AML) patient samples. Here, we describe the development and evaluation of the first CARs specific for human FRβ (m909) in vitro and in vivo. m909 CAR T cells exhibited selective activation and lytic function against engineered C30-FRβ as well as endogenous FRβ(+) AML cell lines in vitro. In mouse models of human AML, m909 CAR T cells mediated the regression of engrafted FRβ(+) THP1 AML in vivo. In addition, we demonstrated that treatment of AML with all-trans retinoic acid (ATRA) enhanced FRβ expression, resulting in improved immune recognition by m909 CAR T cells. Because many cell surface markers are shared between AML blasts and healthy hematopoietic stem and progenitor cells (HSCs), we evaluated FRβ expression and recognition of HSCs by CAR T cells. m909 CAR T cells were not toxic against healthy human CD34(+) HSCs in vitro. Our results indicate that FRβ is a promising target for CAR T-cell therapy of AML, which may be augmented by combination with ATRA. JF - Blood AU - Lynn, Rachel C AU - Poussin, Mathilde AU - Kalota, Anna AU - Feng, Yang AU - Low, Philip S AU - Dimitrov, Dimiter S AU - Powell, Daniel J AD - Ovarian Cancer Research Center, Department of Obstetrics and Gynecology, Perelman School of Medicine, and. ; Division of Hematology/Oncology, Abramson Cancer Center, University of Pennsylvania, Philadelphia, PA; ; Protein Interactions Section, Laboratory of Experimental Immunology, Cancer and Inflammation Program, Center for Cancer Research, National Cancer Institute, Frederick, MD; ; Department of Chemistry, Purdue University, West Lafayette, IN; and. ; Ovarian Cancer Research Center, Department of Obstetrics and Gynecology, Perelman School of Medicine, and Department of Pathology and Laboratory Medicine, Abramson Cancer Center, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA. Y1 - 2015/05/28/ PY - 2015 DA - 2015 May 28 SP - 3466 EP - 3476 VL - 125 IS - 22 KW - Folate Receptor 2 KW - 0 KW - Mutant Chimeric Proteins KW - Receptors, Antigen, T-Cell KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - HEK293 Cells KW - Humans KW - Mice, Inbred NOD KW - Molecular Targeted Therapy KW - Mice KW - Immunotherapy, Adoptive -- methods KW - Mice, Transgenic KW - Mutant Chimeric Proteins -- metabolism KW - Cells, Cultured KW - Genetic Therapy -- methods KW - Mice, SCID KW - Female KW - T-Lymphocytes -- metabolism KW - Leukemia, Myeloid, Acute -- therapy KW - Folate Receptor 2 -- genetics KW - Leukemia, Myeloid, Acute -- genetics KW - Receptors, Antigen, T-Cell -- metabolism KW - Folate Receptor 2 -- antagonists & inhibitors KW - T-Lymphocytes -- drug effects KW - Leukemia, Myeloid, Acute -- pathology KW - T-Lymphocytes -- pathology KW - Leukemia, Myeloid, Acute -- immunology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1684431447?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Targeting+of+folate+receptor+%CE%B2+on+acute+myeloid+leukemia+blasts+with+chimeric+antigen+receptor-expressing+T+cells.&rft.au=Lynn%2C+Rachel+C%3BPoussin%2C+Mathilde%3BKalota%2C+Anna%3BFeng%2C+Yang%3BLow%2C+Philip+S%3BDimitrov%2C+Dimiter+S%3BPowell%2C+Daniel+J&rft.aulast=Lynn&rft.aufirst=Rachel&rft.date=2015-05-28&rft.volume=125&rft.issue=22&rft.spage=3466&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=1528-0020&rft_id=info:doi/10.1182%2Fblood-2014-11-612721 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-25 N1 - Date created - 2015-05-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Blood. 1999 Jun 1;93(11):3940-8 [10339503] Cancer. 1999 Jan 15;85(2):348-57 [10023702] J Immunol. 2004 Dec 15;173(12):7125-30 [15585832] Blood. 2005 Jun 1;105(11):4247-54 [15728125] Cancer Res. 2006 Jun 1;66(11):5875-82 [16740727] Clin Cancer Res. 2006 Oct 15;12(20 Pt 1):6106-15 [17062687] Arthritis Rheum. 2006 Oct;54(10):3126-34 [17009233] Cancer Res. 2006 Nov 15;66(22):10995-1004 [17108138] Blood. 2009 Jan 8;113(2):438-46 [18952896] Cancer Immunol Immunother. 2009 Oct;58(10):1577-86 [19238383] Cancer Res. 2009 Dec 15;69(24):9395-403 [19951991] J Nucl Med. 2010 May;51(5):768-74 [20395331] Blood. 2012 Mar 22;119(12):2709-20 [22160384] J Transl Med. 2012;10:157 [22863016] Curr Opin Oncol. 2012 Nov;24(6):711-9 [23014187] PLoS One. 2012;7(12):e50946 [23284651] N Engl J Med. 2013 Apr 18;368(16):1509-18 [23527958] Cancer Res. 2010 Nov 15;70(22):9053-61 [20926399] Haematologica. 2010 Dec;95(12):2144-52 [20713459] Blood. 2011 Jan 6;117(1):72-82 [20889925] Immunol Lett. 2011 Apr 30;136(1):97-107 [21237205] J Clin Invest. 2011 May;121(5):1822-6 [21540550] Clin Cancer Res. 2013 Jun 15;19(12):3153-64 [23620405] Blood. 2013 Oct 31;122(18):3138-48 [24030378] Blood. 2014 Apr 10;123(15):2343-54 [24596416] Cancer Res. 2011 Jul 1;71(13):4617-27 [21546571] N Engl J Med. 2011 Aug 25;365(8):725-33 [21830940] Arthritis Res Ther. 2011;13(2):R59 [21477314] Blood. 2011 Nov 3;118(18):4817-28 [21849486] Blood. 2012 Jan 19;119(3):696-706 [22117050] Mol Ther. 2012 Mar;20(3):633-43 [22127019] Mod Rheumatol. 2014 Sep;24(5):816-22 [24498991] J Leukoc Biol. 2014 Oct;96(4):563-70 [25015955] Sci Transl Med. 2013 Mar 20;5(177):177ra38 [23515080] Blood. 2000 Nov 15;96(10):3529-36 [11071651] Blood. 2002 Jul 15;100(2):594-602 [12091353] Arthritis Rheum. 2002 Jul;46(7):1947-55 [12124880] J Immunol. 2002 Nov 15;169(10):5555-63 [12421932] Clin Cancer Res. 2003 Jan;9(1):264-72 [12538479] Blood. 2003 Jun 1;101(11):4551-60 [12543860] J Immunol Methods. 2003 Oct 1;281(1-2):65-78 [14580882] Int Immunol. 2004 Mar;16(3):443-53 [14978018] Proc Natl Acad Sci U S A. 1980 May;77(5):2936-40 [6930676] Proc Natl Acad Sci U S A. 1989 Dec;86(24):10024-8 [2513569] Biochemistry. 1989 Oct 3;28(20):8249-54 [2605182] Cancer Res. 1991 Nov 15;51(22):6125-32 [1840502] Proc Natl Acad Sci U S A. 1992 Apr 1;89(7):3070-4 [1348364] Cancer Res. 1993 May 1;53(9):2100-4 [8481912] J Exp Med. 1993 Jul 1;178(1):361-6 [8315392] Biochemistry. 1994 Feb 8;33(5):1209-15 [8110752] J Immunol. 1994 Feb 15;152(4):1515-22 [8120366] Cancer. 1994 May 1;73(9):2432-43 [7513252] J Biol Chem. 1996 Oct 25;271(43):26783-93 [8900159] Immunology. 1997 Mar;90(3):388-96 [9155646] Cell Immunol. 1998 Apr 10;185(1):75-81 [9636685] Arthritis Rheum. 1999 Aug;42(8):1609-16 [10446858] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1182/blood-2014-11-612721 ER - TY - JOUR T1 - Incubation of Methamphetamine Craving Is Associated with Selective Increases in Expression of Bdnf and Trkb, Glutamate Receptors, and Epigenetic Enzymes in Cue-Activated Fos-Expressing Dorsal Striatal Neurons AN - 1735914723; PQ0002270521 AB - Cue-induced methamphetamine seeking progressively increases after withdrawal (incubation of methamphetamine craving), but the underlying mechanisms are largely unknown. We determined whether this incubation is associated with alterations in candidate genes in dorsal striatum (DS), a brain area implicated in cue- and context-induced drug relapse. We first measured mRNA expression of 24 candidate genes in whole DS extracts after short (2 d) or prolonged (1 month) withdrawal in rats following extended-access methamphetamine or saline (control condition) self-administration (9 h/d, 10 d). We found minimal changes. Next, using fluorescence-activated cell sorting, we compared gene expression in Fos-positive dorsal striatal neurons, which were activated during "incubated" cue-induced drug-seeking tests after prolonged withdrawal, with nonactivated Fos-negative neurons. We found significant increases in mRNA expression of immediate early genes (Arc, Egr1), Bdnf and its receptor (rkb), glutamate receptor subunits (Gria1, Gria3, Grm1), and epigenetic enzymes (Hdac3, Hdac4, Hdac5, GLP, Dnmt3a, Kdm1a) in the Fos-positive neurons only. Using RNAscope to determine striatal subregion and cell-type specificity of the activated neurons, we measured colabeling of Fos with Drd1 and Drd2 in three DS subregions. Fos expression was neither subregion nor cell-type specific (52.5 and 39.2% of Fos expression colabeled with Drd1 and Drd2, respectively). Finally, we found that DS injections of SCH23390 (C sub(17)H sub(18)CINO), a D sub(1)-family receptor antagonist known to block cue-induced Fos induction, decreased incubated cue-induced methamphetamine seeking after prolonged withdrawal. Results demonstrate a critical role of DS in incubation of methamphetamine craving and that this incubation is associated with selective gene-expression alterations in cue-activated D sub(1)- and D sub(2)-expressing DS neurons. JF - Journal of Neuroscience AU - Li, Xuan AU - Rubio, F Javier AU - Zeric, Tamara AU - Bossert, Jennifer M AU - Kambhampati, Sarita AU - Cates, Hannah M AU - Kennedy, Pamela J AU - Liu, Qing-Rong AU - Cimbro, Raffaello AU - Hope, Bruce T AU - Nestler, Eric J AU - Shaham, Yavin AD - Behavioral Neuroscience Research Branch, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, U.S. Department of Health and Human Services, Baltimore, Maryland 21224 Y1 - 2015/05/27/ PY - 2015 DA - 2015 May 27 SP - 8232 EP - 8244 PB - Society for Neuroscience, 11 Dupont Circle, N.W. Washington DC 20036 United States VL - 35 IS - 21 SN - 0270-6474, 0270-6474 KW - Toxicology Abstracts; Animal Behavior Abstracts; CSA Neurosciences Abstracts KW - dorsal striatum KW - epigenetics KW - FACS KW - glutamate KW - methamphetamine KW - relapse KW - Dopamine D2 receptors KW - Brain-derived neurotrophic factor KW - Dopamine D1 receptors KW - Enzymes KW - Drug development KW - Drug abuse KW - Glutamic acid receptors KW - Fos protein KW - Flow cytometry KW - Gene expression KW - TrkB receptors KW - Methamphetamine KW - Nervous system KW - Neurons KW - Neostriatum KW - Self-administration KW - Immediate-early proteins KW - Drug addiction KW - EGR-1 protein KW - X 24380:Social Poisons & Drug Abuse KW - N3 11001:Behavioral and Cognitive Neuroscience KW - Y 25050:Genetics and Evolution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1735914723?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Neuroscience&rft.atitle=Incubation+of+Methamphetamine+Craving+Is+Associated+with+Selective+Increases+in+Expression+of+Bdnf+and+Trkb%2C+Glutamate+Receptors%2C+and+Epigenetic+Enzymes+in+Cue-Activated+Fos-Expressing+Dorsal+Striatal+Neurons&rft.au=Li%2C+Xuan%3BRubio%2C+F+Javier%3BZeric%2C+Tamara%3BBossert%2C+Jennifer+M%3BKambhampati%2C+Sarita%3BCates%2C+Hannah+M%3BKennedy%2C+Pamela+J%3BLiu%2C+Qing-Rong%3BCimbro%2C+Raffaello%3BHope%2C+Bruce+T%3BNestler%2C+Eric+J%3BShaham%2C+Yavin&rft.aulast=Li&rft.aufirst=Xuan&rft.date=2015-05-27&rft.volume=35&rft.issue=21&rft.spage=8232&rft.isbn=&rft.btitle=&rft.title=Journal+of+Neuroscience&rft.issn=02706474&rft_id=info:doi/10.1523%2FJNEUROSCI.102215.2015 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-01 N1 - Last updated - 2016-02-29 N1 - SubjectsTermNotLitGenreText - Brain-derived neurotrophic factor; Dopamine D2 receptors; Dopamine D1 receptors; Enzymes; Drug development; Drug abuse; Glutamic acid receptors; Fos protein; Gene expression; Flow cytometry; TrkB receptors; Nervous system; Methamphetamine; epigenetics; Neurons; Neostriatum; Self-administration; Immediate-early proteins; Drug addiction; EGR-1 protein DO - http://dx.doi.org/10.1523/JNEUROSCI.102215.2015 ER - TY - JOUR T1 - The UBC-40 Urothelial Bladder Cancer cell line index: a genomic resource for functional studies. AN - 1689840903; 25997541 AB - Urothelial bladder cancer is a highly heterogeneous disease. Cancer cell lines are useful tools for its study. This is a comprehensive genomic characterization of 40 urothelial bladder carcinoma (UBC) cell lines including information on origin, mutation status of genes implicated in bladder cancer (FGFR3, PIK3CA, TP53, and RAS), copy number alterations assessed using high density SNP arrays, uniparental disomy (UPD) events, and gene expression. Based on gene mutation patterns and genomic changes we identify lines representative of the FGFR3-driven tumor pathway and of the TP53/RB tumor suppressor-driven pathway. High-density array copy number analysis identified significant focal gains (1q32, 5p13.1-12, 7q11, and 7q33) and losses (i.e. 6p22.1) in regions altered in tumors but not previously described as affected in bladder cell lines. We also identify new evidence for frequent regions of UPD, often coinciding with regions reported to be lost in tumors. Previously undescribed chromosome X losses found in UBC lines also point to potential tumor suppressor genes. Cell lines representative of the FGFR3-driven pathway showed a lower number of UPD events. Overall, there is a predominance of more aggressive tumor subtypes among the cell lines. We provide a cell line classification that establishes their relatedness to the major molecularly-defined bladder tumor subtypes. The compiled information should serve as a useful reference to the bladder cancer research community and should help to select cell lines appropriate for the functional analysis of bladder cancer genes, for example those being identified through massive parallel sequencing. JF - BMC genomics AU - Earl, Julie AU - Rico, Daniel AU - Carrillo-de-Santa-Pau, Enrique AU - Rodríguez-Santiago, Benjamín AU - Méndez-Pertuz, Marinela AU - Auer, Herbert AU - Gómez, Gonzalo AU - Grossman, Herbert Barton AU - Pisano, David G AU - Schulz, Wolfgang A AU - Pérez-Jurado, Luis A AU - Carrato, Alfredo AU - Theodorescu, Dan AU - Chanock, Stephen AU - Valencia, Alfonso AU - Real, Francisco X AD - Epithelial Carcinogenesis Group, F BBVA Cancer Cell Biology Programme, CNIO (Spanish National Cancer Research Centre), Madrid, Spain. jearl@ext.cnio.es. ; Structural Computational Biology Group, Structural Biology and Biocomputing Programme, CNIO (Spanish National Cancer Research Centre), Madrid, Spain. drico@cnio.es. ; Epithelial Carcinogenesis Group, F BBVA Cancer Cell Biology Programme, CNIO (Spanish National Cancer Research Centre), Madrid, Spain. ecarrillo@cnio.es. ; Quantitative Genomic Medicine Laboratory, qGenomics, Barcelona, Spain. benjamin.rodriguez@qgenomics.com. ; Epithelial Carcinogenesis Group, F BBVA Cancer Cell Biology Programme, CNIO (Spanish National Cancer Research Centre), Madrid, Spain. mmendez@cnio.es. ; Institut de Recerca Biomèdica de Barcelona, Parc Científic de Barcelona, Barcelona, Spain. herbert.auer@irbbarcelona.org. ; Bioinformatics Unit, Structural Biology and Biocomputing Programme, CNIO (Spanish National Cancer Research Centre), Madrid, Spain. ggomez@cnio.es. ; Department of Urology, MD Anderson Cancer Center, Houston, TX, USA. hbgrossman@mdanderson.org. ; Bioinformatics Unit, Structural Biology and Biocomputing Programme, CNIO (Spanish National Cancer Research Centre), Madrid, Spain. dgpisano@cnio.es. ; Department of Urology, Heinrich-Heine-University, Düsseldorf, Germany. wolfgang.schulz@uni-duesseldorf.de. ; Departament de Ciències Experimentals i de la Salut, Universitat Pompeu Fabra, Barcelona, Spain. luis.perez@upf.edu. ; Servicio de Oncología Médica, Hospital Ramón y Cajal, Madrid, Spain. acarrato@telefonica.net. ; University of Colorado Comprehensive Cancer Center, 80045, Aurora, CO, USA. dan.theodorescu@ucdenver.edu. ; Translational Genomics Laboratory, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, USA. chanocks@mail.nih.gov. ; Structural Computational Biology Group, Structural Biology and Biocomputing Programme, CNIO (Spanish National Cancer Research Centre), Madrid, Spain. avalencia@cnio.es. ; Epithelial Carcinogenesis Group, F BBVA Cancer Cell Biology Programme, CNIO (Spanish National Cancer Research Centre), Madrid, Spain. preal@cnio.es. Y1 - 2015/05/22/ PY - 2015 DA - 2015 May 22 SP - 403 VL - 16 KW - Biomarkers, Tumor KW - 0 KW - TP53 protein, human KW - Tumor Suppressor Protein p53 KW - Phosphatidylinositol 3-Kinases KW - EC 2.7.1.- KW - PIK3CA protein, human KW - EC 2.7.1.137 KW - FGFR3 protein, human KW - EC 2.7.10.1 KW - Receptor, Fibroblast Growth Factor, Type 3 KW - ras Proteins KW - EC 3.6.5.2 KW - Index Medicus KW - ras Proteins -- genetics KW - Biomarkers, Tumor -- genetics KW - DNA Copy Number Variations KW - Phosphatidylinositol 3-Kinases -- genetics KW - Receptor, Fibroblast Growth Factor, Type 3 -- genetics KW - Humans KW - Chromosomes, Human, X KW - Cell Line, Tumor KW - Genomic Instability KW - Tumor Suppressor Protein p53 -- genetics KW - Cluster Analysis KW - Female KW - Male KW - Urinary Bladder Neoplasms -- pathology KW - Genome, Human KW - Urinary Bladder Neoplasms -- genetics KW - Databases, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1689840903?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+genomics&rft.atitle=The+UBC-40+Urothelial+Bladder+Cancer+cell+line+index%3A+a+genomic+resource+for+functional+studies.&rft.au=Earl%2C+Julie%3BRico%2C+Daniel%3BCarrillo-de-Santa-Pau%2C+Enrique%3BRodr%C3%ADguez-Santiago%2C+Benjam%C3%ADn%3BM%C3%A9ndez-Pertuz%2C+Marinela%3BAuer%2C+Herbert%3BG%C3%B3mez%2C+Gonzalo%3BGrossman%2C+Herbert+Barton%3BPisano%2C+David+G%3BSchulz%2C+Wolfgang+A%3BP%C3%A9rez-Jurado%2C+Luis+A%3BCarrato%2C+Alfredo%3BTheodorescu%2C+Dan%3BChanock%2C+Stephen%3BValencia%2C+Alfonso%3BReal%2C+Francisco+X&rft.aulast=Earl&rft.aufirst=Julie&rft.date=2015-05-22&rft.volume=16&rft.issue=&rft.spage=403&rft.isbn=&rft.btitle=&rft.title=BMC+genomics&rft.issn=1471-2164&rft_id=info:doi/10.1186%2Fs12864-015-1450-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-25 N1 - Date created - 2015-06-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Oncogene. 2004 Mar 18;23(12):2250-63 [14968109] Bioinformatics. 2009 Feb 1;25(3):315-21 [19052058] Cancer Res. 2000 Jul 15;60(14):3862-71 [10919661] Br J Cancer. 2000 Oct;83(8):1084-95 [10993658] Clin Cancer Res. 2005 Oct 1;11(19 Pt 1):7012-22 [16203795] Cell Oncol (Dordr). 2012 Aug;35(4):243-57 [22669776] Genes Dev. 1998 Jan 15;12(2):163-74 [9436977] Nat Genet. 1999 Sep;23(1):18-20 [10471491] Oncogene. 2005 Aug 4;24(33):5218-25 [15897885] Biostatistics. 2004 Oct;5(4):557-72 [15475419] Nature. 1983 Feb 3;301(5899):429-30 [6823318] J Urol. 2006 Mar;175(3 Pt 1):1133-7 [16469639] J Clin Oncol. 2006 Aug 1;24(22):3664-71 [16877735] Cancer Res. 2006 Aug 1;66(15):7401-4 [16885334] Int J Cancer. 2006 Oct 1;119(7):1513-8 [16557569] Nat Rev Cancer. 2006 Oct;6(10):813-23 [16990858] Clin Transl Oncol. 2007 Jan;9(1):5-12 [17272224] Bioinformatics. 2007 Apr 1;23(7):892-4 [17267432] Hum Mutat. 2007 Jun;28(6):622-9 [17311302] World J Urol. 2007 Jun;25(3):297-302 [17440731] World J Urol. 2007 Jun;25(3):285-95 [17530260] J Clin Oncol. 2007 Dec 1;25(34):5341-4 [18048811] Urologe A. 2008 Jun;47(6):724-34 [18398596] Clin Pharmacol Ther. 2009 Feb;85(2):217-21 [19005462] Br J Cancer. 1995 Sep;72(3):683-90 [7669581] Mol Cancer Ther. 2009 Apr;8(4):713-24 [19372543] J Clin Invest. 2009 May;119(5):1216-29 [19381019] Biostatistics. 2010 Apr;11(2):242-53 [20097884] Cancer Res. 2010 May 1;70(9):3463-72 [20406976] Nucleic Acids Res. 2010 Jul;38(Web Server issue):W182-7 [20507915] Am J Hum Genet. 2010 Jul 9;87(1):129-38 [20598279] PLoS One. 2010;5(11):e13821 [21072204] Nucleic Acids Res. 2011 Jan;39(Database issue):D945-50 [20952405] Int J Cancer. 2010 Dec 15;127(12):2893-917 [21351269] Clin Cancer Res. 2011 May 1;17(9):2863-73 [21415218] Nat Genet. 2011 Sep;43(9):875-8 [21822268] Nature. 2012 Mar 29;483(7391):603-7 [22460905] Clin Cancer Res. 2012 Jun 15;18(12):3377-86 [22553347] Hum Mol Genet. 2013 Feb 15;22(4):795-803 [23175443] PLoS One. 2013;8(5):e62483 [23650517] J Urol. 2013 Oct;190(4):1404-9 [23500642] Nat Genet. 2013 Dec;45(12):1428-30 [24121789] Nat Genet. 2013 Dec;45(12):1464-9 [24121791] Nat Genet. 2013 Dec;45(12):1459-63 [24121792] Eur Urol. 2014 Feb;65(2):360-6 [24018021] Eur Urol. 2014 Feb;65(2):367-9 [24035680] Nature. 2014 Mar 20;507(7492):315-22 [24476821] Sci Transl Med. 2014 Jul 9;6(244):244ra91 [25009231] Erratum In: BMC Genomics. 2015;16(1):1019 [26621286] BMC Genomics. 2016 Oct 25;17 (1):829 [27782819] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/s12864-015-1450-3 ER - TY - JOUR T1 - A 3.7 kb Fragment of the Mouse Scn10a Gene Promoter Directs Neural Crest But Not Placodal Lineage EGFP Expression in a Transgenic Animal AN - 1735915240; PQ0002270148 AB - Under physiological conditions, the voltage-gated sodium channel Na sub(v)1.8 is expressed almost exclusively in primary sensory neurons. The mechanism restricting Na sub(v)1.8 expression is not entirely clear, but we have previously described a 3.7 kb fragment of the Scn10a promoter capable of recapitulating the tissue-specific expression of Na sub(v)1.8 in transfected neurons and cell lines (Puhl and Ikeda, 2008). To validate these studies in vivo, a transgenic mouse encoding EGFP under the control of this putative sensory neuron specific promoter was generated and characterized in this study. Approximately 45% of dorsal root ganglion neurons of transgenic mice were EGFP-positive (mean diameter = 26.5 mu m). The majority of EGFP-positive neurons bound isolectin B4, although a small percentage (~10%) colabeled with markers of A-fiber neurons. EGFP expression correlated well with the presence of Na sub(v)1.8 transcript (95%), Na sub(v)1.8-immunoreactivity (70%), and TTX-R / sub(Na) (100%), although not all Na sub(v)1.8-expressing neurons expressed EGFP. Several cranial sensory ganglia originating from neurogenic placodes, such as the nodose ganglion, failed to express EGFP, suggesting that additional regulatory elements dictate Scn10a expression in placodal-derived sensory neurons. EGFP was also detected in discrete brain regions of transgenic mice. Quantitative PCR and Na sub(v)1.8-immunoreactivity confirmed Na sub(v)1.8 expression in the amygdala, brainstem, globus pallidus, lateral and paraventricular hypothalamus, and olfactory tubercle. TTX-R / sub(Na) recorded from EGFP-positive hypothalamic neurons demonstrate the usefulness of this transgenic line to study novel roles of Na sub(v)1.8 beyond sensory neurons. Overall, Scn10a-EGFP transgenic mice recapitulate the majority of the Na sub(v)1.8 expression pattern in neural crest-derived sensory neurons. JF - Journal of Neuroscience AU - Lu, Van B AU - Ikeda, Stephen R AU - Puhl, Henry L, III AD - Section on Transmitter Signaling, Laboratory of Molecular Physiology, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland 20892-9411 Y1 - 2015/05/20/ PY - 2015 DA - 2015 May 20 SP - 8021 EP - 8034 PB - Society for Neuroscience, 11 Dupont Circle, N.W. Washington DC 20036 United States VL - 35 IS - 20 SN - 0270-6474, 0270-6474 KW - Biotechnology and Bioengineering Abstracts; Genetics Abstracts; CSA Neurosciences Abstracts KW - dorsal root ganglia KW - nodose ganglion KW - pain KW - sodium channels KW - transgenic KW - Cranial nerves KW - Hypothalamus KW - Sodium channels (voltage-gated) KW - Sensory neurons KW - Regulatory sequences KW - Brain stem KW - Dorsal root ganglia KW - Brain KW - Transcription KW - Transgenic mice KW - Olfactory bulb KW - Promoters KW - Ikeda KW - Globus pallidus KW - Nodose ganglion KW - Peripheral nervous system KW - Polymerase chain reaction KW - Amygdala KW - Hypothalamus (lateral) KW - Neural crest KW - N3 11023:Neurogenetics KW - W 30955:Biosensors KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1735915240?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Neuroscience&rft.atitle=A+3.7+kb+Fragment+of+the+Mouse+Scn10a+Gene+Promoter+Directs+Neural+Crest+But+Not+Placodal+Lineage+EGFP+Expression+in+a+Transgenic+Animal&rft.au=Lu%2C+Van+B%3BIkeda%2C+Stephen+R%3BPuhl%2C+Henry+L%2C+III&rft.aulast=Lu&rft.aufirst=Van&rft.date=2015-05-20&rft.volume=35&rft.issue=20&rft.spage=8021&rft.isbn=&rft.btitle=&rft.title=Journal+of+Neuroscience&rft.issn=02706474&rft_id=info:doi/10.1523%2FJNEUROSCI.021415.2015 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Cranial nerves; Hypothalamus; Sodium channels (voltage-gated); Sensory neurons; Regulatory sequences; Brain stem; Brain; Dorsal root ganglia; Transcription; Transgenic mice; Olfactory bulb; Promoters; Globus pallidus; Peripheral nervous system; Nodose ganglion; Polymerase chain reaction; Amygdala; Hypothalamus (lateral); Neural crest; Ikeda DO - http://dx.doi.org/10.1523/JNEUROSCI.021415.2015 ER - TY - JOUR T1 - Stereoselective Actions of Methylenedioxypyrovalerone (MDPV) To Inhibit Dopamine and Norepinephrine Transporters and Facilitate Intracranial Self-Stimulation in Rats. AN - 1682428183; 25688761 AB - The designer stimulant methylenedioxypyrovalerone (MDPV) is a potent reuptake inhibitor at transporters for dopamine (DAT) and norepinephrine (NET) that produces a constellation of abuse-related behavioral effects. MDPV possesses a chiral center, and the abused formulation of the drug is a racemic mixture, but no data are available on the pharmacology of its isomers. Here, the individual optical isomers of MDPV were prepared and examined with respect to their neurochemical actions on neurotransmitter reuptake and behavioral effects in an assay of intracranial self-stimulation (ICSS) in rats. In assays of DAT uptake inhibition, S(+)MDPV (EC50 = 2.13 nM) was more potent than either (±)MDPV (EC50 = 4.85 nM) or R(-)MDPV (EC50 = 382.80 nM); the three drugs were less potent at NET uptake inhibition, with the same rank order of potency. Neither racemic MDPV nor its optical isomers inhibited the reuptake of serotonin at concentrations up to 10 μM. S(+)MDPV produced an abuse-related and dose-dependent facilitation of ICSS, and the potency of S(+)MDPV (significant facilitation at doses ≥ 0.1 mg/kg) was greater than that of the racemate (significant facilitation at doses ≥ 0.32 mg/kg). R(-)MDPV failed to alter ICSS at doses up to 100 times greater than the lowest effective dose of S(+)MDPV. The results indicate that abuse-related neurochemical and behavioral effects of racemic MDPV reside primarily with its S(+) isomer. JF - ACS chemical neuroscience AU - Kolanos, R AU - Partilla, J S AU - Baumann, M H AU - Hutsell, B A AU - Banks, M L AU - Negus, S S AU - Glennon, R A AD - †Department of Medicinal Chemistry, School of Pharmacy, Virginia Commonwealth University, 800 East Leigh Street, PO Box 980540, Richmond, Virginia 23298, United States. ; ‡Designer Drug Research Unit, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, Maryland 21224, United States. ; §Department of Pharmacology and Toxicology, Virginia Commonwealth University, 410 North 12th Street, PO Box 980613, Richmond, Virginia 23298, United States. Y1 - 2015/05/20/ PY - 2015 DA - 2015 May 20 SP - 771 EP - 777 VL - 6 IS - 5 KW - 3,4-methylenedioxypyrovalerone KW - 0 KW - Benzodioxoles KW - Designer Drugs KW - Dopamine Plasma Membrane Transport Proteins KW - Norepinephrine Plasma Membrane Transport Proteins KW - Pyrrolidines KW - Index Medicus KW - Synthetic cathinones KW - psychomotor stimulants KW - drug abuse KW - MDPV KW - NET KW - cocaine KW - reuptake inhibition KW - ICSS (intracranial self-stimulation) KW - DAT KW - Rats KW - Animals KW - Stereoisomerism KW - Rats, Sprague-Dawley KW - Self Stimulation -- drug effects KW - Designer Drugs -- pharmacology KW - Male KW - Designer Drugs -- chemistry KW - Norepinephrine Plasma Membrane Transport Proteins -- antagonists & inhibitors KW - Pyrrolidines -- chemistry KW - Brain -- drug effects KW - Pyrrolidines -- pharmacology KW - Benzodioxoles -- pharmacology KW - Benzodioxoles -- chemistry KW - Dopamine Plasma Membrane Transport Proteins -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1682428183?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=ACS+chemical+neuroscience&rft.atitle=Stereoselective+Actions+of+Methylenedioxypyrovalerone+%28MDPV%29+To+Inhibit+Dopamine+and+Norepinephrine+Transporters+and+Facilitate+Intracranial+Self-Stimulation+in+Rats.&rft.au=Kolanos%2C+R%3BPartilla%2C+J+S%3BBaumann%2C+M+H%3BHutsell%2C+B+A%3BBanks%2C+M+L%3BNegus%2C+S+S%3BGlennon%2C+R+A&rft.aulast=Kolanos&rft.aufirst=R&rft.date=2015-05-20&rft.volume=6&rft.issue=5&rft.spage=771&rft.isbn=&rft.btitle=&rft.title=ACS+chemical+neuroscience&rft.issn=1948-7193&rft_id=info:doi/10.1021%2Facschemneuro.5b00006 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-07 N1 - Date created - 2015-05-20 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/acschemneuro.5b00006 ER - TY - JOUR T1 - The BRAIN Initiative: developing technology to catalyse neuroscience discovery AN - 1808717282; PQ0003427950 AB - The evolution of the field of neuroscience has been propelled by the advent of novel technological capabilities, and the pace at which these capabilities are being developed has accelerated dramatically in the past decade. Capitalizing on this momentum, the United States launched the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative to develop and apply new tools and technologies for revolutionizing our understanding of the brain. In this article, we review the scientific vision for this initiative set forth by the National Institutes of Health and discuss its implications for the future of neuroscience research. Particular emphasis is given to its potential impact on the mapping and study of neural circuits, and how this knowledge will transform our understanding of the complexity of the human brain and its diverse array of behaviours, perceptions, thoughts and emotions. JF - Philosophical Transactions of the Royal Society of London, Series B: Biological Sciences AU - Jorgenson, Lyric A AU - Newsome, William T AU - Anderson, David J AU - Bargmann, Cornelia I AU - Brown, Emery N AU - Deisseroth, Karl AU - Donoghue, John P AU - Hudson, Kathy L AU - Ling, Geoffrey SF AU - MacLeish, Peter R AU - Marder, Eve AU - Normann, Richard A AU - Sanes, Joshua R AU - Schnitzer, Mark J AU - Sejnowski, Terrence J AU - Tank, David W AU - Tsien, Roger Y AU - Ugurbil, Kamil AU - Wingfield, John C AD - Office of the Director, National Institutes of Health, , Bethesda, MD 20892, USA, jorgensonla@od.nih.gov Y1 - 2015/05/19/ PY - 2015 DA - 2015 May 19 SP - 20140164 PB - Royal Society of London, 6 Carlton House Terrace London SW1Y 5AG United Kingdom VL - 370 IS - 1668 SN - 0962-8436, 0962-8436 KW - CSA Neurosciences Abstracts; Ecology Abstracts KW - BRAIN Initiative KW - neural circuitry KW - neurotechnology KW - Emotions KW - Brain mapping KW - Nervous system KW - Neural networks KW - Perception KW - Vision KW - Reviews KW - Brain KW - Evolution KW - N3 11001:Behavioral and Cognitive Neuroscience KW - D 04040:Ecosystem and Ecology Studies UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808717282?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Philosophical+Transactions+of+the+Royal+Society+of+London%2C+Series+B%3A+Biological+Sciences&rft.atitle=The+BRAIN+Initiative%3A+developing+technology+to+catalyse+neuroscience+discovery&rft.au=Jorgenson%2C+Lyric+A%3BNewsome%2C+William+T%3BAnderson%2C+David+J%3BBargmann%2C+Cornelia+I%3BBrown%2C+Emery+N%3BDeisseroth%2C+Karl%3BDonoghue%2C+John+P%3BHudson%2C+Kathy+L%3BLing%2C+Geoffrey+SF%3BMacLeish%2C+Peter+R%3BMarder%2C+Eve%3BNormann%2C+Richard+A%3BSanes%2C+Joshua+R%3BSchnitzer%2C+Mark+J%3BSejnowski%2C+Terrence+J%3BTank%2C+David+W%3BTsien%2C+Roger+Y%3BUgurbil%2C+Kamil%3BWingfield%2C+John+C&rft.aulast=Jorgenson&rft.aufirst=Lyric&rft.date=2015-05-19&rft.volume=370&rft.issue=1668&rft.spage=20140164&rft.isbn=&rft.btitle=&rft.title=Philosophical+Transactions+of+the+Royal+Society+of+London%2C+Series+B%3A+Biological+Sciences&rft.issn=09628436&rft_id=info:doi/10.1098%2Frstb.2014.0164 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Brain mapping; Emotions; Nervous system; Vision; Perception; Neural networks; Reviews; Brain; Evolution DO - http://dx.doi.org/10.1098/rstb.2014.0164 ER - TY - JOUR T1 - Hormone Therapy and Young-Onset Breast Cancer AN - 1701475593; PQ0001732733 AB - Estrogen plus progestin hormone therapy (HT) is associated with an increased risk of postmenopausal breast cancer, but few studies have examined the impact of HT use on the risk of breast cancer in younger women. We assessed the association between estrogen plus progestin HT or unopposed estrogen HT and young-onset breast cancer using data from the Two Sister Study (2008-2010), a sister-matched study of 1,419 cases diagnosed with breast cancer before the age of 50 years and 1,665 controls. We assessed exposures up to a family-specific index age to ensure comparable opportunities for exposures and used propensity scores to control for birth cohort effects on HT use. Ever HT use was uncommon (7% and 11% in cases and controls, respectively). Use of estrogen plus progestin was not associated with an increased risk of young-onset breast cancer (odds ratio = 0.80, 95% confidence interval: 0.41, 1.59). Unopposed estrogen use was inversely associated with the risk of young-onset breast cancer (odds ratio = 0.58, 95% confidence interval: 0.34, 0.99). Duration of use, age at first use, and recency of use did not modify these associations. JF - American Journal of Epidemiology AU - O'Brien, Katie M AU - Fei, Chunyuan AU - Sandler, Dale P AU - Nichols, Hazel B AU - DeRoo, Lisa A AU - Weinberg, Clarice R AD - Correspondence to Dr. Clarice R. Weinberg, Biostatistics and Computational Biology Branch, National Institute of Environmental Health Sciences, PO Box 12233, Mail Drop A3-03, Research Triangle Park, NC 27709, weinber2@niehs.nih.gov Y1 - 2015/05/15/ PY - 2015 DA - 2015 May 15 SP - 799 EP - 807 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 181 IS - 10 SN - 0002-9262, 0002-9262 KW - Risk Abstracts; Health & Safety Science Abstracts KW - hormone therapy KW - propensity score KW - young-onset breast cancer KW - Risk assessment KW - Health risks KW - Estrogens KW - Age KW - Post-menopause KW - Breast cancer KW - Hormones KW - Cancer KW - H 11000:Diseases/Injuries/Trauma KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701475593?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Hormone+Therapy+and+Young-Onset+Breast+Cancer&rft.au=O%27Brien%2C+Katie+M%3BFei%2C+Chunyuan%3BSandler%2C+Dale+P%3BNichols%2C+Hazel+B%3BDeRoo%2C+Lisa+A%3BWeinberg%2C+Clarice+R&rft.aulast=O%27Brien&rft.aufirst=Katie&rft.date=2015-05-15&rft.volume=181&rft.issue=10&rft.spage=799&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwu347 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2015-09-03 N1 - SubjectsTermNotLitGenreText - Risk assessment; Health risks; Age; Estrogens; Post-menopause; Breast cancer; Hormones; Cancer DO - http://dx.doi.org/10.1093/aje/kwu347 ER - TY - JOUR T1 - Autoantibodies in breast cancer sera are not epiphenomena and may participate in carcinogenesis. AN - 1686070059; 25975273 AB - The objective of this work was to demonstrate that autoantibodies in breast cancer sera are not epiphenomena, and exhibit unique immunologic features resembling the rheumatic autoimmune diseases. We performed a comprehensive study of autoantibodies on a collection of sera from women with breast cancer or benign breast disease, undergoing annual screening mammography. All women in this study had suspicious mammography assessment and underwent a breast biopsy. We used indirect immunofluorescence, the crithidia assay for anti-dsDNA antibodies, and multiple ELISAs for extractable nuclear antigens. Autoantibodies were detected in virtually all patients with breast cancer, predominantly of the IgG1 and IgG3 isotypes. The profile detected in breast cancer sera showed distinctive features, such as antibodies targeting mitochondria, centrosomes, centromeres, nucleoli, cytoskeleton, and multiple nuclear dots. The majority of sera showing anti-mitochondrial antibodies did not react with the M2 component of pyruvate dehydrogenase, characteristic of primary biliary cirrhosis. Anti-centromere antibodies were mainly anti-CENP-B. ELISAs for extractable nuclear antigens and the assays for dsDNA were negative. The distinctive autoantibody profile detected in BC sera is the expression of tumor immunogenicity. Although some of these features resemble those in the rheumatic autoimmune diseases and primary biliary cirrhosis, the data suggest the involvement of an entirely different set of epithelial antigens in breast cancer. High titer autoantibodies targeting centrosomes, centromeres, and mitochondria were detected in a small group of healthy women with suspicious mammography assessment and no cancer by biopsy; this suggests that the process triggering autoantibody formation starts in the pre-malignant phase and that future studies using validated autoantibody panels may allow detection of breast cancer risk in asymptomatic women. Autoantibodies developing in breast cancer are not epiphenomena, but likely reflect an antigen-driven autoimmune response triggered by epitopes developing in the mammary gland during breast carcinogenesis. Our results support the validity of the multiple studies reporting association of autoantibodies with breast cancer. Results further suggest significant promise for the development of panels of breast cancer-specific, premalignant-phase autoantibodies, as well as studies on the autoantibody response to tumor associated antigens in the pathogenesis of cancer. JF - BMC cancer AU - Madrid, Félix Fernández AU - Maroun, Marie-Claire AU - Olivero, Ofelia A AU - Long, Michael AU - Stark, Azadeh AU - Grossman, Lawrence I AU - Binder, Walter AU - Dong, Jingsheng AU - Burke, Matthew AU - Nathanson, S David AU - Zarbo, Richard AU - Chitale, Dhananjay AU - Zeballos-Chávez, Rocío AU - Peebles, Carol AD - Department of Internal Medicine- Division of Rheumatology, Wayne State University School of Medicine, 640 Canfield, Detroit, MI, 48201, USA. fmadrid@med.wayne.edu. ; Department of Internal Medicine- Division of Rheumatology, Wayne State University School of Medicine, 640 Canfield, Detroit, MI, 48201, USA. mmaroun@med.wayne.edu. ; National Cancer Institute, NIH, Laboratory of Cancer Biology and Genetics, 37 Convent Dr. MSC 4255, Bldg 37 Rm 4032, Bethesda, MD, 20892-4255, USA. oliveroo@exchange.nih.gov. ; Department of Pathology, Children's Hospital of Michigan, Wayne State School of Medicine, Detroit, MI, 48201, USA. plong@med.wayne.edu. ; Department of Pathology, Henry Ford Health System, Detroit, MI, 48202, USA. ASTARK1@hfhs.org. ; Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, 540 East Canfield, Detroit, MI, 48201, USA. lgrossman@wayne.edu. ; INOVA Diagnostics Inc, 9900 Old Grove Rd, San Diego, CA, 92131, USA. cpeebles@sd.inovadx.com. ; Department of Internal Medicine- Division of Rheumatology, Wayne State University School of Medicine, 640 Canfield, Detroit, MI, 48201, USA. jinsheng3@gmail.com. ; Department of Diagnostic Radiology, Henry Ford Hospital and Health Network, 2799 West Grand Blvd, Detroit, MI, 48202, USA. MBurke1@hfhs.org. ; Department of Surgery, Henry Ford Health System, 2799 West Grand Boulevard, Detroit, MI, 48202, USA. Dnathan1@hfhs.org. ; Department of Pathology and Laboratory Medicine, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI, 48202, USA. rzarbo1@hfhs.org. ; Department of Pathology and Laboratory Medicine, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI, 48202, USA. dchital1@hfhs.org. ; Department of Pediatrics, Children's Hospital of Michigan, Wayne State School of Medicine, Detroit, MI, USA. plong@med.wayne.edu. Y1 - 2015/05/15/ PY - 2015 DA - 2015 May 15 SP - 407 VL - 15 KW - Antibodies, Antinuclear KW - 0 KW - Antigens, Nuclear KW - Centromere Protein B KW - Immunoglobulin G KW - Index Medicus KW - Centromere -- immunology KW - Humans KW - Breast Diseases -- immunology KW - Centrosome -- immunology KW - Aged KW - Centromere Protein B -- immunology KW - Aged, 80 and over KW - Mitochondria -- immunology KW - Adult KW - Cell Nucleolus -- immunology KW - Middle Aged KW - Female KW - Immunoglobulin G -- blood KW - Breast Neoplasms -- immunology KW - Carcinogenesis -- immunology KW - Antibodies, Antinuclear -- blood KW - Carcinoma in Situ -- immunology KW - Carcinoma, Ductal, Breast -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1686070059?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+cancer&rft.atitle=Autoantibodies+in+breast+cancer+sera+are+not+epiphenomena+and+may+participate+in+carcinogenesis.&rft.au=Madrid%2C+F%C3%A9lix+Fern%C3%A1ndez%3BMaroun%2C+Marie-Claire%3BOlivero%2C+Ofelia+A%3BLong%2C+Michael%3BStark%2C+Azadeh%3BGrossman%2C+Lawrence+I%3BBinder%2C+Walter%3BDong%2C+Jingsheng%3BBurke%2C+Matthew%3BNathanson%2C+S+David%3BZarbo%2C+Richard%3BChitale%2C+Dhananjay%3BZeballos-Ch%C3%A1vez%2C+Roc%C3%ADo%3BPeebles%2C+Carol&rft.aulast=Madrid&rft.aufirst=F%C3%A9lix&rft.date=2015-05-15&rft.volume=15&rft.issue=&rft.spage=407&rft.isbn=&rft.btitle=&rft.title=BMC+cancer&rft.issn=1471-2407&rft_id=info:doi/10.1186%2Fs12885-015-1385-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-01 N1 - Date created - 2015-06-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1995 Dec 5;92(25):11810-3 [8524854] Cancer Res. 1996 Jan 1;56(1):121-6 [8548751] Semin Liver Dis. 1997 Feb;17(1):71-8 [9089912] Arthritis Rheum. 1997 Sep;40(9):1601-11 [9324014] AJR Am J Roentgenol. 2000 Jun;174(6):1769-77 [10845521] J Clin Invest. 2001 Nov;108(10):1411-5 [11714730] Clin Cancer Res. 2002 Mar;8(3):752-8 [11895905] J Immunol. 2002 Sep 1;169(5):2701-11 [12193744] Nat Immunol. 2002 Nov;3(11):991-8 [12407406] Nat Rev Cancer. 2002 Nov;2(11):815-25 [12415252] Nature. 2003 Mar 13;422(6928):226-32 [12634796] Cancer Res. 2003 Mar 15;63(6):1398-404 [12649205] N Engl J Med. 2003 Oct 16;349(16):1526-33 [14561795] Cancer Immunol Immunother. 2003 Dec;52(12):715-38 [12920480] Clin Cancer Res. 2003 Nov 1;9(14):5120-6 [14613989] J Rheumatol. 2004 Mar;31(3):419-21 [14994382] Nat Med. 2004 Aug;10(8):789-99 [15286780] Cancer Res. 2004 Aug 1;64(15):5089-96 [15289310] J Immunol. 1971 Nov;107(5):1281-90 [4330162] Am J Med. 1972 Feb;52(2):148-59 [4621694] Ann N Y Acad Sci. 1975 Jun 30;254:505-15 [52321] Clin Exp Immunol. 1975 Mar;19(3):417-22 [1081928] Proc Natl Acad Sci U S A. 1979 Sep;76(9):4350-4 [388439] J Immunol. 1987 May 15;138(10):3525-31 [3571977] Adv Immunol. 1989;44:93-151 [2646863] J Cell Biol. 1990 Dec;111(6 Pt 2):2839-50 [2176652] Semin Arthritis Rheum. 1995 Apr;24(5):323-58 [7604300] J Clin Invest. 1998 Jan 1;101(1):273-81 [9421490] J Biol Chem. 1999 Jan 29;274(5):2938-52 [9915832] Cancer Res. 1999 Feb 15;59(4):831-42 [10029072] Immunol Lett. 1999 Feb;65(3):143-51 [10065736] Biochim Biophys Acta. 1999 May 31;1454(1):126-31 [10354522] Clin Cancer Res. 1999 Jun;5(6):1393-400 [10389924] Lancet. 1965 Apr 17;1(7390):827-31 [14263538] Cancer Detect Prev. 2005;29(1):59-65 [15734219] Cancer Cell. 2005 May;7(5):411-23 [15894262] Cancer Lett. 2005 Dec 18;230(2):187-98 [16297705] Ann Oncol. 2007 May;18(5):868-73 [17347129] Cell. 2007 Jul 13;130(1):25-35 [17632054] Nature. 2008 Jul 24;454(7203):436-44 [18650914] Future Oncol. 2010 Mar;6(3):471-7 [20222802] Autoimmun Rev. 2011 Feb;10(4):194-200 [20933614] Arthritis Res Ther. 2011;13(2):R38 [21366908] Arthritis Res Ther. 2011;13(2):109 [21554754] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/s12885-015-1385-8 ER - TY - JOUR T1 - Tumor-infiltrating lymphocytes genetically engineered with an inducible gene encoding interleukin-12 for the immunotherapy of metastatic melanoma. AN - 1681911760; 25695689 AB - Infusion of interleukin-12 (IL12) can mediate antitumor immunity in animal models, yet its systemic administration to patients with cancer results in minimal efficacy and severe toxicity. Here, we evaluated the antitumor activity of adoptively transferred human tumor-infiltrating lymphocytes (TILs) genetically engineered to secrete single-chain IL12 selectively at the tumor site. Thirty-three patients with metastatic melanoma were treated in a cell dose-escalation trial of autologous TILs transduced with a gene encoding a single-chain IL12 driven by a nuclear factor of the activated T cells promoter (NFAT.IL12). No IL2 was administered. The administration of 0.001 to 0.1 × 10(9) NFAT.IL12-transduced TILs to 17 patients resulted in a single, objective response (5.9%). However, at doses between 0.3 and 3 × 10(9) cells, 10 of 16 patients (63%) exhibited objective clinical responses. The responses tended to be short, and the administered IL12-producing cells rarely persisted at 1 month. Increasing cell doses were associated with high serum levels of IL12 and IFNγ as well as clinical toxicities, including liver dysfunction, high fevers, and sporadic life-threatening hemodynamic instability. In this first-in-man trial, administration of TILs transduced with an inducible IL12 gene mediated tumor responses in the absence of IL2 administration using cell doses 10- to 100-fold lower than conventional TILs. However, due to toxicities, likely attributable to the secreted IL12, further refinement will be necessary before this approach can be safely used in the treatment of cancer patients. ©2015 American Association for Cancer Research. JF - Clinical cancer research : an official journal of the American Association for Cancer Research AU - Zhang, Ling AU - Morgan, Richard A AU - Beane, Joal D AU - Zheng, Zhili AU - Dudley, Mark E AU - Kassim, Sadik H AU - Nahvi, Azam V AU - Ngo, Lien T AU - Sherry, Richard M AU - Phan, Giao Q AU - Hughes, Marybeth S AU - Kammula, Udai S AU - Feldman, Steven A AU - Toomey, Mary Ann AU - Kerkar, Sid P AU - Restifo, Nicholas P AU - Yang, James C AU - Rosenberg, Steven A AD - Surgery Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. ; Surgery Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. sar@mail.nih.gov. Y1 - 2015/05/15/ PY - 2015 DA - 2015 May 15 SP - 2278 EP - 2288 VL - 21 IS - 10 SN - 1078-0432, 1078-0432 KW - Interleukin-12 KW - 187348-17-0 KW - Index Medicus KW - Young Adult KW - Genetic Engineering KW - Cells, Cultured KW - Immunotherapy KW - Humans KW - Adult KW - Treatment Outcome KW - Aged KW - Middle Aged KW - Transcriptional Activation KW - Male KW - Female KW - Lymphocytes, Tumor-Infiltrating -- physiology KW - Skin Neoplasms -- immunology KW - Interleukin-12 -- biosynthesis KW - Melanoma -- secondary KW - Skin Neoplasms -- therapy KW - Skin Neoplasms -- pathology KW - Melanoma -- therapy KW - Melanoma -- immunology KW - Interleukin-12 -- genetics KW - Lymphocytes, Tumor-Infiltrating -- transplantation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1681911760?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.atitle=Tumor-infiltrating+lymphocytes+genetically+engineered+with+an+inducible+gene+encoding+interleukin-12+for+the+immunotherapy+of+metastatic+melanoma.&rft.au=Zhang%2C+Ling%3BMorgan%2C+Richard+A%3BBeane%2C+Joal+D%3BZheng%2C+Zhili%3BDudley%2C+Mark+E%3BKassim%2C+Sadik+H%3BNahvi%2C+Azam+V%3BNgo%2C+Lien+T%3BSherry%2C+Richard+M%3BPhan%2C+Giao+Q%3BHughes%2C+Marybeth+S%3BKammula%2C+Udai+S%3BFeldman%2C+Steven+A%3BToomey%2C+Mary+Ann%3BKerkar%2C+Sid+P%3BRestifo%2C+Nicholas+P%3BYang%2C+James+C%3BRosenberg%2C+Steven+A&rft.aulast=Zhang&rft.aufirst=Ling&rft.date=2015-05-15&rft.volume=21&rft.issue=10&rft.spage=2278&rft.isbn=&rft.btitle=&rft.title=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-14-2085 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-19 N1 - Date created - 2015-05-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Science. 2002 Oct 25;298(5594):850-4 [12242449] Science. 2006 Oct 6;314(5796):126-9 [16946036] J Exp Med. 1993 Oct 1;178(4):1223-30 [8104230] J Immunol. 1994 Feb 1;152(3):1253-64 [7905500] J Immunol. 1996 Apr 15;156(8):2776-82 [8609396] Hum Gene Ther. 1997 Jun 10;8(9):1125-35 [9189770] Clin Cancer Res. 2006 Oct 15;12(20 Pt 1):6056-63 [17062681] Proc Natl Acad Sci U S A. 2010 Aug 17;107(33):14733-8 [20679213] Cancer Res. 2010 Sep 1;70(17):6725-34 [20647327] J Exp Med. 2010 Sep 27;207(10):2175-86 [20819923] Blood. 2010 Nov 18;116(20):4099-102 [20668228] J Clin Oncol. 2011 Mar 1;29(7):917-24 [21282551] Mol Ther. 2011 Apr;19(4):751-9 [21285960] Blood. 2011 Apr 28;117(17):4501-10 [21385853] Clin Cancer Res. 2011 Jul 1;17(13):4550-7 [21498393] N Engl J Med. 2011 Aug 25;365(8):725-33 [21830940] J Clin Invest. 2011 Dec;121(12):4746-57 [22056381] Clin Cancer Res. 2012 Mar 15;18(6):1672-83 [22291136] J Clin Invest. 2012 Apr;122(4):1271-82 [22426209] Mol Ther. 2012 May;20(5):927-37 [22334018] Blood. 2012 May 3;119(18):4133-41 [22354001] J Immunother. 2012 Jun;35(5):430-9 [22576348] Blood. 2012 Jun 14;119(24):5688-96 [22555974] Nat Immunol. 2012 Aug;13(8):722-8 [22814351] Cancer Gene Ther. 2004 Feb;11(2):81-91 [14685154] Blood. 1997 Oct 1;90(7):2541-8 [9326219] J Immunol. 2004 Dec 15;173(12):7125-30 [15585832] J Clin Oncol. 2013 Jun 10;31(17):2152-9 [23650429] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1078-0432.CCR-14-2085 ER - TY - JOUR T1 - Nonalcoholic Steatohepatitis and Hepatic Fibrosis in HIV-1-Monoinfected Adults With Elevated Aminotransferase Levels on Antiretroviral Therapy. AN - 1677378693; 25681381 AB - Persistent aminotransferase elevations are common in human immunodeficiency virus (HIV)-infected patients on antiretroviral therapy (ART), including those without hepatitis B or C coinfection, but their clinical significance is unknown. HIV-infected adults with aminotransferase levels elevated above the upper limit of normal for ≥6 months while receiving ART, and without chronic viral hepatitis or other known causes of chronic liver disease, underwent a detailed metabolic assessment and liver biopsy. Sixty-two HIV-infected subjects completed the study. Forty (65%) had clinically significant liver pathology, including 34 (55%) with nonalcoholic steatohepatitis (NASH) and 11 (18%) with bridging fibrosis, 10 of whom also had NASH. Nonspecific abnormalities alone were seen in 22 (35%) subjects, including mild steatosis, mild to moderate inflammation, and evidence of drug adaptation. Insulin resistance, obesity, and the presence of either of 2 minor alleles in the PNPLA3 gene were significantly associated with increased risk of NASH and fibrosis. NASH and/or fibrosis were not associated with duration of HIV infection or ART, specific antiretroviral drugs, history of opportunistic infection, immune status, or duration of aminotransferase elevation. HIV-infected adults with chronic aminotransferase elevations while receiving ART have a high rate of liver disease. Noninvasive testing can help identify liver disease in such patients, but liver biopsy is necessary to definitively identify those at risk for liver disease progression and complications. Longitudinal follow-up of this cohort will better characterize the natural history of aminotransferase elevations in this population and identify noninvasive biomarkers of liver disease progression. Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2015. This work is written by (a) US Government employee(s) and is in the public domain in the US. JF - Clinical infectious diseases : an official publication of the Infectious Diseases Society of America AU - Morse, Caryn G AU - McLaughlin, Mary AU - Matthews, Lindsay AU - Proschan, Michael AU - Thomas, Francine AU - Gharib, Ahmed M AU - Abu-Asab, Mones AU - Orenstein, Abigail AU - Engle, Ronald E AU - Hu, Xiaojun AU - Lempicki, Richard AU - Hadigan, Colleen AU - Kleiner, David E AU - Heller, Theo AU - Kovacs, Joseph A AD - Critical Care Medicine Department, AIDS Section, National Institutes of Health (NIH) Clinical Center. ; Laboratory of Immunoregulation. ; Biostatistics Research Branch, National Institute of Allergy and Infectious Diseases (NIAID). ; Diagnostic Radiology, NIH Clinical Center. ; Biomedical and Metabolic Imaging Branch, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). ; Histology Core, National Eye Institute, Bethesda, Maryland. ; Baystate Medical Center, Springfield, Massachusetts. ; Laboratory of Infectious Disease, NIAID, Bethesda. ; Leidos Biomedical Research, Inc, Frederick. ; Laboratory of Pathology, National Cancer Institute. ; Liver Diseases Branch, NIDDK, Bethesda, Maryland. Y1 - 2015/05/15/ PY - 2015 DA - 2015 May 15 SP - 1569 EP - 1578 VL - 60 IS - 10 KW - Anti-Retroviral Agents KW - 0 KW - Transaminases KW - EC 2.6.1.- KW - Index Medicus KW - liver biopsy KW - insulin resistance KW - PNPLA3 KW - hepatotoxicity KW - Young Adult KW - Liver -- pathology KW - Blood Chemical Analysis KW - Humans KW - Cohort Studies KW - Adult KW - Aged KW - Middle Aged KW - Biopsy KW - Histocytochemistry KW - Adolescent KW - Male KW - Female KW - Prevalence KW - Transaminases -- blood KW - HIV Infections -- complications KW - HIV Infections -- drug therapy KW - Antiretroviral Therapy, Highly Active KW - Non-alcoholic Fatty Liver Disease -- epidemiology KW - Liver Cirrhosis -- epidemiology KW - Anti-Retroviral Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1677378693?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+infectious+diseases+%3A+an+official+publication+of+the+Infectious+Diseases+Society+of+America&rft.atitle=Nonalcoholic+Steatohepatitis+and+Hepatic+Fibrosis+in+HIV-1-Monoinfected+Adults+With+Elevated+Aminotransferase+Levels+on+Antiretroviral+Therapy.&rft.au=Morse%2C+Caryn+G%3BMcLaughlin%2C+Mary%3BMatthews%2C+Lindsay%3BProschan%2C+Michael%3BThomas%2C+Francine%3BGharib%2C+Ahmed+M%3BAbu-Asab%2C+Mones%3BOrenstein%2C+Abigail%3BEngle%2C+Ronald+E%3BHu%2C+Xiaojun%3BLempicki%2C+Richard%3BHadigan%2C+Colleen%3BKleiner%2C+David+E%3BHeller%2C+Theo%3BKovacs%2C+Joseph+A&rft.aulast=Morse&rft.aufirst=Caryn&rft.date=2015-05-15&rft.volume=60&rft.issue=10&rft.spage=1569&rft.isbn=&rft.btitle=&rft.title=Clinical+infectious+diseases+%3A+an+official+publication+of+the+Infectious+Diseases+Society+of+America&rft.issn=1537-6591&rft_id=info:doi/10.1093%2Fcid%2Fciv101 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-20 N1 - Date created - 2015-04-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Diabetes Care. 2002 Aug;25(8):1371-7 [12145237] Am J Hum Genet. 2008 Oct;83(4):520-8 [18940312] Hepatology. 2003 Aug;38(2):518-26 [12883497] Diabetologia. 1985 Jul;28(7):412-9 [3899825] Hepatology. 2010 Sep;52(3):894-903 [20684021] JAMA. 2000 Jan 5;283(1):74-80 [10632283] Hepatology. 2010 Sep;52(3):1143-55 [20812358] Proc Natl Acad Sci U S A. 2011 Feb 8;108(6):2438-43 [21262830] Antivir Ther. 2011;16(3):405-11 [21555823] Hepatology. 2011 Oct;54(4):1208-16 [21688282] J Hepatol. 2012 Jun;56(6):1384-91 [22326465] Hepatology. 2012 Jun;55(6):2005-23 [22488764] Nature. 2012 Nov 1;491(7422):56-65 [23128226] J Clin Gastroenterol. 2013 Feb;47(2):182-7 [23059409] Clin Infect Dis. 2013 Mar;56(6):870-9 [23090925] Am J Gastroenterol. 2014 May;109(5):695-704 [24642579] Hepatology. 2014 Jun;59(6):2170-7 [24114809] Am J Physiol Gastrointest Liver Physiol. 2014 Jul 1;307(1):G66-76 [24763554] J Hepatol. 1995 Jun;22(6):696-9 [7560864] J Hepatol. 1997 Jul;27(1):108-13 [9252082] Am J Gastroenterol. 1999 Oct;94(10):3010-4 [10520861] Hepatology. 2005 Jun;41(6):1313-21 [15915461] Hepatology. 2009 Feb;49(2):436-42 [19085967] J Acquir Immune Defic Syndr. 2009 Apr 15;50(5):464-73 [19225402] Clin Infect Dis. 2009 Aug 15;49(4):626-35 [19589079] Clin Gastroenterol Hepatol. 2010 Feb;8(2):183-91 [19800985] Hepatology. 2010 Aug;52(2):612-22 [20683959] J Clin Microbiol. 2002 Dec;40(12):4576-80 [12454155] Gastroenterology. 2005 Jul;129(1):113-21 [16012941] Hepatology. 2006 Jun;43(6):1317-25 [16729309] JAMA. 2006 Aug 16;296(7):844-54 [16905789] Arch Intern Med. 2006 Aug 14-28;166(15):1632-41 [16908797] J Hepatol. 2006 Oct;45(4):592-9 [16837098] Diabetes Care. 2007 Mar;30(3):753-9 [17327355] Hepatology. 2007 Apr;45(4):846-54 [17393509] Am J Hum Genet. 2007 Sep;81(3):559-75 [17701901] Atherosclerosis. 2008 Feb;196(2):696-703 [17254586] Dig Dis Sci. 2008 May;53(5):1375-82 [17939038] Clin Infect Dis. 2008 Jul 15;47(2):250-7 [18532884] Comment In: Clin Infect Dis. 2015 May 15;60(10):1579-81 [25681377] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/cid/civ101 ER - TY - JOUR T1 - ABC transporter-driven pharmacoresistance in Amyotrophic Lateral Sclerosis. AN - 1681501204; 25175835 AB - Amyotrophic Lateral Sclerosis (ALS) is a slowly progressing neurodegenerative disease that affects motor neurons of the nervous system. Despite the identification of many potential therapeutics targeting pathogenic mechanisms in in vitro models, there has been limited progress in translating them into a successful pharmacotherapy in the animal model of ALS. Further, efforts to translate any promising results from preclinical trials to effective pharmacotherapies for patients have been unsuccessful, with the exception of riluzole, the only FDA-approved medication, which only modestly extends survival both in the animal model and in patients. Thus, it is essential to reconsider the strategies for developing ALS pharmacotherapies. Growing evidence suggests that problems identifying highly effective ALS treatments may result from an underestimated issue of drug bioavailability and disease-driven pharmacoresistance, mediated by the ATP-binding cassette (ABC) drug efflux transporters. ABC transporters are predominately localized to the lumen of endothelial cells of the blood-brain and blood-spinal cord barriers (BBB, BSCB) where they limit the entry into the central nervous system (CNS) of a wide range of neurotoxicants and xenobiotics, but also therapeutics. In ALS, expression and function of ABC transporters is increased at the BBB/BSCB and their expression has been detected on neurons and glia in the CNS parenchyma, which may further reduce therapeutic action in target cells. Understanding and accounting for the contribution of these transporters to ALS pharmacoresistance could both improve the modest effects of riluzole and set in motion a re-evaluation of previous ALS drug disappointments. In addition, identifying pathogenic mechanisms regulating ABC transporter expression and function in ALS may lead to the development of new therapeutic strategies. It is likely that novel pharmacological approaches require counteracting pharmacoresistance to improve therapeutic efficacy. This article is part of a Special Issue entitled ALS complex pathogenesis. Copyright © 2014 Elsevier B.V. All rights reserved. JF - Brain research AU - Jablonski, Michael AU - Miller, David S AU - Pasinelli, Piera AU - Trotti, Davide AD - Weinberg Unit for ALS Research, Farber Institute for Neurosciences, Department of Neuroscience, Thomas Jefferson University, 900 Walnut Street, Philadelphia, PA 19004, USA. Electronic address: Michael.jablonski@jefferson.edu. ; Laboratory of Toxicology and Pharmacology, NIH/NIEHS, Research Triangle Park, NC 27709, USA. ; Weinberg Unit for ALS Research, Farber Institute for Neurosciences, Department of Neuroscience, Thomas Jefferson University, 900 Walnut Street, Philadelphia, PA 19004, USA. ; Weinberg Unit for ALS Research, Farber Institute for Neurosciences, Department of Neuroscience, Thomas Jefferson University, 900 Walnut Street, Philadelphia, PA 19004, USA. Electronic address: davide.trotti@jefferson.edu. Y1 - 2015/05/14/ PY - 2015 DA - 2015 May 14 SP - 1 EP - 14 VL - 1607 KW - Index Medicus KW - Amyotrophic Lateral Sclerosis KW - Drug efflux transporters KW - Neurodegeneration KW - Blood–brain barrier KW - Pharmacoresistance KW - Animals KW - Humans KW - Drug Resistance -- physiology KW - Amyotrophic Lateral Sclerosis -- metabolism KW - ATP-Binding Cassette Transporters -- metabolism KW - Amyotrophic Lateral Sclerosis -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1681501204?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+research&rft.atitle=ABC+transporter-driven+pharmacoresistance+in+Amyotrophic+Lateral+Sclerosis.&rft.au=Jablonski%2C+Michael%3BMiller%2C+David+S%3BPasinelli%2C+Piera%3BTrotti%2C+Davide&rft.aulast=Jablonski&rft.aufirst=Michael&rft.date=2015-05-14&rft.volume=1607&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Brain+research&rft.issn=1872-6240&rft_id=info:doi/10.1016%2Fj.brainres.2014.08.060 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-14 N1 - Date created - 2015-04-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Neurosci. 2009 Apr 29;29(17):5463-75 [19403814] Neurobiol Aging. 2009 Nov;30(11):1818-24 [18358568] Neurosci Lett. 2010 Mar 26;472(3):166-70 [20138122] Adv Drug Deliv Rev. 2012 Jul;64(10):943-52 [22210135] Acta Neuropathol. 2012 Sep;124(3):339-52 [22903397] Lancet Neurol. 2010 May;9(5):481-8 [20363190] Mol Pharmacol. 2010 May;77(5):715-23 [20101004] Behav Brain Res. 2010 Nov 12;213(1):82-7 [20450936] J Neuropathol Exp Neurol. 2004 Oct;63(10):1038-47 [15535131] Nat Rev Neurosci. 2005 Aug;6(8):591-602 [16025095] J Clin Invest. 2005 Nov;115(11):3285-90 [16239972] Mol Pharmacol. 2006 Feb;69(2):462-70 [16278373] Neuroscience. 2006;138(1):159-69 [16361063] J Histochem Cytochem. 2006 Oct;54(10):1159-67 [16801529] Mol Pharmacol. 2006 Oct;70(4):1212-9 [16837625] Neurobiol Dis. 2006 Oct;24(1):202-11 [16928449] Science. 2006 Oct 6;314(5796):130-3 [17023659] Mol Pharmacol. 2007 Mar;71(3):667-75 [17132686] Neurobiol Dis. 2007 Apr;26(1):1-13 [17300945] Amyotroph Lateral Scler. 2007 Aug;8(4):217-23 [17653919] J Neurochem. 2007 Oct;103(1):164-73 [17635670] Proc Natl Acad Sci U S A. 2008 Feb 12;105(6):2052-7 [18250315] Mol Pharmacol. 2008 May;73(5):1444-53 [18094072] Neuropharmacology. 2008 May;54(6):1006-16 [18394657] Prog Neurobiol. 2008 May;85(1):94-134 [18282652] Exp Neurol. 2008 Sep;213(1):229-37 [18625223] Trends Pharmacol Sci. 2010 Jun;31(6):246-54 [20417575] Neuron. 2010 Dec 9;68(5):857-64 [21145000] Nat Rev Neurosci. 2011 Mar;12(3):169-82 [21331083] Mediators Inflamm. 2011;2011:670613 [21403895] Curr Pharm Biotechnol. 2011 Apr;12(4):656-73 [21118088] Brain Res. 2011 Jun 29;1398:113-25 [21632035] J Neurochem. 2011 Jul;118(2):163-75 [21517853] Nature. 2011 Sep 8;477(7363):211-5 [21857683] Neuron. 2011 Oct 20;72(2):245-56 [21944778] Neuron. 2011 Oct 20;72(2):257-68 [21944779] Nat Rev Neurol. 2011 Nov;7(11):616-30 [22051914] Acta Myol. 2011 Oct;30(2):117-20 [22106714] Curr Pharm Des. 2011;17(26):2793-802 [21827403] Clin Pharmacol Ther. 2012 Feb;91(2):227-33 [22166851] Brain. 2012 Jan;135(Pt 1):181-9 [22120145] Cochrane Database Syst Rev. 2012;3:CD001447 [22419278] Mol Pharmacol. 2012 Apr;81(4):598-609 [22266374] Drug Resist Updat. 2012 Feb-Apr;15(1-2):62-9 [22409994] Neurobiol Dis. 2012 Aug;47(2):194-200 [22521463] PLoS One. 2012;7(6):e37885 [22715372] CNS Neurosci Ther. 2012 Sep;18(9):791-3 [22712693] Proc Natl Acad Sci U S A. 2012 Sep 25;109(39):15930-5 [22949658] Nature. 2012 Oct 11;490(7419):187-91 [23060188] Mol Imaging Biol. 2012 Dec;14(6):771-6 [22476967] Brain Res. 2013 Jan 23;1491:1-13 [23123212] J Neurotrauma. 2013 Feb 1;30(3):211-26 [22947335] J Cereb Blood Flow Metab. 2013 Mar;33(3):381-8 [23168528] Neuroreport. 2002 Nov 15;13(16):2059-63 [12438926] Ann Neurol. 2003 Feb;53(2):267-70 [12557297] Biochem Pharmacol. 2003 Aug 15;66(4):579-87 [12906922] J Neurochem. 2004 Feb;88(4):821-6 [14756802] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):3178-83 [14981234] Mol Pharmacol. 2004 Sep;66(3):387-94 [15322229] J Pharmacol Exp Ther. 2004 Nov;311(2):449-55 [15218051] Neuroscience. 2004;129(2):349-60 [15501592] Cancer Res. 1989 Dec 15;49(24 Pt 1):6901-5 [2582432] Nature. 1993 Mar 4;362(6415):59-62 [8446170] J Neurochem. 1997 Mar;68(3):1278-85 [9048775] Brain. 2008 Oct;131(Pt 10):2679-89 [18796513] Cell Tissue Res. 2008 Nov;334(2):179-85 [18855017] Neurosci Lett. 2009 Mar 6;452(1):12-6 [19146924] Science. 2009 Feb 27;323(5918):1205-8 [19251627] Science. 2009 Feb 27;323(5918):1208-11 [19251628] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.brainres.2014.08.060 ER - TY - JOUR T1 - Discovery of potent indenoisoquinoline topoisomerase I poisons lacking the 3-nitro toxicophore. AN - 1681261851; 25909279 AB - 3-Nitroindenoisoquinoline human topoisomerase IB (Top1) poisons have potent antiproliferative effects on cancer cells. The undesirable nitro toxicophore could hypothetically be replaced by other functional groups that would retain the desired biological activities and minimize potential safety risks. Eleven series of indenoisoquinolines bearing 3-nitro bioisosteres were synthesized. The molecules were evaluated in the Top1-mediated DNA cleavage assay and in the National Cancer Institute's 60 cell line cytotoxicity assay. The data reveal that fluorine and chlorine may substitute for the 3-nitro group with minimal loss of Top1 poisoning activity. The new information gained from these efforts can be used to design novel indenoisoquinolines with improved safety. JF - Journal of medicinal chemistry AU - Beck, Daniel E AU - Abdelmalak, Monica AU - Lv, Wei AU - Reddy, P V Narasimha AU - Tender, Gabrielle S AU - O'Neill, Elizaveta AU - Agama, Keli AU - Marchand, Christophe AU - Pommier, Yves AU - Cushman, Mark AD - †Department of Medicinal Chemistry and Molecular Pharmacology, College of Pharmacy, and the Purdue Center for Cancer Research, Purdue University, 575 Stadium Mall Drive, West Lafayette, Indiana 47907, United States. ; ‡Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, NCI-Frederick, Frederick, Maryland 21702, United States. Y1 - 2015/05/14/ PY - 2015 DA - 2015 May 14 SP - 3997 EP - 4015 VL - 58 IS - 9 KW - Antineoplastic Agents KW - 0 KW - Indenes KW - Isoquinolines KW - Topoisomerase I Inhibitors KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Quantum Theory KW - Drug Screening Assays, Antitumor KW - Stereoisomerism KW - Thermodynamics KW - Humans KW - DNA -- metabolism KW - Crystallography, X-Ray KW - Cell Line, Tumor KW - Molecular Conformation KW - Protein Binding KW - Hydrogen Bonding KW - Structure-Activity Relationship KW - Topoisomerase I Inhibitors -- pharmacology KW - Indenes -- chemical synthesis KW - Isoquinolines -- pharmacology KW - Isoquinolines -- chemistry KW - Indenes -- pharmacology KW - Topoisomerase I Inhibitors -- chemistry KW - Antineoplastic Agents -- chemical synthesis KW - Indenes -- chemistry KW - Isoquinolines -- chemical synthesis KW - Antineoplastic Agents -- chemistry KW - Antineoplastic Agents -- pharmacology KW - Topoisomerase I Inhibitors -- chemical synthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1681261851?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+medicinal+chemistry&rft.atitle=Discovery+of+potent+indenoisoquinoline+topoisomerase+I+poisons+lacking+the+3-nitro+toxicophore.&rft.au=Beck%2C+Daniel+E%3BAbdelmalak%2C+Monica%3BLv%2C+Wei%3BReddy%2C+P+V+Narasimha%3BTender%2C+Gabrielle+S%3BO%27Neill%2C+Elizaveta%3BAgama%2C+Keli%3BMarchand%2C+Christophe%3BPommier%2C+Yves%3BCushman%2C+Mark&rft.aulast=Beck&rft.aufirst=Daniel&rft.date=2015-05-14&rft.volume=58&rft.issue=9&rft.spage=3997&rft.isbn=&rft.btitle=&rft.title=Journal+of+medicinal+chemistry&rft.issn=1520-4804&rft_id=info:doi/10.1021%2Facs.jmedchem.5b00303 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-06 N1 - Date created - 2015-05-14 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/acs.jmedchem.5b00303 ER - TY - JOUR T1 - Occupational exposure to diesel engine exhaust and alterations in lymphocyte subsets AN - 1808716267; PQ0003429511 AB - BackgroundThe International Agency for Research on Cancer recently classified diesel engine exhaust (DEE) as a Group I carcinogen based largely on its association with lung cancer. However, the exposure-response relationship is still a subject of debate and the underlying mechanism by which DEE causes lung cancer in humans is not well understood.MethodsWe conducted a cross-sectional molecular epidemiology study in a diesel engine truck testing facility of 54 workers exposed to a wide range of DEE (ie, elemental carbon air levels, median range: 49.7, 6.1-107.7 mu g/m3) and 55 unexposed comparable controls.ResultsThe total lymphocyte count (p=0.00044) and three of the four major lymphocyte subsets (ie, CD4+ T cells (p=0.00019), CD8+ T cells (p=0.0058) and B cells (p=0.017)) were higher in exposed versus control workers and findings were highly consistent when stratified by smoking status. In addition, there was evidence of an exposure-response relationship between elemental carbon and these end points (ptrends<0.05), and CD4+ T cell levels were significantly higher in the lowest tertile of DEE exposed workers compared to controls (p=0.012).ConclusionsOur results suggest that DEE exposure is associated with higher levels of cells that play a key role in the inflammatory process, which is increasingly being recognised as contributing to the aetiology of lung cancer.ImpactThis study provides new insights into the underlying mechanism of DEE carcinogenicity. JF - Occupational and Environmental Medicine AU - Lan, Qing AU - Vermeulen, Roel AU - Dai, Yufei AU - Ren, Dianzhi AU - Hu, Wei AU - Duan, Huawei AU - Niu, Yong AU - Xu, Jun AU - Fu, Wei AU - Meliefste, Kees AU - Zhou, Baosen AU - Yang, Jufang AU - Ye, Meng AU - Jia, Xiaowei AU - Meng, Tao AU - Bin, Ping AU - Kim, Christopher AU - Bassig, Bryan A AU - Hosgood, H Dean AU - Silverman, Debra AU - Zheng, Yuxin AU - Rothman, Nathaniel AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA Y1 - 2015/05/11/ PY - 2015 DA - 2015 May 11 SP - 354 EP - 359 PB - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom VL - 72 IS - 5 SN - 1351-0711, 1351-0711 KW - Immunology Abstracts; Toxicology Abstracts; Health & Safety Science Abstracts KW - occupational exposure KW - toxicity KW - Diesel KW - lymphocyte subset KW - Lymphocytes KW - Carcinogens KW - Smoking KW - CD4 antigen KW - Carbon KW - Carcinogenicity KW - Dose-response effects KW - Lymphocytes T KW - Trucks KW - Occupational exposure KW - Lung cancer KW - Cell number KW - Lymphocytes B KW - CD8 antigen KW - Cancer KW - Inflammation KW - Exhausts KW - Epidemiology KW - Diesel engines KW - X 24380:Social Poisons & Drug Abuse KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808716267?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Occupational+and+Environmental+Medicine&rft.atitle=Occupational+exposure+to+diesel+engine+exhaust+and+alterations+in+lymphocyte+subsets&rft.au=Lan%2C+Qing%3BVermeulen%2C+Roel%3BDai%2C+Yufei%3BRen%2C+Dianzhi%3BHu%2C+Wei%3BDuan%2C+Huawei%3BNiu%2C+Yong%3BXu%2C+Jun%3BFu%2C+Wei%3BMeliefste%2C+Kees%3BZhou%2C+Baosen%3BYang%2C+Jufang%3BYe%2C+Meng%3BJia%2C+Xiaowei%3BMeng%2C+Tao%3BBin%2C+Ping%3BKim%2C+Christopher%3BBassig%2C+Bryan+A%3BHosgood%2C+H+Dean%3BSilverman%2C+Debra%3BZheng%2C+Yuxin%3BRothman%2C+Nathaniel&rft.aulast=Lan&rft.aufirst=Qing&rft.date=2015-05-11&rft.volume=72&rft.issue=5&rft.spage=354&rft.isbn=&rft.btitle=&rft.title=Occupational+and+Environmental+Medicine&rft.issn=13510711&rft_id=info:doi/10.1136%2Foemed-2014-102556 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-10-26 N1 - SubjectsTermNotLitGenreText - Cell number; Lymphocytes B; Carcinogens; CD8 antigen; Exhausts; Inflammation; Smoking; CD4 antigen; Carbon; Epidemiology; Carcinogenicity; Dose-response effects; Lymphocytes T; Diesel; Occupational exposure; Lung cancer; Trucks; Lymphocytes; Diesel engines; Cancer DO - http://dx.doi.org/10.1136/oemed-2014-102556 ER - TY - CPAPER T1 - Utilizing Nonhuman Primate SIV Models to Understand The Biology of Primary HIV Infection. T2 - 28th International Conference on Antiviral Research (ICAR 2015) AN - 1684405640; 6351291 JF - 28th International Conference on Antiviral Research (ICAR 2015) AU - Estes, Jacob Y1 - 2015/05/11/ PY - 2015 DA - 2015 May 11 KW - Human immunodeficiency virus KW - Animal models KW - Infection KW - Primates KW - Simian immunodeficiency virus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1684405640?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=28th+International+Conference+on+Antiviral+Research+%28ICAR+2015%29&rft.atitle=Utilizing+Nonhuman+Primate+SIV+Models+to+Understand+The+Biology+of+Primary+HIV+Infection.&rft.au=Estes%2C+Jacob&rft.aulast=Estes&rft.aufirst=Jacob&rft.date=2015-05-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=28th+International+Conference+on+Antiviral+Research+%28ICAR+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://c.ymcdn.com/sites/www.isar-icar.com/resource/resmgr/docs/isar_program2015web.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-29 N1 - Last updated - 2015-06-01 ER - TY - CPAPER T1 - Experimental Ther apies for Ebola Virus Infections: What Has Been Learned. T2 - 28th International Conference on Antiviral Research (ICAR 2015) AN - 1684403965; 6351319 JF - 28th International Conference on Antiviral Research (ICAR 2015) AU - Bray, Mike Y1 - 2015/05/11/ PY - 2015 DA - 2015 May 11 KW - Infection KW - Ebola virus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1684403965?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=28th+International+Conference+on+Antiviral+Research+%28ICAR+2015%29&rft.atitle=Experimental+Ther+apies+for+Ebola+Virus+Infections%3A+What+Has+Been+Learned.&rft.au=Bray%2C+Mike&rft.aulast=Bray&rft.aufirst=Mike&rft.date=2015-05-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=28th+International+Conference+on+Antiviral+Research+%28ICAR+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://c.ymcdn.com/sites/www.isar-icar.com/resource/resmgr/docs/isar_program2015web.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-29 N1 - Last updated - 2015-06-01 ER - TY - JOUR T1 - Generation of a conditionally self-eliminating HAC gene delivery vector through incorporation of a tTA super(VP64) expression cassette AN - 1712772982; PQ0001918154 AB - Human artificial chromosome (HAC)-based vectors represent an alternative technology for gene delivery and expression with a potential to overcome the problems caused by virus-based vectors. The recently developed alphoid super(tetO)-HAC has an advantage over other HAC vectors because it can be easily eliminated from cells by inactivation of the HAC kinetochore via binding of chromatin modifiers, tTA or tTS, to its centromeric tetO sequences. This provides a unique control for phenotypes induced by genes loaded into the HAC. The alphoid super(tetO)-HAC elimination is highly efficient when a high level of chromatin modifiers as tetR fusion proteins is achieved following transfection of cells by a retrovirus vector. However, such vectors are potentially mutagenic and might want to be avoided under some circumstances. Here, we describe a novel system that allows verification of phenotypic changes attributed to expression of genes from the HAC without a transfection step. We demonstrated that a single copy of tTA super(VP64) carrying four tandem repeats of the VP16 domain constitutively expressed from the HAC is capable to generate chromatin changes in the HAC kinetochore that are not compatible with its function. To adopt the alphoid super(tetO)-HAC for routine gene function studies, we constructed a new TAR-BRV- tTA super(VP64) cloning vector that allows a selective isolation of a gene of interest from genomic DNA in yeast followed by its direct transfer to bacterial cells and subsequent loading into the loxP site of the alphoid super(tetO)-HAC in hamster CHO cells from where the HAC may be MMCT-transferred to the recipient human cells. JF - Nucleic Acids Research AU - Kononenko, Artem V AU - Lee, Nicholas CO AU - Liskovykh, Mikhail AU - Masumoto, Hiroshi AU - Earnshaw, William C AU - Larionov, Vladimir AU - Kouprina, Natalay AD - To whom correspondence should be addressed. Tel: +1 301 496 7941; Fax: +1 301 480 2772, kouprinn@mail.nih.gov PY - 2015 SP - e57 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 43 IS - 9 SN - 0305-1048, 0305-1048 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - VP16 protein KW - Chromatin KW - Human artificial chromosomes KW - Cloning vectors KW - Expression vectors KW - Retrovirus KW - Kinetochores KW - Transfection KW - Gene transfer KW - DNA KW - genomics KW - Fusion protein KW - W 30905:Medical Applications KW - N 14820:DNA Metabolism & Structure KW - G 07770:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1712772982?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=Generation+of+a+conditionally+self-eliminating+HAC+gene+delivery+vector+through+incorporation+of+a+tTA+super%28VP64%29+expression+cassette&rft.au=Kononenko%2C+Artem+V%3BLee%2C+Nicholas+CO%3BLiskovykh%2C+Mikhail%3BMasumoto%2C+Hiroshi%3BEarnshaw%2C+William+C%3BLarionov%2C+Vladimir%3BKouprina%2C+Natalay&rft.aulast=Kononenko&rft.aufirst=Artem&rft.date=2015-05-09&rft.volume=43&rft.issue=9&rft.spage=e57&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/10.1093%2Fnar%2Fgkv124 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - VP16 protein; Expression vectors; Retrovirus; Chromatin; Gene transfer; Transfection; Kinetochores; Human artificial chromosomes; DNA; Cloning vectors; Fusion protein; genomics DO - http://dx.doi.org/10.1093/nar/gkv124 ER - TY - CPAPER T1 - The curative potential of T cell transfer immunotherapy for human cancer T2 - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AN - 1669824038; 6340128 JF - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AU - Rosenberg, Steven Y1 - 2015/05/08/ PY - 2015 DA - 2015 May 08 KW - Immunotherapy KW - Lymphocytes T KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669824038?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.atitle=The+curative+potential+of+T+cell+transfer+immunotherapy+for+human+cancer&rft.au=Rosenberg%2C+Steven&rft.aulast=Rosenberg&rft.aufirst=Steven&rft.date=2015-05-08&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://immunology2015.org/program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Opening/meeting interaction T2 - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AN - 1669824023; 6340259 JF - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AU - Ahmed, Mansoor Y1 - 2015/05/08/ PY - 2015 DA - 2015 May 08 KW - Epidemiology KW - Immunology KW - Microbiology KW - Medicine KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669824023?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.atitle=Opening%2Fmeeting+interaction&rft.au=Ahmed%2C+Mansoor&rft.aulast=Ahmed&rft.aufirst=Mansoor&rft.date=2015-05-08&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://immunology2015.org/program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - From mutualism to parasitism: context and consequences T2 - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AN - 1669823995; 6340129 JF - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AU - Belkaid, Yasmine Y1 - 2015/05/08/ PY - 2015 DA - 2015 May 08 KW - Symbiosis KW - Mutualism KW - Parasitism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823995?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.atitle=From+mutualism+to+parasitism%3A+context+and+consequences&rft.au=Belkaid%2C+Yasmine&rft.aulast=Belkaid&rft.aufirst=Yasmine&rft.date=2015-05-08&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://immunology2015.org/program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - A host-directed therapy for TB infection that targets innate cytokines T2 - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AN - 1669823834; 6340174 JF - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AU - Sher, Alan Y1 - 2015/05/08/ PY - 2015 DA - 2015 May 08 KW - Therapy KW - Cytokines KW - Infection UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823834?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.atitle=A+host-directed+therapy+for+TB+infection+that+targets+innate+cytokines&rft.au=Sher%2C+Alan&rft.aulast=Sher&rft.aufirst=Alan&rft.date=2015-05-08&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://immunology2015.org/program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Structure-guided development of an RSV vaccine T2 - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AN - 1669823622; 6340193 JF - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AU - Graham, Barney Y1 - 2015/05/08/ PY - 2015 DA - 2015 May 08 KW - Disease control KW - Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823622?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.atitle=Structure-guided+development+of+an+RSV+vaccine&rft.au=Graham%2C+Barney&rft.aulast=Graham&rft.aufirst=Barney&rft.date=2015-05-08&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://immunology2015.org/program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Recent trends in NIAID-funded, investigator-initiated immunology research T2 - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AN - 1669823362; 6340181 JF - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AU - Rotrosen, Daniel Y1 - 2015/05/08/ PY - 2015 DA - 2015 May 08 KW - Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823362?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.atitle=Recent+trends+in+NIAID-funded%2C+investigator-initiated+immunology+research&rft.au=Rotrosen%2C+Daniel&rft.aulast=Rotrosen&rft.aufirst=Daniel&rft.date=2015-05-08&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://immunology2015.org/program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Developing a quantitative spatiotemporal understanding of immunity using imaging and systems biology T2 - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AN - 1669823194; 6340173 JF - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AU - Germain, Ronald Y1 - 2015/05/08/ PY - 2015 DA - 2015 May 08 KW - Immunity KW - Imaging techniques UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823194?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.atitle=Developing+a+quantitative+spatiotemporal+understanding+of+immunity+using+imaging+and+systems+biology&rft.au=Germain%2C+Ronald&rft.aulast=Germain&rft.aufirst=Ronald&rft.date=2015-05-08&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://immunology2015.org/program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Negative signaling by NK cell inhibitory receptors T2 - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AN - 1669822118; 6340284 JF - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AU - Long, Eric Y1 - 2015/05/08/ PY - 2015 DA - 2015 May 08 KW - Natural killer cells UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669822118?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.atitle=Negative+signaling+by+NK+cell+inhibitory+receptors&rft.au=Long%2C+Eric&rft.aulast=Long&rft.aufirst=Eric&rft.date=2015-05-08&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://immunology2015.org/program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Omics platforms and systems biology in biomarker identification T2 - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AN - 1669821951; 6340271 JF - 2015 Annual Meeting of the American Association of Immunologists (IMMUNOLOGY 2015) AU - Trinchieri, Giorgio Y1 - 2015/05/08/ PY - 2015 DA - 2015 May 08 KW - Bioindicators KW - Biomarkers KW - biomarkers UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669821951?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.atitle=Omics+platforms+and+systems+biology+in+biomarker+identification&rft.au=Trinchieri%2C+Giorgio&rft.aulast=Trinchieri&rft.aufirst=Giorgio&rft.date=2015-05-08&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://immunology2015.org/program/index.html?loc=nav LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - JOUR T1 - Avoidable errors in the modelling of outbreaks of emerging pathogens, with special reference to Ebola AN - 1808707368; PQ0003429592 AB - As an emergent infectious disease outbreak unfolds, public health response is reliant on information on key epidemiological quantities, such as transmission potential and serial interval. Increasingly, transmission models fit to incidence data are used to estimate these parameters and guide policy. Some widely used modelling practices lead to potentially large errors in parameter estimates and, consequently, errors in model-based forecasts. Even more worryingly, in such situations, confidence in parameter estimates and forecasts can itself be far overestimated, leading to the potential for large errors that mask their own presence. Fortunately, straightforward and computationally inexpensive alternatives exist that avoid these problems. Here, we first use a simulation study to demonstrate potential pitfalls of the standard practice of fitting deterministic models to cumulative incidence data. Next, we demonstrate an alternative based on stochastic models fit to raw data from an early phase of 2014 West Africa Ebola virus disease outbreak. We show not only that bias is thereby reduced, but that uncertainty in estimates and forecasts is better quantified and that, critically, lack of model fit is more readily diagnosed. We conclude with a short list of principles to guide the modelling response to future infectious disease outbreaks. JF - Proceedings of the Royal Society of London, Series B: Biological Sciences AU - King, Aaron A AU - Domenech de Celles, Matthieu AU - Magpantay, Felicia MG AU - Rohani, Pejman AD - Fogarty International Center, National Institutes of Health, , Bethesda, MD 20892, USA, kingaa@umich.edu Y1 - 2015/05/07/ PY - 2015 DA - 2015 May 07 SP - 20150347 PB - Royal Society of London, 6 Carlton House Terrace London SW1Y 5AG United Kingdom VL - 282 IS - 1806 SN - 0962-8452, 0962-8452 KW - Virology & AIDS Abstracts; Ecology Abstracts KW - Ebola virus disease KW - forecast KW - emerging infectious disease KW - Data processing KW - Infectious diseases KW - Ebola virus KW - Pathogens KW - Stochasticity KW - Models KW - Disease transmission KW - Public health KW - D 04040:Ecosystem and Ecology Studies KW - V 22400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808707368?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+Royal+Society+of+London%2C+Series+B%3A+Biological+Sciences&rft.atitle=Avoidable+errors+in+the+modelling+of+outbreaks+of+emerging+pathogens%2C+with+special+reference+to+Ebola&rft.au=King%2C+Aaron+A%3BDomenech+de+Celles%2C+Matthieu%3BMagpantay%2C+Felicia+MG%3BRohani%2C+Pejman&rft.aulast=King&rft.aufirst=Aaron&rft.date=2015-05-07&rft.volume=282&rft.issue=1806&rft.spage=20150347&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+Royal+Society+of+London%2C+Series+B%3A+Biological+Sciences&rft.issn=09628452&rft_id=info:doi/10.1098%2Frspb.2015.0347 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Data processing; Infectious diseases; Pathogens; Stochasticity; Public health; Disease transmission; Models; Ebola virus DO - http://dx.doi.org/10.1098/rspb.2015.0347 ER - TY - JOUR T1 - Thymic expression of a T-cell receptor targeting a tumor-associated antigen coexpressed in the thymus induces T-ALL. AN - 1680185209; 25814528 AB - T-cell receptors (TCRs) and chimeric antigen receptors recognizing tumor-associated antigens (TAAs) can now be engineered to be expressed on a wide array of immune effectors. Engineered receptors targeting TAAs have most commonly been expressed on mature T cells, however, some have postulated that receptor expression on immune progenitors could yield T cells with enhanced potency. We generated mice (survivin-TCR-transgenic [Sur-TCR-Tg]) expressing a TCR recognizing the immunodominant epitope (Sur20-28) of murine survivin during early stages of thymopoiesis. Spontaneous T-cell acute lymphoblastic leukemia (T-ALL) occurred in 100% of Sur-TCR-Tg mice derived from 3 separate founders. The leukemias expressed the Sur-TCR and signaled in response to the Sur20-28 peptide. In preleukemic mice, we observed increased cycling of double-negative thymocytes expressing the Sur-TCR and increased nuclear translocation of nuclear factor of activated T cells, consistent with TCR signaling induced by survivin expression in the murine thymus. β2M(-/-) Sur-TCR-Tg mice, which cannot effectively present survivin peptides on class I major histocompatibility complex, had significantly diminished rates of leukemia. We conclude that TCR signaling during the early stages of thymopoiesis mediates an oncogenic signal, and therefore expression of signaling receptors on developing thymocytes with specificity for TAAs expressed in the thymus could pose a risk for neoplasia, independent of insertional mutagenesis. JF - Blood AU - Cui, Yongzhi AU - Onozawa, Masahiro AU - Garber, Haven R AU - Samsel, Leigh AU - Wang, Ziyao AU - McCoy, J Philip AU - Burkett, Sandra AU - Wu, Xiaolin AU - Aplan, Peter D AU - Mackall, Crystal L AD - Pediatric Oncology Branch and. ; Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD; ; Flow Cytometry Core Facility, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD; ; Molecular Cytogenetics Core, Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute-Frederick, Frederick, MD; and. ; Cancer Research Technology Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD. Y1 - 2015/05/07/ PY - 2015 DA - 2015 May 07 SP - 2958 EP - 2967 VL - 125 IS - 19 KW - Antigens, Neoplasm KW - 0 KW - Birc5 protein, mouse KW - Cell Adhesion Molecules KW - Homeodomain Proteins KW - Inhibitor of Apoptosis Proteins KW - Neoplasm Proteins KW - Peptide Fragments KW - RNA, Messenger KW - Receptors, Antigen, T-Cell KW - Repressor Proteins KW - Taa1 protein, mouse KW - RAG-1 protein KW - 128559-51-3 KW - Abridged Index Medicus KW - Index Medicus KW - Peptide Fragments -- metabolism KW - Real-Time Polymerase Chain Reaction KW - Animals KW - Homeodomain Proteins -- physiology KW - Mice KW - Reverse Transcriptase Polymerase Chain Reaction KW - Mice, Transgenic KW - RNA, Messenger -- genetics KW - Lymphocyte Activation KW - Blotting, Western KW - Tumor Cells, Cultured KW - Mice, Inbred C57BL KW - Flow Cytometry KW - Fluorescent Antibody Technique KW - Signal Transduction KW - Precursor T-Cell Lymphoblastic Leukemia-Lymphoma -- metabolism KW - Thymus Gland -- cytology KW - Cell Adhesion Molecules -- genetics KW - Inhibitor of Apoptosis Proteins -- physiology KW - Thymus Gland -- metabolism KW - Receptors, Antigen, T-Cell -- physiology KW - Thymus Gland -- immunology KW - Precursor T-Cell Lymphoblastic Leukemia-Lymphoma -- etiology KW - Precursor T-Cell Lymphoblastic Leukemia-Lymphoma -- pathology KW - Repressor Proteins -- physiology KW - T-Lymphocyte Subsets -- immunology KW - Neoplasm Proteins -- genetics KW - Antigens, Neoplasm -- metabolism KW - Cell Adhesion Molecules -- metabolism KW - Antigens, Neoplasm -- genetics KW - Neoplasm Proteins -- metabolism KW - Cell Transformation, Neoplastic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680185209?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Thymic+expression+of+a+T-cell+receptor+targeting+a+tumor-associated+antigen+coexpressed+in+the+thymus+induces+T-ALL.&rft.au=Cui%2C+Yongzhi%3BOnozawa%2C+Masahiro%3BGarber%2C+Haven+R%3BSamsel%2C+Leigh%3BWang%2C+Ziyao%3BMcCoy%2C+J+Philip%3BBurkett%2C+Sandra%3BWu%2C+Xiaolin%3BAplan%2C+Peter+D%3BMackall%2C+Crystal+L&rft.aulast=Cui&rft.aufirst=Yongzhi&rft.date=2015-05-07&rft.volume=125&rft.issue=19&rft.spage=2958&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=1528-0020&rft_id=info:doi/10.1182%2Fblood-2014-10-609271 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-21 N1 - Date created - 2015-05-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Oncol. 2011 Mar 1;29(7):917-24 [21282551] N Engl J Med. 2013 Apr 18;368(16):1509-18 [23527958] Nat Rev Cancer. 2012 Oct;12(10):671-84 [22996603] J Clin Invest. 2012 Oct;122(10):3398-406 [23023710] J Immunother. 2013 Feb;36(2):133-51 [23377668] Sci Transl Med. 2013 Aug 7;5(197):197ra103 [23926201] Blood. 2013 Aug 8;122(6):863-71 [23770775] Immunol Rev. 2014 Jan;257(1):237-49 [24329801] Sci Transl Med. 2014 Feb 19;6(224):224ra25 [24553386] Stem Cells Transl Med. 2014 May;3(5):636-42 [24682287] Blood. 2014 Jul 10;124(2):188-95 [24876563] N Engl J Med. 2014 Oct 16;371(16):1507-17 [25317870] Lancet. 2015 Feb 7;385(9967):517-28 [25319501] Nat Genet. 1999 Dec;23(4):387-8 [10581018] J Exp Med. 2001 Oct 15;194(8):1043-52 [11602635] Nat Rev Cancer. 2003 Jan;3(1):46-54 [12509766] Science. 2003 Oct 17;302(5644):415-9 [14564000] J Immunol Methods. 2003 Oct 1;281(1-2):65-78 [14580882] Science. 2004 Jan 16;303(5656):333 [14726584] Science. 2004 Oct 8;306(5694):269-71 [15472075] Nature. 1988 Jul 14;334(6178):156-9 [3260351] Cell. 1988 Oct 7;55(1):49-59 [3262424] Cell. 1992 May 1;69(3):529-37 [1316241] Proc Natl Acad Sci U S A. 1992 Dec 1;89(23):11381-5 [1454824] Eur J Immunol. 1993 Jul;23(7):1699-704 [8391988] J Exp Med. 1993 Aug 1;178(2):615-22 [8393478] Eur J Immunol. 1993 Aug;23(8):1922-8 [8344355] J Exp Med. 1994 Feb 1;179(2):661-72 [8294874] J Immunol Methods. 1995 Sep 11;185(1):133-40 [7665895] Eur J Immunol. 1997 Nov;27(11):3039-48 [9394835] J Immunol. 1999 Jan 15;162(2):989-94 [9916724] Proc Natl Acad Sci U S A. 1999 Feb 16;96(4):1457-62 [9990045] Oncogene. 2005 Feb 3;24(6):992-1000 [15592506] J Clin Invest. 2005 Jun;115(6):1616-26 [15931392] Nat Med. 2006 Apr;12(4):401-9 [16582916] Nature. 2006 Apr 27;440(7088):1123 [16641981] J Immunol. 2006 Nov 1;177(9):6548-59 [17056587] Blood. 2007 May 1;109(9):3972-81 [17192390] J Clin Invest. 2007 Aug;117(8):2233-40 [17671653] Clin Cancer Res. 2007 Oct 15;13(20):5991-4 [17947459] Blood. 2008 Jan 1;111(1):344-50 [17890450] J Clin Invest. 2008 Sep;118(9):3132-42 [18688285] J Clin Invest. 2008 Sep;118(9):3143-50 [18688286] Blood. 2008 Sep 15;112(6):2278-86 [18566328] Mol Ther. 2009 Jun;17(6):1031-8 [19337236] Blood. 2009 Jul 16;114(3):535-46 [19451549] Clin Cancer Res. 2009 Sep 1;15(17):5323-37 [19723653] Mol Ther. 2010 Apr;18(4):843-51 [20179677] J Clin Invest. 2010 Nov;120(11):3869-77 [20978348] Proc Natl Acad Sci U S A. 2010 Nov 2;107(44):18939-43 [20956329] Mol Ther. 2013 Apr;21(4):904-12 [23423337] J Immunol. 2011 May 1;186(9):5039-45 [21505216] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1182/blood-2014-10-609271 ER - TY - JOUR T1 - Comparison of magnetic resonance imaging and ultrasound (MRI-US) fusion-guided prostate biopsies obtained from axial and sagittal approaches AN - 1832245319; PQ0001493063 AB - To compare cancer detection rates and concordance between magnetic resonance imaging and ultrasound (MRI-US) fusion-guided prostate biopsy cores obtained from axial and sagittal approaches. Institutional records of MRI-US fusion-guided biopsy were reviewed. Detection rates for all cancers, Gleason greater than or equal to 3 + 4 cancers, and Gleason greater than or equal to 4 + 3 cancers were computed. Agreement between axial and sagittal cores for cancer detection, and frequency where one was upgraded the other was computed on a per-target and per-patient basis. In all, 893 encounters from 791 patients that underwent MRI-US fusion-guided biopsy in 2007-2013 were reviewed, yielding 4688 biopsy cores from 2344 targets for analysis. The mean age and PSA level at each encounter was 61.8 years and 9.7 ng/mL (median 6.45 ng/mL). Detection rates for all cancers, greater than or equal to 3 + 4 cancers, and greater than or equal to 4 + 3 cancers were 25.9%, 17.2%, and 8.1% for axial cores, and 26.1%, 17.6%, and 8.6% for sagittal cores. Per-target agreement was 88.6%, 93.0%, and 96.5%, respectively. On a per-target basis, the rates at which one core upgraded or detected a cancer missed on the other were 8.3% and 8.6% for axial and sagittal cores, respectively. Even with the inclusion of systematic biopsies, omission of axial or sagittal cores would have resulted in missed detection or under-characterisation of cancer in 4.7% or 5.2% of patients, respectively. Cancer detection rates, Gleason scores, and core involvement from axial and sagittal cores are similar, but significant cancer may be missed if only one core is obtained for each target. Discordance between axial and sagittal cores is greatest in intermediate-risk scenarios, where obtaining multiple cores may improve tissue characterisation. JF - BJU International AU - Hong, Cheng W AU - Rais-Bahrami, Soroush AU - Walton-Diaz, Annerleim AU - Shakir, Nabeel AU - Su, Daniel AU - George, Arvin K AU - Merino, Maria J AU - Turkbey, Baris AU - Choyke, Peter L AU - Wood, Bradford J AU - Pinto, Peter A AD - Center for Interventional Oncology Clinical Center. National Institutes of Health (NIH) Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 772 EP - 779 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 115 IS - 5 SN - 1464-4096, 1464-4096 KW - Biotechnology and Bioengineering Abstracts KW - Age KW - Magnetic resonance imaging KW - Discordance KW - Biopsy KW - Prostate KW - Ultrasound KW - Cancer KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1832245319?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BJU+International&rft.atitle=Comparison+of+magnetic+resonance+imaging+and+ultrasound+%28MRI-US%29+fusion-guided+prostate+biopsies+obtained+from+axial+and+sagittal+approaches&rft.au=Hong%2C+Cheng+W%3BRais-Bahrami%2C+Soroush%3BWalton-Diaz%2C+Annerleim%3BShakir%2C+Nabeel%3BSu%2C+Daniel%3BGeorge%2C+Arvin+K%3BMerino%2C+Maria+J%3BTurkbey%2C+Baris%3BChoyke%2C+Peter+L%3BWood%2C+Bradford+J%3BPinto%2C+Peter+A&rft.aulast=Hong&rft.aufirst=Cheng&rft.date=2015-05-01&rft.volume=115&rft.issue=5&rft.spage=772&rft.isbn=&rft.btitle=&rft.title=BJU+International&rft.issn=14644096&rft_id=info:doi/10.1111%2Fbju.12871 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-10-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Age; Discordance; Magnetic resonance imaging; Biopsy; Ultrasound; Prostate; Cancer DO - http://dx.doi.org/10.1111/bju.12871 ER - TY - JOUR T1 - 3D segmentation method combining region growing and graph cut for coronary arteries computed tomography angiography images AN - 1827918023; PQ0001881004 AB - In order to solve the problems that the efficiency is low when the segment of three-dimensional Computed Tomography Angiography (CTA) coronary arteries images with complex structure and small region of interest, a segmentation algorithm combining region growing and graph cut was proposed. Firstly, a method of region growing based on threshold was used to divide images into several regions, which removed irrelevant pixels and simplified structure and protruded regions of interest. Afterwards, according to grey and space information, simplified images were constructed as a network diagram. Finally, network diagram was segmented with theory of graph cut, so the segmentation image of coronary arteries was got. The experimental results show that, compared with traditional graph cut, the increment for the segmentation efficiency is about 51.7%, which reduces the computational complexity. On the aspect of rendering quality, target areas for segmentation images of coronary arteries is complete, which is helpful for doctors to analyze the lesion correctly. JF - Jisuanji Yingyong / Journal of Computer Applications AU - Jiang, Wei AU - Lyu, Xiaoqi AU - Ren, Xiaoying AU - Ren, Guoyin AD - School of Information Engineering, Inner Mongolia University of Science and Technology, Baotou Nei Monggol 014010, China, jwfengye@126.com Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 1462 EP - 1466 PB - Chengdu Institute of Computer Applications, 16 Donghuangchenggen North Street Beijing 100717, [mailto:bib@computerapplications.com.cn], [URL:http://www.computerapplications.com.cn] VL - 35 IS - 5 SN - 1001-9081, 1001-9081 KW - Biotechnology and Bioengineering Abstracts KW - Angiography KW - Computed tomography KW - Segmentation KW - Algorithms KW - Image processing KW - Computer applications KW - coronary artery KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1827918023?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Jisuanji+Yingyong+%2F+Journal+of+Computer+Applications&rft.atitle=3D+segmentation+method+combining+region+growing+and+graph+cut+for+coronary+arteries+computed+tomography+angiography+images&rft.au=Jiang%2C+Wei%3BLyu%2C+Xiaoqi%3BRen%2C+Xiaoying%3BRen%2C+Guoyin&rft.aulast=Jiang&rft.aufirst=Wei&rft.date=2015-05-01&rft.volume=35&rft.issue=5&rft.spage=1462&rft.isbn=&rft.btitle=&rft.title=Jisuanji+Yingyong+%2F+Journal+of+Computer+Applications&rft.issn=10019081&rft_id=info:doi/10.11772%2Fj.issn.1001-9081.2015.05.1462 LA - Chinese DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-10-01 N1 - Number of references - 11 N1 - Last updated - 2017-01-18 N1 - SubjectsTermNotLitGenreText - Angiography; Computed tomography; Algorithms; Segmentation; Image processing; Computer applications; coronary artery DO - http://dx.doi.org/10.11772/j.issn.1001-9081.2015.05.1462 ER - TY - JOUR T1 - Fueling type III secretion: Special Issue: Microbial Translocation AN - 1753471541; PQ0002248462 AB - Type III secretion systems (T3SSs) are complex nanomachines that export proteins from the bacterial cytoplasm across the cell envelope in a single step. They are at the core of the machinery used to assemble the bacterial flagellum, and the needle complex many Gram-negative pathogens use to inject effector proteins into host cells and cause disease. Several models have been put forward to explain how this export is energized, and the mechanism has been the subject of considerable debate. Here we present an overview of these models and discuss their relative merits. Recent evidence suggests that the proton motive force (pmf) is the primary energy source for type III secretion, although contribution from refolding of secreted proteins has not been ruled out. The mechanism by which the pmf is converted to protein export remains enigmatic. JF - Trends in Microbiology AU - Lee, Pei-Chung AU - Rietsch, Arne AD - Cell Biology and Metabolism Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA PY - 2015 SP - 296 EP - 300 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 23 IS - 5 SN - 0966-842X, 0966-842X KW - Microbiology Abstracts B: Bacteriology KW - T3SS KW - needle complex KW - flagellum KW - proton motive force KW - ATPase UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753471541?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+Microbiology&rft.atitle=Fueling+type+III+secretion%3A+Special+Issue%3A+Microbial+Translocation&rft.au=Lee%2C+Pei-Chung%3BRietsch%2C+Arne&rft.aulast=Lee&rft.aufirst=Pei-Chung&rft.date=2015-05-01&rft.volume=23&rft.issue=5&rft.spage=296&rft.isbn=&rft.btitle=&rft.title=Trends+in+Microbiology&rft.issn=0966842X&rft_id=info:doi/10.1016%2Fj.tim.2015.01.012 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Last updated - 2016-01-06 DO - http://dx.doi.org/10.1016/j.tim.2015.01.012 ER - TY - JOUR T1 - Quantitative analysis of PEG-functionalized colloidal gold nanoparticles using charged aerosol detection AN - 1746894631; PQ0001503329 AB - Surface characteristics of a nanoparticle, such as functionalization with polyethylene glycol (PEG), are critical to understand and achieve optimal biocompatibility. Routine physicochemical characterization such as UV-vis spectroscopy (for gold nanoparticles), dynamic light scattering, and zeta potential are commonly used to assess the presence of PEG. However, these techniques are merely qualitative and are not sensitive enough to distinguish differences in PEG quantity, density, or presentation. As an alternative, two methods are described here which allow for quantitative measurement of PEG on PEGylated gold nanoparticles. The first, a displacement method, utilizes dithiothreitol to displace PEG from the gold surface. The dithiothreitol-coated gold nanoparticles are separated from the mixture via centrifugation, and the excess dithiothreitol and dissociated PEG are separated through reversed-phase high-performance liquid chromatography (RP-HPLC). The second, a dissolution method, utilizes potassium cyanide to dissolve the gold nanoparticles and liberate PEG. Excess CN super(-), Au(CN) sub(2) super(-), and free PEG are separated using RP-HPLC. In both techniques, the free PEG can be quantified against a standard curve using charged aerosol detection. The displacement and dissolution methods are validated here using 2-, 5-, 10-, and 20-kDa PEGylated 30-nm colloidal gold nanoparticles. Further value in these techniques is demonstrated not only by quantitating the total PEG fraction but also by being able to be adapted to quantitate the free unbound PEG and the bound PEG fractions. This is an important distinction, as differences in the bound and unbound PEG fractions can affect biocompatibility, which would not be detected in techniques that only quantitate the total PEG fraction. [Figure not available: see fulltext.] JF - Analytical and Bioanalytical Chemistry AU - Smith, Mackensie C AU - Crist, Rachael M AU - Clogston, Jeffrey D AU - McNeil, Scott E AD - Nanotechnology Characterization Laboratory, Cancer Research Technology Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, 21702, USA, clogstonj@mail.nih.gov PY - 2015 SP - 3705 EP - 3716 PB - Springer Science+Business Media, Berlin/Heidelberg Germany VL - 407 IS - 13 SN - 1618-2642, 1618-2642 KW - Aqualine Abstracts; Water Resources Abstracts KW - Aerosols KW - Density KW - Spectroscopy KW - Zeta Potential KW - Centrifugation KW - Cyanide KW - Gold KW - Liquid Chromatography KW - Standards KW - AQ 00001:Water Resources and Supplies KW - SW 0540:Properties of water UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746894631?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Analytical+and+Bioanalytical+Chemistry&rft.atitle=Quantitative+analysis+of+PEG-functionalized+colloidal+gold+nanoparticles+using+charged+aerosol+detection&rft.au=Smith%2C+Mackensie+C%3BCrist%2C+Rachael+M%3BClogston%2C+Jeffrey+D%3BMcNeil%2C+Scott+E&rft.aulast=Smith&rft.aufirst=Mackensie&rft.date=2015-05-01&rft.volume=407&rft.issue=13&rft.spage=3705&rft.isbn=&rft.btitle=&rft.title=Analytical+and+Bioanalytical+Chemistry&rft.issn=16182642&rft_id=info:doi/10.1007%2Fs00216-015-8589-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 49 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Centrifugation; Aerosols; Cyanide; Density; Liquid Chromatography; Gold; Standards; Spectroscopy; Zeta Potential DO - http://dx.doi.org/10.1007/s00216-015-8589-2 ER - TY - JOUR T1 - A Deep Insight into the Sialotranscriptome of the Chagas Disease Vector, Panstrongylus megistus (Hemiptera: Heteroptera) AN - 1701478909; PQ0001758599 AB - Saliva of blood-sucking arthropods contains a complex cocktail of pharmacologically active compounds that assists feeding by counteracting their hosts' hemostatic and inflammatory reactions. Panstrongylus megistus (Burmeister) is an important vector of Chagas disease in South America, but despite its importance there is only one salivary protein sequence publicly deposited in GenBank. In the present work, we used Illumina technology to disclose and publicly deposit 3,703 coding sequences obtained from the assembly of >70 million reads. These sequences should assist proteomic experiments aimed at identifying pharmacologically active proteins and immunological markers of vector exposure. A supplemental file of the transcriptome and deducted protein sequences can be obtained from http://exon.niaid.nih.gov/transcriptome/P_megistus/Pmeg-web.xlsx. JF - Journal of Medical Entomology AU - Ribeiro, Jose MC AU - Schwarz, Alexandra AU - Francischetti, Ivo MB AD - National Institute of Allergy and Infectious Diseases, Laboratory of Malaria and Vector Research, 12735 Twinbrook Parkway, MD 20852., jribeiro@niaid.nih.gov Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 351 EP - 358 PB - Entomological Society of America, 9301 Annapolis Rd. Lanham MD 20706 United States VL - 52 IS - 3 SN - 0022-2585, 0022-2585 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology; Entomology Abstracts KW - Chagas disease KW - vector biology KW - salivary gland KW - transcriptome KW - medical entomology KW - Feeding KW - Deposits KW - Vectors KW - Hosts KW - Entomology KW - Hemiptera KW - Inflammation KW - Disease transmission KW - Public health KW - Gene expression KW - ASW, South America KW - Arthropoda KW - Panstrongylus megistus KW - Saliva KW - proteomics KW - Chagas' disease KW - Amino acid sequence KW - Q1 08484:Species interactions: parasites and diseases KW - Z 05350:Medical, Veterinary, and Agricultural Entomology KW - Q5 08524:Public health, medicines, dangerous organisms KW - K 03310:Genetics & Taxonomy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701478909?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Medical+Entomology&rft.atitle=A+Deep+Insight+into+the+Sialotranscriptome+of+the+Chagas+Disease+Vector%2C+Panstrongylus+megistus+%28Hemiptera%3A+Heteroptera%29&rft.au=Ribeiro%2C+Jose+MC%3BSchwarz%2C+Alexandra%3BFrancischetti%2C+Ivo+MB&rft.aulast=Ribeiro&rft.aufirst=Jose&rft.date=2015-05-01&rft.volume=52&rft.issue=3&rft.spage=351&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medical+Entomology&rft.issn=00222585&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Number of references - 60 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Hosts; Entomology; Public health; Disease transmission; Gene expression; Deposits; Feeding; Vectors; proteomics; Saliva; Amino acid sequence; Inflammation; Chagas' disease; Arthropoda; Panstrongylus megistus; Hemiptera; ASW, South America ER - TY - JOUR T1 - The Role of Expectation in the Therapeutic Outcomes of Alcohol and Drug Addiction Treatments AN - 1698869127 AB - Throughout history, patient–physician relationships have been acknowledged as an important component of the therapeutic effects of any pharmacological treatment. Here, we discuss the role of physiciansʼ expectations in influencing the therapeutic outcomes of alcohol and drug addiction pharmacological treatments. As largely demonstrated, such expectations and attitudes may contribute to produce placebo and nocebo effects that in turn affect the course of the disease and the response to the therapy. This article is aimed at discussing the current insights into expectations, placebo and nocebo mechanisms and their impact on the therapeutic outcomes of alcohol and drug addiction treatments; with the goal of informing physicians and other health care providers about the potentially widespread implications for clinical practice and for a successful treatment regimen. JF - Alcohol and Alcoholism : International Journal of the Medical Council on Alcoholism. AU - Colloca, Luana AU - Heilig, Markus AD - Spagnolo, Primavera A; Corresponding author: Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bldg 10, Clinical Research Center, 10 Center Drive, Bethesda, MD 20892-1540, USA. Tel.: +; Fax: +; E-mail:vera.spagnolo@nih.gov Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 282 EP - 285 CY - Oxford PB - Oxford Publishing Limited(England) VL - 50 IS - 3 SN - 0735-0414 KW - Drug Abuse And Alcoholism KW - Addiction KW - Substance Abuse KW - Attitudes KW - Health Care Services KW - Physicians KW - Health KW - Health Professions KW - Placebo Effect KW - Treatment Methods KW - Alcohol related KW - Alcoholism KW - Clinical outcomes KW - Clinical practice KW - Doctors KW - Health care KW - Health professionals KW - Placebo effect KW - Substance abuse KW - Treatment methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698869127?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol+and+Alcoholism+%3A+International+Journal+of+the+Medical+Council+on+Alcoholism.&rft.atitle=The+Role+of+Expectation+in+the+Therapeutic+Outcomes+of+Alcohol+and+Drug+Addiction+Treatments&rft.au=Spagnolo%2C+Primavera+A%3BColloca%2C+Luana%3BHeilig%2C+Markus&rft.aulast=Spagnolo&rft.aufirst=Primavera&rft.date=2015-05-01&rft.volume=50&rft.issue=3&rft.spage=282&rft.isbn=&rft.btitle=&rft.title=Alcohol+and+Alcoholism+%3A+International+Journal+of+the+Medical+Council+on+Alcoholism.&rft.issn=07350414&rft_id=info:doi/10.1093%2Falcalc%2Fagv015 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-07-20 N1 - Last updated - 2016-05-12 DO - http://dx.doi.org/10.1093/alcalc/agv015 ER - TY - JOUR T1 - Nosologic Comparisons of DSM-IV and DSM-5 Alcohol and Drug Use Disorders: Results From the National Epidemiologic Survey on Alcohol and Related Conditions-III AN - 1698868983 AB - Objective: The purpose of this study was to examine prevalences and concordances between Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV), and Fifth Edition (DSM-5) substance use disorders (SUDs) in a newly completed U.S. epidemiologic survey. Method: The National Epidemiologic Survey on Alcohol and Related Conditions-III surveyed 36,309 civilian, noninstitutionalized adults. SUDs were assessed using the Alcohol Use Disorder and Associated Disabilities Interview Schedule-5. Concordances between DSM-IV and DSM-5 disorders were assessed using kappa statistics. Results: Prevalences of past-year substance-specific DSM-5 disorders (2+ criteria) were modestly higher than those of DSM-IV dependence and abuse combined for alcohol, sedatives/tranquilizers, opioids, and heroin, but lower for cannabis, cocaine, and stimulants. Lifetime prevalences were lower under DSM-5. Prevalences were similar between moderate to severe (4+ criteria) DSM-5 disorders and dependence, whereas prevalences of DSM-5 disorders at 3+ criteria (DSM-5 [3+]) were higher, particularly for cannabis. Past-year concordances were excellent for DSM-IV dependence and abuse combined versus any DSM-5 and DSM-IV dependence versus DSM-5 moderate to severe disorders; lifetime concordances were fair to excellent. Past-year concordances between DSM-IV and DSM-5 (3+) were generally similar to or modestly higher than those with any DSM-5 disorder; lifetime concordances were mostly lower. Conclusions: Findings are consistent with those informing the development of DSM-5. Future research should examine differences in patterns between past-year and lifetime disorders, particularly for cannabis. Other questions warranting investigation include whether different combinations of the same numbers of criteria carry different clinical or nosologic implications, whether changes in nosology yield changes in treatment demand, and whether changes in characteristics of individuals with DSM-5 SUDs dictate modifications to screening and intervention. JF - Journal of Studies on Alcohol and Drugs AU - CHOU, S PATRICIA AU - SMITH, SHARON M AU - JUNG, JEESUN AU - ZHANG, HAITAO AU - SAHA, TULSHI D AU - PICKERING, ROGER P AU - RUAN, W JUNE AU - HUANG, BOJI AU - GRANT, BRIDGET F AD - Laboratory of Epidemiology and Biometry, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland ; Laboratory of Epidemiology and Biometry, Room 3071, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, M.S. 9304, 5635 Fishers Lane, Bethesda, MD 20892-9304, Laboratory of Epidemiology and Biometry, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland ; GOLDSTEIN, RISE B; Laboratory of Epidemiology and Biometry, Room 3071, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, M.S. 9304, 5635 Fishers Lane, Bethesda, MD 20892-9304 Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 378 EP - 388 CY - Piscataway PB - Alcohol Research Documentation, Inc. VL - 76 IS - 3 SN - 1937-1888 KW - Medical Sciences KW - Tests KW - Sedative drugs KW - Stimulants KW - Substance abuse disorders KW - Tranquillizers KW - Alcohol Abuse KW - Substance Abuse KW - Marijuana KW - Cocaine KW - Intervention KW - Mental Illness KW - Drug Abuse KW - Epidemiology KW - Equity KW - Alcohol consumption KW - Alcohol related disorders KW - Cannabis KW - Diagnostic and Statistical Manual KW - Drug abuse KW - Heroin KW - Opioids KW - Psychiatric disorders KW - Screening KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698868983?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Studies+on+Alcohol+and+Drugs&rft.atitle=Nosologic+Comparisons+of+DSM-IV+and+DSM-5+Alcohol+and+Drug+Use+Disorders%3A+Results+From+the+National+Epidemiologic+Survey+on+Alcohol+and+Related+Conditions-III&rft.au=GOLDSTEIN%2C+RISE+B%3BCHOU%2C+S+PATRICIA%3BSMITH%2C+SHARON+M%3BJUNG%2C+JEESUN%3BZHANG%2C+HAITAO%3BSAHA%2C+TULSHI+D%3BPICKERING%2C+ROGER+P%3BRUAN%2C+W+JUNE%3BHUANG%2C+BOJI%3BGRANT%2C+BRIDGET+F&rft.aulast=GOLDSTEIN&rft.aufirst=RISE&rft.date=2015-05-01&rft.volume=76&rft.issue=3&rft.spage=378&rft.isbn=&rft.btitle=&rft.title=Journal+of+Studies+on+Alcohol+and+Drugs&rft.issn=19371888&rft_id=info:doi/ LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-07-07 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - United States--US ER - TY - JOUR T1 - INTERPRETING PHYSICAL AND BEHAVIORAL HEALTH SCORES FROM NEW WORK DISABILITY INSTRUMENTS AN - 1698868467 AB - Objective: To develop a system to guide interpretation of scores generated from 2 new instruments measuring work-related physical and behavioral health functioning (Work Disability — Physical Function (WD-PF) and WD — Behavioral Function (WD-BH)). Design: Cross-sectional, secondary data from 3 independent samples to develop and validate the functional levels for physical and behavioral health functioning. Subjects: Physical group: 999 general adult subjects, 1,017 disability applicants and 497 work-disabled subjects. Behavioral health group: 1,000 general adult subjects, 1,015 disability applicants and 476 work-disabled subjects. Methods: Three-phase analytic approach including item mapping, a modified-Delphi technique, and known-groups validation analysis were used to develop and validate cut-points for functional levels within each of the WD-PF and WD-BH instrumentʼs scales. Results: Four and 5 functional levels were developed for each of the scales in the WD-PF and WD-BH instruments. Distribution of the comparative samples was in the expected direction: the general adult samples consistently demonstrated scores at higher functional levels compared with the claimant and work-disabled samples. Conclusion: Using an item-response theory-based methodology paired with a qualitative process appears to be a feasible and valid approach for translating the WD-BH and WD-PF scores into meaningful levels useful for interpreting a personʼs work-related physical and behavioral health functioning. JF - Journal of Rehabilitation Medicine AU - Ni, Pengsheng AU - Chan, Leighton AU - Rasch, Elizabeth K AU - McDonough, Christine M AU - Brandt, Diane E AU - Bogusz, Kara AU - Jette, Alan M AD - Boston University School of Public Health, Health & Disability Research Institute, Boston, MA ; National Institutes of Health, Rehabilitation Medicine Department, Mark O. Hatfield Clinical Research Center, Bethesda, MD, USA ; Marfeo, Elizabeth E; Boston University School of Public Health, Health & Disability Research Institute, 715 Albany Streeet, T5W Boston, MA 02118, USA Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 394 EP - 402 CY - Stockholm PB - Taylor & Francis Ltd. VL - 47 IS - 5 SN - 1650-1977 KW - Medical Sciences KW - outcome assessment (healthcare) KW - disability evaluation KW - work KW - Adults KW - Physical ability KW - Validation KW - Work KW - Applicants KW - Claimants KW - Disability KW - Health behaviour KW - Health care KW - Health status KW - Mapping KW - Methodology KW - Occupational health and safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698868467?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Rehabilitation+Medicine&rft.atitle=INTERPRETING+PHYSICAL+AND+BEHAVIORAL+HEALTH+SCORES+FROM+NEW+WORK+DISABILITY+INSTRUMENTS&rft.au=Marfeo%2C+Elizabeth+E%3BNi%2C+Pengsheng%3BChan%2C+Leighton%3BRasch%2C+Elizabeth+K%3BMcDonough%2C+Christine+M%3BBrandt%2C+Diane+E%3BBogusz%2C+Kara%3BJette%2C+Alan+M&rft.aulast=Marfeo&rft.aufirst=Elizabeth&rft.date=2015-05-01&rft.volume=47&rft.issue=5&rft.spage=394&rft.isbn=&rft.btitle=&rft.title=Journal+of+Rehabilitation+Medicine&rft.issn=16501977&rft_id=info:doi/10.2340%2F16501977-1947 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-09-22 N1 - Last updated - 2016-05-12 DO - http://dx.doi.org/10.2340/16501977-1947 ER - TY - JOUR T1 - Mothers' guilt responses to children's obesity risk feedback AN - 1695988899; 4687143 AB - This study explored the influence of family health history-based obesity risk feedback for their child on 147 overweight mothers' guilt related to children's lifestyle behaviors and passing down a genetic propensity for overweight. Mothers were randomized to receive, or not, obesity risk feedback for their 4- to 5-year-old child and then made food choices for them using a virtual reality-based buffet. Receipt of risk information increased lifestyle- and genetics-related guilt. Choosing fewer unhealthful foods for the child attenuated both types of guilt. Work in this area may aid in development of obesity risk feedback strategies that enhance child feeding. Reprinted by permission of Sage Publications Ltd JF - Journal of health psychology AU - Persky, Susan AU - McBride, Colleen AU - Faith, Myles AU - Wagner, Laura AU - Ward, Dianne AD - National Human Genome Research Institute ; University of North Carolina Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 649 EP - 658 VL - 20 IS - 5 SN - 1359-1053, 1359-1053 KW - Sociology KW - Obesity KW - Health care KW - Guilt KW - Children KW - Parents KW - Life styles UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1695988899?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+health+psychology&rft.atitle=Mothers%27+guilt+responses+to+children%27s+obesity+risk+feedback&rft.au=Persky%2C+Susan%3BMcBride%2C+Colleen%3BFaith%2C+Myles%3BWagner%2C+Laura%3BWard%2C+Dianne&rft.aulast=Persky&rft.aufirst=Susan&rft.date=2015-05-01&rft.volume=20&rft.issue=5&rft.spage=649&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+psychology&rft.issn=13591053&rft_id=info:doi/10.1177%2F1359105315576608 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-07-14 N1 - Last updated - 2015-07-14 N1 - SubjectsTermNotLitGenreText - 5692 4196; 8823; 9184; 2212; 7404; 5775 13521 DO - http://dx.doi.org/10.1177/1359105315576608 ER - TY - JOUR T1 - Resveratrol supplementation: Where are we now and where should we go? AN - 1692754735; 25625901 AB - Pre-clinical findings have provided mounting evidence that resveratrol, a dietary polyphenol, may confer health benefits and protect against a variety of medical conditions and age-related complications. However, there is no consistent evidence of an increased protection against metabolic disorders and other ailments when comparing studies in laboratory animals and humans. A number of extraneous and potential confounding variables can affect the outcome of clinical research. To date, most of the studies that have investigated the effect of resveratrol administration on patient outcomes have been limited by their sample sizes. In this review, we will survey the latest advances regarding the timing, dosage, formulation, bioavailability, toxicity of resveratrol, and resveratrol-drug interactions in human studies. Moreover, the present report focuses on the actions of resveratrol treatment in combating diseases, such as cancer, diabetes, neurodegeneration, cardiovascular disease, and other age-related ailments. Published by Elsevier B.V. JF - Ageing research reviews AU - Novelle, Marta G AU - Wahl, Devin AU - Diéguez, Carlos AU - Bernier, Michel AU - de Cabo, Rafael AD - Translational Gerontology Branch, National Institute on Aging, NIH, Baltimore, MD 21224, USA; Research Center of Molecular Medicine and Chronic Diseases (CIMUS), University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela 15782, Spain; CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela 15706, Spain. ; Translational Gerontology Branch, National Institute on Aging, NIH, Baltimore, MD 21224, USA. ; Research Center of Molecular Medicine and Chronic Diseases (CIMUS), University of Santiago de Compostela-Instituto de Investigación Sanitaria, Santiago de Compostela 15782, Spain; CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela 15706, Spain. ; Translational Gerontology Branch, National Institute on Aging, NIH, Baltimore, MD 21224, USA. Electronic address: decabora@grc.nia.nih.gov. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 1 EP - 15 VL - 21 KW - Anti-Inflammatory Agents, Non-Steroidal KW - 0 KW - Stilbenes KW - resveratrol KW - Q369O8926L KW - Index Medicus KW - Resveratrol KW - Bioavailability KW - Translational research KW - Clinical trials KW - Metabolism KW - Animals KW - Humans KW - Aging -- drug effects KW - Clinical Trials as Topic KW - Exercise KW - Anti-Inflammatory Agents, Non-Steroidal -- therapeutic use KW - Anti-Inflammatory Agents, Non-Steroidal -- metabolism KW - Stilbenes -- pharmacology KW - Dietary Supplements -- adverse effects KW - Stilbenes -- therapeutic use KW - Chronic Disease -- drug therapy KW - Stilbenes -- metabolism KW - Anti-Inflammatory Agents, Non-Steroidal -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1692754735?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Ageing+research+reviews&rft.atitle=Resveratrol+supplementation%3A+Where+are+we+now+and+where+should+we+go%3F&rft.au=Novelle%2C+Marta+G%3BWahl%2C+Devin%3BDi%C3%A9guez%2C+Carlos%3BBernier%2C+Michel%3Bde+Cabo%2C+Rafael&rft.aulast=Novelle&rft.aufirst=Marta&rft.date=2015-05-01&rft.volume=21&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Ageing+research+reviews&rft.issn=1872-9649&rft_id=info:doi/10.1016%2Fj.arr.2015.01.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-14 N1 - Date created - 2015-05-04 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.arr.2015.01.002 ER - TY - JOUR T1 - Molecular insights into the binding of coenzyme F sub(420) to the conserved protein Rv1155 from Mycobacterium tuberculosis AN - 1687668559; PQ0001496827 AB - Coenzyme F sub(420) is a deazaflavin hydride carrier with a lower reduction potential than most flavins. In Mycobacterium tuberculosis (Mtb), F sub(420) plays an important role in activating PA-824, an antituberculosis drug currently used in clinical trials. Although F sub(420) is important to Mtb redox metabolism, little is known about the enzymes that bind F sub(420) and the reactions that they catalyze. We have identified a novel F sub(420)-binding protein, Rv1155, which is annotated in the Mtb genome sequence as a putative flavin mononucleotide (FMN)-binding protein. Using biophysical techniques, we have demonstrated that instead of binding FMN or other flavins, Rv1155 binds coenzyme F sub(420). The crystal structure of the complex of Rv1155 and F sub(420) reveals one F sub(420) molecule bound to each monomer of the Rv1155 dimer. Structural, biophysical, and bioinformatic analyses of the Rv1155-F sub(420) complex provide clues about its role in the bacterium. PDB Code(s): 4QVB JF - Protein Science AU - Mashalidis, Ellene H AU - Gittis, Apostolos G AU - Tomczak, Aurelie AU - Abell, Chris AU - Barry, Clifton E AU - Garboczi, David N AD - Tuberculosis Research Section, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, 20892. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 729 EP - 740 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 24 IS - 5 SN - 0961-8368, 0961-8368 KW - Microbiology Abstracts B: Bacteriology KW - Genomes KW - Nucleotide sequence KW - Enzymes KW - Flavin mononucleotide KW - Clinical trials KW - Monomers KW - Crystal structure KW - Coenzymes KW - Bioinformatics KW - Drugs KW - Metabolism KW - Mycobacterium tuberculosis KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687668559?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Protein+Science&rft.atitle=Molecular+insights+into+the+binding+of+coenzyme+F+sub%28420%29+to+the+conserved+protein+Rv1155+from+Mycobacterium+tuberculosis&rft.au=Mashalidis%2C+Ellene+H%3BGittis%2C+Apostolos+G%3BTomczak%2C+Aurelie%3BAbell%2C+Chris%3BBarry%2C+Clifton+E%3BGarboczi%2C+David+N&rft.aulast=Mashalidis&rft.aufirst=Ellene&rft.date=2015-05-01&rft.volume=24&rft.issue=5&rft.spage=729&rft.isbn=&rft.btitle=&rft.title=Protein+Science&rft.issn=09618368&rft_id=info:doi/10.1002%2Fpro.2645 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-06-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Genomes; Monomers; Nucleotide sequence; Crystal structure; Enzymes; Coenzymes; Bioinformatics; Flavin mononucleotide; Drugs; Clinical trials; Metabolism; Mycobacterium tuberculosis DO - http://dx.doi.org/10.1002/pro.2645 ER - TY - JOUR T1 - Trimodality therapy in bladder cancer: who, what, and when? AN - 1687348246; 25882559 AB - Radical cystectomy is a standard treatment of nonmetastatic, muscle-invasive bladder cancer. Treatment with trimodality therapy consisting of maximal transurethral resection of the bladder tumor followed by concurrent chemotherapy and radiation has emerged as a method to preserve the native bladder in highly motivated patients. Several factors can affect the likelihood of long-term bladder preservation after trimodality therapy and therefore should be taken into account when selecting patients. New radiation techniques such as intensity modulated radiation therapy and image-guided radiation therapy may decrease the toxicity of radiotherapy in this setting. Novel chemotherapy regimens may improve response rates and minimize toxicity. Published by Elsevier Inc. JF - The Urologic clinics of North America AU - Premo, Christopher AU - Apolo, Andrea B AU - Agarwal, Piyush K AU - Citrin, Deborah E AD - Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, 10 CRC, B2-3500, Bethesda, MD 20892, USA. ; Bladder Cancer Section, Genitourinary Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 10 Center Drive 12N226, MSC 1906, Bethesda, MD 20892, USA. ; Bladder Cancer Section, Urologic Oncology Branch, National Cancer Institute, National Institutes of Health, Building 10, Room 2W-5940, Bethesda, MD 20892-1210, USA. ; Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, 10 CRC, B2-3500, Bethesda, MD 20892, USA. Electronic address: citrind@mail.nih.gov. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 169 EP - 80, vii VL - 42 IS - 2 KW - Antineoplastic Agents KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Muscle-invasive bladder cancer KW - Urothelial carcinoma of the bladder KW - Radiation KW - Bladder preservation KW - Chemoradiation KW - Combined Modality Therapy -- methods KW - Neoplasm Invasiveness KW - Neoplasm Staging KW - Organ Sparing Treatments -- methods KW - Cystectomy KW - Radiotherapy, Image-Guided KW - Humans KW - Checklist KW - Radiotherapy, Intensity-Modulated KW - Neoplasm Recurrence, Local KW - Patient Selection KW - Antineoplastic Agents -- therapeutic use KW - Urinary Bladder Neoplasms -- pathology KW - Urinary Bladder Neoplasms -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687348246?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Urologic+clinics+of+North+America&rft.atitle=Trimodality+therapy+in+bladder+cancer%3A+who%2C+what%2C+and+when%3F&rft.au=Premo%2C+Christopher%3BApolo%2C+Andrea+B%3BAgarwal%2C+Piyush+K%3BCitrin%2C+Deborah+E&rft.aulast=Premo&rft.aufirst=Christopher&rft.date=2015-05-01&rft.volume=42&rft.issue=2&rft.spage=169&rft.isbn=&rft.btitle=&rft.title=The+Urologic+clinics+of+North+America&rft.issn=1558-318X&rft_id=info:doi/10.1016%2Fj.ucl.2015.02.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-15 N1 - Date created - 2015-04-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Urology. 2001 Sep;58(3):380-5 [11549485] Radiother Oncol. 2002 Feb;62(2):215-25 [11937249] Urology. 2002 Jul;60(1):62-7; discussion 67-8 [12100923] J Clin Oncol. 2002 Jul 15;20(14):3061-71 [12118019] N Engl J Med. 2003 Aug 28;349(9):859-66 [12944571] Int J Radiat Oncol Biol Phys. 2003 Nov 1;57(3):665-72 [14529770] J Urol. 2003 Nov;170(5):1772-6 [14532773] Eur Urol. 2004 Mar;45(3):297-303 [15036674] Int J Radiat Oncol Biol Phys. 2004 May 1;59(1):197-207 [15093917] J Clin Oncol. 2004 Jul 1;22(13):2540-5 [15226322] Lancet. 1985 May 4;1(8436):1005-8 [2859462] Int J Radiat Oncol Biol Phys. 1993 Apr 2;25(5):783-90 [8478228] J Clin Oncol. 1996 Jan;14(1):119-26 [8558186] Cancer. 1996 Sep 1;78(5):1089-97 [8780548] J Clin Oncol. 1996 Nov;14(11):2901-7 [8918486] J Clin Oncol. 1997 Mar;15(3):1022-9 [9060542] J Clin Oncol. 1998 Nov;16(11):3576-83 [9817278] J Urol. 1989 Dec;142(6):1448-53; discussion 1453-4 [2585617] J Clin Oncol. 1991 Sep;9(9):1533-42 [1875217] Urology. 2007 Jan;69(1 Suppl):80-92 [17280910] Int J Radiat Oncol Biol Phys. 2007 Jul 15;68(4):1072-80 [17467193] J Urol. 2007 Sep;178(3 Pt 1):807-13; discussion 813 [17631326] Cancer. 2008 Jan 1;112(1):75-83 [18008364] Urology. 2009 Apr;73(4):833-7 [19100600] BJU Int. 2009 Jul;104(2):179-83 [19154448] J Clin Oncol. 2009 Sep 1;27(25):4055-61 [19636019] Int J Radiat Oncol Biol Phys. 2010 Mar 15;76(4):1045-53 [19540057] Cancer Res. 2010 Sep 15;70(18):7017-26 [20843819] BJU Int. 2010 Oct;106(8):1216-22 [20089105] Int J Radiat Oncol Biol Phys. 2005 Jun 1;62(2):309-17 [15890569] J Clin Oncol. 2006 May 20;24(15):2318-24 [16710030] Hum Pathol. 2006 Jun;37(6):726-34 [16733214] Clin Oncol (R Coll Radiol). 2006 Aug;18(6):466-73 [16909970] J Clin Oncol. 2011 Feb 20;29(6):733-8 [21205754] Anticancer Res. 2011 Mar;31(3):985-90 [21498726] Oncologist. 2000;5(6):471-6 [11110598] Radiat Oncol. 2011;6:75 [21679408] Int J Radiat Oncol Biol Phys. 2012 Mar 1;82(3):e457-62 [21945107] Eur Urol. 2012 Apr;61(4):705-11 [22101114] N Engl J Med. 2012 Apr 19;366(16):1477-88 [22512481] Int J Radiat Oncol Biol Phys. 2013 May 1;86(1):77-82 [23332382] J Natl Compr Canc Netw. 2013 Apr 1;11(4):446-75 [23584347] Oncologist. 2013 Jun;18(6):685-6 [23728940] Lancet Oncol. 2013 Aug;14(9):863-72 [23823157] Int J Radiat Oncol Biol Phys. 2014 Feb 1;88(2):326-31 [24411604] CA Cancer J Clin. 2014 Jan-Feb;64(1):9-29 [24399786] Int J Radiat Oncol Biol Phys. 2014 Mar 1;88(3):603-10 [24411628] PLoS One. 2014;9(3):e89754 [24594774] Int J Radiat Oncol Biol Phys. 2014 Apr 1;88(5):1048-56 [24661658] Urology. 2014 Apr;83(4):946-50 [24397940] Eur Urol. 2014 Jul;66(1):120-37 [24613684] J Clin Oncol. 2014 Dec 1;32(34):3801-9 [25366678] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ucl.2015.02.002 ER - TY - JOUR T1 - Methods of Genomic Competency Integration in Practice AN - 1683504135 AB - Purpose Genomics is increasingly relevant to health care, necessitating support for nurses to incorporate genomic competencies into practice. The primary aim of this project was to develop, implement, and evaluate a year-long genomic education intervention that trained, supported, and supervised institutional administrator and educator champion dyads to increase nursing capacity to integrate genomics through assessments of program satisfaction and institutional achieved outcomes. Design Longitudinal study of 23 Magnet Recognition Program® Hospitals (21 intervention, 2 controls) participating in a 1-year new competency integration effort aimed at increasing genomic nursing competency and overcoming barriers to genomics integration in practice. Methods Champion dyads underwent genomic training consisting of one in-person kick-off training meeting followed by monthly education webinars. Champion dyads designed institution-specific action plans detailing objectives, methods or strategies used to engage and educate nursing staff, timeline for implementation, and outcomes achieved. Action plans focused on a minimum of seven genomic priority areas: champion dyad personal development; practice assessment; policy content assessment; staff knowledge needs assessment; staff development; plans for integration; and anticipated obstacles and challenges. Action plans were updated quarterly, outlining progress made as well as inclusion of new methods or strategies. Progress was validated through virtual site visits with the champion dyads and chief nursing officers. Descriptive data were collected on all strategies or methods utilized, and timeline for achievement. Descriptive data were analyzed using content analysis. Findings The complexity of the competency content and the uniqueness of social systems and infrastructure resulted in a significant variation of champion dyad interventions. Conclusions Nursing champions can facilitate change in genomic nursing capacity through varied strategies but require substantial training in order to design and implement interventions. Clinical Relevance Genomics is critical to the practice of all nurses. There is a great opportunity and interest to address genomic knowledge deficits in the practicing nurse workforce as a strategy to improve patient outcomes. Exemplars of champion dyad interventions designed to increase nursing capacity focus on improving education, policy, and healthcare services. JF - Journal of Nursing Scholarship AU - Jenkins, Jean AU - Calzone, Kathleen A AU - Caskey, Sarah AU - Culp, Stacey AU - Weiner, Marsha AU - Badzek, Laurie AD - Kappa , Clinical Advisor, National Institutes of Health, National Human Genome Research Institute, Division of Policy, Communications, and Education, Genomic Healthcare Branch, Bethesda, MD. ; Xi , Senior Nurse Specialist, Research, National Institutes of Health, National Cancer Institute, Center for Cancer Research, Genetics Branch, Bethesda, MD. ; Project Manager, West Virginia University School of Nursing, Morgantown, WV. ; Research Assistant Professor, West Virginia University School of Nursing, Morgantown, WV. ; Xi , Nursing Program Director, Keiser University, Sarasota, FL. ; Alpha Rho , Professor and Senior Author, West Virginia University School of Nursing, Morgantown, WV. ; Kappa , Clinical Advisor, National Institutes of Health, National Human Genome Research Institute, Division of Policy, Communications, and Education, Genomic Healthcare Branch, Bethesda, MD. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 200 EP - 210 CY - Indianapolis PB - Wiley Subscription Services, Inc. VL - 47 IS - 3 SN - 1527-6546 KW - Medical Sciences--Nurses And Nursing KW - Assessment KW - Interventions KW - Labour force KW - Magnet hospitals KW - Needs assessment KW - Nurse led services KW - Nurses KW - Nursing KW - Personal development KW - Professional competence KW - Professional knowledge KW - Professional practices KW - Site visits KW - Social systems KW - Staff development KW - Uniqueness KW - Capacity KW - Chief nursing officers KW - Clinical outcomes KW - Content analysis KW - Health care KW - Hospitals KW - Inclusive education KW - Infrastructure KW - Integrated services UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683504135?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Nursing+Scholarship&rft.atitle=Methods+of+Genomic+Competency+Integration+in+Practice&rft.au=Jenkins%2C+Jean%3BCalzone%2C+Kathleen+A%3BCaskey%2C+Sarah%3BCulp%2C+Stacey%3BWeiner%2C+Marsha%3BBadzek%2C+Laurie&rft.aulast=Jenkins&rft.aufirst=Jean&rft.date=2015-05-01&rft.volume=47&rft.issue=3&rft.spage=200&rft.isbn=&rft.btitle=&rft.title=Journal+of+Nursing+Scholarship&rft.issn=15276546&rft_id=info:doi/10.1111%2Fjnu.12131 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-05-01 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1111/jnu.12131 ER - TY - JOUR T1 - The Science of Caregiver Health AN - 1683501648 JF - Journal of Nursing Scholarship AU - Grady, Patricia A AU - Rosenbaum, Louise M AD - National Institute of Nursing Research, National Institutes of Health, Bethesda, MD. ; National Institute of Nursing Research, National Institutes of Health, Bethesda, MD. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 197 EP - 199 CY - Indianapolis PB - Wiley Subscription Services, Inc. VL - 47 IS - 3 SN - 1527-6546 KW - Medical Sciences--Nurses And Nursing KW - Carers UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683501648?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Nursing+Scholarship&rft.atitle=The+Science+of+Caregiver+Health&rft.au=Grady%2C+Patricia+A%3BRosenbaum%2C+Louise+M&rft.aulast=Grady&rft.aufirst=Patricia&rft.date=2015-05-01&rft.volume=47&rft.issue=3&rft.spage=197&rft.isbn=&rft.btitle=&rft.title=Journal+of+Nursing+Scholarship&rft.issn=15276546&rft_id=info:doi/10.1111%2Fjnu.12137 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-05-01 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1111/jnu.12137 ER - TY - JOUR T1 - Reduction in behavior problems with omega-3 supplementation in children aged 8–16 years: a randomized, double-blind, placebo-controlled, stratified, parallel-group trial AN - 1683500890 AB - Background While limited evidence suggests that omega-3 supplementation may reduce antisocial behavior in children, studies have not reported on posttreatment follow-up and most treatment periods have been of short duration. This study tests the hypothesis that omega-3 supplementation over 6 months will reduce behavior problems in children both at the end of treatment and at 6 months post treatment. Methods In this randomized, double-blind, placebo-controlled, stratified, parallel-group trial, a community sample of 8–16 year old children were randomized into a treatment group ( N = 100) and a placebo-control group ( N = 100). The supplementation consisted of a fruit drink containing 1 g/day of omega-3 or a placebo consisting of the same fruit drink without omega-3. Participants, caregivers, and research assistants were blinded to group assignment. The primary outcome measures of externalizing and internalizing behavior problems were reported by both caregivers and their children in a laboratory setting at 0 months (baseline), 6 months (end of treatment) and 12 months (6 months post treatment), together with the secondary outcome measures of parental antisocial behavior. Data were analyzed on an intention-to-treat basis including all participants. Trial registration: ClinicalTrials.gov: http://clinicaltrials.gov/ct2/show/NCT02016079 Results Significant group × time interactions were observed with the treatment group showing long-term improvements in child behavior problems. The average posttreatment effect size was d = −.59. Effects were documented for parent reports, but with the exception of proactive and reactive aggression, child-report data were nonsignificant. Parents whose children took omega-3 showed significant posttreatment reductions in their own antisocial and aggressive behavior. This improvement in caregiver behavior partly mediated the improvements observed in child behavior. Conclusions Findings provide initial evidence that omega-3 supplementation can produce sustained reductions in externalizing and internalizing behavior problems. Results are the first to report improvements in caregiver behavior, and to establish this improvement as a part-mechanism for the efficacy of omega-3. JF - Journal of Child Psychology and Psychiatry AU - Raine, Adrian AU - Portnoy, Jill AU - Liu, Jianghong AU - Mahoomed, Tashneem AU - Hibbeln, Joseph R AD - Departments of Criminology, Psychiatry and Psychology, University of Pennsylvania, Philadelphia, PA, USA. ; School of Nursing, University of Pennsylvania, Philadelphia, PA, USA. ; Joint Child Health Project, Quatre Bornes, Quatre Bornes, Mauritius. ; Section on Nutritional Neuroscience, National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD, USA. ; Departments of Criminology, Psychiatry and Psychology, University of Pennsylvania, Philadelphia, PA, USA. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 509 EP - 520 CY - Malden PB - Wiley Subscription Services, Inc. VL - 56 IS - 5 KW - Psychology KW - Aggression KW - Behavioural problems KW - Internalizing behaviour KW - Internalizing problems KW - Antisocial behaviour KW - Assistants KW - Behaviour disordered children KW - Carers KW - Children KW - Efficacy KW - Externalizing behaviour KW - Fruit KW - Internalization UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683500890?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Child+Psychology+and+Psychiatry&rft.atitle=Reduction+in+behavior+problems+with+omega-3+supplementation+in+children+aged+8%E2%80%9316%C2%A0years%3A+a+randomized%2C+double-blind%2C+placebo-controlled%2C+stratified%2C+parallel-group+trial&rft.au=Raine%2C+Adrian%3BPortnoy%2C+Jill%3BLiu%2C+Jianghong%3BMahoomed%2C+Tashneem%3BHibbeln%2C+Joseph+R&rft.aulast=Raine&rft.aufirst=Adrian&rft.date=2015-05-01&rft.volume=56&rft.issue=5&rft.spage=509&rft.isbn=&rft.btitle=&rft.title=Journal+of+Child+Psychology+and+Psychiatry&rft.issn=&rft_id=info:doi/10.1111%2Fjcpp.12314 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-05-01 N1 - Last updated - 2016-05-16 DO - http://dx.doi.org/10.1111/jcpp.12314 ER - TY - JOUR T1 - A Novel Tricyclic Ligand-Containing Nonpeptidic HIV-1 Protease Inhibitor, GRL-0739, Effectively Inhibits the Replication of Multidrug-Resistant HIV-1 Variants and Has a Desirable Central Nervous System Penetration Property In Vitro AN - 1683352682; PQ0001539707 AB - We report here that GRL-0739, a novel nonpeptidic HIV-1 protease inhibitor containing a tricycle (cyclohexyl-bis-tetrahydrofuranylurethane [THF]) and a sulfonamide isostere, is highly active against laboratory HIV-1 strains and primary clinical isolates (50% effective concentration [EC50], 0.0019 to 0.0036 mu M), with minimal cytotoxicity (50% cytotoxic concentration [CC50], 21.0 mu M). GRL-0739 blocked the infectivity and replication of HIV-1NL4-3 variants selected by concentrations of up to 5 mu M ritonavir or atazanavir (EC50, 0.035 to 0.058 mu M). GRL-0739 was also highly active against multidrug-resistant clinical HIV-1 variants isolated from patients who no longer responded to existing antiviral regimens after long-term antiretroviral therapy, as well as against the HIV-2ROD variant. The development of resistance against GRL-0739 was substantially delayed compared to that of amprenavir (APV). The effects of the nonspecific binding of human serum proteins on the anti-HIV-1 activity of GRL-0739 were insignificant. In addition, GRL-0739 showed a desirable central nervous system (CNS) penetration property, as assessed using a novel in vitro blood-brain barrier model. Molecular modeling demonstrated that the tricyclic ring and methoxybenzene of GRL-0739 have a larger surface and make greater van der Waals contacts with protease than in the case of darunavir. The present data demonstrate that GRL-0739 has desirable features as a compound with good CNS-penetrating capability for treating patients infected with wild-type and/or multidrug-resistant HIV-1 variants and that the newly generated cyclohexyl-bis-THF moiety with methoxybenzene confers highly desirable anti-HIV-1 potency in the design of novel protease inhibitors with greater CNS penetration profiles. JF - Antimicrobial Agents & Chemotherapy AU - Amano, Masayuki AU - Tojo, Yasushi AU - Salcedo-Gomez, Pedro Miguel AU - Parham, Garth L AU - Nyalapatla, Prasanth R AU - Das, Debananda AU - Ghosh, Arun K AU - Mitsuya, Hiroaki AD - Departments of Infectious Diseases and Hematology, Kumamoto University School of Medicine, Kumamoto, Japan, hm21q@nih.gov. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 2625 EP - 2635 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 59 IS - 5 SN - 0066-4804, 0066-4804 KW - Microbiology Abstracts A: Industrial & Applied Microbiology KW - Clinical isolates KW - Molecular modelling KW - Central nervous system KW - Data processing KW - Blood-brain barrier KW - Replication KW - Drug resistance KW - antiretroviral therapy KW - Proteinase inhibitors KW - Antiviral activity KW - Serum proteins KW - Cytotoxicity KW - Infectivity KW - Antiviral agents KW - Human immunodeficiency virus KW - Ritonavir KW - Human immunodeficiency virus 1 KW - Sulfonamides KW - amprenavir KW - A 01340:Antibiotics & Antimicrobials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683352682?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=A+Novel+Tricyclic+Ligand-Containing+Nonpeptidic+HIV-1+Protease+Inhibitor%2C+GRL-0739%2C+Effectively+Inhibits+the+Replication+of+Multidrug-Resistant+HIV-1+Variants+and+Has+a+Desirable+Central+Nervous+System+Penetration+Property+In+Vitro&rft.au=Amano%2C+Masayuki%3BTojo%2C+Yasushi%3BSalcedo-Gomez%2C+Pedro+Miguel%3BParham%2C+Garth+L%3BNyalapatla%2C+Prasanth+R%3BDas%2C+Debananda%3BGhosh%2C+Arun+K%3BMitsuya%2C+Hiroaki&rft.aulast=Amano&rft.aufirst=Masayuki&rft.date=2015-05-01&rft.volume=59&rft.issue=5&rft.spage=2625&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.04757-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Number of references - 38 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Clinical isolates; Central nervous system; Molecular modelling; Data processing; Replication; Blood-brain barrier; Drug resistance; Proteinase inhibitors; antiretroviral therapy; Antiviral activity; Serum proteins; Infectivity; Cytotoxicity; Antiviral agents; Ritonavir; Sulfonamides; amprenavir; Human immunodeficiency virus; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1128/AAC.04757-14 ER - TY - JOUR T1 - Decreasing pfmdr1 Copy Number Suggests that Plasmodium falciparum in Western Cambodia Is Regaining In Vitro Susceptibility to Mefloquine AN - 1683350050; PQ0001539738 AB - Dihydroartemisinin-piperaquine is the current frontline artemisinin combination therapy (ACT) for Plasmodium falciparum malaria in Cambodia but is now failing in several western provinces. To investigate artesunate plus mefloquine (AS+MQ) as a replacement ACT, we measured the prevalence of multiple pfmdr1 copies-a molecular marker for MQ resistance-in 844 P. falciparum clinical isolates collected in 2008 to 2013. The pfmdr1 copy number is decreasing in Western Cambodia, suggesting that P. falciparum is regaining in vitro susceptibility to MQ. JF - Antimicrobial Agents & Chemotherapy AU - Lim, Pharath AU - Dek, Dalin AU - Try, Vorleak AU - Sreng, Sokunthea AU - Suon, Seila AU - Fairhurst, Rick M AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, USA, rfairhurst@niaid.nih.gov. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 2934 EP - 2937 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 59 IS - 5 SN - 0066-4804, 0066-4804 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Clinical isolates KW - Parasites KW - Human diseases KW - Therapy KW - Malaria KW - Plasmodium falciparum KW - copy number KW - Public health KW - Cambodia KW - artemisinin KW - Mefloquine KW - artesunate KW - A 01340:Antibiotics & Antimicrobials KW - K 03400:Human Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683350050?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Decreasing+pfmdr1+Copy+Number+Suggests+that+Plasmodium+falciparum+in+Western+Cambodia+Is+Regaining+In+Vitro+Susceptibility+to+Mefloquine&rft.au=Lim%2C+Pharath%3BDek%2C+Dalin%3BTry%2C+Vorleak%3BSreng%2C+Sokunthea%3BSuon%2C+Seila%3BFairhurst%2C+Rick+M&rft.aulast=Lim&rft.aufirst=Pharath&rft.date=2015-05-01&rft.volume=59&rft.issue=5&rft.spage=2934&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.05163-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Number of references - 22 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Parasites; Human diseases; Therapy; Malaria; Public health; Clinical isolates; artemisinin; Mefloquine; artesunate; copy number; Plasmodium falciparum; Cambodia DO - http://dx.doi.org/10.1128/AAC.05163-14 ER - TY - JOUR T1 - Infant temperament: stability by age, gender, birth order, term status, and socioeconomic status AN - 1683082026; 4675602 AB - Two complementary studies focused on stability of infant temperament across the 1st year and considered infant age, gender, birth order, term status, and socioeconomic status (SES) as moderators. Study 1 consisted of 73 mothers of firstborn term girls and boys queried at 2, 5, and 13 months of age. Study 2 consisted of 335 mothers of infants of different gender, birth order, term status, and SES queried at 6 and 12 months. Consistent positive and negative affectivity factors emerged at all time points across both studies. Infant temperament proved stable and robust across gender, birth order, term status, and SES. Stability coefficients for temperament factors and scales were medium to large for shorter ( 10 months) intervals. Reprinted by permission of the University of Chicago Press. © All rights reserved JF - Child development AU - Auestad, Nancy AU - O' Connor, Deborah L AU - Bornstein, Marc H AU - Putnick, Diane L AU - Gartstein, Maria A AU - Hahn, Chun-shin AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development ; Washington State University ; National Dairy Research Institute ; University of Toronto Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 844 EP - 863 VL - 86 IS - 3 SN - 0009-3920, 0009-3920 KW - Sociology KW - Birth KW - Age KW - Socioeconomic status KW - Gender KW - Coefficients KW - Infants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683082026?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Child+development&rft.atitle=Infant+temperament%3A+stability+by+age%2C+gender%2C+birth+order%2C+term+status%2C+and+socioeconomic+status&rft.au=Auestad%2C+Nancy%3BO%27+Connor%2C+Deborah+L%3BBornstein%2C+Marc+H%3BPutnick%2C+Diane+L%3BGartstein%2C+Maria+A%3BHahn%2C+Chun-shin&rft.aulast=Auestad&rft.aufirst=Nancy&rft.date=2015-05-01&rft.volume=86&rft.issue=3&rft.spage=844&rft.isbn=&rft.btitle=&rft.title=Child+development&rft.issn=00093920&rft_id=info:doi/10.1111%2Fcdev.12367 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-05-26 N1 - Last updated - 2015-05-26 N1 - SubjectsTermNotLitGenreText - 6495 2212; 1635 11574; 2446 7815 971 2085 2088 10642 2688 2449 10404 12233; 5421 6091; 11988 4011 3974 9390 11932 2328 11935 5837 2360 2688 2449 10404 11936; 646 DO - http://dx.doi.org/10.1111/cdev.12367 ER - TY - JOUR T1 - Cancer information seekers in China: a preliminary profile AN - 1683080448; 4673782 AB - Cancer is now the leading cause of death in China. Effective communication about cancer risk and prevention is an important component of cancer control. Yet, research in this area is very limited in China. This study used probability sample survey data from 2 Chinese cities (Beijing and Hefei, Anhui Province) to investigate potential predictors of self-initiated cancer information seeking. Analysis showed that cancer information seekers in China were likely to be married, relatively educated, earning modest incomes, living in rural areas, smoking occasionally, having a family cancer history, relatively trusting of the media for health information, somewhat knowledgeable about cancer, having nonfatalistic attitudes about cancer, and seeing a personal need for more cancer information. The pattern of results, particularly the lack of influence of personal health and risk perception factors, highlights the possibility that seeking for others might be more prevalent than seeking for self in China. Overall, findings suggest that emphasizing family need and mobilizing family support might be a productive approach to cancer communication interventions in China. Reprinted by permission of Taylor & Francis Ltd. JF - Journal of health communication AU - Zhao, Xiaoquan AU - Mao, Qunan AU - Kreps, Gary L AU - Yu, Guoming AU - Li, Yinghua AU - Chou, Sylvia Wen-ying AU - Perkosie, Alexander AU - Nie, Xueqiong AU - Xu, Zihoa AU - Song, Meijie AU - Kim, Paula AD - George Mason University ; China Ministry of Health ; Renmin University of China ; National Institutes of Health ; National Cancer Institute Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 616 EP - 626 VL - 20 IS - 5 SN - 1081-0730, 1081-0730 KW - Sociology KW - Information KW - Causes of death KW - Health care KW - Survey data KW - Communication KW - China KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683080448?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+health+communication&rft.atitle=Cancer+information+seekers+in+China%3A+a+preliminary+profile&rft.au=Zhao%2C+Xiaoquan%3BMao%2C+Qunan%3BKreps%2C+Gary+L%3BYu%2C+Guoming%3BLi%2C+Yinghua%3BChou%2C+Sylvia+Wen-ying%3BPerkosie%2C+Alexander%3BNie%2C+Xueqiong%3BXu%2C+Zihoa%3BSong%2C+Meijie%3BKim%2C+Paula&rft.aulast=Zhao&rft.aufirst=Xiaoquan&rft.date=2015-05-01&rft.volume=20&rft.issue=5&rft.spage=616&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2015.1012244 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-05-26 N1 - Last updated - 2015-05-26 N1 - SubjectsTermNotLitGenreText - 1939 3617 6220; 2091 3303; 2572; 5775 13521; 6515; 12427 12429; 93 116 30 DO - http://dx.doi.org/10.1080/10810730.2015.1012244 ER - TY - JOUR T1 - Pharmacology of cognitive enhancers for exposure-based therapy of fear, anxiety and trauma-related disorders. AN - 1682205604; 25550231 AB - Pathological fear and anxiety are highly debilitating and, despite considerable advances in psychotherapy and pharmacotherapy they remain insufficiently treated in many patients with PTSD, phobias, panic and other anxiety disorders. Increasing preclinical and clinical evidence indicates that pharmacological treatments including cognitive enhancers, when given as adjuncts to psychotherapeutic approaches [cognitive behavioral therapy including extinction-based exposure therapy] enhance treatment efficacy, while using anxiolytics such as benzodiazepines as adjuncts can undermine long-term treatment success. The purpose of this review is to outline the literature showing how pharmacological interventions targeting neurotransmitter systems including serotonin, dopamine, noradrenaline, histamine, glutamate, GABA, cannabinoids, neuropeptides (oxytocin, neuropeptides Y and S, opioids) and other targets (neurotrophins BDNF and FGF2, glucocorticoids, L-type-calcium channels, epigenetic modifications) as well as their downstream signaling pathways, can augment fear extinction and strengthen extinction memory persistently in preclinical models. Particularly promising approaches are discussed in regard to their effects on specific aspects of fear extinction namely, acquisition, consolidation and retrieval, including long-term protection from return of fear (relapse) phenomena like spontaneous recovery, reinstatement and renewal of fear. We also highlight the promising translational value of the preclinial research and the clinical potential of targeting certain neurochemical systems with, for example d-cycloserine, yohimbine, cortisol, and L-DOPA. The current body of research reveals important new insights into the neurobiology and neurochemistry of fear extinction and holds significant promise for pharmacologically-augmented psychotherapy as an improved approach to treat trauma and anxiety-related disorders in a more efficient and persistent way promoting enhanced symptom remission and recovery. Copyright © 2014. Published by Elsevier Inc. JF - Pharmacology & therapeutics AU - Singewald, N AU - Schmuckermair, C AU - Whittle, N AU - Holmes, A AU - Ressler, K J AD - Department of Pharmacology and Toxicology, Institute of Pharmacy and CMBI, Leopold-Franzens University of Innsbruck, Innrain 80-82, A-6020 Innsbruck, Austria. Electronic address: nicolas.singewald@uibk.ac.at. ; Department of Pharmacology and Toxicology, Institute of Pharmacy and CMBI, Leopold-Franzens University of Innsbruck, Innrain 80-82, A-6020 Innsbruck, Austria. ; Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, MD, USA. ; Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA, USA. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 150 EP - 190 VL - 149 KW - Nootropic Agents KW - 0 KW - Index Medicus KW - Exposure therapy KW - Drug development KW - Cognitive enhancer KW - Reconsolidation KW - Fear extinction KW - Augmented relearning KW - Animals KW - Combined Modality Therapy KW - Humans KW - Signal Transduction -- drug effects KW - Models, Neurological KW - Synaptic Transmission -- drug effects KW - Phobic Disorders -- drug therapy KW - Anxiety -- therapy KW - Anxiety -- drug therapy KW - Implosive Therapy KW - Nootropic Agents -- therapeutic use KW - Extinction, Psychological -- drug effects KW - Nootropic Agents -- pharmacology KW - Stress Disorders, Post-Traumatic -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1682205604?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacology+%26+therapeutics&rft.atitle=Pharmacology+of+cognitive+enhancers+for+exposure-based+therapy+of+fear%2C+anxiety+and+trauma-related+disorders.&rft.au=Singewald%2C+N%3BSchmuckermair%2C+C%3BWhittle%2C+N%3BHolmes%2C+A%3BRessler%2C+K+J&rft.aulast=Singewald&rft.aufirst=N&rft.date=2015-05-01&rft.volume=149&rft.issue=&rft.spage=150&rft.isbn=&rft.btitle=&rft.title=Pharmacology+%26+therapeutics&rft.issn=1879-016X&rft_id=info:doi/10.1016%2Fj.pharmthera.2014.12.004 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-15 N1 - Date created - 2015-03-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Br J Psychiatry. 1993 Jun;162:776-87 [8101126] Nature. 1993 Oct 28;365(6449):855-9 [8413673] Neurosci Lett. 1993 Jun 25;156(1-2):51-3 [8414189] J Consult 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updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.pharmthera.2014.12.004 ER - TY - JOUR T1 - Current concepts of immune based treatments for patients with HCC: from basic science to novel treatment approaches. AN - 1682205213; 25666193 AB - The recent approval of two immune checkpoint inhibitors for the treatment of malignant melanoma has sparked great interest by physicians and basic scientists searching for novel therapeutics for GI cancer. Chronic inflammation is recognised as a major risk factor for the development of hepatocellular carcinoma (HCC) and makes this type of cancer a potentially ideal target for an immune based treatment approach. Further evidence for a critical role of immune responses in patients with HCC is derived from the fact that immune signatures and profiles predict patients' outcome as well as the fact that tumour-induced spontaneous antitumour immunity can be detected. In addition ablative therapies can lead to changes in the number, phenotype and function of different immune cell subsets, which correlate with patients' survival. Various HCC-specific mouse models have been developed, which improve our understanding of hepatocarcinogenesis and tumour-immune cell interactions, and lead to the development of novel immune based treatment approaches, which are currently being evaluated in preclinical and in early clinical settings. Immune checkpoint blockade along with adoptive immune cell therapy and vaccine approaches are currently being evaluated either alone or in combination with other treatments. Here, we provide an overview for the rationale of immunotherapy in HCC, summarise ongoing studies and provide a perspective for immune based approaches in patients with HCC. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions. JF - Gut AU - Greten, Tim F AU - Wang, Xin W AU - Korangy, Firouzeh AD - Gastrointestinal Malignancy Section, Thoracic and Gastrointestinal Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, USA. ; Liver Carcinogenesis Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, USA. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 842 EP - 848 VL - 64 IS - 5 KW - Cancer Vaccines KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - HEPATOCELLULAR CARCINOMA KW - LIVER IMMUNOLOGY KW - Animals KW - Humans KW - Cancer Vaccines -- therapeutic use KW - Disease Models, Animal KW - Translational Medical Research -- methods KW - Immune Tolerance KW - Neoplasm Regression, Spontaneous -- immunology KW - Clinical Trials as Topic -- methods KW - Liver Neoplasms -- therapy KW - Carcinoma, Hepatocellular -- therapy KW - Carcinoma, Hepatocellular -- immunology KW - Liver Neoplasms -- immunology KW - Immunotherapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1682205213?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gut&rft.atitle=Current+concepts+of+immune+based+treatments+for+patients+with+HCC%3A+from+basic+science+to+novel+treatment+approaches.&rft.au=Greten%2C+Tim+F%3BWang%2C+Xin+W%3BKorangy%2C+Firouzeh&rft.aulast=Greten&rft.aufirst=Tim&rft.date=2015-05-01&rft.volume=64&rft.issue=5&rft.spage=842&rft.isbn=&rft.btitle=&rft.title=Gut&rft.issn=1468-3288&rft_id=info:doi/10.1136%2Fgutjnl-2014-307990 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-09 N1 - Date created - 2015-04-04 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1136/gutjnl-2014-307990 ER - TY - JOUR T1 - Persistent organic pollutants (POPs) and fibroids: results from the ENDO study AN - 1680461065; PQ0001495811 AB - To evaluate the association between persistent organic pollutants (POPs) and uterine fibroids, we used previously collected data from a cohort of women aged 18-44 years undergoing laparoscopy or laparotomy at 14 participating hospital surgical centers (n=473). POP concentrations were measured in omental fat and serum. Presence of fibroids was defined on the basis of a postoperative diagnosis (n=99). Odds ratios (OR) and 95% confidence interval (CI) for each POP by biologic medium were estimated using unconditional logistic regression adjusted for identified covariates. Concentrations were higher in omental fat than in serum for all POPs. Serum p,p'-dichlorodiphenyldichloroethylene (p,p'-DDE) was the only POP associated with fibroids (per 1-SD increase in log-transformed p,p'-DDE OR (95% CI): 1.37 (1.05-1.80)). In analyses excluding women diagnosed with endometriosis, a number of polychlorinated biphenyls (PCBs) measured in omental fat were associated with fibroids (PCB 99: 1.64 (1.08, 2.49); PCB 138: 1.64 (1.03, 2.59); PCB 146: 1.54 (1.01, 2.37); PCB 153: 1.88 (1.12, 3.13); PCB 196: 1.60 (1.02, 2.51); PCB 206: 1.52 (1.01, 2.29)). Although exploratory, our study suggests that PCBs may be associated with fibroids in the absence of other gynecologic disorders such as endometriosis, but the associations varied by biologic media with more POPs emerging when quantified in fat. JF - Journal of Exposure Science and Environmental Epidemiology AU - Trabert, Britton AU - Chen, Zhen AU - Kannan, Kurunthachalam AU - Peterson, C Matthew AU - Pollack, Anna Z AU - Sun, Liping AU - Buck Louis, Germaine M AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland, USA Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 278 EP - 285 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 25 IS - 3 SN - 1559-0631, 1559-0631 KW - Toxicology Abstracts; Pollution Abstracts; Health & Safety Science Abstracts; Environment Abstracts KW - Uterus KW - Data processing KW - Laparoscopy KW - Endometriosis KW - polychlorinated biphenyls KW - Pollutants KW - Surgery KW - Persistent organic pollutants KW - PCB compounds KW - PCB KW - Hospitals KW - H 12000:Epidemiology and Public Health KW - X 24350:Industrial Chemicals KW - P 6000:TOXICOLOGY AND HEALTH KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680461065?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.atitle=Persistent+organic+pollutants+%28POPs%29+and+fibroids%3A+results+from+the+ENDO+study&rft.au=Trabert%2C+Britton%3BChen%2C+Zhen%3BKannan%2C+Kurunthachalam%3BPeterson%2C+C+Matthew%3BPollack%2C+Anna+Z%3BSun%2C+Liping%3BBuck+Louis%2C+Germaine+M&rft.aulast=Trabert&rft.aufirst=Britton&rft.date=2015-05-01&rft.volume=25&rft.issue=3&rft.spage=278&rft.isbn=&rft.btitle=&rft.title=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.issn=15590631&rft_id=info:doi/10.1038%2Fjes.2014.31 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Last updated - 2016-03-30 N1 - SubjectsTermNotLitGenreText - Uterus; Data processing; polychlorinated biphenyls; Pollutants; Laparoscopy; Endometriosis; PCB; Hospitals; Surgery; Persistent organic pollutants; PCB compounds DO - http://dx.doi.org/10.1038/jes.2014.31 ER - TY - JOUR T1 - Estrogenic and anti-estrogenic activity of off-the-shelf hair and skin care products AN - 1680458595; PQ0001495812 AB - Use of personal care products is widespread in the United States but tends to be greater among African Americans than whites. Of special concern is the possible hazard of absorption of chemicals with estrogenic activity (EA) or anti-EA (AEA) in these products. Such exposure may have adverse health effects, especially when it occurs during developmental windows (e.g., prepubertally) when estrogen levels are low. We assessed the ethanol extracts of eight commonly used hair and skin products popular among African Americans for EA and AEA using a cell proliferation assay with the estrogen sensitive MCF-7:WS8 cell line derived from a human breast cancer. Four of the eight personal care products tested (Oil Hair Lotion, Extra-dry Skin Lotion, Intensive Skin Lotion, Petroleum Jelly) demonstrated detectable EA, whereas three (Placenta Hair Conditioner, Tea-Tree Hair Conditioner, Cocoa Butter Skin Cream) exhibited AEA. Our data indicate that hair and skin care products can have EA or AEA, and suggest that laboratory studies are warranted to investigate the in vivo activity of such products under chronic exposure conditions as well as epidemiologic studies to investigate potential adverse health effects that might be associated with use of such products. JF - Journal of Exposure Science and Environmental Epidemiology AU - Myers, Sharon L AU - Yang, Chun Z AU - Bittner, George D AU - Witt, Kristine L AU - Tice, Raymond R AU - Baird, Donna D AD - 1] Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA [2] University of California Davis Health System, Sacramento, CA, USA Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 271 EP - 277 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 25 IS - 3 SN - 1559-0631, 1559-0631 KW - Toxicology Abstracts; Health & Safety Science Abstracts KW - Chemicals KW - Consumer products KW - Oil KW - Cocoa butter KW - Chronic exposure KW - Placenta KW - Petroleum KW - Absorption KW - Cream KW - Ethnic groups KW - Ethanol KW - Estrogens KW - Data processing KW - Lotions KW - Skin KW - estrogenic activity KW - Hair KW - Cancer KW - USA KW - Breast cancer KW - Cell proliferation KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - X 24340:Cosmetics, Toiletries & Household Products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680458595?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.atitle=Estrogenic+and+anti-estrogenic+activity+of+off-the-shelf+hair+and+skin+care+products&rft.au=Myers%2C+Sharon+L%3BYang%2C+Chun+Z%3BBittner%2C+George+D%3BWitt%2C+Kristine+L%3BTice%2C+Raymond+R%3BBaird%2C+Donna+D&rft.aulast=Myers&rft.aufirst=Sharon&rft.date=2015-05-01&rft.volume=25&rft.issue=3&rft.spage=271&rft.isbn=&rft.btitle=&rft.title=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.issn=15590631&rft_id=info:doi/10.1038%2Fjes.2014.32 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Estrogens; Skin; Lotions; Data processing; Hair; estrogenic activity; Oil; Cocoa butter; Chronic exposure; Petroleum; Placenta; Cream; Breast cancer; Cell proliferation; Ethanol; Chemicals; Consumer products; Absorption; Cancer; Ethnic groups; USA DO - http://dx.doi.org/10.1038/jes.2014.32 ER - TY - JOUR T1 - Key role for scavenger receptor B-I in the integrative physiology of host defense during bacterial pneumonia. AN - 1680181599; 25336169 AB - Scavenger receptor B-I (SR-BI) is a multirecognition receptor that regulates cholesterol trafficking and cardiovascular inflammation. Although it is expressed by neutrophils (PMNs) and lung-resident cells, no role for SR-BI has been defined in pulmonary immunity. Herein, we report that, compared with SR-BI(+/+) counterparts, SR-BI(-/-) mice suffer markedly increased mortality during bacterial pneumonia associated with higher bacterial burden in the lung and blood, deficient induction of the stress glucocorticoid corticosterone, higher serum cytokines, and increased organ injury. SR-BI(-/-) mice had significantly increased PMN recruitment and cytokine production in the infected airspace. This was associated with defective hematopoietic cell-dependent clearance of lipopolysaccharide from the airspace and increased cytokine production by SR-BI(-/-) macrophages. Corticosterone replacement normalized alveolar neutrophilia but not alveolar cytokines, bacterial burden, or mortality, suggesting that adrenal insufficiency derepresses PMN trafficking to the SR-BI(-/-) airway in a cytokine-independent manner. Despite enhanced alveolar neutrophilia, SR-BI(-/-) mice displayed impaired phagocytic killing. Bone marrow chimeras revealed this defect to be independent of the dyslipidemia and adrenal insufficiency of SR-BI(-/-) mice. During infection, SR-BI(-/-) PMNs displayed deficient oxidant production and CD11b externalization, and increased surface L-selectin, suggesting defective activation. Taken together, SR-BI coordinates several steps in the integrated neutrophilic host defense response to pneumonia. JF - Mucosal immunology AU - Gowdy, K M AU - Madenspacher, J H AU - Azzam, K M AU - Gabor, K A AU - Janardhan, K S AU - Aloor, J J AU - Fessler, M B AD - Division of Intramural Research, Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA. ; 1] Cellular and Molecular Pathology Branch, National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA [2] Integrated Laboratory Systems, Inc., National Institutes of Health, Research Triangle Park, North Carolina, USA. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 559 EP - 571 VL - 8 IS - 3 KW - Antigens, CD11b KW - 0 KW - Cytokines KW - Lipopolysaccharides KW - Scarb1 protein, mouse KW - Scavenger Receptors, Class B KW - L-Selectin KW - 126880-86-2 KW - Corticosterone KW - W980KJ009P KW - Index Medicus KW - Animals KW - Antigens, CD11b -- genetics KW - Lipopolysaccharides -- metabolism KW - Cytokines -- biosynthesis KW - Adrenal Glands -- immunology KW - Cytokines -- immunology KW - Mice KW - Antigens, CD11b -- immunology KW - Bone Marrow Cells -- immunology KW - Adrenal Glands -- pathology KW - Mice, Knockout KW - L-Selectin -- immunology KW - Corticosterone -- biosynthesis KW - L-Selectin -- genetics KW - Klebsiella pneumoniae -- immunology KW - Lipopolysaccharides -- immunology KW - Bone Marrow Cells -- pathology KW - Gene Expression Regulation KW - Bacterial Load KW - Signal Transduction KW - Male KW - Survival Analysis KW - Corticosterone -- immunology KW - Pneumonia, Bacterial -- pathology KW - Klebsiella Infections -- mortality KW - Neutrophils -- pathology KW - Neutrophils -- immunology KW - Pneumonia, Bacterial -- genetics KW - Lung -- pathology KW - Pneumonia, Bacterial -- immunology KW - Pneumonia, Bacterial -- mortality KW - Lung -- immunology KW - Klebsiella Infections -- genetics KW - Scavenger Receptors, Class B -- genetics KW - Klebsiella Infections -- pathology KW - Klebsiella Infections -- immunology KW - Scavenger Receptors, Class B -- immunology KW - Scavenger Receptors, Class B -- deficiency UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680181599?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Mucosal+immunology&rft.atitle=Key+role+for+scavenger+receptor+B-I+in+the+integrative+physiology+of+host+defense+during+bacterial+pneumonia.&rft.au=Gowdy%2C+K+M%3BMadenspacher%2C+J+H%3BAzzam%2C+K+M%3BGabor%2C+K+A%3BJanardhan%2C+K+S%3BAloor%2C+J+J%3BFessler%2C+M+B&rft.aulast=Gowdy&rft.aufirst=K&rft.date=2015-05-01&rft.volume=8&rft.issue=3&rft.spage=559&rft.isbn=&rft.btitle=&rft.title=Mucosal+immunology&rft.issn=1935-3456&rft_id=info:doi/10.1038%2Fmi.2014.88 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-08 N1 - Date created - 2015-05-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Immunol. 2008 Nov 15;181(10):7147-56 [18981136] Cell Host Microbe. 2008 Sep 11;4(3):271-82 [18779053] PLoS One. 2009;4(12):e8448 [20041149] Biochem Biophys Res Commun. 2010 Jan 1;391(1):523-8 [19941833] Lipids Health Dis. 2010;9:16 [20137092] Vet Immunol Immunopathol. 2011 Feb 15;139(2-4):217-28 [21112644] N Engl J Med. 2011 Jan 13;364(2):136-45 [21226579] Am J Respir Crit Care Med. 2011 Jan 15;183(2):157-64 [20693379] J Biol Chem. 2011 Feb 4;286(5):3332-41 [21123180] J Immunol. 2011 Mar 1;186(5):3197-205 [21282514] Nat Cell Biol. 2011 Apr;13(4):423-33 [21423178] Arterioscler Thromb Vasc Biol. 2011 Jun;31(6):1333-41 [21474825] Int J Biochem Cell Biol. 2011 Jul;43(7):1065-70 [19497383] Infect Immun. 2011 Jul;79(7):2865-70 [21576343] Crit Care Clin. 2011 Jul;27(3):589-607 [21742218] Proc Natl Acad Sci U S A. 2011 Sep 20;108(38):16074-9 [21911374] J Exp Med. 2013 May 6;210(5):891-904 [23630228] Free Radic Biol Med. 2013 Jul;60:56-62 [23402870] J Immunol. 2013 Jul 1;191(1):238-48 [23733871] Nat Rev Immunol. 2013 Sep;13(9):621-34 [23928573] Cardiovasc Drugs Ther. 2013 Oct;27(5):425-31 [23812592] Can J Vet Res. 2013 Apr;77(2):120-5 [24082403] Am J Respir Cell Mol Biol. 2014 Feb;50(2):253-62 [24010952] J Immunol. 2012 Feb 1;188(3):1371-80 [22205027] Respir Med. 2012 Jun;106(6):905-8 [22402329] Am J Respir Crit Care Med. 2012 Nov 1;186(9):824-9 [22798317] Arterioscler Thromb Vasc Biol. 2013 Feb;33(2):e39-46 [23202366] Infect Immun. 2007 Aug;75(8):3999-4005 [17548480] Cell Microbiol. 2007 Aug;9(8):2030-9 [17419716] Toxicol Appl Pharmacol. 2007 Jul 15;222(2):227-34 [17602719] Am J Respir Cell Mol Biol. 2000 Jan;22(1):85-91 [10615069] Am J Pathol. 2001 Jan;158(1):179-88 [11141491] Cytokines Cell Mol Ther. 2000 Dec;6(4):177-87 [11565956] Am J Respir Crit Care Med. 2002 Dec 15;166(12 Pt 2):S62-6 [12471091] J Biol Chem. 2003 Jun 20;278(25):22771-80 [12651854] J Med Genet. 2003 Jun;40(6):453-8 [12807968] J Exp Med. 2004 Jul 19;200(2):267-72 [15263032] J Biol Chem. 2004 Aug 20;279(34):36072-82 [15199068] Science. 1996 Jan 26;271(5248):518-20 [8560269] J Immunol. 1996 Sep 15;157(6):2514-20 [8805652] J Lipid Res. 1997 Jul;38(7):1289-98 [9254056] Am J Respir Cell Mol Biol. 2005 Jun;32(6):531-9 [15778492] Curr Drug Targets Inflamm Allergy. 2005 Aug;4(4):455-63 [16101522] Clin Biochem. 2006 Mar;39(3):287-92 [16487950] J Clin Invest. 2008 Jan;118(1):364-75 [18064300] N Engl J Med. 2008 Feb 14;358(7):716-27 [18272895] J Virol. 2008 Apr;82(7):3466-79 [18216094] Cell. 2008 Apr 18;133(2):235-49 [18423196] J Immunol. 2008 Nov 15;181(10):7332-40 [18981156] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/mi.2014.88 ER - TY - JOUR T1 - Systemic Agonistic Anti-CD40 Treatment of Tumor-Bearing Mice Modulates Hepatic Myeloid-Suppressive Cells and Causes Immune-Mediated Liver Damage. AN - 1680175619; 25637366 AB - Immune-stimulatory mAbs are currently being evaluated as antitumor agents. Although overall toxicity from these agents appears to be moderate, liver toxicities have been reported and are not completely understood. We studied the effect of systemic CD40 antibody treatment on myeloid cells in the spleen and liver. Naïve and tumor-bearing mice were treated systemically with agonistic anti-CD40 antibody. Immune cell subsets in the liver and spleen, serum transaminases, and liver histologies were analyzed after antibody administration. Nox2(-/-), Cd40(-/-), and bone marrow chimeric mice were used to study the mechanism by which agonistic anti-CD40 mediates its effects in vivo. Suppressor function of murine and human tumor-induced myeloid-derived suppressor cells (MDSC) was studied upon CD40 ligation. Agonistic CD40 antibody caused liver damage within 24 hours after injection in two unrelated tumor models and mice strains. Using bone marrow chimeras, we demonstrate that CD40 antibody-induced hepatitis in tumor-bearing mice was dependent on the presence of CD40-expressing hematopoietic cells. Agonistic CD40 ligation-dependent liver damage was induced by the generation of reactive oxygen species. Furthermore, agonistic CD40 antibody resulted in increased CD80-positive and CD40-positive liver CD11b(+)Gr-1(+) immature myeloid cells. CD40 ligation on tumor-induced murine and human CD14(+)HLA-DR(low) peripheral blood mononuclear cells from patients with cancer reduced their immune suppressor function. Collectively, agonistic CD40 antibody treatment activated tumor-induced myeloid cells, caused myeloid-dependent hepatotoxicity, and ameliorated the suppressor function of murine and human MDSC. Collectively, our data suggest that CD40 may mature immunosuppressive myeloid cells and thereby cause liver damage in mice with an accumulation of tumor-induced hepatic MDSC. ©2015 American Association for Cancer Research. JF - Cancer immunology research AU - Medina-Echeverz, José AU - Ma, Chi AU - Duffy, Austin G AU - Eggert, Tobias AU - Hawk, Nga AU - Kleiner, David E AU - Korangy, Firouzeh AU - Greten, Tim F AD - Gastrointestinal Malignancy Section, Thoracic and Gastrointestinal Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland. ; Experimental Transplantation and Immunology Branch, NIH, Bethesda, Maryland. ; Laboratory of Pathology, National Cancer Institute, NIH, Bethesda, Maryland. ; Gastrointestinal Malignancy Section, Thoracic and Gastrointestinal Oncology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland. tim.greten@nih.gov. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 557 EP - 566 VL - 3 IS - 5 KW - Antibodies, Monoclonal KW - 0 KW - Antigens, CD40 KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Index Medicus KW - Chemical and Drug Induced Liver Injury -- blood KW - Neoplasms -- drug therapy KW - Animals KW - Liver -- cytology KW - Spleen -- cytology KW - Humans KW - Neoplasms -- blood KW - Cell Line, Tumor KW - Mice, Transgenic KW - Mice, Inbred BALB C KW - Chemical and Drug Induced Liver Injury -- immunology KW - Aspartate Aminotransferases -- blood KW - Alanine Transaminase -- blood KW - Liver -- drug effects KW - Mice, Inbred C57BL KW - Spleen -- drug effects KW - Female KW - Neoplasms -- immunology KW - Myeloid Cells -- immunology KW - Antibodies, Monoclonal -- adverse effects KW - Antibodies, Monoclonal -- pharmacology KW - Myeloid Cells -- drug effects KW - Antigens, CD40 -- antagonists & inhibitors KW - Antigens, CD40 -- immunology KW - Antibodies, Monoclonal -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680175619?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+immunology+research&rft.atitle=Systemic+Agonistic+Anti-CD40+Treatment+of+Tumor-Bearing+Mice+Modulates+Hepatic+Myeloid-Suppressive+Cells+and+Causes+Immune-Mediated+Liver+Damage.&rft.au=Medina-Echeverz%2C+Jos%C3%A9%3BMa%2C+Chi%3BDuffy%2C+Austin+G%3BEggert%2C+Tobias%3BHawk%2C+Nga%3BKleiner%2C+David+E%3BKorangy%2C+Firouzeh%3BGreten%2C+Tim+F&rft.aulast=Medina-Echeverz&rft.aufirst=Jos%C3%A9&rft.date=2015-05-01&rft.volume=3&rft.issue=5&rft.spage=557&rft.isbn=&rft.btitle=&rft.title=Cancer+immunology+research&rft.issn=2326-6074&rft_id=info:doi/10.1158%2F2326-6066.CIR-14-0182 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-08 N1 - Date created - 2015-05-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Med. 1999 Jul;5(7):780-7 [10395323] J Immunol. 2009 Feb 15;182(4):1818-28 [19201833] Int Immunol. 2003 Jul;15(7):817-26 [12807820] Blood. 2003 Aug 15;102(4):1449-57 [12714523] Cancer Res. 2003 Aug 1;63(15):4490-6 [12907622] J Immunol. 2004 Jan 1;172(1):45-53 [14688308] Annu Rev Immunol. 1998;16:111-35 [9597126] Nature. 1998 Jun 4;393(6684):413-4 [9623994] J Exp Med. 1999 Jan 18;189(2):441-6 [9892626] Nat Med. 1999 May;5(5):548-53 [10229232] Nat Med. 1999 Jul;5(7):774-9 [10395322] J Immunol. 2009 May 1;182(9):5693-701 [19380816] Proc Natl Acad Sci U S A. 2009 May 5;106(18):7513-8 [19383782] Cancer Res. 2009 Jul 1;69(13):5514-21 [19549903] Proc Natl Acad Sci U S A. 2009 Nov 17;106(46):19455-60 [19892741] Cancer Res. 2010 Jan 1;70(1):99-108 [19996287] J Leukoc Biol. 2010 Apr;87(4):713-25 [20042467] J Gastroenterol Hepatol. 2011 Jan;26 Suppl 1:173-9 [21199529] Clin Cancer Res. 2011 Apr 15;17(8):2270-80 [21389097] Int Immunopharmacol. 2011 Jul;11(7):802-7 [21237299] Cancer Res. 2011 Jun 15;71(12):4074-84 [21540234] Blood. 2011 Jun 16;117(24):6532-41 [21493801] J Leukoc Biol. 2012 Jan;91(1):167-81 [21954284] Nat Rev Cancer. 2012 Apr;12(4):252-64 [22437870] Nat Rev Immunol. 2012 Apr;12(4):253-68 [22437938] Hepatology. 2013 Feb;57(2):829-39 [23081697] Cancer Immunol Immunother. 2013 Feb;62(2):299-307 [23011590] Clin Cancer Res. 2013 Mar 1;19(5):1035-43 [23460534] Clin Cancer Res. 2013 Mar 1;19(5):1044-53 [23460535] Cancer Res. 2013 Apr 1;73(7):2031-43 [23536564] J Clin Invest. 2013 Apr;123(4):1580-9 [23454751] J Hepatol. 2013 Nov;59(5):1007-13 [23796475] Clin Cancer Res. 2013 Nov 15;19(22):6286-95 [23983255] Int Immunopharmacol. 2013 Dec;17(4):1141-7 [24201083] Nat Rev Clin Oncol. 2014 Feb;11(2):91-9 [24445516] Cancer Gene Ther. 2014 Mar;21(3):95-102 [24481488] Cancer Immunol Res. 2014 Jan;2(1):80-90 [24778163] Cancer Res. 2014 May 1;74(9):2412-21 [24556719] Eur J Immunol. 2014 Aug;44(8):2457-67 [24810636] PLoS One. 2014;9(11):e112717 [25401795] Hepatology. 2005 Aug;42(2):372-80 [16025512] Am J Physiol Gastrointest Liver Physiol. 2006 Apr;290(4):G583-9 [16537970] Cancer Res. 2006 Jul 1;66(13):6807-15 [16818658] J Clin Oncol. 2007 Mar 1;25(7):876-83 [17327609] J Immunol. 2008 Feb 1;180(3):1471-81 [18209042] Gastroenterology. 2008 Jul;135(1):234-43 [18485901] J Immunol. 2008 Oct 15;181(8):5791-802 [18832739] Clin Immunol. 2008 Dec;129(3):471-81 [18790673] Hepatology. 2008 Dec;48(6):1979-88 [18942689] Hepatology. 2003 Jun;37(6):1451-60 [12774025] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/2326-6066.CIR-14-0182 ER - TY - JOUR T1 - Structural and biochemical characterization of a novel aminopeptidase from human intestine. AN - 1677887460; 25752612 AB - N-acetylated α-linked acidic dipeptidase-like protein (NAALADase L), encoded by the NAALADL1 gene, is a close homolog of glutamate carboxypeptidase II, a metallopeptidase that has been intensively studied as a target for imaging and therapy of solid malignancies and neuropathologies. However, neither the physiological functions nor structural features of NAALADase L are known at present. Here, we report a thorough characterization of the protein product of the human NAALADL1 gene, including heterologous overexpression and purification, structural and biochemical characterization, and analysis of its expression profile. By solving the NAALADase L x-ray structure, we provide the first experimental evidence that it is a zinc-dependent metallopeptidase with a catalytic mechanism similar to that of glutamate carboxypeptidase II yet distinct substrate specificity. A proteome-based assay revealed that the NAALADL1 gene product possesses previously unrecognized aminopeptidase activity but no carboxy- or endopeptidase activity. These findings were corroborated by site-directed mutagenesis and identification of bestatin as a potent inhibitor of the enzyme. Analysis of NAALADL1 gene expression at both the mRNA and protein levels revealed the small intestine as the major site of protein expression and points toward extensive alternative splicing of the NAALADL1 gene transcript. Taken together, our data imply that the NAALADL1 gene product's primary physiological function is associated with the final stages of protein/peptide digestion and absorption in the human digestive system. Based on these results, we suggest a new name for this enzyme: human ileal aminopeptidase (HILAP). © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Tykvart, Jan AU - Bařinka, Cyril AU - Svoboda, Michal AU - Navrátil, Václav AU - Souček, Radko AU - Hubálek, Martin AU - Hradilek, Martin AU - Šácha, Pavel AU - Lubkowski, Jacek AU - Konvalinka, Jan AD - From the Gilead Sciences and IOCB Research Centre, Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, Flemingovo n. 2, Prague 6, Czech Republic, the Departments of Biochemistry and. ; the Institute of Biotechnology, Academy of Sciences of the Czech Republic, Vídeňská 1083, Prague 4, Czech Republic, and. ; From the Gilead Sciences and IOCB Research Centre, Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, Flemingovo n. 2, Prague 6, Czech Republic, Physical and Macromolecular Chemistry, Faculty of Natural Science, Charles University, Albertov 6, Prague 2, Czech Republic. ; From the Gilead Sciences and IOCB Research Centre, Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, Flemingovo n. 2, Prague 6, Czech Republic. ; the Center for Cancer Research, Macromolecular Crystallography Laboratory, NCI, National Institutes of Health, Frederick, Maryland 21702-1201. ; From the Gilead Sciences and IOCB Research Centre, Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, Flemingovo n. 2, Prague 6, Czech Republic, the Departments of Biochemistry and jan.konvalinka@uochb.cas.cz. Y1 - 2015/05/01/ PY - 2015 DA - 2015 May 01 SP - 11321 EP - 11336 VL - 290 IS - 18 KW - Endopeptidases KW - EC 3.4.- KW - Dipeptidyl Peptidase 4 KW - EC 3.4.14.5 KW - Glutamate Carboxypeptidase II KW - EC 3.4.17.21 KW - Index Medicus KW - Aminopeptidase KW - Metalloprotease KW - X-ray Crystallography KW - Protein Degradation KW - Intestinal Metabolism KW - DPP IV Activity KW - Molecular Evolution KW - Human Ileal Aminopeptidase KW - PICS KW - Rats KW - Dipeptidyl Peptidase 4 -- metabolism KW - Animals KW - Gene Expression Regulation, Enzymologic KW - Models, Molecular KW - Humans KW - Endopeptidases -- metabolism KW - Molecular Sequence Data KW - Crystallography, X-Ray KW - Amino Acid Sequence KW - Protein Structure, Tertiary KW - Intestines -- enzymology KW - Glutamate Carboxypeptidase II -- chemistry KW - Glutamate Carboxypeptidase II -- metabolism KW - Glutamate Carboxypeptidase II -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1677887460?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Structural+and+biochemical+characterization+of+a+novel+aminopeptidase+from+human+intestine.&rft.au=Tykvart%2C+Jan%3BBa%C5%99inka%2C+Cyril%3BSvoboda%2C+Michal%3BNavr%C3%A1til%2C+V%C3%A1clav%3BSou%C4%8Dek%2C+Radko%3BHub%C3%A1lek%2C+Martin%3BHradilek%2C+Martin%3B%C5%A0%C3%A1cha%2C+Pavel%3BLubkowski%2C+Jacek%3BKonvalinka%2C+Jan&rft.aulast=Tykvart&rft.aufirst=Jan&rft.date=2015-05-01&rft.volume=290&rft.issue=18&rft.spage=11321&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.628149 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-16 N1 - Date created - 2015-05-02 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 3BXM; PDB; 4TWE; 2PVW N1 - SuppNotes - Cited By: Science. 1999 Oct 22;286(5440):779-82 [10531064] FEBS J. 2014 Jul;281(14):3228-42 [24863754] J Neurochem. 2002 Feb;80(3):477-87 [11905994] J Biol Chem. 2003 Nov 7;278(45):44496-504 [12933810] Anal Biochem. 1970 Apr;34(2):595-8 [5443684] Biochem Pharmacol. 1973 Dec 1;22(23):3099-108 [4202581] Anal Biochem. 1976 May 7;72:248-54 [942051] Methods Enzymol. 1986;121:1-947 [3523121] Int J Pept Protein Res. 1991 Jun;37(6):513-20 [1917309] J Biol Chem. 1997 Dec 5;272(49):31006-15 [9388249] J Biol Chem. 1999 Mar 26;274(13):8470-83 [10085079] Acta Crystallogr D Biol Crystallogr. 2004 Dec;60(Pt 12 Pt 1):2126-32 [15572765] EMBO J. 2006 Mar 22;25(6):1375-84 [16467855] Genome Biol. 2006;7 Suppl 1:S12.1-14 [16925834] J Neurochem. 2007 May;101(3):682-96 [17241121] Prostate. 2008 Feb 1;68(2):171-82 [18076021] J Virol. 2008 Jun;82(12):5869-78 [18400858] J Inorg Biochem. 2008 Sep;102(9):1765-76 [18614239] Biochemistry. 2009 May 19;48(19):4126-38 [19301871] Acta Crystallogr D Biol Crystallogr. 2010 Jan;66(Pt 1):12-21 [20057044] Nat Protoc. 2011 Jan;6(1):111-20 [21212787] Protein Expr Purif. 2012 Mar;82(1):106-15 [22178733] Curr Med Chem. 2012;19(9):1300-9 [22304708] Biochim Biophys Acta. 2001 Dec 17;1550(2):107-16 [11755200] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M114.628149 ER - TY - JOUR T1 - The methyltransferases enhancer of zeste homolog (EZH) 1 and EZH2 control hepatocyte homeostasis and regeneration. AN - 1677882328; 25477280 AB - To investigate the role of enhancer of zeste homolog (EZH) 1 and EZH2 in liver homeostasis, mice were generated that carried Ezh1(-/-) and EZH2(fl/fl) alleles and an Alb-Cre transgene. Only the combined loss of EZH1 and EZH2 in mouse hepatocytes caused a depletion of global trimethylation on Lys 27 of histone H3 (H3K27me3) marks and the specific loss of over ∼1900 genes at 3 mo of age. Ezh1(-/-),Ezh2(fl/fl)Alb-Cre mice exhibited progressive liver abnormalities manifested by the development of regenerative nodules and concomitant periportal fibrosis, inflammatory infiltration, and activation of A6-positive hepatic progenitor cells at 8 mo of age. In response to chronic treatment with carbon tetrachloride, all experimental mice, but none of the controls (n = 27 each), showed increased hepatic degeneration associated with liver dysfunction and reduced ability to proliferate. After two-thirds partial hepatectomy, mutant mice (n = 5) displayed increased liver injury and a blunted regenerative response. Genome-wide analyses at 3 mo of age identified 51 genes that had lost H3K27me3 marks, and their expression was significantly increased. These genes were involved in regulation of cell survival, fibrosis, and proliferation. H3K27me3 levels and liver physiology were unaffected in mice lacking either EZH1 globally or EZH2 specifically in hepatocytes. This work demonstrates a critical redundancy of EZH1 and EZH2 in maintaining hepatic homeostasis and regeneration. © FASEB. JF - FASEB journal : official publication of the Federation of American Societies for Experimental Biology AU - Bae, Woo Kyun AU - Kang, Keunsoo AU - Yu, Ji Hoon AU - Yoo, Kyung Hyun AU - Factor, Valentina M AU - Kaji, Kosuke AU - Matter, Matthias AU - Thorgeirsson, Snorri AU - Hennighausen, Lothar AD - *Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, and Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea; Department of Microbiology, Dankook University, Cheonan, Korea; and New Drug Development Center, Daegu-Gyeongbuk Medical Innovation Foundation, Daegu, Korea drwookyun@chonnam.ac.kr lotharh@mail.nih.gov. ; *Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, and Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea; Department of Microbiology, Dankook University, Cheonan, Korea; and New Drug Development Center, Daegu-Gyeongbuk Medical Innovation Foundation, Daegu, Korea. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 1653 EP - 1662 VL - 29 IS - 5 KW - Biomarkers KW - 0 KW - Histones KW - RNA, Messenger KW - Enhancer of Zeste Homolog 2 Protein KW - EC 2.1.1.43 KW - Ezh1 protein, mouse KW - Ezh2 protein, mouse KW - Polycomb Repressive Complex 2 KW - Index Medicus KW - H3-K27 trimethylation KW - liver regeneration KW - fibrosis KW - Real-Time Polymerase Chain Reaction KW - Animals KW - Fibrosis -- etiology KW - Mice KW - Fibrosis -- metabolism KW - Reverse Transcriptase Polymerase Chain Reaction KW - RNA, Messenger -- genetics KW - Cell Proliferation KW - Mice, Knockout KW - Blotting, Western KW - Fibrosis -- pathology KW - Cells, Cultured KW - Histones -- metabolism KW - Inflammation -- etiology KW - Inflammation -- metabolism KW - Fluorescent Antibody Technique KW - Male KW - Inflammation -- pathology KW - High-Throughput Nucleotide Sequencing KW - Biomarkers -- analysis KW - Polycomb Repressive Complex 2 -- physiology KW - Liver Regeneration -- physiology KW - Hepatocytes -- cytology KW - Homeostasis -- physiology KW - Hepatocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1677882328?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.atitle=The+methyltransferases+enhancer+of+zeste+homolog+%28EZH%29+1+and+EZH2+control+hepatocyte+homeostasis+and+regeneration.&rft.au=Bae%2C+Woo+Kyun%3BKang%2C+Keunsoo%3BYu%2C+Ji+Hoon%3BYoo%2C+Kyung+Hyun%3BFactor%2C+Valentina+M%3BKaji%2C+Kosuke%3BMatter%2C+Matthias%3BThorgeirsson%2C+Snorri%3BHennighausen%2C+Lothar&rft.aulast=Bae&rft.aufirst=Woo&rft.date=2015-05-01&rft.volume=29&rft.issue=5&rft.spage=1653&rft.isbn=&rft.btitle=&rft.title=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.issn=1530-6860&rft_id=info:doi/10.1096%2Ffj.14-261537 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-30 N1 - Date created - 2015-05-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Cell. 2010 May 28;38(4):576-89 [20513432] Bioinformatics. 2009 Aug 1;25(15):1952-8 [19505939] Cell Stem Cell. 2010 Sep 3;7(3):299-313 [20804967] Nature. 2011 Jan 20;469(7330):343-9 [21248841] Genes Dev. 2011 Mar 1;25(5):485-98 [21317239] Mol Cell. 2012 Jan 27;45(2):255-62 [22196887] Nat Med. 2012 Feb;18(2):298-301 [22237151] Nat Protoc. 2012 Mar;7(3):562-78 [22383036] Hepatology. 2012 Aug;56(2):622-31 [22370893] Mol Cell. 2012 Nov 30;48(4):572-86 [23063525] Science. 2012 Dec 14;338(6113):1465-9 [23239736] Brief Bioinform. 2013 Mar;14(2):178-92 [22517427] EMBO J. 2013 Jul 17;32(14):1990-2000 [23673358] Hepatology. 2013 Dec;58(6):2176-87 [23813570] Gastroenterology. 2014 Feb;146(2):349-56 [24315991] Hepatology. 2000 Apr;31(4):851-7 [10733539] Nat Immunol. 2003 Feb;4(2):124-31 [12496962] Nature. 2003 May 15;423(6937):302-5 [12714971] Nature. 2003 Oct 30;425(6961):962-7 [14574365] Am J Pathol. 1994 Aug;145(2):409-22 [8053498] Proc Natl Acad Sci U S A. 1999 Jun 22;96(13):7324-9 [10377413] Genes Dev. 2004 Nov 15;18(22):2699-711 [15545627] Annu Rev Genet. 2004;38:413-43 [15568982] J Clin Invest. 2005 Sep;115(9):2330-40 [16110324] Mol Cell. 2008 Nov 21;32(4):491-502 [19026780] Mol Cell. 2008 Nov 21;32(4):503-18 [19026781] Genome Biol. 2009;10(3):R25 [19261174] Genes Dev. 2010 Aug 15;24(16):1718-30 [20675406] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1096/fj.14-261537 ER - TY - JOUR T1 - Involvement of hepatic stellate cell cytoglobin in acute hepatocyte damage through the regulation of CYP2E1-mediated xenobiotic metabolism. AN - 1676591207; 25686096 AB - Oxygen (O2) is required for cytochrome P450 (CYP)-dependent drug metabolism. Cytoglobin (CYGB) is a unique globin expressed exclusively in hepatic stellate cells (HSCs). However, its role in O2-dependent metabolism in neighboring hepatocytes remains unknown. This study provides evidence that CYGB in HSCs is involved in acetaminophen (N-acetyl-p-aminophenol; APAP)-induced hepatotoxicity. Serum alanine aminotransferase levels were higher in wild-type mice than in Cygb-null mice. Wild-type mice exhibited more severe hepatocyte necrosis around the central vein area compared with Cygb-null mice, thus indicating that CYGB deficiency protects against APAP-induced liver damage. Although no difference in the hepatic expression of CYP2E1, a key enzyme involved in APAP toxicity, was observed between wild-type and Cygb-null mice, the serum levels of the APAP metabolites cysteinyl-APAP and N-acetyl-cysteinyl-APAP were decreased in Cygb-null mice, suggesting reduced APAP metabolism in the livers of Cygb-null mice. In primary cultures, APAP-induced hepatocyte damage was increased by co-culturing with wild-type HSCs but not with Cygb-null HSCs. In addition, cell damage was markedly alleviated under low O2 condition (5% O2), suggesting the requirement of O2 for APAP toxicity. Carbon tetrachloride-induced liver injury (CYP2E1-dependent), but not lipopolysaccharide/D-galactosamine-induced injury (CYP2E1-independent), was similarly alleviated in Cygb-null mice. Considering the function of CYGB as O2 carrier, these results strongly support the hypothesis that HSCs are involved in the CYP2E1-mediated xenobiotic activation by augmenting O2 supply to hepatocytes. In conclusion, CYGB in HSCs contributes to the CYP-mediated metabolism of xenobiotics in hepatocytes by supplying O2 for enzymatic oxidation. JF - Laboratory investigation; a journal of technical methods and pathology AU - Teranishi, Yuga AU - Matsubara, Tsutomu AU - Krausz, Kristopher W AU - Le, Thi T T AU - Gonzalez, Frank J AU - Yoshizato, Katsutoshi AU - Ikeda, Kazuo AU - Kawada, Norifumi AD - Department of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan. ; Department of Anatomy and Regenerative Biology, Graduate School of Medicine, Osaka City University, Osaka, Japan. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; 1] Department of Hepatology, Graduate School of Medicine, Osaka City University, Osaka, Japan [2] Phoenixbio Co., Ltd, Hiroshima, Japan. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 515 EP - 524 VL - 95 IS - 5 KW - Lipopolysaccharides KW - 0 KW - Xenobiotics KW - cytoglobin KW - Acetaminophen KW - 362O9ITL9D KW - Globins KW - 9004-22-2 KW - Carbon Tetrachloride KW - CL2T97X0V0 KW - Cytochrome P-450 CYP2E1 KW - EC 1.14.13.- KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Animals KW - Liver -- cytology KW - Liver -- drug effects KW - Xenobiotics -- metabolism KW - Oxygen -- metabolism KW - Mice, Inbred C57BL KW - Liver -- metabolism KW - Mice KW - Xenobiotics -- toxicity KW - Mice, Transgenic KW - Male KW - Hepatic Stellate Cells -- metabolism KW - Globins -- genetics KW - Cytochrome P-450 CYP2E1 -- metabolism KW - Globins -- metabolism KW - Acetaminophen -- metabolism KW - Chemical and Drug Induced Liver Injury -- metabolism KW - Acetaminophen -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676591207?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Laboratory+investigation%3B+a+journal+of+technical+methods+and+pathology&rft.atitle=Involvement+of+hepatic+stellate+cell+cytoglobin+in+acute+hepatocyte+damage+through+the+regulation+of+CYP2E1-mediated+xenobiotic+metabolism.&rft.au=Teranishi%2C+Yuga%3BMatsubara%2C+Tsutomu%3BKrausz%2C+Kristopher+W%3BLe%2C+Thi+T+T%3BGonzalez%2C+Frank+J%3BYoshizato%2C+Katsutoshi%3BIkeda%2C+Kazuo%3BKawada%2C+Norifumi&rft.aulast=Teranishi&rft.aufirst=Yuga&rft.date=2015-05-01&rft.volume=95&rft.issue=5&rft.spage=515&rft.isbn=&rft.btitle=&rft.title=Laboratory+investigation%3B+a+journal+of+technical+methods+and+pathology&rft.issn=1530-0307&rft_id=info:doi/10.1038%2Flabinvest.2015.29 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-03 N1 - Date created - 2015-04-28 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/labinvest.2015.29 ER - TY - JOUR T1 - NCI investment in nanotechnology: achievements and challenges for the future AN - 1676348981; PQ0001433474 AB - Nanotechnology offers an exceptional and unique opportunity for developing a new generation of tools addressing persistent challenges to progress in cancer research and clinical care. The National Cancer Institute (NCI) recognizes this potential, which is why it invests roughly $150 M per year in nanobiotechnology training, research and development. By exploiting the various capacities of nanomaterials, the range of nanoscale vectors and probes potentially available suggests much is possible for precisely investigating, manipulating, and targeting the mechanisms of cancer across the full spectrum of research and clinical care. NCI has played a key role among federal R&D agencies in recognizing early the value of nanobiotechnology in medicine and committing to its development as well as providing training support for new investigators in the field. These investments have allowed many in the research community to pursue breakthrough capabilities that have already yielded broad benefits. Presented here is an overview of how NCI has made these investments with some consideration of how it will continue to work with this research community to pursue paradigm-changing innovations that offer relief from the burdens of cancer. WIREs Nanomed Nanobiotechnol 2015, 7:251-265. doi: 10.1002/wnan.1318 For further resources related to this article, please visit the WIREs website . Conflict of interest: The authors have declared no conflicts of interest for this article. JF - Wiley Interdisciplinary Reviews: Nanomedicine and Nanobiotechnology AU - Dickherber, Anthony AU - Morris, Stephanie A AU - Grodzinski, Piotr AD - Office of the Director, Center for Strategic Scientific Initiatives, NCI/NIH, Bethesda, MD, USA. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 251 EP - 265 PB - Wiley-Blackwell, Baffins Lane Chichester W. Sussex PO19 1UD United Kingdom VL - 7 IS - 3 SN - 1939-5116, 1939-5116 KW - Biotechnology and Bioengineering Abstracts KW - Reviews KW - Probes KW - Cancer KW - nanotechnology KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676348981?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Wiley+Interdisciplinary+Reviews%3A+Nanomedicine+and+Nanobiotechnology&rft.atitle=NCI+investment+in+nanotechnology%3A+achievements+and+challenges+for+the+future&rft.au=Dickherber%2C+Anthony%3BMorris%2C+Stephanie+A%3BGrodzinski%2C+Piotr&rft.aulast=Dickherber&rft.aufirst=Anthony&rft.date=2015-05-01&rft.volume=7&rft.issue=3&rft.spage=251&rft.isbn=&rft.btitle=&rft.title=Wiley+Interdisciplinary+Reviews%3A+Nanomedicine+and+Nanobiotechnology&rft.issn=19395116&rft_id=info:doi/10.1002%2Fwnan.1318 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Reviews; Probes; Cancer; nanotechnology DO - http://dx.doi.org/10.1002/wnan.1318 ER - TY - JOUR T1 - Intensity-modulated proton therapy for elective nodal irradiation and involved-field radiation in the definitive treatment of locally advanced non-small-cell lung cancer: a dosimetric study. AN - 1676340708; 25604729 AB - Photon involved-field (IF) radiation therapy (IFRT), the standard for locally advanced (LA) non-small cell lung cancer (NSCLC), results in favorable outcomes without increased isolated nodal failures, perhaps from scattered dose to elective nodal stations. Because of the high conformality of intensity-modulated proton therapy (IMPT), proton IFRT could increase nodal failures. We investigated the feasibility of IMPT for elective nodal irradiation (ENI) in LA-NSCLC. IMPT IFRT plans were generated to the same total dose of 66.6-72 Gy received by 20 LA-NSCLC patients treated with photon IFRT. IMPT ENI plans were generated to 46 cobalt Gray equivalent (CGE) to elective nodal planning treatment volumes (PTV) plus 24 CGE to IF-PTVs. Proton IFRT and ENI improved the IF-PTV percentage of volume receiving 95% of the prescribed dose (D95) by 4% (P < .01) compared with photon IFRT. All evaluated dosimetric parameters improved significantly with both proton plans. The lung percentage of volume receiving 20 Gy/CGE (V20) and mean lung dose decreased 18% (P < .01) and 36% (P < .01), respectively, with proton IFRT, and 11% (P = .03) and 26% (P < .01) with ENI. The mean esophagus dose decreased 16% with IFRT and 12% with ENI; heart V25 decreased 63% with both (all P < .01). This study demonstrates the feasibility of IMPT for LA-NSCLC ENI. Potential decreased toxicity indicates that IMPT could allow ENI while maintaining a favorable therapeutic ratio compared with photon IFRT. Published by Elsevier Inc. JF - Clinical lung cancer AU - Kesarwala, Aparna H AU - Ko, Christine J AU - Ning, Holly AU - Xanthopoulos, Eric AU - Haglund, Karl E AU - O'Meara, William P AU - Simone, Charles B AU - Rengan, Ramesh AD - Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. Electronic address: aparna.kesarwala@nih.gov. ; Division of Radiation Oncology, Department of Radiology, Walter Reed National Military Medical Center, Bethesda, MD. ; Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD. ; Department of Radiation Oncology, University of Pennsylvania, Philadelphia, PA. ; Department of Radiation Oncology, University of Washington, Seattle, WA. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 237 EP - 244 VL - 16 IS - 3 KW - Index Medicus KW - Radiation therapy KW - NSCLC KW - ENI KW - IFRT KW - IMPT KW - Feasibility Studies KW - Radiometry KW - Radiotherapy Dosage KW - Humans KW - Lymph Nodes -- radiation effects KW - Tumor Burden KW - Aged KW - Middle Aged KW - Male KW - Female KW - Proton Therapy -- adverse effects KW - Lung Neoplasms -- radiotherapy KW - Radiotherapy, Conformal -- methods KW - Radiotherapy, Intensity-Modulated -- methods KW - Proton Therapy -- methods KW - Radiotherapy, Intensity-Modulated -- adverse effects KW - Radiotherapy, Conformal -- adverse effects KW - Lung Neoplasms -- pathology KW - Carcinoma, Non-Small-Cell Lung -- radiotherapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676340708?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+lung+cancer&rft.atitle=Intensity-modulated+proton+therapy+for+elective+nodal+irradiation+and+involved-field+radiation+in+the+definitive+treatment+of+locally+advanced+non-small-cell+lung+cancer%3A+a+dosimetric+study.&rft.au=Kesarwala%2C+Aparna+H%3BKo%2C+Christine+J%3BNing%2C+Holly%3BXanthopoulos%2C+Eric%3BHaglund%2C+Karl+E%3BO%27Meara%2C+William+P%3BSimone%2C+Charles+B%3BRengan%2C+Ramesh&rft.aulast=Kesarwala&rft.aufirst=Aparna&rft.date=2015-05-01&rft.volume=16&rft.issue=3&rft.spage=237&rft.isbn=&rft.btitle=&rft.title=Clinical+lung+cancer&rft.issn=1938-0690&rft_id=info:doi/10.1016%2Fj.cllc.2014.12.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-25 N1 - Date created - 2015-04-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Acta Oncol. 2008;47(1):95-103 [17851862] Radiat Oncol. 2008;3:4 [18218078] Int J Radiat Oncol Biol Phys. 2008 Nov 1;72(3):702-6 [18374513] Int J Radiat Oncol Biol Phys. 2008 Dec 1;72(5):1385-95 [18486357] Int J Radiat Oncol Biol Phys. 2009 Apr 1;73(5):1391-6 [19306748] Int J Radiat Oncol Biol Phys. 2009 May 1;74(1):179-86 [19019562] J Thorac Oncol. 2009 May;4(5):568-77 [19357537] N Engl J Med. 2009 Jul 2;361(1):32-9 [19571281] Lancet. 2009 Aug 1;374(9687):379-86 [19632716] Radiother Oncol. 2010 May;95(2):178-84 [20356642] Int J Radiat Oncol Biol Phys. 2010 Jun 1;77(2):357-66 [19660879] Int J Radiat Oncol Biol Phys. 2010 Jun 1;77(2):337-43 [19775827] Thorax. 2011 Apr;66(4):294-300 [21169287] Cancer. 2011 Jul 1;117(13):3004-13 [21264827] Technol Cancer Res Treat. 2011 Aug;10(4):317-22 [21728388] Int J Radiat Oncol Biol Phys. 2011 Aug 1;80(5):1350-7 [21251767] Int J Radiat Oncol Biol Phys. 2011 Nov 15;81(4):979-84 [20888140] Radiother Oncol. 2011 Dec;101(3):376-82 [21663988] Int J Radiat Oncol Biol Phys. 2012 Jan 1;82(1):435-41.e1 [21075551] Cancer. 2011 Oct 15;117(20):4707-13 [21437893] Pediatr Blood Cancer. 2014 Jan;61(1):89-94 [24000229] Clin Lung Cancer. 2014 Jan;15(1):79-85 [24238934] Int J Radiat Oncol Biol Phys. 2014 Nov 15;90(4):809-18 [25260491] Int J Radiat Oncol Biol Phys. 2002 Nov 15;54(4):999-1006 [12419425] Oncology (Williston Park). 2003 Dec;17(12 Suppl 13):7-14 [14723001] Int J Radiat Oncol Biol Phys. 2004 Nov 1;60(3):741-7 [15465190] Int J Radiat Oncol Biol Phys. 1990 Oct;19(4):967-72 [2170309] N Engl J Med. 1992 Feb 20;326(8):524-30 [1310160] J Clin Oncol. 2005 Sep 1;23(25):5910-7 [16087956] Int J Radiat Oncol Biol Phys. 2005 Oct 1;63(2):324-33 [16168827] Eur J Nucl Med Mol Imaging. 2006 Jun;33(6):697-702 [16612588] Int J Radiat Oncol Biol Phys. 2006 Jul 15;65(4):1087-96 [16682145] Int J Radiat Oncol Biol Phys. 2006 Sep 1;66(1):126-34 [16904518] Int J Radiat Oncol Biol Phys. 2007 Mar 1;67(3):727-34 [17293231] Radiother Oncol. 2007 Feb;82(2):153-9 [17287040] Int J Radiat Oncol Biol Phys. 2007 May 1;68(1):103-10 [17363189] Am J Clin Oncol. 2007 Jun;30(3):239-44 [17551299] J Thorac Cardiovasc Surg. 2007 Jul;134(1):188-93 [17599507] Int J Radiat Oncol Biol Phys. 2007 Oct 1;69(2):580-8 [17869671] J Clin Oncol. 2007 Dec 10;25(35):5557-61 [17984185] J Thorac Oncol. 2008 Feb;3(2):177-86 [18303441] J Clin Oncol. 1999 Sep;17(9):2692-9 [10561343] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.cllc.2014.12.001 ER - TY - JOUR T1 - Polycyclic aromatic hydrocarbons: from metabolism to lung cancer. AN - 1676340072; 25911656 AB - Excessive exposure to polycyclic aromatic hydrocarbons (PAHs) often results in lung cancer, a disease with the highest cancer mortality in the United States. After entry into the lung, PAHs induce phase I metabolic enzymes such as cytochrome P450 (CYP) monooxygenases, i.e. CYP1A1/2 and 1B1, and phase II enzymes such as glutathione S-transferases, UDP glucuronyl transferases, NADPH quinone oxidoreductases (NQOs), aldo-keto reductases (AKRs), and epoxide hydrolases (EHs), via the aryl hydrocarbon receptor (AhR)-dependent and independent pathways. Humans can also be exposed to PAHs through diet, via consumption of charcoal broiled foods. Metabolism of PAHs through the CYP1A1/1B1/EH pathway, CYP peroxidase pathway, and AKR pathway leads to the formation of the active carcinogens diol-epoxides, radical cations, and o-quinones. These reactive metabolites produce DNA adducts, resulting in DNA mutations, alteration of gene expression profiles, and tumorigenesis. Mutations in xenobiotic metabolic enzymes, as well as polymorphisms of tumor suppressor genes (e.g. p53) and/or genes involved in gene expression (e.g. X-ray repair cross-complementing proteins), are associated with lung cancer susceptibility in human populations from different ethnicities, gender, and age groups. Although various metabolic activation/inactivation pathways, AhR signaling, and genetic susceptibilities contribute to lung cancer, the precise points at which PAHs induce tumor initiation remain unknown. The goal of this review is to provide a current state-of-the-science of the mechanisms of human lung carcinogenesis mediated by PAHs, the experimental approaches used to study this complex class of compounds, and future directions for research of these compounds. © The Author 2015. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. JF - Toxicological sciences : an official journal of the Society of Toxicology AU - Moorthy, Bhagavatula AU - Chu, Chun AU - Carlin, Danielle J AD - *Department of Pediatrics, Baylor College of Medicine, Houston, Texas and Division of Extramural Research and Training, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 5 EP - 15 VL - 145 IS - 1 KW - Carcinogens KW - 0 KW - Polycyclic Aromatic Hydrocarbons KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - lung cancer KW - carcinogenesis KW - metabolism KW - genetic susceptibility KW - mixtures KW - polycyclic aromatic hydrocarbons KW - PAH KW - Ah receptor KW - Humans KW - Activation, Metabolic KW - Cytochrome P-450 Enzyme System -- metabolism KW - Polycyclic Aromatic Hydrocarbons -- toxicity KW - Carcinogens -- metabolism KW - Polycyclic Aromatic Hydrocarbons -- pharmacokinetics KW - Carcinogens -- pharmacokinetics KW - Carcinogens -- toxicity KW - Polycyclic Aromatic Hydrocarbons -- metabolism KW - Lung Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676340072?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.atitle=Polycyclic+aromatic+hydrocarbons%3A+from+metabolism+to+lung+cancer.&rft.au=Moorthy%2C+Bhagavatula%3BChu%2C+Chun%3BCarlin%2C+Danielle+J&rft.aulast=Moorthy&rft.aufirst=Bhagavatula&rft.date=2015-05-01&rft.volume=145&rft.issue=1&rft.spage=5&rft.isbn=&rft.btitle=&rft.title=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.issn=1096-0929&rft_id=info:doi/10.1093%2Ftoxsci%2Fkfv040 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-16 N1 - Date created - 2015-04-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Drug Metab Rev. 1993;25(4):503-17 [8313840] Cancer Res. 1994 Dec 1;54(23):6154-9 [7954461] Proc Natl Acad Sci U S A. 1995 Sep 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Dec;22(12):1903-30 [11751421] Cardiovasc Res. 2002 Mar;53(4):1002-9 [11922910] J Chromatogr B Analyt Technol Biomed Life Sci. 2002 Apr 25;770(1-2):3-18 [12013240] Environ Health Perspect. 2002 Jun;110 Suppl 3:451-88 [12060843] J Steroid Biochem Mol Biol. 1997 Jun;62(2-3):223-32 [9393958] Pharmacogenetics. 1998 Dec;8(6):503-11 [9918134] Cancer Res. 1999 Feb 1;59(3):607-14 [9973208] Pharmacogenetics. 1998 Apr;8(2):109-18 [10022748] Chem Res Toxicol. 1992 Mar-Apr;5(2):302-9 [1643262] Sci Total Environ. 1992 Sep 11;126(1-2):17-26 [1439750] Environ Health Perspect. 1992 Nov;98:87-94 [1486868] Carcinogenesis. 1993 May;14(5):879-86 [8504481] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/toxsci/kfv040 ER - TY - JOUR T1 - Post-treatment with an ultra-low dose of NADPH oxidase inhibitor diphenyleneiodonium attenuates disease progression in multiple Parkinson's disease models. AN - 1675873820; 25716193 AB - Nicotinamide adenine dinucleotide phosphate oxidase, a key superoxide-producing enzyme, plays a critical role in microglia-mediated chronic neuroinflammation and subsequent progressive dopaminergic neurodegeneration in Parkinson's disease. Although nicotinamide adenine dinucleotide phosphate oxidase-targeting anti-inflammatory therapy for Parkinson's disease has been proposed, its application in translational research remains limited. The aim of this study was to obtain preclinical evidence supporting this therapeutic strategy by testing the efficacy of an ultra-low dose of the nicotinamide adenine dinucleotide phosphate oxidase inhibitor diphenyleneiodonium in both endotoxin (lipopolysaccharide)- and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-treated mice using post-treatment regimens. Our data revealed that post-treatment with diphenyleneiodonium significantly attenuated progressive dopaminergic degeneration and improved rotarod activity. Remarkably, post-treatment with diphenyleneiodonium 10 months after lipopolysaccharide injection when mice had 30% loss of nigral dopaminergic neurons, showed high efficacy in protecting the remaining neuronal population and restoring motor function. Diphenyleneiodonium-elicited neuroprotection was associated with the inhibition of microglial activation, a reduction in the expression of proinflammatory factors and an attenuation of α-synuclein aggregation. A pathophysiological evaluation of diphenyleneiodonium-treated mice, including assessment of body weight, organs health, and neuronal counts, revealed no overt signs of toxicity. In summary, infusion of ultra-low dose diphenyleneiodonium potently reduced microglia-mediated chronic neuroinflammation by selectively inhibiting nicotinamide adenine dinucleotide phosphate oxidase and halted the progression of neurodegeneration in mouse models of Parkinson's disease. The robust neuroprotective effects and lack of apparent toxic side effects suggest that diphenyleneiodonium at ultra-low dose may be a promising candidate for future clinical trials in Parkinson's disease patients. Published by Oxford University Press on behalf of the Guarantors of Brain 2015. This work is written by US Government employees and is in the public domain in the US. JF - Brain : a journal of neurology AU - Wang, Qingshan AU - Qian, Li AU - Chen, Shih-Heng AU - Chu, Chun-Hsien AU - Wilson, Belinda AU - Oyarzabal, Esteban AU - Ali, Syed AU - Robinson, Bonnie AU - Rao, Deepa AU - Hong, Jau-Shyong AD - 1 Neuropharmacology Section, Laboratory of Neurobiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA wangq4@niehs.nih.gov hong3@niehs.nih.gov. ; 1 Neuropharmacology Section, Laboratory of Neurobiology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. ; 2 Neurochemistry Laboratory, Division of Neurotoxicology, National Centre for Toxicological Research/USFDA, Jefferson, AR 72079, USA. ; 3 National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 1247 EP - 1262 VL - 138 KW - Enzyme Inhibitors KW - 0 KW - Neuroprotective Agents KW - Onium Compounds KW - diphenyleneiodonium KW - 6HJ411TU98 KW - NADPH Oxidase KW - EC 1.6.3.1 KW - Abridged Index Medicus KW - Index Medicus KW - Parkinson’s disease KW - superoxide KW - microglia KW - neuroinflammation KW - NADPH oxidase KW - Substantia Nigra -- metabolism KW - Animals KW - Mice, Inbred C57BL KW - Disease Progression KW - Disease Models, Animal KW - Neuroprotective Agents -- therapeutic use KW - Nerve Degeneration -- drug therapy KW - NADPH Oxidase -- metabolism KW - Onium Compounds -- pharmacology KW - Dopaminergic Neurons -- drug effects KW - NADPH Oxidase -- antagonists & inhibitors KW - Nerve Degeneration -- pathology KW - Enzyme Inhibitors -- pharmacology KW - Microglia -- drug effects KW - Parkinson Disease -- pathology KW - Parkinson Disease -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1675873820?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+%3A+a+journal+of+neurology&rft.atitle=Post-treatment+with+an+ultra-low+dose+of+NADPH+oxidase+inhibitor+diphenyleneiodonium+attenuates+disease+progression+in+multiple+Parkinson%27s+disease+models.&rft.au=Wang%2C+Qingshan%3BQian%2C+Li%3BChen%2C+Shih-Heng%3BChu%2C+Chun-Hsien%3BWilson%2C+Belinda%3BOyarzabal%2C+Esteban%3BAli%2C+Syed%3BRobinson%2C+Bonnie%3BRao%2C+Deepa%3BHong%2C+Jau-Shyong&rft.aulast=Wang&rft.aufirst=Qingshan&rft.date=2015-05-01&rft.volume=138&rft.issue=&rft.spage=1247&rft.isbn=&rft.btitle=&rft.title=Brain+%3A+a+journal+of+neurology&rft.issn=1460-2156&rft_id=info:doi/10.1093%2Fbrain%2Fawv034 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-17 N1 - Date created - 2015-04-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Ann Neurol. 2001 May;49(5):627-35 [11357953] Neuron. 2002 May 16;34(4):521-33 [12062037] J Neurochem. 2002 Jun;81(6):1285-97 [12068076] FASEB J. 2002 Nov;16(13):1713-20 [12409313] Proc Natl Acad Sci U S A. 2003 May 13;100(10):6145-50 [12721370] FASEB J. 2003 Oct;17(13):1954-6 [12897068] J Biol Chem. 2004 Jan 9;279(2):1415-21 [14578353] FASEB J. 2004 Mar;18(3):589-91 [14734632] Nat Rev Immunol. 2004 Mar;4(3):181-9 [15039755] Xenobiotica. 1979 Sep;9(9):539-46 [524914] Trends Neurosci. 1990 Jul;13(7):290-6 [1695406] J Appl Physiol (1985). 1995 Jan;78(1):112-6 [7713799] Free Radic Biol Med. 1996;20(1):75-81 [8903681] Neurobiol Dis. 1997;4(3-4):247-53 [9361301] Annu Rev Neurosci. 1999;22:123-44 [10202534] Prog Neurobiol. 2005 Jun;76(2):77-98 [16081203] Ann Neurol. 2005 Dec;58(6):963-7 [16240369] Neuron. 2006 Oct 5;52(1):33-8 [17015225] Nat Rev Neurosci. 2007 Jan;8(1):57-69 [17180163] Glia. 2007 Apr 1;55(5):453-62 [17203472] Neurobiol Aging. 2007 May;28(5):639-47 [16697488] J Pharmacol Exp Ther. 2007 Sep;322(3):913-22 [17565007] Parkinsonism Relat Disord. 2007;13 Suppl 3:S332-5 [18267260] Semin Immunopathol. 2008 Jul;30(3):339-63 [18509646] Trends Immunol. 2008 Aug;29(8):357-65 [18599350] Curr Drug Metab. 2008 Oct;9(8):686-96 [18855607] Neurotoxicology. 2008 Sep;29(5):864-70 [18471886] J Immunol. 2008 Nov 15;181(10):7194-204 [18981141] Mov Disord. 2009 Apr 15;24(5):647-54 [19117366] Drugs Aging. 2009;26(9):769-79 [19728750] Environ Health Perspect. 2011 Jun;119(6):807-14 [21245015] Eur J Neurol. 2011 Nov;18(11):1336-42 [21457177] Parkinsonism Relat Disord. 2012 Jan;18 Suppl 1:S207-9 [22166436] J Clin Invest. 2012 Apr;122(4):1156-63 [22466657] Trends Pharmacol Sci. 2012 Jun;33(6):295-303 [22503440] J Neuroinflammation. 2012;9:124 [22695044] Glia. 2013 Jun;61(6):855-68 [23536230] Trends Neurosci. 2013 Sep;36(9):543-54 [23876424] Toxicol Pathol. 2014;42(3):487-509 [24135464] J Neurosci. 2014 Sep 10;34(37):12490-503 [25209287] Glia. 2014 Dec;62(12):2034-43 [25043383] Toxicol Pathol. 2000 Jan-Feb;28(1):28-30 [10668987] Synapse. 2001 Feb;39(2):167-74 [11180504] Brain. 2010 Mar;133(Pt 3):808-21 [20123724] Neuroscience. 2010 May 5;167(2):475-81 [20167258] Nat Rev Neurol. 2010 Apr;6(4):193-201 [20234358] Ann Afr Med. 2010 Apr-Jun;9(2):55-61 [20587924] Prog Brain Res. 2010;184:17-33 [20887868] J Neurosci. 2011 Jan 19;31(3):1081-92 [21248133] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/brain/awv034 ER - TY - JOUR T1 - Smoked cannabis' psychomotor and neurocognitive effects in occasional and frequent smokers. AN - 1674959633; 25745105 AB - Δ9-Tetrahydrocannabinol (THC), the primary psychoactive constituent in cannabis, impairs psychomotor performance, cognition and driving ability; thus, driving under the influence of cannabis is a public safety concern. We documented cannabis' psychomotor, neurocognitive, subjective and physiological effects in occasional and frequent smokers to investigate potential differences between these smokers. Fourteen frequent (≥4x/week) and 11 occasional (<2x/week) cannabis smokers entered a secure research unit ∼19 h prior to smoking one 6.8% THC cigarette. Cognitive and psychomotor performance was evaluated with the critical tracking (CTT), divided attention (DAT), n-back (working memory) and Balloon Analog Risk (BART) (risk-taking) tasks at -1.75, 1.5, 3.5, 5.5 and 22.5 h after starting smoking. GLM (General Linear Model) repeated measures ANOVA was utilized to compare scores. Occasional smokers had significantly more difficulty compensating for CTT tracking error compared with frequent smokers 1.5 h after smoking. Divided attention performance declined significantly especially in occasional smokers, with session × group effects for tracking error, hits, false alarms and reaction time. Cannabis smoking did not elicit session × group effects on the n-back or BART. Controlled cannabis smoking impaired psychomotor function, more so in occasional smokers, suggesting some tolerance to psychomotor impairment in frequent users. These data have implications for cannabis-associated impairment in driving under the influence of cannabis cases. Published by Oxford University Press 2015. This work is written by (a) US Government employee(s) and is in the public domain in the US. JF - Journal of analytical toxicology AU - Desrosiers, Nathalie A AU - Ramaekers, Johannes G AU - Chauchard, Emeline AU - Gorelick, David A AU - Huestis, Marilyn A AD - Chemistry and Drug Metabolism Section, Clinical Pharmacology and Therapeutic Research Branch, NIDA IRP, 251 Bayview Boulevard, Suite 200 Room 05A-721, Baltimore, MD 21224, USA Program in Toxicology, University of Maryland Baltimore, Baltimore, MD, USA. ; Department of Neuropsychology and Psychopharmacology, Faculty of Psychology and Neuroscience, Maastricht University, Maastricht, The Netherlands. ; Chemistry and Drug Metabolism Section, Clinical Pharmacology and Therapeutic Research Branch, NIDA IRP, 251 Bayview Boulevard, Suite 200 Room 05A-721, Baltimore, MD 21224, USA Present address: Laboratoire de Psychologie des Pays de la Loire, Faculté de Psychologie, Université de Nantes, Nantes, France. ; Chemistry and Drug Metabolism Section, Clinical Pharmacology and Therapeutic Research Branch, NIDA IRP, 251 Bayview Boulevard, Suite 200 Room 05A-721, Baltimore, MD 21224, USA Present address: Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA. ; Chemistry and Drug Metabolism Section, Clinical Pharmacology and Therapeutic Research Branch, NIDA IRP, 251 Bayview Boulevard, Suite 200 Room 05A-721, Baltimore, MD 21224, USA mhuestis@intra.nida.nih.gov. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 251 EP - 261 VL - 39 IS - 4 KW - Index Medicus KW - Impulsive Behavior -- drug effects KW - Young Adult KW - Heart Rate -- drug effects KW - Risk-Taking KW - Humans KW - Adult KW - Middle Aged KW - Spatial Memory -- drug effects KW - Blood Pressure -- drug effects KW - Adolescent KW - Memory, Short-Term -- drug effects KW - Male KW - Female KW - Marijuana Smoking -- blood KW - Psychomotor Performance -- drug effects KW - Marijuana Smoking -- psychology KW - Cognition -- drug effects KW - Marijuana Smoking -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1674959633?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+analytical+toxicology&rft.atitle=Smoked+cannabis%27+psychomotor+and+neurocognitive+effects+in+occasional+and+frequent+smokers.&rft.au=Desrosiers%2C+Nathalie+A%3BRamaekers%2C+Johannes+G%3BChauchard%2C+Emeline%3BGorelick%2C+David+A%3BHuestis%2C+Marilyn+A&rft.aulast=Desrosiers&rft.aufirst=Nathalie&rft.date=2015-05-01&rft.volume=39&rft.issue=4&rft.spage=251&rft.isbn=&rft.btitle=&rft.title=Journal+of+analytical+toxicology&rft.issn=1945-2403&rft_id=info:doi/10.1093%2Fjat%2Fbkv012 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-21 N1 - Date created - 2015-04-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Pharmacol Biochem Behav. 1988 Nov;31(3):649-55 [2855116] Accid Anal Prev. 1985 Aug;17(4):323-45 [3006718] Psychopharmacology (Berl). 1992;107(2-3):255-62 [1319601] Alcohol Clin Exp Res. 1993 Aug;17(4):762-6 [8214410] J Clin Psychol. 1995 Nov;51(6):768-74 [8778124] Addiction. 1997 Mar;92(3):279-96 [9219390] Neuropsychobiology. 1998;37(2):104-11 [9566276] Lancet. 1998 Nov 14;352(9140):1611-6 [9843121] Can J Public Health. 1999 Jul-Aug;90(4):260-3 [10489724] Psychopharmacology (Berl). 2004 Nov;176(3-4):239-47 [15205869] Am J Psychiatry. 2005 Mar;162(3):507-12 [15741467] Neuropsychopharmacology. 2005 Apr;30(4):800-9 [15775958] Behav Pharmacol. 2005 Sep;16(5-6):487-96 [16148455] Psychopharmacology (Berl). 2006 Sep;187(4):467-75 [16830130] Drug Alcohol Depend. 2006 Nov 8;85(2):114-22 [16723194] Addiction. 2012 Oct;107(10):1837-44 [22553980] Br J Pharmacol. 2013 Dec;170(7):1410-20 [24106872] Clin Chem. 2014 Apr;60(4):631-43 [24563491] Neuropsychopharmacology. 2001 Nov;25(5):757-65 [11682259] J Exp Psychol Appl. 2002 Jun;8(2):75-84 [12075692] Psychopharmacology (Berl). 2002 Oct;164(1):61-70 [12373420] Drug Alcohol Rev. 2007 May;26(3):309-19 [17454021] J Exp Psychol Learn Mem Cogn. 2007 May;33(3):615-22 [17470009] J Clin Exp Neuropsychol. 2007 May;29(4):357-64 [17497559] Exp Clin Psychopharmacol. 2007 Dec;15(6):599-609 [18179313] J Psychopharmacol. 2008 Jun;22(4):441-51 [18635724] Exp Clin Psychopharmacol. 2008 Dec;16(6):565-70 [19086777] J Psychopharmacol. 2009 May;23(3):266-77 [18719045] Arch Clin Neuropsychol. 2009 Nov;24(7):711-7 [19767297] Depress Anxiety. 2009;26(12):1158-64 [19957281] Memory. 2010 May;18(4):394-412 [20408039] Psychopharmacology (Berl). 2010 Jun;210(3):429-38 [20401748] Pharmacol Biochem Behav. 2010 Sep;96(3):333-41 [20600251] Psychopharmacology (Berl). 2011 Mar;214(2):391-401 [21049267] J Psychopharmacol. 2011 Apr;25(4):478-89 [20817749] Clin Chem. 2011 Aug;57(8):1127-36 [21677094] Anal Bioanal Chem. 2011 Sep;401(4):1273-83 [21727996] Clin Chem. 2011 Oct;57(10):1406-14 [21836075] J Cogn Neurosci. 2012 Mar;24(3):588-99 [22066583] Forensic Sci Int. 2012 Feb 10;215(1-3):14-7 [21377816] Mayo Clin Proc. 2012 Feb;87(2):172-86 [22305029] Psychopharmacology (Berl). 2012 Mar;220(2):341-50 [21975580] J Anal Toxicol. 2012 Jul;36(6):405-12 [22589524] Neuropsychopharmacology. 2003 Jul;28(7):1356-65 [12784123] Drug Alcohol Depend. 2004 Feb 7;73(2):109-19 [14725950] J Clin Pharmacol. 2004 Jul;44(7):751-66 [15199080] Psychopharmacology (Berl). 2004 Nov;176(2):214-22 [15502936] Adolescence. 1990 Spring;25(97):171-81 [2333795] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/jat/bkv012 ER - TY - JOUR T1 - A missense variant of the ATP1A2 gene is associated with a novel phenotype of progressive sensorineural hearing loss associated with migraine. AN - 1674201507; 25138102 AB - Hereditary sensorineural hearing loss is an extremely clinical and genetic heterogeneous disorder in humans. Especially, syndromic hearing loss is subdivided by combinations of various phenotypes, and each subtype is related to different genes. We present a new form of progressive hearing loss with migraine found to be associated with a variant in the ATP1A2 gene. The ATP1A2 gene has been reported as the major genetic cause of familial migraine by several previous studies. A Korean family presenting progressive hearing loss with migraine was ascertained. The affected members did not show any aura or other neurologic symptoms during migraine attacks, indicating on a novel phenotype of syndromic hearing loss. To identify the causative gene, linkage analysis and whole-exome sequencing were performed. A novel missense variant, c.571G>A (p.(Val191Met)), was identified in the ATP1A2 gene that showed co-segregation with the phenotype in the family. In silico studies suggest that this variant causes a change in hydrophobic interactions and thereby slightly destabilize the A-domain of Na(+)/K(+)-ATPase. However, functional studies failed to show any effect of the p.(Val191Met) substitution on the catalytic rate of this enzyme. We describe a new phenotype of progressive hearing loss with migraine associated with a variant in the ATP1A2 gene. This study suggests that a variant in Na(+)/K(+)-ATPase can be involved in both migraine and hearing loss. JF - European journal of human genetics : EJHG AU - Oh, Se-Kyung AU - Baek, Jeong-In AU - Weigand, Karl M AU - Venselaar, Hanka AU - Swarts, Herman G P AU - Park, Seong-Hyun AU - Hashim Raza, Muhammad AU - Jung, Da Jung AU - Choi, Soo-Young AU - Lee, Sang-Heun AU - Friedrich, Thomas AU - Vriend, Gert AU - Koenderink, Jan B AU - Kim, Un-Kyung AU - Lee, Kyu-Yup AD - 1] Department of Biology, College of Natural Sciences, Kyungpook National University, Daegu, South Korea [2] School of Life Sciences, KNU Creative BioResearch Group (BK21 plus project), Kyungpook National University, Daegu, South Korea. ; 1] Department of Biology, College of Natural Sciences, Kyungpook National University, Daegu, South Korea [2] Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA. ; Department of Pharmacology and Toxicology, Radboud University Nijmegen Medical Centre, Nijmegen Centre for Molecular Life Sciences, Nijmegen, The Netherlands. ; Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. ; Department of Neurosurgery, Kyungpook National University Hospital, Daegu, South Korea. ; National Institute on Deafness and Other Communication Disorders (NIDCD), National Institutes of Health, Bethesda, MD, USA. ; Department of Otorhinolaryngology-Head and Neck Surgery, College of Medicine, Kyungpook National University, Daegu, South Korea. ; Department of Medicine, University of Pennsylvania, Philadelphia, PA, USA. ; Institute of Chemistry, Technical University of Berlin, Berlin, Germany. ; 1] Department of Biology, College of Natural Sciences, Kyungpook National University, Daegu, South Korea [2] School of Life Sciences, KNU Creative BioResearch Group (BK21 plus project), Kyungpook National University, Daegu, South Korea [3] Advanced Bio-resource Research Center (ABRC), Kyungpook National University, Daegu, South Korea. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 639 EP - 645 VL - 23 IS - 5 KW - ATP1A2 protein, human KW - EC 3.6.1.- KW - Sodium-Potassium-Exchanging ATPase KW - EC 3.6.3.9 KW - Index Medicus KW - Pedigree KW - Genetic Linkage KW - Models, Molecular KW - DNA Mutational Analysis KW - Humans KW - Disease Progression KW - Amino Acid Sequence KW - Base Sequence KW - Sequence Alignment KW - Genes, Dominant KW - Exome KW - Lod Score KW - Adult KW - Molecular Sequence Data KW - Male KW - Protein Conformation KW - High-Throughput Nucleotide Sequencing KW - Phenotype KW - Hearing Loss, Sensorineural -- genetics KW - Migraine Disorders -- diagnosis KW - Sodium-Potassium-Exchanging ATPase -- genetics KW - Migraine Disorders -- etiology KW - Hearing Loss, Sensorineural -- diagnosis KW - Mutation, Missense UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1674201507?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+human+genetics+%3A+EJHG&rft.atitle=A+missense+variant+of+the+ATP1A2+gene+is+associated+with+a+novel+phenotype+of+progressive+sensorineural+hearing+loss+associated+with+migraine.&rft.au=Oh%2C+Se-Kyung%3BBaek%2C+Jeong-In%3BWeigand%2C+Karl+M%3BVenselaar%2C+Hanka%3BSwarts%2C+Herman+G+P%3BPark%2C+Seong-Hyun%3BHashim+Raza%2C+Muhammad%3BJung%2C+Da+Jung%3BChoi%2C+Soo-Young%3BLee%2C+Sang-Heun%3BFriedrich%2C+Thomas%3BVriend%2C+Gert%3BKoenderink%2C+Jan+B%3BKim%2C+Un-Kyung%3BLee%2C+Kyu-Yup&rft.aulast=Oh&rft.aufirst=Se-Kyung&rft.date=2015-05-01&rft.volume=23&rft.issue=5&rft.spage=639&rft.isbn=&rft.btitle=&rft.title=European+journal+of+human+genetics+%3A+EJHG&rft.issn=1476-5438&rft_id=info:doi/10.1038%2Fejhg.2014.154 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-06 N1 - Date created - 2015-04-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Genet. 2008 Jan;73(1):37-43 [18028456] Biosci Rep. 2000 Apr;20(2):51-91 [10965965] Neurol Sci. 2008 May;29 Suppl 1:S52-4 [18545897] Pflugers Arch. 2009 Jan;457(3):623-34 [18324411] J Neurosci. 2009 Jun 24;29(25):8143-55 [19553454] Hum Mutat. 2009 Jul;30(7):E716-27 [19384972] Biochemistry. 2000 Aug 15;39(32):9959-66 [10933816] Cephalalgia. 2013 Jan;33(2):80-6 [23197354] Annu Rev Physiol. 2003;65:817-49 [12524462] Nat Genet. 2003 Feb;33(2):192-6 [12539047] J Biol Chem. 2003 Dec 19;278(51):51213-22 [14532287] Cephalalgia. 2004;24 Suppl 1:9-160 [14979299] Neuron. 2004 Jul 22;43(2):153-4 [15260948] Neuron. 2004 Jul 22;43(2):169-75 [15260953] Proc Natl Acad Sci U S A. 1984 Jun;81(11):3443-6 [6587361] Arch Otolaryngol Head Neck Surg. 1987 Mar;113(3):325-6 [3814380] J Virol. 1993 Aug;67(8):4566-79 [8392598] Headache. 1996 Jan;36(1):24-8 [8666532] Cell. 1996 Nov 1;87(3):543-52 [8898206] Clin Neurosci. 1998;5(1):2-9 [9523051] Genome Res. 1998 Mar;8(3):175-85 [9521921] Genome Res. 1998 Mar;8(3):186-94 [9521922] Curr Pain Headache Rep. 2005 Jun;9(3):213-20 [15907261] Lancet. 2005 Jul 30-Aug 5;366(9483):371-7 [16054936] J Biol Chem. 2005 Sep 16;280(37):32349-55 [16051601] J Assoc Res Otolaryngol. 2007 Dec;8(4):422-34 [17674100] Neurology. 2007 Dec 4;69(23):2170-6 [18056581] Proc Natl Acad Sci U S A. 2009 Aug 18;106(33):13742-7 [19666591] Nature. 2009 Sep 10;461(7261):272-6 [19684571] Proteins. 2009;77 Suppl 9:114-22 [19768677] J Neurophysiol. 2010 May;103(5):2581-6 [20220082] Hum Mol Genet. 2010 Oct 15;19(R2):R119-24 [20846941] Biochim Biophys Acta. 2011 Apr;1812(4):536-43 [20832469] Headache. 2011 Mar;51(3):447-50 [21352219] J Struct Biol. 2011 May;174(2):296-306 [21182963] Eur Arch Otorhinolaryngol. 2012 Jul;269(7):1733-45 [22218850] Pediatr Neurol. 2012 Aug;47(2):133-6 [22759692] Nat Genet. 2012 Sep;44(9):1030-4 [22842232] Neurology. 2012 Oct 9;79(15):1607-14 [23019266] Otol Neurotol. 2008 Jan;29(1):93-6 [18046258] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ejhg.2014.154 ER - TY - JOUR T1 - Does household use of biomass fuel cause lung cancer? A systematic review and evaluation of the evidence for the GBD 2010 study. AN - 1673372021; 25758120 AB - Around 2.4 billion people use traditional biomass fuels for household cooking or heating. In 2006, the International Agency for Research on Cancer (IARC) concluded emissions from household coal combustion are a Group 1 carcinogen, while those from biomass were categorised as 2A due to epidemiologic limitations. This review updates the epidemiologic evidence and provides risk estimates for the 2010 Global Burden of Disease study. Searches were conducted of 10 databases to July 2012 for studies of clinically diagnosed or pathologically confirmed lung cancer associated with household biomass use for cooking and/or heating. Fourteen eligible studies of biomass cooking or heating were identified: 13 had independent estimates (12 cooking only), all were case-control designs and provided 8221 cases and 11 342 controls. The ORs for lung cancer risk with biomass for cooking and/or heating were OR 1.17 (95% CI 1.01 to 1.37) overall, and 1.15 (95% CI 0.97 to 1.37) for cooking only. Publication bias was not detected, but more than half the studies did not explicitly describe a clean reference category. Sensitivity analyses restricted to studies with adequate adjustment and a clean reference category found ORs of 1.21 (95% CI 1.05 to 1.39) for men (two reports, compiling five studies) and 1.95 (95% CI 1.16 to 3.27) for women (five reports, compiling eight studies). Exposure-response evidence was seen for men, and higher risk for women in developing compared with developed countries, consistent with higher exposures in the former. There is now stronger evidence for biomass fuel use causing lung cancer, but future studies need better exposure assessment to strengthen exposure-response evidence. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions. JF - Thorax AU - Bruce, Nigel AU - Dherani, Mukesh AU - Liu, Rui AU - Hosgood, H Dean AU - Sapkota, Amir AU - Smith, Kirk R AU - Straif, Kurt AU - Lan, Qing AU - Pope, Daniel AD - Department of Public Health and Policy, University of Liverpool, Liverpool, UK. ; Environmental Health Sciences, School of Public Health, University of California Berkeley, California, USA. ; Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA Division of Epidemiology, Albert Einstein College of Medicine, Bronx, New York, USA. ; Maryland Institute for Applied Environmental Health, University of Maryland, School of Public Health, College Park, Maryland, USA. ; International Agency for Research on Cancer, Lyon, France. ; Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 433 EP - 441 VL - 70 IS - 5 KW - Index Medicus KW - Clinical Epidemiology KW - Lung Cancer KW - Air Pollution, Indoor -- adverse effects KW - Humans KW - Wood KW - Male KW - Female KW - Lung Neoplasms -- etiology KW - Heating KW - Cooking KW - Biomass KW - Energy-Generating Resources UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673372021?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Thorax&rft.atitle=Does+household+use+of+biomass+fuel+cause+lung+cancer%3F+A+systematic+review+and+evaluation+of+the+evidence+for+the+GBD+2010+study.&rft.au=Bruce%2C+Nigel%3BDherani%2C+Mukesh%3BLiu%2C+Rui%3BHosgood%2C+H+Dean%3BSapkota%2C+Amir%3BSmith%2C+Kirk+R%3BStraif%2C+Kurt%3BLan%2C+Qing%3BPope%2C+Daniel&rft.aulast=Bruce&rft.aufirst=Nigel&rft.date=2015-05-01&rft.volume=70&rft.issue=5&rft.spage=433&rft.isbn=&rft.btitle=&rft.title=Thorax&rft.issn=1468-3296&rft_id=info:doi/10.1136%2Fthoraxjnl-2014-206625 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-22 N1 - Date created - 2015-04-14 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1136/thoraxjnl-2014-206625 ER - TY - JOUR T1 - Disruption of cytochrome P4501A2 in mice leads to increased susceptibility to hyperoxic lung injury. AN - 1671211442; 25680282 AB - Hyperoxia contributes to acute lung injury in diseases such as acute respiratory distress syndrome. Cytochrome P450 (CYP) 1A enzymes have been implicated in hyperoxic lung injury, but the mechanistic role of CYP1A2 in pulmonary injury is not known. We hypothesized that mice lacking the gene Cyp1a2 (which is predominantly expressed in the liver) will be more sensitive to lung injury and inflammation mediated by hyperoxia and that CYP1A2 will play a protective role by attenuating lipid peroxidation and oxidative stress in the lung. Eight- to ten-week-old WT (C57BL/6) or Cyp1a2(-/-) mice were exposed to hyperoxia (>95% O2) or maintained in room air for 24-72 h. Lung injury was assessed by determining the ratio of lung weight/body weight (LW/BW) and by histology. Extent of inflammation was determined by measuring the number of neutrophils in the lung as well as cytokine expression. The Cyp1a2(-/-) mice under hyperoxic conditions showed increased LW/BW ratios, lung injury, neutrophil infiltration, and IL-6 and TNF-α levels and augmented lipid peroxidation, as evidenced by increased formation of malondialdehyde- and 4-hydroxynonenal-protein adducts and pulmonary isofurans compared to WT mice. In vitro experiments showed that the F2-isoprostane PGF2-α is metabolized by CYP1A2 to a dinor metabolite, providing evidence for a catalytic role for CYP1A2 in the metabolism of F2-isoprostanes. In summary, our results support the hypothesis that hepatic CYP1A2 plays a critical role in the attenuation of hyperoxic lung injury by decreasing lipid peroxidation and oxidative stress in vivo. Copyright © 2015 Elsevier Inc. All rights reserved. JF - Free radical biology & medicine AU - Wang, Lihua AU - Lingappan, Krithika AU - Jiang, Weiwu AU - Couroucli, Xanthi I AU - Welty, Stephen E AU - Shivanna, Binoy AU - Barrios, Roberto AU - Wang, Gangduo AU - Firoze Khan, M AU - Gonzalez, Frank J AU - Jackson Roberts, L AU - Moorthy, Bhagavatula AD - Division of Neonatal-Perinatal Medicine, Department of Pediatrics, Texas Children's Hospital, Baylor College of Medicine, Houston, TX 77030, USA. ; Department of Pathology, Houston Methodist Research Institute, Houston, TX 77030, USA. ; Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA. ; Laboratory of Molecular Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37240, USA. ; Division of Neonatal-Perinatal Medicine, Department of Pediatrics, Texas Children's Hospital, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: bmoorthy@bcm.edu. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 147 EP - 159 VL - 82 KW - Aldehydes KW - 0 KW - F2-Isoprostanes KW - Interleukin-6 KW - Tumor Necrosis Factor-alpha KW - Malondialdehyde KW - 4Y8F71G49Q KW - Dinoprost KW - B7IN85G1HY KW - Cytochrome P-450 CYP1A2 KW - EC 1.14.14.1 KW - 4-hydroxy-2-nonenal KW - K1CVM13F96 KW - Index Medicus KW - Oxidative stress KW - Free radicals KW - Acute lung injury KW - ARDS KW - CYP1A2 KW - Animals KW - F2-Isoprostanes -- metabolism KW - Dinoprost -- metabolism KW - Liver -- metabolism KW - Mice KW - Lipid Peroxidation -- physiology KW - Leukocyte Count KW - Mice, Knockout KW - Neutrophil Infiltration KW - Malondialdehyde -- metabolism KW - Oxidative Stress -- physiology KW - Neutrophils KW - Aldehydes -- metabolism KW - Mice, Inbred C57BL KW - Cytochrome P-450 CYP1A2 -- genetics KW - Lung Injury -- metabolism KW - Interleukin-6 -- metabolism KW - Hyperoxia -- metabolism KW - Cytochrome P-450 CYP1A2 -- metabolism KW - Tumor Necrosis Factor-alpha -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1671211442?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Free+radical+biology+%26+medicine&rft.atitle=Disruption+of+cytochrome+P4501A2+in+mice+leads+to+increased+susceptibility+to+hyperoxic+lung+injury.&rft.au=Wang%2C+Lihua%3BLingappan%2C+Krithika%3BJiang%2C+Weiwu%3BCouroucli%2C+Xanthi+I%3BWelty%2C+Stephen+E%3BShivanna%2C+Binoy%3BBarrios%2C+Roberto%3BWang%2C+Gangduo%3BFiroze+Khan%2C+M%3BGonzalez%2C+Frank+J%3BJackson+Roberts%2C+L%3BMoorthy%2C+Bhagavatula&rft.aulast=Wang&rft.aufirst=Lihua&rft.date=2015-05-01&rft.volume=82&rft.issue=&rft.spage=147&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2015.01.019 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-04 N1 - Date created - 2015-04-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Pharmacol. 2002 Mar;61(3):507-15 [11854430] Carcinogenesis. 2002 Jul;23(7):1199-207 [12117779] J Appl Toxicol. 2014 Jul;34(7):743-53 [24532440] PLoS One. 2014;9(7):e101581 [25003466] Toxicol Sci. 2014 Sep;141(1):68-77 [24893714] Antioxid Redox Signal. 2014 Jun 10;20(17):2681-91 [24295151] J Toxicol Environ Health A. 2003 Jan 10;66(1):93-102 [12587293] J Biol Chem. 2004 Jun 4;279(23):23847-50 [15028720] Drug Metab Rev. 2004 May;36(2):159-97 [15237850] J Pharmacol Exp Ther. 2004 Aug;310(2):512-9 [15123765] Free Radic Biol Med. 2004 Sep 1;37(5):724-32 [15288129] Pharmacol Rev. 1971 Jun;23(2):37-133 [4948324] Biochem Pharmacol. 1972 Dec 15;21(24):3249-56 [4405367] Cancer Res. 1974 Sep;34(9):2196-203 [4367284] J Appl Physiol Respir Environ Exerc Physiol. 1978 Nov;45(5):699-704 [730565] Anal Biochem. 1980 Sep 1;107(1):150-5 [6776841] J Biol Chem. 1981 Nov 10;256(21):10986-92 [7287745] FASEB J. 1996 Jun;10(8):809-18 [8666157] Acta Anaesthesiol Scand Suppl. 1996;109:70-3 [8901951] Toxicol Lett. 1997 Jan 15;90(1):67-75 [9020404] J Biol Chem. 1998 Oct 9;273(41):26969-76 [9756946] Intensive Care Med. 1983;9(5):271-3 [6619394] Am Rev Respir Dis. 1988 Mar;137(3):688-94 [2830813] Am J Respir Crit Care Med. 2007 Sep 15;176(6):575-81 [17641159] Am J Respir Cell Mol Biol. 2008 Jan;38(1):88-94 [17673688] Toxicol Appl Pharmacol. 2008 Dec 1;233(2):169-78 [18824009] Pediatr Res. 2009 Jan;65(1):67-71 [18704000] Drug Metab Pharmacokinet. 2009;24(3):269-76 [19571439] Pediatr Res. 2010 Feb;67(2):144-9 [19809377] Crit Care Med. 1988 Jul;16(7):671-8 [3371043] Cancer Res. 1989 Nov 15;49(22):6304-12 [2509067] Crit Rev Biochem Mol Biol. 1990;25(2):97-153 [2183970] EMBO J. 1991 Aug;10(8):2247-58 [2065663] J Appl Physiol (1985). 1993 Apr;74(4):1994-2003 [8514721] Biochem Biophys Res Commun. 1993 Dec 15;197(2):878-85 [8267628] Am J Respir Crit Care Med. 1994 May;149(5):1107-11 [8173748] New Horiz. 1994 Nov;2(4):413-4 [7804789] Chest. 1998 Dec;114(6):1653-9 [9872202] Eur J Anaesthesiol. 1999 Jan;16(1):66-8 [10084104] Am J Respir Crit Care Med. 1999 Jul;160(1):109-16 [10390387] FASEB J. 2004 Dec;18(15):1791-800 [15576482] Free Radic Biol Med. 2005 Feb 1;38(3):325-43 [15629862] Vascul Pharmacol. 2005 Aug;43(2):101-11 [15967733] Toxicol Sci. 2005 Sep;87(1):204-12 [15958656] Am J Physiol Lung Cell Mol Physiol. 2005 Nov;289(5):L807-15 [15951336] N Engl J Med. 2005 Oct 20;353(16):1685-93 [16236739] Pediatr Res. 2006 Jun;59(6):795-800 [16641218] Free Radic Biol Med. 2006 Jul 1;41(1):4-18 [16781448] Am J Physiol Lung Cell Mol Physiol. 2006 Nov;291(5):L1050-8 [16815892] Am J Physiol Lung Cell Mol Physiol. 2010 Jul;299(1):L73-85 [20418384] Free Radic Biol Med. 2010 Oct 15;49(7):1172-81 [20627125] Am J Respir Crit Care Med. 2011 Apr 15;183(8):1043-54 [20959557] Am J Respir Cell Mol Biol. 2011 May;44(5):725-38 [21531958] Toxicol Appl Pharmacol. 2011 Oct 15;256(2):83-94 [21745492] Int J Exp Pathol. 2012 Aug;93(4):269-78 [22804763] Toxicol Appl Pharmacol. 2013 Oct 15;272(2):281-90 [23792423] Am J Physiol Lung Cell Mol Physiol. 2014 Jan;306(2):L152-61 [24285266] J Nutr. 2014 Mar;144(3):258-66 [24453131] Proc Natl Acad Sci U S A. 2002 Dec 24;99(26):16713-8 [12482927] Biochem Biophys Res Commun. 2000 Jan 7;267(1):184-9 [10623596] J Pharmacol Exp Ther. 2000 Feb;292(2):553-60 [10640292] Arch Toxicol. 2000 Jan;73(10-11):540-6 [10663385] N Engl J Med. 2000 May 4;342(18):1301-8 [10793162] Am J Respir Crit Care Med. 2000 Sep;162(3 Pt 1):1175-7 [10988150] Am J Respir Cell Mol Biol. 2002 Feb;26(2):175-82 [11804867] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.freeradbiomed.2015.01.019 ER - TY - JOUR T1 - Towards an HIV cure based on targeted killing of infected cells: different approaches against acute versus chronic infection. AN - 1671210137; 25710815 AB - Current regimens of combination antiretroviral therapy (cART) offer effective control of HIV infection, with maintenance of immune health and near-normal life expectancy. What will it take to progress beyond the status quo, whereby infectious virus can be eradicated (a 'sterilizing cure') or fully controlled without the need for ongoing cART (a 'functional cure')? On the basis of therapeutic advances in the cancer field, we propose that targeted cytotoxic therapy to kill HIV-infected cells represents a logical complement to cART for achieving an HIV cure. This concept is based on the fact that cART effectively blocks replication of the virus, but does not eliminate cells that are already infected; targeted cytotoxic therapy would contribute precisely this missing component. We suggest that different modalities are suited for curing primary acute versus established chronic infection. For acute infection, relatively short-acting potent agents such as recombinant immunotoxins might prove sufficient for HIV eradication, whereas for chronic infection, a long-lasting (lifelong?) modality is required to maintain full virus control, as might be achieved with genetically modified autologous T cells. We present perspectives for complementing cART with targeted cytotoxic therapy, whereby HIV infection is either eradicated or fully controlled, thereby eliminating the need for lifelong cART. JF - Current opinion in HIV and AIDS AU - Dey, Barna AU - Berger, Edward A AD - Laboratory of Viral Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 207 EP - 213 VL - 10 IS - 3 KW - Anti-HIV Agents KW - 0 KW - Index Medicus KW - AIDS/HIV KW - Drug Delivery Systems KW - Animals KW - HIV-1 -- immunology KW - Humans KW - Mice KW - Drug Therapy, Combination KW - HIV Infections -- virology KW - Anti-HIV Agents -- therapeutic use KW - HIV Infections -- immunology KW - Anti-HIV Agents -- pharmacology KW - HIV Infections -- drug therapy KW - T-Lymphocytes -- drug effects KW - T-Lymphocytes -- virology KW - T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1671210137?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+HIV+and+AIDS&rft.atitle=Towards+an+HIV+cure+based+on+targeted+killing+of+infected+cells%3A+different+approaches+against+acute+versus+chronic+infection.&rft.au=Dey%2C+Barna%3BBerger%2C+Edward+A&rft.aulast=Dey&rft.aufirst=Barna&rft.date=2015-05-01&rft.volume=10&rft.issue=3&rft.spage=207&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+HIV+and+AIDS&rft.issn=1746-6318&rft_id=info:doi/10.1097%2FCOH.0000000000000151 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-08 N1 - Date created - 2015-04-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Infect Dis. 2011 Apr 1;203(7):894-7 [21402541] Nat Med. 2012 Nov;18(11):1673-81 [22961108] Nat Immunol. 2013 Jan;14(1):1-5 [23238748] J Exp Med. 2013 Jan 14;210(1):143-56 [23254284] Annu Rev Med. 2013;64:15-29 [23043493] Stem Cells. 2014 Apr;32(4):1021-31 [24307574] Curr Opin HIV AIDS. 2014 May;9(3):250-6 [24638019] Expert Rev Clin Immunol. 2014 May;10(5):553-5 [24734906] Blood. 2014 Apr 17;123(16):2470-7 [24578503] J Med Primatol. 2014 Oct;43(5):341-8 [25138734] Curr Pharm Des. 2014;20(42):6584-643 [25341935] Nat Rev Microbiol. 2014 Nov;12(11):750-64 [25402363] J Immunol. 2014 Dec 1;193(11):5613-25 [25362178] Proc Natl Acad Sci U S A. 1997 Oct 14;94(21):11478-83 [9326635] Eur J Immunol. 1998 Dec;28(12):4177-87 [9862354] Gene Ther. 2005 Feb;12(4):299-310 [15496956] J Immunol. 2007 Mar 1;178(5):2746-54 [17312117] J Immunol. 2007 Jun 1;178(11):6975-83 [17513747] Nat Med. 2008 Dec;14(12):1390-5 [18997777] N Engl J Med. 2009 Feb 12;360(7):692-8 [19213682] Nat Med. 2009 Aug;15(8):901-6 [19448633] Curr Opin HIV AIDS. 2011 May;6(3):181-7 [21460722] Adv Virus Res. 2011;80:103-27 [21762823] Nature. 2012 Jan 5;481(7379):81-4 [22139420] J Immunol. 2012 Apr 1;188(7):3247-56 [22387550] PLoS Pathog. 2012;8(4):e1002649 [22511873] J Virol. 2012 May;86(10):5844-56 [22419808] Sci Transl Med. 2012 May 2;4(132):132ra53 [22553251] Crit Rev Ther Drug Carrier Syst. 2013;30(1):1-49 [23510109] Immunotherapy. 2013 Apr;5(4):407-14 [23557423] Curr Opin HIV AIDS. 2013 May;8(3):224-9 [23454863] PLoS Pathog. 2013;9(5):e1003347 [23671416] Curr Opin Chem Biol. 2013 Jun;17(3):385-92 [23623807] Curr Gene Ther. 2013 Aug;13(4):282-90 [23773178] Virology. 2013 Nov;446(1-2):268-75 [24074590] N Engl J Med. 2013 Nov 7;369(19):1828-35 [24152233] PLoS Pathog. 2014 Jan;10(1):e1003872 [24415939] Nat Med. 2014 Mar;20(3):296-300 [24509526] Proc Natl Acad Sci U S A. 2014 Jun 10;111(23):8571-6 [24799704] Lancet. 2014 Jul 19;384(9939):209-11 [25042220] Nat Rev Cancer. 2014 Aug;14(8):559-67 [24990523] Eur J Cancer. 2014 Sep;50(13):2360-3 [24953565] Nature. 2014 Aug 7;512(7512):74-7 [25042999] Immunol Cell Biol. 2014 Aug;92(7):570-7 [24797582] Curr Top Microbiol Immunol. 2014;382:373-92 [25116109] J Allergy Clin Immunol. 2014 Jul;134(1):12-9 [25117799] Mol Ther. 2014 Sep;22(9):1564-74 [25186558] Vaccine. 2014 Sep 29;32(43):5540-5 [24968157] Curr Opin HIV AIDS. 2015 Jan;10(1):4-11 [25402708] Curr Opin HIV AIDS. 2015 Jan;10(1):18-28 [25415421] Nat Med. 2015 Feb;21(2):132-9 [25599132] AIDS. 2012 Jun 19;26(10):1281-92 [22441256] Proc Natl Acad Sci U S A. 2012 Jul 17;109(29):11782-7 [22753489] J Infect Dis. 2000 Mar;181(3):921-6 [10720513] Blood. 2000 Jul 15;96(2):467-74 [10887107] Blood. 2000 Aug 1;96(3):785-93 [10910888] Mol Ther. 2002 Jun;5(6):788-97 [12027564] J Exp Med. 2004 Sep 20;200(6):749-59 [15365096] Cell. 1991 Mar 8;64(5):1037-46 [1900456] Blood. 1994 Nov 1;84(9):2878-89 [7949163] PLoS Pathog. 2010;6(6):e1000803 [20548940] Blood. 2011 Jan 6;117(1):72-82 [20889925] Curr Opin HIV AIDS. 2011 Jan;6(1):80-5 [21242898] Blood. 2011 Mar 10;117(10):2791-9 [21148083] Immunotherapy. 2011 Mar;3(3):381-94 [21395380] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/COH.0000000000000151 ER - TY - JOUR T1 - SRC family kinase inhibitors antagonize the toxicity of multiple serotypes of botulinum neurotoxin in human embryonic stem cell-derived motor neurons. AN - 1669832914; 25782580 AB - Botulinum neurotoxins (BoNTs), the causative agents of botulism, are potent inhibitors of neurotransmitter release from motor neurons. There are currently no drugs to treat BoNT intoxication after the onset of the disease symptoms. In this study, we explored how modulation of key host pathways affects the process of BoNT intoxication in human motor neurons, focusing on Src family kinase (SFK) signaling. Motor neurons derived from human embryonic stem (hES) cells were treated with a panel of SFK inhibitors and intoxicated with BoNT serotypes A, B, or E (which are responsible for >95 % of human botulism cases). Subsequently, it was found that bosutinib, dasatinib, KX2-391, PP1, PP2, Src inhibitor-1, and SU6656 significantly antagonized all three of the serotypes. Furthermore, the data indicated that the treatment of hES-derived motor neurons with multiple SFK inhibitors increased the antagonistic effect synergistically. Mechanistically, the small molecules appear to inhibit BoNTs by targeting host pathways necessary for intoxication and not by directly inhibiting the toxins' proteolytic activity. Importantly, the identified inhibitors are all well-studied with some in clinical trials while others are FDA-approved drugs. Overall, this study emphasizes the importance of targeting host neuronal pathways, rather than the toxin's enzymatic components, to antagonize multiple BoNT serotypes in motor neurons. JF - Neurotoxicity research AU - Kiris, Erkan AU - Burnett, James C AU - Nuss, Jonathan E AU - Wanner, Laura M AU - Peyser, Brian D AU - Du, Hao T AU - Gomba, Glenn Y AU - Kota, Krishna P AU - Panchal, Rekha G AU - Gussio, Rick AU - Kane, Christopher D AU - Tessarollo, Lino AU - Bavari, Sina AD - Geneva Foundation, Tacoma, WA, USA, erkan.kiris@nih.gov. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 384 EP - 398 VL - 27 IS - 4 KW - src-Family Kinases KW - EC 2.7.10.2 KW - Botulinum Toxins KW - EC 3.4.24.69 KW - Index Medicus KW - Embryonic Stem Cells -- cytology KW - Proteolysis -- drug effects KW - Humans KW - Serogroup KW - Motor Neurons -- metabolism KW - Botulinum Toxins -- toxicity KW - src-Family Kinases -- metabolism KW - Signal Transduction -- drug effects KW - src-Family Kinases -- antagonists & inhibitors KW - Motor Neurons -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669832914?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicity+research&rft.atitle=SRC+family+kinase+inhibitors+antagonize+the+toxicity+of+multiple+serotypes+of+botulinum+neurotoxin+in+human+embryonic+stem+cell-derived+motor+neurons.&rft.au=Kiris%2C+Erkan%3BBurnett%2C+James+C%3BNuss%2C+Jonathan+E%3BWanner%2C+Laura+M%3BPeyser%2C+Brian+D%3BDu%2C+Hao+T%3BGomba%2C+Glenn+Y%3BKota%2C+Krishna+P%3BPanchal%2C+Rekha+G%3BGussio%2C+Rick%3BKane%2C+Christopher+D%3BTessarollo%2C+Lino%3BBavari%2C+Sina&rft.aulast=Kiris&rft.aufirst=Erkan&rft.date=2015-05-01&rft.volume=27&rft.issue=4&rft.spage=384&rft.isbn=&rft.btitle=&rft.title=Neurotoxicity+research&rft.issn=1476-3524&rft_id=info:doi/10.1007%2Fs12640-015-9526-z LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-15 N1 - Date created - 2015-04-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biochemistry. 2001 Feb 20;40(7):2234-42 [11329292] Biochemistry. 2004 Jan 20;43(2):526-32 [14717608] Nat Rev Neurosci. 2004 Apr;5(4):317-28 [15034556] Emerg Infect Dis. 2004 Sep;10(9):1606-11 [15498163] Science. 2006 Apr 28;312(5773):592-6 [16543415] Cell Biochem Biophys. 2006;45(1):111-23 [16679567] Cell Mol Life Sci. 2006 Dec;63(23):2818-28 [17086381] J Gen Physiol. 2007 Mar;129(3):233-44 [17325194] J Biol Chem. 1996 Aug 2;271(31):18322-5 [8702470] Toxicon. 1997 Mar;35(3):433-45 [9080598] FEBS Lett. 1998 Jun 5;429(1):78-82 [9657387] Nat Neurosci. 1999 Apr;2(4):331-8 [10204539] EMBO Rep. 2004 Nov;5(11):1090-5 [15486565] J Biol Chem. 2010 May 28;285(22):17209-17 [20212047] J Cell Sci. 2010 Jul 1;123(Pt 13):2256-65 [20530578] Neoplasia. 2010 Aug;12(8):599-607 [20689754] J Biomol Screen. 2010 Sep;15(8):928-36 [20720092] Molecules. 2011;16(1):202-20 [21193845] Biochem Biophys Res Commun. 2011 Feb 4;405(1):85-90 [21215258] FEBS Lett. 2004 Dec 3;578(1-2):121-7 [15581628] Nature. 2004 Dec 16;432(7019):925-9 [15592454] Curr Opin Pharmacol. 2005 Jun;5(3):274-9 [15907915] Proc Natl Acad Sci U S A. 2005 Jul 12;102(28):9984-9 [15985558] FEBS Lett. 2006 Apr 3;580(8):2011-4 [16545378] Stem Cells. 2007 Aug;25(8):1931-9 [17478583] FEBS Lett. 2007 Oct 16;581(25):4803-8 [17889852] J Neurosci. 2008 Jan 2;28(1):21-30 [18171919] Neurotox Res. 2007 Dec;12(4):275-90 [18201955] Neurobiol Dis. 2008 May;30(2):201-11 [18343677] Stem Cells. 2008 Apr;26(4):886-93 [18238853] J Biol Chem. 2008 Jul 25;283(30):21145-52 [18511418] Cell Mol Life Sci. 2008 Aug;65(15):2296-306 [18425411] Mol Biol Cell. 2008 Dec;19(12):5226-37 [18815274] Proc Natl Acad Sci U S A. 2009 Feb 3;106(5):1330-5 [19164566] J Neurosci. 2009 Apr 29;29(17):5690-700 [19403835] Curr Opin Pharmacol. 2009 Jun;9(3):326-35 [19394272] Biochemistry. 2009 Jun 23;48(24):5631-41 [19476346] J Pharmacol Exp Ther. 2009 Jul;330(1):352-8 [19372387] J Med Chem. 2013 Jul 25;56(14):5860-71 [23815186] Expert Rev Mol Diagn. 2014 Mar;14(2):153-68 [24450833] Expert Opin Drug Discov. 2014 Mar;9(3):319-33 [24520991] FEBS Lett. 2014 Apr 2;588(7):1087-93 [24583011] J Med Chem. 2014 May 22;57(10):4134-53 [24742203] Nat Rev Microbiol. 2014 Aug;12(8):535-49 [24975322] Nat Biotechnol. 2009 Jul;27(7):659-66 [19581876] Mol Cancer Ther. 2009 Nov;8(11):3066-74 [19861409] J Neurosci. 2010 Jan 6;30(1):242-54 [20053906] Cancer Res. 2010 Jan 15;70(2):440-6 [20068163] J Am Chem Soc. 2010 Mar 10;132(9):2868-9 [20158239] Methods Mol Biol. 2010;636:123-37 [20336520] Trends Microbiol. 2010 Apr;18(4):164-72 [20202845] PLoS Pathog. 2011 Mar;7(3):e1002008 [21483489] J Biol Chem. 2011 Apr 29;286(17):15067-72 [21378164] Stem Cell Res. 2011 May;6(3):195-205 [21353660] PLoS One. 2011;6(4):e19126 [21559464] Cell Death Dis. 2011;2:e167 [21633390] Curr Med Chem. 2011;18(19):2921-42 [21651487] Mol Syst Biol. 2011;7:544 [22068327] Toxins (Basel). 2010 May;2(5):978-97 [22069621] Trends Neurosci. 2011 Dec;34(12):629-37 [22051158] Bioorg Med Chem. 2011 Dec 15;19(24):7338-48 [22082667] Trends Pharmacol Sci. 2012 Mar;33(3):122-8 [22153719] Toxicol Sci. 2012 Apr;126(2):426-35 [22223483] Leukemia. 2012 Jun;26(6):1180-8 [22182854] Biochemistry. 2012 Jul 17;51(28):5655-62 [22720883] PLoS One. 2012;7(9):e46185 [23049975] Toxins (Basel). 2012 Oct;4(10):913-39 [23162705] Curr Top Microbiol Immunol. 2013;364:115-37 [23239351] Curr Top Microbiol Immunol. 2013;364:257-85 [23239357] Hum Mol Genet. 2013 Aug 15;22(16):3315-28 [23666528] Neuron. 2013 Oct 30;80(3):675-90 [24183019] Curr Top Med Chem. 2014;14(18):2062-80 [25335886] Curr Top Med Chem. 2014;14(18):2044-61 [25335887] J Vis Exp. 2014;(93):e51915 [25489815] J Appl Toxicol. 1999 Dec;19 Suppl 1:S23-6 [10594895] Infect Immun. 2001 Jan;69(1):570-4 [11119555] JAMA. 2001 Feb 28;285(8):1059-70 [11209178] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s12640-015-9526-z ER - TY - JOUR T1 - Anti-Müllerian hormone and lifestyle, reproductive, and environmental factors among women in rural South Africa. AN - 1669831825; 25710247 AB - Few data exist regarding anti-Müllerian hormone, a marker of ovarian reserve, in relation to environmental factors with potential ovarian toxicity. This analysis included 420 women from Limpopo, South Africa studied in 2010-2011. Women were administered comprehensive questionnaires, and plasma concentrations of anti-Müllerian hormone and dichlorodiphenyltrichloroethane were determined. We used separate multivariable models to examine the associations between natural log-transformed anti-Müllerian hormone concentration (ng/ml) and each of the lifestyle, reproductive, and environmental factors of interest, adjusted for age, body mass index, education, and parity. The median age of women was 24 years (interquartile range [IQR] = 22 to 26); the median anti-Müllerian hormone concentration was 3.1 ng/ml (IQR = 2.0 to 6.0). Women who reported indoor residual spraying in homes with painted walls (indicative of exposure to pyrethroids) had 25% lower (95% confidence interval [CI] = -39%, -8%) anti-Müllerian hormone concentrations compared with women who reported no spraying. Little evidence of decreased anti-Müllerian hormone concentrations was observed among women with the highest dichlorodiphenyltrichloroethane levels. Compared with women who used an electric stove, no association was observed among women who cooked indoors over open wood fires. The findings also suggested lower anti-Müllerian hormone concentrations among women who drank coffee (-19% [95% CI = -31%, -5%]) or alcohol (-21% [95% CI = -36%, -3%]). These are among the first data regarding anti-Müllerian hormone concentrations relative to pesticides and indoor air pollution. Our results are suggestive of decreased ovarian reserve associated with exposure to pyrethroid pesticides, which is consistent with laboratory animal data. JF - Epidemiology (Cambridge, Mass.) AU - Whitworth, Kristina W AU - Baird, Donna D AU - Steiner, Anne Z AU - Bornman, Riana M S AU - Travlos, Gregory S AU - Wilson, Ralph E AU - Longnecker, Matthew P AD - From the aUniversity of Texas School of Public Health, San Antonio Regional Campus, San Antonio, TX; bEpidemiology Branch, cCellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC; dDivision of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, University of North Carolina, Chapel Hill, NC; and eDepartment of Urology, fThe University of Pretoria Centre for Sustainable Malaria Control, University of Pretoria, Pretoria, South Africa. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 429 EP - 435 VL - 26 IS - 3 KW - Insecticides KW - 0 KW - Dichlorodiphenyl Dichloroethylene KW - 4M7FS82U08 KW - Anti-Mullerian Hormone KW - 80497-65-0 KW - DDT KW - CIW5S16655 KW - Index Medicus KW - Young Adult KW - Gravidity -- drug effects KW - Parity -- drug effects KW - South Africa -- epidemiology KW - Rural Population -- statistics & numerical data KW - Humans KW - Adult KW - Surveys and Questionnaires KW - Dichlorodiphenyl Dichloroethylene -- adverse effects KW - Female KW - Dichlorodiphenyl Dichloroethylene -- blood KW - Pregnancy KW - Life Style KW - Insecticides -- adverse effects KW - Anti-Mullerian Hormone -- blood KW - Environmental Exposure -- statistics & numerical data KW - DDT -- blood KW - DDT -- adverse effects KW - Environmental Exposure -- adverse effects KW - Reproductive Health -- statistics & numerical data KW - Insecticides -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669831825?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epidemiology+%28Cambridge%2C+Mass.%29&rft.atitle=Anti-M%C3%BCllerian+hormone+and+lifestyle%2C+reproductive%2C+and+environmental+factors+among+women+in+rural+South+Africa.&rft.au=Whitworth%2C+Kristina+W%3BBaird%2C+Donna+D%3BSteiner%2C+Anne+Z%3BBornman%2C+Riana+M+S%3BTravlos%2C+Gregory+S%3BWilson%2C+Ralph+E%3BLongnecker%2C+Matthew+P&rft.aulast=Whitworth&rft.aufirst=Kristina&rft.date=2015-05-01&rft.volume=26&rft.issue=3&rft.spage=429&rft.isbn=&rft.btitle=&rft.title=Epidemiology+%28Cambridge%2C+Mass.%29&rft.issn=1531-5487&rft_id=info:doi/10.1097%2FEDE.0000000000000265 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-15 N1 - Date created - 2015-04-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Endocrinol Metab. 2001 Jul;86(7):3421-9 [11443219] Fertil Steril. 2002 Feb;77(2):357-62 [11821097] J Toxicol Environ Health A. 2002 Oct 11;65(19):1419-35 [12396874] Hum Reprod. 1992 Nov;7(10):1342-6 [1291557] Endocr Rev. 1993 Apr;14(2):152-64 [8325249] J Clin Endocrinol Metab. 1996 Feb;81(2):571-6 [8636269] Mol Cell Endocrinol. 2005 Apr 29;234(1-2):81-6 [15836956] Chemosphere. 2006 Jan;62(3):333-6 [16005493] Fertil Steril. 2008 Jun;89(6):1836-7 [17603056] Gynecol Endocrinol. 2007;23(8):486-93 [17852428] Toxicology. 2010 Jan 12;267(1-3):1-6 [19892000] Hum Reprod Update. 2010 Mar-Apr;16(2):113-30 [19793843] Menopause. 2010 May-Jun;17(3):571-6 [20065884] Reprod Sci. 2015 May;22(5):519-26 [25228631] Reprod Biomed Online. 2010 Jun;20(6):861-5 [20378408] Ann N Y Acad Sci. 2010 Aug;1204:95-103 [20738279] J Clin Endocrinol Metab. 2010 Nov;95(11):5003-10 [20719830] Fertil Steril. 2011 Jan;95(1):170-5 [20522327] Fertil Steril. 2011 Feb;95(2):736-41.e1-3 [20869051] Fertil Steril. 2011 Feb;95(2):747-50 [21074758] Toxicology. 2011 Mar 28;282(1-2):47-55 [21251947] Hum Reprod Update. 2011 May-Jun;17(3):418-33 [21266373] PLoS One. 2011;6(7):e22024 [21789206] Am J Epidemiol. 2012 Feb 15;175(4):245-9 [22247047] Toxicol Lett. 2012 Apr 25;210(2):155-68 [22020228] Epidemiology. 2012 May;23(3):393-401 [22407137] Eur J Obstet Gynecol Reprod Biol. 2012 Aug;163(2):180-4 [22579227] Hum Reprod. 2012 Oct;27(10):3085-91 [22777530] Am J Hum Biol. 2012 Nov-Dec;24(6):739-45 [22915230] PLoS One. 2012;7(11):e49916 [23209616] Parasit Vectors. 2013;6:118 [23618516] J Clin Endocrinol Metab. 2013 May;98(5):2106-15 [23533229] Reprod Biol Endocrinol. 2013;11:66 [23870423] J Environ Biol. 2013 Jan;34(1):99-105 [24006814] Hum Reprod. 2014 May;29(5):1042-8 [24626805] Environ Health Perspect. 2014 Jun;122(6):545-52 [24577839] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/EDE.0000000000000265 ER - TY - JOUR T1 - No contribution of the ABCB11 p.444A polymorphism in Japanese patients with drug-induced cholestasis. AN - 1666985577; 25713208 AB - European studies have revealed that the ABCB11 c.1331T>C (V444A) polymorphism (rs2287622) C-allele frequency is higher among patients with drug-induced cholestasis. Given the low incidence of this disease, however, this association has not been sufficiently elucidated. We aimed to investigate the significance of this polymorphism in Japanese patients. We determined ABCB11 V444A polymorphism frequencies and HLA genotypes in two independent drug-induced cholestasis cohorts. Expression and taurocholate transport activity of proteins from 444A variants were analyzed using Madin-Darby canine kidney II cells. In cohort 1 (n = 40), the V444A polymorphism C-allele frequency (66%) was lower than that in controls (n = 190, 78%), but this difference was not significant (P = 0.09). In cohort 2 (n = 119), comprising patients with cholestatic (n = 19), hepatocellular (n = 74), and mixed (n = 26) liver injuries, the C-allele frequency was lower among patients with cholestatic liver injury (68%) than among those with hepatocellular (75%) or mixed liver injury (83%), although this difference was not significant. In cohort 1, HLA-A*0201 was observed more frequently in patients (22%) than in controls [11%; P = 0.003; odds ratio, 2.4 (95% confidence interval, 1.4-4.0)]. Taurocholate transport activity of 444A-encoded protein was significantly lower than that of 444V-encoded protein (81% of 444V, P < 0.05) because of the reduced protein stability. In conclusion, ABCB11 444A had slightly reduced transport activity, but it did not contribute to the occurrence of drug-induced cholestasis in Japanese patients. Therefore, genetic susceptibility to acquired cholestasis may differ considerably by ethnicity. Copyright © 2015 by The American Society for Pharmacology and Experimental Therapeutics. JF - Drug metabolism and disposition: the biological fate of chemicals AU - Kagawa, Tatehiro AU - Hirose, Shunji AU - Arase, Yoshitaka AU - Oka, Akira AU - Anzai, Kazuya AU - Tsuruya, Kota AU - Shiraishi, Koichi AU - Orii, Reiko AU - Ieda, Satsuki AU - Nakazawa, Takahide AU - Tomita, Kengo AU - Hokari, Ryota AU - Miura, Soichiro AU - Ebinuma, Hirotoshi AU - Saito, Hidetsugu AU - Kitamura, Tsuneo AU - Horie, Yoshinori AU - Okuse, Chiaki AU - Wasada, Mitsuru AU - Inoko, Hidetoshi AU - Tohkin, Masahiro AU - Saito, Yoshiro AU - Maekawa, Keiko AU - Takikawa, Hajime AU - Mine, Tetsuya AD - Department of Gastroenterology (T.K., S.H., Y.A., K.A., K.T., K.S., R.O., S.I., T.M.), Department of Molecular Life Science, Division of Basic Medical Science and Molecular Medicine (H.I.), and Institute of Medical Science (A.O.), Tokai University School of Medicine, Isehara, Japan; Department of Gastroenterology, Internal Medicine, Kitasato University School of Medicine, Sagamihara, Japan (T.N.); Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan (K.T., R.H., S.M.); Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan (H.E., H.S.); Department of Gastroenterology, Juntendo University Urayasu Hospital, Urayasu, Japan (T.K.); International University of Health and Welfare, Research Centre of Clinical Medicine, Sanno Hospital, Tokyo, Japan (Y.H.); Division of Gastroenterology and Hepatology, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Japan (C.O.); Ikegami General Hospital, Tokyo, Japan (M.W.); Division of Medicinal Safety Science, National Institutes of Health Sciences, Tokyo, Japan (M.T., Y.S., K.M.); and Department of Medicine, Teikyo University School of Medicine, Tokyo, Japan (H.T.) kagawa@tokai.ac.jp. ; Department of Gastroenterology (T.K., S.H., Y.A., K.A., K.T., K.S., R.O., S.I., T.M.), Department of Molecular Life Science, Division of Basic Medical Science and Molecular Medicine (H.I.), and Institute of Medical Science (A.O.), Tokai University School of Medicine, Isehara, Japan; Department of Gastroenterology, Internal Medicine, Kitasato University School of Medicine, Sagamihara, Japan (T.N.); Department of Internal Medicine, National Defense Medical College, Tokorozawa, Japan (K.T., R.H., S.M.); Division of Gastroenterology and Hepatology, Department of Internal Medicine, Keio University School of Medicine, Tokyo, Japan (H.E., H.S.); Department of Gastroenterology, Juntendo University Urayasu Hospital, Urayasu, Japan (T.K.); International University of Health and Welfare, Research Centre of Clinical Medicine, Sanno Hospital, Tokyo, Japan (Y.H.); Division of Gastroenterology and Hepatology, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Japan (C.O.); Ikegami General Hospital, Tokyo, Japan (M.W.); Division of Medicinal Safety Science, National Institutes of Health Sciences, Tokyo, Japan (M.T., Y.S., K.M.); and Department of Medicine, Teikyo University School of Medicine, Tokyo, Japan (H.T.). Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 691 EP - 697 VL - 43 IS - 5 KW - ABCB11 protein, human KW - 0 KW - HLA-A*02:01 antigen KW - HLA-A2 Antigen KW - Index Medicus KW - Madin Darby Canine Kidney Cells KW - Young Adult KW - Animals KW - Humans KW - HLA-A2 Antigen -- genetics KW - Aged KW - Genotype KW - Aged, 80 and over KW - Adult KW - Dogs KW - Middle Aged KW - Gene Frequency -- genetics KW - Male KW - Cell Line KW - Female KW - Cholestasis -- chemically induced KW - Genetic Predisposition to Disease -- genetics KW - ATP-Binding Cassette Transporters -- genetics KW - Cholestasis -- genetics KW - Polymorphism, Single Nucleotide -- genetics KW - Asian Continental Ancestry Group -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1666985577?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+metabolism+and+disposition%3A+the+biological+fate+of+chemicals&rft.atitle=No+contribution+of+the+ABCB11+p.444A+polymorphism+in+Japanese+patients+with+drug-induced+cholestasis.&rft.au=Kagawa%2C+Tatehiro%3BHirose%2C+Shunji%3BArase%2C+Yoshitaka%3BOka%2C+Akira%3BAnzai%2C+Kazuya%3BTsuruya%2C+Kota%3BShiraishi%2C+Koichi%3BOrii%2C+Reiko%3BIeda%2C+Satsuki%3BNakazawa%2C+Takahide%3BTomita%2C+Kengo%3BHokari%2C+Ryota%3BMiura%2C+Soichiro%3BEbinuma%2C+Hirotoshi%3BSaito%2C+Hidetsugu%3BKitamura%2C+Tsuneo%3BHorie%2C+Yoshinori%3BOkuse%2C+Chiaki%3BWasada%2C+Mitsuru%3BInoko%2C+Hidetoshi%3BTohkin%2C+Masahiro%3BSaito%2C+Yoshiro%3BMaekawa%2C+Keiko%3BTakikawa%2C+Hajime%3BMine%2C+Tetsuya&rft.aulast=Kagawa&rft.aufirst=Tatehiro&rft.date=2015-05-01&rft.volume=43&rft.issue=5&rft.spage=691&rft.isbn=&rft.btitle=&rft.title=Drug+metabolism+and+disposition%3A+the+biological+fate+of+chemicals&rft.issn=1521-009X&rft_id=info:doi/10.1124%2Fdmd.114.061325 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-14 N1 - Date created - 2015-03-25 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/dmd.114.061325 ER - TY - JOUR T1 - Extra-hepatic metabolism of 7-ketocholesterol occurs by esterification to fatty acids via cPLA2α and SOAT1 followed by selective efflux to HDL. AN - 1664445980; 25617738 AB - Accumulation of 7-ketocholesterol (7KCh) in tissues has been previously associated with various chronic aging diseases. Orally ingested 7KCh is readily metabolized by the liver and does not pose a toxicity threat. However, 7KCh formed in situ, usually associated with lipoprotein deposits, can adversely affect surrounding tissues by causing inflammation and cytotoxicity. In this study we have investigated various mechanisms for extra-hepatic metabolism of 7KCh (e.g. hydroxylation, sulfation) and found only esterification to fatty acids. The esterification of 7KCh to fatty acids involves the combined action of cytosolic phospholipase A2 alpha (cPLA2α) and sterol O-acyltransferase (SOAT1). Inhibition of either one of these enzymes ablates 7KCh-fatty acid ester (7KFAE) formation. The 7KFAEs are not toxic and do not induce inflammatory responses. However, they can be unstable and re-release 7KCh. The higher the degree of unsaturation, the more unstable the 7KFAE (e.g. 18:0>18:1>18:2>18:3≫20:4). Biochemical inhibition and siRNA knockdown of SOAT1 and cPLA2α ablated the 7KFAE synthesis in cultured ARPE19 cells, but had little effect on the 7KCh-induced inflammatory response. Overexpression of SOAT1 reduced the 7KCh-induced inflammatory response and provided some protection from cell death. This effect is likely due to the increased conversion of 7KCh to 7KFAEs, which reduced the intracellular 7KCh levels. Addition of HDL selectively increased the efflux of 7KFAEs and enhanced the effect of SOAT1 overexpression. Our data suggests an additional function for HDL in aiding extra-hepatic tissues to eliminate 7KCh by returning 7KFAEs to the liver for bile acid formation. Published by Elsevier B.V. JF - Biochimica et biophysica acta AU - Lee, Jung Wha AU - Huang, Jiahn-Dar AU - Rodriguez, Ignacio R AD - Mechanisms of Retinal Diseases Section, Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, MD, USA. Electronic address: leej@nei.nih.gov. ; Mechanisms of Retinal Diseases Section, Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 605 EP - 619 VL - 1851 IS - 5 SN - 0006-3002, 0006-3002 KW - Cholesterol, HDL KW - 0 KW - Enzyme Inhibitors KW - Fatty Acids KW - Ketocholesterols KW - Sterol O-Acyltransferase KW - EC 2.3.1.26 KW - sterol O-acyltransferase 1 KW - Group IV Phospholipases A2 KW - EC 3.1.1.4 KW - PLA2G4A protein, human KW - 7-ketocholesterol KW - O7676FE78M KW - Index Medicus KW - SOAT1 KW - HDL KW - cPLA2α KW - Cultured RPE cell KW - 7-Ketocholesterol fatty acid ester KW - 7-Ketocholesterol KW - Animals KW - Mass Spectrometry KW - Humans KW - Biological Transport KW - Chromatography, High Pressure Liquid KW - Esterification KW - Transfection KW - Biotransformation KW - Cell Death KW - Enzyme Inhibitors -- pharmacology KW - Macaca mulatta KW - RNA Interference KW - Time Factors KW - Cell Line KW - Male KW - Sterol O-Acyltransferase -- metabolism KW - Cholesterol, HDL -- metabolism KW - Sterol O-Acyltransferase -- genetics KW - Group IV Phospholipases A2 -- genetics KW - Retinal Pigment Epithelium -- enzymology KW - Group IV Phospholipases A2 -- antagonists & inhibitors KW - Retinal Pigment Epithelium -- drug effects KW - Group IV Phospholipases A2 -- metabolism KW - Ketocholesterols -- metabolism KW - Sterol O-Acyltransferase -- antagonists & inhibitors KW - Retinal Pigment Epithelium -- pathology KW - Fatty Acids -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664445980?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Extra-hepatic+metabolism+of+7-ketocholesterol+occurs+by+esterification+to+fatty+acids+via+cPLA2%CE%B1+and+SOAT1+followed+by+selective+efflux+to+HDL.&rft.au=Lee%2C+Jung+Wha%3BHuang%2C+Jiahn-Dar%3BRodriguez%2C+Ignacio+R&rft.aulast=Lee&rft.aufirst=Jung&rft.date=2015-05-01&rft.volume=1851&rft.issue=5&rft.spage=605&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbalip.2015.01.007 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-25 N1 - Date created - 2015-03-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biochim Biophys Acta. 2009 Dec;1791(12):1206-15 [19732851] Invest Ophthalmol Vis Sci. 2009 Feb;50(2):523-32 [18936140] J Lipid Res. 2010 Oct;51(10):2847-62 [20567027] Invest Ophthalmol Vis Sci. 2010 Oct;51(10):4942-55 [20554621] Cell Microbiol. 2010 Oct;12(10):1369-77 [20642808] J Steroid Biochem Mol Biol. 1992 Dec;43(8):1055-72 [22217850] Redox Biol. 2013;1:125-30 [24024145] Drug Metab Rev. 2013 Nov;45(4):388-400 [24020383] Prog Retin Eye Res. 2014 Jul;41:64-89 [24704580] PLoS One. 2014;9(7):e100985 [25036103] Cardiovasc Res. 2014 Aug 1;103(3):341-9 [24935434] Exp Eye Res. 2014 Nov;128:151-5 [25261634] J Lipid Res. 1999 Dec;40(12):2195-203 [10588945] J Biol Chem. 1999 Dec 17;274(51):36139-45 [10593897] J Biol Chem. 2000 Jun 2;275(22):16536-42 [10748048] J Biol Chem. 2000 Sep 8;275(36):28083-92 [10846185] J Lipid Res. 2000 Dec;41(12):1991-2001 [11108732] Biochim Biophys Acta. 2001 Feb 26;1530(2-3):209-18 [11239823] Lipids. 2001 Jul;36(7):701-11 [11521968] Biochim Biophys Acta. 2002 Apr 15;1581(3):119-26 [12020639] J Clin Invest. 2002 Jul;110(1):109-17 [12093894] Curr Opin Investig Drugs. 2003 Sep;4(9):1095-9 [14582454] J Biol Chem. 1977 Aug 10;252(15):5186-93 [885845] Biochim Biophys Acta. 1994 Aug 25;1214(1):20-6 [8068724] J Lipid Res. 1996 Feb;37(2):320-35 [9026530] J Biol Chem. 1998 Oct 9;273(41):26755-64 [9756919] J Lipid Res. 2005 Sep;46(9):1933-43 [15995174] Proc Natl Acad Sci U S A. 2005 Feb 22;102(8):2814-9 [15710898] J Lipid Res. 1999 Oct;40(10):1846-57 [10508204] J Steroid Biochem Mol Biol. 2006 Dec;102(1-5):214-21 [17055258] J Lipid Res. 2007 Jun;48(6):1343-52 [17347498] Anal Biochem. 2007 Sep 15;368(2):239-49 [17601482] J Lipid Res. 2009 Oct;50(10):1955-66 [19346330] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbalip.2015.01.007 ER - TY - JOUR T1 - Photoinduced spectral changes of photoluminescent gold nanoclusters. AN - 1639972769; 25517487 AB - Ultrasmall photoluminescent gold nanoclusters (Au NCs), composed of several atoms with sizes up to a few nanometers, have recently stimulated extensive interest. Unique molecule-like behaviors, low toxicity, and facile synthesis make photoluminescent Au NCs a very promising alternative to organic fluorophores and semiconductor quantum dots (QDs) in broad ranges of biomedical applications. However, using gold nanoparticles (Au NPs) for bioimaging might cause their degradation under continuous excitation with UV light, which might result in toxicity. We report spectral changes of photoluminescent 2-(N-morpholino) ethanesulfonic acid (MES)-coated (Au-MES) NCs under irradiation with UV/blue light. Photoluminescent water soluble Au- MES NCs with a photoluminescence (PL) band maximum at 476 nm (λex = 420 nm) were synthesized. Under irradiation with 402 nm wavelength light the size of photoluminescent Au-MES NCs decreased (λem = 430 nm). Irradiating the sample solution with 330 nm wavelength light, nonluminescent Au NPs were disrupted, and photoluminescent Au NCs (λem = 476 nm) were formed. Irradiation with 330 nm wavelength light did not directly affect photoluminescent Au-MES NCs, however, increase in PL intensity indicated the formation of photoluminescent Au NCs from the disrupted nonluminescent Au NPs. This study gives a good insight into the photostability of MES-coated Au NPs under continuous excitation with UV/blue light. JF - Journal of biomedical optics AU - Matulionytė, Marija AU - Marcinonytė, Raminta AU - Rotomskis, Ričardas AD - National Cancer Institute, Biomedical Physics Laboratory, P. Baublio Street 3b, LT-08406 Vilnius, LithuaniabVilnius University, Biophotonics Group of Laser Research Centre, Sauletekio Avenue 9, LT-10222 Vilnius, Lithuania. ; National Cancer Institute, Biomedical Physics Laboratory, P. Baublio Street 3b, LT-08406 Vilnius, Lithuania. Y1 - 2015/05// PY - 2015 DA - May 2015 SP - 051018 VL - 20 IS - 5 KW - Alkanesulfonic Acids KW - 0 KW - Colloids KW - Morpholines KW - Reactive Oxygen Species KW - Water KW - 059QF0KO0R KW - 2-(N-morpholino)ethanesulfonic acid KW - 2GNK67Q0C4 KW - Carbon KW - 7440-44-0 KW - Gold KW - 7440-57-5 KW - Index Medicus KW - Ultraviolet Rays KW - Colloids -- chemistry KW - Particle Size KW - Water -- chemistry KW - Spectrophotometry KW - Light KW - Carbon -- chemistry KW - Luminescence KW - Nanotechnology KW - Photochemistry KW - Metal Nanoparticles -- chemistry KW - Morpholines -- chemistry KW - Alkanesulfonic Acids -- chemistry KW - Gold -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1639972769?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+biomedical+optics&rft.atitle=Photoinduced+spectral+changes+of+photoluminescent+gold+nanoclusters.&rft.au=Matulionyt%C4%97%2C+Marija%3BMarcinonyt%C4%97%2C+Raminta%3BRotomskis%2C+Ri%C4%8Dardas&rft.aulast=Matulionyt%C4%97&rft.aufirst=Marija&rft.date=2015-05-01&rft.volume=20&rft.issue=5&rft.spage=051018&rft.isbn=&rft.btitle=&rft.title=Journal+of+biomedical+optics&rft.issn=1560-2281&rft_id=info:doi/10.1117%2F1.JBO.20.5.051018 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-21 N1 - Date created - 2014-12-18 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1117/1.JBO.20.5.051018 ER - TY - JOUR T1 - Id1 suppresses anti-tumour immune responses and promotes tumour progression by impairing myeloid cell maturation. AN - 1677888173; 25924227 AB - A central mechanism of tumour progression and metastasis involves the generation of an immunosuppressive 'macroenvironment' mediated in part through tumour-secreted factors. Here we demonstrate that upregulation of the Inhibitor of Differentiation 1 (Id1), in response to tumour-derived factors, such as TGFβ, is responsible for the switch from dendritic cell (DC) differentiation to myeloid-derived suppressor cell expansion during tumour progression. Genetic inactivation of Id1 largely corrects the myeloid imbalance, whereas Id1 overexpression in the absence of tumour-derived factors re-creates it. Id1 overexpression leads to systemic immunosuppression by downregulation of key molecules involved in DC differentiation and suppression of CD8 T-cell proliferation, thus promoting primary tumour growth and metastatic progression. Furthermore, advanced melanoma patients have increased plasma TGFβ levels and express higher levels of ID1 in myeloid peripheral blood cells. This study reveals a critical role for Id1 in suppressing the anti-tumour immune response during tumour progression and metastasis. JF - Nature communications AU - Papaspyridonos, Marianna AU - Matei, Irina AU - Huang, Yujie AU - do Rosario Andre, Maria AU - Brazier-Mitouart, Helene AU - Waite, Janelle C AU - Chan, April S AU - Kalter, Julie AU - Ramos, Ilyssa AU - Wu, Qi AU - Williams, Caitlin AU - Wolchok, Jedd D AU - Chapman, Paul B AU - Peinado, Hector AU - Anandasabapathy, Niroshana AU - Ocean, Allyson J AU - Kaplan, Rosandra N AU - Greenfield, Jeffrey P AU - Bromberg, Jacqueline AU - Skokos, Dimitris AU - Lyden, David AD - Children's Cancer and Blood Foundation Laboratories and Departments of Pediatrics and Cell and Developmental Biology, Weill Cornell Medical College, 413 East 69th Street, New York City, New York 10021, USA. ; 1] Children's Cancer and Blood Foundation Laboratories and Departments of Pediatrics and Cell and Developmental Biology, Weill Cornell Medical College, 413 East 69th Street, New York City, New York 10021, USA [2] Department of Neurosurgery, Weill Cornell Medical College, 1300 York Avenue, New York City, New York 10065, USA. ; 1] Children's Cancer and Blood Foundation Laboratories and Departments of Pediatrics and Cell and Developmental Biology, Weill Cornell Medical College, 413 East 69th Street, New York City, New York 10021, USA [2] Department of Genetics, Oncology and Human Toxicology, Faculdade de Ciência Médicas, Universidade Nova de Lisboa, Rua da Junqueira 100, 1349-008 Lisbon, Portugal. ; Regeneron Pharmaceuticals, Tarrytown, New York 10591, USA. ; 1] Melanoma and Immunotherapy Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York City, New York 10065, USA [2] Ludwig Center for Cancer Immunotherapy, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York City, New York 10065, USA. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York City, New York 10065, USA. ; 1] Children's Cancer and Blood Foundation Laboratories and Departments of Pediatrics and Cell and Developmental Biology, Weill Cornell Medical College, 413 East 69th Street, New York City, New York 10021, USA [2] Tumor Metastasis Laboratory, Fundación Centro Nacional de Investigaciones Oncológicas, Calle Melchor Fernández Almagro 3, 28029 Madrid, Spain. ; Brigham and Women's Hospital, Department of Dermatology, Harvard Medical School, 221 Longwood Avenue EBRC, Room 513, Boston, Massachusetts 02118, USA. ; Department of Medicine, Weill Cornell Medical College and Medical Oncology/Solid Tumor Program, 1305 York Avenue, New York City, New York 10021, USA. ; Center for Cancer Research, Pediatric Oncology Branch, National Cancer Institute, National Institutes of Health, Building 10-Hatfield CRC, Room 1-3940, Bethesda, Maryland 20892, USA. ; Department of Neurosurgery, Weill Cornell Medical College, 1300 York Avenue, New York City, New York 10065, USA. ; 1] Children's Cancer and Blood Foundation Laboratories and Departments of Pediatrics and Cell and Developmental Biology, Weill Cornell Medical College, 413 East 69th Street, New York City, New York 10021, USA [2] Department of Pediatrics, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, New York City, New York 10065, USA. Y1 - 2015/04/29/ PY - 2015 DA - 2015 Apr 29 SP - 6840 VL - 6 KW - Inhibitor of Differentiation Protein 1 KW - 0 KW - Interferon Regulatory Factors KW - Transforming Growth Factor beta KW - interferon regulatory factor-8 KW - Index Medicus KW - Gene Expression Regulation, Neoplastic KW - Animals KW - Humans KW - Leukocytes, Mononuclear -- metabolism KW - Neoplasm Metastasis KW - Mice, Inbred C57BL KW - Disease Progression KW - Interferon Regulatory Factors -- metabolism KW - Cell Differentiation KW - Transforming Growth Factor beta -- metabolism KW - Melanoma, Experimental -- secretion KW - Melanoma, Experimental -- metabolism KW - Inhibitor of Differentiation Protein 1 -- physiology KW - Myeloid Cells -- physiology KW - Melanoma, Experimental -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1677888173?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+communications&rft.atitle=Id1+suppresses+anti-tumour+immune+responses+and+promotes+tumour+progression+by+impairing+myeloid+cell+maturation.&rft.au=Papaspyridonos%2C+Marianna%3BMatei%2C+Irina%3BHuang%2C+Yujie%3Bdo+Rosario+Andre%2C+Maria%3BBrazier-Mitouart%2C+Helene%3BWaite%2C+Janelle+C%3BChan%2C+April+S%3BKalter%2C+Julie%3BRamos%2C+Ilyssa%3BWu%2C+Qi%3BWilliams%2C+Caitlin%3BWolchok%2C+Jedd+D%3BChapman%2C+Paul+B%3BPeinado%2C+Hector%3BAnandasabapathy%2C+Niroshana%3BOcean%2C+Allyson+J%3BKaplan%2C+Rosandra+N%3BGreenfield%2C+Jeffrey+P%3BBromberg%2C+Jacqueline%3BSkokos%2C+Dimitris%3BLyden%2C+David&rft.aulast=Papaspyridonos&rft.aufirst=Marianna&rft.date=2015-04-29&rft.volume=6&rft.issue=&rft.spage=6840&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms7840 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-15 N1 - Date created - 2015-04-30 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Oncogene. 2008 Sep 18;27(42):5612-23 [18542061] Cancer Cell. 2010 Dec 14;18(6):655-68 [21156287] Nature. 1999 Oct 14;401(6754):670-7 [10537105] Clin Cancer Res. 2000 May;6(5):1755-66 [10815894] J Immunol. 2001 Jan 1;166(1):678-89 [11123353] Nat Med. 2001 Nov;7(11):1194-201 [11689883] J Immunother. 2001 Nov-Dec;24(6):431-46 [11759067] Am J Pathol. 2003 Feb;162(2):533-46 [12547711] Mol Cell. 2003 Apr;11(4):915-26 [12718878] Oncogene. 2003 May 19;22(20):3180-7 [12789294] Trends Cell Biol. 2003 Aug;13(8):410-8 [12888293] Br J Cancer. 2003 Oct 20;89(8):1463-72 [14562018] J Immunol. 2004 Jan 15;172(2):989-99 [14707072] Trends Mol Med. 2004 Aug;10(8):387-92 [15310459] Cell. 1990 Apr 6;61(1):49-59 [2156629] Nat Rev Immunol. 2004 Dec;4(12):941-52 [15573129] J Immunol. 2005 Feb 15;174(4):1841-50 [15699110] Cancer Res. 2005 Apr 15;65(8):3044-8 [15833831] Blood. 2005 Jun 1;105(11):4272-81 [15701714] Biochem Biophys Res Commun. 2005 Aug 19;334(1):193-8 [16002046] Nat Rev Cancer. 2005 Aug;5(8):603-14 [16034366] Nature. 2005 Dec 8;438(7069):820-7 [16341007] Cancer Res. 2006 Jan 15;66(2):1123-31 [16424049] Curr Opin Genet Dev. 2006 Feb;16(1):30-7 [16377175] Semin Cancer Biol. 2006 Feb;16(1):53-65 [16168663] Proc Natl Acad Sci U S A. 2007 Jan 23;104(4):1260-5 [17227850] Blood. 2007 Mar 1;109(5):1953-61 [17068149] J Clin Invest. 2007 May;117(5):1155-66 [17476345] J Clin Oncol. 2007 Jun 20;25(18):2546-53 [17577033] Nat Biotechnol. 2007 Aug;25(8):911-20 [17664940] Clin Cancer Res. 2007 Aug 15;13(16):4840-8 [17699863] Nature. 2007 Sep 27;449(7161):419-26 [17898760] Science. 2008 Jan 11;319(5860):195-8 [18187653] Immunol Rev. 2008 Apr;222:180-91 [18364002] J Immunol. 2008 Jul 1;181(1):346-53 [18566400] Cancer Res. 2008 Jul 1;68(13):5439-49 [18593947] J Immunol. 2008 Oct 1;181(7):4666-75 [18802069] J Exp Med. 2008 Sep 29;205(10):2235-49 [18809714] J Immunol. 2008 Oct 15;181(8):5791-802 [18832739] Cancer Immunol Immunother. 2009 Jan;58(1):49-59 [18446337] Nat Cell Biol. 2008 Nov;10(11):1349-55 [18820689] Clin Cancer Res. 2008 Dec 15;14(24):8270-8 [19088044] Cell Res. 2009 Jan;19(1):140-8 [19079362] Nat Rev Immunol. 2009 Mar;9(3):162-74 [19197294] J Immunol. 2009 May 1;182(9):5693-701 [19380816] J Immunol. 2009 May 15;182(10):6562-8 [19414811] Ann Oncol. 2009 Aug;20 Suppl 6:vi1-7 [19617292] Haematologica. 2009 Aug;94(8):1075-84 [19644139] PLoS One. 2009;4(11):e7955 [19956687] Cancer Res. 2010 Jan 1;70(1):99-108 [19996287] Prostate. 2010 Mar 1;70(4):443-55 [19902470] Oncogene. 2010 Feb 25;29(8):1093-102 [19946335] J Cell Mol Med. 2009 Sep;13(9B):3939-50 [20196788] Immunol Rev. 2011 Jan;239(1):27-44 [21198663] Semin Cancer Biol. 2011 Apr;21(2):139-46 [21251983] Curr Opin Immunol. 2011 Apr;23(2):279-85 [21227670] N Engl J Med. 2011 Jul 14;365(2):127-38 [21524210] Nat Rev Clin Oncol. 2011 Oct;8(10):577-85 [21808266] Blood. 2012 Mar 1;119(9):2003-12 [22238324] Nat Rev Immunol. 2012 Apr;12(4):253-68 [22437938] Nat Immunol. 2013 Mar;14(3):211-20 [23354483] Prostate. 2013 May;73(6):624-33 [23060149] Cell Rep. 2013 May 30;3(5):1617-28 [23623495] Nat Rev Cancer. 2013 Oct;13(10):739-52 [24060865] J Clin Invest. 2013 Oct;123(10):4464-78 [24091328] Cell Stem Cell. 2010 Mar 5;6(3):265-78 [20207229] Semin Cancer Biol. 2012 Aug;22(4):319-26 [22349515] Cancer Cell. 2012 Jun 12;21(6):777-92 [22698403] Nat Med. 2012 Jun;18(6):883-91 [22635005] Clin Cancer Res. 2012 Sep 15;18(18):4877-82 [22718858] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ncomms7840 ER - TY - JOUR T1 - The implications of the relative risk for road mortality on road safety programmes in Qatar AN - 1808710216; PQ0003427146 AB - The epidemiology of road deaths and in particular the relative risk for road mortality (RRRM) in Qatar has not been fully defined. This study will analyse and compare the proportionate mortality and age-specific death rates from road traffic injuries (RTIs) and make recommendations for targeted injury prevention programmes for road safety in Qatar. Data from the Qatar Statistics Authority (QSA), for the year 2010, was collected and analysed. All deaths classified as 'ICD-10 (V89) Motor- or Nonmotor-Vehicle, Accident Type of Vehicle Unspecified' were included. There were 247 RTI related deaths in Qatar in 2010. An overall death rate was computed at 14.4 deaths per 100000 population. The RRRM varied over 10 times among different populations with Qatari males (QM) having an increased RRRM from 10years of age, those aged 20-29years had the highest RRRM of 10.2. The lowest RRRM was for Qatari females who did not have a single reported road fatality in 2010. Populations with a significantly elevated RRRM (ie, RRRM>1.0) were non-Qatari men older than 50years and Qatari males from the age of 10 onward. Proven and definite programmes must be implemented to reduce these unnecessary deaths among the populations at the highest risk. Multidisciplinary approaches must be implemented and their efficacy evaluated. JF - Injury Prevention AU - Consunji, Rafael J AU - Peralta, Ruben R AU - Al-Thani, Hassan AU - Latifi, Rifat AD - Study Group on Injury Prevention and Control, National Institutes of Health, University of the Philippines Manila, , Manila, Philippines Y1 - 2015/04/28/ PY - 2015 DA - 2015 Apr 28 SP - e105 EP - e108 PB - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom VL - 21 IS - e1 SN - 1353-8047, 1353-8047 KW - Health & Safety Science Abstracts KW - Qatar KW - Mortality KW - Age KW - Prevention KW - Accidents KW - Injuries KW - Traffic safety KW - Traffic KW - H 2000:Transportation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808710216?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Injury+Prevention&rft.atitle=The+implications+of+the+relative+risk+for+road+mortality+on+road+safety+programmes+in+Qatar&rft.au=Consunji%2C+Rafael+J%3BPeralta%2C+Ruben+R%3BAl-Thani%2C+Hassan%3BLatifi%2C+Rifat&rft.aulast=Consunji&rft.aufirst=Rafael&rft.date=2015-04-28&rft.volume=21&rft.issue=e1&rft.spage=e105&rft.isbn=&rft.btitle=&rft.title=Injury+Prevention&rft.issn=13538047&rft_id=info:doi/10.1136%2Finjuryprev-2013-040939 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Mortality; Accidents; Prevention; Age; Injuries; Traffic safety; Traffic; Qatar DO - http://dx.doi.org/10.1136/injuryprev-2013-040939 ER - TY - JOUR T1 - Tissue and species differences in the glucuronidation of glabridin with UDP-glucuronosyltransferases. AN - 1671211860; 25765239 AB - Glabridin (GA) has gained wide application in the cosmetics and food industry. This study was performed to investigate its metabolic inactivation and elimination by glucuronidation by use of liver and intestine microsomes from humans (HLM and HIM) and rats (RLM and RIM), and liver microsomes from cynomolgus monkeys and beagle dogs (CyLM and DLM). Both hydroxyl groups at the C2 and C4 positions of the B ring are conjugated to generate two mono-glucuronides (M1 and M2). HIM, RIM and RLM showed the most robust activity in catalyzing M2 formation with intrinsic clearance values (Clint) above 2000 μL/min/mg, with little measurable M1 formation activity. DLM displayed considerable activity both in M1 and M2 formation, with Clint values of 71 and 214 μL/min/mg, respectively, while HLM and CyLM exhibited low activities in catalyzing M1 and M2 formation, with Clint values all below 20 μL/min/mg. It is revealed that UGT1A1, 1A3, 1A9, 2B7, 2B15 and extrahepatic UGT1A8 and 1A10 are involved in GA glucuronidation. Nearly all UGTs preferred M2 formation except for UGT1A1. Notably, UGT1A8 displayed the highest activity with a Clint value more than 5-fold higher than the other isoforms. Chemical inhibition studies, using selective inhibitors of UGT1A1, 1A9, 2B7 and 1A8, further revealed that UGT1A8 contributed significantly to intestinal GA glucuronidation in humans. In summary, this in vitro study demonstrated large species differences in GA glucuronidation by liver and intestinal microsomes, and that intestinal UGTs are important for the pathway in humans. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. JF - Chemico-biological interactions AU - Guo, Bin AU - Fang, Zhongze AU - Yang, Lu AU - Xiao, Ling AU - Xia, Yangliu AU - Gonzalez, Frank J AU - Zhu, Liangliang AU - Cao, Yunfeng AU - Ge, Guangbo AU - Yang, Ling AU - Sun, Hongzhi AD - The First Affiliated Hospital of Liaoning Medical University, Jinzhou, China; Joint Center for Translational Medicine, Dalian Institute of Chemical Physics, Chinese Academy of Sciences and The First Affiliated Hospital of Liaoning Medical University, Dalian, China. Electronic address: binguo_ln@163.com. ; Department of Toxicology, School of Public Health, Tianjin Medical University, Tianjin, China; Joint Center for Translational Medicine, Dalian Institute of Chemical Physics, Chinese Academy of Sciences and The First Affiliated Hospital of Liaoning Medical University, Dalian, China. ; Joint Center for Translational Medicine, Dalian Institute of Chemical Physics, Chinese Academy of Sciences and The First Affiliated Hospital of Liaoning Medical University, Dalian, China. ; The Centre for Drug and Food Safety Evaluation, School of Life Science, Anqing Normal University, Anqing, China. ; Laboratory of Pharmaceutical Resource Discovery, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian, China. ; Laboratory of Metabolism, Center for Cancer Research, NCI, National Institutes of Health, USA. ; The Centre for Drug and Food Safety Evaluation, School of Life Science, Anqing Normal University, Anqing, China. Electronic address: zhull_better@163.com. ; Joint Center for Translational Medicine, Dalian Institute of Chemical Physics, Chinese Academy of Sciences and The First Affiliated Hospital of Liaoning Medical University, Dalian, China; Key Laboratory of Contraceptives and Devices Research (NPFPC), Shanghai Engineer and Technology Research Center of Reproductive Health Drug and Devices, Shanghai Institute of Planned Parenthood Research, Shanghai, China. ; The First Affiliated Hospital of Liaoning Medical University, Jinzhou, China. Y1 - 2015/04/25/ PY - 2015 DA - 2015 Apr 25 SP - 90 EP - 97 VL - 231 KW - Glucuronides KW - 0 KW - Isoflavones KW - Phenols KW - Glucuronosyltransferase KW - EC 2.4.1.17 KW - UDP-glucuronosyltransferase, UGT1A8 KW - glabridin KW - HOC5567T41 KW - Index Medicus KW - UDP-glucuronosyltransferases KW - Glabridin KW - Glucuronidation KW - Species differences KW - Young Adult KW - Animals KW - Macaca fascicularis KW - Humans KW - Aged KW - Liver -- metabolism KW - Mice KW - Child KW - Intestines -- metabolism KW - Glucuronides -- metabolism KW - Rats, Sprague-Dawley KW - Aged, 80 and over KW - Adult KW - Dogs KW - Middle Aged KW - Adolescent KW - Species Specificity KW - Male KW - Female KW - Microsomes -- metabolism KW - Phenols -- metabolism KW - Glucuronosyltransferase -- metabolism KW - Isoflavones -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1671211860?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemico-biological+interactions&rft.atitle=Tissue+and+species+differences+in+the+glucuronidation+of+glabridin+with+UDP-glucuronosyltransferases.&rft.au=Guo%2C+Bin%3BFang%2C+Zhongze%3BYang%2C+Lu%3BXiao%2C+Ling%3BXia%2C+Yangliu%3BGonzalez%2C+Frank+J%3BZhu%2C+Liangliang%3BCao%2C+Yunfeng%3BGe%2C+Guangbo%3BYang%2C+Ling%3BSun%2C+Hongzhi&rft.aulast=Guo&rft.aufirst=Bin&rft.date=2015-04-25&rft.volume=231&rft.issue=&rft.spage=90&rft.isbn=&rft.btitle=&rft.title=Chemico-biological+interactions&rft.issn=1872-7786&rft_id=info:doi/10.1016%2Fj.cbi.2015.03.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-16 N1 - Date created - 2015-04-07 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.cbi.2015.03.001 ER - TY - JOUR T1 - Cell-to-cell contact facilitates HIV transmission from lymphocytes to astrocytes via CXCR4 AN - 1808696878; PQ0003241723 AB - Objectives: HIV reservoir in the brain represents a major barrier for curing HIV infection. As the most abundant, long-lived cell type, astrocytes play a critical role in maintaining the reservoir; however, the mechanism of infection remains unknown. Here, we determine how viral transmission occurs from HIV-infected lymphocytes to astrocytes by cell-to-cell contact. Design and methods: Human astrocytes were exposed to HIV-infected lymphocytes and monitored by live-imaging, confocal microscopy, transmission and three-dimensional electron microscopy. A panel of receptor antagonists was used to determine the mechanism of viral entry. Results: We found that cell-to-cell contact resulted in efficient transmission of X4 or X4R5-using viruses from T lymphocytes to astrocytes. In co-cultures of astrocytes with HIV-infected lymphocytes, the interaction occurred through a dynamic process of attachment and detachment of the two cell types. Infected lymphocytes invaginated into astrocytes or the contacts occurred via filopodial extensions from either cell type, leading to the formation of virological synapses. In the synapses, budding of immature or incomplete HIV particles from lymphocytes occurred directly onto the membranes of astrocytes. This cell-to-cell transmission could be almost completely blocked by anti-CXCR4 antibody and its antagonist, but only partially inhibited by anti-CD4, ICAM1 antibodies. Conclusion: Cell-to-cell transmission was mediated by a unique mechanism by which immature viral particles initiated a fusion process in a CXCR4-dependent, CD4-independent manner. These observations have important implications for developing approaches to prevent formation of HIV reservoirs in the brain. JF - AIDS AU - Li, Guan-Han AU - Anderson, Caroline AU - Jaeger, Laura AU - Do, Thao AU - Major, Eugene O AU - Nath, Avindra AD - Section of Infections of the Nervous System, National Institute of Neurological Diseases and Stroke, natha@ninds.nih.gov Y1 - 2015/04/24/ PY - 2015 DA - 2015 Apr 24 SP - 755 EP - 766 PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 29 IS - 7 SN - 0269-9370, 0269-9370 KW - CSA Neurosciences Abstracts; Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - astrocyte KW - brain KW - cell-to-cell transmission KW - CXCR4 KW - HIV infection KW - lymphocyte KW - virological synapse KW - Acquired immune deficiency syndrome KW - Astrocytes KW - CXCR4 protein KW - Viruses KW - Lymphocytes KW - Particulates KW - Infection KW - Antagonists KW - Disease transmission KW - CD4 antigen KW - Neurotransmission KW - Synaptogenesis KW - intercellular adhesion molecule 1 KW - Lymphocytes T KW - Reservoirs KW - Electron microscopy KW - Budding KW - Synapses KW - Membranes KW - Brain KW - Antibodies KW - Human immunodeficiency virus KW - Microscopy KW - Confocal microscopy KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - V 22360:AIDS and HIV KW - N3 11027:Neurology & neuropathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808696878?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Cell-to-cell+contact+facilitates+HIV+transmission+from+lymphocytes+to+astrocytes+via+CXCR4&rft.au=Li%2C+Guan-Han%3BAnderson%2C+Caroline%3BJaeger%2C+Laura%3BDo%2C+Thao%3BMajor%2C+Eugene+O%3BNath%2C+Avindra&rft.aulast=Li&rft.aufirst=Guan-Han&rft.date=2015-04-24&rft.volume=29&rft.issue=7&rft.spage=755&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000605 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Synapses; CXCR4 protein; Astrocytes; Brain; Infection; Antagonists; Disease transmission; Antibodies; CD4 antigen; Neurotransmission; Synaptogenesis; Confocal microscopy; intercellular adhesion molecule 1; Lymphocytes T; Electron microscopy; Budding; Acquired immune deficiency syndrome; Membranes; Human immunodeficiency virus; Viruses; Microscopy; Particulates; Lymphocytes; Reservoirs DO - http://dx.doi.org/10.1097/QAD.0000000000000605 ER - TY - JOUR T1 - Safety and Survival With GVAX Pancreas Prime and Listeria Monocytogenes-Expressing Mesothelin (CRS-207) Boost Vaccines for Metastatic Pancreatic Cancer AN - 1827928284; PQ0003429567 AB - PurposeGVAX pancreas, granulocyte-macrophage colony-stimulating factor-secreting allogeneic pancreatic tumor cells, induces T-cell immunity to cancer antigens, including mesothelin. GVAX is administered with low-dose cyclophosphamide (Cy) to inhibit regulatory T cells. CRS-207, live-attenuated Listeria monocytogenes-expressing mesothelin, induces innate and adaptive immunity. On the basis of preclinical synergy, we tested prime/boost vaccination with GVAX and CRS-207 in pancreatic adenocarcinoma.Patients and MethodsPreviously treated patients with metastatic pancreatic adenocarcinoma were randomly assigned at a ratio of 2:1 to two doses of Cy/GVAX followed by four doses of CRS-207 (arm A) or six doses of Cy/GVAX (arm B) every 3 weeks. Stable patients were offered additional courses. The primary end point was overall survival (OS) between arms. Secondary end points were safety and clinical response.ResultsA total of 90 patients were treated (arm A, n = 61; arm B, n = 29); 97% had received prior chemotherapy; 51% had received greater than or equal to two regimens for metastatic disease. Mean number of doses ( plus or minus standard deviation) administered in arms A and B were 5.5 plus or minus 4.5 and 3.7 plus or minus 2.2, respectively. The most frequent grade 3 to 4 related toxicities were transient fevers, lymphopenia, elevated liver enzymes, and fatigue. OS was 6.1 months in arm A versus 3.9 months in arm B (hazard ratio [HR], 0.59; P = .02). In a prespecified per-protocol analysis of patients who received at least three doses (two doses of Cy/GVAX plus one of CRS-207 or three of Cy/GVAX), OS was 9.7 versus 4.6 months (arm A v B; HR, 0.53; P = .02). Enhanced mesothelin-specific CD8 T-cell responses were associated with longer OS, regardless of treatment arm.ConclusionHeterologous prime/boost with Cy/GVAX and CRS-207 extended survival for patients with pancreatic cancer, with minimal toxicity. JF - Journal of Clinical Oncology AU - Le, Dung T AU - Wang-Gillam, Andrea AU - Picozzi, Vincent AU - Greten, Tim F AU - Crocenzi, Todd AU - Springett, Gregory AU - Morse, Michael AU - Zeh, Herbert AU - Cohen, Deirdre AU - Fine, Robert L AU - Onners, Beth AU - Uram, Jennifer N AU - Laheru, Daniel A AU - Lutz, Eric R AU - Solt, Sara AU - Murphy, Aimee Luck AU - Skoble, Justin AU - Lemmens, Ed AU - Grous, John AU - Dubensky, Thomas AU - Brockstedt, Dirk G AU - Jaffee, Elizabeth M AD - Dung T. Le, Beth Onners, Jennifer N. Uram, Daniel A. Laheru, Eric R. Lutz, Sara Solt, and Elizabeth M. Jaffee, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore; Tim F. Greten, National Cancer Institute, Bethesda, MD; Andrea Wang-Gillam, Siteman Cancer Center, Washington University, St Louis, MO; Vincent Picozzi, Virginia Mason Medical Center, Seattle, WA; Todd Crocenzi, Providence Portland Medical Center, Portland, OR; Gregory Springett, Moffitt Cancer Center, Tampa, FL; Michael Morse, Duke University Medical Center, Durham, NC; Herbert Zeh, University of Pittsburgh, Pittsburgh, PA; Deirdre Cohen, New York University Langone Medical Center; Robert L. Fine, Columbia University Medical Center, New York, NY; and Aimee Luck Murphy, Justin Skoble, Ed Lemmens, John Grous, Thomas Dubensky Jr, and Dirk G. Brockstedt, Aduro BioTech, Berkeley, CA, dle2@jhmi.edu Y1 - 2015/04/20/ PY - 2015 DA - 2015 Apr 20 SP - 1325 EP - 1333 PB - American Society of Clinical Oncology VL - 33 IS - 12 SN - 0732-183X, 0732-183X KW - Microbiology Abstracts B: Bacteriology KW - Cell survival KW - Immunoregulation KW - Fatigue KW - Chemotherapy KW - Lymphopenia KW - Pancreatic cancer KW - Enzymes KW - Survival KW - CD8 antigen KW - Toxicity KW - Cyclophosphamide KW - Tumor cells KW - Listeria KW - Metastases KW - Fever KW - Standard deviation KW - Lymphocytes T KW - Liver KW - Vaccines KW - Adenocarcinoma KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1827928284?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Oncology&rft.atitle=Safety+and+Survival+With+GVAX+Pancreas+Prime+and+Listeria+Monocytogenes-Expressing+Mesothelin+%28CRS-207%29+Boost+Vaccines+for+Metastatic+Pancreatic+Cancer&rft.au=Le%2C+Dung+T%3BWang-Gillam%2C+Andrea%3BPicozzi%2C+Vincent%3BGreten%2C+Tim+F%3BCrocenzi%2C+Todd%3BSpringett%2C+Gregory%3BMorse%2C+Michael%3BZeh%2C+Herbert%3BCohen%2C+Deirdre%3BFine%2C+Robert+L%3BOnners%2C+Beth%3BUram%2C+Jennifer+N%3BLaheru%2C+Daniel+A%3BLutz%2C+Eric+R%3BSolt%2C+Sara%3BMurphy%2C+Aimee+Luck%3BSkoble%2C+Justin%3BLemmens%2C+Ed%3BGrous%2C+John%3BDubensky%2C+Thomas%3BBrockstedt%2C+Dirk+G%3BJaffee%2C+Elizabeth+M&rft.aulast=Le&rft.aufirst=Dung&rft.date=2015-04-20&rft.volume=33&rft.issue=12&rft.spage=1325&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Oncology&rft.issn=0732183X&rft_id=info:doi/10.1200%2FJCO.2014.57.4244 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-10-01 N1 - Last updated - 2016-10-12 N1 - SubjectsTermNotLitGenreText - Cell survival; Immunoregulation; Fatigue; Chemotherapy; Pancreatic cancer; Lymphopenia; Survival; Enzymes; Cyclophosphamide; Toxicity; CD8 antigen; Tumor cells; Fever; Metastases; Standard deviation; Liver; Lymphocytes T; Vaccines; Adenocarcinoma; Listeria DO - http://dx.doi.org/10.1200/JCO.2014.57.4244 ER - TY - CPAPER T1 - CCG Tumor Characterization Initiatives: TARGET Pediatric Cancer Genomics Initiative & CGCI Updates T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669824219; 6339823 JF - 2015 American Association for Cancer Research Annual Meeting AU - Auvil, Jaime Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Pediatrics KW - genomics KW - Tumors KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669824219?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=CCG+Tumor+Characterization+Initiatives%3A+TARGET+Pediatric+Cancer+Genomics+Initiative+%26amp%3B+CGCI+Updates&rft.au=Auvil%2C+Jaime&rft.aulast=Auvil&rft.aufirst=Jaime&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - the Microbiota in Carcinogenesis and Cancer Therapy T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669824098; 6339651 JF - 2015 American Association for Cancer Research Annual Meeting AU - Trinchieri, Giorgio Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Carcinogenesis KW - Therapy KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669824098?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=the+Microbiota+in+Carcinogenesis+and+Cancer+Therapy&rft.au=Trinchieri%2C+Giorgio&rft.aulast=Trinchieri&rft.aufirst=Giorgio&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Macrophage migration inhibitory factor (MIF) and miR-301b interactively enhance disease aggressiveness by targeting NR3C2 (nuclear receptor subfamily group c member 2) in human pancreatic cancer T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669824083; 6339532 JF - 2015 American Association for Cancer Research Annual Meeting AU - Yang, Shouhui Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Macrophages KW - macrophage migration inhibitory factor KW - Nuclear receptors KW - Pancreatic cancer KW - Aggressive behavior KW - Migration KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669824083?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Macrophage+migration+inhibitory+factor+%28MIF%29+and+miR-301b+interactively+enhance+disease+aggressiveness+by+targeting+NR3C2+%28nuclear+receptor+subfamily+group+c+member+2%29+in+human+pancreatic+cancer&rft.au=Yang%2C+Shouhui&rft.aulast=Yang&rft.aufirst=Shouhui&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Modulating the Tumor Microenvironment to Enhance the Efficacy of Immunotherapies T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669824078; 6339820 JF - 2015 American Association for Cancer Research Annual Meeting AU - Mackall, Crystal Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Immunotherapy KW - Microenvironments KW - Tumors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669824078?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Modulating+the+Tumor+Microenvironment+to+Enhance+the+Efficacy+of+Immunotherapies&rft.au=Mackall%2C+Crystal&rft.aulast=Mackall&rft.aufirst=Crystal&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Sample suitability for studies with cancer proteomics T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669824077; 6339256 JF - 2015 American Association for Cancer Research Annual Meeting AU - Kinsinger, Christopher Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - proteomics KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669824077?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Sample+suitability+for+studies+with+cancer+proteomics&rft.au=Kinsinger%2C+Christopher&rft.aulast=Kinsinger&rft.aufirst=Christopher&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Plasmonic noble metal-based nanotheranostics T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669824052; 6339836 JF - 2015 American Association for Cancer Research Annual Meeting AU - Chen, Xiaoyuan Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Epidemiology KW - Oncology KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669824052?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Plasmonic+noble+metal-based+nanotheranostics&rft.au=Chen%2C+Xiaoyuan&rft.aulast=Chen&rft.aufirst=Xiaoyuan&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Genomics Data Storage, Access and Analysis for CCG Initiatives: The New CCG Website T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669824050; 6339829 JF - 2015 American Association for Cancer Research Annual Meeting AU - Spaulding, Emma Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Data processing KW - Data storage KW - genomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669824050?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Genomics+Data+Storage%2C+Access+and+Analysis+for+CCG+Initiatives%3A+The+New+CCG+Website&rft.au=Spaulding%2C+Emma&rft.aulast=Spaulding&rft.aufirst=Emma&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - DCE-MRI as a cancer biomarker T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669824037; 6339419 JF - 2015 American Association for Cancer Research Annual Meeting AU - Choyke, Peter Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Bioindicators KW - Biomarkers KW - biomarkers KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669824037?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=DCE-MRI+as+a+cancer+biomarker&rft.au=Choyke%2C+Peter&rft.aulast=Choyke&rft.aufirst=Peter&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Genomics Data Storage, Access and Analysis for CCG Initiatives: NCI Cloud Pilots T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669824031; 6339828 JF - 2015 American Association for Cancer Research Annual Meeting AU - Davidsen, Tanja Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Clouds KW - Data processing KW - Data storage KW - Pilots KW - genomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669824031?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Genomics+Data+Storage%2C+Access+and+Analysis+for+CCG+Initiatives%3A+NCI+Cloud+Pilots&rft.au=Davidsen%2C+Tanja&rft.aulast=Davidsen&rft.aufirst=Tanja&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Alterations of DNA Repair Genes in Cancer Cell Lines and Their Predictive Value for Drug Activity T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669824028; 6339474 JF - 2015 American Association for Cancer Research Annual Meeting AU - Pommier, Yves Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Prediction KW - Tumor cell lines KW - DNA repair KW - Drugs KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669824028?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Alterations+of+DNA+Repair+Genes+in+Cancer+Cell+Lines+and+Their+Predictive+Value+for+Drug+Activity&rft.au=Pommier%2C+Yves&rft.aulast=Pommier&rft.aufirst=Yves&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Clinical genomics and medicine: An informatics perspective T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669824006; 6339277 JF - 2015 American Association for Cancer Research Annual Meeting AU - Kibbe, Warren Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Informatics KW - genomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669824006?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Clinical+genomics+and+medicine%3A+An+informatics+perspective&rft.au=Kibbe%2C+Warren&rft.aulast=Kibbe&rft.aufirst=Warren&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Microbiota and cancer T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823993; 6339345 JF - 2015 American Association for Cancer Research Annual Meeting AU - Trinchieri, Giorgio Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823993?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Microbiota+and+cancer&rft.au=Trinchieri%2C+Giorgio&rft.aulast=Trinchieri&rft.aufirst=Giorgio&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Lung cancer metabolomics identifies metabolites as robust risk biomarkers T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823786; 6339446 JF - 2015 American Association for Cancer Research Annual Meeting AU - Haznadar, Majda AU - Cai, Qiuyin AU - Krausz, Kristopher AU - Bowman, Elise AU - Blot, William AU - Gonzalez, Frank AU - Harris, Curtis Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Bioindicators KW - Health risks KW - Metabolites KW - Biomarkers KW - biomarkers KW - metabolomics KW - Lung cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823786?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Lung+cancer+metabolomics+identifies+metabolites+as+robust+risk+biomarkers&rft.au=Haznadar%2C+Majda%3BCai%2C+Qiuyin%3BKrausz%2C+Kristopher%3BBowman%2C+Elise%3BBlot%2C+William%3BGonzalez%2C+Frank%3BHarris%2C+Curtis&rft.aulast=Haznadar&rft.aufirst=Majda&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Interview Skills T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823762; 6339405 JF - 2015 American Association for Cancer Research Annual Meeting AU - Wiest, Jonathan Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Epidemiology KW - Oncology KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823762?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Interview+Skills&rft.au=Wiest%2C+Jonathan&rft.aulast=Wiest&rft.aufirst=Jonathan&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Late ALL relapse following CD19 CAR immune-pressure demonstrates reversible pan-antigen loss T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823744; 6339984 JF - 2015 American Association for Cancer Research Annual Meeting AU - Jacoby, Elad Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - CD19 antigen UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823744?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Late+ALL+relapse+following+CD19+CAR+immune-pressure+demonstrates+reversible+pan-antigen+loss&rft.au=Jacoby%2C+Elad&rft.aulast=Jacoby&rft.aufirst=Elad&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - A pooled investigation of circulating adiponectin levels and risk of multiple myeloma T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823731; 6339445 JF - 2015 American Association for Cancer Research Annual Meeting AU - Hofmann, Jonathan Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Multiple myeloma KW - Adiponectin UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823731?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=A+pooled+investigation+of+circulating+adiponectin+levels+and+risk+of+multiple+myeloma&rft.au=Hofmann%2C+Jonathan&rft.aulast=Hofmann&rft.aufirst=Jonathan&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Immune cells as targets for pathway inhibition T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823696; 6339730 JF - 2015 American Association for Cancer Research Annual Meeting AU - Restifo, Nicholas Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Epidemiology KW - Oncology KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823696?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acriminaljusticeperiodicals&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+Social+Issues&rft.atitle=Existence+and+Coexistence+in+Acre%3A+The+Power+of+Educational+Activism&rft.au=Hertz-Lazarowitz%2C+Rachel&rft.aulast=Hertz-Lazarowitz&rft.aufirst=Rachel&rft.date=2004-07-02&rft.volume=60&rft.issue=2&rft.spage=357&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Social+Issues&rft.issn=00224537&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - GATA3 modulates chromatin structure to establish active enhancers in breast cancer cells T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823605; 6339526 JF - 2015 American Association for Cancer Research Annual Meeting AU - Takaku, Motoki AU - Grimm, Sara AU - Shimbo, Takashi AU - Perera, Lalith AU - Machida, Shinichi AU - Kurumizaka, Hitoshi AU - Wade, Paul Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Chromatin KW - Breast cancer KW - GATA-3 protein UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823605?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=GATA3+modulates+chromatin+structure+to+establish+active+enhancers+in+breast+cancer+cells&rft.au=Takaku%2C+Motoki%3BGrimm%2C+Sara%3BShimbo%2C+Takashi%3BPerera%2C+Lalith%3BMachida%2C+Shinichi%3BKurumizaka%2C+Hitoshi%3BWade%2C+Paul&rft.aulast=Takaku&rft.aufirst=Motoki&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Transparency and Data Sharing T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823590; 6339961 JF - 2015 American Association for Cancer Research Annual Meeting AU - Zenklusen, Jean Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Transparency KW - Data processing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823590?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Transparency+and+Data+Sharing&rft.au=Zenklusen%2C+Jean&rft.aulast=Zenklusen&rft.aufirst=Jean&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Estrogen metabolism and risk of breast cancer T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823580; 6339693 JF - 2015 American Association for Cancer Research Annual Meeting AU - Ziegler, Regina Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Health risks KW - Estrogens KW - Breast cancer KW - Metabolism KW - Sex hormones UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823580?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Estrogen+metabolism+and+risk+of+breast+cancer&rft.au=Ziegler%2C+Regina&rft.aulast=Ziegler&rft.aufirst=Regina&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Efficacy of the HPV16/18 vaccine against cervical, anal, and oral HPV infection among women with and without previous HPV16/18 exposure T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823578; 6340043 JF - 2015 American Association for Cancer Research Annual Meeting AU - Beachler, Daniel Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Disease control KW - Vaccines KW - Infection KW - Human papillomavirus 16 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823578?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Efficacy+of+the+HPV16%2F18+vaccine+against+cervical%2C+anal%2C+and+oral+HPV+infection+among+women+with+and+without+previous+HPV16%2F18+exposure&rft.au=Beachler%2C+Daniel&rft.aulast=Beachler&rft.aufirst=Daniel&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Drastically reducing HPV-associated cancers through etiologically-based primary and secondary prevention T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823530; 6339392 JF - 2015 American Association for Cancer Research Annual Meeting AU - Lowy, Douglas Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Prevention KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823530?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Drastically+reducing+HPV-associated+cancers+through+etiologically-based+primary+and+secondary+prevention&rft.au=Lowy%2C+Douglas&rft.aulast=Lowy&rft.aufirst=Douglas&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Tumor infiltrating lymphocytes and genetically engineered T cells T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823513; 6339601 JF - 2015 American Association for Cancer Research Annual Meeting AU - Yang, James Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Genetic engineering KW - Lymphocytes T KW - Lymphocytes KW - Tumors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823513?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Tumor+infiltrating+lymphocytes+and+genetically+engineered+T+cells&rft.au=Yang%2C+James&rft.aulast=Yang&rft.aufirst=James&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Molecular imaging in biochemical recurrence T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823479; 6339841 JF - 2015 American Association for Cancer Research Annual Meeting AU - Choyke, Peter Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Biochemistry KW - Imaging techniques UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823479?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Molecular+imaging+in+biochemical+recurrence&rft.au=Choyke%2C+Peter&rft.aulast=Choyke&rft.aufirst=Peter&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Standardized measures of lobular involution and subsequent breast cancer risk among women with benign breast disease T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823477; 6340045 JF - 2015 American Association for Cancer Research Annual Meeting AU - Figueroa, Jonine Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Health risks KW - Breast cancer KW - Standards KW - Benign UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823477?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Standardized+measures+of+lobular+involution+and+subsequent+breast+cancer+risk+among+women+with+benign+breast+disease&rft.au=Figueroa%2C+Jonine&rft.aulast=Figueroa&rft.aufirst=Jonine&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Administrative Roles in Scientific Planning and the Intramural Researcher T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823451; 6339400 JF - 2015 American Association for Cancer Research Annual Meeting AU - Marino, Pamela Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Epidemiology KW - Oncology KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823451?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Administrative+Roles+in+Scientific+Planning+and+the+Intramural+Researcher&rft.au=Marino%2C+Pamela&rft.aulast=Marino&rft.aufirst=Pamela&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Other CCG Initiatives: CDDP, ALCHEMIST& Exceptional Responders T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823448; 6339825 JF - 2015 American Association for Cancer Research Annual Meeting AU - Tarnuzzer, Roy Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Epidemiology KW - Oncology KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823448?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Other+CCG+Initiatives%3A+CDDP%2C+ALCHEMIST%26amp%3B+Exceptional+Responders&rft.au=Tarnuzzer%2C+Roy&rft.aulast=Tarnuzzer&rft.aufirst=Roy&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - PREVENT Cancer Preclinical Drug Development Program T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823356; 6339388 JF - 2015 American Association for Cancer Research Annual Meeting AU - Shoemaker, Robert Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Drug development KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823356?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=PREVENT+Cancer+Preclinical+Drug+Development+Program&rft.au=Shoemaker%2C+Robert&rft.aulast=Shoemaker&rft.aufirst=Robert&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Regulation of tumor microenvironment T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823341; 6339328 JF - 2015 American Association for Cancer Research Annual Meeting AU - Greten, Tim Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Microenvironments KW - Tumors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823341?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Regulation+of+tumor+microenvironment&rft.au=Greten%2C+Tim&rft.aulast=Greten&rft.aufirst=Tim&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Genetically engineered NY-ESO-1-specific T cells in HLA-A2+ patients with synovial sarcoma T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823317; 6339986 JF - 2015 American Association for Cancer Research Annual Meeting AU - Merchant, Melinda Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Histocompatibility antigen HLA KW - Genetic engineering KW - Lymphocytes T KW - synovial sarcoma KW - Sarcoma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823317?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Genetically+engineered+NY-ESO-1-specific+T+cells+in+HLA-A2%2B+patients+with+synovial+sarcoma&rft.au=Merchant%2C+Melinda&rft.aulast=Merchant&rft.aufirst=Melinda&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Nitric oxide signaling pathway as a pathogenic driver in pancreatic cancer T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823276; 6339533 JF - 2015 American Association for Cancer Research Annual Meeting AU - Wang, Jian Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Pancreatic cancer KW - Nitric oxide KW - Signal transduction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823276?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Nitric+oxide+signaling+pathway+as+a+pathogenic+driver+in+pancreatic+cancer&rft.au=Wang%2C+Jian&rft.aulast=Wang&rft.aufirst=Jian&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - CCG Tumor Characterization Initiatives: The Cancer Genome Atlas: A Report on Adult Cancer Genomics T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823233; 6339824 JF - 2015 American Association for Cancer Research Annual Meeting AU - Zenklusen, Jean Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Genomes KW - Atlases KW - genomics KW - Tumors KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823233?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=CCG+Tumor+Characterization+Initiatives%3A+The+Cancer+Genome+Atlas%3A+A+Report+on+Adult+Cancer+Genomics&rft.au=Zenklusen%2C+Jean&rft.aulast=Zenklusen&rft.aufirst=Jean&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Genomics Data Storage, Access and Analysis for CCG Initiatives: Genomics Data Commons T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823205; 6339827 JF - 2015 American Association for Cancer Research Annual Meeting AU - Wang, Zhining Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Data processing KW - Data storage KW - genomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823205?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Genomics+Data+Storage%2C+Access+and+Analysis+for+CCG+Initiatives%3A+Genomics+Data+Commons&rft.au=Wang%2C+Zhining&rft.aulast=Wang&rft.aufirst=Zhining&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Serum lipid metabolites and alpha-ketoglutarate are inversely associated with aggressive prostate cancer T2 - 2015 American Association for Cancer Research Annual Meeting AN - 1669823185; 6339447 JF - 2015 American Association for Cancer Research Annual Meeting AU - Mondul, Alison AU - Moore, Steven AU - Sampson, Joshua AU - Weinstein, Stephanie AU - Albanes, Demetrius Y1 - 2015/04/18/ PY - 2015 DA - 2015 Apr 18 KW - Prostate cancer KW - Serum lipids KW - Lipids KW - Metabolites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669823185?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Serum+lipid+metabolites+and+alpha-ketoglutarate+are+inversely+associated+with+aggressive+prostate+cancer&rft.au=Mondul%2C+Alison%3BMoore%2C+Steven%3BSampson%2C+Joshua%3BWeinstein%2C+Stephanie%3BAlbanes%2C+Demetrius&rft.aulast=Mondul&rft.aufirst=Alison&rft.date=2015-04-18&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={19573A54-AE8F-4E00-9C23-BD6D62268424} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - JOUR T1 - 5-aminolevulinic-acid-based fluorescence spectroscopy and conventional colposcopy for in vivo detection of cervical pre-malignancy. AN - 1675871274; 25887444 AB - Sensitized fluorescence diagnostics are based on selective accumulation of photosensitizer in the tissue where carcinogenesis has started. The present study compared topical 5-aminolevulinic acid (5-ALA)-based fluorescence spectroscopy (FS) in vivo with conventional colposcopy for cervical intraepithelial neoplasia (CIN) detection. We enrolled 48 patients who were referred for colposcopy because of high-grade changes in cervical cytology. Every inspected cervix was divided in to quadrants, and there were 174 quadrants included in the study. Each patient had a cytological smear, colposcopy, FS and histopathological analysis. For FS, 3% 5-ALA cream was used topically and after an average 135 min incubation, fluorescence spectra were recorded from the cervix in vivo. FS and colposcopy results were correlated with histopathology. All spectra were evaluated by a ratio of the protoporphyrin IX fluorescence intensity at 634 nm and autofluorescence intensity at 510 nm. For proper grouping of low-risk and high-risk cases, a threshold of 3.87 was calculated. Data per quadrant showed that FS had higher sensitivity than colposcopy (71.7% vs 67.4%) but specificity was greater for colposcopy (86.6% vs 75.6%). Combination of the methods showed higher sensitivity (88.0% vs 67.4%) but reduced specificity (88.0% and 69.5%), but it had the highest number of correctly identified high-risk changes and the highest (79.3%) accuracy. Data for each patient showed FS sensitivity of 91.2%, which was greater than for colposcopy (88.2%). Higher overdiagnosis resulted in decreased specificity for fluorescence methodology-71.4% versus 78.6% for colposcopy. In both cases, accuracy was 85.4% and effectiveness was >80%, which means that both methods can be used to determine high-risk cervical intraepithelial neoplasia. The diagnostic sensitivity of 97.1% for this complementary diagnosis indicates that it could be the best choice for detection of high-risk changes. 5-ALA-based FS is an objective method, requiring short-term administration for appropriate fluorescence measurements. FS is a promising diagnostic tool with similar accuracy as colposcopy but with the potential advantage of providing objective results. JF - BMC women's health AU - Vansevičiūtė, Rasa AU - Venius, Jonas AU - Žukovskaja, Olga AU - Kanopienė, Daiva AU - Letautienė, Simona AU - Rotomskis, Ričardas AD - National Cancer Institute, Vilnius, Lithuania. rasa.vanseviciute@nvi.lt. ; National Cancer Institute, Vilnius, Lithuania. jonas.venius@nvi.lt. ; Faculty of Medicine, Vilnius University, Vilnius, Lithuania. olga.zukovskaja@gmail.com. ; National Cancer Institute, Vilnius, Lithuania. daiva.kanopiene@nvi.lt. ; National Cancer Institute, Vilnius, Lithuania. simona.letautiene@nvi.lt. ; Laboratory of Biomedical Physics, National Cancer Institute, Vilnius, Lithuania. ricardas.rotomskis@nvi.lt. Y1 - 2015/04/17/ PY - 2015 DA - 2015 Apr 17 SP - 35 VL - 15 KW - Photosensitizing Agents KW - 0 KW - Aminolevulinic Acid KW - 88755TAZ87 KW - Index Medicus KW - Sensitivity and Specificity KW - Colposcopy -- methods KW - Reproducibility of Results KW - Aminolevulinic Acid -- pharmacology KW - Humans KW - Adult KW - Middle Aged KW - Photosensitizing Agents -- pharmacology KW - Early Detection of Cancer -- methods KW - Female KW - Vaginal Smears -- methods KW - Spectrometry, Fluorescence -- methods KW - Cervical Intraepithelial Neoplasia -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1675871274?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=BMC+women%27s+health&rft.atitle=5-aminolevulinic-acid-based+fluorescence+spectroscopy+and+conventional+colposcopy+for+in+vivo+detection+of+cervical+pre-malignancy.&rft.au=Vansevi%C4%8Di%C5%ABt%C4%97%2C+Rasa%3BVenius%2C+Jonas%3B%C5%BDukovskaja%2C+Olga%3BKanopien%C4%97%2C+Daiva%3BLetautien%C4%97%2C+Simona%3BRotomskis%2C+Ri%C4%8Dardas&rft.aulast=Vansevi%C4%8Di%C5%ABt%C4%97&rft.aufirst=Rasa&rft.date=2015-04-17&rft.volume=15&rft.issue=&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=BMC+women%27s+health&rft.issn=1472-6874&rft_id=info:doi/10.1186%2Fs12905-015-0191-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-25 N1 - Date created - 2015-04-22 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Photochem Photobiol. 2000 Jun;71(6):730-6 [10857369] Int J Oral Maxillofac Surg. 2000 Dec;29(6):453-7 [11202330] Photochem Photobiol. 2001 Jun;73(6):636-41 [11421069] J Biomed Opt. 2002 Apr;7(2):215-20 [11966306] Int J Oncol. 2002 Oct;21(4):763-8 [12239614] Oral Oncol. 2003 Feb;39(2):150-6 [12509968] Faraday Discuss. 2004;126:265-79; discussion 303-11 [14992412] Clin Gastroenterol Hepatol. 2004 Sep;2(9):744-53 [15354274] Proc Natl Acad Sci U S A. 1994 Oct 11;91(21):10193-7 [7937860] Lasers Surg Med. 1996;19(1):63-74 [8836997] Medicina (Kaunas). 2004;40(12):1219-30 [15630350] Am J Obstet Gynecol. 2005 Oct;193(4):1331-7 [16202722] Oral Dis. 2005 Nov;11(6):350-9 [16269025] Acta Paediatr. 2007 May;96(5):644-7 [17376185] Am J Clin Pathol. 2008 Jan;129(1):75-80 [18089491] Neoplasia. 2009 Apr;11(4):325-32 [19308287] Photodiagnosis Photodyn Ther. 2008 Dec;5(4):235-7 [19356662] Curr Opin Biotechnol. 2009 Feb;20(1):119-31 [19268567] J Low Genit Tract Dis. 2010 Jan;14(1):5-10 [20040830] Ann Oncol. 2010 Mar;21(3):448-58 [20176693] Int J Cancer. 2011 Apr 15;128(8):1899-907 [20568103] Int J Cancer. 2010 Dec 15;127(12):2893-917 [21351269] Technol Cancer Res Treat. 2011 Apr;10(2):101 [21381787] Best Pract Res Clin Obstet Gynaecol. 2011 Oct;25(5):667-77 [21664876] Head Neck Oncol. 2011;3:38 [21861912] Asian Pac J Cancer Prev. 2011;12(7):1723-6 [22126552] Obstet Gynecol. 2013 Jun;121(6):1209-16 [23812454] Int J Cancer. 2014 Aug 1;135(3):624-34 [24226935] Cancer. 2000 May 15;88(10):2275-82 [10820349] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/s12905-015-0191-4 ER - TY - JOUR T1 - Epidemiology's Continuing Contribution to Public Health: The Power of "Then and Now" AN - 1701475747; PQ0001732828 AB - The 47th annual meeting of the Society for Epidemiologic Research hosted 17 invited speakers charged by the Executive Committee with presenting some of the many ways that epidemiologists have improved the health of the general population. There were 9 "Then and Now" sessions that were structured to focus on how early epidemiologists overcame research hurdles and advanced health through innovative strategies. For most topics, a longstanding expert was paired with an excellent contemporary epidemiologist working in the area, and both were given the freedom to deliver an integrated story about epidemiology's temporal role in protecting and promoting public health. Epidemiologic discoveries in cardiovascular, cancer, and perinatal epidemiology were discussed on day 1, followed by discussions of accomplishments in reducing exposures that adversely impact health (nutrition, environment/occupation, and tobacco use) on day 2. Topics with relevancy for many aspects of epidemiology were presented on day 3, including infectious diseases, social forces, and causal thinking in epidemiologic research. Given the large number of outstanding senior and junior epidemiologists that attended the meeting, choosing speakers was a unique challenge. What became evident from all sessions was the passion that epidemiologists have for population health, tempered with concerns for remaining true to epidemiologic principles, the timely adoption of innovative methods, and the responsible interpretation of research findings. JF - American Journal of Epidemiology AU - Buck Louis, Germaine M AU - Bloom, Michael S AU - Gatto, Nicolle M AU - Hogue, Carol R AU - Westreich, Daniel J AU - Zhang, Cuilin AD - Correspondence to Dr. Germaine M. Buck Louis, Office of the Director, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, 6100 Executive Boulevard, Room 7B03, Rockville, MD 20854, gb156i@nih.gov Y1 - 2015/04/15/ PY - 2015 DA - 2015 Apr 15 SP - e1 EP - e8 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 181 IS - 8 SN - 0002-9262, 0002-9262 KW - Health & Safety Science Abstracts KW - cancer KW - cardiovascular epidemiology KW - environment KW - infection KW - nutrition KW - perinatal epidemiology KW - social epidemiology KW - tobacco KW - Infectious diseases KW - Epidemiology KW - Committees KW - Tobacco KW - Nutrition KW - Cancer KW - Innovations KW - Public health KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701475747?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Epidemiology%27s+Continuing+Contribution+to+Public+Health%3A+The+Power+of+%22Then+and+Now%22&rft.au=Buck+Louis%2C+Germaine+M%3BBloom%2C+Michael+S%3BGatto%2C+Nicolle+M%3BHogue%2C+Carol+R%3BWestreich%2C+Daniel+J%3BZhang%2C+Cuilin&rft.aulast=Buck+Louis&rft.aufirst=Germaine&rft.date=2015-04-15&rft.volume=181&rft.issue=8&rft.spage=e1&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwv043 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2015-09-03 N1 - SubjectsTermNotLitGenreText - Epidemiology; Infectious diseases; Committees; Tobacco; Nutrition; Cancer; Public health; Innovations DO - http://dx.doi.org/10.1093/aje/kwv043 ER - TY - CPAPER T1 - NCI's High Performance Computing (HPC) and High Performance Data (HPD) Computing Platform for Environmental and Earth System Data Science T2 - 2015 European Geosciences Union General Assembly AN - 1684399416; 6348653 JF - 2015 European Geosciences Union General Assembly AU - Evans, Ben AU - Allen, Chris AU - Antony, Joseph AU - Bastrakova, Irina AU - Gohar, Kashif AU - Porter, David AU - Pugh, Tim AU - Santana, Fabiana AU - Smillie, Jon AU - Trenham, Claire AU - Wang, Jingbo AU - Wyborn, Lesley Y1 - 2015/04/12/ PY - 2015 DA - 2015 Apr 12 KW - Data processing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1684399416?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+European+Geosciences+Union+General+Assembly&rft.atitle=NCI%27s+High+Performance+Computing+%28HPC%29+and+High+Performance+Data+%28HPD%29+Computing+Platform+for+Environmental+and+Earth+System+Data+Science&rft.au=Evans%2C+Ben%3BAllen%2C+Chris%3BAntony%2C+Joseph%3BBastrakova%2C+Irina%3BGohar%2C+Kashif%3BPorter%2C+David%3BPugh%2C+Tim%3BSantana%2C+Fabiana%3BSmillie%2C+Jon%3BTrenham%2C+Claire%3BWang%2C+Jingbo%3BWyborn%2C+Lesley&rft.aulast=Evans&rft.aufirst=Ben&rft.date=2015-04-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+European+Geosciences+Union+General+Assembly&rft.issn=&rft_id=info:doi/ L2 - http://meetingorganizer.copernicus.org/egu2015/meetingprogramme LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-29 N1 - Last updated - 2015-06-01 ER - TY - JOUR T1 - Examining the Ethics of Clinical Use of Unproven Interventions Outside of Clinical Trials During the Ebola Epidemic AN - 1687670478; PQ0001543551 AB - The recent Ebola outbreak in West Africa began in the spring of 2014 and has since caused the deaths of over 6,000 people. Since there are no approved treatments or prevention modalities specifically targeted at Ebola Virus Disease (EVD), debate has focused on whether unproven interventions should be offered to Ebola patients outside of clinical trials. Those engaged in the debate have responded rapidly to a complex and evolving crisis, however, and this debate has not provided much opportunity for in-depth analysis. Additionally, the existing literature on access to unproven therapies has focused on contexts like HIV/AIDS and oncology, which are very different than the Ebola epidemic. In this paper, we examine the ethical issues surrounding access to unproven therapies in the context of the recent Ebola outbreak to yield new insights about this controversial and unsettled issue. We argue first that, in this context, the interests of patients in obtaining access to unproven therapies are not fully aligned with the interests of their providers and drug developers. Second, we focus on the resource constraints facing providers, funders, and patients and conclude that they often counsel against the use of unproven interventions against EVD. JF - American Journal of Bioethics AU - Shah, Seema K AU - Wendler, David AU - Danis, Marion AD - Clinical Center Department of Bioethics, Division of AIDS, National Institutes of Health, Bethesda, Maryland, USA Y1 - 2015/04/03/ PY - 2015 DA - 2015 Apr 03 SP - 11 EP - 16 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 15 IS - 4 SN - 1526-5161, 1526-5161 KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Mortality KW - Acquired immune deficiency syndrome KW - Epidemics KW - Crises KW - Intervention KW - Ebola virus KW - Oncology KW - Clinical trials KW - Prevention KW - Human immunodeficiency virus KW - Ethics KW - Africa KW - Outbreaks KW - Drugs KW - V 22360:AIDS and HIV KW - H 4000:Food and Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687670478?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Bioethics&rft.atitle=Examining+the+Ethics+of+Clinical+Use+of+Unproven+Interventions+Outside+of+Clinical+Trials+During+the+Ebola+Epidemic&rft.au=Shah%2C+Seema+K%3BWendler%2C+David%3BDanis%2C+Marion&rft.aulast=Shah&rft.aufirst=Seema&rft.date=2015-04-03&rft.volume=15&rft.issue=4&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Bioethics&rft.issn=15265161&rft_id=info:doi/10.1080%2F15265161.2015.1010996 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-06-01 N1 - Last updated - 2015-08-19 N1 - SubjectsTermNotLitGenreText - Acquired immune deficiency syndrome; Epidemics; Ethics; Oncology; Drugs; Clinical trials; Mortality; Prevention; Crises; Human immunodeficiency virus; Intervention; Outbreaks; Ebola virus; Africa DO - http://dx.doi.org/10.1080/15265161.2015.1010996 ER - TY - JOUR T1 - Modulation of colon cancer by nutmeg. AN - 1669838526; 25712450 AB - Colon cancer is the most common cancer and the third leading cause of cancer mortality in humans. Using mass spectrometry-based metabolomics, the current study revealed the accumulation of four uremic toxins (cresol sulfate, cresol glucuronide, indoxyl sulfate, and phenyl sulfate) in the serum of mice harboring adenomatous polyposis coli (APC) gene mutation-induced colon cancer. These uremic toxins, likely generated from the gut microbiota, were associated with an increase in the expression of the proinflammatory cytokine IL-6 and a disorder of lipid metabolism. Nutmeg, which exhibits antimicrobial activity, attenuated the levels of uremic toxins and decreased intestinal tumorigenesis in Apc(min/+) mice. Nutmeg-treated Apc(min/+) mice had decreased IL-6 levels and normalized dysregulated lipid metabolism, suggesting that uremic toxins are responsible, in part, for the metabolic disorders that occur during tumorigenesis. These studies demonstrate a potential biochemical link among gut microbial metabolism, inflammation, and metabolic disorders and suggest that modulation of gut microbiota and lipid metabolism using dietary intervention or drugs may be effective in colon cancer chemoprevention strategies. JF - Journal of proteome research AU - Li, Fei AU - Yang, Xiu-Wei AU - Krausz, Kristopher W AU - Nichols, Robert G AU - Xu, Wei AU - Patterson, Andrew D AU - Gonzalez, Frank J AD - †Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, United States. ; §State Key Laboratory of Natural and Biomimetic Drugs, Department of Natural Medicines, School of Pharmaceutical Sciences, Peking University Health Science Center, Peking University, Beijing 100191, China. ; ∥Center for Molecular Toxicology and Carcinogenesis, Department of Veterinary and Biomedical Sciences, The Pennsylvania State University, University Park, Pennsylvania 16802, United States. Y1 - 2015/04/03/ PY - 2015 DA - 2015 Apr 03 SP - 1937 EP - 1946 VL - 14 IS - 4 KW - Cresols KW - 0 KW - DNA Primers KW - Glucuronides KW - Interleukin-6 KW - Plant Extracts KW - Sulfuric Acid Esters KW - Toxins, Biological KW - uremia middle molecule toxins KW - phenylsulfate KW - 937-34-8 KW - Indican KW - N187WK1Y1J KW - Index Medicus KW - inflammation KW - mass spectrometry KW - Colon cancer KW - nutmeg KW - uremic toxin KW - metabolomics KW - Metabolomics -- methods KW - Animals KW - Analysis of Variance KW - Blood Chemical Analysis KW - Lipid Metabolism -- drug effects KW - DNA Primers -- genetics KW - Humans KW - Interleukin-6 -- metabolism KW - Mice KW - Caco-2 Cells KW - Gene Expression Profiling KW - Indican -- blood KW - Mice, Inbred C57BL KW - Mass Spectrometry -- methods KW - Glucuronides -- blood KW - Sulfuric Acid Esters -- blood KW - Male KW - Cresols -- blood KW - Toxins, Biological -- metabolism KW - Toxins, Biological -- blood KW - Plant Extracts -- pharmacology KW - Toxins, Biological -- toxicity KW - Myristica fragrans -- chemistry KW - Adenomatous Polyposis Coli -- drug therapy KW - Plant Extracts -- therapeutic use KW - Plant Extracts -- analysis KW - Adenomatous Polyposis Coli -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669838526?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+proteome+research&rft.atitle=Modulation+of+colon+cancer+by+nutmeg.&rft.au=Li%2C+Fei%3BYang%2C+Xiu-Wei%3BKrausz%2C+Kristopher+W%3BNichols%2C+Robert+G%3BXu%2C+Wei%3BPatterson%2C+Andrew+D%3BGonzalez%2C+Frank+J&rft.aulast=Li&rft.aufirst=Fei&rft.date=2015-04-03&rft.volume=14&rft.issue=4&rft.spage=1937&rft.isbn=&rft.btitle=&rft.title=Journal+of+proteome+research&rft.issn=1535-3907&rft_id=info:doi/10.1021%2Fpr5013152 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-07 N1 - Date created - 2015-04-03 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/pr5013152 ER - TY - JOUR T1 - Photoimmunotherapy of hepatocellular carcinoma-targeting Glypican-3 combined with nanosized albumin-bound paclitaxel AN - 1846412061; PQ0003837069 AB - Aim: Effectiveness of Glypican-3 (GPC3)-targeted photoimmunotherapy (PIT) combined with the nanoparticle albumin-bound paclitaxel (nab-paclitaxel) for hepatocellular carcinoma was evaluated. Materials & methods: GPC3 expressing A431/G1 cells were incubated with a phthalocyanine-derivative, IRDye700DX (IR700), conjugated to an anti-GPC3 antibody, IR700-YP7 and exposed to near-infrared light. Therapeutic experiments combining GPC3-targeted PIT with nab-paclitaxel were performed in A431/G1 tumor-bearing mice. Results: IR700-YP7 bound to A431/G1 cells and induced rapid target-specific necrotic cell death by near-infrared light exposure in vitro. IR700-YP7 accumulated in A431/G1 tumors. Tumor growth was inhibited by PIT compared with nontreated control. Additionally, PIT dramatically increased nab-paclitaxel delivery and enhanced the therapeutic effect. Conclusion: PIT targeting GPC3 combined with nab-paclitaxel is a promising method for treating hepatocellular carcinoma. JF - Nanomedicine AU - Hanaoka, Hirofumi AU - Nakajima, Takahito AU - Sato, Kazuhide AU - Watanabe, Rira AU - Phung, Yen AU - Gao, Wei AU - Harada, Toshiko AU - Kim, Insook AU - Paik, Chang H AU - Choyke, Peter L AU - Ho, Mitchell AU - Kobayashi, Hisataka AD - super(1)Molecular Imaging Program, Center for Cancer Research, National Cancer Institute, NIH, Building 10, Room B3B69, MSC1088, Bethesda, MD 20892, USA Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 1139 EP - 1147 PB - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom VL - 10 IS - 7 SN - 1743-5889, 1743-5889 KW - Biotechnology and Bioengineering Abstracts KW - Glypican-3 KW - hepatoma KW - monoclonal antibody KW - nab-paxlitaxel KW - nanodelivery KW - photocyanine dye KW - photoimmunotherapy KW - Cell death KW - Antibodies KW - I.R. radiation KW - Paclitaxel KW - Tumors KW - Heparan sulfate proteoglycans KW - nanoparticles KW - Hepatocellular carcinoma KW - nanotechnology KW - Light effects KW - W 30940:Products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1846412061?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nanomedicine&rft.atitle=Photoimmunotherapy+of+hepatocellular+carcinoma-targeting+Glypican-3+combined+with+nanosized+albumin-bound+paclitaxel&rft.au=Hanaoka%2C+Hirofumi%3BNakajima%2C+Takahito%3BSato%2C+Kazuhide%3BWatanabe%2C+Rira%3BPhung%2C+Yen%3BGao%2C+Wei%3BHarada%2C+Toshiko%3BKim%2C+Insook%3BPaik%2C+Chang+H%3BChoyke%2C+Peter+L%3BHo%2C+Mitchell%3BKobayashi%2C+Hisataka&rft.aulast=Hanaoka&rft.aufirst=Hirofumi&rft.date=2015-04-01&rft.volume=10&rft.issue=7&rft.spage=1139&rft.isbn=&rft.btitle=&rft.title=Nanomedicine&rft.issn=17435889&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-12-01 N1 - Number of references - 18 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Antibodies; Cell death; I.R. radiation; Paclitaxel; Tumors; nanoparticles; Heparan sulfate proteoglycans; Light effects; nanotechnology; Hepatocellular carcinoma ER - TY - JOUR T1 - Prevalence of fatigue symptoms and correlations in the general adult population AN - 1832244629; PQ0001492913 AB - This study sought to clarify the prevalence and associated factors of subjective fatigue symptoms, by analyzing epidemiological data for a sample of the Japanese population. Data from 1224 individuals (539 men and 685 women) aged greater than or equal to 20 years were subsequently analyzed. Prevalence of fatigability was 17.2% (n = 211) and that of residual fatigue was 13.6% (n = 167), with women showing significantly higher prevalence of both symptoms than men (fatigability: men 12.6% vs women 20.9%, chi 2 = 14.43, P = 0.001; residual fatigue: men 10.0% vs women 16.5%, P = 0.001). Multivariate logistic regression analyses revealed that being female, nonrestorative sleep, decreased quality of life, and stress showed significant positive associations with fatigability and residual fatigue. However, a significant positive association was found between depressed mood and fatigability, and short sleep duration and long working hours ( greater than or equal to 9 h) were specifically significantly positively associated with residual fatigue. Sleep hygiene instruction and a psychiatric approach are needed to reduce fatigue in the Japanese population. JF - Sleep and Biological Rhythms AU - Aritake, Sayaka AU - Kaneita, Yoshitaka AU - Ohtsu, Tadahiro AU - Uchiyama, Makoto AU - Mishima, Kazuo AU - Akashiba, Tsuneto AU - Uchimura, Naohisa AU - Nakaji, Shigeyuki AU - Munezawa, Takeshi AU - Ohida, Takashi AD - Department of Psychophysiology National Institute of Mental Health. National Center of Neurology and Psychiatry Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 146 EP - 154 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 13 IS - 2 SN - 1446-9235, 1446-9235 KW - Biotechnology and Bioengineering Abstracts KW - Mood KW - Fatigue KW - Data processing KW - Sleep KW - Regression analysis KW - Stress KW - Hygiene KW - Quality of life KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1832244629?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Sleep+and+Biological+Rhythms&rft.atitle=Prevalence+of+fatigue+symptoms+and+correlations+in+the+general+adult+population&rft.au=Aritake%2C+Sayaka%3BKaneita%2C+Yoshitaka%3BOhtsu%2C+Tadahiro%3BUchiyama%2C+Makoto%3BMishima%2C+Kazuo%3BAkashiba%2C+Tsuneto%3BUchimura%2C+Naohisa%3BNakaji%2C+Shigeyuki%3BMunezawa%2C+Takeshi%3BOhida%2C+Takashi&rft.aulast=Aritake&rft.aufirst=Sayaka&rft.date=2015-04-01&rft.volume=13&rft.issue=2&rft.spage=146&rft.isbn=&rft.btitle=&rft.title=Sleep+and+Biological+Rhythms&rft.issn=14469235&rft_id=info:doi/10.1111%2Fsbr.12099 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-10-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Mood; Data processing; Fatigue; Sleep; Regression analysis; Stress; Hygiene; Quality of life DO - http://dx.doi.org/10.1111/sbr.12099 ER - TY - JOUR T1 - Is the Inverse Association Between Selenium and Bladder Cancer Due to Confounding by Smoking? AN - 1701481526; PQ0001732816 AB - Selenium has been linked to a reduced risk of bladder cancer in some studies. Smoking, a well-established risk factor for bladder cancer, has been associated with lower selenium levels in the body. We investigated the selenium-bladder cancer association in subjects from Maine, New Hampshire, and Vermont in the New England Bladder Cancer Case-Control Study. At interview (2001-2005), participants provided information on a variety of factors, including a comprehensive smoking history, and submitted toenail samples, from which we measured selenium levels. We estimated odds ratios and 95% confidence intervals among 1,058 cases and 1,271 controls using logistic regression. After controlling for smoking, we saw no evidence of an association between selenium levels and bladder cancer (for fourth quartile vs. first quartile, odds ratio (OR) = 0.98, 95% confidence interval (CI): 0.77, 1.25). When results were restricted to regular smokers, there appeared to be an inverse association (OR = 0.76, 95% CI: 0.58, 0.99); however, when pack-years of smoking were considered, this association was attenuated (OR = 0.91, 95% CI: 0.68, 1.20), indicating potential confounding by smoking. Despite some reports of an inverse association between selenium and bladder cancer overall, our results, combined with an in-depth evaluation of other studies, suggested that confounding from smoking intensity or duration could explain this association. Our study highlights the need to carefully evaluate the confounding association of smoking in the selenium-bladder cancer association. JF - American Journal of Epidemiology AU - Beane Freeman, Laura E AU - Karagas, Margaret R AU - Baris, Dalsu AU - Schwenn, Molly AU - Johnson, Alison T AU - Colt, Joanne S AU - Jackson, Brian AU - Hosain, G M Monawar AU - Cantor, Kenneth P AU - Silverman, Debra T AD - Correspondence to Dr. Laura E. Beane Freeman, Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Room 6E136, MSC 9771, Bethesda, MD 20892, freemala@mail.nih.gov Y1 - 2015/04/01/ PY - 2015 DA - 2015 Apr 01 SP - 488 EP - 495 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 181 IS - 7 SN - 0002-9262, 0002-9262 KW - Risk Abstracts; Health & Safety Science Abstracts KW - bladder cancer KW - case-control study KW - selenium KW - smoking KW - Historical account KW - Urinary bladder KW - Risk reduction KW - Cancer KW - Smoking KW - Selenium KW - Health risks KW - USA, New England KW - Risk factors KW - ANW, USA, Maine KW - USA, New Hampshire KW - USA, Vermont KW - H 11000:Diseases/Injuries/Trauma KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701481526?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Is+the+Inverse+Association+Between+Selenium+and+Bladder+Cancer+Due+to+Confounding+by+Smoking%3F&rft.au=Beane+Freeman%2C+Laura+E%3BKaragas%2C+Margaret+R%3BBaris%2C+Dalsu%3BSchwenn%2C+Molly%3BJohnson%2C+Alison+T%3BColt%2C+Joanne+S%3BJackson%2C+Brian%3BHosain%2C+G+M+Monawar%3BCantor%2C+Kenneth+P%3BSilverman%2C+Debra+T&rft.aulast=Beane+Freeman&rft.aufirst=Laura&rft.date=2015-04-01&rft.volume=181&rft.issue=7&rft.spage=488&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwu324 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2015-09-03 N1 - SubjectsTermNotLitGenreText - Historical account; Health risks; Selenium; Smoking; Urinary bladder; Risk factors; Risk reduction; Cancer; USA, New England; USA, New Hampshire; ANW, USA, Maine; USA, Vermont DO - http://dx.doi.org/10.1093/aje/kwu324 ER - TY - JOUR T1 - Bacteremia and Malaria in Tanzanian Children Hospitalized for Acute Febrile Illness AN - 1701476802; PQ0001740849 AB - We recorded the reason for presentation to a rural hospital in an area endemic for malaria in 909 children between January 2006 and March 2009. Blood smears were examined for Plasmodium falciparum parasites, and blood spots dried on filter paper were prepared for 464 children. A PCR assay utilizing the stored blood spots was developed for Streptococcus pneumoniae (lytA) and Haemophilus influenzae (pal). Malaria was present in 299 children whose blood was tested by polymerase chain reaction (PCR); 19 had lytA and 15 had pal. The overall prevalence of lytA was 25 of the 464 children, while that of pal was 18 children. Fever was present in 369 children of whom 19 had lytA DNA while 11 had pal DNA detected. Of the 95 afebrile children, six had lytA and seven pal. We conclude that there are no clinical features that distinguish malaria alone from bacteremia alone or the presence of both infections. JF - Journal of Tropical Pediatrics AU - Lundgren, Ingrid S AU - Heltshe, Sonya L AU - Smith, Arnold L AU - Chibwana, Jerome AU - Fried, Michal W AU - Duffy, Patrick E AD - Correspondence: Arnold L. Smith, Seattle Children's Researh Institute, C9S-8, 1900 Ninth Ave, Seattle, WA 98101, USA. and Patrick E. Duffy, Laboratory of Immunology and Vaccinology, Twinbrook 1, Room1111, 5640 Fishers LaneM, Bethesda, MD 20892-8132, USA.,; duffype@niaid.nih.gov] arnold.smith@seattlechildrens.org Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 81 EP - 85 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 61 IS - 2 SN - 0142-6338, 0142-6338 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts B: Bacteriology; Microbiology Abstracts C: Algology, Mycology & Protozoology; Health & Safety Science Abstracts KW - Bacteremia KW - Malaria KW - Acute febrile illness KW - Parasites KW - Human diseases KW - Nucleotide sequence KW - Infection KW - Public health KW - Fever KW - Endemic species KW - Polymerase chain reaction KW - Haemophilus influenzae KW - Plasmodium falciparum KW - Children KW - Endoparasites KW - Filters KW - Blood KW - Streptococcus pneumoniae KW - Filter paper KW - DNA KW - Rural areas KW - Hospitals KW - K 03400:Human Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - H 13000:Medical Safety KW - J 02400:Human Diseases KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701476802?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Tropical+Pediatrics&rft.atitle=Bacteremia+and+Malaria+in+Tanzanian+Children+Hospitalized+for+Acute+Febrile+Illness&rft.au=Lundgren%2C+Ingrid+S%3BHeltshe%2C+Sonya+L%3BSmith%2C+Arnold+L%3BChibwana%2C+Jerome%3BFried%2C+Michal+W%3BDuffy%2C+Patrick+E&rft.aulast=Lundgren&rft.aufirst=Ingrid&rft.date=2015-04-01&rft.volume=61&rft.issue=2&rft.spage=81&rft.isbn=&rft.btitle=&rft.title=Journal+of+Tropical+Pediatrics&rft.issn=01426338&rft_id=info:doi/10.1093%2Ftropej%2Ffmu069 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Parasites; Endemic species; Human diseases; Nucleotide sequence; DNA; Polymerase chain reaction; Malaria; Endoparasites; Public health; Fever; Blood; Filter paper; Bacteremia; Infection; Children; Hospitals; Filters; Rural areas; Streptococcus pneumoniae; Haemophilus influenzae; Plasmodium falciparum DO - http://dx.doi.org/10.1093/tropej/fmu069 ER - TY - JOUR T1 - Semiparametric Regression Models for a Right-Skewed Outcome Subject to Pooling AN - 1701476034; PQ0001732812 AB - Pooling specimens prior to performing laboratory assays has various benefits. Pooling can help to reduce cost, preserve irreplaceable specimens, meet minimal volume requirements for certain lab tests, and even reduce information loss when a limit of detection is present. Regardless of the motivation for pooling, appropriate analytical techniques must be applied in order to obtain valid inference from composite specimens. When biomarkers are treated as the outcome in a regression model, techniques applicable to individually measured specimens may not be valid when measurements are taken from pooled specimens, particularly when the biomarker is positive and right skewed. In this paper, we propose a novel semiparametric estimation method based on an adaptation of the quasi-likelihood approach that can be applied to a right-skewed outcome subject to pooling. We use simulation studies to compare this method with an existing estimation technique that provides valid estimates only when pools are formed from specimens with identical predictor values. Simulation results and analysis of a motivating example demonstrate that, when appropriate estimation techniques are applied to strategically formed pools, valid and efficient estimation of the regression coefficients can be achieved. JF - American Journal of Epidemiology AU - Mitchell, Emily M AU - Lyles, Robert H AU - Manatunga, Amita K AU - Schisterman, Enrique F AD - Correspondence to Dr. Emily M. Mitchell, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6100 Executive Boulevard, Bethesda, MD 20852, emily.mitchell@nih.gov Y1 - 2015/04/01/ PY - 2015 DA - 2015 Apr 01 SP - 541 EP - 548 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 181 IS - 7 SN - 0002-9262, 0002-9262 KW - Health & Safety Science Abstracts KW - biomarkers KW - design KW - pooled specimens KW - quasi-likelihood KW - skewness KW - statistical analysis KW - Bioindicators KW - Composite materials KW - Adaptability KW - Simulation KW - H 12000:Epidemiology and Public Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701476034?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Semiparametric+Regression+Models+for+a+Right-Skewed+Outcome+Subject+to+Pooling&rft.au=Mitchell%2C+Emily+M%3BLyles%2C+Robert+H%3BManatunga%2C+Amita+K%3BSchisterman%2C+Enrique+F&rft.aulast=Mitchell&rft.aufirst=Emily&rft.date=2015-04-01&rft.volume=181&rft.issue=7&rft.spage=541&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwu301 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Bioindicators; Composite materials; Adaptability; Simulation DO - http://dx.doi.org/10.1093/aje/kwu301 ER - TY - JOUR T1 - Lay theories of smoking and young adult nonsmokers' and smokers' smoking expectations AN - 1695988851; 4687122 AB - This study investigated the relationship between lay theories of cigarette smoking and expectations to smoke. An incremental lay theory of smoking entails the belief that smoking behavior can change; an entity theory entails the belief that smoking behavior cannot change. Undergraduate nonsmokers and smokers completed a survey that assessed lay theories of smoking and smoking expectations. Results demonstrated that lay theories of smoking were differentially associated with smoking expectations for nonsmokers and smokers: stronger incremental beliefs were associated with greater expectations of trying smoking for nonsmokers but lower expectations of becoming a regular smoker for smokers. Implications for interventions are discussed. Reprinted by permission of Sage Publications Ltd JF - Journal of health psychology AU - Fitz, Caroline AU - Kaufman, Annette AU - Moore, Philip AD - George Washington University ; National Cancer Institute Y1 - 2015/04// PY - 2015 DA - Apr 2015 SP - 438 EP - 445 VL - 20 IS - 4 SN - 1359-1053, 1359-1053 KW - Sociology KW - Smoking KW - Surveys KW - Demonstrations KW - Beliefs KW - Youth KW - Expectation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1695988851?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+health+psychology&rft.atitle=Lay+theories+of+smoking+and+young+adult+nonsmokers%27+and+smokers%27+smoking+expectations&rft.au=Fitz%2C+Caroline%3BKaufman%2C+Annette%3BMoore%2C+Philip&rft.aulast=Fitz&rft.aufirst=Caroline&rft.date=2015-04-01&rft.volume=20&rft.issue=4&rft.spage=438&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+psychology&rft.issn=13591053&rft_id=info:doi/10.1177%2F1359105313502694 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-07-14 N1 - Last updated - 2015-07-14 N1 - SubjectsTermNotLitGenreText - 11755 5707 6071 1542 11325; 4614; 1547; 13779 652 5676 646 6091; 12429; 3415 9634 DO - http://dx.doi.org/10.1177/1359105313502694 ER - TY - JOUR T1 - Association between tobacco use and the upper gastrointestinal microbiome among Chinese men AN - 1694979695; PQ0001352628 AB - Purpose: Tobacco causes many adverse health conditions and may alter the upper gastrointestinal (UGI) microbiome. However, the few studies that studied the association between tobacco use and the microbiome were small and underpowered. Therefore, we investigated the association between tobacco use and the UGI microbiome in Chinese men. Methods: We included 278 men who underwent esophageal cancer screening in Henan Province, China. Men were categorized as current, former, or never smokers from questionnaire data. UGI tract bacterial cells were characterized using the Human Oral Microbial Identification Microarray. Counts of unique bacterial species and genera estimated alpha diversity. For beta diversity, principal coordinate (PCoA) vectors were generated from an unweighted UniFrac distance matrix. Polytomous logistic regression models were used for most analyses. Results: Of the 278 men in this study, 46.8 % were current smokers and 12.6 % were former smokers. Current smokers tended to have increased alpha diversity (mean 42.3 species) compared to never smokers (mean 38.9 species). For a 10 species increase, the odds ratio (OR) for current smoking was 1.29 (95 % CI 1.04-1.62). Beta diversity was also associated with current smoking. The first two PCoA vectors were strongly associated with current smoking (PCoA1 OR 0.66; 95 % CI 0.51-0.87; PCoA2 OR 0.73; 95 % CI 0.56-0.95). Furthermore, Dialister invisus and Megasphaera micronuciformis were more commonly detected in current smokers than in never smokers. Conclusions: Current smoking was associated with both alpha and beta diversity in the UGI tract. Future work should consider how the UGI microbiome is associated with smoking-related diseases. JF - Cancer Causes & Control AU - Vogtmann, Emily AU - Flores, Roberto AU - Yu, Guoqin AU - Freedman, Neal D AU - Shi, Jianxin AU - Gail, Mitchell H AU - Dye, Bruce A AU - Wang, Guo-Qing AU - Klepac-Ceraj, Vanja AU - Paster, Bruce J AU - Wei, Wen-Qiang AU - Guo, Hui-Qin AU - Dawsey, Sanford M AU - Qiao, You-Lin AU - Abnet, Christian C AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA, emily.vogtmann@nih.gov Y1 - 2015/04// PY - 2015 DA - Apr 2015 SP - 581 EP - 588 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 26 IS - 4 SN - 0957-5243, 0957-5243 KW - Microbiology Abstracts A: Industrial & Applied Microbiology KW - Esophagus KW - Smoking KW - Inventories KW - Data processing KW - Tobacco KW - Regression analysis KW - Cancer KW - A 01360:Plant Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1694979695?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Causes+%26+Control&rft.atitle=Association+between+tobacco+use+and+the+upper+gastrointestinal+microbiome+among+Chinese+men&rft.au=Vogtmann%2C+Emily%3BFlores%2C+Roberto%3BYu%2C+Guoqin%3BFreedman%2C+Neal+D%3BShi%2C+Jianxin%3BGail%2C+Mitchell+H%3BDye%2C+Bruce+A%3BWang%2C+Guo-Qing%3BKlepac-Ceraj%2C+Vanja%3BPaster%2C+Bruce+J%3BWei%2C+Wen-Qiang%3BGuo%2C+Hui-Qin%3BDawsey%2C+Sanford+M%3BQiao%2C+You-Lin%3BAbnet%2C+Christian+C&rft.aulast=Vogtmann&rft.aufirst=Emily&rft.date=2015-04-01&rft.volume=26&rft.issue=4&rft.spage=581&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-015-0535-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-07-01 N1 - Number of references - 34 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Esophagus; Inventories; Smoking; Data processing; Regression analysis; Tobacco; Cancer DO - http://dx.doi.org/10.1007/s10552-015-0535-2 ER - TY - JOUR T1 - B-cell receptor signaling in diffuse large B-cell lymphoma. AN - 1680757649; 25805587 AB - The importance of understanding the genetic and biochemical basis of B-cell receptor (BCR) survival signaling in diffuse large B-cell lymphoma (DLBCL) is underscored by the recent clinical success of agents that target the BCR pathway. DLBCL is composed of multiple distinct molecular subtypes with divergent clinical outcomes. The activated B-cell-like (ABC) subtype is the most aggressive form of DLBCL and is often resistant to standard chemotherapies. ABC DLBCL expresses numerous genes found in antigen-activated B cells, and genetic and pharmacologic studies have demonstrated that ABC DLBCL tumors are addicted to NF-κB activity. The origins of this NF-κB activity remained obscure until RNA interference screens established that the majority of ABC DLBCL cell lines rely on expression of BCR components and downstream signaling effectors for NF-κB activation. Pharmacological inhibition with ibrutinib of Bruton's tyrosine kinase, a kinase that is required for BCR signaling to engage NF-κB, is selectively toxic for ABC DLBCL tumors; a finding that has now been translated to the clinic. These novel targets not only offer a promising new therapy option for ABC DLBCL, but also demonstrate the value of a deep molecular understanding of oncogenic signaling pathways. Published by Elsevier Inc. JF - Seminars in hematology AU - Young, Ryan M AU - Shaffer, Arthur L AU - Phelan, James D AU - Staudt, Louis M AD - Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD. ; Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD. Electronic address: lstaudt@mail.nih.gov. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 77 EP - 85 VL - 52 IS - 2 KW - NF-kappa B KW - 0 KW - Receptors, Antigen, B-Cell KW - Index Medicus KW - Lymphocyte Activation KW - Humans KW - B-Lymphocytes -- immunology KW - B-Lymphocytes -- metabolism KW - NF-kappa B -- metabolism KW - Lymphoma, Large B-Cell, Diffuse -- drug therapy KW - Receptors, Antigen, B-Cell -- immunology KW - Signal Transduction -- genetics KW - Lymphoma, Large B-Cell, Diffuse -- immunology KW - Lymphoma, Large B-Cell, Diffuse -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680757649?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+hematology&rft.atitle=B-cell+receptor+signaling+in+diffuse+large+B-cell+lymphoma.&rft.au=Young%2C+Ryan+M%3BShaffer%2C+Arthur+L%3BPhelan%2C+James+D%3BStaudt%2C+Louis+M&rft.aulast=Young&rft.aufirst=Ryan&rft.date=2015-04-01&rft.volume=52&rft.issue=2&rft.spage=77&rft.isbn=&rft.btitle=&rft.title=Seminars+in+hematology&rft.issn=1532-8686&rft_id=info:doi/10.1053%2Fj.seminhematol.2015.01.008 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-21 N1 - Date created - 2015-03-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Cell. 2012 Aug 14;22(2):167-79 [22897848] Nature. 2012 Sep 13;489(7415):309-12 [22885698] Nature. 2012 Oct 4;490(7418):116-20 [22885699] Am J Pathol. 2012 Nov;181(5):1879-88 [22982190] PLoS One. 2013;8(1):e54938 [23372794] Proc Natl Acad Sci U S A. 2006 Jul 18;103(29):10961-6 [16832055] J Biol Chem. 2006 Dec 15;281(50):38226-34 [17046816] J Exp Med. 2007 Mar 19;204(3):633-43 [17353367] J Exp Med. 2007 Apr 16;204(4):759-69 [17420266] Science. 2008 Mar 21;319(5870):1676-9 [18323416] Nat Rev Drug Discov. 2013 Mar;12(3):229-43 [23449308] Cancer Cell. 2013 Jun 10;23(6):826-38 [23764004] Proc Natl Acad Sci U S A. 2013 Jul 23;110(30):12420-5 [23840064] Nat Rev Clin Oncol. 2014 Jan;11(1):12-23 [24217204] Cold Spring Harb Perspect Med. 2014 Feb;4(2). pii: a014282. doi: 10.1101/cshperspect.a014282 [24492847] Proc Natl Acad Sci U S A. 2014 Feb 11;111(6):2349-54 [24469833] J Exp Med. 2014 Mar 10;211(3):413-26 [24534189] Blood. 2014 Apr 3;123(14):2199-203 [24497531] Cancer Discov. 2014 Apr;4(4):480-93 [24491438] N Engl J Med. 2014 Jun 12;370(24):2352-4 [24869597] N Engl J Med. 2014 Jun 12;370(24):2286-94 [24869598] Nucleic Acids Res. 2014 Jul;42(12):7591-610 [24875472] Proc Natl Acad Sci U S A. 2014 Aug 5;111(31):11365-70 [25049379] Leukemia. 2015 Apr;29(4):895-900 [25189416] Nature. 2000 Feb 3;403(6769):503-11 [10676951] J Immunol. 2001 Oct 15;167(8):4172-9 [11591737] J Exp Med. 2001 Dec 17;194(12):1861-74 [11748286] Nat Immunol. 2002 Feb;3(2):182-8 [11812996] Nature. 2002 Apr 11;416(6881):603-7 [11948342] N Engl J Med. 2002 Jun 20;346(25):1937-47 [12075054] J Exp Med. 2006 Jul 10;203(7):1785-94 [16818674] Immunity. 2008 Jun;28(6):799-809 [18513998] Proc Natl Acad Sci U S A. 2008 Sep 9;105(36):13520-5 [18765795] Mol Med. 2008 Nov-Dec;14(11-12):665-74 [19009014] Proc Natl Acad Sci U S A. 2008 Dec 30;105(52):20798-803 [19104039] Immunity. 2009 Jan 16;30(1):44-55 [19135393] Cell. 2004 Jun 11;117(6):787-800 [15186779] Mol Immunol. 2004 Jul;41(6-7):599-613 [15219998] Cell. 1989 Mar 10;56(5):777-83 [2493990] Nature. 1989 Mar 30;338(6214):383-4 [2927501] J Biol Chem. 1995 May 12;270(19):11590-4 [7538118] Science. 1996 Feb 9;271(5250):822-5 [8629002] Cell. 1997 Sep 19;90(6):1073-83 [9323135] Immunity. 2005 Jan;22(1):9-18 [15664155] Clin Cancer Res. 2005 Jan 1;11(1):28-40 [15671525] Nat Rev Cancer. 2005 Apr;5(4):251-62 [15803153] Histol Histopathol. 2005 Jul;20(3):945-55 [15944945] Nat Rev Immunol. 2006 Apr;6(4):283-94 [16557260] Nature. 2006 May 4;441(7089):106-10 [16572121] Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6262-7 [19332776] J Immunol. 2009 May 1;182(9):5382-92 [19380785] Nature. 2009 Jun 4;459(7247):717-21 [19412164] Cell. 2009 Oct 30;139(3):573-86 [19879843] Nat Immunol. 2009 Dec;10(12):1292-9 [19855380] Nature. 2010 Jan 7;463(7277):88-92 [20054396] Blood. 2010 May 13;115(19):3907-15 [20110421] Cold Spring Harb Perspect Biol. 2010 Jun;2(6):a000109 [20516126] Immunity. 2010 Jun 25;32(6):778-89 [20620943] Cold Spring Harb Perspect Biol. 2010 Sep;2(9):a003004 [20685844] Proc Natl Acad Sci U S A. 2011 Jan 4;108(1):272-7 [21173233] Nature. 2011 Feb 3;470(7332):115-9 [21179087] Leukemia. 2011 Apr;25(4):681-8 [21233831] Nat Immunol. 2011 Aug;12(8):715-23 [21772280] Annu Rev Immunol. 2012;30:565-610 [22224767] Blood. 2012 May 10;119(19):4467-75 [22415752] Cancer Cell. 2012 Jun 12;21(6):723-37 [22698399] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1053/j.seminhematol.2015.01.008 ER - TY - JOUR T1 - Effects of metformin on energy intake and satiety in obese children AN - 1680440839; PQ0001264692 AB - To investigate the effects of metformin on appetite and energy intake in obese children with hyperinsulinaemia. We conducted a 6-month randomized, double-blind, placebo-controlled trial to evaluate the effects of metformin 1000 mg twice daily on body weight and energy balance in 100 obese children with hyperinsulinaemia aged 6-12 years. The children ate ad libitum from standardized food arrays on two separate occasions before and after 6 months of study medication. The first test meal was consumed after an overnight fast. The second was preceded by a pre-meal load. For each test meal, energy intake was recorded, and the children completed scales of hunger, fullness and desire to eat. Data from the meal studies at baseline and after treatment with study medication were available for 84 children (metformin-treated, n = 45; placebo-treated, n = 39). Compared with placebo, metformin treatment elicited significant reductions from baseline in adjusted mean plus or minus standard error of the mean energy intake after the pre-meal load (metformin: -104.7 plus or minus 83.8 kcal vs. placebo: +144.2 plus or minus 96.9 kcal; p = 0.034) independently of changes in body composition. Metformin also significantly decreased ratings of hunger (-1.5 plus or minus 5.6 vs. +18.6 plus or minus 6.3; p = 0.013) and increased ratings of fullness (+10.1 plus or minus 6.2 vs. -12.8 plus or minus 7.0; p = 0.01) after the pre-meal load. These data suggest that decreased perceived hunger resulting in diminished food intake are among the mechanisms by which metformin treatment reduces body weight in overweight children with hyperinsulinaemia. JF - Diabetes, Obesity and Metabolism AU - Adeyemo, MA AU - McDuffie, J R AU - Kozlosky, M AU - Krakoff, J AU - Calis, KA AU - Brady, S M AU - Yanovski, JA AD - Program in Developmental Endocrinology and Genetics. Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health Y1 - 2015/04// PY - 2015 DA - Apr 2015 SP - 363 EP - 370 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 17 IS - 4 SN - 1462-8902, 1462-8902 KW - Physical Education Index KW - Obesity KW - Weight KW - Medications KW - Work load KW - Diet KW - Children KW - Body composition KW - Diabetes KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680440839?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Diabetes%2C+Obesity+and+Metabolism&rft.atitle=Effects+of+metformin+on+energy+intake+and+satiety+in+obese+children&rft.au=Adeyemo%2C+MA%3BMcDuffie%2C+J+R%3BKozlosky%2C+M%3BKrakoff%2C+J%3BCalis%2C+KA%3BBrady%2C+S+M%3BYanovski%2C+JA&rft.aulast=Adeyemo&rft.aufirst=MA&rft.date=2015-04-01&rft.volume=17&rft.issue=4&rft.spage=363&rft.isbn=&rft.btitle=&rft.title=Diabetes%2C+Obesity+and+Metabolism&rft.issn=14628902&rft_id=info:doi/10.1111%2Fdom.12426 LA - English DB - Physical Education Index N1 - Date revised - 2015-05-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Obesity; Weight; Medications; Work load; Diet; Body composition; Children; Diabetes DO - http://dx.doi.org/10.1111/dom.12426 ER - TY - JOUR T1 - A Trypsin Inhibitor from Rambutan Seeds with Antitumor, Anti-HIV-1 Reverse Transcriptase, and Nitric Oxide-Inducing Properties AN - 1680438202; PQ0001478204 AB - Nephelium lappaceum L., commonly known as "rambutan," is a typical tropical tree and is well known for its juicy and sweet fruit which has an exotic flavor. Chemical studies on rambutan have led to the identification of various components such as monoterpene lactones and volatile compounds. Here, a 22.5-kDa trypsin inhibitor (N . lappaceum trypsin inhibitor (NLTI)) was isolated from fresh rambutan seeds using liquid chromatographical techniques. NLTI reduced the proteolytic activities of both trypsin and alpha -chymotrypsin. Dithiothreitol reduced the trypsin inhibitory activity of NLTI at a concentration of 1 mM, indicating that an intact disulfide bond is essential to the activity. NLTI inhibited HIV-1 reverse transcriptase with an IC sub(50) of 0.73 mu M. In addition, NLTI manifested a time- and dose-dependent inhibitory effect on growth in many tumor cells. NLTI is one of the few trypsin inhibitors with nitric oxide-inducing activity and may find application in tumor therapy. JF - Applied Biochemistry and Biotechnology AU - Fang, Evandro Fei AU - Ng, Tzi Bun AD - School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, Hong Kong, evandro.fang@nih.gov Y1 - 2015/04// PY - 2015 DA - Apr 2015 SP - 3828 EP - 3839 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 175 IS - 8 SN - 0273-2289, 0273-2289 KW - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts KW - Proteolysis KW - Fruits KW - Flavor KW - Sweet taste KW - Seeds KW - Trypsin KW - alpha -Chymotrypsin KW - Trees KW - Disulfide bonds KW - Tumors KW - lactones KW - Tumor cells KW - Nephelium lappaceum KW - Antiviral agents KW - Volatiles KW - Human immunodeficiency virus 1 KW - Monoterpenes KW - RNA-directed DNA polymerase KW - Dithiothreitol KW - V 22360:AIDS and HIV KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680438202?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Applied+Biochemistry+and+Biotechnology&rft.atitle=A+Trypsin+Inhibitor+from+Rambutan+Seeds+with+Antitumor%2C+Anti-HIV-1+Reverse+Transcriptase%2C+and+Nitric+Oxide-Inducing+Properties&rft.au=Fang%2C+Evandro+Fei%3BNg%2C+Tzi+Bun&rft.aulast=Fang&rft.aufirst=Evandro&rft.date=2015-04-01&rft.volume=175&rft.issue=8&rft.spage=3828&rft.isbn=&rft.btitle=&rft.title=Applied+Biochemistry+and+Biotechnology&rft.issn=02732289&rft_id=info:doi/10.1007%2Fs12010-015-1550-1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Number of references - 39 N1 - Last updated - 2015-11-25 N1 - SubjectsTermNotLitGenreText - Proteolysis; Fruits; Seeds; Sweet taste; Flavor; Trypsin; Trees; alpha -Chymotrypsin; Disulfide bonds; lactones; Tumors; Tumor cells; Antiviral agents; Volatiles; Monoterpenes; RNA-directed DNA polymerase; Dithiothreitol; Human immunodeficiency virus 1; Nephelium lappaceum DO - http://dx.doi.org/10.1007/s12010-015-1550-1 ER - TY - JOUR T1 - Comparative Genome Sequencing of Rickettsia rickettsii Strains That Differ in Virulence AN - 1676345661; PQ0001421729 AB - Rickettsia rickettsii is an obligate intracellular pathogen that is the causative agent of Rocky Mountain spotted fever. Strains of R. rickettsii differ dramatically in virulence. In a guinea pig model of infection, the severity of disease as assessed by fever response varies from the most virulent, Sheila Smith, to Iowa, which causes no fever. To identify potential determinants of virulence in R. rickettsii, the genomes of two additional strains were sequenced for comparison to known sequences (comparative genome sequencing [CGS]). R. rickettsii Morgan and R strains were compared to the avirulent R. rickettsii Iowa and virulent R. rickettsii Sheila Smith strains. The Montana strains Sheila Smith and R were found to be highly similar while the eastern strains Iowa and Morgan were most similar to each other. A major surface antigen, rickettsial outer membrane protein A (rOmpA), is severely truncated in the Iowa strain. The region of ompA containing 13 tandem repeats was sequenced, revealing only seven shared SNPs (four nonsynonymous) for R and Morgan strains compared to Sheila Smith, with an additional 17 SNPs identified in Morgan. Another major surface antigen and autotransporter, rOmpB, exhibits a defect in processing in the Iowa strain such that the beta fragment is not cleaved. Sequence analysis of ompB reveals identical sequences between Iowa and Morgan strains and between the R and Sheila Smith strains. The number of SNPs and insertions/deletions between sequences of the two Montana strains and the two eastern strains is low, thus narrowing the field of possible virulence factors. JF - Infection and Immunity AU - Clark, Tina R AU - Noriea, Nicholas F AU - Bublitz, DeAnna C AU - Ellison, Damon W AU - Martens, Craig AU - Lutter, Erika I AU - Hackstadt, Ted Y1 - 2015/04// PY - 2015 DA - Apr 2015 SP - 1568 EP - 1576 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 83 IS - 4 SN - 0019-9567, 0019-9567 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Genomes KW - outer membrane proteins KW - virulence factors KW - Animal models KW - Pathogens KW - Infection KW - Fever KW - Virulence KW - Rocky Mountain spotted fever KW - Single-nucleotide polymorphism KW - surface antigens KW - Rickettsia rickettsii KW - Sheila KW - J 02350:Immunology KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676345661?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Comparative+Genome+Sequencing+of+Rickettsia+rickettsii+Strains+That+Differ+in+Virulence&rft.au=Clark%2C+Tina+R%3BNoriea%2C+Nicholas+F%3BBublitz%2C+DeAnna+C%3BEllison%2C+Damon+W%3BMartens%2C+Craig%3BLutter%2C+Erika+I%3BHackstadt%2C+Ted&rft.aulast=Clark&rft.aufirst=Tina&rft.date=2015-04-01&rft.volume=83&rft.issue=4&rft.spage=1568&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.03140-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Number of references - 46 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Virulence; Fever; Genomes; Rocky Mountain spotted fever; outer membrane proteins; virulence factors; surface antigens; Single-nucleotide polymorphism; Animal models; Pathogens; Infection; Sheila; Rickettsia rickettsii DO - http://dx.doi.org/10.1128/IAI.03140-14 ER - TY - JOUR T1 - Genistein protects female nonobese diabetic mice from developing type 1 diabetes when fed a soy- and alfalfa-free diet. AN - 1674202055; 24713318 AB - The objective of this study was to determine the effects of the phytoestrogen genistein (GEN) on the time of onset and/or the incidence of type 1 diabetes (T1D) in female nonobese diabetic (NOD) mice, when administered GEN by gavage once every day for up to 180 days. Five groups of mice (approximately 24 animals/group; 6-7 weeks of age) were included: naive control, vehicle control (25 mM Na2CO3 in water), and 3 GEN treatment groups (2 mg/kg, 6 mg/kg, and 20 mg/kg). Mice were maintained on a soy- and alfalfa-free diet (5K96) during the study and were monitored for blood glucose changes every week. When compared to the vehicle control, exposure to 2-mg/kg GEN produced significant decreases ranging from 55 to 79% in the total incidences of diabetes (blood glucose ≥ 250 mg/dl) and severe diabetes (blood glucose ≥ 400 mg/dl) starting at week 14 of the study. However, during the later stages of the study (i.e., after week 23), the 2-mg/kg dose had no effect on disease incidence. In animals treated with 6-mg/kg and 20-mg/kg GEN, significant decreases in the total incidence of diabetes were observed starting at week 16, while the incidence of severe diabetes was significantly decreased with the changes being observed initially at weeks 18 and 17 for the 6-mg/kg and 20-mg/kg GEN treatment groups, respectively. Several lines of evidence, including histopathological analysis, suggested that GEN protected the pancreas from autoimmune destruction. However, this protective effect of GEN was absent when female NOD mice were maintained on NTP-2000 rodent diet, which contained 5% soybean meal and 7.5% alfalfa meal (the total concentrations of phytoestrogens ranged between 95 and 134 mg/kg). In summary, oral dosing of GEN reduced the incidence and increased the time to onset of T1D in female NOD mice but only when fed a soy- and alfalfa-free diet. © 2014 by The Author(s). JF - Toxicologic pathology AU - Guo, Tai L AU - Germolec, Dori R AU - Zheng, Jian Feng AU - Kooistra, Linda AU - Auttachoat, Wimolnut AU - Smith, Matthew J AU - White, Kimber L AU - Elmore, Susan A AD - Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, Virginia, USA tlguo1@uga.edu. ; Division of the National Toxicology Program, NIEHS, Research Triangle Park, North Carolina, USA. ; Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, Virginia, USA. ; Charles River Laboratories, Durham, North Carolina, USA. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 435 EP - 448 VL - 43 IS - 3 KW - Autoantibodies KW - 0 KW - Blood Glucose KW - Insulin KW - Phytoestrogens KW - Creatinine KW - AYI8EX34EU KW - Genistein KW - DH2M523P0H KW - Index Medicus KW - genistein KW - type 1 diabetes KW - NOD mouse KW - islet inflammation. KW - Pancreas -- pathology KW - Animals KW - Diabetes Mellitus, Experimental -- genetics KW - Kidney -- pathology KW - Blood Glucose -- metabolism KW - Mice, Inbred NOD KW - Insulin -- blood KW - Mice KW - Creatinine -- blood KW - Diabetes Mellitus, Experimental -- psychology KW - Diabetes Mellitus, Experimental -- pathology KW - Autoantibodies -- analysis KW - Diet KW - Insulin -- immunology KW - Female KW - Diabetes Mellitus, Type 1 -- prevention & control KW - Genistein -- pharmacology KW - Phytoestrogens -- pharmacology KW - Diabetes Mellitus, Type 1 -- pathology KW - Soybeans KW - Medicago sativa UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1674202055?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Genistein+protects+female+nonobese+diabetic+mice+from+developing+type+1+diabetes+when+fed+a+soy-+and+alfalfa-free+diet.&rft.au=Guo%2C+Tai+L%3BGermolec%2C+Dori+R%3BZheng%2C+Jian+Feng%3BKooistra%2C+Linda%3BAuttachoat%2C+Wimolnut%3BSmith%2C+Matthew+J%3BWhite%2C+Kimber+L%3BElmore%2C+Susan+A&rft.aulast=Guo&rft.aufirst=Tai&rft.date=2015-04-01&rft.volume=43&rft.issue=3&rft.spage=435&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623314526318 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-06 N1 - Date created - 2015-04-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Diabetologia. 1999 Dec;42(12):1395-403 [10651256] Rapid Commun Mass Spectrom. 2000;14(8):673-8 [10786906] J Immunol. 2001 Mar 1;166(5):2982-91 [11207247] Int Immunopharmacol. 2001 Apr;1(4):699-712 [11357882] Kidney Int. 2001 Aug;60(2):505-12 [11473633] Cancer Lett. 2001 Oct 22;172(1):1-6 [11595123] J Nutr. 2001 Dec;131(12):3251-8 [11739876] Toxicol Lett. 2002 Mar 10;128(1-3):145-57 [11869825] Proc Natl Acad Sci U S A. 2002 May 28;99(11):7616-21 [12032332] Ann Intern Med. 2003 Jan 7;138(1):1-9 [12513038] Pediatr Pathol Mol Med. 2003 Mar-Apr;22(2):131-41 [12556293] Toxicology. 2003 Jun 30;188(2-3):233-50 [12767694] Clin Endocrinol (Oxf). 2004 May;60(5):541-9 [15104556] BMC Genet. 2004 Apr 2;5:5 [15059244] Am J Epidemiol. 2004 Jul 1;160(1):3-10 [15229111] Diabetes. 1965 Oct;14(10):619-33 [5318831] Jikken Dobutsu. 1980 Jan;29(1):1-13 [6995140] J Biol Chem. 1987 Apr 25;262(12):5592-5 [3106339] Diabetologia. 1988 Jan;31(1):62-4 [3280372] Diabetes. 1990 Sep;39(9):1085-90 [2200729] Kidney Int. 1993 Jan;43(1):114-20 [8433550] Lancet. 1993 Nov 13;342(8881):1209-10 [7901532] J Steroid Biochem Mol Biol. 1994 Jun;49(2-3):153-60 [8031711] Diabetes. 1994 Nov;43(11):1304-10 [7926304] Diabetes. 1996 Jul;45(7):926-33 [8666144] Diabetologia. 1996 Mar;39(3):270-4 [8721771] Can J Physiol Pharmacol. 1997 Apr;75(4):241-54 [9196849] Proc Soc Exp Biol Med. 1998 Mar;217(3):247-53 [9492332] Environ Health Perspect. 1999 Apr;107(4):A182-3 [10383244] Annu Rev Immunol. 2005;23:447-85 [15771578] Diabetes. 2005 Apr;54(4):1245-8 [15793269] Toxicol Sci. 2005 Oct;87(2):399-408 [16049267] Dtsch Tierarztl Wochenschr. 2005 Sep;112(9):323-6 [16240910] Food Chem Toxicol. 2006 Mar;44(3):316-25 [16162389] J Autoimmun. 2006 Mar;26(2):104-15 [16431079] Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9232-7 [16754860] CMAJ. 2006 Jul 18;175(2):165-70 [16847277] Endocrinology. 2007 Jul;148(7):3236-45 [17379646] Carcinogenesis. 2007 Dec;28(12):2560-6 [17916904] Diabetes Metab Res Rev. 2008 Jan-Feb;24(1):74-81 [17932873] Br J Cancer. 2008 Jan 15;98(1):9-14 [18182974] Med Hypotheses. 2008;70(6):1207-9 [18249499] Proc Natl Acad Sci U S A. 2008 Dec 2;105(48):18895-900 [19015530] Pediatr Endocrinol Rev. 2008 Dec;6(2):228-34 [19202509] Cancer Genomics Proteomics. 2009 Mar-Apr;6(2):85-92 [19451092] Scand J Gastroenterol. 2009;44(12):1391-407 [19958057] Int J Environ Res Public Health. 2010 Jul;7(7):2845-52 [20717544] Front Neuroendocrinol. 2010 Oct;31(4):400-19 [20347861] Anat Rec (Hoboken). 2011 Nov;294(11):1930-8 [21965157] Food Funct. 2013 Feb;4(2):200-12 [23160185] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/0192623314526318 ER - TY - JOUR T1 - Agreement of two-dimensional and three-dimensional transvaginal ultrasound with magnetic resonance imaging in assessment of parametrial infiltration in cervical cancer AN - 1673397279; PQ0001383361 AB - Objectives To compare two-dimensional (2D) and three-dimensional (3D) transvaginal ultrasound with magnetic resonance imaging (MRI) as the gold standard in assessment of parametrial infiltration of cervical cancer and to determine if all parts of the cervix are equally assessable with ultrasound. Methods Patients with macroscopically evident and histologically confirmed cervical cancer were staged using International Federation of Gynecology and Obstetrics (FIGO) criteria and underwent MRI and 2D and 3D ultrasound examination before treatment. When assessing parametrial infiltration with 3D ultrasound and MRI, the cervix was (virtually) divided into three cylinders (cranial, middle and caudal) of equal size and each cylinder was then divided into six sectors in a clockwise manner following a consensus between radiologists and ultrasound examiners. The presence and the extent of parametrial invasion were recorded for each sector. Results of 2D ultrasound, 3D ultrasound and MRI were compared and reported in terms of percentage agreement and kappa value. Results A total of 29 consecutive patients were included in the study. The percentage agreement between 2D ultrasound and MRI in assessing parametrial infiltration (yes or no) was 76% (kappa, 0.459) and that between 3D ultrasound and MRI was 79% (kappa, 0.508). The results of 2D ultrasound showed the following agreement with those of MRI: 90% for the ventral parametrium (kappa, 0.720), 72% for the right lateral parametrium (kappa, 0.494), 69% for the left lateral parametrium (kappa, 0.412) and 58.5% for the dorsal parametrium (kappa, 0.017). The results of 3D ultrasound showed the following agreement with those of MRI: 62.5% for the ventral parametrium (kappa, 0.176), 81% for the right lateral parametrium (kappa, 0.595), 70% for the left lateral parametrium (kappa, 0.326) and 52% for the dorsal parametrium (kappa, 0.132). The best agreement between 3D ultrasound and MRI was for the middle cervical cylinder (76%; kappa, 0.438) and the poorest agreement was for the caudal cylinder (42%; kappa, 0.125). Conclusion The results of 2D and 3D ultrasound showed similar moderate agreement with MRI; 2D and 3D ultrasound examinations are less costly and more readily available than MRI and should be considered in the preoperative work-up for cervical cancer. Copyright copyright 2014 ISUOG. Published by John Wiley & Sons Ltd. JF - Ultrasound in Obstetrics and Gynecology AU - Chiappa, V AU - Di Legge, A AU - Valentini, AL AU - Gui, B AU - Micco, M AU - Ludovisi, M AU - Giansiracusa, C AU - Testa, A C AU - Valentin, L AD - Department of Gynecologic Oncology, National Cancer Institute, Milan, Italy. Y1 - 2015/04// PY - 2015 DA - Apr 2015 SP - 459 EP - 469 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 45 IS - 4 SN - 0960-7692, 0960-7692 KW - Biotechnology and Bioengineering Abstracts KW - Gynecology KW - Skull KW - Magnetic resonance imaging KW - Cervical cancer KW - Cervix KW - Ultrasound KW - Obstetrics KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673397279?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Ultrasound+in+Obstetrics+and+Gynecology&rft.atitle=Agreement+of+two-dimensional+and+three-dimensional+transvaginal+ultrasound+with+magnetic+resonance+imaging+in+assessment+of+parametrial+infiltration+in+cervical+cancer&rft.au=Chiappa%2C+V%3BDi+Legge%2C+A%3BValentini%2C+AL%3BGui%2C+B%3BMicco%2C+M%3BLudovisi%2C+M%3BGiansiracusa%2C+C%3BTesta%2C+A+C%3BValentin%2C+L&rft.aulast=Chiappa&rft.aufirst=V&rft.date=2015-04-01&rft.volume=45&rft.issue=4&rft.spage=459&rft.isbn=&rft.btitle=&rft.title=Ultrasound+in+Obstetrics+and+Gynecology&rft.issn=09607692&rft_id=info:doi/10.1002%2Fuog.14637 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Skull; Gynecology; Cervical cancer; Magnetic resonance imaging; Cervix; Obstetrics; Ultrasound DO - http://dx.doi.org/10.1002/uog.14637 ER - TY - JOUR T1 - G-Quadruplex Formation Between G-Rich PNA and Homologous Sequences in Oligonucleotides and Supercoiled Plasmid DNA AN - 1673395392; PQ0001360907 AB - Guanine (G)-rich DNA sequences can adopt four-stranded quadruplex conformations that may play a role in the regulation of genetic processes. To explore the possibility of targeted molecular recognition of DNA sequences with short G-rich peptide nucleic acids (PNA) and to assess the strand arrangement in such complexes, we used PNA and DNA with the Oxytricha nova telomeric sequence d(G4T4G4) as a model. PNA probes were complexed with DNA targets in the following forms: single-stranded oligonucleotides, a loop of DNA in a hairpin conformation, and as supercoiled plasmid with the (G4T4G4)/(C4A4C4) insert. Gel-shift mobility assays demonstrated formation of stable hybrid complexes between the homologous G4T4G4 PNA and DNA with multiple modes of binding. Chemical and enzymatic probing revealed sequence-specific and G-quadruplex dependent binding of G4T4G4 PNA to dsDNA. Spectroscopic and electrophoretic analysis of the complex formed between PNA and the synthetic DNA hairpin containing the G4T4G4 loop showed that the stoichiometry of a prevailing complex is three PNA strands per one DNA strand. We speculate how this new PNA-DNA complex architecture can help to design more selective, quadruplex-specific PNA probes. JF - Nucleic Acid Therapeutics AU - Gaynutdinov, Timur I AU - Englund, Ethan A AU - Appella, Daniel H AU - Onyshchenko, Mykola I AU - Neumann, Ronald D AU - Panyutin, Igor G AD - Department of Radiology and Imaging Sciences, Clinical Center, National Institutes of Health, Bethesda, Maryland. Y1 - 2015/04// PY - 2015 DA - Apr 2015 SP - 78 EP - 84 PB - Mary Ann Liebert, Inc. Publishers, 140 Huguenot St 3rd Fl New Rochelle NY 10801 United States VL - 25 IS - 2 SN - 2159-3337, 2159-3337 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Molecular modelling KW - Guanine KW - Nucleotide sequence KW - DNA probes KW - Hybrids KW - Plasmids KW - Electrophoretic mobility KW - Oxytricha nova KW - Oligonucleotides KW - peptide nucleic acids KW - Conformation KW - W 30905:Medical Applications KW - G 07880:Human Genetics KW - N 14820:DNA Metabolism & Structure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673395392?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acid+Therapeutics&rft.atitle=G-Quadruplex+Formation+Between+G-Rich+PNA+and+Homologous+Sequences+in+Oligonucleotides+and+Supercoiled+Plasmid+DNA&rft.au=Gaynutdinov%2C+Timur+I%3BEnglund%2C+Ethan+A%3BAppella%2C+Daniel+H%3BOnyshchenko%2C+Mykola+I%3BNeumann%2C+Ronald+D%3BPanyutin%2C+Igor+G&rft.aulast=Gaynutdinov&rft.aufirst=Timur&rft.date=2015-04-01&rft.volume=25&rft.issue=2&rft.spage=78&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acid+Therapeutics&rft.issn=21593337&rft_id=info:doi/10.1089%2Fnat.2014.0517 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Number of references - 25 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Molecular modelling; Guanine; Hybrids; DNA probes; Nucleotide sequence; Electrophoretic mobility; Plasmids; Oligonucleotides; Conformation; peptide nucleic acids; Oxytricha nova DO - http://dx.doi.org/10.1089/nat.2014.0517 ER - TY - JOUR T1 - Food Insecurity, Cigarette Smoking, and Acculturation Among Latinos: Data From NHANES 1999-2008 AN - 1673394154; PQ0001354742 AB - Prevalence of food insecurity (FI) among Latinos in the United States is almost double the national average. To better understand FI among Latinos, potential risk factors beyond poverty, including acculturation indicators and smoking status, were explored. Cross-sectional data from 6,681 Latino adults from the 1999-2008 National Health and Nutrition Examination Surveys were used. Partial proportional odds (PPO) models were used to estimate associations of FI, including cigarette smoking and acculturation. The PPO models indicated that compared with never smokers, current smokers had significantly higher odds of FI (odds ratios ranged from 1.32 to 1.51 across models). Lower levels of acculturation and poverty and being a younger or middle-aged adult were also significantly associated with FI. Among Latinos, current smoking and low acculturation are important risk factors for FI. Current smoking and low acculturation may exacerbate nutritional deprivation in a population that is already disproportionally affected by poverty and poor health outcomes. JF - Journal of Immigrant and Minority Health AU - Iglesias-Rios, Lisbeth AU - Bromberg, Julie E AU - Moser, Richard P AU - Augustson, Erik M AD - Tobacco Control Research Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health, 9609 Medical Center Drive, MSC 9761, Bethesda, MD, 20892-9761, USA, Erik.Augustson@nih.gov Y1 - 2015/04// PY - 2015 DA - Apr 2015 SP - 349 EP - 357 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 17 IS - 2 SN - 1557-1912, 1557-1912 KW - Risk Abstracts KW - USA KW - Cigarettes KW - Poverty KW - Risk factors KW - Immigrants KW - Food security KW - Nutrition KW - Ethnic groups KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673394154?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Immigrant+and+Minority+Health&rft.atitle=Food+Insecurity%2C+Cigarette+Smoking%2C+and+Acculturation+Among+Latinos%3A+Data+From+NHANES+1999-2008&rft.au=Iglesias-Rios%2C+Lisbeth%3BBromberg%2C+Julie+E%3BMoser%2C+Richard+P%3BAugustson%2C+Erik+M&rft.aulast=Iglesias-Rios&rft.aufirst=Lisbeth&rft.date=2015-04-01&rft.volume=17&rft.issue=2&rft.spage=349&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immigrant+and+Minority+Health&rft.issn=15571912&rft_id=info:doi/10.1007%2Fs10903-013-9957-7 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Number of references - 39 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Cigarettes; Risk factors; Poverty; Immigrants; Food security; Nutrition; Ethnic groups; USA DO - http://dx.doi.org/10.1007/s10903-013-9957-7 ER - TY - JOUR T1 - Should small papillary thyroid cancer be observed? A population-based study AN - 1673388203; PQ0001291456 AB - BACKGROUND Some centers have advocated selecting patients with small papillary thyroid cancer (PTC) to undergo active surveillance without surgical treatment. The objectives of the current study were to analyze thyroid cancer (TC)-related mortality in a population-based cohort and to determine the impact of small PTCs (defined as tumors less than or equal to 2 cm in greatest dimension) on TC-related mortality. METHODS Data on patients with TC of follicular cell origin from the National Cancer Institute's Surveillance, Epidemiology, and End Results 17 Registries database (1988-2007) were used to analyze the characteristics of PTCs less than or equal to 2 cm in patients who died from TC-related causes. The effects of clinical features on disease-specific survival were analyzed. RESULTS Over the 20-year study period, the rate of TC-related mortality was 2.8% (n=1753 of 61,523 patients). Of the patients who died from TC-related causes, 38% had PTC, 10% had follicular TC, and 31.3% had anaplastic TC. PTCs less than or equal to 2 cm accounted for 12.3% of TC-related mortalities. Compared with patients who did not experience TC-related mortality from PTCs less than or equal to 2 cm, there were significantly higher rates of men (30% vs 17%; P1 cm (59% vs 46%; P<.01), extrathyroid extension (41% vs 11%; P<.01), lymph node metastases (77% vs 28%; P<.01), and distant metastases (31% vs 1%; P<.01) among the patients who died from PTCs less than or equal to 2 cm. Independent risk factors for death from PTCs less than or equal to 2 cm included age greater than or equal to 45 years, lymph node and distant metastases, extrathyroid extension, and undergoing less than thyroid lobectomy. CONCLUSIONS Because 12.3% of patients who experienced TC-related deaths had PTCs less than or equal to 2 cm despite undergoing thyroidectomy, the current results indicate that nonoperative management for patients who have PTCs less than or equal to 2 cm should be used with caution. Patients aged greater than or equal to 45 years with PTCs less than or equal to 2 cm should undergo thyroidectomy. Cancer 2015; 121:1017-1024. copyright 2014 American Cancer Society. Nonoperative management should be used with caution for patients who have papillary thyroid cancers that measure less than or equal to 2 cm in greatest dimension. Patients aged greater than or equal to 45 years with papillary thyroid cancers less than or equal to 2 cm should undergo thyroidectomy. JF - Cancer AU - Nilubol, Naris AU - Kebebew, Electron AD - Endocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. Y1 - 2015/04// PY - 2015 DA - Apr 2015 SP - 1017 EP - 1024 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 121 IS - 7 SN - 0008-543X, 0008-543X KW - Health & Safety Science Abstracts; Risk Abstracts KW - Health risks KW - Mortality KW - Age KW - Surgery KW - Risk factors KW - Thyroid KW - Survival KW - Tumors KW - Cancer KW - Lymph nodes KW - H 11000:Diseases/Injuries/Trauma KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673388203?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Should+small+papillary+thyroid+cancer+be+observed%3F+A+population-based+study&rft.au=Nilubol%2C+Naris%3BKebebew%2C+Electron&rft.aulast=Nilubol&rft.aufirst=Naris&rft.date=2015-04-01&rft.volume=121&rft.issue=7&rft.spage=1017&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.29123 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2015-08-05 N1 - SubjectsTermNotLitGenreText - Mortality; Health risks; Age; Risk factors; Surgery; Thyroid; Survival; Tumors; Lymph nodes; Cancer DO - http://dx.doi.org/10.1002/cncr.29123 ER - TY - JOUR T1 - Pulsed Focused Ultrasound Pretreatment Improves Mesenchymal Stromal Cell Efficacy in Preventing and Rescuing Established Acute Kidney Injury in Mice AN - 1673385855; PQ0001358135 AB - Animal studies have shown that mesenchymal stromal cell (MSC) infusions improve acute kidney injury (AKI) outcomes when administered early after ischemic/reperfusion injury or within 24 hours after cisplatin administration. These findings have spurred several human clinical trials to prevent AKI. However, no specific therapy effectively treats clinically obvious AKI or rescues renal function once advanced injury is established. We investigated if noninvasive image-guided pulsed focused ultrasound (pFUS) could alter the kidney microenvironment to enhance homing of subsequently infused MSC. To examine the efficacy of pFUS-enhanced cell homing in disease, we targeted pFUS to kidneys to enhance MSC homing after cisplatin-induced AKI. We found that pFUS enhanced MSC homing at 1 day post-cisplatin, prior to renal functional deficits, and that enhanced homing improved outcomes of renal function, tubular cell death, and regeneration at 5 days post-cisplatin compared to MSC alone. We then investigated whether pFUS+MSC therapy could rescue established AKI. MSC alone at 3 days post-cisplatin, after renal functional deficits were obvious, significantly improved 7-day survival of animals. Survival was further improved by pFUS and MSC. pFUS prior to MSC injections increased IL-10 production by MSC that homed to kidneys and generated an anti-inflammatory immune cell profile in treated kidneys. This study shows pFUS is a neoadjuvant approach to improve MSC homing to diseased organs. pFUS with MSC better prevents AKI than MSC alone and allows rescue therapy in established AKI, which currently has no meaningful therapeutic options. Stem Cells 2015; 33:1241-1253 JF - Stem Cells AU - Burks, Scott R AU - Nguyen, Ben A AU - Tebebi, Pamela A AU - Kim, Saejeong J AU - Bresler, Michele N AU - Ziadloo, Ali AU - Street, Jonathan M AU - Yuen, Peter ST AU - Star, Robert A AU - Frank, Joseph A AD - Frank Laboratory, Radiology and Imaging Sciences, Clinical Center, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/04// PY - 2015 DA - Apr 2015 SP - 1241 EP - 1253 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 33 IS - 4 SN - 1066-5099, 1066-5099 KW - Biotechnology and Bioengineering Abstracts KW - Cell survival KW - stromal cells KW - Injuries KW - Homing behavior KW - Ischemia KW - Clinical trials KW - Interleukin 10 KW - Inflammation KW - Reperfusion KW - Cell death KW - Stem cells KW - Renal function KW - Cisplatin KW - Microenvironments KW - Cell migration KW - Mesenchyme KW - Ultrasound KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673385855?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+Cells&rft.atitle=Pulsed+Focused+Ultrasound+Pretreatment+Improves+Mesenchymal+Stromal+Cell+Efficacy+in+Preventing+and+Rescuing+Established+Acute+Kidney+Injury+in+Mice&rft.au=Burks%2C+Scott+R%3BNguyen%2C+Ben+A%3BTebebi%2C+Pamela+A%3BKim%2C+Saejeong+J%3BBresler%2C+Michele+N%3BZiadloo%2C+Ali%3BStreet%2C+Jonathan+M%3BYuen%2C+Peter+ST%3BStar%2C+Robert+A%3BFrank%2C+Joseph+A&rft.aulast=Burks&rft.aufirst=Scott&rft.date=2015-04-01&rft.volume=33&rft.issue=4&rft.spage=1241&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.1965 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Cell survival; Injuries; stromal cells; Homing behavior; Ischemia; Clinical trials; Interleukin 10; Inflammation; Reperfusion; Stem cells; Cell death; Cisplatin; Renal function; Microenvironments; Cell migration; Mesenchyme; Ultrasound DO - http://dx.doi.org/10.1002/stem.1965 ER - TY - JOUR T1 - Bone Marrow-Derived Mesenchymal Stromal Cells Harness Purinergenic Signaling to Tolerize Human Th1 Cells In Vivo AN - 1673379773; PQ0001358144 AB - The use of bone marrow-derived mesenchymal stromal cells (BMSC) in the treatment of alloimmune and autoimmune conditions has generated much interest, yet an understanding of the therapeutic mechanism remains elusive. We therefore explored immune modulation by a clinical-grade BMSC product in a model of human-into-mouse xenogeneic graft-versus-host disease (x-GVHD) mediated by human CD4 super(+) Th1 cells. BMSC reversed established, lethal x-GVHD through marked inhibition of Th1 cell effector function. Gene marking studies indicated BMSC engraftment was limited to the lung; furthermore, there was no increase in regulatory T cells, thereby suggesting a paracrine mechanism of BMSC action. BMSC recipients had increased serum CD73 expressing exosomes that promoted adenosine accumulation ex vivo. Importantly, immune modulation mediated by BMSC was fully abrogated by pharmacologic therapy with an adenosine A2A receptor antagonist. To investigate the potential clinical relevance of these mechanistic findings, patient serum samples collected pre- and post-BMSC treatment were studied for exosome content: CD73 expressing exosomes promoting adenosine accumulation were detected in post-BMSC samples. In conclusion, BMSC effectively modulate experimental GVHD through a paracrine mechanism that promotes adenosine-based immune suppression. Stem Cells 2015; 33:1200-1212 Stem Cells 2015; 33:1200-1212 JF - Stem Cells AU - Amarnath, Shoba AU - Foley, Jason E AU - Farthing, Don E AU - Gress, Ronald E AU - Laurence, Arian AU - Eckhaus, Michael A AU - Metais, Jean-Yves AU - Rose, Jeremy J AU - Hakim, Frances T AU - Felizardo, Tania C AU - Cheng, Austin V AU - Robey, Pamela G AU - Stroncek, David E AU - Sabatino, Marianna AU - Battiwalla, Minoo AU - Ito, Sawa AU - Fowler, Daniel H AU - Barrett, Austin J AD - Cytokine biology section, Experimental Transplantation and Immunology Branch, National Cancer Institute, Newcastle Upon Tyne, United Kingdom. Y1 - 2015/04// PY - 2015 DA - Apr 2015 SP - 1200 EP - 1212 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 33 IS - 4 SN - 1066-5099, 1066-5099 KW - Biotechnology and Bioengineering Abstracts KW - Immunoregulation KW - stromal cells KW - exosomes KW - Helper cells KW - Paracrine signalling KW - Autoimmune diseases KW - Bone marrow KW - Graft-versus-host reaction KW - Immunomodulation KW - Lung transplantation KW - Stem cells KW - CD4 antigen KW - Lymphocytes T KW - CD73 antigen KW - Xenografts KW - Adenosine A2A receptors KW - Mesenchyme KW - W 30920:Tissue Engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673379773?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+Cells&rft.atitle=Bone+Marrow-Derived+Mesenchymal+Stromal+Cells+Harness+Purinergenic+Signaling+to+Tolerize+Human+Th1+Cells+In+Vivo&rft.au=Amarnath%2C+Shoba%3BFoley%2C+Jason+E%3BFarthing%2C+Don+E%3BGress%2C+Ronald+E%3BLaurence%2C+Arian%3BEckhaus%2C+Michael+A%3BMetais%2C+Jean-Yves%3BRose%2C+Jeremy+J%3BHakim%2C+Frances+T%3BFelizardo%2C+Tania+C%3BCheng%2C+Austin+V%3BRobey%2C+Pamela+G%3BStroncek%2C+David+E%3BSabatino%2C+Marianna%3BBattiwalla%2C+Minoo%3BIto%2C+Sawa%3BFowler%2C+Daniel+H%3BBarrett%2C+Austin+J&rft.aulast=Amarnath&rft.aufirst=Shoba&rft.date=2015-04-01&rft.volume=33&rft.issue=4&rft.spage=1200&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.1934 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Immunoregulation; exosomes; stromal cells; Helper cells; Autoimmune diseases; Paracrine signalling; Bone marrow; Graft-versus-host reaction; Immunomodulation; Lung transplantation; CD4 antigen; Stem cells; Lymphocytes T; Xenografts; CD73 antigen; Mesenchyme; Adenosine A2A receptors DO - http://dx.doi.org/10.1002/stem.1934 ER - TY - JOUR T1 - Tumor-induced CD11b(+) Gr-1(+) myeloid-derived suppressor cells exacerbate immune-mediated hepatitis in mice in a CD40-dependent manner. AN - 1672610797; 25616156 AB - Immunosuppressive CD11b(+) Gr-1(+) myeloid-derived suppressor cells (MDSCs) accumulate in the livers of tumor-bearing (TB) mice. We studied hepatic MDSCs in two murine models of immune-mediated hepatitis. Unexpectedly, treatment of TB mice with Concanavalin A (Con A) or α-galactosylceramide resulted in increased alanine aminotransferase (ALT) and aspartate aminotransferase (AST) serum levels in comparison to tumor-free mice. Adoptive transfer of hepatic MDSCs into naïve mice exacerbated Con A induced liver damage. Hepatic CD11b(+) Gr-1(+) cells revealed a polarized proinflammatory gene signature after Con A treatment. An IFN-γ-dependent upregulation of CD40 on hepatic CD11b(+) Gr-1(+) cells along with an upregulation of CD80, CD86, and CD1d after Con A treatment was observed. Con A treatment resulted in a loss of suppressor function by tumor-induced CD11b(+) Gr-1(+) MDSCs as well as enhanced reactive oxygen species (ROS)-mediated hepatotoxicity. CD40 knockdown in hepatic MDSCs led to increased arginase activity upon Con A treatment and lower ALT/AST serum levels. Finally, blockade of arginase activity in Cd40(-/-) tumor-induced myeloid cells resulted in exacerbation of hepatitis and increased ROS production in vivo. Our findings indicate that in a setting of acute hepatitis, tumor-induced hepatic MDSCs act as proinflammatory immune effector cells capable of killing hepatocytes in a CD40-dependent manner. Published 2015. This article is a U.S. Government work and is in the public domain in the USA. JF - European journal of immunology AU - Kapanadze, Tamar AU - Medina-Echeverz, José AU - Gamrekelashvili, Jaba AU - Weiss, Jonathan M AU - Wiltrout, Robert H AU - Kapoor, Veena AU - Hawk, Nga AU - Terabe, Masaki AU - Berzofsky, Jay A AU - Manns, Michael P AU - Wang, Ena AU - Marincola, Francesco M AU - Korangy, Firouzeh AU - Greten, Tim F AD - Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA; Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 1148 EP - 1158 VL - 45 IS - 4 KW - Antigens, CD11b KW - 0 KW - Antigens, CD1d KW - Antigens, CD40 KW - Antigens, CD80 KW - Antigens, CD86 KW - CD1d antigen, mouse KW - Cd86 protein, mouse KW - Galactosylceramides KW - Gr-1 protein, mouse KW - Mitogens KW - Reactive Oxygen Species KW - Receptors, Chemokine KW - alpha-galactosylceramide KW - Concanavalin A KW - 11028-71-0 KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Arginase KW - EC 3.5.3.1 KW - Index Medicus KW - Immune-mediated hepatitis KW - Reactive oxygen species KW - Myeloid-derived suppressor cells KW - CD40 KW - α-Galactosylceramide KW - Reactive Oxygen Species -- metabolism KW - Animals KW - Galactosylceramides -- pharmacology KW - Liver -- cytology KW - Antigens, CD11b -- metabolism KW - Mice, Inbred BALB C KW - Mice, Knockout KW - Antigens, CD86 -- biosynthesis KW - Hepatocytes -- immunology KW - Arginase -- biosynthesis KW - Arginase -- antagonists & inhibitors KW - Liver Neoplasms -- immunology KW - Mitogens -- pharmacology KW - Antigens, CD1d -- biosynthesis KW - Liver -- injuries KW - Receptors, Chemokine -- metabolism KW - Mice KW - Hepatocytes -- pathology KW - Aspartate Aminotransferases -- blood KW - Alanine Transaminase -- blood KW - Antigens, CD80 -- biosynthesis KW - Adoptive Transfer KW - Arginase -- metabolism KW - Mice, Inbred C57BL KW - Cell Line KW - Concanavalin A -- pharmacology KW - Female KW - Antigens, CD40 -- biosynthesis KW - Hepatitis -- immunology KW - Myeloid Cells -- transplantation KW - Myeloid Cells -- immunology KW - Hepatitis -- genetics KW - Antigens, CD40 -- metabolism KW - Antigens, CD40 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1672610797?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+immunology&rft.atitle=Tumor-induced+CD11b%28%2B%29+Gr-1%28%2B%29+myeloid-derived+suppressor+cells+exacerbate+immune-mediated+hepatitis+in+mice+in+a+CD40-dependent+manner.&rft.au=Kapanadze%2C+Tamar%3BMedina-Echeverz%2C+Jos%C3%A9%3BGamrekelashvili%2C+Jaba%3BWeiss%2C+Jonathan+M%3BWiltrout%2C+Robert+H%3BKapoor%2C+Veena%3BHawk%2C+Nga%3BTerabe%2C+Masaki%3BBerzofsky%2C+Jay+A%3BManns%2C+Michael+P%3BWang%2C+Ena%3BMarincola%2C+Francesco+M%3BKorangy%2C+Firouzeh%3BGreten%2C+Tim+F&rft.aulast=Kapanadze&rft.aufirst=Tamar&rft.date=2015-04-01&rft.volume=45&rft.issue=4&rft.spage=1148&rft.isbn=&rft.btitle=&rft.title=European+journal+of+immunology&rft.issn=1521-4141&rft_id=info:doi/10.1002%2Feji.201445093 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-18 N1 - Date created - 2015-04-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Immunol. 2008 Dec;129(3):471-81 [18790673] J Clin Invest. 2008 Dec;118(12):4036-48 [19033672] J Immunol. 2009 May 1;182(9):5693-701 [19380816] Cancer Res. 2009 Jul 1;69(13):5514-21 [19549903] Immunology. 2009 Sep;128(1):141-9 [19689743] Proc Natl Acad Sci U S A. 2009 Nov 17;106(46):19455-60 [19892741] Cancer Res. 2010 Jan 1;70(1):99-108 [19996287] Methods Mol Biol. 2010;594:57-72 [20072909] J Leukoc Biol. 2010 Apr;87(4):713-25 [20042467] Cancer Res. 2010 Apr 15;70(8):3052-61 [20388795] Gastroenterology. 2002 Jun;122(7):2049-63 [12055609] Circulation. 2002 Aug 20;106(8):981-6 [12186804] J Immunol. 2004 Jan 1;172(1):45-53 [14688308] Cancer Res. 2004 Sep 1;64(17):6337-43 [15342423] Hepatology. 2004 Nov;40(5):1190-6 [15486936] J Clin Invest. 1992 Jul;90(1):196-203 [1634608] J Exp Med. 1993 Aug 1;178(2):669-74 [7688031] J Exp Med. 1994 May 1;179(5):1529-37 [8163936] Hepatology. 1995 Jan;21(1):190-8 [7806154] Gastroenterology. 1996 Aug;111(2):462-71 [8690213] Cell. 2005 Mar 11;120(5):649-61 [15766528] J Immunol. 2005 Aug 1;175(3):1540-50 [16034092] Cancer Res. 2006 Jul 1;66(13):6807-15 [16818658] J Immunol. 2008 Oct 15;181(8):5791-802 [18832739] Gastroenterology. 2008 Sep;135(3):871-81, 881.e1-5 [18674538] Cancer Res. 2007 Jan 1;67(1):425; author reply 426 [17210725] Dig Dis. 2010;28(1):86-92 [20460895] J Immunol. 2010 Jul 1;185(1):203-10 [20525890] Eur J Immunol. 2010 Nov;40(11):2969-75 [21061430] Blood. 2010 Dec 16;116(25):5738-47 [20807889] PLoS One. 2011;6(4):e18281 [21483776] Int Immunopharmacol. 2011 Jul;11(7):816-26 [21376153] Free Radic Biol Med. 2012 Jan 1;52(1):59-69 [22064361] J Leukoc Biol. 2012 Jan;91(1):167-81 [21954284] World J Gastroenterol. 2012 Jan 14;18(2):119-25 [22253517] Nat Rev Immunol. 2012 Apr;12(4):253-68 [22437938] Semin Cancer Biol. 2012 Aug;22(4):282-8 [22313876] Clin Cancer Res. 2012 Sep 15;18(18):4877-82 [22718858] Immunol Invest. 2012;41(6-7):581-94 [23017136] Cell Rep. 2012 Sep 27;2(3):628-39 [22959433] Gut. 2012 Dec;61(12):1733-43 [22267597] J Leukoc Biol. 2012 Dec;92(6):1199-206 [23077247] Hepatology. 2007 Feb;45(2):475-85 [17256743] J Exp Med. 2007 Jun 11;204(6):1463-74 [17548519] J Immunol. 2008 Feb 1;180(3):1471-81 [18209042] Gastroenterology. 2008 Jul;135(1):234-43 [18485901] Immunity. 2013 Mar 21;38(3):541-54 [23477736] Cancer Res. 2013 Apr 15;73(8):2435-44 [23423978] Nat Rev Immunol. 2013 May;13(5):349-61 [23618831] Nat Rev Cancer. 2013 Oct;13(10):739-52 [24060865] Hepatology. 2013 Oct;58(4):1436-50 [23564603] J Hepatol. 2013 Nov;59(5):1007-13 [23796475] J Immunol. 2014 Apr 1;192(7):3068-79 [24567529] Protein Cell. 2014 Sep;5(9):714-24 [24981055] Hepatology. 2014 Dec;60(6):2109-17 [24913836] J Immunol. 2009 Feb 15;182(4):1818-28 [19201833] Eur J Immunol. 2000 Jul;30(7):1919-28 [10940881] J Exp Med. 2000 Oct 2;192(7):921-30 [11015434] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/eji.201445093 ER - TY - JOUR T1 - Sensitization of cisplatin therapy by a naphthalimide based organoselenium compound through modulation of antioxidant enzymes and p53 mediated apoptosis. AN - 1672610178; 25730340 AB - The widely used anti-cancer drug cisplatin imparts various toxic manifestations in the host, with nephrotoxicity being the most severe one. The trace element selenium shows antioxidant activity in both human and animals. The present study was designed to assess the chemoprotecting and chemoenhancing efficacy of a naphthalimide based organoselenium compound 2-(5-selenocyanato-pentyl)-benzo[de]isoquinoline 1,3-dione during cisplatin chemotherapy in mice bearing Ehrlich ascites carcinoma cells. Cisplatin (5 mg/kg b.w.) was administered intraperitoneally and the organoselenium compound (3 mg/kg b.w.) was given by oral gavage in concomitant and pretreatment schedule. The effects of the test compound was evaluated by assaying biochemical, hematological, histological, genotoxicity parameters and by investigating induction of apoptosis in tumor cells, and calculating tumor growth response in the host. The organoselenium compound significantly prevented cisplatin induced generation of reactive oxygen species (ROS), reactive nitrogen species, and onset of lipid peroxidation in the kidney tissue of the experimental mice. In addition, the test compound was also substantially restored cisplatin induced depleted activities of the renal antioxidant enzymes and reduced glutathione level; prevented the serum blood urea nitrogen level, creatinine level, chromosomal aberration, DNA damage, histological alterations of kidney, and normalized the hematological profile of the tumor bearing mice. Furthermore, the organoselenium compound alone or during combination therapy induced apoptosis in tumor cells through mitochondria mediated and DNA damage mediated pathway and ultimately increased the life span of the tumor bearing host. Hence, the results showed that the test compound not only reduced the toxicity of cisplatin but also enhanced its anti-tumor efficacy. JF - Free radical research AU - Ghosh, P AU - Singha Roy, S AU - Basu, A AU - Bhattacharjee, A AU - Bhattacharya, S AD - Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute , Kolkata, West Bengal , India. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 453 EP - 471 VL - 49 IS - 4 KW - 2-(5-selenocyanatopentyl)benzo(de)isoquinoline-1,3-dione KW - 0 KW - Anticarcinogenic Agents KW - Antioxidants KW - Naphthalimides KW - Organoselenium Compounds KW - Tumor Suppressor Protein p53 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - anti-cancer drug KW - selenium KW - apoptosis KW - antioxidant KW - oxidative stress KW - Animals KW - Carcinoma, Ehrlich Tumor -- enzymology KW - Kidney -- metabolism KW - Anticarcinogenic Agents -- therapeutic use KW - Carcinoma, Ehrlich Tumor -- drug therapy KW - Kidney -- drug effects KW - Mice KW - Tumor Suppressor Protein p53 -- metabolism KW - DNA Damage -- drug effects KW - Chromosome Aberrations -- drug effects KW - Carcinoma, Ehrlich Tumor -- metabolism KW - Apoptosis -- drug effects KW - Female KW - Cisplatin -- therapeutic use KW - Organoselenium Compounds -- therapeutic use KW - Cisplatin -- toxicity KW - Antioxidants -- therapeutic use KW - Oxidative Stress -- drug effects KW - Naphthalimides -- therapeutic use KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1672610178?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Free+radical+research&rft.atitle=Sensitization+of+cisplatin+therapy+by+a+naphthalimide+based+organoselenium+compound+through+modulation+of+antioxidant+enzymes+and+p53+mediated+apoptosis.&rft.au=Ghosh%2C+P%3BSingha+Roy%2C+S%3BBasu%2C+A%3BBhattacharjee%2C+A%3BBhattacharya%2C+S&rft.aulast=Ghosh&rft.aufirst=P&rft.date=2015-04-01&rft.volume=49&rft.issue=4&rft.spage=453&rft.isbn=&rft.btitle=&rft.title=Free+radical+research&rft.issn=1029-2470&rft_id=info:doi/10.3109%2F10715762.2015.1012079 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-15 N1 - Date created - 2015-04-10 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3109/10715762.2015.1012079 ER - TY - JOUR T1 - Gefitinib and erlotinib in metastatic non-small cell lung cancer: a meta-analysis of toxicity and efficacy of randomized clinical trials. AN - 1672603246; 25795635 AB - Tyrosine kinase inhibitors (TKIs) targeting the epidermal growth factor receptor (EGFR) have been evaluated in patients with metastatic and advanced non-small cell lung cancer (NSCLC). The U.S. Food and Drug Administration initially granted accelerated approval to gefitinib but subsequently rescinded the authorization. Erlotinib and afatinib are similar compounds approved for the treatment of metastatic NSCLC. The objective of this study was to compare the efficacy and toxicity of erlotinib, gefitinib, and afatinib in NSCLC. We tabulated efficacy variables including overall response rate (ORR), progression-free survival (PFS), and overall survival (OS) and quantitated toxicities and rates of dose reductions and discontinuation. Summary odds ratios were calculated using random and fixed-effects models. An odds ratio was the summary measure used for pooling of studies. We examined 28 studies including three randomized trials with afatinib. Clinical toxicities, including pruritus, rash, anorexia, diarrhea, nausea, fatigue, mucositis, paronychia, and anemia, were similar between erlotinib and gefitinib, although some statistical differences were observed. Afatinib treatment resulted in more diarrhea, rash, and paronychia compared with erlotinib and gefitinib. Regarding efficacy, similar outcomes were recorded for ORR, PFS, or OS in the total population and in specific subgroups of patients between erlotinib and gefitinib. All three TKIs demonstrated higher ORRs in first line in tumors harboring EGFR mutations. Gefitinib has similar activity and toxicity compared with erlotinib and offers a valuable alternative to patients with NSCLC. Afatinib has similar efficacy compared with erlotinib and gefitinib in first-line treatment of tumors harboring EGFR mutations but may be associated with more toxicity, although further studies are needed. Gefitinib deserves consideration for U.S. marketing as a primary treatment for EGFR-mutant NSCLC. ©AlphaMed Press. JF - The oncologist AU - Burotto, Mauricio AU - Manasanch, Elisabet E AU - Wilkerson, Julia AU - Fojo, Tito AD - Medical Oncology and Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; Department of Lymphoma and Myeloma, University of Texas MD Anderson Cancer Center, Houston, Texas, USA mauricio.burottopichun@nih.gov mauricioburotto@yahoo.com. ; Medical Oncology and Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA; Department of Lymphoma and Myeloma, University of Texas MD Anderson Cancer Center, Houston, Texas, USA. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 400 EP - 410 VL - 20 IS - 4 KW - Quinazolines KW - 0 KW - afatinib KW - 41UD74L59M KW - Erlotinib Hydrochloride KW - DA87705X9K KW - gefitinib KW - S65743JHBS KW - Index Medicus KW - Erlotinib KW - Afatinib KW - Tyrosine kinase inhibitors KW - Gefitinib KW - Lung cancer KW - Quinazolines -- administration & dosage KW - Erlotinib Hydrochloride -- administration & dosage KW - Randomized Controlled Trials as Topic KW - Disease-Free Survival KW - Humans KW - Treatment Outcome KW - Publication Bias KW - Erlotinib Hydrochloride -- adverse effects KW - Quinazolines -- adverse effects KW - Carcinoma, Non-Small-Cell Lung -- mortality KW - Lung Neoplasms -- drug therapy KW - Lung Neoplasms -- mortality KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Carcinoma, Non-Small-Cell Lung -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1672603246?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+oncologist&rft.atitle=Gefitinib+and+erlotinib+in+metastatic+non-small+cell+lung+cancer%3A+a+meta-analysis+of+toxicity+and+efficacy+of+randomized+clinical+trials.&rft.au=Burotto%2C+Mauricio%3BManasanch%2C+Elisabet+E%3BWilkerson%2C+Julia%3BFojo%2C+Tito&rft.aulast=Burotto&rft.aufirst=Mauricio&rft.date=2015-04-01&rft.volume=20&rft.issue=4&rft.spage=400&rft.isbn=&rft.btitle=&rft.title=The+oncologist&rft.issn=1549-490X&rft_id=info:doi/10.1634%2Ftheoncologist.2014-0154 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-25 N1 - Date created - 2015-04-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: N Engl J Med. 2004 May 20;350(21):2129-39 [15118073] Science. 2004 Jun 4;304(5676):1497-500 [15118125] Clin Ther. 2004 Oct;26(10):1630-6 [15598479] N Engl J Med. 2005 Jul 14;353(2):123-32 [16014882] Lancet. 2005 Oct 29-Nov 4;366(9496):1527-37 [16257339] Clin Cancer Res. 2007 Jun 15;13(12):3731-7 [17575239] Anticancer Drugs. 2008 Feb;19(2):209-16 [18176118] J Clin Oncol. 2008 May 20;26(15):2450-6 [18378568] J Clin Oncol. 2008 Sep 10;26(26):4253-60 [18779612] Lancet. 2008 Nov 22;372(9652):1809-18 [19027483] J Clin Oncol. 2009 May 1;27(13):2253-60 [19289623] N Engl J Med. 2009 Sep 3;361(10):947-57 [19692680] J Thorac Oncol. 2010 Feb;5(2):179-84 [20101144] J Clin Oncol. 2010 Feb 10;28(5):753-60 [20038730] Lancet Oncol. 2010 Feb;11(2):121-8 [20022809] Lancet Oncol. 2014 Feb;15(2):213-22 [24439929] N Engl J Med. 2014 Mar 27;370(13):1189-97 [24670165] Lancet Oncol. 2015 Feb;16(2):141-51 [25589191] J Clin Oncol. 2003 Jun 15;21(12):2237-46 [12748244] Clin Cancer Res. 2004 Feb 15;10(4):1212-8 [14977817] J Clin Oncol. 2004 Mar 1;22(5):777-84 [14990632] Clin Cancer Res. 2010 Feb 15;16(4):1307-14 [20145166] J Cell Mol Med. 2010 Jan;14(1-2):51-69 [20015198] Lancet Oncol. 2010 Jun;11(6):521-9 [20493771] N Engl J Med. 2010 Jun 24;362(25):2380-8 [20573926] N Engl J Med. 2010 Oct 28;363(18):1693-703 [20979469] Lung Cancer. 2010 Dec;70(3):301-7 [20400201] J Thorac Oncol. 2011 Jan;6(1):148-55 [21107294] N Engl J Med. 2011 Mar 10;364(10):947-55 [21388312] Drug Resist Updat. 2011 Jun;14(3):177-90 [21435938] Lancet Oncol. 2011 Aug;12(8):735-42 [21783417] J Thorac Oncol. 2011 Sep;6(9):1569-77 [21716146] Eur J Cancer. 2011 Oct;47(15):2331-40 [21802939] Br J Cancer. 2011 Oct 11;105(8):1123-30 [21934690] Lancet. 2011 Nov 12;378(9804):1727-40 [21565398] Anticancer Drugs. 2006 Apr;17(4):401-9 [16549997] Curr Med Res Opin. 2006 Mar;22(3):561-73 [16574039] Cancer Cell. 2007 Mar;11(3):217-27 [17349580] J Biomed Biotechnol. 2011;2011:415641 [22219656] J Thorac Oncol. 2012 Feb;7(2):412-8 [22157367] Clin Lung Cancer. 2012 Mar;13(2):107-14 [22056888] Lancet Oncol. 2012 Mar;13(3):300-8 [22277837] Lancet Oncol. 2012 Mar;13(3):239-46 [22285168] Lancet Oncol. 2012 May;13(5):442-3 [22452893] Lancet Oncol. 2012 May;13(5):528-38 [22452896] Lancet Oncol. 2012 May;13(5):466-75 [22512843] J Thorac Oncol. 2012 Jun;7(6):1041-8 [22534814] Lung Cancer. 2012 Jul;77(1):97-103 [22405570] Lung Cancer. 2012 Aug;77(2):346-52 [22534669] J Clin Oncol. 2012 Aug 20;30(24):3002-11 [22778317] J Clin Oncol. 2012 Oct 1;30(28):3516-24 [22949150] Cancer. 2012 Dec 15;118(24):6234-42 [22674612] Eur J Cancer. 2013 Jan;49(1):106-14 [22897841] Ann Oncol. 2013 Mar;24(3):577-85 [23131389] J Clin Oncol. 2013 Mar 10;31(8):1039-49 [23401433] PLoS One. 2013;8(3):e59314 [23555654] J Natl Cancer Inst. 2013 May 1;105(9):595-605 [23594426] N Engl J Med. 2013 Jun 20;368(25):2385-94 [23724913] Lung Cancer. 2013 Aug;81(2):155-61 [23664448] Lancet Oncol. 2013 Sep;14(10):981-8 [23883922] J Clin Oncol. 2013 Sep 20;31(27):3327-34 [23816960] J Clin Oncol. 2013 Sep 20;31(27):3335-41 [23816963] J Clin Oncol. 2013 Sep 20;31(27):3303-6 [23980079] CA Cancer J Clin. 2014 Jan-Feb;64(1):9-29 [24399786] Crit Rev Oncol Hematol. 2014 Feb;89(2):300-13 [24041630] Comment In: Oncologist. 2015 Apr;20(4):335-6 [25795633] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1634/theoncologist.2014-0154 ER - TY - JOUR T1 - Estimating burden and disease costs of exposure to endocrine-disrupting chemicals in the European union. AN - 1671216970; 25742516 AB - Rapidly increasing evidence has documented that endocrine-disrupting chemicals (EDCs) contribute substantially to disease and disability. The objective was to quantify a range of health and economic costs that can be reasonably attributed to EDC exposures in the European Union (EU). A Steering Committee of scientists adapted the Intergovernmental Panel on Climate Change weight-of-evidence characterization for probability of causation based upon levels of available epidemiological and toxicological evidence for one or more chemicals contributing to disease by an endocrine disruptor mechanism. To evaluate the epidemiological evidence, the Steering Committee adapted the World Health Organization Grading of Recommendations Assessment, Development and Evaluation (GRADE) Working Group criteria, whereas the Steering Committee adapted definitions recently promulgated by the Danish Environmental Protection Agency for evaluating laboratory and animal evidence of endocrine disruption. Expert panels used the Delphi method to make decisions on the strength of the data. Expert panels achieved consensus at least for probable (>20%) EDC causation for IQ loss and associated intellectual disability, autism, attention-deficit hyperactivity disorder, childhood obesity, adult obesity, adult diabetes, cryptorchidism, male infertility, and mortality associated with reduced testosterone. Accounting for probability of causation and using the midpoint of each range for probability of causation, Monte Carlo simulations produced a median cost of €157 billion (or $209 billion, corresponding to 1.23% of EU gross domestic product) annually across 1000 simulations. Notably, using the lowest end of the probability range for each relationship in the Monte Carlo simulations produced a median range of €109 billion that differed modestly from base case probability inputs. EDC exposures in the EU are likely to contribute substantially to disease and dysfunction across the life course with costs in the hundreds of billions of Euros per year. These estimates represent only those EDCs with the highest probability of causation; a broader analysis would have produced greater estimates of burden of disease and costs. JF - The Journal of clinical endocrinology and metabolism AU - Trasande, Leonardo AU - Zoeller, R Thomas AU - Hass, Ulla AU - Kortenkamp, Andreas AU - Grandjean, Philippe AU - Myers, John Peterson AU - DiGangi, Joseph AU - Bellanger, Martine AU - Hauser, Russ AU - Legler, Juliette AU - Skakkebaek, Niels E AU - Heindel, Jerrold J AD - New York University (NYU) School of Medicine (L.T.), New York, New York 10016; NYU Wagner School of Public Service (L.T.), New York, New York 10012; NYU Steinhardt School of Culture, Education, and Human Development (L.T.), Department of Nutrition, Food & Public Health, New York, New York 10003; NYU Global Institute of Public Health (L.T.), New York, New York 10003; University of Massachusetts (R.T.Z.), Amherst, Massachusetts 01003; National Food Institute (U.H.), Technical University of Denmark, 19 2860 Søborg, Denmark; Brunel University (A.K., R.H.), Institute of Environment, Health and Societies, Uxbridge, Middlesex UB8 3PH, United Kingdom; Department of Environmental Health (P.G.), Harvard T.H. Chan School of Public Health, Boston, Massachusetts 02115; University of Southern Denmark (P.G.), 5000 Odense, Denmark; Environmental Health Sciences (J.P.M.), Charlottesville, Virginia 22902; IPEN (J.D.), SE-402 35 Gothenburg, Sweden; EHESP School of Public Health (M.B.), 75014 Paris, France; Department of Chemistry and Biology (J.L.), Institute for Environmental Studies, VU University, 1081 HV Amsterdam, The Netherlands; Department of Growth and Reproduction (N.E.S.), Rigshospitalet, Endocrine Disruption of Male Reproduction and Child Health (EDMaRC) and University of Copenhagen, DK-2100 Copenhagen, Denmark; and National Institute of Environmental Health Sciences (J.J.H.), Division of Extramural Research and Training, Research Triangle Park, North Carolina 27709. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 1245 EP - 1255 VL - 100 IS - 4 KW - Endocrine Disruptors KW - 0 KW - Environmental Pollutants KW - Abridged Index Medicus KW - Index Medicus KW - Attention Deficit Disorder with Hyperactivity -- economics KW - Autistic Disorder -- economics KW - Environmental Pollutants -- toxicity KW - Humans KW - Aged KW - Child KW - Autistic Disorder -- epidemiology KW - Attention Deficit Disorder with Hyperactivity -- epidemiology KW - Autistic Disorder -- chemically induced KW - Adult KW - Middle Aged KW - Attention Deficit Disorder with Hyperactivity -- chemically induced KW - Male KW - Female KW - Endocrine Disruptors -- toxicity KW - European Union -- economics KW - Endocrine System Diseases -- economics KW - Cost of Illness KW - Environmental Exposure -- statistics & numerical data KW - Environmental Exposure -- economics KW - European Union -- statistics & numerical data KW - Endocrine System Diseases -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1671216970?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+endocrinology+and+metabolism&rft.atitle=Estimating+burden+and+disease+costs+of+exposure+to+endocrine-disrupting+chemicals+in+the+European+union.&rft.au=Trasande%2C+Leonardo%3BZoeller%2C+R+Thomas%3BHass%2C+Ulla%3BKortenkamp%2C+Andreas%3BGrandjean%2C+Philippe%3BMyers%2C+John+Peterson%3BDiGangi%2C+Joseph%3BBellanger%2C+Martine%3BHauser%2C+Russ%3BLegler%2C+Juliette%3BSkakkebaek%2C+Niels+E%3BHeindel%2C+Jerrold+J&rft.aulast=Trasande&rft.aufirst=Leonardo&rft.date=2015-04-01&rft.volume=100&rft.issue=4&rft.spage=1245&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+endocrinology+and+metabolism&rft.issn=1945-7197&rft_id=info:doi/10.1210%2Fjc.2014-4324 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-06 N1 - Date created - 2015-04-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nature. 1999 Oct 21;401(6755):763-4 [10548101] J Clin Endocrinol Metab. 2015 Apr;100(4):1278-88 [25742518] J Allergy Clin Immunol. 2000 Sep;106(3):493-9 [10984369] Toxicol Sci. 2001 May;61(1):76-82 [11294977] J Epidemiol Community Health. 2001 Jul;55(7):508-14 [11413183] Am J Epidemiol. 2002 Feb 15;155(4):313-22 [11836195] Mol Cell Endocrinol. 2002 Jun 28;192(1-2):157-70 [12088877] Occup Environ Med. 2002 Oct;59(10):651-2 [12356922] Pediatrics. 2003 Jun;111(6 Pt 1):1467-74 [12777573] Environ Health Perspect. 2004 Jun;112(9):944-9 [15198913] BMJ. 2004 Jun 19;328(7454):1490 [15205295] Ann N Y Acad Sci. 1981;363:189-204 [6942722] Milbank Mem Fund Q Health Soc. 1982 Summer;60(3):429-62 [6923138] Am J Public Health. 1986 Apr;76(4):392-6 [3082226] Milbank Q. 1986;64(4):489-547 [3102916] Med Care. 1992 Nov;30(11 Suppl):NS1-12 [1434963] JAMA. 1996 Oct 16;276(15):1253-8 [8849754] Health Econ. 1996 Sep-Oct;5(5):447-67 [8922972] Epidemiology. 1999 Sep;10(5):573-84 [10468437] Proc R Soc Med. 1965 May;58:295-300 [14283879] Endocrinology. 2005 Feb;146(2):607-12 [15498886] BMC Health Serv Res. 2004 Dec 22;4(1):38 [15615589] Toxicology. 2005 Jun 1;210(2-3):223-33 [15840436] Semin Reprod Med. 2006 Jul;24(3):156-67 [16804814] J Natl Cancer Inst. 2006 Nov 15;98(22):1623-33 [17105985] Ann N Y Acad Sci. 2006 Sep;1076:911-23 [17119266] Environ Health Perspect. 2007 Oct;115(10):1406-14 [17938728] BMJ. 2008 May 17;336(7653):1106-10 [18483053] Birth Defects Res B Dev Reprod Toxicol. 2008 Jun;83(3):157-395 [18613034] Econ Hum Biol. 2008 Jul;6(2):281-92 [18619930] Environ Health Perspect. 2008 Oct;116(10):1376-82 [18941581] J Expo Sci Environ Epidemiol. 2009 Feb;19(2):223-34 [18665197] Mol Cell Endocrinol. 2009 May 25;304(1-2):43-8 [19433246] Mol Cell Endocrinol. 2009 May 25;304(1-2):63-8 [19433249] BMC Health Serv Res. 2010;10:97 [20403173] Environ Health Perspect. 2010 Oct;118(10):1444-9 [20562054] Mt Sinai J Med. 2011 Jan-Feb;78(1):98-106 [21259266] Health Aff (Millwood). 2011 May;30(5):863-70 [21543421] Med Care. 2011 Aug;49(8):679-85 [21478780] Environ Res. 2011 Aug;111(6):825-30 [21676388] Eur Neuropsychopharmacol. 2011 Oct;21(10):718-79 [21924589] Health Aff (Millwood). 2011 Dec;30(12):2400-9 [22147869] Endocrinology. 2012 Sep;153(9):4097-110 [22733974] JAMA. 2012 Sep 19;308(11):1113-21 [22990270] Environ Res. 2013 May;123:17-24 [23473920] Toxicol Lett. 2013 Dec 16;223(3):295-305 [24177261] Obesity (Silver Spring). 2014 Feb;22(2):488-96 [23963708] Environ Int. 2015 Jan;74:144-51 [25454231] J Clin Endocrinol Metab. 2015 Apr;100(4):1256-66 [25742515] J Clin Endocrinol Metab. 2015 Apr;100(4):1267-77 [25742517] Med Decis Making. 2000 Jul-Sep;20(3):332-42 [10929856] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1210/jc.2014-4324 ER - TY - JOUR T1 - Male reproductive disorders, diseases, and costs of exposure to endocrine-disrupting chemicals in the European Union. AN - 1671214491; 25742517 AB - Increasing evidence suggests that endocrine-disrupting chemicals (EDCs) contribute to male reproductive diseases and disorders. To estimate the incidence/prevalence of selected male reproductive disorders/diseases and associated economic costs that can be reasonably attributed to specific EDC exposures in the European Union (EU). An expert panel evaluated evidence for probability of causation using the Intergovernmental Panel on Climate Change weight-of-evidence characterization. Exposure-response relationships and reference levels were evaluated, and biomarker data were organized from carefully identified studies from the peer-reviewed literature to represent European exposure and approximate burden of disease as it occurred in 2010. The cost-of-illness estimation utilized multiple peer-reviewed sources. The expert panel identified low epidemiological and strong toxicological evidence for male infertility attributable to phthalate exposure, with a 40-69% probability of causing 618,000 additional assisted reproductive technology procedures, costing €4.71 billion annually. Low epidemiological and strong toxicological evidence was also identified for cryptorchidism due to prenatal polybrominated diphenyl ether exposure, resulting in a 40-69% probability that 4615 cases result, at a cost of €130 million (sensitivity analysis, €117-130 million). A much more modest (0-19%) probability of causation in testicular cancer by polybrominated diphenyl ethers was identified due to very low epidemiological and weak toxicological evidence, with 6830 potential cases annually and costs of €848 million annually (sensitivity analysis, €313-848 million). The panel assigned 40-69% probability of lower T concentrations in 55- to 64-year-old men due to phthalate exposure, with 24 800 associated deaths annually and lost economic productivity of €7.96 billion. EDCs may contribute substantially to male reproductive disorders and diseases, with nearly €15 billion annual associated costs in the EU. These estimates represent only a few EDCs for which there were sufficient epidemiological studies and those with the highest probability of causation. These public health costs should be considered as the EU contemplates regulatory action on EDCs. JF - The Journal of clinical endocrinology and metabolism AU - Hauser, Russ AU - Skakkebaek, Niels E AU - Hass, Ulla AU - Toppari, Jorma AU - Juul, Anders AU - Andersson, Anna Maria AU - Kortenkamp, Andreas AU - Heindel, Jerrold J AU - Trasande, Leonardo AD - Department of Environmental Health (R.H.), Harvard T.H. Chan School of Public Health, Boston, Massachusetts 02115; Department of Growth and Reproduction (N.E.S., A.J., A.M.A.), Rigshospitalet, EDMaRC and University of Copenhagen, DK-2100 Copenhagen, Denmark; National Food Institute (U.H.), Technical University of Denmark, 2800 Kgs Søborg, Denmark; Departments of Physiology and Pediatrics (J.T.), University of Turku, 20014 Turku, Finland; Brunel University (A.K.), London UB8 3PH, United Kingdom; National Institute of Environmental Health Sciences (J.J.H.), Division of Extramural Research and Training, Research Triangle Park, North Carolina 27709; New York University (NYU) School of Medicine (L.T.), New York, New York 10016; NYU Wagner School of Public Service (L.T.), New York, New York 10012; NYU Steinhardt School of Culture, Education, and Human Development (L.T.), Department of Nutrition, Food, and Public Health, New York, New York 10003; and NYU Global Institute of Public Health (L.T.), New York, New York 10003. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 1267 EP - 1277 VL - 100 IS - 4 KW - Endocrine Disruptors KW - 0 KW - Water Pollutants, Chemical KW - Abridged Index Medicus KW - Index Medicus KW - Environmental Exposure -- statistics & numerical data KW - Water Pollutants, Chemical -- toxicity KW - Humans KW - Environmental Exposure -- economics KW - Cryptorchidism -- economics KW - Eunuchism -- epidemiology KW - Testicular Neoplasms -- chemically induced KW - Cryptorchidism -- epidemiology KW - Cryptorchidism -- chemically induced KW - Testicular Neoplasms -- economics KW - Neoplasms, Germ Cell and Embryonal -- epidemiology KW - Climate Change KW - Eunuchism -- economics KW - Adult KW - Neoplasms, Germ Cell and Embryonal -- economics KW - Neoplasms, Germ Cell and Embryonal -- chemically induced KW - Eunuchism -- chemically induced KW - Testicular Neoplasms -- epidemiology KW - Male KW - Endocrine Disruptors -- toxicity KW - European Union -- economics KW - Cost of Illness KW - Infertility, Male -- economics KW - Infertility, Male -- chemically induced KW - Infertility, Male -- epidemiology KW - European Union -- statistics & numerical data UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1671214491?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+endocrinology+and+metabolism&rft.atitle=Male+reproductive+disorders%2C+diseases%2C+and+costs+of+exposure+to+endocrine-disrupting+chemicals+in+the+European+Union.&rft.au=Hauser%2C+Russ%3BSkakkebaek%2C+Niels+E%3BHass%2C+Ulla%3BToppari%2C+Jorma%3BJuul%2C+Anders%3BAndersson%2C+Anna+Maria%3BKortenkamp%2C+Andreas%3BHeindel%2C+Jerrold+J%3BTrasande%2C+Leonardo&rft.aulast=Hauser&rft.aufirst=Russ&rft.date=2015-04-01&rft.volume=100&rft.issue=4&rft.spage=1267&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+endocrinology+and+metabolism&rft.issn=1945-7197&rft_id=info:doi/10.1210%2Fjc.2014-4325 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-08-06 N1 - Date created - 2015-04-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Toxicol Appl Pharmacol. 2005 Aug 22;207(1):78-88 [16005038] Environ Health Perspect. 2005 Aug;113(8):1056-61 [16079079] J Clin Oncol. 2005 Aug 20;23(24):5757-61 [16110032] Int J Androl. 2006 Feb;29(1):96-104; discussion 105-8 [16466529] Int J Androl. 2006 Feb;29(1):228-34 [16371110] Hum Reprod Update. 2006 May-Jun;12(3):303-23 [16540528] Epidemiology. 2006 Nov;17(6):682-91 [17003688] Environ Health Perspect. 2006 Nov;114(11):1643-8 [17107847] J Clin Endocrinol Metab. 2007 Jan;92(1):196-202 [17062768] Hum Reprod. 2007 Jun;22(6):1506-12 [17376819] Environ Health Perspect. 2007 Oct;115(10):1519-26 [17938745] J Clin Endocrinol Metab. 2007 Dec;92(12):4696-705 [17895324] Hum Reprod Update. 2008 Jan-Feb;14(1):49-58 [18032558] Environ Health Perspect. 2007 Dec;115 Suppl 1:122-8 [18174960] Reprod Biomed Online. 2008 Feb;16(2):289-303 [18284889] Environ Sci Technol. 2008 Feb 15;42(4):1377-84 [18351120] J Clin Invest. 2008 Apr;118(4):1479-90 [18340380] BMJ. 2008 May 17;336(7653):1106-10 [18483053] Syst Biol Reprod Med. 2008 May-Jun;54(3):143-54 [18570050] J Clin Endocrinol Metab. 2008 Jul;93(7):2737-45 [18270261] J Androl. 2009 May-Jun;30(3):287-97 [19059903] Cancer Res. 2009 Jun 15;69(12):5241-50 [19491264] Nat Genet. 2009 Jul;41(7):811-5 [19483682] Arch Dis Child. 2009 Nov;94(11):868-72 [19542061] Future Oncol. 2009 Nov;5(9):1389-402 [19903067] Toxicol Sci. 2010 Jul;116(1):297-312 [20375078] N Engl J Med. 2010 Jul 8;363(2):109-22 [20592293] Birth Defects Res A Clin Mol Teratol. 2010 Oct;88(10):910-9 [20865786] Environ Health. 2011;10:9 [21255392] Environ Health Perspect. 2011 Jul;119(7):958-63 [21377950] Int J Androl. 2011 Aug;34(4):369-78 [20633195] Int J Androl. 2011 Oct;34(5 Pt 2):e397-406 [21790659] J Clin Endocrinol Metab. 2011 Oct;96(10):3007-19 [21816776] J Urol. 2012 Feb;187(2):594-8 [22177168] Mol Cell Endocrinol. 2012 May 22;355(2):208-20 [22127307] Hum Reprod. 2012 May;27(5):1451-9 [22402212] Int J Androl. 2012 Jun;35(3):303-16 [22372636] Eur J Endocrinol. 2012 Jun;166(6):983-91 [22423144] J Androl. 2012 May-Jun;33(3):488-98 [21597090] Chemosphere. 2012 Nov;89(8):911-8 [22868196] Environ Health Perspect. 2012 Oct;120(10):1397-403 [22832070] Eur J Endocrinol. 2013 Feb;168(2):227-33 [23161753] Sci Total Environ. 2013 Feb 15;445-446:299-305 [23340023] Eur J Endocrinol. 2013 Apr;168(4):R67-76 [23504510] Environ Health Perspect. 2013 Apr;121(4):A104-6 [23548368] J Clin Endocrinol Metab. 2013 Jun;98(6):2223-9 [23589523] Andrology. 2013 Sep;1(5):741-8 [23843214] JAMA. 2013 Nov 6;310(17):1829-36 [24193080] Nat Rev Endocrinol. 2013 Dec;9(12):699-712 [24042328] Reprod Toxicol. 2013 Dec;42:232-41 [24140385] Int J Hyg Environ Health. 2014 Mar;217(2-3):271-8 [23906849] Hum Reprod Update. 2014 Mar-Apr;20(2):231-49 [24077978] Eur J Cancer. 2014 Mar;50(4):831-9 [24369860] Environ Health Perspect. 2014 Mar;122(3):235-41 [24425099] Reproduction. 2014;147(4):R119-29 [24497529] Environ Int. 2014 May;66:146-56 [24583187] Fertil Steril. 2014 May;101(5):1359-66 [24534276] Toxicol Appl Pharmacol. 2014 Aug 1;278(3):201-8 [24055644] Nat Rev Endocrinol. 2014 Sep;10(9):553-62 [24935122] J Clin Endocrinol Metab. 2014 Nov;99(11):4346-52 [25121464] Environ Health Perspect. 2015 Jan;123(1):101-7 [25353625] J Clin Endocrinol Metab. 2015 Apr;100(4):1245-55 [25742516] J Clin Endocrinol Metab. 2015 Apr;100(4):1278-88 [25742518] Environ Res. 2015 Aug;141:77-85 [25440295] Hum Reprod. 2001 May;16(5):972-8 [11331648] N Engl J Med. 2001 Nov 8;345(19):1388-93 [11794171] Hum Reprod. 2002 Feb;17(2):503-15 [11821304] Int J Cancer. 2002 May 10;99(2):218-28 [11979437] Hum Reprod. 2003 Jul;18(7):1383-94 [12832361] Hum Reprod. 2003 Sep;18(9):1959-66 [12923157] BMJ. 2004 Jun 19;328(7454):1490 [15205295] Acta Pathol Microbiol Scand. 1968;72(2):348-9 [5661531] N Engl J Med. 1997 Jul 10;337(2):91-5 [9211678] Lancet. 1998 Oct 10;352(9135):1172-7 [9777833] JAMA. 1998 Nov 18;280(19):1690-1 [9832001] Toxicol Appl Pharmacol. 1999 Apr 15;156(2):81-95 [10198273] Environ Health Perspect. 1999 May;107(5):397-405 [10210696] Ugeskr Laeger. 2004 Nov 22;166(48):4372-5 [15587631] Hum Reprod. 2005 Mar;20(3):604-10 [15591081] Int J Cancer. 2005 Jul 10;115(5):822-7 [15704170] Epidemiology. 2005 Jul;16(4):487-93 [15951666] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1210/jc.2014-4325 ER - TY - JOUR T1 - Global analysis of posttranscriptional gene expression in response to sodium arsenite. AN - 1669841604; 25493608 AB - Inorganic arsenic species are potent environmental toxins and causes of numerous health problems. Most studies have assumed that arsenic-induced changes in mRNA levels result from effects on gene transcription. We evaluated the prevalence of changes in mRNA stability in response to sodium arsenite in human fibroblasts. We used microarray analyses to determine changes in steady-state mRNA levels and mRNA decay rates following 24-hr exposure to noncytotoxic concentrations of sodium arsenite, and we confirmed some of these changes using real-time reverse-transcription polymerase chain reaction (RT-PCR). In arsenite-exposed cells, 186 probe set-identified transcripts were significantly increased and 167 were significantly decreased. When decay rates were analyzed after actinomycin D treatment, only 4,992 (9.1%) of probe set-identified transcripts decayed by > 25% after 4 hr. Of these, 70 were among the 353 whose steady-state levels were altered by arsenite, and of these, only 4 exhibited significantly different decay rates between arsenite and control treatment. Real-time RT-PCR confirmed a major, significant arsenite-induced stabilization of the mRNA encoding δ aminolevulinate synthase 1 (ALAS1), the rate-limiting enzyme in heme biosynthesis. This change presumably accounted for at least part of the 2.7-fold increase in steady-state ALAS1 mRNA levels seen after arsenite treatment. This could reflect decreases in cellular heme caused by the massive induction by arsenite of heme oxygenase mRNA (HMOX1; 68-fold increase), the rate-limiting enzyme in heme catabolism. We conclude that arsenite modification of mRNA stability is relatively uncommon, but in some instances can result in significant changes in gene expression. JF - Environmental health perspectives AU - Qiu, Lian-Qun AU - Abey, Sarah AU - Harris, Shawn AU - Shah, Ruchir AU - Gerrish, Kevin E AU - Blackshear, Perry J AD - Laboratory of Signal Transduction, National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, North Carolina, USA. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 324 EP - 330 VL - 123 IS - 4 KW - Arsenites KW - 0 KW - Environmental Pollutants KW - RNA, Messenger KW - Sodium Compounds KW - Dactinomycin KW - 1CC1JFE158 KW - sodium arsenite KW - 48OVY2OC72 KW - Heme Oxygenase-1 KW - EC 1.14.14.18 KW - 5-Aminolevulinate Synthetase KW - EC 2.3.1.37 KW - Index Medicus KW - Dactinomycin -- pharmacology KW - Cells, Cultured KW - Humans KW - Male KW - Fibroblasts -- drug effects KW - Environmental Pollutants -- toxicity KW - Heme Oxygenase-1 -- metabolism KW - Arsenites -- toxicity KW - Sodium Compounds -- toxicity KW - 5-Aminolevulinate Synthetase -- metabolism KW - 5-Aminolevulinate Synthetase -- genetics KW - Heme Oxygenase-1 -- genetics KW - Gene Expression Regulation -- drug effects KW - Fibroblasts -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669841604?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Global+analysis+of+posttranscriptional+gene+expression+in+response+to+sodium+arsenite.&rft.au=Qiu%2C+Lian-Qun%3BAbey%2C+Sarah%3BHarris%2C+Shawn%3BShah%2C+Ruchir%3BGerrish%2C+Kevin+E%3BBlackshear%2C+Perry+J&rft.aulast=Qiu&rft.aufirst=Lian-Qun&rft.date=2015-04-01&rft.volume=123&rft.issue=4&rft.spage=324&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1408626 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-27 N1 - Date created - 2015-04-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Toxicol Appl Pharmacol. 2005 Sep 1;207(2 Suppl):557-64 [15996700] Bioinformatics. 2005 Oct 15;21(20):3933-4 [16109745] Cancer Res. 2005 Dec 1;65(23):10977-83 [16322246] Nucleic Acids Res. 2006;34(2):485-95 [16421274] Toxicol Appl Pharmacol. 2006 Nov 1;216(3):407-15 [16876216] Mol Cell Biol. 2006 Dec;26(24):9196-208 [17030620] Biostatistics. 2007 Apr;8(2):414-32 [16928955] Tohoku J Exp Med. 2007 Sep;213(1):1-16 [17785948] J Cell Physiol. 2008 Mar;214(3):796-809 [17849448] Exp Biol Med (Maywood). 2008 Mar;233(3):377-84 [18296743] Toxicol Appl Pharmacol. 2008 Mar 15;227(3):400-16 [18191166] Environ Health Perspect. 2008 Apr;116(4):524-31 [18414638] Cytokine Growth Factor Rev. 2008 Jun-Aug;19(3-4):245-51 [18524667] Toxicol Appl Pharmacol. 2008 Dec 15;233(3):389-403 [18929588] Toxicol In Vitro. 2009 Feb;23(1):148-57 [19000923] BMC Genomics. 2010;11:282 [20444259] Arch Toxicol. 2010 Aug;84(8):585-96 [20502880] J Appl Toxicol. 2011 Mar;31(2):95-107 [21321970] BMC Genomics. 2011;12:173 [21457566] BMC Biol. 2011;9:34 [21627854] J Biol Chem. 2011 Jul 29;286(30):26424-30 [21659532] Toxicol Sci. 2011 Oct;123(2):305-32 [21750349] Biol Pharm Bull. 2011;34(11):1748-52 [22040890] J Immunol. 2012 May 15;188(10):5150-9 [22491258] Toxicol Lett. 2012 Jul 20;212(2):169-79 [22641096] J Biol Chem. 2000 May 19;275(20):15336-42 [10809768] Hepatology. 2001 May;33(5):1217-22 [11343251] Toxicol Sci. 2001 Jun;61(2):314-20 [11353140] Carcinogenesis. 2002 May;23(5):867-76 [12016162] Science. 2002 Jun 21;296(5576):2143-5 [12077387] Toxicol Lett. 2002 Jul 7;133(1):33-45 [12076508] Nucleic Acids Res. 2001 May 1;29(9):e45 [11328886] Environ Health Perspect. 2002 Oct;110 Suppl 5:883-6 [12426152] Carcinogenesis. 2003 Apr;24(4):747-56 [12727804] Toxicol Lett. 2003 Jul 20;143(2):155-62 [12749819] Mol Cell Biochem. 2004 Jan;255(1-2):57-66 [14971646] Toxicol Appl Pharmacol. 2004 Aug 1;198(3):394-404 [15276419] J Cell Biol. 1971 Sep;50(3):746-61 [4398631] Cancer Res. 1973 Nov;33(11):2658-61 [4748426] Cancer Res. 1989 Jul 15;49(14):3776-82 [2736519] Mol Cell Biol. 1990 Sep;10(9):4967-9 [2388632] Folia Med Cracov. 1993;34(1-4):29-47 [8175062] Environ Health Perspect. 1998 Aug;106 Suppl 4:1005-15 [9703486] Methods Mol Biol. 2013;1064:91-100 [23996251] Nat Rev Immunol. 2014 Jun;14(6):361-76 [24854588] RNA Biol. 2014;11(8):1019-30 [25531407] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1289/ehp.1408626 ER - TY - JOUR T1 - Enhanced antitumor activity of 3-bromopyruvate in combination with rapamycin in vivo and in vitro. AN - 1669840175; 25644152 AB - 3-Bromopyruvate (3-BrPA) is an alkylating agent and a well-known inhibitor of energy metabolism. Rapamycin is an inhibitor of the serine/threonine protein kinase mTOR. Both 3-BrPA and rapamycin show chemopreventive efficacy in mouse models of lung cancer. Aerosol delivery of therapeutic drugs for lung cancer has been reported to be an effective route of delivery with little systemic distribution in humans. In this study, 3-BrPA and rapamycin were evaluated in combination for their preventive effects against lung cancer in mice by aerosol treatment, revealing a synergistic ability as measured by tumor multiplicity and tumor load compared treatment with either single-agent alone. No evidence of liver toxicity was detected by monitoring serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) enzymes. To understand the mechanism in vitro experiments were performed using human non-small cell lung cancer (NSCLC) cell lines. 3-BrPA and rapamycin also synergistically inhibited cell proliferation. Rapamycin alone blocked the mTOR signaling pathway, whereas 3-BrPA did not potentiate this effect. Given the known role of 3-BrPA as an inhibitor of glycolysis, we investigated mitochondrial bioenergetics changes in vitro in 3-BrPA-treated NSCLC cells. 3-BrPA significantly decreased glycolytic activity, which may be due to adenosine triphosphate (ATP) depletion and decreased expression of GAPDH. Our results demonstrate that rapamycin enhanced the antitumor efficacy of 3-BrPA, and that dual inhibition of mTOR signaling and glycolysis may be an effective therapeutic strategy for lung cancer chemoprevention. ©2015 American Association for Cancer Research. JF - Cancer prevention research (Philadelphia, Pa.) AU - Zhang, Qi AU - Pan, Jing AU - Lubet, Ronald A AU - Komas, Steven M AU - Kalyanaraman, Balaraman AU - Wang, Yian AU - You, Ming AD - Medical College of Wisconsin Cancer Center, Medical College of Wisconsin, Milwaukee, Wisconsin. Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin. ; Chemoprevention Branch, National Cancer Institute, Bethesda, Maryland. ; Department of Biophysics, Medical College of Wisconsin, Milwaukee, Wisconsin. ; Medical College of Wisconsin Cancer Center, Medical College of Wisconsin, Milwaukee, Wisconsin. Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, Wisconsin. myou@mcw.edu. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 318 EP - 326 VL - 8 IS - 4 KW - Antibiotics, Antineoplastic KW - 0 KW - Enzyme Inhibitors KW - Pyruvates KW - bromopyruvate KW - 63JMV04GRK KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - MTOR protein, human KW - EC 2.7.1.1 KW - TOR Serine-Threonine Kinases KW - Sirolimus KW - W36ZG6FT64 KW - Index Medicus KW - Animals KW - Oxygen Consumption -- drug effects KW - TOR Serine-Threonine Kinases -- antagonists & inhibitors KW - TOR Serine-Threonine Kinases -- metabolism KW - Humans KW - Mice KW - Mice, Inbred A KW - Blotting, Western KW - Glycolysis -- drug effects KW - Tumor Cells, Cultured KW - Antibiotics, Antineoplastic -- pharmacology KW - Energy Metabolism -- drug effects KW - Mitochondria -- drug effects KW - Adenosine Triphosphate -- metabolism KW - Antineoplastic Combined Chemotherapy Protocols KW - Xenograft Model Antitumor Assays KW - Enzyme Inhibitors -- pharmacology KW - Female KW - Cell Proliferation -- drug effects KW - Carcinoma, Non-Small-Cell Lung -- metabolism KW - Pyruvates -- pharmacology KW - Sirolimus -- pharmacology KW - Lung Neoplasms -- drug therapy KW - Apoptosis -- drug effects KW - Carcinoma, Non-Small-Cell Lung -- drug therapy KW - Lung Neoplasms -- pathology KW - Lung Neoplasms -- metabolism KW - Carcinoma, Non-Small-Cell Lung -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669840175?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+prevention+research+%28Philadelphia%2C+Pa.%29&rft.atitle=Enhanced+antitumor+activity+of+3-bromopyruvate+in+combination+with+rapamycin+in+vivo+and+in+vitro.&rft.au=Zhang%2C+Qi%3BPan%2C+Jing%3BLubet%2C+Ronald+A%3BKomas%2C+Steven+M%3BKalyanaraman%2C+Balaraman%3BWang%2C+Yian%3BYou%2C+Ming&rft.aulast=Zhang&rft.aufirst=Qi&rft.date=2015-04-01&rft.volume=8&rft.issue=4&rft.spage=318&rft.isbn=&rft.btitle=&rft.title=Cancer+prevention+research+%28Philadelphia%2C+Pa.%29&rft.issn=1940-6215&rft_id=info:doi/10.1158%2F1940-6207.CAPR-14-0142 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-21 N1 - Date created - 2015-04-02 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1940-6207.CAPR-14-0142 ER - TY - JOUR T1 - How a homolog of high-fidelity replicases conducts mutagenic DNA synthesis. AN - 1669832718; 25775266 AB - All DNA replicases achieve high fidelity by a conserved mechanism, but each translesion polymerase carries out mutagenic DNA synthesis in its own way. Here we report crystal structures of human DNA polymerase ν (Pol ν), which is homologous to high-fidelity replicases yet is error prone. Instead of a simple open-to-closed movement of the O helix upon binding of a correct incoming nucleotide, Pol ν has a different open state and requires the finger domain to swing sideways and undergo both opening and closing motions to accommodate the nascent base pair. A single-amino acid substitution in the O helix of the finger domain improves the fidelity of Pol ν nearly ten-fold. A unique cavity and the flexibility of the thumb domain allow Pol ν to generate and accommodate a looped-out primer strand. Primer loop-out may be a mechanism for DNA trinucloetide-repeat expansion. JF - Nature structural & molecular biology AU - Lee, Young-Sam AU - Gao, Yang AU - Yang, Wei AD - Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 298 EP - 303 VL - 22 IS - 4 KW - DNA KW - 9007-49-2 KW - DNA polymerase N, human KW - EC 2.7.7.7 KW - DNA-Directed DNA Polymerase KW - Index Medicus KW - Sequence Alignment KW - Models, Molecular KW - Molecular Sequence Data KW - Crystallography, X-Ray KW - Amino Acid Sequence KW - Protein Structure, Tertiary KW - DNA -- biosynthesis KW - DNA-Directed DNA Polymerase -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669832718?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+structural+%26+molecular+biology&rft.atitle=How+a+homolog+of+high-fidelity+replicases+conducts+mutagenic+DNA+synthesis.&rft.au=Lee%2C+Young-Sam%3BGao%2C+Yang%3BYang%2C+Wei&rft.aulast=Lee&rft.aufirst=Young-Sam&rft.date=2015-04-01&rft.volume=22&rft.issue=4&rft.spage=298&rft.isbn=&rft.btitle=&rft.title=Nature+structural+%26+molecular+biology&rft.issn=1545-9985&rft_id=info:doi/10.1038%2Fnsmb.2985 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-02 N1 - Date created - 2015-04-03 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 4XVI; PDB; 4XVK; 4XVL; 4XVM N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2014 Feb 25;111(8):2954-9 [24449906] Nat Commun. 2014;5:3216 [24496117] Biochemistry. 2014 May 6;53(17):2752-67 [24720884] Biochemistry. 2014 May 6;53(17):2793-803 [24716551] Curr Biol. 2000 Oct 5;10(19):1221-4 [11050393] Nat Genet. 2002 May;31(1):37-46 [11967533] Science. 2002 Nov 15;298(5597):1387-95 [12242451] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3895-900 [12649320] J Biol Chem. 2003 Aug 22;278(34):32014-9 [12794064] Nucleic Acids Res. 2003 Nov 1;31(21):6117-26 [14576298] Mol Cell. 1998 Mar;1(4):583-93 [9660942] EMBO J. 1998 Dec 15;17(24):7514-25 [9857206] Structure. 1999 Feb 15;7(2):R31-5 [10368292] Genomics. 1999 Jul 1;59(1):90-6 [10395804] EMBO J. 2004 Nov 10;23(22):4484-94 [15496986] Acta Crystallogr D Biol Crystallogr. 2004 Dec;60(Pt 12 Pt 1):2126-32 [15572765] Nat Struct Mol Biol. 2005 Jan;12(1):97-8 [15608652] EMBO J. 2006 Aug 9;25(15):3458-68 [16900098] J Biol Chem. 2006 Aug 18;281(33):23445-55 [16787914] Acta Crystallogr D Biol Crystallogr. 2006 Oct;62(Pt 10):1243-50 [17001101] DNA Repair (Amst). 2007 Feb 4;6(2):213-23 [17118716] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15591-8 [17898175] DNA Repair (Amst). 2007 Dec 1;6(12):1709-25 [17631059] DNA Repair (Amst). 2008 Jan 1;7(1):119-27 [17920341] Nucleic Acids Res. 2008 Jun;36(11):3847-56 [18503084] Proc Natl Acad Sci U S A. 2008 Dec 30;105(52):20695-700 [19106298] Curr Opin Struct Biol. 2009 Jun;19(3):294-9 [19481445] Nat Struct Mol Biol. 2009 Sep;16(9):979-86 [19718023] Cell. 2009 Oct 16;139(2):312-24 [19837034] Cell. 2009 Dec 24;139(7):1279-89 [20064374] Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):213-21 [20124702] Protein Expr Purif. 2010 Apr;70(2):163-71 [19853037] Biochim Biophys Acta. 2010 May;1804(5):1049-63 [19545649] Nucleic Acids Res. 2010 Jun;38(10):3233-44 [20144948] J Cell Biol. 2010 Jun 28;189(7):1117-27 [20584917] Nature. 2010 Oct 7;467(7316):678-83 [20729832] J Mol Biol. 2011 Jan 21;405(3):642-52 [21050863] J Biol Chem. 2011 Jun 3;286(22):19758-67 [21454515] Proc Natl Acad Sci U S A. 2011 Oct 25;108(43):17644-8 [22006298] Biochemistry. 2011 Nov 22;50(46):10126-35 [22008035] Proc Natl Acad Sci U S A. 2012 May 8;109(19):7269-74 [22529383] DNA Repair (Amst). 2013 Jan 1;12(1):1-9 [23219161] Proc Natl Acad Sci U S A. 2013 Feb 19;110(8):E687-96 [23386725] Proc Natl Acad Sci U S A. 2013 May 14;110(20):8146-51 [23630267] Methods Mol Biol. 2013;1010:3-17 [23754215] Yale J Biol Med. 2013 Dec;86(4):507-16 [24348215] Nat Struct Mol Biol. 2014 Jan;21(1):49-55 [24292646] Mol Cell. 2014 Jan 9;53(1):1-3 [24411078] Comment In: Nat Struct Mol Biol. 2015 Apr;22(4):273-5 [25837870] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nsmb.2985 ER - TY - JOUR T1 - Marine ω-3 polyunsaturated fatty acids and risk of colorectal cancer according to microsatellite instability. AN - 1667348145; 25810492 AB - Chronic inflammation is involved in the development of colorectal cancer (CRC) and microsatellite instability (MSI), a distinct phenotype of CRC. Experimental evidence indicates an anti-inflammatory and antineoplastic effect of marine ω-3 polyunsaturated fatty acids (PUFAs). However, epidemiologic data remain inconclusive. We investigated whether the association between marine ω-3 PUFAs and CRC varies by MSI-defined subtypes of tumors in the Nurses' Health Study and Health Professionals Follow-up Study. We documented and classified 1125 CRC cases into either MSI-high tumors, in which 30% or more of the 10 microsatellite markers demonstrated instability, or microsatellite-stable (MSS) tumors. Cox proportional hazards model was used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs) of MSS tumors and MSI-high tumors in relation to marine ω-3 PUFA intake. All statistical tests were two-sided. Marine ω-3 PUFA intake was not associated with overall incidence of CRC. However, a statistically significant difference was detected by MSI status (P heterogeneity = .02): High marine ω-3 PUFA intake was associated with a lower risk of MSI-high tumors (comparing ≥0.30g/d with <0.10g/d: multivariable HR = 0.54, 95% CI = 0.35 to 0.83, P linearity = .03) but not MSS tumors (HR = 0.97, 95% CI = 0.78 to 1.20, P linearity = .28). This differential association appeared to be independent of CpG island methylator phenotype and BRAF mutation status. High marine ω-3 PUFA intake is associated with lower risk of MSI-high CRC but not MSS tumors, suggesting a potential role of ω-3 PUFAs in protection against CRC through DNA mismatch repair. Further research is needed to confirm our findings and elucidate potential underlying mechanisms. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. JF - Journal of the National Cancer Institute AU - Song, Mingyang AU - Nishihara, Reiko AU - Wu, Kana AU - Qian, Zhi Rong AU - Kim, Sun A AU - Sukawa, Yasutaka AU - Mima, Kosuke AU - Inamura, Kentaro AU - Masuda, Atsuhiro AU - Yang, Juhong AU - Fuchs, Charles S AU - Giovannucci, Edward L AU - Ogino, Shuji AU - Chan, Andrew T AD - Department of Nutrition (MS, RN, KW, ELG) and Department of Epidemiology (MS, ELG, SO), Harvard School of Public Health, Boston, MA; Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA (RN, ZRQ, SAK, YS, KM, AM, JY, CSF, SO); Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD (KI); Channing Division of Network Medicine, Department of Medicine (CSF, ELG, SO, ATC) and Department of Pathology (SO), Harvard Medical School, Brigham and Women's Hospital, Boston, MA; Division of Gastroenterology, Massachusetts General Hospital and Harvard Medical School, Boston, MA (ATC). Y1 - 2015/04// PY - 2015 DA - April 2015 VL - 107 IS - 4 KW - Anti-Inflammatory Agents KW - 0 KW - Antineoplastic Agents KW - Fatty Acids, Omega-3 KW - BRAF protein, human KW - EC 2.7.11.1 KW - Proto-Oncogene Proteins B-raf KW - Index Medicus KW - Humans KW - Proto-Oncogene Proteins B-raf -- genetics KW - Phenotype KW - Risk KW - Inflammation -- prevention & control KW - DNA Methylation KW - Adult KW - CpG Islands -- genetics KW - Incidence KW - Follow-Up Studies KW - Middle Aged KW - Mutation KW - Female KW - Inflammation -- complications KW - Male KW - Proportional Hazards Models KW - Microsatellite Instability KW - Fatty Acids, Omega-3 -- therapeutic use KW - Anti-Inflammatory Agents -- therapeutic use KW - Colorectal Neoplasms -- genetics KW - Colorectal Neoplasms -- epidemiology KW - Antineoplastic Agents -- therapeutic use KW - Colorectal Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1667348145?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Marine+%CF%89-3+polyunsaturated+fatty+acids+and+risk+of+colorectal+cancer+according+to+microsatellite+instability.&rft.au=Song%2C+Mingyang%3BNishihara%2C+Reiko%3BWu%2C+Kana%3BQian%2C+Zhi+Rong%3BKim%2C+Sun+A%3BSukawa%2C+Yasutaka%3BMima%2C+Kosuke%3BInamura%2C+Kentaro%3BMasuda%2C+Atsuhiro%3BYang%2C+Juhong%3BFuchs%2C+Charles+S%3BGiovannucci%2C+Edward+L%3BOgino%2C+Shuji%3BChan%2C+Andrew+T&rft.aulast=Song&rft.aufirst=Mingyang&rft.date=2015-04-01&rft.volume=107&rft.issue=4&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdjv007 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-01 N1 - Date created - 2015-03-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Immunol. 2003 Feb 15;170(4):2214-20 [12574395] Gut. 2012 Jun;61(6):847-54 [22427238] Am J Clin Nutr. 2004 Jun;79(6):935-45 [15159222] Gut. 2004 Aug;53(8):1137-44 [15247181] Am J Epidemiol. 1992 May 15;135(10):1114-26; discussion 1127-36 [1632423] Science. 1993 May 7;260(5109):816-9 [8484122] Biometrics. 1995 Jun;51(2):524-32 [7662841] Cancer Res. 1996 Mar 15;56(6):1237-40 [8640805] Lipids. 1996 Mar;31 Suppl:S313-7 [8729142] J Womens Health. 1997 Feb;6(1):49-62 [9065374] Am J Clin Nutr. 1997 Apr;65(4 Suppl):1220S-1228S; discussion 1229S-1231S [9094926] Am J Clin Nutr. 1998 Jan;67(1):25-30 [9440371] Proc Natl Acad Sci U S A. 1998 Oct 13;95(21):12468-73 [9770509] Am J Epidemiol. 2004 Nov 15;160(10):1011-22 [15522858] J Clin Oncol. 2005 Jan 20;23(3):609-18 [15659508] Mol Cell. 2005 Mar 18;17(6):793-803 [15780936] J Natl Cancer Inst. 2005 Jun 15;97(12):906-16 [15956652] Mod Pathol. 2006 Jan;19(1):59-68 [16118624] Histopathology. 2007 Jan;50(1):113-30 [17204026] Int J Colorectal Dis. 2007 Jul;22(7):765-76 [17216221] Nat Rev Immunol. 2008 May;8(5):349-61 [18437155] Br J Nutr. 2012 Nov 14;108(9):1550-6 [22906228] Nutr Cancer. 2014;66(4):716-27 [24053119] Int J Cancer. 2014 Nov 15;135(10):2413-23 [24706410] Cancer Res. 2000 Sep 1;60(17):4864-8 [10987299] JAMA. 2001 Jan 17;285(3):304-12 [11176840] Gut. 2001 Jun;48(6):821-9 [11358903] J Clin Pathol. 2001 Jul;54(7):526-32 [11429424] Cancer Epidemiol Biomarkers Prev. 2001 Aug;10(8):913-4 [11489762] Cancer Res. 2001 Oct 15;61(20):7444-8 [11606378] Am J Physiol Cell Physiol. 2002 Jul;283(1):C148-54 [12055083] Cancer Res. 2002 Nov 1;62(21):6011-4 [12414620] Cancer Epidemiol Biomarkers Prev. 2008 May;17(5):1136-43 [18483335] Int J Cancer. 2009 Feb 1;124(3):678-86 [18973226] Cancer Epidemiol Biomarkers Prev. 2009 Feb;18(2):516-25 [19190143] Cancer Res. 2009 Aug 15;69(16):6423-9 [19638594] J Natl Cancer Inst. 2010 Mar 17;102(6):365-7 [20208016] Lancet. 2010 Mar 20;375(9719):1030-47 [20304247] Gastroenterology. 2010 Jun;138(6):2073-2087.e3 [20420947] Lancet. 1991 Aug 24;338(8765):464-8 [1678444] Stat Med. 1989 May;8(5):551-61 [2657958] Gastroenterology. 2010 Jun;138(6):2101-2114.e5 [20420949] Am J Epidemiol. 1992 Feb 15;135(4):418-27 [1550093] Gut. 2010 Jul;59(7):918-25 [20348368] Proc Natl Acad Sci U S A. 2010 Aug 10;107(32):14298-303 [20660763] CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855] Biometrics. 2011 Mar;67(1):50-8 [20486928] Int J Cancer. 2011 Oct 1;129(7):1718-29 [21120874] Gut. 2012 Jan;61(1):135-49 [21490374] Contemp Clin Trials. 2012 Jan;33(1):159-71 [21986389] Nat Med. 2012 Feb;18(2):224-6 [22270723] FASEB J. 2003 Nov;17(14):2115-7 [12958148] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/jnci/djv007 ER - TY - JOUR T1 - Adolescents' medicine use for headache: secular trends in 20 countries from 1986 to 2010. AN - 1666990373; 25805794 AB - This study reports secular trends in medicine use for headache among adolescents in 20 countries from 1986 to 2010. The international Health Behaviour in School-aged Children (HBSC) survey includes self-reported data about medicine use for headaches among nationally representative samples of 11-, 13- and 15-year-olds. We included 20 countries with data from at least three data collection waves, with a total of 380 129 participants. The prevalence of medicine use for headaches varied from 16.5% among Hungarian boys in 1994 to 62.9% among girls in Wales in 1998. The prevalence was higher among girls than boys in every country and data collection year. The prevalence of medicine use for headaches increased in 12 of 20 countries, most notably in the Czech Republic, Poland, Russia, Sweden and Wales. The prevalence of medicine use for headaches among adolescents is high and increasing in many countries. As some medicines are toxic this may constitute a public health problem. © The Author 2015. Published by Oxford University Press on behalf of the European Public Health Association. All rights reserved. JF - European journal of public health AU - Holstein, Bjørn E AU - Andersen, Anette AU - Fotiou, Anastasios AU - Gobina, Inese AU - Godeau, Emmanuelle AU - Holme Hansen, Ebba AU - Iannotti, Ron AU - Levin, Kate AU - Gabhainn, Saoirse Nic AU - Ravens-Sieberer, Ulrike AU - Välimaa, Raili AU - Medicine Use Writing Group AD - 1 University of Southern Denmark, National Institute of Public Health, Copenhagen, Denmark bho@niph.dk. ; 1 University of Southern Denmark, National Institute of Public Health, Copenhagen, Denmark. ; 2 University Mental Health Research Institute, Athens, Greece. ; 3 Department of Public Health and Epidemiology, Riga Stradins University, Riga, Latvia. ; 4 French Institute of Health and Medical Research, Paris, France. ; 5 Department of Pharmacy, University of Copenhagen, Copenhagen, Denmark. ; 6 Eunice Kennedy Shriver National Institute of Child Health and Human Development, Prevention Research Branch, Bethesda MD, USA. ; 7 School of Medicine, Medical & Biological Sciences, University of St Andrews, St Andrews, Scotland. ; 8 Health Promotion Research Centre, School of Health Sciences, National University of Ireland, Galway, Ireland. ; 9 Department of Child and Adolescent Psychiatry, Psychotherapy, and Psychosomatics, University Medical Centre Hamburg-Eppendorf, Hamburg, Germany. ; 10 Department of Health Sciences, University of Jyväskylä, Jyväskylän Yliopisto, Finland. ; Medicine Use Writing Group Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 76 EP - 79 VL - 25 Suppl 2 KW - Analgesics KW - 0 KW - Index Medicus KW - North America KW - Sex Factors KW - Humans KW - Health Surveys KW - Europe KW - Child KW - Adolescent KW - Male KW - Female KW - Adolescent Behavior KW - Headache -- drug therapy KW - Analgesics -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1666990373?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+public+health&rft.atitle=Adolescents%27+medicine+use+for+headache%3A+secular+trends+in+20+countries+from+1986+to+2010.&rft.au=Holstein%2C+Bj%C3%B8rn+E%3BAndersen%2C+Anette%3BFotiou%2C+Anastasios%3BGobina%2C+Inese%3BGodeau%2C+Emmanuelle%3BHolme+Hansen%2C+Ebba%3BIannotti%2C+Ron%3BLevin%2C+Kate%3BGabhainn%2C+Saoirse+Nic%3BRavens-Sieberer%2C+Ulrike%3BV%C3%A4limaa%2C+Raili%3BMedicine+Use+Writing+Group&rft.aulast=Holstein&rft.aufirst=Bj%C3%B8rn&rft.date=2015-04-01&rft.volume=25+Suppl+2&rft.issue=&rft.spage=76&rft.isbn=&rft.btitle=&rft.title=European+journal+of+public+health&rft.issn=1464-360X&rft_id=info:doi/10.1093%2Feurpub%2Fckv035 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-15 N1 - Date created - 2015-03-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Int J Public Health. 2009 Sep;54 Suppl 2:131-9 [19639260] Ugeskr Laeger. 2009 Jan 5;171(1-2):24-8 [19128560] Res Social Adm Pharm. 2008 Jun;4(2):98-114 [18555964] J Child Psychol Psychiatry. 2008 Apr;49(4):441-8 [18081755] Qual Health Res. 2008 Feb;18(2):234-43 [18216342] Ann Pharmacother. 2007 Apr;41(4):581-6 [17389663] Patient Educ Couns. 2006 Feb;60(2):171-8 [15939568] Br J Clin Pharmacol. 2009 Oct;68(4):599-608 [19843063] Pediatrics. 2004 Sep;114(3):e378-83 [15342901] Ann Pharmacother. 2003 Mar;37(3):361-6 [12639163] Pharmacoepidemiol Drug Saf. 2011 Apr;20(4):424-31 [21246643] Acad Pediatr. 2010 Jul-Aug;10(4):228-32 [20542751] Med Anthropol Q. 1999 Mar;13(1):51-68 [10322601] Int J Public Health. 2009 Sep;54 Suppl 2:140-50 [19639259] Pediatrics. 2009 Aug;124(2):446-54 [19651573] Pharmacoepidemiol Drug Saf. 2009 Jul;18(7):619-23 [19358227] Qual Health Res. 2009 Jun;19(6):829-39 [19366860] Clin Ther. 2009 Feb;31(2):436-45 [19302916] Br J Clin Pharmacol. 2009 Sep;68(3):455-61 [19740404] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/eurpub/ckv035 ER - TY - JOUR T1 - High-throughput viability assay using an autonomously bioluminescent cell line with a bacterial Lux reporter. AN - 1665495842; 25447977 AB - Cell viability assays are extensively used to determine cell health, evaluate growth conditions, and assess compound cytotoxicity. Most existing assays are endpoint assays, in which data are collected at one time point after termination of the experiment. The time point at which toxicity of a compound is evident, however, depends on the mechanism of that compound. An ideal cell viability assay allows the determination of compound toxicity kinetically without having to terminate the assay prematurely. We optimized and validated a reagent-addition-free cell viability assay using an autoluminescent HEK293 cell line that stably expresses bacterial luciferase and all substrates necessary for bioluminescence. This cell viability assay can be used for real-time, long-term measurement of compound cytotoxicity in live cells with a signal-to-basal ratio of 20- to 200-fold and Z-factors of ~0.6 after 24-, 48- 72-, or 96-h incubation with compound. We also found that the potencies of nine cytotoxic compounds correlated well with those measured by four other commonly used cell viability assays. The results demonstrated that this kinetic cell viability assay using the HEK293(lux) autoluminescent cell line is useful for high-throughput evaluation of compound cytotoxicity. © 2014 Society for Laboratory Automation and Screening. JF - Journal of laboratory automation AU - Class, Bradley AU - Thorne, Natasha AU - Aguisanda, Francis AU - Southall, Noel AU - McKew, John C AU - Zheng, Wei AD - National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD, USA. ; National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD, USA thornen@mail.nih.gov wzheng@mail.nih.gov. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 164 EP - 174 VL - 20 IS - 2 KW - Bacterial Proteins KW - 0 KW - Luminescent Proteins KW - Recombinant Proteins KW - Index Medicus KW - bioluminescent assay KW - cell viability KW - high-throughput screening KW - cytotoxicity KW - autonomously bioluminescent assay KW - Epithelial Cells -- physiology KW - Epithelial Cells -- drug effects KW - Cell Survival -- drug effects KW - Recombinant Proteins -- metabolism KW - Humans KW - Genes, Reporter KW - Recombinant Proteins -- genetics KW - Cell Line KW - Luminescent Measurements -- methods KW - Bacterial Proteins -- genetics KW - Bacterial Proteins -- metabolism KW - High-Throughput Screening Assays -- methods KW - Toxicology -- methods KW - Luminescent Proteins -- metabolism KW - Drug Evaluation, Preclinical -- methods KW - Luminescent Proteins -- genetics KW - Cytological Techniques -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665495842?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+laboratory+automation&rft.atitle=High-throughput+viability+assay+using+an+autonomously+bioluminescent+cell+line+with+a+bacterial+Lux+reporter.&rft.au=Class%2C+Bradley%3BThorne%2C+Natasha%3BAguisanda%2C+Francis%3BSouthall%2C+Noel%3BMcKew%2C+John+C%3BZheng%2C+Wei&rft.aulast=Class&rft.aufirst=Bradley&rft.date=2015-04-01&rft.volume=20&rft.issue=2&rft.spage=164&rft.isbn=&rft.btitle=&rft.title=Journal+of+laboratory+automation&rft.issn=2211-0690&rft_id=info:doi/10.1177%2F2211068214560608 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-22 N1 - Date created - 2015-03-21 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/2211068214560608 ER - TY - JOUR T1 - Hamburger polyomaviruses. AN - 1664776443; 25568187 AB - Epidemiological studies have suggested that consumption of beef may correlate with an increased risk of colorectal cancer. One hypothesis to explain this proposed link might be the presence of a carcinogenic infectious agent capable of withstanding cooking. Polyomaviruses are a ubiquitous family of thermostable non-enveloped DNA viruses that are known to be carcinogenic. Using virion enrichment, rolling circle amplification (RCA) and next-generation sequencing, we searched for polyomaviruses in meat samples purchased from several supermarkets. Ground beef samples were found to contain three polyomavirus species. One species, bovine polyomavirus 1 (BoPyV1), was originally discovered as a contaminant in laboratory FCS. A previously unknown species, BoPyV2, occupies the same clade as human Merkel cell polyomavirus and raccoon polyomavirus, both of which are carcinogenic in their native hosts. A third species, BoPyV3, is related to human polyomaviruses 6 and 7. Examples of additional DNA virus families, including herpesviruses, adenoviruses, circoviruses and gyroviruses were also detected either in ground beef samples or in comparison samples of ground pork and ground chicken. The results suggest that the virion enrichment/RCA approach is suitable for random detection of essentially any DNA virus with a detergent-stable capsid. It will be important for future studies to address the possibility that animal viruses commonly found in food might be associated with disease. JF - The Journal of general virology AU - Peretti, Alberto AU - FitzGerald, Peter C AU - Bliskovsky, Valery AU - Buck, Christopher B AU - Pastrana, Diana V AD - National Cancer Institute, Bethesda, MD, USA. ; National Cancer Institute, Bethesda, MD, USA buckc@mail.nih.gov pastrand@mail.nih.gov. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 833 EP - 839 VL - 96 KW - Index Medicus KW - Swine KW - Phylogeny KW - Animals KW - Chickens KW - Cattle KW - Food Microbiology KW - Cattle Diseases -- virology KW - Humans KW - Polyomavirus Infections -- virology KW - Molecular Sequence Data KW - Genome, Viral KW - Polyomavirus Infections -- veterinary KW - Meat -- virology KW - Polyomavirus -- genetics KW - Polyomavirus -- isolation & purification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664776443?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+general+virology&rft.atitle=Hamburger+polyomaviruses.&rft.au=Peretti%2C+Alberto%3BFitzGerald%2C+Peter+C%3BBliskovsky%2C+Valery%3BBuck%2C+Christopher+B%3BPastrana%2C+Diana+V&rft.aulast=Peretti&rft.aufirst=Alberto&rft.date=2015-04-01&rft.volume=96&rft.issue=&rft.spage=833&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+general+virology&rft.issn=1465-2099&rft_id=info:doi/10.1099%2Fvir.0.000033 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-21 N1 - Date created - 2015-03-18 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - KM496326; GENBANK; KM496324; KM496325; KM496323 N1 - SuppNotes - Cited By: Nature. 1977 Sep 8;269(5624):171-3 [909583] Virology. 2014 Nov;468-470:303-10 [25217712] Arch Virol. 1984;80(2-3):131-46 [6326710] Arch Virol. 1986;87(3-4):287-96 [3004390] J Gen Virol. 1991 Nov;72 ( Pt 11):2739-45 [1658200] Science. 2008 Feb 22;319(5866):1096-100 [18202256] Nucleic Acids Res. 2008 Jul 1;36(Web Server issue):W465-9 [18424797] Arch Virol. 2009;154(1):115-9 [19039515] Virology. 2009 Feb 20;384(2):260-5 [19135222] Trends Microbiol. 2009 May;17(5):205-11 [19375325] Angew Chem Int Ed Engl. 2009;48(32):5798-808 [19588476] Cell Host Microbe. 2010 Jun 25;7(6):509-15 [20542254] J Bacteriol. 2010 Oct;192(20):5441-53 [20709901] Cancer Res. 2010 Nov 1;70(21):8388-97 [20959478] J Virol. 2011 Jan;85(2):916-24 [21047967] Nat Biotechnol. 2011 Jul;29(7):644-52 [21572440] Arch Virol. 2011 Sep;156(9):1627-34 [21562881] Int J Cancer. 2012 Jun 1;130(11):2475-83 [22212999] Nat Methods. 2012 Apr;9(4):357-9 [22388286] Lancet Oncol. 2012 Apr;13(4):339-40 [22577663] Emerg Infect Dis. 2013 Jan;19(1):77-84 [23260029] Biologicals. 2013 Mar;41(2):63-70 [23116715] J Gen Virol. 2013 Jun;94(Pt 6):1357-64 [23426354] Proc Natl Acad Sci U S A. 2013 Jul 30;110(31):12744-9 [23847207] J Virol. 2013 Sep;87(18):10105-13 [23843634] PLoS Pathog. 2013;9(8):e1003558 [23990782] Vet Rec. 2014 Mar 15;174(11):264 [24627501] Water Res. 2014 Aug 1;59:119-29 [24793110] J Virol. 1979 Apr;30(1):400-3 [90163] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1099/vir.0.000033 ER - TY - JOUR T1 - Chiral resolution and absolute configuration of the enantiomers of the psychoactive "designer drug" 3,4-methylenedioxypyrovalerone. AN - 1664774469; 25727807 AB - Illicit rac-MDPV (3,4-methylenedioxypyrovalerone), manufactured in clandestine labs, has become widely abused for its cocaine-like stimulant properties. It has recently been found as one of the toxic materials in the so-called "bath salts," producing, among other effects, psychosis and tachycardia in humans when introduced by any of the several routes of administration (e.g., intravenous, oral, etc.). The considerable toxicity of this "designer drug" probably resides in one of the enantiomers of the racemate. In order to obtain a sufficient amount of the enantiomers of rac-MDPV to determine their activity, we improved the known synthesis of rac-MDPV and found chemical resolving agents, (+)- and (-)-2'-bromotetranilic acid, that gave the MDPV enantiomers in >96% enantiomeric excess as determined by (1) H nuclear magnetic resonance and chiral high-performance liquid chromatography. The absolute stereochemistry of these enantiomers was determined by single-crystal X-ray diffraction studies. Published 2015. This article is a U.S. Government work and is in the public domain in the USA. JF - Chirality AU - Suzuki, Masaki AU - Deschamps, Jeffrey R AU - Jacobson, Arthur E AU - Rice, Kenner C AD - Drug Design and Synthesis Section, Molecular Targets and Medications Discovery Branch, National Institute on Drug Abuse, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 287 EP - 293 VL - 27 IS - 4 KW - 3,4-methylenedioxypyrovalerone KW - 0 KW - Benzodioxoles KW - Designer Drugs KW - Psychotropic Drugs KW - Pyrrolidines KW - Hydrochloric Acid KW - QTT17582CB KW - Index Medicus KW - euphoric stimulant KW - bath salts KW - designer drug KW - synthesis KW - non-chromatographic chiral resolution KW - 3,4-methylenedioxypyrovalerone (MDPV) KW - Stereoisomerism KW - Hydrochloric Acid -- chemistry KW - Limit of Detection KW - Pyrrolidines -- analysis KW - Psychotropic Drugs -- isolation & purification KW - Designer Drugs -- isolation & purification KW - Psychotropic Drugs -- chemistry KW - Pyrrolidines -- chemistry KW - Benzodioxoles -- isolation & purification KW - Benzodioxoles -- analysis KW - Psychotropic Drugs -- analysis KW - Pyrrolidines -- isolation & purification KW - Benzodioxoles -- chemistry KW - Designer Drugs -- chemistry KW - Designer Drugs -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664774469?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chirality&rft.atitle=Chiral+resolution+and+absolute+configuration+of+the+enantiomers+of+the+psychoactive+%22designer+drug%22+3%2C4-methylenedioxypyrovalerone.&rft.au=Suzuki%2C+Masaki%3BDeschamps%2C+Jeffrey+R%3BJacobson%2C+Arthur+E%3BRice%2C+Kenner+C&rft.aulast=Suzuki&rft.aufirst=Masaki&rft.date=2015-04-01&rft.volume=27&rft.issue=4&rft.spage=287&rft.isbn=&rft.btitle=&rft.title=Chirality&rft.issn=1520-636X&rft_id=info:doi/10.1002%2Fchir.22423 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-30 N1 - Date created - 2015-03-18 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/chir.22423 ER - TY - JOUR T1 - Fetal consequences of maternal antiretroviral nucleoside reverse transcriptase inhibitor use in human and nonhuman primate pregnancy. AN - 1664208554; 25635584 AB - Here we present fetal genotoxicity and mitochondrial toxicity, induced by nucleoside reverse transcriptase inhibitors (NRTIs), in HIV-1-infected pregnant women treated to prevent mother-to-child HIV-1 transmission, and in virus-free pregnant patas monkeys. In the offspring of pregnant patas monkeys given human-equivalent NRTI protocols, aneuploidy was found in cultured bone marrow cells taken at birth, 1, and 3 years of age. In some newborn human infants, the offspring of HIV-1-infected mothers given zidovudine (AZT) therapy, aneuploidy, mitochondrial DNA (mtDNA) depletion, morphologically damaged mitochondria, and reduction in cardiac left ventricular muscle were observed. NRTI-exposed human and patas umbilical cords had similar levels of mtDNA depletion and mitochondrial morphological damage. NRTI-exposed patas offspring showed a compensatory increase in heart mtDNA, and a 50% loss of brain mtDNA at 1 year of age. Mitochondrial morphological damage and mtDNA loss were persistent in blood cells of NRTI-exposed infants up to 2 years of age, and in heart and brain from NRTI-exposed patas up to 3 years of age (human equivalent of 15 years). Whereas use of NRTIs in human pregnancy protects many thousands of children worldwide, some HIV-1-uninfected infants born to HIV-1-infected mothers receiving antiretroviral drug therapy sustain toxicities that may have adverse consequences later in life. JF - Current opinion in pediatrics AU - Poirier, Miriam C AU - Gibbons, Alexander T AU - Rugeles, Maria T AU - Andre-Schmutz, Isabelle AU - Blanche, Stephane AD - aCarcinogen-DNA Interactions Section, Laboratory of Cancer Biology and Genetics, CCR, National Cancer Institute, NIH, Bethesda, Maryland, USA bGrupo Imunovirologia, School of Medicine Universidad de Antioquia, Medellin, Colombia cInstitut National de la Sante et de la Recherche Medicale, Universite Paris Descartes, Sorbonne Paris Cite, Paris, France dUnite d'Immunologie-Hematologie Pediatrique, Hopital Necker-Enfants Malades, Paris, France. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 233 EP - 239 VL - 27 IS - 2 KW - DNA, Mitochondrial KW - 0 KW - Reverse Transcriptase Inhibitors KW - Zidovudine KW - 4B9XT59T7S KW - Index Medicus KW - Infant KW - Maternal-Fetal Exchange KW - Animals, Newborn KW - Animals KW - Aneuploidy KW - Humans KW - Infant, Newborn KW - Disease Models, Animal KW - Erythrocebus patas KW - Female KW - Pregnancy KW - Reverse Transcriptase Inhibitors -- adverse effects KW - Infectious Disease Transmission, Vertical -- prevention & control KW - DNA, Mitochondrial -- drug effects KW - Zidovudine -- toxicity KW - Zidovudine -- adverse effects KW - Reverse Transcriptase Inhibitors -- pharmacology KW - DNA, Mitochondrial -- physiology KW - Zidovudine -- pharmacology KW - HIV Infections -- prevention & control KW - HIV Infections -- drug therapy KW - Reverse Transcriptase Inhibitors -- toxicity KW - Pregnancy Complications, Infectious -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664208554?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+pediatrics&rft.atitle=Fetal+consequences+of+maternal+antiretroviral+nucleoside+reverse+transcriptase+inhibitor+use+in+human+and+nonhuman+primate+pregnancy.&rft.au=Poirier%2C+Miriam+C%3BGibbons%2C+Alexander+T%3BRugeles%2C+Maria+T%3BAndre-Schmutz%2C+Isabelle%3BBlanche%2C+Stephane&rft.aulast=Poirier&rft.aufirst=Miriam&rft.date=2015-04-01&rft.volume=27&rft.issue=2&rft.spage=233&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+pediatrics&rft.issn=1531-698X&rft_id=info:doi/10.1097%2FMOP.0000000000000193 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-21 N1 - Date created - 2015-03-13 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Curr Pharm Des. 2010 Oct;16(30):3339-51 [20687890] Toxicol Sci. 2010 Nov;118(1):191-201 [20702595] Mitochondrion. 2011 May;11(3):520-7 [21303702] Pediatr Infect Dis J. 2011 Dec;30(12):1069-74 [22051859] Crit Rev Biochem Mol Biol. 2012 Jan-Feb;47(1):64-74 [22176657] HIV Med. 2012 Feb;13(2):98-106 [22103263] Expert Rev Anti Infect Ther. 2012 Jun;10(6):661-74 [22734956] J Infect Dis. 2013 Jul 15;208(2):244-8 [23559463] J Infect Dis. 2013 Jul 15;208(2):235-43 [23559464] J Int AIDS Soc. 2013;16:18597 [23782480] AIDS. 2013 Apr 24;27(7):1099-108 [23211773] J Infect. 2014 Jan;68 Suppl 1:S57-62 [24139190] Clin Exp Immunol. 2014 Apr;176(1):11-22 [24325737] JAMA. 2014 Jul 23-30;312(4):339-40 [25038347] AIDS Care. 2014;26(11):1327-35 [24878112] AIDS. 2004 Apr 30;18(7):1013-21 [15096804] J Acquir Immune Defic Syndr. 2003 Jun 1;33(2):175-83 [12794551] J Acquir Immune Defic Syndr. 2014 Jul 1;66(3):245-55 [24732876] Toxicol Appl Pharmacol. 2004 Sep 1;199(2):151-61 [15313587] Nat Med. 1995 May;1(5):417-22 [7585087] J Natl Cancer Inst. 1997 Nov 5;89(21):1602-8 [9362158] Cardiovasc Toxicol. 2005;5(3):333-46 [16244378] Environ Mol Mutagen. 2007 Apr-May;48(3-4):201-9 [16538687] AIDS. 2007 May 11;21(8):929-38 [17457086] J Antimicrob Chemother. 2008 Jan;61(1):8-12 [17999978] Toxicol Appl Pharmacol. 2008 Jan 15;226(2):206-11 [17949768] AIDS. 2008 Oct 18;22(16):2165-77 [18832880] Mutat Res. 2009 Jun 1;665(1-2):67-74 [19427513] Antivir Ther. 2009;14(3):331-8 [19474467] J Am Coll Cardiol. 2011 Jan 4;57(1):76-85 [21185505] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/MOP.0000000000000193 ER - TY - JOUR T1 - Nodal signaling from the visceral endoderm is required to maintain Nodal gene expression in the epiblast and drive DVE/AVE migration. AN - 1664205580; 25536399 AB - In the early mouse embryo, a specialized population of extraembryonic visceral endoderm (VE) cells called the distal VE (DVE) arises at the tip of the egg cylinder stage embryo and then asymmetrically migrates to the prospective anterior, recruiting additional distal cells. Upon migration these cells, called the anterior VE (AVE), establish the anterior posterior (AP) axis by restricting gastrulation-inducing signals to the opposite pole. The Nodal-signaling pathway has been shown to have a critical role in the generation and migration of the DVE/AVE. The Nodal gene is expressed in both the VE and in the pluripotent epiblast, which gives rise to the germ layers. Previous findings have provided conflicting evidence as to the relative importance of Nodal signaling from the epiblast vs. VE for AP patterning. Here we show that conditional mutagenesis of the Nodal gene specifically within the VE leads to reduced Nodal expression levels in the epiblast and incomplete or failed DVE/AVE migration. These results support a required role for VE Nodal to maintain normal levels of expression in the epiblast, and suggest signaling from both VE and epiblast is important for DVE/AVE migration. Published by Elsevier Inc. JF - Developmental biology AU - Kumar, Amit AU - Lualdi, Margaret AU - Lyozin, George T AU - Sharma, Prashant AU - Loncarek, Jadranka AU - Fu, Xin-Yuan AU - Kuehn, Michael R AD - Laboratory of Protein Dynamics and Signaling, Center for Cancer Research, National Cancer Institute, National Institutes of Health, United States. ; Laboratory Animal Sciences Program, SAIC-Frederick, Frederick, MD 21702, United States. ; Department of Pediatrics (Neonatology), The University of Utah, Salt Lake City, UT 84112, United States. ; Cancer Science Institute of Singapore, Singapore 117599, Singapore. ; Laboratory of Protein Dynamics and Signaling, Center for Cancer Research, National Cancer Institute, National Institutes of Health, United States. Electronic address: mkuehn@mail.nih.gov. Y1 - 2015/04/01/ PY - 2015 DA - 2015 Apr 01 SP - 1 EP - 9 VL - 400 IS - 1 KW - Galactosides KW - 0 KW - Indoles KW - Nodal Protein KW - Nodal protein, mouse KW - 5-bromo-4-chloro-3-indolyl beta-galactoside KW - V595OG374W KW - Index Medicus KW - Ttr-Cre KW - Epiblast KW - Nodal signaling KW - DVE/AVE KW - Visceral endoderm KW - Microscopy, Fluorescence KW - Animals KW - In Situ Hybridization KW - Genes, Reporter -- genetics KW - Mice, Inbred C57BL KW - Mice KW - Mutagenesis KW - Signal Transduction -- physiology KW - Gene Expression Regulation, Developmental -- physiology KW - Nodal Protein -- genetics KW - Cell Movement -- physiology KW - Body Patterning -- physiology KW - Endoderm -- physiology KW - Endoderm -- cytology KW - Germ Layers -- metabolism KW - Nodal Protein -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664205580?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Developmental+biology&rft.atitle=Nodal+signaling+from+the+visceral+endoderm+is+required+to+maintain+Nodal+gene+expression+in+the+epiblast+and+drive+DVE%2FAVE+migration.&rft.au=Kumar%2C+Amit%3BLualdi%2C+Margaret%3BLyozin%2C+George+T%3BSharma%2C+Prashant%3BLoncarek%2C+Jadranka%3BFu%2C+Xin-Yuan%3BKuehn%2C+Michael+R&rft.aulast=Kumar&rft.aufirst=Amit&rft.date=2015-04-01&rft.volume=400&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Developmental+biology&rft.issn=1095-564X&rft_id=info:doi/10.1016%2Fj.ydbio.2014.12.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-19 N1 - Date created - 2015-03-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Dev Biol. 2004 Sep 1;273(1):149-59 [15302604] Mech Dev. 2004 Nov;121(11):1403-15 [15454269] Curr Biol. 1996 Nov 1;6(11):1487-96 [8939602] Development. 1997 Mar;124(5):1033-44 [9056778] Nat Genet. 1999 Jan;21(1):70-1 [9916792] Genes Dev. 1999 Jun 15;13(12):1575-88 [10385626] Genes Dev. 1999 Jun 15;13(12):1589-600 [10385627] Proc Natl Acad Sci U S A. 2004 Nov 2;101(44):15656-60 [15505202] Dev Biol. 2001 Jun 15;234(2):304-16 [11397001] Development. 2001 May;128(10):1831-43 [11311163] Nat Methods. 2014 Sep;11(9):966-70 [25028895] Development. 2002 Jul;129(14):3455-68 [12091315] Dev Cell. 2002 Nov;3(5):745-56 [12431380] Nat Cell Biol. 2002 Dec;4(12):981-5 [12447384] Genes Dev. 2003 Jul 1;17(13):1646-62 [12842913] Dev Biol. 2003 Sep 15;261(2):470-87 [14499654] Mech Dev. 2002 Dec;119 Suppl 1:S97-S101 [14516668] BMC Dev Biol. 2001;1:4 [11299042] Development. 2004 Mar;131(5):1157-64 [14973277] Nature. 2004 Mar 25;428(6981):387-92 [15004567] Dev Dyn. 2005 Apr;232(4):1031-6 [15736223] Development. 2005 Jun;132(11):2513-20 [15857911] Dev Cell. 2005 Nov;9(5):639-50 [16256739] Dev Cell. 2006 Apr;10(4):451-9 [16580991] Development. 2006 Jul;133(13):2497-505 [16728477] Dev Cell. 2006 Sep;11(3):313-23 [16950123] Lab Invest. 2007 Oct;87(10):1018-28 [17660847] Genesis. 2007 Dec;45(12):729-36 [18064671] Dev Dyn. 2008 Dec;237(12):3591-601 [18773491] J Cell Biol. 2009 Jan 26;184(2):323-34 [19153222] Nat Rev Genet. 2009 Jul;10(7):467-77 [19536196] Nature. 2001 Jun 21;411(6840):965-9 [11418863] Genesis. 2009 Jul;47(7):447-55 [19415627] Int J Biol Sci. 2010;6(6):569-83 [20941375] Dev Biol. 2011 Jan 15;349(2):350-62 [21047506] Development. 2011 Apr;138(8):1521-30 [21427142] Nat Cell Biol. 2011 Jul;13(7):743-52 [21623358] Development. 2012 Jan;139(1):3-14 [22147950] Nat Commun. 2012;3:673 [22334076] Development. 2012 Mar;139(6):1059-69 [22354839] Dev Cell. 2013 Oct 28;27(2):131-44 [24176640] Cell. 2014 Feb 27;156(5):1032-44 [24529478] Dev Dyn. 2014 Jul;243(7):937-47 [24633704] PLoS Biol. 2014 Jun;12(6):e1001890 [24960041] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ydbio.2014.12.016 ER - TY - JOUR T1 - A phase II study of GW786034 (pazopanib) with or without bicalutamide in patients with castration-resistant prostate cancer. AN - 1664202498; 24993934 AB - Pazopanib is an oral vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor. In this randomized, open label phase II study, pazopanib alone or in combination with bicalutamide was evaluated in patients with chemotherapy-naive castration-resistant prostate cancer (CRPC). Patients received either pazopanib 800 mg daily (arm A) or pazopanib 800 mg plus bicalutamide 50 mg daily (arm B). A 2-stage study design was used, and the primary endpoint was prostate-specific antigen (PSA) response rate (defined as a confirmed ≥ 50% decline from baseline). A total of 23 patients (arm A, 10; arm B, 13) were accrued. The main grade 3+ toxicities were hypertension, fatigue, decreased lymphocytes, and increased alanine transaminase. Owing to significant toxicity, the protocol was amended after the first 11 patients and the pazopanib starting dose was reduced to 600 mg daily. In arm A, of 9 evaluable patients, there was 1 patient (11%) with a PSA response, 3 (33%) with stable PSA, and 5 (56%) with PSA progression; in arm B, of 12 evaluable patients, there were 2 patients (17%) with PSA responses, 6 (50%) with stable PSA, and 4 (33%) with PSA progression. Median progression-free survival was similar in both arms at 7.3 months (95% CI, 2.5 months to not reached). Long-term stable disease was seen in 4 patients who remained on treatment for 18 months (arm A), 26 months (arm A), 35 months (arm B), and 52 months (arm B). In this unselected patient population, pazopanib either alone or in combination with bicalutamide failed to show sufficient activity to warrant further evaluation. However, 4 patients had long-term benefit, suggesting that targeting the VEGFR pathway may still be relevant in selected patients and emphasizing the need for improved predictive markers for patients with CRPC. Copyright © 2015 Elsevier Inc. All rights reserved. JF - Clinical genitourinary cancer AU - Sridhar, Srikala S AU - Joshua, Anthony M AU - Gregg, Richard AU - Booth, Christopher M AU - Murray, Nevin AU - Golubovic, Jovana AU - Wang, Lisa AU - Harris, Pamela AU - Chi, Kim N AD - Princess Margaret Hospital, Phase II Consortium, Toronto, ON. ; Department of Oncology, Queen's University, Kingston, ON. ; BC Cancer Agency, Vancouver, BC. ; Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, MD. ; BC Cancer Agency, Vancouver, BC. Electronic address: kchi@bccancer.bc.ca. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 124 EP - 129 VL - 13 IS - 2 KW - Angiogenesis Inhibitors KW - 0 KW - Anilides KW - Antineoplastic Agents KW - Nitriles KW - Pyrimidines KW - Sulfonamides KW - Tosyl Compounds KW - pazopanib KW - 7RN5DR86CK KW - bicalutamide KW - A0Z3NAU9DP KW - Kallikreins KW - EC 3.4.21.- KW - kallikrein-related peptidase 3, human KW - Prostate-Specific Antigen KW - EC 3.4.21.77 KW - Index Medicus KW - Patient selection KW - PSA response KW - Angiogenesis inhibitors KW - CRPC KW - Drug Administration Schedule KW - Kallikreins -- metabolism KW - Aged, 80 and over KW - Prostate-Specific Antigen -- metabolism KW - Humans KW - Treatment Outcome KW - Aged KW - Middle Aged KW - Male KW - Angiogenesis Inhibitors -- therapeutic use KW - Pyrimidines -- adverse effects KW - Pyrimidines -- therapeutic use KW - Antineoplastic Agents -- administration & dosage KW - Tosyl Compounds -- adverse effects KW - Nitriles -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Sulfonamides -- administration & dosage KW - Nitriles -- therapeutic use KW - Tosyl Compounds -- administration & dosage KW - Sulfonamides -- therapeutic use KW - Pyrimidines -- administration & dosage KW - Angiogenesis Inhibitors -- administration & dosage KW - Antineoplastic Agents -- adverse effects KW - Sulfonamides -- adverse effects KW - Anilides -- therapeutic use KW - Prostatic Neoplasms, Castration-Resistant -- metabolism KW - Tosyl Compounds -- therapeutic use KW - Anilides -- adverse effects KW - Angiogenesis Inhibitors -- adverse effects KW - Nitriles -- adverse effects KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Anilides -- administration & dosage KW - Prostatic Neoplasms, Castration-Resistant -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664202498?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+genitourinary+cancer&rft.atitle=A+phase+II+study+of+GW786034+%28pazopanib%29+with+or+without+bicalutamide+in+patients+with+castration-resistant+prostate+cancer.&rft.au=Sridhar%2C+Srikala+S%3BJoshua%2C+Anthony+M%3BGregg%2C+Richard%3BBooth%2C+Christopher+M%3BMurray%2C+Nevin%3BGolubovic%2C+Jovana%3BWang%2C+Lisa%3BHarris%2C+Pamela%3BChi%2C+Kim+N&rft.aulast=Sridhar&rft.aufirst=Srikala&rft.date=2015-04-01&rft.volume=13&rft.issue=2&rft.spage=124&rft.isbn=&rft.btitle=&rft.title=Clinical+genitourinary+cancer&rft.issn=1938-0682&rft_id=info:doi/10.1016%2Fj.clgc.2014.06.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-03 N1 - Date created - 2015-03-16 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00486642; ClinicalTrials.gov N1 - SuppNotes - Cited By: N Engl J Med. 2013 Aug 22;369(8):722-31 [23964934] N Engl J Med. 2013 Oct 24;369(17):1659-60 [24152265] PLoS One. 2013;8(10):e78881 [24205338] Clin Cancer Res. 2014 Feb 1;20(3):617-30 [24097861] Clin Genitourin Cancer. 2014 Apr;12(2):100-5 [24169494] J Clin Oncol. 1999 Nov;17(11):3461-7 [10550143] Cancer Res. 2001 Mar 15;61(6):2533-6 [11289126] Urology. 2001 Jul;58(1):53-8 [11445479] Clin Cancer Res. 2001 Jul;7(7):1932-6 [11448906] J Cell Biochem. 2004 Jan 1;91(1):125-50 [14689586] Am J Pathol. 1993 Aug;143(2):401-9 [7688183] Cancer. 1997 Feb 15;79(4):772-9 [9024715] J Clin Oncol. 1997 Aug;15(8):2928-38 [9256137] Prostate. 1997 Sep 15;33(1):38-45 [9294625] J Urol. 1998 Jan;159(1):149-53 [9400459] J Clin Oncol. 1998 May;16(5):1835-43 [9586898] Clin Cancer Res. 1997 Dec;3(12 Pt 1):2507-11 [9815654] Urology. 1999 Sep;54(3):523-7 [10475365] Urology. 1999 Sep;54(3):567-72 [10475375] Br J Cancer. 2007 Dec 3;97(11):1480-5 [18040273] Ann Oncol. 2008 Apr;19(4):746-51 [18056648] Eur J Cancer. 2009 Jan;45(2):228-47 [19097774] Prostate Cancer Prostatic Dis. 2009;12(3):241-6 [19597531] N Engl J Med. 2010 Jul 29;363(5):411-22 [20818862] Lancet. 2010 Oct 2;376(9747):1147-54 [20888992] N Engl J Med. 2011 May 26;364(21):1995-2005 [21612468] Ann Oncol. 2012 Mar;23(3):688-94 [21821830] J Clin Oncol. 2012 May 1;30(13):1534-40 [22454414] Invest New Drugs. 2012 Aug;30(4):1652-9 [21785998] N Engl J Med. 2012 Sep 27;367(13):1187-97 [22894553] Cold Spring Harb Perspect Med. 2012 Oct;2(10). pii: a006577. doi: 10.1101/cshperspect.a006577 [23028128] J Nucl Med. 2012 Nov;53(11):1670-5 [22984218] Cancer J. 2013 Jan-Feb;19(1):90-8 [23337762] Cancer J. 2013 Jan-Feb;19(1):99-106 [23337763] CA Cancer J Clin. 2013 Jan;63(1):11-30 [23335087] J Clin Oncol. 2013 Feb 1;31(4):412-9 [23169517] Int J Radiat Oncol Biol Phys. 2013 Jul 1;86(3):540-5 [23541810] Clin Cancer Res. 2013 Jun 1;19(11):3088-94 [23553848] Lancet Oncol. 2013 Jul;14(8):760-8 [23742877] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.clgc.2014.06.001 ER - TY - JOUR T1 - Transcriptional and epigenetic substrates of methamphetamine addiction and withdrawal: evidence from a long-access self-administration model in the rat. AN - 1664193652; 24939695 AB - Methamphetamine use disorder is a chronic neuropsychiatric disorder characterized by recurrent binge episodes, intervals of abstinence, and relapses to drug use. Humans addicted to methamphetamine experience various degrees of cognitive deficits and other neurological abnormalities that complicate their activities of daily living and their participation in treatment programs. Importantly, models of methamphetamine addiction in rodents have shown that animals will readily learn to give themselves methamphetamine. Rats also accelerate their intake over time. Microarray studies have also shown that methamphetamine taking is associated with major transcriptional changes in the striatum measured within a short or longer time after cessation of drug taking. After a 2-h withdrawal time, there was increased expression of genes that participate in transcription regulation. These included cyclic AMP response element binding (CREB), ETS domain-containing protein (ELK1), and members of the FOS family of transcription factors. Other genes of interest include brain-derived neurotrophic factor (BDNF), tyrosine kinase receptor, type 2 (TrkB), and synaptophysin. Methamphetamine-induced transcription was found to be regulated via phosphorylated CREB-dependent events. After a 30-day withdrawal from methamphetamine self-administration, however, there was mostly decreased expression of transcription factors including junD. There was also downregulation of genes whose protein products are constituents of chromatin-remodeling complexes. Altogether, these genome-wide results show that methamphetamine abuse might be associated with altered regulation of a diversity of gene networks that impact cellular and synaptic functions. These transcriptional changes might serve as triggers for the neuropsychiatric presentations of humans who abuse this drug. Better understanding of the way that gene products interact to cause methamphetamine addiction will help to develop better pharmacological treatment of methamphetamine addicts. JF - Molecular neurobiology AU - Cadet, Jean Lud AU - Brannock, Christie AU - Jayanthi, Subramaniam AU - Krasnova, Irina N AD - Molecular Neuropsychiatry Research Branch, Intramural Research Program, National Institute on Drug Abuse, NIH, DHHS, 251 Bayview Boulevard, Baltimore, MD, 21224, USA, JCADET@intra.nida.nih.gov. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 696 EP - 717 VL - 51 IS - 2 KW - Transcription Factors KW - 0 KW - Methamphetamine KW - 44RAL3456C KW - Index Medicus KW - Rats KW - Gene Regulatory Networks -- genetics KW - Animals KW - Self Administration KW - Gene Regulatory Networks -- drug effects KW - Humans KW - Time Factors KW - Epigenesis, Genetic -- genetics KW - Methamphetamine -- administration & dosage KW - Behavior, Addictive -- chemically induced KW - Epigenesis, Genetic -- drug effects KW - Disease Models, Animal KW - Transcription Factors -- genetics KW - Behavior, Addictive -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664193652?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+neurobiology&rft.atitle=Transcriptional+and+epigenetic+substrates+of+methamphetamine+addiction+and+withdrawal%3A+evidence+from+a+long-access+self-administration+model+in+the+rat.&rft.au=Cadet%2C+Jean+Lud%3BBrannock%2C+Christie%3BJayanthi%2C+Subramaniam%3BKrasnova%2C+Irina+N&rft.aulast=Cadet&rft.aufirst=Jean&rft.date=2015-04-01&rft.volume=51&rft.issue=2&rft.spage=696&rft.isbn=&rft.btitle=&rft.title=Molecular+neurobiology&rft.issn=1559-1182&rft_id=info:doi/10.1007%2Fs12035-014-8776-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-14 N1 - Date created - 2015-03-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2005 Jan 11;102(2):491-6 [15608059] Genomics. 2005 Aug;86(2):242-51 [15922553] Gene Expr Patterns. 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2013 Apr;16(4):434-40 [23475113] BMC Genomics. 2013;14:92 [23398888] Neurobiol Learn Mem. 2013 May;102:34-42 [23567105] Psychiatr Clin North Am. 2013 Jun;36(2):261-75 [23688691] Biochem Soc Trans. 2013 Jun;41(3):741-9 [23697933] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s12035-014-8776-8 ER - TY - JOUR T1 - Rotenone decreases intracellular aldehyde dehydrogenase activity: implications for the pathogenesis of Parkinson's disease. AN - 1664193646; 25645689 AB - Repeated systemic administration of the mitochondrial complex I inhibitor rotenone produces a rodent model of Parkinson's disease (PD). Mechanisms of relatively selective rotenone-induced damage to nigrostriatal dopaminergic neurons remain incompletely understood. According to the 'catecholaldehyde hypothesis,' buildup of the autotoxic dopamine metabolite 3,4-dihydroxyphenylacetaldehyde (DOPAL) contributes to PD pathogenesis. Vesicular uptake blockade increases DOPAL levels, and DOPAL is detoxified mainly by aldehyde dehydrogenase (ALDH). We tested whether rotenone interferes with vesicular uptake and intracellular ALDH activity. Endogenous and F-labeled catechols were measured in PC12 cells incubated with rotenone (0-1000 nM, 180 min), without or with F-dopamine (2 μM) to track vesicular uptake and catecholamine metabolism. Rotenone dose dependently increased DOPAL, F-DOPAL, and 3,4-dihydroxyphenylethanol (DOPET) levels while decreasing dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) levels and the ratio of dopamine to the sum of its deaminated metabolites. In test tubes, rotenone did not affect conversion of DOPAL to DOPAC by ALDH when NAD(+) was supplied, whereas the direct-acting ALDH inhibitor benomyl markedly increased DOPAL and decreased DOPAC concentrations in the reaction mixtures. We propose that rotenone builds up intracellular DOPAL by decreasing ALDH activity and attenuating vesicular sequestration of cytoplasmic catecholamines. The results provide a novel mechanism for selective rotenone-induced toxicity in dopaminergic neurons. We report that rotenone, a mitochondrial complex I inhibitor that produces an animal model of Parkinson's disease, increases intracellular levels of the toxic dopamine metabolite 3,4-dihydroxyphenyl-acetaldehyde (DOPAL), via decreased DOPAL metabolism by aldehyde dehydrogenase (ALDH) and decreased vesicular sequestration of cytoplasmic dopamine by the vesicular monoamine transporter (VMAT). The results provide a novel mechanism for rotenone-induced toxicity in dopaminergic neurons. © 2015 International Society for Neurochemistry. JF - Journal of neurochemistry AU - Goldstein, David S AU - Sullivan, Patti AU - Cooney, Adele AU - Jinsmaa, Yunden AU - Kopin, Irwin J AU - Sharabi, Yehonatan AD - Clinical Neurocardiology Section, CNP/DIR/NINDS/NIH, Bethesda, Maryland, USA. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 14 EP - 25 VL - 133 IS - 1 KW - Uncoupling Agents KW - 0 KW - Rotenone KW - 03L9OT429T KW - NAD KW - 0U46U6E8UK KW - 3,4-Dihydroxyphenylacetic Acid KW - 102-32-9 KW - Aldehyde Dehydrogenase KW - EC 1.2.1.3 KW - Electron Transport Complex I KW - EC 1.6.5.3 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - 3,4-dihydroxyphenyl-acetaldehyde KW - Parkinson's disease KW - rotenone KW - aldehyde dehydrogenase KW - vesicular monoamine transporter KW - Rats KW - NAD -- metabolism KW - Electron Transport Complex I -- drug effects KW - Animals KW - 3,4-Dihydroxyphenylacetic Acid -- metabolism KW - Humans KW - Glioblastoma -- metabolism KW - Brain Neoplasms -- metabolism KW - Dopamine -- metabolism KW - Glioma -- metabolism KW - PC12 Cells KW - Parkinson Disease, Secondary -- chemically induced KW - Parkinson Disease, Secondary -- enzymology KW - Aldehyde Dehydrogenase -- metabolism KW - Uncoupling Agents -- pharmacology KW - Rotenone -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664193646?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neurochemistry&rft.atitle=Rotenone+decreases+intracellular+aldehyde+dehydrogenase+activity%3A+implications+for+the+pathogenesis+of+Parkinson%27s+disease.&rft.au=Goldstein%2C+David+S%3BSullivan%2C+Patti%3BCooney%2C+Adele%3BJinsmaa%2C+Yunden%3BKopin%2C+Irwin+J%3BSharabi%2C+Yehonatan&rft.aulast=Goldstein&rft.aufirst=David&rft.date=2015-04-01&rft.volume=133&rft.issue=1&rft.spage=14&rft.isbn=&rft.btitle=&rft.title=Journal+of+neurochemistry&rft.issn=1471-4159&rft_id=info:doi/10.1111%2Fjnc.13042 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-27 N1 - Date created - 2015-03-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Neurosci Res. 2000 May 15;60(4):552-8 [10797558] Brain Res. 2000 Jun 23;868(2):191-201 [10854571] Nat Neurosci. 2000 Dec;3(12):1301-6 [11100151] Exp Neurol. 2003 Jan;179(1):9-16 [12504863] J Neurochem. 2003 Feb;84(3):491-502 [12558969] Brain Res. 2003 Nov 7;989(2):205-13 [14556942] Chem Res Toxicol. 2004 Sep;17(9):1272-9 [15377162] N Engl J Med. 1988 Apr 7;318(14):876-80 [3352672] Ann Neurol. 1990 Apr;27(4):373-85 [1972319] J Chromatogr B Biomed Appl. 1994 Mar 4;653(2):131-8 [8205240] Brain Res. 1997 Apr 4;753(1):157-62 [9125443] Nature. 1997 Aug 28;388(6645):839-40 [9278044] Adv Pharmacol. 1998;42:250-3 [9327891] Acta Pharmacol Sin. 2005 Jan;26(1):17-26 [15659109] Antioxid Redox Signal. 2005 May-Jun;7(5-6):630-8 [15890007] Neurotoxicology. 2007 Jan;28(1):143-9 [17010440] J Pharmacol Exp Ther. 2007 Nov;323(2):499-507 [17726156] Acta Neuropathol. 2008 Feb;115(2):193-203 [17965867] Mov Disord. 2008 Apr 30;23(6):777-83 [18383531] Toxicol In Vitro. 2008 Sep;22(6):1461-8 [18579341] Mol Pharmacol. 2008 Oct;74(4):933-40 [18599602] Arch Neurol. 2008 Dec;65(12):1577-81 [19064744] PLoS One. 2010;5(12):e15251 [21179455] Ann N Y Acad Sci. 2011 Jan;1216:86-98 [21272013] Environ Health Perspect. 2011 Jun;119(6):866-72 [21269927] J Biol Chem. 2011 Jul 29;286(30):26978-86 [21642436] Neuroscience. 2011 Nov 10;195:138-44 [21884756] J Neurochem. 2012 Dec;123(6):932-43 [22906103] Proc Natl Acad Sci U S A. 2013 Jan 8;110(2):636-41 [23267077] J Neurochem. 2013 Sep;126(5):591-603 [23786406] Neuropharmacology. 2014 Jan;76 Pt A:97-105 [24025942] Neurology. 2014 Feb 4;82(5):419-26 [24491970] Neurosci Lett. 2014 May 21;569:27-32 [24670480] Pharmacol Ther. 2014 Dec;144(3):268-82 [24945828] Exp Neurol. 2015 Jan;263:244-53 [25263579] Chem Res Toxicol. 2014 Aug 18;27(8):1359-61 [25045800] J Neurochem. 2014 Oct;131(2):219-28 [24848581] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/jnc.13042 ER - TY - JOUR T1 - E-mentoring for violence and injury prevention: early lessons from a global programme AN - 1663902467; 4655939 AB - To address the growing burden of violence and injuries, especially in low- and middle-income countries, in 2007 the World Health Organization launched MENTOR-VIP, a global violence and injury prevention (VIP)-mentoring programme. The programme aims to develop human resource capacity through 12-month mentoring arrangements between individual VIP experts (mentors) and less-experienced injury practitioners (mentees). In this paper, we review the first five years of the programme (2007-2011) using a systems analysis and SWOT (Strengths, Weaknesses, Opportunities and Threats) frameworks, discuss programme findings and make recommendations. A well-defined programme with clear instructions, successful matching of mentorship pairs with similar interests and language, a formal accord agreement, institutional support and effective communication were identified as programme strengths. Overambitious projects, lack of funds and difficulties with communications were identified as programme weaknesses. Mentorship projects that require institutional permissions or resources could be potential threats to the success of mentorship. The study resulted in the four following recommendations to strengthen the programme: (1) institute additional steps in selection and matching mentor-mentee pair; (2) train mentors on e-mentoring; (3) conduct special orientation for mentees to the programme; and (4) maintain effective and open communication throughout the programme. Reprinted by permission of Taylor & Francis Ltd. JF - Global public health AU - Wadhwaniya, Shirin AU - Meddings, David AU - Gururaj, Gopalkrishna AU - Ozanne-Smith, Joan AU - Ameratunga, Shanthi AU - Hyder, Adnan A AD - Johns Hopkins University ; World Health Organization ; National Institute of Mental Health and Neuro Sciences, Bangalore ; Monash University ; University of Auckland Y1 - 2015/04// PY - 2015 DA - Apr 2015 SP - 501 EP - 519 VL - 10 IS - 4 SN - 1744-1692, 1744-1692 KW - Sociology KW - Human resources KW - World Health Organization KW - Prevention KW - Injuries KW - Training KW - Communication KW - Violence KW - Low income UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1663902467?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Global+public+health&rft.atitle=E-mentoring+for+violence+and+injury+prevention%3A+early+lessons+from+a+global+programme&rft.au=Wadhwaniya%2C+Shirin%3BMeddings%2C+David%3BGururaj%2C+Gopalkrishna%3BOzanne-Smith%2C+Joan%3BAmeratunga%2C+Shanthi%3BHyder%2C+Adnan+A&rft.aulast=Wadhwaniya&rft.aufirst=Shirin&rft.date=2015-04-01&rft.volume=10&rft.issue=4&rft.spage=501&rft.isbn=&rft.btitle=&rft.title=Global+public+health&rft.issn=17441692&rft_id=info:doi/10.1080%2F17441692.2014.1001766 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-03-16 N1 - Last updated - 2015-03-17 N1 - SubjectsTermNotLitGenreText - 13325; 6555 6220; 10072; 13737 6772 9030; 6099; 12894; 2572; 7553 6271 DO - http://dx.doi.org/10.1080/17441692.2014.1001766 ER - TY - JOUR T1 - Sirolimus for progressive neurofibromatosis type 1-associated plexiform neurofibromas: a neurofibromatosis Clinical Trials Consortium phase II study. AN - 1663657556; 25314964 AB - Plexiform neurofibromas (PNs) are benign peripheral nerve sheath tumors that arise in one-third of individuals with neurofibromatosis type 1 (NF1). They may cause significant disfigurement, compression of vital structures, neurologic dysfunction, and/or pain. Currently, the only effective management strategy is surgical resection. Converging evidence has demonstrated that the NF1 tumor suppressor protein, neurofibromin, negatively regulates activity in the mammalian Target of Rapamycin pathway. We employed a 2-strata clinical trial design. Stratum 1 included subjects with inoperable, NF1-associated progressive PN and sought to determine whether sirolimus safely and tolerably increases time to progression (TTP). Volumetric MRI analysis conducted at regular intervals was used to determine TTP relative to baseline imaging. The estimated median TTP of subjects receiving sirolimus was 15.4 months (95% CI: 14.3-23.7 mo), which was significantly longer than 11.9 months (P < .001), the median TTP of the placebo arm of a previous PN clinical trial with similar eligibility criteria. This study demonstrated that sirolimus prolongs TTP by almost 4 months in patients with NF1-associated progressive PN. Although the improvement in TTP is modest, given the lack of significant or frequent toxicity and the availability of few other treatment options, the use of sirolimus to slow the growth of progressive PN could be considered in select patients. © The Author(s) 2014. Published by Oxford University Press on behalf of the Society for Neuro-Oncology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com. JF - Neuro-oncology AU - Weiss, Brian AU - Widemann, Brigitte C AU - Wolters, Pamela AU - Dombi, Eva AU - Vinks, Alexander AU - Cantor, Alan AU - Perentesis, John AU - Schorry, Elizabeth AU - Ullrich, Nicole AU - Gutmann, David H AU - Tonsgard, James AU - Viskochil, David AU - Korf, Bruce AU - Packer, Roger J AU - Fisher, Michael J AD - Division of Oncology, Cincinnati Children's Hospital Medical Center, Cancer and Blood Diseases Institute, Cincinnati, Ohio (B.W., J.P.); Division of Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio (E.S.); Division of Clinical Pharmacology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio (A.V.); National Cancer Institute, Pediatric Oncology Branch, Bethesda, Maryland (B.C.W, E.D., P.W.); Department of Genetics, University of Alabama at Birmingham, Birmingham, Alabama (B.K.); Department of Preventitive Medicine, University of Alabama at Birmingham, Birmingham, Alabama (A.C.); Department of Neurology, Boston Children's Hospital, Boston, Massachusetts (N.U.); Department of Neurology, Washington University, St. Louis, Missouri (D.H.G.); Children's National Health System, Center for Neuroscience and Behavioral Medicine, Washington, DC (R.J.P.); Division of Oncology, The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania (M.J.F.); Division of Genetics, Primary Children's Hospital, Salt Lake City, Utah (D.V.); Division of Neurology, The University of Chicago Medicine Comer Children's Hospital, Chicago, Illinois (J.T.). Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 596 EP - 603 VL - 17 IS - 4 KW - Sirolimus KW - W36ZG6FT64 KW - Index Medicus KW - neurofibromatosis KW - NF1 KW - mTOR KW - sirolimus KW - rapamycin KW - plexiform neurofibroma KW - Young Adult KW - Disease-Free Survival KW - Humans KW - Adult KW - Treatment Outcome KW - Middle Aged KW - Child KW - Adolescent KW - Male KW - Female KW - Child, Preschool KW - Sirolimus -- adverse effects KW - Neurofibromatosis 1 -- drug therapy KW - Neurofibroma, Plexiform -- drug therapy KW - Spinal Neoplasms -- drug therapy KW - Sirolimus -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1663657556?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuro-oncology&rft.atitle=Sirolimus+for+progressive+neurofibromatosis+type+1-associated+plexiform+neurofibromas%3A+a+neurofibromatosis+Clinical+Trials+Consortium+phase+II+study.&rft.au=Weiss%2C+Brian%3BWidemann%2C+Brigitte+C%3BWolters%2C+Pamela%3BDombi%2C+Eva%3BVinks%2C+Alexander%3BCantor%2C+Alan%3BPerentesis%2C+John%3BSchorry%2C+Elizabeth%3BUllrich%2C+Nicole%3BGutmann%2C+David+H%3BTonsgard%2C+James%3BViskochil%2C+David%3BKorf%2C+Bruce%3BPacker%2C+Roger+J%3BFisher%2C+Michael+J&rft.aulast=Weiss&rft.aufirst=Brian&rft.date=2015-04-01&rft.volume=17&rft.issue=4&rft.spage=596&rft.isbn=&rft.btitle=&rft.title=Neuro-oncology&rft.issn=1523-5866&rft_id=info:doi/10.1093%2Fneuonc%2Fnou235 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-23 N1 - Date created - 2015-03-12 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Pediatr Blood Cancer. 2014 Sep;61(9):1598-602 [24753394] Am J Med Genet. 2000 May 15;92(2):132-5 [10797438] Oncologist. 2000;5(6):477-85 [11110599] Kidney Int. 2001 Jan;59(1):3-16 [11135052] Arch Dermatol. 2001 Nov;137(11):1421-5 [11708944] Curr Top Microbiol Immunol. 2004;279:339-59 [14560967] J Pain. 2003 Sep;4(7):407-14 [14622683] Comput Med Imaging Graph. 2004 Jul;28(5):257-65 [15249071] Brain. 1988 Dec;111 ( Pt 6):1355-81 [3145091] J Pediatr. 1997 Nov;131(5):678-82 [9403645] Am J Med Genet. 1999 Mar 26;89(1):1-6 [10469430] Am J Med Genet. 1999 Mar 26;89(1):31-7 [10469434] Cancer Res. 2005 Apr 1;65(7):2755-60 [15805275] Proc Natl Acad Sci U S A. 2005 Jun 14;102(24):8573-8 [15937108] Ann Neurol. 2006 Mar;59(3):490-8 [16453317] Am J Med Genet A. 2006 Sep 15;140(18):1893-8 [16906549] Neurology. 2007 Feb 27;68(9):643-7 [17215493] Cancer Res. 2008 Mar 1;68(5):1520-8 [18316617] Mol Cancer Ther. 2008 May;7(5):1237-45 [18483311] J Med Genet. 2009 Feb;46(2):81-5 [18930997] BMB Rep. 2009 May 31;42(5):239-44 [19470236] Neurology. 2009 Oct 20;73(16):1273-9 [19841379] Int J Cancer. 2010 Jan 15;126(2):563-71 [19634141] Transplant Proc. 2009 Dec;41(10):4285-8 [20005385] Cell Cycle. 2012 Jan 15;11(2):236-48 [22214661] PLoS One. 2012;7(4):e35711 [22558206] Neuroscience. 2012 Oct 25;223:102-13 [22750207] Pediatr Blood Cancer. 2013 Jan;60(1):59-64 [22645095] Lancet Oncol. 2012 Dec;13(12):1218-24 [23099009] Ther Drug Monit. 2013 Jun;35(3):332-7 [23666574] Neurology. 2013 Nov 19;81(21 Suppl 1):S6-14 [24249806] Neuro Oncol. 2014 May;16(5):707-18 [24500418] Am J Med Genet A. 2014 Jun;164A(6):1431-7 [24664633] Pediatr Blood Cancer. 2014 Jun;61(6):982-6 [24851266] Oncotarget. 2014 Mar 30;5(6):1502-14 [24681606] Pediatrics. 2014 Jun;133(6):e1792-7 [24864177] Erratum In: Neuro Oncol. 2015 Jun;17(6):905 [26023102] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/neuonc/nou235 ER - TY - JOUR T1 - Insights into the mechanism of inhibition of CXCR4: identification of Piperidinylethanamine analogs as anti-HIV-1 inhibitors. AN - 1663656945; 25583709 AB - The cellular entry of HIV-1 into CD4(+) T cells requires ordered interactions of HIV-1 envelope glycoprotein with C-X-C chemokine receptor type 4 (CXCR4) receptors. However, such interactions, which should be critical for rational structure-based discovery of new CXCR4 inhibitors, remain poorly understood. Here we first determined the effects of amino acid substitutions in CXCR4 on HIV-1NL 4 - 3 glycoprotein-elicited fusion events using site-directed mutagenesis-based fusion assays and identified 11 potentially key amino acid substitutions, including D97A and E288A, which caused >30% reductions in fusion. We subsequently carried out a computational search of a screening library containing ∼604,000 compounds, in order to identify potential CXCR4 inhibitors. The computational search used the shape of IT1t, a known CXCR4 inhibitor, as a reference and employed various algorithms, including shape similarity, isomer generation, and docking against a CXCR4 crystal structure. Sixteen small molecules were identified for biological assays based on their high shape similarity to IT1t, and their putative binding modes formed hydrogen bond interactions with the amino acids identified above. Three compounds with piperidinylethanamine cores showed activity and were resynthesized. One molecule, designated CX6, was shown to significantly inhibit fusion elicited by X4 HIV-1NL 4 - 3 glycoprotein (50% inhibitory concentration [IC50], 1.9 μM), to inhibit Ca(2+) flux elicited by stromal cell-derived factor 1α (SDF-1α) (IC50, 92 nM), and to exert anti-HIV-1 activity (IC50, 1.5 μM). Structural modeling demonstrated that CX6 bound to CXCR4 through hydrogen bond interactions with Asp97 and Glu288. Our study suggests that targeting CXCR4 residues important for fusion elicited by HIV-1 envelope glycoprotein should be a useful and feasible approach to identifying novel CXCR4 inhibitors, and it provides important insights into the mechanism by which small-molecule CXCR4 inhibitors exert their anti-HIV-1 activities. Copyright © 2015, American Society for Microbiology. All Rights Reserved. JF - Antimicrobial agents and chemotherapy AU - Das, Debananda AU - Maeda, Kenji AU - Hayashi, Yasuhiro AU - Gavande, Navnath AU - Desai, Darshan V AU - Chang, Simon B AU - Ghosh, Arun K AU - Mitsuya, Hiroaki AD - Experimental Retrovirology Section, HIV and AIDS Malignancy Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA dasd@mail.nih.gov. ; Experimental Retrovirology Section, HIV and AIDS Malignancy Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. ; Departments of Chemistry and Medicinal Chemistry, Purdue University, West Lafayette, Indiana, USA. ; Experimental Retrovirology Section, HIV and AIDS Malignancy Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA Departments of Hematology and Infectious Diseases, Kumamoto University Graduate School of Medical and Pharmaceutical Sciences, Kumamoto, Japan. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 1895 EP - 1904 VL - 59 IS - 4 KW - Anti-HIV Agents KW - 0 KW - CX6 compound KW - HIV Fusion Inhibitors KW - Piperidines KW - Receptors, CXCR4 KW - Small Molecule Libraries KW - Viral Envelope Proteins KW - Index Medicus KW - Mutagenesis, Site-Directed KW - High-Throughput Screening Assays KW - Cell Survival -- drug effects KW - Humans KW - Algorithms KW - Viral Envelope Proteins -- metabolism KW - Hydrogen Bonding KW - Amino Acid Substitution KW - Piperidines -- pharmacology KW - Piperidines -- chemical synthesis KW - Anti-HIV Agents -- chemical synthesis KW - HIV Fusion Inhibitors -- chemical synthesis KW - Receptors, CXCR4 -- chemistry KW - Anti-HIV Agents -- pharmacology KW - Receptors, CXCR4 -- antagonists & inhibitors KW - HIV-1 -- drug effects KW - HIV Fusion Inhibitors -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1663656945?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+agents+and+chemotherapy&rft.atitle=Insights+into+the+mechanism+of+inhibition+of+CXCR4%3A+identification+of+Piperidinylethanamine+analogs+as+anti-HIV-1+inhibitors.&rft.au=Das%2C+Debananda%3BMaeda%2C+Kenji%3BHayashi%2C+Yasuhiro%3BGavande%2C+Navnath%3BDesai%2C+Darshan+V%3BChang%2C+Simon+B%3BGhosh%2C+Arun+K%3BMitsuya%2C+Hiroaki&rft.aulast=Das&rft.aufirst=Debananda&rft.date=2015-04-01&rft.volume=59&rft.issue=4&rft.spage=1895&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+agents+and+chemotherapy&rft.issn=1098-6596&rft_id=info:doi/10.1128%2FAAC.04654-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-15 N1 - Date created - 2015-03-12 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Virol. 2000 Feb;74(4):1787-93 [10644351] J Biol Chem. 2000 Aug 4;275(31):23736-44 [10825158] J Biol Chem. 2001 Apr 27;276(17):14153-60 [11154697] J Biol Chem. 2001 Sep 14;276(37):35194-200 [11454872] J Med Chem. 2004 Mar 25;47(7):1739-49 [15027865] Science. 1986 Jul 18;233(4761):343-6 [2425430] J Virol. 1986 Aug;59(2):284-91 [3016298] J Virol. 1992 Apr;66(4):2232-9 [1548759] Virology. 1997 Jun 23;233(1):193-8 [9201229] Nat Med. 1998 Jan;4(1):72-7 [9427609] Mol Pharmacol. 1998 Feb;53(2):340-5 [9463493] Biochem Biophys Res Commun. 1998 Dec 30;253(3):877-82 [9918823] J Biol Chem. 2006 May 5;281(18):12688-98 [16476734] Curr Top Med Chem. 2006;6(13):1319-33 [16918451] J Med Chem. 2006 Oct 19;49(21):6177-96 [17034125] J Med Chem. 2007 Jan 11;50(1):74-82 [17201411] J Biol Chem. 2007 Feb 23;282(8):5111-5 [17197449] Antimicrob Agents Chemother. 2007 Jul;51(7):2351-8 [17452489] J Biol Chem. 2007 Aug 31;282(35):25677-86 [17591774] J Biol Chem. 2007 Sep 14;282(37):27354-65 [17599916] Antimicrob Agents Chemother. 2008 Jun;52(6):2111-9 [18378711] J Mol Biol. 2008 Sep 12;381(4):956-74 [18590744] J Med Chem. 2008 Dec 25;51(24):7915-20 [19053768] Clin Infect Dis. 2009 Mar 15;48(6):798-805 [19193109] Biochem Pharmacol. 2009 Dec 1;78(11):1382-90 [19631193] Antimicrob Agents Chemother. 2010 Feb;54(2):817-24 [19949058] J Med Chem. 2010 Feb 11;53(3):1250-60 [20043638] J Med Chem. 2010 Apr 22;53(8):3376-88 [20297846] J Chem Inf Model. 2010 Apr 26;50(4):572-84 [20235588] J Med Chem. 2010 May 27;53(10):3862-86 [20158188] Science. 2010 Nov 19;330(6007):1066-71 [20929726] Antimicrob Agents Chemother. 2011 Apr;55(4):1717-27 [21282450] ChemMedChem. 2011 May 2;6(5):834-9 [21312334] Expert Opin Investig Drugs. 2012 Mar;21(3):341-53 [22283809] Br J Pharmacol. 2012 Mar;165(6):1688-703 [21864311] Curr Pharm Des. 2012;18(9):1311-6 [22316155] Expert Opin Emerg Drugs. 2012 Jun;17(2):135-45 [22533737] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/AAC.04654-14 ER - TY - JOUR T1 - Exposure assessment of adult intake of bisphenol A (BPA) with emphasis on canned food dietary exposures. AN - 1662001048; 25645382 AB - Bisphenol A (BPA) is a high-volume, synthetic compound found in epoxy resins and plastics used in food packaging. Food is believed to be a major source of BPA intake. In this study, we measured the concentration of BPA in convenience samplings of foodstuffs purchased in Dallas, Texas. Sampling entailed collection of 204 samples of fresh, frozen, and canned foods in two rounds in 2010. BPA was positive in 73% of the canned food samples, while it was found in only 7% of non-canned foods at low concentrations. The results of this food sampling program were used to calculate adult dietary intakes of BPA. A pathway approach combined food intakes, a "canned fraction" parameter which described what portion of total intake of that food came from canned products, and measured food concentrations. Dietary intakes were calculated as 12.6 ng/kg-day, of which 12.4 ng/kg-day was from canned foods. Canned vegetable intakes alone were 11.9 ng/kg-day. This dietary intake was compared to total intakes of BPA estimated from urine measurements of the National Health and Nutrition Examination Survey (NHANES). Total adult central tendency intakes ranged from 30 to 70 ng/kg-day for NHANES cycles between 2005 and 2010. Three possibilities were explored to explain the difference between these two approaches for intake estimation. Not all foods which may have been canned, particularly canned beverages such as soft drinks, were sampled in our food sampling program. Second, non-food pathways of exposure may be important for adults, including thermal paper exposures, and dust and air exposures. Finally, our canned food concentrations may not be adequately representative of canned foods in the United States; they were found to be generally lower compared to canned food concentrations measured in six other worldwide food surveys including three in North America. Our finding that canned food concentrations greatly exceeded non-canned concentrations was consistent with other studies, and underscores the importance of canned foods in the overall exposure of adults of BPA. Copyright © 2015. Published by Elsevier Ltd. JF - Environment international AU - Lorber, Matthew AU - Schecter, Arnold AU - Paepke, Olaf AU - Shropshire, William AU - Christensen, Krista AU - Birnbaum, Linda AD - National Center for Environmental Assessment, US Environmental Protection Agency, Washington, DC, USA. Electronic address: lorber.matthew@epa.gov. ; Dept of Pharmacology and Toxicology, University of Louisville, 2363 Valleta Lane, Louisville, KY, USA. ; Eurofins GfA Lab Service, Hamburg, Germany. ; Environmental and Occupational Health Sciences Program, University of Texas School of Public Health, Dallas, TX, USA. ; Wisconsin Division of Public Health, Bureau of Environmental and Occupational Health, 1 West Wilson Street, Room 145, Madison, WI, USA. ; NCI/NIH, Research Triangle Park, NC, USA. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 55 EP - 62 VL - 77 KW - Benzhydryl Compounds KW - 0 KW - Phenols KW - bisphenol A KW - MLT3645I99 KW - Index Medicus KW - Bisphenol A KW - NHANES KW - Dietary exposure KW - BPA KW - Frozen Foods -- analysis KW - Vegetables -- chemistry KW - Humans KW - Food Packaging -- methods KW - Adult KW - Diet Surveys KW - Texas KW - Nutrition Surveys KW - Diet KW - Food, Preserved -- analysis KW - Food Contamination -- statistics & numerical data KW - Environmental Exposure -- analysis KW - Phenols -- urine KW - Phenols -- analysis KW - Benzhydryl Compounds -- urine KW - Benzhydryl Compounds -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1662001048?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environment+international&rft.atitle=Exposure+assessment+of+adult+intake+of+bisphenol+A+%28BPA%29+with+emphasis+on+canned+food+dietary+exposures.&rft.au=Lorber%2C+Matthew%3BSchecter%2C+Arnold%3BPaepke%2C+Olaf%3BShropshire%2C+William%3BChristensen%2C+Krista%3BBirnbaum%2C+Linda&rft.aulast=Lorber&rft.aufirst=Matthew&rft.date=2015-04-01&rft.volume=77&rft.issue=&rft.spage=55&rft.isbn=&rft.btitle=&rft.title=Environment+international&rft.issn=1873-6750&rft_id=info:doi/10.1016%2Fj.envint.2015.01.008 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-24 N1 - Date created - 2015-03-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Anal Sci. 2003 Dec;19(12):1663-6 [14696933] Proc Natl Acad Sci U S A. 2015 Feb 3;112(5):1475-80 [25583509] Food Addit Contam. 2005 Jan;22(1):65-72 [15895613] Toxicology. 2006 Sep 21;226(2-3):79-89 [16860916] Environ Res. 2007 Jan;103(1):9-20 [16750524] Reprod Toxicol. 2007 Aug-Sep;24(2):139-77 [17825522] J Chromatogr A. 2008 Aug 22;1202(2):189-95 [18639882] J Expo Sci Environ Epidemiol. 2008 Nov;18(6):608-15 [18414515] J Agric Food Chem. 2009 Feb 25;57(4):1307-11 [19170636] Environ Res. 2009 Jul;109(5):629-33 [19426969] Chemosphere. 2009 Aug;76(6):755-60 [19535125] Biomed Chromatogr. 2009 Nov;23(11):1186-90 [19444800] J Expo Sci Environ Epidemiol. 2010 Mar;20(2):115-6 [20160736] J Dent Hyg. 2010 Summer;84(3):145-50 [20579427] Anal Bioanal Chem. 2010 Sep;398(1):571-6 [20623271] Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2010 Nov;27(11):1627-37 [20835936] Pediatrics. 2010 Oct;126(4):760-8 [20819896] Environ Sci Technol. 2010 Dec 15;44(24):9425-30 [21038926] Public Health Nutr. 2011 Apr;14(4):575-83 [21070685] J Expo Sci Environ Epidemiol. 2011 May-Jun;21(3):272-9 [20237498] Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2011 Jun;28(6):791-8 [21623504] Arch Environ Contam Toxicol. 2011 Jul;61(1):68-73 [21221962] J Agric Food Chem. 2011 Jul 13;59(13):7178-85 [21598963] Environ Sci Technol. 2011 Aug 15;45(16):7044-50 [21732633] J Expo Sci Environ Epidemiol. 2012 May-Jun;22(3):219-26 [22333730] Environ Sci Technol. 2012 Jun 19;46(12):6515-22 [22591511] J Agric Food Chem. 2013 May 15;61(19):4655-62 [23614805] Reprod Toxicol. 2013 Dec;42:132-55 [23994667] Food Chem Toxicol. 2013 Dec;62:935-48 [23867546] Biomed Chromatogr. 2004 Oct;18(8):501-7 [15386523] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.envint.2015.01.008 ER - TY - JOUR T1 - SLC13A5 is a novel transcriptional target of the pregnane X receptor and sensitizes drug-induced steatosis in human liver. AN - 1658708638; 25628225 AB - The solute carrier family 13 member 5 (SLC13A5) is a sodium-coupled transporter that mediates cellular uptake of citrate, which plays important roles in the synthesis of fatty acids and cholesterol. Recently, the pregnane X receptor (PXR, NR1I2), initially characterized as a xenobiotic sensor, has been functionally linked to the regulation of various physiologic processes that are associated with lipid metabolism and energy homeostasis. Here, we show that the SLC13A5 gene is a novel transcriptional target of PXR, and altered expression of SLC13A5 affects lipid accumulation in human liver cells. The prototypical PXR activator rifampicin markedly induced the mRNA and protein expression of SLC13A5 in human primary hepatocytes. Utilizing cell-based luciferase reporter assays, electrophoretic mobility shift assays, and chromatin immunoprecipitation assays, we identified and functionally characterized two enhancer modules located upstream of the SLC13A5 gene transcription start site that are associated with regulation of PXR-mediated SLC13A5 induction. Functional analysis further revealed that rifampicin can enhance lipid accumulation in human primary hepatocytes, and knockdown of SLC13A5 expression alone leads to a significant decrease of the lipid content in HepG2 cells. Overall, our results uncover SLC13A5 as a novel target gene of PXR and may contribute to drug-induced steatosis and metabolic disorders in humans. U.S. Government work not protected by U.S. copyright. JF - Molecular pharmacology AU - Li, Linhao AU - Li, Haishan AU - Garzel, Brandy AU - Yang, Hui AU - Sueyoshi, Tatsuya AU - Li, Qing AU - Shu, Yan AU - Zhang, Junran AU - Hu, Bingfang AU - Heyward, Scott AU - Moeller, Timothy AU - Xie, Wen AU - Negishi, Masahiko AU - Wang, Hongbing AD - Department of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, Maryland (L.L., H.L., B.G., H.Y., Q.L., Y.S., H.W.); Pharmacogenetics Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental and Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina (T.S., M.N.); Department of Radiation Oncology, Case Western Reserve University, Cleveland, Ohio (J.Z.); Bioreclamation In Vitro Technologies, Baltimore, Maryland (S.H., T.M.); and Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh School of Pharmacy, Pittsburgh, Pennsylvania (B.H., W.X.). ; Department of Pharmaceutical Sciences, University of Maryland School of Pharmacy, Baltimore, Maryland (L.L., H.L., B.G., H.Y., Q.L., Y.S., H.W.); Pharmacogenetics Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental and Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina (T.S., M.N.); Department of Radiation Oncology, Case Western Reserve University, Cleveland, Ohio (J.Z.); Bioreclamation In Vitro Technologies, Baltimore, Maryland (S.H., T.M.); and Center for Pharmacogenetics and Department of Pharmaceutical Sciences, University of Pittsburgh School of Pharmacy, Pittsburgh, Pennsylvania (B.H., W.X.) hwang@rx.umaryland.edu. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 674 EP - 682 VL - 87 IS - 4 KW - Receptors, Steroid KW - 0 KW - SLC13A5 protein, human KW - Symporters KW - pregnane X receptor KW - Rifampin KW - VJT6J7R4TR KW - Index Medicus KW - Rifampin -- toxicity KW - Animals KW - Gene Knockdown Techniques KW - Hep G2 Cells KW - Humans KW - Enhancer Elements, Genetic KW - Transcription, Genetic KW - Response Elements KW - Mice, Transgenic KW - Transcriptional Activation KW - Lipid Metabolism KW - Hepatocytes -- metabolism KW - Fatty Liver -- chemically induced KW - Receptors, Steroid -- antagonists & inhibitors KW - Fatty Liver -- metabolism KW - Symporters -- metabolism KW - Symporters -- genetics KW - Receptors, Steroid -- metabolism KW - Liver -- metabolism KW - Receptors, Steroid -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658708638?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+pharmacology&rft.atitle=SLC13A5+is+a+novel+transcriptional+target+of+the+pregnane+X+receptor+and+sensitizes+drug-induced+steatosis+in+human+liver.&rft.au=Li%2C+Linhao%3BLi%2C+Haishan%3BGarzel%2C+Brandy%3BYang%2C+Hui%3BSueyoshi%2C+Tatsuya%3BLi%2C+Qing%3BShu%2C+Yan%3BZhang%2C+Junran%3BHu%2C+Bingfang%3BHeyward%2C+Scott%3BMoeller%2C+Timothy%3BXie%2C+Wen%3BNegishi%2C+Masahiko%3BWang%2C+Hongbing&rft.aulast=Li&rft.aufirst=Linhao&rft.date=2015-04-01&rft.volume=87&rft.issue=4&rft.spage=674&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=1521-0111&rft_id=info:doi/10.1124%2Fmol.114.097287 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-26 N1 - Date created - 2015-02-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Pharmacokinet. 2003;42(15):1331-57 [14674787] Biochem J. 2003 Aug 15;374(Pt 1):21-6 [12826022] Histochemistry. 1992 Jul;97(6):493-7 [1385366] J Biol Chem. 1995 Mar 17;270(11):5779-85 [7890707] J Biol Chem. 1998 Aug 14;273(33):20972-81 [9694847] Mol Cell Biol. 1998 Oct;18(10):5652-8 [9742082] Annu Rev Physiol. 2006;68:159-91 [16460270] Biochem J. 2006 Jul 1;397(1):25-9 [16608441] J Pharmacol Exp Ther. 2007 Jan;320(1):72-80 [17041008] Mol Pharmacol. 2007 Jan;71(1):220-9 [17028159] Am J Physiol Gastrointest Liver Physiol. 2007 Jan;292(1):G402-8 [16973915] Oncogene. 2007 Jan 11;26(2):258-68 [16819505] J Biol Chem. 2007 Mar 30;282(13):9768-76 [17267396] Nat Protoc. 2007;2(7):1722-33 [17641637] World J Gastroenterol. 2008 Jan 7;14(1):22-8 [18176957] Gastroenterology. 2008 Feb;134(2):556-67 [18242221] Drug Metab Pharmacokinet. 2008;23(1):8-13 [18305370] Pharm Res. 2009 Aug;26(8):1807-15 [19415465] Trends Endocrinol Metab. 2009 Aug;20(6):273-9 [19595610] Chem Biol Interact. 2010 Mar 30;184(3):376-87 [20079722] Adv Drug Deliv Rev. 2010 Oct 30;62(13):1238-49 [20727377] BMC Genomics. 2010;11:701 [21156036] Biochem Biophys Res Commun. 2011 Mar 18;406(3):371-6 [21329659] Pharmacol Res. 2011 Jul;64(1):4-10 [21397695] Cell Metab. 2011 Aug 3;14(2):184-95 [21803289] J Pharmacol Exp Ther. 2011 Nov;339(2):487-98 [21856859] Trends Mol Med. 2011 Nov;17(11):641-9 [21764377] Carcinogenesis. 2012 Aug;33(8):1487-93 [22610075] FASEB J. 2012 Sep;26(9):3625-36 [22661004] Diabetes. 2013 Jun;62(6):1876-87 [23349477] Pflugers Arch. 2014 Jan;466(1):119-30 [24114175] Mol Pharmacol. 1999 Dec;56(6):1329-39 [10570062] Nature. 2000 Jul 27;406(6794):435-9 [10935643] Genes Dev. 2000 Dec 1;14(23):3014-23 [11114890] J Biol Chem. 2001 May 4;276(18):14581-7 [11297522] Cell Tissue Res. 2001 Oct;306(1):85-99 [11683185] Semin Liver Dis. 2002;22(2):185-94 [12016549] Nat Rev Drug Discov. 2002 Apr;1(4):259-66 [12120277] Biochem J. 2002 Oct 15;367(Pt 2):313-9 [12186628] J Biol Chem. 2002 Oct 18;277(42):39469-76 [12177002] Biochem Biophys Res Commun. 2002 Dec 6;299(3):465-71 [12445824] J Biol Chem. 2003 Apr 18;278(16):14146-52 [12571232] Biochem J. 2004 Mar 15;378(Pt 3):949-57 [14656221] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/mol.114.097287 ER - TY - JOUR T1 - Phase 1 trial and pharmacokinetic study of the oral platinum analog satraplatin in children and young adults with refractory solid tumors including brain tumors. AN - 1658425450; 25556988 AB - Based on pre-clinical and clinical activity in adult refractory tumors, and absence of significant neuro-, nephro-, or oto-toxicity, we conducted a pediatric phase 1 trial to determine the toxicities, maximum tolerated dose (MTD), and pharmacokinetics of satraplatin, an oral platinum analogue, in children and young adults with refractory solid tumors. Satraplatin was administered orally once daily on days 1-5 of a 28-day cycle at dose level (DL) 1 (60 mg/m(2) /dose), and DL2 (80 mg/m(2) /dose). Toxicities, responses, satraplatin pharmacokinetics, and pharmacogenomic expression of specific DNA repair genes were evaluated. Nine patients received 1-15 cycles (median = 2). The MTD was exceeded at DL2 with delayed prolonged myelosuppression as dose-limiting toxicity (DLT) in 2/4 patients. At DL1, 0/5 patients had DLTs. Common non-DLTs included myelosuppression, gastrointestinal toxicities, fatigue, headache, liver enzyme elevation, and electrolyte abnormalities. No significant neuro-, nephro-, or oto-toxicity was observed. No objective responses were observed but 2 patients experienced prolonged disease stabilization (---6-15 cycles). Satraplatin exposure (day 1 plasma ultrafiltrate area under the curve) was similar at DL1 and DL2. A strong correlation between estimated creatinine clearance and satraplatin pharmacokinetic parameters (clearance, area under the curve, and peak concentration) was observed. The MTD of oral satraplatin in children with solid tumors was 60 mg/m(2) /dose daily ×5 days every 28 days, which is lower than the adult recommended dose of 80-120 mg/m(2) /dose. The toxicity profile was similar to adults and delayed myelosuppression was the DLT. No significant neuro-, nephro- or oto-toxicities were observed. © 2015 Wiley Periodicals, Inc. JF - Pediatric blood & cancer AU - Akshintala, Srivandana AU - Marcus, Leigh AU - Warren, Katherine E AU - Murphy, Robert F AU - Sissung, Tristan M AU - Srivastava, Anjali AU - Goodspeed, Wendy J AU - Goodwin, Anne AU - Brewer, Carmen C AU - Zalewski, Christopher AU - King, Kelly A AU - Kim, AeRang AU - Figg, William D AU - Widemann, Brigitte C AD - Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 603 EP - 610 VL - 62 IS - 4 KW - Antineoplastic Agents KW - 0 KW - Organoplatinum Compounds KW - satraplatin KW - 8D7B37T28G KW - Index Medicus KW - phase 1 trial KW - solid tumors KW - pediatric KW - Administration, Oral KW - Young Adult KW - Dose-Response Relationship, Drug KW - Humans KW - Child KW - Maximum Tolerated Dose KW - Adolescent KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Male KW - Female KW - DNA Repair -- drug effects KW - Child, Preschool KW - Organoplatinum Compounds -- pharmacokinetics KW - Brain Neoplasms -- pathology KW - Organoplatinum Compounds -- adverse effects KW - Organoplatinum Compounds -- administration & dosage KW - Brain Neoplasms -- drug therapy KW - Antineoplastic Agents -- administration & dosage KW - Antineoplastic Agents -- pharmacokinetics KW - Brain Neoplasms -- metabolism KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658425450?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pediatric+blood+%26+cancer&rft.atitle=Phase+1+trial+and+pharmacokinetic+study+of+the+oral+platinum+analog+satraplatin+in+children+and+young+adults+with+refractory+solid+tumors+including+brain+tumors.&rft.au=Akshintala%2C+Srivandana%3BMarcus%2C+Leigh%3BWarren%2C+Katherine+E%3BMurphy%2C+Robert+F%3BSissung%2C+Tristan+M%3BSrivastava%2C+Anjali%3BGoodspeed%2C+Wendy+J%3BGoodwin%2C+Anne%3BBrewer%2C+Carmen+C%3BZalewski%2C+Christopher%3BKing%2C+Kelly+A%3BKim%2C+AeRang%3BFigg%2C+William+D%3BWidemann%2C+Brigitte+C&rft.aulast=Akshintala&rft.aufirst=Srivandana&rft.date=2015-04-01&rft.volume=62&rft.issue=4&rft.spage=603&rft.isbn=&rft.btitle=&rft.title=Pediatric+blood+%26+cancer&rft.issn=1545-5017&rft_id=info:doi/10.1002%2Fpbc.25344 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-11 N1 - Date created - 2015-02-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437] J Clin Oncol. 1997 Jul;15(7):2691-700 [9215842] Cancer Chemother Pharmacol. 1998;42(2):142-8 [9654114] Br J Cancer. 1998 Nov;78(9):1170-4 [9820175] Ann Oncol. 1998 Dec;9(12):1315-22 [9932162] Invest New Drugs. 2005 Jan;23(1):79-84 [15528984] Cancer Chemother Pharmacol. 2006 Apr;57(4):483-90 [16172904] Expert Rev Anticancer Ther. 2006 Jul;6(7):973-82 [16831070] J Clin Oncol. 1999 Dec;17(12):3822-7 [10577855] J Natl Cancer Inst. 2000 Feb 2;92(3):179-81 [10655425] Biochem Pharmacol. 2006 Sep 14;72(6):693-700 [16844093] Cancer Chemother Pharmacol. 2007 Sep;60(4):589-600 [17541592] J Clin Oncol. 2008 Sep 20;26(27):4394-400 [18802151] Clin Cancer Res. 2009 Jun 1;15(11):3866-71 [19458055] J Clin Oncol. 2009 Nov 10;27(32):5431-8 [19805692] Clin Cancer Res. 2011 Mar 15;17(6):1632-40 [21278243] Cancer Chemother Pharmacol. 2012 Jan;69(1):247-52 [21706317] Ann Oncol. 2012 Apr;23(4):1037-44 [21828377] Anticancer Res. 2014 Jan;34(1):435-42 [24403499] Cancer Lett. 2014 May 1;346(2):163-71 [24462818] J Clin Oncol. 2012 Jul 1;30(19):2408-17 [22547603] Clin Genitourin Cancer. 2013 Sep;11(3):229-37 [23684781] Cancer Res. 1992 Oct 15;52(20):5674-80 [1327513] Cancer Res. 1993 Jun 1;53(11):2581-6 [8388318] Br J Cancer. 1993 Aug;68(2):240-50 [8347478] Br J Cancer. 1994 Sep;70(3):415-20 [8080724] Cancer Chemother Pharmacol. 1995;36(6):451-8 [7554035] Anticancer Res. 1996 Jul-Aug;16(4A):1857-62 [8712713] Jpn J Clin Oncol. 2000 Sep;30(9):377-84 [11095134] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/pbc.25344 ER - TY - JOUR T1 - Attenuation of cyclophosphamide-induced pulmonary toxicity in Swiss albino mice by naphthalimide-based organoselenium compound 2-(5-selenocyanatopentyl)-benzo[de]isoquinoline 1,3-dione. AN - 1652425040; 25471377 AB - The widely used antineoplastic drug cyclophosphamide causes pulmonary toxicity by inducing oxidative stress. Selenium, a dietary micronutrient, has been found to protect various organs from oxidative injuries. This study was designed to investigate the protective efficacy of an organoselenium compound 2-(5-selenocyanato-pentyl)-benzo[de]isoquinoline 1,3-dione against cyclophosphamide-induced pulmonary toxicity in Swiss albino mice. Cyclophosphamide (25 mg/kg b.w.) was administered intraperitoneally for 10 d and the organoselenium compound (3 mg/kg b.w.) was given by oral gavage in concomitant and pretreatment schedules. Various biochemical parameters related to oxidative stress and antioxidant enzymes along with histology of lungs were evaluated to assess the effect of the test compound. The oral LD50 of the test compound was more than 1000 mg/kg b.w. in Swiss albino mice. The test compound substantially ameliorated cyclophosphamide-induced pulmonary injury by reducing the levels of reactive oxygen species, reactive nitrogen species, and lipid peroxidation, respectively, by 14.88, 18.54, and 21.10% in concomitant treatment schedule and by 23.89, 35.73, and 30.76% in the pretreatment schedule as well as by restoring the level of reduced glutathione and activities of glutathione-S-transferase, superoxide dismutase, catalase, and glutathione peroxidase, respectively, by 36.88, 42.43, 38.0, 35.0, and 34.06% in the concomitant treatment schedule and by 66.02, 59.29, 57.23, 71.59, and 57.22% in the pretreatment schedule. The test compound also attenuated cyclophosphamide-induced histological alterations of lung tissue. The test compound emerged as an efficient antioxidant protecting lungs tissue from cyclophosphamide-induced injury. JF - Pharmaceutical biology AU - Ghosh, Prosenjit AU - Bhattacharjee, Arin AU - Basu, Abhishek AU - Singha Roy, Somnath AU - Bhattacharya, Sudin AD - Department of Cancer Chemoprevention, Chittaranjan National Cancer Institute , Kolkata, West Bengal , India. Y1 - 2015/04// PY - 2015 DA - April 2015 SP - 524 EP - 532 VL - 53 IS - 4 KW - 2-(5-selenocyanatopentyl)benzo(de)isoquinoline-1,3-dione KW - 0 KW - Antineoplastic Agents, Alkylating KW - Antioxidants KW - Naphthalimides KW - Organoselenium Compounds KW - Reactive Oxygen Species KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - lung KW - selenium KW - reactive oxygen species KW - lung toxicity KW - antioxidant KW - oxidative stress KW - Anticancer drug KW - Molecular Structure KW - Reactive Oxygen Species -- metabolism KW - Animals KW - Lethal Dose 50 KW - Mice KW - Female KW - Lung Injury -- chemically induced KW - Antioxidants -- toxicity KW - Cyclophosphamide -- toxicity KW - Naphthalimides -- therapeutic use KW - Naphthalimides -- toxicity KW - Lung -- pathology KW - Organoselenium Compounds -- therapeutic use KW - Lung Injury -- metabolism KW - Lung Injury -- prevention & control KW - Organoselenium Compounds -- toxicity KW - Antioxidants -- therapeutic use KW - Lung -- drug effects KW - Lung -- enzymology KW - Antineoplastic Agents, Alkylating -- toxicity KW - Lung Injury -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652425040?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmaceutical+biology&rft.atitle=Attenuation+of+cyclophosphamide-induced+pulmonary+toxicity+in+Swiss+albino+mice+by+naphthalimide-based+organoselenium+compound+2-%285-selenocyanatopentyl%29-benzo%5Bde%5Disoquinoline+1%2C3-dione.&rft.au=Ghosh%2C+Prosenjit%3BBhattacharjee%2C+Arin%3BBasu%2C+Abhishek%3BSingha+Roy%2C+Somnath%3BBhattacharya%2C+Sudin&rft.aulast=Ghosh&rft.aufirst=Prosenjit&rft.date=2015-04-01&rft.volume=53&rft.issue=4&rft.spage=524&rft.isbn=&rft.btitle=&rft.title=Pharmaceutical+biology&rft.issn=1744-5116&rft_id=info:doi/10.3109%2F13880209.2014.931440 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-14 N1 - Date created - 2015-01-29 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3109/13880209.2014.931440 ER - TY - JOUR T1 - The CDX1-microRNA-215 axis regulates colorectal cancer stem cell differentiation. AN - 1669447788; 25775580 AB - The transcription factor caudal-type homeobox 1 (CDX1) is a key regulator of differentiation in the normal colon and in colorectal cancer (CRC). CDX1 activates the expression of enterocyte genes, but it is not clear how the concomitant silencing of stem cell genes is achieved. MicroRNAs (miRNAs) are important mediators of gene repression and have been implicated in tumor suppression and carcinogenesis, but the roles of miRNAs in differentiation, particularly in CRC, remain poorly understood. Here, we identified microRNA-215 (miR-215) as a direct transcriptional target of CDX1 by using high-throughput small RNA sequencing to profile miRNA expression in two pairs of CRC cell lines: CDX1-low HCT116 and HCT116 with stable CDX1 overexpression, and CDX1-high LS174T and LS174T with stable CDX1 knockdown. Validation of candidate miRNAs identified by RNA-seq in a larger cell-line panel revealed miR-215 to be most significantly correlated with CDX1 expression. Quantitative ChIP-PCR and promoter luciferase assays confirmed that CDX1 directly activates miR-215 transcription. miR-215 expression is depleted in FACS-enriched cancer stem cells compared with unsorted samples. Overexpression of miR-215 in poorly differentiated cell lines causes a decrease in clonogenicity, whereas miR-215 knockdown increases clonogenicity and impairs differentiation in CDX1-high cell lines. We identified the genome-wide targets of miR-215 and found that miR-215 mediates the repression of cell cycle and stemness genes downstream of CDX1. In particular, the miR-215 target gene BMI1 has been shown to promote stemness and self-renewal and to vary inversely with CDX1. Our work situates miR-215 as a link between CDX1 expression and BMI1 repression that governs differentiation in CRC. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Jones, Matthew F AU - Hara, Toshifumi AU - Francis, Princy AU - Li, Xiao Ling AU - Bilke, Sven AU - Zhu, Yuelin AU - Pineda, Marbin AU - Subramanian, Murugan AU - Bodmer, Walter F AU - Lal, Ashish AD - Cancer and Immunogenetics Laboratory, Weatherall Institute of Molecular Medicine, Department of Oncology, University of Oxford, John Radcliffe Hospital, Oxford, OX3 9DS, United Kingdom; and Regulatory RNAs and Cancer Section and. ; Regulatory RNAs and Cancer Section and. ; Molecular Genetics Section, Genetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. ; Cancer and Immunogenetics Laboratory, Weatherall Institute of Molecular Medicine, Department of Oncology, University of Oxford, John Radcliffe Hospital, Oxford, OX3 9DS, United Kingdom; and walter.bodmer@hertford.ox.ac.uk ashish.lal@nih.gov. ; Regulatory RNAs and Cancer Section and walter.bodmer@hertford.ox.ac.uk ashish.lal@nih.gov. Y1 - 2015/03/31/ PY - 2015 DA - 2015 Mar 31 SP - E1550 EP - E1558 VL - 112 IS - 13 KW - BMI1 protein, human KW - 0 KW - CDX1 protein, human KW - Homeodomain Proteins KW - MIRN215 microRNA, human KW - MicroRNAs KW - Polycomb Repressive Complex 1 KW - EC 2.3.2.27 KW - Index Medicus KW - CDX1 KW - miRNA KW - miR-215 KW - colorectal cancer KW - cancer stem cells KW - Gene Expression Profiling KW - Transfection KW - Humans KW - CpG Islands KW - Colon -- metabolism KW - Sequence Analysis, RNA KW - Cell Differentiation KW - Cell Line, Tumor KW - HCT116 Cells KW - Polycomb Repressive Complex 1 -- metabolism KW - Gene Expression Regulation, Neoplastic KW - MicroRNAs -- metabolism KW - Colorectal Neoplasms -- metabolism KW - Homeodomain Proteins -- metabolism KW - Neoplastic Stem Cells -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669447788?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=The+CDX1-microRNA-215+axis+regulates+colorectal+cancer+stem+cell+differentiation.&rft.au=Jones%2C+Matthew+F%3BHara%2C+Toshifumi%3BFrancis%2C+Princy%3BLi%2C+Xiao+Ling%3BBilke%2C+Sven%3BZhu%2C+Yuelin%3BPineda%2C+Marbin%3BSubramanian%2C+Murugan%3BBodmer%2C+Walter+F%3BLal%2C+Ashish&rft.aulast=Jones&rft.aufirst=Matthew&rft.date=2015-03-31&rft.volume=112&rft.issue=13&rft.spage=E1550&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=1091-6490&rft_id=info:doi/10.1073%2Fpnas.1503370112 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-22 N1 - Date created - 2015-04-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Rev Cancer. 2011 Dec;11(12):849-64 [22113163] PLoS Genet. 2011 Nov;7(11):e1002363 [22102825] Proc Natl Acad Sci U S A. 2012 Jan 10;109(2):466-71 [22190486] PLoS One. 2012;7(1):e29275 [22238599] Nature. 2012 Feb 23;482(7386):524-8 [22358842] Am J Pathol. 2012 Apr;180(4):1509-21 [22349300] Nat Rev Cancer. 2012 Sep;12(9):613-26 [22898542] RNA Biol. 2012 Jun;9(6):781-91 [22664917] Proc Natl Acad Sci U S A. 2012 Dec 11;109(50):20584-9 [23112162] PLoS One. 2013;8(1):e55214 [23358900] Cell Stem Cell. 2013 May 2;12(5):602-15 [23642368] Nature. 2013 May 16;497(7449):378-82 [23644459] Nat Rev Mol Cell Biol. 2013 Aug;14(8):475-88 [23800994] Cancer Res. 2013 Sep 15;73(18):5798-809 [23867471] Mol Cell Biol. 2014 Feb;34(3):533-50 [24277930] Nat Med. 2014 Jan;20(1):29-36 [24292392] Genes Dev. 2014 Mar 1;28(5):438-50 [24532687] Oncogene. 2014 Mar 20;33(12):1601-8 [23584479] J Pathol. 2014 Sep;234(1):34-45 [24797403] Gut. 2014 Dec;63(12):1854-63 [24550372] Oncogene. 2015 Feb 26;34(9):1094-104 [24662829] Nat Genet. 2003 Jul;34(3):267-73 [12808457] Nucleic Acids Res. 2003 Sep 15;31(18):5238-46 [12954759] Proc Natl Acad Sci U S A. 2004 Jan 13;101(2):574-9 [14704280] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):2999-3004 [14973191] Gut. 2004 Oct;53(10):1416-23 [15361487] J Pathol. 2004 Nov;204(3):289-95 [15378566] Proc Natl Acad Sci U S A. 2005 May 24;102(21):7565-70 [15894614] Nature. 2005 Jun 9;435(7043):828-33 [15944707] Nature. 2005 Jun 9;435(7043):834-8 [15944708] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517] Biochim Biophys Acta. 2005 Dec 20;1731(3):168-78 [16321657] Mol Cell. 2007 Jun 8;26(5):745-52 [17540599] Curr Protoc Bioinformatics. 2008 Mar;Chapter 2:Unit 2.6 [18428685] Nat Genet. 2008 Jul;40(7):915-20 [18536716] Cancer Res. 2008 Dec 15;68(24):10094-104 [19074875] Cancer Res. 2008 Dec 15;68(24):10105-12 [19074876] Nat Rev Mol Cell Biol. 2009 Feb;10(2):126-39 [19165215] Proc Natl Acad Sci U S A. 2009 Feb 10;106(6):1936-41 [19188603] Brief Bioinform. 2009 Sep;10(5):490-7 [19332473] Genes Dev. 2009 Dec 1;23(23):2700-4 [19903759] Proc Natl Acad Sci U S A. 2010 Feb 23;107(8):3722-7 [20133591] Br J Surg. 2010 Jun;97(6):853-61 [20301167] Cancer Cell. 2010 Oct 19;18(4):367-81 [20951946] Proc Natl Acad Sci U S A. 2011 Mar 15;108(11):4382-7 [21368208] Nature. 2011 Oct 13;478(7368):255-9 [21927002] Gene Ther. 2011 Dec;18(12):1104-10 [21525952] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1073/pnas.1503370112 ER - TY - CPAPER T1 - Implicating the Alpha-2 Receptor in Unique Actions of Drugs T2 - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AN - 1669822717; 6341295 JF - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AU - Potter, William Y1 - 2015/03/28/ PY - 2015 DA - 2015 Mar 28 KW - Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669822717?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.atitle=Implicating+the+Alpha-2+Receptor+in+Unique+Actions+of+Drugs&rft.au=Potter%2C+William&rft.aulast=Potter&rft.aufirst=William&rft.date=2015-03-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/Annual_Meeting_EB_2015/Program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Cryo-Electron Microscopy Comes of Age: Applications to Molecular Pharmacology T2 - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AN - 1669822714; 6341299 JF - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AU - Subramaniam, Sriram Y1 - 2015/03/28/ PY - 2015 DA - 2015 Mar 28 KW - Age KW - Pharmacology KW - Microscopy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669822714?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.atitle=Cryo-Electron+Microscopy+Comes+of+Age%3A+Applications+to+Molecular+Pharmacology&rft.au=Subramaniam%2C+Sriram&rft.aulast=Subramaniam&rft.aufirst=Sriram&rft.date=2015-03-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/Annual_Meeting_EB_2015/Program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - The Scientific Review Officer and Program Officer Career Paths T2 - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AN - 1669822124; 6341146 JF - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AU - Pawlyk, Aaron Y1 - 2015/03/28/ PY - 2015 DA - 2015 Mar 28 KW - Reviews KW - Careers UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669822124?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.atitle=The+Scientific+Review+Officer+and+Program+Officer+Career+Paths&rft.au=Pawlyk%2C+Aaron&rft.aulast=Pawlyk&rft.aufirst=Aaron&rft.date=2015-03-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/Annual_Meeting_EB_2015/Program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Inflammatory Cell Dynamics in Cancer and Infection: Interrogating the Role of the Microbiome T2 - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AN - 1669822067; 6341259 JF - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AU - Goldszmid, Romina Y1 - 2015/03/28/ PY - 2015 DA - 2015 Mar 28 KW - Infection KW - Cancer KW - Inflammation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669822067?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.atitle=Inflammatory+Cell+Dynamics+in+Cancer+and+Infection%3A+Interrogating+the+Role+of+the+Microbiome&rft.au=Goldszmid%2C+Romina&rft.aulast=Goldszmid&rft.aufirst=Romina&rft.date=2015-03-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/Annual_Meeting_EB_2015/Program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Dynamic Regulation of the Nitrosothiol Proteome in Cardiovascular Disease T2 - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AN - 1669822051; 6341336 JF - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AU - Murphy, Elizabeth Y1 - 2015/03/28/ PY - 2015 DA - 2015 Mar 28 KW - Cardiovascular diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669822051?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.atitle=Dynamic+Regulation+of+the+Nitrosothiol+Proteome+in+Cardiovascular+Disease&rft.au=Murphy%2C+Elizabeth&rft.aulast=Murphy&rft.aufirst=Elizabeth&rft.date=2015-03-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/Annual_Meeting_EB_2015/Program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Science Policy as a Biomedical Career Path T2 - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AN - 1669821896; 6341145 JF - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AU - Fox, Meredith Y1 - 2015/03/28/ PY - 2015 DA - 2015 Mar 28 KW - Policies KW - Careers KW - Science policy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669821896?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.atitle=Science+Policy+as+a+Biomedical+Career+Path&rft.au=Fox%2C+Meredith&rft.aulast=Fox&rft.aufirst=Meredith&rft.date=2015-03-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/Annual_Meeting_EB_2015/Program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Training Future Biomedical Researchers: Challenges and Opportunities T2 - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AN - 1669821873; 6341159 JF - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AU - Desmond, Nancy Y1 - 2015/03/28/ PY - 2015 DA - 2015 Mar 28 KW - Training UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669821873?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.atitle=Training+Future+Biomedical+Researchers%3A+Challenges+and+Opportunities&rft.au=Desmond%2C+Nancy&rft.aulast=Desmond&rft.aufirst=Nancy&rft.date=2015-03-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/Annual_Meeting_EB_2015/Program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - The NINDS Anticonvulsant Screening Program--Background and Overview T2 - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AN - 1669821842; 6341214 JF - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AU - Kehne, John Y1 - 2015/03/28/ PY - 2015 DA - 2015 Mar 28 KW - Screening KW - Reviews KW - Anticonvulsants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669821842?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.atitle=The+NINDS+Anticonvulsant+Screening+Program--Background+and+Overview&rft.au=Kehne%2C+John&rft.aulast=Kehne&rft.aufirst=John&rft.date=2015-03-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/Annual_Meeting_EB_2015/Program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - A Medicinal Chemical Approach to Design of A1 Adenosine Receptor Agonists for Seizure Treatment T2 - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AN - 1669821160; 6341218 JF - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AU - Jacobson, Kenneth Y1 - 2015/03/28/ PY - 2015 DA - 2015 Mar 28 KW - Adenosine receptors KW - Seizures UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669821160?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.atitle=A+Medicinal+Chemical+Approach+to+Design+of+A1+Adenosine+Receptor+Agonists+for+Seizure+Treatment&rft.au=Jacobson%2C+Kenneth&rft.aulast=Jacobson&rft.aufirst=Kenneth&rft.date=2015-03-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/Annual_Meeting_EB_2015/Program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - New Directions in Supporting Science T2 - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AN - 1669821127; 6341162 JF - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AU - Rogers, Michael Y1 - 2015/03/28/ PY - 2015 DA - 2015 Mar 28 KW - Pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669821127?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.atitle=New+Directions+in+Supporting+Science&rft.au=Rogers%2C+Michael&rft.aulast=Rogers&rft.aufirst=Michael&rft.date=2015-03-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/Annual_Meeting_EB_2015/Program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Science: A Constant Rewrite T2 - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AN - 1669821044; 6341148 JF - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AU - Thomas, Christopher Y1 - 2015/03/28/ PY - 2015 DA - 2015 Mar 28 KW - Pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669821044?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.atitle=Science%3A+A+Constant+Rewrite&rft.au=Thomas%2C+Christopher&rft.aulast=Thomas&rft.aufirst=Christopher&rft.date=2015-03-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/Annual_Meeting_EB_2015/Program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - NIH Vascular Biology and Hypertension Branch Interest in Vascular Stiffness T2 - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AN - 1669820929; 6341202 JF - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AU - Oh, Young Y1 - 2015/03/28/ PY - 2015 DA - 2015 Mar 28 KW - Hypertension UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669820929?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.atitle=NIH+Vascular+Biology+and+Hypertension+Branch+Interest+in+Vascular+Stiffness&rft.au=Oh%2C+Young&rft.aulast=Oh&rft.aufirst=Young&rft.date=2015-03-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/Annual_Meeting_EB_2015/Program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Biomedical Careers in the Pharmaceutical Industry T2 - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AN - 1669820920; 6341142 JF - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AU - Clark, Janet Y1 - 2015/03/28/ PY - 2015 DA - 2015 Mar 28 KW - Careers KW - Pharmaceuticals KW - Pharmaceutical industry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669820920?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.atitle=Biomedical+Careers+in+the+Pharmaceutical+Industry&rft.au=Clark%2C+Janet&rft.aulast=Clark&rft.aufirst=Janet&rft.date=2015-03-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/Annual_Meeting_EB_2015/Program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Assuring a Bright Future for Biomedical Research T2 - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AN - 1669820686; 6341160 JF - 2015 Annual Meeting of the American Society of Pharmacology and Experimental Therapeutics (ASPET 2015) AU - Silberberg, Shai Y1 - 2015/03/28/ PY - 2015 DA - 2015 Mar 28 KW - Pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669820686?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.atitle=Assuring+a+Bright+Future+for+Biomedical+Research&rft.au=Silberberg%2C+Shai&rft.aulast=Silberberg&rft.aufirst=Shai&rft.date=2015-03-28&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Society+of+Pharmacology+and+Experimental+Therapeutics+%28ASPET+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.aspet.org/Annual_Meeting_EB_2015/Program/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - JOUR T1 - Ubiquilin1 represses migration and epithelial-to-mesenchymal transition of human non-small cell lung cancer cells. AN - 1667347119; 24747970 AB - Ubiquilin1 (UBQLN1) is a ubiquitin-like domain and a ubiquitin-associated domain containing protein that has been reported to be involved in shuttling proteins to the proteasome, especially during endoplasmic reticulum-associated protein degradation. Thus, UBQLN1 function has been shown to be critical for combating a number of neurological disorders caused by protein aggregation, such as amyotrophic lateral sclerosis, Alzheimer's disease and Huntington's disease. A role for UBQLN1 in regulating processes involved in tumorigenesis has not been demonstrated. Herein, we show that loss of UBQLN1 causes increased cell migration and invasion, actin cytoskeleton reorganization and induction of epithelial-to-mesenchymal transition (EMT). Loss of UBQLN1 results in a significant decrease in the expression of epithelial markers including E-cadherin and claudin1, whereas expression of mesenchymal markers including Vimentin, Snail and ZEB1 are significantly elevated. Interestingly, we found that ZEB1 is required for induction of mesenchymal-like properties following loss of UBQLN1 and ZEB1 is capable of repressing expression of UBQLN1, suggesting a physiological, reciprocal regulation of EMT by UBQLN1 and ZEB1. Further, we find evidence for a role for UBQLN2 in also regulating EMT and cell migration. These observations have potential clinical relevance because the UBQLN1 gene is lost and underexpressed in a large percentage of human cancer cell lines, and primary human lung cancer samples and recurrent mutations in all five UBQLN family members have been identified in human lung cancers. Taken together, our results suggest for the first time a role for UBQLN family members in cancer biology. JF - Oncogene AU - Shah, P P AU - Lockwood, W W AU - Saurabh, K AU - Kurlawala, Z AU - Shannon, S P AU - Waigel, S AU - Zacharias, W AU - Beverly, L J AD - James Graham Brown Cancer Center, University of Louisville, Louisville, KY, USA. ; Cancer Biology and Genetics Section, Cancer Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA. ; 1] James Graham Brown Cancer Center, University of Louisville, Louisville, KY, USA [2] Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY, USA. ; 1] James Graham Brown Cancer Center, University of Louisville, Louisville, KY, USA [2] Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY, USA [3] Division of Hematology and Oncology, Department of Medicine, University of Louisville School of Medicine, Louisville, KY, USA. Y1 - 2015/03/26/ PY - 2015 DA - 2015 Mar 26 SP - 1709 EP - 1717 VL - 34 IS - 13 KW - Carrier Proteins KW - 0 KW - Cell Cycle Proteins KW - Homeodomain Proteins KW - Transcription Factors KW - UBQLN1 protein, human KW - ZEB1 protein, human KW - Zinc Finger E-box-Binding Homeobox 1 KW - Adenosine Triphosphatases KW - EC 3.6.1.- KW - CDC48 protein KW - Index Medicus KW - Transcription Factors -- physiology KW - Neoplasm Invasiveness KW - Adenosine Triphosphatases -- physiology KW - Humans KW - Homeodomain Proteins -- physiology KW - Endoplasmic Reticulum Stress KW - Cell Line, Tumor KW - Cell Movement KW - Cell Cycle Proteins -- physiology KW - Carrier Proteins -- physiology KW - Lung Neoplasms -- pathology KW - Epithelial-Mesenchymal Transition KW - Carcinoma, Non-Small-Cell Lung -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1667347119?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Ubiquilin1+represses+migration+and+epithelial-to-mesenchymal+transition+of+human+non-small+cell+lung+cancer+cells.&rft.au=Shah%2C+P+P%3BLockwood%2C+W+W%3BSaurabh%2C+K%3BKurlawala%2C+Z%3BShannon%2C+S+P%3BWaigel%2C+S%3BZacharias%2C+W%3BBeverly%2C+L+J&rft.aulast=Shah&rft.aufirst=P&rft.date=2015-03-26&rft.volume=34&rft.issue=13&rft.spage=1709&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2014.97 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-04 N1 - Date created - 2015-03-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Mol Neurosci. 2009 May;38(1):19-30 [18953672] J Clin Invest. 2009 Jun;119(6):1420-8 [19487818] J Clin Invest. 2009 Jun;119(6):1429-37 [19487819] J Clin Invest. 2009 Jun;119(6):1438-49 [19487820] J Cell Biol. 2009 Oct 19;187(2):201-17 [19822669] Cell. 2009 Nov 25;139(5):871-90 [19945376] J Am Soc Nephrol. 2010 Feb;21(2):212-22 [20019167] Cancer Sci. 2010 Feb;101(2):293-9 [19961486] J Cell Sci. 2010 Apr 1;123(Pt 7):1031-8 [20332119] J Biol Chem. 2010 May 28;285(22):17098-111 [20338999] Free Radic Res. 2011 Jun;45(6):692-8 [21417786] Proc Natl Acad Sci U S A. 2012 Jan 17;109(3):E119-26 [22233804] J Surg Oncol. 2012 Jun 15;105(8):830-4 [22213004] Oncogene. 2012 Jun 28;31(26):3124-35 [22081074] PLoS One. 2012;7(12):e53209 [23300891] Brain Res. 2013 Aug 2;1524:62-73 [23774650] Oncogene. 2000 Aug 3;19(33):3823-8 [10949939] Nature. 2002 Dec 12;420(6916):629-35 [12478284] Curr Opin Cell Biol. 2003 Dec;15(6):740-6 [14644200] Nature. 2004 Jun 24;429(6994):834-40 [15215855] J Proteome Res. 2006 May;5(5):1143-54 [16674103] Cancer Res. 2006 May 15;66(10):5338-45 [16707460] Cancer Res. 2006 Sep 1;66(17):8319-26 [16951136] J Cell Biol. 2006 Sep 25;174(7):963-71 [17000876] Mol Biol Cell. 2006 Nov;17(11):4606-18 [16914519] Cancer Res. 2007 Apr 1;67(7):3461-7 [17409457] Neurosci Lett. 2007 Aug 31;424(1):1-5 [17709205] Curr Med Chem. 2008;15(1):47-60 [18220762] Cell Mol Life Sci. 2009 Mar;66(5):773-87 [19011757] J Biol Chem. 2009 Mar 20;284(12):8083-92 [19112176] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/onc.2014.97 ER - TY - CPAPER T1 - Prioritization and Predictive Toxicology: Estrogen Receptor Active Compounds T2 - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AN - 1669822449; 6340554 JF - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AU - Casey, W Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Prediction KW - Estrogen receptors KW - Toxicology KW - Sex hormones UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669822449?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.atitle=Prioritization+and+Predictive+Toxicology%3A+Estrogen+Receptor+Active+Compounds&rft.au=Casey%2C+W&rft.aulast=Casey&rft.aufirst=W&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2015Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Opportunities for Improving Clinical and Nonclinical Approaches to Managing Cardiovascular Risk in Cancer Patients T2 - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AN - 1669822219; 6340600 JF - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AU - Davis, M Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Health risks KW - Cardiovascular diseases KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669822219?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.atitle=Opportunities+for+Improving+Clinical+and+Nonclinical+Approaches+to+Managing+Cardiovascular+Risk+in+Cancer+Patients&rft.au=Davis%2C+M&rft.aulast=Davis&rft.aufirst=M&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2015Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Assessing Confidence in Tox21 T2 - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AN - 1669822059; 6340772 JF - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AU - Bucher, J AU - Tice, R AU - Paules, R AU - Casey, W AU - Rooney, A AU - Thayer, K AU - DeVito, M Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Toxicology KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669822059?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.atitle=Assessing+Confidence+in+Tox21&rft.au=Bucher%2C+J%3BTice%2C+R%3BPaules%2C+R%3BCasey%2C+W%3BRooney%2C+A%3BThayer%2C+K%3BDeVito%2C+M&rft.aulast=Bucher&rft.aufirst=J&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2015Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Toxicity of Subchronic Aspergillus fumigatus Exposures in BALB/cJ and B6C3F1/N Mouse Strains T2 - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AN - 1669821168; 6340841 JF - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AU - Germolec, D Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Insecticides KW - Toxicity KW - Strains KW - Aspergillus fumigatus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669821168?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.atitle=Toxicity+of+Subchronic+Aspergillus+fumigatus+Exposures+in+BALB%2FcJ+and+B6C3F1%2FN+Mouse+Strains&rft.au=Germolec%2C+D&rft.aulast=Germolec&rft.aufirst=D&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2015Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Transcriptional Effects of DNA Damage: Gene Expression Changes Associated with Tamoxifen Exposure in Humans and Nonhuman Primates T2 - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AN - 1669821080; 6340860 JF - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AU - Poirier, M Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Gene expression KW - DNA damage KW - Transcription KW - Tamoxifen KW - Primates UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669821080?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.atitle=Transcriptional+Effects+of+DNA+Damage%3A+Gene+Expression+Changes+Associated+with+Tamoxifen+Exposure+in+Humans+and+Nonhuman+Primates&rft.au=Poirier%2C+M&rft.aulast=Poirier&rft.aufirst=M&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2015Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Increasing Environmental Health Literacy: A Model for High School and Undergraduate Summer Internship Programs in Government T2 - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AN - 1669821053; 6340814 JF - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AU - Collins, T Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Environmental health KW - Summer KW - Models UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669821053?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.atitle=Increasing+Environmental+Health+Literacy%3A+A+Model+for+High+School+and+Undergraduate+Summer+Internship+Programs+in+Government&rft.au=Collins%2C+T&rft.aulast=Collins&rft.aufirst=T&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2015Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Tox21 Phase III: Improving on Biological Coverage, Relevance, and Public Outreach T2 - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AN - 1669820836; 6340553 JF - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AU - Paules, R Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Toxicology KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669820836?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.atitle=Tox21+Phase+III%3A+Improving+on+Biological+Coverage%2C+Relevance%2C+and+Public+Outreach&rft.au=Paules%2C+R&rft.aulast=Paules&rft.aufirst=R&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2015Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Using Reverse Toxicokinetic Models to Correlate In Vitro and In Vivo Estrogen Receptor Activity T2 - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AN - 1669820791; 6340701 JF - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AU - Casey, W Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Estrogen receptors KW - Models KW - Sex hormones UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669820791?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.atitle=Using+Reverse+Toxicokinetic+Models+to+Correlate+In+Vitro+and+In+Vivo+Estrogen+Receptor+Activity&rft.au=Casey%2C+W&rft.aulast=Casey&rft.aufirst=W&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2015Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Using Bioactivity-Based Read-Across (BaBRA) to Characterize the ToxCast Library T2 - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AN - 1669820761; 6340766 JF - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AU - Casey, W AU - Allen, D AU - Kleinstreuer, N Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Toxicology KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669820761?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.atitle=Using+Bioactivity-Based+Read-Across+%28BaBRA%29+to+Characterize+the+ToxCast+Library&rft.au=Casey%2C+W%3BAllen%2C+D%3BKleinstreuer%2C+N&rft.aulast=Casey&rft.aufirst=W&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2015Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Evaluating and Quantifying Stress for Inclusion in Cumulative Risk Assessment T2 - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AN - 1669820680; 6340613 JF - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AU - Rider, C AU - Simmons, J Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Risk assessment KW - Stress UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669820680?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.atitle=Evaluating+and+Quantifying+Stress+for+Inclusion+in+Cumulative+Risk+Assessment&rft.au=Rider%2C+C%3BSimmons%2C+J&rft.aulast=Rider&rft.aufirst=C&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2015Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - An NIEHS/NTP Perspective on the Future of Toxicity and Carcinogenesis Testing T2 - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AN - 1669820675; 6340852 JF - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AU - Birnbaum, L Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Bioaccumulation KW - Carcinogenesis KW - Pollution effects KW - Pollution indicators KW - Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669820675?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.atitle=An+NIEHS%2FNTP+Perspective+on+the+Future+of+Toxicity+and+Carcinogenesis+Testing&rft.au=Birnbaum%2C+L&rft.aulast=Birnbaum&rft.aufirst=L&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2015Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Moving forward on Complex Herbal Mixtures at the National Toxicology Program T2 - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AN - 1669820654; 6340759 JF - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AU - Rider, C AU - Collins, B AU - Auerbach, S AU - DeVito, M AU - Blystone, C AU - Waidyanatha, S Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Toxicology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669820654?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.atitle=Moving+forward+on+Complex+Herbal+Mixtures+at+the+National+Toxicology+Program&rft.au=Rider%2C+C%3BCollins%2C+B%3BAuerbach%2C+S%3BDeVito%2C+M%3BBlystone%2C+C%3BWaidyanatha%2C+S&rft.aulast=Rider&rft.aufirst=C&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2015Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - The US Tox21 Collaboration: Advances Made and Lessons Learned T2 - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AN - 1669820621; 6340550 JF - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AU - Birnbaum, L AU - Kavlock, R Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Toxicology KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669820621?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.atitle=The+US+Tox21+Collaboration%3A+Advances+Made+and+Lessons+Learned&rft.au=Birnbaum%2C+L%3BKavlock%2C+R&rft.aulast=Birnbaum&rft.aufirst=L&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2015Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - Berenbaum and Beyond: Concepts and Theories Underlying Mixtures Research and Cumulative Risk Assessment T2 - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AN - 1669820614; 6340463 JF - 54rd Annual Meeting of the Society of Toxicology (SOT 2015) AU - Rider, C Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Risk assessment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669820614?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.atitle=Berenbaum+and+Beyond%3A+Concepts+and+Theories+Underlying+Mixtures+Research+and+Cumulative+Risk+Assessment&rft.au=Rider%2C+C&rft.aulast=Rider&rft.aufirst=C&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=54rd+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/Pub/Prog/2015Program.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - CPAPER T1 - The Effects of Tomatidine on Three Cell Models of Differentiation T2 - Keystone Symposia Meeting on Obesity and the Metabolic Syndrome: Mitochondria and Energy Expenditure AN - 1658697993; 6336009 JF - Keystone Symposia Meeting on Obesity and the Metabolic Syndrome: Mitochondria and Energy Expenditure AU - Becker, Kevin Y1 - 2015/03/22/ PY - 2015 DA - 2015 Mar 22 KW - Differentiation KW - Cell culture KW - tomatidine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658697993?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=Keystone+Symposia+Meeting+on+Obesity+and+the+Metabolic+Syndrome%3A+Mitochondria+and+Energy+Expenditure&rft.atitle=The+Effects+of+Tomatidine+on+Three+Cell+Models+of+Differentiation&rft.au=Becker%2C+Kevin&rft.aulast=Becker&rft.aufirst=Kevin&rft.date=2015-03-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Keystone+Symposia+Meeting+on+Obesity+and+the+Metabolic+Syndrome%3A+Mitochondria+and+Energy+Expenditure&rft.issn=&rft_id=info:doi/ L2 - http://www.keystonesymposia.org/15X7 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-28 N1 - Last updated - 2015-02-27 ER - TY - JOUR T1 - Modulation of Alzheimer's Aβ protofilament-membrane interactions by lipid headgroups. AN - 1664774553; 25581460 AB - The molecular pathogenesis of Alzheimer's disease (AD) is complex and sparsely understood. The relationship between AD's amyloid β (Aβ) peptides and neuronal membranes is central to Aβ's cytotoxicity and is directly modulated by the composition of the lipid headgroups. Molecular studies of the insertion of model Aβ40 protofilaments in lipid bilayers revealed strong interactions that affect the structural integrity of both the membranes and the ordered amyloid aggregates. In particular, electrostatics plays a crucial role in the interaction between Aβ protofilaments and palmytoil-oleoyl-phosphatidylethanolamine (POPE) lipids, a common component of neuronal plasma membranes. Here, we use all-atom molecular dynamics and steered molecular dynamics simulations to systematically compare the effects that POPE and palmytoil-oleoyl-phosphatidylcholine (POPC) headgroups have on the Aβ-lipid interactions. We find that Aβ protofilaments exhibit weaker electrostatic interactions with POPC headgroups and establish significantly shorter-lived contacts with the POPC bilayer. This illustrates the crucial yet complex role of electrostatic and hydrogen bonding interactions in modulating the anchoring and insertion of Aβ peptides into lipid bilayers. Our study reveals the atomistic details behind the barrier created by the lipid headgroup region in impeding solution-aggregated fibrillar oligomers to spontaneously insert into POPC bilayers, in contrast to the POPE case. While the biological reality is notoriously more complex (e.g., including other factors such as cholesterol), our results evidence a simple experimentally and computationally testable case for probing the factors that control the insertion of Aβ oligomeric aggregates in neuronal cell membranes--a process central to their neurotoxicity. JF - ACS chemical neuroscience AU - Tofoleanu, Florentina AU - Brooks, Bernard R AU - Buchete, Nicolae-Viorel AD - †Laboratory of Computational Biology, Biochemistry and Biophysics Center, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, United States. Y1 - 2015/03/18/ PY - 2015 DA - 2015 Mar 18 SP - 446 EP - 455 VL - 6 IS - 3 KW - Amyloid beta-Peptides KW - 0 KW - Lipid Bilayers KW - Phosphatidylcholines KW - Phosphatidylethanolamines KW - 1-palmitoyl-2-oleoylphosphatidylethanolamine KW - 10015-88-0 KW - 1-palmitoyl-2-oleoylphosphatidylcholine KW - TE895536Y5 KW - Index Medicus KW - molecular dynamics simulations KW - Alzheimer’s disease KW - amyloid β-peptide fibrils KW - amyloid peptide-lipid membrane interactions KW - toxic amyloid channels KW - Aβ fibrillar oligomers KW - Static Electricity KW - Computer Simulation KW - Phosphatidylethanolamines -- metabolism KW - Humans KW - Phosphatidylcholines -- metabolism KW - Statistics, Nonparametric KW - Structure-Activity Relationship KW - Amyloid beta-Peptides -- metabolism KW - Amyloid beta-Peptides -- chemistry KW - Molecular Dynamics Simulation KW - Alzheimer Disease -- metabolism KW - Lipid Bilayers -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664774553?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=ACS+chemical+neuroscience&rft.atitle=Modulation+of+Alzheimer%27s+A%CE%B2+protofilament-membrane+interactions+by+lipid+headgroups.&rft.au=Tofoleanu%2C+Florentina%3BBrooks%2C+Bernard+R%3BBuchete%2C+Nicolae-Viorel&rft.aulast=Tofoleanu&rft.aufirst=Florentina&rft.date=2015-03-18&rft.volume=6&rft.issue=3&rft.spage=446&rft.isbn=&rft.btitle=&rft.title=ACS+chemical+neuroscience&rft.issn=1948-7193&rft_id=info:doi/10.1021%2Fcn500277f LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-08 N1 - Date created - 2015-03-18 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1021/cn500277f ER - TY - JOUR T1 - 7-Ketocholesterol increases retinal microglial migration, activation, and angiogenicity: a potential pathogenic mechanism underlying age-related macular degeneration. AN - 1664444724; 25775051 AB - Age-related macular degeneration (AMD) has been associated with both accumulation of lipid and lipid oxidative products, as well as increased neuroinflammatory changes and microglial activation in the outer retina. However, the relationships between these factors are incompletely understood. 7-Ketocholesterol (7KCh) is a cholesterol oxidation product localized to the outer retina with prominent pro-inflammatory effects. To explore the potential relationship between 7KCh and microglial activation, we localized 7KCh and microglia to the outer retina of aged mice and investigated 7KCh effects on retinal microglia in both in vitro and in vivo systems. We found that retinal microglia demonstrated a prominent chemotropism to 7KCh and readily internalized 7KCh. Sublethal concentrations of 7KCh resulted in microglial activation and polarization to a pro-inflammatory M1 state via NLRP3 inflammasome activation. Microglia exposed to 7KCh reduced expression of neurotrophic growth factors but increased expression of angiogenic factors, transitioning to a more neurotoxic and pro-angiogenic phenotype. Finally, subretinal transplantation of 7KCh-exposed microglia promoted choroidal neovascularization (CNV) relative to control microglia in a Matrigel-CNV model. The interaction of retinal microglia with 7KCh in the aged retina may thus underlie how outer retinal lipid accumulation in intermediate AMD results in neuroinflammation that ultimately drives progression towards advanced AMD. JF - Scientific reports AU - Indaram, Maanasa AU - Ma, Wenxin AU - Zhao, Lian AU - Fariss, Robert N AU - Rodriguez, Ignacio R AU - Wong, Wai T AD - Unit on Neuron-Glia Interactions in Retinal Disease, Laboratory of Retinal Cell and Molecular Biology, National Eye institute, National Institutes of Health, Bethesda, MD, USA. ; Biological Imaging Core, Laboratory of Retinal Cell and Molecular Biology, National Eye institute, National Institutes of Health, Bethesda, MD, USA. ; Mechanism of Retinal Diseases Section, Laboratory of Retinal Cell and Molecular Biology, National Eye institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2015/03/16/ PY - 2015 DA - 2015 Mar 16 SP - 9144 VL - 5 KW - Chemotactic Factors KW - 0 KW - Cx3cr1 protein, mouse KW - Ketocholesterols KW - Nerve Growth Factors KW - Receptors, Chemokine KW - 7-ketocholesterol KW - O7676FE78M KW - Index Medicus KW - Cell Proliferation -- drug effects KW - Animals KW - Nerve Growth Factors -- metabolism KW - Nerve Growth Factors -- genetics KW - Cell Survival -- drug effects KW - Receptors, Chemokine -- metabolism KW - Disease Models, Animal KW - Receptors, Chemokine -- genetics KW - Mice KW - Gene Expression Regulation -- drug effects KW - Chemotactic Factors -- metabolism KW - Mice, Transgenic KW - Chemotactic Factors -- pharmacology KW - Retina -- metabolism KW - Ketocholesterols -- pharmacology KW - Macular Degeneration -- pathology KW - Retina -- drug effects KW - Microglia -- immunology KW - Macular Degeneration -- etiology KW - Retina -- pathology KW - Neovascularization, Pathologic KW - Ketocholesterols -- metabolism KW - Microglia -- drug effects KW - Microglia -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664444724?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scientific+reports&rft.atitle=7-Ketocholesterol+increases+retinal+microglial+migration%2C+activation%2C+and+angiogenicity%3A+a+potential+pathogenic+mechanism+underlying+age-related+macular+degeneration.&rft.au=Indaram%2C+Maanasa%3BMa%2C+Wenxin%3BZhao%2C+Lian%3BFariss%2C+Robert+N%3BRodriguez%2C+Ignacio+R%3BWong%2C+Wai+T&rft.aulast=Indaram&rft.aufirst=Maanasa&rft.date=2015-03-16&rft.volume=5&rft.issue=&rft.spage=9144&rft.isbn=&rft.btitle=&rft.title=Scientific+reports&rft.issn=2045-2322&rft_id=info:doi/10.1038%2Fsrep09144 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-04 N1 - Date created - 2015-03-17 N1 - Date revised - 2017-01-14 N1 - 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Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/srep09144 ER - TY - JOUR T1 - Dynamin regulates metaphase furrow formation and plasma membrane compartmentalization in the syncytial Drosophila embryo AN - 1808718083; PQ0003426027 AB - The successive nuclear division cycles in the syncytial Drosophila embryo are accompanied by ingression and regression of plasma membrane furrows, which surround individual nuclei at the embryo periphery, playing a central role in embryo compartmentalization prior to cellularization. Here, we demonstrate that cell cycle changes in dynamin localization and activity at the plasma membrane (PM) regulate metaphase furrow formation and PM organization in the syncytial embryo. Dynamin was localized on short PM furrows during interphase, mediating endocytosis of PM components. Dynamin redistributed off ingressed PM furrows in metaphase, correlating with stabilized PM components and the associated actin regulatory machinery on long furrows. Acute inhibition of dynamin in the temperature sensitive shibire mutant embryo resulted in morphogenetic consequences in the syncytial division cycle. These included inhibition of metaphase furrow ingression, randomization of proteins normally polarized to intercap PM and disruption of the diffusion barrier separating PM domains above nuclei. Based on these findings, we propose that cell cycle changes in dynamin orchestrate recruitment of actin regulatory machinery for PM furrow dynamics during the early mitotic cycles in the Drosophila embryo. JF - Biology Open AU - Rikhy, Richa AU - Mavrakis, Manos AU - Lippincott-Schwartz, Jennifer AD - Present address: Indian Institute of Science Education and Research, Homi Bhabha Road, Pashan, Pune, 411008, India, lippincj@mail.nih.gov Y1 - 2015/03/15/ PY - 2015 DA - 2015 Mar 15 SP - 301 EP - 311 PB - The Company of Biologists Ltd., 140 Cowley Rd Cambridge, CB4 0DL United Kingdom VL - 4 IS - 3 SN - 2046-6390, 2046-6390 KW - Biotechnology and Bioengineering Abstracts KW - Dynamin KW - Endocytosis KW - Drosophila KW - Polarity KW - Actin KW - Compartmentalization KW - Syncytium KW - Temperature effects KW - Cell cycle KW - Interphase KW - Metaphase KW - Nuclear division KW - Plasma membranes KW - Embryos KW - Diffusion KW - Nuclei KW - W 30940:Products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808718083?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biology+Open&rft.atitle=Dynamin+regulates+metaphase+furrow+formation+and+plasma+membrane+compartmentalization+in+the+syncytial+Drosophila+embryo&rft.au=Rikhy%2C+Richa%3BMavrakis%2C+Manos%3BLippincott-Schwartz%2C+Jennifer&rft.aulast=Rikhy&rft.aufirst=Richa&rft.date=2015-03-15&rft.volume=4&rft.issue=3&rft.spage=301&rft.isbn=&rft.btitle=&rft.title=Biology+Open&rft.issn=20466390&rft_id=info:doi/10.1242%2Fbio.20149936 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Temperature effects; Endocytosis; Dynamin; Plasma membranes; Cell cycle; Interphase; Diffusion; Actin; Embryos; Nuclei; Metaphase; Nuclear division; Drosophila DO - http://dx.doi.org/10.1242/bio.20149936 ER - TY - JOUR T1 - Filarial Infection Modulates the Immune Response to Mycobacterium tuberculosis through Expansion of CD4+ IL-4 Memory T Cells AN - 1808717620; PQ0003425235 AB - Exaggerated CD4+ T helper 2-specific cytokine producing memory T cell responses developing concomitantly with a T helper 1 response might have a detrimental role in immunity to infection caused by Mycobacterium tuberculosis. To assess the dynamics of Ag-specific memory T cell compartments in the context of filarial infection, we used multiparameter flow cytometry on PBMCs from 25 microfilaremic filarial-infected (Inf) and 14 filarial-uninfected (Uninf) subjects following stimulation with filarial Ag (BmA) or with the M. tuberculosis-specific Ag culture filtrate protein-10 (CFP-10). Our data demonstrated that the Inf group had a marked increase in BmA-specific CD4+IL-4+ cells (median net frequency compared with baseline [Fo] = 0.09% versus 0.01%; p = 0.038) but also to CFP-10 (Fo = 0.16% versus 0.007%; p = 0.04) and staphylococcal enterotoxin B (Fo = 0.49% versus 0.26%; p = 0.04). The Inf subjects showed a BmA-specific expansion of CD4+CD45RO+IL-4+ producing central memory (TCM, CD45RO+CCR7+CD27+; Fo = 1.1% versus 0.5%; p = 0.04) as well as effector memory (TEM, CD45RO+CCR7-CD27-; Fo = 1.5% versus 0.2%; p = 0.03) with a similar but nonsignificant response to CFP-10. In addition, there was expansion of CD4+IL-4+CD45RA+CCR7+CD27+ (naive-like) in Inf individuals compared with Uninf subjects. Among Inf subjects with definitive latent tuberculosis, there were no differences in frequencies of IL-4-producing cells within any of the memory compartments compared with the Uninf group. Our data suggest that filarial infection induces Ag-specific, exaggerated IL-4 responses in distinct T cell memory compartments to M. tuberculosis-specific Ags, which are attenuated in subjects who are able to mount a delayed type hypersensitivity reaction to M. tuberculosis. JF - Journal of Immunology AU - Chatterjee, Soumya AU - Clark, Carolyn E AU - Lugli, Enrico AU - Roederer, Mario AU - Nutman, Thomas B AD - Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892; and Y1 - 2015/03/15/ PY - 2015 DA - 2015 Mar 15 SP - 2706 EP - 2714 PB - American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 United States VL - 194 IS - 6 SN - 0022-1767, 0022-1767 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Interleukin 4 KW - Data processing KW - Memory cells KW - Immunological memory KW - Cell culture KW - Staphylococcal enterotoxin B KW - Infection KW - Flow cytometry KW - Memory KW - CD4 antigen KW - Hypersensitivity (delayed) KW - Lymphocytes T KW - Tuberculosis KW - Mycobacterium tuberculosis KW - J 02350:Immunology KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808717620?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Immunology&rft.atitle=Filarial+Infection+Modulates+the+Immune+Response+to+Mycobacterium+tuberculosis+through+Expansion+of+CD4%2B+IL-4+Memory+T+Cells&rft.au=Chatterjee%2C+Soumya%3BClark%2C+Carolyn+E%3BLugli%2C+Enrico%3BRoederer%2C+Mario%3BNutman%2C+Thomas+B&rft.aulast=Chatterjee&rft.aufirst=Soumya&rft.date=2015-03-15&rft.volume=194&rft.issue=6&rft.spage=2706&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunology&rft.issn=00221767&rft_id=info:doi/10.4049%2Fjimmunol.1402718 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-10-12 N1 - SubjectsTermNotLitGenreText - Interleukin 4; Data processing; Immunological memory; Memory cells; Cell culture; Infection; Staphylococcal enterotoxin B; Flow cytometry; CD4 antigen; Memory; Hypersensitivity (delayed); Lymphocytes T; Tuberculosis; Mycobacterium tuberculosis DO - http://dx.doi.org/10.4049/jimmunol.1402718 ER - TY - JOUR T1 - Bone Marrow Plasma Cells Are a Primary Source of Serum HIV-1-Specific Antibodies in Chronically Infected Individuals AN - 1808642242; PQ0003425280 AB - Several potent and broadly neutralizing Abs to HIV-1 have been isolated recently from peripheral blood B cells of infected individuals, based on prescreening of Ab activity in the serum. However, little is known regarding the cells that make the Abs that circulate in the blood. Accordingly, we investigated the most likely source, the bone marrow, of chronically HIV-1-infected individuals who were not receiving antiretroviral therapy. Increased frequencies of plasma cells, as well as B cell precursors, namely preB-I and preB-II, and decreased frequencies of mature B cells were observed in bone marrow aspirates of these individuals compared with HIV-negative counterparts. Increased frequencies of bone marrow plasma cells are consistent with known hallmarks of HIV-1 infection, namely hypergammaglobulinemia and increased frequencies of peripheral blood plasmablasts. Levels of HIV-1 envelope (Env)-binding and HIV-1-neutralizing Abs were measured in serum, and corresponding frequencies of Ab-secreting or Env-binding cells were measured in the blood (plasmablasts and memory B cells) and in the bone marrow (plasma cells). A strong correlation was observed between serum HIV-1-specific Abs and Env-specific bone marrow-derived plasma cells, but not circulating plasmablasts or memory B cells. These findings demonstrate that, despite HIV-1-induced phenotypic and functional B cell dysregulation in the peripheral blood and secondary lymphoid tissues, bone marrow plasma cells remain a primary source for circulating HIV-1-specific Abs in HIV-1-infected individuals. JF - Journal of Immunology AU - Montezuma-Rusca, Jairo M AU - Moir, Susan AU - Kardava, Lela AU - Buckner, Clarisa M AU - Louie, Aaron AU - Kim, Leo JY AU - Santich, Brian H AU - Wang, Wei AU - Fankuchen, Olivia R AU - Diaz, Gabriella AU - Daub, Janine R AU - Rosenzweig, Sergio D AU - Chun, Tae-Wook AU - Li, Yuxing AU - Braylan, Raul C AU - Calvo, Katherine R AU - Fauci, Anthony S AD - Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 Y1 - 2015/03/15/ PY - 2015 DA - 2015 Mar 15 SP - 2561 EP - 2568 PB - American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 United States VL - 194 IS - 6 SN - 0022-1767, 0022-1767 KW - Toxicology Abstracts; Immunology Abstracts KW - Lymphocytes B KW - antiretroviral therapy KW - Bone marrow KW - Immunological memory KW - Memory cells KW - Peripheral blood KW - Hypergammaglobulinemia KW - Infection KW - Lymphoid tissue KW - Antibodies KW - Envelopes KW - Human immunodeficiency virus KW - Human immunodeficiency virus 1 KW - Plasma cells KW - X 24310:Pharmaceuticals KW - F 06915:Cancer Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808642242?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Immunology&rft.atitle=Bone+Marrow+Plasma+Cells+Are+a+Primary+Source+of+Serum+HIV-1-Specific+Antibodies+in+Chronically+Infected+Individuals&rft.au=Montezuma-Rusca%2C+Jairo+M%3BMoir%2C+Susan%3BKardava%2C+Lela%3BBuckner%2C+Clarisa+M%3BLouie%2C+Aaron%3BKim%2C+Leo+JY%3BSantich%2C+Brian+H%3BWang%2C+Wei%3BFankuchen%2C+Olivia+R%3BDiaz%2C+Gabriella%3BDaub%2C+Janine+R%3BRosenzweig%2C+Sergio+D%3BChun%2C+Tae-Wook%3BLi%2C+Yuxing%3BBraylan%2C+Raul+C%3BCalvo%2C+Katherine+R%3BFauci%2C+Anthony+S&rft.aulast=Montezuma-Rusca&rft.aufirst=Jairo&rft.date=2015-03-15&rft.volume=194&rft.issue=6&rft.spage=2561&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunology&rft.issn=00221767&rft_id=info:doi/10.4049%2Fjimmunol.1402424 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Antibodies; Envelopes; Lymphocytes B; antiretroviral therapy; Memory cells; Immunological memory; Bone marrow; Peripheral blood; Hypergammaglobulinemia; Infection; Plasma cells; Lymphoid tissue; Human immunodeficiency virus; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.4049/jimmunol.1402424 ER - TY - JOUR T1 - Immunotoxin targeting glypican-3 regresses liver cancer via dual inhibition of Wnt signalling and protein synthesis. AN - 1662636430; 25758784 AB - Glypican-3 is a cell surface glycoprotein that associates with Wnt in liver cancer. We develop two antibodies targeting glypican-3, HN3 and YP7. The first antibody recognizes a functional epitope and inhibits Wnt signalling, whereas the second antibody recognizes a C-terminal epitope but does not inhibit Wnt signalling. Both are fused to a fragment of Pseudomonas exotoxin A (PE38) to create immunotoxins. Interestingly, the immunotoxin based on HN3 (HN3-PE38) has superior antitumor activity as compared with YP7 (YP7-PE38) both in vitro and in vivo. Intravenous administration of HN3-PE38 alone, or in combination with chemotherapy, induces regression of Hep3B and HepG2 liver tumour xenografts in mice. This study establishes glypican-3 as a promising candidate for immunotoxin-based liver cancer therapy. Our results demonstrate immunotoxin-induced tumour regression via dual mechanisms: inactivation of cancer signalling via the antibody and inhibition of protein synthesis via the toxin. JF - Nature communications AU - Gao, Wei AU - Tang, Zhewei AU - Zhang, Yi-Fan AU - Feng, Mingqian AU - Qian, Min AU - Dimitrov, Dimiter S AU - Ho, Mitchell AD - Antibody Therapy Section, Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. ; 1] Antibody Therapy Section, Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA [2] Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai 200062, China. ; Institute of Biomedical Sciences, School of Life Sciences, East China Normal University, Shanghai 200062, China. ; Protein Interaction Group, Laboratory of Experimental Immunology, Center for Cancer Research, National Cancer Institute, Frederick, Maryland 21702, USA. Y1 - 2015/03/11/ PY - 2015 DA - 2015 Mar 11 SP - 6536 VL - 6 KW - Antibodies, Monoclonal KW - 0 KW - Antineoplastic Agents KW - Bacterial Toxins KW - Exotoxins KW - GPC3 protein, mouse KW - Glypicans KW - Immunotoxins KW - Recombinant Fusion Proteins KW - Single-Domain Antibodies KW - Virulence Factors KW - Wnt Proteins KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Animals KW - Antibodies, Monoclonal -- genetics KW - Liver -- immunology KW - Virulence Factors -- chemistry KW - Humans KW - Gene Expression KW - Antibodies, Monoclonal -- immunology KW - ADP Ribose Transferases -- genetics KW - Bacterial Toxins -- genetics KW - Immunotoxins -- chemistry KW - ADP Ribose Transferases -- chemistry KW - Single-Domain Antibodies -- genetics KW - Tumor Burden -- drug effects KW - Liver -- drug effects KW - Xenograft Model Antitumor Assays KW - Immunotoxins -- genetics KW - Signal Transduction KW - Exotoxins -- genetics KW - Liver -- pathology KW - ADP Ribose Transferases -- immunology KW - Single-Domain Antibodies -- immunology KW - Molecular Targeted Therapy KW - Virulence Factors -- genetics KW - Exotoxins -- chemistry KW - Mice KW - Exotoxins -- immunology KW - Bacterial Toxins -- immunology KW - Virulence Factors -- immunology KW - Hep G2 Cells KW - Bacterial Toxins -- chemistry KW - Female KW - Remission Induction KW - Wnt Proteins -- antagonists & inhibitors KW - Glypicans -- genetics KW - Antineoplastic Agents -- administration & dosage KW - Recombinant Fusion Proteins -- immunology KW - Hepatoblastoma -- immunology KW - Wnt Proteins -- immunology KW - Glypicans -- immunology KW - Recombinant Fusion Proteins -- administration & dosage KW - Glypicans -- antagonists & inhibitors KW - Wnt Proteins -- genetics KW - Protein Biosynthesis -- drug effects KW - Antineoplastic Agents -- immunology KW - Liver Neoplasms -- pathology KW - Hepatoblastoma -- genetics KW - Liver Neoplasms -- drug therapy KW - Recombinant Fusion Proteins -- genetics KW - Hepatoblastoma -- drug therapy KW - Antineoplastic Agents -- chemistry KW - Hepatoblastoma -- pathology KW - Liver Neoplasms -- immunology KW - Liver Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1662636430?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+communications&rft.atitle=Immunotoxin+targeting+glypican-3+regresses+liver+cancer+via+dual+inhibition+of+Wnt+signalling+and+protein+synthesis.&rft.au=Gao%2C+Wei%3BTang%2C+Zhewei%3BZhang%2C+Yi-Fan%3BFeng%2C+Mingqian%3BQian%2C+Min%3BDimitrov%2C+Dimiter+S%3BHo%2C+Mitchell&rft.aulast=Gao&rft.aufirst=Wei&rft.date=2015-03-11&rft.volume=6&rft.issue=&rft.spage=6536&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms7536 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-09 N1 - Date created - 2015-03-11 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Eur J Cancer. 2012 Oct;48(15):2417-30 [22244830] Hepatology. 2014 Aug;60(2):576-87 [24492943] Proc Natl Acad Sci U S A. 2013 Mar 19;110(12):E1083-91 [23471984] Sci Transl Med. 2013 Oct 23;5(208):208ra147 [24154601] PLoS One. 2013;8(11):e81919 [24260587] J Cell Sci. 2014 Apr 1;127(Pt 7):1565-75 [24496449] Cancer Immun. 2007;7:20 [18088084] Cancer Res. 2008 Aug 1;68(15):6300-5 [18676854] J Mol Biol. 2008 Oct 10;382(3):779-89 [18687338] J Hepatol. 2008 Dec;49(6):985-97 [18930332] Cancer. 2001 Jan 1;91(1):101-5 [11148565] J Cell Biol. 2003 Nov 10;163(3):625-35 [14610063] Oncogene. 2004 Jan 29;23(4):945-55 [14661052] Eur J Cancer. 2004 Apr;40(6):852-7 [15120041] Gastroenterology. 2004 Nov;127(5 Suppl 1):S5-S16 [15508102] J Bacteriol. 1987 Nov;169(11):4967-71 [2889718] In Vitro Cell Dev Biol. 1992 Feb;28A(2):136-42 [1371504] Int J Cancer. 1992 Apr 22;51(1):108-15 [1563830] Biochem J. 1995 Oct 15;311 ( Pt 2):561-5 [7487896] Cancer Res. 1997 Nov 15;57(22):5179-84 [9371521] Proc Natl Acad Sci U S A. 1998 Jul 21;95(15):8847-51 [9671767] J Biol Chem. 2005 Jan 7;280(1):607-17 [15491997] Cancer Res. 2005 Jul 15;65(14):6245-54 [16024626] Eur J Cancer. 2006 Mar;42(4):456-9 [16427779] Nat Rev Cancer. 2006 Jul;6(7):559-65 [16794638] Clin Cancer Res. 2006 Aug 1;12(15):4695-701 [16899620] Mol Cancer Ther. 2006 Oct;5(10):2435-43 [17041086] Annu Rev Med. 2007;58:221-37 [17059365] Cancer Res. 2008 Dec 1;68(23):9832-8 [19047163] Biochem Biophys Res Commun. 2009 Jan 9;378(2):279-84 [19022220] Cancer Res. 2009 May 15;69(10):4294-300 [19401447] Cancer Sci. 2009 Aug;100(8):1403-7 [19496787] Int J Cancer. 2010 Mar 15;126(6):1291-301 [19816934] Ann Oncol. 2010 May;21 Suppl 5:v93-7 [20555112] Eur J Cancer. 2011 Feb;47(3):333-8 [21112773] Int J Cancer. 2011 May 1;128(9):2246-7 [20617511] Int J Cancer. 2011 May 1;128(9):2020-30 [20635390] J Pharmacol Exp Ther. 2011 Apr;337(1):155-61 [21205925] BioDrugs. 2011 Oct 1;25(5):275-84 [21942912] Clin Cancer Res. 2011 Oct 15;17(20):6398-405 [22003067] Cancer Cell. 2012 Feb 14;21(2):212-26 [22340594] Lancet. 2012 Mar 31;379(9822):1245-55 [22353262] Anticancer Res. 2012 Apr;32(4):1379-86 [22493374] J Biol Chem. 2012 Apr 6;287(15):11730-9 [22337891] MAbs. 2012 Sep-Oct;4(5):592-9 [22820551] Proc Natl Acad Sci U S A. 2014 Jun 10;111(23):8571-6 [24799704] Cell. 2014 Jul 3;158(1):157-70 [24976009] Eur J Cancer. 2012 Dec;48(18):3456-64 [22835780] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ncomms7536 ER - TY - JOUR T1 - Whole-genome RNAi screen highlights components of the endoplasmic reticulum/Golgi as a source of resistance to immunotoxin-mediated cytotoxicity. AN - 1662636166; 25713356 AB - Immunotoxins (antibody-toxin fusion proteins) target surface antigens on cancer cells and kill these cells via toxin-mediated inhibition of protein synthesis. To identify genes controlling this process, an RNAi whole-genome screen (∼ 22,000 genes at three siRNAs per gene) was conducted via monitoring the cytotoxicity of the mesothelin-directed immunotoxin SS1P. SS1P, a Pseudomonas exotoxin-based immunotoxin, was chosen because it is now in clinical trials and has produced objective tumor regressions in patients. High and low concentrations of SS1P were chosen to allow for the identification of both mitigators and sensitizers. As expected, silencing known essential genes in the immunotoxin pathway, such as mesothelin, furin, KDEL receptor 2, or members of the diphthamide pathway, protected cells. Of greater interest was the observation that many RNAi targets increased immunotoxin sensitivity, indicating that these gene products normally contribute to inefficiencies in the killing pathway. Of the top sensitizers, many genes encode proteins that locate to either the endoplasmic reticulum (ER) or Golgi and are annotated as part of the secretory system. Genes related to the ER-associated degradation system were not among high-ranking mitigator or sensitizer candidates. However, the p97 inhibitor eeyarestatin 1 enhanced immunotoxin killing. Our results highlight potential targets for chemical intervention that could increase immunotoxin killing of cancer cells and enhance our understanding of toxin trafficking. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Pasetto, Matteo AU - Antignani, Antonella AU - Ormanoglu, Pinar AU - Buehler, Eugen AU - Guha, Rajarshi AU - Pastan, Ira AU - Martin, Scott E AU - FitzGerald, David J AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4264; and. ; Division of Preclinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, Rockville, MD 20850. ; Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4264; and pastani@mail.nih.gov fitzgerd@helix.nih.gov. Y1 - 2015/03/10/ PY - 2015 DA - 2015 Mar 10 SP - E1135 EP - E1142 VL - 112 IS - 10 KW - Immunotoxins KW - 0 KW - Index Medicus KW - screen KW - toxin KW - immunotoxin KW - RNAi KW - genome KW - Animals KW - Humans KW - Endoplasmic Reticulum -- metabolism KW - RNA Interference KW - Immunotoxins -- pharmacology KW - Golgi Apparatus -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1662636166?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Whole-genome+RNAi+screen+highlights+components+of+the+endoplasmic+reticulum%2FGolgi+as+a+source+of+resistance+to+immunotoxin-mediated+cytotoxicity.&rft.au=Pasetto%2C+Matteo%3BAntignani%2C+Antonella%3BOrmanoglu%2C+Pinar%3BBuehler%2C+Eugen%3BGuha%2C+Rajarshi%3BPastan%2C+Ira%3BMartin%2C+Scott+E%3BFitzGerald%2C+David+J&rft.aulast=Pasetto&rft.aufirst=Matteo&rft.date=2015-03-10&rft.volume=112&rft.issue=10&rft.spage=E1135&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=1091-6490&rft_id=info:doi/10.1073%2Fpnas.1501958112 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-11 N1 - Date created - 2015-03-11 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 1117281; PubChem-BioAssay N1 - SuppNotes - Cited By: Infect Immun. 1991 Jan;59(1):407-14 [1702764] Cancer Res. 1992 Jan 1;52(1):181-6 [1727378] J Biol Chem. 1994 Jul 8;269(27):18167-76 [8027078] Biochem J. 1995 Apr 1;307 ( Pt 1):29-37 [7717988] Biochemistry. 1997 Sep 16;36(37):11051-4 [9333321] J Biol Chem. 1997 Dec 12;272(50):31707-11 [9395513] J Cell Biol. 1999 Jul 12;146(1):71-84 [10402461] Appl Immunohistochem Mol Morphol. 2005 Sep;13(3):243-7 [16082249] J Biol Chem. 2006 Apr 14;281(15):10540-7 [16484228] Clin Cancer Res. 2007 Mar 1;13(5):1571-5 [17332303] Nucleic Acids Res. 2007;35(8):e57 [17392344] Mol Biol Cell. 2007 Jul;18(7):2400-10 [17429068] Nat Methods. 2007 Oct;4(10):847-9 [17828270] J Biol Chem. 2008 Mar 21;283(12):7445-54 [18199748] Cancer Res. 2008 Aug 1;68(15):6300-5 [18676854] Nucleic Acids Res. 2009 Jan;37(Database issue):D412-6 [18940858] Blood. 2009 Apr 16;113(16):3792-800 [18988862] PLoS Pathog. 2009 May;5(5):e1000437 [19478882] J Cell Sci. 2009 Dec 1;122(Pt 23):4393-400 [19903691] Nat Rev Cancer. 2010 Feb;10(2):130-7 [20094047] PLoS One. 2010;5(2):e9078 [20140093] Nat Rev Immunol. 2010 May;10(5):317-27 [20414205] Nature. 2010 Jun 17;465(7300):891-6 [20559380] J Biol Chem. 2010 Sep 17;285(38):29367-74 [20647305] PLoS One. 2010;5(11):e15479 [21124757] ACS Chem Biol. 2011 Jan 21;6(1):47-60 [21142076] PLoS One. 2011;6(7):e22713 [21799938] Dev Cell. 2011 Aug 16;21(2):231-44 [21782526] J Biol Chem. 2011 Oct 14;286(41):35634-42 [21844198] Cancer Res. 2011 Oct 15;71(20):6300-9 [21998010] Pathol Int. 2011 Nov;61(11):638-44 [22029674] Toxins (Basel). 2010 Mar;2(3):310-25 [22069586] FEBS J. 2011 Dec;278(23):4683-700 [21585657] J Biomol Screen. 2012 Mar;17(3):370-8 [22086724] Proc Natl Acad Sci U S A. 2012 May 1;109(18):6898-903 [22509046] Nature. 2012 Jun 7;486(7401):80-4 [22678283] PLoS One. 2012;7(7):e41119 [22829918] J Biol Chem. 2012 Aug 24;287(35):29921-30 [22787145] Breast Cancer Res. 2010;12(5):R85 [20946665] Annu Rev Med. 2013;64:15-29 [23043493] PLoS Genet. 2013;9(2):e1003334 [23468660] J Biol Chem. 2013 Apr 26;288(17):12305-12 [23486472] Toxins (Basel). 2013 May;5(5):958-68 [23645155] Toxins (Basel). 2013 Aug;5(8):1486-502 [23965432] Nat Cell Biol. 2013 Dec;15(12):1473-85 [24185178] Biochem J. 2014 Feb 1;457(3):485-96 [24200403] Cancer Genomics Proteomics. 2014 Jan-Feb;11(1):25-38 [24633317] Oncotarget. 2014 Feb 28;5(4):860-71 [24658219] Blood. 2014 Apr 10;123(15):2293-301 [24578502] Blood. 2014 Apr 17;123(16):2470-7 [24578503] J Neurosci. 2014 May 14;34(20):6772-89 [24828632] Gene. 2014 Jul 25;545(2):282-9 [24835311] Proc Natl Acad Sci U S A. 2014 Jun 17;111(24):8838-43 [24876273] Oncotarget. 2014 Jul 15;5(13):5165-76 [24970821] PLoS Pathog. 2014 Jul;10(7):e1004295 [25078082] BMJ Open. 2014;4(8):e004930 [25107436] Cancer. 2014 Nov 1;120(21):3311-9 [24989332] Br J Haematol. 2014 Nov;167(4):524-8 [25098371] Cell. 2014 Oct 23;159(3):647-61 [25307932] Biochemistry. 1999 Dec 14;38(50):16507-13 [10600112] Clin Cancer Res. 2001 Dec;7(12):3862-8 [11751476] Carcinogenesis. 2002 Jun;23(6):967-75 [12082018] Cancer Res. 2003 Dec 15;63(24):8614-22 [14695172] Methods Mol Biol. 2004;248:503-18 [14970517] Clin Cancer Res. 2004 Jun 15;10(12 Pt 1):3937-42 [15217923] Bioconjug Chem. 2004 Jul-Aug;15(4):765-73 [15264863] Cell. 1978 Sep;15(1):245-50 [699044] Somat Cell Mol Genet. 1985 Mar;11(2):117-26 [3856953] Proc Natl Acad Sci U S A. 1990 Jan;87(1):308-12 [2104981] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1073/pnas.1501958112 ER - TY - JOUR T1 - Characterization of the Host Response to Pichinde Virus Infection in the Syrian Golden Hamster by Species-Specific Kinome Analysis AN - 1808625157; PQ0003424707 AB - The Syrian golden hamster has been increasingly used to study viral hemorrhagic fever (VHF) pathogenesis and countermeasure efficacy. As VHFs are a global health concern, well-characterized animal models are essential for both the development of therapeutics and vaccines as well as for increasing our understanding of the molecular events that underlie viral pathogenesis. However, the paucity of reagents or platforms that are available for studying hamsters at a molecular level limits the ability to extract biological information from this important animal model. As such, there is a need to develop platforms/technologies for characterizing host responses of hamsters at a molecular level. To this end, we developed hamster-specific kinome peptide arrays to characterize the molecular host response of the Syrian golden hamster. After validating the functionality of the arrays using immune agonists of defined signaling mechanisms (lipopolysaccharide (LPS) and tumor necrosis factor (TNF)- alpha ), we characterized the host response in a hamster model of VHF based on Pichinde virus (PICV) infection by performing temporal kinome analysis of lung tissue. Our analysis revealed key roles for vascular endothelial growth factor (VEGF), interleukin (IL) responses, nuclear factor kappa-light-chain-enhancer of activated B cells (NF- Kappa B) signaling, and Toll-like receptor (TLR) signaling in the response to PICV infection. These findings were validated through phosphorylation-specific Western blot analysis. Overall, we have demonstrated that hamster-specific kinome arrays are a robust tool for characterizing the species-specific molecular host response in a VHF model. Further, our results provide key insights into the hamster host response to PICV infection and will inform future studies with high-consequence VHF pathogens. JF - Molecular and Cellular Proteomics AU - Falcinelli, Shane AU - Gowen, Brian B AU - Trost, Brett AU - Napper, Scott AU - Kusalik, Anthony AU - Johnson, Reed F AU - Safronetz, David AU - Prescott, Joseph AU - Wahl-Jensen, Victoria AU - Jahrling, Peter B AU - Kindrachuk, Jason AD - From the Emerging Viral Pathogens Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA; , kindrachuk.kenneth@nih.gov Y1 - 2015/03/08/ PY - 2015 DA - 2015 Mar 08 SP - 646 EP - 657 PB - American Society for Biochemistry and Molecular Biology, 9650 Rockville Pike Bethesda MD 20814-3996 United States VL - 14 IS - 3 SN - 1535-9476, 1535-9476 KW - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts KW - Vascular endothelial growth factor KW - Western blotting KW - Molecular modelling KW - Lymphocytes B KW - Tumor necrosis factor KW - Interleukins KW - Animal models KW - Drug development KW - Pathogens KW - Infection KW - NF- Kappa B protein KW - Lung KW - Information processing KW - Hemorrhagic fever KW - Lipopolysaccharides KW - Pichinde virus KW - proteomics KW - Vaccines KW - Toll-like receptors KW - W 30960:Bioinformatics & Computer Applications KW - V 22370:Oncology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808625157?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+Cellular+Proteomics&rft.atitle=Characterization+of+the+Host+Response+to+Pichinde+Virus+Infection+in+the+Syrian+Golden+Hamster+by+Species-Specific+Kinome+Analysis&rft.au=Falcinelli%2C+Shane%3BGowen%2C+Brian+B%3BTrost%2C+Brett%3BNapper%2C+Scott%3BKusalik%2C+Anthony%3BJohnson%2C+Reed+F%3BSafronetz%2C+David%3BPrescott%2C+Joseph%3BWahl-Jensen%2C+Victoria%3BJahrling%2C+Peter+B%3BKindrachuk%2C+Jason&rft.aulast=Falcinelli&rft.aufirst=Shane&rft.date=2015-03-08&rft.volume=14&rft.issue=3&rft.spage=646&rft.isbn=&rft.btitle=&rft.title=Molecular+and+Cellular+Proteomics&rft.issn=15359476&rft_id=info:doi/10.1074%2Fmcp.M114.045443 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Vascular endothelial growth factor; Molecular modelling; Western blotting; Lymphocytes B; Tumor necrosis factor; Animal models; Interleukins; Drug development; Pathogens; Infection; NF- Kappa B protein; Lung; Information processing; Lipopolysaccharides; Hemorrhagic fever; Vaccines; proteomics; Toll-like receptors; Pichinde virus DO - http://dx.doi.org/10.1074/mcp.M114.045443 ER - TY - JOUR T1 - Variations of gastric corpus microbiota are associated with early esophageal squamous cell carcinoma and squamous dysplasia. AN - 1661326862; 25743945 AB - Observational studies revealed a relationship between changes in gastric mucosa and risk of esophageal squamous cell carcinoma (ESCC) which suggested a possible role for gastric microbiota in ESCC carcinogenesis. In this study we aimed to compare pattern of gastric corpus microbiota in ESCC with normal esophagus. Cases were included subjects with early ESCC (stage I-II) and esophageal squamous dysplasia (ESD) as the cancer precursor. Control groups included age and sex-matched subjects with mid-esophagus esophagitis (diseased-control), and histologically normal esophagus (healthy-control). DNA was extracted from snap-frozen gastric corpus tissues and 16S rRNA was sequenced on GS-FLX Titanium. After noise removal, an average of 3004 reads per sample was obtained from 93 subjects. We applied principal coordinate analysis to ordinate distances from beta diversity data. Pattern of gastric microbiota using Unifrac (p = 0.004) and weighted Unifrac distances (p = 0.018) statistically varied between cases and healthy controls. Sequences were aligned to SILVA database and Clostridiales and Erysipelotrichales orders were more abundant among cases after controling for multiple testing (p = 0.011). No such difference was observed between mid-esophagitis and healthy controls. This study is the first to show that composition of gastric corpus mucosal microbiota differs in early ESCC and ESD from healthy esophagus. JF - Scientific reports AU - Nasrollahzadeh, Dariush AU - Malekzadeh, Reza AU - Ploner, Alexander AU - Shakeri, Ramin AU - Sotoudeh, Masoud AU - Fahimi, Saman AU - Nasseri-Moghaddam, Siavosh AU - Kamangar, Farin AU - Abnet, Christian C AU - Winckler, Björn AU - Islami, Farhad AU - Boffetta, Paolo AU - Brennan, Paul AU - Dawsey, Sanford M AU - Ye, Weimin AD - 1] Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm 17177, Sweden [2] Digestive Oncology Research Center, Digestive Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran. ; Digestive Oncology Research Center, Digestive Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran. ; Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm 17177, Sweden. ; Department of Public Health Analysis, School of Community Health and Policy, Morgan State University, Baltimore, Maryland, USA. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda MD 20892-7335, USA. ; 1] Digestive Oncology Research Center, Digestive Diseases Research Institute, Tehran University of Medical Sciences, Tehran, Iran [2] Institute for Translational Epidemiology and Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, NY 10029-6574, USA. ; Institute for Translational Epidemiology and Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, NY 10029-6574, USA. ; International Agency for Research on Cancer, Lyon, France. Y1 - 2015/03/06/ PY - 2015 DA - 2015 Mar 06 SP - 8820 VL - 5 KW - Index Medicus KW - Neoplasm Staging KW - Humans KW - Case-Control Studies KW - Biodiversity KW - Aged KW - Middle Aged KW - Metagenome KW - Male KW - Female KW - Gastric Mucosa -- microbiology KW - Carcinoma, Squamous Cell -- etiology KW - Precancerous Conditions KW - Microbiota KW - Carcinoma, Squamous Cell -- pathology KW - Esophageal Neoplasms -- etiology KW - Gastric Mucosa -- pathology KW - Esophageal Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1661326862?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Scientific+reports&rft.atitle=Variations+of+gastric+corpus+microbiota+are+associated+with+early+esophageal+squamous+cell+carcinoma+and+squamous+dysplasia.&rft.au=Nasrollahzadeh%2C+Dariush%3BMalekzadeh%2C+Reza%3BPloner%2C+Alexander%3BShakeri%2C+Ramin%3BSotoudeh%2C+Masoud%3BFahimi%2C+Saman%3BNasseri-Moghaddam%2C+Siavosh%3BKamangar%2C+Farin%3BAbnet%2C+Christian+C%3BWinckler%2C+Bj%C3%B6rn%3BIslami%2C+Farhad%3BBoffetta%2C+Paolo%3BBrennan%2C+Paul%3BDawsey%2C+Sanford+M%3BYe%2C+Weimin&rft.aulast=Nasrollahzadeh&rft.aufirst=Dariush&rft.date=2015-03-06&rft.volume=5&rft.issue=&rft.spage=8820&rft.isbn=&rft.btitle=&rft.title=Scientific+reports&rft.issn=2045-2322&rft_id=info:doi/10.1038%2Fsrep08820 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-25 N1 - Date created - 2015-03-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Eur J Gastroenterol Hepatol. 2000 Feb;12(2):165-73 [10741930] Br J Cancer. 1973 Sep;28(3):197-214 [4743904] Br J Cancer. 2007 Jan 15;96(1):172-6 [17179990] J Microbiol Methods. 2007 May;69(2):330-9 [17391789] Am J Gastroenterol. 2007 Aug;102(8):1603-9 [17488251] Genome Biol. 2007;8(7):R143 [17659080] Cell Host Microbe. 2008 Apr 17;3(4):213-23 [18407065] Br J Cancer. 2008 Jun 3;98(11):1857-63 [18475303] Cancer Epidemiol Biomarkers Prev. 2008 Nov;17(11):3062-8 [18990747] Int J Cancer. 2009 May 1;124(9):2135-8 [19107937] PLoS One. 2009;4(11):e7985 [19956741] Environ Microbiol. 2010 Jan;12(1):118-23 [19725865] Gastroenterology. 2010 Jul;139(1):73-83; quiz e11-2 [20399210] Scand J Gastroenterol. 1997 Dec;32(12):1215-21 [9438319] Am J Gastroenterol. 2005 Mar;100(3):588-93 [15743356] Appl Environ Microbiol. 2005 Dec;71(12):8228-35 [16332807] Proc Natl Acad Sci U S A. 2006 Jan 17;103(3):732-7 [16407106] Appl Environ Microbiol. 2007 Jan;73(1):278-88 [17071787] Nat Methods. 2010 Oct;7(10):813-9 [20818378] BMC Bioinformatics. 2011;12:38 [21276213] CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855] ISME J. 2011 Oct;5(10):1571-9 [21472016] Am J Gastroenterol. 2011 Nov;106(11):1923-9 [21931379] Bioinformatics. 2012 Jul 15;28(14):1823-9 [22556368] Br J Cancer. 2012 Aug 21;107(5):888-94 [22814581] Nucleic Acids Res. 2013 Jan;41(Database issue):D590-6 [23193283] Cancer Epidemiol Biomarkers Prev. 2013 Apr;22(4):540-52 [23549398] Infect Immun. 2013 May;81(5):1382-9 [23429529] ISME J. 2013 Jul;7(7):1354-66 [23466701] J Natl Cancer Inst. 2013 Dec 18;105(24):1907-11 [24316595] Dig Surg. 2013;30(4-6):331-6 [24051550] ISME J. 2014 May;8(5):1101-14 [24401855] Cancer Epidemiol Biomarkers Prev. 2014 May;23(5):735-41 [24700175] ISME J. 2012 Jun;6(6):1176-85 [22170420] Crit Rev Oral Biol Med. 2001;12(4):301-14 [11603503] Clin Med (Lond). 2002 Mar-Apr;2(2):147-52 [11991099] Gastroenterology. 2003 May;124(5):1193-201 [12730860] World J Gastroenterol. 2003 Nov;9(11):2501-4 [14606084] Nucleic Acids Res. 2004;32(4):1363-71 [14985472] J Natl Cancer Inst. 2004 Mar 3;96(5):388-96 [14996860] Br J Cancer. 2000 Nov;83(9):1249-54 [11027442] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/srep08820 ER - TY - JOUR T1 - Goserelin for ovarian protection during breast-cancer adjuvant chemotherapy. AN - 1661330576; 25738668 AB - Ovarian failure is a common toxic effect of chemotherapy. Studies of the use of gonadotropin-releasing hormone (GnRH) agonists to protect ovarian function have shown mixed results and lack data on pregnancy outcomes. We randomly assigned 257 premenopausal women with operable hormone-receptor-negative breast cancer to receive standard chemotherapy with the GnRH agonist goserelin (goserelin group) or standard chemotherapy without goserelin (chemotherapy-alone group). The primary study end point was the rate of ovarian failure at 2 years, with ovarian failure defined as the absence of menses in the preceding 6 months and levels of follicle-stimulating hormone (FSH) in the postmenopausal range. Rates were compared with the use of conditional logistic regression. Secondary end points included pregnancy outcomes and disease-free and overall survival. At baseline, 218 patients were eligible and could be evaluated. Among 135 with complete primary end-point data, the ovarian failure rate was 8% in the goserelin group and 22% in the chemotherapy-alone group (odds ratio, 0.30; 95% confidence interval [CI], 0.09 to 0.97; two-sided P=0.04). Owing to missing primary end-point data, sensitivity analyses were performed, and the results were consistent with the main findings. Missing data did not differ according to treatment group or according to the stratification factors of age and planned chemotherapy regimen. Among the 218 patients who could be evaluated, pregnancy occurred in more women in the goserelin group than in the chemotherapy-alone group (21% vs. 11%, P=0.03); women in the goserelin group also had improved disease-free survival (P=0.04) and overall survival (P=0.05). Although missing data weaken interpretation of the findings, administration of goserelin with chemotherapy appeared to protect against ovarian failure, reducing the risk of early menopause and improving prospects for fertility. (Funded by the National Cancer Institute and others; POEMS/S0230 ClinicalTrials.gov number, NCT00068601.). JF - The New England journal of medicine AU - Moore, Halle C F AU - Unger, Joseph M AU - Phillips, Kelly-Anne AU - Boyle, Frances AU - Hitre, Erika AU - Porter, David AU - Francis, Prudence A AU - Goldstein, Lori J AU - Gomez, Henry L AU - Vallejos, Carlos S AU - Partridge, Ann H AU - Dakhil, Shaker R AU - Garcia, Agustin A AU - Gralow, Julie AU - Lombard, Janine M AU - Forbes, John F AU - Martino, Silvana AU - Barlow, William E AU - Fabian, Carol J AU - Minasian, Lori AU - Meyskens, Frank L AU - Gelber, Richard D AU - Hortobagyi, Gabriel N AU - Albain, Kathy S AU - POEMS/S0230 Investigators AD - From the Cleveland Clinic Foundation, Cleveland (H.C.F.M.); SWOG Cancer Research Group Statistical Center, Fred Hutchinson Cancer Research Center (J.M.U., W.E.B.), and Seattle Cancer Care Alliance and University of Washington (J.G.) - all in Seattle; Peter MacCallum Cancer Centre, University of Melbourne, Melbourne, VIC (K.-A.P., P.A.F.), Australia and New Zealand Breast Cancer Trials Group (ANZBCTG) (K.-A.P., P.A.F., J.F.F.), Calvary Mater Hospital, Newcastle, NSW (F.B., J.M.L., J.F.F.), and University of Sydney, Sydney (F.B.) - all in Australia; International Breast Cancer Study Group (IBCSG), Bern, Switzerland (K.-A.P., P.A.F.); National Institute of Oncology, Budapest, Hungary (E.H.); Auckland Regional Cancer and Blood Service, Auckland, New Zealand (D.P.); Fox Chase Cancer Center, Philadelphia (L.J.G.); Instituto de Enfermedades Neoplasicas (H.L.G.) and Oncosalud SAC (C.S.V.), Lima, Peru; Dana-Farber Cancer Institute (A.H.P., R.D.G.) and IBCSG Statistical Center (R.D.G.) - both in Boston; Wichita Community Clinical Oncology Program, Wichita (S.R.D.), and University of Kansas, Westwood (C.J.F.) - both in Kansas; University of Southern California Norris Cancer Center, Los Angeles (A.A.G.), the Angeles Clinic and Research Institute, Santa Monica (S.M.), and University of California at Irvine Chao Family Comprehensive Cancer Center, Orange (F.L.M) - all in California; National Cancer Institute, Division of Cancer Prevention, Bethesda, MD (L.M.); M.D. Anderson Cancer Center, Houston (G.N.H.); and Loyola University Medical Center, Cardinal Bernardin Cancer Center, Maywood, IL (K.S.A.). ; POEMS/S0230 Investigators Y1 - 2015/03/05/ PY - 2015 DA - 2015 Mar 05 SP - 923 EP - 932 VL - 372 IS - 10 KW - Goserelin KW - 0F65R8P09N KW - Gonadotropin-Releasing Hormone KW - 33515-09-2 KW - Abridged Index Medicus KW - Index Medicus KW - Regression Analysis KW - Pregnancy Rate KW - Disease-Free Survival KW - Premenopause KW - Humans KW - Adult KW - Middle Aged KW - Female KW - Chemotherapy, Adjuvant KW - Pregnancy KW - Breast Neoplasms -- drug therapy KW - Gonadotropin-Releasing Hormone -- agonists KW - Breast Neoplasms -- mortality KW - Primary Ovarian Insufficiency -- prevention & control KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Breast Neoplasms -- surgery KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Goserelin -- therapeutic use KW - Goserelin -- adverse effects KW - Primary Ovarian Insufficiency -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1661330576?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+New+England+journal+of+medicine&rft.atitle=Goserelin+for+ovarian+protection+during+breast-cancer+adjuvant+chemotherapy.&rft.au=Moore%2C+Halle+C+F%3BUnger%2C+Joseph+M%3BPhillips%2C+Kelly-Anne%3BBoyle%2C+Frances%3BHitre%2C+Erika%3BPorter%2C+David%3BFrancis%2C+Prudence+A%3BGoldstein%2C+Lori+J%3BGomez%2C+Henry+L%3BVallejos%2C+Carlos+S%3BPartridge%2C+Ann+H%3BDakhil%2C+Shaker+R%3BGarcia%2C+Agustin+A%3BGralow%2C+Julie%3BLombard%2C+Janine+M%3BForbes%2C+John+F%3BMartino%2C+Silvana%3BBarlow%2C+William+E%3BFabian%2C+Carol+J%3BMinasian%2C+Lori%3BMeyskens%2C+Frank+L%3BGelber%2C+Richard+D%3BHortobagyi%2C+Gabriel+N%3BAlbain%2C+Kathy+S%3BPOEMS%2FS0230+Investigators&rft.aulast=Moore&rft.aufirst=Halle+C&rft.date=2015-03-05&rft.volume=372&rft.issue=10&rft.spage=923&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=1533-4406&rft_id=info:doi/10.1056%2FNEJMoa1413204 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-16 N1 - Date created - 2015-03-05 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00068601; ClinicalTrials.gov N1 - SuppNotes - Cited By: N Engl J Med. 2014 Jul 10;371(2):107-18 [24881463] Ann Oncol. 2013 Sep;24(9):2224-35 [23709175] J Clin Oncol. 2014 Apr 10;32(11):1151-6 [24567428] Psychooncology. 2014 Feb;23(2):173-82 [24038775] N Engl J Med. 2015 Jan 29;372(5):436-46 [25495490] Eur J Cancer. 2000 Jan;36(1):43-8 [10741293] Eur J Cancer. 1998 Apr;34(5):632-40 [9713266] J Clin Oncol. 2006 Jun 20;24(18):2917-31 [16651642] Oncologist. 2007 Sep;12(9):1055-66 [17914075] Fertil Steril. 2009 Mar;91(3):694-7 [18675959] Int J Oncol. 2009 Oct;35(4):789-96 [19724914] Breast Cancer Res Treat. 2009 Oct;117(3):561-7 [19153828] Lancet. 2009 Dec 19;374(9707):2055-63 [20004966] N Engl J Med. 2010 Jun 3;362(22):2053-65 [20519679] Breast Cancer Res. 2010;12(4):R49 [20630060] J Clin Oncol. 2011 Jun 10;29(17):2334-41 [21537042] JAMA. 2011 Jul 20;306(3):269-76 [21771987] Breast Cancer Res Treat. 2011 Dec;130(3):783-90 [21279682] J Clin Oncol. 2012 Feb 10;30(5):533-8 [22231041] Obstet Gynecol. 2013 Jan;121(1):78-86 [23262931] Cancer Treat Rev. 2014 Jun;40(5):675-83 [24360817] Comment In: BMJ. 2015;350:h1274 [25752307] Nat Rev Clin Oncol. 2015 May;12(5):252 [25801817] N Engl J Med. 2015 Jun 4;372(23):2269-70 [26039609] N Engl J Med. 2015 Jun 4;372(23):2268 [26039610] N Engl J Med. 2015 Jun 4;372(23):2268-9 [26039611] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1056/NEJMoa1413204 ER - TY - CPAPER T1 - The Development and Utility of PRO Tools: The PRO-CTCAE Measurement System T2 - 2015 American Society for Clinical Pharmacology and Therapeutics (ASCPT 2015) AN - 1669820611; 6340387 JF - 2015 American Society for Clinical Pharmacology and Therapeutics (ASCPT 2015) AU - Minasian, Lori Y1 - 2015/03/03/ PY - 2015 DA - 2015 Mar 03 KW - Pharmacology KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669820611?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+American+Society+for+Clinical+Pharmacology+and+Therapeutics+%28ASCPT+2015%29&rft.atitle=The+Development+and+Utility+of+PRO+Tools%3A+The+PRO-CTCAE+Measurement+System&rft.au=Minasian%2C+Lori&rft.aulast=Minasian&rft.aufirst=Lori&rft.date=2015-03-03&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+American+Society+for+Clinical+Pharmacology+and+Therapeutics+%28ASCPT+2015%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascpt.org/Portals/8/docs/Meetings/2015%20Annual%20Meeting/Final%20Program%20-%20FINAL.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-31 N1 - Last updated - 2015-04-06 ER - TY - JOUR T1 - Infertility and incident endometrial cancer risk: a pooled analysis from the epidemiology of endometrial cancer consortium (E2C2) AN - 1668250545; PQ0001223578 AB - Background: Nulliparity is an endometrial cancer risk factor, but whether or not this association is due to infertility is unclear. Although there are many underlying infertility causes, few studies have assessed risk relations by specific causes. Methods: We conducted a pooled analysis of 8153 cases and 11 713 controls from 2 cohort and 12 case-control studies. All studies provided self-reported infertility and its causes, except for one study that relied on data from national registries. Logistic regression was used to estimate adjusted odds ratios (OR) and 95% confidence intervals (CI). Results: Nulliparous women had an elevated endometrial cancer risk compared with parous women, even after adjusting for infertility (OR=1.76; 95% CI: 1.59-1.94). Women who reported infertility had an increased risk compared with those without infertility concerns, even after adjusting for nulliparity (OR=1.22; 95% CI: 1.13-1.33). Among women who reported infertility, none of the individual infertility causes were substantially related to endometrial cancer. Conclusions: Based on mainly self-reported infertility data that used study-specific definitions of infertility, nulliparity and infertility appeared to independently contribute to endometrial cancer risk. Understanding residual endometrial cancer risk related to infertility, its causes and its treatments may benefit from large studies involving detailed data on various infertility parameters. JF - British Journal of Cancer AU - Yang, H P AU - Cook, L S AU - Weiderpass, E AU - Adami, H-O AU - Anderson, K E AU - Cai, H AU - Cerhan, J R AU - Clendenen, T V AU - Felix, A S AU - Friedenreich, C M AU - Garcia-Closas, M AU - Goodman, M T AU - Liang, X AU - Lissowska, J AU - Lu, L AU - Magliocco, A M AU - McCann, S E AU - Moysich, K B AU - Olson, S H AU - Petruzella, S AU - Pike, M C AU - Polidoro, S AU - Ricceri, F AU - Risch, H A AU - Sacerdote, C AU - Setiawan, V W AU - Shu, X O AU - Spurdle, A B AU - Trabert, B AU - Webb, P M AU - Wentzensen, N AU - Xiang, Y-B AU - Xu, Y AU - Yu, H AU - Zeleniuch-Jacquotte, A AU - Brinton, L A AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892, USA Y1 - 2015/03/03/ PY - 2015 DA - 2015 Mar 03 SP - 925 EP - 933 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 112 IS - 5 SN - 0007-0920, 0007-0920 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Risk assessment KW - Infertility KW - Health risks KW - Epidemiology KW - Risk factors KW - Cancer KW - H 11000:Diseases/Injuries/Trauma KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668250545?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+Journal+of+Cancer&rft.atitle=Infertility+and+incident+endometrial+cancer+risk%3A+a+pooled+analysis+from+the+epidemiology+of+endometrial+cancer+consortium+%28E2C2%29&rft.au=Yang%2C+H+P%3BCook%2C+L+S%3BWeiderpass%2C+E%3BAdami%2C+H-O%3BAnderson%2C+K+E%3BCai%2C+H%3BCerhan%2C+J+R%3BClendenen%2C+T+V%3BFelix%2C+A+S%3BFriedenreich%2C+C+M%3BGarcia-Closas%2C+M%3BGoodman%2C+M+T%3BLiang%2C+X%3BLissowska%2C+J%3BLu%2C+L%3BMagliocco%2C+A+M%3BMcCann%2C+S+E%3BMoysich%2C+K+B%3BOlson%2C+S+H%3BPetruzella%2C+S%3BPike%2C+M+C%3BPolidoro%2C+S%3BRicceri%2C+F%3BRisch%2C+H+A%3BSacerdote%2C+C%3BSetiawan%2C+V+W%3BShu%2C+X+O%3BSpurdle%2C+A+B%3BTrabert%2C+B%3BWebb%2C+P+M%3BWentzensen%2C+N%3BXiang%2C+Y-B%3BXu%2C+Y%3BYu%2C+H%3BZeleniuch-Jacquotte%2C+A%3BBrinton%2C+L+A&rft.aulast=Yang&rft.aufirst=H&rft.date=2015-03-03&rft.volume=112&rft.issue=5&rft.spage=925&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2015.24 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-04-29 N1 - SubjectsTermNotLitGenreText - Risk assessment; Health risks; Infertility; Epidemiology; Risk factors; Cancer DO - http://dx.doi.org/10.1038/bjc.2015.24 ER - TY - JOUR T1 - Isoflavones enhance interleukin-17 gene expression via retinoic acid receptor-related orphan receptors α and γ. AN - 1657319212; 25583575 AB - The retinoic acid receptor-related orphan receptors α and γ (RORα and RORγ), are key regulators of helper T (Th)17 cell differentiation, which is involved in the innate immune system and autoimmune disorders. In this study, we investigated the effects of isoflavones on RORα/γ activity and the gene expression of interleukin (IL)-17, which mediates the function of Th17 cells. In doxycycline-inducible CHO stable cell lines, we found that four isoflavones, biochanin A (BA), genistein, formononetin, and daidzein, enhanced RORα- or RORγ-mediated transcriptional activity in a dose-dependent manner. In an activation assay of the Il17a promoter using Jurkat cells, these compounds enhanced the RORα- or RORγ-mediated activation of the Il17a promoter at concentrations of 1 × 10(-6)M to 1 × 10(-5)M. In mammalian two-hybrid assays, the four isoflavones enhanced the interaction between the RORα- or RORγ-ligand binding domain and the co-activator LXXLL peptide in a dose-dependent manner. In addition, these isoflavones potently enhanced Il17a mRNA expression in mouse T lymphoma EL4 cells treated with phorbol myristate acetate and ionomycin, but showed slight enhancement of Il17a gene expression in RORα/γ-knockdown EL4 cells. Immunoprecipitation and immunoblotting assays also revealed that BA enhanced the interaction between RORγt and SRC-1, which is a co-activator for nuclear receptors. Taken together, these results suggest that the isoflavones have the ability to enhance IL-17 gene expression by stabilizing the interactions between RORα/γ and co-activators. This also provides the first evidence that dietary chemicals can enhance IL-17 gene expression in immune cells. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved. JF - Toxicology AU - Kojima, Hiroyuki AU - Takeda, Yukimasa AU - Muromoto, Ryuta AU - Takahashi, Miki AU - Hirao, Toru AU - Takeuchi, Shinji AU - Jetten, Anton M AU - Matsuda, Tadashi AD - Hokkaido Institute of Public Health, Kita-19, Nishi-12, Kita-ku, Sapporo 060-0819, Japan. Electronic address: kojima@iph.pref.hokkaido.jp. ; National Institute of Environmental Health Sciences, National Institutes of Health, 111 T. W. Alexander Drive, Research Triangle Park, NC 27709, USA. ; Graduate School of Pharmaceutical Sciences, Hokkaido University, Kita-12, Nishi-6, Kita-ku, Sapporo 060-0812, Japan. ; Hokkaido Institute of Public Health, Kita-19, Nishi-12, Kita-ku, Sapporo 060-0819, Japan. Y1 - 2015/03/02/ PY - 2015 DA - 2015 Mar 02 SP - 32 EP - 39 VL - 329 KW - Interleukin-17 KW - 0 KW - Isoflavones KW - Nuclear Receptor Subfamily 1, Group F, Member 1 KW - Nuclear Receptor Subfamily 1, Group F, Member 3 KW - RNA, Messenger KW - Receptors, Cytoplasmic and Nuclear KW - formononetin KW - 295DQC67BJ KW - daidzein KW - 6287WC5J2L KW - Genistein KW - DH2M523P0H KW - biochanin A KW - U13J6U390T KW - Index Medicus KW - Interleukin 17 KW - Isoflavone KW - Retinoic acid receptor-related orphan receptor KW - Th17 KW - Luciferase assay KW - Animals KW - Cricetulus KW - HeLa Cells KW - Humans KW - Jurkat Cells KW - Receptors, Cytoplasmic and Nuclear -- genetics KW - Cell Line, Tumor KW - Mice KW - RNA, Messenger -- genetics KW - RNA, Messenger -- metabolism KW - Th17 Cells -- drug effects KW - Genistein -- pharmacology KW - Receptors, Cytoplasmic and Nuclear -- metabolism KW - CHO Cells KW - Gene Expression Regulation KW - Cell Differentiation -- drug effects KW - Th17 Cells -- metabolism KW - Cricetinae KW - Nuclear Receptor Subfamily 1, Group F, Member 1 -- genetics KW - Nuclear Receptor Subfamily 1, Group F, Member 3 -- genetics KW - Interleukin-17 -- metabolism KW - Isoflavones -- pharmacology KW - Nuclear Receptor Subfamily 1, Group F, Member 3 -- metabolism KW - Interleukin-17 -- genetics KW - Nuclear Receptor Subfamily 1, Group F, Member 1 -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1657319212?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology&rft.atitle=Isoflavones+enhance+interleukin-17+gene+expression+via+retinoic+acid+receptor-related+orphan+receptors+%CE%B1+and+%CE%B3.&rft.au=Kojima%2C+Hiroyuki%3BTakeda%2C+Yukimasa%3BMuromoto%2C+Ryuta%3BTakahashi%2C+Miki%3BHirao%2C+Toru%3BTakeuchi%2C+Shinji%3BJetten%2C+Anton+M%3BMatsuda%2C+Tadashi&rft.aulast=Kojima&rft.aufirst=Hiroyuki&rft.date=2015-03-02&rft.volume=329&rft.issue=&rft.spage=32&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=1879-3185&rft_id=info:doi/10.1016%2Fj.tox.2015.01.007 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-13 N1 - Date created - 2015-02-16 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.tox.2015.01.007 ER - TY - JOUR T1 - Reverse zoonosis of influenza to swine: new perspectives on the human-animal interface AN - 1746891714; PQ0002195345 AB - The origins of the 2009 influenza A (H1N1) pandemic in swine are unknown, highlighting gaps in our understanding of influenza A virus (IAV) ecology and evolution. We review how recently strengthened influenza virus surveillance in pigs has revealed that influenza virus transmission from humans to swine is far more frequent than swine-to-human zoonosis, and is central in seeding swine globally with new viral diversity. The scale of global human-to-swine transmission represents the largest 'reverse zoonosis' of a pathogen documented to date. Overcoming the bias towards perceiving swine as sources of human viruses, rather than recipients, is key to understanding how the bidirectional nature of the human-animal interface produces influenza threats to both hosts. JF - Trends in Microbiology AU - Nelson, Martha I AU - Vincent, Amy L AD - Fogarty International Center, National Institutes of Health, Bethesda, MD 20892, USA Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 142 EP - 153 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 23 IS - 3 SN - 0966-842X, 0966-842X KW - Microbiology Abstracts B: Bacteriology; Virology & AIDS Abstracts KW - influenza A virus KW - swine KW - pandemic KW - evolution KW - human-animal interface KW - pandemics KW - Influenza A virus KW - Reviews KW - Influenza A KW - Seeding KW - Pathogens KW - Evolution KW - V 22410:Animal Diseases KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1746891714?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+Microbiology&rft.atitle=Reverse+zoonosis+of+influenza+to+swine%3A+new+perspectives+on+the+human-animal+interface&rft.au=Nelson%2C+Martha+I%3BVincent%2C+Amy+L&rft.aulast=Nelson&rft.aufirst=Martha&rft.date=2015-03-01&rft.volume=23&rft.issue=3&rft.spage=142&rft.isbn=&rft.btitle=&rft.title=Trends+in+Microbiology&rft.issn=0966842X&rft_id=info:doi/10.1016%2Fj.tim.2014.12.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - pandemics; Influenza A; Reviews; Seeding; Pathogens; Evolution; Influenza A virus DO - http://dx.doi.org/10.1016/j.tim.2014.12.002 ER - TY - JOUR T1 - Acoustic Separation and Biomedical Research: Lessons from Indian Regulation of Compensation for Research Injury AN - 1718059716; 2011-839613 AB - In early 2013, the Indian government introduced new rules governing the conduct of clinical trials involving human participants. Among other provisions, the law requires that sponsors of research compensate participants who are injured during the course of their research participation. This article examines the effects of India's compensation law and the efforts that policymakers in India have made to tailor the law since its passage. I use the legal concept of acoustic separation as a framework to explain and justify the approach that India has taken in refining its regulation of research related injuries. I conclude that India's example may provide useful lessons for research sponsors and lawmakers in other regulatory states seeking to promote a well-regulated biomedical research industry. Adapted from the source document. JF - The Journal of Law, Medicine & Ethics AU - Larkin, Megan E AD - Post-doctoral fellow in the Clinical Center Department of Bioethics at the National Institutes of Health. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 105 EP - 115 PB - Wiley-Blackwell, UK VL - 43 IS - 1 SN - 1073-1105, 1073-1105 KW - Economic conditions and policy - Economic policy, planning, and development KW - Law and ethics - Law and jurisprudence KW - Health conditions and policy - Medicine and health care KW - Culture and religion - Intellectual life KW - Politics - Politics and policy-making KW - Manufacturing and heavy industry - Industry and industrial policy KW - Medical research KW - Law KW - Regulation KW - Clinical trials KW - Decision-making KW - Industry KW - India KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1718059716?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apais&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+Law%2C+Medicine+%26+Ethics&rft.atitle=Acoustic+Separation+and+Biomedical+Research%3A+Lessons+from+Indian+Regulation+of+Compensation+for+Research+Injury&rft.au=Larkin%2C+Megan+E&rft.aulast=Larkin&rft.aufirst=Megan&rft.date=2015-03-01&rft.volume=43&rft.issue=1&rft.spage=105&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Law%2C+Medicine+%26+Ethics&rft.issn=10731105&rft_id=info:doi/10.1111%2Fjlme.12199 LA - English DB - PAIS Index N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-09-28 N1 - SubjectsTermNotLitGenreText - India; Regulation; Law; Medical research; Decision-making; Clinical trials; Industry DO - http://dx.doi.org/10.1111/jlme.12199 ER - TY - JOUR T1 - Mass spectrometry-based protein identification with accurate statistical significance assignment AN - 1701473937; PQ0001733173 AB - Motivation: Assigning statistical significance accurately has become increasingly important as metadata of many types, often assembled in hierarchies, are constructed and combined for further biological analyses. Statistical inaccuracy of metadata at any level may propagate to downstream analyses, undermining the validity of scientific conclusions thus drawn. From the perspective of mass spectrometry-based proteomics, even though accurate statistics for peptide identification can now be achieved, accurate protein level statistics remain challenging.Results: We have constructed a protein ID method that combines peptide evidences of a candidate protein based on a rigorous formula derived earlier; in this formula the database P-value of every peptide is weighted, prior to the final combination, according to the number of proteins it maps to. We have also shown that this protein ID method provides accurate protein level E-value, eliminating the need of using empirical post-processing methods for type-I error control. Using a known protein mixture, we find that this protein ID method, when combined with the Soric formula, yields accurate values for the proportion of false discoveries. In terms of retrieval efficacy, the results from our method are comparable with other methods tested.Availability and implementation: The source code, implemented in C++ on a linux system, is available for download at ftp://ftp.ncbi.nlm.nih.gov/pub/qmbp/qmbp_ms/RAId/RAId_Linux_64Bit. Supplementary information: Supplementary data are available at Bioinformatics online. JF - Bioinformatics AU - Alves, Gelio AU - Yu, Yi-Kuo AD - *To whom correspondence should be addressed., yyu@ncbi.nlm.nih.gov Y1 - 2015/03/01/ PY - 2015 DA - 2015 Mar 01 SP - 699 EP - 706 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 31 IS - 5 SN - 1367-4803, 1367-4803 KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - Databases KW - Statistics KW - Data processing KW - Bioinformatics KW - proteomics KW - Maps KW - Internet KW - N 14810:Methods KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1701473937?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioinformatics&rft.atitle=Mass+spectrometry-based+protein+identification+with+accurate+statistical+significance+assignment&rft.au=Alves%2C+Gelio%3BYu%2C+Yi-Kuo&rft.aulast=Alves&rft.aufirst=Gelio&rft.date=2015-03-01&rft.volume=31&rft.issue=5&rft.spage=699&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtu717 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Last updated - 2016-07-07 N1 - SubjectsTermNotLitGenreText - Databases; Data processing; Statistics; proteomics; Bioinformatics; Maps; Internet DO - http://dx.doi.org/10.1093/bioinformatics/btu717 ER - TY - JOUR T1 - Caregiver burden is associated with disability in schizophrenia: Results of a study from a rural setting of south India AN - 1698867368 AB - Background: Taking care of patients with schizophrenia is a major source of burden to the family. Research on burden experienced by family members of patients living in rural communities is sparse.Methods: Data were obtained from a community intervention program for psychoses in a rural community of south India, where persons with severe mental disorders were identified, treated and followed up. As part of the program, caregivers of 245 schizophrenia patients were interviewed using the Burden Assessment Schedule. Psychopathology (Positive and Negative Syndrome Scale; PANSS), treatment status and disability (Indian Disability Evaluation and Assessment Scale; IDEAS) experienced by the patients were also assessed. Univariate and multivariate analyses were used to study the influence of different factors on the caregiver burden.Results: Level of burden had a significant direct correlation with disability (Pearson’s r = .35; p < .01) and severity of psychopathology (r = .21; p < .01). Duration of treatment had an inverse correlation with burden (Pearson’s r = −.16; p < .01). Multivariate analysis revealed that total IDEAS score (Beta = .28; t = 4.37; p ≤ .01), duration of treatment (Beta = −.17; t = −2.58; p = .01), age of the family caregiver (Beta = .15; t = 2.4; p = .02) and gender of the patient (Beta = −.13; t = −2.1; p = .04) were significant predictors of burden. The model including total IDEAS score explained 14% of variance (adjusted R 2 = .139; p < .01). Conclusion: Burden experienced by family caregivers of schizophrenia patients depends on the level of disability experienced by the patient, age of the family caregivers and gender of the patient. Interventions to reduce disability of the patients may reduce the caregiver burden. JF - The International Journal of Social Psychiatry AU - Kumar, Channaveerachari N AU - Suresha, Kudumallige K AU - Thirthalli, Jagadisha AU - Arunachala, Udupi AU - Gangadhar, Bangalore N AD - Department of Psychiatry, National Institute of Mental Health and Neuro Sciences, Bangalore, India ; Manasa Nursing Home, Thirthahalli, India ; Department of Psychiatry, National Institute of Mental Health and Neuro Sciences, Bangalore, India Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 157 EP - 163 CY - London PB - SAGE PUBLICATIONS, INC. VL - 61 IS - 2 SN - 0020-7640 KW - Medical Sciences--Psychiatry And Neurology KW - Schizophrenia KW - caregiver burden KW - disability KW - rural community KW - Caregivers KW - Rural Areas KW - Caregiver Burden KW - Physically Handicapped KW - Caretaker syndrome KW - Disability KW - Carers KW - Rural communities KW - Burden KW - India UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1698867368?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+International+Journal+of+Social+Psychiatry&rft.atitle=Caregiver+burden+is+associated+with+disability+in+schizophrenia%3A+Results+of+a+study+from+a+rural+setting+of+south+India&rft.au=Kumar%2C+Channaveerachari+N%3BSuresha%2C+Kudumallige+K%3BThirthalli%2C+Jagadisha%3BArunachala%2C+Udupi%3BGangadhar%2C+Bangalore+N&rft.aulast=Kumar&rft.aufirst=Channaveerachari&rft.date=2015-03-01&rft.volume=61&rft.issue=2&rft.spage=157&rft.isbn=&rft.btitle=&rft.title=The+International+Journal+of+Social+Psychiatry&rft.issn=00207640&rft_id=info:doi/10.1177%2F0020764014537637 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-07-07 N1 - Last updated - 2016-09-08 N1 - SubjectsTermNotLitGenreText - India DO - http://dx.doi.org/10.1177/0020764014537637 ER - TY - JOUR T1 - The Real Challenge for Cookstoves and Health: More Evidence AN - 1680450654; PQ0001534673 JF - EcoHealth AU - Rosenthal, Joshua AD - Division of Epidemiology and Population Studies, Fogarty International Center, National Institutes of Health, Bethesda, MD, 20892-2220, USA, joshua_rosenthal@nih.gov Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 8 EP - 11 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 12 IS - 1 SN - 1612-9202, 1612-9202 KW - Ecology Abstracts UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680450654?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=EcoHealth&rft.atitle=The+Real+Challenge+for+Cookstoves+and+Health%3A+More+Evidence&rft.au=Rosenthal%2C+Joshua&rft.aulast=Rosenthal&rft.aufirst=Joshua&rft.date=2015-03-01&rft.volume=12&rft.issue=1&rft.spage=8&rft.isbn=&rft.btitle=&rft.title=EcoHealth&rft.issn=16129202&rft_id=info:doi/10.1007%2Fs10393-014-0997-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Number of references - 17 N1 - Last updated - 2015-11-16 DO - http://dx.doi.org/10.1007/s10393-014-0997-9 ER - TY - JOUR T1 - Epidemiology of Japanese Encephalitis in the Philippines: A Systematic Review AN - 1676365747; PQ0001407953 AB - Japanese encephalitis virus (JEV) is an important cause of neurologic infections in Asia, resulting in substantial disability and deaths. Although believed to be endemic in the Philippines, little is known of the epidemiology and geographic distribution of this disease in the country. We reviewed data from clinical studies, prevalence surveys and animal studies since the 1950s. Based on this review, JEV is an important cause of encephalitis and febrile illness in all three major island groups of the country. The majority of cases were seen in children younger than 15 years and males were more often affected than females. The national laboratory initiated testing of referred cases in 2009 and surveillance for acute encephalitis syndrome (AES) with laboratory confirmation of a subset of cases was established in 2011. From 2011 to 2014, there were 1,032 cases of suspected JE. Of 497 cases with specimens tested, 73 (15%) had laboratory-confirmed JE. Our findings confirm that JE has an extensive geographic distribution in the Philippines. These findings support the introduction of JE vaccine into the country's routine immunization program. JF - PLoS Neglected Tropical Diseases AU - Lopez, Anna Lena AU - Aldaba, Josephine G AU - Roque, Vito G AU - Tandoc, Amado O AU - Sy, Ava Kristy AU - Espino, Fe Esperanza AU - DeQuiroz-Castro, Maricel AU - Jee, Youngmee AU - Ducusin, Maria Joyce AU - Fox, Kimberley K AD - University of the Philippines Manila-National Institutes of Health, Institute of Child Health and Human Development, Manila, Philippines PY - 2015 PB - Public Library of Science, 185 Berry Street San Francisco CA 94107 United States VL - 9 IS - 3 SN - 1935-2727, 1935-2727 KW - Virology & AIDS Abstracts; Health & Safety Science Abstracts KW - Philippines KW - Mortality KW - Geographical distribution KW - Data processing KW - Infection KW - Children KW - Encephalitis KW - Immunization KW - Islands KW - Epidemiology KW - Disabilities KW - Reviews KW - Japanese encephalitis virus KW - Vaccines KW - Asia KW - H 4000:Food and Drugs KW - V 22400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676365747?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+Neglected+Tropical+Diseases&rft.atitle=Epidemiology+of+Japanese+Encephalitis+in+the+Philippines%3A+A+Systematic+Review&rft.au=Lopez%2C+Anna+Lena%3BAldaba%2C+Josephine+G%3BRoque%2C+Vito+G%3BTandoc%2C+Amado+O%3BSy%2C+Ava+Kristy%3BEspino%2C+Fe+Esperanza%3BDeQuiroz-Castro%2C+Maricel%3BJee%2C+Youngmee%3BDucusin%2C+Maria+Joyce%3BFox%2C+Kimberley+K&rft.aulast=Lopez&rft.aufirst=Anna&rft.date=2015-03-01&rft.volume=9&rft.issue=3&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+Neglected+Tropical+Diseases&rft.issn=19352727&rft_id=info:doi/10.1371%2Fjournal.pntd.0003630 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Geographical distribution; Data processing; Islands; Epidemiology; Reviews; Vaccines; Children; Infection; Immunization; Encephalitis; Mortality; Disabilities; Japanese encephalitis virus; Philippines; Asia DO - http://dx.doi.org/10.1371/journal.pntd.0003630 ER - TY - JOUR T1 - Infant attachment security and early childhood behavioral inhibition interact to predict adolescent social anxiety symptoms AN - 1676089875; 4666068 AB - Insecure attachment and behavioral inhibition (BI) increase risk for internalizing problems, but few longitudinal studies have examined their interaction in predicting adolescent anxiety. This study included 165 adolescents (ages 14-17 years) selected based on their reactivity to novelty at 4 months. Infant attachment was assessed with the Strange Situation. Multimethod BI assessments were conducted across childhood. Adolescents and their parents independently reported on anxiety. The interaction of attachment and BI significantly predicted adolescent anxiety symptoms, such that BI and anxiety were only associated among adolescents with histories of insecure attachment. Exploratory analyses revealed that this effect was driven by insecure‐ ;resistant attachment and that the association between BI and social anxiety was significant only for insecure males. Clinical implications are discussed. Reprinted by permission of the University of Chicago Press. © All rights reserved JF - Child development AU - Pine, Daniel S AU - Henderson, Heather A AU - Fox, Nathan A AU - Lewis-Morrarty, Erin AU - Degnan, Kathryn A AU - Chronis-Tuscano, Andrea AD - University of Maryland ; National Institute of Mental Health ; University of Waterloo Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 598 EP - 613 VL - 86 IS - 2 SN - 0009-3920, 0009-3920 KW - Sociology KW - Longitudinal studies KW - Early childhood KW - Anxiety KW - Social interaction KW - Adolescents KW - Infants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676089875?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Child+development&rft.atitle=Infant+attachment+security+and+early+childhood+behavioral+inhibition+interact+to+predict+adolescent+social+anxiety+symptoms&rft.au=Pine%2C+Daniel+S%3BHenderson%2C+Heather+A%3BFox%2C+Nathan+A%3BLewis-Morrarty%2C+Erin%3BDegnan%2C+Kathryn+A%3BChronis-Tuscano%2C+Andrea&rft.aulast=Pine&rft.aufirst=Daniel&rft.date=2015-03-01&rft.volume=86&rft.issue=2&rft.spage=598&rft.isbn=&rft.btitle=&rft.title=Child+development&rft.issn=00093920&rft_id=info:doi/10.1111%2Fcdev.12336 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-04-27 N1 - Last updated - 2015-04-28 N1 - SubjectsTermNotLitGenreText - 3827 2211 652 5676 646 6091 2212; 593; 1147 4196; 7541 7537 971; 6495 2212; 11860 11907 DO - http://dx.doi.org/10.1111/cdev.12336 ER - TY - JOUR T1 - Saving lives by building bridges between user needs and clean cooking technology AN - 1676088352; 4666517 JF - Journal of health communication AU - Rosenthal, Joshua P AU - Borrazzo, John AD - National Institutes of Health, USA ; USAID Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 1 EP - 2 VL - 20 IS - Supp.1 SN - 1081-0730, 1081-0730 KW - Sociology KW - Air pollution KW - Mortality KW - Household equipment KW - Traditional technology KW - Cooking KW - Food safety KW - Hygiene KW - Aid KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1676088352?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+health+communication&rft.atitle=Saving+lives+by+building+bridges+between+user+needs+and+clean+cooking+technology&rft.au=Rosenthal%2C+Joshua+P%3BBorrazzo%2C+John&rft.aulast=Rosenthal&rft.aufirst=Joshua&rft.date=2015-03-01&rft.volume=20&rft.issue=Supp.1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/10.1080%2F10810730.2014.996304 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-04-27 N1 - Last updated - 2015-04-28 N1 - SubjectsTermNotLitGenreText - 6156 5772; 2854 5129; 5142 10449 5772; 879; 8291 3409 6306; 6035 4379; 891 9818; 12885 12622; 10449 5772 DO - http://dx.doi.org/10.1080/10810730.2014.996304 ER - TY - JOUR T1 - Garlic and onions: their cancer prevention properties. AN - 1675872663; 25586902 AB - The Allium genus includes garlic, onions, shallots, leeks, and chives. These vegetables are popular in cuisines worldwide and are valued for their potential medicinal properties. Epidemiologic studies, while limited in their abilities to assess Allium consumption, indicate some associations of Allium vegetable consumption with decreased risk of cancer, particularly cancers of the gastrointestinal tract. Limited intervention studies have been conducted to support these associations. The majority of supportive evidence on Allium vegetables cancer-preventive effects comes from mechanistic studies. These studies highlight potential mechanisms of individual sulfur-containing compounds and of various preparations and extracts of these vegetables, including decreased bioactivation of carcinogens, antimicrobial activities, and redox modification. Allium vegetables and their components have effects at each stage of carcinogenesis and affect many biologic processes that modify cancer risk. This review discusses the cancer-preventive effects of Allium vegetables, particularly garlic and onions, and their bioactive sulfur compounds and highlights research gaps. ©2015 American Association for Cancer Research. JF - Cancer prevention research (Philadelphia, Pa.) AU - Nicastro, Holly L AU - Ross, Sharon A AU - Milner, John A AD - Cancer Prevention Fellowship Program, Nutritional Science Research Group, Division of Cancer Prevention, National Cancer Institute, Bethesda, MD. holly.nicastro@nih.gov. ; Nutritional Science Research Group, Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland. ; USDA/ARS Beltsville Human Nutrition Research Center, Beltsville, Maryland. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 181 EP - 189 VL - 8 IS - 3 KW - Plant Extracts KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Onions -- chemistry KW - Plant Extracts -- therapeutic use KW - Neoplasms -- prevention & control KW - Garlic -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1675872663?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+prevention+research+%28Philadelphia%2C+Pa.%29&rft.atitle=Garlic+and+onions%3A+their+cancer+prevention+properties.&rft.au=Nicastro%2C+Holly+L%3BRoss%2C+Sharon+A%3BMilner%2C+John+A&rft.aulast=Nicastro&rft.aufirst=Holly&rft.date=2015-03-01&rft.volume=8&rft.issue=3&rft.spage=181&rft.isbn=&rft.btitle=&rft.title=Cancer+prevention+research+%28Philadelphia%2C+Pa.%29&rft.issn=1940-6215&rft_id=info:doi/10.1158%2F1940-6207.CAPR-14-0172 LA - 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Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1940-6207.CAPR-14-0172 ER - TY - JOUR T1 - Food Insecurity, Cigarette Smoking, and Acculturation Among Latinos: Data From NHANES 1999–2008 AN - 1673613819 AB - Prevalence of food insecurity (FI) among Latinos in the United States is almost double the national average. To better understand FI among Latinos, potential risk factors beyond poverty, including acculturation indicators and smoking status, were explored. Cross-sectional data from 6,681 Latino adults from the 1999–2008 National Health and Nutrition Examination Surveys were used. Partial proportional odds (PPO) models were used to estimate associations of FI, including cigarette smoking and acculturation. The PPO models indicated that compared with never smokers, current smokers had significantly higher odds of FI (odds ratios ranged from 1.32 to 1.51 across models). Lower levels of acculturation and poverty and being a younger or middle-aged adult were also significantly associated with FI. Among Latinos, current smoking and low acculturation are important risk factors for FI. Current smoking and low acculturation may exacerbate nutritional deprivation in a population that is already disproportionally affected by poverty and poor health outcomes. JF - Journal of Immigrant and Minority Health AU - Iglesias-Rios, Lisbeth AU - Bromberg, Julie E AU - Moser, Richard P AU - Augustson, Erik M AD - Tobacco Control Research Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health, 9609 Medical Center Drive, MSC 9761, Bethesda, MD, 20892-9761, USA Erik.Augustson@nih.gov Erik.Augustson@nih.gov; BLH Technologies, Inc., 1803 Research Boulevard, Suite 300, Rockville, MD, 20850, USA ; Science of Research and Technology Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health, 9606 Medical Center Drive, MSC 9761, Bethesda, MD, 20892-9761, USA ; Tobacco Control Research Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health, 9609 Medical Center Drive, MSC 9761, Bethesda, MD, 20892-9761, USA Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 349 EP - 357 CY - New York PB - Springer Science & Business Media VL - 17 IS - 2 SN - 1557-1912 KW - Medical Sciences KW - Acculturation KW - Deprivation KW - Health status KW - Healthy food KW - Insecurity KW - Latin American people KW - Middle aged people KW - Nutrition KW - Poverty KW - Risk factors KW - Smokers KW - Smoking KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673613819?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Immigrant+and+Minority+Health&rft.atitle=Food+Insecurity%2C+Cigarette+Smoking%2C+and+Acculturation+Among+Latinos%3A+Data+From+NHANES+1999%E2%80%932008&rft.au=Iglesias-Rios%2C+Lisbeth%3BBromberg%2C+Julie+E%3BMoser%2C+Richard+P%3BAugustson%2C+Erik+M&rft.aulast=Iglesias-Rios&rft.aufirst=Lisbeth&rft.date=2015-03-01&rft.volume=17&rft.issue=2&rft.spage=349&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immigrant+and+Minority+Health&rft.issn=15571912&rft_id=info:doi/10.1007%2Fs10903-013-9957-7 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-03-31 N1 - Last updated - 2016-05-12 N1 - SubjectsTermNotLitGenreText - United States--US DO - http://dx.doi.org/10.1007/s10903-013-9957-7 ER - TY - JOUR T1 - Measurement of Nonverbal IQ in Autism Spectrum Disorder: Scores in Young Adulthood Compared to Early Childhood AN - 1673612808 AB - Nonverbal IQ (NVIQ) was examined in 84 individuals with autism spectrum disorder (ASD) followed from age 2 to 19. Most adults who scored in the range of intellectual disability also received scores below 70 as children, and the majority of adults with scores in the average range had scored in this range by age 3. However, within the lower ranges of ability, actual scores declined from age 2 to 19, likely due in part to limitations of appropriate tests. Use of Vineland-II daily living skills scores in place of NVIQ did not statistically improve the correspondence between age 2 and age 19 scores. Clinicians and researchers should use caution when making comparisons based on exact scores or specific ability ranges within or across individuals with ASD of different ages. JF - Journal of Autism and Developmental Disorders AU - Bishop, Somer L AU - Farmer, Cristan AU - Thurm, Audrey AD - Center for Autism and the Developing Brain, Weill Cornell Medical College, 21 Bloomingdale Rd-Rogers Building, White Plains, NY, 10605, USA slb9013@med.cornell.edu; Pediatrics and Developmental Neuroscience Branch, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, Bethesda, MD, 20892, USA ; Center for Autism and the Developing Brain, Weill Cornell Medical College, 21 Bloomingdale Rd-Rogers Building, White Plains, NY, 10605, USA Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 966 EP - 974 CY - New York PB - Springer Science & Business Media VL - 45 IS - 4 SN - 0162-3257 KW - Children And Youth - About KW - Adulthood KW - Age KW - Autism KW - Autistic children KW - Autistic spectrum disorders KW - Autistic young children KW - Childhood KW - Children KW - Disability KW - Intelligence quotient KW - Learning disabilities KW - Life course KW - Living skills KW - Measurement KW - Young adulthood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673612808?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Autism+and+Developmental+Disorders&rft.atitle=Measurement+of+Nonverbal+IQ+in+Autism+Spectrum+Disorder%3A+Scores+in+Young+Adulthood+Compared+to+Early+Childhood&rft.au=Bishop%2C+Somer+L%3BFarmer%2C+Cristan%3BThurm%2C+Audrey&rft.aulast=Bishop&rft.aufirst=Somer&rft.date=2015-03-01&rft.volume=45&rft.issue=4&rft.spage=966&rft.isbn=&rft.btitle=&rft.title=Journal+of+Autism+and+Developmental+Disorders&rft.issn=01623257&rft_id=info:doi/10.1007%2Fs10803-014-2250-3 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-03-31 N1 - Last updated - 2016-05-12 DO - http://dx.doi.org/10.1007/s10803-014-2250-3 ER - TY - JOUR T1 - HIV-associated nephropathies: epidemiology, pathology, mechanisms and treatment. AN - 1673078205; 25686569 AB - HIV is a highly adaptive, rapidly evolving virus, which is associated with renal diseases including collapsing glomerulopathy-the classic histomorphological form of HIV-associated nephropathy. Other nephropathies related to viral factors include HIV-immune-complex kidney disease and thrombotic microangiopathy. The distribution of HIV-associated kidney diseases has changed over time and continues to vary across geographic regions worldwide. The reasons for this diversity are complex and include a critical role of APOL1 variants and possibly other genetic factors, disparities in access to effective antiviral therapies, and likely other factors that we do not yet fully understand. The mechanisms responsible for HIVAN, including HIV infection of podocytes and tubular epithelial cells, the molecules responsible for HIV entry, and diverse mechanisms of cell injury, have been the focus of much study. Although combined antiretroviral therapy is effective at preventing and reversing HIVAN, focal segmental glomerulosclerosis, arterionephrosclerosis and diabetic nephropathy are increasingly common in individuals who have received such therapy for many years. These diseases are associated with metabolic syndrome, obesity and premature ageing. Future directions for HIV-related kidney disease will involve regular screening for drug nephrotoxicity and incipient renal disease, as well as further research into the mechanisms by which chronic inflammation can lead to glomerular disease. JF - Nature reviews. Nephrology AU - Rosenberg, Avi Z AU - Naicker, Saraladevi AU - Winkler, Cheryl A AU - Kopp, Jeffrey B AD - Department of Pathology, Johns Hopkins Medical Institutions, 720 Rutland Avenue, Baltimore, MD 21287, USA. ; School of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand, 7 York Road, Parktown, Johannesburg 2193, South Africa. ; Basic Research Laboratory, Center for Cancer Research, National Cancer Institute, Leidos Biomedical Research, Frederick National Laboratory, Frederick, MD 21702, USA. ; Kidney Disease Section, NIDDK, NIH, 10 Center Drive, 3N116 Bethesda, MD 20892-1268, USA. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 150 EP - 160 VL - 11 IS - 3 KW - Index Medicus KW - Humans KW - AIDS-Associated Nephropathy -- epidemiology KW - AIDS-Associated Nephropathy -- etiology KW - AIDS-Associated Nephropathy -- pathology KW - AIDS-Associated Nephropathy -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673078205?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+reviews.+Nephrology&rft.atitle=HIV-associated+nephropathies%3A+epidemiology%2C+pathology%2C+mechanisms+and+treatment.&rft.au=Rosenberg%2C+Avi+Z%3BNaicker%2C+Saraladevi%3BWinkler%2C+Cheryl+A%3BKopp%2C+Jeffrey+B&rft.aulast=Rosenberg&rft.aufirst=Avi&rft.date=2015-03-01&rft.volume=11&rft.issue=3&rft.spage=150&rft.isbn=&rft.btitle=&rft.title=Nature+reviews.+Nephrology&rft.issn=1759-507X&rft_id=info:doi/10.1038%2Fnrneph.2015.9 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-23 N1 - Date created - 2015-02-24 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nrneph.2015.9 ER - TY - JOUR T1 - Balancing activity and tolerability of neoadjuvant paclitaxel- and docetaxel-based chemotherapy for HER2-positive early stage breast cancer: sensitivity analysis of randomized trials. AN - 1672603043; 25683304 AB - Paclitaxel and docetaxel represent the most adopted taxanes in the neoadjuvant treatment of HER2-positive breast cancer. Questions still remain with regard to their difference in terms of activity and tolerability. Events for pathological complete response (pCR), severe and febrile neutropenia (FN), and severe neurotoxicity were pooled by adopting a fixed- and random-effect model. A sensitivity analysis to test for the interaction between paclitaxel and docetaxel was accomplished. Absolute differences with 95% confidence intervals (CIs) and the number of patients needed to treat/harm (NNT/NNH) were calculated to derive the Likelihood of being Helped or Harmed (LHH). Data from 15 trials (3601 patients) were included. Paclitaxel significantly increases pCR rate by 6.8% in comparison with docetaxel (43.4%, 95% CI 41.1-45.7% versus 36.6%, 95% CI 34.3-39.0%, p=0.0001), regardless of the chemotherapy backbone, with an absolute difference of 9% and 9.2% for anthracycline-based or free-regimens. Paclitaxel significantly improves pCR versus docetaxel with a single HER2-inhibition by 6.7% (p=0.0012), with no difference if combined with a dual HER2-inhibition. Severe neutropenia and FN are significantly lower with paclitaxel, with an absolute difference of 32.4% (p<0.0001) and 2.5% (p=0.0059), respectively. Conversely, severe neurotoxicity is slightly higher with paclitaxel (3%, p=0.0001). The LHH ratio calculated for pCR and severe neutropenia is 2.0 and 0.7 for paclitaxel and docetaxel. Although the activity of neoadjuvant paclitaxel and docetaxel HER2-positive breast cancer is considered similar, the slight advantage in pCR, the significantly lower neutropenia and FN, do favor paclitaxel (in the weekly fashion) over docetaxel, despite the slightly worst neurotoxicity. Copyright © 2015 Elsevier Ltd. All rights reserved. JF - Cancer treatment reviews AU - Carbognin, Luisa AU - Sperduti, Isabella AU - Nortilli, Rolando AU - Brunelli, Matteo AU - Vicentini, Cecilia AU - Pellini, Francesca AU - Pollini, Giovanni Paolo AU - Giannarelli, Diana AU - Tortora, Giampaolo AU - Bria, Emilio AD - Medical Oncology, University of Verona, Azienda Ospedaliera Universitaria Integrata, Verona, Italy. Electronic address: luisa.carbognin@gmail.com. ; Biostatistics, Regina Elena National Cancer Institute, Roma, Italy. Electronic address: isperduti@yahoo.it. ; Medical Oncology, University of Verona, Azienda Ospedaliera Universitaria Integrata, Verona, Italy. Electronic address: rolando.nortilli@ospedaleuniverona.it. ; Department of Pathology and Diagnostic, University of Verona, Azienda Ospedaliera Universitaria Integrata, Verona, Italy. Electronic address: matteo.brunelli@univr.it. ; Medical Oncology, University of Verona, Azienda Ospedaliera Universitaria Integrata, Verona, Italy. Electronic address: cecivice@gmail.com. ; Chirurgia 'A', Department of Surgery and Oncology, University of Verona, Azienda Ospedaliera Universitaria Integrata, Verona, Italy. Electronic address: francesca.pellini@ospedaleuniverona.it. ; Chirurgia 'A', Department of Surgery and Oncology, University of Verona, Azienda Ospedaliera Universitaria Integrata, Verona, Italy. Electronic address: giovanni.pollini@ospedaleuniverona.it. ; Biostatistics, Regina Elena National Cancer Institute, Roma, Italy. Electronic address: giannarelli@ifo.it. ; Medical Oncology, University of Verona, Azienda Ospedaliera Universitaria Integrata, Verona, Italy. Electronic address: giampaolo.tortora@univr.it. ; Medical Oncology, University of Verona, Azienda Ospedaliera Universitaria Integrata, Verona, Italy. Electronic address: emilio.bria@univr.it. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 262 EP - 270 VL - 41 IS - 3 KW - Taxoids KW - 0 KW - docetaxel KW - 15H5577CQD KW - ERBB2 protein, human KW - EC 2.7.10.1 KW - Receptor, ErbB-2 KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Docetaxel KW - Neoadjuvant KW - Sensitivity analysis KW - Breast cancer KW - HER2-positive KW - Paclitaxel -- administration & dosage KW - Randomized Controlled Trials as Topic KW - Paclitaxel -- adverse effects KW - Neoplasm Staging KW - Humans KW - Neoadjuvant Therapy KW - Taxoids -- adverse effects KW - Female KW - Chemotherapy, Adjuvant KW - Taxoids -- administration & dosage KW - Breast Neoplasms -- drug therapy KW - Breast Neoplasms -- pathology KW - Receptor, ErbB-2 -- metabolism KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Breast Neoplasms -- enzymology KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1672603043?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+treatment+reviews&rft.atitle=Balancing+activity+and+tolerability+of+neoadjuvant+paclitaxel-+and+docetaxel-based+chemotherapy+for+HER2-positive+early+stage+breast+cancer%3A+sensitivity+analysis+of+randomized+trials.&rft.au=Carbognin%2C+Luisa%3BSperduti%2C+Isabella%3BNortilli%2C+Rolando%3BBrunelli%2C+Matteo%3BVicentini%2C+Cecilia%3BPellini%2C+Francesca%3BPollini%2C+Giovanni+Paolo%3BGiannarelli%2C+Diana%3BTortora%2C+Giampaolo%3BBria%2C+Emilio&rft.aulast=Carbognin&rft.aufirst=Luisa&rft.date=2015-03-01&rft.volume=41&rft.issue=3&rft.spage=262&rft.isbn=&rft.btitle=&rft.title=Cancer+treatment+reviews&rft.issn=1532-1967&rft_id=info:doi/10.1016%2Fj.ctrv.2015.02.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-14 N1 - Date created - 2015-02-24 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ctrv.2015.02.003 ER - TY - JOUR T1 - Surface-enhanced Raman spectroscopy of the anti-cancer drug irinotecan in presence of human serum albumin. AN - 1667964570; 25645751 AB - The development of nanotechnological devices and their clinical application in medicine has become increasingly important, especially in the context of targeted and personalized therapy. This is particularly important in cancer therapy, where antitumor drugs are highly cytotoxic and often exert their therapeutic effect at concentrations close to systemic toxicity. In the last years a growing number of studies has started to report the use of plasmonic nanoprobes in the field of theranostics, broadening the application of vibrational spectroscopies like Raman scattering and surface enhanced Raman scattering (SERS) in biomedicine. The present work aims to identify and characterize the vibrational profiles of a widely used anticancer drug, irinotecan (CPT-11). With a rational approach, SERS experiments have been performed on this analyte employing both Au and Ag colloids, starting from simple aqueous solutions up to albumin mixtures. A major step forward for drug detection in albumin solutions has been taken with the adoption of a simple deproteinization strategy, and a two-in-one-step separation and identification by coupling thin layer chromatography, TLC, with SERS (TLC-SERS). The latter has revealed to be a valid system for protein separation and simultaneous analyte detection, showing a potential to become an innovative, sensitive and low cost method for antineoplastic drug profiling in patients' body fluids. Copyright © 2015 Elsevier B.V. All rights reserved. JF - Colloids and surfaces. B, Biointerfaces AU - Vicario, A AU - Sergo, V AU - Toffoli, G AU - Bonifacio, A AD - Department of Engineering and Architecture, University of Trieste, Via Valerio 6a, 34127 Trieste, TS, Italy; Experimental and Clinical Pharmacology Division, Department of Translational Research, IRCCS-National Cancer Institute, Aviano, PN, Italy. ; Department of Engineering and Architecture, University of Trieste, Via Valerio 6a, 34127 Trieste, TS, Italy. ; Experimental and Clinical Pharmacology Division, Department of Translational Research, IRCCS-National Cancer Institute, Aviano, PN, Italy. ; Department of Engineering and Architecture, University of Trieste, Via Valerio 6a, 34127 Trieste, TS, Italy. Electronic address: abonifacio@units.it. Y1 - 2015/03/01/ PY - 2015 DA - 2015 Mar 01 SP - 41 EP - 46 VL - 127 KW - Antineoplastic Agents KW - 0 KW - Serum Albumin KW - Solutions KW - irinotecan KW - 0H43101T0J KW - Camptothecin KW - XT3Z54Z28A KW - Index Medicus KW - Thin layer chromatography KW - Irinotecan KW - Albumin KW - SERS KW - Humans KW - Chromatography, Thin Layer KW - Serum Albumin -- metabolism KW - Camptothecin -- chemistry KW - Camptothecin -- pharmacology KW - Camptothecin -- analogs & derivatives KW - Spectrum Analysis, Raman KW - Antineoplastic Agents -- chemistry KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1667964570?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Colloids+and+surfaces.+B%2C+Biointerfaces&rft.atitle=Surface-enhanced+Raman+spectroscopy+of+the+anti-cancer+drug+irinotecan+in+presence+of+human+serum+albumin.&rft.au=Vicario%2C+A%3BSergo%2C+V%3BToffoli%2C+G%3BBonifacio%2C+A&rft.aulast=Vicario&rft.aufirst=A&rft.date=2015-03-01&rft.volume=127&rft.issue=&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=Colloids+and+surfaces.+B%2C+Biointerfaces&rft.issn=1873-4367&rft_id=info:doi/10.1016%2Fj.colsurfb.2015.01.023 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-21 N1 - Date created - 2015-03-30 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.colsurfb.2015.01.023 ER - TY - JOUR T1 - Reproductive consequences of a matrilineal overthrow in rhesus monkeys AN - 1667352810; 4658994 AB - Matrilineal overthrows in macaque societies are rare but devastating events, often resulting in severe morbidity, mortality, and loss of individual and group fitness. The handful of documented macaque overthrows provides scant evidence to reveal the severity or longevity of reproductive consequences resulting from such violent events. We analyzed archival records from semi-free ranging rhesus monkeys, Macaca mulatta, across 6 years (55≤ ;N≤107, from 2007 to 2012) during which time a matrilineal overthrow occurred (in 2009) to test the hypothesis that extremely violent interactions such as a matrilineal overthrow would significantly reduce reproductive fitness for the involved matrilines and for the troop collectively. The matrilineal overthrow resulted in a significant increase in infant loss for the population from the previous year (χ ;2=8.117, df=1, P=0.004), as evidenced by the fact that in 2009, but not in other years, the proportion of infants lost was greater than the proportion of viable infants (χ2=4.55, df=1, P=0.03). Moreover, the deposed matriline suffered 100% infant loss in 2009, a significant change from the previous year (χ2=7.87, df=1, P  ;=0.005) while the attacking matriline suffered 50% infant loss (also a significant change from the previous year; χ ;2=4.44, df=1, P=0.035), with the uninvolved, lowest-ranking matriline showing no change in infant loss from the previous year (χ2=  ;0.008, df=1, P=0.93). The deposed matriline did not produce viable offspring again until 3 years later. We further found that rates of severe fighting (as indicated by the number of fight wounds requiring medical treatment) were positively correlated with infant loss across the 6 years of the study (r[s]=0.943, P=0.005). Our data indicate that extreme periods of intra-group conflict, such as the matrilineal overthrow, have marked short-term consequences for individual fitness, and may be extreme examples of the long-term influences that group violence exerts on the mean fitness within a primate troop. Am. J. Primatol. 77:346– ;352, 2015. Published 2014. This article is a U.S. Government work and is in the public domain in the USA. Copyright John Wiley & Sons. Reproduced with permission. An electronic version of this article is available online at http://www.interscience.wiley.com JF - American journal of primatology AU - Suomi, Stephen J AU - Dettmer, Amanda M AU - Woodward, Ruth A AD - National Institutes of Health Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 346 EP - 352 VL - 77 IS - 3 SN - 0275-2565, 0275-2565 KW - Anthropology KW - Mortality KW - Primatology KW - Medical treatment KW - U.S.A. KW - Violence KW - Animal behaviour KW - Primate reproduction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1667352810?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+primatology&rft.atitle=Reproductive+consequences+of+a+matrilineal+overthrow+in+rhesus+monkeys&rft.au=Suomi%2C+Stephen+J%3BDettmer%2C+Amanda+M%3BWoodward%2C+Ruth+A&rft.aulast=Suomi&rft.aufirst=Stephen&rft.date=2015-03-01&rft.volume=77&rft.issue=3&rft.spage=346&rft.isbn=&rft.btitle=&rft.title=American+journal+of+primatology&rft.issn=02752565&rft_id=info:doi/10.1002%2Fajp.22350 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-03-30 N1 - Last updated - 2015-03-30 N1 - SubjectsTermNotLitGenreText - 8291 3409 6306; 1025 1542 11325; 10149; 13325; 10147 10148 10149 11574; 7890 5792 10484; 433 293 14 DO - http://dx.doi.org/10.1002/ajp.22350 ER - TY - JOUR T1 - A RecA protein surface required for activation of DNA polymerase V. AN - 1667347401; 25811184 AB - DNA polymerase V (pol V) of Escherichia coli is a translesion DNA polymerase responsible for most of the mutagenesis observed during the SOS response. Pol V is activated by transfer of a RecA subunit from the 3'-proximal end of a RecA nucleoprotein filament to form a functional complex called DNA polymerase V Mutasome (pol V Mut). We identify a RecA surface, defined by residues 112-117, that either directly interacts with or is in very close proximity to amino acid residues on two distinct surfaces of the UmuC subunit of pol V. One of these surfaces is uniquely prominent in the active pol V Mut. Several conformational states are populated in the inactive and active complexes of RecA with pol V. The RecA D112R and RecA D112R N113R double mutant proteins exhibit successively reduced capacity for pol V activation. The double mutant RecA is specifically defective in the ATP binding step of the activation pathway. Unlike the classic non-mutable RecA S117F (recA1730), the RecA D112R N113R variant exhibits no defect in filament formation on DNA and promotes all other RecA activities efficiently. An important pol V activation surface of RecA protein is thus centered in a region encompassing amino acid residues 112, 113, and 117, a surface exposed at the 3'-proximal end of a RecA filament. The same RecA surface is not utilized in the RecA activation of the homologous and highly mutagenic RumA'2B polymerase encoded by the integrating-conjugative element (ICE) R391, indicating a lack of structural conservation between the two systems. The RecA D112R N113R protein represents a new separation of function mutant, proficient in all RecA functions except SOS mutagenesis. JF - PLoS genetics AU - Gruber, Angela J AU - Erdem, Aysen L AU - Sabat, Grzegorz AU - Karata, Kiyonobu AU - Jaszczur, Malgorzata M AU - Vo, Dan D AU - Olsen, Tayla M AU - Woodgate, Roger AU - Goodman, Myron F AU - Cox, Michael M AD - Department of Biochemistry, University of Wisconsin-Madison, Madison, Wisconsin, United States of America. ; Departments of Biological Sciences and Chemistry, University of Southern California, Los Angeles, California, United States of America. ; Biotechnology Center, University of Wisconsin-Madison, Madison, Wisconsin, United States of America. ; Laboratory of Genomic Integrity, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States of America. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 1 VL - 11 IS - 3 KW - Escherichia coli Proteins KW - 0 KW - Nucleoproteins KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Rec A Recombinases KW - EC 2.7.7.- KW - DNA polymerase V, E coli KW - EC 2.7.7.7 KW - DNA-Directed DNA Polymerase KW - Index Medicus KW - Nucleoproteins -- genetics KW - DNA Damage KW - Escherichia coli KW - Amino Acid Sequence KW - Adenosine Triphosphate -- genetics KW - Mutagenesis -- genetics KW - Mutation KW - DNA Replication KW - Escherichia coli Proteins -- metabolism KW - Rec A Recombinases -- genetics KW - SOS Response (Genetics) KW - Transcriptional Activation -- genetics KW - Rec A Recombinases -- metabolism KW - DNA-Directed DNA Polymerase -- genetics KW - Escherichia coli Proteins -- genetics KW - DNA-Directed DNA Polymerase -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1667347401?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+genetics&rft.atitle=A+RecA+protein+surface+required+for+activation+of+DNA+polymerase+V.&rft.au=Gruber%2C+Angela+J%3BErdem%2C+Aysen+L%3BSabat%2C+Grzegorz%3BKarata%2C+Kiyonobu%3BJaszczur%2C+Malgorzata+M%3BVo%2C+Dan+D%3BOlsen%2C+Tayla+M%3BWoodgate%2C+Roger%3BGoodman%2C+Myron+F%3BCox%2C+Michael+M&rft.aulast=Gruber&rft.aufirst=Angela&rft.date=2015-03-01&rft.volume=11&rft.issue=3&rft.spage=e1005066&rft.isbn=&rft.btitle=&rft.title=PLoS+genetics&rft.issn=1553-7404&rft_id=info:doi/10.1371%2Fjournal.pgen.1005066 LA - 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Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pgen.1005066 ER - TY - JOUR T1 - Individual Differences in Situation Awareness: Validation of the Situationism Scale AN - 1665166562 AB - This article concerns the construct of lay situationism—an individual’s belief in the importance of a behavior’s context. Study 1 identified a 13-item Situationism Scale, which demonstrated good reliability and validity. In particular, higher situationism was associated with greater situation-control (strategies to manipulate the environment in order to avoid temptation). Subsequent laboratory studies indicated that people higher on the situationism subscales used greater situation-control by sitting farther from junk food (Study 2) and choosing to drink non-alcoholic beverages before a cognitive task (Study 3). Overall, findings provide preliminary support for the psychometric validity and predictive utility of the Situationism Scale and offer this individual difference construct as a means to expand self-regulation theory. JF - The Journal of Social Psychology AU - Roberts, Megan E AU - Gibbons, Frederick X AU - Gerrard, Meg AU - Klein, William M P AD - Dartmouth College, Dartmouth Medical School, National Cancer Institute ; Dartmouth College; Dartmouth Medical School; National Cancer Institute Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 143 EP - 162 CY - Philadelphia PB - Taylor & Francis Ltd. VL - 155 IS - 2 SN - 0022-4545 KW - Psychology KW - Alcoholic beverages KW - Cognitive tasks KW - Drinks KW - Individual differences KW - Regulation theory KW - Reliability KW - Selfregulation KW - Temptation KW - Validation KW - Validity KW - Scales KW - Situation KW - Psychometric Analysis KW - 0312:social psychology; personality & social roles (individual traits, social identity, adjustment, conformism, & deviance) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665166562?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+Social+Psychology&rft.atitle=Individual+Differences+in+Situation+Awareness%3A+Validation+of+the+Situationism+Scale&rft.au=Roberts%2C+Megan+E%3BGibbons%2C+Frederick+X%3BGerrard%2C+Meg%3BKlein%2C+William+M+P&rft.aulast=Roberts&rft.aufirst=Megan&rft.date=2015-03-01&rft.volume=155&rft.issue=2&rft.spage=143&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Social+Psychology&rft.issn=00224545&rft_id=info:doi/10.1080%2F00224545.2014.977762 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA); Sociological Abstracts N1 - Date revised - 2015-02-26 N1 - Last updated - 2016-09-05 DO - http://dx.doi.org/10.1080/00224545.2014.977762 ER - TY - JOUR T1 - Using infrared thermography to assess emotional responses to infants AN - 1665162129 AB - Adult–infant interactions operate simultaneously across multiple domains and at multiple levels – from physiology to behaviour. Unpackaging and understanding them, therefore, involve analysis of multiple data streams. In this study, we tested physiological responses and cognitive preferences for infant and adult faces in adult females and males. Infrared thermography was used to assess facial temperature changes as a measure of emotional valence, and we used a behavioural rating system to assess adultsʼ expressed preferences. We found greater physiological activation in response to infant stimuli in females than males. As for cognitive preferences, we found greater responses to adult stimuli than to infant stimuli, both in males and females. The results are discussed in light of the Life History Theory. Finally, we discuss the importance of integrating the two data streams on our conclusions. JF - Early Child Development and Care : ECDC AU - Esposito, Gianluca AU - Nakazawa, Jun AU - Ogawa, Shota AU - Stival, Rita AU - Putnick, Diane L AU - Bornstein, Marc H AD - Department of Psychology and Cognitive Science, University of Trento, Trento, Italy, RIKEN Brain Science Institute, Unit for Affiliative Social Behavior, Wako-Shi, Japan, Department of Developmental Science, Faculty of Education, Chiba University, Chiba, Japan, The United Graduate School of Education, Tokyo Gakugei University, Chiba, Japan, Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD, USA ; Department of Psychology and Cognitive Science, University of Trento, Trento, Italy; RIKEN Brain Science Institute, Unit for Affiliative Social Behavior, Wako-Shi, Japan; Department of Developmental Science, Faculty of Education, Chiba University, Chiba, Japan; The United Graduate School of Education, Tokyo Gakugei University, Chiba, Japan; Eunice Kennedy Shriver National Institute of Child Health and Human Development, NIH, Bethesda, MD, USA Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 438 EP - 447 CY - Abingdon PB - Taylor & Francis Ltd. VL - 185 IS - 3 SN - 0300-4430 KW - Medical Sciences--Pediatrics KW - Behaviour KW - Adults KW - Emotional responses KW - Infants KW - Physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665162129?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Early+Child+Development+and+Care+%3A+ECDC&rft.atitle=Using+infrared+thermography+to+assess+emotional+responses+to+infants&rft.au=Esposito%2C+Gianluca%3BNakazawa%2C+Jun%3BOgawa%2C+Shota%3BStival%2C+Rita%3BPutnick%2C+Diane+L%3BBornstein%2C+Marc+H&rft.aulast=Esposito&rft.aufirst=Gianluca&rft.date=2015-03-01&rft.volume=185&rft.issue=3&rft.spage=438&rft.isbn=&rft.btitle=&rft.title=Early+Child+Development+and+Care+%3A+ECDC&rft.issn=03004430&rft_id=info:doi/10.1080%2F03004430.2014.932153 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-02-05 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1080/03004430.2014.932153 ER - TY - JOUR T1 - Methodological Challenges of Validating a Clinical Decision-Making Tool in the Practice Environment AN - 1665154692 AB - Validating a measurement tool intended for use in the practice environment poses challenges that may not be present when validating a tool intended solely for research purposes. The aim of this article is to describe the methodological challenges of validating a clinical decision-making tool, the Oncology Acuity Tool, which nurses use to make nurse assignment and staffing decisions prospectively each shift. Data were derived from a larger validation study, during which several methodological challenges arose. Revisions to the tool, including conducting iterative feedback cycles with end users, were necessary before the validation study was initiated. The “true” value of patient acuity is unknown, and thus, two approaches to inter-rater reliability assessment were used. Discordant perspectives existed between experts and end users. Balancing psychometric rigor with clinical relevance may be achieved through establishing research–practice partnerships, seeking active and continuous feedback with end users, and weighing traditional statistical rules of thumb with practical considerations. JF - Western Journal of Nursing Research AU - Brennan, Caitlin W AU - Daly, Barbara J AD - National Institutes of Health Clinical Center, Bethesda, MD, USA ; Case Western Reserve University, Cleveland, OH, USA ; National Institutes of Health Clinical Center, Bethesda, MD, USA Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 536 EP - 545 CY - Beverly Hills PB - SAGE PUBLICATIONS, INC. VL - 37 IS - 4 SN - 0193-9459 KW - Medical Sciences--Nurses And Nursing KW - oncology KW - acute care KW - instrument development KW - nurse staffing KW - acuity KW - Acute services KW - Challenges KW - Weighing KW - Clinical decision making KW - Decision making KW - End users KW - Experts KW - Feedback KW - Heuristics KW - Measurement KW - Nurses KW - Oncology KW - Partnerships KW - Reliability KW - Revisions KW - Staffing KW - Validation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665154692?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Western+Journal+of+Nursing+Research&rft.atitle=Methodological+Challenges+of+Validating+a+Clinical+Decision-Making+Tool+in+the+Practice+Environment&rft.au=Brennan%2C+Caitlin+W%3BDaly%2C+Barbara+J&rft.aulast=Brennan&rft.aufirst=Caitlin&rft.date=2015-03-01&rft.volume=37&rft.issue=4&rft.spage=536&rft.isbn=&rft.btitle=&rft.title=Western+Journal+of+Nursing+Research&rft.issn=01939459&rft_id=info:doi/10.1177%2F0193945914539738 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-03-05 N1 - Last updated - 2016-05-12 DO - http://dx.doi.org/10.1177/0193945914539738 ER - TY - JOUR T1 - Distributed MRI reconstruction using gadgetron-based cloud computing AN - 1664212474; PQ0001221355 AB - Purpose To expand the open source Gadgetron reconstruction framework to support distributed computing and to demonstrate that a multinode version of the Gadgetron can be used to provide nonlinear reconstruction with clinically acceptable latency. Methods The Gadgetron framework was extended with new software components that enable an arbitrary number of Gadgetron instances to collaborate on a reconstruction task. This cloud-enabled version of the Gadgetron was deployed on three different distributed computing platforms ranging from a heterogeneous collection of commodity computers to the commercial Amazon Elastic Compute Cloud. The Gadgetron cloud was used to provide nonlinear, compressed sensing reconstruction on a clinical scanner with low reconstruction latency (eg, cardiac and neuroimaging applications). Results The proposed setup was able to handle acquisition and 1 sub(1)-SPIRiT reconstruction of nine high temporal resolution real-time, cardiac short axis cine acquisitions, covering the ventricles for functional evaluation, in under 1 min. A three-dimensional high-resolution brain acquisition with 1 mm super(3) isotropic pixel size was acquired and reconstructed with nonlinear reconstruction in less than 5 min. Conclusion A distributed computing enabled Gadgetron provides a scalable way to improve reconstruction performance using commodity cluster computing. Nonlinear, compressed sensing reconstruction can be deployed clinically with low image reconstruction latency. Magn Reson Med 73:1015-1025, 2015. copyright 2014 Wiley Periodicals, Inc. JF - Magnetic Resonance in Medicine AU - Xue, Hui AU - Inati, Souheil AU - Soerensen, Thomas Sangild AU - Kellman, Peter AU - Hansen, Michael S AD - Magnetic Resonance Technology Program, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 1015 EP - 1025 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 73 IS - 3 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Clouds KW - Heart KW - Computer programs KW - Neuroimaging KW - software KW - Computers KW - Magnetic resonance imaging KW - Image processing KW - N.M.R. KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664212474?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Magnetic+Resonance+in+Medicine&rft.atitle=Distributed+MRI+reconstruction+using+gadgetron-based+cloud+computing&rft.au=Xue%2C+Hui%3BInati%2C+Souheil%3BSoerensen%2C+Thomas+Sangild%3BKellman%2C+Peter%3BHansen%2C+Michael+S&rft.aulast=Xue&rft.aufirst=Hui&rft.date=2015-03-01&rft.volume=73&rft.issue=3&rft.spage=1015&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.25213 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Heart; Clouds; Computer programs; software; Neuroimaging; Computers; Magnetic resonance imaging; Image processing; N.M.R. DO - http://dx.doi.org/10.1002/mrm.25213 ER - TY - JOUR T1 - Potent Plasmodium falciparum Gametocytocidal Activity of Diaminonaphthoquinones, Lead Antimalarial Chemotypes Identified in an Antimalarial Compound Screen AN - 1664197800; PQ0001232434 AB - Forty percent of the world's population is threatened by malaria, which is caused by Plasmodium parasites and results in an estimated 200 million clinical cases and 650,000 deaths each year. Drug resistance has been reported for all commonly used antimalarials and has prompted screens to identify new drug candidates. However, many of these new candidates have not been evaluated against the parasite stage responsible for transmission, gametocytes. If Plasmodium falciparum gametocytes are not eliminated, patients continue to spread malaria for weeks after asexual parasite clearance. Asymptomatic individuals can also harbor gametocyte burdens sufficient for transmission, and a safe, effective gametocytocidal agent could also be used in community-wide malaria control programs. Here, we identify 15 small molecules with nanomolar activity against late-stage gametocytes. Fourteen are diaminonaphthoquinones (DANQs), and one is a 2-imino-benzo[d]imidazole (IBI). One of the DANQs identified, SJ000030570, is a lead antimalarial candidate. In contrast, 94% of the 650 compounds tested are inactive against late-stage gametocytes. Consistent with the ineffectiveness of most approved antimalarials against gametocytes, of the 19 novel compounds with activity against known anti-asexual-stage targets, only 3 had any strong effect on gametocyte viability. These data demonstrate the distinct biology of the transmission stages and emphasize the importance of screening for gametocytocidal activity. The potent gametocytocidal activity of DANQ and IBI coupled with their efficacy against asexual parasites provides leads for the development of antimalarials with the potential to prevent both the symptoms and the spread of malaria. JF - Antimicrobial Agents & Chemotherapy AU - Tanaka, Takeshi Q AU - Guiguemde, W Armand AU - Barnett, David S AU - Maron, Maxim I AU - Min, Jaeki AU - Connelly, Michele C AU - Suryadevara, Praveen Kumar AU - Guy, R Kiplin AU - Williamson, Kim C AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA, kwilli4@luc.edu. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 1389 EP - 1397 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 59 IS - 3 SN - 0066-4804, 0066-4804 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Screening KW - Parasites KW - Symptoms KW - Human diseases KW - Data processing KW - Gametocytes KW - Drug resistance KW - Control programs KW - Drug development KW - Malaria KW - Plasmodium falciparum KW - Public health KW - Screens KW - Antimalarial agents KW - Drugs KW - A 01340:Antibiotics & Antimicrobials KW - Q1 08485:Species interactions: pests and control KW - Q5 08524:Public health, medicines, dangerous organisms KW - K 03420:Plant Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664197800?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Potent+Plasmodium+falciparum+Gametocytocidal+Activity+of+Diaminonaphthoquinones%2C+Lead+Antimalarial+Chemotypes+Identified+in+an+Antimalarial+Compound+Screen&rft.au=Tanaka%2C+Takeshi+Q%3BGuiguemde%2C+W+Armand%3BBarnett%2C+David+S%3BMaron%2C+Maxim+I%3BMin%2C+Jaeki%3BConnelly%2C+Michele+C%3BSuryadevara%2C+Praveen+Kumar%3BGuy%2C+R+Kiplin%3BWilliamson%2C+Kim+C&rft.aulast=Tanaka&rft.aufirst=Takeshi&rft.date=2015-03-01&rft.volume=59&rft.issue=3&rft.spage=1389&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.01930-13 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Number of references - 43 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Screening; Symptoms; Parasites; Screens; Human diseases; Malaria; Drugs; Public health; Data processing; Gametocytes; Control programs; Drug resistance; Antimalarial agents; Drug development; Plasmodium falciparum DO - http://dx.doi.org/10.1128/AAC.01930-13 ER - TY - JOUR T1 - Noise propagation in region of interest measurements AN - 1664190439; PQ0001221349 AB - Purpose The purpose of this work was to develop and validate a technique for predicting the standard deviation (SD) associated with thermal noise propagation in region of interest measurements. Theory and Methods Standard methods for error propagation estimation were used to derive equations for the SDs of linear combinations of complex, magnitude, or phase pixel values. The equations were applied to common imaging scenarios in which the image pixels were correlated due to anisotropic pixel resolutions and parallel imaging. All SD estimates were evaluated efficiently using only vector-vector multiplications and Fourier transforms. The estimated SDs were compared to those obtained using repeated experiments and pseudo replica reconstructions. Results The proposed method was able to predict region of interest SDs in all the tested analysis scenarios. Positive and negative noise correlations caused by different parallel-imaging aliasing point spread functions were accurately predicted, and the method predicted the confidence intervals (CI) of time-intensity curves for in vivo cardiac perfusion measurements. Conclusion An intuitive technique for region of interest CIs was developed and validated using phantom experiments and in vivo data. Magn Reson Med 73:1300-1308, 2015. copyright 2014 Wiley Periodicals, Inc. JF - Magnetic Resonance in Medicine AU - Hansen, Michael S AU - Inati, Souheil J AU - Kellman, Peter AD - National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 1300 EP - 1308 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 73 IS - 3 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Heart KW - Mathematical models KW - Anisotropy KW - Data processing KW - Perfusion KW - Standard deviation KW - Image processing KW - N.M.R. KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664190439?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Magnetic+Resonance+in+Medicine&rft.atitle=Noise+propagation+in+region+of+interest+measurements&rft.au=Hansen%2C+Michael+S%3BInati%2C+Souheil+J%3BKellman%2C+Peter&rft.aulast=Hansen&rft.aufirst=Michael&rft.date=2015-03-01&rft.volume=73&rft.issue=3&rft.spage=1300&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.25194 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Heart; Standard deviation; Perfusion; Data processing; Anisotropy; Mathematical models; Image processing; N.M.R. DO - http://dx.doi.org/10.1002/mrm.25194 ER - TY - JOUR T1 - Prevention of tumor growth driven by PIK3CA and HPV oncogenes by targeting mTOR signaling with metformin in oral squamous carcinomas expressing OCT3. AN - 1661996057; 25681087 AB - Most squamous cell carcinomas of the head and neck (HNSCC) exhibit a persistent activation of the PI3K-mTOR signaling pathway. We have recently shown that metformin, an oral antidiabetic drug that is also used to treat lipodystrophy in HIV-infected (HIV(+)) individuals, diminishes mTOR activity and prevents the progression of chemically induced experimental HNSCC premalignant lesions. Here, we explored the preclinical activity of metformin in HNSCCs harboring PIK3CA mutations and HPV oncogenes, both representing frequent HNSCC alterations, aimed at developing effective targeted preventive strategies. The biochemical and biologic effects of metformin were evaluated in representative HNSCC cells expressing mutated PIK3CA or HPV oncogenes (HPV(+)). The oral delivery of metformin was optimized to achieve clinical relevant blood levels. Molecular determinants of metformin sensitivity were also investigated, and their expression levels were examined in a large collection of HNSCC cases. We found that metformin inhibits mTOR signaling and tumor growth in HNSCC cells expressing mutated PIK3CA and HPV oncogenes, and that these activities require the expression of organic cation transporter 3 (OCT3/SLC22A3), a metformin uptake transporter. Coexpression of OCT3 and the mTOR pathway activation marker pS6 were observed in most HNSCC cases, including those arising in HIV(+) patients. Activation of the PI3K-mTOR pathway is a widespread event in HNSCC, including HPV(-) and HPV(+) lesions arising in HIV(+) patients, all of which coexpress OCT3. These observations may provide a rationale for the clinical evaluation of metformin to halt HNSCC development from precancerous lesions, including in HIV(+) individuals at risk of developing HPV(-) associated cancers. ©2015 American Association for Cancer Research. JF - Cancer prevention research (Philadelphia, Pa.) AU - Madera, Dmitri AU - Vitale-Cross, Lynn AU - Martin, Daniel AU - Schneider, Abraham AU - Molinolo, Alfredo A AU - Gangane, Nitin AU - Carey, Thomas E AU - McHugh, Jonathan B AU - Komarck, Christine M AU - Walline, Heather M AU - William, William N AU - Seethala, Raja R AU - Ferris, Robert L AU - Gutkind, J Silvio AD - Molecular Carcinogenesis Section, Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, NIH, Bethesda, Maryland. ; Department of Oncology and Diagnostic Sciences, School of Dentistry and Greenebaum Cancer Center, Program in Oncology, University of Maryland, Baltimore, Maryland. ; Department of Pathology, Mahatma Gandhi Institute of Medical Sciences, Wardha, Maharashtra, India. ; Department of Otolaryngology-Head Neck Surgery, and the Head and Neck SPORE Tissue Core, University of Michigan, Ann Arbor, Michigan. ; Department of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas. ; University of Pittsburgh School of Medicine, Pathology Program, Pittsburgh, Philadelphia. ; Otolaryngology, Immunology, Cancer Immunology Program, University of Pittsburgh School of Medicine, Pittsburgh, Philadelphia. ; Molecular Carcinogenesis Section, Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, NIH, Bethesda, Maryland. sg39v@nih.gov. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 197 EP - 207 VL - 8 IS - 3 KW - Hypoglycemic Agents KW - 0 KW - Octamer Transcription Factor-3 KW - Oncogene Proteins, Viral KW - POU5F1 protein, human KW - Metformin KW - 9100L32L2N KW - Phosphatidylinositol 3-Kinases KW - EC 2.7.1.- KW - MTOR protein, human KW - EC 2.7.1.1 KW - TOR Serine-Threonine Kinases KW - PIK3CA protein, human KW - EC 2.7.1.137 KW - Index Medicus KW - Animals KW - Apoptosis KW - Head and Neck Neoplasms -- prevention & control KW - Papillomaviridae -- physiology KW - Humans KW - Head and Neck Neoplasms -- pathology KW - Mice, Nude KW - Mice KW - Hypoglycemic Agents -- pharmacology KW - Papillomavirus Infections -- prevention & control KW - Cell Proliferation KW - Papillomavirus Infections -- pathology KW - Blotting, Western KW - Tumor Cells, Cultured KW - Tissue Array Analysis KW - Head and Neck Neoplasms -- etiology KW - Head and Neck Neoplasms -- metabolism KW - Signal Transduction -- drug effects KW - Papillomavirus Infections -- etiology KW - Case-Control Studies KW - Xenograft Model Antitumor Assays KW - Cell Cycle KW - Papillomavirus Infections -- metabolism KW - Immunoenzyme Techniques KW - Female KW - Metformin -- pharmacology KW - Carcinoma, Squamous Cell -- etiology KW - Phosphatidylinositol 3-Kinases -- metabolism KW - TOR Serine-Threonine Kinases -- metabolism KW - Carcinoma, Squamous Cell -- metabolism KW - Oncogene Proteins, Viral -- metabolism KW - Mouth Neoplasms -- metabolism KW - Carcinoma, Squamous Cell -- pathology KW - Mouth Neoplasms -- etiology KW - Mouth Neoplasms -- prevention & control KW - Carcinoma, Squamous Cell -- prevention & control KW - Octamer Transcription Factor-3 -- metabolism KW - Mouth Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1661996057?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+prevention+research+%28Philadelphia%2C+Pa.%29&rft.atitle=Prevention+of+tumor+growth+driven+by+PIK3CA+and+HPV+oncogenes+by+targeting+mTOR+signaling+with+metformin+in+oral+squamous+carcinomas+expressing+OCT3.&rft.au=Madera%2C+Dmitri%3BVitale-Cross%2C+Lynn%3BMartin%2C+Daniel%3BSchneider%2C+Abraham%3BMolinolo%2C+Alfredo+A%3BGangane%2C+Nitin%3BCarey%2C+Thomas+E%3BMcHugh%2C+Jonathan+B%3BKomarck%2C+Christine+M%3BWalline%2C+Heather+M%3BWilliam%2C+William+N%3BSeethala%2C+Raja+R%3BFerris%2C+Robert+L%3BGutkind%2C+J+Silvio&rft.aulast=Madera&rft.aufirst=Dmitri&rft.date=2015-03-01&rft.volume=8&rft.issue=3&rft.spage=197&rft.isbn=&rft.btitle=&rft.title=Cancer+prevention+research+%28Philadelphia%2C+Pa.%29&rft.issn=1940-6215&rft_id=info:doi/10.1158%2F1940-6207.CAPR-14-0348 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-01 N1 - Date created - 2015-03-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Ann Intern Med. 2008 May 20;148(10):728-36 [18490686] Cancer Prev Res (Phila). 2009 Jan;2(1):27-36 [19139015] Acta Physiol (Oxf). 2009 May;196(1):65-80 [19245654] Cell Metab. 2010 May 5;11(5):390-401 [20444419] J Natl Cancer Inst. 2009 Aug 19;101(16):1120-30 [19648510] Br Dent J. 2009 Nov 28;207(10):471-5 [19946320] Am J Obstet Gynecol. 2010 Apr;202(4):383.e1-7 [20350646] Cell Cycle. 2012 Apr 1;11(7):1374-82 [22421144] Clin Cancer Res. 2012 May 1;18(9):2558-68 [22409888] Gynecol Endocrinol. 2012 Dec;28(12):956-60 [22808990] BMC Cancer. 2012;12:517 [23151022] Biochem Biophys Res Commun. 2013 Jan 4;430(1):352-7 [23159620] CA Cancer J Clin. 2013 Jan;63(1):11-30 [23335087] J Natl Cancer Inst. 2013 Feb 6;105(3):175-201 [23297039] J Oral Pathol Med. 2013 Mar;42(3):250-6 [22861817] Eur J Cancer. 2013 Apr;49(6):1479-90 [23228442] Neoplasia. 2013 Jun;15(6):620-30 [23730210] J Infect Dis. 2013 Aug 1;208(3):454-62 [23624362] Otolaryngol Head Neck Surg. 2013 Aug;149(2):252-60 [23585151] J Clin Invest. 2013 Sep;123(9):3693-700 [23999444] J Med Virol. 2014 Mar;86(3):419-25 [24154930] Pharmacol Ther. 2014 Apr;142(1):88-98 [24280066] Diabetes Care. 2014;37(5):1367-74 [24623020] Transplant Rev (Orlando). 2014 Jul;28(3):126-33 [24685370] Oral Oncol. 2014 Oct;50(10):930-41 [24177052] Drugs Today (Barc). 2014 Sep;50(9):623-40 [25313369] Head Neck. 2015 Jan;37(1):134-50 [24481720] Head Neck. 2015 Sep;37(9):1268-73 [24801563] JAMA. 2000 Jul 26;284(4):472-7 [10904511] J Pharm Sci. 2001 Aug;90(8):1176-85 [11536222] J Clin Invest. 2001 Oct;108(8):1167-74 [11602624] J Clin Pathol. 2002 Apr;55(4):244-65 [11919208] Genes Dev. 2003 Aug 1;17(15):1829-34 [12869586] J Clin Pharmacol. 1996 Nov;36(11):1012-21 [8973990] Science. 2005 Feb 18;307(5712):1098-101 [15718470] AIDS. 2005 Sep 2;19(13):1407-14 [16103772] Cancer Res. 2005 Nov 1;65(21):9953-61 [16267020] BMC Infect Dis. 2010;10:183 [20573187] J Clin Endocrinol Metab. 2010 Oct;95(10):E204-8 [20660041] Pharmacogenet Genomics. 2010 Nov;20(11):687-99 [20859243] Handb Exp Pharmacol. 2011;(201):105-67 [21103969] Int J Oncol. 2011 Jan;38(1):189-200 [21109940] Clin Pharmacokinet. 2011 Feb;50(2):81-98 [21241070] Cancer Res. 2011 Jul 1;71(13):4366-72 [21540236] Pharmacogenet Genomics. 2011 Dec;21(12):837-50 [21989078] J Clin Oncol. 2011 Nov 10;29(32):4294-301 [21969503] Curr Treat Options Oncol. 2012 Mar;13(1):71-81 [22282394] Cancer Prev Res (Phila). 2012 Apr;5(4):562-73 [22467081] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1940-6207.CAPR-14-0348 ER - TY - JOUR T1 - Lack of effect of metformin on mammary carcinogenesis in nondiabetic rat and mouse models. AN - 1661995629; 25681088 AB - Epidemiologic studies have shown that diabetics receiving the biguanide metformin, as compared with sulfonylureas or insulin, have a lower incidence of breast cancer. Metformin increases levels of activated AMPK (AMP-activated protein kinase) and decreases circulating IGF-1; encouraging its potential use in both cancer prevention and therapeutic settings. In anticipation of clinical trials in nondiabetic women, the efficacy of metformin in nondiabetic rat and mouse mammary cancer models was evaluated. Metformin was administered by gavage or in the diet, at a human equivalent dose, in standard mammary cancer models: (i) methylnitrosourea (MNU)-induced estrogen receptor-positive (ER(+)) mammary cancers in rats, and (ii) MMTV-Neu/p53KO ER(-) (estrogen receptor-negative) mammary cancers in mice. In the MNU rat model, metformin dosing (150 or 50 mg/kg BW/d, by gavage) was ineffective in decreasing mammary cancer multiplicity, latency, or weight. Pharmacokinetic studies of metformin (150 mg/kg BW/d, by gavage) yielded plasma levels (Cmax and AUC) higher than humans taking 1.5 g/d. In rats bearing small palpable mammary cancers, short-term metformin (150 mg/kg BW/d) treatment increased levels of phospho-AMPK and phospho-p53 (Ser20), but failed to reduce Ki67 labeling or expression of proliferation-related genes. In the mouse model, dietary metformin (1,500 mg/kg diet) did not alter final cancer incidence, multiplicity, or weight. Metformin did not prevent mammary carcinogenesis in two mammary cancer models, raising questions about metformin efficacy in breast cancer in nondiabetic populations. ©2015 American Association for Cancer Research. JF - Cancer prevention research (Philadelphia, Pa.) AU - Thompson, Matthew D AU - Grubbs, Clinton J AU - Bode, Ann M AU - Reid, Joel M AU - McGovern, Renee AU - Bernard, Philip S AU - Stijleman, Inge J AU - Green, Jeffrey E AU - Bennett, Christina AU - Juliana, M Margaret AU - Moeinpour, Fariba AU - Steele, Vernon E AU - Lubet, Ronald A AD - National Cancer Institute, Bethesda, Maryland. ; University of Alabama at Birmingham, Birmingham, Alabama. clintongrubbs@uabmc.edu. ; Hormel Institute, University of Minnesota, Austin, Minnesota. ; Mayo Clinic Cancer Center, Rochester, Minnesota. ; Huntsman Cancer Institute, Salt Lake City, Utah. ; Laboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, Maryland. ; University of Alabama at Birmingham, Birmingham, Alabama. ; CARDG, Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 231 EP - 239 VL - 8 IS - 3 KW - Alkylating Agents KW - 0 KW - Biomarkers, Tumor KW - Hypoglycemic Agents KW - RNA, Messenger KW - Methylnitrosourea KW - 684-93-5 KW - Metformin KW - 9100L32L2N KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Animals KW - Biomarkers, Tumor -- genetics KW - Humans KW - Methylnitrosourea -- toxicity KW - Hypoglycemic Agents -- pharmacology KW - Mice KW - Tissue Distribution KW - Reverse Transcriptase Polymerase Chain Reaction KW - RNA, Messenger -- genetics KW - Mice, Transgenic KW - Hypoglycemic Agents -- pharmacokinetics KW - Rats KW - Rats, Sprague-Dawley KW - Tumor Cells, Cultured KW - Mice, Inbred C57BL KW - Alkylating Agents -- toxicity KW - Mice, SCID KW - Female KW - Metformin -- pharmacology KW - Mammary Neoplasms, Experimental -- chemically induced KW - Mammary Neoplasms, Experimental -- drug therapy KW - Disease Models, Animal KW - Metformin -- pharmacokinetics KW - Mammary Neoplasms, Experimental -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1661995629?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+prevention+research+%28Philadelphia%2C+Pa.%29&rft.atitle=Lack+of+effect+of+metformin+on+mammary+carcinogenesis+in+nondiabetic+rat+and+mouse+models.&rft.au=Thompson%2C+Matthew+D%3BGrubbs%2C+Clinton+J%3BBode%2C+Ann+M%3BReid%2C+Joel+M%3BMcGovern%2C+Renee%3BBernard%2C+Philip+S%3BStijleman%2C+Inge+J%3BGreen%2C+Jeffrey+E%3BBennett%2C+Christina%3BJuliana%2C+M+Margaret%3BMoeinpour%2C+Fariba%3BSteele%2C+Vernon+E%3BLubet%2C+Ronald+A&rft.aulast=Thompson&rft.aufirst=Matthew&rft.date=2015-03-01&rft.volume=8&rft.issue=3&rft.spage=231&rft.isbn=&rft.btitle=&rft.title=Cancer+prevention+research+%28Philadelphia%2C+Pa.%29&rft.issn=1940-6215&rft_id=info:doi/10.1158%2F1940-6207.CAPR-14-0181-T LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-01 N1 - Date created - 2015-03-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Neoplasma. 2009;56(3):269-74 [19309231] Cancer Prev Res (Phila). 2009 Feb;2(2):161-7 [19196723] Cancer Prev Res (Phila). 2010 Sep;3(9):1066-76 [20810672] Clin Cancer Res. 2010 Nov 1;16(21):5222-32 [20837693] Cancer Epidemiol Biomarkers Prev. 2011 Jan;20(1):101-11 [21119073] Breast Cancer Res Treat. 2011 Feb;126(1):215-20 [20976543] Oncogene. 2011 Mar 10;30(10):1174-82 [21102522] BMC Med. 2011;9:33 [21470407] Breast Cancer Res Treat. 2011 Aug;128(3):783-94 [21655990] Ann N Y Acad Sci. 2011 Dec;1243:54-68 [22211893] Nat Rev Cancer. 2012 Mar;12(3):159-69 [22337149] Nat Rev Mol Cell Biol. 2012 Apr;13(4):251-62 [22436748] Exp Mol Pathol. 2001 Jun;70(3):183-93 [11417997] Cancer Res. 2002 Nov 15;62(22):6376-80 [12438218] J Natl Cancer Inst. 2003 Dec 17;95(24):1825-33 [14679152] Br J Clin Pharmacol. 1981 Aug;12(2):235-46 [7306436] Cancer Res. 1987 Aug 1;47(15):4020-4 [3607747] Hum Pathol. 1997 Oct;28(10):1180-8 [9343325] Int J Oncol. 1998 Feb;12(2):449-53 [9458374] Carcinogenesis. 1998 Aug;19(8):1345-51 [9744527] J Biol Chem. 1962 Mar;237:904-9 [13891416] N Engl J Med. 2004 Dec 30;351(27):2817-26 [15591335] BMJ. 2005 Jun 4;330(7503):1304-5 [15849206] Carcinogenesis. 2005 Aug;26(8):1343-53 [15845649] Exp Gerontol. 2005 Aug-Sep;40(8-9):685-93 [16125352] PLoS One. 2012;7(3):e33411 [22448244] Cell. 2012 Apr 13;149(2):274-93 [22500797] J Clin Oncol. 2012 Jul 20;30(21):2593-600 [22564993] J Clin Oncol. 2012 Aug 10;30(23):2844-52 [22689798] Breast Cancer Res Treat. 2012 Oct;135(3):821-30 [22933030] Cancer Discov. 2012 Sep;2(9):778-90 [22926251] Breast Cancer. 2012 Oct;19(4):309-14 [21725655] Nature. 2013 Feb 14;494(7436):256-60 [23292513] Eur J Surg Oncol. 2013 Jun;39(6):619-26 [23473851] Clin Cancer Res. 2014 Mar 1;20(5):1298-305 [24520097] Genome Biol. 2013;14(11):R125 [24220145] Science. 2005 Dec 9;310(5754):1642-6 [16308421] Cancer Res. 2007 Jul 15;67(14):6745-52 [17638885] Clin Cancer Res. 2007 Sep 15;13(18 Pt 1):5488-96 [17875779] J Clin Invest. 2010 Jul;120(7):2355-69 [20577053] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/1940-6207.CAPR-14-0181-T ER - TY - JOUR T1 - Macrophage solubilization and cytotoxicity of indium-containing particles as in vitro correlates to pulmonary toxicity in vivo. AN - 1661332475; 25527823 AB - Macrophage-solubilized indium-containing particles (ICPs) were previously shown in vitro to be cytotoxic. In this study, we compared macrophage solubilization and cytotoxicity of indium phosphide (InP) and indium-tin oxide (ITO) with similar particle diameters (∼ 1.5 µm) and then determined if relative differences in these in vitro parameters correlated with pulmonary toxicity in vivo. RAW 264.7 macrophages were treated with InP or ITO particles and cytotoxicity was assayed at 24 h. Ionic indium was measured in 24 h culture supernatants. Macrophage cytotoxicity and particle solubilization in vitro were much greater for InP compared with ITO. To correlate changes in vivo, B6C3F1 mice were treated with InP or ITO by oropharyngeal aspiration. On Days 14 and 28, bronchoalveolar lavage (BAL) and pleural lavage (PL) fluids were collected and assayed for total leukocytes. Cell differentials, lactate dehydrogenase activity, and protein levels were also measured in BAL. All lavage parameters were greatly increased in mice treated with InP compared with ITO. These data suggest that macrophage solubilization and cytotoxicity of some ICPs in vitro are capable of predicting pulmonary toxicity in vivo. In addition, these differences in toxicity were observed despite the two particulate compounds containing similar amounts of indium suggesting that solubilization, not total indium content, better reflects the toxic potential of some ICPs. Soluble InCl3 was shown to be more cytotoxic than InP to macrophages and lung epithelial cells in vitro further suggesting that ionic indium is the primary cytotoxic component of InP. Published by Oxford University Press on behalf of the Society of Toxicology 2014. This work is written by US Government employees and is in the public domain in the US. JF - Toxicological sciences : an official journal of the Society of Toxicology AU - Gwinn, William M AU - Qu, Wei AU - Bousquet, Ronald W AU - Price, Herman AU - Shines, Cassandra J AU - Taylor, Genie J AU - Waalkes, Michael P AU - Morgan, Daniel L AD - *NTP Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences; and Alion Science and Technology Corporation, Research Triangle Park, North Carolina 27709, USA gwinnwm@niehs.nih.gov. ; *NTP Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences; and Alion Science and Technology Corporation, Research Triangle Park, North Carolina 27709, USA. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 17 EP - 26 VL - 144 IS - 1 KW - Air Pollutants, Occupational KW - 0 KW - Phosphines KW - Tin Compounds KW - Indium KW - 045A6V3VFX KW - indium phosphide KW - 22398-80-7 KW - indium trichloride KW - 31JB8MKF8Z KW - indium tin oxide KW - 71243-84-0 KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - Index Medicus KW - sintered ITO KW - indium KW - macrophage cytotoxicity KW - solubilization KW - pulmonary toxicity KW - InP KW - Leukocytes -- metabolism KW - Animals KW - Solubility KW - Dose-Response Relationship, Drug KW - Particle Size KW - Mice KW - Leukocytes -- drug effects KW - Bronchoalveolar Lavage Fluid -- chemistry KW - Cell Survival -- drug effects KW - Inhalation Exposure KW - Time Factors KW - RAW 264.7 Cells KW - Bronchoalveolar Lavage Fluid -- cytology KW - L-Lactate Dehydrogenase -- metabolism KW - Male KW - Phosphines -- chemistry KW - Tin Compounds -- toxicity KW - Indium -- toxicity KW - Lung Diseases -- pathology KW - Lung Diseases -- metabolism KW - Air Pollutants, Occupational -- toxicity KW - Tin Compounds -- chemistry KW - Macrophages -- drug effects KW - Air Pollutants, Occupational -- chemistry KW - Lung Diseases -- chemically induced KW - Macrophages -- pathology KW - Indium -- chemistry KW - Phosphines -- toxicity KW - Phagocytosis KW - Macrophages -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1661332475?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.atitle=Macrophage+solubilization+and+cytotoxicity+of+indium-containing+particles+as+in+vitro+correlates+to+pulmonary+toxicity+in+vivo.&rft.au=Gwinn%2C+William+M%3BQu%2C+Wei%3BBousquet%2C+Ronald+W%3BPrice%2C+Herman%3BShines%2C+Cassandra+J%3BTaylor%2C+Genie+J%3BWaalkes%2C+Michael+P%3BMorgan%2C+Daniel+L&rft.aulast=Gwinn&rft.aufirst=William&rft.date=2015-03-01&rft.volume=144&rft.issue=1&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.issn=1096-0929&rft_id=info:doi/10.1093%2Ftoxsci%2Fkfu273 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-30 N1 - Date created - 2015-03-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Int Arch Occup Environ Health. 2012 May;85(4):447-53 [21833746] Part Fibre Toxicol. 2011;8:27 [21896169] Toxicol Sci. 2013 Oct;135(2):414-24 [23872580] Int J Mol Sci. 2014;15(4):6815-30 [24758926] Toxicol Sci. 2001 Nov;64(1):28-40 [11606799] Natl Toxicol Program Tech Rep Ser. 2001 Jul;(499):7-340 [12087422] J Occup Health. 2003 May;45(3):137-9 [14646287] J Occup Health. 2003 Jul;45(4):228-30 [14646281] Cancer Res. 1989 Aug 1;49(15):4237-41 [2743310] Eur Respir J. 2005 Jan;25(1):200-4 [15640342] Eur Respir J. 2007 Feb;29(2):317-24 [17050566] Sci Total Environ. 2007 Nov 15;387(1-3):155-65 [17804041] Occup Environ Med. 2008 Jan;65(1):51-5 [17626138] Toxicol Sci. 2009 Apr;108(2):472-81 [19176593] Exp Lung Res. 2009 Dec;35(10):858-82 [19995279] J Occup Health. 2009;51(6):513-21 [19834281] J Occup Health. 2010;52(1):14-22 [19940388] Am J Respir Crit Care Med. 2010 Mar 1;181(5):458-64 [20019344] Chin Med J (Engl). 2010 May 20;123(10):1347-50 [20529594] Met Ions Life Sci. 2011;8:375-401 [21473387] J Occup Health. 2011;53(2):51-63 [21233592] Nanoscale. 2011 Jun;3(6):2552-9 [21509403] J Occup Health. 2011;53(3):234-9 [21422720] J Occup Health. 2011;53(3):175-87 [21471693] Environ Toxicol. 2013 Oct;28(10):595-600 [24022999] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/toxsci/kfu273 ER - TY - JOUR T1 - Diversity Outbred Mice Identify Population-Based Exposure Thresholds and Genetic Factors that Influence Benzene-Induced Genotoxicity. AN - 1660660084; 25376053 AB - Inhalation of benzene at levels below the current exposure limit values leads to hematotoxicity in occupationally exposed workers. We sought to evaluate Diversity Outbred (DO) mice as a tool for exposure threshold assessment and to identify genetic factors that influence benzene-induced genotoxicity. We exposed male DO mice to benzene (0, 1, 10, or 100 ppm; 75 mice/exposure group) via inhalation for 28 days (6 hr/day for 5 days/week). The study was repeated using two independent cohorts of 300 animals each. We measured micronuclei frequency in reticulocytes from peripheral blood and bone marrow and applied benchmark concentration modeling to estimate exposure thresholds. We genotyped the mice and performed linkage analysis. We observed a dose-dependent increase in benzene-induced chromosomal damage and estimated a benchmark concentration limit of 0.205 ppm benzene using DO mice. This estimate is an order of magnitude below the value estimated using B6C3F1 mice. We identified a locus on Chr 10 (31.87 Mb) that contained a pair of overexpressed sulfotransferases that were inversely correlated with genotoxicity. The genetically diverse DO mice provided a reproducible response to benzene exposure. The DO mice display interindividual variation in toxicity response and, as such, may more accurately reflect the range of response that is observed in human populations. Studies using DO mice can localize genetic associations with high precision. The identification of sulfotransferases as candidate genes suggests that DO mice may provide additional insight into benzene-induced genotoxicity. JF - Environmental health perspectives AU - French, John E AU - Gatti, Daniel M AU - Morgan, Daniel L AU - Kissling, Grace E AU - Shockley, Keith R AU - Knudsen, Gabriel A AU - Shepard, Kim G AU - Price, Herman C AU - King, Deborah AU - Witt, Kristine L AU - Pedersen, Lars C AU - Munger, Steven C AU - Svenson, Karen L AU - Churchill, Gary A AD - Division of the National Toxicology Program, National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH), Department of Health and Human Resources (DHHS), Research Triangle Park, North Carolina, USA. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 237 EP - 245 VL - 123 IS - 3 KW - Hazardous Substances KW - 0 KW - Sulfotransferases KW - EC 2.8.2.- KW - Benzene KW - J64922108F KW - Index Medicus KW - Sulfotransferases -- genetics KW - Bone Marrow Cells -- drug effects KW - Animals KW - Animals, Outbred Strains KW - Genetic Linkage -- drug effects KW - Dose-Response Relationship, Drug KW - Mice KW - DNA Damage -- genetics KW - DNA Damage -- drug effects KW - Risk Assessment KW - Reticulocytes -- drug effects KW - Micronucleus Tests KW - Inhalation Exposure KW - Benzene -- toxicity KW - Hazardous Substances -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660660084?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+health+perspectives&rft.atitle=Diversity+Outbred+Mice+Identify+Population-Based+Exposure+Thresholds+and+Genetic+Factors+that+Influence+Benzene-Induced+Genotoxicity.&rft.au=French%2C+John+E%3BGatti%2C+Daniel+M%3BMorgan%2C+Daniel+L%3BKissling%2C+Grace+E%3BShockley%2C+Keith+R%3BKnudsen%2C+Gabriel+A%3BShepard%2C+Kim+G%3BPrice%2C+Herman+C%3BKing%2C+Deborah%3BWitt%2C+Kristine+L%3BPedersen%2C+Lars+C%3BMunger%2C+Steven+C%3BSvenson%2C+Karen+L%3BChurchill%2C+Gary+A&rft.aulast=French&rft.aufirst=John&rft.date=2015-03-01&rft.volume=123&rft.issue=3&rft.spage=237&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1408202 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-16 N1 - Date created - 2015-03-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nature. 2011 Sep 15;477(7364):289-94 [21921910] Risk Anal. 1987 Dec;7(4):415-26 [3444929] Pharmacogenomics. 2012 Jan;13(1):91-111 [22111604] Carcinogenesis. 2012 Feb;33(2):240-52 [22166497] J Natl Cancer Inst. 2012 Nov 21;104(22):1724-37 [23111193] Leukemia. 2012 Dec;26(12):2494-8 [22643707] Environ Health Perspect. 2013 Jan;121(1):23-31 [23086705] Nat Genet. 2013 Jul;45(7):767-75 [23708188] Nucleic Acids Res. 2014 Jan;42(Database issue):D810-7 [24285300] Genetics. 1994 Nov;138(3):963-71 [7851788] BMJ. 1996 Apr 27;312(7038):1079 [8616417] Am J Ind Med. 1996 Mar;29(3):236-46 [8833776] Mutagenesis. 1996 Sep;11(5):455-62 [8921506] Behav Genet. 1998 Jan;28(1):29-38 [9573644] Biochemistry. 1999 Aug 10;38(32):10474-9 [10441143] Science. 2004 Dec 3;306(5702):1774-6 [15576619] Food Chem Toxicol. 2005 Feb;43(2):203-16 [15621332] Cancer Res. 2005 Oct 15;65(20):9574-81 [16230423] Toxicol Sci. 2006 Mar;90(1):5-22 [16322073] Carcinogenesis. 2006 Oct;27(10):2083-9 [16728435] Toxicol Pathol. 2006;34(6):802-5 [17162538] Hum Mol Genet. 2007 Mar 1;16(5):463-70 [17189289] Genetics. 2007 May;176(1):675-83 [17409088] Pharmacogenet Genomics. 2007 Oct;17(10):789-801 [17885617] Mutat Res. 2007 Dec 1;634(1-2):235-40 [17851117] Mutat Res. 2008 Jan 8;649(1-2):101-13 [17869571] J Natl Cancer Inst Monogr. 2008;(39):74-7 [18648008] J Toxicol Environ Health A. 2008;71(22):1482-9 [18836923] Carcinogenesis. 2009 Jan;30(1):50-8 [18978339] PLoS One. 2009;4(3):e4729 [19266100] Genomics. 2009 Apr;93(4):343-9 [19162166] Genome Biol. 2009;10(11):R130 [19919682] Toxicol Pathol. 2010 Jan;38(1):180-1 [20019353] Chem Biol Interact. 2010 Mar 19;184(1-2):58-66 [20056112] PLoS Genet. 2010 Sep;6(9):e1001085 [20838427] ILAR J. 2011;52(1):24-31 [21411855] BMC Genet. 2011;12:66 [21794153] Genetics. 2012 Feb;190(2):389-401 [22345608] Genetics. 2012 Feb;190(2):437-47 [22345611] G3 (Bethesda). 2014 Sep;4(9):1623-33 [25237114] Genetics. 2014 Sep;198(1):59-73 [25236449] Genetics. 2001 Sep;159(1):371-87 [11560912] Epidemiology. 2003 Sep;14(5):569-77 [14501272] Genome Res. 2004 Oct;14(10A):1880-7 [15466288] Mutat Res. 1973 May;18(2):187-90 [4351282] Fundam Appl Toxicol. 1984 Oct;4(5):854-71 [6510615] Nature. 2011 Sep 15;477(7364):326-9 [21921916] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1289/ehp.1408202 ER - TY - JOUR T1 - Comparison of calculated and acquired high b value diffusion-weighted imaging in prostate cancer AN - 1660435338; PQ0001112609 AB - Purpose: To determine whether the performance of calculated high b value diffusion-weighted images (DWI) derived from regular lower b value DWI using exponential diffusion decay models (intravoxel incoherent motion = IVIM and diffusional kurtosis = DK) is comparable to acquired high b value DWI in prostate cancer detection. Materials and Methods: One hundred six patients underwent diagnostic multiparametric prostate MRI at 3T using an endorectal coil. Five b value (b = 0, 188, 375, 563, 750 s/mm super(2)) DWI and high b value (b = 0, 1000 and 2000 s/mm super(2)) DWI were acquired. Calculated high b value (b = 1000 s/mm super(2) and b = 2000 s/mm super(2) ) DWI were derived from the DWI dataset using DK and IVIM models. Calculated and acquired high b value DWI images were compared for lesion visibility and image quality by two experienced radiologists (1 and 6 years of experience). GEE with Wald test was used to compare the image quality among the four calculated high b value DWI by comparing the proportion of lesions in each model which were comparable to the acquired images. This comparison was done for all lesions and by lesion location (PZ or CG; low apical/anterior or apical/mid/base) Results: More lesions were visible on acquired b = 2000 s/mm super(2) compared to b = 1000 s/mm super(2) DWI. Calculated high b value DWI using the IVIM model had approximately the same number of lesions as acquired high b value DWI, whereas the DK model had fewer lesions than acquired images. The image quality of calculated high b value DWI was comparable to that of acquired images, and the highest quality images were obtained with b1000 sub(IVIM). The image quality of calculated b1000 sub(IVIM) was the same as that of acquired DWI in apical/mid/base (98%) locations and comparable in low apical and anterior (95.4%) locations. The image quality of calculated b2000 sub(IVIM) was inferior in both apical/mid/base (86.2%) locations and comparable in low apical and anterior (83.9%) locations. Conclusion: Calculated high b value DWI obtained using IVIM model has same lesion visibility as that of acquired DWI. The image quality of calculated high b value DWI relative to corresponding acquired DWI decreases with increase in b value. JF - Abdominal Imaging AU - Grant, Kinzya B AU - Agarwal, Harsh K AU - Shih, Joanna H AU - Bernardo, Marcelino AU - Pang, Yuxi AU - Daar, Dagane AU - Merino, Maria J AU - Wood, Bradford J AU - Pinto, Peter A AU - Choyke, Peter L AU - Turkbey, Baris AD - Molecular Imaging Program, National Cancer Institute (NCI), NIH 10 Center Dr, MSC 1182, Bldg 10, Room B3B85, Bethesda, MD, 20892-1088, USA, turkbeyi@mail.nih.gov Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 578 EP - 586 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 40 IS - 3 SN - 0942-8925, 0942-8925 KW - Biotechnology and Bioengineering Abstracts KW - Prostate cancer KW - Magnetic resonance imaging KW - Diffusion KW - Models KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660435338?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Abdominal+Imaging&rft.atitle=Comparison+of+calculated+and+acquired+high+b+value+diffusion-weighted+imaging+in+prostate+cancer&rft.au=Grant%2C+Kinzya+B%3BAgarwal%2C+Harsh+K%3BShih%2C+Joanna+H%3BBernardo%2C+Marcelino%3BPang%2C+Yuxi%3BDaar%2C+Dagane%3BMerino%2C+Maria+J%3BWood%2C+Bradford+J%3BPinto%2C+Peter+A%3BChoyke%2C+Peter+L%3BTurkbey%2C+Baris&rft.aulast=Grant&rft.aufirst=Kinzya&rft.date=2015-03-01&rft.volume=40&rft.issue=3&rft.spage=578&rft.isbn=&rft.btitle=&rft.title=Abdominal+Imaging&rft.issn=09428925&rft_id=info:doi/10.1007%2Fs00261-014-0246-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Number of references - 33 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Prostate cancer; Magnetic resonance imaging; Diffusion; Models DO - http://dx.doi.org/10.1007/s00261-014-0246-2 ER - TY - JOUR T1 - Crystal structure of a fully glycosylated HIV-1 gp120 core reveals a stabilizing role for the glycan at Asn262 AN - 1660399210; PQ0001110182 AB - The crystal structure of a fully glycosylated HIV-1 gp120 core in complex with CD4 receptor and Fab 17b at 4.5-Aa resolution reveals 9 of the 15 N-linked glycans of core gp120 to be partially ordered. The glycan at position Asn262 had the most extensive and well-ordered electron density, and a GlcNAc sub(2)Man sub(7) was modeled. The GlcNAc stem of this glycan is largely buried in a cleft in gp120, suggesting a role in gp120 folding and stability. Its arms interact with the stems of neighboring glycans from the oligomannose patch, which is a major target for broadly neutralizing antibodies. Proteins 2015; 83:590-596. copyright 2014 Wiley Periodicals, Inc. JF - Proteins: Structure, Function and Bioinformatics AU - Kong, Leopold AU - Wilson, Ian A AU - Kwong, Peter D AD - Vaccine Research Center, National Institutes of Health, Bethesda, Maryland, 20892. Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 590 EP - 596 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030 United States VL - 83 IS - 3 SN - 0887-3585, 0887-3585 KW - Biotechnology and Bioengineering Abstracts KW - Protein structure KW - Glycoprotein gp120 KW - Antibodies KW - CD4 antigen KW - N-linked glycans KW - Human immunodeficiency virus 1 KW - Crystal structure KW - Bioinformatics KW - Polysaccharides KW - Fab KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660399210?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.atitle=Crystal+structure+of+a+fully+glycosylated+HIV-1+gp120+core+reveals+a+stabilizing+role+for+the+glycan+at+Asn262&rft.au=Kong%2C+Leopold%3BWilson%2C+Ian+A%3BKwong%2C+Peter+D&rft.aulast=Kong&rft.aufirst=Leopold&rft.date=2015-03-01&rft.volume=83&rft.issue=3&rft.spage=590&rft.isbn=&rft.btitle=&rft.title=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.issn=08873585&rft_id=info:doi/10.1002%2Fprot.24747 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Protein structure; Glycoprotein gp120; CD4 antigen; Antibodies; N-linked glycans; Crystal structure; Bioinformatics; Fab; Polysaccharides; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1002/prot.24747 ER - TY - JOUR T1 - Sustained reprogramming of the estrogen response after chronic exposure to endocrine disruptors. AN - 1660031317; 25594248 AB - The pervasive nature of estrogenic industrial and dietary compounds is a growing health concern linked to cancer, obesity, and neurological disorders. Prior analyses of endocrine disruptor action have focused primarily on the short-term consequences of exposure. However, these studies are unlikely to reflect the consequences of constant exposures common to industrialized countries. Here we examined the global effects of long-term endocrine disruption on gene transcription and estrogen signaling. Estrogen-dependent breast cancer cell lines were chronically treated with physiologically relevant levels of bisphenol A or genistein for more than 70 passages. Microarray analysis demonstrated global reprogramming of the transcriptome when compared with a similarly cultured control cell line. Estrogen-responsive targets showed diminished expression in both the presence and absence of estrogen. Estrogen receptor recruitment, H3K4 monomethylation, and deoxyribonuclease accessibility were reduced at nearby response elements. Based on these observations, we investigated the potential of long-term endocrine disruptor exposure to initiate persistent transcriptional reprogramming. Culture of chronically exposed cell lines in the absence of the endocrine disruptors did not reverse many of the signaling defects that accumulated during treatment. Taken together, these data demonstrate that chronic exposure to endocrine disrupting compounds can permanently alter physiological hormone signaling. JF - Molecular endocrinology (Baltimore, Md.) AU - Patterson, Andrea R AU - Mo, Xiaokui AU - Shapiro, Ali AU - Wernke, Karen E AU - Archer, Trevor K AU - Burd, Craig J AD - Department of Molecular Genetics (A.R.P., A.S., K.E.W., C.J.B.), The Ohio State University, Center for Biostatistics (X.M.), Ohio State University Wexner Medical Center, and The Arthur G. James Comprehensive Cancer Center (A.R.P., A.S., C.J.B.), Columbus, Ohio 43210; and Laboratory of Molecular Carcinogenesis (T.K.A.), National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 384 EP - 395 VL - 29 IS - 3 KW - EGR3 protein, human KW - 0 KW - Endocrine Disruptors KW - Estrogens KW - Ligands KW - Receptors, Estrogen KW - Early Growth Response Protein 3 KW - 144516-98-3 KW - Index Medicus KW - Genetic Loci KW - Humans KW - Signal Transduction -- drug effects KW - Epigenesis, Genetic -- drug effects KW - Cell Line, Tumor KW - Receptors, Estrogen -- metabolism KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Early Growth Response Protein 3 -- genetics KW - Endocrine Disruptors -- toxicity KW - Estrogens -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660031317?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.atitle=Sustained+reprogramming+of+the+estrogen+response+after+chronic+exposure+to+endocrine+disruptors.&rft.au=Patterson%2C+Andrea+R%3BMo%2C+Xiaokui%3BShapiro%2C+Ali%3BWernke%2C+Karen+E%3BArcher%2C+Trevor+K%3BBurd%2C+Craig+J&rft.aulast=Patterson&rft.aufirst=Andrea&rft.date=2015-03-01&rft.volume=29&rft.issue=3&rft.spage=384&rft.isbn=&rft.btitle=&rft.title=Molecular+endocrinology+%28Baltimore%2C+Md.%29&rft.issn=1944-9917&rft_id=info:doi/10.1210%2Fme.2014-1237 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-29 N1 - Date created - 2015-02-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Cell Endocrinol. 2013 Nov 5;380(1-2):25-31 [23545159] Cell Death Dis. 2013;4:e676 [23788033] BMC Cancer. 2014;14:379 [24884420] Neurosci Biobehav Rev. 1999 Nov;23(7):1011-27 [10580314] N Engl J Med. 2001 Jan 25;344(4):276-85 [11172156] Cancer Res. 2001 Jul 1;61(13):5045-50 [11431339] Mol Pharmacol. 2001 Sep;60(3):595-602 [11502892] In Vitro Cell Dev Biol Anim. 2001 May;37(5):275-82 [11513082] Cancer Epidemiol Biomarkers Prev. 2004 May;13(5):698-708 [15159299] Cell. 1983 May;33(1):65-76 [6088056] Mol Pharmacol. 1988 Jan;33(1):120-6 [3122017] Environ Health Perspect. 1991 May;92:167-73 [1935846] Endocrinology. 1993 Jun;132(6):2279-86 [8504731] Reprod Toxicol. 2007 Aug-Sep;24(2):131-8 [17768031] Reprod Toxicol. 2007 Aug-Sep;24(2):139-77 [17825522] Environ Health Perspect. 2008 Jan;116(1):39-44 [18197297] Cancer Lett. 2008 Oct 8;269(2):226-42 [18492603] Environ Int. 2009 Jan;35(1):21-6 [18640724] Endocr Rev. 2009 Feb;30(1):75-95 [19074586] N Engl J Med. 2009 Feb 5;360(6):573-87 [19196674] PLoS Comput Biol. 2009 Nov;5(11):e1000566 [19918365] Ethn Dis. 2010 Winter;20(1 Suppl 1):S1-50-4 [20521385] Hormones (Athens). 2010 Jul-Sep;9(3):191-205 [20688617] Trends Biochem Sci. 2011 May;36(5):272-81 [21315607] Horm Cancer. 2010 Jun;1(3):146-55 [21761357] J Steroid Biochem Mol Biol. 2011 Nov;127(3-5):204-15 [21899826] J Neuroendocrinol. 2012 Feb;24(2):319-30 [22053957] Mol Pharmacol. 1998 Jul;54(1):105-12 [9658195] Endocrinology. 1998 Oct;139(10):4252-63 [9751507] Reprod Biol Endocrinol. 2006;4:49 [17010207] Mol Cell Biol. 2012 May;32(10):1805-17 [22451486] Genome Res. 2012 Jun;22(6):1015-25 [22508765] Carcinogenesis. 2012 Sep;33(9):1684-91 [22791811] Genome Res. 2012 Nov;22(11):2153-62 [23019147] Endocrinology. 2013 Jan;154(1):184-92 [23183185] Environ Health Perspect. 2013 Apr;121(4):459-66 [23384675] Environ Int. 2014 Mar;64:83-90 [24382480] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1210/me.2014-1237 ER - TY - JOUR T1 - Language analysis as a window to bereaved parents' emotions during a parent-physician bereavement meeting AN - 1660029603; 4650782 AB - Parent-physician bereavement meetings may benefit parents by facilitating sense making, which is associated with healthy adjustment after a traumatic event. Prior research suggests a reciprocal relationship between sense making and positive emotions. We analyzed parents' use of emotion words during bereavement meetings to better understand parents' emotional reactions during the meeting and how their emotional reactions related to their appraisals of the meeting. Parents' use of positive emotion words increased, suggesting the meetings help parents make sense of the death. Parents' use of positive emotion words was negatively related to their own and/or their spouse's appraisals of the meeting, suggesting that parents who have a positive emotional experience during the meeting may also have a short-term negative reaction. Language analysis can be an effective tool to understand individuals' ongoing emotions and meaning making processes during interventions to reduce adverse consequences of a traumatic event, such as a child's death. Reprinted by permission of Sage publications Ltd JF - Journal of language and social psychology AU - Eggly, Susan AU - Manning, Mark AU - Slatcher, Richard AU - Berg, Robert AU - Wessel, David AU - Newth, Christopher AU - Shanley, Thomas AU - Harrison, Rick AU - Dalton, Heidi AU - Dean, J AU - Doctor, Allan AU - Jenkins, Tammara AU - Meert, Kathleen AD - Wayne State University ; Children's Hospital Los Angeles ; University of Michigan ; University of California, Los Angeles ; Phoenix Children's Hospital ; University of Utah ; St. Louis Children's Hospital ; Eunice Kennedy Shriver National Institute of Child Health and Human Development Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 181 EP - 199 VL - 34 IS - 2 SN - 0261-927X, 0261-927X KW - Sociology KW - Emotions KW - Social psychology KW - Doctors KW - Family KW - Health KW - Bereavement UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660029603?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+language+and+social+psychology&rft.atitle=Language+analysis+as+a+window+to+bereaved+parents%27+emotions+during+a+parent-physician+bereavement+meeting&rft.au=Eggly%2C+Susan%3BManning%2C+Mark%3BSlatcher%2C+Richard%3BBerg%2C+Robert%3BWessel%2C+David%3BNewth%2C+Christopher%3BShanley%2C+Thomas%3BHarrison%2C+Rick%3BDalton%2C+Heidi%3BDean%2C+J%3BDoctor%2C+Allan%3BJenkins%2C+Tammara%3BMeert%2C+Kathleen&rft.aulast=Eggly&rft.aufirst=Susan&rft.date=2015-03-01&rft.volume=34&rft.issue=2&rft.spage=181&rft.isbn=&rft.btitle=&rft.title=Journal+of+language+and+social+psychology&rft.issn=0261927X&rft_id=info:doi/10.1177%2F0261927X14555549 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-03-02 N1 - Last updated - 2015-03-03 N1 - SubjectsTermNotLitGenreText - 1561; 5772; 4748; 3675 10299 13682 7883 8864; 11901 10404; 4196 DO - http://dx.doi.org/10.1177/0261927X14555549 ER - TY - JOUR T1 - Toward gene therapy for growth hormone deficiency via salivary gland expression of growth hormone. AN - 1658420223; 24320050 AB - Salivary glands are useful targets for gene therapeutics. After gene transfer into salivary glands, regulated secretory pathway proteins, such as human growth hormone, are secreted into saliva, whereas constitutive secretory pathway proteins, such as erythropoietin, are secreted into the bloodstream. Secretion of human growth hormone (hGH) into the saliva is not therapeutically useful. In this study, we attempted to redirect the secretion of transgenic hGH from the saliva to the serum by site-directed mutagenesis. We tested hGH mutants first in vitro with AtT20 cells, a model endocrine cell line that exhibits polarized secretion of regulated secretory pathway proteins. Selected mutants were further studied in vivo using adenoviral-mediated gene transfer to rat submandibular glands. We identified two mutants with differences in secretion behavior compared to wild-type hGH. One mutant, ΔN1-6 , was detected in the serum of transduced rats, demonstrating that expression of this mutant in the salivary gland resulted in its secretion through the constitutive secretory pathway. This study demonstrates that mutagenesis of therapeutic proteins normally destined for the regulated secretory pathway may result in their secretion via the constitutive secretory pathway into the circulation for potential therapeutic benefit. © Published 2013. This article is a U.S. Government work and is in the public domain in the USA. JF - Oral diseases AU - Racz, G Z AU - Zheng, C AU - Goldsmith, C M AU - Baum, B J AU - Cawley, N X AD - Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 149 EP - 155 VL - 21 IS - 2 KW - Erythropoietin KW - 11096-26-7 KW - Human Growth Hormone KW - 12629-01-5 KW - Dentistry KW - gene therapy KW - gene engineering KW - cell biology KW - endocrinology KW - Animals KW - Submandibular Gland -- metabolism KW - Humans KW - Transgenes KW - Erythropoietin -- secretion KW - Gene Expression KW - Secretory Pathway -- genetics KW - Submandibular Gland -- secretion KW - Adenoviridae -- genetics KW - Rats KW - Erythropoietin -- blood KW - Transfection KW - Mutagenesis, Site-Directed -- methods KW - Saliva -- metabolism KW - Genetic Vectors -- genetics KW - Cell Line KW - Human Growth Hormone -- deficiency KW - Human Growth Hormone -- genetics KW - Human Growth Hormone -- secretion KW - Genetic Therapy -- methods KW - Salivary Glands -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658420223?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oral+diseases&rft.atitle=Toward+gene+therapy+for+growth+hormone+deficiency+via+salivary+gland+expression+of+growth+hormone.&rft.au=Racz%2C+G+Z%3BZheng%2C+C%3BGoldsmith%2C+C+M%3BBaum%2C+B+J%3BCawley%2C+N+X&rft.aulast=Racz&rft.aufirst=G&rft.date=2015-03-01&rft.volume=21&rft.issue=2&rft.spage=149&rft.isbn=&rft.btitle=&rft.title=Oral+diseases&rft.issn=1601-0825&rft_id=info:doi/10.1111%2Fodi.12217 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-12-13 N1 - Date created - 2015-02-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 1996 Oct 11;271(41):25284-91 [8810291] Expert Opin Biol Ther. 2013 Jun;13(6):927-32 [23662811] J Biol Chem. 1995 Apr 14;270(15):8723-9 [7721777] Hum Gene Ther. 1999 Nov 20;10(17):2789-97 [10584925] Endocrinology. 2000 Mar;141(3):883-90 [10698162] J Clin Endocrinol Metab. 2001 Aug;86(8):3941-7 [11502836] J Clin Endocrinol Metab. 2002 Feb;87(2):847-52 [11836331] Mol Endocrinol. 2003 Sep;17(9):1856-67 [12829804] Nature. 1986 May 22-28;321(6068):443-6 [3012361] Annu Rev Cell Biol. 1987;3:243-93 [3318877] EMBO J. 1993 May;12(5):2159-68 [8491204] Hum Gene Ther. 1996 Nov 10;7(17):2177-84 [8934231] Hum Gene Ther. 1996 Dec 1;7(18):2255-61 [8953316] Crit Rev Oral Biol Med. 1998;9(1):4-22 [9488245] Gene Ther. 1998 Apr;5(4):537-41 [9614579] Biochem J. 1998 Jun 15;332 ( Pt 3):593-610 [9620860] J Dent Res. 2005 Jun;84(6):500-9 [15914585] Hum Gene Ther. 2005 May;16(5):571-83 [15916482] Pituitary. 2007;10(4):351-7 [17965963] Hum Gene Ther. 2008 Mar;19(3):279-86 [18303958] Mol Ther. 2008 Jun;16(6):1089-97 [18388914] Biochem Biophys Res Commun. 2008 Aug 15;373(1):136-9 [18544341] J Clin Endocrinol Metab. 2010 Feb;95(2):731-9 [19952226] Int J Biochem Cell Biol. 2010 Jun;42(6):773-7 [20219693] Clin Cancer Res. 2011 May 1;17(9):2842-51 [21367751] Endocr Rev. 2012 Apr;33(2):254-70 [22357343] Proc Natl Acad Sci U S A. 2012 Nov 20;109(47):19403-7 [23129637] Exp Diabetes Res. 2012;2012:768760 [23431286] PLoS One. 2013;8(3):e59222 [23554999] Hum Gene Ther. 2013 Apr;24(4):417-23 [23402345] J Cell Sci. 1996 Oct;109 ( Pt 10):2591-9 [8923220] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/odi.12217 ER - TY - JOUR T1 - Herbal dietary supplement associated hepatotoxicity: an upcoming workshop and need for research. AN - 1658417484; 25579757 JF - Gastroenterology AU - Vuppalanchi, Raj AU - Navarro, Victor AU - Vega, Maricruz AU - Bonkovsky, Herbert L AU - Seeff, Leonard AU - Serrano, Jose AU - Drug-Induced Liver Injury Network (DILIN) AD - Division of Gastroenterology & Hepatology, Indiana University, Indianapolis, Indiana. ; Division of Hepatology, Einstein Medical Center, Philadelphia, Pennsylvania. ; Department of Internal Medicine, Sections on Gastroenterology and Molecular Medicine and Translational Science, Wake Forest University School of Medicine, Winston-Salem, North Carolina. ; National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland. ; Drug-Induced Liver Injury Network (DILIN) Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 480 EP - 482 VL - 148 IS - 3 KW - Plant Preparations KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Chemical and Drug Induced Liver Injury -- etiology KW - Plant Preparations -- adverse effects KW - Liver Diseases -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658417484?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gastroenterology&rft.atitle=Herbal+dietary+supplement+associated+hepatotoxicity%3A+an%C2%A0upcoming+workshop+and+need+for+research.&rft.au=Vuppalanchi%2C+Raj%3BNavarro%2C+Victor%3BVega%2C+Maricruz%3BBonkovsky%2C+Herbert+L%3BSeeff%2C+Leonard%3BSerrano%2C+Jose%3BDrug-Induced+Liver+Injury+Network+%28DILIN%29&rft.aulast=Vuppalanchi&rft.aufirst=Raj&rft.date=2015-03-01&rft.volume=148&rft.issue=3&rft.spage=480&rft.isbn=&rft.btitle=&rft.title=Gastroenterology&rft.issn=1528-0012&rft_id=info:doi/10.1053%2Fj.gastro.2015.01.004 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-14 N1 - Date created - 2015-02-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Dig Dis Sci. 2013 Sep;58(9):2682-90 [23625293] Hepatology. 2014 Oct;60(4):1399-408 [25043597] Gastroenterology. 2015 Mar;148(3):517-532.e3 [25500423] J Hepatol. 2009 Jan;50(1):111-7 [19010564] Adv Data. 2004 May 27;(343):1-19 [15188733] Am J Gastroenterol. 2012 Sep;107(9):1380-7 [22733303] J Am Diet Assoc. 2006 Dec;106(12):1966-74 [17126626] Liver Int. 2007 May;27(4):465-74 [17403186] JAMA. 2008 Aug 27;300(8):915-23 [18728265] JAMA. 1998 Nov 11;280(18):1569-75 [9820257] Rev Esp Enferm Dig. 2008 Nov;100(11):688-95 [19159172] Comment On: Gastroenterology. 2015 Mar;148(3):517-532.e3 [25500423] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1053/j.gastro.2015.01.004 ER - TY - JOUR T1 - Association of TGF-β2 levels in breast milk with severity of breast biopsy diagnosis. AN - 1657325858; 25604865 AB - TGF-β plays a dual role in breast carcinogenesis, acting at early stages as tumor-suppressors and later as tumor-promoters. TGF-β isoforms are expressed in breast tissues and secreted in milk, suggesting that analysis of levels in milk might be informative for breast cancer risk. Accordingly, we assessed TGF-β2 levels in milk from women who had undergone a breast biopsy and related the concentrations to diagnosis. Milk donated by women who had undergone or were scheduled for a breast biopsy was shipped on ice for processing and testing. Breast cancer risk factors were obtained through a self-administered questionnaire, and biopsy diagnoses were extracted from pathology reports. TGF-β2 levels in milk, assessed as absolute levels and in relation to total protein, were analyzed in bilateral samples donated by 182 women. Linear regression was used to estimate relationships of log-transformed TGF-β2 levels and TGF-β2/ total protein ratios to biopsy category. Milk TGF-β2 levels from biopsied and non-biopsied breasts within women were highly correlated (r (2) = 0.77). Higher mean TGF-β2 milk levels (based on average of bilateral samples) were marginally associated with more severe breast pathological diagnosis, after adjusting for duration of nursing current child (adjusted p trend = 0.07). Our exploratory analysis suggests a borderline significant association between higher mean TGF-β2 levels in breast milk and more severe pathologic diagnoses. Further analysis of TGF-β signaling in milk may increase understanding of postpartum remodeling and advance efforts to analyze milk as a means of assessing risk of breast pathology. JF - Cancer causes & control : CCC AU - Yang, Hannah P AU - Schneider, Sallie Smith AU - Chisholm, Christina M AU - Browne, Eva P AU - Mahmood, Sidra AU - Gierach, Gretchen L AU - Lenington, Sarah AU - Anderton, Douglas L AU - Sherman, Mark E AU - Arcaro, Kathleen F AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, 9609 Medical Center Drive, Room 7E-238 , Bethesda, MD, 20892, USA, yanghan@mail.nih.gov. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 345 EP - 354 VL - 26 IS - 3 KW - Protein Isoforms KW - 0 KW - TGFB2 protein, human KW - Transforming Growth Factor beta2 KW - Index Medicus KW - Risk KW - Breast Feeding KW - Risk Factors KW - Humans KW - Adult KW - Surveys and Questionnaires KW - Female KW - Breast Neoplasms -- diagnosis KW - Transforming Growth Factor beta2 -- chemistry KW - Milk, Human -- metabolism KW - Transforming Growth Factor beta2 -- biosynthesis KW - Breast Neoplasms -- metabolism KW - Biopsy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1657325858?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+causes+%26+control+%3A+CCC&rft.atitle=Association+of+TGF-%CE%B22+levels+in+breast+milk+with+severity+of+breast+biopsy+diagnosis.&rft.au=Yang%2C+Hannah+P%3BSchneider%2C+Sallie+Smith%3BChisholm%2C+Christina+M%3BBrowne%2C+Eva+P%3BMahmood%2C+Sidra%3BGierach%2C+Gretchen+L%3BLenington%2C+Sarah%3BAnderton%2C+Douglas+L%3BSherman%2C+Mark+E%3BArcaro%2C+Kathleen+F&rft.aulast=Yang&rft.aufirst=Hannah&rft.date=2015-03-01&rft.volume=26&rft.issue=3&rft.spage=345&rft.isbn=&rft.btitle=&rft.title=Cancer+causes+%26+control+%3A+CCC&rft.issn=1573-7225&rft_id=info:doi/10.1007%2Fs10552-014-0498-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-29 N1 - Date created - 2015-02-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cold Spring Harb Perspect Biol. 2011 Jan;3(1):a003277 [20810549] J Mammary Gland Biol Neoplasia. 2011 Jun;16(2):97-108 [21494783] Pediatr Allergy Immunol. 2011 Dec;22(8):853-61 [21929601] Indian J Exp Biol. 2011 Nov;49(11):879-87 [22126020] Epigenetics. 2011 Dec;6(12):1425-35 [22139572] Pediatr Res. 2012 Jul;72(1):77-85 [22453296] BMC Cancer. 2012;12:100 [22436421] J Hum Lact. 2012 Nov;28(4):543-6 [22914689] Breastfeed Med. 2013 Feb;8(1):120-6 [23373436] J Natl Cancer Inst. 2013 Feb 6;105(3):166-74 [23264680] Oncologist. 2013;18(4):e13-5 [23633450] Breastfeed Med. 2013 Jun;8(3):249-56 [23259645] Am J Physiol Gastrointest Liver Physiol. 2013 Jun 15;304(12):G1055-65 [23558011] J Natl Cancer Inst. 2014 Feb;106(2):djt369 [24511106] Pediatr Res. 2010 Oct;68(4):330-4 [20581738] Cytokine. 2002 Feb 21;17(4):182-6 [11991670] Proc Natl Acad Sci U S A. 2003 Jul 22;100(15):8621-3 [12861075] Cancer Lett. 2006 Apr 8;235(1):100-13 [15949894] Biochim Biophys Acta. 2007 Jan;1775(1):21-62 [16904831] J Mammary Gland Biol Neoplasia. 2007 Dec;12(4):249-57 [18027075] Cancer Res. 2007 Dec 15;67(24):11517-27 [18089780] Cell. 2008 Jul 25;134(2):215-30 [18662538] Future Oncol. 2008 Oct;4(5):595-7 [18922115] J Natl Cancer Inst. 2008 Nov 19;100(22):1643-8 [19001605] J Mammary Gland Biol Neoplasia. 2009 Jun;14(2):131-44 [19396528] Cytokine Growth Factor Rev. 2009 Aug;20(4):305-17 [19656717] J Clin Oncol. 2009 Nov 10;27(32):5308-11 [19826117] J Pediatr. 2010 Feb;156(2 Suppl):S21-5 [20105660] Pediatr Allergy Immunol. 2010 Feb;21(1 Pt 1):47-59 [19594862] Breast Cancer Res Treat. 2010 Jun;121(3):727-35 [19937272] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s10552-014-0498-8 ER - TY - JOUR T1 - SU2C phase Ib study of paclitaxel and MK-2206 in advanced solid tumors and metastatic breast cancer. AN - 1657318988; 25688104 AB - There is preclinical synergism between taxanes and MK-2206. We aim to determine the maximum tolerated dose, safety, and activity of combining MK-2206 and paclitaxel in metastatic cancer. Patients received weekly doses of paclitaxel at 80mg/m2 on day 1, followed by MK-2206 orally on day 2 escalated at 90mg, 135mg, and 200mg. Treatment continued until progression, excessive toxicity, or patient request. Blood and tissue were collected for pharmacokinetic and pharmacodynamics markers. A cycle consisted of three weeks of therapy. Dose-limiting toxicity (DLT) was defined as unacceptable toxicity during the first cycle. All statistical tests were two-sided. Twenty-two patients were treated, nine in dose escalation and 13 in dose expansion. Median age was 55 years. Median number of cycles was four. Dose escalation was completed with no DLT. CTCAE Grade 3 or higher adverse events were fatigue (n = 2), rash (n = 2), hyperglycemia (n = 1), and neutropenia (n = 7). Four patients in the expansion phase required MK-2206 dose reduction. Phase II recommended dose was established as paclitaxel 80mg/m2 weekly on day 1, and MK-2206 135mg weekly on day 2. Paclitaxel systemic exposure was similar in the presence or absence of MK-2206. Plasma MK-2206 concentrations were similar to data from previous phase I monotherapy. There was a statistically significant decrease in expression of pAKT S473 (P = .01) and pAKT T308 (P = .002) after therapy. PI3K/AKT/mTOR downregulation in tumor tissues and circulating markers did not correlate with tumor response or clinical benefit. There were five objective responses, and nine patients had stable disease. MK-2206 was well tolerated with paclitaxel. Preliminary antitumor activity was documented. © The Author 2015. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. JF - Journal of the National Cancer Institute AU - Gonzalez-Angulo, Ana M AU - Krop, Ian AU - Akcakanat, Argun AU - Chen, Huiqin AU - Liu, Shuying AU - Li, Yisheng AU - Culotta, Kirk S AU - Tarco, Emily AU - Piha-Paul, Sarina AU - Moulder-Thompson, Stacy AU - Velez-Bravo, Vivianne AU - Sahin, Aysegul A AU - Doyle, Laurence A AU - Do, Kim-Anh AU - Winer, Eric P AU - Mills, Gordon B AU - Kurzrock, Razelle AU - Meric-Bernstam, Funda AD - Departments of Breast Medical Oncology (AMGA, SL, SMT), Systems Biology (AMGA, GBM), Biostatistics (HC, YL, K-AD), Experimental Therapeutics (KSC), Investigational Cancer Therapeutics (AA, ET, SPP, VV-B, FMB), Pathology (AAS) and Surgical Oncology (FMB), The University of Texas MD Anderson Cancer Center, Houston, TX; Division of Hematology-Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA (IK, EPW); Division of Hematology-Oncology, University of California, San Diego, CA (RK); Cancer Therapy Evaluation Program, NIH/National Cancer Institute, Rockville, MD (LAD). ; Departments of Breast Medical Oncology (AMGA, SL, SMT), Systems Biology (AMGA, GBM), Biostatistics (HC, YL, K-AD), Experimental Therapeutics (KSC), Investigational Cancer Therapeutics (AA, ET, SPP, VV-B, FMB), Pathology (AAS) and Surgical Oncology (FMB), The University of Texas MD Anderson Cancer Center, Houston, TX; Division of Hematology-Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA (IK, EPW); Division of Hematology-Oncology, University of California, San Diego, CA (RK); Cancer Therapy Evaluation Program, NIH/National Cancer Institute, Rockville, MD (LAD). fmeric@mdanderson.org. Y1 - 2015/03// PY - 2015 DA - March 2015 VL - 107 IS - 3 KW - Biomarkers, Tumor KW - 0 KW - Heterocyclic Compounds, 3-Ring KW - MK 2206 KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Severity of Illness Index KW - Paclitaxel -- administration & dosage KW - Drug Administration Schedule KW - Drug Eruptions -- etiology KW - Humans KW - Fatigue -- chemically induced KW - Heterocyclic Compounds, 3-Ring -- administration & dosage KW - Neutropenia -- chemically induced KW - Aged KW - Paclitaxel -- adverse effects KW - Hyperglycemia -- chemically induced KW - Adult KW - Treatment Outcome KW - Biomarkers, Tumor -- analysis KW - Middle Aged KW - Maximum Tolerated Dose KW - Heterocyclic Compounds, 3-Ring -- adverse effects KW - Female KW - Male KW - Breast Neoplasms -- drug therapy KW - Neoplasms -- drug therapy KW - Neoplasms -- pathology KW - Neoplasms -- chemistry KW - Breast Neoplasms -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- pharmacokinetics KW - Breast Neoplasms -- chemistry KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1657318988?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=SU2C+phase+Ib+study+of+paclitaxel+and+MK-2206+in+advanced+solid+tumors+and+metastatic+breast+cancer.&rft.au=Gonzalez-Angulo%2C+Ana+M%3BKrop%2C+Ian%3BAkcakanat%2C+Argun%3BChen%2C+Huiqin%3BLiu%2C+Shuying%3BLi%2C+Yisheng%3BCulotta%2C+Kirk+S%3BTarco%2C+Emily%3BPiha-Paul%2C+Sarina%3BMoulder-Thompson%2C+Stacy%3BVelez-Bravo%2C+Vivianne%3BSahin%2C+Aysegul+A%3BDoyle%2C+Laurence+A%3BDo%2C+Kim-Anh%3BWiner%2C+Eric+P%3BMills%2C+Gordon+B%3BKurzrock%2C+Razelle%3BMeric-Bernstam%2C+Funda&rft.aulast=Gonzalez-Angulo&rft.aufirst=Ana&rft.date=2015-03-01&rft.volume=107&rft.issue=3&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdju493 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-06 N1 - Date created - 2015-02-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437] J Clin Oncol. 2001 Nov 15;19(22):4216-23 [11709565] Tumori. 2002 Nov-Dec;88(6):470-3 [12597140] Jpn J Clin Oncol. 2003 Aug;33(8):371-6 [14523055] Tumori. 2004 May-Jun;90(3):285-8 [15315306] Cancer Cell. 2004 Aug;6(2):117-27 [15324695] J Clin Oncol. 1998 Oct;16(10):3353-61 [9779712] Cancer Res. 2005 Apr 1;65(7):2554-9 [15805248] Nat Rev Drug Discov. 2005 Dec;4(12):988-1004 [16341064] Clin Cancer Res. 2007 Jun 15;13(12):3623-9 [17510207] Cancer Cell. 2007 Oct;12(4):395-402 [17936563] Cancer Res. 2008 Aug 1;68(15):6084-91 [18676830] J Clin Oncol. 2009 May 1;27(13):2278-87 [19332717] Cancer Res. 2009 May 15;69(10):4192-201 [19435893] Cancer Cell. 2009 Jul 7;16(1):21-32 [19573809] Jpn J Clin Oncol. 2009 Sep;39(9):569-75 [19520687] Clin Cancer Res. 2010 May 1;16(9):2656-65 [20406837] Mol Cancer Ther. 2010 Jul;9(7):1956-67 [20571069] J Clin Oncol. 2011 Dec 10;29(35):4688-95 [22025163] Cancer. 2012 May 1;118(9):2378-84 [22006179] Clin Cancer Res. 2012 Oct 15;18(20):5816-28 [22932669] Clin Cancer Res. 2013 Oct 1;19(19):5413-22 [23888070] J Hematol Oncol. 2014;7:1 [24387695] Ann Oncol. 2014 Jun;25(6):1122-7 [24669015] Breast Cancer Res. 2013;15(6):R110 [24252402] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/jnci/dju493 ER - TY - JOUR T1 - Using infrared thermography to assess emotional responses to infants AN - 1655760358; 4645018 AB - Adult-infant interactions operate simultaneously across multiple domains and at multiple levels - from physiology to behaviour. Unpackaging and understanding them, therefore, involve analysis of multiple data streams. In this study, we tested physiological responses and cognitive preferences for infant and adult faces in adult females and males. Infrared thermography was used to assess facial temperature changes as a measure of emotional valence, and we used a behavioural rating system to assess adults' expressed preferences. We found greater physiological activation in response to infant stimuli in females than males. As for cognitive preferences, we found greater responses to adult stimuli than to infant stimuli, both in males and females. The results are discussed in light of the Life History Theory. Finally, we discuss the importance of integrating the two data streams on our conclusions. Reprinted by permission of Carfax Publishing, Taylor and Francis Ltd. JF - Early child development and care AU - Esposito, Gianluca AU - Nakazawa, Jun AU - Ogawa, Shota AU - Stival, Rita AU - Putnick, Diane L AU - Bornstein, Marc H AD - Università degli Studi di Trento ; Chiba University ; Tokyo Gakugei University ; Eunice Kennedy Shriver National Institute of Child Health and Human Development Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 438 EP - 447 VL - 185 IS - 3 SN - 0300-4430, 0300-4430 KW - Sociology KW - Preferences KW - Social behaviour KW - Gender KW - Social interaction KW - Cognition KW - Infants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1655760358?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Early+child+development+and+care&rft.atitle=Using+infrared+thermography+to+assess+emotional+responses+to+infants&rft.au=Esposito%2C+Gianluca%3BNakazawa%2C+Jun%3BOgawa%2C+Shota%3BStival%2C+Rita%3BPutnick%2C+Diane+L%3BBornstein%2C+Marc+H&rft.aulast=Esposito&rft.aufirst=Gianluca&rft.date=2015-03-01&rft.volume=185&rft.issue=3&rft.spage=438&rft.isbn=&rft.btitle=&rft.title=Early+child+development+and+care&rft.issn=03004430&rft_id=info:doi/10.1080%2F03004430.2014.932153 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-02-18 N1 - Last updated - 2015-02-18 N1 - SubjectsTermNotLitGenreText - 6495 2212; 2449 10404; 10016; 11776; 11860 11907; 5421 6091 DO - http://dx.doi.org/10.1080/03004430.2014.932153 ER - TY - JOUR T1 - Paternalism and utilitarianism in research with human participants AN - 1655759300; 4645181 AB - In this article I defend a rule utilitarian approach to paternalistic policies in research with human participants. Some rules that restrict individual autonomy can be justified on the grounds that they help to maximize the overall balance of benefits over risks in research. The consequences that should be considered when formulating policy include not only likely impacts on research participants, but also impacts on investigators, institutions, sponsors, and the scientific community. The public reaction to adverse events in research (such as significant injury to participants or death) is a crucial concern that must be taken into account when assessing the consequences of different policy options, because public backlash can lead to outcomes that have a negative impact on science, such as cuts in funding, overly restrictive regulation and oversight, and reduced willingness of individuals to participate in research. I argue that concern about the public reaction to adverse events justifies some restrictions on the risks that competent, adult volunteers can face in research that offers them no significant benefits. The paternalism defended here is not pure, because it involves restrictions on the rights of investigators in order to protect participants. It also has a mixed rationale, because individual autonomy may be restricted not only to protect participants from harm but also to protect other stakeholders. Utility is not the sole justification for paternalistic research policies, since other considerations, such as justice and respect for individual rights/autonomy, must also be taken into account. Reprinted by permission of Springer JF - Health care analysis AU - Resnik, David B AD - National Institute of Environmental Health Sciences Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - 19 EP - 31 VL - 23 IS - 1 SN - 1065-3058, 1065-3058 KW - Sociology KW - Community KW - Risk KW - Injuries KW - Utilitarianism KW - Justice KW - Paternalism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1655759300?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+care+analysis&rft.atitle=Paternalism+and+utilitarianism+in+research+with+human+participants&rft.au=Resnik%2C+David+B&rft.aulast=Resnik&rft.aufirst=David&rft.date=2015-03-01&rft.volume=23&rft.issue=1&rft.spage=19&rft.isbn=&rft.btitle=&rft.title=Health+care+analysis&rft.issn=10653058&rft_id=info:doi/10.1007%2Fs10728-012-0233-0 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-02-18 N1 - Last updated - 2015-02-18 N1 - SubjectsTermNotLitGenreText - 7032 9705; 9267; 11035; 13216 9485 9486; 2603; 6555 6220 DO - http://dx.doi.org/10.1007/s10728-012-0233-0 ER - TY - JOUR T1 - Subconjunctival sirolimus in the treatment of autoimmune non-necrotizing anterior scleritis: results of a phase I/II clinical trial. AN - 1655520386; 25526946 AB - To investigate the safety, tolerability and efficacy of subconjunctival sirolimus injections as a treatment for active, autoimmune, non-necrotizing anterior scleritis. Phase I/II, single-center, open-label, nonrandomized, prospective pilot study. Five participants with active, autoimmune, non-necrotizing anterior scleritis with scleral inflammatory grade of ≥1+ in at least 1 quadrant with a history of flares were enrolled. A baseline injection was given, with the primary outcome measure of at least a 2-step reduction or reduction to grade zero in the study eye by 8 weeks. Secondary outcomes included changes in visual acuity and intraocular pressure, ability to taper concomitant immunosuppressive regimen, and number of participants who experienced a disease flare requiring reinjection. Safety outcomes included the number and severity of systemic and ocular toxicities, and vision loss ≥15 ETDRS letters. The study included 6 visits over 4 months with an extension phase to 1 year for participants who met the primary outcome. All participants (N = 5, 100%; 95% CI [0.60, 1.00]) met the primary outcome in the study eye by the week 8 visit. There was no significant change in mean visual acuity or intraocular pressure. Three out of 5 patients (60%) experienced flares requiring reinjection. No systemic toxicities were observed. Two participants (40%) experienced a localized sterile inflammatory reaction at the site of the injection, which resolved without complication. Subconjunctival sirolimus leads to a short-term reduction in scleral inflammation, though relapses requiring reinjection do occur. There were no serious adverse events, though a local sterile conjunctival inflammatory reaction was observed. Published by Elsevier Inc. JF - American journal of ophthalmology AU - Bhatt, Nirali AU - Dalal, Monica AU - Tucker, William AU - Obiyor, Dominic AU - Nussenblatt, Robert AU - Sen, H Nida AD - National Eye Institute, National Institutes of Health, Bethesda, Maryland. ; National Eye Institute, National Institutes of Health, Bethesda, Maryland. Electronic address: senh@nei.nih.gov. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 601 EP - 606 VL - 159 IS - 3 KW - Immunosuppressive Agents KW - 0 KW - Sirolimus KW - W36ZG6FT64 KW - Abridged Index Medicus KW - Index Medicus KW - Intraocular Pressure -- drug effects KW - Anterior Eye Segment KW - Prospective Studies KW - Injections, Intraocular KW - Humans KW - Visual Acuity -- drug effects KW - Adult KW - Aged KW - Pilot Projects KW - Middle Aged KW - Male KW - Female KW - Sirolimus -- adverse effects KW - Autoimmune Diseases -- drug therapy KW - Sirolimus -- therapeutic use KW - Scleritis -- drug therapy KW - Immunosuppressive Agents -- therapeutic use KW - Conjunctiva -- drug effects KW - Immunosuppressive Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1655520386?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+ophthalmology&rft.atitle=Subconjunctival+sirolimus+in+the+treatment+of+autoimmune+non-necrotizing+anterior+scleritis%3A+results+of+a+phase+I%2FII+clinical+trial.&rft.au=Bhatt%2C+Nirali%3BDalal%2C+Monica%3BTucker%2C+William%3BObiyor%2C+Dominic%3BNussenblatt%2C+Robert%3BSen%2C+H+Nida&rft.aulast=Bhatt&rft.aufirst=Nirali&rft.date=2015-03-01&rft.volume=159&rft.issue=3&rft.spage=601&rft.isbn=&rft.btitle=&rft.title=American+journal+of+ophthalmology&rft.issn=1879-1891&rft_id=info:doi/10.1016%2Fj.ajo.2014.12.009 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-17 N1 - Date created - 2015-02-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Ophthalmology. 2005 Oct;112(10):1814-20 [16199269] Br J Ophthalmol. 1976 Mar;60(3):163-91 [1268179] Curr Eye Res. 1988 May;7(5):483-6 [3409715] Br J Ophthalmol. 1991 Jun;75(6):340-1 [2043575] Ophthalmology. 1991 Apr;98(4):472-9 [1828871] Am J Ophthalmol. 2009 Oct;148(4):500-509.e2 [19570522] Am J Ophthalmol. 2010 Jan;149(1):77-81 [19875093] Ophthalmology. 2011 Apr;118(4):768-71 [21093921] Ophthalmology. 2011 Oct;118(10):1932-7 [21708408] Ophthalmology. 2012 Jan;119(1):124-31 [22115710] Am J Ophthalmol. 2012 Jun;153(6):1038-42 [22465364] Am J Ophthalmol. 2008 Mar;145(3):487-492 [18282493] Am J Ophthalmol. 2000 Oct;130(4):469-76 [11024419] Am J Ophthalmol. 2000 Oct;130(4):492-513 [11024423] Ophthalmology. 2003 Sep;110(9):1750-5 [13129873] Ophthalmology. 1992 Sep;99(9):1419-23 [1407973] Br J Ophthalmol. 1994 May;78(5):381-5 [8025072] Br J Ophthalmol. 1996 Apr;80(4):332-6 [8703885] Clin Biochem. 1998 Jul;31(5):335-40 [9721431] Br J Ophthalmol. 2005 Jun;89(6):666-9 [15923497] Ophthalmology. 1984 Oct;91(10):1253-63 [6514289] Br J Ophthalmol. 2005 Jul;89(7):917-8 [15965178] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ajo.2014.12.009 ER - TY - JOUR T1 - Intrauterine devices and endometrial cancer risk: A pooled analysis of the Epidemiology of Endometrial Cancer Consortium AN - 1654671551; 21180124 AB - Intrauterine devices (IUDs), long-acting and reversible contraceptives, induce a number of immunological and biochemical changes in the uterine environment that could affect endometrial cancer (EC) risk. We addressed this relationship through a pooled analysis of data collected in the Epidemiology of Endometrial Cancer Consortium. We combined individual-level data from 4 cohort and 14 case-control studies, in total 8,801 EC cases and 15,357 controls. Using multivariable logistic regression, we estimated pooled odds ratios (pooled-ORs) and 95% confidence intervals (CIs) for EC risk associated with ever use, type of device, ages at first and last use, duration of use and time since last use, stratified by study and adjusted for confounders. Ever use of IUDs was inversely related to EC risk (pooled-OR=0.81, 95% CI=0.74-0.90). Compared with never use, reduced risk of EC was observed for inert IUDs (pooled-OR=0.69, 95% CI=0.58-0.82), older age at first use ( greater than or equal to 35 years pooled-OR=0.53, 95% CI=0.43-0.67), older age at last use ( greater than or equal to 45 years pooled-OR=0.60, 95% CI=0.50-0.72), longer duration of use ( greater than or equal to 10 years pooled-OR=0.61, 95% CI=0.52-0.71) and recent use (within 1 year of study entry pooled-OR=0.39, 95% CI=0.30-0.49). Future studies are needed to assess the respective roles of detection biases and biologic effects related to foreign body responses in the endometrium, heavier bleeding (and increased clearance of carcinogenic cells) and localized hormonal changes. What's new? Are IUDs associated with endometrial cancer? Around the world, the intrauterine device is gaining popularity as a long-term birth control strategy. Positioned as it is embedded in the uterine lining, an IUD could affect endometrial tissue. This study builds on previous work by considering the type of device used, in addition to factors such as duration of use. The authors found that women who had used an IUD, particularly an inert IUD, had less risk of endometrial cancer. The longer the device was used, they found, the more the cancer risk decreased. JF - International Journal of Cancer AU - Felix, Ashley S AU - Gaudet, Mia M AU - Vecchia, Carlo La AU - Nagle, Christina M AU - Shu, Xiao Ou AU - Weiderpass, Elisabete AU - Adami, Hans Olov AU - Beresford, Shirley AU - Bernstein, Leslie AU - Chen, Chu AU - Cook, Linda S AU - Vivo, Immaculata De AU - Doherty, Jennifer A AU - Friedenreich, Christine M AU - Gapstur, Susan M AU - Hill, Dierdre AU - Horn-Ross, Pamela L AU - Lacey, James V AU - Levi, Fabio AU - Liang, Xiaolin AU - Lu, Lingeng AU - Magliocco, Anthony AU - McCann, Susan E AU - Negri, Eva AU - Olson, Sara H AU - Palmer, Julie R AU - Patel, Alpa V AU - Petruzella, Stacey AU - Prescott, Jennifer AU - Risch, Harvey A AU - Rosenberg, Lynn AU - Sherman, Mark E AU - Spurdle, Amanda B AU - Webb, Penelope M AU - Wise, Lauren A AU - Xiang, Yong-Bing AU - Xu, Wanghong AU - Yang, Hannah P AU - Yu, Herbert AU - Zeleniuch-Jacquotte, Anne AU - Brinton, Louise A AD - Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD. Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - E410 EP - E422 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 136 IS - 5 SN - 0020-7136, 0020-7136 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Risk assessment KW - Health risks KW - Age KW - Biochemistry KW - Epidemiology KW - Carcinogenicity KW - Risk factors KW - Risk reduction KW - Cancer KW - Contraceptives KW - R2 23060:Medical and environmental health KW - H 4000:Food and Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654671551?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=Intrauterine+devices+and+endometrial+cancer+risk%3A+A+pooled+analysis+of+the+Epidemiology+of+Endometrial+Cancer+Consortium&rft.au=Felix%2C+Ashley+S%3BGaudet%2C+Mia+M%3BVecchia%2C+Carlo+La%3BNagle%2C+Christina+M%3BShu%2C+Xiao+Ou%3BWeiderpass%2C+Elisabete%3BAdami%2C+Hans+Olov%3BBeresford%2C+Shirley%3BBernstein%2C+Leslie%3BChen%2C+Chu%3BCook%2C+Linda+S%3BVivo%2C+Immaculata+De%3BDoherty%2C+Jennifer+A%3BFriedenreich%2C+Christine+M%3BGapstur%2C+Susan+M%3BHill%2C+Dierdre%3BHorn-Ross%2C+Pamela+L%3BLacey%2C+James+V%3BLevi%2C+Fabio%3BLiang%2C+Xiaolin%3BLu%2C+Lingeng%3BMagliocco%2C+Anthony%3BMcCann%2C+Susan+E%3BNegri%2C+Eva%3BOlson%2C+Sara+H%3BPalmer%2C+Julie+R%3BPatel%2C+Alpa+V%3BPetruzella%2C+Stacey%3BPrescott%2C+Jennifer%3BRisch%2C+Harvey+A%3BRosenberg%2C+Lynn%3BSherman%2C+Mark+E%3BSpurdle%2C+Amanda+B%3BWebb%2C+Penelope+M%3BWise%2C+Lauren+A%3BXiang%2C+Yong-Bing%3BXu%2C+Wanghong%3BYang%2C+Hannah+P%3BYu%2C+Herbert%3BZeleniuch-Jacquotte%2C+Anne%3BBrinton%2C+Louise+A&rft.aulast=Felix&rft.aufirst=Ashley&rft.date=2015-03-01&rft.volume=136&rft.issue=5&rft.spage=E410&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.29229 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2015-02-18 N1 - SubjectsTermNotLitGenreText - Risk assessment; Health risks; Age; Epidemiology; Biochemistry; Carcinogenicity; Risk factors; Risk reduction; Contraceptives; Cancer DO - http://dx.doi.org/10.1002/ijc.29229 ER - TY - JOUR T1 - Relationship between ambient ultraviolet radiation and non-Hodgkin lymphoma subtypes: A U.S. population-based study of racial and ethnic groups AN - 1654666065; 21180146 AB - Associations between ultraviolet radiation (UVR) exposure and non-Hodgkin lymphoma (NHL) have been inconsistent, but few studies have examined these associations for specific subtypes or across race/ethnicities. We evaluated the relationship between ambient UVR exposure and subtype-specific NHL incidence for whites, Hispanics and blacks in the United States for years 2001-2010 (n=187,778 cases). Incidence rate ratios (IRRs) and 95% confidence intervals (CIs) were calculated for UVR quintiles using Poisson regression. Incidence was lower for the highest UVR quintile for chronic/small lymphocytic/leukemia (CLL/SLL) (IRR=0.87, 95% CI: 0.77-0.97), mantle cell (IRR=0.82, 95% CI: 0.69-0.97), lymphoplasmacytic (IRR=0.58, 95% CI: 0.42-0.80), mucosa-associated lymphoid tissue (MZLMALT) (IRR=0.74, 95% CI: 0.60-0.90), follicular (FL) (IRR=0.76, 95% CI: 0.68-0.86), diffuse large B-cell (IRR=0.84, 95% CI: 0.76-0.94; ), peripheral T-cell other (PTCL) (IRR=0.76, 95% CI: 0.61-0.95) and PTCL not otherwise specified (PNOS) (IRR=0.77, 95% CI: 0.61-0.98). Trends were significant for MZLMALT, FL, DLBCL, BNOS and PTCL, with FL and DLBCL still significant after Bonferroni correction. We found interaction by race/ethnicity for CLL/SLL, FL, Burkitt, PNOS and MF/SS, with CLL/SLL and FL still significant after Bonferroni correction. Some B-cell lymphomas (CLL/SLL, FL and Burkitt) suggested significant inverse relationships in whites and Hispanics, but not in blacks. Some T-cell lymphomas suggested the most reduced risk for the highest quintile of UVR among blacks (PNOS and MF/SS), though trends were not significant. These findings strengthen the case for an inverse association of UVR exposure, support modest heterogeneity between NHL subtypes and suggest some differences by race/ethnicity. What's new? Studies have yielded mix results as to whether exposure to ultraviolet radiation (UVR) increases or decreases risk of non-Hodgkin lymphoma (NHL). In the present analysis of data from population-based cancer registries in the United States, increasing ambient UVR exposure was associated with a reduction in risk of most NHL subtypes, The reduction occurred for all races, including non-Hispanic whites, Hispanic whites, and blacks. The findings emphasize the importance of exploring NHL etiology according to subtypes and across races and ethnicities, as NHL is increasingly recognized as comprising a diverse group of cancers, each potentially involving unique mechanisms. JF - International Journal of Cancer AU - Cahoon, Elizabeth K AU - Pfeiffer, Ruth M AU - Wheeler, David C AU - Arhancet, Juan AU - Lin, Shih-Wen AU - Alexander, Bruce H AU - Linet, Martha S AU - Freedman, DMichal AD - Radiation Epidemiology Branch, National Cancer Institute, Division of Cancer Epidemiology and Genetics, U.S. Department of Health and Human Services, National Institutes of Health, Bethesda, MD. Y1 - 2015/03// PY - 2015 DA - Mar 2015 SP - E432 EP - E441 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 136 IS - 5 SN - 0020-7136, 0020-7136 KW - Health & Safety Science Abstracts; Immunology Abstracts; Risk Abstracts KW - Risk reduction KW - Non-Hodgkin's lymphoma KW - Leukemia KW - U.V. radiation KW - Risk factors KW - Ultraviolet radiation KW - Lymphocytes T KW - Lymphoma KW - Races KW - Ethnic groups KW - B-cell lymphoma KW - Etiology KW - Data processing KW - Lymphocytes B KW - Population studies KW - Race differences KW - Cancer KW - Health risks KW - USA KW - T-cell lymphoma KW - Chronic lymphatic leukemia KW - H 8000:Radiation Safety/Electrical Safety KW - F 06915:Cancer Immunology KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654666065?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Cancer&rft.atitle=Relationship+between+ambient+ultraviolet+radiation+and+non-Hodgkin+lymphoma+subtypes%3A+A+U.S.+population-based+study+of+racial+and+ethnic+groups&rft.au=Cahoon%2C+Elizabeth+K%3BPfeiffer%2C+Ruth+M%3BWheeler%2C+David+C%3BArhancet%2C+Juan%3BLin%2C+Shih-Wen%3BAlexander%2C+Bruce+H%3BLinet%2C+Martha+S%3BFreedman%2C+DMichal&rft.aulast=Cahoon&rft.aufirst=Elizabeth&rft.date=2015-03-01&rft.volume=136&rft.issue=5&rft.spage=E432&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.29237 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2015-08-05 N1 - SubjectsTermNotLitGenreText - Etiology; B-cell lymphoma; Data processing; Lymphocytes B; Population studies; Race differences; Cancer; Leukemia; U.V. radiation; Risk factors; Lymphocytes T; T-cell lymphoma; Chronic lymphatic leukemia; Ethnic groups; Races; Non-Hodgkin's lymphoma; Health risks; Ultraviolet radiation; Risk reduction; Lymphoma; USA DO - http://dx.doi.org/10.1002/ijc.29237 ER - TY - JOUR T1 - Semimetal nanomaterials of antimony as highly efficient agent for photoacoustic imaging and photothermal therapy. AN - 1653131156; 25662491 AB - In this study we report semimetal nanomaterials of antimony (Sb) as highly efficient agent for photoacoustic imaging (PAI) and photothermal therapy (PTT). The Sb nanorod bundles have been synthesized through a facile route by mixing 1-octadecane (ODE) and oleyl amine (OAm) as the solvent. The aqueous dispersion of PEGylated Sb NPs, due to its broad and strong photoabsorption ranging from ultraviolet (UV) to near-infrared (NIR) wavelengths, is applicable as a photothermal agent driven by 808 nm laser with photothermal conversion efficiency up to 41%, noticeably higher than most of the PTT agents reported before. Our in vitro experiments also showed that cancer cell ablation effect of PEGylated Sb NPs was dependent on laser power. By intratumoral administration of PEGylated Sb NPs, 100% tumor ablation can be realized by using NIR laser irradiation with a lower power of 1 W/cm(2) for 5 min (or 0.5 W/cm(2) for 10 min) and no obvious toxic side effect is identified after photothermal treatment. Moreover, intense PA signal was also observed after intratumoral injection of PEGylated Sb NPs and NIR laser irradiation due to their strong NIR photoabsorption, suggesting PEGylated Sb NPs as a potential NIR PA agent. Based on the findings of this work, further development of using other semimetal nanocrystals as highly efficient NIR agents can be achieved for vivo tumor imaging and PTT. Published by Elsevier Ltd. JF - Biomaterials AU - Li, Wanwan AU - Rong, Pengfei AU - Yang, Kai AU - Huang, Peng AU - Sun, Kang AU - Chen, Xiaoyuan AD - State Key Lab of Metal Matrix Composites, School of Materials Science and Engineering, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai 200240, China; Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), Bethesda, MD 20892, USA. Electronic address: wwli@sjtu.edu.cn. ; Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), Bethesda, MD 20892, USA; State Key Laboratory for Powder Metallurgy, Central South University, Changsha, Hunan 410083, China; Department of Radiology, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, China. ; Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), Bethesda, MD 20892, USA; School of Radiation Medicine and Protection (SRMP) and School of Radiological and Interdisciplinary Sciences (RAD-X), Soochow University, Suzhou, Jiangsu 215123, China. ; Department of Radiology, The Third Xiangya Hospital, Central South University, Changsha, Hunan 410013, China. ; State Key Lab of Metal Matrix Composites, School of Materials Science and Engineering, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai 200240, China. ; Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), Bethesda, MD 20892, USA. Electronic address: shawn.chen@nih.gov. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 18 EP - 26 VL - 45 KW - Polyethylene Glycols KW - 30IQX730WE KW - Antimony KW - 9IT35J3UV3 KW - Index Medicus KW - Nanorod bundles KW - Semimetal KW - Photothermal therapy (PTT) KW - Photoacoustic imaging (PAI) KW - Cell Proliferation -- drug effects KW - Animals KW - Spectrometry, X-Ray Emission KW - Cell Survival -- drug effects KW - X-Ray Diffraction KW - Polyethylene Glycols -- chemistry KW - Spectrophotometry, Ultraviolet KW - Mice, Nude KW - Cell Line, Tumor KW - Spectroscopy, Near-Infrared KW - Nanostructures -- ultrastructure KW - Nanostructures -- chemistry KW - Hyperthermia, Induced KW - Diagnostic Imaging KW - Antimony -- pharmacology KW - Phototherapy KW - Photoacoustic Techniques UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1653131156?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biomaterials&rft.atitle=Semimetal+nanomaterials+of+antimony+as+highly+efficient+agent+for+photoacoustic+imaging+and+photothermal+therapy.&rft.au=Li%2C+Wanwan%3BRong%2C+Pengfei%3BYang%2C+Kai%3BHuang%2C+Peng%3BSun%2C+Kang%3BChen%2C+Xiaoyuan&rft.aulast=Li&rft.aufirst=Wanwan&rft.date=2015-03-01&rft.volume=45&rft.issue=&rft.spage=18&rft.isbn=&rft.btitle=&rft.title=Biomaterials&rft.issn=1878-5905&rft_id=info:doi/10.1016%2Fj.biomaterials.2014.12.037 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-27 N1 - Date created - 2015-02-09 N1 - Date revised - 2017-01-24 N1 - Last updated - 2017-01-25 DO - http://dx.doi.org/10.1016/j.biomaterials.2014.12.037 ER - TY - JOUR T1 - Cyclic depsipeptides as potential cancer therapeutics. AN - 1652435995; 25419631 AB - Cyclic depsipeptides are polypeptides in which one or more amino acid is replaced by a hydroxy acid, resulting in the formation of at least one ester bond in the core ring structure. Many natural cyclic depsipeptides possessing intriguing structural and biological properties, including antitumor, antifungal, antiviral, antibacterial, anthelmintic, and anti-inflammatory activities, have been identified from fungi, plants, and marine organisms. In particular, the potent effects of cyclic depsipeptides on tumor cells have led to a number of clinical trials evaluating their potential as chemotherapeutic agents. Although many of the trials have not achieved the desired results, romidepsin (FK228), a bicyclic depsipeptide that inhibits histone deacetylase, has been shown to have clinical efficacy in patients with refractory cutaneous T-cell lymphoma and has received Food and Drug Administration approval for use in treatment. In this review, we discuss antitumor cyclic depsipeptides that have undergone clinical trials and focus on their structural features, mechanisms, potential applications in chemotherapy, and pharmacokinetic and toxicity data. The results of this study indicate that cyclic depsipeptides could be a rich source of new cancer therapeutics. JF - Anti-cancer drugs AU - Kitagaki, Jirouta AU - Shi, Genbin AU - Miyauchi, Shizuka AU - Murakami, Shinya AU - Yang, Yili AD - aDepartment of Periodontology, Division of Oral Biology and Disease Control, Osaka University Graduate School of Dentistry bChallenge to Intractable Oral Diseases, Center for Translational Dental Research, Osaka University Dental Hospital, Suita, Osaka, Japan cMacromolecular Crystallography Laboratory, National Cancer Institute, National Institutes of Health, Frederick, Maryland, USA dCenter for Translational Medicine, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, People's Republic of China. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 259 EP - 271 VL - 26 IS - 3 KW - Antineoplastic Agents KW - 0 KW - Depsipeptides KW - Histone Deacetylase Inhibitors KW - Lactams KW - Lactones KW - cryptophycin 1 KW - cryptophycin 52 KW - elisidepsin KW - 0FWR494EC9 KW - kahalalide F KW - 149204-42-2 KW - didemnins KW - 77327-04-9 KW - romidepsin KW - CX3T89XQBK KW - aplidine KW - Y76ID234HW KW - Index Medicus KW - Lactones -- adverse effects KW - Lactams -- adverse effects KW - Animals KW - Lactones -- pharmacokinetics KW - Histone Deacetylase Inhibitors -- pharmacology KW - Humans KW - Clinical Trials as Topic KW - Lactams -- pharmacokinetics KW - Lymphoma, T-Cell, Cutaneous -- drug therapy KW - Lactams -- pharmacology KW - Lactones -- pharmacology KW - Antineoplastic Agents -- pharmacokinetics KW - Depsipeptides -- pharmacology KW - Depsipeptides -- pharmacokinetics KW - Depsipeptides -- adverse effects KW - Antineoplastic Agents -- pharmacology KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652435995?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Anti-cancer+drugs&rft.atitle=Cyclic+depsipeptides+as+potential+cancer+therapeutics.&rft.au=Kitagaki%2C+Jirouta%3BShi%2C+Genbin%3BMiyauchi%2C+Shizuka%3BMurakami%2C+Shinya%3BYang%2C+Yili&rft.aulast=Kitagaki&rft.aufirst=Jirouta&rft.date=2015-03-01&rft.volume=26&rft.issue=3&rft.spage=259&rft.isbn=&rft.btitle=&rft.title=Anti-cancer+drugs&rft.issn=1473-5741&rft_id=info:doi/10.1097%2FCAD.0000000000000183 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-03 N1 - Date created - 2015-01-28 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/CAD.0000000000000183 ER - TY - JOUR T1 - Steatogenesis in adult-onset type II citrullinemia is associated with down-regulation of PPARα. AN - 1652433257; 25533124 AB - SLC25A13 (citrin or aspartate-glutamate carrier 2) is located in the mitochondrial membrane in the liver and its genetic deficiency causes adult-onset type II citrullinemia (CTLN2). CTLN2 is one of the urea cycle disorders characterized by sudden-onset hyperammonemia due to reduced argininosuccinate synthase activity. This disorder is frequently accompanied with hepatosteatosis in the absence of obesity and ethanol consumption. However, the precise mechanism of steatogenesis remains unclear. The expression of genes associated with fatty acid (FA) and triglyceride (TG) metabolism was examined using liver samples obtained from 16 CTLN2 patients and compared with 7 healthy individuals. Although expression of hepatic genes associated with lipogenesis and TG hydrolysis was not changed, the mRNAs encoding enzymes/proteins involved in FA oxidation (carnitine palmitoyl-CoA transferase 1α, medium- and very-long-chain acyl-CoA dehydrogenases, and acyl-CoA oxidase 1), very-low-density lipoprotein secretion (microsomal TG transfer protein), and FA transport (CD36 and FA-binding protein 1), were markedly suppressed in CTLN2 patients. Serum concentrations of ketone bodies were also decreased in these patients, suggesting reduced mitochondrial β-oxidation activity. Consistent with these findings, the expression of peroxisome proliferator-activated receptor α (PPARα), a master regulator of hepatic lipid metabolism, was significantly down-regulated. Hepatic PPARα expression was inversely correlated with severity of steatosis and circulating ammonia and citrulline levels. Additionally, phosphorylation of c-Jun-N-terminal kinase was enhanced in CTLN2 livers, which was likely associated with lower hepatic PPARα. Collectively, down-regulation of PPARα is associated with steatogenesis in CTLN2 patients. These findings provide a novel link between urea cycle disorder, lipid metabolism, and PPARα. Copyright © 2014 Elsevier B.V. All rights reserved. JF - Biochimica et biophysica acta AU - Komatsu, Michiharu AU - Kimura, Takefumi AU - Yazaki, Masahide AU - Tanaka, Naoki AU - Yang, Yang AU - Nakajima, Takero AU - Horiuchi, Akira AU - Fang, Zhong-Ze AU - Joshita, Satoru AU - Matsumoto, Akihiro AU - Umemura, Takeji AU - Tanaka, Eiji AU - Gonzalez, Frank J AU - Ikeda, Shu-Ichi AU - Aoyama, Toshifumi AD - Department of Medicine (Gastroenterology), Shinshu University School of Medicine, Japan. ; Department of Medicine (Gastroenterology), Shinshu University School of Medicine, Japan; Department of Metabolic Regulation, Shinshu University Graduate School of Medicine, Japan. ; Department of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine, Japan; Department of Biological Sciences for Intractable Neurological Diseases, Institute for Biomedical Sciences, Shinshu University, Japan. ; Department of Medicine (Gastroenterology), Shinshu University School of Medicine, Japan; Department of Metabolic Regulation, Shinshu University Graduate School of Medicine, Japan. Electronic address: naopi@shinshu-u.ac.jp. ; Department of Metabolic Regulation, Shinshu University Graduate School of Medicine, Japan. ; Digestive Disease Center, Showa Inan General Hospital, Japan. ; Department of Toxicology, School of Public Health, Tianjin Medical University, China. ; Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, USA. ; Department of Medicine (Neurology and Rheumatology), Shinshu University School of Medicine, Japan. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 473 EP - 481 VL - 1852 IS - 3 SN - 0006-3002, 0006-3002 KW - Fatty Acids KW - 0 KW - Ketone Bodies KW - Mitochondrial Membrane Transport Proteins KW - PPAR alpha KW - RNA, Messenger KW - SLC25A13 protein, human KW - Triglycerides KW - JNK Mitogen-Activated Protein Kinases KW - EC 2.7.11.24 KW - Index Medicus KW - Urea cycle disorder KW - NAFLD KW - JNK KW - SLC25A13 KW - Mitochondrial β-oxidation KW - PPARα KW - Ketone Bodies -- metabolism KW - Triglycerides -- genetics KW - Humans KW - Ketone Bodies -- genetics KW - RNA, Messenger -- genetics KW - RNA, Messenger -- biosynthesis KW - Fatty Acids -- metabolism KW - Fatty Acids -- genetics KW - Triglycerides -- metabolism KW - Adult KW - JNK Mitogen-Activated Protein Kinases -- genetics KW - Middle Aged KW - Female KW - Male KW - JNK Mitogen-Activated Protein Kinases -- metabolism KW - Fatty Liver -- etiology KW - Citrullinemia -- complications KW - Fatty Liver -- metabolism KW - Citrullinemia -- genetics KW - Mitochondria, Liver -- metabolism KW - Mitochondria, Liver -- pathology KW - Citrullinemia -- pathology KW - PPAR alpha -- biosynthesis KW - Citrullinemia -- metabolism KW - PPAR alpha -- genetics KW - Down-Regulation KW - Mitochondria, Liver -- genetics KW - Fatty Liver -- genetics KW - Fatty Liver -- pathology KW - Lipid Metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652433257?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Steatogenesis+in+adult-onset+type+II+citrullinemia+is+associated+with+down-regulation+of+PPAR%CE%B1.&rft.au=Komatsu%2C+Michiharu%3BKimura%2C+Takefumi%3BYazaki%2C+Masahide%3BTanaka%2C+Naoki%3BYang%2C+Yang%3BNakajima%2C+Takero%3BHoriuchi%2C+Akira%3BFang%2C+Zhong-Ze%3BJoshita%2C+Satoru%3BMatsumoto%2C+Akihiro%3BUmemura%2C+Takeji%3BTanaka%2C+Eiji%3BGonzalez%2C+Frank+J%3BIkeda%2C+Shu-Ichi%3BAoyama%2C+Toshifumi&rft.aulast=Komatsu&rft.aufirst=Michiharu&rft.date=2015-03-01&rft.volume=1852&rft.issue=3&rft.spage=473&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbadis.2014.12.011 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-16 N1 - Date created - 2015-01-31 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.bbadis.2014.12.011 ER - TY - JOUR T1 - Therapeutic efficacy of Wuzhi tablet (Schisandra sphenanthera Extract) on acetaminophen-induced hepatotoxicity through a mechanism distinct from N-acetylcysteine. AN - 1652414797; 25534769 AB - Acetaminophen (APAP) hepatotoxicity is the most common cause of drug-induced liver injury and N-acetylcysteine (NAC) is the primary antidote of APAP poisoning. Wuzhi tablet (WZ), the active constituents well identified and quantified, is a preparation of an ethanol extract of Schisandra sphenanthera and exerts a protective effect toward APAP-induced hepatotoxicity in mice. However, the clinical use of WZ to rescue APAP-induced acute liver injury and the mechanisms involved in the therapeutic effect of WZ remain unclear. Therefore, the effect of WZ on APAP hepatotoxicity was compared with NAC in mice, and molecular pathways contributing to its therapeutic action were investigated. Administration of WZ 4 hours after APAP treatment significantly attenuated APAP hepatotoxicity and exerted much better therapeutic effect than NAC, as revealed by morphologic, histologic, and biochemical assessments. Both WZ and NAC prevented APAP-induced c-Jun N-terminal protein kinase activation and mitochondrial glutathione depletion in livers. The protein expression of nuclear factor erythroid 2-related factor 2 target genes including Gclc, Gclm, Ho-1, and Nqo1 was increased by WZ administration. Furthermore, p53 and p21 levels were upregulated upon APAP exposure, which were completely reversed by postdosing of WZ 4 hours after APAP treatment over 48 hours. In comparison with NAC, WZ significantly increased the expression of cyclin D1, cyclin D-dependent kinase 4, proliferating cell nuclear antigen, and augmenter of liver regeneration in APAP-injured livers. This study demonstrated that WZ possessed a therapeutic efficacy against APAP-induced liver injury by inhibiting oxidative stress and stimulating a regenerative response after liver injury. Thus WZ may represent a new therapy for APAP-induced acute liver injury. U.S. Government work not protected by U.S. copyright. JF - Drug metabolism and disposition: the biological fate of chemicals AU - Fan, Xiaomei AU - Chen, Pan AU - Jiang, Yiming AU - Wang, Ying AU - Tan, Huasen AU - Zeng, Hang AU - Wang, Yongtao AU - Qu, Aijuan AU - Gonzalez, Frank J AU - Huang, Min AU - Bi, Huichang AD - School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China (X.F., Y.J., Yi.W., H.T., H.Z., Yo.W., M.H., H.B.); The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China (P.C.); and Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD (A.Q., F.J.G). ; School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China (X.F., Y.J., Yi.W., H.T., H.Z., Yo.W., M.H., H.B.); The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China (P.C.); and Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD (A.Q., F.J.G) bihchang@mail.sysu.edu.cn. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 317 EP - 324 VL - 43 IS - 3 KW - Drugs, Chinese Herbal KW - 0 KW - Plant Extracts KW - Tablets KW - wuzhi KW - Acetaminophen KW - 362O9ITL9D KW - Glutathione KW - GAN16C9B8O KW - Acetylcysteine KW - WYQ7N0BPYC KW - Index Medicus KW - Animals KW - Hepatocytes -- drug effects KW - Liver -- drug effects KW - Glutathione -- metabolism KW - Signal Transduction -- drug effects KW - Oxidative Stress -- drug effects KW - Mice, Inbred C57BL KW - Liver -- metabolism KW - Mice KW - Male KW - Hepatocytes -- metabolism KW - Tablets -- pharmacology KW - Plant Extracts -- pharmacology KW - Schisandra -- chemistry KW - Acetaminophen -- adverse effects KW - Acetylcysteine -- metabolism KW - Plant Extracts -- chemistry KW - Drugs, Chinese Herbal -- pharmacology KW - Chemical and Drug Induced Liver Injury -- metabolism KW - Chemical and Drug Induced Liver Injury -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652414797?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Drug+metabolism+and+disposition%3A+the+biological+fate+of+chemicals&rft.atitle=Therapeutic+efficacy+of+Wuzhi+tablet+%28Schisandra+sphenanthera+Extract%29+on+acetaminophen-induced+hepatotoxicity+through+a+mechanism+distinct+from+N-acetylcysteine.&rft.au=Fan%2C+Xiaomei%3BChen%2C+Pan%3BJiang%2C+Yiming%3BWang%2C+Ying%3BTan%2C+Huasen%3BZeng%2C+Hang%3BWang%2C+Yongtao%3BQu%2C+Aijuan%3BGonzalez%2C+Frank+J%3BHuang%2C+Min%3BBi%2C+Huichang&rft.aulast=Fan&rft.aufirst=Xiaomei&rft.date=2015-03-01&rft.volume=43&rft.issue=3&rft.spage=317&rft.isbn=&rft.btitle=&rft.title=Drug+metabolism+and+disposition%3A+the+biological+fate+of+chemicals&rft.issn=1521-009X&rft_id=info:doi/10.1124%2Fdmd.114.062067 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-10 N1 - Date created - 2015-01-16 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/dmd.114.062067 ER - TY - JOUR T1 - Detection of phosphorylated insulin receptor in colorectal adenoma and adenocarcinoma: implications for prognosis and clinical outcome. AN - 1627952851; 25102778 AB - Colorectal carcinoma remains among the most frequent causes of cancer death. Besides the well-known genetic predisposition, a key role in colorectal adenoma and adenocarcinoma etio-pathogenesis, mainly in sporadic cases, is played by definite risk factors, such as obesity, type 2 diabetes, insulin resistance, hyper-insulinemia, and insulin therapy. These epidemiological data motivated us to determine, by means of immunohistochemistry, the amount of activated (phosphorylated) insulin receptor in archival samples from 22 colorectal adenoma and 117 adenocarcinoma patients, with the objective to estimate the role of this factor in colorectal epithelium transformation and cancer progression. Statistical analysis of the results clearly showed that positive staining for phosphorylated insulin receptor was significantly more frequent in adenomas than adenocarcinomas (P < 0.0001) and, within the adenocarcinoma cohort, it was more frequent in low-grade tumors (P = 0.005). In adenomas, staining was exclusively cytoplasmic, while in adenocarcinomas it was cytoplasmic and/or nuclear (P < 0.0001). Interestingly, disease-free survival in colorectal adenocarcinoma patients pointed out a significantly better prognosis for those bearing a positive staining for phosphorylated insulin receptor (P = 0.02). From these data, we can argue that activated insulin receptor plays a fundamental role at the early stages of tumorigenesis, where late stages could be characterized by a shift toward more active oncogenic drivers. Determining the amount of phosphorylated insulin receptor could thus represent a novel prognostic/predictive tool in colorectal adenocarcinoma patients. © 2014 Wiley Periodicals, Inc., A Wiley Company. JF - Journal of cellular physiology AU - Abbruzzese, Claudia AU - Diodoro, Maria Grazia AU - Sperduti, Isabella AU - Mileo, Anna Maria AU - Pattaro, Giada AU - De Salvo, Laura AU - Cosimelli, Maurizio AU - Perrotti, Nicola AU - Paggi, Marco G AD - Department of Experimental Oncology, Regina Elena National Cancer Institute, IRCCS, Rome, Italy. Y1 - 2015/03// PY - 2015 DA - March 2015 SP - 562 EP - 567 VL - 230 IS - 3 KW - Receptor, Insulin KW - EC 2.7.10.1 KW - Index Medicus KW - Disease-Free Survival KW - Cell Transformation, Neoplastic -- pathology KW - Phosphorylation KW - Humans KW - Adult KW - Treatment Outcome KW - Neoplasm Grading KW - HCT116 Cells KW - Cell Transformation, Neoplastic -- genetics KW - Adenomatous Polyposis Coli -- pathology KW - Adenomatous Polyposis Coli -- genetics KW - Receptor, Insulin -- isolation & purification KW - Prognosis KW - Adenomatous Polyposis Coli -- therapy KW - Receptor, Insulin -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627952851?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+physiology&rft.atitle=Detection+of+phosphorylated+insulin+receptor+in+colorectal+adenoma+and+adenocarcinoma%3A+implications+for+prognosis+and+clinical+outcome.&rft.au=Abbruzzese%2C+Claudia%3BDiodoro%2C+Maria+Grazia%3BSperduti%2C+Isabella%3BMileo%2C+Anna+Maria%3BPattaro%2C+Giada%3BDe+Salvo%2C+Laura%3BCosimelli%2C+Maurizio%3BPerrotti%2C+Nicola%3BPaggi%2C+Marco+G&rft.aulast=Abbruzzese&rft.aufirst=Claudia&rft.date=2015-03-01&rft.volume=230&rft.issue=3&rft.spage=562&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+physiology&rft.issn=1097-4652&rft_id=info:doi/10.1002%2Fjcp.24733 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-10 N1 - Date created - 2014-11-24 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/jcp.24733 ER - TY - JOUR T1 - Withanolide E sensitizes renal carcinoma cells to TRAIL-induced apoptosis by increasing cFLIP degradation. AN - 1669450944; 25719250 AB - Withanolide E, a steroidal lactone from Physalis peruviana, was found to be highly active for sensitizing renal carcinoma cells and a number of other human cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis. Withanolide E, the most potent and least toxic of five TRAIL-sensitizing withanolides identified, enhanced death receptor-mediated apoptotic signaling by a rapid decline in the levels of cFLIP proteins. Other mechanisms by which TRAIL sensitizers have been reported to work: generation of reactive oxygen species (ROS), changes in pro-and antiapoptotic protein expression, death receptor upregulation, activation of intrinsic (mitochondrial) apoptotic pathways, ER stress, and proteasomal inhibition proved to be irrelevant to withanolide E activity. Loss of cFLIP proteins was not due to changes in expression, but rather destabilization and/or aggregation, suggesting impairment of chaperone proteins leading to degradation. Indeed, withanolide E treatment altered the stability of a number of HSP90 client proteins, but with greater apparent specificity than the well-known HSP90 inhibitor geldanamycin. As cFLIP has been reported to be an HSP90 client, this provides a potentially novel mechanism for sensitizing cells to TRAIL. Sensitization of human renal carcinoma cells to TRAIL-induced apoptosis by withanolide E and its lack of toxicity were confirmed in animal studies. Owing to its novel activity, withanolide E is a promising reagent for the analysis of mechanisms of TRAIL resistance, for understanding HSP90 function, and for further therapeutic development. In marked contrast to bortezomib, among the best currently available TRAIL sensitizers, withanolide E's more specific mechanism of action suggests minimal toxic side effects. JF - Cell death & disease AU - Henrich, C J AU - Brooks, A D AU - Erickson, K L AU - Thomas, C L AU - Bokesch, H R AU - Tewary, P AU - Thompson, C R AU - Pompei, R J AU - Gustafson, K R AU - McMahon, J B AU - Sayers, T J AD - 1] Molecular Targets Laboratory, NCI-Frederick, Frederick, MD, USA [2] Basic Research Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA. ; 1] Basic Research Program, Leidos Biomedical Research, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD, USA [2] Laboratory for Experimental Immunology and Cancer Inflammation Program, NCI-Frederick, Frederick, MD, USA. ; 1] Molecular Targets Laboratory, NCI-Frederick, Frederick, MD, USA [2] Department of Chemistry, Clark University, Worcester, MA, USA. ; Molecular Targets Laboratory, NCI-Frederick, Frederick, MD, USA. ; Laboratory for Experimental Immunology and Cancer Inflammation Program, NCI-Frederick, Frederick, MD, USA. Y1 - 2015/02/26/ PY - 2015 DA - 2015 Feb 26 SP - 1 VL - 6 KW - Reactive Oxygen Species KW - 0 KW - TNF-Related Apoptosis-Inducing Ligand KW - Withanolides KW - Index Medicus KW - Animals KW - Blotting, Western KW - Humans KW - Immunoprecipitation KW - Cell Line, Tumor KW - Mice, Inbred BALB C KW - Reactive Oxygen Species -- pharmacology KW - Endoplasmic Reticulum Stress -- drug effects KW - TNF-Related Apoptosis-Inducing Ligand -- pharmacology KW - Carcinoma, Renal Cell -- metabolism KW - Apoptosis -- drug effects KW - Withanolides -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1669450944?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+death+%26+disease&rft.atitle=Withanolide+E+sensitizes+renal+carcinoma+cells+to+TRAIL-induced+apoptosis+by+increasing+cFLIP+degradation.&rft.au=Henrich%2C+C+J%3BBrooks%2C+A+D%3BErickson%2C+K+L%3BThomas%2C+C+L%3BBokesch%2C+H+R%3BTewary%2C+P%3BThompson%2C+C+R%3BPompei%2C+R+J%3BGustafson%2C+K+R%3BMcMahon%2C+J+B%3BSayers%2C+T+J&rft.aulast=Henrich&rft.aufirst=C&rft.date=2015-02-26&rft.volume=6&rft.issue=&rft.spage=e1666&rft.isbn=&rft.btitle=&rft.title=Cell+death+%26+disease&rft.issn=2041-4889&rft_id=info:doi/10.1038%2Fcddis.2015.38 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-22 N1 - Date created - 2015-02-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Apoptosis. 2011 Oct;16(10):1014-27 [21710254] J Hepatol. 2011 Dec;55(6):1272-80 [21703207] Mol Cancer Ther. 2012 Jan;11(1):3-13 [22234808] Apoptosis. 2012 Apr;17(4):349-63 [22072062] Clin Exp Dermatol. 2012 Apr;37(3):259-65 [22103668] J Nat Prod. 2012 Mar 23;75(3):394-9 [22313254] Biochem Pharmacol. 2012 Jun 1;83(11):1475-83 [22230480] Exp Cell Res. 2012 Jul 1;318(11):1324-31 [22309778] PLoS One. 2012;7(5):e37764 [22701533] Expert Opin Ther Targets. 2012 Aug;16(8):801-17 [22762543] Eur J Med Chem. 2012 Aug;54:499-511 [22705001] Exp Oncol. 2012 Oct;34(3):176-84 [23070002] Biochem Pharmacol. 2012 Nov 15;84(10):1282-91 [22981382] Oncogene. 2012 Nov 1;31(44):4677-88 [22266862] PLoS One. 2012;7(11):e50547 [23226310] Sci Signal. 2012 Dec 18;5(255):ra93 [23250397] Crit Rev Oncol Hematol. 2013 Mar;85(3):363-72 [22944363] Oncogene. 2013 Mar 14;32(11):1341-50 [22580613] Cell Death Differ. 2013 Jul;20(7):858-68 [23579241] Br J Pharmacol. 2013 Aug;169(8):1723-44 [23638798] Cell Death Differ. 2008 Apr;15(4):751-61 [18219321] Oncogene. 2008 May 15;27(22):3211-20 [18084329] Free Radic Biol Med. 2009 Jun 15;46(12):1639-49 [19345731] Cancer Immunol Immunother. 2009 Aug;58(8):1229-44 [19089423] Cell Death Dis. 2013;4:e778 [23969857] Gastroenterology. 2013 Dec;145(6):1369-79 [24036366] Trends Cell Biol. 2013 Dec;23(12):612-9 [24060597] Cancer Res. 2013 Dec 1;73(23):7022-33 [24121490] Cell Rep. 2013 Oct 31;5(2):397-408 [24209745] J Biol Chem. 2014 Jan 17;289(3):1852-65 [24297176] Invest New Drugs. 2014 Feb;32(1):68-74 [23887853] J Med Chem. 2014 Apr 10;57(7):2851-63 [24625088] Adv Exp Med Biol. 2014;818:167-80 [25001536] Cell Death Differ. 2014 Sep;21(9):1350-64 [24948009] Mol Carcinog. 2015 Jun;54(6):417-29 [24293234] Apoptosis. 2007 Nov;12(11):2115-33 [17874299] Neoplasia. 2002 Nov-Dec;4(6):551-7 [12407450] J Clin Oncol. 2002 Nov 15;20(22):4420-7 [12431963] Blood. 2003 Jul 1;102(1):303-10 [12637321] Lab Invest. 2003 Jul;83(7):1033-43 [12861043] Proc Natl Acad Sci U S A. 1991 May 1;88(9):3671-5 [2023917] Cancer Immunol Immunother. 2005 May;54(5):499-505 [15614529] J Biol Chem. 2005 May 13;280(19):19401-9 [15760909] Mol Cancer Ther. 2006 Jun;5(6):1434-45 [16818501] Clin Cancer Res. 2007 Jun 1;13(11):3403-12 [17545549] J Nat Prod. 2007 Jul;70(7):1146-52 [17580910] Cancer Res. 2007 Oct 1;67(19):9482-9 [17909058] Molecules. 2009;14(7):2373-93 [19633611] Biochem Pharmacol. 2010 Feb 15;79(4):542-51 [19769945] Mol Cancer Res. 2010 May;8(5):729-38 [20442297] Nat Rev Cancer. 2010 Aug;10(8):537-49 [20651736] Mol Cancer. 2010;9:239 [20836852] J Nat Prod. 2010 Dec 27;73(12):2013-8 [21067210] Cancer Cell. 2011 Jan 18;19(1):101-13 [21251615] Cancer Res. 2011 Mar 1;71(5):1883-92 [21363923] Nat Prod Rep. 2011 Apr;28(4):705-40 [21344104] Cancer Immunol Immunother. 2011 Aug;60(8):1173-80 [21626033] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/cddis.2015.38 ER - TY - JOUR T1 - A mutant p53/let-7i-axis-regulated gene network drives cell migration, invasion and metastasis. AN - 1659767959; 24662829 AB - Most p53 mutations in human cancers are missense mutations resulting in a full-length mutant p53 protein. Besides losing tumor suppressor activity, some hotspot p53 mutants gain oncogenic functions. This effect is mediated in part, through gene expression changes due to inhibition of p63 and p73 by mutant p53 at their target gene promoters. Here, we report that the tumor suppressor microRNA let-7i is downregulated by mutant p53 in multiple cell lines expressing endogenous mutant p53. In breast cancer patients, significantly decreased let-7i levels were associated with missense mutations in p53. Chromatin immunoprecipitation and promoter luciferase assays established let-7i as a transcriptional target of mutant p53 through p63. Introduction of let-7i to mutant p53 cells significantly inhibited migration, invasion and metastasis by repressing a network of oncogenes including E2F5, LIN28B, MYC and NRAS. Our findings demonstrate that repression of let-7i expression by mutant p53 has a key role in enhancing migration, invasion and metastasis. JF - Oncogene AU - Subramanian, M AU - Francis, P AU - Bilke, S AU - Li, X L AU - Hara, T AU - Lu, X AU - Jones, M F AU - Walker, R L AU - Zhu, Y AU - Pineda, M AU - Lee, C AU - Varanasi, L AU - Yang, Y AU - Martinez, L A AU - Luo, J AU - Ambs, S AU - Sharma, S AU - Wakefield, L M AU - Meltzer, P S AU - Lal, A AD - Genetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Department of Biochemistry and Molecular Biology, College of Medicine, Howard University, Washington, DC, USA. ; Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Department of Biochemistry, University of Mississippi Cancer Institute, University of Mississippi Medical Center, Jackson, MS, USA. ; Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Laboratory of Human Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2015/02/26/ PY - 2015 DA - 2015 Feb 26 SP - 1094 EP - 1104 VL - 34 IS - 9 KW - MicroRNAs KW - 0 KW - RNA, Small Interfering KW - TP53 protein, human KW - TP63 protein, human KW - Transcription Factors KW - Tumor Suppressor Protein p53 KW - Tumor Suppressor Proteins KW - mirnlet7 microRNA, human KW - Index Medicus KW - Cell Movement KW - Animals KW - Transcription Factors -- metabolism KW - DNA Mutational Analysis KW - Humans KW - Cell Line, Tumor KW - Mice KW - Mice, Nude KW - Neoplasm Invasiveness -- genetics KW - Mutation, Missense KW - Neoplasm Transplantation KW - Neoplasm Metastasis -- genetics KW - Down-Regulation KW - Neoplasm Invasiveness -- pathology KW - Tumor Suppressor Proteins -- metabolism KW - RNA, Small Interfering -- pharmacology KW - Neoplasm Metastasis -- pathology KW - Female KW - Neoplasms -- pathology KW - MicroRNAs -- genetics KW - Gene Regulatory Networks -- drug effects KW - Tumor Suppressor Protein p53 -- genetics KW - MicroRNAs -- antagonists & inhibitors KW - Tumor Suppressor Protein p53 -- metabolism KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1659767959?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=A+mutant+p53%2Flet-7i-axis-regulated+gene+network+drives+cell+migration%2C+invasion+and+metastasis.&rft.au=Subramanian%2C+M%3BFrancis%2C+P%3BBilke%2C+S%3BLi%2C+X+L%3BHara%2C+T%3BLu%2C+X%3BJones%2C+M+F%3BWalker%2C+R+L%3BZhu%2C+Y%3BPineda%2C+M%3BLee%2C+C%3BVaranasi%2C+L%3BYang%2C+Y%3BMartinez%2C+L+A%3BLuo%2C+J%3BAmbs%2C+S%3BSharma%2C+S%3BWakefield%2C+L+M%3BMeltzer%2C+P+S%3BLal%2C+A&rft.aulast=Subramanian&rft.aufirst=M&rft.date=2015-02-26&rft.volume=34&rft.issue=9&rft.spage=1094&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2014.46 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-24 N1 - Date created - 2015-02-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Cell Biol. 2012 Apr;14(4):366-74 [22407364] Nature. 1989 Dec 7;342(6250):705-8 [2531845] Mol Cell Biol. 1998 Jul;18(7):3735-43 [9632756] Mol Cell Biol. 1999 Feb;19(2):1438-49 [9891077] Genes Dev. 1999 Oct 1;13(19):2490-501 [10521394] Cell. 2005 Mar 11;120(5):635-47 [15766527] Mol Cell Biol. 2005 Nov;25(22):10097-110 [16260623] Cell. 2006 Jan 13;124(1):207-19 [16413492] Cancer Cell. 2006 Sep;10(3):191-202 [16959611] Gene. 2006 Dec 15;384:51-61 [16971064] Int J Cancer. 2007 Feb 15;120(4):796-805 [17096325] Oncogene. 2007 Apr 2;26(15):2220-5 [17401431] Mol Cell. 2007 Jun 8;26(5):731-43 [17540598] Mol Cell. 2007 Jun 8;26(5):745-52 [17540599] Nature. 2007 Jun 28;447(7148):1130-4 [17554337] Cancer Res. 2007 Aug 15;67(16):7713-22 [17699775] Cancer Res. 2007 Oct 15;67(20):9762-70 [17942906] Cell Cycle. 2008 Mar 15;7(6):759-64 [18344688] Nature. 2008 Sep 4;455(7209):64-71 [18668037] Proc Natl Acad Sci U S A. 2008 Sep 30;105(39):14879-84 [18812516] Trends Cell Biol. 2008 Oct;18(10):505-16 [18774294] Cell. 2009 Jan 23;136(2):215-33 [19167326] Cell. 2009 Apr 3;137(1):87-98 [19345189] Mol Cell. 2009 Sep 11;35(5):610-25 [19748357] J Biol Chem. 2010 Jan 1;285(1):216-25 [19903813] Cell. 2009 Dec 24;139(7):1327-41 [20064378] Cancer Cell. 2010 Mar 16;17(3):273-85 [20227041] Nat Struct Mol Biol. 2010 Oct;17(10):1169-74 [20924405] Cancer Res. 2011 Mar 15;71(6):2034-7 [21406394] Cancer Cell. 2011 Jul 12;20(1):79-91 [21741598] Blood. 2011 Jul 28;118(4):903-15 [21653321] Cell. 2011 Sep 30;147(1):81-94 [21962509] Oncogene. 2011 Oct 6;30(40):4185-93 [21625210] Mol Cell Biol. 2011 Nov;31(22):4464-81 [21930790] PLoS Genet. 2011 Nov;7(11):e1002363 [22102825] Cell. 2012 Jan 20;148(1-2):244-58 [22265415] Br J Cancer. 2012 Apr 10;106(8):1415-23 [22433967] Science. 2012 Apr 13;336(6078):237-40 [22499947] Genes Dev. 2012 Apr 15;26(8):830-45 [22508727] Cell Death Differ. 2012 Jun;19(6):1038-48 [22193543] Genes Dev. 2012 Jun 15;26(12):1268-86 [22713868] Nat Rev Cancer. 2012 Sep;12(9):613-26 [22898542] Nat Cell Biol. 2013 Jan;15(1):2-8 [23263379] PLoS One. 2013;8(1):e55214 [23358900] Oncogene. 2013 Mar 7;32(10):1252-65 [22580601] Cell Death Dis. 2013;4:e574 [23559009] Oncogene. 2013 Jun 13;32(24):2992-3000 [22797073] Oncogene. 2013 Jul 4;32(27):3286-95 [22847613] Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3384-9 [19211792] Nat Genet. 2000 May;25(1):47-54 [10802655] Mol Cell Biol. 2001 Mar;21(5):1874-87 [11238924] J Biol Chem. 2001 Oct 19;276(42):39359-67 [11483599] J Biol Chem. 2002 May 24;277(21):18817-26 [11893750] Nat Rev Cancer. 2002 Aug;2(8):594-604 [12154352] Cancer Cell. 2003 Apr;3(4):403-10 [12726865] Nat Struct Mol Biol. 2012 Mar;19(3):321-7 [22343717] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/onc.2014.46 ER - TY - JOUR T1 - Adenovirus vectors as HIV-1 vaccines: where are we? What next? AN - 1808693022; PQ0003241689 AB - Although antibody studies have moved to the forefront of HIV-1 vaccine research since the RV144 trial [1,2], it seems likely that complementary CD8 super(+) T-cell immunity will be necessary. This is the best defined protective factor in established HIV-1 infection, based on numerous lines of evidence, including reduced simian immunodeficiency virus (SIV) containment after depletion of CD8 super(+) cells in infected macaques [3-5], HIV-1 sequence evolution predominately in CD8 super(+) T-cell epitopes [6], class I human leukocyte antigen (HLA-I) locus being the greatest genetic determinant of immune control [7] and temporal correlation of the CD8 super(+) T-cell response to drop of viremia during acute infection [8,9]. Although less certain, this arm of immunity may contribute to preventing HIV-1 infection as well. HIV-1-specific CD8 super(+) T cells can kill infected cells before virion production and sterilize viral cultures in vitro [10,11], and have been observed in some highly exposed yet uninfected persons such as a cohort of commercial sex workers in Nairobi [12]. JF - AIDS AU - D'Souza, Marie Patricia AU - Yang, Otto O AD - Division of AIDS, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland, oyang@mednet.ucla.edu. Y1 - 2015/02/20/ PY - 2015 DA - 2015 Feb 20 SP - 395 EP - 400 PB - Lippincott Williams & Wilkins, Inc, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 29 IS - 4 SN - 0269-9370, 0269-9370 KW - Health & Safety Science Abstracts; Immunology Abstracts; Virology & AIDS Abstracts KW - adenovirus KW - HIV-1 KW - HVTN 505 KW - Step trial KW - vaccine KW - Virions KW - Histocompatibility antigen HLA KW - Acquired immune deficiency syndrome KW - Cell culture KW - Infection KW - Swine influenza virus KW - Expression vectors KW - Human immunodeficiency virus 1 KW - Lymphocytes T KW - Containment KW - Epitopes KW - Macaca KW - Adenovirus KW - Kenya, Nairobi KW - Prostitution KW - CD8 antigen KW - Immunity KW - Antibodies KW - Human immunodeficiency virus KW - Viremia KW - Vaccines KW - Simian immunodeficiency virus KW - Evolution KW - V 22360:AIDS and HIV KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808693022?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=AIDS&rft.atitle=Adenovirus+vectors+as+HIV-1+vaccines%3A+where+are+we%3F+What+next%3F&rft.au=D%27Souza%2C+Marie+Patricia%3BYang%2C+Otto+O&rft.aulast=D%27Souza&rft.aufirst=Marie&rft.date=2015-02-20&rft.volume=29&rft.issue=4&rft.spage=395&rft.isbn=&rft.btitle=&rft.title=AIDS&rft.issn=02699370&rft_id=info:doi/10.1097%2FQAD.0000000000000548 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-04 N1 - SubjectsTermNotLitGenreText - Histocompatibility antigen HLA; Virions; Prostitution; Cell culture; Immunity; CD8 antigen; Infection; Expression vectors; Antibodies; Lymphocytes T; Vaccines; Viremia; Evolution; Epitopes; Acquired immune deficiency syndrome; Containment; Human immunodeficiency virus; Macaca; Human immunodeficiency virus 1; Adenovirus; Swine influenza virus; Simian immunodeficiency virus; Kenya, Nairobi DO - http://dx.doi.org/10.1097/QAD.0000000000000548 ER - TY - JOUR T1 - How I treat classical Hodgkin lymphoma in patients infected with human immunodeficiency virus. AN - 1657321112; 25499453 AB - HIV-associated classical Hodgkin lymphoma (HIV-cHL) is an important complication of HIV disease in the era of effective combination antiretroviral therapy (cART). Generally, newly diagnosed HIV-cHL should be managed with curative intent. With modern HIV therapeutics, HIV-cHL treatment outcomes are largely comparable to those of the background population with cHL (non-HIV-cHL). To achieve these outcomes, particular attention must be given to managing HIV. This management includes understanding HIV as a comorbid condition with a spectrum of impact that is unique to each patient. Meticulous attention to drug-drug interactions is required to avoid toxicity and pharmacokinetic effects that can undermine cure. Relapsed and refractory HIV-cHL poses additional therapeutic challenges. The standard management in this setting should also be based on that for non-HIV-cHL, and includes the use of salvage chemotherapy followed by autologous stem cell transplant in chemosensitive disease. The role of allogeneic hematopoietic stem cell transplant is less clear but may be useful in select cases. Newer agents with activity in cHL are being tested as part of primary and salvage therapy and are also highly relevant for HIV-cHL. JF - Blood AU - Uldrick, Thomas S AU - Little, Richard F AD - HIV and AIDS Malignancy Branch, Center for Cancer Research, and. ; HIV and AIDS Malignancy Branch, Center for Cancer Research, and Clinical Investigations Branch, Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, MD. Y1 - 2015/02/19/ PY - 2015 DA - 2015 Feb 19 SP - 1226 EP - 35; quiz 1355 VL - 125 IS - 8 KW - Anti-Retroviral Agents KW - 0 KW - Bleomycin KW - 11056-06-7 KW - Vinblastine KW - 5V9KLZ54CY KW - Dacarbazine KW - 7GR28W0FJI KW - Doxorubicin KW - 80168379AG KW - Abridged Index Medicus KW - Index Medicus KW - Vinblastine -- therapeutic use KW - Dacarbazine -- therapeutic use KW - Lymphatic Metastasis KW - Humans KW - Adult KW - Doxorubicin -- therapeutic use KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - HIV-1 KW - Bleomycin -- therapeutic use KW - Male KW - Anti-Retroviral Agents -- therapeutic use KW - Hodgkin Disease -- pathology KW - HIV Infections -- virology KW - HIV Infections -- complications KW - HIV Infections -- therapy KW - Hodgkin Disease -- virology KW - Hodgkin Disease -- therapy KW - Hodgkin Disease -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1657321112?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=How+I+treat+classical+Hodgkin+lymphoma+in+patients+infected+with+human+immunodeficiency+virus.&rft.au=Uldrick%2C+Thomas+S%3BLittle%2C+Richard+F&rft.aulast=Uldrick&rft.aufirst=Thomas&rft.date=2015-02-19&rft.volume=125&rft.issue=8&rft.spage=1226&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=1528-0020&rft_id=info:doi/10.1182%2Fblood-2014-08-551598 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-24 N1 - Date created - 2015-02-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Leuk Lymphoma. 2012 Dec;53(12):2383-9 [22642936] J Clin Oncol. 2012 Nov 20;30(33):4111-6 [23045581] J Clin Oncol. 2012 Nov 20;30(33):4117-23 [23045592] Blood. 2012 Nov 29;120(23):4488-95 [22821764] J Clin Oncol. 2013 Feb 20;31(6):692-700 [23182984] PLoS One. 2013;8(10):e77409 [24098586] Lancet Oncol. 2013 Dec;14(13):1348-56 [24239220] Hematology Am Soc Hematol Educ Program. 2013;2013:382-8 [24319208] Mod Pathol. 2013 May;26(5):648-57 [23307058] J Clin Oncol. 2014 Sep 20;32(27):3048-58 [25113771] J Acquir Immune Defic Syndr. 2000 Aug 15;24(5):444-50 [11035615] JAMA. 2001 Apr 4;285(13):1736-45 [11277828] Blood. 2001 Oct 15;98(8):2339-44 [11588028] Clin Infect Dis. 2002 Apr 15;34(8):1115-21 [11915001] AIDS. 2002 May 24;16(8):1155-61 [12004274] AIDS. 2002 Sep 27;16(14):1973-6 [12351963] AIDS. 2003 Jan 3;17(1):81-7 [12478072] N Engl J Med. 1998 Nov 19;339(21):1506-14 [9819449] Blood. 1999 Apr 1;93(7):2319-26 [10090942] Ann Oncol. 1999 Feb;10(2):189-95 [10093688] Blood. 2005 Jan 15;105(2):874-8 [15388574] Blood. 2003 Jun 15;101(12):4653-9 [12609827] Lancet. 2003 Sep 20;362(9388):959-61 [14511930] HIV Med. 2013 Sep;14(8):481-90 [23560682] J Natl Cancer Inst. 2013 Aug 21;105(16):1221-9 [23892362] Ann Hematol. 2005 Oct;84(10):661-6 [15875183] Blood. 2006 Jan 1;107(1):52-9 [16150944] AIDS. 2006 Apr 24;20(7):985-93 [16603850] Cancer Res. 2006 Jun 1;66(11):5716-22 [16740709] Blood. 2006 Dec 1;108(12):3786-91 [16917006] Ann Oncol. 2007 Feb;18(2):376-80 [17071938] J Clin Oncol. 2007 Feb 10;25(5):579-86 [17242396] J Clin Oncol. 2007 Aug 20;25(24):3746-52 [17646666] Blood. 2007 Nov 15;110(10):3715-21 [17682125] Biol Blood Marrow Transplant. 2008 Jan;14(1):59-66 [18158962] Blood. 2008 Feb 15;111(4):2339-46 [18070985] J Clin Oncol. 2008 Mar 1;26(7):1027-32 [18309938] J Acquir Immune Defic Syndr. 2008 Apr 1;47(4):422-8 [18434957] Am J Pathol. 2008 Jul;173(1):195-204 [18502823] Blood. 2009 Mar 19;113(12):2765-3775 [19096012] J Clin Oncol. 2009 May 1;27(13):2192-8 [19332732] Blood. 2009 Aug 13;114(7):1306-13 [19451551] Leuk Lymphoma. 2009 Oct;50(10):1718-20 [19757300] N Engl J Med. 2010 Mar 11;362(10):875-85 [20220182] Blood. 2010 Apr 15;115(15):3017-24 [20130244] AIDS. 2010 Jun 1;24(9):1299-306 [20559036] Ann Intern Med. 2010 Oct 5;153(7):452-60 [20921544] Q J Nucl Med Mol Imaging. 2010 Dec;54(6):698-703 [21150859] Haematologica. 2011 Feb;96(2):269-76 [21071500] Cancer. 2011 Mar 1;117(5):1089-96 [20960504] J Natl Cancer Inst. 2011 May 4;103(9):753-62 [21483021] Blood. 2011 Jun 9;117(23):6100-8 [21368291] Blood. 2011 Jul 7;118(1):44-9 [21551234] N Engl J Med. 2011 Jul 21;365(3):203-12 [21774708] J Acquir Immune Defic Syndr. 2011 Apr 15;56(5):460-6 [21239997] J Clin Virol. 2011 Dec;52(4):328-32 [21924674] Pathol Int. 2012 Feb;62(2):77-83 [22243776] Cancer Epidemiol Biomarkers Prev. 2014 Feb;23(2):274-81 [24326629] AIDS. 2014 Mar 27;28(6):881-90 [24300545] Haematologica. 2014 Jun;99(6):1107-13 [24658820] Clin Infect Dis. 2014 Jul 15;59(2):279-86 [24755860] Cancer Epidemiol. 2014 Aug;38(4):386-92 [24947588] Br J Haematol. 2014 Sep;166(6):875-90 [25041527] J Clin Oncol. 2014 Sep 1;32(25):2705-11 [25071108] Histopathology. 2014 Dec;65(6):749-56 [24809535] Br J Haematol. 2004 May;125(4):455-62 [15142115] Am J Clin Pathol. 2004 May;121(5):727-38 [15151213] Leuk Lymphoma. 2003;44 Suppl 3:S63-8 [15202527] N Engl J Med. 1986 Apr 3;314(14):874-9 [3005862] Lancet. 1991 Feb 9;337(8737):320-2 [1671232] Blood. 1992 Jul 15;80(2):484-91 [1320954] J Pathol. 1992 Aug;167(4):381-4 [1328576] Am J Pathol. 1993 Apr;142(4):1073-9 [8386441] Proc Natl Acad Sci U S A. 1993 Oct 1;90(19):9150-4 [8415670] Cancer. 1994 Jan 15;73(2):437-44 [7507401] J Clin Oncol. 1995 Jul;13(7):1758-67 [7541452] J Exp Med. 1996 Oct 1;184(4):1495-505 [8879220] AIDS. 1998 Jan 1;12(1):65-74 [9456256] AIDS Patient Care STDS. 2013 May;27(5):259-65 [23600703] AIDS. 2013 Mar 27;27(6):1033-5 [23698067] N Engl J Med. 2012 Feb 2;366(5):399-408 [22149921] AIDS. 2012 Apr 24;26(7):861-5 [22333746] J Acquir Immune Defic Syndr. 2012 Jun 1;60(2):150-7 [22395672] J Clin Oncol. 2012 Jun 20;30(18):2183-9 [22454421] Blood. 2012 Oct 18;120(16):3280-7 [22948049] Blood. 2012 Oct 25;120(17):3530-40 [22955918] Leuk Lymphoma. 2012 Dec;53(12):2390-6 [22642935] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1182/blood-2014-08-551598 ER - TY - JOUR T1 - The POLD3 subunit of DNA polymerase δ can promote translesion synthesis independently of DNA polymerase ζ. AN - 1657315152; 25628356 AB - The replicative DNA polymerase Polδ consists of a catalytic subunit POLD1/p125 and three regulatory subunits POLD2/p50, POLD3/p66 and POLD4/p12. The ortholog of POLD3 in Saccharomyces cerevisiae, Pol32, is required for a significant proportion of spontaneous and UV-induced mutagenesis through its additional role in translesion synthesis (TLS) as a subunit of DNA polymerase ζ. Remarkably, chicken DT40 B lymphocytes deficient in POLD3 are viable and able to replicate undamaged genomic DNA with normal kinetics. Like its counterpart in yeast, POLD3 is required for fully effective TLS, its loss resulting in hypersensitivity to a variety of DNA damaging agents, a diminished ability to maintain replication fork progression after UV irradiation and a significant decrease in abasic site-induced mutagenesis in the immunoglobulin loci. However, these defects appear to be largely independent of Polζ, suggesting that POLD3 makes a significant contribution to TLS independently of Polζ in DT40 cells. Indeed, combining polη, polζ and pold3 mutations results in synthetic lethality. Additionally, we show in vitro that POLD3 promotes extension beyond an abasic by the Polδ holoenzyme suggesting that while POLD3 is not required for normal replication, it may help Polδ to complete abasic site bypass independently of canonical TLS polymerases. © The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research. JF - Nucleic acids research AU - Hirota, Kouji AU - Yoshikiyo, Kazunori AU - Guilbaud, Guillaume AU - Tsurimoto, Toshiki AU - Murai, Junko AU - Tsuda, Masataka AU - Phillips, Lara G AU - Narita, Takeo AU - Nishihara, Kana AU - Kobayashi, Kaori AU - Yamada, Kouich AU - Nakamura, Jun AU - Pommier, Yves AU - Lehmann, Alan AU - Sale, Julian E AU - Takeda, Shunichi AD - Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshidakonoe, Sakyo-ku, Kyoto 606-8501, Japan Department of Chemistry, GraduateSchool of Science and Engineering, Tokyo Metropolitan University, Minami-Osawa, Hachioji- shi, Tokyo 192-0397, Japan. ; Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshidakonoe, Sakyo-ku, Kyoto 606-8501, Japan. ; Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK. ; Department of Biology, School of Sciences, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan. ; Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshidakonoe, Sakyo-ku, Kyoto 606-8501, Japan Laboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. ; Department of Chemistry, GraduateSchool of Science and Engineering, Tokyo Metropolitan University, Minami-Osawa, Hachioji- shi, Tokyo 192-0397, Japan. ; Division of Genetic Biochemistry, National Institute of Health and Nutrition, Tokyo 162-8636, Japan. ; Department of Environmental Sciences and Engineering, University of North Carolina, Chapel Hill, NC 27599, USA. ; Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton BN1 9RQ, UK. ; Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge CB2 0QH, UK jes@mrc-lmb.cam.ac.uk. ; Department of Radiation Genetics, Graduate School of Medicine, Kyoto University, Yoshidakonoe, Sakyo-ku, Kyoto 606-8501, Japan stakeda@rg.med.kyoto-u.ac.jp. Y1 - 2015/02/18/ PY - 2015 DA - 2015 Feb 18 SP - 1671 EP - 1683 VL - 43 IS - 3 KW - DNA Primers KW - 0 KW - DNA Polymerase III KW - EC 2.7.7.- KW - DNA polymerase zeta KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Index Medicus KW - Polymerase Chain Reaction KW - Animals KW - Chickens KW - Base Sequence KW - S Phase KW - Reverse Transcriptase Polymerase Chain Reaction KW - Cell Line KW - DNA-Directed DNA Polymerase -- metabolism KW - DNA Repair KW - DNA Damage KW - DNA Polymerase III -- chemistry KW - DNA Polymerase III -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1657315152?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=The+POLD3+subunit+of+DNA+polymerase+%CE%B4+can+promote+translesion+synthesis+independently+of+DNA+polymerase+%CE%B6.&rft.au=Hirota%2C+Kouji%3BYoshikiyo%2C+Kazunori%3BGuilbaud%2C+Guillaume%3BTsurimoto%2C+Toshiki%3BMurai%2C+Junko%3BTsuda%2C+Masataka%3BPhillips%2C+Lara+G%3BNarita%2C+Takeo%3BNishihara%2C+Kana%3BKobayashi%2C+Kaori%3BYamada%2C+Kouich%3BNakamura%2C+Jun%3BPommier%2C+Yves%3BLehmann%2C+Alan%3BSale%2C+Julian+E%3BTakeda%2C+Shunichi&rft.aulast=Hirota&rft.aufirst=Kouji&rft.date=2015-02-18&rft.volume=43&rft.issue=3&rft.spage=1671&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=1362-4962&rft_id=info:doi/10.1093%2Fnar%2Fgkv023 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-18 N1 - Date created - 2015-02-18 N1 - Date revised - 2017-01-24 N1 - SuppNotes - Cited By: Biochimie. 2009 Sep;91(9):1163-72 [19540301] Proc Natl Acad Sci U S A. 2009 Jun 16;106(24):9631-6 [19487673] Cell Cycle. 2010 Feb 15;9(4):729-35 [20139724] J Cell Biol. 2010 Jun 28;189(7):1117-27 [20584917] PLoS Genet. 2010 Oct;6(10). pii: e1001151. doi: 10.1371/journal.pgen.1001151 [20949111] J Mol Biol. 2010 Nov 19;404(1):34-44 [20888339] Genes Cells. 2010 Dec;15(12):1228-39 [21070511] Nat Chem Biol. 2012 Jan;8(1):125-32 [22119860] PLoS Comput Biol. 2011 Dec;7(12):e1002322 [22219720] J Biol Chem. 2012 May 18;287(21):17281-7 [22465957] PLoS One. 2012;7(6):e39156 [22723953] Proc Natl Acad Sci U S A. 2012 Jul 31;109(31):12455-60 [22711820] Methods Mol Biol. 2012;920:417-32 [22941620] Environ Mol Mutagen. 2012 Dec;53(9):666-82 [23065663] Nucleic Acids Res. 2012 Dec;40(22):11618-26 [23066099] Nucleic Acids Res. 2013 May;41(9):4913-25 [23535143] Science. 2014 Jan 3;343(6166):88-91 [24310611] Cell Cycle. 2014;13(1):23-31 [24300032] DNA Repair (Amst). 2014 Dec;24:138-49 [24819597] Curr Genet. 2000 Nov;38(4):178-87 [11126776] Genes Dev. 2001 Apr 15;15(8):945-54 [11316789] J Biochem. 2001 May;129(5):699-708 [11328591] Nature. 2001 Aug 30;412(6850):921-6 [11528482] J Biol Chem. 2002 Feb 8;277(6):3894-901 [11711545] Science. 2002 Feb 15;295(5558):1301-6 [11847344] Genetics. 2002 Apr;160(4):1409-22 [11973297] Nature. 2002 Sep 5;419(6902):43-8 [12214226] J Biol Chem. 2002 Sep 27;277(39):36853-62 [12124382] EMBO J. 2002 Oct 15;21(20):5558-66 [12374756] J Biol Chem. 2002 Dec 13;277(50):48690-5 [12356753] EMBO J. 2003 Apr 1;22(7):1654-64 [12660171] EMBO J. 2003 Jun 16;22(12):3188-97 [12805232] DNA Repair (Amst). 2004 Jul 2;3(7):693-702 [15177178] Nat Immunol. 2004 Jul;5(7):707-12 [15195091] EMBO J. 1989 Jun;8(6):1849-54 [2670563] Cell. 1992 Apr 17;69(2):367-74 [1348971] Proc Natl Acad Sci U S A. 1994 Sep 13;91(19):9047-51 [8090767] Carcinogenesis. 1997 Apr;18(4):605-10 [9111189] J Cell Biol. 1998 Mar 23;140(6):1285-95 [9508763] J Biol Chem. 1998 Jul 31;273(31):19747-55 [9677405] Genetics. 2005 Feb;169(2):575-82 [15520252] Genetics. 2005 Apr;169(4):1939-55 [15687278] J Immunol. 2006 Jan 1;176(1):365-71 [16365429] J Exp Med. 2006 Feb 20;203(2):319-23 [16476771] Mol Immunol. 2006 Apr;43(10):1587-94 [16263170] J Biol Chem. 2006 May 12;281(19):13388-95 [16497663] Mol Cell. 2006 Oct 6;24(1):115-25 [17018297] PLoS Biol. 2006 Nov;4(11):e366 [17105346] J Biol Chem. 2006 Dec 15;281(50):38244-56 [17050527] Nature. 2007 Aug 16;448(7155):820-3 [17671506] Mol Cell. 2008 Apr 25;30(2):137-44 [18439893] Mol Cell. 2008 May 23;30(4):519-29 [18498753] Mol Cell Biol. 2008 Oct;28(19):6113-22 [18662998] PLoS One. 2009;4(1):e4184 [19145245] Nucleic Acids Res. 2009 Feb;37(2):647-57 [19074196] PLoS Genet. 2009 Jan;5(1):e1000356 [19180185] Adv Exp Med Biol. 2008;637:28-38 [19181108] DNA Repair (Amst). 2009 Dec 3;8(12):1444-51 [19783229] N1 - Last updated - 2017-01-25 DO - http://dx.doi.org/10.1093/nar/gkv023 ER - TY - JOUR T1 - Effect of Biofilms on Recalcitrance of Staphylococcal Joint Infection to Antibiotic Treatment AN - 1687676599; PQ0001530158 AB - The pathogenesis of joint infections is not well understood. In particular, we do not know why these infections respond poorly to antibiotic treatment. Here we show that methicillin-resistant Staphylococcus aureus, a major cause of joint infections, forms exceptionally strong biofilmlike aggregates in human synovial fluid (SF), to an extent significantly exceeding biofilm formation observed in growth medium or serum. Screening a transposon bank identified bacterial fibronectin- and fibrinogen-binding proteins as important for the formation of macroscopic clumps in SF, suggesting an important role of fibrin-containing clots in the formation of bacterial aggregates during joint infection. Pretreatment of SF with plasmin led to a strongly reduced formation of aggregates and increased susceptibility to antibiotics. These results give important insight into the pathogenesis of staphylococcal joint infection and the mechanisms underlying resistance to treatment. Furthermore, they point toward a potential novel approach for treating joint infections. JF - Journal of Infectious Diseases AU - Dastgheyb, Sana AU - Parvizi, Javad AU - Shapiro, Irving M AU - Hickok, Noreen J AU - Otto, Michael AD - National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland; Department of Orthopedic Surgery, Thomas Jefferson University, motto@niaid.nih.gov Y1 - 2015/02/15/ PY - 2015 DA - 2015 Feb 15 SP - 641 EP - 650 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 211 IS - 4 SN - 0022-1899, 0022-1899 KW - Microbiology Abstracts B: Bacteriology KW - Staphylococcus aureus KW - MRSA KW - antibiotic resistance KW - joint infection KW - septic arthritis KW - biofilm KW - Transposons KW - Plasmin KW - Synovial fluid KW - Drug resistance KW - Joint diseases KW - Antibiotics KW - Biofilms KW - Infection KW - Fibrinogen-binding protein KW - J 02320:Cell Biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687676599?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Effect+of+Biofilms+on+Recalcitrance+of+Staphylococcal+Joint+Infection+to+Antibiotic+Treatment&rft.au=Dastgheyb%2C+Sana%3BParvizi%2C+Javad%3BShapiro%2C+Irving+M%3BHickok%2C+Noreen+J%3BOtto%2C+Michael&rft.aulast=Dastgheyb&rft.aufirst=Sana&rft.date=2015-02-15&rft.volume=211&rft.issue=4&rft.spage=641&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiu514 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-06-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Transposons; Plasmin; Synovial fluid; Drug resistance; Joint diseases; Antibiotics; Biofilms; Infection; Fibrinogen-binding protein; Staphylococcus aureus DO - http://dx.doi.org/10.1093/infdis/jiu514 ER - TY - JOUR T1 - Bortezomib reduces pre-existing antibodies to recombinant immunotoxins in mice. AN - 1653125542; 25560410 AB - Recombinant immunotoxin (RIT) therapy is limited in patients by neutralizing Ab responses. Ninety percent of patients with normal immune systems make neutralizing Abs after one cycle of RIT, preventing repeated dosing. Furthermore, some patients have pre-existing Abs from environmental exposure to Pseudomonas exotoxin, the component of the RIT that elicits the neutralizing Ab response. Bortezomib is an U.S. Food and Drug Administration-approved proteasome inhibitor that selectively targets and kills plasma cells that are necessary for the neutralizing Ab response. We hypothesized that bortezomib may abrogate neutralizing Ab levels, making dosing of RIT possible in mice already immune to RIT. We immunized BALB/c mice with multiple doses of SS1P, a RIT whose Ab portion targets mesothelin. Mice with elevated Ab levels were separated into groups to receive saline, bortezomib, the pentostatin/cyclophosphamide (PC) regimen, or the bortezomib/PC (BPC) combination regimen. Four weeks after finishing therapy, plasma Ab levels were assayed, and bone marrow was harvested. The bortezomib and PC regimens significantly reduced Ab levels, and we observed fewer plasma cells in the bone marrow of bortezomib-treated mice but not in PC-treated mice. The BPC combination regimen almost completely eliminated Abs and further reduced plasma cells in the bone marrow. This regimen is more effective than individual regimens and may reduce Ab levels in patients with pre-existing neutralizing Abs to Pseudomonas exotoxin, allowing RIT treatment. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Manning, Michael L AU - Mason-Osann, Emily AU - Onda, Masanori AU - Pastan, Ira AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20894. ; Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20894 pastani@mail.nih.gov. Y1 - 2015/02/15/ PY - 2015 DA - 2015 Feb 15 SP - 1695 EP - 1701 VL - 194 IS - 4 KW - Antibodies, Monoclonal KW - 0 KW - Antibodies, Neutralizing KW - Bacterial Toxins KW - Boronic Acids KW - Exotoxins KW - Proteasome Inhibitors KW - Pyrazines KW - Recombinant Proteins KW - SS1(dsFv)PE38 KW - Virulence Factors KW - Bortezomib KW - 69G8BD63PP KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - ADP Ribose Transferases -- immunology KW - Recombinant Proteins -- immunology KW - Enzyme-Linked Immunosorbent Assay KW - Mice KW - Exotoxins -- immunology KW - Bacterial Toxins -- immunology KW - Virulence Factors -- immunology KW - Mice, Inbred BALB C KW - Female KW - Immunotherapy -- methods KW - Boronic Acids -- pharmacology KW - Proteasome Inhibitors -- pharmacology KW - Pyrazines -- pharmacology KW - Antibodies, Neutralizing -- blood KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1653125542?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Bortezomib+reduces+pre-existing+antibodies+to+recombinant+immunotoxins+in+mice.&rft.au=Manning%2C+Michael+L%3BMason-Osann%2C+Emily%3BOnda%2C+Masanori%3BPastan%2C+Ira&rft.aulast=Manning&rft.aufirst=Michael&rft.date=2015-02-15&rft.volume=194&rft.issue=4&rft.spage=1695&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=1550-6606&rft_id=info:doi/10.4049%2Fjimmunol.1402324 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-22 N1 - Date created - 2015-02-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Immunology. 1977 Apr;32(4):427-34 [608677] J Immunol. 2014 Jul 1;193(1):48-55 [24890727] Nephrol Dial Transplant. 2005 Jun;20 Suppl 6:vi3-9 [15958824] Clin Cancer Res. 2005 Aug 15;11(16):5840-6 [16115924] Blood. 2006 Jun 15;107(12):4907-16 [16507771] Nat Rev Immunol. 2006 Oct;6(10):741-50 [16977339] J Immunol. 2006 Dec 15;177(12):8822-34 [17142785] Cancer Res. 2007 Feb 15;67(4):1783-92 [17308121] Clin Cancer Res. 2007 Sep 1;13(17):5144-9 [17785569] Nat Med. 2008 Jul;14(7):748-55 [18542049] Nat Biotechnol. 2008 Aug;26(8):901-8 [18688246] Proc Natl Acad Sci U S A. 2008 Aug 12;105(32):11311-6 [18678888] Blood. 2008 Sep 1;112(5):1593-9 [18574024] Immunol Rev. 2010 Sep;237(1):140-59 [20727034] Proc Natl Acad Sci U S A. 2011 Apr 5;108(14):5742-7 [21436054] Lancet Oncol. 2011 May;12(5):431-40 [21507715] Clin Cancer Res. 2011 Jun 1;17(11):3697-705 [21521777] J Immunol. 2011 Oct 1;187(7):3840-53 [21880982] Protein Eng Des Sel. 2012 Jan;25(1):1-6 [22101015] J Clin Oncol. 2012 May 20;30(15):1822-8 [22355053] Ann N Y Acad Sci. 2012 Dec;1274:48-59 [23252897] Mol Cancer Ther. 2013 Jan;12(1):48-57 [23136186] J Neural Transm (Vienna). 2013 Feb;120(2):275-90 [23008029] Genet Med. 2013 Feb;15(2):123-31 [23060045] Transplantation. 2013 Jun 15;95(11):1331-7 [23624544] Toxins (Basel). 2013 Aug;5(8):1486-502 [23965432] Sci Transl Med. 2013 Oct 23;5(208):208ra147 [24154601] Blood. 2014 Jul 3;124(1):63-9 [24855212] Eur J Immunol. 1988 Feb;18(2):313-6 [3350037] Blood. 2014 Apr 17;123(16):2470-7 [24578503] J Clin Oncol. 2003 Apr 1;21(7):1278-84 [12663715] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.4049/jimmunol.1402324 ER - TY - JOUR T1 - Genome-wide association study identified SNP on 15q24 associated with bladder cancer risk in Japanese population. AN - 1652399639; 25281661 AB - Through genome-wide association analysis and an independent replication study using a total of 1131 bladder cancer cases and 12 558 non-cancer controls of Japanese populations, we identified a susceptibility locus on chromosome 15q24. SNP rs11543198 was associated with bladder cancer risk with odds ratio (OR) of 1.41 and P-value of 4.03 × 10(-9). Subgroup analysis revealed rs11543198 to have a stronger effect in male smokers with OR of 1.66. SNP rs8041357, which is in complete linkage disequilibrium (r(2) = 1) with rs11543198, was also associated with bladder cancer risk in Europeans (P = 0.045 for an additive and P = 0.025 for a recessive model), despite much lower minor allele frequency in Europeans (3.7%) compared with the Japanese (22.2%). Imputational analysis in this region suggested CYP1A2, which metabolizes tobacco-derived carcinogen, as a causative candidate gene. We also confirmed the association of previously reported loci, namely SLC14A1, APOBEC3A, PSCA and MYC, with bladder cancer. Our finding implies the crucial roles of genetic variations on the chemically associated development of bladder cancer. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com. JF - Human molecular genetics AU - Matsuda, Koichi AU - Takahashi, Atsushi AU - Middlebrooks, Candace D AU - Obara, Wataru AU - Nasu, Yasutomo AU - Inoue, Keiji AU - Tamura, Kenji AU - Yamasaki, Ichiro AU - Naya, Yoshio AU - Tanikawa, Chizu AU - Cui, Ri AU - Figueroa, Jonine D AU - Silverman, Debra T AU - Rothman, Nathaniel AU - Namiki, Mikio AU - Tomita, Yoshihiko AU - Nishiyama, Hiroyuki AU - Kohri, Kenjiro AU - Deguchi, Takashi AU - Nakagawa, Masayuki AU - Yokoyama, Masayoshi AU - Miki, Tsuneharu AU - Kumon, Hiromi AU - Fujioka, Tomoaki AU - Prokunina-Olsson, Ludmila AU - Kubo, Michiaki AU - Nakamura, Yusuke AU - Shuin, Taro AD - Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan. ; Center for Integrative Medical Science, The Institute of Physical and Chemical Research (RIKEN), Kanagawa, Japan. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, USA. ; Department of Urology, Iwate Medical University School of Medicine, Iwate, Japan. ; Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan. ; Department of Urology, School of Medicine, Kochi University, Koichi, Japan. ; Department of Urology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan. ; Department of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Ishikawa, Japan. ; Department of Urology, Yamagata University Faculty of Medicine, Yamagata, Japan. ; Department of Urology, Faculty of Medicine, University of Tsukuba, Ibaragi, Japan. ; Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, Aichi, Japan. ; Department of Urology, Graduate School of Medicine, Gifu University, Gifu, Japan. ; Department of Urology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, Japan. ; Department of Urology, Ehime University Graduate School of Medicine, Ehime, Japan. ; Department of Medicine and Department of Surgery, Center for Personalized Therapeutics, The University of Chicago, Chicago, IL, USA ynakamura@bsd.uchicago.edu. Y1 - 2015/02/15/ PY - 2015 DA - 2015 Feb 15 SP - 1177 EP - 1184 VL - 24 IS - 4 KW - Index Medicus KW - Genotype KW - Smoking KW - Odds Ratio KW - Alleles KW - Reproducibility of Results KW - Humans KW - Genetic Association Studies KW - Case-Control Studies KW - Male KW - Japan KW - Female KW - Polymorphism, Single Nucleotide KW - Chromosomes, Human, Pair 15 KW - Urinary Bladder Neoplasms -- genetics KW - Genetic Predisposition to Disease KW - Asian Continental Ancestry Group -- genetics KW - Genome-Wide Association Study UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652399639?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+molecular+genetics&rft.atitle=Genome-wide+association+study+identified+SNP+on+15q24+associated+with+bladder+cancer+risk+in+Japanese+population.&rft.au=Matsuda%2C+Koichi%3BTakahashi%2C+Atsushi%3BMiddlebrooks%2C+Candace+D%3BObara%2C+Wataru%3BNasu%2C+Yasutomo%3BInoue%2C+Keiji%3BTamura%2C+Kenji%3BYamasaki%2C+Ichiro%3BNaya%2C+Yoshio%3BTanikawa%2C+Chizu%3BCui%2C+Ri%3BFigueroa%2C+Jonine+D%3BSilverman%2C+Debra+T%3BRothman%2C+Nathaniel%3BNamiki%2C+Mikio%3BTomita%2C+Yoshihiko%3BNishiyama%2C+Hiroyuki%3BKohri%2C+Kenjiro%3BDeguchi%2C+Takashi%3BNakagawa%2C+Masayuki%3BYokoyama%2C+Masayoshi%3BMiki%2C+Tsuneharu%3BKumon%2C+Hiromi%3BFujioka%2C+Tomoaki%3BProkunina-Olsson%2C+Ludmila%3BKubo%2C+Michiaki%3BNakamura%2C+Yusuke%3BShuin%2C+Taro&rft.aulast=Matsuda&rft.aufirst=Koichi&rft.date=2015-02-15&rft.volume=24&rft.issue=4&rft.spage=1177&rft.isbn=&rft.btitle=&rft.title=Human+molecular+genetics&rft.issn=1460-2083&rft_id=info:doi/10.1093%2Fhmg%2Fddu512 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-22 N1 - Date created - 2015-01-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855] Nature. 2010 Oct 28;467(7319):1061-73 [20981092] Hum Mol Genet. 2011 Nov 1;20(21):4268-81 [21750109] Hum Mol Genet. 2011 Nov 1;20(21):4282-9 [21824976] Proc Natl Acad Sci U S A. 2012 Mar 27;109(13):4974-9 [22416122] Nat Genet. 2012 Apr;44(4):430-4, S1-2 [22387998] Nat Genet. 2012 Aug;44(8):955-9 [22820512] Eur J Cancer Prev. 2013 Nov;22(6):607-19 [23462460] Asian Pac J Cancer Prev. 2013;14(5):3155-8 [23803095] Gene. 2013 Jul 25;524(2):168-74 [23628800] Genes Chromosomes Cancer. 2014 Jan;53(1):98-105 [24155119] Hum Mol Genet. 2014 Mar 1;23(5):1387-98 [24163127] Tumour Biol. 2014 Mar;35(3):2253-7 [24293373] Int J Cancer. 2014 Dec 1;135(11):2653-60 [24740636] Jpn J Cancer Res. 1999 Sep;90(9):899-902 [10551315] Oncogene. 2000 Mar 2;19(10):1288-96 [10713670] J Natl Cancer Inst. 2001 Apr 4;93(7):538-45 [11287448] Int J Cancer. 2002 Mar 10;98(2):274-8 [11857419] Mutat Res. 2002 Sep 30;506-507:65-77 [12351146] World J Urol. 2004 Feb;21(6):424-32 [14689225] Cancer Causes Control. 2003 Dec;14(10):907-14 [14750529] Cancer Causes Control. 2004 Oct;15(8):759-69 [15456989] Semin Cancer Biol. 2004 Dec;14(6):473-86 [15489140] Lancet. 1988 Feb 20;1(8582):414-5 [2893213] IARC Sci Publ. 1987;(82):1-406 [3329634] Carcinogenesis. 1991 Oct;12(10):1945-7 [1934275] Cancer Res. 1994 Jan 1;54(1):89-94 [8261468] Toxicol Lett. 1994 Feb 1;70(2):133-8 [8296317] Cancer Epidemiol Biomarkers Prev. 1994 Jul-Aug;3(5):413-21 [7920209] Eur J Cancer Prev. 1995 Feb;4(1):45-59 [7728097] Hum Mol Genet. 1995 Feb;4(2):231-6 [7757072] Mutat Res. 1997 Aug 1;378(1-2):51-63 [9288885] J Biochem. 1999 Apr;125(4):803-8 [10101295] Bioinformatics. 2005 Jan 15;21(2):263-5 [15297300] Lancet. 2005 Aug 20-26;366(9486):649-59 [16112301] Proc Natl Acad Sci U S A. 2006 Jun 6;103(23):8780-5 [16728505] Nat Genet. 2006 Aug;38(8):904-9 [16862161] Arch Toxicol. 2007 Mar;81(3):169-82 [16906435] Science. 2007 Jun 1;316(5829):1341-5 [17463248] Cancer Epidemiol Biomarkers Prev. 2007 Aug;16(8):1595-600 [17684133] Chem Res Toxicol. 2008 Jan;21(1):70-83 [18052394] Carcinogenesis. 2009 Jun;30(6):991-6 [19369583] Nat Genet. 2009 Sep;41(9):991-5 [19648920] Nat Genet. 2010 Mar;42(3):210-5 [20139978] Nat Genet. 2010 Nov;42(11):978-84 [20972438] JAMA. 2011 Aug 17;306(7):737-45 [21846855] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/hmg/ddu512 ER - TY - CPAPER T1 - NIH Response to the Two Reports of Advisory Committee to the Director T2 - 2015 Annual Meeting of the American Association for the Advancement of Science (AAAS 2015) AN - 1658699753; 6339026 JF - 2015 Annual Meeting of the American Association for the Advancement of Science (AAAS 2015) AU - Bourne, Philip Y1 - 2015/02/12/ PY - 2015 DA - 2015 Feb 12 KW - Advisory committees UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658699753?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2015%29&rft.atitle=NIH+Response+to+the+Two+Reports+of+Advisory+Committee+to+the+Director&rft.au=Bourne%2C+Philip&rft.aulast=Bourne&rft.aufirst=Philip&rft.date=2015-02-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://aaas.confex.com/aaas/2015/webprogram/meeting2015-02-11.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-28 N1 - Last updated - 2015-02-27 ER - TY - CPAPER T1 - Direct Imaging of Molecular Structures with Electron Microscopes T2 - 2015 Annual Meeting of the American Association for the Advancement of Science (AAAS 2015) AN - 1658699386; 6338638 JF - 2015 Annual Meeting of the American Association for the Advancement of Science (AAAS 2015) AU - Subramaniam, Sriram Y1 - 2015/02/12/ PY - 2015 DA - 2015 Feb 12 KW - Molecular structure KW - Microscopes KW - Imaging techniques UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658699386?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2015%29&rft.atitle=Direct+Imaging+of+Molecular+Structures+with+Electron+Microscopes&rft.au=Subramaniam%2C+Sriram&rft.aulast=Subramaniam&rft.aufirst=Sriram&rft.date=2015-02-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://aaas.confex.com/aaas/2015/webprogram/meeting2015-02-11.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-28 N1 - Last updated - 2015-02-27 ER - TY - CPAPER T1 - Reproducibility: An NIH Perspective T2 - 2015 Annual Meeting of the American Association for the Advancement of Science (AAAS 2015) AN - 1658698874; 6338947 JF - 2015 Annual Meeting of the American Association for the Advancement of Science (AAAS 2015) AU - Silberberg, Shai Y1 - 2015/02/12/ PY - 2015 DA - 2015 Feb 12 KW - Information sciences KW - Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658698874?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2015%29&rft.atitle=Reproducibility%3A+An+NIH+Perspective&rft.au=Silberberg%2C+Shai&rft.aulast=Silberberg&rft.aufirst=Shai&rft.date=2015-02-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://aaas.confex.com/aaas/2015/webprogram/meeting2015-02-11.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-28 N1 - Last updated - 2015-02-27 ER - TY - CPAPER T1 - Big Data in Health Policy T2 - 2015 Annual Meeting of the American Association for the Advancement of Science (AAAS 2015) AN - 1658698377; 6338922 JF - 2015 Annual Meeting of the American Association for the Advancement of Science (AAAS 2015) AU - Russell, Beth Y1 - 2015/02/12/ PY - 2015 DA - 2015 Feb 12 KW - Policies KW - Data processing KW - Health policy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658698377?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2015%29&rft.atitle=Big+Data+in+Health+Policy&rft.au=Russell%2C+Beth&rft.aulast=Russell&rft.aufirst=Beth&rft.date=2015-02-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://aaas.confex.com/aaas/2015/webprogram/meeting2015-02-11.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-28 N1 - Last updated - 2015-02-27 ER - TY - CPAPER T1 - Challenges and Opportunities for the World's Largest Clinical Trials Database T2 - 2015 Annual Meeting of the American Association for the Advancement of Science (AAAS 2015) AN - 1658698068; 6338942 JF - 2015 Annual Meeting of the American Association for the Advancement of Science (AAAS 2015) AU - Zarin, Deborah Y1 - 2015/02/12/ PY - 2015 DA - 2015 Feb 12 KW - Databases KW - Clinical trials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658698068?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2015%29&rft.atitle=Challenges+and+Opportunities+for+the+World%27s+Largest+Clinical+Trials+Database&rft.au=Zarin%2C+Deborah&rft.aulast=Zarin&rft.aufirst=Deborah&rft.date=2015-02-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://aaas.confex.com/aaas/2015/webprogram/meeting2015-02-11.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-28 N1 - Last updated - 2015-02-27 ER - TY - CPAPER T1 - Towards Fully Automated Abdominal CT Image Interpretation T2 - 2015 Annual Meeting of the American Association for the Advancement of Science (AAAS 2015) AN - 1658698037; 6338999 JF - 2015 Annual Meeting of the American Association for the Advancement of Science (AAAS 2015) AU - Summers, Ronald Y1 - 2015/02/12/ PY - 2015 DA - 2015 Feb 12 KW - Automation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658698037?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2015%29&rft.atitle=Towards+Fully+Automated+Abdominal+CT+Image+Interpretation&rft.au=Summers%2C+Ronald&rft.aulast=Summers&rft.aufirst=Ronald&rft.date=2015-02-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://aaas.confex.com/aaas/2015/webprogram/meeting2015-02-11.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-28 N1 - Last updated - 2015-02-27 ER - TY - CPAPER T1 - Understanding Nicotine Addiction and Its Brain Reward Systems T2 - 2015 Annual Meeting of the American Association for the Advancement of Science (AAAS 2015) AN - 1658697175; 6338548 JF - 2015 Annual Meeting of the American Association for the Advancement of Science (AAAS 2015) AU - Compton, Wilson Y1 - 2015/02/12/ PY - 2015 DA - 2015 Feb 12 KW - Nicotine KW - Reinforcement KW - Brain KW - Addiction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658697175?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2015%29&rft.atitle=Understanding+Nicotine+Addiction+and+Its+Brain+Reward+Systems&rft.au=Compton%2C+Wilson&rft.aulast=Compton&rft.aufirst=Wilson&rft.date=2015-02-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Annual+Meeting+of+the+American+Association+for+the+Advancement+of+Science+%28AAAS+2015%29&rft.issn=&rft_id=info:doi/ L2 - https://aaas.confex.com/aaas/2015/webprogram/meeting2015-02-11.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-28 N1 - Last updated - 2015-02-27 ER - TY - JOUR T1 - A recurrent mutation in PARK2 is associated with familial lung cancer. AN - 1653131647; 25640678 AB - PARK2, a gene associated with Parkinson disease, is a tumor suppressor in human malignancies. Here, we show that c.823C>T (p.Arg275Trp), a germline mutation in PARK2, is present in a family with eight cases of lung cancer. The resulting amino acid change, p.Arg275Trp, is located in the highly conserved RING finger 1 domain of PARK2, which encodes an E3 ubiquitin ligase. Upon further analysis, the c.823C>T mutation was detected in three additional families affected by lung cancer. The effect size for PARK2 c.823C>T (odds ratio = 5.24) in white individuals was larger than those reported for variants from lung cancer genome-wide association studies. These data implicate this PARK2 germline mutation as a genetic susceptibility factor for lung cancer. Our results provide a rationale for further investigations of this specific mutation and gene for evaluation of the possibility of developing targeted therapies against lung cancer in individuals with PARK2 variants by compensating for the loss-of-function effect caused by the associated variation. Copyright © 2015 The American Society of Human Genetics. Published by Elsevier Inc. All rights reserved. JF - American journal of human genetics AU - Xiong, Donghai AU - Wang, Yian AU - Kupert, Elena AU - Simpson, Claire AU - Pinney, Susan M AU - Gaba, Colette R AU - Mandal, Diptasri AU - Schwartz, Ann G AU - Yang, Ping AU - de Andrade, Mariza AU - Pikielny, Claudio AU - Byun, Jinyoung AU - Li, Yafang AU - Stambolian, Dwight AU - Spitz, Margaret R AU - Liu, Yanhong AU - Amos, Christopher I AU - Bailey-Wilson, Joan E AU - Anderson, Marshall AU - You, Ming AD - Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, USA; Cancer Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA. ; Cancer Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA; Department of Medicine, Medical College of Wisconsin, Milwaukee, WI 53226, USA. ; Computational and Statistical Genomics Branch, National Human Genome Research Institute, NIH, Baltimore, MD 20892, USA. ; Department of Environmental Health, College of Medicine, University of Cincinnati, Cincinnati, OH 45267, USA. ; College of Medicine, University of Toledo, Toledo, OH 43614, USA. ; Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA. ; Karmanos Cancer Institute, Detroit, MI 48201, USA. ; Mayo Clinic, Rochester, MN 55905, USA. ; Department of Community and Family Medicine, Geisel School of Medicine, Dartmouth College, Lebanon, NH 03755, USA. ; Department of Ophthalmology and Genetics, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Baylor College of Medicine, Houston, TX 77030, USA. ; Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, USA; Cancer Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA. Electronic address: myou@mcw.edu. Y1 - 2015/02/05/ PY - 2015 DA - 2015 Feb 05 SP - 301 EP - 308 VL - 96 IS - 2 KW - DNA Primers KW - 0 KW - Ubiquitin-Protein Ligases KW - EC 2.3.2.27 KW - parkin protein KW - Index Medicus KW - Pedigree KW - Odds Ratio KW - Base Sequence KW - DNA Primers -- genetics KW - Humans KW - Mutation, Missense -- genetics KW - Molecular Sequence Data KW - Sequence Analysis, DNA KW - Exome -- genetics KW - Male KW - Germ-Line Mutation -- genetics KW - Female KW - Genetic Predisposition to Disease -- genetics KW - Ubiquitin-Protein Ligases -- genetics KW - Lung Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1653131647?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+journal+of+human+genetics&rft.atitle=A+recurrent+mutation+in+PARK2+is+associated+with+familial+lung+cancer.&rft.au=Xiong%2C+Donghai%3BWang%2C+Yian%3BKupert%2C+Elena%3BSimpson%2C+Claire%3BPinney%2C+Susan+M%3BGaba%2C+Colette+R%3BMandal%2C+Diptasri%3BSchwartz%2C+Ann+G%3BYang%2C+Ping%3Bde+Andrade%2C+Mariza%3BPikielny%2C+Claudio%3BByun%2C+Jinyoung%3BLi%2C+Yafang%3BStambolian%2C+Dwight%3BSpitz%2C+Margaret+R%3BLiu%2C+Yanhong%3BAmos%2C+Christopher+I%3BBailey-Wilson%2C+Joan+E%3BAnderson%2C+Marshall%3BYou%2C+Ming&rft.aulast=Xiong&rft.aufirst=Donghai&rft.date=2015-02-05&rft.volume=96&rft.issue=2&rft.spage=301&rft.isbn=&rft.btitle=&rft.title=American+journal+of+human+genetics&rft.issn=1537-6605&rft_id=info:doi/10.1016%2Fj.ajhg.2014.12.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-09 N1 - Date created - 2015-02-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Ann Neurol. 2002 Sep;52(3):276-84 [12205639] Neuron. 2002 Dec 19;36(6):1007-19 [12495618] Hum Mol Genet. 2003 Nov 15;12(22):2957-65 [14519684] Am J Epidemiol. 1968 Sep;88(2):149-58 [5673487] Mov Disord. 1987;2(2):73-91 [3504266] BMJ. 1995 Jun 10;310(6993):1500-1 [7787596] Nature. 1998 Apr 9;392(6676):605-8 [9560156] Br J Cancer. 2005 Jan 17;92(1):201-5 [15583688] Hum Mol Genet. 2005 Sep 1;14(17):2571-86 [16049031] Cancer Epidemiol Biomarkers Prev. 2007 Jun;16(6):1260-5 [17548694] Nature. 2008 Apr 3;452(7187):638-42 [18385739] Genome Res. 2012 Mar;22(3):568-76 [22300766] Cancer Discov. 2012 May;2(5):401-4 [22588877] Carcinogenesis. 2012 Sep;33(9):1797-805 [22696596] J Mol Med (Berl). 2014 Jan;92(1):31-42 [24297497] Nat Genet. 2014 Jun;46(6):588-94 [24793136] Nat Genet. 2014 Jun;46(6):527-8 [24866187] Nat Genet. 2014 Jul;46(7):736-41 [24880342] CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855] Eur J Epidemiol. 2011 Jun;26 Suppl 1:S1-58 [21626386] Nat Genet. 2011 Aug;43(8):792-6 [21725308] Nature. 2011 Dec 1;480(7375):99-103 [22080950] N Engl J Med. 2000 May 25;342(21):1560-7 [10824074] Science. 2001 May 25;292(5521):1552-5 [11375494] J Neurochem. 2002 Apr;81(2):301-6 [12064477] Nat Genet. 2008 May;40(5):616-22 [18385676] Nat Genet. 2008 Dec;40(12):1407-9 [18978787] Clin Cancer Res. 2009 Apr 15;15(8):2666-74 [19351763] Bioinformatics. 2009 Jul 15;25(14):1754-60 [19451168] Nat Genet. 2010 Jan;42(1):77-82 [19946270] Cancer Res. 2010 Mar 15;70(6):2359-67 [20215501] Genome Res. 2010 Sep;20(9):1297-303 [20644199] Nucleic Acids Res. 2010 Sep;38(16):e164 [20601685] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ajhg.2014.12.016 ER - TY - JOUR T1 - MnSOD upregulation sustains the Warburg effect via mitochondrial ROS and AMPK-dependent signalling in cancer. AN - 1652451916; 25651975 AB - Manganese superoxide dismutase (MnSOD/SOD2) is a mitochondria-resident enzyme that governs the types of reactive oxygen species egressing from the organelle to affect cellular signalling. Here we demonstrate that MnSOD upregulation in cancer cells establishes a steady flow of H2O2 originating from mitochondria that sustains AMP-activated kinase (AMPK) activation and the metabolic shift to glycolysis. Restricting MnSOD expression or inhibiting AMPK suppresses the metabolic switch and dampens the viability of transformed cells indicating that the MnSOD/AMPK axis is critical to support cancer cell bioenergetics. Recapitulating in vitro findings, clinical and epidemiologic analyses of MnSOD expression and AMPK activation indicated that the MnSOD/AMPK pathway is most active in advanced stage and aggressive breast cancer subtypes. Taken together, our results indicate that MnSOD serves as a biomarker of cancer progression and acts as critical regulator of tumour cell metabolism. JF - Nature communications AU - Hart, Peter C AU - Mao, Mao AU - de Abreu, Andre Luelsdorf P AU - Ansenberger-Fricano, Kristine AU - Ekoue, Dede N AU - Ganini, Douglas AU - Kajdacsy-Balla, Andre AU - Diamond, Alan M AU - Minshall, Richard D AU - Consolaro, Marcia E L AU - Santos, Janine H AU - Bonini, Marcelo G AD - 1] Department of Medicine, University of Illinois at Chicago, 909 South Wolcott Avenue, COMRB 1131, Chicago, Illinois 60612, USA [2] Department of Pathology, University of Illinois at Chicago, 909 South Wolcott Avenue, COMRB 1131, Chicago, Illinois 60612, USA. ; 1] Department of Medicine, University of Illinois at Chicago, 909 South Wolcott Avenue, COMRB 1131, Chicago, Illinois 60612, USA [2] Department of Pharmacology, University of Illinois at Chicago, 909 South Wolcott Avenue, COMRB 1131, Chicago, Illinois 60612, USA. ; 1] Department of Medicine, University of Illinois at Chicago, 909 South Wolcott Avenue, COMRB 1131, Chicago, Illinois 60612, USA [2] Department of Pharmacology, University of Illinois at Chicago, 909 South Wolcott Avenue, COMRB 1131, Chicago, Illinois 60612, USA [3] Universidade Estadual de Maringa, Avenida Colombo, 5790, CEP, 87020-900 Maringa, PR, Brazil. ; Department of Pathology, University of Illinois at Chicago, 909 South Wolcott Avenue, COMRB 1131, Chicago, Illinois 60612, USA. ; Free Radical Metabolite Section, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences/NIH, 111T.W., Alexander Drive MD-F02, Research Triangle Park, North Carolina 27709, USA. ; 1] Department of Pharmacology, University of Illinois at Chicago, 909 South Wolcott Avenue, COMRB 1131, Chicago, Illinois 60612, USA [2] Department of Anesthesiology, University of Illinois at Chicago, 909 South Wolcott Avenue, COMRB 1131, Chicago, Illinois 60612, USA. ; Universidade Estadual de Maringa, Avenida Colombo, 5790, CEP, 87020-900 Maringa, PR, Brazil. ; Department of Physiology and Pharmacology, University of Medicine and Dentistry of New Jersey, 185 South Orange Avenue, Newark, New Jersey 07103, USA. ; 1] Department of Medicine, University of Illinois at Chicago, 909 South Wolcott Avenue, COMRB 1131, Chicago, Illinois 60612, USA [2] Department of Pathology, University of Illinois at Chicago, 909 South Wolcott Avenue, COMRB 1131, Chicago, Illinois 60612, USA [3] Department of Pharmacology, University of Illinois at Chicago, 909 South Wolcott Avenue, COMRB 1131, Chicago, Illinois 60612, USA. Y1 - 2015/02/05/ PY - 2015 DA - 2015 Feb 05 SP - 6053 VL - 6 KW - RNA, Small Interfering KW - 0 KW - Reactive Oxygen Species KW - Hydrogen Peroxide KW - BBX060AN9V KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Hexokinase KW - EC 2.7.1.1 KW - Phosphofructokinase-1 KW - EC 2.7.1.11 KW - Pyruvate Kinase KW - EC 2.7.1.40 KW - AMP-Activated Protein Kinases KW - EC 2.7.11.1 KW - Index Medicus KW - Neoplasm Staging KW - Humans KW - Hydrogen Peroxide -- metabolism KW - Mitochondria -- enzymology KW - RNA, Small Interfering -- genetics KW - Cell Line, Tumor KW - RNA, Small Interfering -- metabolism KW - Transcriptional Activation KW - Oxidation-Reduction KW - Phosphofructokinase-1 -- metabolism KW - Pyruvate Kinase -- genetics KW - Hexokinase -- genetics KW - Hexokinase -- metabolism KW - Glycolysis -- genetics KW - Signal Transduction KW - Female KW - Male KW - Mitochondria -- genetics KW - Pyruvate Kinase -- metabolism KW - Phosphofructokinase-1 -- genetics KW - Breast Neoplasms -- genetics KW - Reactive Oxygen Species -- metabolism KW - AMP-Activated Protein Kinases -- antagonists & inhibitors KW - AMP-Activated Protein Kinases -- genetics KW - Colonic Neoplasms -- genetics KW - AMP-Activated Protein Kinases -- metabolism KW - Superoxide Dismutase -- metabolism KW - Prostatic Neoplasms -- genetics KW - Colonic Neoplasms -- enzymology KW - Gene Expression Regulation, Neoplastic KW - Prostatic Neoplasms -- pathology KW - Superoxide Dismutase -- antagonists & inhibitors KW - Breast Neoplasms -- pathology KW - Superoxide Dismutase -- genetics KW - Prostatic Neoplasms -- enzymology KW - Breast Neoplasms -- enzymology KW - Colonic Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652451916?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+communications&rft.atitle=MnSOD+upregulation+sustains+the+Warburg+effect+via+mitochondrial+ROS+and+AMPK-dependent+signalling+in+cancer.&rft.au=Hart%2C+Peter+C%3BMao%2C+Mao%3Bde+Abreu%2C+Andre+Luelsdorf+P%3BAnsenberger-Fricano%2C+Kristine%3BEkoue%2C+Dede+N%3BGanini%2C+Douglas%3BKajdacsy-Balla%2C+Andre%3BDiamond%2C+Alan+M%3BMinshall%2C+Richard+D%3BConsolaro%2C+Marcia+E+L%3BSantos%2C+Janine+H%3BBonini%2C+Marcelo+G&rft.aulast=Hart&rft.aufirst=Peter&rft.date=2015-02-05&rft.volume=6&rft.issue=&rft.spage=6053&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms7053 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-29 N1 - Date created - 2015-02-05 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Pathol. 2011 Dec;225(4):475-8 [22025211] Cancer Res. 2011 Nov 1;71(21):6684-95 [22009531] Am J Pathol. 2012 Jan;180(1):24-31 [22056359] Nature. 2012 Jan 19;481(7381):385-8 [22101431] J Exp Med. 2012 Feb 13;209(2):211-5 [22330683] Cancer Cell. 2012 Mar 20;21(3):297-308 [22439925] Antioxid Redox Signal. 2008 Mar;10(3):635-40 [17999628] Shock. 2008 Feb;29(2):300-8 [17693941] Cell. 2008 May 2;133(3):462-74 [18455987] Arch Biochem Biophys. 2008 Aug 15;476(2):171-7 [18424257] Semin Cancer Biol. 2009 Feb;19(1):25-31 [19130886] Am J Physiol Regul Integr Comp Physiol. 2009 May;296(5):R1496-502 [19297546] Cancer Sci. 2009 Jun;100(6):1026-33 [19385967] Int J Cancer. 2009 Oct 1;125(7):1497-504 [19507253] Cancer Biol Ther. 2008 Nov;7(11):1732-43 [19151587] Oncogene. 2010 May 20;29(20):2962-72 [20228846] Proc Natl Acad Sci U S A. 2010 Jul 13;107(28):12564-9 [20538976] Circulation. 2001 Aug 28;104(9):979-81 [11524388] J Biol Chem. 2002 Mar 29;277(13):11392-400 [11751868] Oncogene. 2002 Jun 27;21(28):4392-402 [12080470] Cancer Epidemiol Biomarkers Prev. 2004 Jan;13(1):146-9 [14744747] J Biol Chem. 2004 Feb 6;279(6):4305-12 [14627695] Biochem Biophys Res Commun. 1994 Jun 30;201(3):1356-65 [8024580] Science. 1997 Mar 28;275(5308):1943-7 [9072974] Genes Chromosomes Cancer. 1999 Jul;25(3):251-60 [10379871] Am J Physiol. 1999 Jul;277(1 Pt 1):E1-10 [10409121] J Cell Biochem. 2012 Jun;113(6):1966-76 [22253064] Mol Cancer Ther. 2012 Sep;11(9):1863-72 [22772423] Neuroscience. 2012 Dec 13;226:21-8 [22982624] Free Radic Biol Med. 2012 Nov 15;53(10):1838-47 [23000060] Free Radic Biol Med. 2013 Jan;54:116-24 [22982047] Proc Natl Acad Sci U S A. 2013 Jan 15;110(3):972-7 [23277563] Cell. 2013 Jan 17;152(1-2):224-35 [23332757] Food Chem Toxicol. 2013 Mar;53:294-8 [23261675] Proc Natl Acad Sci U S A. 2013 Mar 12;110(11):E1026-34 [23431153] Cardiovasc Drugs Ther. 2013 Jun;27(3):189-98 [23358928] Mol Cancer Ther. 2013 Oct;12(10):2067-77 [23960096] Cell Cycle. 2014;13(3):347-8 [24335489] Free Radic Biol Med. 2014 Feb;67:342-52 [24269899] J Mol Cell Cardiol. 2014 Aug;73:112-6 [24530899] Curr Biol. 2000 Oct 19;10(20):1247-55 [11069105] Science. 1964 Feb 28;143(3609):929-33 [14090142] Science. 1956 Aug 10;124(3215):269-70 [13351639] Mol Cell. 2004 Dec 3;16(5):819-30 [15574336] JAMA. 2006 Jun 7;295(21):2492-502 [16757721] Free Radic Biol Med. 2007 Jan 1;42(1):64-78 [17157194] Am J Physiol Cell Physiol. 2007 Jan;292(1):C125-36 [16971499] J Cell Biochem. 2007 Jun 1;101(3):723-34 [17211854] Cancer Cell. 2007 Aug;12(2):108-13 [17692803] Circ Res. 2008 Feb 15;102(3):328-37 [18063812] Cell Metab. 2012 Apr 4;15(4):451-65 [22482728] FASEB J. 2012 May;26(5):2175-86 [22321727] Nature. 2012 May 31;485(7400):661-5 [22660331] Cell Metab. 2012 Jun 6;15(6):827-37 [22682223] Mol Cell Biol. 2012 Jul;32(13):2570-84 [22547685] Cancer Res. 2012 Aug 1;72(15):3807-16 [22710435] Oncogene. 2001 Jan 25;20(4):430-9 [11313974] J Exp Med. 2001 Jun 18;193(12):1351-9 [11413190] Ann N Y Acad Sci. 2010 Jul;1201:72-8 [20649542] Cell Signal. 2011 Jan;23(1):6-13 [20633638] Mitochondrion. 2010 Nov;10(6):649-61 [20601193] Cancer Res. 2010 Dec 15;70(24):10351-61 [20961996] Proc Natl Acad Sci U S A. 2011 Jan 25;108(4):1397-402 [21220315] Am J Physiol Cell Physiol. 2011 Mar;300(3):C385-93 [21123733] Proc Natl Acad Sci U S A. 2011 Mar 8;108(10):4129-34 [21325052] BMC Cancer. 2011;11:143 [21501481] Free Radic Biol Med. 2011 Jun 15;50(12):1771-9 [21419216] Cell Death Differ. 2011 Sep;18(9):1414-24 [21415859] Cell Metab. 2011 Oct 5;14(4):537-44 [21982713] Dev Cell. 2011 Oct 18;21(4):783-95 [22014527] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ncomms7053 ER - TY - JOUR T1 - Systemic uptake, albumin and hemoglobin binding of [(14)C]2,3-butanedione administered by intratracheal instillation in male Harlan Sprague Dawley rats and oropharyngeal aspiration in male B6C3F1/N mice. AN - 1652446229; 25559854 AB - 2,3-Butanedione (BD) is a reactive diketone in artificial butter flavors that is thought to cause bronchiolitis obliterans in workers in microwave popcorn manufacturing. Bronchiolitis obliterans is generally not diagnosed until irreversible damage has occurred; therefore a biomarker of early exposure is needed. The potential systemic uptake of BD from inhalation exposure has not been evaluated. The objective here was to evaluate the systemic exposure of BD and binding to hemoglobin and albumin. [(14)C]BD was administered to male Harlan Sprague Dawley rats (100 mg/kg, intratracheal instillation) and B6C3F1/N mice (157 mg/kg, oropharyngeal aspiration). Blood and plasma was collected 24 h after administration and analyzed for (14)C content. At 24h, 0.88±0.07% of the administered dose was in rat blood, 0.66±0.06% in rat plasma, 0.38±0.13% in mouse blood and 0.17±0.05% in mouse plasma. Albumin binding in rats was 269±24.2 ng equiv./mg, which accounts for 38% of the radioactivity in plasma. In mice, binding was 85.0±22.3 ng equiv./mg albumin, which accounts for 51% of the radioactivity in plasma. The binding to hemoglobin in rats was 38.2±17.6 ng equiv./mg, and to globin was 29.1±3.96 ng equiv./mg. In mice, the binding to hemoglobin was 16.2±9.0 ng equiv./mg. The site(s) of adduction on hemoglobin and albumin was investigated by mass spectrometry. In rat globin, arginine adducts were detected at R-30 and R-104 of the beta chain in vitro and in vivo. In rat albumin, adducts were detected in vitro on R-219/221, R-360, and R-368, and in vivo on a variety of arginine residues. This study demonstrated that BD enters the systemic circulation and reacts with arginine on hemoglobin and albumin. These results indicate that hemoglobin and albumin adducts may be useful as biomarkers of BD exposure in humans. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved. JF - Chemico-biological interactions AU - Fennell, Timothy R AU - Morgan, Daniel L AU - Watson, Scott L AU - Dhungana, Suraj AU - Waidyanatha, Suramya AD - RTI International, Research Triangle Park, NC, United States. ; Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, United States. ; Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, United States. Electronic address: waidyanathas@niehs.nih.gov. Y1 - 2015/02/05/ PY - 2015 DA - 2015 Feb 05 SP - 112 EP - 119 VL - 227 KW - Carbon Radioisotopes KW - 0 KW - Hemoglobins KW - Serum Albumin KW - Arginine KW - 94ZLA3W45F KW - Diacetyl KW - K324J5K4HM KW - Index Medicus KW - Albumin binding KW - Hemoglobin binding KW - 2,3-Butanedione KW - Systemic uptake KW - Rats KW - Arginine -- analysis KW - Animals KW - Rats, Sprague-Dawley KW - Arginine -- chemistry KW - Intubation, Intratracheal KW - Mice KW - Tandem Mass Spectrometry KW - Protein Binding KW - Male KW - Chromatography, High Pressure Liquid KW - Carbon Radioisotopes -- chemistry KW - Diacetyl -- chemistry KW - Serum Albumin -- metabolism KW - Hemoglobins -- analysis KW - Serum Albumin -- analysis KW - Hemoglobins -- metabolism KW - Diacetyl -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652446229?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemico-biological+interactions&rft.atitle=Systemic+uptake%2C+albumin+and+hemoglobin+binding+of+%5B%2814%29C%5D2%2C3-butanedione+administered+by+intratracheal+instillation+in+male+Harlan+Sprague+Dawley+rats+and+oropharyngeal+aspiration+in+male+B6C3F1%2FN+mice.&rft.au=Fennell%2C+Timothy+R%3BMorgan%2C+Daniel+L%3BWatson%2C+Scott+L%3BDhungana%2C+Suraj%3BWaidyanatha%2C+Suramya&rft.aulast=Fennell&rft.aufirst=Timothy&rft.date=2015-02-05&rft.volume=227&rft.issue=&rft.spage=112&rft.isbn=&rft.btitle=&rft.title=Chemico-biological+interactions&rft.issn=1872-7786&rft_id=info:doi/10.1016%2Fj.cbi.2014.12.029 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-14 N1 - Date created - 2015-02-04 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.cbi.2014.12.029 ER - TY - JOUR T1 - Mechanism of RNA polymerase II bypass of oxidative cyclopurine DNA lesions. AN - 1652442351; 25605892 AB - In human cells, the oxidative DNA lesion 8,5'-cyclo-2'-deoxyadenosine (CydA) induces prolonged stalling of RNA polymerase II (Pol II) followed by transcriptional bypass, generating both error-free and mutant transcripts with AMP misincorporated immediately downstream from the lesion. Here, we present biochemical and crystallographic evidence for the mechanism of CydA recognition. Pol II stalling results from impaired loading of the template base (5') next to CydA into the active site, leading to preferential AMP misincorporation. Such predominant AMP insertion, which also occurs at an abasic site, is unaffected by the identity of the 5'-templating base, indicating that it derives from nontemplated synthesis according to an A rule known for DNA polymerases and recently identified for Pol II bypass of pyrimidine dimers. Subsequent to AMP misincorporation, Pol II encounters a major translocation block that is slowly overcome. Thus, the translocation block combined with the poor extension of the dA.rA mispair reduce transcriptional mutagenesis. Moreover, increasing the active-site flexibility by mutation in the trigger loop, which increases the ability of Pol II to accommodate the bulky lesion, and addition of transacting factor TFIIF facilitate CydA bypass. Thus, blocking lesion entry to the active site, translesion A rule synthesis, and translocation block are common features of transcription across different bulky DNA lesions. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Walmacq, Celine AU - Wang, Lanfeng AU - Chong, Jenny AU - Scibelli, Kathleen AU - Lubkowska, Lucyna AU - Gnatt, Averell AU - Brooks, Philip J AU - Wang, Dong AU - Kashlev, Mikhail AD - Center for Cancer Research, National Cancer Institute, Frederick, MD 21702; ; Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, CA 92093; ; Biopolcore, Inc., Baltimore, MD 21208; and. ; Laboratory of Neurogenetics and Division of Metabolism and Health Effects, National Institute on Alcohol Abuse and Alcoholism, and Office of Rare Diseases Research, National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD 20892. ; Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California, San Diego, La Jolla, CA 92093; dongwang@ucsd.edu kashlevm@mail.nih.gov. ; Center for Cancer Research, National Cancer Institute, Frederick, MD 21702; dongwang@ucsd.edu kashlevm@mail.nih.gov. Y1 - 2015/02/03/ PY - 2015 DA - 2015 Feb 03 SP - E410 EP - E419 VL - 112 IS - 5 KW - Purines KW - 0 KW - DNA KW - 9007-49-2 KW - RNA Polymerase II KW - EC 2.7.7.- KW - Index Medicus KW - RNA polymerase II KW - translesion transcription KW - oxidative DNA damage KW - transcription factor TFIIF KW - transcriptional mutagenesis KW - Oxidation-Reduction KW - Base Sequence KW - DNA -- chemistry KW - Transcription, Genetic KW - Purines -- metabolism KW - RNA Polymerase II -- metabolism KW - DNA Damage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652442351?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Mechanism+of+RNA+polymerase+II+bypass+of+oxidative+cyclopurine+DNA+lesions.&rft.au=Walmacq%2C+Celine%3BWang%2C+Lanfeng%3BChong%2C+Jenny%3BScibelli%2C+Kathleen%3BLubkowska%2C+Lucyna%3BGnatt%2C+Averell%3BBrooks%2C+Philip+J%3BWang%2C+Dong%3BKashlev%2C+Mikhail&rft.aulast=Walmacq&rft.aufirst=Celine&rft.date=2015-02-03&rft.volume=112&rft.issue=5&rft.spage=E410&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=1091-6490&rft_id=info:doi/10.1073%2Fpnas.1415186112 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-28 N1 - Date created - 2015-02-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Annu Rev Biochem. 1996;65:15-42 [8811173] Oncogene. 1996 Aug 15;13(4):823-31 [8761304] Mol Cell. 2004 Dec 22;16(6):955-65 [15610738] FEBS Lett. 2005 Feb 7;579(4):873-6 [15680966] Chem Rev. 2006 Feb;106(2):474-88 [16464015] Proc Natl Acad Sci U S A. 2006 Jun 20;103(25):9506-11 [16769904] Mol Cell. 2006 Oct 20;24(2):257-66 [17052459] Cell. 2006 Dec 1;127(5):941-54 [17129781] EMBO J. 2006 Nov 29;25(23):5481-91 [17110932] Science. 2007 Feb 9;315(5813):859-62 [17290000] EMBO Rep. 2007 Apr;8(4):388-93 [17363972] Nat Struct Mol Biol. 2007 Dec;14(12):1127-33 [17994106] Proc Natl Acad Sci U S A. 2008 Jan 29;105(4):1170-5 [18202176] Chem Res Toxicol. 2008 Feb;21(2):276-81 [18189366] Mol Cell. 2008 Jun 6;30(5):557-66 [18538654] DNA Repair (Amst). 2008 Jul 1;7(7):1168-79 [18495558] DNA Repair (Amst). 2008 Sep 1;7(9):1413-25 [18603018] Microbiol Mol Biol Rev. 2009 Mar;73(1):134-54 [19258535] J Biol Chem. 2009 Jul 17;284(29):19601-12 [19439405] J Biol Chem. 2009 Nov 13;284(46):31658-63 [19758983] Biochemistry. 2010 Feb 16;49(6):1053-5 [20067321] Proc Natl Acad Sci U S A. 2010 May 25;107(21):9584-9 [20448203] Nat Rev Cancer. 2011 Mar;11(3):218-27 [21346784] Mol Cell. 2012 Apr 13;46(1):18-29 [22405652] Aging Cell. 2012 Aug;11(4):714-6 [22530741] Nat Chem Biol. 2012 Oct;8(10):817-22 [22902614] J Am Chem Soc. 2013 Sep 4;135(35):13054-61 [23927577] Proc Natl Acad Sci U S A. 2014 May 6;111(18):6642-7 [24733897] Proc Natl Acad Sci U S A. 2014 May 6;111(18):E1823-32 [24757057] Proc Natl Acad Sci U S A. 2014 May 27;111(21):7665-70 [24753580] Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):3832-7 [10759556] J Biol Chem. 2000 Jul 21;275(29):22355-62 [10801836] Nature. 2001 May 17;411(6835):366-74 [11357144] Science. 2001 Jun 8;292(5523):1876-82 [11313499] J Photochem Photobiol B. 2001 Oct;63(1-3):88-102 [11684456] Mutat Res. 2002 Dec 29;510(1-2):55-70 [12459443] Mutat Res. 2002 Dec 29;510(1-2):131-40 [12459449] Nature. 2003 Aug 28;424(6952):1083-7 [12904819] J Mol Biol. 2004 Sep 24;342(4):1085-99 [15351637] Annu Rev Genet. 1986;20:201-30 [3545059] Bioessays. 1991 Feb;13(2):79-84 [2029269] Protein Expr Purif. 1993 Jun;4(3):207-14 [8390879] Proc Natl Acad Sci U S A. 1994 Aug 30;91(18):8502-6 [8078911] Ann N Y Acad Sci. 1994 Jul 29;726:132-42; discussion 142-3 [8092671] Cell. 2004 Nov 12;119(4):481-9 [15537538] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1073/pnas.1415186112 ER - TY - JOUR T1 - Microtubule-targeting agents augment the toxicity of DNA-damaging agents by disrupting intracellular trafficking of DNA repair proteins. AN - 1652441497; 25605897 AB - The paradigm that microtubule-targeting agents (MTAs) cause cell death via mitotic arrest applies to rapidly dividing cells but cannot explain MTA activity in slowly growing human cancers. Many preferred cancer regimens combine a MTA with a DNA-damaging agent (DDA). We hypothesized that MTAs synergize with DDAs by interfering with trafficking of DNA repair proteins on interphase microtubules. We investigated nine proteins involved in DNA repair: ATM, ATR, DNA-PK, Rad50, Mre11, p95/NBS1, p53, 53BP1, and p63. The proteins were sequestered in the cytoplasm by vincristine and paclitaxel but not by an aurora kinase inhibitor, colocalized with tubulin by confocal microscopy and coimmunoprecipitated with the microtubule motor dynein. Furthermore, adding MTAs to radiation, doxorubicin, or etoposide led to more sustained γ-H2AX levels. We conclude DNA damage-repair proteins traffic on microtubules and addition of MTAs sequesters them in the cytoplasm, explaining why MTA/DDA combinations are common anticancer regimens. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Poruchynsky, Marianne S AU - Komlodi-Pasztor, Edina AU - Trostel, Shana AU - Wilkerson, Julia AU - Regairaz, Marie AU - Pommier, Yves AU - Zhang, Xu AU - Kumar Maity, Tapan AU - Robey, Robert AU - Burotto, Mauricio AU - Sackett, Dan AU - Guha, Udayan AU - Fojo, Antonio Tito AD - Center for Cancer Research. ; National Cancer Institute, Developmental Therapeutics Branch, National Cancer Institute, and. ; Program in Physical Biology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892. ; Center for Cancer Research, fojot@mail.nih.gov. Y1 - 2015/02/03/ PY - 2015 DA - 2015 Feb 03 SP - 1571 EP - 1576 VL - 112 IS - 5 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - targeted therapies KW - microtubule targeting agents KW - DNA-damaging agents KW - combination chemotherapy KW - DNA repair protein trafficking KW - Humans KW - Cell Line, Tumor KW - Fluorescent Antibody Technique KW - DNA Repair KW - DNA Damage KW - Microtubules -- drug effects KW - DNA -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652441497?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Microtubule-targeting+agents+augment+the+toxicity+of+DNA-damaging+agents+by+disrupting+intracellular+trafficking+of+DNA+repair+proteins.&rft.au=Poruchynsky%2C+Marianne+S%3BKomlodi-Pasztor%2C+Edina%3BTrostel%2C+Shana%3BWilkerson%2C+Julia%3BRegairaz%2C+Marie%3BPommier%2C+Yves%3BZhang%2C+Xu%3BKumar+Maity%2C+Tapan%3BRobey%2C+Robert%3BBurotto%2C+Mauricio%3BSackett%2C+Dan%3BGuha%2C+Udayan%3BFojo%2C+Antonio+Tito&rft.aulast=Poruchynsky&rft.aufirst=Marianne&rft.date=2015-02-03&rft.volume=112&rft.issue=5&rft.spage=1571&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=1091-6490&rft_id=info:doi/10.1073%2Fpnas.1416418112 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-28 N1 - Date created - 2015-02-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10855-60 [12145320] Mol Biol Cell. 2012 Jan;23(1):1-6 [22210845] Biochem Pharmacol. 2012 Jun 15;83(12):1602-12 [22414726] Mol Cell Endocrinol. 2012 Sep 5;360(1-2):68-75 [21986558] Cell Cycle. 2012 Mar 1;11(5):963-73 [22333583] Cancer Res. 2012 Sep 15;72(18):4611-5 [22987486] N Engl J Med. 2012 Sep 27;367(13):1187-97 [22894553] Biochem Biophys Res Commun. 2012 Dec 7;429(1-2):57-62 [23131551] N Engl J Med. 2013 Jan 10;368(2):138-48 [23228172] Eur Urol. 2013 Mar;63(3):428-35 [23084329] Radiat Res. 2014 Jan;181(1):1-8 [24320053] Biochem Pharmacol. 2014 Mar 1;88(1):58-65 [24418411] Biochim Biophys Acta. 2014 May;1843(5):985-1001 [24486332] Proc Natl Acad Sci U S A. 2014 Apr 15;111(15):5723-8 [24706788] Cell Mol Life Sci. 2014 Jun;71(12):2289-97 [24448903] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213] Biochem Pharmacol. 1988 Oct 15;37(20):3995-4000 [3190743] Cancer Chemother Pharmacol. 1995;35(4):297-303 [7828272] Mol Cancer Ther. 2006 Feb;5(2):450-6 [16505120] Cell Cycle. 2006 Oct;5(19):2253-9 [16969106] Cytometry A. 2007 Sep;71(9):648-61 [17622968] Int J Oncol. 2008 Feb;32(2):435-9 [18202766] Cell Cycle. 2008 Apr 1;7(7):940-9 [18414063] Semin Oncol. 2008 Jun;35(3 Suppl 3):S6-S12 [18538179] Proc Natl Acad Sci U S A. 2008 Sep 16;105(37):14112-7 [18776048] Nucleic Acids Res. 2008 Oct;36(17):5678-94 [18772227] Cancer Immunol Immunother. 2010 May;59(5):663-74 [19890632] Mol Cancer Ther. 2010 May;9(5):1339-48 [20442307] Cancer Res. 2010 Jul 15;70(14):5870-9 [20587529] Lancet. 2010 Oct 2;376(9747):1147-54 [20888992] Mol Cancer Ther. 2010 Oct;9(10):2700-13 [20937595] Cancer Res. 2010 Oct 15;70(20):7992-8002 [20807808] Mol Cancer Ther. 2011 Feb;10(2):303-12 [21216936] Nat Rev Clin Oncol. 2011 Apr;8(4):244-50 [21283127] Biochim Biophys Acta. 2011 Jun;1807(6):679-88 [21216222] Cell Cycle. 2010 Mar 15;9(6):1207-13 [20237434] N Engl J Med. 2011 May 26;364(21):1995-2005 [21612468] Cancer Res. 2011 Sep 15;71(18):6019-29 [21799031] Clin Cancer Res. 2012 Jan 1;18(1):51-63 [22215906] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1073/pnas.1416418112 ER - TY - JOUR T1 - The V Gene Repertoires of Classical and Atypical Memory B Cells in Malaria-Susceptible West African Children AN - 1808687415; PQ0003460505 AB - Immunity to Plasmodium falciparum malaria is naturally acquired in individuals living in malaria-endemic areas of Africa. Abs play a key role in mediating this immunity; however, the acquisition of the components of Ab immunity, long-lived plasma cells and memory B cells (MBCs), is remarkably inefficient, requiring years of malaria exposure. Although long-lived classical MBCs (CD19+/CD20+/CD21+/CD27+/CD10-) are gradually acquired in response to natural infection, exposure to P. falciparum also results in a large expansion of what we have termed atypical MBCs (CD19+/CD20+/CD21-/CD27-/CD10-). At present, the function of atypical MBCs in malaria is not known, nor are the factors that drive their differentiation. To gain insight into the relationship between classical and atypical IgG+ MBCs, we compared the Ab H and L chain V gene repertoires of children living in a malaria-endemic region in Mali. We found that these repertoires were remarkably similar by a variety of criteria, including V gene usage, rate of somatic hypermutation, and CDR-H3 length and composition. The similarity in these repertoires suggests that classical MBCs and atypical MBCs differentiate in response to similar Ag-dependent selective pressures in malaria-exposed children and that atypical MBCs do not express a unique V gene repertoire. JF - Journal of Immunology AU - Zinocker, Severin AU - Schindler, Christine E AU - Skinner, Jeff AU - Rogosch, Tobias AU - Waisberg, Michael AU - Schickel, Jean-Nicolas AU - Meffre, Eric AU - Kayentao, Kassoum AU - Ongoiba, Aissata AU - Traore, Boubacar AU - Pierce, Susan K AD - Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852 Y1 - 2015/02/01/ PY - 2015 DA - 2015 Feb 01 SP - 929 EP - 939 PB - American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 United States VL - 194 IS - 3 SN - 0022-1767, 0022-1767 KW - Genetics Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts KW - Parasites KW - Human diseases KW - Mali KW - Lymphocytes B KW - Immunology KW - Immunological memory KW - Memory cells KW - Malaria KW - Plasmodium falciparum KW - Immunity KW - Children KW - Infection KW - Public health KW - Differentiation KW - Antibodies KW - Genes KW - somatic hypermutation KW - Plasma cells KW - G 07720:Immunogenetics KW - K 03400:Human Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - F 06910:Microorganisms & Parasites KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808687415?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Immunology&rft.atitle=The+V+Gene+Repertoires+of+Classical+and+Atypical+Memory+B+Cells+in+Malaria-Susceptible+West+African+Children&rft.au=Zinocker%2C+Severin%3BSchindler%2C+Christine+E%3BSkinner%2C+Jeff%3BRogosch%2C+Tobias%3BWaisberg%2C+Michael%3BSchickel%2C+Jean-Nicolas%3BMeffre%2C+Eric%3BKayentao%2C+Kassoum%3BOngoiba%2C+Aissata%3BTraore%2C+Boubacar%3BPierce%2C+Susan+K&rft.aulast=Zinocker&rft.aufirst=Severin&rft.date=2015-02-01&rft.volume=194&rft.issue=3&rft.spage=929&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunology&rft.issn=00221767&rft_id=info:doi/10.4049%2Fjimmunol.1402168 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Parasites; Human diseases; Genes; Immunology; Malaria; Immunity; Public health; Differentiation; Antibodies; Lymphocytes B; Memory cells; Immunological memory; somatic hypermutation; Infection; Children; Plasma cells; Plasmodium falciparum; Mali DO - http://dx.doi.org/10.4049/jimmunol.1402168 ER - TY - JOUR T1 - Log-odds sequence logos AN - 1776668087; PQ0002761999 AB - Motivation: DNA and protein patterns are usefully represented by sequence logos. However, the methods for logo generation in common use lack a proper statistical basis, and are non-optimal for recognizing functionally relevant alignment columns.Results: We redefine the information at a logo position as a per-observation multiple alignment log-odds score. Such scores are positive or negative, depending on whether a column's observations are better explained as arising from relatedness or chance. Within this framework, we propose distinct normalized maximum likelihood and Bayesian measures of column information. We illustrate these measures on High Mobility Group B (HMGB) box proteins and a dataset of enzyme alignments. Particularly in the context of protein alignments, our measures improve the discrimination of biologically relevant positions.Availability and implementation: Our new measures are implemented in an open-source Web-based logo generation program, which is available at http://www.ncbi.nlm.nih.gov/CBBresearch/Yu/logoddslogo/index.html. A stand-alone version of the program is also available from this site. Supplementary information: Supplementary data are available at Bioinformatics online. JF - Bioinformatics AU - Yu, Yi-Kuo AU - Capra, John A AU - Stojmirovic, Aleksandar AU - Landsman, David AU - Altschul, Stephen F AD - *To whom correspondence should be addressed., altschul@ncbi.nlm.nih.gov Y1 - 2015/02/01/ PY - 2015 DA - 2015 Feb 01 SP - 324 EP - 331 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 31 IS - 3 SN - 1367-4803, 1367-4803 KW - Biochemistry Abstracts 2: Nucleic Acids; Biotechnology and Bioengineering Abstracts KW - Computer programs KW - Statistics KW - Data processing KW - Bayesian analysis KW - Nucleotide sequence KW - High mobility group proteins KW - DNA KW - Enzymes KW - Bioinformatics KW - Internet KW - N 14810:Methods KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1776668087?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioinformatics&rft.atitle=Log-odds+sequence+logos&rft.au=Yu%2C+Yi-Kuo%3BCapra%2C+John+A%3BStojmirovic%2C+Aleksandar%3BLandsman%2C+David%3BAltschul%2C+Stephen+F&rft.aulast=Yu&rft.aufirst=Yi-Kuo&rft.date=2015-02-01&rft.volume=31&rft.issue=3&rft.spage=324&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtu634 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Computer programs; Data processing; Statistics; Bayesian analysis; Nucleotide sequence; DNA; High mobility group proteins; Enzymes; Bioinformatics; Internet DO - http://dx.doi.org/10.1093/bioinformatics/btu634 ER - TY - JOUR T1 - Clinical Presentation of Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections in Research and Community Settings AN - 1773834997; PQ0002687332 AB - Background: The first cases of pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) were described>15 years ago. Since that time, the literature has been divided between studies that successfully demonstrate an etiologic relationship between Group A streptococcal (GAS) infections and childhood-onset obsessive-compulsive disorder (OCD), and those that fail to find an association. One possible explanation for the conflicting reports is that the diagnostic criteria proposed for PANDAS are not specific enough to describe a unique and homogeneous cohort of patients. To evaluate the validity of the PANDAS criteria, we compared clinical characteristics of PANDAS patients identified in two community practices with a sample of children meeting full research criteria for PANDAS. Methods: A systematic review of clinical records was used to identify the presence or absence of selected symptoms in children evaluated for PANDAS by physicians in Hinsdale, Illinois (n=52) and Bethesda, Maryland (n=40). Results were compared against data from participants in National Institute of Mental Health (NIMH) research investigations of PANDAS (n=48). Results: As described in the original PANDAS cohort, males outnumbered females (95:45) by 2:1, and symptoms began in early childhood (7.3 plus or minus 2.7 years). Clinical presentations were remarkably similar across sites, with all children reporting acute onset of OCD symptoms and multiple comorbidities, including separation anxiety (86-92%), school issues (75-81%), sleep disruptions (71%), tics (60-65%), urinary symptoms (42-81%), and others. Twenty of the community cases (22%) failed to meet PANDAS criteria because of an absence of documentation of GAS infections. Conclusions: The diagnostic criteria for PANDAS can be used by clinicians to accurately identify patients with common clinical features and shared etiology of symptoms. Although difficulties in documenting an association between GAS infection and symptom onset/exacerbations may preclude a diagnosis of PANDAS in some children with acute-onset OCD, they do appear to meet criteria for pediatric acute-onset neuropsychiatric syndrome (PANS). JF - Journal of Child and Adolescent Psychopharmacology AU - Swedo, Susan E AU - Seidlitz, Jakob AU - Kovacevic, Miro AU - Latimer, MElizabeth AU - Hommer, Rebecca AU - Lougee, Lorraine AU - Grant, Paul AD - Pediatrics & Developmental Neuroscience Branch, National Institute of Mental Health, Bethesda Maryland. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 26 EP - 30 PB - Mary Ann Liebert, Inc., 2 Madison Ave Larchmont NY 10538 United States VL - 25 IS - 1 SN - 1044-5463, 1044-5463 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Streptococcus KW - Etiology KW - Data processing KW - Anxiety KW - Pediatrics KW - Adolescence KW - Infection KW - Children KW - Mental disorders KW - Sleep KW - Obsessive compulsive disorder KW - Pans KW - J 02310:Genetics & Taxonomy KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1773834997?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Child+and+Adolescent+Psychopharmacology&rft.atitle=Clinical+Presentation+of+Pediatric+Autoimmune+Neuropsychiatric+Disorders+Associated+with+Streptococcal+infections+in+Research+and+Community+Settings&rft.au=Swedo%2C+Susan+E%3BSeidlitz%2C+Jakob%3BKovacevic%2C+Miro%3BLatimer%2C+MElizabeth%3BHommer%2C+Rebecca%3BLougee%2C+Lorraine%3BGrant%2C+Paul&rft.aulast=Swedo&rft.aufirst=Susan&rft.date=2015-02-01&rft.volume=25&rft.issue=1&rft.spage=26&rft.isbn=&rft.btitle=&rft.title=Journal+of+Child+and+Adolescent+Psychopharmacology&rft.issn=10445463&rft_id=info:doi/10.1089%2Fcap.2014.0073 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Number of references - 21 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Etiology; Mental disorders; Data processing; Anxiety; Pediatrics; Sleep; Adolescence; Obsessive compulsive disorder; Children; Infection; Pans; Streptococcus DO - http://dx.doi.org/10.1089/cap.2014.0073 ER - TY - JOUR T1 - Interactions between ethanol and the endocannabinoid system at GABAergic synapses on basolateral amygdala principal neurons AN - 1758247138; PQ0002436947 AB - The basolateral amygdala (BLA) plays crucial roles in stimulus value coding, as well as drug and alcohol dependence. Ethanol alters synaptic transmission in the BLA, while endocannabinoids (eCBs) produce presynaptic depression at BLA synapses. Recent studies suggest interactions between ethanol and eCBs that have important consequences for alcohol drinking behavior. To determine how ethanol and eCBs interact in the BLA, we examined the physiology and pharmacology of GABAergic synapses onto BLA pyramidal neurons in neurons from young rats. Application of ethanol at concentrations relevant to intoxication increased, in both young and adult animals, the frequency of spontaneous and miniature GABAergic inhibitory postsynaptic currents, indicating a presynaptic site of ethanol action. Ethanol did not potentiate sIPSCs during inhibition of adenylyl cyclase while still exerting its effect during inhibition of protein kinase A. Activation of type 1 cannabinoid receptors (CB1) in the BLA inhibited GABAergic transmission via an apparent presynaptic mechanism, and prevented ethanol potentiation. Surprisingly, ethanol potentiation was also prevented by CB1 antagonists/inverse agonists. Brief depolarization of BLA pyramidal neurons suppressed GABAergic transmission (depolarization-induced suppression of inhibition [DSI]), an effect previously shown to be mediated by postsynaptic eCB release and presynaptic CB1 activation. A CB1-mediated suppression of GABAergic transmission was also produced by combined afferent stimulation at 0.1 Hz (LFS), and postsynaptic loading with the eCB arachidonoyl ethanolamide (AEA). Both DSI and LFS-induced synaptic depression were prevented by ethanol. Our findings indicate antagonistic interactions between ethanol and eCB/CB1 modulation at GABAergic BLA synapses that may contribute to eCB roles in ethanol seeking and drinking. JF - Alcohol AU - Talani, Giuseppe AU - Lovinger, David M AD - Section on Synaptic Pharmacology, Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA PY - 2015 SP - 781 EP - 794 PB - Elsevier B.V., Box 882 New York NY 10159 United States VL - 49 IS - 8 SN - 0741-8329, 0741-8329 KW - CSA Neurosciences Abstracts; Toxicology Abstracts KW - Alcohol KW - CB1 receptor KW - Synapse KW - Inhibition KW - Arachidonoyl ethanolamide KW - Cyclic AMP KW - Intoxication KW - Inverse agonists KW - Coding KW - Protein kinase A KW - Sensory neurons KW - synaptic depression KW - Pharmacology KW - Potentiation KW - gamma -Aminobutyric acid KW - Inhibitory postsynaptic potentials KW - Drug abuse KW - Antagonists KW - Drug dependence KW - Neurotransmission KW - Drinking behavior KW - Amygdala KW - Cannabinoid CB1 receptors KW - Pyramidal cells KW - Ethanol KW - X 24380:Social Poisons & Drug Abuse KW - N3 11001:Behavioral and Cognitive Neuroscience UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1758247138?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcohol&rft.atitle=Interactions+between+ethanol+and+the+endocannabinoid+system+at+GABAergic+synapses+on+basolateral+amygdala+principal+neurons&rft.au=Talani%2C+Giuseppe%3BLovinger%2C+David+M&rft.aulast=Talani&rft.aufirst=Giuseppe&rft.date=2015-02-01&rft.volume=49&rft.issue=8&rft.spage=781&rft.isbn=&rft.btitle=&rft.title=Alcohol&rft.issn=07418329&rft_id=info:doi/10.1016%2Fj.alcohol.2015.08.006 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Number of references - 94 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Inverse agonists; Intoxication; Coding; Protein kinase A; Sensory neurons; Pharmacology; synaptic depression; Potentiation; Inhibitory postsynaptic potentials; gamma -Aminobutyric acid; Drug abuse; Antagonists; Drug dependence; Neurotransmission; Drinking behavior; Amygdala; Cannabinoid CB1 receptors; Pyramidal cells; Ethanol DO - http://dx.doi.org/10.1016/j.alcohol.2015.08.006 ER - TY - JOUR T1 - Target enhanced 2D similarity search by using explicit biological activity annotations and profiles AN - 1751217320; PQ0002365703 AB - The enriched biological activity information of compounds in large and freely-accessible chemical databases like the PubChem Bioassay Database has become a powerful research resource for the scientific research community. Currently, 2D fingerprint based conventional similarity search (CSS) is the most common widely used approach for database screening, but it does not typically incorporate the relative importance of fingerprint bits to biological activity. In this study, a large-scale similarity search investigation has been carried out on 208 well-defined compound activity classes extracted from PubChem Bioassay Database. An analysis was performed to compare the search performance of three types of 2D similarity search approaches: 2D fingerprint based conventional similarity search approach (CSS), iterative similarity search approach with multiple active compounds as references (ISS), and fingerprint based iterative similarity search with classification (ISC), which can be regarded as the combination of iterative similarity search with active references and a reversed iterative similarity search with inactive references. Compared to the search results returned by CSS, ISS improves recall but not precision. Although ISC causes the false rejection of active hits, it improves the precision with statistical significance, and outperforms both ISS and CSS. In a second part of this study, we introduce the profile concept into the three types of searches. We find that the profile based non-iterative search can significantly improve the search performance by increasing the recall rate. We also find that profile based ISS (PBISS) and profile based ISC (PBISC) significantly decreases ISS search time without sacrificing search performance. On the basis of our large-scale investigation directed against a wide spectrum of pharmaceutical targets, we conclude that ISC and ISS searches perform better than 2D fingerprint similarity searching and that profile based versions of these algorithms do nearly as well in less time. We also suggest that the profile version of the iterative similarity searches are both better performing and potentially quicker than the standard algorithm. JF - Journal of Cheminformatics AU - Yu, Xiang AU - Geer, Lewis Y AU - Han, Lianyi AU - Bryant, Stephen H AD - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, 8600 Rockville Pike, Bethesda, MD, 20894, USA, lewisg@ncbi.nlm.nih.gov PY - 2015 SP - 1 EP - 12 PB - Springer-Verlag (Heidelberg), Tiergartenstrasse 17 Heidelberg 69121 Germany VL - 7 IS - 1 KW - Biotechnology and Bioengineering Abstracts KW - Databases KW - Statistics KW - Classification KW - Informatics KW - Algorithms KW - Pharmaceuticals KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751217320?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Cheminformatics&rft.atitle=Target+enhanced+2D+similarity+search+by+using+explicit+biological+activity+annotations+and+profiles&rft.au=Yu%2C+Xiang%3BGeer%2C+Lewis+Y%3BHan%2C+Lianyi%3BBryant%2C+Stephen+H&rft.aulast=Yu&rft.aufirst=Xiang&rft.date=2015-02-01&rft.volume=7&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+Cheminformatics&rft.issn=1758-2946&rft_id=info:doi/10.1186%2Fs13321-015-0103-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 41 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Databases; Statistics; Classification; Informatics; Algorithms; Pharmaceuticals DO - http://dx.doi.org/10.1186/s13321-015-0103-5 ER - TY - JOUR T1 - A prospective study of occupational physical activity and breast cancer risk AN - 1751214910; PQ0002272398 AB - Physical activity has been associated with reduced breast cancer risk, but studies of occupational activity have produced inconsistent results. The purpose of this study was to evaluate the relationship between occupational physical activity and breast cancer in a prospective study of women with a family history of breast cancer. We studied breast cancer risk in 47,649 Sister Study participants with an occupational history. Information on occupational activity and breast cancer risk factors was collected during baseline interviews (2004-2009). Physical activity at each job was self-reported and categorized as mostly sitting, sitting and standing equally, mostly standing, and active. Multivariable Cox proportional hazards regression was used to evaluate associations between lifetime occupational activity and incident breast cancer, after adjusting for established risk factors and recreational activity. During follow-up, a total of 1,798 breast cancer diagnoses were reported. Compared with women who did not spend any time in active jobs, women who spent a high proportion ( greater than or equal to 75 %) of their working years in active jobs had a reduced risk of breast cancer (HR 0.72; 95 % CI 0.52-0.98). Associations were strongest among overweight (HR 0.64; 95 % CI 0.42-0.98) and postmenopausal (HR 0.67; 95 % CI 0.45-0.98) women. Occupational activity was associated with a reduced risk of breast cancer. Occupational activity is a domain of physical activity that should be further examined in studies of postmenopausal breast cancer risk. Additional research is necessary to better understand the mechanisms underlying the relationships between occupational activity, body size, and breast cancer. JF - Cancer Causes & Control AU - Ekenga, Christine C AU - Parks, Christine G AU - Sandler, Dale P AD - Division of Public Health Sciences, Department of Surgery, Washington University School of Medicine, Campus Box 8100, 600 South Taylor Avenue, Saint Louis, MO, 63110, USA, sandler@niehs.nih.gov PY - 2015 SP - 1779 EP - 1789 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 26 IS - 12 SN - 0957-5243, 0957-5243 KW - Toxicology Abstracts KW - Body weight KW - Post-menopause KW - Physical activity KW - Risk factors KW - Body size KW - Breast cancer KW - X 24490:Other UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1751214910?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Causes+%26+Control&rft.atitle=A+prospective+study+of+occupational+physical+activity+and+breast+cancer+risk&rft.au=Ekenga%2C+Christine+C%3BParks%2C+Christine+G%3BSandler%2C+Dale+P&rft.aulast=Ekenga&rft.aufirst=Christine&rft.date=2015-02-01&rft.volume=26&rft.issue=12&rft.spage=1779&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-015-0671-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-12-01 N1 - Number of references - 51 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Body weight; Post-menopause; Risk factors; Physical activity; Body size; Breast cancer DO - http://dx.doi.org/10.1007/s10552-015-0671-8 ER - TY - JOUR T1 - Genetic Counselors' Implicit Racial Attitudes and Their Relationship to Communication AN - 1732813149; PQ0002197763 AB - Objective: Implicit racial attitudes are thought to shape interpersonal interactions and may contribute to health-care disparities. This study explored the relationship between genetic counselors' implicit racial attitudes and their communication during simulated genetic counseling sessions. Method: A nationally representative sample of genetic counselors completed a web-based survey that included the Race Implicit Association Test (IAT; Greenwald, McGhee, & Schwartz, 1998; Cooper et al., 2012). A subset of these counselors (n = 67) had participated in an earlier study in which they were video recorded counseling Black, Hispanic, and non-Hispanic White SCs about their prenatal or cancer risks. The counselors' IAT scores were related to their session communications through robust regression modeling. Results: Genetic counselors showed a moderate to strong pro-White bias on the Race IAT (M = 0.41, SD = 0.35). Counselors with stronger pro-White bias were rated as displaying lower levels of positive affect (p < .05) and tended to use less emotionally responsive communication (p < .10) when counseling minority SCs. When counseling White SCs, pro-White bias was associated with lower levels of verbal dominance during sessions (p < .10). Stronger pro-White bias was also associated with more positive ratings of counselors' nonverbal effectiveness by White SCs. Conclusion: Implicit racial bias is associated with negative markers of communication in minority client sessions and may contribute to racial disparities in processes of care related to genetic services. JF - Health Psychology AU - Schaa, Kendra L AU - Biesecker, Barbara B AU - Roter, Debra L AU - Cooper, Lisa A AU - Erby, Lori H AD - The Johns Hopkins Bloomberg School of Public Health and National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, lori.erby@nih.gov Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 111 EP - 119 PB - American Psychological Association, 750 First St., N.E. Washington DC 20002-4242 United States VL - 34 IS - 2 SN - 0278-6133, 0278-6133 KW - Genetics Abstracts; Health & Safety Science Abstracts; Risk Abstracts KW - implicit attitudes KW - race/ethnicity KW - genetic counseling KW - RIAS KW - patient-provider communication KW - Emotions KW - Prenatal experience KW - Communication KW - Cancer KW - Dominance KW - Health risks KW - Attitudes KW - Communications KW - Genetic screening KW - Ethnic groups KW - Races KW - Genetic counselling KW - G 07880:Human Genetics KW - H 11000:Diseases/Injuries/Trauma KW - R2 23110:Psychological aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732813149?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Psychology&rft.atitle=Genetic+Counselors%27+Implicit+Racial+Attitudes+and+Their+Relationship+to+Communication&rft.au=Schaa%2C+Kendra+L%3BBiesecker%2C+Barbara+B%3BRoter%2C+Debra+L%3BCooper%2C+Lisa+A%3BErby%2C+Lori+H&rft.aulast=Schaa&rft.aufirst=Kendra&rft.date=2015-02-01&rft.volume=34&rft.issue=2&rft.spage=111&rft.isbn=&rft.btitle=&rft.title=Health+Psychology&rft.issn=02786133&rft_id=info:doi/10.1037%2Fhea0000155 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Emotions; Communication; Cancer; Races; Dominance; Genetic counselling; Health risks; Attitudes; Prenatal experience; Communications; Genetic screening; Ethnic groups DO - http://dx.doi.org/10.1037/hea0000155 ER - TY - JOUR T1 - Bisphenol A, benzophenone-type ultraviolet filters, and phthalates in relation to uterine leiomyoma AN - 1727679009; PQ0002193729 AB - Bisphenol A, benzophenone-type UV filters, and phthalates are chemicals in high production and use including in a range of personal care products. Exposure of humans to these chemicals has been shown to affect endocrine function. Although short-lived, widespread exposure may lead to continual opportunity for these chemicals to elicit health effects in humans. The association of these chemicals with incident uterine leiomyoma, an estrogen sensitive disease, is not known. Urinary concentrations of bisphenol A (BPA), five benzophenone-type UV filters (2-hydroxy-4-methoxybenzophenone (2OH-4MeO-BP), 2,4-dihydroxybenzophenone (2,4OH-BP), 2,2 super(3)-dihydroxybenzophenone (2,2 super(3)OH-4MeO-BP), 2,2 super(3)4,4 super(3)-tetrahydroxybenzophenone (2,2 super(3)4,4 super(3)OH-BP), and 4-hydroxybenzophenone (4OH-BP), and 14 phthalate monoesters were quantified in 495 women who later underwent laparoscopy/laparotomy at 14 clinical sites for the diagnosis of fibroids. Significantly higher geometric mean creatinine-corrected concentrations of BPA, 2,4OH-BP, and 2OH-4MeO-BP were observed in women with than without fibroids [BPA: 2.09 mu g/g vs. 1.46 mu g/g p=0.004; 2,4OH-BP:11.10 mu g/g vs. 6.71 mu g/g p=0.01; 2OH-4MeO-BP: 11.31 mu g/g vs. 6.10 mu g/g p=0.01]. Mono-methyl phthalate levels were significantly lower in women with than without fibroids (1.78 mu g/g vs. 2.40 mu g/g). However, none of the exposures were associated with a significant odds ratio even when adjusting for relevant covariates. There was a lack of an association between select nonpersistent chemicals and the odds of a fibroid diagnosis. JF - Environmental Research AU - Pollack, A Z AU - Buck Louis, GM AU - Chen, Z AU - Sun, L AU - Trabert, B AU - Guo, Y AU - Kannan, K AD - Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6100 Executive Blvd. Suite 7B03, Rockville, MD 20852 USA PY - 2015 SP - 101 EP - 107 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 137 SN - 0013-9351, 0013-9351 KW - Environment Abstracts KW - (2OH-4MeO-BP) 2-hydroxy-4-methoxybenzophenone KW - (2,4OH-BP) 2,4-dihydroxybenzophenone KW - (2,2 super(3)OH-4MeO-BP) 2,2 super(3)-dihydroxybenzophenone KW - (2,2 super(3)4,4 super(3)OH-BP) 2,2 super(3)4,4 super(3)-tetrahydroxybenzophenone KW - (4OH-BP) 4-hydroxybenzophenone KW - (BMI) body mass index KW - (BPA) bisphenol A KW - (CI) confidence interval KW - (DEHP) di-2-ethylhexyl phthalate KW - (MBzP) mono-benzyl phthalate KW - (MnBP) mono-n-butyl phthalate KW - (MiBP) mono-isobutyl phthalate KW - (MCHP) mono-cyclohexyl phthalate KW - (MEP) mono-ethyl phthalate KW - (MEHP) mono-2-ethylhexyl phthalate KW - (MEHHP) mono-(2-ethyl-5-hydroxyhexyl) phthalate KW - (MEOHP) mono-(2-ethyl-5-oxohexyl) phthalate KW - (MECPP) mono-(2-ethyl-5-carboxypentyl) phthalate KW - (MiNP) mono-isononyl phthalate KW - (MCNP) mono-(carboxynonyl) phthalate KW - (MMP) mono-methyl phthalate KW - (MCPP) mono-(3-carboxypropyl) phthalate KW - (MOP) mono-n-octyl phthalate KW - (NHANES) National Health and Nutrition Examination Survey KW - odds ratio (OR) KW - polycystic ovary syndrome (PCOS) KW - Benzophenone KW - Bisphenol A KW - Fibroid KW - Phthalate KW - Ultraviolet filter KW - Chemicals KW - Filters KW - Estrogens KW - Consumer products KW - Phthalates KW - Urine KW - Laparoscopy KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727679009?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvabstractsmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Research&rft.atitle=Bisphenol+A%2C+benzophenone-type+ultraviolet+filters%2C+and+phthalates+in+relation+to+uterine+leiomyoma&rft.au=Pollack%2C+A+Z%3BBuck+Louis%2C+GM%3BChen%2C+Z%3BSun%2C+L%3BTrabert%2C+B%3BGuo%2C+Y%3BKannan%2C+K&rft.aulast=Pollack&rft.aufirst=A&rft.date=2015-02-01&rft.volume=137&rft.issue=&rft.spage=101&rft.isbn=&rft.btitle=&rft.title=Environmental+Research&rft.issn=00139351&rft_id=info:doi/10.1016%2Fj.envres.2014.06.028 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Bisphenol A; Filters; Chemicals; Estrogens; Consumer products; Laparoscopy; Urine; Phthalates DO - http://dx.doi.org/10.1016/j.envres.2014.06.028 ER - TY - JOUR T1 - Couples' urinary bisphenol A and phthalate metabolite concentrations and the secondary sex ratio AN - 1727677944; PQ0002193733 AB - With limited research focusing on non-persistent chemicals as exogenous factors affecting human sex selection, this study aimed to evaluate the association of urinary bisphenol A (BPA) and phthalate metabolite concentrations with the secondary sex ratio (SSR), defined as the ratio of male to female live births. The current analysis is limited to singleton live births (n=220, 43.9%) from the Longitudinal Investigation of Fertility and the Environment (LIFE) Study, in which couples discontinuing contraception with the intention of becoming pregnant were enrolled and followed while trying for pregnancy and through delivery for those achieving pregnancy. Using modified Poisson regression models accounting for potential confounders, we estimated the relative risks (RRs) of a male birth per standard deviation change in the log-transformed maternal, paternal, and couple urinary BPA and 14 phthalate metabolite concentrations (ng/mL) measured upon enrollment. When maternal and paternal chemical concentrations were modeled jointly, paternal BPA (RR, 0.77; 95% confidence interval [CI], 0.62-0.95) and mono-isobutyl phthalate (RR, 0.82; 95% CI, 0.67-1.00) were significantly associated with a female excess. Contrarily, maternal BPA (RR, 1.16; 95% CI, 1.03-1.31), mono-isobutyl phthalate (RR, 1.28; 95% CI, 1.06-1.54), mono-benzyl phthalate (RR, 1.31; 95% CI, 1.08-1.58), and mono-n-butyl phthalate (RR, 1.24; 95% CI, 1.01-1.51) were significantly associated with a male excess. These findings underscore varying patterns for the SSR in relation to parental exposures. Given the absence of previous investigation, these partner-specific associations of non-persistent chemicals with the SSR need future corroboration. JF - Environmental Research AU - Bae, Jisuk AU - Kim, Sungduk AU - Kannan, Kurunthachalam AU - Buck Louis, Germaine M AD - Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6100 Executive Boulevard, Rockville, MD 20852, USA Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 450 EP - 457 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 137 SN - 0013-9351, 0013-9351 KW - Risk Abstracts; Environment Abstracts KW - BPA bisphenol A KW - BzBP benzylbutyl phthalate KW - CI confidence interval KW - DBP dibutyl phthalate KW - DEHP di-2-ethylhexyl phthalate KW - DiBP di-isobutyl phthalate KW - EDC endocrine-disrupting chemical KW - GED General Educational Development KW - GM geometric mean KW - LIFE Longitudinal Investigation of Fertility and the Environment KW - LOD limit of detection KW - MBzP mono-benzyl phthalate KW - MCHP mono-cyclohexyl phthalate KW - MCMHP mono-[(2-carboxymethyl) hexyl] phthalate KW - MCPP mono-(3-carboxypropyl) phthalate KW - MECPP mono-(2-ethyl-5-carboxypentyl) phthalate KW - MEHHP mono-(2-ethyl-5-hydroxyhexyl) phthalate KW - MEHP mono-2-ethylhexyl phthalate KW - MEOHP mono-(2-ethyl-5-oxohexyl) phthalate KW - MEP mono-ethyl phthalate KW - MiBP mono-isobutyl phthalate KW - MiNP mono-isononyl phthalate KW - MMP mono-methyl phthalate KW - MnBP mono-n-butyl phthalate KW - MOP mono-n-octyl phthalate KW - PCB polychlorinated biphenyl KW - RR relative risk KW - SD standard deviation KW - SSR secondary sex ratio KW - Bisphenol A KW - Endocrine disruptors KW - Fertility KW - Phthalates KW - Sex ratio KW - Chemicals KW - Urine KW - Risk factors KW - Metabolites KW - Pregnancy KW - ENA 13:Population Planning & Control KW - R2 23050:Environment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727677944?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Research&rft.atitle=Couples%27+urinary+bisphenol+A+and+phthalate+metabolite+concentrations+and+the+secondary+sex+ratio&rft.au=Bae%2C+Jisuk%3BKim%2C+Sungduk%3BKannan%2C+Kurunthachalam%3BBuck+Louis%2C+Germaine+M&rft.aulast=Bae&rft.aufirst=Jisuk&rft.date=2015-02-01&rft.volume=137&rft.issue=&rft.spage=450&rft.isbn=&rft.btitle=&rft.title=Environmental+Research&rft.issn=00139351&rft_id=info:doi/10.1016%2Fj.envres.2014.11.011 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-07-07 N1 - SubjectsTermNotLitGenreText - Bisphenol A; Chemicals; Fertility; Sex ratio; Urine; Phthalates; Risk factors; Metabolites; Pregnancy DO - http://dx.doi.org/10.1016/j.envres.2014.11.011 ER - TY - JOUR T1 - Preconception and early pregnancy air pollution exposures and risk of gestational diabetes mellitus AN - 1727677615; PQ0002193714 AB - Background Air pollution has been linked to gestational diabetes mellitus (GDM) but no studies have evaluated impact of preconception and early pregnancy air pollution exposures on GDM risk. Methods Electronic medical records provided data on 219,952 singleton deliveries to mothers with (n=11,334) and without GDM (n=208,618). Average maternal exposures to particulate matter (PM) less than or equal to 2.5 mu m (PM2.5) and PM2.5 constituents, PM less than or equal to 10 mu m (PM10), nitrogen oxides (NO x ), carbon monoxide, sulfur dioxide (SO2) and ozone (O3) were estimated for the 3-month preconception window, first trimester, and gestational weeks 1-24 based on modified Community Multiscale Air Quality models for delivery hospital referral regions. Binary regression models with robust standard errors estimated relative risks (RR) for GDM per interquartile range (IQR) increase in pollutant concentrations adjusted for study site, maternal age and race/ethnicity. Results Preconception maternal exposure to NO X (RR=1.09, 95% CI: 1.04, 1.13) and SO2 (RR=1.05, 1.01, 1.09) were associated with increased risk of subsequent GDM and risk estimates remained elevated for first trimester exposure. Preconception O3 was associated with lower risk of subsequent GDM (RR=0.93, 0.90, 0.96) but risks increased later in pregnancy. Conclusion Maternal exposures to NO x and SO2 preconception and during the first few weeks of pregnancy were associated with increased GDM risk. O3 appeared to increase GDM risk in association with mid-pregnancy exposure but not in earlier time windows. These common exposures merit further investigation. JF - Environmental Research AU - Robledo, Candace A AU - Mendola, Pauline AU - Yeung, Edwina AU - Maennisto, Tuija AU - Sundaram, Rajeshwari AU - Liu, Danping AU - Ying, Qi AU - Sherman, Seth AU - Grantz, Katherine L AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Division of Intramural Population Health Research, Epidemiology Branch, Rockville, MD 20892, USA PY - 2015 SP - 316 EP - 322 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 137 SN - 0013-9351, 0013-9351 KW - Risk Abstracts; Pollution Abstracts; Environment Abstracts KW - AQRH Air Quality and Reproductive Health Study KW - BMI body mass index KW - CI confidence interval KW - CMAQ Community Multi-scale Air Quality Model KW - CO carbon monoxide KW - CSL Consortium on Safe Labor Study KW - EPA US Environmental Protection Agency KW - GDM gestational diabetes mellitus KW - LMP last menstrual period KW - PM10 particulate matter less than or equal to 10 mu m KW - PM2.5 fine particulate matter less than or equal to 2.5 mu m KW - RR relative risk KW - O3 ozone KW - NO X nitrogen oxides KW - SO2 sulfur dioxides KW - Preconception KW - Pregnancy KW - Air pollution KW - Gestational diabetes KW - Particle size KW - Age KW - Air quality KW - Particulates KW - Nitrogen oxides KW - Diabetes mellitus KW - Carbon monoxide KW - Photochemicals KW - Sulfur dioxide KW - Ethnic groups KW - Ozone KW - Hospitals KW - P 0000:AIR POLLUTION KW - R2 23050:Environment KW - ENA 01:Air Pollution UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1727677615?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Research&rft.atitle=Preconception+and+early+pregnancy+air+pollution+exposures+and+risk+of+gestational+diabetes+mellitus&rft.au=Robledo%2C+Candace+A%3BMendola%2C+Pauline%3BYeung%2C+Edwina%3BMaennisto%2C+Tuija%3BSundaram%2C+Rajeshwari%3BLiu%2C+Danping%3BYing%2C+Qi%3BSherman%2C+Seth%3BGrantz%2C+Katherine+L&rft.aulast=Robledo&rft.aufirst=Candace&rft.date=2015-02-01&rft.volume=137&rft.issue=&rft.spage=316&rft.isbn=&rft.btitle=&rft.title=Environmental+Research&rft.issn=00139351&rft_id=info:doi/10.1016%2Fj.envres.2014.12.020 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Particle size; Age; Air quality; Particulates; Nitrogen oxides; Pregnancy; Air pollution; Carbon monoxide; Diabetes mellitus; Sulfur dioxide; Photochemicals; Ethnic groups; Hospitals; Ozone DO - http://dx.doi.org/10.1016/j.envres.2014.12.020 ER - TY - JOUR T1 - Motor Neuron Differentiation from Pluripotent Stem Cells and Other Intermediate Proliferative Precursors that can be Discriminated by Lineage Specific Reporters AN - 1709174559; PQ0001224467 AB - We have used a four stage protocol to generate spinal motor neurons (MNs) from human embryonic stem cells (ESCs) and human induced pluripotent stem cells (iPSCs). These stages include the pluripotent stem cell (PSC) stage, neural stem cell (NSC) stage, OLIG2 expressing motor neuron precursor (MNP) stage, and HB9 expressing mature-MN stage. To optimize the differentiation protocol reporter lines marking the NSC and MNP stages were used. The NSC stage is a pro-proliferative precursor stage at which cells can be directed to differentiate to other neural types like cortical neurons also, in addition to MNs; thus, NSCs can be expanded and stored for future differentiation to different neural types thereby, shortening the differentiation interval as compared to the complete process of differentiation from ESCs or iPSCs. Additionally, we find that OLIG2 positive cells at the MNP stage can be cryopreserved and then recovered to continue the process of MN differentiation, thereby providing a highly stable and reproducible technique for bulk differentiation. MNPs were differentiated to MNs expressing the marker HB9 demonstrating that mature-MNs can be generated with this protocol. JF - Stem Cell Reviews AU - Jha, Balendu Shekhar AU - Rao, Mahendra AU - Malik, Nasir AD - Laboratory of Stem Cell Biology, National Institutes of Health (NIH), Bethesda, MD, USA, malikn@mail.nih.gov PY - 2015 SP - 194 EP - 204 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 11 IS - 1 SN - 1550-8943, 1550-8943 KW - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts KW - Differentiation KW - Motor neurons KW - Stem cells KW - Cortex KW - Embryo cells KW - Inhibitory postsynaptic potentials KW - Olig2 protein KW - Neural stem cells KW - Cryopreservation KW - N3 11003:Developmental neuroscience KW - W 30945:Fermentation & Cell Culture UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1709174559?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+Cell+Reviews&rft.atitle=Motor+Neuron+Differentiation+from+Pluripotent+Stem+Cells+and+Other+Intermediate+Proliferative+Precursors+that+can+be+Discriminated+by+Lineage+Specific+Reporters&rft.au=Jha%2C+Balendu+Shekhar%3BRao%2C+Mahendra%3BMalik%2C+Nasir&rft.aulast=Jha&rft.aufirst=Balendu&rft.date=2015-02-01&rft.volume=11&rft.issue=1&rft.spage=194&rft.isbn=&rft.btitle=&rft.title=Stem+Cell+Reviews&rft.issn=15508943&rft_id=info:doi/10.1007%2Fs12015-014-9541-0 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-09-01 N1 - Number of references - 40 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Motor neurons; Differentiation; Stem cells; Cortex; Embryo cells; Inhibitory postsynaptic potentials; Olig2 protein; Cryopreservation; Neural stem cells DO - http://dx.doi.org/10.1007/s12015-014-9541-0 ER - TY - JOUR T1 - Women Caregivers of Persons with Brain Tumour: A Psychosocial Needs Assessment in a Tertiary Care Hospital in Bangalore AN - 1690397231; 4680520 AB - The diagnosis of a brain tumour poses severe challenges to patients as well as their caregivers. As caregivers, women play an important role. However, most of the literature on brain tumours has failed to emphasise the invaluable services of women caregivers, and their psychosocial needs have been overlooked. The current study aims to highlight this neglected aspect. Thirty women caregivers were selected through purposive sampling and their needs were assessed using a semi-structured questionnaire under five heads such as, professional service needs, informational needs, psychological/emotional needs, personal and spiritual needs and social support needs. It was found that some of their needs were unmet, especially their psychological/emotional and informational needs. Thus, gender-specific interventions are recommended across neuro-oncological settings. Reprinted by permission of Sage Publications India JF - Indian journal of gender studies AU - Amaresha, Anekal AU - Reddy, N AU - Ahmed, Atiq AU - Ross, Diana AU - Arthur, Julian AD - National Institute of Mental Health and Neurosciences ; Central University of Rajasthan ; Richmond Fellowship Post Graduate College for Psycho-Social Rehabilitation Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 41 EP - 62 VL - 22 IS - 1 SN - 0971-5215, 0971-5215 KW - Sociology KW - India KW - Gendered space KW - Women homeworkers KW - Karnataka KW - Cancer KW - Gender roles KW - Community care UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1690397231?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Indian+journal+of+gender+studies&rft.atitle=Women+Caregivers+of+Persons+with+Brain+Tumour%3A+A+Psychosocial+Needs+Assessment+in+a+Tertiary+Care+Hospital+in+Bangalore&rft.au=Amaresha%2C+Anekal%3BReddy%2C+N%3BAhmed%2C+Atiq%3BRoss%2C+Diana%3BArthur%2C+Julian&rft.aulast=Amaresha&rft.aufirst=Anekal&rft.date=2015-02-01&rft.volume=22&rft.issue=1&rft.spage=41&rft.isbn=&rft.btitle=&rft.title=Indian+journal+of+gender+studies&rft.issn=09715215&rft_id=info:doi/10.1177%2F0971521514556944 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-06-23 N1 - Last updated - 2015-06-23 N1 - SubjectsTermNotLitGenreText - 2604 11949 13521; 13600 13682; 5428; 5430 5421 6091 12092; 1939 3617 6220; 197 175 387 30 DO - http://dx.doi.org/10.1177/0971521514556944 ER - TY - JOUR T1 - Fetal Origins of Malarial Disease: Cord Blood Cytokines as Risk Markers for Pediatric Severe Malarial Anemia AN - 1687673895; PQ0001568806 AB - Background. Severe malarial anemia (SMA) remains a major cause of pediatric illness and mortality in Sub-Saharan Africa. Here we test the hypothesis that prenatal exposures, reflected by soluble inflammatory mediators in cord blood, can condition an individual's susceptibility to SMA. Methods. In a Tanzanian birth cohort (n = 743), we measured cord blood concentrations of tumor necrosis factor (TNF), TNF receptors I and II (TNF-RI and TNF-RII), interleukin (IL)-1 beta , IL-4, IL-5, IL-6, IL-10, and interferon gamma (IFN- gamma ). After adjusting for conventional covariates, we calculated the hazard ratios (HR) for time to first SMA event with log(e) cytokine concentrations dichotomized at the median, by quartile, and per standard deviation (SD) increase. Results. Low levels of TNF, TNF-RI, IL-1 beta , and IL-5 and high levels of TNF-RII were associated statistically significantly and respectively with approximately 3-fold, 2-fold, 8-fold, 4-fold, and 3-fold increased risks of SMA (Hb < 50 g/L). TNF, TNF-RI, and IL-1 beta concentrations were inversely and log-linearly associated with SMA risk; the HR (95% confidence interval [CI]) per 1-SD increase were respectively 0.81 (.65, 1.02), 0.76 (.62, .92), and 0.50 (.40, .62). Conclusions. These data suggest that proinflammatory cytokine levels at birth are inversely associated with SMA risk and support the hypothesis that pediatric malarial disease has fetal origins. JF - Journal of Infectious Diseases AU - Brickley, Elizabeth B AU - Wood, Angela M AU - Kabyemela, Edward AU - Morrison, Robert AU - Kurtis, Jonathan D AU - Fried, Michal AU - Duffy, Patrick E AD - Laboratory of Malaria Immunology and Vaccinology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland; Department of Public Health and Primary Care, Strangeways Research Laboratories, University of Cambridge, United Kingdom, patrick.duffy@nih.gov Y1 - 2015/02/01/ PY - 2015 DA - 2015 Feb 01 SP - 436 EP - 444 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 211 IS - 3 SN - 0022-1899, 0022-1899 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Immunology Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - malaria KW - anemia KW - cord blood KW - inflammation KW - cytokines KW - developmental programming KW - risk marker KW - Interleukin 6 KW - gamma -Interferon KW - Interleukin 4 KW - Human diseases KW - Prenatal experience KW - Interleukin 5 KW - Tumor necrosis factor KW - Interleukin 1 KW - Parturition KW - Malaria KW - Tumor necrosis factor receptors KW - Interleukin 10 KW - Risks KW - Public health KW - Cord blood KW - Infectious diseases KW - Mortality KW - Data processing KW - Pediatrics KW - Anemia KW - Fetuses KW - Inflammation KW - Blood KW - Standard deviation KW - Anaemia KW - Africa KW - Mortality causes KW - K 03400:Human Diseases KW - Q1 08604:Stock assessment and management KW - F 06910:Microorganisms & Parasites KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687673895?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Fetal+Origins+of+Malarial+Disease%3A+Cord+Blood+Cytokines+as+Risk+Markers+for+Pediatric+Severe+Malarial+Anemia&rft.au=Brickley%2C+Elizabeth+B%3BWood%2C+Angela+M%3BKabyemela%2C+Edward%3BMorrison%2C+Robert%3BKurtis%2C+Jonathan+D%3BFried%2C+Michal%3BDuffy%2C+Patrick+E&rft.aulast=Brickley&rft.aufirst=Elizabeth&rft.date=2015-02-01&rft.volume=211&rft.issue=3&rft.spage=436&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiu454 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-06-01 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Blood; Human diseases; Anaemia; Infectious diseases; Parturition; Malaria; Risks; Mortality causes; Public health; Interleukin 6; Mortality; gamma -Interferon; Interleukin 4; Data processing; Interleukin 5; Prenatal experience; Pediatrics; Tumor necrosis factor; Interleukin 1; Anemia; Interleukin 10; Tumor necrosis factor receptors; Fetuses; Inflammation; Cord blood; Standard deviation; Africa DO - http://dx.doi.org/10.1093/infdis/jiu454 ER - TY - JOUR T1 - Realizing the Promise of Social Psychology in Improving Public Health AN - 1683352589; PQ0001536880 AB - The theories, phenomena, empirical findings, and methodological approaches that characterize contemporary social psychology hold much promise for addressing enduring problems in public health. Indeed, social psychologists played a major role in the development of the discipline of health psychology during the 1970s and 1980s. The health domain allows for the testing, refinement, and application of many interesting and important research questions in social psychology, and offers the discipline a chance to enhance its reach and visibility. Nevertheless, in a review of recent articles in two major social-psychological journals (Personality and Social Psychology Bulletin and Journal of Personality and Social Psychology), we found that only 3.2% of 467 studies explored health-related topics. In this article, we identify opportunities for research at the interface of social psychology and health, delineate barriers, and offer strategies that can address these barriers as the discipline continues to evolve. JF - Personality and Social Psychology Review AU - Klein, William MP AU - Shepperd, James A AU - Suls, Jerry AU - Rothman, Alexander J AU - Croyle, Robert T AD - National Cancer Institute, Rockville, MD, USA Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 77 EP - 92 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 19 IS - 1 SN - 1088-8683, 1088-8683 KW - Health & Safety Science Abstracts KW - social psychology KW - health psychology KW - health behavior KW - public health KW - Psychology KW - Reviews KW - Personality KW - Visibility KW - Public health KW - H 12000:Epidemiology and Public Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683352589?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Personality+and+Social+Psychology+Review&rft.atitle=Realizing+the+Promise+of+Social+Psychology+in+Improving+Public+Health&rft.au=Klein%2C+William+MP%3BShepperd%2C+James+A%3BSuls%2C+Jerry%3BRothman%2C+Alexander+J%3BCroyle%2C+Robert+T&rft.aulast=Klein&rft.aufirst=William&rft.date=2015-02-01&rft.volume=19&rft.issue=1&rft.spage=77&rft.isbn=&rft.btitle=&rft.title=Personality+and+Social+Psychology+Review&rft.issn=10888683&rft_id=info:doi/10.1177%2F1088868314539852 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Number of references - 112 N1 - Last updated - 2015-07-23 N1 - SubjectsTermNotLitGenreText - Psychology; Reviews; Personality; Visibility; Public health DO - http://dx.doi.org/10.1177/1088868314539852 ER - TY - JOUR T1 - FGF-21, a novel metabolic regulator, has a robust neuroprotective role and is markedly elevated in neurons by mood stabilizers AN - 1683349208; PQ0001549986 AB - Fibroblast growth factor-21 (FGF-21) is a new member of the FGF super-family and an important endogenous regulator of glucose and lipid metabolism. It has been proposed as a therapeutic target for diabetes and obesity. Its function in the central nervous system (CNS) remains unknown. Previous studies from our laboratory demonstrated that aging primary neurons are more vulnerable to glutamate-induced excitotoxicity, and that co-treatment with the mood stabilizers lithium and valproic acid (VPA) induces synergistic neuroprotective effects. This study sought to identify molecule(s) involved in these synergistic effects. We found that FGF-21 mRNA was selectively and markedly elevated by co-treatment with lithium and VPA in primary rat brain neurons. FGF-21 protein levels were also robustly increased in neuronal lysates and culture medium following lithium-VPA co-treatment. Combining glycogen synthase kinase-3 (GSK-3) inhibitors with VPA or histone deacetylase (HDAC) inhibitors with lithium synergistically increased FGF-21 mRNA levels, supporting that synergistic effects of lithium and VPA are mediated via GSK-3 and HDAC inhibition, respectively. Exogenous FGF-21 protein completely protected aging neurons from glutamate challenge. This neuroprotection was associated with enhanced Akt-1 activation and GSK-3 inhibition. Lithium-VPA co-treatment markedly prolonged lithium-induced Akt-1 activation and augmented GSK-3 inhibition. Akt-1 knockdown markedly decreased FGF-21 mRNA levels and reduced the neuroprotection induced by FGF-21 or lithium-VPA co-treatment. In addition, FGF-21 knockdown reduced lithium-VPA co-treatment-induced Akt-1 activation and neuroprotection against excitotoxicity. Together, our novel results suggest that FGF-21 is a key mediator of the effects of these mood stabilizers and a potential new therapeutic target for CNS disorders. JF - Molecular Psychiatry AU - Leng, Y AU - Wang, Z AU - Tsai, L-K AU - Leeds, P AU - Fessler, E B AU - Wang, J AU - Chuang, D-M AD - Section on Molecular Neurobiology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 215 EP - 223 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 20 IS - 2 SN - 1359-4184, 1359-4184 KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - Central nervous system KW - Histone deacetylase KW - Obesity KW - Aging KW - Brain KW - Neuroprotection KW - Glycogen synthase kinase 3 KW - Glucose metabolism KW - mRNA KW - Lipid metabolism KW - Mood KW - Diabetes mellitus KW - Neurons KW - Valproic acid KW - AKT1 protein KW - Glutamic acid KW - Excitotoxicity KW - Lithium KW - X 24310:Pharmaceuticals KW - N3 11001:Behavioral and Cognitive Neuroscience UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683349208?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Psychiatry&rft.atitle=FGF-21%2C+a+novel+metabolic+regulator%2C+has+a+robust+neuroprotective+role+and+is+markedly+elevated+in+neurons+by+mood+stabilizers&rft.au=Leng%2C+Y%3BWang%2C+Z%3BTsai%2C+L-K%3BLeeds%2C+P%3BFessler%2C+E+B%3BWang%2C+J%3BChuang%2C+D-M&rft.aulast=Leng&rft.aufirst=Y&rft.date=2015-02-01&rft.volume=20&rft.issue=2&rft.spage=215&rft.isbn=&rft.btitle=&rft.title=Molecular+Psychiatry&rft.issn=13594184&rft_id=info:doi/10.1038%2Fmp.2013.192 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Obesity; Histone deacetylase; Central nervous system; Aging; Brain; Neuroprotection; Glucose metabolism; Glycogen synthase kinase 3; Lipid metabolism; mRNA; Diabetes mellitus; Mood; Valproic acid; Neurons; AKT1 protein; Glutamic acid; Lithium; Excitotoxicity DO - http://dx.doi.org/10.1038/mp.2013.192 ER - TY - JOUR T1 - Infant Attachment Security and Early Childhood Behavioral Inhibition Interact to Predict Adolescent Social Anxiety Symptoms AN - 1673612459 AB - Insecure attachment and behavioral inhibition (BI) increase risk for internalizing problems, but few longitudinal studies have examined their interaction in predicting adolescent anxiety. This study included 165 adolescents (ages 14–17 years) selected based on their reactivity to novelty at 4 months. Infant attachment was assessed with the Strange Situation. Multimethod BI assessments were conducted across childhood. Adolescents and their parents independently reported on anxiety. The interaction of attachment and BI significantly predicted adolescent anxiety symptoms, such that BI and anxiety were only associated among adolescents with histories of insecure attachment. Exploratory analyses revealed that this effect was driven by insecure-resistant attachment and that the association between BI and social anxiety was significant only for insecure males. Clinical implications are discussed. JF - Child Development AU - Lewis-Morrarty, Erin AU - Degnan, Kathryn A AU - Chronis-Tuscano, Andrea AU - Pine, Daniel S AU - Henderson, Heather A AU - Fox, Nathan A AD - University of Maryland. ; National Institute of Mental Health. ; University of Waterloo. ; University of Maryland. Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 598 EP - 613 CY - Ann Arbor PB - Wiley Subscription Services, Inc. VL - 86 IS - 2 SN - 0009-3920 KW - Psychology KW - Adolescents KW - Risk behaviour KW - Anxiety KW - Attachment KW - Childhood KW - Inhibition KW - Internalization KW - Internalizing problems KW - Men KW - Parents KW - Reactivity KW - Social anxiety KW - Symptoms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673612459?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Child+Development&rft.atitle=Infant+Attachment+Security+and+Early+Childhood+Behavioral+Inhibition+Interact+to+Predict+Adolescent+Social+Anxiety+Symptoms&rft.au=Lewis-Morrarty%2C+Erin%3BDegnan%2C+Kathryn+A%3BChronis-Tuscano%2C+Andrea%3BPine%2C+Daniel+S%3BHenderson%2C+Heather+A%3BFox%2C+Nathan+A&rft.aulast=Lewis-Morrarty&rft.aufirst=Erin&rft.date=2015-02-01&rft.volume=86&rft.issue=2&rft.spage=598&rft.isbn=&rft.btitle=&rft.title=Child+Development&rft.issn=00093920&rft_id=info:doi/10.1111%2Fcdev.12336 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-03-31 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1111/cdev.12336 ER - TY - JOUR T1 - Predicting Anxiety Diagnoses and Severity with the CBCL-A: Improvement Relative to Other CBCL Scales? AN - 1673612293 AB - The Child Behavior Checklist (CBCL) is a widely used parent-report of child and adolescent behavior. We examined the ability of the CBCL-A scale, a previously published subset of CBCL items, to predict the presence of generalized anxiety disorder (GAD), separation anxiety disorder (SAD), and social phobia (SoP), as well as anxiety severity, among 488 youth randomized in the Child Anxiety Multimodal Study (CAMS). We predicted that the CBCL-A’s unique inclusion of items related to somatic symptoms would better identify anxiety disorder and severity than other CBCL scales, given that somatic complaints are often key features of anxiety among youth. Results support the use of the anxiety-based CBCL subscales as first-line screeners for generally elevated symptoms of anxiety, rather than tools to identify specific anxiety disorders. Although somatic symptoms are often reported and included in diagnostic criteria for certain anxiety disorders (e.g., SAD, GAD), the unique combination of somatic and non-somatic symptoms for the CBCL-A subscale did not increase its ability to consistently predict the presence of specific anxiety disorders. JF - Journal of Psychopathology and Behavioral Assessment AU - Read, Kendra L AU - Settipani, Cara A AU - Peterman, Jeremy AU - Kendall, Philip C AU - Compton, Scott AU - Piacentini, John AU - McCracken, James AU - Bergman, Lindsey AU - Walkup, John AU - Sakolsky, Dara AU - Birmaher, Boris AU - Albano, Anne Marie AU - Rynn, Moira AU - Ginsburg, Golda AU - Keeton, Courtney AU - Gosch, Elizabeth AU - Suveg, Cynthia AU - Sherrill, Joel AU - March, John AD - Department of Psychology, Temple University, 1701 N. 13th Street, Philadelphia, PA, 19122, USA kendra.read@temple.edu kendra.read@temple.edu kendra.read@temple.edu kendra.read@temple.edu; Department of Psychology, Duke University, 1701 N. 13th Street, Philadelphia, PA, 19122, USA ; Department of Psychology, University of California, Los Angeles, 1701 N. 13th Street, Philadelphia, PA, 19122, USA ; Department of Psychology, Cornell University, 1701 N. 13th Street, Philadelphia, PA, 19122, USA ; Department of Psychology, University of Pittsburgh, 1701 N. 13th Street, Philadelphia, PA, 19122, USA ; Department of Psychology, Columbia University, 1701 N. 13th Street, Philadelphia, PA, 19122, USA ; Department of Psychology, The John Hopkins University, School of Medicine, 1701 N. 13th Street, Philadelphia, PA, 19122, USA ; Department of Psychology, Philadelphia College of Osteopathic Medicine, 1701 N. 13th Street, Philadelphia, PA, 19122, USA ; Department of Psychology, University of Georgia, 1701 N. 13th Street, Philadelphia, PA, 19122, USA ; Department of Psychology, Temple University, 1701 N. 13th Street, Philadelphia, PA, 19122, USA, Department of Psychology, The National Institute of Mental Health, 1701 N. 13th Street, Philadelphia, PA, 19122, USA ; Department of Psychology, Temple University, 1701 N. 13th Street, Philadelphia, PA, 19122, USA Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 100 EP - 111 CY - New York PB - Springer Science & Business Media VL - 37 IS - 1 SN - 0882-2689 KW - Psychology KW - Adolescents KW - Behaviour KW - Child Behaviour Checklist KW - Children KW - Clinical assessment KW - Complaints KW - Generalized anxiety disorders KW - Separation anxiety KW - Severity KW - Social anxiety KW - Social phobia KW - Somatic symptoms KW - Symptoms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673612293?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Psychopathology+and+Behavioral+Assessment&rft.atitle=Predicting+Anxiety+Diagnoses+and+Severity+with+the+CBCL-A%3A+Improvement+Relative+to+Other+CBCL+Scales%3F&rft.au=Read%2C+Kendra+L%3BSettipani%2C+Cara+A%3BPeterman%2C+Jeremy%3BKendall%2C+Philip+C%3BCompton%2C+Scott%3BPiacentini%2C+John%3BMcCracken%2C+James%3BBergman%2C+Lindsey%3BWalkup%2C+John%3BSakolsky%2C+Dara%3BBirmaher%2C+Boris%3BAlbano%2C+Anne+Marie%3BRynn%2C+Moira%3BGinsburg%2C+Golda%3BKeeton%2C+Courtney%3BGosch%2C+Elizabeth%3BSuveg%2C+Cynthia%3BSherrill%2C+Joel%3BMarch%2C+John&rft.aulast=Read&rft.aufirst=Kendra&rft.date=2015-02-01&rft.volume=37&rft.issue=1&rft.spage=100&rft.isbn=&rft.btitle=&rft.title=Journal+of+Psychopathology+and+Behavioral+Assessment&rft.issn=08822689&rft_id=info:doi/10.1007%2Fs10862-014-9439-9 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-03-24 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1007/s10862-014-9439-9 ER - TY - JOUR T1 - BIOLOGICAL EFFECTIVENESS OF PHOTONS AND ELECTRONS AS A FUNCTION OF ENERGY AN - 1668255872; PQ0001237862 AB - AN UNRESOLVED question in evaluating the risk of cancer in humans from exposure to low linear-energy transfer (LET) radiation (i.e., photons and electrons) is the dependence of the biological effectiveness on energy. This dependence is relevant for estimating the level of cancer risk from exposure to low-LET radiation at lower energies in mammography and other medical imaging procedures as well as certain sources of occupational and public radiation exposure (NCRP 2012). Because of the broad importance of this topic to the basic responsibilities and interests of NCRP, the Council created a Scientific Committee (SC 1-20) to evaluate this question. Numerous other expert groups have also considered this question, and several have concluded that the biological effectiveness of lower-energy, low-LET radiation based on chromosomal aberration data and biophysical considerations may be two or more times greater than for higher-energy, low-LET radiation (NCRP 1990; ICRP 2003). However, biological systems used in the experiments and biophysical analysis provide only indirect evidence and may not be strictly applicable to cancer in humans. JF - Health Physics AU - Simon, Steven L AU - Braby, Leslie A AU - Chang, Polly Y AU - Goodhead, Dudley T AU - Hora, Stephen AU - Kocher, David C AU - Mabuchi, Kiyohiko AU - Puskin, Jerome S AU - Richardson, David AU - Rosenstein, Marvin AU - Tucker, James AU - Vano, Eliseo AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892-7238, ssimon@mail.nih.gov Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 143 EP - 144 PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States VL - 108 IS - 2 SN - 0017-9078, 0017-9078 KW - Health & Safety Science Abstracts; Risk Abstracts KW - National Council on Radiation Protection and Measurements KW - cancer KW - radiation risk KW - relative biological effectiveness KW - Health risks KW - Radiation KW - Biological effects KW - Responsibility KW - Energy KW - Committees KW - Chromosome aberrations KW - Councils KW - Cancer KW - H 1000:Occupational Safety and Health KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668255872?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Physics&rft.atitle=BIOLOGICAL+EFFECTIVENESS+OF+PHOTONS+AND+ELECTRONS+AS+A+FUNCTION+OF+ENERGY&rft.au=Simon%2C+Steven+L%3BBraby%2C+Leslie+A%3BChang%2C+Polly+Y%3BGoodhead%2C+Dudley+T%3BHora%2C+Stephen%3BKocher%2C+David+C%3BMabuchi%2C+Kiyohiko%3BPuskin%2C+Jerome+S%3BRichardson%2C+David%3BRosenstein%2C+Marvin%3BTucker%2C+James%3BVano%2C+Eliseo&rft.aulast=Simon&rft.aufirst=Steven&rft.date=2015-02-01&rft.volume=108&rft.issue=2&rft.spage=143&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0000000000000256 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-08-05 N1 - SubjectsTermNotLitGenreText - Health risks; Biological effects; Radiation; Responsibility; Committees; Energy; Councils; Chromosome aberrations; Cancer DO - http://dx.doi.org/10.1097/HP.0000000000000256 ER - TY - JOUR T1 - PUBLIC HEALTH AND MEDICAL PREPAREDNESS FOR A NUCLEAR DETONATION: THE NUCLEAR INCIDENT MEDICAL ENTERPRISE AN - 1668253928; PQ0001237865 AB - Resilience and the ability to mitigate the consequences of a nuclear incident are enhanced by (1) effective planning, preparation and training; (2) ongoing interaction, formal exercises, and evaluation among the sectors involved; (3) effective and timely response and communication; and (4) continuous improvements based on new science, technology, experience, and ideas. Public health and medical planning require a complex, multi-faceted systematic approach involving federal, state, local, tribal, and territorial governments; private sector organizations; academia; industry; international partners; and individual experts and volunteers. The approach developed by the U.S. Department of Health and Human Services Nuclear Incident Medical Enterprise (NIME) is the result of efforts from government and nongovernment experts. It is a "bottom-up" systematic approach built on the available and emerging science that considers physical infrastructure damage, the spectrum of injuries, a scarce resources setting, the need for decision making in the face of a rapidly evolving situation with limited information early on, timely communication, and the need for tools and just-in-time information for responders who will likely be unfamiliar with radiation medicine and uncertain and overwhelmed in the face of the large number of casualties and the presence of radioactivity. The components of NIME can be used to support planning for, response to, and recovery from the effects of a nuclear incident Recognizing that it is a continuous work-in-progress, the current status of the public health and medical preparedness and response for a nuclear incident is provided. JF - Health Physics AU - Coleman, C Norman AU - Sullivan, Julie M AU - Bader, Judith L AU - Murrain-Hill, Paula AU - Koemer, John F AU - Garrett, Andrew L AU - Weinstock, David M AU - Case, Cullen Jr AU - Hrdina, Chad AU - Adams, Steven A AD - Office of Emergency Management, Office of the Assistant Secretary for Preparedness and Response, Department of Health and Human Services, Washington, DC; Radiation Research Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, MD, ccoleman@mail.nih.gov Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 149 EP - 160 PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States VL - 108 IS - 2 SN - 0017-9078, 0017-9078 KW - Health & Safety Science Abstracts KW - National Council on Radiation Protection and Measurements KW - emergency planning KW - nuclear war KW - radiological terrorism KW - France, Languedoc-Roussillon, Nimes KW - Infrastructure KW - Decision making KW - Communications KW - Radiation KW - Injuries KW - Training KW - Radioactivity KW - Private sector KW - Public health KW - Technology KW - H 6000:Natural Disasters/Civil Defense/Emergency Management UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668253928?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Physics&rft.atitle=PUBLIC+HEALTH+AND+MEDICAL+PREPAREDNESS+FOR+A+NUCLEAR+DETONATION%3A+THE+NUCLEAR+INCIDENT+MEDICAL+ENTERPRISE&rft.au=Coleman%2C+C+Norman%3BSullivan%2C+Julie+M%3BBader%2C+Judith+L%3BMurrain-Hill%2C+Paula%3BKoemer%2C+John+F%3BGarrett%2C+Andrew+L%3BWeinstock%2C+David+M%3BCase%2C+Cullen+Jr%3BHrdina%2C+Chad%3BAdams%2C+Steven+A&rft.aulast=Coleman&rft.aufirst=C&rft.date=2015-02-01&rft.volume=108&rft.issue=2&rft.spage=149&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0000000000000249 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-05-27 N1 - SubjectsTermNotLitGenreText - Infrastructure; Decision making; Communications; Injuries; Radiation; Training; Radioactivity; Private sector; Technology; Public health; France, Languedoc-Roussillon, Nimes DO - http://dx.doi.org/10.1097/HP.0000000000000249 ER - TY - JOUR T1 - DOSE RECONSTRUCTION FOR THE MILLION WORKER STUDY: STATUS AND GUIDELINES AN - 1668250564; PQ0001237871 AB - The primary aim of the epidemiologic study of one million U.S. radiation workers and veterans [the Million Worker Study (MWS)] is to provide scientifically valid information on the level of radiation risk when exposures are received gradually over time and not within seconds, as was the case for Japanese atomic bomb survivors. The primary outcome of the epidemiologic study is cancer mortality, but other causes of death such as cardiovascular disease and cerebrovascular disease will be evaluated. This paper focuses on the description of the various components of the MWS, the available dosimetry results, and the challenges that have been encountered. It is expected that the Committee will complete its report in 2016. JF - Health Physics AU - Bouville, Andre AU - Toohey, Richard E AU - Boice, John D AU - Beck, Harold L AU - Dauer, Larry T AU - Eckerman, Keith F AU - Hagemeyer, Derek AU - Leggett, Richard W AU - Mumma, Michael T AU - Napier, Bruce AD - National Cancer Institute, 9609 Medical Center Drive, Room 7E590, MSC 9778, Rockville, MD 20850, andre.bouville@nih.gov Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 206 EP - 220 PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States VL - 108 IS - 2 SN - 0017-9078, 0017-9078 KW - Health & Safety Science Abstracts; Risk Abstracts KW - National Council on Radiation Protection and Measurements KW - dose assessment KW - exposure occupational KW - radiation risk KW - INW, Japan KW - Mortality KW - Health risks KW - Radiation KW - Committees KW - Guidelines KW - Dosimetry KW - Atomic bombs KW - Cardiovascular diseases KW - Japan KW - Cancer KW - H 1000:Occupational Safety and Health KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668250564?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Physics&rft.atitle=DOSE+RECONSTRUCTION+FOR+THE+MILLION+WORKER+STUDY%3A+STATUS+AND+GUIDELINES&rft.au=Bouville%2C+Andre%3BToohey%2C+Richard+E%3BBoice%2C+John+D%3BBeck%2C+Harold+L%3BDauer%2C+Larry+T%3BEckerman%2C+Keith+F%3BHagemeyer%2C+Derek%3BLeggett%2C+Richard+W%3BMumma%2C+Michael+T%3BNapier%2C+Bruce&rft.aulast=Bouville&rft.aufirst=Andre&rft.date=2015-02-01&rft.volume=108&rft.issue=2&rft.spage=206&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0000000000000231 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-08-05 N1 - SubjectsTermNotLitGenreText - Health risks; Mortality; Radiation; Committees; Atomic bombs; Dosimetry; Guidelines; Cardiovascular diseases; Cancer; INW, Japan; Japan DO - http://dx.doi.org/10.1097/HP.0000000000000231 ER - TY - JOUR T1 - Identification of emotional facial expressions among behaviorally inhibited adolescents with lifetime anxiety disorders AN - 1665167140 AB - The current study examined differences in emotion expression identification between adolescents characterised with behavioural inhibition (BI) in childhood with and without a lifetime history of anxiety disorder. Participants were originally assessed for BI during toddlerhood and for social reticence during childhood. During adolescence, participants returned to the laboratory and completed a facial emotion identification task and a clinical psychiatric interview. Results revealed that behaviorally inhibited adolescents with a lifetime history of anxiety disorder displayed a lower threshold for identifying fear relative to anger emotion expressions compared to non-anxious behaviorally inhibited adolescents and non-inhibited adolescents with or without anxiety. These findings were specific to behaviorally inhibited adolescents with a lifetime history of social anxiety disorder. Thus, adolescents with a history of both BI and anxiety, specifically social anxiety, are more likely to differ from other adolescents in their identification of fearful facial expressions. This offers further evidence that perturbations in the processing of emotional stimuli may underlie the aetiology of anxiety disorders. JF - Cognition & Emotion AU - Reeb-Sutherland, Bethany C AU - Rankin Williams, Lela AU - Degnan, Kathryn A AU - Pérez-Edgar, Koraly AU - Chronis-Tuscano, Andrea AU - Leibenluft, Ellen AU - Pine, Daniel S AU - Pollak, Seth D AU - Fox, Nathan A AD - Department of Psychology, Florida International University, Miami, FL, USA, School of Social Work, Arizona State University, Phoenix, AZ, USA, Department of Human Development and Quantitative Methodology, University of Maryland, College Park, MD, USA, Department of Psychology, The Pennsylvania State University, University Park, PA, USA, Department of Psychology, University of Maryland, College Park, MD, USA, Mood and Anxiety Disorders Program, National Institute of Mental Health (NIH), Bethesda, MD, USA, Department of Psychology, Waisman Center, University of Wisconsin–Madison, Madison, WI, USA ; Department of Psychology, Florida International University, Miami, FL, USA; School of Social Work, Arizona State University, Phoenix, AZ, USA; Department of Human Development and Quantitative Methodology, University of Maryland, College Park, MD, USA; Department of Psychology, The Pennsylvania State University, University Park, PA, USA; Department of Psychology, University of Maryland, College Park, MD, USA; Mood and Anxiety Disorders Program, National Institute of Mental Health (NIH), Bethesda, MD, USA; Department of Psychology, Waisman Center, University of Wisconsin–Madison, Madison, WI, USA Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 372 EP - 382 CY - Hove PB - Taylor & Francis Ltd. VL - 29 IS - 2 SN - 0269-9931 KW - Psychology KW - Adolescence KW - Emotional-Behavioural problems KW - Adolescents KW - Aetiology KW - Anger KW - Behaviour KW - Childhood KW - Facial expressions KW - Fear KW - Identification KW - Inhibition KW - Social anxiety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665167140?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cognition+%26+Emotion&rft.atitle=Identification+of+emotional+facial+expressions+among+behaviorally+inhibited+adolescents+with+lifetime+anxiety+disorders&rft.au=Reeb-Sutherland%2C+Bethany+C%3BRankin+Williams%2C+Lela%3BDegnan%2C+Kathryn+A%3BP%C3%A9rez-Edgar%2C+Koraly%3BChronis-Tuscano%2C+Andrea%3BLeibenluft%2C+Ellen%3BPine%2C+Daniel+S%3BPollak%2C+Seth+D%3BFox%2C+Nathan+A&rft.aulast=Reeb-Sutherland&rft.aufirst=Bethany&rft.date=2015-02-01&rft.volume=29&rft.issue=2&rft.spage=372&rft.isbn=&rft.btitle=&rft.title=Cognition+%26+Emotion&rft.issn=02699931&rft_id=info:doi/10.1080%2F02699931.2014.913552 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1080/02699931.2014.913552 ER - TY - JOUR T1 - Understanding the elevated suicide risk of female soldiers during deployments AN - 1665158759 AB - The Army Study to Assess Risk and Resilience in Servicemembers (Army STARRS) has found that the proportional elevation in the US Army enlisted soldier suicide rate during deployment (compared with the never-deployed or previously deployed) is significantly higher among women than men, raising the possibility of gender differences in the adverse psychological effects of deployment. Person-month survival models based on a consolidated administrative database for active duty enlisted Regular Army soldiers in 2004–2009 ( n = 975 057) were used to characterize the gender × deployment interaction predicting suicide. Four explanatory hypotheses were explored involving the proportion of females in each soldierʼs occupation, the proportion of same-gender soldiers in each soldierʼs unit, whether the soldier reported sexual assault victimization in the previous 12 months, and the soldierʼs pre-deployment history of treated mental/behavioral disorders. The suicide rate of currently deployed women (14.0/100 000 person-years) was 3.1–3.5 times the rates of other (i.e. never-deployed/previously deployed) women. The suicide rate of currently deployed men (22.6/100 000 person-years) was 0.9–1.2 times the rates of other men. The adjusted (for time trends, sociodemographics, and Army career variables) female:male odds ratio comparing the suicide rates of currently deployed v. other women v. men was 2.8 (95% confidence interval 1.1–6.8), became 2.4 after excluding soldiers with Direct Combat Arms occupations, and remained elevated (in the range 1.9–2.8) after adjusting for the hypothesized explanatory variables. These results are valuable in excluding otherwise plausible hypotheses for the elevated suicide rate of deployed women and point to the importance of expanding future research on the psychological challenges of deployment for women. JF - Psychological Medicine AU - Street, A E AU - Gilman, S E AU - Rosellini, A J AU - Stein, M B AU - Bromet, E J AU - Cox, K L AU - Colpe, L J AU - Fullerton, C S AU - Gruber, M J AU - Heeringa, S G AU - Lewandowski-Romps, L AU - Little, R J A AU - Naifeh, J A AU - Nock, M K AU - Sampson, N A AU - Schoenbaum, M AU - Ursano, R J AU - Zaslavsky, A M AU - Kessler, R C AD - National Center for PTSD, VA Boston Healthcare System, Boston, MA, USA ; Departments of Social and Behavioral Sciences, and Epidemiology, Harvard School of Public Health, Boston, MA, USA ; Department of Health Care Policy, Harvard Medical School, Boston, MA, USA ; Departments of Psychiatry and Family and Preventive Medicine, University of California San Diego, La Jolla, CA, USA ; Department of Psychiatry, Stony Brook University School of Medicine, Stony Brook, NY, USA ; US Army Public Health Command, Aberdeen Proving Ground, MD, USA ; Division of Services and Intervention Research, National Institute of Mental Health, Bethesda, MD, USA ; National Center for PTSD, VA Boston Healthcare System, Boston, MA, USA, Department of Psychiatry, Uniformed Services University School of Medicine, Center for the Study of Traumatic Stress, Bethesda, MD, USA ; National Center for PTSD, VA Boston Healthcare System, Boston, MA, USA, Institute for Social Research, University of Michigan, Ann Arbor, MI, USA ; National Center for PTSD, VA Boston Healthcare System, Boston, MA, USA, Department of Biostatistics, University of Michigan, Ann Arbor, MI, USA ; National Center for PTSD, VA Boston Healthcare System, Boston, MA, USA, Department of Psychology, Harvard University, Cambridge, MA, USA ; National Center for PTSD, VA Boston Healthcare System, Boston, MA, USA, Office of Science Policy, Planning and Communications, National Institute of Mental Health, Bethesda, MD, USA ; National Center for PTSD, VA Boston Healthcare System, Boston, MA, USA Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 717 EP - 726 CY - Cambridge PB - Cambridge University Press VL - 45 IS - 4 SN - 0033-2917 KW - Psychology KW - Arms KW - Armies KW - Soldiers KW - Suicide KW - Victimization KW - Assault KW - Behaviour disorders KW - Deployment KW - Elevation KW - Gender KW - Gender differences KW - Occupations KW - Psychiatric disorders KW - Psychological aspects KW - Resilience KW - Risk assessment KW - Same sex KW - Sexual assault KW - Sexual violence KW - United States--US UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665158759?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychological+Medicine&rft.atitle=Understanding+the+elevated+suicide+risk+of+female+soldiers+during+deployments&rft.au=Street%2C+A+E%3BGilman%2C+S+E%3BRosellini%2C+A+J%3BStein%2C+M+B%3BBromet%2C+E+J%3BCox%2C+K+L%3BColpe%2C+L+J%3BFullerton%2C+C+S%3BGruber%2C+M+J%3BHeeringa%2C+S+G%3BLewandowski-Romps%2C+L%3BLittle%2C+R+J+A%3BNaifeh%2C+J+A%3BNock%2C+M+K%3BSampson%2C+N+A%3BSchoenbaum%2C+M%3BUrsano%2C+R+J%3BZaslavsky%2C+A+M%3BKessler%2C+R+C&rft.aulast=Street&rft.aufirst=A&rft.date=2015-02-01&rft.volume=45&rft.issue=4&rft.spage=717&rft.isbn=&rft.btitle=&rft.title=Psychological+Medicine&rft.issn=00332917&rft_id=info:doi/10.1017%2FS003329171400258X LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Name - Army-US N1 - Date revised - 2015-03-05 N1 - Last updated - 2016-05-16 N1 - SubjectsTermNotLitGenreText - United States--US DO - http://dx.doi.org/10.1017/S003329171400258X ER - TY - JOUR T1 - Temperature-sensitive liposome-mediated delivery of thrombolytic agents. AN - 1665122976; 25766387 AB - Clinical efficacy of thrombolytic drugs is limited by lack of specific delivery and requires large therapeutic doses which increase toxicity. Encapsulating these drugs in temperature-sensitive liposomes and applying hyperthermia to deliver thrombolytic agents locally to thrombus might theoretically favourably alter the therapeutic window. The objectives of this study were to formulate liposomes encapsulating thrombolytics and assess thrombolytic activity following hyperthermia. Three liposome formulations were investigated: temperature-sensitive liposome (TSL, DPPC:DSPE-PEG2000 (mol% 95:5)), low temperature-sensitive liposome (LTSL, DPPC:MSPC:DSPE-PEG2000 (mol% 85.3:9.7:5)), and traditional temperature-sensitive liposome (TTSL, DPPC:HSPC:Chol:DSPE-PEG2000 (mol% 55:25:15:5)). To characterise temperature-dependent release of high molecular weight cargo from each formulation, fluorescein-conjugated dextrans (70 kDa) were loaded and release was quantified via spectrophotometry. Staphylokinase (SAK), urokinase, and tissue-type plasminogen activator were also loaded individually into each liposome formulation. Leakage at 37 °C and release at 38-44 °C were quantified via chromogenic enzymatic activity assay. Clot lysis was evaluated by measuring mass of blood clots before and after thrombolytic liposome treatment. The LTSL formulation had optimal release characteristics with maximum release at 41.3 °C. Release of dextrans from LTSLs was observed to be 11.5 ± 1.5%, 79.7 ± 1.6%, and 93.6 ± 3.7% after 15 min in plasma at 37°, 39°, and 41.3 °C, respectively. The SAK LTSL had the highest release/leakage ratio and demonstrated greater clot lysis. The SAK LTSL achieves significant clot lysis in vitro. When combined with local hyperthermia, the SAK LTSL potentially produces sufficient thrombolysis while minimising systemic side effects. JF - International journal of hyperthermia : the official journal of European Society for Hyperthermic Oncology, North American Hyperthermia Group AU - Saxena, Vishal AU - Gacchina Johnson, Carmen AU - Negussie, Ayele H AU - Sharma, Karun V AU - Dreher, Matthew R AU - Wood, Bradford J AD - Center for Interventional Oncology, Radiology and Imaging Sciences, Clinical Centre, National Cancer Institute, National Institutes of Health, Bethesda , Maryland , USA . Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 67 EP - 73 VL - 31 IS - 1 KW - Fibrinolytic Agents KW - 0 KW - Lipids KW - Liposomes KW - Polyethylene Glycols KW - 30IQX730WE KW - Tissue Plasminogen Activator KW - EC 3.4.21.68 KW - Urokinase-Type Plasminogen Activator KW - EC 3.4.21.73 KW - Metalloendopeptidases KW - EC 3.4.24.- KW - auR protein, Staphylococcus aureus KW - EC 3.4.24.29 KW - Index Medicus KW - Staphylokinase KW - thrombolysis KW - temperature sensitive liposomes KW - tissue plasminogen activator KW - Polyethylene Glycols -- chemistry KW - Lipids -- chemistry KW - Humans KW - Hyperthermia, Induced KW - Temperature KW - Male KW - Urokinase-Type Plasminogen Activator -- administration & dosage KW - Tissue Plasminogen Activator -- chemistry KW - Fibrinolytic Agents -- administration & dosage KW - Blood Coagulation -- drug effects KW - Urokinase-Type Plasminogen Activator -- chemistry KW - Tissue Plasminogen Activator -- administration & dosage KW - Metalloendopeptidases -- administration & dosage KW - Metalloendopeptidases -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665122976?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+hyperthermia+%3A+the+official+journal+of+European+Society+for+Hyperthermic+Oncology%2C+North+American+Hyperthermia+Group&rft.atitle=Temperature-sensitive+liposome-mediated+delivery+of+thrombolytic+agents.&rft.au=Saxena%2C+Vishal%3BGacchina+Johnson%2C+Carmen%3BNegussie%2C+Ayele+H%3BSharma%2C+Karun+V%3BDreher%2C+Matthew+R%3BWood%2C+Bradford+J&rft.aulast=Saxena&rft.aufirst=Vishal&rft.date=2015-02-01&rft.volume=31&rft.issue=1&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=International+journal+of+hyperthermia+%3A+the+official+journal+of+European+Society+for+Hyperthermic+Oncology%2C+North+American+Hyperthermia+Group&rft.issn=1464-5157&rft_id=info:doi/10.3109%2F02656736.2014.991428 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-23 N1 - Date created - 2015-03-19 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3109/02656736.2014.991428 ER - TY - JOUR T1 - Temporal variation in the acute effects of air pollution on blood pressure measured at admission to labor/delivery AN - 1664214823; PQ0001239824 AB - Same day or recent air pollution exposure increases blood pressure in pregnant women. Temporal blood pressure variation associated with hourly air pollution is unstudied. We randomly selected 500 women (249 normotensive, 191 with hypertensive disorders, and 60 with chronic hypertension) with singleton pregnancies and blood pressure measured at labor/delivery admission from a large cohort, the Consortium on Safe Labor. Community multiscale air quality models estimated hourly air pollutant exposures for the admission hour (lag 0) and for the 24 h preceding labor/delivery admission (lags 1-24). Linear regression estimated the effect of 10 % increase in pollutants on blood pressure at each time point, adjusting for maternal characteristics, labor type, and time of day. Women with chronic hypertension had higher systolic blood pressure with exposure to particulate matter <10 mu m (by 1.0-1.3 mmHg at 0-4 h), sulfur dioxide (by 0.7-0.9 mmHg at 0-3, 16-20, and 22-23 h) and with some air toxics. Diastolic blood pressure was higher in normotensive women with ozone exposure (by 0.1-0.4 mmHg at 0-1 and 23-24 h). Similar effects for systolic blood pressure were seen among women with hypertensive disorders (by 0.6 mmHg at 19-20 h), but most pollutants were associated with lower blood pressure in these women. Substantial variation in the impact of hourly air pollutant measures on blood pressure was observed during the day prior to labor/delivery admission, both by mothers' hypertensive status and by the lag time prior to BP measurement. Effects were largest near admission (lags 0-4) and among women with chronic hypertension. JF - Air Quality, Atmosphere and Health AU - Maennisto, Tuija AU - Mendola, Pauline AU - Liu, Danping AU - Leishear, Kira AU - Ying, Qi AU - Sundaram, Rajeshwari AD - Epidemiology Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6100 Executive Blvd, 7B05, Rockville, MD, 20852, USA, pauline.mendola@nih.gov Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 13 EP - 28 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 8 IS - 1 SN - 1873-9318, 1873-9318 KW - Health & Safety Science Abstracts; Pollution Abstracts; Meteorological & Geoastrophysical Abstracts KW - Atmospheric pollution variations KW - Ozone measurements KW - Atmospheric pollution models KW - Atmospheric pollution KW - Sulfur in atmosphere KW - Statistical analysis KW - Atmospheric pollution effects KW - Pollution effects KW - Air quality KW - Particulates KW - Atmosphere KW - Particulate atmospheric pollution KW - Blood pressure KW - Pregnancy KW - Air quality models KW - Air pollution KW - Particulate matter in atmosphere KW - Sulfur dioxide KW - Atmospheric pollution and health KW - Pressure variations KW - Hypertension KW - Ozone KW - M2 551.510.42:Air Pollution (551.510.42) KW - P 0000:AIR POLLUTION KW - H 12000:Epidemiology and Public Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664214823?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Apollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Air+Quality%2C+Atmosphere+and+Health&rft.atitle=Temporal+variation+in+the+acute+effects+of+air+pollution+on+blood+pressure+measured+at+admission+to+labor%2Fdelivery&rft.au=Maennisto%2C+Tuija%3BMendola%2C+Pauline%3BLiu%2C+Danping%3BLeishear%2C+Kira%3BYing%2C+Qi%3BSundaram%2C+Rajeshwari&rft.aulast=Maennisto&rft.aufirst=Tuija&rft.date=2015-02-01&rft.volume=8&rft.issue=1&rft.spage=13&rft.isbn=&rft.btitle=&rft.title=Air+Quality%2C+Atmosphere+and+Health&rft.issn=18739318&rft_id=info:doi/10.1007%2Fs11869-014-0268-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Number of references - 37 N1 - Last updated - 2015-04-29 N1 - SubjectsTermNotLitGenreText - Atmospheric pollution variations; Ozone measurements; Atmospheric pollution; Atmospheric pollution models; Sulfur in atmosphere; Atmospheric pollution effects; Statistical analysis; Air quality; Particulate atmospheric pollution; Air quality models; Particulate matter in atmosphere; Atmospheric pollution and health; Pressure variations; Air pollution; Sulfur dioxide; Pollution effects; Particulates; Atmosphere; Blood pressure; Ozone; Pregnancy; Hypertension DO - http://dx.doi.org/10.1007/s11869-014-0268-5 ER - TY - JOUR T1 - Gene Expression of Mesothelioma in Vinylidene Chloride-exposed F344/N Rats Reveal Immune Dysfunction, Tissue Damage, and Inflammation Pathways AN - 1664209047; PQ0001203197 AB - A majority (80%) of human malignant mesotheliomas are asbestos-related. However, non-asbestos risk factors (radiation, chemicals, and genetic factors) account for up to 30% of cases. A recent 2-year National Toxicology Program carcinogenicity bioassay showed that male F344/N rats exposed to the industrial toxicant vinylidene chloride (VDC) resulted in a marked increase in malignant mesothelioma. Global gene expression profiles of these tumors were compared to spontaneous mesotheliomas and the F344/N rat mesothelial cell line (Fred-PE) in order to characterize the molecular features and chemical-specific profiles of mesothelioma in VDC-exposed rats. As expected, mesotheliomas from control and VDC-exposed rats shared pathways associated with tumorigenesis, including cellular and tissue development, organismal injury, embryonic development, inflammatory response, cell cycle regulation, and cellular growth and proliferation, while mesotheliomas from VDC-exposed rats alone showed overrepresentation of pathways associated with pro-inflammatory pathways and immune dysfunction such as the nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway, interleukin (IL)-8 and IL-12 signaling, interleukin responses, Fc receptor signaling, and natural killer and dendritic cells signaling, as well as overrepresentation of DNA damage and repair. These data suggest that a chronic, pro-inflammatory environment associated with VDC exposure may exacerbate disturbances in oncogene, growth factor, and cell cycle regulation, resulting in an increased incidence of mesothelioma. JF - Toxicologic Pathology AU - Blackshear, Pamela E AU - Pandiri, Arun R AU - Nagai, Hiroaki AU - Bhusari, Sachin AU - Hong, Hue-Hua AU - Ton, Thai-Vu T AU - Clayton, Natasha P AU - Wyde, Michael AU - Shockley, Keith R AU - Peddada, Shyamal D AU - Gerrish, Kevin E AU - Sills, Robert C AU - Hoenerhoff, Mark J AD - Cellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, Integrated Laboratory Systems, Inc., Research Triangle Park, North Carolina, USA, hoenerho@med.umich.edu Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 171 EP - 185 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 43 IS - 2 SN - 0192-6233, 0192-6233 KW - Genetics Abstracts; Immunology Abstracts; Toxicology Abstracts KW - vinylidene chloride KW - mesothelioma KW - F344/N rat KW - National Toxicology Program KW - microarray KW - gene expression KW - mesothelial cell KW - Fred-PE cells KW - Genetic factors KW - Data processing KW - Toxicants KW - Injuries KW - Lymphocytes B KW - Vinylidene chloride KW - Tumorigenesis KW - Cell cycle KW - Natural killer cells KW - Inflammation KW - Fc receptors KW - Gene expression KW - Dendritic cells KW - DNA damage KW - Interleukin 12 KW - Embryogenesis KW - Oncogenes KW - Carcinogenicity KW - Risk factors KW - Growth factors KW - Cell proliferation KW - Signal transduction KW - F 06915:Cancer Immunology KW - G 07730:Development & Cell Cycle KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664209047?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Gene+Expression+of+Mesothelioma+in+Vinylidene+Chloride-exposed+F344%2FN+Rats+Reveal+Immune+Dysfunction%2C+Tissue+Damage%2C+and+Inflammation+Pathways&rft.au=Blackshear%2C+Pamela+E%3BPandiri%2C+Arun+R%3BNagai%2C+Hiroaki%3BBhusari%2C+Sachin%3BHong%2C+Hue-Hua%3BTon%2C+Thai-Vu+T%3BClayton%2C+Natasha+P%3BWyde%2C+Michael%3BShockley%2C+Keith+R%3BPeddada%2C+Shyamal+D%3BGerrish%2C+Kevin+E%3BSills%2C+Robert+C%3BHoenerhoff%2C+Mark+J&rft.aulast=Blackshear&rft.aufirst=Pamela&rft.date=2015-02-01&rft.volume=43&rft.issue=2&rft.spage=171&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623314537885 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Number of references - 62 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Genetic factors; Data processing; Injuries; Toxicants; Lymphocytes B; Vinylidene chloride; Cell cycle; Tumorigenesis; Natural killer cells; Fc receptors; Inflammation; Gene expression; Interleukin 12; DNA damage; Dendritic cells; Embryogenesis; Oncogenes; Carcinogenicity; Risk factors; mesothelioma; Growth factors; Cell proliferation; Signal transduction DO - http://dx.doi.org/10.1177/0192623314537885 ER - TY - JOUR T1 - Clinical and pharmacogenomic implications of genetic variation in a Southern Ethiopian population AN - 1664207307; PQ0001183704 AB - Africa is home to genetically diverse human populations. We compared the genetic structure of the Wolaita ethnic population from Southern Ethiopia (WETH, n=120) with HapMap populations using genome-wide variants. We investigated allele frequencies of 443 clinically and pharmacogenomically relevant genetic variants in WETH compared with HapMap populations. We found that WETH were genetically most similar to the Kenya Maasai and least similar to the Japanese in HapMap. Variant alleles associated with increased risk of adverse reactions to drugs used for treating tuberculosis (rs1799929 and rs1495741 in NAT2), thromboembolism (rs7294, rs9923231 and rs9934438 in VKORC1), and HIV/AIDS and solid tumors (rs2242046 in SLC28A1) had significantly higher frequencies in WETH compared with African ancestry HapMap populations. Our results illustrate that clinically relevant pharmacogenomic loci display allele frequency differences among African populations. We conclude that drug dosage guidelines for important global health diseases should be validated in genetically diverse African populations. JF - Pharmacogenomics Journal AU - Tekola-Ayele, F AU - Adeyemo, A AU - Aseffa, A AU - Hailu, E AU - Finan, C AU - Davey, G AU - Rotimi, C N AU - Newport, M J AD - Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA PY - 2015 SP - 101 EP - 108 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 15 IS - 1 SN - 1470-269X, 1470-269X KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Acquired immune deficiency syndrome KW - Mycobacterium KW - pharmacogenomics KW - Solid tumors KW - Genetic diversity KW - Thromboembolism KW - Population genetics KW - Human immunodeficiency virus KW - Gene frequency KW - Tuberculosis KW - Drugs KW - Genetic structure KW - Side effects KW - G 07880:Human Genetics KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664207307?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pharmacogenomics+Journal&rft.atitle=Clinical+and+pharmacogenomic+implications+of+genetic+variation+in+a+Southern+Ethiopian+population&rft.au=Tekola-Ayele%2C+F%3BAdeyemo%2C+A%3BAseffa%2C+A%3BHailu%2C+E%3BFinan%2C+C%3BDavey%2C+G%3BRotimi%2C+C+N%3BNewport%2C+M+J&rft.aulast=Tekola-Ayele&rft.aufirst=F&rft.date=2015-02-01&rft.volume=15&rft.issue=1&rft.spage=101&rft.isbn=&rft.btitle=&rft.title=Pharmacogenomics+Journal&rft.issn=1470269X&rft_id=info:doi/10.1038%2Ftpj.2014.39 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Population genetics; Acquired immune deficiency syndrome; Solid tumors; pharmacogenomics; Genetic diversity; Tuberculosis; Gene frequency; Genetic structure; Drugs; Thromboembolism; Side effects; Mycobacterium; Human immunodeficiency virus DO - http://dx.doi.org/10.1038/tpj.2014.39 ER - TY - JOUR T1 - Prevalence and Correlates of Receiving and Sharing High-Penetrance Cancer Genetic Test Results: Findings from the Health Information National Trends Survey AN - 1664203360; PQ0001238334 AB - Background/Aims: The aim of this study was to explore the prevalence and correlates of receiving and sharing high-penetrance cancer genetic test results. Methods: Participants completed the population-based, cross-sectional 2013 Health Information National Trends Survey. We examined sociodemographic characteristics of participants reporting having had BRCA1/2 or Lynch syndrome genetic testing, and sociodemographic and psychosocial correlates of sharing test results with health professionals and family members. Results: Participants who underwent BRCA1/2 or Lynch syndrome genetic testing (n = 77; 2.42% of respondents) were more likely to be female and to have a family or personal history of cancer than those not undergoing testing. Approximately three-quarters of participants shared results with health professionals and three-quarters with their family; only 4% did not share results with anyone. Participants who shared results with health professionals reported greater optimism, self-efficacy for health management, and trust in information from their doctors. Participants who shared results with their family were more likely to be female and to have a personal history of cancer, and had greater self-efficacy for health management, perceived less ambiguity in cancer prevention recommendations, and lower cancer prevention fatalism. Conclusions: We identified several novel psychosocial correlates of sharing genetic information. Health professionals may use this information to identify patients less likely to share information with at-risk family members. copyright 2014 S. Karger AG, Basel JF - Public Health Genomics AU - Taber, Jennifer M AU - Chang, Christine Q AU - Lam, Tram K AU - Gillanders, Elizabeth M AU - Hamilton, Jada G AU - Schully, Sheri D AD - Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health, Bethesda, Md. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 67 EP - 77 PB - S. Karger AG, P.O. Box Basel CH-4009 Switzerland VL - 18 IS - 2 SN - 1662-4246, 1662-4246 KW - Genetics Abstracts; Risk Abstracts; Health & Safety Science Abstracts KW - BRCA1/2 KW - Communication of test results KW - Genetic testing KW - Health Information National Trends Survey KW - Hereditary cancer KW - Hereditary nonpolyposis colorectal cancer KW - Lynch syndrome KW - Historical account KW - Prevention KW - Perception KW - Genetic screening KW - BRCA1 protein KW - Medical personnel KW - Cancer KW - Public health KW - G 07880:Human Genetics KW - H 11000:Diseases/Injuries/Trauma KW - R2 23110:Psychological aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664203360?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Public+Health+Genomics&rft.atitle=Prevalence+and+Correlates+of+Receiving+and+Sharing+High-Penetrance+Cancer+Genetic+Test+Results%3A+Findings+from+the+Health+Information+National+Trends+Survey&rft.au=Taber%2C+Jennifer+M%3BChang%2C+Christine+Q%3BLam%2C+Tram+K%3BGillanders%2C+Elizabeth+M%3BHamilton%2C+Jada+G%3BSchully%2C+Sheri+D&rft.aulast=Taber&rft.aufirst=Jennifer&rft.date=2015-02-01&rft.volume=18&rft.issue=2&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=Public+Health+Genomics&rft.issn=16624246&rft_id=info:doi/10.1159%2F000368745 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2016-09-14 N1 - SubjectsTermNotLitGenreText - BRCA1 protein; Genetic screening; Cancer; Public health; Historical account; Prevention; Perception; Medical personnel DO - http://dx.doi.org/10.1159/000368745 ER - TY - JOUR T1 - Nitrate in drinking water and bladder cancer risk in Spain. AN - 1662003271; 25601732 AB - Nitrate is a widespread contaminant in drinking water and ingested nitrate under conditions resulting in endogenous nitrosation is suspected to be carcinogenic. However, the suggested association between nitrate in drinking water and bladder cancer remains inconsistent. We evaluated the long-term exposure to drinking water nitrate as a risk factor for bladder cancer, considering endogenous nitrosation modifiers and other covariables. We conducted a hospital-based case-control study of bladder cancer in Spain (1998-2001). Residential histories and water consumption information were ascertained through personal interviews. Historical nitrate levels (1940-2000) were estimated in study municipalities based on monitoring records and water source. Residential histories of study subjects were linked with nitrate estimates by year and municipality to calculate individual exposure from age 18 to recruitment. We calculated odds ratios (OR) and 95% confidence intervals (CI) for bladder cancer among 531 cases and 556 controls with reliable interviews and nitrate exposure information covering at least 70% of years from age 18 to interview. Average residential levels ranged from 2.1mg/L to 12.0mg/L among regions. Adjusted OR (95%CI) for average residential levels relative to ≤ 5 mg/L were 1.2 (0.7-2.0) for >5-10mg/L and 1.1 (0.6-1.9) for >10mg/L. The OR for subjects with longest exposure duration (>20 years) to highest levels (>9.5mg/L) was 1.4 (0.9-2.3). Stratification by intake of vitamin C, vitamin E, meat, and gastric ulcer diagnosis did not modify these results. A non-significant negative association was found with waterborne ingested nitrate with an OR of 0.7 (0.4-1.0) for >8 vs. ≤ 4 mg/day. Adjustment for several covariables showed similar results to crude analyses. Bladder cancer risk was inconsistently associated with chronic exposure to drinking water nitrate at levels below the current regulatory limit. Elevated risk is suggested only among subjects with longest exposure duration to the highest levels. No evidence of interaction with endogenous nitrosation modifiers was observed. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Environmental research AU - Espejo-Herrera, Nadia AU - Cantor, Kenneth P AU - Malats, Nuria AU - Silverman, Debra T AU - Tardón, Adonina AU - García-Closas, Reina AU - Serra, Consol AU - Kogevinas, Manolis AU - Villanueva, Cristina M AD - Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain; Universitat Pompeu Fabra, Departament de Ciències Experimentals i de la Salut, Barcelona, Spain; CIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain. ; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA. ; Genetic and Molecular Epidemiology Group, Spanish National Cancer Research Center (CNIO), Madrid, Spain. ; Universidad de Oviedo, Oviedo, Spain. ; Hospital Universitario de Canarias, La Laguna, Spain. ; Universitat Pompeu Fabra, Departament de Ciències Experimentals i de la Salut, Barcelona, Spain; Consorci Hospitalari Parc Taulí, Sabadell, Spain. ; Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain; Universitat Pompeu Fabra, Departament de Ciències Experimentals i de la Salut, Barcelona, Spain; CIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain; IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain; National School of Public Health, Athens, Greece. ; Centre for Research in Environmental Epidemiology (CREAL), Barcelona, Spain; Universitat Pompeu Fabra, Departament de Ciències Experimentals i de la Salut, Barcelona, Spain; CIBER Epidemiología y Salud Pública (CIBERESP), Barcelona, Spain; IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain. Electronic address: cvillanueva@creal.cat. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 299 EP - 307 VL - 137 KW - Carcinogens KW - 0 KW - Drinking Water KW - Nitrates KW - Water Pollutants, Chemical KW - Index Medicus KW - Nitrate KW - Drinking wáter KW - Case-control study KW - Bladder cáncer KW - Water contaminants KW - Environmental Monitoring KW - Animals KW - Risk Factors KW - Humans KW - Cats KW - Adult KW - Case-Control Studies KW - Aged KW - Middle Aged KW - Spain -- epidemiology KW - Male KW - Female KW - Drinking Water -- analysis KW - Water Pollutants, Chemical -- toxicity KW - Urinary Bladder Neoplasms -- epidemiology KW - Nitrates -- toxicity KW - Environmental Exposure KW - Carcinogens -- toxicity KW - Urinary Bladder Neoplasms -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1662003271?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+research&rft.atitle=Nitrate+in+drinking+water+and+bladder+cancer+risk+in+Spain.&rft.au=Espejo-Herrera%2C+Nadia%3BCantor%2C+Kenneth+P%3BMalats%2C+Nuria%3BSilverman%2C+Debra+T%3BTard%C3%B3n%2C+Adonina%3BGarc%C3%ADa-Closas%2C+Reina%3BSerra%2C+Consol%3BKogevinas%2C+Manolis%3BVillanueva%2C+Cristina+M&rft.aulast=Espejo-Herrera&rft.aufirst=Nadia&rft.date=2015-02-01&rft.volume=137&rft.issue=&rft.spage=299&rft.isbn=&rft.btitle=&rft.title=Environmental+research&rft.issn=1096-0953&rft_id=info:doi/10.1016%2Fj.envres.2014.10.034 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-04 N1 - Date created - 2015-03-09 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.envres.2014.10.034 ER - TY - JOUR T1 - Antiviral Potential of ERK/MAPK and PI3K/AKT/mTOR Signaling Modulation for Middle East Respiratory Syndrome Coronavirus Infection as Identified by Temporal Kinome Analysis AN - 1660439447; PQ0001092173 AB - Middle East respiratory syndrome coronavirus (MERS-CoV) is a lineage C betacoronavirus, and infections with this virus can result in acute respiratory syndrome with renal failure. Globally, MERS-CoV has been responsible for 877 laboratory-confirmed infections, including 317 deaths, since September 2012. As there is a paucity of information regarding the molecular pathogenesis associated with this virus or the identities of novel antiviral drug targets, we performed temporal kinome analysis on human hepatocytes infected with the Erasmus isolate of MERS-CoV with peptide kinome arrays. bioinformatics analysis of our kinome data, including pathway overrepresentation analysis (ORA) and functional network analysis, suggested that extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) and phosphoinositol 3-kinase (PI3K)/serine-threonine kinase (AKT)/mammalian target of rapamycin (mTOR) signaling responses were specifically modulated in response to MERS-CoV infection in vitro throughout the course of infection. The overrepresentation of specific intermediates within these pathways determined by pathway and functional network analysis of our kinome data correlated with similar patterns of phosphorylation determined through Western blot array analysis. In addition, analysis of the effects of specific kinase inhibitors on MERS-CoV infection in tissue culture models confirmed these cellular response observations. Further, we have demonstrated that a subset of licensed kinase inhibitors targeting the ERK/MAPK and PI3K/AKT/mTOR pathways significantly inhibited MERS-CoV replication in vitro whether they were added before or after viral infection. Taken together, our data suggest that ERK/MAPK and PI3K/AKT/mTOR signaling responses play important roles in MERS-CoV infection and may represent novel drug targets for therapeutic intervention strategies. JF - Antimicrobial Agents & Chemotherapy AU - Kindrachuk, Jason AU - Ork, Britini AU - Hart, Brit J AU - Mazur, Steven AU - Holbrook, Michael R AU - Frieman, Matthew B AU - Traynor, Dawn AU - Johnson, Reed F AU - Dyall, Julie AU - Kuhn, Jens H AD - Integrated Research Facility, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Frederick, Maryland, USA, kindrachuk.kenneth@nih.gov. Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 1088 EP - 1099 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 59 IS - 2 SN - 0066-4804, 0066-4804 KW - Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Western blotting KW - MAP kinase KW - Data processing KW - Coronavirus KW - Protein-serine/threonine kinase KW - Hepatocytes KW - Replication KW - Renal failure KW - Therapeutic applications KW - Tissue culture KW - Infection KW - Computer programs KW - Extracellular signal-regulated kinase KW - 1-Phosphatidylinositol 3-kinase KW - Antiviral agents KW - Phosphorylation KW - AKT protein KW - Bioinformatics KW - TOR protein KW - Signal transduction KW - A 01340:Antibiotics & Antimicrobials KW - V 22320:Replication UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660439447?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Antiviral+Potential+of+ERK%2FMAPK+and+PI3K%2FAKT%2FmTOR+Signaling+Modulation+for+Middle+East+Respiratory+Syndrome+Coronavirus+Infection+as+Identified+by+Temporal+Kinome+Analysis&rft.au=Kindrachuk%2C+Jason%3BOrk%2C+Britini%3BHart%2C+Brit+J%3BMazur%2C+Steven%3BHolbrook%2C+Michael+R%3BFrieman%2C+Matthew+B%3BTraynor%2C+Dawn%3BJohnson%2C+Reed+F%3BDyall%2C+Julie%3BKuhn%2C+Jens+H&rft.aulast=Kindrachuk&rft.aufirst=Jason&rft.date=2015-02-01&rft.volume=59&rft.issue=2&rft.spage=1088&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.03659-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Number of references - 48 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Western blotting; MAP kinase; Data processing; Protein-serine/threonine kinase; Replication; Hepatocytes; Therapeutic applications; Renal failure; Tissue culture; Infection; Extracellular signal-regulated kinase; Computer programs; 1-Phosphatidylinositol 3-kinase; Phosphorylation; Antiviral agents; AKT protein; Bioinformatics; TOR protein; Signal transduction; Coronavirus DO - http://dx.doi.org/10.1128/AAC.03659-14 ER - TY - JOUR T1 - Prion Infection of Mouse Brain Reveals Multiple New Upregulated Genes Involved in Neuroinflammation or Signal Transduction AN - 1660438932; PQ0001092568 AB - Gliosis is often a preclinical pathological finding in neurodegenerative diseases, including prion diseases, but the mechanisms facilitating gliosis and neuronal damage in these diseases are not understood. To expand our knowledge of the neuroinflammatory response in prion diseases, we assessed the expression of key genes and proteins involved in the inflammatory response and signal transduction in mouse brain at various times after scrapie infection. In brains of scrapie-infected mice at pre- and postclinical stages, we identified 15 previously unreported differentially expressed genes related to inflammation or activation of the STAT signal transduction pathway. Levels for the majority of differentially expressed genes increased with time postinfection. In quantitative immunoblotting experiments of STAT proteins, STAT1 alpha , phosphorylated-STAT1 alpha (pSTAT1 alpha ), and pSTAT3 were increased between 94 and 131 days postinfection (p.i.) in brains of mice infected with strain 22L. Furthermore, a select group of STAT-associated genes was increased preclinically during scrapie infection, suggesting early activation of the STAT signal transduction pathway. Comparison of inflammatory markers between mice infected with scrapie strains 22L and RML indicated that the inflammatory responses and gene expression profiles in the brains were strikingly similar, even though these scrapie strains infect different brain regions. The endogenous interleukin-1 receptor antagonist (IL-1Ra), an inflammatory marker, was newly identified as increasing preclinically in our model and therefore might influence scrapie pathogenesis in vivo. However, in IL-1Ra-deficient or overexpressor transgenic mice inoculated with scrapie, neither loss nor overexpression of IL-1Ra demonstrated any observable effect on gliosis, protease-resistant prion protein (PrPres) formation, disease tempo, pathology, or expression of the inflammatory genes analyzed. IMPORTANCE Prion infection leads to PrPres deposition, gliosis, and neuroinflammation in the central nervous system before signs of clinical illness. Using a scrapie mouse model of prion disease to assess various time points postinoculation, we identified 15 unreported genes that were increased in the brains of scrapie-infected mice and were associated with inflammation and/or JAK-STAT activation. Comparison of mice infected with two scrapie strains (22L and RML), which have dissimilar neuropathologies, indicated that the inflammatory responses and gene expression profiles in the brains were similar. Genes that increased prior to clinical signs might be involved in controlling scrapie infection or in facilitating damage to host tissues. We tested the possible role of the endogenous IL-1Ra, which was increased at 70 days p.i. In scrapie-infected mice deficient in or overexpressing IL-1Ra, there was no observable effect on gliosis, PrPres formation, disease tempo, pathology, or expression of inflammatory genes analyzed. JF - Journal of Virology AU - Carroll, James A AU - Striebel, James F AU - Race, Brent AU - Phillips, Katie AU - Chesebro, Bruce PY - 2015 SP - 2388 EP - 2404 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 89 IS - 4 SN - 0022-538X, 0022-538X KW - Biotechnology and Bioengineering Abstracts; Genetics Abstracts; Virology & AIDS Abstracts KW - Central nervous system KW - Immunoblotting KW - Animal models KW - Brain KW - Stat protein KW - Scrapie KW - Transgenic mice KW - Infection KW - Interleukin 1 receptor antagonist KW - Inflammation KW - Gene expression KW - Neurodegenerative diseases KW - Prion protein KW - Gliosis KW - Interleukin 1 receptors KW - Neuropathology KW - Signal transduction KW - W 30925:Genetic Engineering KW - G 07870:Mammals KW - V 22380:Prions UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660438932?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Virology&rft.atitle=Prion+Infection+of+Mouse+Brain+Reveals+Multiple+New+Upregulated+Genes+Involved+in+Neuroinflammation+or+Signal+Transduction&rft.au=Carroll%2C+James+A%3BStriebel%2C+James+F%3BRace%2C+Brent%3BPhillips%2C+Katie%3BChesebro%2C+Bruce&rft.aulast=Carroll&rft.aufirst=James&rft.date=2015-02-01&rft.volume=89&rft.issue=4&rft.spage=2388&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.02952-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Number of references - 95 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Immunoblotting; Central nervous system; Stat protein; Brain; Animal models; Scrapie; Infection; Transgenic mice; Interleukin 1 receptor antagonist; Inflammation; Gene expression; Neurodegenerative diseases; Prion protein; Interleukin 1 receptors; Gliosis; Neuropathology; Signal transduction DO - http://dx.doi.org/10.1128/JVI.02952-14 ER - TY - JOUR T1 - Coxiella burnetii Effector Proteins That Localize to the Parasitophorous Vacuole Membrane Promote Intracellular Replication AN - 1660435131; PQ0001092376 AB - The intracellular bacterial pathogen Coxiella burnetii directs biogenesis of a parasitophorous vacuole (PV) that acquires host endolysosomal components. Formation of a PV that supports C. burnetii replication requires a Dot/Icm type 4B secretion system (T4BSS) that delivers bacterial effector proteins into the host cell cytosol. Thus, a subset of T4BSS effectors are presumed to direct PV biogenesis. Recently, the PV-localized effector protein CvpA was found to promote C. burnetii intracellular growth and PV expansion. We predict additional C. burnetii effectors localize to the PV membrane and regulate eukaryotic vesicle trafficking events that promote pathogen growth. To identify these vacuolar effector proteins, a list of predicted C. burnetii T4BSS substrates was compiled using bioinformatic criteria, such as the presence of eukaryote-like coiled-coil domains. Adenylate cyclase translocation assays revealed 13 proteins were secreted in a Dot/Icm-dependent fashion by C. burnetii during infection of human THP-1 macrophages. Four of the Dot/Icm substrates, termed Coxiella vacuolar protein B (CvpB), CvpC, CvpD, and CvpE, labeled the PV membrane and LAMP1-positive vesicles when ectopically expressed as fluorescently tagged fusion proteins. C. burnetii Delta cvpB, Delta cvpC, Delta cvpD, and Delta cvpE mutants exhibited significant defects in intracellular replication and PV formation. Genetic complementation of the Delta cvpD and Delta cvpE mutants rescued intracellular growth and PV generation, whereas the growth of C. burnetii Delta cvpB and Delta cvpC was rescued upon cohabitation with wild-type bacteria in a common PV. Collectively, these data indicate C. burnetii encodes multiple effector proteins that target the PV membrane and benefit pathogen replication in human macrophages. JF - Infection and Immunity AU - Larson, Charles L AU - Beare, Paul A AU - Voth, Daniel E AU - Howe, Dale AU - Cockrell, Diane C AU - Bastidas, Robert J AU - Valdivia, Raphael H AU - Heinzen, Robert A AD - Coxiella Pathogenesis Section, Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA, rheinzen@niaid.nih.gov. Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 661 EP - 670 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 83 IS - 2 SN - 0019-9567, 0019-9567 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Macrophages KW - Data processing KW - Replication KW - protein B KW - Pathogens KW - Infection KW - parasitophorous vacuole KW - Coxiella burnetii KW - Complementation KW - Cytosol KW - Membrane vesicles KW - Vesicles KW - Fusion protein KW - Bioinformatics KW - Translocation KW - Adenylate cyclase KW - J 02350:Immunology KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660435131?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Coxiella+burnetii+Effector+Proteins+That+Localize+to+the+Parasitophorous+Vacuole+Membrane+Promote+Intracellular+Replication&rft.au=Larson%2C+Charles+L%3BBeare%2C+Paul+A%3BVoth%2C+Daniel+E%3BHowe%2C+Dale%3BCockrell%2C+Diane+C%3BBastidas%2C+Robert+J%3BValdivia%2C+Raphael+H%3BHeinzen%2C+Robert+A&rft.aulast=Larson&rft.aufirst=Charles&rft.date=2015-02-01&rft.volume=83&rft.issue=2&rft.spage=661&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.02763-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Number of references - 63 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Macrophages; Data processing; Replication; protein B; Pathogens; Infection; parasitophorous vacuole; Complementation; Membrane vesicles; Cytosol; Vesicles; Bioinformatics; Fusion protein; Translocation; Adenylate cyclase; Coxiella burnetii DO - http://dx.doi.org/10.1128/IAI.02763-14 ER - TY - JOUR T1 - Transcriptional Profiling of Human Epithelial Cells Infected with Plasmid-Bearing and Plasmid-Deficient Chlamydia trachomatis AN - 1660430885; PQ0001092377 AB - Chlamydia trachomatis is an obligate intracellular epitheliotropic bacterial pathogen of humans. Infection of the eye can result in trachoma, the leading cause of preventable blindness in the world. The pathophysiology of blinding trachoma is driven by multiple episodes of reinfection of conjunctival epithelial cells, producing an intense chronic inflammatory response resulting in submucosal tissue remodeling and scarring. Recent reports have shown that infection with trachoma organisms lacking the cryptic chlamydial plasmid is highly attenuated in macaque eyes, a relevant experimental model of human trachoma infection. To better understand the molecular basis of plasmid-mediated infection attenuation and the potential modulation of host immunity, we conducted transcriptional profiling of human epithelial cells infected with C. trachomatis plasmid-bearing (A2497) and plasmid-deficient (A2497P-) organisms. Infection of human epithelial cells with either strain increased the expression of host genes coding for proinflammatory (granulocyte-macrophage colony-stimulating factor [GM-CSF], macrophage colony-stimulating factor [MCSF], interleukin-6 [IL-6], IL-8, IL-1 alpha , CXCL1, CXCL2, CXCL3, intercellular adhesion molecule 1 [ICAM1]), chemoattraction (CCL20, CCL5, CXCL10), immune suppression (PD-L1, NFKB1B, TNFAIP3, CGB), apoptosis (CASP9, FAS, IL-24), and cell growth and fibrosis (EGR1 and IL-20) proteins. Statistically significant increases in the levels of expression of many of these genes were found in A2497-infected cells compared to the levels of expression in A2497P-infected cells. Our findings suggest that the chlamydial plasmid plays a focal role in the host cell inflammatory response to infection and immune avoidance. These results provide new insights into the role of the chlamydial plasmid as a chlamydial virulence factor and its contributions to trachoma pathogenesis. JF - Infection and Immunity AU - Porcella, Stephen F AU - Carlson, John H AU - Sturdevant, Daniel E AU - Sturdevant, Gail L AU - Kanakabandi, Kishore AU - Virtaneva, Kimmo AU - Wilder, Hannah AU - Whitmire, William M AU - Song, Lihua AU - Caldwell, Harlan D AD - Laboratory of Intracellular Parasites, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA, sporcella@niaid.nih.gov. Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 534 EP - 543 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 83 IS - 2 SN - 0019-9567, 0019-9567 KW - Genetics Abstracts; Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Interleukin 6 KW - Epithelial cells KW - Apoptosis KW - virulence factors KW - Eye KW - Fibrosis KW - Interleukin 1 KW - Statistical analysis KW - PD-L1 protein KW - Chlamydia trachomatis KW - Macrophage colony-stimulating factor KW - Interleukin 8 KW - Trachoma KW - intercellular adhesion molecule 1 KW - CD95 antigen KW - CCL20 protein KW - Macaca KW - Granulocyte-macrophage colony-stimulating factor KW - Transcription KW - Pathogens KW - Immunity KW - Blindness KW - Plasmids KW - Interleukin 20 KW - Inflammation KW - Interleukin 24 KW - CXCL10 protein KW - Fas antigen KW - EGR-1 protein KW - J 02350:Immunology KW - F 06910:Microorganisms & Parasites KW - G 07770:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660430885?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Infection+and+Immunity&rft.atitle=Transcriptional+Profiling+of+Human+Epithelial+Cells+Infected+with+Plasmid-Bearing+and+Plasmid-Deficient+Chlamydia+trachomatis&rft.au=Porcella%2C+Stephen+F%3BCarlson%2C+John+H%3BSturdevant%2C+Daniel+E%3BSturdevant%2C+Gail+L%3BKanakabandi%2C+Kishore%3BVirtaneva%2C+Kimmo%3BWilder%2C+Hannah%3BWhitmire%2C+William+M%3BSong%2C+Lihua%3BCaldwell%2C+Harlan+D&rft.aulast=Porcella&rft.aufirst=Stephen&rft.date=2015-02-01&rft.volume=83&rft.issue=2&rft.spage=534&rft.isbn=&rft.btitle=&rft.title=Infection+and+Immunity&rft.issn=00199567&rft_id=info:doi/10.1128%2FIAI.02764-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Number of references - 35 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Interleukin 6; Epithelial cells; Apoptosis; Eye; virulence factors; Fibrosis; Interleukin 1; PD-L1 protein; Statistical analysis; Macrophage colony-stimulating factor; Interleukin 8; Trachoma; intercellular adhesion molecule 1; CD95 antigen; CCL20 protein; Granulocyte-macrophage colony-stimulating factor; Transcription; Blindness; Immunity; Pathogens; Plasmids; Interleukin 20; Inflammation; CXCL10 protein; Interleukin 24; Fas antigen; EGR-1 protein; Macaca; Chlamydia trachomatis DO - http://dx.doi.org/10.1128/IAI.02764-14 ER - TY - JOUR T1 - Hyper-Acetylation of Histone H3K56 Limits Break-Induced Replication by Inhibiting Extensive Repair Synthesis. AN - 1658422729; 25705897 AB - Break-induced replication (BIR) has been implicated in restoring eroded telomeres and collapsed replication forks via single-ended invasion and extensive DNA synthesis on the recipient chromosome. Unlike other recombination subtypes, DNA synthesis in BIR likely relies heavily on mechanisms enabling efficient fork progression such as chromatin modification. Herein we report that deletion of HST3 and HST4, two redundant de-acetylases of histone H3 Lysine 56 (H3K56), inhibits BIR, sensitizes checkpoint deficient cells to deoxyribonucleotide triphosphate pool depletion, and elevates translocation-type gross chromosomal rearrangements (GCR). The basis for deficiency in BIR and gene conversion with long gap synthesis in hst3Δ hst4Δ cells can be traced to a defect in extensive DNA synthesis. Distinct from other cellular defects associated with deletion of HST3 and HST4 including thermo-sensitivity and elevated spontaneous mutagenesis, the BIR defect in hst3Δ hst4Δ cannot be offset by the deletion of RAD17 or MMS22, but rather by the loss of RTT109 or ASF1, or in combination with the H3K56R mutation, which also restores tolerance to replication stress in mrc1 mutants. Our studies suggest that acetylation of H3K56 limits extensive repair synthesis and interferes with efficient fork progression in BIR. JF - PLoS genetics AU - Che, Jun AU - Smith, Stephanie AU - Kim, Yoo Jung AU - Shim, Eun Yong AU - Myung, Kyungjae AU - Lee, Sang Eun AD - Department of Cellular and Structural Biology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America; Program of Radiation Biology, Department of Radiation Oncology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America. ; Genome Instability Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Program of Radiation Biology, Department of Radiation Oncology, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America; Department of Molecular Medicine, Institute of Biotechnology, Universsity of Texas Health Science Center at San Antonio, San Antonio, Texas, United States of America. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 1 VL - 11 IS - 2 KW - Chromatin KW - 0 KW - Histones KW - Saccharomyces cerevisiae Proteins KW - Hst3 protein, S cerevisiae KW - EC 3.5.1.- KW - Hst4 protein, S cerevisiae KW - Histone Deacetylases KW - EC 3.5.1.98 KW - Index Medicus KW - Saccharomyces cerevisiae -- genetics KW - DNA Repair -- genetics KW - Acetylation KW - Humans KW - Telomere -- genetics KW - DNA Breaks, Double-Stranded KW - Mutation KW - DNA Damage -- genetics KW - Chromosomes -- genetics KW - Histones -- genetics KW - Chromatin -- genetics KW - DNA Replication -- genetics KW - Saccharomyces cerevisiae Proteins -- genetics KW - Recombination, Genetic -- genetics KW - Histone Deacetylases -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658422729?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+genetics&rft.atitle=Hyper-Acetylation+of+Histone+H3K56+Limits+Break-Induced+Replication+by+Inhibiting+Extensive+Repair+Synthesis.&rft.au=Che%2C+Jun%3BSmith%2C+Stephanie%3BKim%2C+Yoo+Jung%3BShim%2C+Eun+Yong%3BMyung%2C+Kyungjae%3BLee%2C+Sang+Eun&rft.aulast=Che&rft.aufirst=Jun&rft.date=2015-02-01&rft.volume=11&rft.issue=2&rft.spage=e1004990&rft.isbn=&rft.btitle=&rft.title=PLoS+genetics&rft.issn=1553-7404&rft_id=info:doi/10.1371%2Fjournal.pgen.1004990 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-07 N1 - Date created - 2015-02-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Science. 2007 Feb 2;315(5812):653-5 [17272723] Cell. 2007 Feb 23;128(4):721-33 [17320509] Nature. 2007 Apr 12;446(7137):806-10 [17314980] Nature. 2007 May 3;447(7140):102-5 [17410126] Nature. 2007 Aug 16;448(7155):820-3 [17671506] EMBO J. 2007 Sep 19;26(18):4113-25 [17762868] J Biol Chem. 2007 Sep 28;282(39):28587-96 [17690098] J Biol Chem. 2007 Dec 28;282(52):37805-14 [17977840] Cell Cycle. 2008 Apr 1;7(7):859-64 [18414031] Mol Cell. 2008 May 9;30(3):325-35 [18471978] EMBO J. 2008 May 21;27(10):1502-12 [18418382] Proc Natl Acad Sci U S A. 2008 Jul 1;105(26):9000-5 [18577595] Cell. 2008 Jul 25;134(2):231-43 [18662539] Cell. 2008 Jul 25;134(2):244-55 [18662540] Genetics. 2008 Aug;179(4):1769-84 [18579506] Genetics. 2008 Aug;179(4):1845-60 [18689895] Mol Biol Cell. 2008 Nov;19(11):4993-5005 [18799617] PLoS Genet. 2008 Nov;4(11):e1000270 [19023413] Genes Dev. 2009 Jan 1;23(1):67-79 [19136626] Nat Struct Mol Biol. 2013 Jul;20(7):836-42 [23728291] Proc Natl Acad Sci U S A. 2013 Aug 13;110(33):13475-80 [23898170] Nature. 2013 Oct 17;502(7471):393-6 [24025768] Nature. 2013 Oct 17;502(7471):389-92 [24025772] Mutat Res. 2013 Oct;750(1-2):5-14 [23916969] PLoS Genet. 2013 Oct;9(10):e1003899 [24204308] Nat Commun. 2014;5:4091 [24909977] Mol Cell Biol. 2005 May;25(10):3934-44 [15870268] Mol Cell. 2009 Feb 27;33(4):417-27 [19250903] EMBO J. 2009 Apr 22;28(8):1131-41 [19322196] Cell. 2001 Feb 9;104(3):397-408 [11239397] Nature. 2001 Aug 2;412(6846):557-61 [11484058] Nat Cell Biol. 2001 Nov;3(11):958-65 [11715016] Mol Cell. 2002 Aug;10(2):373-85 [12191482] Proc Natl Acad Sci U S A. 2003 May 27;100(11):6640-5 [12750463] Genes Dev. 2003 Jul 15;17(14):1755-67 [12865299] Nature. 2003 Aug 28;424(6952):1078-83 [12944972] Proc Natl Acad Sci U S A. 2009 Jan 27;106(4):1151-6 [19164567] Genes Dev. 2009 Feb 1;23(3):291-303 [19204116] Nature. 2009 May 7;459(7243):113-7 [19270680] Mol Cell. 2009 Oct 9;36(1):153-63 [19818718] Biochim Biophys Acta. 2010 May-Jun;1799(5-6):480-6 [20100606] PLoS Genet. 2010 May;6(5):e1000948 [20485519] Genes Dev. 2010 Jun 1;24(11):1133-44 [20516198] PLoS Genet. 2010 May;6(5):e1000973 [20523895] Science. 2010 Jul 2;329(5987):82-5 [20595613] PLoS Genet. 2010 Jul;6(7):e1001007 [20628570] Mol Cell. 2010 Sep 10;39(5):724-35 [20832724] PLoS Biol. 2011;9(2):e1000594 [21347245] Mol Cell Biol. 2012 Jan;32(1):154-72 [22025679] Mol Cell. 2012 Apr 13;46(1):7-17 [22387026] Nature. 2012 Sep 27;489(7417):576-80 [22960743] PLoS Genet. 2012;8(11):e1003026 [23144625] PLoS Genet. 2013;9(1):e1003237 [23357952] Science. 2013 Apr 12;340(6129):195-9 [23580526] PLoS Genet. 2013 Apr;9(4):e1003410 [23593017] Sci STKE. 2004 Mar 9;2004(223):PL8 [15010550] Genes Dev. 1995 Dec 1;9(23):2888-902 [7498786] Cell. 1998 Aug 7;94(3):399-409 [9708741] Microbiol Mol Biol Rev. 1999 Jun;63(2):349-404 [10357855] Cell. 2005 May 6;121(3):375-85 [15882620] Nature. 2005 Jul 14;436(7048):294-8 [16015338] Mol Cell. 2005 Sep 2;19(5):699-706 [16137625] Mol Cell Biol. 2005 Oct;25(19):8430-43 [16166626] Proc Natl Acad Sci U S A. 2006 May 2;103(18):6988-93 [16627621] Mol Cell Biol. 2006 Jun;26(11):4086-94 [16705162] Annu Rev Biochem. 2006;75:111-35 [16756487] Mol Cell. 2006 Jul 7;23(1):109-19 [16818235] Curr Biol. 2006 Jul 11;16(13):1280-9 [16815704] Methods. 2007 Feb;41(2):168-76 [17189859] Science. 2007 Feb 2;315(5812):649-52 [17272722] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pgen.1004990 ER - TY - JOUR T1 - A multi-megabase copy number gain causes maternal transmission ratio distortion on mouse chromosome 2. AN - 1656045089; 25679959 AB - Significant departures from expected Mendelian inheritance ratios (transmission ratio distortion, TRD) are frequently observed in both experimental crosses and natural populations. TRD on mouse Chromosome (Chr) 2 has been reported in multiple experimental crosses, including the Collaborative Cross (CC). Among the eight CC founder inbred strains, we found that Chr 2 TRD was exclusive to females that were heterozygous for the WSB/EiJ allele within a 9.3 Mb region (Chr 2 76.9 - 86.2 Mb). A copy number gain of a 127 kb-long DNA segment (designated as responder to drive, R2d) emerged as the strongest candidate for the causative allele. We mapped R2d sequences to two loci within the candidate interval. R2d1 is located near the proximal boundary, and contains a single copy of R2d in all strains tested. R2d2 maps to a 900 kb interval, and the number of R2d copies varies from zero in classical strains (including the mouse reference genome) to more than 30 in wild-derived strains. Using real-time PCR assays for the copy number, we identified a mutation (R2d2WSBdel1) that eliminates the majority of the R2d2WSB copies without apparent alterations of the surrounding WSB/EiJ haplotype. In a three-generation pedigree segregating for R2d2WSBdel1, the mutation is transmitted to the progeny and Mendelian segregation is restored in females heterozygous for R2d2WSBdel1, thus providing direct evidence that the copy number gain is causal for maternal TRD. We found that transmission ratios in R2d2WSB heterozygous females vary between Mendelian segregation and complete distortion depending on the genetic background, and that TRD is under genetic control of unlinked distorter loci. Although the R2d2WSB transmission ratio was inversely correlated with average litter size, several independent lines of evidence support the contention that female meiotic drive is the cause of the distortion. We discuss the implications and potential applications of this novel meiotic drive system. JF - PLoS genetics AU - Didion, John P AU - Morgan, Andrew P AU - Clayshulte, Amelia M-F AU - Mcmullan, Rachel C AU - Yadgary, Liran AU - Petkov, Petko M AU - Bell, Timothy A AU - Gatti, Daniel M AU - Crowley, James J AU - Hua, Kunjie AU - Aylor, David L AU - Bai, Ling AU - Calaway, Mark AU - Chesler, Elissa J AU - French, John E AU - Geiger, Thomas R AU - Gooch, Terry J AU - Garland, Theodore AU - Harrill, Alison H AU - Hunter, Kent AU - McMillan, Leonard AU - Holt, Matt AU - Miller, Darla R AU - O'Brien, Deborah A AU - Paigen, Kenneth AU - Pan, Wenqi AU - Rowe, Lucy B AU - Shaw, Ginger D AU - Simecek, Petr AU - Sullivan, Patrick F AU - Svenson, Karen L AU - Weinstock, George M AU - Threadgill, David W AU - Pomp, Daniel AU - Churchill, Gary A AU - Pardo-Manuel de Villena, Fernando AD - Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America; Carolina Center for Genome Science, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America. ; Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America. ; The Jackson Laboratory, Bar Harbor, Maine, United States of America. ; Department of Genetics, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America; Carolina Center for Genome Science, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America; Department of Cell Biology and Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America. ; Department of Biological Sciences, North Carolina State University, Raleigh, North Carolina, United States of America. ; Laboratory of Cancer Biology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; National Toxicology Program, National Institute of Environmental Sciences, NIH, Research Triangle Park, North Carolina, United States of America. ; Department of Biology, University of California Riverside, Riverside, California, United States of America. ; Department of Environmental and Occupational Health, University of Arkansas for Medical Sciences, Little Rock, Arkansas, United States of America. ; Department of Computer Science, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America. ; Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America; Department of Cell Biology and Physiology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America. ; Jackson Laboratory for Genomic Medicine, Farmington, Connecticut, United States of America. ; Department of Veterinary Pathobiology and Department of Molecular and Cellular Medicine, Texas A&M University, College Station, Texas, United States of America. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 1 VL - 11 IS - 2 KW - Index Medicus KW - Genotyping Techniques KW - Animals KW - Haplotypes -- genetics KW - Alleles KW - Crosses, Genetic KW - Mice KW - Mutation KW - Chromosomes -- genetics KW - Male KW - Female KW - Inheritance Patterns -- genetics KW - Meiosis -- genetics KW - DNA Copy Number Variations -- genetics KW - Genomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1656045089?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+genetics&rft.atitle=A+multi-megabase+copy+number+gain+causes+maternal+transmission+ratio+distortion+on+mouse+chromosome+2.&rft.au=Didion%2C+John+P%3BMorgan%2C+Andrew+P%3BClayshulte%2C+Amelia+M-F%3BMcmullan%2C+Rachel+C%3BYadgary%2C+Liran%3BPetkov%2C+Petko+M%3BBell%2C+Timothy+A%3BGatti%2C+Daniel+M%3BCrowley%2C+James+J%3BHua%2C+Kunjie%3BAylor%2C+David+L%3BBai%2C+Ling%3BCalaway%2C+Mark%3BChesler%2C+Elissa+J%3BFrench%2C+John+E%3BGeiger%2C+Thomas+R%3BGooch%2C+Terry+J%3BGarland%2C+Theodore%3BHarrill%2C+Alison+H%3BHunter%2C+Kent%3BMcMillan%2C+Leonard%3BHolt%2C+Matt%3BMiller%2C+Darla+R%3BO%27Brien%2C+Deborah+A%3BPaigen%2C+Kenneth%3BPan%2C+Wenqi%3BRowe%2C+Lucy+B%3BShaw%2C+Ginger+D%3BSimecek%2C+Petr%3BSullivan%2C+Patrick+F%3BSvenson%2C+Karen+L%3BWeinstock%2C+George+M%3BThreadgill%2C+David+W%3BPomp%2C+Daniel%3BChurchill%2C+Gary+A%3BPardo-Manuel+de+Villena%2C+Fernando&rft.aulast=Didion&rft.aufirst=John&rft.date=2015-02-01&rft.volume=11&rft.issue=2&rft.spage=e1004850&rft.isbn=&rft.btitle=&rft.title=PLoS+genetics&rft.issn=1553-7404&rft_id=info:doi/10.1371%2Fjournal.pgen.1004850 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-03 N1 - Date created - 2015-02-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Science. 2008 Dec 5;322(5907):1559-62 [19056989] Science. 2009 Jan 16;323(5912):373-5 [19074312] Bioinformatics. 2009 Aug 15;25(16):2078-9 [19505943] Nat Methods. 2009 Sep;6(9):663-6 [19668205] Bioinformatics. 2010 Jun 15;26(12):i199-207 [20529906] Mamm Genome. 2010 Jun;21(5-6):231-46 [20473506] Physiol Genomics. 2010 Jul 7;42(2):190-200 [20388837] Science. 2010 Aug 6;329(5992):682-5 [20616234] BMC Genet. 2010;11:98 [21044349] Nat Genet. 2011 Jul;43(7):648-55 [21623374] Genome Res. 2011 Aug;21(8):1213-22 [21406540] BMC Genomics. 2012;13:34 [22260749] Nat Methods. 2012 Apr;9(4):357-9 [22388286] Cell Rep. 2012 Sep 27;2(3):454-61 [22959432] Physiol Genomics. 2012 Dec 1;44(23):1141-53 [23048196] Mamm Genome. 2013 Feb;24(1-2):1-20 [23223940] Hum Genet. 2013 Mar;132(3):245-63 [23242375] Dis Model Mech. 2013 May;6(3):571-9 [23519032] Genetics. 2013 May;194(1):81-9 [23457233] Cell. 2013 May 9;153(4):910-8 [23643243] PLoS Genet. 2013;9(10):e1003853 [24098153] Genetics. 2013 Dec;195(4):1385-95 [24056412] Science. 2013 Dec 20;342(6165):1508-12 [24357318] Mamm Genome. 2014 Apr;25(3-4):95-108 [24487921] Genetics. 2014 May;197(1):91-106 [24578350] Genome Biol. 2012;13(8):R72 [22916792] Curr Biol. 2014 Oct 6;24(19):2295-300 [25242031] Trends Genet. 2003 Jan;19(1):24-31 [12493245] Mamm Genome. 2000 Mar;11(3):225-30 [10723728] Genetics. 2000 May;155(1):283-9 [10790402] Hum Genet. 2001 Jan;108(1):31-6 [11214904] Mamm Genome. 2001 May;12(5):331-9 [11331939] Mamm Genome. 2001 Aug;12(8):590-4 [11471051] Science. 2001 Aug 10;293(5532):1098-102 [11498581] Genome Res. 2003 Jan;13(1):122-33 [12529315] Bioinformatics. 2003 May 1;19(7):889-90 [12724300] Proc Natl Acad Sci U S A. 2004 Apr 20;101(16):6062-7 [15075390] Genome Res. 2004 Sep;14(9):1806-11 [15342563] Chromosoma. 1976 Jul 30;56(4):381-91 [949923] Cell. 1984 Jun;37(2):621-8 [6722884] Genetics. 1991 Aug;128(4):813-21 [1916246] Annu Rev Genet. 1991;25:511-57 [1812815] Hereditas. 1993;119(1):39-46 [8244755] Mamm Genome. 1994 May;5(5):253-74 [8075499] Mamm Genome. 1995 May;6(5):315-20 [7626881] Nature. 1996 Mar 14;380(6570):149-52 [8600386] Chromosoma. 2001 Aug;110(4):247-52 [11534816] Genetics. 2001 Nov;159(3):1179-89 [11729161] Genome Res. 2002 Apr;12(4):656-64 [11932250] Nature. 2002 Dec 5;420(6915):520-62 [12466850] Genetics. 1996 Aug;143(4):1739-52 [8844160] Genetics. 1997 Nov;147(3):1279-87 [9383070] Behav Genet. 1998 May;28(3):227-37 [9670598] Genetics. 1999 Sep;153(1):415-26 [10471723] Genetics. 1961 Dec;46:1699-712 [14456042] Mol Phylogenet Evol. 2004 Dec;33(3):626-46 [15522792] Mamm Genome. 2004 Nov;15(11):878-86 [15672592] Genetics. 2005 Jan;169(1):347-53 [15466426] Genetics. 2005 Aug;170(4):1863-77 [15944354] Heredity (Edinb). 1992 Oct;69(4):315-24 [16718932] Genes Immun. 2006 Dec;7(8):684-7 [17024129] Genetics. 2007 Dec;177(4):2321-33 [17947429] Genome Res. 2011 Aug;21(8):1239-48 [21493779] Curr Biol. 2011 Aug 9;21(15):1296-301 [21782438] Nature. 2011 Sep 15;477(7364):289-94 [21921910] Nature. 2011 Sep 15;477(7364):326-9 [21921916] Genetics. 2012 Feb;190(2):389-401 [22345608] Genetics. 2012 Feb;190(2):437-47 [22345611] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pgen.1004850 ER - TY - JOUR T1 - Significant clinical impact of recurrent BRCA1 and BRCA2 mutations in Mexico AN - 1655728934; PQ0001057626 AB - BACKGROUND Frequent recurrent mutations in the breast and ovarian cancer susceptibility (BRCA) genes BRCA1 and BRCA2 among Hispanics, including a large rearrangement Mexican founder mutation (BRCA1 exon 9-12 deletion [ex9-12del]), suggest that an ancestry-informed BRCA-testing strategy could reduce disparities and promote cancer prevention by enabling economic screening for hereditary breast and ovarian cancer in Mexico. METHODS In a multistage approach, 188 patients with cancer who were unselected for family cancer history (92 with ovarian cancer and 96 with breast cancer) were screened for BRCA mutations using a Hispanic mutation panel (HISPANEL) of 115 recurrent mutations in a multiplex assay (114 were screened on a mass spectroscopy platform, and a polymerase chain reaction assay was used to screen for the BRCA1 ex9-12del mutation). This was followed by sequencing of all BRCA exons and adjacent intronic regions and a BRCA1 multiplex ligation-dependent probe amplification assay (MLPA) for HISPANEL-negative patients. BRCA mutation prevalence was calculated and correlated with histology and tumor receptor status, and HISPANEL sensitivity was estimated. RESULTS BRCA mutations were detected in 26 of 92 patients (28%) with ovarian cancer, in 14 of 96 patients (15%) with breast cancer overall, and in 9 of 33 patients (27%) who had tumors that were negative for estrogen receptor, progesterone receptor, and human epithelial growth factor 2 (triple-negative breast cancer). Most patients with breast cancer were diagnosed with locally advanced disease. The Mexican founder mutation (BRCA1 ex9-12del) accounted for 35% of BRCA-associated ovarian cancers and 29% of BRCA-associated breast cancers. At 2% of the sequencing and MLPA cost, HISPANEL detected 68% of all BRCA mutations. CONCLUSIONS In this study, a remarkably high prevalence of BRCA mutations was observed among patients with ovarian cancer and breast cancer who were not selected for family history, and the BRCA1 ex9-12del mutation explained 33% of the total. The remarkable frequency of BRCA1 ex9-12del in Mexico City supports a nearby origin of this Mexican founder mutation and may constitute a regional public health problem. The HISPANEL mutation panel presents a translational opportunity for cost-effective genetic testing to enable breast and ovarian cancer prevention. Cancer 2015; 121:372-378. copyright 2014 American Cancer Society. This is the first study of BRCA mutation prevalence among unselected breast cancer and ovarian cancer cases in Mexico, demonstrating a remarkably high frequency of BRCA mutations, including a high percentage with the Mexican founder mutation, BRCA1 ex9-12del. The HISPANEL, an economic and sensitive tool that detects recurrent BRCA mutations, has the potential to provide cost-effective cancer prevention and management by improving access to genetic cancer risk assessment among underserved populations like Mexico. JF - Cancer AU - Villarreal-Garza, Cynthia AU - Alvarez-Gomez, Rosa Maria AU - Perez-Plasencia, Carlos AU - Herrera, Luis A AU - Herzog, Josef AU - Castillo, Danielle AU - Mohar, Alejandro AU - Castro, Clementina AU - Gallardo, Lenny N AU - Gallardo, Dolores AU - Santibanez, Miguel AU - Blazer, Kathleen R AU - Weitzel, Jeffrey N AD - Unit of Biomedical Cancer Research, National Cancer Institute-Institute for Biomedical Research, National Autonomous University of Mexico, Mexico Federal District, Mexico. Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 372 EP - 378 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 121 IS - 3 SN - 0008-543X, 0008-543X KW - Risk Abstracts; Health & Safety Science Abstracts KW - Sensitivity KW - Estrogens KW - Mexico, Distrito Federal, Mexico City KW - Tumors KW - Mass spectroscopy KW - Cancer KW - Genetics KW - Health risks KW - Prevention KW - Mexico KW - Economics KW - Genetic screening KW - Breast cancer KW - Ovarian carcinoma KW - Mutation KW - Ethnic groups KW - Urban areas KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1655728934?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer&rft.atitle=Significant+clinical+impact+of+recurrent+BRCA1+and+BRCA2+mutations+in+Mexico&rft.au=Villarreal-Garza%2C+Cynthia%3BAlvarez-Gomez%2C+Rosa+Maria%3BPerez-Plasencia%2C+Carlos%3BHerrera%2C+Luis+A%3BHerzog%2C+Josef%3BCastillo%2C+Danielle%3BMohar%2C+Alejandro%3BCastro%2C+Clementina%3BGallardo%2C+Lenny+N%3BGallardo%2C+Dolores%3BSantibanez%2C+Miguel%3BBlazer%2C+Kathleen+R%3BWeitzel%2C+Jeffrey+N&rft.aulast=Villarreal-Garza&rft.aufirst=Cynthia&rft.date=2015-02-01&rft.volume=121&rft.issue=3&rft.spage=372&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.29058 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2015-04-29 N1 - SubjectsTermNotLitGenreText - Sensitivity; Estrogens; Tumors; Cancer; Mass spectroscopy; Health risks; Genetics; Prevention; Economics; Breast cancer; Genetic screening; Ovarian carcinoma; Mutation; Ethnic groups; Urban areas; Mexico; Mexico, Distrito Federal, Mexico City DO - http://dx.doi.org/10.1002/cncr.29058 ER - TY - JOUR T1 - Cutaneous adverse effects associated with the tyrosine-kinase inhibitor cabozantinib. AN - 1655260024; 25427282 AB - Cabozantinib S-malate is a vascular endothelial growth factor receptor 2, c-MET, and RET multitargeted tyrosine kinase inhibitor that has antiangiogenic and antitumorigenic properties with potential efficacy for the treatment of several cancers. Cutaneous reactions, one of the most frequently observed adverse effects associated with tyrosine kinase inhibitors, can significantly affect patients' quality of life and drug adherence and represent a major therapeutic challenge to maximizing the efficacy of targeted cancer therapy. To describe the frequency and spectrum of skin reactions in patients with urothelial carcinoma receiving cabozantinib as monotherapy. A single-institution study at the Clinical Research Center at the National Institutes of Health included 41 consecutive adults with metastatic, progressive urothelial carcinoma enrolled in a National Cancer Institute open-label, nonrandomized, phase 2 clinical trial. Patients receiving cabozantinib were evaluated for the development of skin reactions at each treatment visit from October 2012 to June 2014 by the primary oncology team and referred for dermatologic evaluation as appropriate. A detailed history, full-body physical examination, and clinical photographs of cutaneous lesions were obtained. Of 41 consecutive patients who received cabozantinib, 30 (73%) developed 1 or more cutaneous toxic effects. Adverse events included hand-foot skin reaction (22 [54%]), generalized pigment dilution and/or hair depigmentation (18 [44%]), xerosis (8 [20%]), scrotal erythema/ulceration (6 [15%]), and nail splinter hemorrhages (5 [12%]). Eighteen patients (44%) had 2 or more cutaneous adverse events. Reactions developed in 17 of 30 patients (57%) during the first month of cabozantinib treatment and in 24 of 30 (80%) by the second month. Of patients with skin toxic effects, dose reduction was required for symptom management in 9 of 30 patients (30%), and treatment discontinuation was required in 4 of 30 (13%). Cabozantinib monotherapy is associated with 1 or more cutaneous adverse events in most patients. Early detection and prompt treatment may increase patients' adherence to tyrosine kinase inhibitor therapy. clinicaltrials.gov Identifier: NCT01688999. JF - JAMA dermatology AU - Zuo, Rena C AU - Apolo, Andrea B AU - DiGiovanna, John J AU - Parnes, Howard L AU - Keen, Corrine M AU - Nanda, Swati AU - Dahut, William L AU - Cowen, Edward W AD - Dermatology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. ; Genitourinary Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. ; Prostate and Urologic Cancer Research Group, Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. ; Dermatology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland4section editor, JAMA Dermatology. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 170 EP - 177 VL - 151 IS - 2 KW - Anilides KW - 0 KW - Protein Kinase Inhibitors KW - Pyridines KW - cabozantinib KW - 1C39JW444G KW - Receptor Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Abridged Index Medicus KW - Index Medicus KW - Protein Kinase Inhibitors -- adverse effects KW - Dose-Response Relationship, Drug KW - Aged, 80 and over KW - Humans KW - Protein Kinase Inhibitors -- administration & dosage KW - Adult KW - Retrospective Studies KW - Quality of Life KW - Aged KW - Middle Aged KW - Follow-Up Studies KW - Receptor Protein-Tyrosine Kinases -- antagonists & inhibitors KW - Male KW - Female KW - Skin -- drug effects KW - Drug Eruptions -- etiology KW - Pyridines -- administration & dosage KW - Urinary Bladder Neoplasms -- secondary KW - Skin -- pathology KW - Urinary Bladder Neoplasms -- drug therapy KW - Anilides -- adverse effects KW - Pyridines -- adverse effects KW - Drug Eruptions -- diagnosis KW - Anilides -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1655260024?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA+dermatology&rft.atitle=Cutaneous+adverse+effects+associated+with+the+tyrosine-kinase+inhibitor+cabozantinib.&rft.au=Zuo%2C+Rena+C%3BApolo%2C+Andrea+B%3BDiGiovanna%2C+John+J%3BParnes%2C+Howard+L%3BKeen%2C+Corrine+M%3BNanda%2C+Swati%3BDahut%2C+William+L%3BCowen%2C+Edward+W&rft.aulast=Zuo&rft.aufirst=Rena&rft.date=2015-02-01&rft.volume=151&rft.issue=2&rft.spage=170&rft.isbn=&rft.btitle=&rft.title=JAMA+dermatology&rft.issn=2168-6084&rft_id=info:doi/10.1001%2Fjamadermatol.2014.2734 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-21 N1 - Date created - 2015-02-12 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT01688999; ClinicalTrials.gov N1 - SuppNotes - Comment In: JAMA Oncol. 2015 Jul;1(4):535-6 [26181263] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1001/jamadermatol.2014.2734 ER - TY - JOUR T1 - Liver is the major source of elevated serum lipocalin-2 levels after bacterial infection or partial hepatectomy: A critical role for IL-6/STAT3 AN - 1654679871; PQ0001048671 AB - Lipocalin-2 (LCN2) was originally isolated from human neutrophils and termed neutrophil gelatinase-associated lipocalin (NGAL). However, the functions of LCN2 and the cell types that are primarily responsible for LCN2 production remain unclear. To address these issues, hepatocyte-specific Lcn2 knockout (Lcn2 super(Hep-/-)) mice were generated and subjected to bacterial infection (with Klesbsiella pneumoniae or Escherichia coli) or partial hepatectomy (PHx). Studies of Lcn2 super(Hep-/-) mice revealed that hepatocytes contributed to 25% of the low basal serum level of LCN2 protein (62 ng/mL) but were responsible for more than 90% of the highly elevated serum LCN2 protein level (6,000 ng/mL) postinfection and more than 60% post-PHx (700 ng/mL). Interestingly, both Lcn2 super(Hep-/-) and global Lcn2 knockout (Lcn2 super(-/-)) mice demonstrated comparable increases in susceptibility to infection with K. pneumoniae or E. coli. These mice also had increased enteric bacterial translocation from the gut to the mesenteric lymph nodes and exhibited reduced liver regeneration after PHx. Treatment with interleukin (IL)-6 stimulated hepatocytes to produce LCN2 in vitro and in vivo. Hepatocyte-specific ablation of the IL-6 receptor or Stat3, a major downstream effector of IL-6, markedly abrogated LCN2 elevation in vivo. Furthermore, chromatin immunoprecipitation (ChIP) assay revealed that STAT3 was recruited to the promoter region of the Lcn2 gene upon STAT3 activation by IL-6. Conclusion: Hepatocytes are the major cell type responsible for LCN2 production after bacterial infection or PHx, and this response is dependent on IL-6 activation of the STAT3 signaling pathway. Thus, hepatocyte-derived LCN2 plays an important role in inhibiting bacterial infection and promoting liver regeneration. (Hepatology 2015; 61:692-702) JF - Hepatology AU - Xu, Ming-Jiang AU - Feng, Dechun AU - Wu, Hailong AU - Wang, Hua AU - Chan, Yvonne AU - Kolls, Jay AU - Borregaard, Niels AU - Porse, Bo AU - Berger, Thorsten AU - Mak, Tak W AU - Cowland, Jack B AU - Kong, Xiaoni AU - Gao, Bin AD - Laboratory of Liver Diseases, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 692 EP - 702 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 61 IS - 2 SN - 0270-9139, 0270-9139 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Interleukin 6 KW - Chromatin KW - Hepatocytes KW - Stat3 protein KW - Immunoprecipitation KW - Leukocytes (neutrophilic) KW - Infection KW - Lymph nodes KW - Serum levels KW - Promoters KW - Digestive tract KW - Interleukin 6 receptors KW - Escherichia coli KW - Liver KW - Lipocalin KW - Translocation KW - Transcription activation KW - Klebsiella pneumoniae KW - Signal transduction KW - J 02410:Animal Diseases KW - A 01490:Miscellaneous KW - F 06915:Cancer Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654679871?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hepatology&rft.atitle=Liver+is+the+major+source+of+elevated+serum+lipocalin-2+levels+after+bacterial+infection+or+partial+hepatectomy%3A+A+critical+role+for+IL-6%2FSTAT3&rft.au=Xu%2C+Ming-Jiang%3BFeng%2C+Dechun%3BWu%2C+Hailong%3BWang%2C+Hua%3BChan%2C+Yvonne%3BKolls%2C+Jay%3BBorregaard%2C+Niels%3BPorse%2C+Bo%3BBerger%2C+Thorsten%3BMak%2C+Tak+W%3BCowland%2C+Jack+B%3BKong%2C+Xiaoni%3BGao%2C+Bin&rft.aulast=Xu&rft.aufirst=Ming-Jiang&rft.date=2015-02-01&rft.volume=61&rft.issue=2&rft.spage=692&rft.isbn=&rft.btitle=&rft.title=Hepatology&rft.issn=02709139&rft_id=info:doi/10.1002%2Fhep.27447 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Interleukin 6; Chromatin; Stat3 protein; Hepatocytes; Leukocytes (neutrophilic); Immunoprecipitation; Infection; Lymph nodes; Serum levels; Promoters; Interleukin 6 receptors; Digestive tract; Liver; Lipocalin; Translocation; Transcription activation; Signal transduction; Escherichia coli; Klebsiella pneumoniae DO - http://dx.doi.org/10.1002/hep.27447 ER - TY - JOUR T1 - Optimized three-dimensional sodium imaging of the human heart on a clinical 3T scanner AN - 1654678626; PQ0001033843 AB - Purpose Optimization of sequence and sequence parameters to allow three-dimensional (3D) sodium imaging of the entire human heart in vivo in a clinically reasonable time. Theory and Methods A stack of spirals pulse sequence was optimized for cardiac imaging by considering factors such as spoiling, nutation angles, repetition time, echo time, T1/T2 relaxation, off-resonance, data acquisition window, motion, and segmented k-space acquisition. Simulations based on Bloch equations as well as the exact trajectory used for data acquisition provided the basis for choice of parameter combinations for sodium imaging. Sodium phantom scanning was used to validate the choice of parameters and for corroboration with simulations. In vivo cardiac imaging in six volunteers was also performed with an optimized sequence. Results Phantom studies showed good correlation with simulation results. Images obtained from human volunteers showed that the heart can be imaged with a nominal resolution of 5 5 10 mm super(3) and with a signal-to-noise ratio >15 (in the septum) in about 6-10 minutes. Long axis views of the reformatted human heart show true 3D imaging capability. Conclusion Optimization of the sequence and its parameters allowed in vivo 3D sodium imaging of the entire human heart in a clinically reasonable time. Magn Reson Med 73:623-632, 2015. copyright 2014 Wiley Periodicals, Inc. JF - Magnetic Resonance in Medicine AU - Gai, Neville D AU - Rochitte, Carlos AU - Nacif, Marcelo S AU - Bluemke, David A AD - Radiology & Imaging Sciences, National Institutes of Health, Bethesda, MD, USA. Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 623 EP - 632 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 73 IS - 2 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Heart KW - Sodium KW - Repetition KW - Mathematical models KW - Scanning KW - N.M.R. KW - Septum KW - imaging KW - Data acquisition KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654678626?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Magnetic+Resonance+in+Medicine&rft.atitle=Optimized+three-dimensional+sodium+imaging+of+the+human+heart+on+a+clinical+3T+scanner&rft.au=Gai%2C+Neville+D%3BRochitte%2C+Carlos%3BNacif%2C+Marcelo+S%3BBluemke%2C+David+A&rft.aulast=Gai&rft.aufirst=Neville&rft.date=2015-02-01&rft.volume=73&rft.issue=2&rft.spage=623&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.25175 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Sodium; Heart; Repetition; Mathematical models; Scanning; N.M.R.; Septum; imaging; Data acquisition DO - http://dx.doi.org/10.1002/mrm.25175 ER - TY - JOUR T1 - Immunological aspects of antiviral therapy of chronic hepatitis B virus and hepatitis C virus infections AN - 1654675162; PQ0001048672 AB - Hepatitis B virus (HBV) and hepatitis C virus (HCV) cause a large proportion of acute and chronic liver disease worldwide. Over the past decades many immunological studies defined host immune responses that mediate spontaneous clearance of acute HBV and HCV infection. However, host immune responses are also relevant in the context of treatment-induced clearance of chronic HBV and HCV infection. First, the pretreatment level of interferon-stimulated genes as well as genetic determinants of innate immune responses, such as single nucleotide polymorphisms near the IFNL3 gene, are strong predictors of the response to interferon-alpha (IFN- alpha )-based therapy. Second, IFN- alpha , which has been a mainstay of HBV and HCV therapy over decades, and ribavirin, which has also been included in interferon-free direct antiviral therapy for HCV, modulate host immune responses. Third, both IFN- alpha -based and IFN- alpha -free treatment regimens of HBV and HCV infection alter the short-term and long-term adaptive immune response against these viruses. Finally, treatment studies have not just improved the clinical outcomes, but also provided opportunities to study virus-host interaction. This review summarizes our current knowledge on how a patient's immune response affects the treatment outcome of HBV and HCV infection and how innate and adaptive immune responses themselves are altered by the different treatment regimens. ( Hepatology 2015; 61:712-721) JF - Hepatology AU - Rehermann, Barbara AU - Bertoletti, Antonio AD - Immunology Section, Liver Diseases Branch, NIDDK, National Institutes of Health, DHHS, Bethesda, MD, USA. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 712 EP - 721 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 61 IS - 2 SN - 0270-9139, 0270-9139 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts; Immunology Abstracts KW - Liver diseases KW - Hepatitis B virus KW - Hepatitis C virus KW - Single-nucleotide polymorphism KW - alpha -Interferon KW - Chronic infection KW - Ribavirin KW - Immune response KW - Immunological aspects KW - A 01340:Antibiotics & Antimicrobials KW - V 22350:Immunology KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654675162?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hepatology&rft.atitle=Immunological+aspects+of+antiviral+therapy+of+chronic+hepatitis+B+virus+and+hepatitis+C+virus+infections&rft.au=Rehermann%2C+Barbara%3BBertoletti%2C+Antonio&rft.aulast=Rehermann&rft.aufirst=Barbara&rft.date=2015-02-01&rft.volume=61&rft.issue=2&rft.spage=712&rft.isbn=&rft.btitle=&rft.title=Hepatology&rft.issn=02709139&rft_id=info:doi/10.1002%2Fhep.27323 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Liver diseases; Single-nucleotide polymorphism; Ribavirin; Chronic infection; alpha -Interferon; Immune response; Immunological aspects; Hepatitis C virus; Hepatitis B virus DO - http://dx.doi.org/10.1002/hep.27323 ER - TY - JOUR T1 - Detection of glutamate, glutamine, and glutathione by radiofrequency suppression and echo time optimization at 7 tesla AN - 1654673866; PQ0001033829 AB - Purpose To achieve detection of glutamate (Glu), glutamine (Gln), and glutathione (GSH) by minimizing the N-acetyl-aspartate (NAA) multiplet signals at 2.49 ppm using a echo time (TE) -optimized PRESS pulse sequence and a novel J-suppression radiofrequency pulse. Methods Using density matrix simulations, a PRESS sequence with (TE sub(1), TE sub(2))=(69, 37) ms and an inserted 90 degree J-suppression pulse were found to minimize the NAA multiplet at 2.49 ppm. Results NAA phantom experiments confirmed the successful suppression of the NAA multiplet at 2.49 ppm. A study of eight healthy volunteers found both Glu and Gln to be significantly higher in gray matter (GM) dominant medial prefrontal cortex voxels than in white matter (WM) dominant right frontal cortex voxels. Time-course super(1)H spectra acquired during intravenous [U- super(13)C sub(6)]glucose infusion showed gradually changing Glu C4 and Gln C4 proton resonance signals in a spectral pattern predicted by numerical simulations. Conclusion Reliable detection of Glu, Gln, and GSH was achieved. Glu and Gln levels were significantly higher in frontal lobe GM than in frontal lobe WM. It is feasible to use the proposed proton MR spectroscopy method to measure the kinetics of super(13)C incorporation into Glu and Gln during infusion of super(13)C labeled glucose. Magn Reson Med 73:451-458, 2015. copyright 2014 Wiley Periodicals, Inc. JF - Magnetic Resonance in Medicine AU - An, Li AU - Li, Shizhe AU - Murdoch, James B AU - Araneta, Maria Ferraris AU - Johnson, Christopher AU - Shen, Jun AD - National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 451 EP - 458 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 73 IS - 2 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Intravenous administration KW - Glutamine KW - Mathematical models KW - Glutathione KW - Protons KW - Glucose KW - Substantia alba KW - Cortex (frontal) KW - Frontal lobe KW - Kinetics KW - Magnetic resonance spectroscopy KW - N.M.R. KW - Glutamic acid KW - Cortex (prefrontal) KW - Substantia grisea KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654673866?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Magnetic+Resonance+in+Medicine&rft.atitle=Detection+of+glutamate%2C+glutamine%2C+and+glutathione+by+radiofrequency+suppression+and+echo+time+optimization+at+7+tesla&rft.au=An%2C+Li%3BLi%2C+Shizhe%3BMurdoch%2C+James+B%3BAraneta%2C+Maria+Ferraris%3BJohnson%2C+Christopher%3BShen%2C+Jun&rft.aulast=An&rft.aufirst=Li&rft.date=2015-02-01&rft.volume=73&rft.issue=2&rft.spage=451&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.25150 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Glutamine; Intravenous administration; Mathematical models; Protons; Glutathione; Glucose; Cortex (frontal); Substantia alba; Frontal lobe; Magnetic resonance spectroscopy; Kinetics; N.M.R.; Glutamic acid; Cortex (prefrontal); Substantia grisea DO - http://dx.doi.org/10.1002/mrm.25150 ER - TY - JOUR T1 - Investing in prospective cohorts for etiologic study of occupational exposures AN - 1654670133; PQ0001048141 AB - Prospective cohorts have played a major role in understanding the contribution of diet, physical activity, medical conditions, and genes to the development of many diseases, but have not been widely used for occupational exposures. Studies in agriculture are an exception. We draw upon our experience using this design to study agricultural workers to identify conditions that might foster use of prospective cohorts to study other occupational settings. Prospective cohort studies are perceived by many as the strongest epidemiologic design. It allows updating of information on exposure and other factors, collection of biologic samples before disease diagnosis for biomarker studies, assessment of effect modification by genes, lifestyle, and other occupational exposures, and evaluation of a wide range of health outcomes. Increased use of prospective cohorts would be beneficial in identifying hazardous exposures in the workplace. Occupational epidemiologists should seek opportunities to initiate prospective cohorts to investigate high priority, occupational exposures. Am. J. Ind. Med. 58:113-122, 2015. copyright 2015 Wiley Periodicals, Inc. JF - American Journal of Industrial Medicine AU - Blair, A AU - Hines, C J AU - Thomas, K W AU - Alavanja, MCR AU - Freeman, LEBeane AU - Hoppin, JA AU - Kamel, F AU - Lynch, C F AU - Lubin, J H AU - Silverman, D T AU - Whelan, E AU - Zahm, SH AU - Sandler, D P AD - Division of Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland. Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 113 EP - 122 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 58 IS - 2 SN - 0271-3586, 0271-3586 KW - Toxicology Abstracts; Health & Safety Science Abstracts KW - Bioindicators KW - Agriculture KW - Diets KW - Physical activity KW - biomarkers KW - Perception KW - Priorities KW - Occupational exposure KW - H 1000:Occupational Safety and Health KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654670133?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Industrial+Medicine&rft.atitle=Investing+in+prospective+cohorts+for+etiologic+study+of+occupational+exposures&rft.au=Blair%2C+A%3BHines%2C+C+J%3BThomas%2C+K+W%3BAlavanja%2C+MCR%3BFreeman%2C+LEBeane%3BHoppin%2C+JA%3BKamel%2C+F%3BLynch%2C+C+F%3BLubin%2C+J+H%3BSilverman%2C+D+T%3BWhelan%2C+E%3BZahm%2C+SH%3BSandler%2C+D+P&rft.aulast=Blair&rft.aufirst=A&rft.date=2015-02-01&rft.volume=58&rft.issue=2&rft.spage=113&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Industrial+Medicine&rft.issn=02713586&rft_id=info:doi/10.1002%2Fajim.22403 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2015-04-02 N1 - SubjectsTermNotLitGenreText - Diets; Agriculture; Physical activity; biomarkers; Occupational exposure; Bioindicators; Perception; Priorities DO - http://dx.doi.org/10.1002/ajim.22403 ER - TY - JOUR T1 - Engineered Mesenchymal Stem Cells with Enhanced Tropism and Paracrine Secretion of Cytokines and Growth Factors to Treat Traumatic Brain Injury AN - 1654665431; PQ0001057742 AB - Traumatic brain injury (TBI) is the leading cause of death and disability worldwide. Mesenchymal stem cells (MSCs) are promising for the treatment of various diseases and injuries. Many strategies have been applied to attract MSCs to injury site after systemic infusion. In this study, we evidenced that the CXC chemokine receptor 4 (CXCR4)-SDF1 alpha (stromal cell-derived factor 1 alpha ) axis in engineered MSCs serves not only to attract MSC migration to TBI but also to activate Akt kinase signaling pathway in MSCs to promote paracrine secretion of cytokines and growth factors. This leads to enhanced vasculogenesis and neuroprotection at the boundary of TBI for improved blood supply, recovery of axon connectivity, and behavioral ability and results in positive feedback loop to enhance additional MSC tropism to injury. These findings indicate a new aspect of SDF1 alpha in mediating CXCR4 engineered MSCs for brain trauma homing and recovery. This potential mechanism may be applicable to other injuries, where CXCR4-SDF1 alpha interaction is highly associated. Stem Cells 2015; 33:456-467 JF - Stem Cells AU - Wang, Zhe AU - Wang, Yu AU - Wang, Zhiyong AU - Gutkind, JSilvio AU - Wang, Zhongliang AU - Wang, Fu AU - Lu, Jie AU - Niu, Gang AU - Teng, Gaojun AU - Chen, Xiaoyuan AD - Laboratory of Molecular Imaging and Nanomedicine, National Institute of Biomedical Imaging and Bioengineering, National Institutes of Health, Bethesda, Maryland, USA. PY - 2015 SP - 456 EP - 467 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 33 IS - 2 SN - 1066-5099, 1066-5099 KW - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts KW - SDF-1 protein KW - CXC chemokine receptors KW - Brain injury KW - CXCR4 protein KW - Neural networks KW - Paracrine signalling KW - Tropism KW - Neuroprotection KW - Stem cells KW - AKT protein KW - Boundaries KW - Cytokines KW - Feedback KW - Axons KW - Cell migration KW - Growth factors KW - Mesenchyme KW - Traumatic brain injury KW - Signal transduction KW - W 30910:Imaging KW - N3 11001:Behavioral and Cognitive Neuroscience UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654665431?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+Cells&rft.atitle=Engineered+Mesenchymal+Stem+Cells+with+Enhanced+Tropism+and+Paracrine+Secretion+of+Cytokines+and+Growth+Factors+to+Treat+Traumatic+Brain+Injury&rft.au=Wang%2C+Zhe%3BWang%2C+Yu%3BWang%2C+Zhiyong%3BGutkind%2C+JSilvio%3BWang%2C+Zhongliang%3BWang%2C+Fu%3BLu%2C+Jie%3BNiu%2C+Gang%3BTeng%2C+Gaojun%3BChen%2C+Xiaoyuan&rft.aulast=Wang&rft.aufirst=Zhe&rft.date=2015-02-01&rft.volume=33&rft.issue=2&rft.spage=456&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.1878 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - SDF-1 protein; CXC chemokine receptors; Brain injury; CXCR4 protein; Neural networks; Tropism; Paracrine signalling; Neuroprotection; Stem cells; Boundaries; AKT protein; Cytokines; Axons; Feedback; Growth factors; Cell migration; Traumatic brain injury; Mesenchyme; Signal transduction DO - http://dx.doi.org/10.1002/stem.1878 ER - TY - JOUR T1 - A methods review on use of nonsense suppression to study 3' end formation and other aspects of tRNA biogenesis. AN - 1652766097; 25447915 AB - Suppressor tRNAs bear anticodon mutations that allow them to decode premature stop codons in metabolic marker gene mRNAs, that can be used as in vivo reporters of functional tRNA biogenesis. Here, we review key components of a suppressor tRNA system specific to Schizosaccharomyces pombe and its adaptations for use to study specific steps in tRNA biogenesis. Eukaryotic tRNA biogenesis begins with transcription initiation by RNA polymerase (pol) III. The nascent pre-tRNAs must undergo folding, 5' and 3' processing to remove the leader and trailer, nuclear export, and splicing if applicable, while multiple complex chemical modifications occur throughout the process. We review evidence that precursor-tRNA processing begins with transcription termination at the oligo(T) terminator element, which forms a 3' oligo(U) tract on the nascent RNA, a sequence-specific binding site for the RNA chaperone, La protein. The processing pathway bifurcates depending on a poorly understood property of pol III termination that determines the 3' oligo(U) length and therefore the affinity for La. We thus review the pol III termination process and the factors involved including advances using gene-specific random mutagenesis by dNTP analogs that identify key residues important for transcription termination in certain pol III subunits. The review ends with a 'technical approaches' section that includes a parts lists of suppressor-tRNA alleles, strains and plasmids, and graphic examples of its diverse uses. Published by Elsevier B.V. JF - Gene AU - Rijal, Keshab AU - Maraia, Richard J AU - Arimbasseri, Aneeshkumar G AD - Intramural Research Program on Genomics of Differentiation, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA. ; Intramural Research Program on Genomics of Differentiation, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA. Electronic address: maraiar@mail.nih.gov. ; Intramural Research Program on Genomics of Differentiation, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA. Electronic address: arimbasseriag@mail.nih.gov. Y1 - 2015/02/01/ PY - 2015 DA - 2015 Feb 01 SP - 35 EP - 50 VL - 556 IS - 1 KW - Codon, Nonsense KW - 0 KW - RNA Precursors KW - RNA, Transfer KW - 9014-25-9 KW - RNA Polymerase III KW - EC 2.7.7.6 KW - Index Medicus KW - RPC53 KW - Transcription termination KW - RPC37 KW - RNA polymerase III KW - RPC2 KW - RPC11 KW - RNA Precursors -- metabolism KW - Animals KW - Mutagenesis, Site-Directed -- methods KW - Humans KW - RNA Polymerase III -- metabolism KW - RNA 3' End Processing KW - RNA Precursors -- genetics KW - Codon, Nonsense -- genetics KW - Schizosaccharomyces -- genetics KW - Transcription Termination, Genetic KW - Schizosaccharomyces -- metabolism KW - RNA, Transfer -- biosynthesis KW - Suppression, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652766097?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene&rft.atitle=A+methods+review+on+use+of+nonsense+suppression+to+study+3%27+end+formation+and+other+aspects+of+tRNA+biogenesis.&rft.au=Rijal%2C+Keshab%3BMaraia%2C+Richard+J%3BArimbasseri%2C+Aneeshkumar+G&rft.aulast=Rijal&rft.aufirst=Keshab&rft.date=2015-02-01&rft.volume=556&rft.issue=1&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=Gene&rft.issn=1879-0038&rft_id=info:doi/10.1016%2Fj.gene.2014.11.034 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-03 N1 - Date created - 2014-12-19 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Biol Chem. 2000 Oct 6;275(40):31480-7 [10906331] Mol Cell Biol. 2001 Oct;21(20):6870-81 [11564871] Biochim Biophys Acta. 2013 Mar-Apr;1829(3-4):318-30 [23099421] Proc Natl Acad Sci U S A. 2002 Feb 5;99(3):1218-22 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http://dx.doi.org/10.1016/j.gene.2014.11.034 ER - TY - JOUR T1 - Identification of a functional SNP in the 3'UTR of CXCR2 that is associated with reduced risk of lung cancer. AN - 1652450899; 25480945 AB - Global changes in gene expression accompany the development of cancer. Thus, inherited variants in miRNA-binding sites are likely candidates for conferring inherited susceptibility. Using an in silico approach, we compiled a comprehensive list of SNPs predicted to modulate miRNA binding in genes from several key lung cancer pathways. We then investigated whether these SNPs were associated with lung cancer risk in two independent populations. In general, SNPs in miRNA-binding sites are rare. However, some allelic variation was observed. We found that rs1126579 in CXCR2 was associated with a reduced risk of lung cancer in both European American [ORTT vs. CC 0.56 (0.37-0.88); P = 0.008] and Japanese [ORTT vs. CC 0.62 (0.38-1.00); P = 0.049] populations. Furthermore, we found that the SNP disrupted a novel binding site for miR-516a-3p, led to a moderate increase in CXCR2 mRNA and protein expression, and increased MAPK signaling. Moreover, analysis of rs1126579 with serum levels of IL8, its endogenous ligand, supported an interaction whereby rs1126579-T and high serum IL8 conferred synergistic protection from lung cancer. Our findings demonstrate a function for a 3'UTR SNP in modulating CXCR2 expression, signaling, and susceptibility to lung cancer. ©2014 American Association for Cancer Research. JF - Cancer research AU - Ryan, Bríd M AU - Robles, Ana I AU - McClary, Andrew C AU - Haznadar, Majda AU - Bowman, Elise D AU - Pine, Sharon R AU - Brown, Derek AU - Khan, Mohammed AU - Shiraishi, Kouya AU - Kohno, Takashi AU - Okayama, Hirokazu AU - Modali, Ramakrishna AU - Yokota, Jun AU - Harris, Curtis C AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. Department of Pathology, Stanford University Hospital and Clinics, Stanford, California. ; Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, New Brunswick, New Jersey. ; Division of Genome Biology, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. Division of Genome Biology, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan. ; BioServe Ltd., Beltsville, Maryland. ; Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. Curtis_Harris@nih.gov. Y1 - 2015/02/01/ PY - 2015 DA - 2015 Feb 01 SP - 566 EP - 575 VL - 75 IS - 3 KW - 3' Untranslated Regions KW - 0 KW - Interleukin-8 KW - Ligands KW - MicroRNAs KW - Receptors, Interleukin-8B KW - Index Medicus KW - Genetic Variation KW - Humans KW - Aged KW - Binding Sites KW - Gene Expression Regulation, Neoplastic KW - Genotype KW - Gene Expression Profiling KW - Alleles KW - MicroRNAs -- metabolism KW - Risk Factors KW - Case-Control Studies KW - Middle Aged KW - Interleukin-8 -- metabolism KW - Signal Transduction KW - Male KW - Female KW - Japan KW - Polymorphism, Single Nucleotide KW - Receptors, Interleukin-8B -- genetics KW - Lung Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652450899?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+research&rft.atitle=Identification+of+a+functional+SNP+in+the+3%27UTR+of+CXCR2+that+is+associated+with+reduced+risk+of+lung+cancer.&rft.au=Ryan%2C+Br%C3%ADd+M%3BRobles%2C+Ana+I%3BMcClary%2C+Andrew+C%3BHaznadar%2C+Majda%3BBowman%2C+Elise+D%3BPine%2C+Sharon+R%3BBrown%2C+Derek%3BKhan%2C+Mohammed%3BShiraishi%2C+Kouya%3BKohno%2C+Takashi%3BOkayama%2C+Hirokazu%3BModali%2C+Ramakrishna%3BYokota%2C+Jun%3BHarris%2C+Curtis+C&rft.aulast=Ryan&rft.aufirst=Br%C3%ADd&rft.date=2015-02-01&rft.volume=75&rft.issue=3&rft.spage=566&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-14-2101 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-08 N1 - Date created - 2015-02-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Res. 2013 Mar 15;73(6):1867-75 [23378343] Genes Dev. 2013 Nov 1;27(21):2380-96 [24145798] Proc Natl Acad Sci U S A. 2013 Dec 17;110(51):20705-10 [24248364] Hum Mol Genet. 2014 Sep 1;23(17):4569-80 [24722204] J Immunol. 2000 Nov 1;165(9):5269-77 [11046061] Carcinogenesis. 2003 Feb;24(2):269-74 [12584177] Am J Epidemiol. 2003 Aug 1;158(3):251-8 [12882947] Cell. 2003 Dec 26;115(7):787-98 [14697198] Cell. 2004 Jan 23;116(2):281-97 [14744438] Br J Cancer. 2004 Jul 19;91(2):355-8 [15188009] Science. 1992 Dec 11;258(5089):1798-801 [1281554] Clin Cancer Res. 2004 Nov 1;10(21):7157-62 [15534087] Cell. 2004 Nov 24;119(5):591-602 [15550242] Nature. 2005 Aug 4;436(7051):642 [16079833] Science. 2005 Oct 14;310(5746):317-20 [16224024] Nature. 2012 Jul 19;487(7407):330-7 [22810696] J Clin Invest. 2012 Sep;122(9):3127-44 [22922255] Biochem Biophys Res Commun. 2013 Jan 11;430(2):529-34 [23232114] Cancer Res. 2013 Jan 15;73(2):571-82 [23204236] Cancer Epidemiol Biomarkers Prev. 2005 Nov;14(11 Pt 1):2487-93 [16284368] Science. 2006 May 26;312(5777):1215-7 [16728641] Nat Genet. 2006 Jun;38 Suppl:S8-13 [16736023] Bioinformatics. 2014 Aug 15;30(16):2243-6 [24764460] Nat Genet. 2006 Jul;38(7):813-8 [16751773] Nucleic Acids Res. 2006 Jul 1;34(Web Server issue):W451-4 [16845047] Nat Genet. 2006 Dec;38(12):1452-6 [17072316] Nucleic Acids Res. 2007 Jan;35(Database issue):D51-4 [17099235] Proc Natl Acad Sci U S A. 2007 Feb 27;104(9):3300-5 [17360642] Cancer Res. 2007 Jul 15;67(14):6854-62 [17638896] Am J Hum Genet. 2007 Aug;81(2):405-13 [17668390] Nat Rev Mol Cell Biol. 2007 Sep;8(9):729-40 [17667954] Carcinogenesis. 2008 Mar;29(3):579-84 [18192692] Cell. 2008 Jun 13;133(6):1006-18 [18555777] Biochem Biophys Res Commun. 2008 Sep 12;374(1):101-5 [18602895] Cancer Res. 2008 Oct 15;68(20):8535-40 [18922928] Cancer Res. 2009 Mar 15;69(6):2167-70 [19276354] Cell. 2009 May 15;137(4):647-58 [19409607] Proc Natl Acad Sci U S A. 2009 Jul 21;106(29):12085-90 [19597153] Epidemiology. 2009 Nov;20(6):863-71 [19806059] Nucleic Acids Res. 2010 Jan;38(Database issue):D640-51 [19906729] Nat Rev Cancer. 2010 Jan;10(1):51-7 [20029423] Carcinogenesis. 2010 Jan;31(1):37-49 [19955394] Carcinogenesis. 2010 May;31(5):834-41 [20061363] Nat Rev Cancer. 2010 Jun;10(6):389-402 [20495573] PLoS One. 2011;6(4):e17944 [21533135] Eur J Epidemiol. 2011 Jun;26(6):433-8 [21344323] J Natl Cancer Inst. 2011 Jul 20;103(14):1112-22 [21685357] Cancer Res. 2011 Aug 1;71(15):5175-81 [21676885] Cancer Res. 2012 Jan 1;72(1):100-11 [22080568] Nat Rev Genet. 2012 Apr;13(4):271-82 [22411466] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1158/0008-5472.CAN-14-2101 ER - TY - JOUR T1 - Metallothionein blocks oxidative DNA damage induced by acute inorganic arsenic exposure. AN - 1652444841; 25485709 AB - We studied how protein metallothionein (MT) impacts arsenic-induced oxidative DNA damage (ODD) using cells that poorly express MT (MT-I/II double knockout embryonic cells; called MT-null cells) and wild-type (WT) MT competent cells. Arsenic (as NaAsO2) was less cytolethal over 24h in WT cells (LC50=11.0±1.3μM; mean±SEM) than in MT-null cells (LC50=5.6±1.2μM). ODD was measured by the immuno-spin trapping method. Arsenic (1 or 5μM; 24h) induced much less ODD in WT cells (121% and 141% of control, respectively) than in MT-null cells (202% and 260%). In WT cells arsenic caused concentration-dependent increases in MT expression (transcript and protein), and in the metal-responsive transcription factor-1 (MTF-1), which is required to induce the MT gene. In contrast, basal MT levels were not detectable in MT-null cells and unaltered by arsenic exposure. Transfection of MT-I gene into the MT-null cells markedly reduced arsenic-induced ODD levels. The transport genes, Abcc1 and Abcc2 were increased by arsenic in WT cells but either showed no or very limited increases in MT-null cells. Arsenic caused increases in oxidant stress defense genes HO-1 and GSTα2 in both WT and MT-null cells, but to much higher levels in WT cells. WT cells appear more adept at activating metal transport systems and oxidant response genes, although the role of MT in these responses is unclear. Overall, MT protects against arsenic-induced ODD in MT competent cells by potential sequestration of scavenging oxidant radicals and/or arsenic. Published by Elsevier Inc. JF - Toxicology and applied pharmacology AU - Qu, Wei AU - Waalkes, Michael P AD - National Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. Electronic address: qu@niehs.nih.gov. ; National Toxicology Program Laboratory, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. Y1 - 2015/02/01/ PY - 2015 DA - 2015 Feb 01 SP - 267 EP - 274 VL - 282 IS - 3 KW - Carcinogens KW - 0 KW - DNA-Binding Proteins KW - Environmental Pollutants KW - Isoenzymes KW - Membrane Proteins KW - Multidrug Resistance-Associated Proteins KW - Transcription Factors KW - transcription factor MTF-1 KW - multidrug resistance-associated protein 2 KW - 4AF605U6JN KW - Metallothionein KW - 9038-94-2 KW - Heme Oxygenase-1 KW - EC 1.14.14.18 KW - Hmox1 protein, mouse KW - Glutathione Transferase KW - EC 2.5.1.18 KW - glutathione S-transferase alpha KW - Arsenic KW - N712M78A8G KW - multidrug resistance-associated protein 1 KW - Y49M64GZ4Q KW - Index Medicus KW - Oxidative DNA damage KW - Reactive oxygen species KW - Cell Proliferation -- drug effects KW - Animals KW - DNA-Binding Proteins -- genetics KW - Glutathione Transferase -- genetics KW - Heme Oxygenase-1 -- genetics KW - Mice KW - Membrane Proteins -- genetics KW - Transcription Factors -- genetics KW - Isoenzymes -- genetics KW - Cell Survival -- drug effects KW - Oxidative Stress KW - Multidrug Resistance-Associated Proteins -- genetics KW - Gene Expression Regulation -- drug effects KW - Cell Line KW - Environmental Pollutants -- toxicity KW - Arsenic -- toxicity KW - Carcinogens -- toxicity KW - Metallothionein -- genetics KW - DNA Damage -- genetics KW - Metallothionein -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652444841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=Metallothionein+blocks+oxidative+DNA+damage+induced+by+acute+inorganic+arsenic+exposure.&rft.au=Qu%2C+Wei%3BWaalkes%2C+Michael+P&rft.aulast=Qu&rft.aufirst=Wei&rft.date=2015-02-01&rft.volume=282&rft.issue=3&rft.spage=267&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2014.11.014 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-16 N1 - Date created - 2015-02-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Toxicol Sci. 2000 Jun;55(2):460-7 [10828279] Antiviral Res. 2000 Sep;47(3):207-14 [10974373] J Biol Chem. 2000 Oct 27;275(43):33404-8 [10938093] Proc Natl Acad Sci U S A. 2001 Feb 13;98(4):1643-8 [11172004] Biochem Pharmacol. 2001 Jun 1;61(11):1387-91 [11331074] Am J Pathol. 2002 Mar;160(3):1047-56 [11891201] Chem Res Toxicol. 2002 Dec;15(12):1627-34 [12482246] Carcinogenesis. 2003 Jun;24(6):1123-32 [12807749] Mutat Res. 2003 Dec 10;533(1-2):107-20 [14643415] Mutat Res. 2003 Dec 10;533(1-2):211-26 [14643422] J Pharmacol Exp Ther. 2004 Jan;308(1):260-7 [14569069] Mol Cell Biochem. 2004 Jan;255(1-2):67-78 [14971647] J Biol Chem. 2004 Jul 30;279(31):32700-8 [15161912] Fundam Appl Toxicol. 1994 Jul;23(1):32-7 [7958560] J Biol Chem. 1995 Mar 10;270(10):5506-10 [7890668] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8103-7 [9653147] Curr Med Chem. 2005;12(10):1161-208 [15892631] Nat Methods. 2006 Feb;3(2):123-7 [16432522] Mol Pharmacol. 2006 Apr;69(4):1499-505 [16434618] Curr Med Chem. 2009;16(5):522-37 [19199919] Cancer Sci. 2009 Mar;100(3):382-8 [19154403] J Biol Chem. 2009 May 8;284(19):12609-21 [19276070] Toxicol Appl Pharmacol. 2009 Aug 1;238(3):215-20 [19362100] Toxicol Sci. 2009 Sep;111(1):100-8 [19542206] J Natl Cancer Inst. 2009 Dec 16;101(24):1670-81 [19933942] Free Radic Res. 2010 Jun;44(6):605-13 [20380594] Biometals. 2010 Oct;23(5):927-40 [20361350] J Biochem Mol Toxicol. 2010 Sep-Oct;24(5):330-4 [20979157] Biochim Biophys Acta. 2011 Jan;1809(1):56-62 [21035574] J Appl Toxicol. 2011 Mar;31(2):95-107 [21321970] Toxicology. 2011 May 10;283(2-3):65-87 [21414382] J Inorg Biochem. 2012 Mar;108:141-9 [22197475] Arch Toxicol. 2012 Jun;86(6):879-96 [22488045] Biochim Biophys Acta. 2012 Sep;1823(9):1416-25 [22289350] Biol Trace Elem Res. 2012 Dec;149(3):331-9 [22555517] Arch Toxicol. 2013 Feb;87(2):311-21 [22914987] Biochem Biophys Res Commun. 2013 Apr 19;433(4):477-83 [23523794] Toxicol Lett. 2013 Jul 18;220(3):277-85 [23664956] Biochem Biophys Res Commun. 2013 Nov 8;441(1):208-13 [24140052] Arch Toxicol. 2014 Feb;88(2):249-61 [24091636] Neurochem Int. 2014 Sep;75:79-88 [24932697] Toxicol Sci. 2006 May;91(1):70-81 [16436460] Int J Cancer. 2006 Jul 1;119(1):28-32 [16432836] J Am Chem Soc. 2006 Sep 27;128(38):12473-83 [16984198] Nat Protoc. 2007;2(3):512-22 [17406615] Arch Biochem Biophys. 2007 Jul 15;463(2):201-10 [17462582] Environ Health Perspect. 2007 Jul;115(7):1101-6 [17637929] Kidney Int. 2008 May;73(9):994-1007 [18272962] Chembiochem. 2009 Jan 5;10(1):55-62 [19089881] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.taap.2014.11.014 ER - TY - JOUR T1 - Hydroxylated tropolones inhibit hepatitis B virus replication by blocking viral ribonuclease H activity. AN - 1652441270; 25451058 AB - Hepatitis B virus (HBV) remains a major human pathogen despite the development of both antiviral drugs and a vaccine, in part because the current therapies do not suppress HBV replication far enough to eradicate the virus. Here, we screened 51 troponoid compounds for their ability to suppress HBV RNaseH activity and HBV replication based on the activities of α-hydroxytropolones against HIV RNaseH, with the goal of determining whether the tropolone pharmacophore may be a promising scaffold for anti-HBV drug development. Thirteen compounds inhibited HBV RNaseH, with the best 50% inhibitory concentration (IC50) being 2.3 μM. Similar inhibition patterns were observed against HBV genotype D and C RNaseHs, implying limited genotype specificity. Six of 10 compounds tested against HBV replication in culture suppressed replication via blocking of viral RNaseH activity, with the best 50% effective concentration (EC50) being 0.34 μM. Eighteen compounds inhibited recombinant human RNaseH1, and moderate cytotoxicity was observed for all compounds (50% cytotoxic concentration [CC50]=25 to 79 μM). Therapeutic indexes ranged from 3.8 to 94. Efficient inhibition required an intact α-hydroxytropolone moiety plus one or more short appendages on the tropolone ring, but a wide variety of constituents were permissible. These data indicate that troponoids and specifically α-hydroxytropolones are promising lead candidates for development as anti-HBV drugs, providing that toxicity can be minimized. Potential anti-RNaseH drugs are envisioned to be employed in combination with the existing nucleos(t)ide analogs to suppress HBV replication far enough to block genomic maintenance, with the goal of eradicating infection. Copyright © 2015, American Society for Microbiology. All Rights Reserved. JF - Antimicrobial agents and chemotherapy AU - Lu, Gaofeng AU - Lomonosova, Elena AU - Cheng, Xiaohong AU - Moran, Eileen A AU - Meyers, Marvin J AU - Le Grice, Stuart F J AU - Thomas, Craig J AU - Jiang, Jian-kang AU - Meck, Christine AU - Hirsch, Danielle R AU - D'Erasmo, Michael P AU - Suyabatmaz, Duygu M AU - Murelli, Ryan P AU - Tavis, John E AD - Department of Gastroenterology, the Second Affiliated Hospital, Zhengzhou University, Zhengzhou, Henan, China Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, Saint Louis, Missouri, USA. ; Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, Saint Louis, Missouri, USA Saint Louis University Liver Center, Saint Louis University School of Medicine, Saint Louis, Missouri, USA. ; Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, Saint Louis, Missouri, USA. ; Center for World Health and Medicine, Saint Louis University School of Medicine, Saint Louis, Missouri, USA. ; Basic Research Laboratory, National Cancer Institute, Frederick, Maryland, USA. ; NIH Chemical Genomics Center, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA. ; Department of Chemistry, Brooklyn College, The City University of New York, Brooklyn, New York, USA Department of Chemistry, The Graduate Center, The City University of New York, New York, New York, USA. ; Department of Chemistry, Brooklyn College, The City University of New York, Brooklyn, New York, USA. ; Department of Molecular Microbiology and Immunology, Saint Louis University School of Medicine, Saint Louis, Missouri, USA Saint Louis University Liver Center, Saint Louis University School of Medicine, Saint Louis, Missouri, USA tavisje@slu.edu. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 1070 EP - 1079 VL - 59 IS - 2 KW - Tropolone KW - 7L6DL16P1T KW - Ribonuclease H KW - EC 3.1.26.4 KW - Index Medicus KW - Humans KW - Virus Replication -- drug effects KW - Ribonuclease H -- antagonists & inhibitors KW - Ribonuclease H -- metabolism KW - Tropolone -- pharmacology KW - Hepatitis B virus -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652441270?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+agents+and+chemotherapy&rft.atitle=Hydroxylated+tropolones+inhibit+hepatitis+B+virus+replication+by+blocking+viral+ribonuclease+H+activity.&rft.au=Lu%2C+Gaofeng%3BLomonosova%2C+Elena%3BCheng%2C+Xiaohong%3BMoran%2C+Eileen+A%3BMeyers%2C+Marvin+J%3BLe+Grice%2C+Stuart+F+J%3BThomas%2C+Craig+J%3BJiang%2C+Jian-kang%3BMeck%2C+Christine%3BHirsch%2C+Danielle+R%3BD%27Erasmo%2C+Michael+P%3BSuyabatmaz%2C+Duygu+M%3BMurelli%2C+Ryan+P%3BTavis%2C+John+E&rft.aulast=Lu&rft.aufirst=Gaofeng&rft.date=2015-02-01&rft.volume=59&rft.issue=2&rft.spage=1070&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+agents+and+chemotherapy&rft.issn=1098-6596&rft_id=info:doi/10.1128%2FAAC.04617-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-08 N1 - Date created - 2015-01-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: ACS Chem Biol. 2008 Oct 17;3(10):635-44 [18831589] J Virol. 2007 Nov;81(22):12472-84 [17804499] EMBO Rep. 2009 Feb;10(2):144-51 [19165139] J Mol Biol. 2009 May 8;388(3):462-74 [19289131] Hepatology. 2009 Sep;50(3):661-2 [19714720] J Med Chem. 2009 Oct 8;52(19):5781-4 [19791799] Structure. 2009 Dec 9;17(12):1625-35 [20004166] Hepatology. 2010 Jan;51(1):73-80 [19998272] J Med Chem. 2009 Mar 12;52(5):1380-7 [19178289] J Virol. 2010 Aug;84(15):7625-33 [20484498] J Am Chem Soc. 2010 Sep 15;132(36):12711-6 [20726553] J Antibiot (Tokyo). 2011 Feb;64(2):183-8 [21063422] J Med Chem. 2011 Mar 24;54(6):1812-24 [21366258] J Med Chem. 2011 Jul 14;54(13):4462-73 [21568335] Biochim Biophys Acta. 2011 Dec;1813(12):2000-7 [21878356] Org Lett. 2012 Dec 7;14(23):5988-91 [23167954] PLoS Pathog. 2013 Jan;9(1):e1003125 [23349632] Antiviral Res. 2013 Apr;98(1):27-34 [23391846] Expert Rev Anti Infect Ther. 2013 Aug;11(8):755-7 [23977931] PLoS One. 2013;8(8):e71006 [23990920] Antiviral Res. 2013 Sep;99(3):221-9 [23796982] J Org Chem. 2013 Dec 6;78(23):11707-13 [24171600] Biochem Biophys Res Commun. 2014 Jan 17;443(3):808-13 [24342612] J Hepatol. 2014 Apr;60(4):715-22 [24295873] Antiviral Res. 2014 Aug;108:48-55 [24858512] Intervirology. 2014;57(3-4):158-62 [25034483] Antimicrob Agents Chemother. 2014 Jul;58(7):4086-93 [24798282] Antimicrob Agents Chemother. 2014 Dec;58(12):7451-61 [25267681] Bioorg Med Chem Lett. 2014 Nov 1;24(21):4943-7 [25283553] J Org Chem. 2000 Jul 28;65(15):4509-14 [10959851] Am J Gastroenterol. 2002 Nov;97(11):2886-95 [12425564] Mol Cell. 2003 Mar;11(3):807-15 [12667461] J Viral Hepat. 2004 Mar;11(2):97-107 [14996343] N Engl J Med. 2004 Mar 11;350(11):1118-29 [15014185] Antimicrob Agents Chemother. 1982 Nov;22(5):824-31 [6185088] J Antibiot (Tokyo). 1988 Jul;41(7):862-8 [3417559] J Virol. 1990 Nov;64(11):5553-8 [1698997] Structure. 1995 Feb 15;3(2):131-4 [7735828] Mol Biol Evol. 1995 Jul;12(4):657-70 [7544864] J Virol. 1996 Jul;70(7):4269-74 [8676448] Chem Biol Interact. 1998 Nov 6;116(1-2):45-60 [9877200] Nucleic Acids Res. 2005;33(4):1249-56 [15741178] Antimicrob Agents Chemother. 2005 Dec;49(12):4884-94 [16304149] Mol Pharmacol. 2006 Apr;69(4):1454-60 [16418335] Epidemiol Rev. 2006;28:112-25 [16754644] ACS Chem Biol. 2006 Dec 20;1(11):702-12 [17184135] Ann Intern Med. 2009 Jan 20;150(2):104-10 [19124811] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/AAC.04617-14 ER - TY - JOUR T1 - FutureTox II: in vitro data and in silico models for predictive toxicology. AN - 1652440978; 25628403 AB - FutureTox II, a Society of Toxicology Contemporary Concepts in Toxicology workshop, was held in January, 2014. The meeting goals were to review and discuss the state of the science in toxicology in the context of implementing the NRC 21st century vision of predicting in vivo responses from in vitro and in silico data, and to define the goals for the future. Presentations and discussions were held on priority concerns such as predicting and modeling of metabolism, cell growth and differentiation, effects on sensitive subpopulations, and integrating data into risk assessment. Emerging trends in technologies such as stem cell-derived human cells, 3D organotypic culture models, mathematical modeling of cellular processes and morphogenesis, adverse outcome pathway development, and high-content imaging of in vivo systems were discussed. Although advances in moving towards an in vitro/in silico based risk assessment paradigm were apparent, knowledge gaps in these areas and limitations of technologies were identified. Specific recommendations were made for future directions and research needs in the areas of hepatotoxicity, cancer prediction, developmental toxicity, and regulatory toxicology. © The Author 2015. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. JF - Toxicological sciences : an official journal of the Society of Toxicology AU - Knudsen, Thomas B AU - Keller, Douglas A AU - Sander, Miriam AU - Carney, Edward W AU - Doerrer, Nancy G AU - Eaton, David L AU - Fitzpatrick, Suzanne Compton AU - Hastings, Kenneth L AU - Mendrick, Donna L AU - Tice, Raymond R AU - Watkins, Paul B AU - Whelan, Maurice AD - United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711, Sanofi, Bridgewater, New Jersey 08807, Page One Editorial Services, Boulder, Colorado 80304, Dow Chemical Company, Midland, Michigan 48674, Health and Environmental Sciences Institute, Washington, District of Columbia 20005, University of Washington, Seattle, Washington 98105, United States Food and Drug Administration, Silver Spring, Maryland 20993, Sanofi, Bethesda, Maryland 20814, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, University of North Carolina, Chapel Hill, North Carolina 27599, The Hamner Institutes, Research Triangle Park, North Carolina 27709, and European Commission Joint Research Centre, I-21027 Ispra, Italy. ; United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711, Sanofi, Bridgewater, New Jersey 08807, Page One Editorial Services, Boulder, Colorado 80304, Dow Chemical Company, Midland, Michigan 48674, Health and Environmental Sciences Institute, Washington, District of Columbia 20005, University of Washington, Seattle, Washington 98105, United States Food and Drug Administration, Silver Spring, Maryland 20993, Sanofi, Bethesda, Maryland 20814, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, University of North Carolina, Chapel Hill, North Carolina 27599, The Hamner Institutes, Research Triangle Park, North Carolina 27709, and European Commission Joint Research Centre, I-21027 Ispra, Italy douglas.keller@sanofi.com. ; United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711, Sanofi, Bridgewater, New Jersey 08807, Page One Editorial Services, Boulder, Colorado 80304, Dow Chemical Company, Midland, Michigan 48674, Health and Environmental Sciences Institute, Washington, District of Columbia 20005, University of Washington, Seattle, Washington 98105, United States Food and Drug Administration, Silver Spring, Maryland 20993, Sanofi, Bethesda, Maryland 20814, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, University of North Carolina, Chapel Hill, North Carolina 27599, The Hamner Institutes, Research Triangle Park, North Carolina 27709, and European Commission Joint Research Centre, I-21027 Ispra, Italy United States Environmental Protection Agency, Research Triangle Park, North Carolina 27711, Sanofi, Bridgewater, New Jersey 08807, Page One Editorial Services, Boulder, Colorado 80304, Dow Chemical Company, Midland, Michigan 48674, Health and Environmental Sciences Institute, Washington, District of Columbia 20005, University of Washington, Seattle, Washington 98105, United States Food and Drug Administration, Silver Spring, Maryland 20993, Sanofi, Bethesda, Maryland 20814, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, University of North Carolina, Chapel Hill, North Carolina 27599, The Hamner Institutes, Research Triangle Park, North Carolina 27709, and European Commission Joint Research Centre, I-21027 Ispra, Italy. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 256 EP - 267 VL - 143 IS - 2 KW - Index Medicus KW - predictive toxicology KW - in silico KW - modeling KW - in vitro KW - risk assessment KW - United States KW - Societies, Scientific KW - Predictive Value of Tests KW - Congresses as Topic KW - Computer Simulation KW - Toxicology -- trends KW - In Vitro Techniques KW - Toxicology -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652440978?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.atitle=FutureTox+II%3A+in+vitro+data+and+in+silico+models+for+predictive+toxicology.&rft.au=Knudsen%2C+Thomas+B%3BKeller%2C+Douglas+A%3BSander%2C+Miriam%3BCarney%2C+Edward+W%3BDoerrer%2C+Nancy+G%3BEaton%2C+David+L%3BFitzpatrick%2C+Suzanne+Compton%3BHastings%2C+Kenneth+L%3BMendrick%2C+Donna+L%3BTice%2C+Raymond+R%3BWatkins%2C+Paul+B%3BWhelan%2C+Maurice&rft.aulast=Knudsen&rft.aufirst=Thomas&rft.date=2015-02-01&rft.volume=143&rft.issue=2&rft.spage=256&rft.isbn=&rft.btitle=&rft.title=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.issn=1096-0929&rft_id=info:doi/10.1093%2Ftoxsci%2Fkfu234 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-01 N1 - Date created - 2015-01-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Environ Toxicol Chem. 2011 Jan;30(1):9-21 [20963854] Nat Biotechnol. 2014 Jun;32(6):583-91 [24837663] Toxicol Sci. 2011 Sep;123(1):281-9 [21693436] Environ Health Perspect. 2015 Mar;123(3):237-45 [25376053] Birth Defects Res C Embryo Today. 2011 Dec;93(4):312-23 [22271680] Genetics. 2012 Feb;190(2):389-401 [22345608] Toxicol Sci. 2012 Apr;126(2):291-7 [22262567] Nat Rev Cancer. 2007 Jan;7(1):54-60 [17186018] Genome Biol. 2006;7(7):R61 [16859521] Arch Intern Med. 2007 Sep 10;167(16):1752-9 [17846394] Science. 2008 Feb 15;319(5865):906-7 [18276874] Toxicol Sci. 2009 Mar;108(1):19-21 [19168570] Environ Health Perspect. 2009 Apr;117(4):624-31 [19440503] Toxicol Sci. 2009 Jul;110(1):40-6 [19435982] Toxicol Sci. 2009 Aug;110(2):251-4 [19468057] Toxicol Sci. 2009 Nov;112(1):17-22 [19703945] Toxicol Sci. 2009 Dec;112(2):297-302 [19805406] Toxicol Sci. 2010 Mar;114(1):20-4 [20026472] Toxicol Sci. 2010 Sep;117(1):17-24 [20573784] Environ Toxicol Chem. 2010 Mar;29(3):730-41 [20821501] N Engl J Med. 2010 Oct 7;363(15):1397-409 [20660394] Environ Toxicol Chem. 2011 Jan;30(1):64-76 [20963853] Toxicol Sci. 2011 Oct;123(2):349-58 [21750347] BMC Syst Biol. 2011;5:190 [22074594] Toxicol Sci. 2012 Jan;125(1):157-74 [21948869] Methods Cell Biol. 2012;110:325-66 [22482955] J Mol Cell Cardiol. 2012 May;52(5):998-1008 [22353256] J Pharmacol Exp Ther. 2012 May;341(2):510-7 [22353878] Chem Res Toxicol. 2012 Jul 16;25(7):1287-302 [22519603] Trends Biotechnol. 2012 Aug;30(8):421-5 [22652049] Environ Health Perspect. 2013 Jan;121(1):7-14 [23052129] Environ Health Perspect. 2013 Jan;121(1):23-31 [23086705] Methods Mol Biol. 2013;969:3-28 [23296924] Toxicol Sci. 2013 Apr;132(2):327-46 [23358191] Am J Physiol Cell Physiol. 2013 Jun 1;304(11):C1053-63 [23485712] Toxicol Sci. 2013 Jul;134(1):180-94 [23596260] Environ Health Perspect. 2013 Jul;121(7):756-65 [23603828] Nat Rev Drug Discov. 2013 Aug;12(8):565-7 [23903208] Science. 2013 Aug 9;341(6146):651-4 [23868920] Toxicol Appl Pharmacol. 2013 Sep 15;271(3):309-23 [20353796] Toxicology. 2013 Oct 4;312:158-65 [23978457] Chem Res Toxicol. 2013 Dec 16;26(12):1840-61 [24206190] Toxicol Sci. 2014 Feb;137(2):269-77 [24204016] Stem Cell Res Ther. 2013;4 Suppl 1:I1 [24565163] J Appl Toxicol. 2014 Jan;34(1):1-18 [24166207] Chem Res Toxicol. 2014 Mar 17;27(3):314-29 [24446777] J Chem Inf Model. 2014 Jan 27;54(1):1-4 [24251851] Chem Res Toxicol. 2011 Aug 15;24(8):1251-62 [21699217] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/toxsci/kfu234 ER - TY - JOUR T1 - The role of Abcb5 alleles in susceptibility to haloperidol-induced toxicity in mice and humans. AN - 1652439320; 25647612 AB - We know very little about the genetic factors affecting susceptibility to drug-induced central nervous system (CNS) toxicities, and this has limited our ability to optimally utilize existing drugs or to develop new drugs for CNS disorders. For example, haloperidol is a potent dopamine antagonist that is used to treat psychotic disorders, but 50% of treated patients develop characteristic extrapyramidal symptoms caused by haloperidol-induced toxicity (HIT), which limits its clinical utility. We do not have any information about the genetic factors affecting this drug-induced toxicity. HIT in humans is directly mirrored in a murine genetic model, where inbred mouse strains are differentially susceptible to HIT. Therefore, we genetically analyzed this murine model and performed a translational human genetic association study. A whole genome SNP database and computational genetic mapping were used to analyze the murine genetic model of HIT. Guided by the mouse genetic analysis, we demonstrate that genetic variation within an ABC-drug efflux transporter (Abcb5) affected susceptibility to HIT. In situ hybridization results reveal that Abcb5 is expressed in brain capillaries, and by cerebellar Purkinje cells. We also analyzed chromosome substitution strains, imaged haloperidol abundance in brain tissue sections and directly measured haloperidol (and its metabolite) levels in brain, and characterized Abcb5 knockout mice. Our results demonstrate that Abcb5 is part of the blood-brain barrier; it affects susceptibility to HIT by altering the brain concentration of haloperidol. Moreover, a genetic association study in a haloperidol-treated human cohort indicates that human ABCB5 alleles had a time-dependent effect on susceptibility to individual and combined measures of HIT. Abcb5 alleles are pharmacogenetic factors that affect susceptibility to HIT, but it is likely that additional pharmacogenetic susceptibility factors will be discovered. ABCB5 alleles alter susceptibility to HIT in mouse and humans. This discovery leads to a new model that (at least in part) explains inter-individual differences in susceptibility to a drug-induced CNS toxicity. JF - PLoS medicine AU - Zheng, Ming AU - Zhang, Haili AU - Dill, David L AU - Clark, J David AU - Tu, Susan AU - Yablonovitch, Arielle L AU - Tan, Meng How AU - Zhang, Rui AU - Rujescu, Dan AU - Wu, Manhong AU - Tessarollo, Lino AU - Vieira, Wilfred AU - Gottesman, Michael M AU - Deng, Suhua AU - Eberlin, Livia S AU - Zare, Richard N AU - Billard, Jean-Martin AU - Gillet, Jean-Pierre AU - Li, Jin Billy AU - Peltz, Gary AD - Department of Anesthesia, Stanford University School of Medicine, Stanford, California, United States of America. ; Computer Science, Stanford University, Stanford, California, United States of America. ; Veterans Affairs Palo Alto Health Care System, Palo Alto, California, United States of America. ; Department of Genetics, Stanford University School of Medicine, Stanford, California, United States of America. ; Department of Psychiatry, University Of Halle, Halle, Germany. ; Center for Cancer Research, National Cancer Institute, Frederick, Maryland, United States of America. ; Laboratory of Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. ; Department of Pathology, Stanford University, Stanford, California, United States of America. ; Department of Chemistry, Stanford University, Stanford, California, United States of America. ; Laboratory of Molecular Cancer Biology, Molecular Physiology Research Unit (URPhyM), Namur Research Institute for Life Sciences (NARILIS), Faculty of Medicine, University of Namur, Belgium. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 1 VL - 12 IS - 2 KW - ABCB5 protein, human KW - 0 KW - ABCB5 protein, mouse KW - Antipsychotic Agents KW - P-Glycoprotein KW - Haloperidol KW - J6292F8L3D KW - Index Medicus KW - Young Adult KW - Animals KW - Humans KW - Blood-Brain Barrier -- metabolism KW - Genetic Association Studies KW - Mice KW - Adult KW - Middle Aged KW - Genetic Predisposition to Disease KW - Adolescent KW - Female KW - Male KW - Antipsychotic Agents -- toxicity KW - Polymorphism, Single Nucleotide KW - Alleles KW - P-Glycoprotein -- genetics KW - P-Glycoprotein -- metabolism KW - ATP-Binding Cassette Transporters -- metabolism KW - ATP-Binding Cassette Transporters -- genetics KW - Brain -- metabolism KW - Neurotoxicity Syndromes -- genetics KW - Haloperidol -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652439320?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+medicine&rft.atitle=The+role+of+Abcb5+alleles+in+susceptibility+to+haloperidol-induced+toxicity+in+mice+and+humans.&rft.au=Zheng%2C+Ming%3BZhang%2C+Haili%3BDill%2C+David+L%3BClark%2C+J+David%3BTu%2C+Susan%3BYablonovitch%2C+Arielle+L%3BTan%2C+Meng+How%3BZhang%2C+Rui%3BRujescu%2C+Dan%3BWu%2C+Manhong%3BTessarollo%2C+Lino%3BVieira%2C+Wilfred%3BGottesman%2C+Michael+M%3BDeng%2C+Suhua%3BEberlin%2C+Livia+S%3BZare%2C+Richard+N%3BBillard%2C+Jean-Martin%3BGillet%2C+Jean-Pierre%3BLi%2C+Jin+Billy%3BPeltz%2C+Gary&rft.aulast=Zheng&rft.aufirst=Ming&rft.date=2015-02-01&rft.volume=12&rft.issue=2&rft.spage=e1001782&rft.isbn=&rft.btitle=&rft.title=PLoS+medicine&rft.issn=1549-1676&rft_id=info:doi/10.1371%2Fjournal.pmed.1001782 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-28 N1 - Date created - 2015-02-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Curr Drug Metab. 2011 Oct;12(8):732-41 [21623707] Proc Natl Acad Sci U S A. 2011 Dec 20;108(51):20766-71 [22143804] Trends Genet. 2012 Feb;28(2):62-9 [22118772] Biochem Biophys Res Commun. 2012 Feb 24;418(4):736-41 [22306008] FEBS J. 2012 Apr;279(7):1156-66 [22251459] Pharmacogenomics J. 2012 Apr;12(2):147-55 [21079646] Mamm Genome. 2012 Jun;23(5-6):322-35 [22207321] Nature. 2013 Sep 26;501(7468):506-11 [24037378] Nat Med. 2013 Dec;19(12):1584-96 [24309662] Curr Opin Psychiatry. 2008 Mar;21(2):151-6 [18332662] Nat Genet. 2000 Mar;24(3):221-5 [10700173] Nat Genet. 2000 Aug;25(4):381-4 [10932178] Acta Psychiatr Scand. 2001 Nov;104(5):375-9 [11722319] J Psychiatry Neurosci. 2002 Nov;27(6):406-15 [12491573] J Biol Chem. 2003 Nov 21;278(47):47156-65 [12960149] Science. 2004 Oct 22;306(5696):690-5 [15499019] Proc Natl Acad Sci U S A. 1984 Jul;81(14):4591-5 [6611553] Nature. 1984 Oct 4-10;311(5985):464-7 [6332988] Eur J Pharmacol. 1984 Nov 13;106(2):455-6 [6335692] Life Sci. 1985 Jul 1;36(26):2503-8 [2861548] Biochem Biophys Res Commun. 1986 Jan 29;134(2):743-8 [2868716] J Biol Chem. 1986 Jun 15;261(17):7585-7 [3486869] Drugs. 1987 Jan;33(1):31-49 [3545764] J Pharmacol Exp Ther. 1994 Jan;268(1):380-7 [8301579] J Pharmacol Exp Ther. 1994 Aug;270(2):822-30 [8071874] Neurotoxicology. 1994 Spring;15(1):61-73 [8090363] Life Sci. 1995 Nov 17;57(26):2439-46 [8847965] Life Sci. 1997;60(8):529-34 [9042387] Nat Rev Genet. 2005 Apr;6(4):271-86 [15803197] Cancer Res. 2005 May 15;65(10):4320-33 [15899824] Pharmacogenomics. 2005 Dec;6(8):857-64 [16296948] Semin Neurol. 2007 Apr;27(2):159-69 [17390261] Genetics. 2007 Apr;175(4):1999-2008 [17277361] Mol Psychiatry. 2007 Aug;12(8):707-47 [17549063] Pharm Res. 2007 Sep;24(9):1745-58 [17619998] J Neural Transm Suppl. 2007;(72):159-63 [17982890] Mol Psychiatry. 2008 May;13(5):544-56 [18180754] Genetics. 2008 Nov;180(3):1609-16 [18791257] Biochim Biophys Acta. 2009 May;1794(5):725-37 [19135557] Bioinformatics. 2009 Jul 15;25(14):1754-60 [19451168] Bioinformatics. 2009 Aug 15;25(16):2078-9 [19505943] Biol Psychiatry. 2010 Feb 1;67(3):279-82 [19875103] Mamm Genome. 2010 Apr;21(3-4):143-52 [20135320] PLoS Biol. 2010;8(6):e1000412 [20613859] Oncogene. 2010 Nov 18;29(46):6115-24 [20729912] PLoS One. 2011;6(1):e16318 [21298007] Psychopharmacology (Berl). 2011 Apr;214(3):719-28 [21079921] Cancer Res. 2011 Aug 1;71(15):5307-16 [21652540] Handb Clin Neurol. 2012;103:201-13 [21827890] Chembiochem. 2011 Sep 19;12(14):2129-32 [21793152] Nature. 2011 Sep 15;477(7364):289-94 [21921910] Infect Immun. 2011 Nov;79(11):4472-9 [21875959] Nat Rev Drug Discov. 2011 Nov;10(11):817-33 [22037040] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pmed.1001782 ER - TY - JOUR T1 - Systematic and endothelial inflammation and endothelial progenitor cell levels in emphysematous rats exposed to intermittent hypoxia. AN - 1652438960; 25587169 AB - This study aimed to develop an overlap syndrome rat model with intermittent hypoxia (IH) exposure as seen in obstructive sleep apnea, on a base of preexisting emphysema caused by 16 wk of smoke exposure to determine whether IH and emphysema existing simultaneously play overlapped roles on systematic/endothelial inflammation and endothelial damage. Sixty male Wistar rats were divided into 4 groups of 15 each, labeled according to exposure conditions as control, IH, emphysema, and overlap groups. In these animals, electroencephalogram monitoring and preliminary experiments to obtain arterial blood gas values were performed. Serum concentrations of tumor necrosis factor (TNF)-α and interleukin (IL)-6, TNF-α and IL-6 concentrations in the culture medium, Ras homology A mRNA expression levels of endothelial cells from right common carotid artery, and ratio of carotid intima-media thickness of whole thickness of vascular wall expressed in percent (C-IMT) (%) values were evaluated. Subsequently, circulating endothelial progenitor cells (EPCs) within rat peripheral blood and bone marrow were measured with flow cytometry. The serum and endothelial concentrations of TNF-α and IL-6 and the levels of endothelial Ras homology A mRNA have statistically significant results described as overlap>emphysema>IH>control. The levels of EPCs in rat peripheral blood and bone marrow have statistically significant results described as overlap>IH>emphysema>control. C-IMT (%) values from right common carotid artery are the highest in the overlap group and the lowest in the control group. There is no statistical difference when comparing the IH and the emphysema groups. Regardless of whether IH and emphysema exposure are mechanistically synergistic, this overlap elicits a more severe systematic/endothelial inflammation and endothelial damage; meanwhile, a robust mobilization of EPCs is demonstrated, which is not to mean a robust adherent and repairing capability. Copyright © 2015 by Daedalus Enterprises. JF - Respiratory care AU - Yang, Qing-chan AU - Sun, Xin AU - Wang, Yong-mei AU - Wu, Qi AU - Feng, Jing AU - Chen, Bao-yuan AD - Tianjin Haihe Hospital, Tianjin, China. ; Tianjin Haihe Hospital, Tianjin, China. zyyhxkfj@126.com tjshhyywym@126.com. ; Respiratory Department, Tianjin Medical University General Hospital, Tianjin, China. Neuropharmacology Section, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina. zyyhxkfj@126.com tjshhyywym@126.com. ; Respiratory Department, Tianjin Medical University General Hospital, Tianjin, China. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 279 EP - 289 VL - 60 IS - 2 KW - Interleukin-6 KW - 0 KW - RNA, Messenger KW - Tumor Necrosis Factor-alpha KW - rhoA GTP-Binding Protein KW - EC 3.6.5.2 KW - Index Medicus KW - inflammation KW - endothelial progenitor cell KW - emphysema KW - endothelial dysfunction KW - intermittent hypoxia KW - Animals KW - Bone Marrow -- pathology KW - rhoA GTP-Binding Protein -- genetics KW - Carotid Artery, Common -- diagnostic imaging KW - Carotid Artery, Common -- pathology KW - Cell Count KW - Interleukin-6 -- metabolism KW - Disease Models, Animal KW - Rats KW - RNA, Messenger -- metabolism KW - Cells, Cultured KW - Rats, Wistar KW - Sleep Apnea, Obstructive -- complications KW - Tumor Necrosis Factor-alpha -- metabolism KW - Carotid Intima-Media Thickness KW - Male KW - Hypoxia -- pathology KW - Pulmonary Emphysema -- pathology KW - Inflammation -- blood KW - Hypoxia -- blood KW - Inflammation -- etiology KW - Endothelial Progenitor Cells -- metabolism KW - Pulmonary Emphysema -- blood KW - Hypoxia -- genetics KW - Pulmonary Emphysema -- genetics KW - Inflammation -- pathology KW - Endothelium -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652438960?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Respiratory+care&rft.atitle=Systematic+and+endothelial+inflammation+and+endothelial+progenitor+cell+levels+in+emphysematous+rats+exposed+to+intermittent+hypoxia.&rft.au=Yang%2C+Qing-chan%3BSun%2C+Xin%3BWang%2C+Yong-mei%3BWu%2C+Qi%3BFeng%2C+Jing%3BChen%2C+Bao-yuan&rft.aulast=Yang&rft.aufirst=Qing-chan&rft.date=2015-02-01&rft.volume=60&rft.issue=2&rft.spage=279&rft.isbn=&rft.btitle=&rft.title=Respiratory+care&rft.issn=1943-3654&rft_id=info:doi/10.4187%2Frespcare.03492 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-09 N1 - Date created - 2015-01-30 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.4187/respcare.03492 ER - TY - JOUR T1 - Ibrutinib for previously untreated and relapsed or refractory chronic lymphocytic leukaemia with TP53 aberrations: a phase 2, single-arm trial. AN - 1652437385; 25555420 AB - Patients with chronic lymphocytic leukaemia (CLL) with TP53 aberrations respond poorly to first-line chemoimmunotherapy, resulting in early relapse and short survival. We investigated the safety and activity of ibrutinib in previously untreated and relapsed or refractory CLL with TP53 aberrations. In this investigator-initiated, single-arm phase 2 study, we enrolled eligible adult patients with active CLL with TP53 aberrations at the National Institutes of Health Clinical Center (Bethesda, MD, USA). Patients received 28-day cycles of ibrutinib 420 mg orally once daily until disease progression or the occurrence of limiting toxicities. The primary endpoint was overall response to treatment at 24 weeks in all evaluable patients. This study is registered with ClinicalTrials.gov, number NCT01500733, and is fully enrolled. Between Dec 22, 2011, and Jan 2, 2014, we enrolled 51 patients; 47 had CLL with deletion 17p13.1 and four carried a TP53 mutation in the absence of deletion 17p13.1. All patients had active disease requiring therapy. 35 enrolled patients had previously untreated CLL and 16 had relapsed or refractory disease. Median follow-up was 24 months (IQR 12.9-27.0). 33 previously untreated patients and 15 patients with relapsed or refractory CLL were evaluable for response at 24 weeks. 32 (97%; 95% CI 86-100) of 33 previously untreated patients achieved an objective response, including partial response in 18 patients (55%) and partial response with lymphocytosis in 14 (42%). One patient had progressive disease at 0.4 months. 12 (80%; 95% CI 52-96) of the 15 patients with relapsed or refractory CLL had an objective response: six (40%) achieved a partial response and six (40%) a partial response with lymphocytosis; the remaining three (20%) patients had stable disease. Grade 3 or worse treatment-related adverse events were neutropenia in 12 (24%) patients (grade 4 in one [2%] patient), anaemia in seven (14%) patients, and thrombocytopenia in five (10%) patients (grade 4 in one [2%] patient). Grade 3 pneumonia occurred in three (6%) patients, and grade 3 rash in one (2%) patient. The activity and safety profile of single-agent ibrutinib in CLL with TP53 aberrations is encouraging and supports its consideration as a novel treatment option for patients with this high-risk disease in both first-line and second-line settings. Intramural Research Program of the National Heart, Lung, and Blood Institute and the National Cancer Institute, Danish Cancer Society, Novo Nordisk Foundation, National Institutes of Health Medical Research Scholars Program, and Pharmacyclics Inc. Copyright © 2015 Elsevier Ltd. All rights reserved. JF - The Lancet. Oncology AU - Farooqui, Mohammed Z H AU - Valdez, Janet AU - Martyr, Sabrina AU - Aue, Georg AU - Saba, Nakhle AU - Niemann, Carsten U AU - Herman, Sarah E M AU - Tian, Xin AU - Marti, Gerald AU - Soto, Susan AU - Hughes, Thomas E AU - Jones, Jade AU - Lipsky, Andrew AU - Pittaluga, Stefania AU - Stetler-Stevenson, Maryalice AU - Yuan, Constance AU - Lee, Yuh Shan AU - Pedersen, Lone B AU - Geisler, Christian H AU - Calvo, Katherine R AU - Arthur, Diane C AU - Maric, Irina AU - Childs, Richard AU - Young, Neal S AU - Wiestner, Adrian AD - Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. ; Office of Biostatistics Research, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. ; Clinical Center Pharmacy Department, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. ; Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA; Medical Scholars Research Program, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. ; Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Department of Hematology, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark. ; Department of Laboratory Medicine, Clinical Research Center, National Institutes of Health, Bethesda, MD, USA. ; Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. Electronic address: wiestnera@mail.nih.gov. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 169 EP - 176 VL - 16 IS - 2 KW - PCI 32765 KW - 0 KW - Pyrazoles KW - Pyrimidines KW - TP53 protein, human KW - Tumor Suppressor Protein p53 KW - Index Medicus KW - Survival Rate KW - Single-Blind Method KW - Neoplasm Staging KW - Aged, 80 and over KW - Humans KW - Adult KW - Prognosis KW - Aged KW - Middle Aged KW - Follow-Up Studies KW - Male KW - Female KW - Pyrimidines -- therapeutic use KW - Pyrazoles -- therapeutic use KW - Leukemia, Lymphocytic, Chronic, B-Cell -- genetics KW - Leukemia, Lymphocytic, Chronic, B-Cell -- drug therapy KW - Neoplasm Recurrence, Local -- drug therapy KW - Drug Resistance, Neoplasm -- genetics KW - Mutation -- genetics KW - Leukemia, Lymphocytic, Chronic, B-Cell -- pathology KW - Tumor Suppressor Protein p53 -- genetics KW - Leukemia, Lymphocytic, Chronic, B-Cell -- mortality KW - Neoplasm Recurrence, Local -- genetics KW - Neoplasm Recurrence, Local -- mortality KW - Neoplasm Recurrence, Local -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652437385?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Lancet.+Oncology&rft.atitle=Ibrutinib+for+previously+untreated+and+relapsed+or+refractory+chronic+lymphocytic+leukaemia+with+TP53+aberrations%3A+a+phase+2%2C+single-arm+trial.&rft.au=Farooqui%2C+Mohammed+Z+H%3BValdez%2C+Janet%3BMartyr%2C+Sabrina%3BAue%2C+Georg%3BSaba%2C+Nakhle%3BNiemann%2C+Carsten+U%3BHerman%2C+Sarah+E+M%3BTian%2C+Xin%3BMarti%2C+Gerald%3BSoto%2C+Susan%3BHughes%2C+Thomas+E%3BJones%2C+Jade%3BLipsky%2C+Andrew%3BPittaluga%2C+Stefania%3BStetler-Stevenson%2C+Maryalice%3BYuan%2C+Constance%3BLee%2C+Yuh+Shan%3BPedersen%2C+Lone+B%3BGeisler%2C+Christian+H%3BCalvo%2C+Katherine+R%3BArthur%2C+Diane+C%3BMaric%2C+Irina%3BChilds%2C+Richard%3BYoung%2C+Neal+S%3BWiestner%2C+Adrian&rft.aulast=Farooqui&rft.aufirst=Mohammed+Z&rft.date=2015-02-01&rft.volume=16&rft.issue=2&rft.spage=169&rft.isbn=&rft.btitle=&rft.title=The+Lancet.+Oncology&rft.issn=1474-5488&rft_id=info:doi/10.1016%2FS1470-2045%2814%2971182-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-31 N1 - Date created - 2015-02-02 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT01500733; ClinicalTrials.gov N1 - SuppNotes - Cited By: Blood. 2014 Mar 20;123(12):1810-7 [24415539] Blood. 2014 May 22;123(21):3247-54 [24652989] Blood. 2014 Dec 18;124(26):3841-9 [25301705] Leukemia. 2014 Nov;28(11):2188-96 [24699307] Blood. 2014 May 22;123(21):3286-95 [24659631] J Clin Oncol. 2007 Dec 10;25(35):5616-23 [17984186] Blood. 2008 Jun 15;111(12):5446-56 [18216293] Blood. 2008 Aug 15;112(4):975-80 [18411418] J Clin Oncol. 2009 Dec 10;27(35):6012-8 [19826119] Lancet. 2010 Oct 2;376(9747):1164-74 [20888994] Blood. 2010 Oct 7;116(14):2438-47 [20595516] Lancet Oncol. 2014 Jan;15(1):48-58 [24332241] Semin Cancer Biol. 2014 Feb;24:43-8 [23831274] Leukemia. 2014 Mar;28(3):649-57 [24270740] N Engl J Med. 2014 Mar 13;370(11):997-1007 [24450857] Curr Hematol Malig Rep. 2011 Mar;6(1):36-46 [21153774] J Clin Oncol. 2011 Jun 1;29(16):2223-9 [21483000] Blood. 2011 Sep 29;118(13):3489-98 [21725050] Int Rev Immunol. 2012 Apr;31(2):119-32 [22449073] J Clin Oncol. 2012 May 10;30(14):1647-55 [22493413] Blood. 2012 Dec 6;120(24):4684-91 [22875912] Hematol Oncol Clin North Am. 2013 Apr;27(2):289-301 [23561474] N Engl J Med. 2013 Jul 4;369(1):32-42 [23782158] N Engl J Med. 2014 Jun 12;370(24):2352-4 [24869597] N Engl J Med. 2014 Jun 12;370(24):2286-94 [24869598] N Engl J Med. 2014 Jul 17;371(3):213-23 [24881631] Semin Hematol. 2014 Jul;51(3):168-76 [25048781] Haematologica. 2014 Aug;99(8):1350-5 [24859876] Lancet Oncol. 2014 Sep;15(10):1090-9 [25150798] Comment In: Lancet Oncol. 2015 Feb;16(2):122-4 [25638674] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/S1470-2045(14)71182-9 ER - TY - JOUR T1 - Sunitinib in patients with chemotherapy-refractory thymoma and thymic carcinoma: an open-label phase 2 trial. AN - 1652434306; 25592632 AB - No standard treatments are available for advanced thymic epithelial tumours after failure of platinum-based chemotherapy. We investigated the activity of sunitinib, an orally administered tyrosine kinase inhibitor. Between May 15, 2012, and Oct 2, 2013, we did an open-label phase 2 trial in patients with histologically confirmed chemotherapy-refractory thymic epithelial tumours. Patients were eligible if they had disease progression after at least one previous regimen of platinum-containing chemotherapy, an Eastern Cooperative Oncology Group performance status of two or lower, measurable disease, and adequate organ function. Patients received 50 mg of sunitinib orally once a day, in 6-week cycles (ie, 4 weeks of treatment followed by 2 weeks without treatment), until tumour progression or unacceptable toxic effects arose. The primary endpoint was investigator-assessed best tumour response at any point, which we analysed separately in thymoma and thymic carcinoma cohorts. Patients who had received at least one cycle of treatment and had their disease reassessed were included in the analyses of response. The trial was registered with ClinicalTrials.gov, number NCT01621568. 41 patients were enrolled, 25 with thymic carcinoma and 16 with thymoma. One patient with thymic carcinoma was deemed ineligible after enrolment and did not receive protocol treatment. Of patients who received treatment, one individual with thymic carcinoma was not assessable because she died. Median follow-up on trial was 17 months (IQR 14.0-18.4). Of 23 assessable patients with thymic carcinoma, six (26%, 90% CI 12.1-45.3, 95% CI 10.2-48.4) had partial responses, 15 (65%, 95% CI 42.7-83.6) achieved stable disease, and two (9%, 1.1-28.0) had progressive disease. Of 16 patients with thymoma, one (6%, 95% CI 0.2-30.2) had a partial response, 12 (75%, 47.6-92.7) had stable disease, and three (19%, 4.1-45.7) had progressive disease. The most common grade 3 and 4 treatment-related adverse events were lymphocytopenia (eight [20%] of 40 patients), fatigue (eight [20%]), and oral mucositis (eight [20%]). Five (13%) patients had decreases in left-ventricular ejection fraction, of which three (8%) were grade 3 events. Three (8%) patients died during treatment, including one individual who died of cardiac arrest that was possibly treatment-related. Sunitinib is active in previously treated patients with thymic carcinoma. Further studies are needed to identify potential biomarkers of activity. National Cancer Institute (Cancer Therapy Evaluation Program). Copyright © 2015 Elsevier Ltd. All rights reserved. JF - The Lancet. Oncology AU - Thomas, Anish AU - Rajan, Arun AU - Berman, Arlene AU - Tomita, Yusuke AU - Brzezniak, Christina AU - Lee, Min-Jung AU - Lee, Sunmin AU - Ling, Alexander AU - Spittler, Aaron J AU - Carter, Corey A AU - Guha, Udayan AU - Wang, Yisong AU - Szabo, Eva AU - Meltzer, Paul AU - Steinberg, Seth M AU - Trepel, Jane B AU - Loehrer, Patrick J AU - Giaccone, Giuseppe AD - Thoracic and GI Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Developmental Therapeutics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Department of Hematology and Oncology, Walter Reed National Military Medical Center, Bethesda, MD, USA. ; Radiology and Imaging Sciences, Warren Grant Magnuson Clinical Center, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Division of Hematology/Oncology, Indiana University Medical Center, Indianapolis, IN, USA. ; Division of Hematology/Oncology, Lombardi Cancer Center, Georgetown University, Washington, DC, USA. ; Division of Cancer Prevention, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Genetics Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Biostatistics and Data Management Section, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. ; Division of Hematology/Oncology, Lombardi Cancer Center, Georgetown University, Washington, DC, USA. Electronic address: gg496@georgetown.edu. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 177 EP - 186 VL - 16 IS - 2 KW - Antineoplastic Agents KW - 0 KW - Indoles KW - Pyrroles KW - sunitinib KW - V99T50803M KW - Index Medicus KW - Survival Rate KW - Neoplasm Staging KW - Aged, 80 and over KW - Humans KW - Adult KW - Prognosis KW - Aged KW - Middle Aged KW - Follow-Up Studies KW - Male KW - Female KW - Neuroendocrine Tumors -- pathology KW - Thymoma -- drug therapy KW - Pyrroles -- therapeutic use KW - Thymus Neoplasms -- pathology KW - Thymoma -- pathology KW - Neoplasm Recurrence, Local -- drug therapy KW - Thymoma -- mortality KW - Neuroendocrine Tumors -- drug therapy KW - Indoles -- therapeutic use KW - Thymus Neoplasms -- drug therapy KW - Antineoplastic Agents -- therapeutic use KW - Thymus Neoplasms -- mortality KW - Drug Resistance, Neoplasm -- drug effects KW - Neoplasm Recurrence, Local -- mortality KW - Neoplasm Recurrence, Local -- pathology KW - Neuroendocrine Tumors -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652434306?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Lancet.+Oncology&rft.atitle=Sunitinib+in+patients+with+chemotherapy-refractory+thymoma+and+thymic+carcinoma%3A+an+open-label+phase+2+trial.&rft.au=Thomas%2C+Anish%3BRajan%2C+Arun%3BBerman%2C+Arlene%3BTomita%2C+Yusuke%3BBrzezniak%2C+Christina%3BLee%2C+Min-Jung%3BLee%2C+Sunmin%3BLing%2C+Alexander%3BSpittler%2C+Aaron+J%3BCarter%2C+Corey+A%3BGuha%2C+Udayan%3BWang%2C+Yisong%3BSzabo%2C+Eva%3BMeltzer%2C+Paul%3BSteinberg%2C+Seth+M%3BTrepel%2C+Jane+B%3BLoehrer%2C+Patrick+J%3BGiaccone%2C+Giuseppe&rft.aulast=Thomas&rft.aufirst=Anish&rft.date=2015-02-01&rft.volume=16&rft.issue=2&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=The+Lancet.+Oncology&rft.issn=1474-5488&rft_id=info:doi/10.1016%2FS1470-2045%2814%2971181-7 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-31 N1 - Date created - 2015-02-02 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT01621568; ClinicalTrials.gov N1 - SuppNotes - Cited By: Br J Cancer. 2010 Jul 13;103(2):196-200 [20571495] Int J Exp Pathol. 2011 Oct;92(5):340-4 [21645144] Curr Oncol Rep. 2012 Jun;14(3):221-9 [22434312] Ann Thorac Surg. 2010 Jan;89(1):245-52; discussion 252 [20103246] J Thorac Oncol. 2009 Jun;4(6):773-5 [19461405] Cancer Res. 2009 Mar 15;69(6):2514-22 [19276342] Clin Cancer Res. 2008 Oct 15;14(20):6674-82 [18927310] Ann Anat. 2008;190(3):238-45 [18356031] Science. 2008 Jan 11;319(5860):195-8 [18187653] Lancet. 2007 Dec 15;370(9604):2011-9 [18083403] J Clin Oncol. 1994 Jun;12(6):1164-8 [8201378] Biometrics. 1985 Sep;41(3):741-4 [4074823] J Pathol. 2004 Mar;202(3):375-81 [14991904] Int J Cancer. 2003 Jul 1;105(4):546-51 [12712448] Blood. 2003 May 1;101(9):3597-605 [12531805] J Thorac Cardiovasc Surg. 2002 Sep;124(3):493-8 [12202865] Surg Today. 2001;31(11):1038-40 [11766079] Blood. 2000 Dec 1;96(12):3872-9 [11090072] Am J Pathol. 2000 Jul;157(1):257-66 [10880395] J Thorac Oncol. 2010 Oct;5(10 Suppl 4):S291-5 [20859122] J Thorac Oncol. 2010 Sep;5(9):1447-53 [20651610] N Engl J Med. 2010 Aug 19;363(8):711-23 [20525992] N Engl J Med. 2012 Jun 28;366(26):2455-65 [22658128] J Thorac Oncol. 2013 Feb;8(2):246-9 [23328550] Lung Cancer. 2013 Apr;80(1):75-80 [23313005] Lancet Oncol. 2014 Feb;15(2):191-200 [24439931] Cancer Discov. 2014 Jun;4(6):650-61 [24801577] Nat Genet. 2014 Aug;46(8):844-9 [24974848] Sci Rep. 2014;4:7336 [25482724] J Cancer Res Clin Oncol. 2015 Feb;141(2):323-31 [25146529] Comment In: Lancet Oncol. 2015 Feb;16(2):124-5 [25592633] Erratum In: Lancet Oncol. 2015 Mar;16(3):e105 [25752557] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/S1470-2045(14)71181-7 ER - TY - JOUR T1 - Subjective and objective screening tests for hydroxychloroquine toxicity. AN - 1652428291; 25444344 AB - To compare subjective and objective clinical tests used in the screening for hydroxychloroquine retinal toxicity to multifocal electroretinography (mfERG) reference testing. Prospective, single-center, case control study. Fifty-seven patients with a previous or current history of hydroxychloroquine treatment of more than 5 years' duration. Participants were evaluated with a detailed medical history, dilated ophthalmologic examination, color fundus photography, fundus autofluorescence (FAF) imaging, spectral-domain (SD) optical coherence tomography (OCT), automated visual field testing (10-2 visual field mean deviation [VFMD]), and mfERG testing. We used mfERG test parameters as a gold standard to divide participants into 2 groups: those affected by hydroxychloroquine-induced retinal toxicity and those unaffected. We assessed the association of various imaging and psychophysical variables in the affected versus the unaffected group. Fifty-seven study participants (91.2% female; mean age, 55.7±10.4 years; mean duration of hydroxychloroquine treatment, 15.0±7.5 years) were divided into affected (n = 19) and unaffected (n = 38) groups based on mfERG criteria. Mean age and duration of hydroxychloroquine treatment did not differ statistically between groups. Mean OCT retinal thickness measurements in all 9 macular subfields were significantly lower (<40 μm) in the affected group (P < 0.01 for all comparisons) compared with those in the unaffected group. Mean VFMD was 11 dB lower in the affected group (P < 0.0001). Clinical features indicative of retinal toxicity were scored for the 2 groups and were detected in 68.4% versus 0.0% using color fundus photographs, 73.3% versus 9.1% using FAF images, and 84.2% versus 0.0% on the scoring for the perifoveal loss of the photoreceptor ellipsoid zone on SD-OCT for affected and unaffected participants, respectively. Using a polynomial modeling approach, OCT inner ring retinal thickness measurements and Humphrey 10-2 VFMD were identified as the variables associated most strongly with the presence of hydroxychloroquine as defined by mfERG testing. Optical coherence tomography retinal thickness and 10-2 VFMD are objective measures demonstrating clinically useful sensitivity and specificity for the detection of hydroxychloroquine toxicity as identified by mfERG, and thus may be suitable surrogate tests. Published by Elsevier Inc. JF - Ophthalmology AU - Cukras, Catherine AU - Huynh, Nancy AU - Vitale, Susan AU - Wong, Wai T AU - Ferris, Fredrick L AU - Sieving, Paul A AD - Division of Epidemiology and Clinical Research, National Eye Institute, National Institutes of Health, Bethesda, Maryland. Electronic address: cukrasc@nei.nih.gov. ; Ophthalmic Genetics and Visual Function Branch, National Eye Institute, National Institutes of Health, Bethesda, Maryland. ; Division of Epidemiology and Clinical Research, National Eye Institute, National Institutes of Health, Bethesda, Maryland. ; Office of the Scientific Director, National Eye Institute, National Institutes of Health, Bethesda, Maryland. ; Ophthalmic Genetics and Visual Function Branch, National Eye Institute, National Institutes of Health, Bethesda, Maryland; Section for Translational Research in Retinal and Macular Degeneration, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 356 EP - 366 VL - 122 IS - 2 KW - Antirheumatic Agents KW - 0 KW - Hydroxychloroquine KW - 4QWG6N8QKH KW - Index Medicus KW - Sensitivity and Specificity KW - Arthritis, Rheumatoid -- drug therapy KW - Humans KW - Fluorescein Angiography KW - Aged KW - Electroretinography -- drug effects KW - Prospective Studies KW - Lupus Erythematosus, Systemic -- drug therapy KW - Visual Acuity -- drug effects KW - Adult KW - Case-Control Studies KW - Visual Fields -- drug effects KW - Middle Aged KW - Female KW - Male KW - Retinal Diseases -- diagnosis KW - Antirheumatic Agents -- toxicity KW - Retina -- drug effects KW - Tomography, Optical Coherence KW - Retina -- pathology KW - Hydroxychloroquine -- toxicity KW - Diagnostic Techniques, Ophthalmological KW - Retinal Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652428291?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Ophthalmology&rft.atitle=Subjective+and+objective+screening+tests+for+hydroxychloroquine%C2%A0toxicity.&rft.au=Cukras%2C+Catherine%3BHuynh%2C+Nancy%3BVitale%2C+Susan%3BWong%2C+Wai+T%3BFerris%2C+Fredrick+L%3BSieving%2C+Paul+A&rft.aulast=Cukras&rft.aufirst=Catherine&rft.date=2015-02-01&rft.volume=122&rft.issue=2&rft.spage=356&rft.isbn=&rft.btitle=&rft.title=Ophthalmology&rft.issn=1549-4713&rft_id=info:doi/10.1016%2Fj.ophtha.2014.07.056 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-14 N1 - Date created - 2015-01-27 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ophtha.2014.07.056 ER - TY - JOUR T1 - In vivo 2H2O administration reveals impaired triglyceride storage in adipose tissue of insulin-resistant humans. AN - 1652419146; 25418322 AB - Indirect evidence suggests that impaired triglyceride storage in the subcutaneous fat depot contributes to the development of insulin resistance via lipotoxicity. We directly tested this hypothesis by measuring, in vivo, TG synthesis, de novo lipogenesis (DNL), adipocyte proliferation, and insulin suppression of lipolysis in subcutaneous adipose tissue of BMI-matched individuals classified as insulin resistant (IR) or insulin sensitive (IS). Nondiabetic, moderately obese subjects with BMI 25-35 kg/m(2), classified as IR or IS by the modified insulin suppression test, consumed deuterated water ((2)H2O) for 4 weeks. Deuterium incorporation into glycerol, palmitate, and DNA indicated TG synthesis, DNL, and adipocyte proliferation, respectively. Net TG synthesis and DNL in adipose cells were significantly lower in IR as compared with IS subjects, whereas adipocyte proliferation did not differ significantly. Plasma FFAs measured during an insulin suppression test were 2.5-fold higher in IR subjects, indicating resistance to insulin suppression of lipolysis. Adipose TG synthesis correlated directly with DNL but not with proliferation. These results provide direct in vivo evidence for impaired TG storage in subcutaneous adipose tissue of IR as compared with IS. Relative inability to store TG in the subcutaneous depot may represent a mechanism contributing to the development of insulin resistance in the setting of obesity. Copyright © 2015 by the American Society for Biochemistry and Molecular Biology, Inc. JF - Journal of lipid research AU - Allister, Candice A AU - Liu, Li-fen AU - Lamendola, Cindy A AU - Craig, Colleen M AU - Cushman, Samuel W AU - Hellerstein, Marc K AU - McLaughlin, Tracey L AD - Department of Nutritional Science and Toxicology, University of California at Berkeley, Berkeley, CA. ; Department of Medicine, Stanford University School of Medicine, Stanford, CA. ; Diabetes, Endocrinology, and Obesity Branch, National Institute of Digestive Diseases and Kidney Disease, National Institutes of Health, Bethesda, MD. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 435 EP - 439 VL - 56 IS - 2 KW - Triglycerides KW - 0 KW - Deuterium Oxide KW - J65BV539M3 KW - Index Medicus KW - lipolysis KW - obesity KW - lipogenesis KW - subcutaneous adipose KW - insulin resistance KW - de novo KW - triglycerides KW - Obesity -- metabolism KW - Lipolysis -- physiology KW - Humans KW - Middle Aged KW - Body Mass Index KW - Male KW - Female KW - Adipose Tissue -- metabolism KW - Triglycerides -- metabolism KW - Deuterium Oxide -- metabolism KW - Insulin Resistance -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652419146?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+lipid+research&rft.atitle=In+vivo+2H2O+administration+reveals+impaired+triglyceride+storage+in+adipose+tissue+of+insulin-resistant+humans.&rft.au=Allister%2C+Candice+A%3BLiu%2C+Li-fen%3BLamendola%2C+Cindy+A%3BCraig%2C+Colleen+M%3BCushman%2C+Samuel+W%3BHellerstein%2C+Marc+K%3BMcLaughlin%2C+Tracey+L&rft.aulast=Allister&rft.aufirst=Candice&rft.date=2015-02-01&rft.volume=56&rft.issue=2&rft.spage=435&rft.isbn=&rft.btitle=&rft.title=Journal+of+lipid+research&rft.issn=1539-7262&rft_id=info:doi/10.1194%2Fjlr.M052860 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-10-20 N1 - Date created - 2015-01-31 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Diabetes. 2013 Sep;62(9):2997-3004 [23970518] Am J Physiol Endocrinol Metab. 2013 Oct 15;305(8):E999-E1006 [23982159] N Engl J Med. 2014 Sep 18;371(12):1131-41 [25229917] J Biol Chem. 2000 Mar 24;275(12):8456-60 [10722680] Am J Physiol Endocrinol Metab. 2003 Oct;285(4):E790-803 [12824084] Am J Physiol Endocrinol Metab. 2004 Apr;286(4):E577-88 [14600072] Metabolism. 2004 Apr;53(4):495-9 [15045698] Biochem Biophys Res Commun. 2004 May 14;317(4):1045-51 [15094374] J Clin Endocrinol Metab. 1991 Jan;72(1):96-107 [1986032] J Biol Chem. 1964 Feb;239:375-80 [14169133] Nutr Rev. 2007 Jun;65(6 Pt 2):S7-12 [17605308] Diabetologia. 2007 Aug;50(8):1707-15 [17549449] J Clin Invest. 2007 Sep;117(9):2621-37 [17717599] J Clin Endocrinol Metab. 2011 Nov;96(11):E1756-60 [21865361] Metabolism. 2011 Dec;60(12):1741-7 [21820141] J Clin Endocrinol Metab. 2012 Jul;97(7):E1219-23 [22492868] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1194/jlr.M052860 ER - TY - JOUR T1 - Exploring allosteric activation of LigAB from Sphingobium sp. strain SYK-6 through kinetics, mutagenesis and computational studies. AN - 1652411234; 25562402 AB - The protocatechuate 4,5-dioxygenase (LigAB) from Sphingobium sp. strain SYK-6 is the defining member of the Type II extradiol dioxygenase superfamily (a.k.a. PCA Dioxygenase Superfamily or PCADSF) and plays a key aromatic ring-opening role in the metabolism of several lignin derived aromatic compounds. In our search for alternate substrates and inhibitors of LigAB, we discovered allosteric rate enhancement in the presence of non-substrate protocatechuate-like aldehydes such as vanillin. LigAB has the broadest substrate utilization profile of all protocatechuate (PCA) 4,5-dioxygenase described in the literature, however, the rate enhancement is only observed with PCA, with vanillin increasing kcat for LigAB by 36%. Computational docking has identified a potential site of allosteric binding near the entrance to the active site. Examination of a multiple sequence alignment reveals that many of the residues contributing to this newly identified allosteric pocket are highly conserved within the LigB family of the PCADSF. Point mutants of Phe103α and Ala18β, two residues located in the putative allosteric pocket, display altered rate enhancement as compared to LigAB-WT, providing support for the computationally identified allosteric binding site. Further investigation of this binding site may provide insight into the mechanism of this never before observed allosteric activation in extradiol dioxygenases. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Archives of biochemistry and biophysics AU - Barry, Kevin Patrick AU - Ngu, Abraham AU - Cohn, Erin Frances AU - Cote, Joy Marie AU - Burroughs, A Maxwell AU - Gerbino, Jason Paul AU - Taylor, Erika Anne AD - Department of Chemistry, Wesleyan University, Middletown, CT 06459, USA. ; National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD 20894, USA. ; Department of Chemistry, Wesleyan University, Middletown, CT 06459, USA. Electronic address: eataylor@wesleyan.edu. Y1 - 2015/02/01/ PY - 2015 DA - 2015 Feb 01 SP - 35 EP - 45 VL - 567 KW - Benzaldehydes KW - 0 KW - vanillin KW - CHI530446X KW - Dioxygenases KW - EC 1.13.11.- KW - protocatechuate 4,5-dioxygenase KW - EC 1.13.11.8 KW - Index Medicus KW - Protocatechuate 4,5-dioxygenase KW - Allosteric activation KW - Lignin KW - PCAD superfamily KW - Dioxygenase KW - Vanillin KW - Benzaldehydes -- metabolism KW - Enzyme Activation KW - Kinetics KW - Allosteric Site KW - Protein Conformation KW - Mutagenesis, Site-Directed KW - Dioxygenases -- genetics KW - Dioxygenases -- chemistry KW - Molecular Docking Simulation KW - Sphingomonadaceae -- enzymology KW - Dioxygenases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652411234?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+biochemistry+and+biophysics&rft.atitle=Exploring+allosteric+activation+of+LigAB+from+Sphingobium+sp.+strain+SYK-6+through+kinetics%2C+mutagenesis+and+computational+studies.&rft.au=Barry%2C+Kevin+Patrick%3BNgu%2C+Abraham%3BCohn%2C+Erin+Frances%3BCote%2C+Joy+Marie%3BBurroughs%2C+A+Maxwell%3BGerbino%2C+Jason+Paul%3BTaylor%2C+Erika+Anne&rft.aulast=Barry&rft.aufirst=Kevin&rft.date=2015-02-01&rft.volume=567&rft.issue=&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=Archives+of+biochemistry+and+biophysics&rft.issn=1096-0384&rft_id=info:doi/10.1016%2Fj.abb.2014.12.019 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-24 N1 - Date created - 2015-01-27 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.abb.2014.12.019 ER - TY - JOUR T1 - Use of an endogenous plasmid locus for stable in trans complementation in Borrelia burgdorferi. AN - 1652393609; 25452278 AB - Targeted mutagenesis and complementation are important tools for studying genes of unknown function in the Lyme disease spirochete Borrelia burgdorferi. A standard method of complementation is reintroduction of a wild-type copy of the targeted gene on a shuttle vector. However, shuttle vectors are present at higher copy numbers than B. burgdorferi plasmids and are potentially unstable in the absence of selection, thereby complicating analyses in the mouse-tick infectious cycle. B. burgdorferi has over 20 plasmids, with some, such as linear plasmid 25 (lp25), carrying genes required by the spirochete in vivo but relatively unstable during in vitro cultivation. We propose that complementation on an endogenous plasmid such as lp25 would overcome the copy number and in vivo stability issues of shuttle vectors. In addition, insertion of a selectable marker on lp25 could ensure its stable maintenance by spirochetes in culture. Here, we describe the construction of a multipurpose allelic-exchange vector containing a multiple-cloning site and either of two selectable markers. This suicide vector directs insertion of the complementing gene into the bbe02 locus, a site on lp25 that was previously shown to be nonessential during both in vitro and in vivo growth. We demonstrate the functional utility of this strategy by restoring infectivity to an ospC mutant through complementation at this site on lp25 and stable maintenance of the ospC gene throughout mouse infection. We conclude that this represents a convenient and widely applicable method for stable gene complementation in B. burgdorferi. Copyright © 2015, American Society for Microbiology. All Rights Reserved. JF - Applied and environmental microbiology AU - Kasumba, Irene N AU - Bestor, Aaron AU - Tilly, Kit AU - Rosa, Patricia A AD - Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA kasumba.irene@nih.gov. ; Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 1038 EP - 1046 VL - 81 IS - 3 KW - Index Medicus KW - Animals KW - Lyme Disease -- microbiology KW - Genomic Instability KW - Disease Models, Animal KW - Mice KW - Borrelia burgdorferi -- genetics KW - Borrelia burgdorferi -- growth & development KW - Genetic Vectors KW - Genetics, Microbial -- methods KW - Genetic Complementation Test KW - Molecular Biology -- methods KW - Plasmids UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652393609?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Applied+and+environmental+microbiology&rft.atitle=Use+of+an+endogenous+plasmid+locus+for+stable+in+trans+complementation+in+Borrelia+burgdorferi.&rft.au=Kasumba%2C+Irene+N%3BBestor%2C+Aaron%3BTilly%2C+Kit%3BRosa%2C+Patricia+A&rft.aulast=Kasumba&rft.aufirst=Irene&rft.date=2015-02-01&rft.volume=81&rft.issue=3&rft.spage=1038&rft.isbn=&rft.btitle=&rft.title=Applied+and+environmental+microbiology&rft.issn=1098-5336&rft_id=info:doi/10.1128%2FAEM.03657-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-08 N1 - Date created - 2015-01-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Infect Immun. 2003 Jun;71(6):3138-45 [12761092] PLoS One. 2014;9(3):e93141 [24671196] J Mol Microbiol Biotechnol. 2003;6(1):29-40 [14593251] J Bacteriol. 2003 Nov;185(22):6723-7 [14594849] Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):3142-7 [14970347] Infect Immun. 2004 Oct;72(10):5938-46 [15385497] Science. 1982 Jun 18;216(4552):1317-9 [7043737] Infect Immun. 1988 Aug;56(8):1831-6 [3397175] Gene. 1991 Apr;100:189-94 [1905257] J Bacteriol. 1994 May;176(10):3072-5 [8188609] Methods Mol Biol. 1995;47:253-9 [7550741] Infect Immun. 1996 Sep;64(9):3870-6 [8751941] J Bacteriol. 1996 Oct;178(20):5946-53 [8830691] Microbiology. 1997 Feb;143 ( Pt 2):519-22 [9043127] Nature. 1997 Dec 11;390(6660):580-6 [9403685] Infect Immun. 1999 Jul;67(7):3181-7 [10377088] Infect Immun. 2004 Dec;72(12):7147-54 [15557639] Proc Natl Acad Sci U S A. 2005 May 10;102(19):6972-7 [15860579] J Bacteriol. 2005 Jul;187(14):4822-9 [15995197] Nature. 2005 Jul 28;436(7050):573-7 [16049492] J Med Entomol. 2005 Jul;42(4):676-84 [16119559] Vector Borne Zoonotic Dis. 2005 Fall;5(3):237-45 [16187892] Mol Microbiol. 2006 Mar;59(5):1591-601 [16468997] Infect Immun. 2006 Jun;74(6):3547-53 [16714587] Infect Immun. 2006 Jun;74(6):3678-81 [16714602] Mol Microbiol. 2007 Feb;63(3):694-710 [17181780] Infect Immun. 2007 Mar;75(3):1517-9 [17158906] Mol Microbiol. 2007 Jun;64(5):1358-74 [17542926] Mol Microbiol. 2007 Sep;65(5):1193-217 [17645733] Mol Microbiol. 2008 Jul;69(1):15-29 [18452586] J Bacteriol. 2008 Dec;190(24):7885-91 [18849429] J Infect Dis. 2009 Oct 15;200(8):1318-30 [19754308] Appl Environ Microbiol. 2010 Nov;76(22):7407-12 [20851957] J Bacteriol. 2011 Mar;193(5):1161-71 [21193609] Infect Immun. 2011 Sep;79(9):3510-7 [21708994] Infect Immun. 2006 Jun;74(6):3554-64 [16714588] Mol Microbiol. 2000 Feb;35(3):490-516 [10672174] J Bacteriol. 2000 May;182(9):2445-52 [10762244] Proc Natl Acad Sci U S A. 2000 Apr 25;97(9):4850-5 [10781091] J Bacteriol. 2000 May;182(10):2909-18 [10781562] Proc Natl Acad Sci U S A. 2000 Dec 5;97(25):13865-70 [11106398] Mol Microbiol. 2001 Feb;39(3):714-21 [11169111] J Bacteriol. 2001 Oct;183(19):5544-53 [11544216] J Bacteriol. 2001 Nov;183(22):6558-64 [11673425] Proc Natl Acad Sci U S A. 2001 Oct 23;98(22):12724-9 [11675503] Infect Immun. 2002 Apr;70(4):2139-50 [11895980] Mol Microbiol. 2002 Jan;43(2):281-95 [11985709] Infect Immun. 2002 Sep;70(9):4798-804 [12183522] Mol Microbiol. 2003 May;48(3):753-64 [12694619] Microbiology. 2011 Oct;157(Pt 10):2831-40 [21778210] Infect Immun. 2012 Oct;80(10):3501-11 [22851744] Mol Microbiol. 2013 Jul;89(2):216-27 [23692497] PLoS One. 2013;8(12):e83276 [24358270] Infect Immun. 2003 Aug;71(8):4608-13 [12874340] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/AEM.03657-14 ER - TY - JOUR T1 - Discovery of a novel general anesthetic chemotype using high-throughput screening. AN - 1652392444; 25603205 AB - The development of novel anesthetics has historically been a process of combined serendipity and empiricism, with most recent new anesthetics developed via modification of existing anesthetic structures. Using a novel high-throughput screen employing the fluorescent anesthetic 1-aminoanthracene and apoferritin as a surrogate for on-pathway anesthetic protein target(s), we screened a 350,000 compound library for competition with 1-aminoanthracene-apoferritin binding. Hit compounds meeting structural criteria had their binding affinities for apoferritin quantified with isothermal titration calorimetry and were tested for γ-aminobutyric acid type A receptor binding using a flunitrazepam binding assay. Chemotypes with a strong presence in the top 700 and exhibiting activity via isothermal titration calorimetry were selected for medicinal chemistry optimization including testing for anesthetic potency and toxicity in an in vivo Xenopus laevis tadpole assay. Compounds with low toxicity and high potency were tested for anesthetic potency in mice. From an initial chemical library of more than 350,000 compounds, we identified 2,600 compounds that potently inhibited 1-aminoanthracene binding to apoferritin. A subset of compounds chosen by structural criteria (700) was successfully reconfirmed using the initial assay. Based on a strong presence in both the initial and secondary screens the 6-phenylpyridazin-3(2H)-one chemotype was assessed for anesthetic activity in tadpoles. Medicinal chemistry efforts identified four compounds with high potency and low toxicity in tadpoles, two were found to be effective novel anesthetics in mice. The authors demonstrate the first use of a high-throughput screen to successfully identify a novel anesthetic chemotype and show mammalian anesthetic activity for members of that chemotype. JF - Anesthesiology AU - McKinstry-Wu, Andrew R AU - Bu, Weiming AU - Rai, Ganesha AU - Lea, Wendy A AU - Weiser, Brian P AU - Liang, David F AU - Simeonov, Anton AU - Jadhav, Ajit AU - Maloney, David J AU - Eckenhoff, Roderic G AD - From the Department of Anesthesiology and Critical Care (A.R.M.-W., W.B., R.G.E.) and Department of Pharmacology (B.P.W.), University of Pennsylvania, Philadelphia, Pennsylvania; National Institutes of Health Chemical Genomics Center, National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, Maryland (G.R., W.A.L., A.S., A.J., D.J.M.); and College of Arts and Sciences, University of Pennsylvania, Philadelphia, Pennsylvania (D.F.L.). Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 325 EP - 333 VL - 122 IS - 2 KW - Anesthetics KW - 0 KW - Phenols KW - Receptors, GABA-A KW - Flunitrazepam KW - 620X0222FQ KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Reflex -- drug effects KW - Phenols -- pharmacology KW - Larva KW - Phenols -- chemistry KW - Mice, Inbred C57BL KW - Xenopus KW - Calorimetry KW - Receptors, GABA-A -- drug effects KW - Mice KW - Flunitrazepam -- metabolism KW - Female KW - Anesthetics -- pharmacology KW - Anesthetics -- chemistry KW - High-Throughput Screening Assays -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652392444?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Anesthesiology&rft.atitle=Discovery+of+a+novel+general+anesthetic+chemotype+using+high-throughput+screening.&rft.au=McKinstry-Wu%2C+Andrew+R%3BBu%2C+Weiming%3BRai%2C+Ganesha%3BLea%2C+Wendy+A%3BWeiser%2C+Brian+P%3BLiang%2C+David+F%3BSimeonov%2C+Anton%3BJadhav%2C+Ajit%3BMaloney%2C+David+J%3BEckenhoff%2C+Roderic+G&rft.aulast=McKinstry-Wu&rft.aufirst=Andrew&rft.date=2015-02-01&rft.volume=122&rft.issue=2&rft.spage=325&rft.isbn=&rft.btitle=&rft.title=Anesthesiology&rft.issn=1528-1175&rft_id=info:doi/10.1097%2FALN.0000000000000505 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-24 N1 - Date created - 2015-01-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Neurosci. 2003 Sep 17;23(24):8608-17 [13679430] J Pharmacol Exp Ther. 2001 Apr;297(1):338-51 [11259561] Proc Natl Acad Sci U S A. 2009 Apr 21;106(16):6501-6 [19346473] Bioorg Med Chem. 2009 Jul 15;17(14):5133-8 [19520579] J Biol Chem. 2009 Sep 4;284(36):24176-84 [19605349] PLoS One. 2009;4(9):e7150 [19777064] Anesthesiology. 2010 Apr;112(4):834-41 [20234312] Proc Natl Acad Sci U S A. 2010 Aug 10;107(32):14122-7 [20660787] Methods Cell Biol. 2011;105:517-24 [21951545] Methods Cell Biol. 2011;105:525-41 [21951546] FASEB J. 2012 Jun;26(6):2394-400 [22362897] J Biol Chem. 2013 Jul 5;288(27):19343-57 [23677991] Mol Pharmacol. 2013 Nov;84(5):670-8 [23950219] Anesthesiology. 2004 Sep;101(3):703-9 [15329595] J Neurochem. 1985 Apr;44(4):1162-7 [2983028] Nature. 1997 Sep 25;389(6649):385-9 [9311780] Pharmacol Rev. 1997 Dec;49(4):343-67 [9443162] Science. 1999 Jan 1;283(5398):70-4 [9872743] J Pharmacol Exp Ther. 2006 May;317(2):615-26 [16397088] Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11473-8 [16864780] J Neurosci. 2006 Nov 8;26(45):11599-605 [17093081] J Neurosci. 2007 Feb 7;27(6):1247-54 [17287498] Lancet. 2008 Jul 12;372(9633):139-44 [18582931] J Neurosci. 2001 Mar 15;21(6):RC136 [11245705] Drug Discov Today. 2004 May 15;9(10):430-1 [15109945] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/ALN.0000000000000505 ER - TY - JOUR T1 - BCL-2 family protein, BAD is down-regulated in breast cancer and inhibits cell invasion. AN - 1652390757; 25499972 AB - We have previously demonstrated that the anti-apoptotic protein BAD is expressed in normal human breast tissue and shown that BAD inhibits expression of cyclin D1 to delay cell-cycle progression in breast cancer cells. Herein, expression of proteins in breast tissues was studied by immunohistochemistry and results were analyzed statistically to obtain semi-quantitative data. Biochemical and functional changes in BAD-overexpressing MCF7 breast cancer cells were evaluated using PCR, reporter assays, western blotting, ELISA and extracellular matrix invasion assays. Compared to normal tissues, Grade II breast cancers expressed low total/phosphorylated forms of BAD in both cytoplasmic and nuclear compartments. BAD overexpression decreased the expression of β-catenin, Sp1, and phosphorylation of STATs. BAD inhibited Ras/MEK/ERK and JNK signaling pathways, without affecting the p38 signaling pathway. Expression of the metastasis-related proteins, MMP10, VEGF, SNAIL, CXCR4, E-cadherin and TlMP2 was regulated by BAD with concomitant inhibition of extracellular matrix invasion. Inhibition of BAD by siRNA increased invasion and Akt/p-Akt levels. Clinical data and the results herein suggest that in addition to the effect on apoptosis, BAD conveys anti-metastatic effects and is a valuable prognostic marker in breast cancer. Copyright © 2014 Elsevier Inc. All rights reserved. JF - Experimental cell research AU - Cekanova, Maria AU - Fernando, Romaine I AU - Siriwardhana, Nalin AU - Sukhthankar, Mugdha AU - De la Parra, Columba AU - Woraratphoka, Jirayus AU - Malone, Christine AU - Ström, Anders AU - Baek, Seung J AU - Wade, Paul A AU - Saxton, Arnold M AU - Donnell, Robert M AU - Pestell, Richard G AU - Dharmawardhane, Suranganie AU - Wimalasena, Jay AD - Department of Small Animal Clinical Sciences, College of Veterinary Medicine, The University of Tennessee, Knoxville, TN, USA. Electronic address: mcekanov@utk.edu. ; Department of Obstetrics and Gynecology, Graduate School of Medicine, Medical Center, The University of Tennessee, Knoxville, TN, USA. ; Department of Animal Science, The University of Tennessee, Knoxville, TN, USA. ; Department of Biomedical and Diagnostics Sciences, College of Veterinary Medicine, The University of Tennessee, Knoxville, TN, USA. ; Department of Biochemistry, School of Medicine, University of Puerto Rico, Medical Sciences Campus, San Juan, PR, USA. ; Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA. ; Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, Houston, TX, USA. ; Department of Cancer Biology, Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA. ; Department of Obstetrics and Gynecology, Graduate School of Medicine, Medical Center, The University of Tennessee, Knoxville, TN, USA. Electronic address: jwimalas@gmail.com. Y1 - 2015/02/01/ PY - 2015 DA - 2015 Feb 01 SP - 1 EP - 10 VL - 331 IS - 1 KW - BAD protein, human KW - 0 KW - RNA, Messenger KW - STAT Transcription Factors KW - bcl-Associated Death Protein KW - beta Catenin KW - Proto-Oncogene Proteins c-akt KW - EC 2.7.11.1 KW - Index Medicus KW - Extracellular matrix invasion KW - Breast cancer KW - BAD KW - Metastasis KW - Real-Time Polymerase Chain Reaction KW - Proto-Oncogene Proteins c-akt -- genetics KW - STAT Transcription Factors -- metabolism KW - Proto-Oncogene Proteins c-akt -- metabolism KW - Humans KW - Reverse Transcriptase Polymerase Chain Reaction KW - RNA, Messenger -- genetics KW - Cell Proliferation KW - Epithelial-Mesenchymal Transition KW - Blotting, Western KW - Tumor Cells, Cultured KW - Phosphorylation KW - beta Catenin -- metabolism KW - MCF-7 Cells KW - Enzyme-Linked Immunosorbent Assay KW - beta Catenin -- genetics KW - STAT Transcription Factors -- genetics KW - Flow Cytometry KW - Female KW - Immunoenzyme Techniques KW - Cell Movement KW - Down-Regulation KW - bcl-Associated Death Protein -- antagonists & inhibitors KW - bcl-Associated Death Protein -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652390757?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Experimental+cell+research&rft.atitle=BCL-2+family+protein%2C+BAD+is+down-regulated+in+breast+cancer+and+inhibits+cell+invasion.&rft.au=Cekanova%2C+Maria%3BFernando%2C+Romaine+I%3BSiriwardhana%2C+Nalin%3BSukhthankar%2C+Mugdha%3BDe+la+Parra%2C+Columba%3BWoraratphoka%2C+Jirayus%3BMalone%2C+Christine%3BStr%C3%B6m%2C+Anders%3BBaek%2C+Seung+J%3BWade%2C+Paul+A%3BSaxton%2C+Arnold+M%3BDonnell%2C+Robert+M%3BPestell%2C+Richard+G%3BDharmawardhane%2C+Suranganie%3BWimalasena%2C+Jay&rft.aulast=Cekanova&rft.aufirst=Maria&rft.date=2015-02-01&rft.volume=331&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Experimental+cell+research&rft.issn=1090-2422&rft_id=info:doi/10.1016%2Fj.yexcr.2014.11.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-26 N1 - Date created - 2015-01-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Invest. 2009 Jun;119(6):1429-37 [19487819] PLoS One. 2009;4(7):e6224 [19593445] Clin Exp Metastasis. 2009;26(6):505-16 [19294520] Oncogene. 2008 Dec;27 Suppl 1:S53-70 [19641507] J Biol Chem. 2009 Oct 9;284(41):28004-20 [19667065] J Biol Chem. 2010 Mar 12;285(11):8218-26 [20053993] Cancer Res. 1994 May 1;54(9):2468-71 [8162596] Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9545-52 [8790367] Oncogene. 1996 Oct 3;13(7):1511-9 [8875989] Cell. 1996 Nov 15;87(4):619-28 [8929531] EMBO J. 1997 Aug 1;16(15):4628-38 [9303307] Science. 1998 Mar 20;279(5358):1954-8 [9506948] EMBO J. 1999 Mar 1;18(5):1367-77 [10064602] Trends Biochem Sci. 2010 Mar;35(3):161-8 [19884009] Cell Res. 2010 Apr;20(4):458-69 [20142842] PLoS One. 2010;5(7):e11772 [20668552] Mol Cancer Res. 2010 Aug;8(8):1116-25 [20647330] J Exp Clin Cancer Res. 2010;29:107 [20691103] Oncogene. 2010 Sep 30;29(39):5381-91 [20603619] Mol Cancer Res. 2004 Oct;2(10):551-6 [15498929] J Natl Cancer Inst. 1973 Nov;51(5):1409-16 [4357757] Cancer Res. 1993 Oct 1;53(19):4701-14 [8402648] Cell. 1999 Aug 6;98(3):295-303 [10458605] Pathol Int. 1999 Sep;49(9):775-80 [10504548] EMBO J. 2004 Nov 24;23(23):4679-89 [15526035] Nature. 2003 Aug 21;424(6951):952-6 [12931191] Biochem J. 2003 Oct 15;375(Pt 2):263-74 [12871207] Oncogene. 2003 Nov 24;22(53):8590-607 [14634621] Nat Rev Cancer. 2003 Nov;3(11):859-68 [14668816] Anticancer Res. 1999 Sep-Oct;19(5C):4555-63 [10650810] Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):4262-6 [10759547] Mol Cell Biol. 2000 Jul;20(13):4745-53 [10848600] Annu Rev Biochem. 2000;69:217-45 [10966458] Breast Cancer Res Treat. 2000 Sep;63(1):23-9 [11079156] J Biol Chem. 2000 Dec 15;275(50):39458-65 [10978339] Oncogene. 2001 Jul 27;20(33):4507-18 [11494146] Nature. 2004 May 6;429(6987):75-9 [15129283] Mol Biol Cell. 2004 Jul;15(7):3266-84 [15121878] Carcinogenesis. 2004 Aug;25(8):1371-6 [15033904] J Biol Chem. 2004 Oct 1;279(40):42240-9 [15231831] Mod Pathol. 2002 Jan;15(1):26-34 [11796838] Methods. 2001 Dec;25(4):402-8 [11846609] Pathol Oncol Res. 2002;8(1):26-30 [11994759] Nature. 2002 Sep 26;419(6905):395-9 [12353035] Mol Endocrinol. 2004 Dec;18(12):2937-49 [15358836] J Clin Invest. 2004 Dec;114(12):1704-13 [15599395] J Biol Chem. 2004 Dec 24;279(52):54470-8 [15471874] J Immunol. 2005 Sep 1;175(5):3033-44 [16116191] Cancer J. 2005 Sep-Oct;11(5):404-11 [16259871] Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):8995-9000 [16754849] Carcinogenesis. 2006 Aug;27(8):1682-91 [16597645] Am J Pathol. 2006 Sep;169(3):729-37 [16936249] Dig Liver Dis. 2006 Sep;38(9):683-7 [16807152] Mol Cell Biol. 2006 Dec;26(23):9071-82 [17000778] Mol Cancer Ther. 2006 Nov;5(11):2747-56 [17121921] Mol Cell Biol. 2007 Feb;27(4):1356-69 [17145782] Proc Natl Acad Sci U S A. 2007 Mar 6;104(10):3787-92 [17360431] Breast Cancer Res Treat. 2007 Apr;102(2):173-9 [17004114] Nature. 2011 Jun 2;474(7349):96-9 [21552281] Cancer Res. 2006 Oct 15;66(20):9986-94 [17047061] Proc Natl Acad Sci U S A. 2007 May 1;104(18):7438-43 [17460049] APMIS. 2007 Aug;115(8):976-81 [17696955] J Biol Chem. 2007 Sep 28;282(39):28864-73 [17670745] Mol Biol Cell. 2008 Jun;19(6):2566-78 [18367547] Cell Death Differ. 2008 Jul;15(7):1113-23 [18309324] BMC Cancer. 2008;8:153 [18510726] Clin Cancer Res. 2008 Jul 1;14(13):4128-33 [18593990] Nat Rev Cancer. 2008 Aug;8(8):592-603 [18650835] Breast Cancer Res Treat. 2008 Nov;112(2):287-96 [18158619] Eur J Cancer. 2009 Mar;45(4):694-704 [19138840] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.yexcr.2014.11.016 ER - TY - JOUR T1 - Identification and mutagenesis of the adeno-associated virus 5 sialic acid binding region. AN - 1652384027; 25410855 AB - As a genus, the dependoviruses use a diverse group of cell surface carbohydrates for attachment and entry. Despite the fact that a majority of adeno-associated viruses (AAVs) utilize sialic acid (SIA) for binding and transduction, this virus-carbohydrate interaction is poorly understood. Utilizing X-ray crystallography, two SIA binding regions were mapped for AAV5. The first site mapped to the depression in the center of the 3-fold axis of symmetry, while the second site was located under the βHI loop close to the 5-fold axis. Mutagenesis of amino acids 569 and 585 or 587 within the 3-fold depression resulted in elimination or alteration in SIA-dependent transduction, respectively. This change in SIA binding was confirmed using glycan microarrays. Mutagenesis of the second site identified a role in transduction that was SIA independent. Further studies of the mutants at the 3-fold site demonstrated a change in transduction activity and cell tropism in vivo as well as resistance to neutralization by a polyclonal antibody raised against the wild-type virus. Despite the fact that a majority of AAVs utilize sialic acid for binding and transduction, this virus-carbohydrate interaction is poorly understood. Utilizing X-ray crystallography, the sialic acid binding regions of AAV5 were identified and studied using a variety of approaches. Mutagenesis of this region resulted in elimination or alteration in sialic acid-dependent transduction in cell lines. This change in sialic acid glycan binding was confirmed using glycan arrays. Further study also demonstrated a change in transduction and activity and cell tropism in vivo as well as resistance to neutralization by antibodies raised against the wild-type virus. Copyright © 2015, American Society for Microbiology. All Rights Reserved. JF - Journal of virology AU - Afione, Sandra AU - DiMattia, Michael A AU - Halder, Sujata AU - Di Pasquale, Giovanni AU - Agbandje-McKenna, Mavis AU - Chiorini, John A AD - NIDCR, NIH, Molecular Physiology and Therapeutics Branch, Bethesda, Maryland, USA. ; University of Florida, Department of Biochemistry and Molecular Biology, Gainesville, Florida, USA. ; University of Florida, Department of Biochemistry and Molecular Biology, Gainesville, Florida, USA mckenna@ufl.edu jchiorini@dir.nidcr.nih.gov. ; NIDCR, NIH, Molecular Physiology and Therapeutics Branch, Bethesda, Maryland, USA mckenna@ufl.edu jchiorini@dir.nidcr.nih.gov. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 1660 EP - 1672 VL - 89 IS - 3 KW - Antibodies, Neutralizing KW - 0 KW - Antibodies, Viral KW - Capsid Proteins KW - N-Acetylneuraminic Acid KW - GZP2782OP0 KW - Index Medicus KW - Animals KW - Models, Molecular KW - Viral Tropism KW - Humans KW - DNA Mutational Analysis KW - Transduction, Genetic KW - Crystallography, X-Ray KW - Antibodies, Neutralizing -- immunology KW - Cell Line KW - Antibodies, Viral -- immunology KW - Mutagenesis KW - Binding Sites KW - Virus Attachment KW - Dependovirus -- physiology KW - Capsid Proteins -- metabolism KW - Dependovirus -- genetics KW - N-Acetylneuraminic Acid -- metabolism KW - Dependovirus -- chemistry KW - Dependovirus -- immunology KW - Capsid Proteins -- genetics KW - Capsid Proteins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652384027?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+virology&rft.atitle=Identification+and+mutagenesis+of+the+adeno-associated+virus+5+sialic+acid+binding+region.&rft.au=Afione%2C+Sandra%3BDiMattia%2C+Michael+A%3BHalder%2C+Sujata%3BDi+Pasquale%2C+Giovanni%3BAgbandje-McKenna%2C+Mavis%3BChiorini%2C+John+A&rft.aulast=Afione&rft.aufirst=Sandra&rft.date=2015-02-01&rft.volume=89&rft.issue=3&rft.spage=1660&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=1098-5514&rft_id=info:doi/10.1128%2FJVI.02503-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-07 N1 - Date created - 2015-01-13 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Med. 1999 Sep;5(9):1052-6 [10470084] Acta Crystallogr D Biol Crystallogr. 1998 Sep 1;54(Pt 5):905-21 [9757107] J Virol. 2006 Feb;80(3):1563-73 [16415031] Acta Crystallogr Sect F Struct Biol Cryst Commun. 2005 Oct 1;61(Pt 10):917-21 [16511195] Gene Ther. 2006 Apr;13(7):594-601 [16341060] J Virol. 2006 Jun;80(11):5516-22 [16699032] J Virol. 2006 Sep;80(17):8482-92 [16912298] J Virol. 2006 Sep;80(18):9093-103 [16940521] J Virol. 2006 Nov;80(22):11393-7 [16943302] Acta Crystallogr D Biol Crystallogr. 2007 Jan;63(Pt 1):94-100 [17164531] J Virol Methods. 2007 Mar;140(1-2):17-24 [17126418] J Struct Biol. 2007 May;158(2):182-7 [17116403] J Virol. 2008 Sep;82(17):8911-6 [18524816] Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):213-21 [20124702] Acta Crystallogr D Biol Crystallogr. 2010 Apr;66(Pt 4):486-501 [20383002] J Virol. 2010 Aug;84(15):7782-92 [20484503] Acta Crystallogr D Biol Crystallogr. 2010 Jul;66(Pt 7):797-805 [20606260] Mol Ther. 2011 Nov;19(11):1990-8 [21829176] J Gen Virol. 2012 Feb;93(Pt 2):347-55 [22071509] J Virol. 2012 Apr;86(7):3452-65 [22258256] J Virol. 2013 Oct;87(20):11187-99 [23926356] J Virol. 2013 Dec;87(24):13206-13 [24067974] J Virol. 2014 Mar;88(5):2991-3003 [24371066] Curr Opin Virol. 2014 Aug;7:108-18 [25047752] J Virol. 2000 Apr;74(8):3852-8 [10729159] J Gen Virol. 2000 Aug;81(Pt 8):2077-84 [10900047] J Virol. 2001 Jul;75(14):6615-24 [11413329] J Virol. 2001 Aug;75(15):6884-93 [11435568] J Virol. 2002 Jan;76(2):791-801 [11752169] J Biol Chem. 2002 Jun 28;277(26):23709-13 [11925433] Hum Gene Ther. 2002 Jul 1;13(10):1235-43 [12133276] Biotechniques. 2002 Jul;33(1):204-6, 208, 210-1 [12139247] J Virol. 2002 Oct;76(20):10437-43 [12239320] J Virol. 2003 Jun;77(12):6995-7006 [12768018] J Virol. 2003 Oct;77(20):11072-81 [14512555] Nat Med. 2003 Oct;9(10):1306-12 [14502277] Cancer Res. 1990 Mar 1;50(5):1403-10 [2302705] Virology. 1992 Nov;191(1):301-8 [1329321] Virology. 1997 May 26;232(1):19-31 [9185585] J Virol. 1998 Feb;72(2):1438-45 [9445046] J Gen Virol. 1998 Sep;79 ( Pt 9):2163-9 [9747725] Hum Gene Ther. 2006 Jan;17(1):10-9 [16409121] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/JVI.02503-14 ER - TY - JOUR T1 - Duodenal ischemia and upper GI bleeding are dose-limiting toxicities of 24-h continuous intra-arterial pancreatic perfusion of gemcitabine following vascular isolation of the pancreatic head: early results from the Regional Chemotherapy in Locally Advanced Pancreatic Cancer (RECLAP) study. AN - 1652382780; 25236592 AB - Regional chemotherapy is used successfully in the treatment of both primary and secondary malignancies, in particular of the peritoneal surface and the liver, and is currently explored as an attractive approach for patients with locally advanced pancreatic ductal adenocarcinoma. To establish the feasibility and toxicity of regional intra-arterial gemcitabine delivered as a 24-h continuous infusion to the pancreas as a novel treatment option for patients with locally advanced PDAC a phase I clinical trial was conducted. Between April 2011 and September 2013 six patients with biopsy confirmed, borderline or unresectable pancreatic adenocarcinoma, and having received at least one line of systemic chemotherapy, underwent vascular redistribution of the inflow to the head of the pancreas by arterial coil embolization followed by perfusion catheter placement within the splenic artery. Patients were treated with increasing doses of gemcitabine administered by continuous splenic arterial infusion over 24 h with inter-patient and intra-patient dose escalation scheme. The primary endpoint was toxicity of the intra-arterial gemcitabine regimen and to establish the maximum tolerated dose. Catheter placement and gemcitabine infusion was successful in all patients enrolled to date (n = 6). Four out of six patients experienced catheter tip migration requiring replacement or revision. Patients received a median of four doses of 24-h gemcitabine infusion. Two patients developed grade 3 and 4 duodenal ischemia and upper gastrointestinal bleeding. Median overall survival was 15.3 months and median time to progression was 3 months. Three patients (50 %, n = 3/6) progressed systemically. Two patients had stable disease >4 months following treatment and underwent pancreaticoduodenectomy. While technically feasible to treat locally advanced pancreatic ductal adenocarcinoma, prolonged regional pancreatic perfusion with gemcitabine following pancreatic arterial redistribution carries a high risk for gastrointestinal toxicity. Shorter infusion schedules with frequent on treatment evaluations should be considered for future clinical trials. JF - Investigational new drugs AU - Beane, Joal D AU - Griffin, Kayla F AU - Levy, Elliot B AU - Pandalai, Prakash AU - Wood, Bradford AU - Abi-Jaoudeh, Nadine AU - Beresnev, Tatiana AU - Shutack, Yvonne AU - Webb, Carole C AU - Avital, Itzhak AU - Rudloff, Udo AD - Thoracic & GI Oncology Branch, National Cancer Institute, Hatfield Center, CCR - 4 West/5940 10 Center Drive, Bethesda, MD, 20892-0001, USA. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 109 EP - 118 VL - 33 IS - 1 KW - Antimetabolites, Antineoplastic KW - 0 KW - Deoxycytidine KW - 0W860991D6 KW - gemcitabine KW - B76N6SBZ8R KW - Index Medicus KW - Perfusion KW - Carcinoma, Pancreatic Ductal -- drug therapy KW - Humans KW - Aged KW - Duodenum -- blood supply KW - Catheterization KW - Duodenum -- drug effects KW - Pancreas -- blood supply KW - Treatment Outcome KW - Splenic Artery KW - Middle Aged KW - Maximum Tolerated Dose KW - Pancreatic Neoplasms -- drug therapy KW - Female KW - Male KW - Antimetabolites, Antineoplastic -- administration & dosage KW - Duodenal Diseases -- chemically induced KW - Deoxycytidine -- adverse effects KW - Antimetabolites, Antineoplastic -- adverse effects KW - Deoxycytidine -- analogs & derivatives KW - Deoxycytidine -- therapeutic use KW - Deoxycytidine -- administration & dosage KW - Ischemia -- chemically induced KW - Gastrointestinal Hemorrhage -- chemically induced KW - Antimetabolites, Antineoplastic -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652382780?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Investigational+new+drugs&rft.atitle=Duodenal+ischemia+and+upper+GI+bleeding+are+dose-limiting+toxicities+of+24-h+continuous+intra-arterial+pancreatic+perfusion+of+gemcitabine+following+vascular+isolation+of+the+pancreatic+head%3A+early+results+from+the+Regional+Chemotherapy+in+Locally+Advanced+Pancreatic+Cancer+%28RECLAP%29+study.&rft.au=Beane%2C+Joal+D%3BGriffin%2C+Kayla+F%3BLevy%2C+Elliot+B%3BPandalai%2C+Prakash%3BWood%2C+Bradford%3BAbi-Jaoudeh%2C+Nadine%3BBeresnev%2C+Tatiana%3BShutack%2C+Yvonne%3BWebb%2C+Carole+C%3BAvital%2C+Itzhak%3BRudloff%2C+Udo&rft.aulast=Beane&rft.aufirst=Joal&rft.date=2015-02-01&rft.volume=33&rft.issue=1&rft.spage=109&rft.isbn=&rft.btitle=&rft.title=Investigational+new+drugs&rft.issn=1573-0646&rft_id=info:doi/10.1007%2Fs10637-014-0157-7 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-18 N1 - Date created - 2015-01-15 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s10637-014-0157-7 ER - TY - JOUR T1 - Joint analysis of longitudinal and survival data measured on nested timescales by using shared parameter models: an application to fecundity data AN - 1652368933; 4643511 AB - We consider the joint modelling, analysis and prediction of a longitudinal binary process and a discrete time-to-event outcome. We consider data from a prospective pregnancy study, which provides day level information regarding the behaviour of couples attempting to conceive. Reproductive epidemiologists are particularly interested in developing a model for individualized predictions of time to pregnancy (TTP). A couple's intercourse behaviour should be an integral part of such a model and is one of the main focuses of the paper. In our motivating data, the intercourse observations are a long series of binary data with a periodic probability of success and the amount of available intercourse data is a function of both the menstrual cycle length and TTP. Moreover, these variables are dependent and observed on different, and nested, timescales (TTP is measured in menstrual cycles whereas intercourse is measured on days within a menstrual cycle) further complicating its analysis. Here, we propose a semiparametric shared parameter model for the joint modelling of the binary longitudinal data (intercourse behaviour) and the discrete survival outcome (TTP). Further, we develop couple-based dynamic predictions for the intercourse profiles, which in turn are used to assess the risk for subfertility (i.e. TTP longer than six menstrual cycles). Reprinted by permission of Blackwell Publishers JF - Journal of the Royal Statistical Society AU - Sundaram, Rajeshwari AU - Buck Louis, Germaine M AU - Mclain, Alexander C AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development Y1 - 2015/02// PY - 2015 DA - Feb 2015 SP - 339 EP - 357 VL - 64 IS - 2 SN - 0035-9254, 0035-9254 KW - Sociology KW - Longitudinal studies KW - Epidemiology KW - Menstruation KW - Sexual intercourse KW - Pregnancy KW - Modelling UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652368933?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+Royal+Statistical+Society&rft.atitle=Joint+analysis+of+longitudinal+and+survival+data+measured+on+nested+timescales+by+using+shared+parameter+models%3A+an+application+to+fecundity+data&rft.au=Sundaram%2C+Rajeshwari%3BBuck+Louis%2C+Germaine+M%3BMclain%2C+Alexander+C&rft.aulast=Sundaram&rft.aufirst=Rajeshwari&rft.date=2015-02-01&rft.volume=64&rft.issue=2&rft.spage=339&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+Royal+Statistical+Society&rft.issn=00359254&rft_id=info:doi/10.1111%2Frssc.12075 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-02-09 N1 - Last updated - 2015-02-09 N1 - SubjectsTermNotLitGenreText - 8162 8163; 10020; 4357 7894; 11567 11563 1025 1542 11325 6071; 7541 7537 971; 7941 13598 5421 6091 DO - http://dx.doi.org/10.1111/rssc.12075 ER - TY - JOUR T1 - Treatment of pediatric acute lymphoblastic leukemia. AN - 1645230127; 25435112 AB - Acute lymphoblastic leukemia (ALL) is the most common pediatric oncologic diagnosis, and advances in its treatment have led to progressive improvements in survival. The 4 main components of therapy are remission induction, consolidation, maintenance, and central nervous system-directed therapy, and usually last 2 to 3 years. Treatment intensity based on risk-based stratification is the cornerstone of treatment. Patients with features of more favorable disease are spared the more toxic effects of chemotherapy, whereas more aggressive regimens are reserved for those with higher-risk disease. Prognosis of relapsed pediatric ALL depends primarily on duration of remission and site of relapse. Copyright © 2015 Elsevier Inc. All rights reserved. JF - Pediatric clinics of North America AU - Cooper, Stacy L AU - Brown, Patrick A AD - Pediatric Hematology/Oncology, Johns Hopkins/National Institutes of Health, Bloomberg 11379, 1800 Orleans Street, Baltimore, MD 21287, USA. ; Pediatric Leukemia Program, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, 1650 Orleans Street, CRB1 Room 2M49, Baltimore, MD 21231, USA. Electronic address: pbrown2@jhmi.edu. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 61 EP - 73 VL - 62 IS - 1 KW - Antineoplastic Agents KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Leukemia treatment KW - Risk-based stratification KW - Acute lymphoblastic leukemia KW - Humans KW - Treatment Outcome KW - Prognosis KW - Child KW - Risk Assessment KW - Antineoplastic Agents -- therapeutic use KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- drug therapy KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645230127?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pediatric+clinics+of+North+America&rft.atitle=Treatment+of+pediatric+acute+lymphoblastic+leukemia.&rft.au=Cooper%2C+Stacy+L%3BBrown%2C+Patrick+A&rft.aulast=Cooper&rft.aufirst=Stacy&rft.date=2015-02-01&rft.volume=62&rft.issue=1&rft.spage=61&rft.isbn=&rft.btitle=&rft.title=Pediatric+clinics+of+North+America&rft.issn=1557-8240&rft_id=info:doi/10.1016%2Fj.pcl.2014.09.006 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-29 N1 - Date created - 2014-12-01 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Oncol. 1995 Feb;13(2):345-51 [7531219] Blood. 1994 Nov 1;84(9):3122-33 [7949185] Br J Haematol. 1998 Jul;102(2):423-38 [9695956] J Clin Oncol. 2005 May 20;23(15):3376-82 [15908649] Br J Haematol. 2005 Jun;129(6):734-45 [15952999] Klin Padiatr. 2005 Nov-Dec;217(6):310-20 [16307416] Blood. 2006 Jul 15;108(2):441-51 [16556894] Blood. 2006 Aug 15;108(4):1165-73 [16609069] Br J Haematol. 2006 Dec;135(5):595-602 [17054672] Nat Rev Drug Discov. 2007 Feb;6(2):149-65 [17268486] Lancet. 2007 Jul 21;370(9583):240-50 [17658395] Blood. 2008 Mar 1;111(5):2548-55 [18039957] J Clin Oncol. 2008 May 1;26(13):2186-91 [18445843] Blood. 2008 Jun 15;111(12):5477-85 [18388178] Bone Marrow Transplant. 2008 Aug;42(3):201-5 [18490913] Clin Cancer Res. 2011 Oct 15;17(20):6398-405 [22003067] N Engl J Med. 2012 Apr 12;366(15):1371-81 [22494120] Am J Hematol. 2012 May;87(5):472-8 [22388572] J Clin Oncol. 2012 Jun 10;30(17):2094-101 [22564992] Blood. 2012 Oct 4;120(14):2807-16 [22896001] Haematologica. 2012 Nov;97(11):1743-50 [22580999] Hematology Am Soc Hematol Educ Program. 2012;2012:143-51 [23233573] Pediatr Blood Cancer. 2013 Feb;60(2):254-7 [22948968] Br J Haematol. 2013 Apr;161(1):27-42 [23384118] Curr Opin Hematol. 2013 Jul;20(4):369-73 [23695450] Leukemia. 2008 Dec;22(12):2142-50 [18818707] Blood. 2009 May 21;113(21):5083-9 [19131545] N Engl J Med. 2009 Jun 25;360(26):2730-41 [19553647] J Clin Oncol. 2009 Nov 1;27(31):5175-81 [19805687] Leukemia. 2010 Feb;24(2):285-97 [20016531] Leukemia. 2010 Apr;24(4):715-20 [20130603] Blood. 2010 Apr 22;115(16):3206-14 [20154213] Br J Haematol. 2010 Apr;149(1):84-92 [20085575] Br J Haematol. 2010 Jun;149(5):722-33 [20331462] Lancet. 2010 Dec 11;376(9757):2009-17 [21131038] Eur J Cancer. 2011 Jan;47(2):239-47 [21095115] J Pediatr. 2011 Jul;159(1):133-7 [21353248] J Clin Oncol. 2011 Aug 10;29(23):3185-93 [21747090] Br J Haematol. 2013 May;161(4):556-65 [23480776] Blood. 1992 Jun 15;79(12):3316-24 [1596572] J Clin Oncol. 2013 Sep 20;31(27):3397-402 [23940221] Pediatr Blood Cancer. 2014 Jun;61(6):1114-7 [24376133] Eur J Cancer. 2013 Apr;49(6):1346-55 [23265714] J Clin Oncol. 2000 Feb;18(4):813-23 [10673523] J Clin Oncol. 2001 Jul 1;19(13):3188-93 [11432885] Blood. 2002 Mar 15;99(6):1986-94 [11877270] Leukemia. 2004 Mar;18(3):499-504 [14981525] Cancer. 1970 Aug;26(2):404-9 [5271211] J Clin Oncol. 1992 Apr;10(4):624-30 [1548525] Blood. 1996 Aug 1;88(3):831-7 [8704238] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.pcl.2014.09.006 ER - TY - JOUR T1 - Enhanced fluorescence imaging guided photodynamic therapy of sinoporphyrin sodium loaded graphene oxide. AN - 1641018085; 25542797 AB - Extensive research indicates that graphene oxide (GO) can effectively deliver photosensitives (PSs) by π-π stacking for photodynamic therapy (PDT). However, due to the tight complexes of GO and PSs, the fluorescence of PSs are often drastically quenched via an energy/charge transfer process, which limits GO-PS systems for photodiagnostics especially in fluorescence imaging. To solve this problem, we herein strategically designed and prepared a novel photo-theranostic agent based on sinoporphyrin sodium (DVDMS) loaded PEGylated GO (GO-PEG-DVDMS) with improved fluorescence property for enhanced optical imaging guided PDT. The fluorescence of loaded DVDMS is drastically enhanced via intramolecular charge transfer. Meanwhile, the GO-PEG vehicles can significantly increase the tumor accumulation efficiency of DVDMS and lead to an improved PDT efficacy as compared to DVDMS alone. The cancer theranostic capability of the as-prepared GO-PEG-DVDMS was carefully investigated both in vitro and in vivo. Most intriguingly, 100% in vivo tumor elimination was achieved by intravenous injection of GO-PEG-DVDMS (2 mg/kg of DVDMS, 50 J) without tumor recurrence, loss of body weight or other noticeable toxicity. This novel GO-PEG-DVDMS theranostics is well suited for enhanced fluorescence imaging guided PDT. Published by Elsevier Ltd. JF - Biomaterials AU - Yan, Xuefeng AU - Niu, Gang AU - Lin, Jing AU - Jin, Albert J AU - Hu, Hao AU - Tang, Yuxia AU - Zhang, Yujie AU - Wu, Aiguo AU - Lu, Jie AU - Zhang, Shaoliang AU - Huang, Peng AU - Shen, Baozhong AU - Chen, Xiaoyuan AD - Department of Radiology, The Fourth Hospital of Harbin Medical University, Harbin, Heilongjiang, China; National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), 31 Center Drive, Bethesda, MD 20892, United States; Molecular Imaging Center of Harbin Medical University, Harbin, Heilongjiang, China. ; National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), 31 Center Drive, Bethesda, MD 20892, United States. ; Laboratory of Cellular Imaging and Macromolecular Biophysics, National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health, Bethesda, MD 20892, United States. ; Key Laboratory of Magnetic Materials and Devices, & Division of Functional Materials and Nanodevices, Ningbo Institute of Materials Technology and Engineering, Chinese Academy of Sciences, Ningbo, Zhejiang 315201, China. ; Jiangxi Qinglong Group Co., Ltd., No. 283 Dongfeng Street, Yichun, Jiangxi 336000, China. ; National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), 31 Center Drive, Bethesda, MD 20892, United States. Electronic address: peng.huang@nih.gov. ; Department of Radiology, The Fourth Hospital of Harbin Medical University, Harbin, Heilongjiang, China; Molecular Imaging Center of Harbin Medical University, Harbin, Heilongjiang, China. Electronic address: shenbzh@vip.sina.com. ; National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), 31 Center Drive, Bethesda, MD 20892, United States. Electronic address: shawn.chen@nih.gov. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 94 EP - 102 VL - 42 KW - Oxides KW - 0 KW - Porphyrins KW - sinoporphyrin sodium KW - Singlet Oxygen KW - 17778-80-2 KW - Polyethylene Glycols KW - 30IQX730WE KW - Graphite KW - 7782-42-5 KW - Index Medicus KW - Photodynamic therapy KW - Sinoporphyrin sodium (DVDMS) KW - Graphene oxide (GO) KW - Photosensitizer KW - Fluorescence imaging KW - Animals KW - Spectrometry, Fluorescence KW - Intracellular Space -- metabolism KW - Humans KW - Cell Line, Tumor KW - Mice, Nude KW - Cell Death -- drug effects KW - Singlet Oxygen -- chemistry KW - Cell Survival -- drug effects KW - Polyethylene Glycols -- chemistry KW - Endocytosis -- drug effects KW - Microscopy, Atomic Force KW - Flow Cytometry KW - Tissue Distribution -- drug effects KW - Polyethylene Glycols -- chemical synthesis KW - Graphite -- chemical synthesis KW - Oxides -- chemical synthesis KW - Porphyrins -- chemical synthesis KW - Porphyrins -- chemistry KW - Photochemotherapy KW - Diagnostic Imaging KW - Graphite -- chemistry KW - Porphyrins -- therapeutic use KW - Oxides -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1641018085?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biomaterials&rft.atitle=Enhanced+fluorescence+imaging+guided+photodynamic+therapy+of+sinoporphyrin+sodium+loaded+graphene+oxide.&rft.au=Yan%2C+Xuefeng%3BNiu%2C+Gang%3BLin%2C+Jing%3BJin%2C+Albert+J%3BHu%2C+Hao%3BTang%2C+Yuxia%3BZhang%2C+Yujie%3BWu%2C+Aiguo%3BLu%2C+Jie%3BZhang%2C+Shaoliang%3BHuang%2C+Peng%3BShen%2C+Baozhong%3BChen%2C+Xiaoyuan&rft.aulast=Yan&rft.aufirst=Xuefeng&rft.date=2015-02-01&rft.volume=42&rft.issue=&rft.spage=94&rft.isbn=&rft.btitle=&rft.title=Biomaterials&rft.issn=1878-5905&rft_id=info:doi/10.1016%2Fj.biomaterials.2014.11.040 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-08 N1 - Date created - 2014-12-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer J. 2002 Mar-Apr;8(2):154-63 [11999949] J Fluoresc. 2013 Jan;23(1):41-7 [22914972] Biomaterials. 2013 Apr;34(12):3002-9 [23374706] Biomaterials. 2013 Jun;34(19):4643-54 [23523428] Adv Mater. 2013 Jun 11;25(22):3055-61 [23404693] ACS Nano. 2013 Jun 25;7(6):5320-9 [23721576] Nanoscale. 2013 Aug 7;5(15):6857-66 [23770832] Nat Protoc. 2013 Dec;8(12):2392-403 [24202553] Anticancer Drugs. 2014 Feb;25(2):174-82 [24100280] Acc Chem Res. 2013 Oct 15;46(10):2211-24 [23480658] Theranostics. 2014;4(3):229-39 [24505232] Small. 2013 Nov 11;9(21):3678-84 [23661612] J Natl Cancer Inst. 1998 Jun 17;90(12):889-905 [9637138] Int J Nanomedicine. 2014;9:3077-90 [25028547] J Am Chem Soc. 2008 Aug 20;130(33):10856-7 [18661988] Trends Biotechnol. 2008 Nov;26(11):612-21 [18804298] Nanotechnology. 2009 Apr 1;20(13):135102 [19420486] Anal Chem. 2010 Mar 15;82(6):2341-6 [20180560] Langmuir. 2010 May 4;26(9):6083-5 [20297789] Chem Rev. 2010 May 12;110(5):2839-57 [20104890] Chem Rev. 2010 May 12;110(5):2795-838 [20353192] Angew Chem Int Ed Engl. 2010 Aug 2;49(33):5703-7 [20818755] Nano Lett. 2010 Sep 8;10(9):3318-23 [20684528] Adv Drug Deliv Rev. 2010 Aug 30;62(11):1094-124 [20858520] Biomaterials. 2011 May;32(13):3447-58 [21303717] Nat Mater. 2011 Apr;10(4):324-32 [21423187] ACS Nano. 2011 Jun 28;5(6):4550-61 [21539346] Chemistry. 2011 Oct 17;17(43):12084-91 [21915922] Biomaterials. 2012 Mar;33(7):2206-14 [22169821] ACS Nano. 2012 Mar 27;6(3):2361-70 [22339280] Nanoscale. 2012 Jul 7;4(13):3833-42 [22653227] ACS Nano. 2012 Jun 26;6(6):5070-7 [22631052] Adv Mater. 2012 Sep 25;24(37):5104-10 [22718562] Anal Chem. 2013 Feb 5;85(3):1424-30 [23278187] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.biomaterials.2014.11.040 ER - TY - JOUR T1 - Effects of μ-opioid receptor agonists in assays of acute pain-stimulated and pain-depressed behavior in male rats: role of μ-agonist efficacy and noxious stimulus intensity. AN - 1639496714; 25406170 AB - Pain is associated with stimulation of some behaviors and depression of others, and μ-opioid receptor agonists are among the most widely used analgesics. This study used parallel assays of pain-stimulated and pain-depressed behavior in male Sprague-Dawley rats to compare antinociception profiles for six μ-agonists that varied in efficacy at μ-opioid receptors (from highest to lowest: methadone, fentanyl, morphine, hydrocodone, buprenorphine, and nalbuphine). Intraperitoneal injection of diluted lactic acid served as an acute noxious stimulus to either stimulate stretching or depress operant responding maintained by electrical stimulation in an intracranial self-stimulation (ICSS). All μ-agonists blocked both stimulation of stretching and depression of ICSS produced by 1.8% lactic acid. The high-efficacy agonists methadone and fentanyl were more potent at blocking acid-induced depression of ICSS than acid-stimulated stretching, whereas lower-efficacy agonists displayed similar potency across assays. All μ-agonists except morphine also facilitated ICSS in the absence of the noxious stimulus at doses similar to those that blocked acid-induced depression of ICSS. The potency of the low-efficacy μ-agonist nalbuphine, but not the high-efficacy μ-agonist methadone, to block acid-induced depression of ICSS was significantly reduced by increasing the intensity of the noxious stimulus to 5.6% acid. These results demonstrate sensitivity of acid-induced depression of ICSS to a range of clinically effective μ-opioid analgesics and reveal distinctions between opioids based on efficacy at the μ-receptor. These results also support the use of parallel assays of pain-stimulated and -depressed behaviors to evaluate analgesic efficacy of candidate drugs. U.S. Government work not protected by U.S. copyright. JF - The Journal of pharmacology and experimental therapeutics AU - Altarifi, Ahmad A AU - Rice, Kenner C AU - Negus, S Stevens AD - Department of Pharmacology, School of Medicine, Jordan University of Science and Technology, Irbid, Jordan (A.A.A.); Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, Virginia (A.A.A., S.S.N.); and Chemical Biology Research Branch, National Institute on Drug Abuse and National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland (K.C.R.) altarifiaa@vcu.edu. ; Department of Pharmacology, School of Medicine, Jordan University of Science and Technology, Irbid, Jordan (A.A.A.); Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, Virginia (A.A.A., S.S.N.); and Chemical Biology Research Branch, National Institute on Drug Abuse and National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland (K.C.R.). Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 208 EP - 217 VL - 352 IS - 2 KW - Analgesics, Opioid KW - 0 KW - Receptors, Opioid, mu KW - Lactic Acid KW - 33X04XA5AT KW - Index Medicus KW - Conditioning, Operant -- drug effects KW - Animals KW - Rats, Sprague-Dawley KW - Self Stimulation KW - Dose-Response Relationship, Drug KW - Brain -- drug effects KW - Brain -- metabolism KW - Electric Stimulation KW - Male KW - Lactic Acid -- pharmacology KW - Behavior, Animal -- drug effects KW - Receptors, Opioid, mu -- agonists KW - Analgesics, Opioid -- pharmacology KW - Acute Pain -- psychology KW - Analgesics, Opioid -- therapeutic use KW - Analgesics, Opioid -- administration & dosage KW - Acute Pain -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1639496714?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.atitle=Effects+of+%CE%BC-opioid+receptor+agonists+in+assays+of+acute+pain-stimulated+and+pain-depressed+behavior+in+male+rats%3A+role+of+%CE%BC-agonist+efficacy+and+noxious+stimulus+intensity.&rft.au=Altarifi%2C+Ahmad+A%3BRice%2C+Kenner+C%3BNegus%2C+S+Stevens&rft.aulast=Altarifi&rft.aufirst=Ahmad&rft.date=2015-02-01&rft.volume=352&rft.issue=2&rft.spage=208&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=1521-0103&rft_id=info:doi/10.1124%2Fjpet.114.219873 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-08 N1 - Date created - 2014-12-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Pharmacol Rev. 2014 Jul;66(3):869-917 [24973197] Pharmacol Rep. 2014 Jun;66(3):459-65 [24905524] Arch Intern Med. 2003 Nov 10;163(20):2433-45 [14609780] J Pharmacol Exp Ther. 2004 Feb;308(2):547-54 [14600248] Psychopharmacology (Berl). 2004 Apr;172(4):463-70 [14727002] Anesthesiology. 2004 Jul;101(1):191-203 [15220791] Hum Psychopharmacol. 2004 Oct;19 Suppl 1:S3-7 [15378670] Arch Invest Med (Mex). 1974;5 SUPPL 1:207-14 [4155611] Br J Pharmacol. 1977 Aug;60(4):537-45 [409448] J Pharmacol Exp Ther. 1991 Nov;259(2):582-9 [1658305] Drug Metabol Drug Interact. 1991;9(2):77-102 [1686855] J Pharmacol Exp Ther. 1992 Jul;262(1):1-9 [1625189] J Pharmacol Exp Ther. 1993 Oct;267(1):280-6 [7901396] Mol Pharmacol. 1994 Feb;45(2):330-4 [8114680] Ann Acad Med Singapore. 1994 Mar;23(2):129-38 [8080219] J Pharmacol Exp Ther. 1994 Dec;271(3):1630-7 [7996478] Mol Pharmacol. 1997 Jan;51(1):87-96 [9016350] J Clin Pharmacol. 1997 Oct;37(10):908-15 [9505982] J Pharmacol Exp Ther. 1998 May;285(2):496-505 [9580589] J Pharmacol Exp Ther. 1998 May;285(2):595-601 [9580603] J Pharmacol Exp Ther. 1999 Feb;288(2):827-33 [9918595] J Pharmacol Exp Ther. 1999 May;289(2):965-75 [10215676] J Pharmacol Exp Ther. 1999 Sep;290(3):1132-40 [10454487] Vital Health Stat 10. 2004 Jul;(222):1-151 [15791763] Behav Brain Res. 2006 Jun 30;170(2):308-15 [16675039] J Pain. 2006 Jun;7(6):408-16 [16750797] Am J Physiol Regul Integr Comp Physiol. 2006 Aug;291(2):R300-6 [16497818] J Pharmacol Exp Ther. 2006 Nov;319(2):507-14 [16751251] Nat Rev Neurosci. 2008 Apr;9(4):314-20 [18354400] Neuropharmacology. 2008 Apr;54(5):767-75 [18289614] J Am Vet Med Assoc. 2008 Oct 15;233(8):1278-83 [19180716] Eur J Pharmacol. 2009 Feb 14;604(1-3):58-65 [19133255] Nat Rev Neurosci. 2009 Apr;10(4):283-94 [19259101] Brain Res Rev. 2009 Apr;60(1):226-42 [19162070] Pain. 2009 Jul;144(1-2):170-7 [19435650] Pharmacol Rep. 2009 May-Jun;61(3):424-35 [19605941] Life Sci. 2009 Aug 12;85(7-8):309-15 [19559034] Chin Med J (Engl). 2010 Jan 20;123(2):142-5 [20137360] Methods Mol Biol. 2010;617:79-91 [20336415] Psychopharmacology (Berl). 2010 Jun;210(2):149-59 [20101391] J Midwifery Womens Health. 2011 May-Jun;56(3):222-39 [21535371] Behav Pharmacol. 2011 Oct;22(7):663-73 [21921839] Emerg Med Pract. 2011 Jul;13(7):1-17; quiz 18 [22164398] J Pharmacol Exp Ther. 2012 Mar;340(3):501-9 [22128346] Pain. 2012 Apr;153(4):876-84 [22341563] Drugs Aging. 2012 Apr 1;29(4):285-305 [22462628] Behav Pharmacol. 2012 Oct;23(7):678-92 [22914074] J Opioid Manag. 2012 Nov-Dec;8(6):403-13 [23264318] J Pain. 2013 Mar;14(3):246-59 [23332494] Lab Anim (NY). 2013 Aug;42(8):292-300 [23877610] Behav Pharmacol. 2013 Sep;24(5-6):459-70 [23881045] J Pain Palliat Care Pharmacother. 2013 Dec;27(4):402-5 [24245573] Neuropsychopharmacology. 2014 Feb;39(3):614-24 [24008352] Anesthesiology. 2014 May;120(5):1262-74 [24509068] Case Manager. 2000 Sep-Oct;11(5):50-3 [11942280] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1124/jpet.114.219873 ER - TY - JOUR T1 - Evaluation of developmental toxicity and teratogenicity of diclofenac using Xenopus embryos. AN - 1634271608; 24992311 AB - Diclofenac is a non-steroidal anti-inflammatory drug (NSAID) with analgesic and anti-pyretic properties. This compound is therefore used to treat pain, inflammatory disorders, and dysmenorrhea. Due to its multimodal mechanism of action and ability to penetrate placenta, diclofenac is known to have undesirable side effects including teratogenicity. However, limited data exist on its teratogenicity, and a detailed investigation regarding harmful effects of this drug during embryogenesis is warranted. Here, we analyzed the developmental toxic effects of diclofenac using Xenopus embryos according to the Frog Embryo Teratogenesis Assay-Xenopus (FETAX) protocol. Diclofenac treatment exerted a teratogenic effect on Xenopus embryos with a teratogenic index (TI) value of 2.64 TI; if this value is higher than 1.2, the cut-off value indicative of toxicity. In particular, mortality of embryos treated with diclofenac increased in a concentration-dependent manner and a broad spectrum of malformations such as shortening and kinking of the axis, abdominal bulging, and prominent blister formation, was observed. The shape and length of internal organs also differed compared to the control group embryos and show developmental retardation on histological label. However, the expression of major tissue-specific markers did not change when analyzed by reverse transcription-polymerase chain reaction (RT-PCR). In conclusion, diclofenac treatment can promote teratogenicity that results in morphological anomalies, but not disrupt the developmental tissue arrangement during Xenopus embryogenesis. Copyright © 2014 Elsevier Ltd. All rights reserved. JF - Chemosphere AU - Chae, Jeong-Pil AU - Park, Mi Seon AU - Hwang, Yoo-Seok AU - Min, Byung-Hwa AU - Kim, Sang-Hyun AU - Lee, Hyun-Shik AU - Park, Mae-Ja AD - Department of Anatomy, College of Medicine, Kyungpook National University, Daegu 700-422, South Korea. ; Aquaculture Management Division, National Fisheries Research and Development Institute, Busan 619-705, South Korea. ; Laboratory of Cell and Developmental Signaling, National Cancer Institute-Frederick, Frederick, MD 21702, USA. ; Department of Pharmacology, College of Medicine, Kyungpook National University, Daegu 700-422, South Korea. ; ABRC, School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University, Daegu 702-701, South Korea. Electronic address: leeh@knu.ac.kr. ; Department of Anatomy, College of Medicine, Kyungpook National University, Daegu 700-422, South Korea. Electronic address: mjpark@knu.ac.kr. Y1 - 2015/02// PY - 2015 DA - February 2015 SP - 52 EP - 58 VL - 120 KW - Anti-Inflammatory Agents, Non-Steroidal KW - 0 KW - Teratogens KW - Diclofenac KW - 144O8QL0L1 KW - Index Medicus KW - Xenopus laevis KW - Teratogenicity KW - Embryotoxicity KW - FETAX KW - Animals KW - Reverse Transcriptase Polymerase Chain Reaction KW - Embryo, Nonmammalian -- drug effects KW - Female KW - Abnormalities, Drug-Induced -- pathology KW - Xenopus -- embryology KW - Diclofenac -- toxicity KW - Teratogens -- toxicity KW - Anti-Inflammatory Agents, Non-Steroidal -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1634271608?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemosphere&rft.atitle=Evaluation+of+developmental+toxicity+and+teratogenicity+of+diclofenac+using+Xenopus+embryos.&rft.au=Chae%2C+Jeong-Pil%3BPark%2C+Mi+Seon%3BHwang%2C+Yoo-Seok%3BMin%2C+Byung-Hwa%3BKim%2C+Sang-Hyun%3BLee%2C+Hyun-Shik%3BPark%2C+Mae-Ja&rft.aulast=Chae&rft.aufirst=Jeong-Pil&rft.date=2015-02-01&rft.volume=120&rft.issue=&rft.spage=52&rft.isbn=&rft.btitle=&rft.title=Chemosphere&rft.issn=1879-1298&rft_id=info:doi/10.1016%2Fj.chemosphere.2014.05.063 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-22 N1 - Date created - 2014-12-04 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.chemosphere.2014.05.063 ER - TY - JOUR T1 - Home kitchen ventilation, cooking fuels, and lung cancer risk in a prospective cohort of never smoking women in Shanghai, China. AN - 1625340229; 24917360 AB - Indoor air pollution (IAP) caused by cooking has been associated with lung cancer risk in retrospective case-control studies in developing and rural countries. We report the association of cooking conditions, fuel use, oil use, and risk of lung cancer in a developed urban population in a prospective cohort of women in Shanghai. A total of 71,320 never smoking women were followed from 1996 through 2009 and 429 incident lung cancer cases were identified. Questionnaires collected information on household living and cooking practices for the three most recent residences and utilization of cooking fuel and oil, and ventilation conditions. Cox proportional hazards regression estimated the association for kitchen ventilation conditions, cooking fuels, and use of cooking oils for the risk of lung cancer by hazard ratios (HR) with 95% confidence intervals (95% CI). Ever poor kitchen ventilation was associated with a 49% increase in lung cancer risk (HR: 1.49; 95% CI: 1.15-1.95) compared to never poor ventilation. Ever use of coal was not significantly associated. However, ever coal use with poor ventilation (HR: 1.69; 95% CI: 1.22-2.35) and 20 or more years of using coal with poor ventilation (HR: 2.03; 95% CI: 1.35-3.05) was significantly associated compared to no exposure to coal or poor ventilation. Cooking oil use was not significantly associated. These results demonstrate that IAP from poor ventilation of coal combustion increases the risk of lung cancer and is an important public health issue in cities across China where people may have lived in homes with inadequate kitchen ventilation. © 2014 UICC. JF - International journal of cancer AU - Kim, Christopher AU - Gao, Yu-Tang AU - Xiang, Yong-Bing AU - Barone-Adesi, Francesco AU - Zhang, Yawei AU - Hosgood, H Dean AU - Ma, Shuangge AU - Shu, Xiao-ou AU - Ji, Bu-Tian AU - Chow, Wong-Ho AU - Seow, Wei Jie AU - Bassig, Bryan AU - Cai, Qiuyin AU - Zheng, Wei AU - Rothman, Nathaniel AU - Lan, Qing AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD; School of Public Health, Yale University, New Haven, CT. Y1 - 2015/02/01/ PY - 2015 DA - 2015 Feb 01 SP - 632 EP - 638 VL - 136 IS - 3 KW - Coal KW - 0 KW - Index Medicus KW - ventilation KW - lung cancer KW - coal KW - Shanghai KW - never smoking KW - women KW - China KW - Risk KW - Prospective Studies KW - Ventilation KW - Humans KW - Cohort Studies KW - Adult KW - Aged KW - Middle Aged KW - Female KW - Proportional Hazards Models KW - Air Pollution, Indoor -- adverse effects KW - Lung Neoplasms -- etiology KW - Cooking UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1625340229?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+cancer&rft.atitle=Home+kitchen+ventilation%2C+cooking+fuels%2C+and+lung+cancer+risk+in+a+prospective+cohort+of+never+smoking+women+in+Shanghai%2C+China.&rft.au=Kim%2C+Christopher%3BGao%2C+Yu-Tang%3BXiang%2C+Yong-Bing%3BBarone-Adesi%2C+Francesco%3BZhang%2C+Yawei%3BHosgood%2C+H+Dean%3BMa%2C+Shuangge%3BShu%2C+Xiao-ou%3BJi%2C+Bu-Tian%3BChow%2C+Wong-Ho%3BSeow%2C+Wei+Jie%3BBassig%2C+Bryan%3BCai%2C+Qiuyin%3BZheng%2C+Wei%3BRothman%2C+Nathaniel%3BLan%2C+Qing&rft.aulast=Kim&rft.aufirst=Christopher&rft.date=2015-02-01&rft.volume=136&rft.issue=3&rft.spage=632&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.29020 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-23 N1 - Date created - 2014-11-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Br J Cancer. 1990 Dec;62(6):982-7 [2257230] Int J Epidemiol. 1991 Mar;20(1):26-31 [2066232] Mutat Res. 1992 Dec;298(2):105-11 [1282206] JAMA. 1994 Jun 8;271(22):1752-9 [8196118] J Natl Cancer Inst. 1995 Jun 7;87(11):836-41 [7791233] Int J Epidemiol. 1997 Feb;26(1):24-31 [9126500] BMJ. 1997 Oct 18;315(7114):980-8 [9365295] Mutat Res. 1997 Nov 28;381(2):157-61 [9434872] Environ Res. 1999 Jul;81(1):18-22 [10361022] Epidemiology. 1999 Sep;10(5):488-94 [10468420] Toxicol Appl Pharmacol. 2005 Aug 1;206(1):73-93 [15963346] Am J Epidemiol. 2005 Aug 15;162(4):326-33 [16014775] Toxicol Sci. 2005 Oct;87(2):337-43 [16014734] Cancer Causes Control. 2005 Nov;16(9):1085-90 [16184474] Am J Epidemiol. 2005 Dec 1;162(11):1123-31 [16236996] J Food Prot. 2006 Jan;69(1):199-204 [16416919] Cancer Res. 2006 May 1;66(9):4961-7 [16651454] BMJ. 2006 Aug 19;333(7564):376 [16837487] Environ Health Perspect. 2007 Jun;115(6):848-55 [17589590] Methods Mol Biol. 2009;472:397-411 [19107445] Occup Environ Med. 2009 Oct;66(10):672-8 [19625285] Eur Respir J. 2010 Mar;35(3):667-75 [19797125] Environ Mol Mutagen. 2010 May;51(4):315-21 [20143344] N Engl J Med. 2011 Jun 23;364(25):2469-70 [21696322] Proc Natl Acad Sci U S A. 2011 Jul 5;108(27):11028-33 [21690396] Int J Epidemiol. 2011 Jun;40(3):719-28 [21278196] BMJ. 2012;345:e5414 [22936785] Nat Genet. 2012 Dec;44(12):1330-5 [23143601] Am J Epidemiol. 2000 Jan 15;151(2):140-7 [10645816] BMJ. 2000 Aug 5;321(7257):323-9 [10926586] Cancer Epidemiol Biomarkers Prev. 2000 Nov;9(11):1215-21 [11097230] Lung Cancer. 2002 Feb;35(2):111-7 [11804682] J Natl Cancer Inst. 2002 Jun 5;94(11):826-35 [12048270] Environ Health Perspect. 2004 Jun;112(9):970-8 [15198916] Occup Environ Med. 2004 Oct;61(10):799-805 [15377764] Science. 1987 Jan 9;235(4785):217-20 [3798109] Int J Cancer. 1987 Nov 15;40(5):604-9 [2824385] Cancer Causes Control. 2013 Mar;24(3):439-50 [23314675] Am J Epidemiol. 2007 Mar 15;165(6):634-42 [17189590] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ijc.29020 ER - TY - JOUR T1 - Uncovering the polymerase-induced cytotoxicity of an oxidized nucleotide. AN - 1652423965; 25409153 AB - Oxidative stress promotes genomic instability and human diseases. A common oxidized nucleoside is 8-oxo-7,8-dihydro-2'-deoxyguanosine, which is found both in DNA (8-oxo-G) and as a free nucleotide (8-oxo-dGTP). Nucleotide pools are especially vulnerable to oxidative damage. Therefore cells encode an enzyme (MutT/MTH1) that removes free oxidized nucleotides. This cleansing function is required for cancer cell survival and to modulate Escherichia coli antibiotic sensitivity in a DNA polymerase (pol)-dependent manner. How polymerases discriminate between damaged and non-damaged nucleotides is not well understood. This analysis is essential given the role of oxidized nucleotides in mutagenesis, cancer therapeutics, and bacterial antibiotics. Even with cellular sanitizing activities, nucleotide pools contain enough 8-oxo-dGTP to promote mutagenesis. This arises from the dual coding potential where 8-oxo-dGTP(anti) base pairs with cytosine and 8-oxo-dGTP(syn) uses its Hoogsteen edge to base pair with adenine. Here we use time-lapse crystallography to follow 8-oxo-dGTP insertion opposite adenine or cytosine with human pol β, to reveal that insertion is accommodated in either the syn- or anti-conformation, respectively. For 8-oxo-dGTP(anti) insertion, a novel divalent metal relieves repulsive interactions between the adducted guanine base and the triphosphate of the oxidized nucleotide. With either templating base, hydrogen-bonding interactions between the bases are lost as the enzyme reopens after catalysis, leading to a cytotoxic nicked DNA repair intermediate. Combining structural snapshots with kinetic and computational analysis reveals how 8-oxo-dGTP uses charge modulation during insertion that can lead to a blocked DNA repair intermediate. JF - Nature AU - Freudenthal, Bret D AU - Beard, William A AU - Perera, Lalith AU - Shock, David D AU - Kim, Taejin AU - Schlick, Tamar AU - Wilson, Samuel H AD - Laboratory of Structural Biology, National Institute of Environmental Health Sciences, National Institutes of Health, PO Box 12233, Research Triangle Park, North Carolina 27709-2233, USA. ; 1] Department of Chemistry, New York University, and NYU-ECNU Center for Computational Chemistry at NYU Shanghai, 10th Floor Silver Center, 100 Washington Square East, New York, New York 10003, USA [2] Courant Institute of Mathematical Sciences, New York University, 251 Mercer Street, New York, New York 10012, USA. Y1 - 2015/01/29/ PY - 2015 DA - 2015 Jan 29 SP - 635 EP - 639 VL - 517 IS - 7536 KW - Cytotoxins KW - 0 KW - Deoxyguanine Nucleotides KW - 8-oxodeoxyguanosine triphosphate KW - 139307-94-1 KW - 8-hydroxyguanine KW - 5614-64-2 KW - Guanine KW - 5Z93L87A1R KW - Cytosine KW - 8J337D1HZY KW - DNA KW - 9007-49-2 KW - DNA Polymerase beta KW - EC 2.7.7.- KW - Adenine KW - JAC85A2161 KW - Index Medicus KW - Guanine -- chemistry KW - Humans KW - Catalytic Domain KW - DNA -- biosynthesis KW - Guanine -- metabolism KW - Neoplasms -- genetics KW - Cytosine -- metabolism KW - Oxidation-Reduction KW - Adenine -- metabolism KW - Oxidative Stress KW - DNA -- chemistry KW - Time Factors KW - Hydrogen Bonding KW - DNA Replication KW - DNA Repair KW - Neoplasms -- enzymology KW - Cytosine -- chemistry KW - Models, Molecular KW - Adenine -- chemistry KW - Static Electricity KW - Base Pairing KW - Kinetics KW - Guanine -- analogs & derivatives KW - Crystallography, X-Ray KW - Substrate Specificity KW - Molecular Conformation KW - Deoxyguanine Nucleotides -- chemistry KW - Cytotoxins -- chemistry KW - Cytotoxins -- metabolism KW - Deoxyguanine Nucleotides -- metabolism KW - Cytotoxins -- toxicity KW - DNA Damage KW - DNA Polymerase beta -- chemistry KW - Deoxyguanine Nucleotides -- toxicity KW - DNA Polymerase beta -- metabolism KW - Mutagenesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652423965?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature&rft.atitle=Uncovering+the+polymerase-induced+cytotoxicity+of+an+oxidized+nucleotide.&rft.au=Freudenthal%2C+Bret+D%3BBeard%2C+William+A%3BPerera%2C+Lalith%3BShock%2C+David+D%3BKim%2C+Taejin%3BSchlick%2C+Tamar%3BWilson%2C+Samuel+H&rft.aulast=Freudenthal&rft.aufirst=Bret&rft.date=2015-01-29&rft.volume=517&rft.issue=7536&rft.spage=635&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=1476-4687&rft_id=info:doi/10.1038%2Fnature13886 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-05-11 N1 - Date created - 2015-01-29 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - 4UAY; PDB; 4UAZ; 4UB1; 4UBC; 4UB2; 4UBB; 4UB3; 4UB4; 4UB5; 4UAW N1 - SuppNotes - Cited By: Mutagenesis. 2004 May;19(3):169-85 [15123782] Biochemistry. 2014 May 6;53(17):2768-80 [24717170] Proc Natl Acad Sci U S A. 1982 Apr;79(7):2211-5 [6954535] Proc Natl Acad Sci U S A. 1990 Jun;87(12):4533-7 [2352934] EMBO J. 1991 Jan;10(1):25-33 [1989886] Nature. 1991 Jan 31;349(6308):431-4 [1992344] Nucleic Acids Res. 1991 Apr 11;19(7):1407-12 [2027747] Methods Enzymol. 1995;262:98-107 [8594388] Biochemistry. 1997 Sep 16;36(37):11205-15 [9287163] Acta Crystallogr D Biol Crystallogr. 2004 Dec;60(Pt 12 Pt 1):2126-32 [15572765] J Comput Chem. 2005 Dec;26(16):1781-802 [16222654] Protein Sci. 2006 Jan;15(1):135-51 [16322565] Structure. 2006 Apr;14(4):757-66 [16615916] BMC Struct Biol. 2007;7:7 [17313689] J Mol Biol. 2007 Apr 13;367(5):1258-69 [17321545] Biochemistry. 2008 Jan 22;47(3):870-9 [18161950] Nucleic Acids Res. 2008 Apr;36(7):2174-81 [18276636] Hum Mol Genet. 2009 Nov 1;18(21):4102-17 [19643912] Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):213-21 [20124702] Nucleic Acids Res. 2010 May;38(9):2878-90 [20071746] Nat Struct Mol Biol. 2010 Jul;17(7):889-90 [20526335] Free Radic Biol Med. 2010 Dec 1;49(11):1603-16 [20840865] Science. 2012 Apr 20;336(6079):315-9 [22517853] Biochemistry. 2000 Feb 8;39(5):1029-33 [10653647] J Biol Chem. 2002 Mar 8;277(10):8235-42 [11756435] Curr Biol. 2002 Jun 4;12(11):912-8 [12062055] Carcinogenesis. 2002 Sep;23(9):1419-25 [12189182] Structure. 2003 May;11(5):489-96 [12737815] J Biol Chem. 2012 Jul 6;287(28):23830-9 [22577134] Nature. 2012 Jul 12;487(7406):196-201 [22785315] Nucleic Acids Res. 2013 Feb 1;41(3):1848-58 [23267011] Cell. 2013 Jul 3;154(1):157-68 [23827680] J Biol Chem. 2014 Feb 28;289(9):6289-98 [24425881] Biochemistry. 2014 Apr 8;53(13):2075-7 [24649945] Nature. 2014 Apr 10;508(7495):215-21 [24695224] Nature. 2014 Apr 10;508(7495):222-7 [24695225] J Biol Chem. 2004 Jul 23;279(30):31921-9 [15145936] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/nature13886 ER - TY - JOUR T1 - Natural variations of copper and sulfur stable isotopes in blood of hepatocellular carcinoma patients. AN - 1652422898; 25583489 AB - The widespread hypoxic conditions of the tumor microenvironment can impair the metabolism of bioessential elements such as copper and sulfur, notably by changing their redox state and, as a consequence, their ability to bind specific molecules. Because competing redox state is known to drive isotopic fractionation, we have used here the stable isotope compositions of copper ((65)Cu/(63)Cu) and sulfur ((34)S/(32)S) in the blood of patients with hepatocellular carcinoma (HCC) as a tool to explore the cancer-driven copper and sulfur imbalances. We report that copper is (63)Cu-enriched by ∼0.4‰ and sulfur is (32)S-enriched by ∼1.5‰ in the blood of patients compared with that of control subjects. As expected, HCC patients have more copper in red blood cells and serum compared with control subjects. However, the isotopic signature of this blood extra copper burden is not in favor of a dietary origin but rather suggests a reallocation in the body of copper bound to cysteine-rich proteins such as metallothioneins. The magnitude of the sulfur isotope effect is similar in red blood cells and serum of HCC patients, implying that sulfur fractionation is systemic. The (32)S-enrichment of sulfur in the blood of HCC patients is compatible with the notion that sulfur partly originates from tumor-derived sulfides. The measurement of natural variations of stable isotope compositions, using techniques developed in the field of Earth sciences, can provide new means to detect and quantify cancer metabolic changes and provide insights into underlying mechanisms. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Balter, Vincent AU - Nogueira da Costa, Andre AU - Bondanese, Victor Paky AU - Jaouen, Klervia AU - Lamboux, Aline AU - Sangrajrang, Suleeporn AU - Vincent, Nicolas AU - Fourel, François AU - Télouk, Philippe AU - Gigou, Michelle AU - Lécuyer, Christophe AU - Srivatanakul, Petcharin AU - Bréchot, Christian AU - Albarède, Francis AU - Hainaut, Pierre AD - UMR 5276, Laboratoire de Géologie de Lyon, École Normale Supérieure de Lyon, CNRS, Université de Lyon 1, BP 7000 Lyon, France; vincent.balter@ens-lyon.fr. ; Mechanistic Toxicology & Molecular Pathology Department of Non-Clinical Development, UCB BioPharma, SPRL Chemin du Foriest 1, B-1420 Braine L'Alleud, Belgium; ; UMR 5276, Laboratoire de Géologie de Lyon, École Normale Supérieure de Lyon, CNRS, Université de Lyon 1, BP 7000 Lyon, France; ; Department of Human Evolution, Max Planck Institute for Evolutionary Anthropology, 04103 Leipzig, Germany; ; National Cancer Institute, Bangkok 10400, Thailand; ; Unité 785, Pathogénèse et Traitement de l'Hépatite Fulminante et du Cancer du Foie, INSERM, Université Paris-Sud, 94800 Villejuif, France; ; UMR 5276, Laboratoire de Géologie de Lyon, École Normale Supérieure de Lyon, CNRS, Université de Lyon 1, BP 7000 Lyon, France; Institut Universitaire de France, 75005 Paris, France; ; Unité 785, Pathogénèse et Traitement de l'Hépatite Fulminante et du Cancer du Foie, INSERM, Université Paris-Sud, 94800 Villejuif, France; Institut Pasteur, 75015 Paris, France; ; Unité 823, Ontogenèse et Oncogenèse Moléculaire, Institut Albert Bonniot, INSERM, Université Joseph Fourier, 38706 Grenoble, France; and Strathclyde Institute of Global Public Health, International Prevention Research Institute, 69006 Lyon, France. Y1 - 2015/01/27/ PY - 2015 DA - 2015 Jan 27 SP - 982 EP - 985 VL - 112 IS - 4 KW - Sulfur Isotopes KW - 0 KW - Sulfur KW - 70FD1KFU70 KW - Copper KW - 789U1901C5 KW - Index Medicus KW - copper KW - sulfur KW - liver KW - stable isotopes KW - cancer KW - Sulfur Isotopes -- blood KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Male KW - Female KW - Tumor Microenvironment KW - Carcinoma, Hepatocellular -- blood KW - Sulfur -- blood KW - Copper -- blood KW - Liver Neoplasms -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652422898?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=Natural+variations+of+copper+and+sulfur+stable+isotopes+in+blood+of+hepatocellular+carcinoma+patients.&rft.au=Balter%2C+Vincent%3BNogueira+da+Costa%2C+Andre%3BBondanese%2C+Victor+Paky%3BJaouen%2C+Klervia%3BLamboux%2C+Aline%3BSangrajrang%2C+Suleeporn%3BVincent%2C+Nicolas%3BFourel%2C+Fran%C3%A7ois%3BT%C3%A9louk%2C+Philippe%3BGigou%2C+Michelle%3BL%C3%A9cuyer%2C+Christophe%3BSrivatanakul%2C+Petcharin%3BBr%C3%A9chot%2C+Christian%3BAlbar%C3%A8de%2C+Francis%3BHainaut%2C+Pierre&rft.aulast=Balter&rft.aufirst=Vincent&rft.date=2015-01-27&rft.volume=112&rft.issue=4&rft.spage=982&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=1091-6490&rft_id=info:doi/10.1073%2Fpnas.1415151112 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-23 N1 - Date created - 2015-01-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Eur J Biochem. 2000 Feb;267(4):1008-18 [10672009] Int J Cancer. 2015 Jan 1;136(1):172-81 [24803312] Annu Rev Biochem. 1975;44:147-59 [1094908] Cancer Res. 1981 Jul;41(7):2962-6 [7248954] Nature. 1983 Nov 17-23;306(5940):284-7 [6316150] Gynecol Obstet Invest. 1993;35(3):175-8 [8505012] Oncogene. 1995 Jan 5;10(1):27-32 [7824276] Nature. 1995 Aug 24;376(6542):660-9 [7651515] Blood. 2005 May 15;105(10):3812-6 [15665115] Science. 2007 Sep 14;317(5844):1534-7 [17872441] Nat Chem Biol. 2008 Mar;4(3):176-85 [18277979] Cancer Treat Rev. 2009 Feb;35(1):32-46 [18774652] Metallomics. 2011 Sep;3(9):926-33 [21789323] PLoS One. 2012;7(6):e37707 [22675488] Am J Phys Anthropol. 2012 Jul;148(3):334-40 [22576060] Proc Natl Acad Sci U S A. 2012 Jun 19;109(25):9989-94 [22652567] Nat Rev Cancer. 2013 Jun;13(6):425-31 [23660784] Metallomics. 2013 Aug;5(8):1016-24 [23727706] Proc Natl Acad Sci U S A. 2013 Jul 23;110(30):12474-9 [23836652] Metallomics. 2013 Nov;5(11):1470-82 [23963064] Proc Natl Acad Sci U S A. 2013 Nov 26;110(48):19507-12 [24218578] Am J Phys Anthropol. 2014 Feb;153(2):280-5 [24263674] Nature. 2014 May 22;509(7501):492-6 [24717435] Annu Rev Nutr. 2002;22:439-58 [12055353] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1073/pnas.1415151112 ER - TY - JOUR T1 - Griffithsin tandemers: flexible and potent lectin inhibitors of the human immunodeficiency virus. AN - 1680187434; 25613831 AB - The lectin griffithsin (GRFT) is a potent antiviral agent capable of prevention and treatment of infections caused by a number of enveloped viruses and is currently under development as an anti-HIV microbicide. In addition to its broad antiviral activity, GRFT is stable at high temperature and at a broad pH range, displays little toxicity and immunogenicity, and is amenable to large-scale manufacturing. Native GRFT is a domain-swapped homodimer that binds to viral envelope glycoproteins and has displayed mid-picomolar activity in cell-based anti-HIV assays. Previously, we have engineered and analyzed several monomeric forms of this lectin (mGRFT) with anti-HIV EC50 values ranging up to 323 nM. Based on our previous analysis of mGRFT, we hypothesized that the orientation and spacing of the carbohydrate binding domains GRFT were key to its antiviral activity. Here we present data on engineered tandem repeats of mGRFT (mGRFT tandemers) with antiviral activity at concentrations as low as one picomolar in whole-cell anti-HIV assays. mGRFT tandemers were analyzed thermodynamically, both individually and in complex with HIV-1 gp120. We also demonstrate by dynamic light scattering and cryo-electron microscopy that mGRFT tandemers do not aggregate HIV virions. This establishes that, although the intra-virion crosslinking of HIV envelope glycoproteins is likely integral to their activity, the antiviral activity of these lectins is not due to virus aggregation caused by inter-virion crosslinking. The engineered tandemer constructs of mGRFT may provide novel and powerful agents for prevention of infection by HIV and other enveloped viruses. JF - Retrovirology AU - Moulaei, Tinoush AU - Alexandre, Kabamba B AU - Shenoy, Shilpa R AU - Meyerson, Joel R AU - Krumpe, Lauren Rh AU - Constantine, Brian AU - Wilson, Jennifer AU - Buckheit, Robert W AU - McMahon, James B AU - Subramaniam, Sriram AU - Wlodawer, Alexander AU - O'Keefe, Barry R AD - Molecular Targets Laboratory, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702-1201, USA. tinoush@umd.edu. ; Molecular Targets Laboratory, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702-1201, USA. AAlexandre@csir.co.za. ; Molecular Targets Laboratory, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702-1201, USA. kuriansh@mail.nih.gov. ; Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892, USA. meyersonj@mail.nih.gov. ; Molecular Targets Laboratory, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702-1201, USA. Lauren.HaughKrumpe@nih.gov. ; Molecular Targets Laboratory, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702-1201, USA. brian.constantine@nih.gov. ; Molecular Targets Laboratory, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702-1201, USA. wilsonje@mail.nih.gov. ; Imquest BioSciences, Frederick, MD, 21704, USA. rbuckheit@imquestbio.com. ; Molecular Targets Laboratory, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702-1201, USA. mcmahon@ncifcrf.gov. ; Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892, USA. subramas@mail.nih.gov. ; Protein Structure Section, Macromolecular Crystallography Laboratory, National Cancer Institute at Frederick, Frederick, MD, 21702-1201, USA. wlodawer@nih.gov. ; Molecular Targets Laboratory, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, 21702-1201, USA. okeefeba@mail.nih.gov. Y1 - 2015/01/23/ PY - 2015 DA - 2015 Jan 23 SP - 6 VL - 12 KW - Antiviral Agents KW - 0 KW - Plant Lectins KW - Recombinant Proteins KW - griffithsin protein, Griffithsia KW - Index Medicus KW - Recombinant Proteins -- pharmacology KW - Models, Molecular KW - Humans KW - Recombinant Proteins -- chemistry KW - Microbial Sensitivity Tests KW - Cell Line KW - Protein Conformation KW - Plant Lectins -- pharmacology KW - Antiviral Agents -- pharmacology KW - Antiviral Agents -- chemistry KW - HIV-1 -- drug effects KW - Plant Lectins -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680187434?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Retrovirology&rft.atitle=Griffithsin+tandemers%3A+flexible+and+potent+lectin+inhibitors+of+the+human+immunodeficiency+virus.&rft.au=Moulaei%2C+Tinoush%3BAlexandre%2C+Kabamba+B%3BShenoy%2C+Shilpa+R%3BMeyerson%2C+Joel+R%3BKrumpe%2C+Lauren+Rh%3BConstantine%2C+Brian%3BWilson%2C+Jennifer%3BBuckheit%2C+Robert+W%3BMcMahon%2C+James+B%3BSubramaniam%2C+Sriram%3BWlodawer%2C+Alexander%3BO%27Keefe%2C+Barry+R&rft.aulast=Moulaei&rft.aufirst=Tinoush&rft.date=2015-01-23&rft.volume=12&rft.issue=&rft.spage=6&rft.isbn=&rft.btitle=&rft.title=Retrovirology&rft.issn=1742-4690&rft_id=info:doi/10.1186%2Fs12977-014-0127-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-15 N1 - Date created - 2015-05-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biochemistry. 2000 Sep 19;39(37):11194-204 [10985765] Acta Biochim Pol. 2006;53(4):617-26 [17128290] Nature. 2002 Dec 12;420(6916):678-82 [12478295] Nature. 2003 Mar 20;422(6929):307-12 [12646921] J Virol. 2003 Oct;77(19):10557-65 [12970440] Cell. 1986 Jun 6;45(5):637-48 [2423250] J Biol Chem. 1990 Jun 25;265(18):10373-82 [2355006] J Virol Methods. 1991 Jun;33(1-2):87-100 [1719015] J Virol. 1993 Jan;67(1):584-8 [8416385] J Gen Virol. 1995 Jun;76 ( Pt 6):1509-14 [7782780] Antivir Chem Chemother. 2007;18(1):1-11 [17354647] Protein Sci. 2007 Jul;16(7):1485-9 [17567736] J Struct Biol. 2008 Mar;161(3):260-75 [17855124] Antimicrob Agents Chemother. 2013 May;57(5):2076-86 [23403432] J Virol. 2013 Jun;87(11):6257-69 [23536670] Antimicrob Agents Chemother. 2013 Aug;57(8):3976-89 [23752505] Nat Struct Mol Biol. 2013 Dec;20(12):1352-7 [24154805] Antimicrob Agents Chemother. 2014;58(1):120-7 [24145548] Neonatology. 2008;93(4):288-94 [18525212] Nature. 2008 Sep 4;455(7209):109-13 [18668044] Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6099-104 [19332801] Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6029-30 [19357305] J Virol. 2010 Mar;84(5):2511-21 [20032190] Virology. 2010 Jun 20;402(1):187-96 [20392471] J Am Chem Soc. 2010 Jun 30;132(25):8682-9 [20524663] Structure. 2010 Sep 8;18(9):1104-15 [20826337] PLoS Pathog. 2010;6(12):e1001249 [21203482] Proc Natl Acad Sci U S A. 2011 Jul 12;108(28):11440-5 [21709254] PLoS One. 2011;6(8):e22635 [21829638] PLoS One. 2011;6(8):e23521 [21858152] Virology. 2011 Sep 1;417(2):253-8 [21802104] J Gen Virol. 2011 Oct;92(Pt 10):2367-73 [21715597] Antimicrob Agents Chemother. 2011 Nov;55(11):5159-67 [21896910] J Virol. 2011 Dec;85(23):12114-23 [21937655] PLoS Pathog. 2012;8(7):e1002797 [22807678] Mol Pharm. 2012 Sep 4;9(9):2613-25 [22827601] AIDS Res Hum Retroviruses. 2012 Nov;28(11):1513-23 [22607556] Proc Natl Acad Sci U S A. 2013 Jan 8;110(2):513-8 [23267106] Biochem J. 2002 May 15;364(Pt 1):173-80 [11988090] J Virol. 1996 Mar;70(3):1863-72 [8627711] J Struct Biol. 1996 Jan-Feb;116(1):71-6 [8742726] Adv Protein Chem. 1997;50:61-122 [9338079] Science. 1998 Jun 19;280(5371):1884-8 [9632381] Nature. 1998 Jun 18;393(6686):648-59 [9641677] Glycobiology. 2004 Dec;14(12):1229-46 [15175256] J Biol Chem. 2005 Mar 11;280(10):9345-53 [15613479] Structure. 2006 Jul;14(7):1127-35 [16843894] Arch Virol. 2013 Feb;158(2):349-58 [23053519] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1186/s12977-014-0127-3 ER - TY - JOUR T1 - Prolonged fasting identifies heat shock protein 10 as a Sirtuin 3 substrate: elucidating a new mechanism linking mitochondrial protein acetylation to fatty acid oxidation enzyme folding and function. AN - 1652429531; 25505263 AB - Although Sirtuin 3 (SIRT3), a mitochondrially enriched deacetylase and activator of fat oxidation, is down-regulated in response to high fat feeding, the rate of fatty acid oxidation and mitochondrial protein acetylation are invariably enhanced in this dietary milieu. These paradoxical data implicate that additional acetylation modification-dependent levels of regulation may be operational under nutrient excess conditions. Because the heat shock protein (Hsp) Hsp10-Hsp60 chaperone complex mediates folding of the fatty acid oxidation enzyme medium-chain acyl-CoA dehydrogenase, we tested whether acetylation-dependent mitochondrial protein folding contributes to this regulatory discrepancy. We demonstrate that Hsp10 is a functional SIRT3 substrate and that, in response to prolonged fasting, SIRT3 levels modulate mitochondrial protein folding. Acetyl mutagenesis of Hsp10 lysine 56 alters Hsp10-Hsp60 binding, conformation, and protein folding. Consistent with Hsp10-Hsp60 regulation of fatty acid oxidation enzyme integrity, medium-chain acyl-CoA dehydrogenase activity and fat oxidation are elevated by Hsp10 acetylation. These data identify acetyl modification of Hsp10 as a nutrient-sensing regulatory node controlling mitochondrial protein folding and metabolic function. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Lu, Zhongping AU - Chen, Yong AU - Aponte, Angel M AU - Battaglia, Valentina AU - Gucek, Marjan AU - Sack, Michael N AD - From the Cardiovascular and Pulmonary Branch and the Department of Biochemistry and Molecular Medicine, George Washington University, Washington, D. C. 20052, and the Veterans Affairs Medical Center, Washington, D. C. 20422 luz@gwu.edu. ; Proteomic Core Facility, NHLBI, National Institutes of Health, Bethesda, Maryland 20892. ; the Department of Biochemistry and Molecular Medicine, George Washington University, Washington, D. C. 20052, and the Veterans Affairs Medical Center, Washington, D. C. 20422. ; From the Cardiovascular and Pulmonary Branch and sackm@nih.gov. Y1 - 2015/01/23/ PY - 2015 DA - 2015 Jan 23 SP - 2466 EP - 2476 VL - 290 IS - 4 KW - Chaperonin 10 KW - 0 KW - Fatty Acids KW - Mitochondrial Proteins KW - Molecular Chaperones KW - Reactive Oxygen Species KW - Sirt3 protein, mouse KW - Sirtuin 3 KW - EC 3.5.1.- KW - Oxygen KW - S88TT14065 KW - Index Medicus KW - Sirtuin KW - Heat Shock Protein (HSP) KW - Protein Folding KW - Fatty Acid Oxidation KW - Mitochondria KW - SIRT3 KW - Reactive Oxygen Species -- metabolism KW - Animals KW - Oxygen -- metabolism KW - Mice KW - Mutagenesis KW - Fatty Acids -- metabolism KW - Mice, Knockout KW - Acetylation KW - Chromatography, Gel KW - Electrophoresis, Gel, Two-Dimensional KW - Mitochondria -- metabolism KW - Flow Cytometry KW - Gene Expression Regulation KW - Mitochondrial Proteins -- metabolism KW - Chaperonin 10 -- genetics KW - Chaperonin 10 -- metabolism KW - Sirtuin 3 -- metabolism KW - Fasting UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652429531?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Prolonged+fasting+identifies+heat+shock+protein+10+as+a+Sirtuin+3+substrate%3A+elucidating+a+new+mechanism+linking+mitochondrial+protein+acetylation+to+fatty+acid+oxidation+enzyme+folding+and+function.&rft.au=Lu%2C+Zhongping%3BChen%2C+Yong%3BAponte%2C+Angel+M%3BBattaglia%2C+Valentina%3BGucek%2C+Marjan%3BSack%2C+Michael+N&rft.aulast=Lu&rft.aufirst=Zhongping&rft.date=2015-01-23&rft.volume=290&rft.issue=4&rft.spage=2466&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.606228 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-21 N1 - Date created - 2015-01-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Diabetes. 2013 Oct;62(10):3404-17 [23835326] J Proteome Res. 2012 Mar 2;11(3):1633-43 [22309199] J Biol Chem. 2013 Nov 22;288(47):33837-47 [24121500] Mol Cell Biol. 2014 Feb;34(4):699-710 [24324009] Biochim Biophys Acta. 2014 Apr 4;1841(4):525-34 [24525425] Cell Metab. 2014 Aug 5;20(2):214-25 [24930971] Cardiovasc Res. 2014 Sep 1;103(4):485-97 [24966184] Science. 2009 Feb 20;323(5917):1063-6 [19229036] Curr Opin Lipidol. 2009 Apr;20(2):98-105 [19276888] Cell. 2009 May 1;137(3):560-70 [19410549] J Mol Cell Cardiol. 2009 Jun;46(6):842-9 [19217910] PLoS One. 2009;4(7):e6449 [19649258] Q Rev Biophys. 2009 May;42(2):83-116 [19638247] Endocr Rev. 2010 Feb;31(1):25-51 [19861693] Science. 2010 Feb 19;327(5968):1000-4 [20167786] Mol Genet Metab. 2003 Feb;78(2):112-8 [12618083] J Biol Chem. 2003 Apr 18;278(16):14543-9 [12578827] J Biol Chem. 1994 Feb 11;269(6):4401-8 [7905878] Proc Natl Acad Sci U S A. 1997 Aug 19;94(17):9011-6 [9256426] Proc Natl Acad Sci U S A. 2005 Mar 1;102(9):3242-7 [15728349] Mol Genet Metab. 2005 Aug;85(4):260-70 [15927499] J Clin Invest. 2006 Apr;116(4):1071-80 [16528409] Crit Rev Biochem Mol Biol. 2006 Jul-Aug;41(4):211-39 [16849107] Genes Dev. 2007 Sep 1;21(17):2172-81 [17785525] Cell Metab. 2008 Jan;7(1):45-56 [18177724] Cell Death Differ. 2009 Mar;16(3):449-64 [19023330] Oncogene. 2012 Mar 22;31(12):1546-57 [21841822] Cold Spring Harb Symp Quant Biol. 2011;76:175-82 [22096028] Essays Biochem. 2012;52:23-35 [22708561] Cold Spring Harb Perspect Biol. 2012 Dec;4(12). pii: a013102. doi: 10.1101/cshperspect.a013102 [23209156] Proc Natl Acad Sci U S A. 2013 Apr 16;110(16):6601-6 [23576753] Cell. 2013 Jun 6;153(6):1354-65 [23746846] Cell. 2013 Jul 18;154(2):430-41 [23870130] PLoS One. 2013;8(9):e73457 [24039949] Nature. 2010 Mar 4;464(7285):121-5 [20203611] J Cell Biochem. 2010 May;110(1):238-47 [20235147] Free Radic Biol Med. 2010 Oct 15;49(7):1230-7 [20647045] Biochem J. 2011 Feb 1;433(3):505-14 [21044047] Mol Cell. 2011 Jan 21;41(2):139-49 [21255725] Mol Cell. 2011 Jun 24;42(6):719-30 [21700219] Mol Cell. 2011 Jul 8;43(1):33-44 [21726808] EMBO Rep. 2011 Aug;12(8):840-6 [21720390] PLoS One. 2011;6(8):e24068 [21901160] Cell Stress Chaperones. 2011 Nov;16(6):633-40 [21717087] Proc Natl Acad Sci U S A. 2013 Nov 12;110(46):E4298-305 [24167279] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M114.606228 ER - TY - JOUR T1 - Epigenetic modification of histone 3 lysine 27: mediator subunit MED25 is required for the dissociation of polycomb repressive complex 2 from the promoter of cytochrome P450 2C9. AN - 1652429393; 25391650 AB - The Mediator complex is vital for the transcriptional regulation of eukaryotic genes. Mediator binds to nuclear receptors at target response elements and recruits chromatin-modifying enzymes and RNA polymerase II. Here, we examine the involvement of Mediator subunit MED25 in the epigenetic regulation of human cytochrome P450 2C9 (CYP2C9). MED25 is recruited to the CYP2C9 promoter through association with liver-enriched HNF4α, and we show that MED25 influences the H3K27 status of the HNF4α binding region. This region was enriched for the activating marker H3K27ac and histone acetyltransferase CREBBP after MED25 overexpression but was trimethylated when MED25 expression was silenced. The epigenetic regulator Polycomb repressive complex (PRC2), which represses expression by methylating H3K27, plays an important role in target gene regulation. Silencing MED25 correlated with increased association of PRC2 not only with the promoter region chromatin but with HNF4α itself. We confirmed the involvement of MED25 for fully functional preinitiation complex recruitment and transcriptional output in vitro. Formaldehyde-assisted isolation of regulatory elements (FAIRE) revealed chromatin conformation changes that were reliant on MED25, indicating that MED25 induced a permissive chromatin state that reflected increases in CYP2C9 mRNA. For the first time, we showed evidence that a functionally relevant human gene is transcriptionally regulated by HNF4α via MED25 and PRC2. CYP2C9 is important for the metabolism of many exogenous chemicals including pharmaceutical drugs as well as endogenous substrates. Thus, MED25 is important for regulating the epigenetic landscape resulting in transcriptional activation of a highly inducible gene, CYP2C9. © 2015 by The American Society for Biochemistry and Molecular Biology, Inc. JF - The Journal of biological chemistry AU - Englert, Neal A AU - Luo, George AU - Goldstein, Joyce A AU - Surapureddi, Sailesh AD - From the Laboratory of Toxicology and Pharmacology, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709. ; From the Laboratory of Toxicology and Pharmacology, NIEHS, National Institutes of Health, Research Triangle Park, North Carolina 27709 goldste1@niehs.nih.gov. Y1 - 2015/01/23/ PY - 2015 DA - 2015 Jan 23 SP - 2264 EP - 2278 VL - 290 IS - 4 KW - Chromatin KW - 0 KW - HNF4A protein, human KW - Hepatocyte Nuclear Factor 4 KW - Histones KW - MED25 protein, human KW - Mediator Complex KW - Nucleosomes KW - Formaldehyde KW - 1HG84L3525 KW - Jumonji Domain-Containing Histone Demethylases KW - EC 1.14.11.- KW - KDM6B protein, human KW - Cytochrome P-450 CYP2C9 KW - EC 1.14.13.- KW - Index Medicus KW - Histone Methylation KW - Drug Metabolism KW - Chromatin Modification KW - Nuclear Receptor KW - Epigenetics KW - Microscopy, Confocal KW - Animals KW - Promoter Regions, Genetic KW - Chromatin -- metabolism KW - Hep G2 Cells KW - Gene Silencing KW - Humans KW - Formaldehyde -- chemistry KW - Nucleosomes -- metabolism KW - Chromatin Immunoprecipitation KW - Mice KW - Protein Binding KW - Protein Conformation KW - Cytochrome P-450 CYP2C9 -- metabolism KW - Mediator Complex -- genetics KW - Histones -- metabolism KW - Mediator Complex -- metabolism KW - Jumonji Domain-Containing Histone Demethylases -- metabolism KW - Jumonji Domain-Containing Histone Demethylases -- genetics KW - Hepatocyte Nuclear Factor 4 -- metabolism KW - Epigenesis, Genetic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652429393?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+biological+chemistry&rft.atitle=Epigenetic+modification+of+histone+3+lysine+27%3A+mediator+subunit+MED25+is+required+for+the+dissociation+of+polycomb+repressive+complex+2+from+the+promoter+of+cytochrome+P450+2C9.&rft.au=Englert%2C+Neal+A%3BLuo%2C+George%3BGoldstein%2C+Joyce+A%3BSurapureddi%2C+Sailesh&rft.aulast=Englert&rft.aufirst=Neal&rft.date=2015-01-23&rft.volume=290&rft.issue=4&rft.spage=2264&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M114.579474 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-21 N1 - Date created - 2015-01-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Development. 2009 Sep;136(18):3131-41 [19700617] Mol Cancer Res. 2009 Dec;7(12):1937-45 [19934271] Nat Genet. 2010 Mar;42(3):255-9 [20118932] J Lipid Res. 2010 Apr;51(4):832-42 [19965590] Exp Biol Med (Maywood). 2010 Jan;235(1):32-9 [20404016] Nat Genet. 2010 Aug;42(8):722-6 [20601953] Nat Struct Mol Biol. 2010 Oct;17(10):1279-86 [20835241] Nat Rev Genet. 2010 Nov;11(11):761-72 [20940737] Cell. 2010 Oct 29;143(3):470-84 [21029866] Genes Dev. 2010 Dec 1;24(23):2615-20 [21123648] Nat Cell Biol. 2011 Jan;13(1):87-94 [21131960] Mol Cell Biol. 2011 Feb;31(3):466-81 [21135126] Cold Spring Harb Symp Quant Biol. 2010;75:11-22 [21502408] Cell. 2011 Jul 8;146(1):92-104 [21729782] Genome Res. 2011 Oct;21(10):1757-67 [21750106] Curr Opin Cell Biol. 2012 Jun;24(3):405-14 [22336329] Biochim Biophys Acta. 2012 Aug;1824(8):974-82 [22627143] J Biol Chem. 2012 Oct 19;287(43):35784-94 [22910904] Pharmacol Rep. 2012;64(4):927-39 [23087145] Genome Res. 2013 Jan;23(1):60-73 [22964890] Mol Pharmacol. 2013 Mar;83(3):709-18 [23295386] Mol Cell. 2013 Mar 7;49(5):808-24 [23473600] Pharmacol Ther. 2013 Apr;138(1):103-41 [23333322] Transcription. 2013 Jan-Feb;4(1):18-23 [23131664] Mol Pharmacol. 2000 Dec;58(6):1441-50 [11093784] Proc Natl Acad Sci U S A. 2002 Sep 3;99(18):11836-41 [12189208] Curr Drug Metab. 2002 Dec;3(6):561-97 [12369887] Mol Cell Biol. 2003 Sep;23(17):6229-42 [12917344] EMBO J. 2003 Oct 15;22(20):5323-35 [14532106] Mol Cell. 2004 Mar 26;13(6):887-93 [15053881] Mol Cell. 2004 Apr 23;14(2):183-93 [15099518] EMBO J. 2004 Oct 13;23(20):4061-71 [15385962] Nucleic Acids Res. 1983 Mar 11;11(5):1475-89 [6828386] EMBO J. 1999 Oct 1;18(19):5380-8 [10508170] Science. 2004 Nov 26;306(5701):1574-7 [15567868] Trends Biochem Sci. 2005 May;30(5):250-5 [15896743] J Pharmacol Exp Ther. 2005 Sep;314(3):1125-33 [15919766] Mol Pharmacol. 2005 Sep;68(3):747-57 [15933212] J Biol Chem. 2005 Sep 9;280(36):31686-98 [16006652] Cell. 2006 Apr 21;125(2):213-7 [16630806] Nature. 2006 Aug 17;442(7104):772-8 [16862119] BMC Genomics. 2006;7:181 [16854234] Mol Cell. 2007 Jul 6;27(1):121-33 [17612495] EMBO J. 2007 Aug 8;26(15):3545-57 [17641689] Drug Metab Dispos. 2007 Sep;35(9):1700-10 [17576804] Nat Genet. 2008 Jul;40(7):897-903 [18552846] Mol Pharmacol. 2008 Sep;74(3):913-23 [18552123] Nucleic Acids Res. 2009 Feb;37(3):778-92 [19074951] Nature. 2009 May 7;459(7243):108-12 [19295514] Pharmacogenomics. 2009 Jul;10(7):1067-76 [19604079] J Biol Chem. 2013 Mar 22;288(12):8332-41 [23362253] Mol Cell Biol. 2013 Jun;33(11):2202-11 [23530060] Genome Res. 2013 Jul;23(7):1130-41 [23570689] Mol Cell Biol. 2013 Sep;33(18):3594-610 [23836885] J Biol Chem. 2013 Sep 6;288(36):26179-87 [23864652] J Biol Chem. 2013 Sep 27;288(39):27898-911 [23943624] Nat Struct Mol Biol. 2013 Oct;20(10):1147-55 [24096405] Crit Rev Biochem Mol Biol. 2013 Nov-Dec;48(6):575-608 [24088064] Mol Cell. 2014 Jan 9;53(1):49-62 [24289921] Proc Natl Acad Sci U S A. 2014 Jan 28;111(4):1355-60 [24474760] Genome Biol. 2013;14(8):R91 [23987249] Genes Dev. 2000 Oct 1;14(19):2452-60 [11018013] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1074/jbc.M114.579474 ER - TY - JOUR T1 - Dual suppression of estrogenic and inflammatory activities for targeting of endometriosis. AN - 1652426310; 25609169 AB - Estrogenic and inflammatory components play key roles in a broad range of diseases including endometriosis, a common estrogen-dependent gynecological disorder in which endometrial tissue creates inflammatory lesions at extrauterine sites, causing pelvic pain and reduced fertility. Current medical therapies focus primarily on reducing systemic levels of estrogens, but these are of limited effectiveness and have considerable side effects. We developed estrogen receptor (ER) ligands, chloroindazole (CLI) and oxabicycloheptene sulfonate (OBHS), which showed strong ER-dependent anti-inflammatory activity in a preclinical model of endometriosis that recapitulates the estrogen dependence and inflammatory responses of the disease in immunocompetent mice and in primary human endometriotic stromal cells in culture. Estrogen-dependent phenomena, including cell proliferation, cyst formation, vascularization, and lesion growth, were all arrested by CLI or OBHS, which prevented lesion expansion and also elicited regression of established lesions, suppressed inflammation, angiogenesis, and neurogenesis in the lesions, and interrupted crosstalk between lesion cells and infiltrating macrophages. Studies in ERα or ERβ knockout mice indicated that ERα is the major mediator of OBHS effectiveness and ERβ is dominant in CLI actions, implying involvement of both ERs in endometriosis. Neither ligand altered estrous cycling or fertility at doses that were effective for suppression of endometriosis. Hence, CLI and OBHS are able to restrain endometriosis by dual suppression of the estrogen-inflammatory axis. Our findings suggest that these compounds have the desired characteristics of preventive and therapeutic agents for clinical endometriosis and possibly other estrogen-driven and inflammation-promoted disorders. Copyright © 2015, American Association for the Advancement of Science. JF - Science translational medicine AU - Zhao, Yuechao AU - Gong, Ping AU - Chen, Yiru AU - Nwachukwu, Jerome C AU - Srinivasan, Sathish AU - Ko, CheMyong AU - Bagchi, Milan K AU - Taylor, Robert N AU - Korach, Kenneth S AU - Nettles, Kendall W AU - Katzenellenbogen, John A AU - Katzenellenbogen, Benita S AD - Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA. ; Department of Cancer Biology, Scripps Research Institute, Jupiter, FL 33458, USA. ; Department of Comparative Biosciences, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA. ; Department of Obstetrics and Gynecology, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA. ; Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. ; Department of Chemistry, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA. ; Department of Molecular and Integrative Physiology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA. katzenel@illinois.edu. Y1 - 2015/01/21/ PY - 2015 DA - 2015 Jan 21 VL - 7 IS - 271 KW - Anti-Inflammatory Agents KW - 0 KW - Estrogens KW - Indazoles KW - Ligands KW - Nitriles KW - Receptors, Estrogen KW - Triazoles KW - letrozole KW - 7LKK855W8I KW - Index Medicus KW - Animals KW - Humans KW - Neurons -- drug effects KW - Disease Progression KW - Disease Models, Animal KW - Macrophages -- drug effects KW - Mice, Transgenic KW - Neurons -- pathology KW - Cell Survival -- drug effects KW - Treatment Outcome KW - Triazoles -- therapeutic use KW - Nitriles -- pharmacology KW - Triazoles -- pharmacology KW - Receptors, Estrogen -- metabolism KW - Nitriles -- therapeutic use KW - Drug Therapy, Combination KW - Embryonic Stem Cells -- metabolism KW - Embryonic Stem Cells -- drug effects KW - Macrophages -- pathology KW - Cells, Cultured KW - Stromal Cells -- drug effects KW - Mice, Inbred C57BL KW - Female KW - Fertility -- drug effects KW - Endometriosis -- pathology KW - Estrogens -- metabolism KW - Endometriosis -- prevention & control KW - Anti-Inflammatory Agents -- therapeutic use KW - Endometriosis -- drug therapy KW - Inflammation -- pathology KW - Anti-Inflammatory Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652426310?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+translational+medicine&rft.atitle=Dual+suppression+of+estrogenic+and+inflammatory+activities+for+targeting+of+endometriosis.&rft.au=Zhao%2C+Yuechao%3BGong%2C+Ping%3BChen%2C+Yiru%3BNwachukwu%2C+Jerome+C%3BSrinivasan%2C+Sathish%3BKo%2C+CheMyong%3BBagchi%2C+Milan+K%3BTaylor%2C+Robert+N%3BKorach%2C+Kenneth+S%3BNettles%2C+Kendall+W%3BKatzenellenbogen%2C+John+A%3BKatzenellenbogen%2C+Benita+S&rft.aulast=Zhao&rft.aufirst=Yuechao&rft.date=2015-01-21&rft.volume=7&rft.issue=271&rft.spage=271ra9&rft.isbn=&rft.btitle=&rft.title=Science+translational+medicine&rft.issn=1946-6242&rft_id=info:doi/10.1126%2Fscitranslmed.3010626 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-21 N1 - Date created - 2015-01-22 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: N Engl J Med. 2009 Jan 15;360(3):268-79 [19144942] Semin Reprod Med. 2012 Jan;30(1):39-45 [22271293] Endocrinology. 2012 Aug;153(8):3960-71 [22700766] Fertil Steril. 2012 Sep;98(3):520-8 [22771029] Nat Med. 2012 Jul;18(7):1102-11 [22660634] Endocrinology. 2013 Mar;154(3):1349-60 [23392257] Proc Natl Acad Sci U S A. 2013 Feb 26;110(9):3543-8 [23401502] PLoS One. 2013;8(5):e64049 [23691144] Hum Reprod Update. 2013 Jul-Aug;19(4):406-18 [23539633] Development. 2000 Oct;127(19):4277-91 [10976058] J Clin Endocrinol Metab. 2000 Feb;85(2):896-904 [10690908] Sci Transl Med. 2014 Feb 5;6(222):222ra16 [24500404] Fertil Steril. 2001 Mar;75(3):489-95 [11239529] Hum Reprod. 2002 Jul;17(7):1895-900 [12093857] J Clin Endocrinol Metab. 2002 Jul;87(7):3460-6 [12107266] Neurosci Lett. 2004 May 6;361(1-3):168-71 [15135920] Int J Fertil. 1988 Jan-Feb;33(1):48-51 [2896174] J Clin Endocrinol Metab. 1994 Mar;78(3):642-9 [8126136] J Clin Invest. 1996 Jul 15;98(2):482-9 [8755660] Hum Reprod. 1996 Oct;11(10):2269-75 [8943541] Am J Pathol. 2009 Aug;175(2):547-56 [19574425] J Clin Endocrinol Metab. 1997 May;82(5):1621-8 [9141560] Lancet. 2004 Nov 13-19;364(9447):1789-99 [15541453] J Med Chem. 2005 Feb 24;48(4):1132-44 [15715479] Hum Reprod. 2005 Apr;20(4):936-41 [15618247] Science. 2005 Jun 10;308(5728):1587-9 [15947176] J Med Chem. 2005 Nov 17;48(23):7261-74 [16279785] Hum Reprod Update. 2006 Jan-Feb;12(1):49-56 [16123052] Fertil Steril. 2006 May;85(5):1307-18 [16647373] Am J Pathol. 2006 Jun;168(6):2074-84 [16723720] Fertil Steril. 2007 Sep;88(3):581-7 [17412328] Endocrinology. 2008 Mar;149(3):1190-204 [18048499] Nat Chem Biol. 2008 Apr;4(4):241-7 [18344977] Pain. 2009 Dec 15;147(1-3):255-64 [19819623] Semin Reprod Med. 2010 Jan;28(1):36-43 [20104427] J Mol Med (Berl). 2010 Mar;88(3):223-5 [20174777] Fertil Steril. 2010 May 15;93(8):2513-8 [19819437] J Immunol. 2010 Jul 15;185(2):1169-76 [20554954] FASEB J. 2010 Dec;24(12):4660-7 [20667977] Annu Rev Physiol. 2011;73:163-82 [21054165] Gynecol Obstet Invest. 2011;71(2):112-7 [21150161] Cell. 2011 May 13;145(4):584-95 [21565615] Reprod Biol Endocrinol. 2011;9:89 [21693038] Endocrinology. 2011 Aug;152(8):3226-32 [21586552] J Immunol. 2011 Sep 1;187(5):2386-93 [21810607] Erratum In: Sci Transl Med. 2015 Feb 11;7(274):274er1 [25673758] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1126/scitranslmed.3010626 ER - TY - JOUR T1 - Trends in US newspaper and television coverage of tobacco AN - 1808660794; PQ0003458244 AB - PurposeThe news media plays an important role in agenda setting and framing of stories about tobacco control. The purpose of this study was to examine newspaper, newswire and television coverage of tobacco issues in the USA over a 7-year period.MethodsAnalyses of 2004-2010 news media surveillance system data from the US Centers for Disease Control and Prevention's Office on Smoking and Health, based on content analysis and quantitative methods. Information on extent of news coverage, and types of tobacco-related themes, were examined from articles in 10 newspapers and 2 major newswires, as well as transcripts from 6 national television networks.ResultsThe overall extent of newspaper, newswire and television stories about tobacco, and level of coverage by specific media outlets, varied over time, especially for newspapers. Nevertheless, there was an average of 3 newspaper stories, 4 newswire stories, and 1 television tobacco-related story each day. Television stories were more likely to contain cessation/addiction or health effects/statistics themes and less likely to contain secondhand smoke or policy/regulation themes than newspaper/newswire stories. There was more variation in the choice of tobacco theme among individual newspapers/newswires than television media outlets.ConclusionsNews coverage of tobacco in the USA was relatively constant from 2004 to 2010. Audiences were more likely to be exposed to different tobacco themes in newspapers/newswires than on television. Tracking information about tobacco news stories can be used by advocates, programs and others for planning and evaluation, and by researchers for hypothesis generation. JF - Tobacco Control AU - Nelson, David E AU - Pederson, Linda L AU - Mowery, Paul AU - Bailey, Sarah AU - Sevilimedu, Varadan AU - London, Joel AU - Babb, Stephen AU - Pechacek, Terry AD - Cancer Prevention Fellowship Program, Division of Cancer Prevention, National Cancer Institute, , Bethesda, Maryland, USA Y1 - 2015/01/17/ PY - 2015 DA - 2015 Jan 17 SP - 94 EP - 99 PB - BMJ Publishing Group Ltd. VL - 24 IS - 1 SN - 0964-4563, 0964-4563 KW - Toxicology Abstracts KW - Media KW - Prevention KW - Advertising and Promotion KW - Smoke KW - Smoking KW - Data processing KW - Tobacco KW - Statistical analysis KW - Disease control KW - Addiction KW - X 24380:Social Poisons & Drug Abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1808660794?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Tobacco+Control&rft.atitle=Trends+in+US+newspaper+and+television+coverage+of+tobacco&rft.au=Nelson%2C+David+E%3BPederson%2C+Linda+L%3BMowery%2C+Paul%3BBailey%2C+Sarah%3BSevilimedu%2C+Varadan%3BLondon%2C+Joel%3BBabb%2C+Stephen%3BPechacek%2C+Terry&rft.aulast=Nelson&rft.aufirst=David&rft.date=2015-01-17&rft.volume=24&rft.issue=1&rft.spage=94&rft.isbn=&rft.btitle=&rft.title=Tobacco+Control&rft.issn=09644563&rft_id=info:doi/10.1136%2Ftobaccocontrol-2013-050963 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-07-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Smoke; Smoking; Data processing; Disease control; Statistical analysis; Tobacco; Addiction DO - http://dx.doi.org/10.1136/tobaccocontrol-2013-050963 ER - TY - JOUR T1 - Vaccine-elicited CD4 T cells induce immunopathology after chronic LCMV infection. AN - 1652409238; 25593185 AB - CD4 T cells promote innate and adaptive immune responses, but how vaccine-elicited CD4 T cells contribute to immune protection remains unclear. We evaluated whether induction of virus-specific CD4 T cells by vaccination would protect mice against infection with chronic lymphocytic choriomeningitis virus (LCMV). Immunization with vaccines that selectively induced CD4 T cell responses resulted in catastrophic inflammation and mortality after challenge with a persistent strain of LCMV. Immunopathology required antigen-specific CD4 T cells and was associated with a cytokine storm, generalized inflammation, and multi-organ system failure. Virus-specific CD8 T cells or antibodies abrogated the pathology. These data demonstrate that vaccine-elicited CD4 T cells in the absence of effective antiviral immune responses can trigger lethal immunopathology. Copyright © 2015, American Association for the Advancement of Science. JF - Science (New York, N.Y.) AU - Penaloza-MacMaster, Pablo AU - Barber, Daniel L AU - Wherry, E John AU - Provine, Nicholas M AU - Teigler, Jeffrey E AU - Parenteau, Lily AU - Blackmore, Stephen AU - Borducchi, Erica N AU - Larocca, Rafael A AU - Yates, Kathleen B AU - Shen, Hao AU - Haining, W Nicholas AU - Sommerstein, Rami AU - Pinschewer, Daniel D AU - Ahmed, Rafi AU - Barouch, Dan H AD - Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. ; Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD 20892, USA. ; Department of Microbiology and Institute for Immunology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. ; Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA. ; Department of Pathology and Immunology, WHO Collaborating Centre for Vaccine Immunology, University of Geneva, 1211 Geneva, Switzerland. ; Department of Pathology and Immunology, WHO Collaborating Centre for Vaccine Immunology, University of Geneva, 1211 Geneva, Switzerland. Department of Biomedicine-Haus Petersplatz, Division of Experimental Virology, University of Basel, 4009 Basel, Switzerland. ; Emory Vaccine Center and Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322, USA. ; Center for Virology and Vaccine Research, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. Ragon Institute of MGH, MIT, and Harvard, Boston, MA 02114, USA. dbarouch@bidmc.harvard.edu. Y1 - 2015/01/16/ PY - 2015 DA - 2015 Jan 16 SP - 278 EP - 282 VL - 347 IS - 6219 KW - Antibodies, Viral KW - 0 KW - Antigens, Viral KW - Cytokines KW - Epitopes, T-Lymphocyte KW - Viral Vaccines KW - Index Medicus KW - Virus Replication KW - Cytokines -- blood KW - Animals KW - Adaptive Immunity KW - Epitopes, T-Lymphocyte -- immunology KW - Vaccination KW - Antibodies, Viral -- immunology KW - Multiple Organ Failure -- etiology KW - Viral Load KW - CD8-Positive T-Lymphocytes -- immunology KW - Antigens, Viral -- immunology KW - Immunologic Memory KW - Mice, Inbred C57BL KW - Lymphocytic choriomeningitis virus -- immunology KW - Viral Vaccines -- adverse effects KW - CD4-Positive T-Lymphocytes -- immunology KW - Viral Vaccines -- immunology KW - Immune System Diseases -- pathology KW - Immune System Diseases -- etiology KW - Lymphocytic choriomeningitis virus -- physiology KW - Arenaviridae Infections -- immunology KW - Arenaviridae Infections -- virology KW - Immune System Diseases -- immunology KW - Inflammation -- etiology KW - Inflammation -- immunology KW - Inflammation -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652409238?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28New+York%2C+N.Y.%29&rft.atitle=Vaccine-elicited+CD4+T+cells+induce+immunopathology+after+chronic+LCMV+infection.&rft.au=Penaloza-MacMaster%2C+Pablo%3BBarber%2C+Daniel+L%3BWherry%2C+E+John%3BProvine%2C+Nicholas+M%3BTeigler%2C+Jeffrey+E%3BParenteau%2C+Lily%3BBlackmore%2C+Stephen%3BBorducchi%2C+Erica+N%3BLarocca%2C+Rafael+A%3BYates%2C+Kathleen+B%3BShen%2C+Hao%3BHaining%2C+W+Nicholas%3BSommerstein%2C+Rami%3BPinschewer%2C+Daniel+D%3BAhmed%2C+Rafi%3BBarouch%2C+Dan+H&rft.aulast=Penaloza-MacMaster&rft.aufirst=Pablo&rft.date=2015-01-16&rft.volume=347&rft.issue=6219&rft.spage=278&rft.isbn=&rft.btitle=&rft.title=Science+%28New+York%2C+N.Y.%29&rft.issn=1095-9203&rft_id=info:doi/10.1126%2Fscience.aaa2148 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-26 N1 - Date created - 2015-01-16 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - GSE63825; GEO N1 - SuppNotes - Cited By: J Virol. 2003 Apr;77(8):4911-27 [12663797] Nature. 2003 Feb 20;421(6925):852-6 [12594515] Science. 2003 Apr 11;300(5617):339-42 [12690202] Science. 2003 Oct 24;302(5645):659-62 [14576438] J Virol. 2004 Apr;78(8):3811-6 [15047796] Nat Immunol. 2004 Sep;5(9):934-42 [15300247] Proc Natl Acad Sci U S A. 2004 Aug 31;101(35):13026-31 [15326293] Virology. 1983 Oct 15;130(1):247-51 [6636539] J Exp Med. 1984 Aug 1;160(2):521-40 [6332167] J Exp Med. 1988 May 1;167(5):1719-24 [3367096] J Virol. 1994 Jul;68(7):4700-4 [7911534] J Virol. 1994 Dec;68(12):8056-63 [7966595] Eur J Immunol. 1996 Feb;26(2):435-43 [8617315] J Exp Med. 1996 Sep 1;184(3):863-71 [9064346] Virology. 1997 Sep 1;235(2):286-92 [9281508] Nature. 2005 Mar 3;434(7029):88-93 [15744305] Nat Immunol. 2005 May;6(5):472-80 [15834410] Nat Med. 2005 Jul;11(7):748-56 [15951824] Proc Natl Acad Sci U S A. 2006 Mar 21;103(12):4663-8 [16537369] Nat Immunol. 2007 Feb;8(2):191-7 [17136045] Virology. 2007 Jun 20;363(1):113-23 [17320138] PLoS Comput Biol. 2007 Mar 23;3(3):e39 [17381235] Clin Cancer Res. 2007 Aug 1;13(15 Pt 1):4547-55 [17671141] Immunity. 2008 Apr;28(4):533-45 [18356084] J Virol. 2008 Dec;82(23):11734-41 [18829752] Immunity. 2009 Jan 16;30(1):155-67 [19144320] BMC Bioinformatics. 2009;10:48 [19192299] PLoS One. 2009;4(8):e6730 [19707583] J Immunol. 2010 Jul 1;185(1):190-202 [20525889] Nat Med. 2010 Oct;16(10):1147-51 [20890291] J Exp Med. 2011 May 9;208(5):987-99 [21536743] J Acquir Immune Defic Syndr. 2012 Jan 1;59(1):1-9 [21963936] Proc Natl Acad Sci U S A. 2011 Dec 27;108(52):21182-7 [22160724] Nature. 2012 Jan 19;481(7381):394-8 [22101430] Nat Med. 2013 Feb;19(2):143-9 [23389614] Methods Mol Biol. 2013;979:161-73 [23397395] Immunity. 2014 Feb 20;40(2):289-302 [24530057] Science. 2014 Apr 4;344(6179):49-51 [24700849] J Exp Med. 2014 Aug 25;211(9):1905-18 [25113973] Science. 2001 Mar 23;291(5512):2413-7 [11264538] J Virol. 2001 Nov;75(21):10421-30 [11581410] Science. 2003 Apr 11;300(5617):337-9 [12690201] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1126/science.aaa2148 ER - TY - JOUR T1 - Non-hematopoietic PAR-2 is essential for matriptase-driven pre-malignant progression and potentiation of ras-mediated squamous cell carcinogenesis. AN - 1652380655; 24469043 AB - The membrane-anchored serine protease, matriptase, is consistently dysregulated in a range of human carcinomas, and high matriptase activity correlates with poor prognosis. Furthermore, matriptase is unique among tumor-associated proteases in that epithelial stem cell expression of the protease suffices to induce malignant transformation. Here, we use genetic epistasis analysis to identify proteinase-activated receptor (PAR)-2-dependent inflammatory signaling as an essential component of matriptase-mediated oncogenesis. In cell-based assays, matriptase was a potent activator of PAR-2, and PAR-2 activation by matriptase caused robust induction of nuclear factor (NF)κB through Gαi. Importantly, genetic elimination of PAR-2 from mice completely prevented matriptase-induced pre-malignant progression, including inflammatory cytokine production, inflammatory cell recruitment, epidermal hyperplasia and dermal fibrosis. Selective ablation of PAR-2 from bone marrow-derived cells did not prevent matriptase-driven pre-malignant progression, indicating that matriptase activates keratinocyte stem cell PAR-2 to elicit its pro-inflammatory and pro-tumorigenic effects. When combined with previous studies, our data suggest that dual induction of PAR-2-NFκB inflammatory signaling and PI3K-Akt-mTor survival/proliferative signaling underlies the transforming potential of matriptase and may contribute to pro-tumorigenic signaling in human epithelial carcinogenesis. JF - Oncogene AU - Sales, K U AU - Friis, S AU - Konkel, J E AU - Godiksen, S AU - Hatakeyama, M AU - Hansen, K K AU - Rogatto, S R AU - Szabo, R AU - Vogel, L K AU - Chen, W AU - Gutkind, J S AU - Bugge, T H AD - 1] Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA [2] Clinical Research Core, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA. ; 1] Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA [2] Department of Cellular and Molecular Medicine, Faculty of Health and Medical Science, University of Copenhagen, Copenhagen, Denmark. ; Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA. ; 1] Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA [2] Department of Cellular and Molecular Medicine, Faculty of Health and Medical Science, University of Copenhagen, Copenhagen, Denmark [3] Department of Biology, Faculty of Science, University of Copenhagen, Copenhagen, Denmark. ; 1] Department of Urology, Faculty of Medicine, Sao Paulo State University (UNESP), Botucatu, Sao Paulo, Brazil [2] AC Camargo Cancer Center, Sao Paulo, Brazil. ; Department of Cellular and Molecular Medicine, Faculty of Health and Medical Science, University of Copenhagen, Copenhagen, Denmark. Y1 - 2015/01/15/ PY - 2015 DA - 2015 Jan 15 SP - 346 EP - 356 VL - 34 IS - 3 KW - Cytokines KW - 0 KW - NF-kappa B KW - Receptor, PAR-2 KW - Serine Endopeptidases KW - EC 3.4.21.- KW - matriptase KW - GTP-Binding Protein alpha Subunits, Gi-Go KW - EC 3.6.5.1 KW - ras Proteins KW - EC 3.6.5.2 KW - Index Medicus KW - Animals KW - GTP-Binding Protein alpha Subunits, Gi-Go -- metabolism KW - Cytokines -- genetics KW - GTP-Binding Protein alpha Subunits, Gi-Go -- genetics KW - HEK293 Cells KW - Humans KW - Disease Progression KW - Carcinoma, Squamous Cell -- metabolism KW - Cytokines -- metabolism KW - Precancerous Conditions -- metabolism KW - Reverse Transcriptase Polymerase Chain Reaction KW - Skin Neoplasms -- metabolism KW - Precancerous Conditions -- pathology KW - NF-kappa B -- genetics KW - Mice, Knockout KW - Skin Neoplasms -- genetics KW - Precancerous Conditions -- genetics KW - Cells, Cultured KW - Mice, Inbred C57BL KW - Carcinoma, Squamous Cell -- genetics KW - Keratinocytes -- metabolism KW - Immunohistochemistry KW - Cell Line KW - NF-kappa B -- metabolism KW - Epithelial Cells -- metabolism KW - ras Proteins -- genetics KW - Serine Endopeptidases -- metabolism KW - Serine Endopeptidases -- genetics KW - Epithelial Cells -- pathology KW - Cell Transformation, Neoplastic -- metabolism KW - Receptor, PAR-2 -- genetics KW - Receptor, PAR-2 -- metabolism KW - ras Proteins -- metabolism KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652380655?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Non-hematopoietic+PAR-2+is+essential+for+matriptase-driven+pre-malignant+progression+and+potentiation+of+ras-mediated+squamous+cell+carcinogenesis.&rft.au=Sales%2C+K+U%3BFriis%2C+S%3BKonkel%2C+J+E%3BGodiksen%2C+S%3BHatakeyama%2C+M%3BHansen%2C+K+K%3BRogatto%2C+S+R%3BSzabo%2C+R%3BVogel%2C+L+K%3BChen%2C+W%3BGutkind%2C+J+S%3BBugge%2C+T+H&rft.aulast=Sales&rft.aufirst=K&rft.date=2015-01-15&rft.volume=34&rft.issue=3&rft.spage=346&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2013.563 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-22 N1 - Date created - 2015-01-15 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Arterioscler Thromb Vasc Biol. 2007 Apr;27(4):769-75 [17255532] J Biol Chem. 2006 Oct 27;281(43):32095-112 [16885167] Semin Thromb Hemost. 2008 Mar;34(2):147-53 [18645919] J Biol Chem. 2008 Oct 24;283(43):29495-504 [18713750] Future Oncol. 2009 Feb;5(1):97-104 [19243302] J Exp Med. 2009 May 11;206(5):1135-47 [19414552] J Invest Dermatol. 2009 Jul;129(7):1816-23 [19242518] J Biol Chem. 2009 Aug 28;284(35):23177-81 [19487698] Carcinogenesis. 2009 Sep;30(9):1487-96 [19546160] Dev Cell. 2010 Jan 19;18(1):25-38 [20152175] Nat Rev Cancer. 2010 Apr;10(4):278-92 [20300104] Oncogene. 2011 Apr 28;30(17):2003-16 [21217780] Semin Immunopathol. 2012 Jan;34(1):133-49 [21971685] J Exp Med. 2012 Aug 27;209(9):1689-702 [22908325] PLoS Genet. 2012;8(8):e1002937 [22952456] Proc Natl Acad Sci U S A. 2013 Jan 2;110(1):93-8 [23248318] J Biol Chem. 2013 Jun 28;288(26):19028-39 [23673661] Proc Natl Acad Sci U S A. 2000 May 9;97(10):5255-60 [10805786] J Biol Chem. 2000 Aug 25;275(34):26333-42 [10831593] J Immunol. 2000 Dec 1;165(11):6504-10 [11086091] Am J Pathol. 2001 Apr;158(4):1301-11 [11290548] J Biol Chem. 2001 Aug 24;276(34):31657-66 [11413129] J Biol Chem. 2002 Mar 22;277(12):10539-46 [11792696] Clin Cancer Res. 2002 Apr;8(4):1101-7 [11948120] J Biol Chem. 2002 May 3;277(18):16081-7 [11850418] J Immunol. 2002 Nov 1;169(9):5315-21 [12391252] J Clin Invest. 2003 Jan;111(1):25-7 [12511583] Cancer Res. 2003 Mar 1;63(5):1101-5 [12615728] Expert Rev Mol Diagn. 2003 May;3(3):331-8 [12779007] J Invest Dermatol. 2003 Sep;121(3):529-41 [12925212] Am J Respir Cell Mol Biol. 2004 Apr;30(4):470-8 [14500256] Chest. 2004 May;125(5):1843-52 [15136399] J Invest Dermatol. 2004 May;122(5):1214-24 [15140225] Proc Natl Acad Sci U S A. 1994 Sep 27;91(20):9208-12 [7937743] Proc Natl Acad Sci U S A. 1995 Sep 26;92(20):9151-5 [7568091] J Biol Chem. 1996 Nov 15;271(46):29034-42 [8910556] J Biol Chem. 1997 Feb 14;272(7):4043-9 [9020112] Proc Assoc Am Physicians. 1997 Mar;109(2):190-207 [9069588] Immunology. 1998 Jul;94(3):356-62 [9767417] J Invest Dermatol. 2005 Jan;124(1):38-45 [15654951] Br J Cancer. 2005 Jan 31;92(2):278-83 [15611789] Biochem J. 2005 Jun 15;388(Pt 3):967-72 [15537383] Hum Pathol. 2005 Jun;36(6):626-33 [16021568] Genes Dev. 2005 Aug 15;19(16):1934-50 [16103220] Cell. 2006 Feb 10;124(3):631-44 [16469707] Mod Pathol. 2006 Mar;19(3):447-52 [16439987] Int J Surg Pathol. 2006 Jan;14(1):65-72 [16501837] Am J Pathol. 2006 May;168(5):1513-25 [16651618] BMC Cancer. 2006;6:176 [16820046] J Biol Chem. 2008 May 2;283(18):12293-304 [18308730] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/onc.2013.563 ER - TY - JOUR T1 - Translating bioinformatics in oncology: guilt-by-profiling analysis and identification of KIF18B and CDCA3 as novel driver genes in carcinogenesis. AN - 1645779288; 25236463 AB - Co-regulated genes are not identified in traditional microarray analyses, but may theoretically be closely functionally linked [guilt-by-association (GBA), guilt-by-profiling]. Thus, bioinformatics procedures for guilt-by-profiling/association analysis have yet to be applied to large-scale cancer biology. We analyzed 2158 full cancer transcriptomes from 163 diverse cancer entities in regard of their similarity of gene expression, using Pearson's correlation coefficient (CC). Subsequently, 428 highly co-regulated genes (|CC| ≥ 0.8) were clustered unsupervised to obtain small co-regulated networks. A major subnetwork containing 61 closely co-regulated genes showed highly significant enrichment of cancer bio-functions. All genes except kinesin family member 18B (KIF18B) and cell division cycle associated 3 (CDCA3) were of confirmed relevance for tumor biology. Therefore, we independently analyzed their differential regulation in multiple tumors and found severe deregulation in liver, breast, lung, ovarian and kidney cancers, thus proving our GBA hypothesis. Overexpression of KIF18B and CDCA3 in hepatoma cells and subsequent microarray analysis revealed significant deregulation of central cell cycle regulatory genes. Consistently, RT-PCR and proliferation assay confirmed the role of both genes in cell cycle progression. Finally, the prognostic significance of the identified KIF18B- and CDCA3-dependent predictors (P = 0.01, P = 0.04) was demonstrated in three independent HCC cohorts and several other tumors. In summary, we proved the efficacy of large-scale guilt-by-profiling/association strategies in oncology. We identified two novel oncogenes and functionally characterized them. The strong prognostic importance of downstream predictors for HCC and many other tumors indicates the clinical relevance of our findings. Supplementary data are available at Bioinformatics online. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. JF - Bioinformatics (Oxford, England) AU - Itzel, Timo AU - Scholz, Peter AU - Maass, Thorsten AU - Krupp, Markus AU - Marquardt, Jens U AU - Strand, Susanne AU - Becker, Diana AU - Staib, Frank AU - Binder, Harald AU - Roessler, Stephanie AU - Wang, Xin Wei AU - Thorgeirsson, Snorri AU - Müller, Martina AU - Galle, Peter R AU - Teufel, Andreas AD - Department of Medicine I, University of Regensburg, 93053, Regensburg, Department of Medicine I, Institute of Medical Biostatistics, Epidemiology and Informatics (IMBEI), University Medical Center, Johannes Gutenberg University, 55131, Mainz, Department of Pathology, University of Heidelberg, 69120, Germany and Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, 20892 MD, USA. Y1 - 2015/01/15/ PY - 2015 DA - 2015 Jan 15 SP - 216 EP - 224 VL - 31 IS - 2 KW - Biomarkers, Tumor KW - 0 KW - CDCA3 protein, human KW - Cell Cycle Proteins KW - KIF18B protein, human KW - EC 3.6.1.- KW - Kinesin KW - EC 3.6.4.4 KW - Index Medicus KW - Oligonucleotide Array Sequence Analysis KW - Humans KW - Liver Neoplasms -- mortality KW - Prognosis KW - Disease Progression KW - Cell Proliferation KW - Cell Cycle Proteins -- metabolism KW - Gene Expression Profiling KW - Liver Neoplasms -- pathology KW - Blotting, Western KW - Tumor Cells, Cultured KW - Survival Rate KW - Cell Cycle Proteins -- genetics KW - Carcinoma, Hepatocellular -- genetics KW - Carcinogenesis KW - Carcinoma, Hepatocellular -- pathology KW - Flow Cytometry KW - Tumor Stem Cell Assay KW - Cell Cycle KW - Carcinoma, Hepatocellular -- mortality KW - Liver Neoplasms -- genetics KW - Gene Expression Regulation, Neoplastic KW - Biomarkers, Tumor -- metabolism KW - Biomarkers, Tumor -- genetics KW - Neoplasms -- pathology KW - Neoplasms -- mortality KW - Computational Biology -- methods KW - Kinesin -- genetics KW - Kinesin -- metabolism KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645779288?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Bioinformatics+%28Oxford%2C+England%29&rft.atitle=Translating+bioinformatics+in+oncology%3A+guilt-by-profiling+analysis+and+identification+of+KIF18B+and+CDCA3+as+novel+driver+genes+in+carcinogenesis.&rft.au=Itzel%2C+Timo%3BScholz%2C+Peter%3BMaass%2C+Thorsten%3BKrupp%2C+Markus%3BMarquardt%2C+Jens+U%3BStrand%2C+Susanne%3BBecker%2C+Diana%3BStaib%2C+Frank%3BBinder%2C+Harald%3BRoessler%2C+Stephanie%3BWang%2C+Xin+Wei%3BThorgeirsson%2C+Snorri%3BM%C3%BCller%2C+Martina%3BGalle%2C+Peter+R%3BTeufel%2C+Andreas&rft.aulast=Itzel&rft.aufirst=Timo&rft.date=2015-01-15&rft.volume=31&rft.issue=2&rft.spage=216&rft.isbn=&rft.btitle=&rft.title=Bioinformatics+%28Oxford%2C+England%29&rft.issn=1367-4811&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbtu586 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-09 N1 - Date created - 2015-01-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nature. 2000 Feb 10;403(6770):601-3 [10688178] Genome Res. 2004 Jun;14(6):1085-94 [15173114] Nucleic Acids Res. 2001 Jan 1;29(1):152-5 [11125075] Yeast. 2001 Apr;18(6):523-31 [11284008] Nat Genet. 2002 Jul;31(3):255-65 [12089522] Bioinformatics. 2007 Jul 15;23(14):1846-7 [17496320] J Mol Diagn. 2003 May;5(2):73-81 [12707371] Curr Opin Struct Biol. 2003 Jun;13(3):370-6 [12831889] Gene. 2007 Oct 15;401(1-2):12-8 [17651921] Br J Cancer. 2008 Feb 12;98(3):523-8 [18231106] Front Biosci. 2008;13:4097-121 [18508502] Genome Biol. 2008;9 Suppl 1:S2 [18613946] Cancer Res. 2009 Jun 15;69(12):4974-82 [19509229] CA Cancer J Clin. 2009 Jul-Aug;59(4):225-49 [19474385] Int J Oncol. 2009 Dec;35(6):1257-64 [19885547] Hepatology. 2010 Apr;51(4):1401-9 [20054870] Gastroenterology. 2010 May;138(5):1920-30 [20100483] J Clin Epidemiol. 2010 Sep;63(9):945-9 [20573481] Cold Spring Harb Perspect Biol. 2010 Oct;2(10):a003236 [20719876] J Biol Chem. 1996 Aug 16;271(33):19935-42 [8702708] Science. 1996 Dec 6;274(5293):1672-7 [8939849] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981] BMC Bioinformatics. 2005;6:227 [16162296] Bioinformatics. 2005 Sep 1;21 Suppl 2:ii59-65 [16204126] BMC Genomics. 2010;11 Suppl 4:S19 [21143802] Nucleic Acids Res. 2011 Jan;39(Database issue):D1002-4 [21071405] J Surg Oncol. 2011 May 1;103(6):563-73 [21480251] BMC Med Genomics. 2011;4:53 [21718500] Biochem Biophys Res Commun. 2011 Sep 16;413(1):36-40 [21875573] Lab Invest. 2011 Nov;91(11):1634-42 [21876534] J Hepatol. 2012 Jan;56(1):267-75 [21782758] Nucleic Acids Res. 2012 Jan;40(Database issue):D13-25 [22140104] Nucleic Acids Res. 2013 Jan;41(Database issue):D991-5 [23193258] Cancer Res. 2010 Dec 15;70(24):10202-12 [21159642] Nat Biotechnol. 2003 Sep;21(9):1055-62 [12923548] Ann Med. 2003;35(6):391-7 [14572162] BMC Bioinformatics. 2003 Dec 10;4:61 [14667255] Cell. 2000 Jul 7;102(1):109-26 [10929718] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/bioinformatics/btu586 ER - TY - JOUR T1 - Activating mutations of STAT5B and STAT3 in lymphomas derived from γδ-T or NK cells. AN - 1652396527; 25586472 AB - Lymphomas arising from NK or γδ-T cells are very aggressive diseases and little is known regarding their pathogenesis. Here we report frequent activating mutations of STAT3 and STAT5B in NK/T-cell lymphomas (n=51), γδ-T-cell lymphomas (n=43) and their cell lines (n=9) through next generation and/or Sanger sequencing. STAT5B N642H is particularly frequent in all forms of γδ-T-cell lymphomas. STAT3 and STAT5B mutations are associated with increased phosphorylated protein and a growth advantage to transduced cell lines or normal NK cells. Growth-promoting activity of the mutants can be partially inhibited by a JAK1/2 inhibitor. Molecular modelling and surface plasmon resonance measurements of the N642H mutant indicate a marked increase in binding affinity of the phosphotyrosine-Y699 with the mutant histidine. This is associated with the prolonged persistence of the mutant phosphoSTAT5B and marked increase of binding to target sites. Our findings suggest that JAK-STAT pathway inhibition may represent a therapeutic strategy. JF - Nature communications AU - Küçük, Can AU - Jiang, Bei AU - Hu, Xiaozhou AU - Zhang, Wenyan AU - Chan, John K C AU - Xiao, Wenming AU - Lack, Nathan AU - Alkan, Can AU - Williams, John C AU - Avery, Kendra N AU - Kavak, Pınar AU - Scuto, Anna AU - Sen, Emel AU - Gaulard, Philippe AU - Staudt, Lou AU - Iqbal, Javeed AU - Zhang, Weiwei AU - Cornish, Adam AU - Gong, Qiang AU - Yang, Qunpei AU - Sun, Hong AU - d'Amore, Francesco AU - Leppä, Sirpa AU - Liu, Weiping AU - Fu, Kai AU - de Leval, Laurence AU - McKeithan, Timothy AU - Chan, Wing C AD - Department of Pathology, City of Hope Medical Center, Duarte, California 91010, USA. ; Department of Pathology, West China Hospital of Sichuan University, Chengdu 610041, China. ; Department of Pathology, Queen Elizabeth Hospital, Hong Kong, China. ; Division of Bioinformatics and Biostatistics, National Center for Toxicological Research, Food and Drug Administration, Maryland 20993, USA. ; Department of Pharmacology, Koc University, Istanbul 34450, Turkey. ; Department of Computer Engineering, Bilkent University, Ankara 06800, Turkey. ; Department of Molecular Medicine, Beckman Research Institute of City of Hope, Duarte, California 91010, USA. ; Department of Computer Engineering, Boğaziçi University, İstanbul 34342, Turkey. ; Département de Pathologie, Groupe Henri-Mondor Albert-Chenevier, Inserm U955, Université Paris Est, Créteil 94000, France. ; Molecular Biology of Lymphoid Malignancies Section, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892, USA. ; Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, Nebraska 68198-3135, USA. ; Department of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, Nebraska 68198-5805, USA. ; Beijing Institute of Genomics, Chinese Academy of Sciences, Beijing 100029, China. ; Department of Hematology, Aarhus University Hospital, Aarhus 8000, Denmark. ; Department of Oncology, Helsinki University Central Hospital, PO Box 180, Helsinki 00029, Finland. ; Pathologie Clinique Institut, Universitaire de Pathologie rue du Bugnon 25, CH 1011 Lausanne, Switzerland. Y1 - 2015/01/14/ PY - 2015 DA - 2015 Jan 14 SP - 6025 VL - 6 KW - IL2 protein, human KW - 0 KW - Interleukin-2 KW - Receptors, Antigen, T-Cell, gamma-delta KW - STAT3 Transcription Factor KW - STAT3 protein, human KW - STAT5 Transcription Factor KW - STAT5B protein, human KW - Phosphotyrosine KW - 21820-51-9 KW - Histidine KW - 4QD397987E KW - JAK1 protein, human KW - EC 2.7.10.2 KW - Janus Kinase 1 KW - Index Medicus KW - Histidine -- chemistry KW - Janus Kinase 1 -- metabolism KW - Interleukin-2 -- metabolism KW - Phosphotyrosine -- chemistry KW - Humans KW - HEK293 Cells KW - Receptors, Antigen, T-Cell, gamma-delta -- metabolism KW - Protein Structure, Tertiary KW - Mutation KW - Binding Sites KW - T-Lymphocyte Subsets -- cytology KW - Gene Expression Regulation, Neoplastic KW - STAT5 Transcription Factor -- genetics KW - STAT3 Transcription Factor -- genetics KW - Killer Cells, Natural -- cytology KW - Lymphoma, T-Cell -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652396527?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nature+communications&rft.atitle=Activating+mutations+of+STAT5B+and+STAT3+in+lymphomas+derived+from+%CE%B3%CE%B4-T+or+NK+cells.&rft.au=K%C3%BC%C3%A7%C3%BCk%2C+Can%3BJiang%2C+Bei%3BHu%2C+Xiaozhou%3BZhang%2C+Wenyan%3BChan%2C+John+K+C%3BXiao%2C+Wenming%3BLack%2C+Nathan%3BAlkan%2C+Can%3BWilliams%2C+John+C%3BAvery%2C+Kendra+N%3BKavak%2C+P%C4%B1nar%3BScuto%2C+Anna%3BSen%2C+Emel%3BGaulard%2C+Philippe%3BStaudt%2C+Lou%3BIqbal%2C+Javeed%3BZhang%2C+Weiwei%3BCornish%2C+Adam%3BGong%2C+Qiang%3BYang%2C+Qunpei%3BSun%2C+Hong%3Bd%27Amore%2C+Francesco%3BLepp%C3%A4%2C+Sirpa%3BLiu%2C+Weiping%3BFu%2C+Kai%3Bde+Leval%2C+Laurence%3BMcKeithan%2C+Timothy%3BChan%2C+Wing+C&rft.aulast=K%C3%BC%C3%A7%C3%BCk&rft.aufirst=Can&rft.date=2015-01-14&rft.volume=6&rft.issue=&rft.spage=6025&rft.isbn=&rft.btitle=&rft.title=Nature+communications&rft.issn=2041-1723&rft_id=info:doi/10.1038%2Fncomms7025 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-08 N1 - Date created - 2015-01-14 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - SRA200820; SRA N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/ncomms7025 ER - TY - CPAPER T1 - Mechanisms of Ibrutinib Resistance in the Aggressive, ABC-subtype of Diffuse Large B Cell Lymphoma: PI3K and Pathways to new Therapeutic Options T2 - 2015 Keystone Symposia on PI 3-Kinase Signaling Pathways in Disease AN - 1658697759; 6335120 JF - 2015 Keystone Symposia on PI 3-Kinase Signaling Pathways in Disease AU - Shaffer III, Arthur Y1 - 2015/01/13/ PY - 2015 DA - 2015 Jan 13 KW - B-cell lymphoma KW - 1-Phosphatidylinositol 3-kinase KW - Lymphoma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658697759?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Keystone+Symposia+on+PI+3-Kinase+Signaling+Pathways+in+Disease&rft.atitle=Mechanisms+of+Ibrutinib+Resistance+in+the+Aggressive%2C+ABC-subtype+of+Diffuse+Large+B+Cell+Lymphoma%3A+PI3K+and+Pathways+to+new+Therapeutic+Options&rft.au=Shaffer+III%2C+Arthur&rft.aulast=Shaffer+III&rft.aufirst=Arthur&rft.date=2015-01-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Keystone+Symposia+on+PI+3-Kinase+Signaling+Pathways+in+Disease&rft.issn=&rft_id=info:doi/ L2 - https://www.keystonesymposia.org/index.cfm?e=Web.Meeting.Program&meetingid=1310&subTab=program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-28 N1 - Last updated - 2015-02-27 ER - TY - CPAPER T1 - Lymphoproliferation and CD8 T Cell Senescence in Primary Human Immunodeficiencies caused by Gene Mutations that Activate PI3K Signaling T2 - 2015 Keystone Symposia on PI 3-Kinase Signaling Pathways in Disease AN - 1658696143; 6335132 JF - 2015 Keystone Symposia on PI 3-Kinase Signaling Pathways in Disease AU - Lucas, Carrie Y1 - 2015/01/13/ PY - 2015 DA - 2015 Jan 13 KW - 1-Phosphatidylinositol 3-kinase KW - Point mutation KW - Immunodeficiency KW - Lymphocytes T KW - Senescence KW - CD8 antigen UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658696143?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=2015+Keystone+Symposia+on+PI+3-Kinase+Signaling+Pathways+in+Disease&rft.atitle=Lymphoproliferation+and+CD8+T+Cell+Senescence+in+Primary+Human+Immunodeficiencies+caused+by+Gene+Mutations+that+Activate+PI3K+Signaling&rft.au=Lucas%2C+Carrie&rft.aulast=Lucas&rft.aufirst=Carrie&rft.date=2015-01-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2015+Keystone+Symposia+on+PI+3-Kinase+Signaling+Pathways+in+Disease&rft.issn=&rft_id=info:doi/ L2 - https://www.keystonesymposia.org/index.cfm?e=Web.Meeting.Program&meetingid=1310&subTab=program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-28 N1 - Last updated - 2015-02-27 ER - TY - JOUR T1 - miR-155 augments CD8+ T-cell antitumor activity in lymphoreplete hosts by enhancing responsiveness to homeostatic γc cytokines. AN - 1652401814; 25548153 AB - Lymphodepleting regimens are used before adoptive immunotherapy to augment the antitumor efficacy of transferred T cells by removing endogenous homeostatic "cytokine sinks." These conditioning modalities, however, are often associated with severe toxicities. We found that microRNA-155 (miR-155) enabled tumor-specific CD8(+) T cells to mediate profound antitumor responses in lymphoreplete hosts that were not potentiated by immune-ablation. miR-155 enhanced T-cell responsiveness to limited amounts of homeostatic γc cytokines, resulting in delayed cellular contraction and sustained cytokine production. miR-155 restrained the expression of the inositol 5-phosphatase Ship1, an inhibitor of the serine-threonine protein kinase Akt, and multiple negative regulators of signal transducer and activator of transcription 5 (Stat5), including suppressor of cytokine signaling 1 (Socs1) and the protein tyrosine phosphatase Ptpn2. Expression of constitutively active Stat5a recapitulated the survival advantages conferred by miR-155, whereas constitutive Akt activation promoted sustained effector functions. Our results indicate that overexpression of miR-155 in tumor-specific T cells can be used to increase the effectiveness of adoptive immunotherapies in a cell-intrinsic manner without the need for life-threatening, lymphodepleting maneuvers. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Ji, Yun AU - Wrzesinski, Claudia AU - Yu, Zhiya AU - Hu, Jinhui AU - Gautam, Sanjivan AU - Hawk, Nga V AU - Telford, William G AU - Palmer, Douglas C AU - Franco, Zulmarie AU - Sukumar, Madhusudhanan AU - Roychoudhuri, Rahul AU - Clever, David AU - Klebanoff, Christopher A AU - Surh, Charles D AU - Waldmann, Thomas A AU - Restifo, Nicholas P AU - Gattinoni, Luca AD - Experimental Transplantation and Immunology Branch and tawald@helix.nih.gov jiyun@mail.nih.gov gattinol@mail.nih.gov. ; Surgery Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892; ; Experimental Transplantation and Immunology Branch and. ; Academy of Immunology and Microbiology (AIM), Institute for Basic Science (IBS), Pohang, 790-784, Korea; and. ; Lymphoid Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 tawald@helix.nih.gov jiyun@mail.nih.gov gattinol@mail.nih.gov. Y1 - 2015/01/13/ PY - 2015 DA - 2015 Jan 13 SP - 476 EP - 481 VL - 112 IS - 2 KW - Cytokines KW - 0 KW - MicroRNAs KW - Mirn155 microRNA, mouse KW - STAT5 Transcription Factor KW - Stat5a protein, mouse KW - gp100 Melanoma Antigen KW - Proto-Oncogene Proteins c-akt KW - EC 2.7.11.1 KW - Index Medicus KW - microRNA-155 KW - lymphodepletion KW - homeostatic cytokines KW - adoptive immunotherapy KW - STAT5 Transcription Factor -- metabolism KW - Proto-Oncogene Proteins c-akt -- metabolism KW - Animals KW - HEK293 Cells KW - Humans KW - Cell Line, Tumor KW - Mice KW - Mice, Transgenic KW - Melanoma, Experimental -- immunology KW - Melanoma, Experimental -- therapy KW - Mice, Knockout KW - Base Sequence KW - gp100 Melanoma Antigen -- immunology KW - gp100 Melanoma Antigen -- genetics KW - Immunotherapy, Adoptive KW - Mice, Inbred C57BL KW - Melanoma, Experimental -- genetics KW - Signal Transduction KW - MicroRNAs -- metabolism KW - MicroRNAs -- immunology KW - MicroRNAs -- genetics KW - CD8-Positive T-Lymphocytes -- immunology KW - Cytokines -- biosynthesis KW - Cytokines -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652401814?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.atitle=miR-155+augments+CD8%2B+T-cell+antitumor+activity+in+lymphoreplete+hosts+by+enhancing+responsiveness+to+homeostatic+%CE%B3c+cytokines.&rft.au=Ji%2C+Yun%3BWrzesinski%2C+Claudia%3BYu%2C+Zhiya%3BHu%2C+Jinhui%3BGautam%2C+Sanjivan%3BHawk%2C+Nga+V%3BTelford%2C+William+G%3BPalmer%2C+Douglas+C%3BFranco%2C+Zulmarie%3BSukumar%2C+Madhusudhanan%3BRoychoudhuri%2C+Rahul%3BClever%2C+David%3BKlebanoff%2C+Christopher+A%3BSurh%2C+Charles+D%3BWaldmann%2C+Thomas+A%3BRestifo%2C+Nicholas+P%3BGattinoni%2C+Luca&rft.aulast=Ji&rft.aufirst=Yun&rft.date=2015-01-13&rft.volume=112&rft.issue=2&rft.spage=476&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences+of+the+United+States+of+America&rft.issn=1091-6490&rft_id=info:doi/10.1073%2Fpnas.1422916112 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-30 N1 - Date created - 2015-01-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Res. 2012 Apr 15;72(8):1986-95 [22367213] Nat Immunol. 2011 Dec;12(12):1230-7 [22057288] Blood. 2012 Jun 14;119(24):5688-96 [22555974] Cell Rep. 2012 Dec 27;2(6):1697-709 [23200854] Immunol Rev. 2013 May;253(1):146-57 [23550644] Immunity. 2013 Apr 18;38(4):742-53 [23601686] Nat Immunol. 2013 Jun;14(6):593-602 [23603793] Cell Cycle. 2013 Jun 15;12(12):1939-47 [23676217] Immunity. 2013 Jul 25;39(1):49-60 [23890063] Nat Commun. 2014;5:3073 [24445916] J Exp Med. 2003 Aug 18;198(4):569-80 [12925674] J Immunol. 2005 Mar 1;174(5):2591-601 [15728465] J Clin Oncol. 2005 Apr 1;23(10):2346-57 [15800326] J Exp Med. 2005 Oct 3;202(7):907-12 [16203864] Nat Rev Immunol. 2006 May;6(5):383-93 [16622476] Proc Natl Acad Sci U S A. 2006 May 2;103(18):7024-9 [16641092] Nat Clin Pract Oncol. 2006 Dec;3(12):668-81 [17139318] J Clin Invest. 2007 Feb;117(2):492-501 [17273561] Science. 2007 Apr 27;316(5824):608-11 [17463290] J Clin Invest. 2007 Aug;117(8):2197-204 [17657310] Immunity. 2007 Dec;27(6):847-59 [18055230] J Immunother. 2008 Jul-Aug;31(6):569-76 [18528297] J Clin Oncol. 2008 Nov 10;26(32):5233-9 [18809613] Immunity. 2009 Jan 16;30(1):80-91 [19144316] Cell. 2009 Jan 23;136(2):215-33 [19167326] Proc Natl Acad Sci U S A. 2009 Apr 28;106(17):7113-8 [19359473] Nat Med. 2009 Jul;15(7):808-13 [19525962] Blood. 2009 Oct 1;114(14):2888-99 [19589923] J Immunother. 2010 Jan;33(1):1-7 [19952961] Nat Rev Immunol. 2010 Feb;10(2):111-22 [20098459] Nat Genet. 2010 Jun;42(6):530-5 [20473312] Cancer Res. 2010 Sep 1;70(17):6725-34 [20647327] Proc Natl Acad Sci U S A. 2010 Sep 21;107(38):16601-6 [20823247] Immunity. 2010 Oct 29;33(4):607-19 [20888269] Mol Ther. 2011 Apr;19(4):751-9 [21285960] Clin Cancer Res. 2011 Jul 1;17(13):4550-7 [21498393] Sci Transl Med. 2011 Aug 10;3(95):95ra73 [21832238] Curr Opin Immunol. 2011 Oct;23(5):598-604 [21889323] N Engl J Med. 2011 Nov 3;365(18):1673-83 [22047558] Blood. 2012 May 3;119(18):4133-41 [22354001] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1073/pnas.1422916112 ER - TY - JOUR T1 - A flexible reporter system for direct observation and isolation of cancer stem cells. AN - 1652397385; 25497455 AB - Many tumors are hierarchically organized with a minority cell population that has stem-like properties and enhanced ability to initiate tumorigenesis and drive therapeutic relapse. These cancer stem cells (CSCs) are typically identified by complex combinations of cell-surface markers that differ among tumor types. Here, we developed a flexible lentiviral-based reporter system that allows direct visualization of CSCs based on functional properties. The reporter responds to the core stem cell transcription factors OCT4 and SOX2, with further selectivity and kinetic resolution coming from use of a proteasome-targeting degron. Cancer cells marked by this reporter have the expected properties of self-renewal, generation of heterogeneous offspring, high tumor- and metastasis-initiating activity, and resistance to chemotherapeutics. With this approach, the spatial distribution of CSCs can be assessed in settings that retain microenvironmental and structural cues, and CSC plasticity and response to therapeutics can be monitored in real time. Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved. JF - Stem cell reports AU - Tang, Binwu AU - Raviv, Asaf AU - Esposito, Dominic AU - Flanders, Kathleen C AU - Daniel, Catherine AU - Nghiem, Bao Tram AU - Garfield, Susan AU - Lim, Langston AU - Mannan, Poonam AU - Robles, Ana I AU - Smith, William I AU - Zimmerberg, Joshua AU - Ravin, Rea AU - Wakefield, Lalage M AD - Laboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, MD 20892, USA. ; Protein Expression Laboratory, Advanced Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD 21701, USA. ; Confocal Microscopy Core, National Cancer Institute, Bethesda, MD 20892, USA. ; Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD 20892 USA. ; Department of Pathology, Suburban Hospital, Bethesda, MD 20814, USA. ; Program in Physical Biology, National Institute of Child Health and Human Development, Bethesda, MD 20892, USA. ; Laboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, MD 20892, USA. Electronic address: lw34g@nih.gov. Y1 - 2015/01/13/ PY - 2015 DA - 2015 Jan 13 SP - 155 EP - 169 VL - 4 IS - 1 KW - Antineoplastic Agents KW - 0 KW - Transcription Factors KW - Index Medicus KW - Heterografts KW - Asymmetric Cell Division KW - Animals KW - Embryonic Stem Cells -- cytology KW - Transcription Factors -- metabolism KW - Cell Tracking KW - Humans KW - Cell Differentiation KW - Mice KW - Cell Line, Tumor KW - Cell Movement -- genetics KW - Protein Binding KW - Gene Order KW - Phenotype KW - Promoter Regions, Genetic KW - Embryonic Stem Cells -- metabolism KW - Tumor Cells, Cultured KW - Genetic Vectors KW - Drug Resistance, Neoplasm -- genetics KW - Response Elements KW - Immunophenotyping KW - Antineoplastic Agents -- pharmacology KW - Cell Transformation, Neoplastic -- genetics KW - Neoplastic Stem Cells -- pathology KW - Genes, Reporter KW - Gene Expression KW - Neoplastic Stem Cells -- metabolism KW - Neoplastic Stem Cells -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652397385?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+cell+reports&rft.atitle=A+flexible+reporter+system+for+direct+observation+and+isolation+of+cancer+stem+cells.&rft.au=Tang%2C+Binwu%3BRaviv%2C+Asaf%3BEsposito%2C+Dominic%3BFlanders%2C+Kathleen+C%3BDaniel%2C+Catherine%3BNghiem%2C+Bao+Tram%3BGarfield%2C+Susan%3BLim%2C+Langston%3BMannan%2C+Poonam%3BRobles%2C+Ana+I%3BSmith%2C+William+I%3BZimmerberg%2C+Joshua%3BRavin%2C+Rea%3BWakefield%2C+Lalage+M&rft.aulast=Tang&rft.aufirst=Binwu&rft.date=2015-01-13&rft.volume=4&rft.issue=1&rft.spage=155&rft.isbn=&rft.btitle=&rft.title=Stem+cell+reports&rft.issn=2213-6711&rft_id=info:doi/10.1016%2Fj.stemcr.2014.11.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-23 N1 - Date created - 2015-01-17 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Protein Eng. 1999 Dec;12(12):1035-40 [10611396] Cell. 2013 Jan 17;152(1-2):25-38 [23273993] J Clin Invest. 2003 Oct;112(7):1116-24 [14523048] Cancer Res. 1988 Apr 15;48(8):1996-2004 [2450643] J Biol Chem. 1998 Dec 25;273(52):34970-5 [9857028] Mol Cell Biol. 2005 Mar;25(6):2475-85 [15743839] Cell. 2005 May 6;121(3):465-77 [15882627] Nat Rev Cancer. 2005 Sep;5(9):744-9 [16148886] Cancer Res. 2005 Oct 1;65(19):8944-50 [16204067] PLoS Biol. 2007 May;5(5):e102 [17439301] Genes Dev. 2007 Dec 15;21(24):3238-43 [18079172] Cell Cycle. 2008 Mar 15;7(6):725-8 [18239456] Nat Genet. 2008 May;40(5):499-507 [18443585] Cell. 2008 May 16;133(4):704-15 [18485877] Breast Cancer Res. 2008;10(2):R25 [18366788] Cell Stem Cell. 2007 Nov;1(5):555-67 [18371393] Stem Cells. 2008 Dec;26(12):3068-74 [18787205] Cell Stem Cell. 2009 Feb 6;4(2):129-40 [19200802] J Natl Cancer Inst. 2009 Mar 4;101(5):350-9 [19244169] Nat Methods. 2009 May;6(5):370-6 [19404254] Stem Cells. 2009 Jan;27(1):40-8 [18948646] Cancer Res. 2009 Jul 15;69(14):5648-55 [19584295] J Immunol Methods. 2009 Aug 15;347(1-2):70-8 [19567251] Proc Natl Acad Sci U S A. 2010 Feb 2;107(5):2195-200 [20080668] Nat Med. 2011 Mar;17(3):313-9 [21386835] Cell. 2011 Mar 18;144(6):940-54 [21414485] Breast Cancer Res Treat. 2011 Jul;128(1):45-55 [20665103] Proc Natl Acad Sci U S A. 2011 Jun 28;108(26):10544-9 [21670270] Clin Cancer Res. 2011 Oct 1;17(19):6125-9 [21685479] Immunity. 2013 Sep 19;39(3):611-21 [24012420] Nat Med. 2013 Nov;19(11):1423-37 [24202395] Genome Biol. 2012;13(10):251 [23088445] Cell Stem Cell. 2011 Oct 4;9(4):317-29 [21982232] Proc Natl Acad Sci U S A. 2012 Feb 21;109(8):2784-9 [22308314] Cancer Cell. 2012 Mar 20;21(3):283-96 [22439924] Stem Cells. 2012 May;30(5):833-44 [22489015] Breast Cancer Res. 2011;13(5):R94 [21952072] Cancer Treat Rev. 2012 Oct;38(6):589-98 [22469558] Cell Stem Cell. 2012 Jun 14;10(6):717-28 [22704512] Mol Cell. 2012 Aug 24;47(4):570-84 [22819326] J Mammary Gland Biol Neoplasia. 2012 Jun;17(2):111-7 [22665270] Breast Cancer Res Treat. 2001 Jan;65(2):101-10 [11261825] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.stemcr.2014.11.002 ER - TY - JOUR T1 - Epidemiology of Cholera in the Philippines AN - 1660410718; PQ0001041737 AB - Cholera has been increasingly reported in the past decade. It is most feared because of its tendency to spread rapidly resulting in deaths in a short time, if appropriate treatment is not provided. For fear of trade and travel sanctions, countries were disinclined to report cholera, unless large outbreaks ensued. Although countries in Asia have been reporting cholera, it is believed that more cases are not being identified and instead being reported as acute watery diarrhea. Cholera is endemic in the Philippines however data on cholera in the country remained sparse, until 2008 when surveillance was strengthened. From 2008 to 2013, 42,071 suspected and confirmed cholera cases were reported in 87% of provinces and metropolitan areas in the country, confirming the endemicity of cholera in the Philippines. Poor access to improved sanitation was associated with cholera. On the other hand despite access to improved water sources, cholera remains to be seen. The latter is most probably due to the breakdown and non-chlorination of water systems. We identified areas where cholera has been known to occur in the Philippines, this will assist in the development and implementation of policies to minimize the morbidity and mortality due to this disease. JF - PLoS Neglected Tropical Diseases AU - Lopez, Anna Lena AU - Macasaet, Lino Y AU - Ylade, Michelle AU - Tayag, Enrique A AU - Ali, Mohammad AD - University of the Philippines Manila-National Institutes of Health, Philippines Y1 - 2015/01/08/ PY - 2015 DA - 2015 Jan 08 PB - Public Library of Science, 185 Berry Street San Francisco CA 94107 United States VL - 9 IS - 1 SN - 1935-2727, 1935-2727 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Health & Safety Science Abstracts; Microbiology Abstracts B: Bacteriology KW - Travel KW - Trade KW - Fear KW - Disease control KW - Morbidity KW - Disease transmission KW - Endemic species KW - Sanitation KW - ISEW, Philippines KW - Cholera KW - Asia KW - Mortality KW - Data processing KW - Diarrhea KW - Pathogenic bacteria KW - Bacterial diseases KW - Surveillance and enforcement KW - Epidemiology KW - Endemism KW - Outbreaks KW - Metropolitan areas KW - Mortality causes KW - Q1 08604:Stock assessment and management KW - H 12000:Epidemiology and Public Health KW - J 02400:Human Diseases KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660410718?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+Neglected+Tropical+Diseases&rft.atitle=Epidemiology+of+Cholera+in+the+Philippines&rft.au=Lopez%2C+Anna+Lena%3BMacasaet%2C+Lino+Y%3BYlade%2C+Michelle%3BTayag%2C+Enrique+A%3BAli%2C+Mohammad&rft.aulast=Lopez&rft.aufirst=Anna&rft.date=2015-01-08&rft.volume=9&rft.issue=1&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+Neglected+Tropical+Diseases&rft.issn=19352727&rft_id=info:doi/10.1371%2Fjournal.pntd.0003440 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Endemic species; Endemism; Epidemiology; Pathogenic bacteria; Bacterial diseases; Surveillance and enforcement; Disease control; Mortality causes; Disease transmission; Travel; Mortality; Diarrhea; Sanitation; Data processing; Fear; Cholera; Morbidity; Trade; Outbreaks; Metropolitan areas; ISEW, Philippines; Asia DO - http://dx.doi.org/10.1371/journal.pntd.0003440 ER - TY - JOUR T1 - A phase I trial of vertical inhibition of IGF signalling using cixutumumab, an anti-IGF-1R antibody, and selumetinib, an MEK 1/2 inhibitor, in advanced solid tumours. AN - 1643406679; 25268371 AB - We completed a phase I clinical trial to test the safety and toxicity of combined treatment with cixutumumab (anti-IGF-1R antibody) and selumetinib (MEK 1/2 inhibitor). Patients with advanced solid tumours, refractory to standard therapy received selumetinib hydrogen sulphate capsules orally twice daily, and cixutumumab intravenously on days 1 and 15 of each 28-day cycle. The study used a 3+3 design, with a dose-finding cohort followed by an expansion cohort at the maximally tolerated dose that included pharmacokinetic and pharmacodynamic correlative studies. Thirty patients were enrolled, with 16 in the dose-finding cohort and 14 in the expansion cohort. Grade 3 or greater toxicities included nausea and vomiting, anaemia, CVA, hypertension, hyperglycaemia, and ophthalmic symptoms. The maximally tolerated combination dose was 50 mg twice daily of selumetinib and 12 mg kg(-1) every 2 weeks of cixutumumab. Two patients achieved a partial response (one unconfirmed), including a patient with BRAF wild-type thyroid carcinoma, and a patient with squamous cell carcinoma of the tongue, and six patients achieved time to progression of >6 months, including patients with thyroid carcinoma, colorectal carcinoma, and basal cell carcinoma. Comparison of pre- and on-treatment biopsies showed significant suppression of pERK and pS6 activity with treatment. Our study of anti-IGF-1R antibody cixutumumab and MEK 1/2 inhibitor selumetinib showed that the combination is safe and well-tolerated at these doses, with preliminary evidence of clinical benefit and pharmacodynamic evidence of target inhibition. JF - British journal of cancer AU - Wilky, B A AU - Rudek, M A AU - Ahmed, S AU - Laheru, D A AU - Cosgrove, D AU - Donehower, R C AU - Nelkin, B AU - Ball, D AU - Doyle, L A AU - Chen, H AU - Ye, X AU - Bigley, G AU - Womack, C AU - Azad, N S AD - Department of Oncology, Sidney Kimmel Comprehensive Cancer Center at The Johns Hopkins University School of Medicine, 1650 Orleans Street, Baltimore, MD 21231, USA. ; National Cancer Institute, 9609 Medical Center Drive, MSC 9379, Bethesda, MD 20892, USA. ; Oncology iMed, AstraZeneca, Mereside, Alderley Park, Maccelsfield, Cheshire SK104TG, UK. Y1 - 2015/01/06/ PY - 2015 DA - 2015 Jan 06 SP - 24 EP - 31 VL - 112 IS - 1 KW - AZD 6244 KW - 0 KW - Antibodies, Monoclonal KW - Benzimidazoles KW - anti-IGF-1R antibody A12 KW - Receptor, IGF Type 1 KW - EC 2.7.10.1 KW - MAP Kinase Kinase Kinases KW - EC 2.7.11.25 KW - Index Medicus KW - Disease-Free Survival KW - Benzimidazoles -- administration & dosage KW - Benzimidazoles -- adverse effects KW - Humans KW - Aged KW - Benzimidazoles -- pharmacokinetics KW - Antibodies, Monoclonal -- administration & dosage KW - MAP Kinase Kinase Kinases -- antagonists & inhibitors KW - Antibodies, Monoclonal -- pharmacokinetics KW - Cohort Studies KW - Treatment Outcome KW - Receptor, IGF Type 1 -- antagonists & inhibitors KW - Middle Aged KW - Antibodies, Monoclonal -- adverse effects KW - Male KW - Female KW - Neoplasms -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- pharmacokinetics KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1643406679?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+cancer&rft.atitle=A+phase+I+trial+of+vertical+inhibition+of+IGF+signalling+using+cixutumumab%2C+an+anti-IGF-1R+antibody%2C+and+selumetinib%2C+an+MEK+1%2F2+inhibitor%2C+in+advanced+solid+tumours.&rft.au=Wilky%2C+B+A%3BRudek%2C+M+A%3BAhmed%2C+S%3BLaheru%2C+D+A%3BCosgrove%2C+D%3BDonehower%2C+R+C%3BNelkin%2C+B%3BBall%2C+D%3BDoyle%2C+L+A%3BChen%2C+H%3BYe%2C+X%3BBigley%2C+G%3BWomack%2C+C%3BAzad%2C+N+S&rft.aulast=Wilky&rft.aufirst=B&rft.date=2015-01-06&rft.volume=112&rft.issue=1&rft.spage=24&rft.isbn=&rft.btitle=&rft.title=British+journal+of+cancer&rft.issn=1532-1827&rft_id=info:doi/10.1038%2Fbjc.2014.515 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-23 N1 - Date created - 2015-01-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Clin Cancer Res. 2007 Mar 1;13(5):1576-83 [17332304] Cancer Lett. 2007 Apr 18;248(2):269-79 [16996205] Clin Cancer Res. 2007 Sep 15;13(18 Pt 2):5549s-5555s [17875788] J Clin Oncol. 2008 May 1;26(13):2139-46 [18390968] Thyroid. 2008 Aug;18(8):853-64 [18651802] Cancer Res. 2008 Oct 15;68(20):8322-32 [18922904] Expert Opin Investig Drugs. 2009 Jul;18(7):1025-33 [19548856] Clin Cancer Res. 2010 Mar 1;16(5):1613-23 [20179232] Cancer Cell. 2010 Dec 14;18(6):683-95 [21156289] Sci Signal. 2011;4(166):pe16 [21447797] J Clin Oncol. 2011 Jun 10;29(17):2350-6 [21519015] Cancer Chemother Pharmacol. 2011 Dec;68(6):1619-28 [21953275] Curr Med Chem. 2012;19(8):1164-76 [22257058] Cancer Res. 2012 Jul 1;72(13):3228-37 [22552284] Methods Mol Biol. 2012;929:377-89 [23007438] Clin Cancer Res. 2012 Oct 1;18(19):5290-303 [22872574] Cancer Discov. 2013 May;3(5):548-63 [23454899] Cancer Discov. 2013 May;3(5):491-3 [23658296] Cancer Chemother Pharmacol. 2013 Jun;71(6):1395-409 [23443307] Mol Cancer Ther. 2013 Jun;12(6):1131-9 [23515613] Eur J Cancer. 2013 Oct;49(15):3219-28 [23835252] Clin Cancer Res. 2013 Nov 1;19(21):5940-51 [23918606] Clin Cancer Res. 2013 Nov 15;19(22):6219-29 [24045180] Exp Cell Res. 1999 Nov 25;253(1):1-6 [10579905] Nature. 2001 Mar 1;410(6824):37-40 [11242034] Cell Cycle. 2004 Mar;3(3):372-9 [14726697] Biometrics. 1989 Sep;45(3):925-37 [2790129] Cell. 1998 May 15;93(4):605-15 [9604935] Cancer Res. 2006 Feb 1;66(3):1500-8 [16452206] Leukemia. 2006 Jul;20(7):1254-60 [16642049] Breast Cancer Res. 2006;8(2):R18 [16584539] Comment In: Br J Cancer. 2015 Jan 6;112(1):1-3 [25562565] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1038/bjc.2014.515 ER - TY - CPAPER T1 - From the Pump Handle to the Fire Hose: Applying Health Sciences to Understanding the Impacts of Climate Change on Human Health T2 - 95th American Meteorological Society Annual Meeting AN - 1658698692; 6337553 JF - 95th American Meteorological Society Annual Meeting AU - Balbus, John Y1 - 2015/01/04/ PY - 2015 DA - 2015 Jan 04 KW - Fires KW - Climatic changes KW - Pumps KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658698692?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=95th+American+Meteorological+Society+Annual+Meeting&rft.atitle=From+the+Pump+Handle+to+the+Fire+Hose%3A+Applying+Health+Sciences+to+Understanding+the+Impacts+of+Climate+Change+on+Human+Health&rft.au=Balbus%2C+John&rft.aulast=Balbus&rft.aufirst=John&rft.date=2015-01-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=95th+American+Meteorological+Society+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - https://ams.confex.com/ams/95Annual/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-28 N1 - Last updated - 2015-02-27 ER - TY - CPAPER T1 - The HHS Sustainable and Climate Resilient Health Care Facilities Initiative T2 - 95th American Meteorological Society Annual Meeting AN - 1658696995; 6337228 JF - 95th American Meteorological Society Annual Meeting AU - Balbus, John Y1 - 2015/01/04/ PY - 2015 DA - 2015 Jan 04 KW - Health care KW - Climate KW - Sustainable development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1658696995?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Acpi&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=conference&rft.jtitle=95th+American+Meteorological+Society+Annual+Meeting&rft.atitle=The+HHS+Sustainable+and+Climate+Resilient+Health+Care+Facilities+Initiative&rft.au=Balbus%2C+John&rft.aulast=Balbus&rft.aufirst=John&rft.date=2015-01-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=95th+American+Meteorological+Society+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - https://ams.confex.com/ams/95Annual/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-28 N1 - Last updated - 2015-02-27 ER - TY - JOUR T1 - Do we still need the Rational Formula? An alternative empirical procedure for peak discharge estimation in small and ungauged basins AN - 1680460870; PQ0001491378 AB - The Rational Formula is the most applied equation in practical hydrology due to its simplicity and the effective compromise between theory and data availability. Although the Rational Formula has several drawbacks, it is reliable and surprisingly accurate considering the paucity of input information. However, after more than a century, the recent progress in computational ability, theory and large-scale monitoring compel us to try to suggest a more advanced yet still empirical procedure for estimating peak discharge in small and ungauged basins. In this paper, an alternative empirical procedure is described and discussed, and then a discussion as to whether the Rational Formula is still necessary is presented. The presented methodology integrates the three standard steps of the common event-based approach (design hyetograph, rainfall excess and rainfall-runoff transformation) accurately adapted for application with a lack of observed data. The proposed procedure requires the same input information as necessary for application of the Rational Formula (soil properties, intensity-duration-frequency rainfall curves and T sub(c)) and provides both the peak discharge and the design hydrograph shape and, most importantly, reduces the subjectivity of the hydrologist in its application.Editor D. Koutsoyiannis JF - Hydrological Sciences Journal/Journal des Sciences Hydrologiques AU - Grimaldi, Salvatore AU - Petroselli, Andrea AD - Dipartimento per la innovazione nei sistemi biologici, agroalimentari e forestali (DIBAF), University of Tuscia, I-01100 Viterbo, Italy Y1 - 2015/01/02/ PY - 2015 DA - 2015 Jan 02 SP - 67 EP - 77 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 60 IS - 1 SN - 0262-6667, 0262-6667 KW - Water Resources Abstracts; ASFA 2: Ocean Technology Policy & Non-Living Resources; Meteorological & Geoastrophysical Abstracts; Environment Abstracts; Aqualine Abstracts KW - Hydrograph analysis KW - Rainfall KW - Basins KW - Stormwater runoff KW - Soil properties KW - Hydrology KW - Flood Peak KW - Hyetographs KW - Soil Properties KW - Hydrologic Data KW - Hydrologic analysis KW - Mathematical models KW - Rainfall-runoff Relationships KW - Rainfall runoff KW - River discharge KW - Rational Formula KW - Standards KW - Monitoring KW - SW 5010:Network design KW - AQ 00006:Sewage KW - Q2 09241:General KW - M2 556.16:Runoff (556.16) KW - ENA 15:Renewable Resources-Terrestrial UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680460870?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hydrological+Sciences+Journal%2FJournal+des+Sciences+Hydrologiques&rft.atitle=Do+we+still+need+the+Rational+Formula%3F+An+alternative+empirical+procedure+for+peak+discharge+estimation+in+small+and+ungauged+basins&rft.au=Grimaldi%2C+Salvatore%3BPetroselli%2C+Andrea&rft.aulast=Grimaldi&rft.aufirst=Salvatore&rft.date=2015-01-02&rft.volume=60&rft.issue=1&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=Hydrological+Sciences+Journal%2FJournal+des+Sciences+Hydrologiques&rft.issn=02626667&rft_id=info:doi/10.1080%2F02626667.2014.880546 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-05-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Mathematical models; River discharge; Hydrology; Hydrograph analysis; Hydrologic analysis; Rainfall runoff; Soil properties; Hyetographs; Stormwater runoff; Rainfall; Basins; Rational Formula; Rainfall-runoff Relationships; Standards; Flood Peak; Soil Properties; Monitoring; Hydrologic Data DO - http://dx.doi.org/10.1080/02626667.2014.880546 ER - TY - JOUR T1 - Meat Consumption and Risk of Squamous Cell Carcinoma of the Lung: A Case-Control Study in Uruguayan Men AN - 1654677775; 21314782 AB - In the period 1995-2004, a hospital-based case-control study on meat consumption and squamous cell carcinoma of the lung in men was conducted in Montevideo, Uruguay. The study included 300 cases and 600 controls, frequency matched on age and residence. The results showed that total meat [odds ratio (OR) = 1.72, 95% confidence interval (CI): 1.05-2.81, P value for trend = 0.03], red meat (OR = 1.82, 95% CI: 1.13-2.91, P value for trend = 0.01), beef consumption (OR = 2.22, 95% CI: 1.42-3.45, P value for trend = 0.0004), bacon (OR = 1.50, 95% CI: 1.00-2.24, P value for trend = 0.03), saucisson (OR = 1.69, 95% CI: 1.07-2.67, P value for trend = 0.01), and salted meat intake (OR = 2.70, 95% CI: 1.63-4.46, P value for trend = 0.0001) were positively associated with squamous cell lung cancer. These results are discussed and we suggest that meat consumption could be considered as a strong risk factor for squamous cell lung cancer. JF - Nutrition and Cancer AU - Deneo-Pellegrini, Hugo AU - Ronco, Alvaro L AU - De Stefani, Eduardo AD - Department of Pathology, National Cancer Institute, Montevideo, Uruguay Y1 - 2015/01/02/ PY - 2015 DA - 2015 Jan 02 SP - 82 EP - 88 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 67 IS - 1 SN - 0163-5581, 0163-5581 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Meat KW - Uruguay, Montevideo KW - Health risks KW - Age KW - Risk factors KW - Males KW - Uruguay KW - Cancer KW - Lung cancer KW - H 11000:Diseases/Injuries/Trauma KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654677775?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nutrition+and+Cancer&rft.atitle=Meat+Consumption+and+Risk+of+Squamous+Cell+Carcinoma+of+the+Lung%3A+A+Case-Control+Study+in+Uruguayan+Men&rft.au=Deneo-Pellegrini%2C+Hugo%3BRonco%2C+Alvaro+L%3BDe+Stefani%2C+Eduardo&rft.aulast=Deneo-Pellegrini&rft.aufirst=Hugo&rft.date=2015-01-02&rft.volume=67&rft.issue=1&rft.spage=82&rft.isbn=&rft.btitle=&rft.title=Nutrition+and+Cancer&rft.issn=01635581&rft_id=info:doi/10.1080%2F01635581.2015.970290 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2015-08-05 N1 - SubjectsTermNotLitGenreText - Meat; Health risks; Age; Males; Risk factors; Cancer; Lung cancer; Uruguay, Montevideo; Uruguay DO - http://dx.doi.org/10.1080/01635581.2015.970290 ER - TY - JOUR T1 - Genome-Wide Association Studies in Africans and African Americans: Expanding the Framework of the Genomics of Human Traits and Disease AN - 1780521473; PQ0002841245 AB - Genomic research is one of the tools for elucidating the pathogenesis of diseases of global health relevance and paving the research dimension to clinical and public health translation. Recent advances in genomic research and technologies have increased our understanding of human diseases, genes associated with these disorders, and the relevant mechanisms. Genome-wide association studies (GWAS) have proliferated since the first studies were published several years ago and have become an important tool in helping researchers comprehend human variation and the role genetic variants play in disease. However, the need to expand the diversity of populations in GWAS has become increasingly apparent as new knowledge is gained about genetic variation. Inclusion of diverse populations in genomic studies is critical to a more complete understanding of human variation and elucidation of the underpinnings of complex diseases. In this review, we summarize the available data on GWAS in recent African ancestry populations within the western hemisphere (i.e. African Americans and peoples of the Caribbean) and continental African populations. Furthermore, we highlight ways in which genomic studies in populations of recent African ancestry have led to advances in the areas of malaria, HIV, prostate cancer, and other diseases. Finally, we discuss the advantages of conducting GWAS in recent African ancestry populations in the context of addressing existing and emerging global health conditions. copyright 2014 S. Karger AG, Basel JF - Public Health Genomics AU - Peprah, Emmanuel AU - Xu, Huichun AU - Tekola-Ayele, Fasil AU - Royal, Charmaine D AD - Center for Translation Research and Implementation Science, National Heart, Lung, and Blood Institute Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 40 EP - 51 PB - S. Karger AG, P.O. Box Basel CH-4009 Switzerland VL - 18 IS - 1 SN - 1662-4246, 1662-4246 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Genetics Abstracts; Health & Safety Science Abstracts KW - African American KW - African ancestry KW - African populations KW - Genetic conditions KW - Genome-wide association studies KW - Genomics KW - Global health KW - Health KW - Translation KW - Human diseases KW - Genetic diversity KW - Malaria KW - Public health KW - Genetics KW - Population genetics KW - ASW, Caribbean Sea KW - Genes KW - genomics KW - Ethnic groups KW - Data processing KW - Population studies KW - Translations KW - Prostate cancer KW - Human immunodeficiency virus KW - Reviews KW - Technology KW - Q1 08443:Population genetics KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - G 07880:Human Genetics KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780521473?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Public+Health+Genomics&rft.atitle=Genome-Wide+Association+Studies+in+Africans+and+African+Americans%3A+Expanding+the+Framework+of+the+Genomics+of+Human+Traits+and+Disease&rft.au=Peprah%2C+Emmanuel%3BXu%2C+Huichun%3BTekola-Ayele%2C+Fasil%3BRoyal%2C+Charmaine+D&rft.aulast=Peprah&rft.aufirst=Emmanuel&rft.date=2015-01-01&rft.volume=18&rft.issue=1&rft.spage=40&rft.isbn=&rft.btitle=&rft.title=Public+Health+Genomics&rft.issn=16624246&rft_id=info:doi/10.1159%2F000367962 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Population genetics; Genetics; Translations; Human diseases; Genes; Malaria; Public health; Translation; Prostate cancer; Data processing; Reviews; Genetic diversity; Population studies; genomics; Human immunodeficiency virus; Ethnic groups; Technology; ASW, Caribbean Sea DO - http://dx.doi.org/10.1159/000367962 ER - TY - JOUR T1 - Thyroid tuberculosis AN - 1773833006; PQ0001740544 JF - QJM: An International Journal of Medicine AU - Chuang, T-J AU - Liu, J-S AU - Hung, Y-J AU - Hsieh, C-H AD - Address correspondence to Chang-Hsun Hsieh, Division of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, #325, Section 2, Cheng-Gong Rd., Nei-Hu, Taipei, Taiwan., 10324@yahoo.com.tw Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 47 EP - 48 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 108 IS - 1 SN - 1460-2725, 1460-2725 KW - Microbiology Abstracts B: Bacteriology KW - Mycobacterium KW - Thyroid KW - Tuberculosis KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1773833006?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=QJM%3A+An+International+Journal+of+Medicine&rft.atitle=Thyroid+tuberculosis&rft.au=Chuang%2C+T-J%3BLiu%2C+J-S%3BHung%2C+Y-J%3BHsieh%2C+C-H&rft.aulast=Chuang&rft.aufirst=T-J&rft.date=2015-01-01&rft.volume=108&rft.issue=1&rft.spage=47&rft.isbn=&rft.btitle=&rft.title=QJM%3A+An+International+Journal+of+Medicine&rft.issn=14602725&rft_id=info:doi/10.1093%2Fqjmed%2Fhcu154 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Last updated - 2016-03-30 N1 - SubjectsTermNotLitGenreText - Thyroid; Tuberculosis; Mycobacterium DO - http://dx.doi.org/10.1093/qjmed/hcu154 ER - TY - JOUR T1 - The Biomarkers of Exposure and Effect in Agriculture (BEEA) Study: Rationale, Design, Methods, and Participant Characteristics AN - 1753460860; PQ0002432403 AB - Agricultural exposures including pesticides, endotoxin, and allergens have been associated with risk of various cancers and other chronic diseases, although the biological mechanisms underlying these associations are generally unclear. To facilitate future molecular epidemiologic investigations, in 2010 the study of Biomarkers of Exposure and Effect in Agriculture (BEEA) was initiated within the Agricultural Health Study, a large prospective cohort in Iowa and North Carolina. Here the design and methodology of BEEA are described and preliminary frequencies for participant characteristics and current agricultural exposures are reported. At least 1,600 male farmers over 50 years of age will be enrolled in the BEEA study. During a home visit, participants are asked to complete a detailed interview about recent agricultural exposures and provide samples of blood, urine, and (since 2013) house dust. As of mid-September 2014, in total, 1,233 participants have enrolled. Most of these participants (83%) were still farming at the time of interview. Among those still farming, the most commonly reported crops were corn (81%) and soybeans (74%), and the most frequently noted animals were beef cattle (35%) and hogs (13%). There were 861 (70%) participants who reported occupational pesticide use in the 12 months prior to interview; among these participants, the most frequently noted herbicides were glyphosate (83%) and 2,4-D (72%), and most commonly reported insecticides were malathion (21%), cyfluthrin (13%), and permethrin (12%). Molecular epidemiologic investigations within BEEA have the potential to yield important new insights into the biological mechanisms through which these or other agricultural exposures influence disease risk. JF - Journal of Toxicology and Environmental Health, Part A: Current Issues AU - Hofmann, Jonathan N AU - Beane Freeman, Laura E AU - Lynch, Charles F AU - Andreotti, Gabriella AU - Thomas, Kent W AU - Sandler, Dale P AU - Savage, Sharon A AU - Alavanja, Michael C AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA Y1 - 2015///0, PY - 2015 DA - 0, 2015 SP - 1338 EP - 1347 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 78 IS - 21-22 SN - 1528-7394, 1528-7394 KW - Pollution Abstracts; Environment Abstracts; Health & Safety Science Abstracts; Toxicology Abstracts KW - 2,4-D KW - Agriculture KW - Endotoxins KW - Age KW - Crops KW - Malathion KW - Insecticides KW - Allergens KW - Bioindicators KW - ANW, USA, North Carolina KW - Permethrin KW - Herbicides KW - biomarkers KW - Cancer KW - Soybeans KW - Health risks KW - Blood KW - Cattle KW - House dust KW - USA, Iowa KW - Urine KW - Beef KW - Pesticides KW - Glyphosate KW - P 0000:AIR POLLUTION KW - X 24320:Food Additives & Contaminants KW - H 1000:Occupational Safety and Health KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1753460860?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Toxicology+and+Environmental+Health%2C+Part+A%3A+Current+Issues&rft.atitle=The+Biomarkers+of+Exposure+and+Effect+in+Agriculture+%28BEEA%29+Study%3A+Rationale%2C+Design%2C+Methods%2C+and+Participant+Characteristics&rft.au=Hofmann%2C+Jonathan+N%3BBeane+Freeman%2C+Laura+E%3BLynch%2C+Charles+F%3BAndreotti%2C+Gabriella%3BThomas%2C+Kent+W%3BSandler%2C+Dale+P%3BSavage%2C+Sharon+A%3BAlavanja%2C+Michael+C&rft.aulast=Hofmann&rft.aufirst=Jonathan&rft.date=2015-01-01&rft.volume=78&rft.issue=21-22&rft.spage=1338&rft.isbn=&rft.btitle=&rft.title=Journal+of+Toxicology+and+Environmental+Health%2C+Part+A%3A+Current+Issues&rft.issn=15287394&rft_id=info:doi/10.1080%2F15287394.2015.1091414 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Last updated - 2016-07-20 N1 - SubjectsTermNotLitGenreText - Endotoxins; Agriculture; 2,4-D; Age; Permethrin; Herbicides; biomarkers; Malathion; Crops; Cancer; Soybeans; Blood; Insecticides; House dust; Beef; Urine; Allergens; Pesticides; Glyphosate; Bioindicators; Health risks; Cattle; ANW, USA, North Carolina; USA, Iowa DO - http://dx.doi.org/10.1080/15287394.2015.1091414 ER - TY - JOUR T1 - Copper and sulfur isotope variations in liver cancer AN - 1752576914; 2016-001738 JF - V.M. Goldschmidt Conference - Program and Abstracts AU - Balter, Vincent AU - da Costa, Andre Nogueira AU - Bondanese, Victor Paky AU - Jaouen, Klervia AU - Lamboux, Aline AU - Sangrajrang, Suleeporn AU - Vincent, Nicolas AU - Fourel, Francois AU - Telouk, Philippe AU - Gigou, Michelle AU - Lecuyer, Christophe AU - Srivatanakul, Petcharin AU - Brechot, Christian AU - Albarede, Francis AU - Hainaut, Pierre AU - Anonymous Y1 - 2015 PY - 2015 DA - 2015 SP - 185 PB - Goldschmidt Conference, [varies] VL - 25 SN - 1042-7287, 1042-7287 KW - medical geology KW - isotopes KW - copper KW - Cu-63 KW - S-32 KW - stable isotopes KW - variations KW - metals KW - sulfur KW - ecology KW - cancer KW - public health KW - 02D:Isotope geochemistry KW - 22:Environmental geology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1752576914?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ageorefmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=V.M.+Goldschmidt+Conference+-+Program+and+Abstracts&rft.atitle=Copper+and+sulfur+isotope+variations+in+liver+cancer&rft.au=Balter%2C+Vincent%3Bda+Costa%2C+Andre+Nogueira%3BBondanese%2C+Victor+Paky%3BJaouen%2C+Klervia%3BLamboux%2C+Aline%3BSangrajrang%2C+Suleeporn%3BVincent%2C+Nicolas%3BFourel%2C+Francois%3BTelouk%2C+Philippe%3BGigou%2C+Michelle%3BLecuyer%2C+Christophe%3BSrivatanakul%2C+Petcharin%3BBrechot%2C+Christian%3BAlbarede%2C+Francis%3BHainaut%2C+Pierre%3BAnonymous&rft.aulast=Balter&rft.aufirst=Vincent&rft.date=2015-01-01&rft.volume=25&rft.issue=&rft.spage=185&rft.isbn=&rft.btitle=&rft.title=V.M.+Goldschmidt+Conference+-+Program+and+Abstracts&rft.issn=10427287&rft_id=info:doi/ L2 - http://goldschmidt.info/2015/uploads/abstracts/finalPDFs/185.pdf LA - English DB - GeoRef N1 - Conference title - Goldschmidt 2015 N1 - Copyright - GeoRef, Copyright 2016, American Geosciences Institute. N1 - Date revised - 2016-01-01 N1 - Last updated - 2015-12-31 N1 - SubjectsTermNotLitGenreText - cancer; copper; Cu-63; ecology; isotopes; medical geology; metals; public health; S-32; stable isotopes; sulfur; variations ER - TY - JOUR T1 - Pesticide Exposures and Body Mass Index (BMI) of Pesticide Applicators From the Agricultural Health Study. AN - 1735333679; 26479458 AB - Endocrine-disrupting chemicals, including pesticides, may be associated with weight gain. This is the first longitudinal study to examine a potential association between weight gain and pesticides using data on 8,365 male pesticide applicators from the Agricultural Health Study (AHS) cohort established in 1993. The relationship between total cumulative days of exposure to pesticide functional/chemical classes and to the four most frequently used individual pesticides was studied in relation to body mass index (BMI) at the time of 5-yr follow-up (beginning in 1998) with the length of the exposure period dating back to age 20 yr. Multiple regression, Spearman correlation, ordinal logistic regression, and logistic regression models all utilized a Bonferroni-adjusted p value, were adjusted for relevant covariates, and were stratified by state of residence (Iowa/North Carolina) and presence/absence of weight-related health conditions. Adjusted multiple regression yielded statistically significant positive parameter estimates for the study sample and Iowa subgroups with consistent findings for triazine herbicides and atrazine: Change in BMI per 100 cumulative pesticide exposure days ranged from 0.07 to 0.11 for triazine herbicides and from 0.10 to 0.19 for atrazine. Ordinal logistic regression compared normal weight with overweight and with obese using the zero exposure category as referent. Statistically significant adjusted odds ratios identified for the study sample and both state subgroups for the highest level of atrazine exposure ranged from 1.4 to 1.7. Further investigation is warranted to evaluate the associations identified here. JF - Journal of toxicology and environmental health. Part A AU - LaVerda, Nancy L AU - Goldsmith, David F AU - Alavanja, Michael C R AU - Hunting, Katherine L AD - a Department of Environmental and Occupational Health , Milken Institute School of Public Health, George Washington University , Washington , DC , USA. ; b National Cancer Institute , Rockville , Maryland , USA. Y1 - 2015 PY - 2015 DA - 2015 SP - 1255 EP - 1276 VL - 78 IS - 20 SN - 1528-7394, 1528-7394 KW - Pesticides KW - 0 KW - Index Medicus KW - Young Adult KW - Prospective Studies KW - Aged, 80 and over KW - Humans KW - North Carolina KW - Adult KW - Aged KW - Middle Aged KW - Longitudinal Studies KW - Iowa KW - Male KW - Occupational Exposure KW - Farmers KW - Body Mass Index KW - Pesticides -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1735333679?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+toxicology+and+environmental+health.+Part+A&rft.atitle=Pesticide+Exposures+and+Body+Mass+Index+%28BMI%29+of+Pesticide+Applicators+From+the+Agricultural+Health+Study.&rft.au=LaVerda%2C+Nancy+L%3BGoldsmith%2C+David+F%3BAlavanja%2C+Michael+C+R%3BHunting%2C+Katherine+L&rft.aulast=LaVerda&rft.aufirst=Nancy&rft.date=2015-01-01&rft.volume=78&rft.issue=20&rft.spage=1255&rft.isbn=&rft.btitle=&rft.title=Journal+of+toxicology+and+environmental+health.+Part+A&rft.issn=15287394&rft_id=info:doi/10.1080%2F15287394.2015.1074844 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-25 N1 - Date created - 2015-11-20 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1080/15287394.2015.1074844 ER - TY - JOUR T1 - Obatoclax in combination with fludarabine and rituximab is well-tolerated and shows promising clinical activity in relapsed chronic lymphocytic leukemia. AN - 1735332410; 25971907 AB - Obatoclax is a small molecule mimetic of the BH3 domain of BCL-2 family proteins. This phase 1 study combining obatoclax with FR was undertaken in chronic lymphocytic leukemia (CLL) patients relapsed after at least one prior therapy. Obatoclax was given as a 3-h infusion on days 1 and 3 and escalated through three dose levels, with standard dose FR days 1-5. Thirteen patients were enrolled, with a median of two prior therapies. One dose-limiting toxicity (DLT) of a 2-week treatment delay for persistent grade 2-3 neutropenia was observed at the highest obatoclax dose (20 mg/m2), but no maximum tolerated dose (MTD) was reached. The overall response rate (ORR) was 85%, with 15% complete responses (CRs) by NCI-96 criteria and 54% by IWCLL 2008 criteria. Median time to progression was 20 months. It is concluded that obatoclax can be safely administered to relapsed CLL patients in combination with FR and shows promising clinical activity. JF - Leukemia & lymphoma AU - Brown, Jennifer R AU - Tesar, Bethany AU - Yu, Lijian AU - Werner, Lillian AU - Takebe, Naoko AU - Mikler, Evgeny AU - Reynolds, Hazel M AU - Thompson, Christina AU - Fisher, David C AU - Neuberg, Donna AU - Freedman, A S AD - a Department of Medical Oncology , Boston , MA , USA. ; b Department of Biostatistics and Computational Biology , Dana-Farber Cancer Institute , Boston , MA , USA. ; d Investigational Drug Branch, National Cancer Institute, National Institutes of Health , Bethesda , MD , USA. Y1 - 2015 PY - 2015 DA - 2015 SP - 3336 EP - 3342 VL - 56 IS - 12 KW - Biomarkers KW - 0 KW - Pyrroles KW - obatoclax KW - Rituximab KW - 4F4X42SYQ6 KW - Vidarabine KW - FA2DM6879K KW - fludarabine KW - P2K93U8740 KW - Index Medicus KW - Chronic lymphocytic leukemia KW - phase I–III trials KW - BCL-2 KW - rituximab KW - Vidarabine -- analogs & derivatives KW - Neoplasm Staging KW - Combined Modality Therapy KW - Humans KW - Disease Progression KW - Aged KW - Vidarabine -- administration & dosage KW - Recurrence KW - Pyrroles -- administration & dosage KW - Adult KW - Treatment Outcome KW - Chromosome Aberrations KW - Rituximab -- administration & dosage KW - Middle Aged KW - Retreatment KW - Mutation KW - Female KW - Male KW - Leukemia, Lymphocytic, Chronic, B-Cell -- drug therapy KW - Leukemia, Lymphocytic, Chronic, B-Cell -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Leukemia, Lymphocytic, Chronic, B-Cell -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1735332410?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Leukemia+%26+lymphoma&rft.atitle=Obatoclax+in+combination+with+fludarabine+and+rituximab+is+well-tolerated+and+shows+promising+clinical+activity+in+relapsed+chronic+lymphocytic+leukemia.&rft.au=Brown%2C+Jennifer+R%3BTesar%2C+Bethany%3BYu%2C+Lijian%3BWerner%2C+Lillian%3BTakebe%2C+Naoko%3BMikler%2C+Evgeny%3BReynolds%2C+Hazel+M%3BThompson%2C+Christina%3BFisher%2C+David+C%3BNeuberg%2C+Donna%3BFreedman%2C+A+S&rft.aulast=Brown&rft.aufirst=Jennifer&rft.date=2015-01-01&rft.volume=56&rft.issue=12&rft.spage=3336&rft.isbn=&rft.btitle=&rft.title=Leukemia+%26+lymphoma&rft.issn=1029-2403&rft_id=info:doi/10.3109%2F10428194.2015.1048441 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-09-20 N1 - Date created - 2015-11-21 N1 - Date revised - 2017-02-02 N1 - Last updated - 2017-02-02 DO - http://dx.doi.org/10.3109/10428194.2015.1048441 ER - TY - JOUR T1 - Variations in Glycogen Synthesis in Human Pluripotent Stem Cells with Altered Pluripotent States. AN - 1734284591; 26565809 AB - Human pluripotent stem cells (hPSCs) represent very promising resources for cell-based regenerative medicine. It is essential to determine the biological implications of some fundamental physiological processes (such as glycogen metabolism) in these stem cells. In this report, we employ electron, immunofluorescence microscopy, and biochemical methods to study glycogen synthesis in hPSCs. Our results indicate that there is a high level of glycogen synthesis (0.28 to 0.62 μg/μg proteins) in undifferentiated human embryonic stem cells (hESCs) compared with the glycogen levels (0 to 0.25 μg/μg proteins) reported in human cancer cell lines. Moreover, we found that glycogen synthesis was regulated by bone morphogenetic protein 4 (BMP-4) and the glycogen synthase kinase 3 (GSK-3) pathway. Our observation of glycogen bodies and sustained expression of the pluripotent factor Oct-4 mediated by the potent GSK-3 inhibitor CHIR-99021 reveals an altered pluripotent state in hPSC culture. We further confirmed glycogen variations under different naïve pluripotent cell growth conditions based on the addition of the GSK-3 inhibitor BIO. Our data suggest that primed hPSCs treated with naïve growth conditions acquire altered pluripotent states, similar to those naïve-like hPSCs, with increased glycogen synthesis. Furthermore, we found that suppression of phosphorylated glycogen synthase was an underlying mechanism responsible for altered glycogen synthesis. Thus, our novel findings regarding the dynamic changes in glycogen metabolism provide new markers to assess the energetic and various pluripotent states in hPSCs. The components of glycogen metabolic pathways offer new assays to delineate previously unrecognized properties of hPSCs under different growth conditions. JF - PloS one AU - Chen, Richard J AU - Zhang, Guofeng AU - Garfield, Susan H AU - Shi, Yi-Jun AU - Chen, Kevin G AU - Robey, Pamela G AU - Leapman, Richard D AD - Laboratory of Cellular Imaging and Macromolecular Biophysics, National Institute of Biomedical Imaging and Bioengineering, National Institutes of Health, Bethesda, MD, 20892, United States of America. ; Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, United States of America. ; NIH Stem Cell Unit, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, United States of America. ; Craniofacial and Skeletal Diseases Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, 20892, United States of America. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 11 KW - Bone Morphogenetic Protein 4 KW - 0 KW - Glycogen KW - 9005-79-2 KW - Glycogen Synthase KW - EC 2.4.1.11 KW - Glycogen Synthase Kinase 3 KW - EC 2.7.11.26 KW - Index Medicus KW - Induced Pluripotent Stem Cells -- metabolism KW - Glycogen Synthase -- metabolism KW - Humans KW - Bone Morphogenetic Protein 4 -- metabolism KW - Cell Differentiation KW - Induced Pluripotent Stem Cells -- cytology KW - Glycogen Synthase Kinase 3 -- metabolism KW - Cell Proliferation KW - Cell Line KW - Glycogen -- metabolism KW - Pluripotent Stem Cells -- metabolism KW - Pluripotent Stem Cells -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1734284591?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Variations+in+Glycogen+Synthesis+in+Human+Pluripotent+Stem+Cells+with+Altered+Pluripotent+States.&rft.au=Chen%2C+Richard+J%3BZhang%2C+Guofeng%3BGarfield%2C+Susan+H%3BShi%2C+Yi-Jun%3BChen%2C+Kevin+G%3BRobey%2C+Pamela+G%3BLeapman%2C+Richard+D&rft.aulast=Chen&rft.aufirst=Richard&rft.date=2015-01-01&rft.volume=10&rft.issue=11&rft.spage=e0142554&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0142554 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-07-06 N1 - Date created - 2015-11-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cell. 2007 Dec 14;131(6):1204 [18083108] Science. 1998 Nov 6;282(5391):1145-7 [9804556] Nature. 2008 May 22;453(7194):519-23 [18497825] Glycoconj J. 2008 Aug;25(6):503-10 [17973187] Cell Stem Cell. 2008 Aug 7;3(2):196-206 [18682241] Stem Cells Dev. 2009 Jun;18(5):749-58 [19284351] Cell Stem Cell. 2009 Jun 5;4(6):487-92 [19497275] PLoS One. 2010;5(3):e9644 [20300197] Cold Spring Harb Perspect Biol. 2010 Apr;2(4):a001040 [20452943] Science. 2010 Sep 17;329(5998):1492-9 [20847263] FEBS Lett. 2010 Oct 22;584(20):4366-72 [20888814] PLoS One. 2010;5(10):e13703 [21060825] Cell. 2011 Feb 4;144(3):439-52 [21295703] Cell Res. 2011 Mar;21(3):518-29 [21243013] Int J Dev Biol. 2010;54(11-12):1729-41 [21305470] PLoS One. 2011;6(6):e20914 [21698063] EMBO J. 2011 Dec 14;30(24):4860-73 [22085932] Proc Natl Acad Sci U S A. 2012 Mar 20;109(12):4485-90 [22392999] EMBO J. 2012 May 2;31(9):2103-16 [22446391] PLoS One. 2012;7(5):e35997 [22563476] Stem Cells. 2012 Oct;30(10):2175-87 [22887864] Cell Stem Cell. 2012 Nov 2;11(5):589-95 [23122286] Stem Cell Res. 2012 Nov;9(3):237-48 [22910561] Cell Metab. 2012 Dec 5;16(6):751-64 [23177934] Stem Cell Res. 2013 Jan;10(1):57-66 [23117585] Cell Stem Cell. 2013 Dec 5;13(6):663-75 [24315441] Nature. 2013 Dec 12;504(7479):282-6 [24172903] Br J Cancer. 2004 Dec 13;91(12):2094-100 [15599384] Development. 2005 Mar;132(6):1273-82 [15703277] Nat Methods. 2005 Mar;2(3):185-90 [15782187] J Cell Sci. 2005 Oct 1;118(Pt 19):4495-509 [16179608] Nat Protoc. 2007;2(3):753-62 [17406637] Exp Biol Med (Maywood). 2007 Jun;232(6):833-43 [17526776] Cell. 2007 Jun 29;129(7):1261-74 [17604717] Dev Biol. 2007 Jul 15;307(2):446-59 [17560561] Science. 2007 Dec 21;318(5858):1917-20 [18029452] Stem Cell Reports. 2014 Mar 11;2(3):366-81 [24672758] J Vis Exp. 2014;(89). doi: 10.3791/51519 [25077932] Regen Med. 2014;9(4):401-3 [25159054] Cell Stem Cell. 2014 Oct 2;15(4):471-87 [25090446] Cell. 2007 Nov 30;131(5):861-72 [18035408] Ann Clin Biochem. 2002 Nov;39(Pt 6):612-3 [12564847] Cell. 2003 Oct 31;115(3):281-92 [14636556] Nat Med. 2004 Jan;10(1):55-63 [14702635] Cancer Res. 1981 Mar;41(3):1165-70 [7459858] Am J Physiol. 1981 Feb;240(2):E197-202 [6781362] Nature. 1995 Dec 21-28;378(6559):785-9 [8524413] Nat Biotechnol. 2007 Jul;25(7):803-16 [17572666] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0142554 ER - TY - JOUR T1 - Advances in Anticancer Immunotoxin Therapy AN - 1732830806; PQ0002237623 AB - Immunotoxins are a novel class of antibody-conjugated therapeutics currently in clinical development for a variety of malignancies. They consist of an antibody-based targeting domain fused to a bacterial toxin payload for cell killing. Immunotoxins kill cells by inhibiting protein synthesis, a unique mechanism of action that is toxic to both dividing and nondividing cells. Recent advances in the design and administration of immunotoxins are overcoming historical challenges in the field, leading to renewed interest in these therapeutics. JF - Oncologist AU - Alewine, Christine AU - Hassan, Raffit AU - Pastan, Ira AD - Laboratory of Molecular Biology, pastani@mail.nih.gov Y1 - 2015///0, PY - 2015 DA - 0, 2015 SP - 176 EP - 185 PB - AlphaMed Press, Inc., One Prestige Pl, Ste 290 Miamisburg OH 45342-3758 United States VL - 20 IS - 2 SN - 1083-7159, 1083-7159 KW - Biotechnology and Bioengineering Abstracts; Immunology Abstracts; Oncogenes & Growth Factors Abstracts KW - Antibody conjugate KW - Recombinant immunotoxin KW - Vascular leak syndrome KW - Antidrug antibody KW - Malignancy KW - Protein biosynthesis KW - Immunotoxins KW - Toxins KW - W 30940:Products KW - F 06915:Cancer Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732830806?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncologist&rft.atitle=Advances+in+Anticancer+Immunotoxin+Therapy&rft.au=Alewine%2C+Christine%3BHassan%2C+Raffit%3BPastan%2C+Ira&rft.aulast=Alewine&rft.aufirst=Christine&rft.date=2015-01-01&rft.volume=20&rft.issue=2&rft.spage=176&rft.isbn=&rft.btitle=&rft.title=Oncologist&rft.issn=10837159&rft_id=info:doi/10.1634%2Ftheoncologist.2014-0358 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-01 N1 - Last updated - 2016-02-29 N1 - SubjectsTermNotLitGenreText - Malignancy; Protein biosynthesis; Toxins; Immunotoxins DO - http://dx.doi.org/10.1634/theoncologist.2014-0358 ER - TY - JOUR T1 - Incorporation of nonzero echo times in the SPGR and bSSFP signal models used in mcDESPOT AN - 1732829857; PQ0002211280 AB - Purpose To analyze the effect of neglecting nonzero echo times (TEs) in the conventional model of multicomponent driven equilibrium single pulse observation of T sub(1) and T sub(2) (mcDESPOT). Theory and Methods Formulations of the two-component spoiled gradient recalled echo (SPGR) and balanced steady state free precession (bSSFP) models that incorporate nonzero TE effects are presented in the context of mcDESPOT and compared with the conventionally used SPGR and bSSFP models which ignore nonzero TEs. Relative errors in derived parameter estimates from conventional mcDESPOT, omitting TE effects, are assessed using simulations over a wide range of experimental and sample parameters. Results The neglect of nonzero TE leads to an overestimate of the SPGR signal and an underestimate of the bSSFP signal. These effects can introduce large errors in parameter estimates derived from conventional mcDESPOT under realistic imaging conditions. Conclusion SPGR and bSSFP signal models accounting for nonzero TE effects should be incorporated into quantitative mcDESPOT analyses. Magn Reson Med 74:1227-1235, 2015. JF - Magnetic Resonance in Medicine AU - Bouhrara, Mustapha AU - Spencer, Richard G AD - Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA. PY - 2015 SP - 1227 EP - 1235 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 74 IS - 5 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - N.M.R. KW - imaging KW - Models KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1732829857?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Magnetic+Resonance+in+Medicine&rft.atitle=Incorporation+of+nonzero+echo+times+in+the+SPGR+and+bSSFP+signal+models+used+in+mcDESPOT&rft.au=Bouhrara%2C+Mustapha%3BSpencer%2C+Richard+G&rft.aulast=Bouhrara&rft.aufirst=Mustapha&rft.date=2015-01-01&rft.volume=74&rft.issue=5&rft.spage=1227&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.25984 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-01 N1 - Last updated - 2015-12-09 N1 - SubjectsTermNotLitGenreText - N.M.R.; imaging; Models DO - http://dx.doi.org/10.1002/mrm.25984 ER - TY - JOUR T1 - Nitric Oxide Down-Regulates Topoisomerase I and Induces Camptothecin Resistance in Human Breast MCF-7 Tumor Cells. AN - 1731781254; 26540186 AB - Camptothecin (CPT), a topoisomerase I poison, is an important drug for the treatment of solid tumors in the clinic. Nitric oxide (·NO), a physiological signaling molecule, is involved in many cellular functions, including cell proliferation, survival and death. We have previously shown that ·NO plays a significant role in the detoxification of etoposide (VP-16), a topoisomerase II poison in vitro and in human melanoma cells. ·NO/·NO-derived species are reported to modulate activity of several important cellular proteins. As topoisomerases contain a number of free sulfhydryl groups which may be targets of ·NO/·NO-derived species, we have investigated the roles of ·NO/·NO-derived species in the stability and activity of topo I. Here we show that ·NO/·NO-derived species induces a significant down-regulation of topoisomerase I protein via the ubiquitin/26S proteasome pathway in human colon (HT-29) and breast (MCF-7) cancer cell lines. Importantly, ·NO treatment induced a significant resistance to CPT only in MCF-7 cells. This resistance to CPT did not result from loss of topoisomerase I activity as there were no differences in topoisomerase I-induced DNA cleavage in vitro or in tumor cells, but resulted from the stabilization/induction of bcl2 protein. This up-regulation of bcl2 protein in MCF-7 cells was wtp53 dependent as pifithrine-α, a small molecule inhibitor of wtp53 function, completely reversed CPT resistance, suggesting that wtp53 and bcl2 proteins played important roles in CPT resistance. Because tumors in vivo are heterogeneous and contaminated by infiltrating macrophages, ·NO-induced down-regulation of topoisomerase I protein combined with bcl2 protein stabilization could render certain tumors highly resistant to CPT and drugs derived from it in the clinic. JF - PloS one AU - Sharma, Nilesh K AU - Kumar, Ashutosh AU - Kumari, Amrita AU - Tokar, Erik J AU - Waalkes, Michael P AU - Bortner, Carl D AU - Williams, Jason AU - Ehrenshaft, Marilyn AU - Mason, Ronald P AU - Sinha, Birandra K AD - Immunity, Inflammation and Disease Laboratory, National Institute of Environmental Health Sciences, NIH, Research Triangle, Park, Durham, North Carolina, United States of America. ; National Toxicology Program, National Institute of Environmental Health Sciences, NIH, Research Triangle, Park, Durham, North Carolina, United States of America. ; Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, NIH, Research Triangle, Park, Durham, North Carolina, United States of America. ; Laboratory of Structural Biology, National Institute of Environmental Health Sciences, NIH, Research Triangle, Park, Durham, North Carolina, United States of America. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 11 KW - Topoisomerase I Inhibitors KW - 0 KW - Nitric Oxide KW - 31C4KY9ESH KW - Etoposide KW - 6PLQ3CP4P3 KW - DNA Topoisomerases, Type I KW - EC 5.99.1.2 KW - TOP1 protein, human KW - Camptothecin KW - XT3Z54Z28A KW - Index Medicus KW - Topoisomerase I Inhibitors -- pharmacology KW - Etoposide -- pharmacology KW - Tumor Cells, Cultured KW - Cell Survival -- genetics KW - Cell Survival -- drug effects KW - Humans KW - Up-Regulation -- drug effects KW - MCF-7 Cells KW - Up-Regulation -- genetics KW - HT29 Cells KW - Breast Neoplasms -- genetics KW - Breast Neoplasms -- drug therapy KW - Down-Regulation -- genetics KW - Camptothecin -- pharmacology KW - Drug Resistance, Neoplasm -- genetics KW - Nitric Oxide -- metabolism KW - Down-Regulation -- drug effects KW - DNA Topoisomerases, Type I -- genetics KW - Drug Resistance, Neoplasm -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1731781254?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Nitric+Oxide+Down-Regulates+Topoisomerase+I+and+Induces+Camptothecin+Resistance+in+Human+Breast+MCF-7+Tumor+Cells.&rft.au=Sharma%2C+Nilesh+K%3BKumar%2C+Ashutosh%3BKumari%2C+Amrita%3BTokar%2C+Erik+J%3BWaalkes%2C+Michael+P%3BBortner%2C+Carl+D%3BWilliams%2C+Jason%3BEhrenshaft%2C+Marilyn%3BMason%2C+Ronald+P%3BSinha%2C+Birandra+K&rft.aulast=Sharma&rft.aufirst=Nilesh&rft.date=2015-01-01&rft.volume=10&rft.issue=11&rft.spage=e0141897&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0141897 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-13 N1 - Date created - 2015-11-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Anticancer Res. 1998 Jul-Aug;18(4C):2919-32 [9713486] Cell Res. 2002 Dec;12(5-6):311-20 [12528889] Int J Cancer. 1999 Jul 30;82(3):396-404 [10399957] Proc Natl Acad Sci U S A. 1999 Aug 31;96(18):10355-60 [10468612] Science. 1999 Sep 10;285(5434):1733-7 [10481009] Curr Mol Med. 2004 Nov;4(7):741-51 [15579021] Eur J Cancer. 2005 Jan;41(2):265-71 [15661552] Toxicology. 2005 Mar 15;208(2):223-33 [15691587] Mol Pharmacol. 2005 Mar;67(3):937-47 [15602006] Cancer Res. 2006 Jan 15;66(2):605-12 [16423985] Cancer Res. 2006 Jun 15;66(12):6353-60 [16778213] Antioxid Redox Signal. 2006 Jul-Aug;8(7-8):1329-37 [16910780] Chem Res Toxicol. 2006 Sep;19(9):1160-74 [16978020] Mol Cell. 2007 Apr 13;26(1):63-74 [17434127] Nitric Oxide. 2009 Sep;21(2):92-103 [19602444] Proc Natl Acad Sci U S A. 2012 Dec 11;109(50):20373-8 [23185001] Chem Res Toxicol. 2012 Oct 15;25(10):2194-202 [22971010] J Clin Invest. 2010 Nov;120(11):3843-54 [20978357] Oncogene. 2003 Dec 8;22(56):9030-40 [14663481] J Biol Chem. 2004 Jun 11;279(24):25535-43 [15054096] J Biol Chem. 1983 Dec 25;258(24):15365-70 [6317692] Annu Rev Biochem. 1985;54:665-97 [2992360] Science. 1989 Nov 24;246(4933):1046-8 [2555920] J Natl Cancer Inst. 1994 Jun 1;86(11):836-42 [8182764] Cancer Invest. 1994;12(5):530-42 [7922710] Drugs. 1995 Jan;49(1):11-9 [7705211] Cancer Res. 1995 Apr 15;55(8):1649-54 [7712469] Mol Pharmacol. 1995 May;47(5):907-14 [7538195] J Biol Chem. 1995 Sep 15;270(37):21429-32 [7665550] Proc Natl Acad Sci U S A. 1996 May 14;93(10):4736-41 [8643472] Biochemistry. 1996 May 7;35(18):5778-86 [8639538] Cancer Res. 1996 Feb 15;56(4):892-8 [8631030] Br J Pharmacol. 1995 Dec;116(7):2866-72 [8680718] Cancer Res. 1996 Oct 1;56(19):4430-7 [8813137] Cancer Res. 1997 Aug 15;57(16):3365-9 [9269997] J Biol Chem. 1997 Sep 26;272(39):24159-64 [9305865] Science. 1998 Mar 6;279(5356):1534-41 [9488652] Chem Res Toxicol. 2013 Mar 18;26(3):379-87 [23402364] J Am Coll Cardiol. 2013 Jul 9;62(2):89-95 [23665095] J Pharmacol Exp Ther. 2013 Dec;347(3):607-14 [24049059] Chem Res Toxicol. 2013 Jan 18;26(1):96-105 [23137061] ACS Chem Biol. 2014 Mar 21;9(3):821-30 [24397869] Proc Natl Acad Sci U S A. 2014 Apr 29;111(17):6323-8 [24733928] Cancer Res. 2000 Jan 1;60(1):184-90 [10646872] Biochem Biophys Res Commun. 2000 Jan 19;267(2):609-13 [10631110] Nat Cell Biol. 2000 Jun;2(6):339-45 [10854324] Biochem Biophys Res Commun. 2001 Mar 2;281(3):766-71 [11237724] Annu Rev Pharmacol Toxicol. 2001;41:203-36 [11264456] Cancer Res. 2001 Aug 1;61(15):5926-32 [11479235] Cancer Res. 2001 Sep 1;61(17):6388-93 [11522631] Clin Cancer Res. 1997 Sep;3(9):1653-60 [9815856] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0141897 ER - TY - JOUR T1 - Suppression of Rat Oral Carcinogenesis by Agonists of Peroxisome Proliferator Activated Receptor γ. AN - 1729350094; 26516762 AB - Peroxisome-proliferator-activated receptor γ (PPARγ) is a ligand-activated transcription factor that regulates cell proliferation, differentiation, and apoptosis. In vivo studies were performed to evaluate the activities of two thiazolidinedione PPARγ agonists, rosiglitazone and pioglitazone, as inhibitors of oral carcinogenesis in rats. Oral squamous cell carcinomas (OSCC) were induced in male F344 rats by 4-nitroquinoline-1-oxide (NQO; 20 ppm in the drinking water for 10 weeks). In each study, groups of 30 NQO-treated rats were exposed to a PPARγ agonist beginning at week 10 (one day after completion of NQO administration) or at week 17 (7 weeks post-NQO); chemopreventive agent exposure was continued until study termination at week 22 (rosiglitazone study) or week 24 (pioglitazone study). Administration of rosiglitazone (800 mg/kg diet) beginning at week 10 increased survival, reduced oral cancer incidence, and reduced oral cancer invasion score in comparison to dietary controls; however, chemopreventive activity was largely lost when rosiglitazone administration was delayed until week 17. Administration of pioglitazone (500 mg/kg diet beginning at week 10 or 1000 mg/kg diet beginning at week 17) induced significant reductions in oral cancer incidence without significant effects on OSCC invasion scores. Transcript levels of PPARγ and its three transcriptional variants (PPARγv1, PPARγv2, and PPARγv3) were not significantly different in OSCC versus age- and site-matched phenotypically normal oral tissues from rats treated with NQO. These data suggest that PPARγ provides a useful molecular target for oral cancer chemoprevention, and that overexpression of PPARγ at the transcriptional level in neoplastic lesions is not essential for chemopreventive efficacy. JF - PloS one AU - McCormick, David L AU - Horn, Thomas L AU - Johnson, William D AU - Peng, Xinjian AU - Lubet, Ronald A AU - Steele, Vernon E AD - Life Sciences Group, IIT Research Institute, Chicago, Illinois 60616, United States of America. ; Chemopreventive Agent Development Research Group, Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland 20852, United States of America. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 10 KW - 4-nitroquinolone-1-oxide KW - 0 KW - Antineoplastic Agents KW - PPAR gamma KW - Quinolones KW - Thiazolidinediones KW - rosiglitazone KW - 05V02F2KDG KW - 4-Nitroquinoline-1-oxide KW - 56-57-5 KW - pioglitazone KW - X4OV71U42S KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - 4-Nitroquinoline-1-oxide -- therapeutic use KW - Antineoplastic Agents -- administration & dosage KW - Antineoplastic Agents -- therapeutic use KW - Male KW - 4-Nitroquinoline-1-oxide -- administration & dosage KW - Quinolones -- therapeutic use KW - PPAR gamma -- metabolism KW - Thiazolidinediones -- therapeutic use KW - Mouth Neoplasms -- drug therapy KW - Carcinoma, Squamous Cell -- drug therapy KW - Thiazolidinediones -- administration & dosage KW - Quinolones -- administration & dosage KW - PPAR gamma -- genetics KW - PPAR gamma -- agonists UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1729350094?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Suppression+of+Rat+Oral+Carcinogenesis+by+Agonists+of+Peroxisome+Proliferator+Activated+Receptor+%CE%B3.&rft.au=McCormick%2C+David+L%3BHorn%2C+Thomas+L%3BJohnson%2C+William+D%3BPeng%2C+Xinjian%3BLubet%2C+Ronald+A%3BSteele%2C+Vernon+E&rft.aulast=McCormick&rft.aufirst=David&rft.date=2015-01-01&rft.volume=10&rft.issue=10&rft.spage=e0141849&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0141849 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-17 N1 - Date created - 2015-10-31 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - GSE51125; GEO N1 - SuppNotes - Cited By: J Clin Invest. 1997 May 15;99(10):2416-22 [9153284] Cancer Epidemiol Biomarkers Prev. 2009 Feb;18(2):541-50 [19190158] Cancer Epidemiol Biomarkers Prev. 2004 Nov;13(11 Pt 1):1704-9 [15533896] Lancet. 2005 Nov 19;366(9499):1784-93 [16298215] Biochim Biophys Acta. 2007 Aug;1771(8):1065-81 [17428730] JAMA. 2007 Sep 12;298(10):1189-95 [17848653] Oral Oncol. 2008 May;44(5):446-54 [17933578] Int J Cancer. 2008 Nov 15;123(10):2254-9 [18712722] Am Heart J. 2012 Nov;164(5):672-80 [23137497] Nat Med. 2013 May;19(5):557-66 [23652116] Angiogenesis. 2008;11(4):361-7 [18810647] J Pharmacol Exp Ther. 2015 Jun;353(3):573-81 [25876909] Metabolism. 2009 Dec;58(12):1694-702 [19767038] Cancer Prev Res (Phila). 2010 Jan;3(1):73-81 [20051374] Head Neck Pathol. 2009 Mar;3(1):78-81 [20596995] Cancer Sci. 2011 Feb;102(2):460-7 [21129124] J Biol Chem. 2011 Dec 2;286(48):41626-35 [21979952] Front Biosci (Landmark Ed). 2012;17:1816-34 [22201838] Nat Rev Cancer. 2012 Mar;12(3):181-95 [22318237] J Chronic Dis. 1972 Dec;25(12):711-6 [4648515] Cancer Res. 1988 Jun 1;48(11):3282-7 [3365707] NCI Monogr. 1989;(8):13-6 [2654650] Mol Carcinog. 2013 Jul;52(7):514-25 [22389237] Am J Epidemiol. 2013 Sep 1;178(5):679-90 [23817919] Anticancer Res. 2014 Feb;34(2):1021-5 [24511049] Oral Oncol. 2014 May;50(5):380-6 [24461628] Oral Oncol. 2014 Oct;50(10):924-9 [24434068] PLoS One. 2014;9(11):e113385 [25411778] Biochem Pharmacol. 2014 Nov 1;92(1):73-89 [25083916] CA Cancer J Clin. 2015 Jan-Feb;65(1):5-29 [25559415] PLoS One. 2015;10(1):e0116285 [25635769] CA Cancer J Clin. 2015 Mar;65(2):87-108 [25651787] Biomed Res Int. 2015;2015:845340 [25866814] J Natl Cancer Inst. 1998 Nov 4;90(21):1626-36 [9811312] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0141849 ER - TY - JOUR T1 - Clinical and Neuroimaging Features in Two Children with Mutations in the Mitochondrial ND5 Gene AN - 1722183644; PQ0002050501 AB - Mutations in the mitochondrial-encoded nicotinamide adenine dinucleotide dehydrogenase 5 gene (MT-ND5) has been implicated as an important genetic cause of childhood mitochondrial encephalomyopathies. This study reports the clinical and magnetic resonance imaging findings in two pediatric patients with mutations in the ND5 gene of mitochondrial DNA. The 8-month-old boy with m.13513 G > A mutation presented with infantile basal ganglia stroke syndrome secondary to mineralizing angiopathy. The 7-year-old girl with the m.13514A > G mutation had episodic regression, progressive ataxia, optic atrophy, and hyperactivity. Magnetic resonance imaging of the brain showed bilateral symmetrical signal intensity changes in the thalamus, tectal plate, and inferior olivary nucleus, which subsided on follow-up image. Both the patients had a stable course. Familiarity with the various phenotypic and magnetic resonance imaging findings and the clinical course in childhood mitochondrial encephalomyopathies may help the physician in targeted metabolic-genetic testing and prognostication. JF - Neuropediatrics AU - Sonam, Kothari AU - Bindu, P S AU - Taly, Arun B AU - Govindaraju, Chikkanna AU - Gayathri, Narayanappa AU - Arvinda, Hanumanthapura R AU - Nagappa, Madhu AU - Sinha, Sanjib AU - Khan, Nahid Akthar AU - Govindaraj, Periyasamy AU - Thangaraj, Kumarasamy AD - Department of Clinical Neurosciences, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, Karnataka, India Y1 - 2015///0, PY - 2015 DA - 0, 2015 SP - 277 EP - 281 PB - Georg Thieme Verlag, Ruedigerstr. 14 Stuttgart 70469 Germany VL - 46 IS - 04 SN - 0174-304X, 0174-304X KW - Biotechnology and Bioengineering Abstracts; Genetics Abstracts; CSA Neurosciences Abstracts KW - mitochondrial encephalmyopathy KW - ND5 mutation KW - m.13513G > A KW - m.13514A > G Mineralizing angiopathy KW - Neuroimaging KW - Pediatrics KW - Stroke KW - Magnetic resonance imaging KW - Mitochondria KW - Familiarity KW - Children KW - Thalamus KW - dehydrogenase KW - Mitochondrial DNA KW - ND5 gene KW - NAD KW - Ataxia KW - Inferior olivary nucleus KW - Mutation KW - Basal ganglia KW - optic atrophy KW - Hyperactivity KW - W 30910:Imaging KW - G 07880:Human Genetics KW - N3 11003:Developmental neuroscience UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1722183644?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuropediatrics&rft.atitle=Clinical+and+Neuroimaging+Features+in+Two+Children+with+Mutations+in+the+Mitochondrial+ND5+Gene&rft.au=Sonam%2C+Kothari%3BBindu%2C+P+S%3BTaly%2C+Arun+B%3BGovindaraju%2C+Chikkanna%3BGayathri%2C+Narayanappa%3BArvinda%2C+Hanumanthapura+R%3BNagappa%2C+Madhu%3BSinha%2C+Sanjib%3BKhan%2C+Nahid+Akthar%3BGovindaraj%2C+Periyasamy%3BThangaraj%2C+Kumarasamy&rft.aulast=Sonam&rft.aufirst=Kothari&rft.date=2015-01-01&rft.volume=46&rft.issue=04&rft.spage=277&rft.isbn=&rft.btitle=&rft.title=Neuropediatrics&rft.issn=0174304X&rft_id=info:doi/10.1055%2Fs-0035-1550149 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-10-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Neuroimaging; Pediatrics; Magnetic resonance imaging; Stroke; Mitochondria; Children; Familiarity; dehydrogenase; Thalamus; ND5 gene; Mitochondrial DNA; NAD; Ataxia; Inferior olivary nucleus; Mutation; Basal ganglia; Hyperactivity; optic atrophy DO - http://dx.doi.org/10.1055/s-0035-1550149 ER - TY - JOUR T1 - Nonnutritive Sweeteners in Breast Milk. AN - 1711538303; 26267522 AB - Nonnutritive sweeteners (NNS), including saccharin, sucralose, aspartame, and acesulfame-potassium, are commonly consumed in the general population, and all except for saccharin are considered safe for use during pregnancy and lactation. Sucralose (Splenda) currently holds the majority of the NNS market share and is often combined with acesulfame-potassium in a wide variety of foods and beverages. To date, saccharin is the only NNS reported to be found in human breast milk after maternal consumption, while there is no apparent information on the other NNS. Breast milk samples were collected from 20 lactating volunteers, irrespective of their habitual NNS intake. Saccharin, sucralose, and acesulfame-potassium were present in 65% of participants' milk samples, whereas aspartame was not detected. These data indicate that NNS are frequently ingested by nursing infants, and thus prospective clinical studies are necessary to determine whether early NNS exposure via breast milk may have clinical implications. JF - Journal of toxicology and environmental health. Part A AU - Sylvetsky, Allison C AU - Gardner, Alexandra L AU - Bauman, Viviana AU - Blau, Jenny E AU - Garraffo, H Martin AU - Walter, Peter J AU - Rother, Kristina I AD - a Section on Pediatric Diabetes and Metabolism , National Institute for Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda , Maryland , USA. ; c Clinical Mass Spectrometry Core , National Institute for Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda , Maryland , USA. Y1 - 2015 PY - 2015 DA - 2015 SP - 1029 EP - 1032 VL - 78 IS - 16 SN - 1528-7394, 1528-7394 KW - Non-Nutritive Sweeteners KW - 0 KW - Thiazines KW - Sucrose KW - 57-50-1 KW - trichlorosucrose KW - 96K6UQ3ZD4 KW - Saccharin KW - FST467XS7D KW - acetosulfame KW - MA3UYZ6K1H KW - Aspartame KW - Z0H242BBR1 KW - Index Medicus KW - Thiazines -- metabolism KW - Saccharin -- metabolism KW - Sucrose -- analysis KW - Humans KW - Aspartame -- analysis KW - Sucrose -- metabolism KW - Aspartame -- metabolism KW - Lactation KW - Environmental Monitoring KW - Sucrose -- analogs & derivatives KW - Saccharin -- analysis KW - Thiazines -- analysis KW - Female KW - Non-Nutritive Sweeteners -- metabolism KW - Milk, Human -- chemistry KW - Non-Nutritive Sweeteners -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1711538303?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+toxicology+and+environmental+health.+Part+A&rft.atitle=Nonnutritive+Sweeteners+in+Breast+Milk.&rft.au=Sylvetsky%2C+Allison+C%3BGardner%2C+Alexandra+L%3BBauman%2C+Viviana%3BBlau%2C+Jenny+E%3BGarraffo%2C+H+Martin%3BWalter%2C+Peter+J%3BRother%2C+Kristina+I&rft.aulast=Sylvetsky&rft.aufirst=Allison&rft.date=2015-01-01&rft.volume=78&rft.issue=16&rft.spage=1029&rft.isbn=&rft.btitle=&rft.title=Journal+of+toxicology+and+environmental+health.+Part+A&rft.issn=15287394&rft_id=info:doi/10.1080%2F15287394.2015.1053646 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-03 N1 - Date created - 2015-09-12 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1080/15287394.2015.1053646 ER - TY - JOUR T1 - Identification of a Cryptic Bacterial Promoter in Mouse (mdr1a) P-Glycoprotein cDNA. AN - 1708893792; 26309032 AB - The efflux transporter P-glycoprotein (P-gp) is an important mediator of various pharmacokinetic parameters, being expressed at numerous physiological barriers and also in multidrug-resistant cancer cells. Molecular cloning of homologous cDNAs is an important tool for the characterization of functional differences in P-gp between species. However, plasmids containing mouse mdr1a cDNA display significant genetic instability during cloning in bacteria, indicating that mdr1a cDNA may be somehow toxic to bacteria, allowing only clones containing mutations that abrogate this toxicity to survive transformation. We demonstrate here the presence of a cryptic promoter in mouse mdr1a cDNA that causes mouse P-gp expression in bacteria. This expression may account for the observed toxicity of mdr1a DNA to bacteria. Sigma 70 binding site analysis and GFP reporter plasmids were used to identify sequences in the first 321 bps of mdr1a cDNA capable of initiating bacterial protein expression. An mdr1a M107L cDNA containing a single residue mutation at the proposed translational start site was shown to allow sub-cloning of mdr1a in E. coli while retaining transport properties similar to wild-type P-gp. This mutant mdr1a cDNA may prove useful for efficient cloning of mdr1a in E. coli. JF - PloS one AU - Pluchino, Kristen M AU - Esposito, Dominic AU - Moen, Janna K AU - Hall, Matthew D AU - Madigan, James P AU - Shukla, Suneet AU - Procter, Lauren V AU - Wall, Vanessa E AU - Schneider, Thomas D AU - Pringle, Ian AU - Ambudkar, Suresh V AU - Gill, Deborah R AU - Hyde, Steven C AU - Gottesman, Michael M AD - Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States of America. ; Protein Expression Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research, Inc., Frederick, MD, United States of America. ; Gene Regulation and Chromosome Biology Laboratory, National Cancer Institute, Molecular Information Theory Group, Frederick, MD, United States of America. ; Gene Medicine Research Group, NDCLS, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 8 KW - DNA, Complementary KW - 0 KW - P-Glycoproteins KW - Sigma Factor KW - multidrug resistance protein 3 KW - RNA polymerase sigma 70 KW - EC 2.7.7.- KW - DNA-Directed RNA Polymerases KW - EC 2.7.7.6 KW - Index Medicus KW - Microscopy, Confocal KW - Animals KW - Blotting, Western KW - Spectrometry, Fluorescence KW - Sigma Factor -- metabolism KW - Plasmids -- genetics KW - Humans KW - HEK293 Cells KW - DNA-Directed RNA Polymerases -- metabolism KW - Mice KW - Flow Cytometry KW - Protein Conformation KW - Binding Sites KW - P-Glycoproteins -- genetics KW - Escherichia coli -- metabolism KW - DNA, Complementary -- genetics KW - Escherichia coli -- genetics KW - Promoter Regions, Genetic -- genetics KW - Escherichia coli -- growth & development KW - P-Glycoproteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1708893792?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Identification+of+a+Cryptic+Bacterial+Promoter+in+Mouse+%28mdr1a%29+P-Glycoprotein+cDNA.&rft.au=Pluchino%2C+Kristen+M%3BEsposito%2C+Dominic%3BMoen%2C+Janna+K%3BHall%2C+Matthew+D%3BMadigan%2C+James+P%3BShukla%2C+Suneet%3BProcter%2C+Lauren+V%3BWall%2C+Vanessa+E%3BSchneider%2C+Thomas+D%3BPringle%2C+Ian%3BAmbudkar%2C+Suresh+V%3BGill%2C+Deborah+R%3BHyde%2C+Steven+C%3BGottesman%2C+Michael+M&rft.aulast=Pluchino&rft.aufirst=Kristen&rft.date=2015-01-01&rft.volume=10&rft.issue=8&rft.spage=e0136396&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0136396 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-26 N1 - Date created - 2015-08-28 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Invest. 1995 Oct;96(4):1698-705 [7560060] Essays Biochem. 2011 Sep 7;50(1):161-78 [21967057] Science. 1997 Sep 5;277(5331):1453-62 [9278503] Biochemistry. 1998 Apr 7;37(14):5010-9 [9538020] Methods Enzymol. 1998;292:370-82 [9711568] Methods Enzymol. 1998;292:504-14 [9711578] Physiol Rev. 1999 Jan;79(1 Suppl):S3-S22 [9922374] Nat Rev Drug Discov. 2006 Mar;5(3):219-34 [16518375] Biochem Soc Symp. 2006;(73):1-10 [16626282] Mol Pharm. 2006 Jan-Feb;3(1):78-86 [16686372] Pharm Res. 2006 Jul;23(7):1460-72 [16779700] Nucleic Acids Res. 2007;35(3):771-88 [17189297] Mini Rev Med Chem. 2008 Mar;8(3):193-200 [18336339] Drug Metab Dispos. 2009 Mar;37(3):635-43 [19047468] Science. 2009 Mar 27;323(5922):1718-22 [19325113] PLoS One. 2011;6(12):e29191 [22216205] Nature. 2012 Oct 25;490(7421):566-9 [23000902] Proc Natl Acad Sci U S A. 2013 Aug 13;110(33):13386-91 [23901103] Protein Sci. 2014 Jan;23(1):34-46 [24155053] Genes Dev. 2014 Feb 1;28(3):214-9 [24449106] Acta Crystallogr D Biol Crystallogr. 2015 Mar;71(Pt 3):732-41 [25760620] J Gene Med. 1999 Sep-Oct;1(5):312-21 [10738548] FEBS Lett. 2000 May 12;473(2):149-53 [10812063] J Mol Biol. 2001 Oct 12;313(1):215-28 [11601857] Nat Rev Cancer. 2002 Jan;2(1):48-58 [11902585] Clin Pharmacokinet. 2003;42(1):59-98 [12489979] Biochim Biophys Acta. 2004 Jan 28;1660(1-2):53-65 [14757220] Proc Natl Acad Sci U S A. 1999 Nov 23;96(24):13679-84 [10570132] Oncogene. 2003 Oct 20;22(47):7468-85 [14576852] Proc Natl Acad Sci U S A. 1974 Apr;71(4):1342-6 [4598299] Somat Cell Mol Genet. 1985 Mar;11(2):117-26 [3856953] J Mol Biol. 1986 Apr 5;188(3):415-31 [3525846] J Biol Chem. 1989 Aug 25;264(24):14376-81 [2569468] Science. 1989 Sep 8;245(4922):1066-73 [2475911] Mol Cell Biol. 1990 Apr;10(4):1652-63 [1969610] Nature. 1990 Sep 27;347(6291):382-6 [1699127] Cell. 1990 Nov 16;63(4):827-34 [1699669] Biochemistry. 1992 Jul 7;31(26):6103-10 [1352702] J Bacteriol. 1993 May;175(9):2613-24 [8478327] Proc Natl Acad Sci U S A. 1993 Oct 1;90(19):9209-13 [8105473] Biochemistry. 1995 Jan 10;34(1):32-9 [7819214] J Bioenerg Biomembr. 1995 Feb;27(1):43-52 [7629051] Clin Pharmacol Ther. 2009 Oct;86(4):368-77 [19625998] Microb Biotechnol. 2010 Jul;3(4):403-11 [21255339] PLoS One. 2011;6(3):e18197 [21483867] PLoS One. 2011;6(8):e22577 [21826197] Proc Natl Acad Sci U S A. 1996 Jun 11;93(12):5969-74 [8650203] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0136396 ER - TY - JOUR T1 - Disposition of bisphenol AF, a bisphenol A analogue, in hepatocytes in vitro and in male and female Harlan Sprague-Dawley rats and B6C3F1/N mice following oral and intravenous administration. AN - 1706578325; 25923777 AB - 1. Bisphenol AF (BPAF) is used as a crosslinking agent for polymers and is being considered as a replacement for bisphenol A (BPA). 2. In this study, comparative clearance and metabolism of BPAF and BPA in hepatocytes and the disposition and metabolism of BPAF in rodents following oral administration of 3.4, 34 or 340 mg/kg [(14)C]BPAF were investigated. 3. BPAF was cleared more slowly than BPA in hepatocytes with the rate: rat > mouse > human. 4. [(14)C]BPAF was excreted primarily in feces by 72 h after oral administration to rats (65-80%) and mice (63-72%). Females excreted more in urine (rat, 15%; mouse, 24%) than males (rat, 1-4%; mouse, 10%). Residual tissue radioactivity was 94% of fecal radioactivity was present as BPAF, suggesting extensive deconjugation in the intestine. 6. Metabolites identified in bile were BPAF-glucuronide, -diglucuronide, -glucuronide sulfate and -sulfate. 7. In conclusion, BPAF was well absorbed following gavage administration and highly metabolized and excreted mostly in the feces as BPAF. JF - Xenobiotica; the fate of foreign compounds in biological systems AU - Waidyanatha, Suramya AU - Mathews, James M AU - Patel, Purvi R AU - Black, Sherry R AU - Snyder, Rodney W AU - Fennell, Timothy R AD - a Division of National Toxicology Program , National Institute of Environmental Health Sciences, Research Triangle Park , NC , USA and. Y1 - 2015 PY - 2015 DA - 2015 SP - 811 EP - 819 VL - 45 IS - 9 KW - 4,4'-hexafluorisopropylidene diphenol KW - 0 KW - Benzhydryl Compounds KW - Carbon Radioisotopes KW - Phenols KW - bisphenol A KW - MLT3645I99 KW - Index Medicus KW - oral absorption KW - metabolism KW - hepatocytes KW - disposition KW - Bisphenol AF KW - Administration, Oral KW - Animals KW - Rats, Sprague-Dawley KW - Metabolome KW - Metabolic Networks and Pathways KW - Humans KW - Mice KW - Tissue Distribution KW - Administration, Intravenous KW - Male KW - Female KW - Phenols -- administration & dosage KW - Benzhydryl Compounds -- chemistry KW - Phenols -- metabolism KW - Phenols -- chemistry KW - Benzhydryl Compounds -- metabolism KW - Benzhydryl Compounds -- administration & dosage KW - Hepatocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1706578325?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Xenobiotica%3B+the+fate+of+foreign+compounds+in+biological+systems&rft.atitle=Disposition+of+bisphenol+AF%2C+a+bisphenol+A+analogue%2C+in+hepatocytes+in+vitro+and+in+male+and+female+Harlan+Sprague-Dawley+rats+and+B6C3F1%2FN+mice+following+oral+and+intravenous+administration.&rft.au=Waidyanatha%2C+Suramya%3BMathews%2C+James+M%3BPatel%2C+Purvi+R%3BBlack%2C+Sherry+R%3BSnyder%2C+Rodney+W%3BFennell%2C+Timothy+R&rft.aulast=Waidyanatha&rft.aufirst=Suramya&rft.date=2015-01-01&rft.volume=45&rft.issue=9&rft.spage=811&rft.isbn=&rft.btitle=&rft.title=Xenobiotica%3B+the+fate+of+foreign+compounds+in+biological+systems&rft.issn=1366-5928&rft_id=info:doi/10.3109%2F00498254.2015.1021732 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-06-07 N1 - Date created - 2015-08-24 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3109/00498254.2015.1021732 ER - TY - JOUR T1 - Yeast Prions: Structure, Biology, and Prion-Handling Systems AN - 1705064570; PQ0001232686 JF - Microbiology and Molecular Biology Reviews AU - Wickner, Reed B AU - Shewmaker, Frank P AU - Bateman, David A AU - Edskes, Herman K AU - Gorkovskiy, Anton AU - Dayani, Yaron AU - Bezsonov, Evgeny E AD - Laboratory of Biochemistry and Genetics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA, wickner@helix.nih.gov. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 1 EP - 17 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 79 IS - 1 SN - 1092-2172, 1092-2172 KW - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - Prion protein KW - K 03330:Biochemistry KW - J 02490:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1705064570?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Microbiology+and+Molecular+Biology+Reviews&rft.atitle=Yeast+Prions%3A+Structure%2C+Biology%2C+and+Prion-Handling+Systems&rft.au=Wickner%2C+Reed+B%3BShewmaker%2C+Frank+P%3BBateman%2C+David+A%3BEdskes%2C+Herman+K%3BGorkovskiy%2C+Anton%3BDayani%2C+Yaron%3BBezsonov%2C+Evgeny+E&rft.aulast=Wickner&rft.aufirst=Reed&rft.date=2015-01-01&rft.volume=79&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Microbiology+and+Molecular+Biology+Reviews&rft.issn=10922172&rft_id=info:doi/10.1128%2FMMBR.00041-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-08-01 N1 - Number of references - 217 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Prion protein DO - http://dx.doi.org/10.1128/MMBR.00041-14 ER - TY - JOUR T1 - The Role of Grape Seed Extract in the Treatment of Chemo/Radiotherapy Induced Toxicity: A Systematic Review of Preclinical Studies. AN - 1692751397; 25880972 AB - Grapes are one of the most consumed fruits in the world and are rich in polyphenols. Grape seed proanthocyanidins (GSP) have demonstrated chemopreventive and/or chemotherapeutic effects in various cancer cell cultures and animal models. The clinical efficacy of chemotherapy is often limited by its adverse effects. Several studies show that reactive oxygen species mediate the cardiotoxicity and neurotoxicity induced by various cancer chemotherapeutic agents. This implies that concomitant administration of antioxidants may prevent these adverse effects. The review was carried out in accordance with the PRISMA guidelines. An electronic search strategy in Medline and Embase databases was conducted. Of the 41 studies reviewed, 27 studied GSP while the remainder (14) studied grape seed or skin extracts (GSE). All the studies were published in English, except 2 in Chinese. A significant percentage (34%) of the studies we reviewed assessed the effect of GSE or GSP on cardiotoxicity induced by chemotherapy. Doxorubicin was the most common chemotherapeutic drug studied followed by cisplatin. Research studies that assessed the effect of GSE or GSP on radiation treatment accounted for 22% of the articles reviewed. GSE/GSP ameliorates some of the cytotoxic effects on normal cells/tissues induced by chemo/radiotherapy. JF - Nutrition and cancer AU - Olaku, Oluwadamilola O AU - Ojukwu, Mary O AU - Zia, Farah Z AU - White, Jeffrey D AD - a Office of Cancer Complementary and Alternative Medicine, National Cancer Institute , Bethesda , Maryland , USA and Kelly Services , Rockville , Maryland , USA. Y1 - 2015 PY - 2015 DA - 2015 SP - 730 EP - 740 VL - 67 IS - 5 KW - Grape Seed Extract KW - 0 KW - Grape Seed Proanthocyanidins KW - Proanthocyanidins KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Rats, Wistar KW - Mice KW - Drug Evaluation, Preclinical KW - Proanthocyanidins -- therapeutic use KW - Grape Seed Extract -- therapeutic use KW - Drug-Related Side Effects and Adverse Reactions -- etiology KW - Drug-Related Side Effects and Adverse Reactions -- drug therapy KW - Radiation Injuries, Experimental -- etiology KW - Radiation Injuries, Experimental -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1692751397?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nutrition+and+cancer&rft.atitle=The+Role+of+Grape+Seed+Extract+in+the+Treatment+of+Chemo%2FRadiotherapy+Induced+Toxicity%3A+A+Systematic+Review+of+Preclinical+Studies.&rft.au=Olaku%2C+Oluwadamilola+O%3BOjukwu%2C+Mary+O%3BZia%2C+Farah+Z%3BWhite%2C+Jeffrey+D&rft.aulast=Olaku&rft.aufirst=Oluwadamilola&rft.date=2015-01-01&rft.volume=67&rft.issue=5&rft.spage=730&rft.isbn=&rft.btitle=&rft.title=Nutrition+and+cancer&rft.issn=1532-7914&rft_id=info:doi/10.1080%2F01635581.2015.1029639 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-05-03 N1 - Date created - 2015-06-30 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1080/01635581.2015.1029639 ER - TY - JOUR T1 - Use of Ethanol in the Trans-Arterial Lipiodol Embolization (TAELE) of Intermediated-Stage HCC: Is This Safer than Conventional Trans-Arterial Chemo-Embolization (c-TACE)? AN - 1691602047; 26110810 AB - To evaluate safety and efficacy of Trans-Arterial Ethanol-Lipiodol Embolization (TAELE) compared with conventional Trans-Arterial Chemo-Embolization (cTACE) in the treatment of small intermediate-HCC (BCLC-Stage B). A random sample of 87 patients (37.93% male; 62.07% female; age range, 36-86 years) with documented small intermediate-HCC and treated with TAELE (mixture 1:1 of Ethanol and Lipiodol) or cTACE (mixture of 50mg-Epirubicin and 5cc-Lipiodol) were retrospectively studied in an institutional review board approved protocol. The two procedures were compared with χ2-test, χ2-test with Yates correction, McNemar's exact test, ANOVA test and log-rank test. TAELE and cTACE therapies were performed in 45 and 42 patients, respectively. Thirty days after the procedure, a Multi-Detector Computed Tomography (MDCT) showed no significant difference in the number of patients with partial and complete response between the two groups (p-value = 0.958), according to mRECIST. Contrary, significant differences were found in tumor-devascularization, lesion-reduction and post-embolization syndrome occurrence (p-value = 0.0004, p-value = 0.0003 and p-value = 0.009, respectively). Similar survival was observed during 36-month follow-up (p-value = 0.884). Compared to cTACE, TAELE showed a better toxicity profile with similar 36-month survival and similar one-month anti-tumor effects, which makes it better tolerated by patients, especially in case of more than one treatment. JF - PloS one AU - Somma, Francesco AU - D'Angelo, Roberto AU - Serra, Nicola AU - Gatta, Gianluca AU - Grassi, Roberto AU - Fiore, Francesco AD - Department of Medicine and Surgery "Magrassi and Lanzara", Section of Radiology, Second University of Naples (SUN), Napoli, Italy. ; Department of Interventional Radiology, National Cancer Institute of Naples "Fondazione Pascale", Napoli, Italy. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 6 KW - Ethanol KW - 3K9958V90M KW - Epirubicin KW - 3Z8479ZZ5X KW - Ethiodized Oil KW - 8008-53-5 KW - Index Medicus KW - Aged, 80 and over KW - Humans KW - Adult KW - Treatment Outcome KW - Retrospective Studies KW - Aged KW - Middle Aged KW - Male KW - Female KW - Chemoembolization, Therapeutic -- adverse effects KW - Ethiodized Oil -- administration & dosage KW - Liver Neoplasms -- therapy KW - Epirubicin -- therapeutic use KW - Chemoembolization, Therapeutic -- methods KW - Ethiodized Oil -- therapeutic use KW - Carcinoma, Hepatocellular -- therapy KW - Ethanol -- administration & dosage KW - Epirubicin -- administration & dosage KW - Ethanol -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1691602047?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Use+of+Ethanol+in+the+Trans-Arterial+Lipiodol+Embolization+%28TAELE%29+of+Intermediated-Stage+HCC%3A+Is+This+Safer+than+Conventional+Trans-Arterial+Chemo-Embolization+%28c-TACE%29%3F&rft.au=Somma%2C+Francesco%3BD%27Angelo%2C+Roberto%3BSerra%2C+Nicola%3BGatta%2C+Gianluca%3BGrassi%2C+Roberto%3BFiore%2C+Francesco&rft.aulast=Somma&rft.aufirst=Francesco&rft.date=2015-01-01&rft.volume=10&rft.issue=6&rft.spage=e0129573&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0129573 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-06 N1 - Date created - 2015-06-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: World J Surg. 2000 Jul;24(7):844-50; discussion 850 [10833253] J Vasc Interv Radiol. 2001 Mar;12(3):321-6 [11287509] J Hepatol. 2001 Sep;35(3):421-30 [11592607] Lancet. 2002 May 18;359(9319):1734-9 [12049862] Radiology. 2002 Jul;224(1):47-54 [12091661] Cancer Treat Rev. 2003 Apr;29(2):99-104 [12670452] Br J Cancer. 2003 Oct 20;89(8):1423-7 [14562011] Lancet. 2003 Dec 6;362(9399):1907-17 [14667750] Gastroenterology. 2004 Apr;126(4):1005-14 [15057740] Gastroenterology. 2004 Nov;127(5 Suppl 1):S179-88 [15508083] J Vasc Interv Radiol. 1993 May-Jun;4(3):333-9 [8390316] Ann Surg. 1994 Mar;219(3):236-47 [8147605] Hepatology. 1994 Sep;20(3):643-50 [7521316] Radiology. 1996 Jan;198(1):33-40 [8539401] N Engl J Med. 1999 Mar 11;340(10):745-50 [10072408] Am J Pathol. 1954 Sep-Oct;30(5):969-77 [13197542] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078] J Gastroenterol. 2005 Mar;40(3):225-35 [15830281] World J Gastroenterol. 2005 May 14;11(18):2792-5 [15884125] Hepatology. 2005 Nov;42(5):1208-36 [16250051] Cardiovasc Intervent Radiol. 2007 Jan-Feb;30(1):6-25 [17103105] J Clin Oncol. 2007 Mar 10;25(8):978-86 [17350947] Lancet. 2009 Feb 21;373(9664):614-6 [19231618] J Vasc Interv Radiol. 2009 Mar;20(3):352-9 [19167240] Cochrane Database Syst Rev. 2011;(3):CD004787 [21412886] Oncology. 2011;81 Suppl 1:141-7 [22212948] J Hepatol. 2012 Apr;56(4):908-43 [22424438] Eur J Gastroenterol Hepatol. 2012 Nov;24(11):1325-32 [22872074] Endocrine. 2014 Sep;47(1):177-82 [24385266] Am J Transplant. 2009 Aug;9(8):1920-8 [19552767] Semin Liver Dis. 2010 Feb;30(1):52-60 [20175033] Semin Liver Dis. 2010 Feb;30(1):61-74 [20175034] Psychometrika. 1947 Jun;12(2):153-7 [20254758] Radiology. 2010 Jun;255(3):955-65 [20501733] World J Gastroenterol. 2010 Dec 7;16(45):5766-72 [21128329] Radiology. 2008 Oct;249(1):346-54 [18796686] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0129573 ER - TY - JOUR T1 - Defining the Pharmacodynamic Profile and Therapeutic Index of NHS-IL12 Immunocytokine in Dogs with Malignant Melanoma. AN - 1690648096; 26091536 AB - Interleukin (IL)-12 is a pro-inflammatory cytokine that mediates T-helper type 1 responses and cytotoxic T-cell activation, contributing to its utility as anti-cancer agent. Systemic administration of IL-12 often results in unacceptable toxicity; therefore, strategies to direct delivery of IL-12 to tumors are under investigation. The objective of this study was to assist the preclinical development of NHS-IL12, an immunocytokine consisting of an antibody, which targets necrotic tumor regions, linked to IL-12. Specifically this study sought to evaluate the safety, serum pharmacokinetics, anti-tumor activity, and immune modulation of NHS-IL12 in dogs with naturally occurring cancers. A rapid dose-escalation study of NHS-IL12 administered subcutaneously to dogs with melanoma was conducted through the Comparative Oncology Trials Consortium (COTC). Eleven dogs were enrolled in four dose-escalation cohorts; thereafter, an additional seven dogs were treated at the defined tolerable dose of 0.8 mg/m2. The expanded cohort at this fixed dose (ten dogs in total) was accrued for further pharmacokinetics and pharmacodynamics assessment. NHS-IL12 levels, serum cytokine concentrations, and peripheral blood mononuclear cell characterization (post-treatment) and draining lymph node immune profiling, and tumor biopsies (pre- and post-treatment) were collected. Adverse events included thrombocytopenia, liver enzymopathies, fever, and vasculitis. Correlation between interferon (IFN)-γ induction, adverse events, and NHS-IL12 exposure (maximum concentration and area under the concentration-time curve) were dose-dependent. Serum IL-10 levels and intratumoral CD8+ populations increased after treatment. Partial responses, according to Response Evaluation Criteria in Solid Tumors (RECIST) criteria, were observed in two dogs treated with NHS-IL12 0.8 mg/m2 and 1.6 mg/m2. NHS-IL12 was administered safely to dogs with melanoma and both immunologic and clinical activity was observed. This study successfully defined a narrow therapeutic window for systemic delivery of NHS-IL12 via the subcutaneous route. Results will inform the design and implementation of first-in-human clinical trials of NHS-IL12 in cancer patients. JF - PloS one AU - Paoloni, Melissa AU - Mazcko, Christina AU - Selting, Kimberly AU - Lana, Susan AU - Barber, Lisa AU - Phillips, Jeffrey AU - Skorupski, Katherine AU - Vail, David AU - Wilson, Heather AU - Biller, Barbara AU - Avery, Anne AU - Kiupel, Matti AU - LeBlanc, Amy AU - Bernhardt, Anna AU - Brunkhorst, Beatrice AU - Tighe, Robert AU - Khanna, Chand AD - Comparative Oncology Program, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, United States of America. ; College of Veterinary Medicine, University of Missouri-Columbia, Columbia, Missouri, United States of America. ; College of Veterinary Medicine and Biological Sciences, Colorado State University, Fort Collins, Colorado, United States of America. ; School of Veterinary Medicine, Tufts University, North Grafton, Massachusetts, United States of America. ; College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee, United States of America. ; School of Veterinary Medicine, University of California Davis, Davis, California, United States of America. ; School of Veterinary Medicine, University of Wisconsin-Madison, Madison, Wisconsin, United States of America. ; College of Veterinary Medicine, Texas A&M University, College Station, Texas, United States of America. ; College of Veterinary Medicine, Michigan State University, East Lansing, Michigan, United States of America. ; EMD-Serono Research and Development Institute, Billerica, Massachusetts, United States of America. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 6 KW - Antineoplastic Agents KW - 0 KW - Cytokines KW - Immunoglobulin G KW - Immunologic Factors KW - NHS-IL12 immunocytokine KW - Recombinant Fusion Proteins KW - Interleukin-12 KW - 187348-17-0 KW - Index Medicus KW - Cytokines -- blood KW - Animals KW - Lymph Nodes -- metabolism KW - Lymphocytes, Tumor-Infiltrating -- immunology KW - CD8-Positive T-Lymphocytes -- metabolism KW - Lymph Nodes -- pathology KW - Leukocytes, Mononuclear -- immunology KW - Lymphocytes, Tumor-Infiltrating -- metabolism KW - Infusions, Subcutaneous KW - CD8-Positive T-Lymphocytes -- immunology KW - Leukocytes, Mononuclear -- metabolism KW - Treatment Outcome KW - Dogs KW - Immunophenotyping KW - Male KW - Female KW - Lymph Nodes -- immunology KW - Recombinant Fusion Proteins -- pharmacokinetics KW - Antineoplastic Agents -- administration & dosage KW - Immunologic Factors -- administration & dosage KW - Interleukin-12 -- administration & dosage KW - Antineoplastic Agents -- pharmacokinetics KW - Immunoglobulin G -- pharmacology KW - Dog Diseases -- drug therapy KW - Dog Diseases -- pathology KW - Recombinant Fusion Proteins -- administration & dosage KW - Interleukin-12 -- pharmacokinetics KW - Immunoglobulin G -- administration & dosage KW - Melanoma -- veterinary KW - Immunologic Factors -- pharmacokinetics KW - Immunologic Factors -- pharmacology KW - Recombinant Fusion Proteins -- pharmacology KW - Interleukin-12 -- pharmacology KW - Dog Diseases -- blood KW - Antineoplastic Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1690648096?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Defining+the+Pharmacodynamic+Profile+and+Therapeutic+Index+of+NHS-IL12+Immunocytokine+in+Dogs+with+Malignant+Melanoma.&rft.au=Paoloni%2C+Melissa%3BMazcko%2C+Christina%3BSelting%2C+Kimberly%3BLana%2C+Susan%3BBarber%2C+Lisa%3BPhillips%2C+Jeffrey%3BSkorupski%2C+Katherine%3BVail%2C+David%3BWilson%2C+Heather%3BBiller%2C+Barbara%3BAvery%2C+Anne%3BKiupel%2C+Matti%3BLeBlanc%2C+Amy%3BBernhardt%2C+Anna%3BBrunkhorst%2C+Beatrice%3BTighe%2C+Robert%3BKhanna%2C+Chand&rft.aulast=Paoloni&rft.aufirst=Melissa&rft.date=2015-01-01&rft.volume=10&rft.issue=6&rft.spage=e0129954&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0129954 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-13 N1 - Date created - 2015-06-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Lancet. 1998 Jun 27;351(9120):1901-3 [9654253] Clin Cancer Res. 1995 Dec;1(12):1595-601 [9815961] J Clin Oncol. 1999 Jul;17(7):2105-16 [10561265] Clin Exp Immunol. 2000 Jan;119(1):28-37 [10606961] Cytokine Growth Factor Rev. 2001 Dec;12(4):375-91 [11544106] Cytokine Growth Factor Rev. 2002 Apr;13(2):155-68 [11900991] Clin Cancer Res. 2003 Jan;9(1):76-83 [12538454] Nat Rev Immunol. 2003 Feb;3(2):133-46 [12563297] Cancer Immun. 2003 Jul 16;3:7 [12862418] Clin Cancer Res. 2003 Oct 15;9(13):4653-65 [14581334] Immunity. 2003 Nov;19(5):641-4 [14614851] N Engl J Med. 1988 Dec 22;319(25):1676-80 [3264384] Immunol Ser. 1994;61:239-50 [7516716] Science. 1995 Nov 10;270(5238):908 [7481785] Cancer. 1997 Apr 1;79(7):1409-21 [9083164] J Immunol. 1998 Jun 15;160(12):6195-203 [9637539] J Clin Oncol. 1999 Mar;17(3):968-75 [10071291] Cancer Gene Ther. 1999 Jan-Feb;6(1):26-36 [10078961] Curr Cancer Drug Targets. 2006 Mar;6(2):123-33 [16529542] Oncologist. 2006 Apr;11(4):397-408 [16614236] Vaccine. 2006 May 22;24(21):4582-5 [16188351] Clin Cancer Res. 2007 Aug 15;13(16):4677-85 [17699845] Mol Ther. 2007 Nov;15(11):2044-50 [17726460] Food Chem Toxicol. 2008 Jan;46(1):203-11 [17868966] Nat Rev Cancer. 2008 Feb;8(2):147-56 [18202698] Gene Ther. 2008 Feb;15(4):267-76 [18033308] Eur J Cancer. 2009 Jan;45(2):228-47 [19097774] PLoS One. 2009;4(3):e4972 [19330034] PLoS Med. 2009 Oct;6(10):e1000161 [19823573] Cancer Biol Ther. 2010 Jan;9(1):20-2 [20023419] PLoS One. 2010;5(6):e11013 [20543980] Curr Opin Allergy Clin Immunol. 2010 Dec;10(6):534-41 [20966748] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0129954 ER - TY - JOUR T1 - Phosphatase Inhibitors Function as Novel, Broad Spectrum Botulinum Neurotoxin Antagonists in Mouse and Human Embryonic Stem Cell-Derived Motor Neuron-Based Assays. AN - 1687995138; 26061731 AB - There is an urgent need to develop novel treatments to counter Botulinum neurotoxin (BoNT) poisoning. Currently, the majority of BoNT drug development efforts focus on directly inhibiting the proteolytic components of BoNT, i.e. light chains (LC). Although this is a rational approach, previous research has shown that LCs are extremely difficult drug targets and that inhibiting multi-serotype BoNTs with a single LC inhibitor may not be feasible. An alternative approach would target neuronal pathways involved in intoxication/recovery, rather than the LC itself. Phosphorylation-related mechanisms have been implicated in the intoxication pathway(s) of BoNTs. However, the effects of phosphatase inhibitors upon BoNT activity in the physiological target of BoNTs, i.e. motor neurons, have not been investigated. In this study, a small library of phosphatase inhibitors was screened for BoNT antagonism in the context of mouse embryonic stem cell-derived motor neurons (ES-MNs). Four inhibitors were found to function as BoNT/A antagonists. Subsequently, we confirmed that these inhibitors protect against BoNT/A in a dose-dependent manner in human ES-MNs. Additionally, these compounds provide protection when administered in post-intoxication scenario. Importantly, the inhibitors were also effective against BoNT serotypes B and E. To the best of our knowledge, this is the first study showing phosphatase inhibitors as broad-spectrum BoNT antagonists. JF - PloS one AU - Kiris, Erkan AU - Nuss, Jonathan E AU - Stanford, Stephanie M AU - Wanner, Laura M AU - Cazares, Lisa AU - Maestre, Michael F AU - Du, Hao T AU - Gomba, Glenn Y AU - Burnett, James C AU - Gussio, Rick AU - Bottini, Nunzio AU - Panchal, Rekha G AU - Kane, Christopher D AU - Tessarollo, Lino AU - Bavari, Sina AD - Geneva Foundation, Tacoma, WA, United States of America; Department of Molecular and Translational Sciences, US Army Medical Research Institute of Infectious Diseases, Frederick, MD, United States of America; Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute (NCI), Frederick, MD, United States of America. ; Department of Molecular and Translational Sciences, US Army Medical Research Institute of Infectious Diseases, Frederick, MD, United States of America. ; Division of Cellular Biology, La Jolla Institute for Allergy and Immunology, La Jolla, CA, United States of America. ; Leidos Biomedical Research, Inc., Computational Drug Development Group (CDDG), NCI, Frederick, MD, United States of America; CDDG, Developmental Therapeutics Program, NCI, Frederick, MD, United States of America. ; CDDG, Developmental Therapeutics Program, NCI, Frederick, MD, United States of America. ; Department of Molecular and Translational Sciences, US Army Medical Research Institute of Infectious Diseases, Frederick, MD, United States of America; Henry M. Jackson Foundation, Bethesda, MD, United States of America; DoD Biotechnology High Performance Computing Software Applications Institute (BHSAI), Telemedicine and Advanced Technology Research Center (TATRC), US Army Medical Research and Materiel Command (USAMRMC), Frederick, MD, United States of America. ; Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute (NCI), Frederick, MD, United States of America. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 6 KW - Enzyme Inhibitors KW - 0 KW - SNARE Proteins KW - Small Molecule Libraries KW - Phosphoric Monoester Hydrolases KW - EC 3.1.3.2 KW - Botulinum Toxins KW - EC 3.4.24.69 KW - Index Medicus KW - Animals KW - Dose-Response Relationship, Drug KW - Humans KW - Mice KW - Drug Evaluation, Preclinical KW - SNARE Proteins -- metabolism KW - Phosphoric Monoester Hydrolases -- antagonists & inhibitors KW - Motor Neurons -- metabolism KW - Embryonic Stem Cells -- metabolism KW - Embryonic Stem Cells -- drug effects KW - Small Molecule Libraries -- pharmacology KW - Botulinum Toxins -- toxicity KW - Enzyme Inhibitors -- pharmacology KW - Botulinum Toxins -- antagonists & inhibitors KW - Motor Neurons -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687995138?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Phosphatase+Inhibitors+Function+as+Novel%2C+Broad+Spectrum+Botulinum+Neurotoxin+Antagonists+in+Mouse+and+Human+Embryonic+Stem+Cell-Derived+Motor+Neuron-Based+Assays.&rft.au=Kiris%2C+Erkan%3BNuss%2C+Jonathan+E%3BStanford%2C+Stephanie+M%3BWanner%2C+Laura+M%3BCazares%2C+Lisa%3BMaestre%2C+Michael+F%3BDu%2C+Hao+T%3BGomba%2C+Glenn+Y%3BBurnett%2C+James+C%3BGussio%2C+Rick%3BBottini%2C+Nunzio%3BPanchal%2C+Rekha+G%3BKane%2C+Christopher+D%3BTessarollo%2C+Lino%3BBavari%2C+Sina&rft.aulast=Kiris&rft.aufirst=Erkan&rft.date=2015-01-01&rft.volume=10&rft.issue=6&rft.spage=e0129264&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0129264 LA - 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Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0129264 ER - TY - JOUR T1 - Editing the Plasmodium vivax Genome, Using Zinc-Finger Nucleases AN - 1687673771; PQ0001517486 AB - Plasmodium vivax is a major cause of malaria morbidity worldwide yet has remained genetically intractable. To stably modify this organism, we used zinc-finger nucleases (ZFNs), which take advantage of homology-directed DNA repair mechanisms at the site of nuclease action. Using ZFNs specific to the gene encoding P. vivax dihydrofolate reductase (pvdhfr), we transfected blood specimens from Saimiri boliviensis monkeys infected with the pyrimethamine (Pyr)-susceptible Chesson strain with a ZFN plasmid carrying a Pyr-resistant mutant pvdhfr sequence. We obtained Pyr-resistant parasites in vivo that carried mutant pvdhfr and additional silent mutations designed to confirm editing. These results herald the era of stable P. vivax genetic modifications. JF - Journal of Infectious Diseases AU - Barros, Roberto R Moraes AU - Straimer, Judith AU - Sa, Juliana M AU - Salzman, Rebecca E AU - Melendez-Muniz, Viviana A AU - Mu, Jianbing AU - Fidock, David A AU - Wellems, Thomas E AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, twellems@niaid.nih.gov Y1 - 2015/01/01/ PY - 2015 DA - 2015 Jan 01 SP - 125 EP - 129 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 211 IS - 1 SN - 0022-1899, 0022-1899 KW - Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources KW - malaria KW - transfection KW - allelic modification KW - dihydrofolate reductase-thymidylate synthase KW - pyrimethamine KW - Saimiri boliviensis KW - Pyrimethamine KW - Genomes KW - Parasites KW - Mutations KW - Nucleotide sequence KW - Nuclease KW - Plasmodium vivax KW - Malaria KW - DNA repair KW - Plasmids KW - Morbidity KW - Public health KW - Saimiri KW - Blood KW - Dihydrofolate reductase KW - Infectious diseases KW - DNA KW - Mutation KW - N 14820:DNA Metabolism & Structure KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08524:Public health, medicines, dangerous organisms KW - K 03310:Genetics & Taxonomy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687673771?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Editing+the+Plasmodium+vivax+Genome%2C+Using+Zinc-Finger+Nucleases&rft.au=Barros%2C+Roberto+R+Moraes%3BStraimer%2C+Judith%3BSa%2C+Juliana+M%3BSalzman%2C+Rebecca+E%3BMelendez-Muniz%2C+Viviana+A%3BMu%2C+Jianbing%3BFidock%2C+David+A%3BWellems%2C+Thomas+E&rft.aulast=Barros&rft.aufirst=Roberto+R&rft.date=2015-01-01&rft.volume=211&rft.issue=1&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjiu423 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-06-01 N1 - Last updated - 2016-10-26 N1 - SubjectsTermNotLitGenreText - Genomes; Parasites; Infectious diseases; Mutations; Nucleotide sequence; DNA; Plasmids; Public health; Pyrimethamine; Blood; Dihydrofolate reductase; Nuclease; Malaria; DNA repair; Mutation; Morbidity; Saimiri; Plasmodium vivax DO - http://dx.doi.org/10.1093/infdis/jiu423 ER - TY - JOUR T1 - Higher AgNOR Expression in Metaplastic and Dysplastic Airway Epithelial Cells Predicts the Risk of Developing Lung Cancer in Women Chronically Exposed to Biomass Smoke AN - 1687665192; PQ0001579764 AB - We evaluated AgNOR expression in airway epithelial cells (AECs) as a risk factor of lung carcinogenesis in 228 nonsmoking women exposed to biomass fuel (BMF). A total of 185 age-matched women who cooked with cleaner fuel (liquefied petroleum gas [LPG]) were enrolled as study controls. Compared with controls, Papanicolaou-stained sputum samples showed 4 and 8 times higher prevalence of metaplasia and dysplasia, respectively, in AECs of BMF users. AgNOR staining showed significantly larger numbers of dots and larger size and percentage of AgNOR-occupied nuclear area in normal AECs of BMF users than in controls. Interestingly, AgNOR parameters increased dramatically when the cells were transformed from normalcy to metaplasia and dysplasia. Compared with LPG users, BMF users showed a marked rise in reactive oxygen species (ROS) generation and a depletion of superoxide dismutase (SOD), indicating oxidative stress. Indoor air of BMF-using households had 2-5 times more particulate pollutants (PM sub(10) and PM sub(2.5)), 73% more nitrogen dioxide (NO sub(2)), and 4 times more particulate-laden benzo(a)pyrene [B(a)P], but no difference in sulfur dioxide was observed. A high-performance liquid chromatography (HPLC) study estimated a 6-fold rise in benzene metabolite trans, trans-muconic acid (t,t-MA) in urine of BMF users. After controlling confounding foctors using multivariate logistic regression, positive associations were observed between cellular changes, AgNOR parameters, and PM sub(10), PM sub(2.5), NO sub(2), B(a)P, and t,t-MA levels, especially the concentration of B(a)P. In conclusion, cumulative exposure to biomass smoke causes oxidative stress and enhances AgNOR expression in precancerous metaplastic and dysplastic AECs and appears to be a risk factor for developing lung cancer. JF - Journal of Environmental Pathology, Toxicology and Oncology AU - Mondal, Nandan Kumar AU - Roychoudhury, Sanghita AU - Ray, Manas Ranjan AD - Artificial Organs Laboratory, Department of Surgery, University of Maryland School of Medicine, Baltimore, Maryland; Department of Experimental Hematology, Chittaranjan National Cancer Institute, Kolkata, India; Department of Zoology, Kabi Nazrul College Y1 - 2015 PY - 2015 DA - 2015 SP - 35 EP - 51 PB - Begell House Inc., 79 Madison Avenue, Suite 1201 New York NY 10016-7892 United States VL - 34 IS - 1 SN - 0731-8898, 0731-8898 KW - Toxicology Abstracts; Health & Safety Science Abstracts; Risk Abstracts; Pollution Abstracts KW - Indoor air pollution KW - biomass fuel KW - particulate matter KW - oxidative stress KW - AgNOR KW - airway epithelial cells KW - metaplasia KW - dysplasia KW - carcinogenesis KW - lung cancer KW - High-performance liquid chromatography KW - Epithelial cells KW - Fuels KW - Metabolites KW - Particulates KW - Nitrogen dioxide KW - Sulfur dioxide KW - Reactive oxygen species KW - Superoxide dismutase KW - Oxidative stress KW - Risk factors KW - Metaplasia KW - Petroleum KW - Lung cancer KW - Respiratory tract KW - Particle size KW - Dysplasia KW - Biomass KW - Cancer KW - Smoke KW - Health risks KW - Liquid chromatography KW - Households KW - Nuclear fuels KW - Carcinogenesis KW - Sputum KW - H 8000:Radiation Safety/Electrical Safety KW - P 0000:AIR POLLUTION KW - R2 23060:Medical and environmental health KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1687665192?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Environmental+Pathology%2C+Toxicology+and+Oncology&rft.atitle=Higher+AgNOR+Expression+in+Metaplastic+and+Dysplastic+Airway+Epithelial+Cells+Predicts+the+Risk+of+Developing+Lung+Cancer+in+Women+Chronically+Exposed+to+Biomass+Smoke&rft.au=Mondal%2C+Nandan+Kumar%3BRoychoudhury%2C+Sanghita%3BRay%2C+Manas+Ranjan&rft.aulast=Mondal&rft.aufirst=Nandan&rft.date=2015-01-01&rft.volume=34&rft.issue=1&rft.spage=35&rft.isbn=&rft.btitle=&rft.title=Journal+of+Environmental+Pathology%2C+Toxicology+and+Oncology&rft.issn=07318898&rft_id=info:doi/10.1615%2FJEnvironPatholToxicolOncol.2015010708 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-06-01 N1 - Last updated - 2015-08-19 N1 - SubjectsTermNotLitGenreText - High-performance liquid chromatography; Epithelial cells; Dysplasia; Fuels; Metabolites; Biomass; Nitrogen dioxide; Smoke; Sulfur dioxide; Reactive oxygen species; Oxidative stress; Superoxide dismutase; Petroleum; Metaplasia; Risk factors; Carcinogenesis; Sputum; Respiratory tract; Lung cancer; Particle size; Particulates; Cancer; Health risks; Liquid chromatography; Households; Nuclear fuels DO - http://dx.doi.org/10.1615/JEnvironPatholToxicolOncol.2015010708 ER - TY - JOUR T1 - Neuronal Cx3cr1 Deficiency Protects against Amyloid β-Induced Neurotoxicity. AN - 1686409719; 26038823 AB - Cx3cr1, the receptor for the chemokine Cx3cl1 (fractalkine), has been implicated in the progression and severity of Alzheimer's disease-like pathology in mice, but the underlying mechanisms remain unclear. A complicating factor is that Cx3cr1 has been demonstrated in both neurons and microglia. Here, we have dissected the differences between neuronal and microglial Cx3cr1, specifically by comparing direct amyloid-β-induced toxicity in cultured, mature, microglia-depleted hippocampal neurons from wild-type and Cx3cr1-/- mice. Wild-type neurons expressed both Cx3cl1 and Cx3cr1 and released Cx3cl1 in response to amyloid-β. Knockout of neuronal Cx3cr1 abated amyloid-β-induced lactate dehydrogenase release. Furthermore, amyloid-β differentially induced depression of pre- and postsynaptic components of miniature excitatory postsynaptic currents, in a peptide conformation-dependent manner. Knockout of neuronal Cx3cr1 abated effects of both amyloid-β conformational states, which were differentiable by aggregation kinetics and peptide morphology. We obtained similar results after both acute and chronic treatment of cultured neurons with the Cx3cr1 antagonist F1. Thus, neuronal Cx3cr1 may impact Alzheimer's disease-like pathology by modulating conformational state-dependent amyloid-β-induced synaptotoxicity. JF - PloS one AU - Dworzak, Jenny AU - Renvoisé, Benoît AU - Habchi, Johnny AU - Yates, Emma V AU - Combadière, Christophe AU - Knowles, Tuomas P AU - Dobson, Christopher M AU - Blackstone, Craig AU - Paulsen, Ole AU - Murphy, Philip M AD - Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America; Neuronal Oscillations Group, Department of Physiology, Development, and Neuroscience, University of Cambridge, Cambridge, United Kingdom; Cell Biology Section, Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America. ; Cell Biology Section, Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America. ; Department of Chemistry, University of Cambridge, Cambridge, United Kingdom. ; Centre d'Immunologie et des Maladies Infectieuses-Paris, Institut National de la Santé et de la Recherche Médicale, Paris, France. ; Neuronal Oscillations Group, Department of Physiology, Development, and Neuroscience, University of Cambridge, Cambridge, United Kingdom. ; Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, United States of America. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 6 KW - Amyloid beta-Peptides KW - 0 KW - Cx3cr1 protein, mouse KW - Receptors, Chemokine KW - Index Medicus KW - Animals KW - Disease Models, Animal KW - Mice KW - Mice, Knockout KW - Protein Aggregation, Pathological -- metabolism KW - Receptors, Chemokine -- deficiency KW - Amyloid beta-Peptides -- genetics KW - Alzheimer Disease -- genetics KW - Neurons -- metabolism KW - Amyloid beta-Peptides -- metabolism KW - Protein Aggregation, Pathological -- pathology KW - Protein Aggregation, Pathological -- genetics KW - Alzheimer Disease -- metabolism KW - Synaptic Transmission KW - Neurons -- pathology KW - Alzheimer Disease -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1686409719?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Neuronal+Cx3cr1+Deficiency+Protects+against+Amyloid+%CE%B2-Induced+Neurotoxicity.&rft.au=Dworzak%2C+Jenny%3BRenvois%C3%A9%2C+Beno%C3%AEt%3BHabchi%2C+Johnny%3BYates%2C+Emma+V%3BCombadi%C3%A8re%2C+Christophe%3BKnowles%2C+Tuomas+P%3BDobson%2C+Christopher+M%3BBlackstone%2C+Craig%3BPaulsen%2C+Ole%3BMurphy%2C+Philip+M&rft.aulast=Dworzak&rft.aufirst=Jenny&rft.date=2015-01-01&rft.volume=10&rft.issue=6&rft.spage=e0127730&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0127730 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-22 N1 - Date created - 2015-06-04 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Eur J Neurosci. 2004 Dec;20(12):3222-32 [15610155] Neuron. 2006 Dec 7;52(5):831-43 [17145504] Neurobiol Dis. 2005 Nov;20(2):187-98 [16242627] J Neurosci. 2005 Nov 30;25(48):11061-70 [16319306] Proc Natl Acad Sci U S A. 2006 Feb 28;103(9):3410-5 [16492745] J Neurosci. 2006 May 31;26(22):6011-8 [16738244] J Immunol. 2000 Feb 1;164(3):1333-9 [10640747] Nat Rev Neurosci. 2001 Aug;2(8):595-8 [11484003] Glia. 2002 Mar 15;37(4):314-27 [11870871] J Neurosci. 2000 Aug 1;20(15):RC87 [10899174] Nature. 2002 Apr 4;416(6880):535-9 [11932745] J Neuroimmunol. 2002 Mar;124(1-2):16-28 [11958818] J Neurosci Res. 2002 Aug 1;69(3):418-26 [12125082] Science. 2002 Oct 25;298(5594):789-91 [12399581] Nat Neurosci. 2002 Nov;5 Suppl:1035-8 [12403980] Brain Res. 2003 Apr 11;968(2):263-72 [12663096] Brain Res. 2003 Jul 25;979(1-2):65-70 [12850572] Proc Natl Acad Sci U S A. 1998 May 26;95(11):6448-53 [9600986] Proc Natl Acad Sci U S A. 1998 Nov 24;95(24):14500-5 [9826729] Methods Enzymol. 1999;309:189-204 [10507025] Am J Pathol. 2010 Nov;177(5):2549-62 [20864679] J Neurosci. 2010 Dec 15;30(50):17091-101 [21159979] Nat Neurosci. 2010 Apr;13(4):411-3 [20305648] Arch Biochem Biophys. 2010 Apr 15;496(2):84-92 [20153288] Nat Rev Neurol. 2010 Apr;6(4):193-201 [20234358] J Vis Exp. 2010;(41). pii: 1884. doi: 10.3791/1884 [20644518] J Neuroimmunol. 2010 Jul 27;224(1-2):85-92 [20570369] Neuron. 2010 Oct 6;68(1):19-31 [20920788] J Neurosci. 2006 Oct 11;26(41):10488-98 [17035533] J Biol Chem. 2011 Sep 16;286(37):32713-22 [21771791] Synapse. 2007 Jun;61(6):367-74 [17372971] Brain Res. 2007 May 30;1150:200-6 [17397805] J Neurochem. 2007 Jun;101(5):1172-84 [17286590] Int Rev Neurobiol. 2007;82:187-204 [17678962] J Neurosci. 2008 Jan 23;28(4):788-97 [18216187] Exp Neurol. 2008 Mar;210(1):7-13 [18053990] Nat Med. 2008 Aug;14(8):837-42 [18568035] FEBS J. 2009 Mar;276(5):1266-81 [19175671] J Biol Chem. 2009 Apr 17;284(16):10639-49 [19240035] Neurotox Res. 2009 Jul;16(1):1-13 [19526294] J Leukoc Biol. 2009 Oct;86(4):903-11 [19571253] Proc Natl Acad Sci U S A. 2009 Sep 1;106(35):14745-50 [19706468] Neurochem Int. 2009 Dec;55(8):741-6 [19631247] Science. 2009 Dec 11;326(5959):1533-7 [20007899] J Biol Chem. 2010 Jan 22;285(4):2506-14 [19915004] J Biol Chem. 2010 Mar 5;285(10):7619-32 [20032460] J Neurosci. 2011 Nov 9;31(45):16241-50 [22072675] Neurobiol Aging. 2013 Dec;34(12):2843-52 [23855980] Exp Neurol. 2014 Jan;251:127-38 [23333589] J Neurosci. 2011 Feb 2;31(5):1688-92 [21289177] Nat Chem. 2009 Jul;1(4):326-31 [20703363] Neurobiol Aging. 2011 Mar;32(3):443-58 [19368990] Arterioscler Thromb Vasc Biol. 2011 Jul;31(7):e11-8 [21527754] J Chem Phys. 2011 Aug 14;135(6):065105 [21842954] J Neuroimmunol. 2005 Sep;166(1-2):19-28 [16019082] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0127730 ER - TY - JOUR T1 - Terminated Trials in the ClinicalTrials.gov Results Database: Evaluation of Availability of Primary Outcome Data and Reasons for Termination. AN - 1683759730; 26011295 AB - Clinical trials that end prematurely (or "terminate") raise financial, ethical, and scientific concerns. The extent to which the results of such trials are disseminated and the reasons for termination have not been well characterized. A cross-sectional, descriptive study of terminated clinical trials posted on the ClinicalTrials.gov results database as of February 2013 was conducted. The main outcomes were to characterize the availability of primary outcome data on ClinicalTrials.gov and in the published literature and to identify the reasons for trial termination. Approximately 12% of trials with results posted on the ClinicalTrials.gov results database (905/7,646) were terminated. Most trials were terminated for reasons other than accumulated data from the trial (68%; 619/905), with an insufficient rate of accrual being the lead reason for termination among these trials (57%; 350/619). Of the remaining trials, 21% (193/905) were terminated based on data from the trial (findings of efficacy or toxicity) and 10% (93/905) did not specify a reason. Overall, data for a primary outcome measure were available on ClinicalTrials.gov and in the published literature for 72% (648/905) and 22% (198/905) of trials, respectively. Primary outcome data were reported on the ClinicalTrials.gov results database and in the published literature more frequently (91% and 46%, respectively) when the decision to terminate was based on data from the trial. Trials terminate for a variety of reasons, not all of which reflect failures in the process or an inability to achieve the intended goals. Primary outcome data were reported most often when termination was based on data from the trial. Further research is needed to identify best practices for disseminating the experience and data resulting from terminated trials in order to help ensure maximal societal benefit from the investments of trial participants and others involved with the study. JF - PloS one AU - Williams, Rebecca J AU - Tse, Tony AU - DiPiazza, Katelyn AU - Zarin, Deborah A AD - National Library of Medicine (NLM), National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Bethesda, Maryland, United States of America. ; Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland, United States of America. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 5 KW - Index Medicus KW - Humans KW - Treatment Outcome KW - Outcome Assessment (Health Care) KW - Early Termination of Clinical Trials KW - Databases, Factual KW - Clinical Trials as Topic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683759730?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Terminated+Trials+in+the+ClinicalTrials.gov+Results+Database%3A+Evaluation+of+Availability+of+Primary+Outcome+Data+and+Reasons+for+Termination.&rft.au=Williams%2C+Rebecca+J%3BTse%2C+Tony%3BDiPiazza%2C+Katelyn%3BZarin%2C+Deborah+A&rft.aulast=Williams&rft.aufirst=Rebecca&rft.date=2015-01-01&rft.volume=10&rft.issue=5&rft.spage=e0127242&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0127242 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-04-18 N1 - Date created - 2015-05-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: BMJ. 2010;340:c869 [20332511] JAMA. 2014 Mar 12;311(10):1045-51 [24618966] J Clin Oncol. 2010 Dec 10;28(35):5197-201 [21060029] N Engl J Med. 2011 Mar 3;364(9):852-60 [21366476] Am J Bioeth. 2011 Mar;11(3):2-10 [21400374] Kennedy Inst Ethics J. 2011 Mar;21(1):51-78 [21598846] Acad Med. 2011 Nov;86(11):1360-6 [21952064] BMJ. 2012;344:d7292 [22214755] Clin Cancer Res. 2012 Jan 1;18(1):256-62 [21976533] JAMA. 2012 May 2;307(17):1838-47 [22550198] N Engl J Med. 2013 Nov 14;369(20):1926-34 [24224625] Ann Intern Med. 2014 Apr 1;160(7):477-83 [24687070] Am Heart J. 2014 Aug;168(2):213-9.e1 [25066561] J Natl Cancer Inst. 2014 Sep;106(9). pii: dju229. doi: 10.1093/jnci/dju229 [25190726] BMJ. 2014;349:g6870 [25491195] BMJ. 2014;349:g7089 [25499097] Clin Trials. 2015 Feb;12(1):77-83 [25475878] JAMA. 2014 Mar 12;311(10):1063-5 [24618969] JAMA. 2003 Apr 23-30;289(16):2128-31 [12709471] CMAJ. 2004 Sep 28;171(7):735-40 [15451835] Lancet. 1991 Apr 13;337(8746):867-72 [1672966] Circulation. 1994 Jun;89(6):2892-907 [8205706] JAMA. 2005 Nov 2;294(17):2203-9 [16264162] J Am Med Inform Assoc. 2007 May-Jun;14(3):253-63 [17329729] JAMA. 2007 May 16;297(19):2112-20 [17507347] N Engl J Med. 2008 Jan 17;358(3):252-60 [18199864] PLoS Med. 2008 Sep 23;5(9):e191 [18816163] Chest. 2009 Jul;136(1):295-303 [19584212] Chest. 2009 Jul;136(1):304-5 [19584213] J Oncol Pract. 2013 Nov;9(6):267-76 [24130252] PLoS Med. 2013 Dec;10(12):e1001566; discussion e1001566 [24311990] JAMA. 2010 Mar 24;303(12):1180-7 [20332404] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0127242 ER - TY - JOUR T1 - Caregiving Networks-Using a Network Approach to Identify Missed Opportunities AN - 1683500794 AB - Objectives. This study demonstrates the added value to caregiving research by using a multi-informant social network approach within the context of Alzheimerʼs disease and related dementia. Method. Sixty-six informants from 24 families enumerated caregiving network members in 2012. Comparisons were made between networks based on a single informant versus multiple informants in terms of network composition and caregiving roles, core-periphery structure, and identification of "missed opportunities" in recruitment. Results. On average, each informant beyond the index enumerated 6.2 new members, resulting in about 10 new members per family network when the multiple-informant approach is used. Compared with index informantsʼ networks, multi-informant networks showed an 85% increase in identification of direct care providers (1.71 compared with 3.42) and a 48% increase in identification of those involved in care decision making (3.33 compared with 4.92). Informants from the same network generally showed agreement in reported participation in caregiving activities. However, the reports of non-participation in these roles were less consistent among the informants. Resulting structure indicated a core caregiving network (M = 6.12 members), with semi-peripheral and peripheral members (M = 5.19 and M = 14.83 members, respectively). Discussion. Results suggest that an iterative, targeted sampling approach with at least three informants allows for a more comprehensive assessment of caregiving processes. Applying this approach in future research will greatly enhance our knowledge and better inform future interventions to facilitate family adaptation. JF - The Journals of Gerontology. Series B, Psychological Sciences and Social Sciences AU - Ashida, Sato AU - Schafer, Ellen J AU - Ludden, Amanda AD - Koehly, Laura M; Social and Behavioral Research Branch, National Human Genome Research Institute, National Institutes of Health, 31 Center Dr., Building 31, Room B1B37D, Bethesda, MD 20892 Y1 - 2015 PY - 2015 DA - 2015 SP - 143 EP - 154 CY - Washington PB - Oxford University Press, UK VL - 70 IS - 1 SN - 1079-5014 KW - Gerontology And Geriatrics KW - Alzheimerʼs disease KW - Caregiving KW - Dementia KW - Family structure KW - Social networks KW - Participation KW - Approaches KW - Interventions KW - Recruitment KW - Sampling KW - Social Science Research KW - Caregivers KW - Knowledge KW - Decision Making KW - Family Structure KW - Kinship Networks KW - Social Networks KW - Senility KW - Alzheimer's disease KW - Carers KW - Composition KW - Decision making KW - Health professionals KW - Identification KW - In care KW - Informants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1683500794?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journals+of+Gerontology.+Series+B%2C+Psychological+Sciences+and+Social+Sciences&rft.atitle=Caregiving+Networks-Using+a+Network+Approach+to+Identify+Missed+Opportunities&rft.au=Koehly%2C+Laura+M%3BAshida%2C+Sato%3BSchafer%2C+Ellen+J%3BLudden%2C+Amanda&rft.aulast=Koehly&rft.aufirst=Laura&rft.date=2015-01-01&rft.volume=70&rft.issue=1&rft.spage=143&rft.isbn=&rft.btitle=&rft.title=The+Journals+of+Gerontology.+Series+B%2C+Psychological+Sciences+and+Social+Sciences&rft.issn=10795014&rft_id=info:doi/10.1093%2Fgeronb%2Fgbu111 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-05-12 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1093/geronb/gbu111 ER - TY - JOUR T1 - Small molecule inhibitors of the annexin A2 heterotetramer prevent human papillomavirus type 16 infection. AN - 1682887288; 25712315 AB - High-risk human papillomavirus (HPV) infection leads to the development of several human cancers that cause significant morbidity and mortality worldwide. HPV type 16 (HPV16) is the most common of the cancer-causing genotypes and gains entry to the basal cells of the epithelium through a non-canonical endocytic pathway that involves the annexin A2/S100A10 heterotetramer (A2t). A2t is composed of two annexin A2 monomers bound to an S100A10 dimer and this interaction is a potential target to block HPV16 infection. Here, recently identified small molecule inhibitors of A2t (A2ti) were investigated for their ability to prevent HPV16 infection in vitro. A2ti were added to HeLa cells in increasing concentrations prior to the addition of HPV16. Cytotoxicity was evaluated via trypan blue exclusion. HPV16 pseudovirion infection and fluorescently labelled HPV16 capsid internalization was measured with flow cytometry. A2ti blocked HPV16 infection by 100% without substantial cellular toxicity or reduction in cell growth. Furthermore, A2ti blocked HPV16 entry into epithelial cells by 65%, indicating that the observed inhibition of HPV16 infection is in part due to a block in entry and that non-infectious entry may occur in the absence of A2t binding. These results demonstrate that targeting A2t may be an effective strategy to prevent HPV16 infection. © The Author 2015. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. JF - The Journal of antimicrobial chemotherapy AU - Woodham, Andrew W AU - Taylor, Julia R AU - Jimenez, Andrew I AU - Skeate, Joseph G AU - Schmidt, Thomas AU - Brand, Heike E AU - Da Silva, Diane M AU - Kast, W Martin AD - Department of Molecular Microbiology & Immunology, University of Southern California, 2011 Zonal Avenue HMR 401, Los Angeles, CA, USA. ; Norris Comprehensive Cancer Center, University of Southern California, 1441 Eastlake Avenue, Los Angeles, CA, USA. ; Laboratories of Chemical Physics and Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA. ; Norris Comprehensive Cancer Center, University of Southern California, 1441 Eastlake Avenue, Los Angeles, CA, USA Department of Obstetrics & Gynecology, University of Southern California, 2020 Zonal Avenue Room 220, Los Angeles, CA, USA. ; Department of Molecular Microbiology & Immunology, University of Southern California, 2011 Zonal Avenue HMR 401, Los Angeles, CA, USA Norris Comprehensive Cancer Center, University of Southern California, 1441 Eastlake Avenue, Los Angeles, CA, USA Department of Obstetrics & Gynecology, University of Southern California, 2020 Zonal Avenue Room 220, Los Angeles, CA, USA mkast@usc.edu. Y1 - 2015 PY - 2015 DA - 2015 SP - 1686 EP - 1690 VL - 70 IS - 6 KW - ANXA2 protein, human KW - 0 KW - Annexin A2 KW - Antiviral Agents KW - Index Medicus KW - A2t KW - HPV16 KW - annexin A2/S100A10 heterotetramer KW - Cell Survival -- drug effects KW - HeLa Cells KW - Humans KW - Human papillomavirus 16 -- physiology KW - Annexin A2 -- antagonists & inhibitors KW - Antiviral Agents -- pharmacology KW - Endocytosis -- drug effects KW - Virus Internalization -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1682887288?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+antimicrobial+chemotherapy&rft.atitle=Small+molecule+inhibitors+of+the+annexin+A2+heterotetramer+prevent+human+papillomavirus+type+16+infection.&rft.au=Woodham%2C+Andrew+W%3BTaylor%2C+Julia+R%3BJimenez%2C+Andrew+I%3BSkeate%2C+Joseph+G%3BSchmidt%2C+Thomas%3BBrand%2C+Heike+E%3BDa+Silva%2C+Diane+M%3BKast%2C+W+Martin&rft.aulast=Woodham&rft.aufirst=Andrew&rft.date=2015-01-01&rft.volume=70&rft.issue=6&rft.spage=1686&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+antimicrobial+chemotherapy&rft.issn=1460-2091&rft_id=info:doi/10.1093%2Fjac%2Fdkv045 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-05 N1 - Date created - 2015-05-21 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Physiol Rev. 2002 Apr;82(2):331-71 [11917092] J Exp Med. 2004 Nov 15;200(10):1337-46 [15545357] EMBO J. 1990 Dec;9(13):4207-13 [2148288] Biochem Biophys Res Commun. 1994 Feb 15;198(3):983-9 [8117306] Curr Protoc Cell Biol. 2004 Sep;Chapter 17:Unit 17.8 [18228446] Curr Protoc Cell Biol. 2007 Dec;Chapter 26:Unit 26.1 [18228512] J Med Chem. 2011 Apr 14;54(7):2080-94 [21375334] J Virol. 2011 Nov;85(22):11809-20 [21900167] Ann Oncol. 2011 Dec;22(12):2675-86 [21471563] ChemMedChem. 2012 Aug;7(8):1435-46 [22644793] PLoS One. 2012;7(8):e43519 [22927980] Vaccine. 2012 Nov 20;30 Suppl 5:F12-23 [23199955] Oncol Rep. 2013 May;29(5):1962-8 [23467841] J Virol. 2013 Jun;87(11):6062-72 [23536685] J Virol. 2013 Jul;87(13):7502-15 [23637395] Radiother Oncol. 2013 Sep;108(3):397-402 [23830197] J Mol Biol. 2014 Oct 23;426(21):3670-80 [25178257] Microbes Infect. 2003 Feb;5(2):123-33 [12650770] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/jac/dkv045 ER - TY - JOUR T1 - Hair mercury concentrations and in vitro fertilization (IVF) outcomes among women from a fertility clinic. AN - 1680177812; 25601638 AB - Total hair mercury (Hg) was measured among 205 women undergoing in vitro fertilization (IVF) treatment and the association with prospectively collected IVF outcomes (229 IVF cycles) was evaluated. Hair Hg levels (median=0.62ppm, range: 0.03-5.66ppm) correlated with fish intake (r=0.59), and exceeded the recommended EPA reference of 1ppm in 33% of women. Generalized linear mixed models with random intercepts accounting for within-woman correlations across treatment cycles were used to evaluate the association of hair Hg with IVF outcomes adjusted for age, body mass index, race, smoking status, infertility diagnosis, and protocol type. Hair Hg levels were not related to ovarian stimulation outcomes (peak estradiol levels, total and mature oocyte yields) or to fertilization rate, embryo quality, clinical pregnancy rate or live birth rate. Copyright © 2015 Elsevier Inc. All rights reserved. JF - Reproductive toxicology (Elmsford, N.Y.) AU - Wright, Diane L AU - Afeiche, Myriam C AU - Ehrlich, Shelley AU - Smith, Kristen AU - Williams, Paige L AU - Chavarro, Jorge E AU - Batsis, Maria AU - Toth, Thomas L AU - Hauser, Russ AD - Vincent Department of Obstetrics and Gynecology Service, Division of Reproductive Medicine and IVF, Massachusetts General Hospital Fertility Center, Harvard Medical School, Boston, MA, USA. Electronic address: dwright4@mgh.harvard.edu. ; Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA. ; Division of Biostatistics and Epidemiology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA. ; Department of Biostatistics, Harvard School of Public Health, Boston, MA, USA; Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA. ; Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA; Channing Division of Network Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; Department of Nutrition, Harvard School of Public Health, Boston, MA, USA. ; Vincent Department of Obstetrics and Gynecology Service, Division of Reproductive Medicine and IVF, Massachusetts General Hospital Fertility Center, Harvard Medical School, Boston, MA, USA; Section on Endocrinology and Genetics, Program on Developmental Endocrinology and Genetics & Pediatric Endocrinology Inter-Institute Training Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA. ; Vincent Department of Obstetrics and Gynecology Service, Division of Reproductive Medicine and IVF, Massachusetts General Hospital Fertility Center, Harvard Medical School, Boston, MA, USA. ; Vincent Department of Obstetrics and Gynecology Service, Division of Reproductive Medicine and IVF, Massachusetts General Hospital Fertility Center, Harvard Medical School, Boston, MA, USA; Department of Environmental Health, Harvard School of Public Health, Boston, MA, USA; Department of Epidemiology, Harvard School of Public Health, Boston, MA, USA. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 125 EP - 132 VL - 51 KW - Environmental Pollutants KW - 0 KW - Mercury KW - FXS1BY2PGL KW - Index Medicus KW - Fertilization KW - Implantation KW - Oocyte KW - Human KW - In vitro fertilization (IVF) KW - Mercury (Hg) KW - Animals KW - Ovulation Induction KW - Humans KW - Fishes KW - Adult KW - Pectinidae KW - Decapoda (Crustacea) KW - Seafood KW - Diet KW - Female KW - Pregnancy Outcome KW - Pregnancy KW - Hair -- chemistry KW - Mercury -- analysis KW - Fertilization in Vitro KW - Environmental Pollutants -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1680177812?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.atitle=Hair+mercury+concentrations+and+in+vitro+fertilization+%28IVF%29+outcomes+among+women+from+a+fertility+clinic.&rft.au=Wright%2C+Diane+L%3BAfeiche%2C+Myriam+C%3BEhrlich%2C+Shelley%3BSmith%2C+Kristen%3BWilliams%2C+Paige+L%3BChavarro%2C+Jorge+E%3BBatsis%2C+Maria%3BToth%2C+Thomas+L%3BHauser%2C+Russ&rft.aulast=Wright&rft.aufirst=Diane&rft.date=2015-01-01&rft.volume=51&rft.issue=&rft.spage=125&rft.isbn=&rft.btitle=&rft.title=Reproductive+toxicology+%28Elmsford%2C+N.Y.%29&rft.issn=1873-1708&rft_id=info:doi/10.1016%2Fj.reprotox.2015.01.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-16 N1 - Date created - 2015-05-08 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Assist Reprod Genet. 2010 Aug;27(8):463-8 [20508982] Int J Androl. 2010 Apr;33(2):385-93 [20002217] Neurotoxicol Teratol. 2011 Mar-Apr;33(2):325-8 [21145963] Hum Reprod. 2011 Jan;26(1):245-52 [21071489] J Toxicol Sci. 2012 Feb;37(1):123-30 [22293416] Hum Reprod. 2012 May;27(5):1401-10 [22381621] Reprod Toxicol. 2012 Nov;34(3):471-81 [22732149] Aging Cell. 2012 Dec;11(6):1046-54 [22978268] Hum Reprod. 2012 Dec;27(12):3583-92 [23014629] J Assist Reprod Genet. 2012 Dec;29(12):1369-79 [23229520] Environ Toxicol Pharmacol. 2013 Jul;36(1):30-4 [23538324] Reprod Toxicol. 2011 Feb;31(2):164-70 [21115110] BJOG. 2002 Oct;109(10):1121-5 [12387464] Environ Health Perspect. 2004 Aug;112(11):1165-71 [15289161] Pediatrics. 1974 Nov;54(5):587-95 [4480317] Br J Ind Med. 1985 Jul;42(7):488-94 [4015997] Int Arch Occup Environ Health. 1987;59(6):551-7 [3679554] Int J Epidemiol. 1989 Dec;18(4):858-67 [2621022] Am J Epidemiol. 1992 May 15;135(10):1114-26; discussion 1127-36 [1632423] Occup Environ Med. 1994 Jan;51(1):28-34 [8124459] Crit Rev Toxicol. 1995;25(1):1-24 [7734058] Sci Total Environ. 1998 Jun 18;214:165-74 [9646524] Scand J Work Environ Health. 1999 Jun;25(3):285-90 [10450781] Reprod Toxicol. 2006 Jul;22(1):13-9 [16439098] JAMA. 2006 Oct 18;296(15):1885-99 [17047219] Curr Opin Obstet Gynecol. 2008 Jun;20(3):281-91 [18460944] Int J Hyg Environ Health. 2008 Oct;211(5-6):560-79 [18160343] N Engl J Med. 2009 Jan 15;360(3):236-43 [19144939] Environ Health Perspect. 2009 Mar;117(3):367-72 [19337510] Am J Epidemiol. 2009 May 15;169(10):1182-90 [19363102] Reprod Toxicol. 2010 Jun;29(3):298-305 [20096775] J Assist Reprod Genet. 2011 Dec;28(12):1223-8 [22071884] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.reprotox.2015.01.003 ER - TY - JOUR T1 - Long-term dietary supplementation of pomegranates, figs and dates alleviate neuroinflammation in a transgenic mouse model of Alzheimer's disease. AN - 1667349181; 25807081 AB - Alzheimer's disease (AD) is a devastating age-related neurodegenerative disease with no specific treatment at present. The APPsw/Tg2576 mice exhibit age-related deterioration in memory and learning as well as amyloid-beta (Aβ) accumulation, and this mouse strain is considered an effective model for studying the mechanism of accelerated brain aging and senescence. The present study was aimed to investigate the beneficial effects of dietary supplements pomegranate, figs, or the dates on suppressing inflammatory cytokines in APPsw/Tg2576 mice. Changes in the plasma cytokines and Aβ, ATP, and inflammatory cytokines were investigated in the brain of transgenic mice. Significantly enhanced levels of inflammatory cytokines IL-1β, IL-2, IL-3, IL-4, IL-5, IL-6, IL-9, IL-10, TNF-α and Eotaxin activity were decreased by administration of the diet supplements containing pomegranates, figs, or dates. In addition, putative delays in the formation of senile plaques, as indicated by a decreasing tendency of brain Aβ1-40 and Aβ1-42 contents, were observed. Thus, novel results mediated by reducing inflammatory cytokines during aging may represent one mechanism by which these supplements exert their beneficial effects against neurodegenerative diseases such as AD. JF - PloS one AU - Essa, Musthafa Mohamed AU - Subash, Selvaraju AU - Akbar, Mohammed AU - Al-Adawi, Samir AU - Guillemin, Gilles J AD - Dept of Food Science and Nutrition, College of Agriculture and Marine Sciences, Sultan Qaboos University, Muscat, Oman; Ageing and Dementia Research Group, Sultan Qaboos University, Muscat, Oman; Neuropharmacology group, MND and Neurodegenerative Diseases Research Centre, Macquarie University, Sydney, NSW, Australia. ; Dept of Food Science and Nutrition, College of Agriculture and Marine Sciences, Sultan Qaboos University, Muscat, Oman; Ageing and Dementia Research Group, Sultan Qaboos University, Muscat, Oman. ; Section of Molecular Pharmacology and Toxicology, Laboratory of Membrane Biochemistry and Biophysics, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Rockville, MD, United States of America. ; Ageing and Dementia Research Group, Sultan Qaboos University, Muscat, Oman; College of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Oman. ; Neuropharmacology group, MND and Neurodegenerative Diseases Research Centre, Macquarie University, Sydney, NSW, Australia. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 3 KW - Amyloid beta-Peptides KW - 0 KW - Cytokines KW - Adenosine Triphosphate KW - 8L70Q75FXE KW - Index Medicus KW - Cytokines -- blood KW - Animals KW - Adenosine Triphosphate -- metabolism KW - Enzyme-Linked Immunosorbent Assay KW - Disease Models, Animal KW - Mice KW - Dietary Supplements KW - Brain -- metabolism KW - Fruit -- metabolism KW - Amyloid beta-Peptides -- analysis KW - Mice, Transgenic KW - Fruit -- chemistry KW - Female KW - Phoeniceae -- chemistry KW - Phoeniceae -- metabolism KW - Ficus -- chemistry KW - Punicaceae -- chemistry KW - Punicaceae -- metabolism KW - Alzheimer Disease -- metabolism KW - Ficus -- metabolism KW - Alzheimer Disease -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1667349181?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Long-term+dietary+supplementation+of+pomegranates%2C+figs+and+dates+alleviate+neuroinflammation+in+a+transgenic+mouse+model+of+Alzheimer%27s+disease.&rft.au=Essa%2C+Musthafa+Mohamed%3BSubash%2C+Selvaraju%3BAkbar%2C+Mohammed%3BAl-Adawi%2C+Samir%3BGuillemin%2C+Gilles+J&rft.aulast=Essa&rft.aufirst=Musthafa&rft.date=2015-01-01&rft.volume=10&rft.issue=3&rft.spage=e0120964&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0120964 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-03-04 N1 - Date created - 2015-03-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Food Funct. 2014 Feb;5(2):310-8 [24336779] Nutr Neurosci. 2015 Aug;18(6):281-8 [24954036] Proc Natl Acad Sci U S A. 1997 Feb 18;94(4):1500-5 [9037082] Prog Neurobiol. 1997 Feb;51(2):195-222 [9247964] J Neurosci. 1998 Apr 15;18(8):2974-81 [9526014] Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7778-83 [9636227] Mycopathologia. 1998;142(3):119-23 [10052161] Phytother Res. 1999 May;13(3):188-91 [10353154] J Am Coll Nutr. 2005 Feb;24(1):44-50 [15670984] Int J Food Sci Nutr. 2004 Sep;55(6):511-6 [15762315] Phytother Res. 2014 Feb;28(2):193-9 [23519910] Biomed Res Int. 2014;2014:546357 [25050360] Pak J Biol Sci. 2014 Dec;17(12):1209-18 [26027167] Trends Neurosci. 2005 Apr;28(4):202-8 [15808355] Zhonghua Yu Fang Yi Xue Za Zhi. 2005 Mar;39(2):80-3 [15842822] Zhong Yao Cai. 2004 Oct;27(10):754-6 [15850358] Neurology. 2005 Apr 26;64(8):1371-7 [15851726] Pediatr Res. 2005 Jun;57(6):858-64 [15774834] J Agric Food Chem. 2005 Sep 21;53(19):7586-91 [16159190] Science. 2006 Jun 2;312(5778):1372-4 [16741119] J Agric Food Chem. 2006 Oct 4;54(20):7717-23 [17002444] Neurobiol Dis. 2006 Dec;24(3):506-15 [17010630] Science. 2006 Dec 15;314(5806):1683; author reply 1683 [17170278] Neurochem Res. 2011 Nov;36(11):2096-103 [21706234] Nat Rev Neurosci. 2011 Dec;12(12):723-38 [22048062] Neurochem Res. 2012 Sep;37(9):1829-42 [22614926] J Ethnopharmacol. 2000 Jul;71(1-2):89-92 [10904150] J Struct Biol. 2000 Jun;130(2-3):184-208 [10940225] Acta Physiol Hung. 2000;87(1):71-6 [11032050] J Neurosci. 2001 Jan 15;21(2):372-81 [11160418] J Biol Chem. 2001 Apr 20;276(16):12991-8 [11152675] J Nat Prod. 2001 Jul;64(7):993-6 [11473446] N Engl J Med. 2001 Nov 22;345(21):1515-21 [11794217] J Agric Food Chem. 2002 Jan 30;50(3):610-7 [11804538] Ann Neurol. 2002 Aug;52(2):168-74 [12210786] Neurobiol Aging. 2002 Sep-Oct;23(5):655-64 [12392766] Br J Haematol. 2002 Dec;119(4):1042-51 [12472586] Neurology. 2003 Jul 8;61(1):76-80 [12847160] J Neurol. 2003 Jul;250(7):788-92 [12883918] Arch Neurol. 2004 May;61(5):668-72 [15148142] Neurobiol Aging. 2004 Nov-Dec;25(10):1293-8 [15465625] Science. 1983 Mar 11;219(4589):1184-90 [6338589] Microbios. 1989;59(240-241):203-10 [2512469] Neurosci Lett. 1991 Aug 19;129(2):318-20 [1745413] Lab Invest. 1992 Feb;66(2):223-30 [1370967] Neurology. 1993 Aug;43(8):1609-11 [8351023] Neurology. 1994 Feb;44(2):227-32 [8309563] J Neuropathol Exp Neurol. 1995 Mar;54(2):276-81 [7876895] Nature. 1995 Apr 13;374(6523):647-50 [7715705] Trends Neurosci. 1995 Mar;18(3):130-6 [7754524] Acta Neuropathol. 1995;89(6):544-51 [7676810] Curr Opin Neurobiol. 1995 Oct;5(5):642-6 [8580716] Blood. 1996 Mar 15;87(6):2095-147 [8630372] Endocr Rev. 1996 Feb;17(1):64-102 [8641224] Neurology. 1996 Aug;47(2):425-32 [8757015] Neurosci Lett. 1995 Dec 29;202(1-2):17-20 [8787820] Brain Res. 1996 Jun 3;723(1-2):231-4 [8813406] J Ethnopharmacol. 2011 Feb 16;133(3):1021-6 [21094237] J Alzheimers Dis. 2010;21(4):1263-9 [21504122] Exp Toxicol Pathol. 2011 Jul;63(5):433-41 [20359872] Nutrition. 2008 Jul-Aug;24(7-8):733-43 [18490140] J Ethnopharmacol. 2008 Sep 2;119(1):1-5 [18586078] Pak J Pharm Sci. 2010 Jan;23(1):53-8 [20067867] Behav Brain Res. 2010 May 1;209(1):73-9 [20096732] J Agric Food Chem. 2010 Jun 9;58(11):6660-5 [20443626] J Agric Food Chem. 2010 Jun 23;58(12):7158-65 [20443568] Neuron. 2010 Nov 4;68(3):409-27 [21040844] Arch Neurol. 2010 Dec;67(12):1485-90 [20697031] FASEB J. 2011 Jan;25(1):5-13 [21205781] Br J Nutr. 2013 Mar 14;109(5):802-9 [22676910] J Nutr. 2013 May;143(5):597-605 [23468550] Inflamm Res. 2013 Nov;62(11):971-80 [23979691] Oxid Med Cell Longev. 2013;2013:685909 [24223235] Eur Rev Med Pharmacol Sci. 2013 Nov;17(22):2988-93 [24302176] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0120964 ER - TY - JOUR T1 - Methylation-associated partial down-regulation of mesothelin causes resistance to anti-mesothelin immunotoxins in a pancreatic cancer cell line. AN - 1666988368; 25803818 AB - Anti-mesothelin Pseudomonas exotoxin A-based recombinant immunotoxins (RITs) present a potential treatment modality for pancreatic ductal adenocarcinoma (PDAC). To study mechanisms of resistance, the sensitive PDAC cell line KLM-1 was intermittently exposed to the anti-mesothelin SS1-LR-GGS RIT. Surviving cells were resistant to various anti-mesothelin RITs (IC50s >1 μg/ml), including the novel de-immunized RG7787. These resistant KLM-1-R cells were equally sensitive to the anti-CD71 HB21(Fv)-PE40 RIT as KLM-1, indicating resistance was specific to anti-mesothelin RITs. Mesothelin gene expression was partially down-regulated in KLM-1-R, resulting in 5-fold lower surface protein levels and decreased cellular uptake of RG7787 compared to KLM-1. Bisulfite sequencing analysis found that the mesothelin promoter region was significantly more methylated in KLM-1-R (59 ± 3.6%) compared to KLM-1 (41 ± 4.8%), indicating hypermethylation as a mechanism of mesothelin downregulation. The DNA methyltransferase inhibitor 5-azacytidine restored original mesothelin surface expression to more than half in KLM-1-R and increased sensitivity to RG7787 (IC50 = 722.4 ± 232.6 ng/ml), although cells remained significantly less sensitive compared to parental KLM-1 cells (IC50 = 4.41 ± 0.38 ng/ml). Mesothelin cDNA introduction in KLM-1-R led to 5-fold higher surface protein levels and significantly higher RG7887 uptake compared to KLM-1. As a result, the original sensitivity to RG7787 was fully restored (IC50 = 4.49 ± 1.11 ng/ml). A significantly higher RG7787 uptake was thus required to reach the original cytotoxicity in resistant cells, hinting that intracellular RIT trafficking is also a limiting factor. RNA deep sequencing analysis of KLM-1 and KLM-1-R cells supported our experimental findings; compared to KLM-1, resistant cells displayed differential expression of genes linked to intracellular transport and an expression pattern that matched a more general hypermethylation status. In conclusion, resistance to anti-mesothelin RITs in KLM-1 is linked to a methylation-associated down-regulation of mesothelin, while aberrations in RIT trafficking could also play a role. JF - PloS one AU - Hollevoet, Kevin AU - Mason-Osann, Emily AU - Müller, Fabian AU - Pastan, Ira AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States of America; Laboratory for Therapeutic and Diagnostic Antibodies, Department of Pharmaceutical and Pharmacological Sciences, KU Leuven, Leuven University, Leuven, Belgium. ; Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, United States of America. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 3 KW - Bacterial Toxins KW - 0 KW - Exotoxins KW - GPI-Linked Proteins KW - Immunoglobulin Variable Region KW - Immunotoxins KW - Recombinant Proteins KW - Virulence Factors KW - mesothelin KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Cell Proliferation -- drug effects KW - ADP Ribose Transferases -- immunology KW - Cell Count KW - Humans KW - Immunoglobulin Variable Region -- immunology KW - Cell Line, Tumor KW - Bacterial Toxins -- immunology KW - Exotoxins -- immunology KW - Virulence Factors -- immunology KW - Reverse Transcriptase Polymerase Chain Reaction KW - Base Sequence KW - Blotting, Western KW - Apoptosis -- drug effects KW - Molecular Sequence Data KW - Sequence Analysis, RNA KW - Flow Cytometry KW - Recombinant Proteins -- pharmacology KW - Pancreatic Neoplasms -- metabolism KW - GPI-Linked Proteins -- metabolism KW - DNA Methylation KW - Immunotoxins -- immunology KW - Gene Expression Regulation, Neoplastic -- physiology KW - Recombinant Proteins -- immunology KW - Drug Resistance, Neoplasm -- physiology KW - Immunotoxins -- pharmacology KW - GPI-Linked Proteins -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1666988368?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Methylation-associated+partial+down-regulation+of+mesothelin+causes+resistance+to+anti-mesothelin+immunotoxins+in+a+pancreatic+cancer+cell+line.&rft.au=Hollevoet%2C+Kevin%3BMason-Osann%2C+Emily%3BM%C3%BCller%2C+Fabian%3BPastan%2C+Ira&rft.aulast=Hollevoet&rft.aufirst=Kevin&rft.date=2015-01-01&rft.volume=10&rft.issue=3&rft.spage=e0122462&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0122462 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-16 N1 - Date created - 2015-03-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Cancer Ther. 2013 Jan;12(1):48-57 [23136186] Clin Cancer Res. 2009 Aug 15;15(16):5274-9 [19671873] Sci Transl Med. 2013 Oct 23;5(208):208ra147 [24154601] Blood. 1999 Nov 15;94(10):3340-8 [10552943] Int J Oncol. 2000 Oct;17(4):643-51 [10995873] Clin Cancer Res. 2001 Dec;7(12):3862-8 [11751476] Cancer Res. 2003 Jul 15;63(14):4158-66 [12874021] Am J Surg Pathol. 2003 Nov;27(11):1418-28 [14576474] Methods Mol Biol. 2004;248:503-18 [14970517] Proc Natl Acad Sci U S A. 1977 Feb;74(2):565-9 [265522] Proc Natl Acad Sci U S A. 1996 Jan 9;93(1):136-40 [8552591] Int J Pancreatol. 1996 Aug;20(1):43-50 [8872523] Oncogene. 2005 Jan 6;24(1):199-211 [15637593] Clin Cancer Res. 2005 May 15;11(10):3814-20 [15897581] Proc Natl Acad Sci U S A. 2005 Oct 25;102(43):15545-50 [16199517] Br J Cancer. 2006 Apr 24;94(8):1087-92 [16495912] Nat Rev Cancer. 2006 Jul;6(7):559-65 [16794638] Eur J Gynaecol Oncol. 2010;31(1):63-71 [20349783] Mol Cell Biol. 2010 Jul;30(14):3444-52 [20457813] Nat Rev Drug Discov. 2011 Mar;10(3):221-37 [21358741] Carcinogenesis. 2011 Jul;32(7):1013-24 [21515913] FEBS J. 2011 Aug;278(15):2613-24 [21624055] Clin Cancer Res. 2011 Sep 15;17(18):5926-34 [21813632] Epigenetics. 2011 Aug;6(8):1029-34 [21775819] FEBS J. 2011 Dec;278(23):4683-700 [21585657] Protein Eng Des Sel. 2012 Jan;25(1):1-6 [22101015] J Am Chem Soc. 2012 Jan 18;134(2):773-6 [22188241] Proc Natl Acad Sci U S A. 2012 May 1;109(18):6898-903 [22509046] Nat Rev Genet. 2012 Jul;13(7):484-92 [22641018] Proc Natl Acad Sci U S A. 2012 Jul 17;109(29):11782-7 [22753489] PLoS One. 2012;7(10):e47320 [23056628] Proc Natl Acad Sci U S A. 2012 Dec 18;109(51):E3597-603 [23213206] Leuk Res. 2013 Nov;37(11):1551-6 [24070652] J Immunother. 2014 Jan;37(1):8-15 [24316551] Nucleic Acids Res. 2014 Jan;42(Database issue):D756-63 [24259432] Cancer Res. 2014 Jun 1;74(11):2907-12 [24824231] J Biol Chem. 2013 Apr 26;288(17):12305-12 [23486472] Clin Cancer Res. 2007 Sep 1;13(17):5144-9 [17785569] Nucleic Acids Res. 2009 Jan;37(Database issue):D412-6 [18940858] Mol Cancer Ther. 2014 Aug;13(8):2040-9 [24928849] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0122462 ER - TY - JOUR T1 - Treatment Patterns of Youth with Bipolar Disorder: Results from the National Comorbidity Survey—Adolescent Supplement (NCS-A) AN - 1665161547 AB - Despite growing evidence that bipolar disorder often emerges in adolescence, there are limited data regarding treatment patterns of youth with bipolar disorder in community samples. Our objective was to present the prevalence and clinical correlates of treatment utilization for a nationally representative sample of US adolescents with bipolar disorder. Analyses are based on data from the National Comorbidity Survey-Adolescent Supplement, a face-to-face survey of 10,123 adolescents (ages 13–18) identified in household and school settings. We found that of adolescents meeting DSM-IV criteria for bipolar I or II disorder (N=250), 49 % were treated for depression or mania, 13 % were treated for conditions other than depression or mania, and 38 % did not report receiving treatment. Treatment for depression or mania was associated with increased rates of suicide attempts, as well as greater role disability and more comorbid alcohol use relative to those who had not received treatment. Treated adolescents had triple the rate of ADHD and double the rates of behavior disorders than those without treatment. Our findings demonstrate that a substantial proportion of youth with bipolar disorder do not receive treatment, and of those who do, many receive treatment for comorbid conditions rather than for their mood-related symptoms. Treatment was more common among youth with severe manifestations and consequences of bipolar disorder and those with behavior problems. These trends highlight the need to identify barriers to treatment for adolescents with bipolar disorder and demonstrate that those in treatment are not representative of youth with bipolar disorder in the general population. JF - Journal of Abnormal Child Psychology AU - Khazanov, Gabriela Kattan AU - Cui, Lihong AU - Merikangas, Kathleen Ries AU - Angst, Jules AD - Genetic Epidemiology Research Branch, National Institute of Mental Health, Bldg. 35A, Rm 2E410, 35 Convent Dr. MSC 3720, Bethesda, MD, 20892-0001, USA merikank@mail.nih.gov merikank@mail.nih.gov merikank@mail.nih.gov; Zurich University Psychiatric Hospital, Zurich, Switzerland ; Genetic Epidemiology Research Branch, National Institute of Mental Health, Bldg. 35A, Rm 2E410, 35 Convent Dr. MSC 3720, Bethesda, MD, 20892-0001, USA Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 391 EP - 400 CY - New York PB - Springer Science & Business Media VL - 43 IS - 2 SN - 0091-0627 KW - Medical Sciences--Physical Medicine And Rehabilitation KW - Adolescence KW - Adolescents KW - Alcohol consumption KW - Attention deficit hyperactivity disorder KW - Behaviour disorders KW - Bipolar affective disorder KW - Comorbidity KW - Depression KW - Disability KW - Mania KW - Suicidal behaviour KW - Suicide KW - Symptoms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665161547?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Abnormal+Child+Psychology&rft.atitle=Treatment+Patterns+of+Youth+with+Bipolar+Disorder%3A+Results+from+the+National+Comorbidity+Survey%E2%80%94Adolescent+Supplement+%28NCS-A%29&rft.au=Khazanov%2C+Gabriela+Kattan%3BCui%2C+Lihong%3BMerikangas%2C+Kathleen+Ries%3BAngst%2C+Jules&rft.aulast=Khazanov&rft.aufirst=Gabriela&rft.date=2015-01-01&rft.volume=43&rft.issue=2&rft.spage=391&rft.isbn=&rft.btitle=&rft.title=Journal+of+Abnormal+Child+Psychology&rft.issn=00910627&rft_id=info:doi/10.1007%2Fs10802-014-9885-6 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-02-05 N1 - Last updated - 2015-12-14 DO - http://dx.doi.org/10.1007/s10802-014-9885-6 ER - TY - JOUR T1 - Membrane-active macromolecules resensitize NDM-1 gram-negative clinical isolates to tetracycline antibiotics. AN - 1665124375; 25789871 AB - Gram-negative 'superbugs' such as New Delhi metallo-beta-lactamase-1 (blaNDM-1) producing pathogens have become world's major public health threats. Development of molecular strategies that can rehabilitate the 'old antibiotics' and halt the antibiotic resistance is a promising approach to target them. We report membrane-active macromolecules (MAMs) that restore the antibacterial efficacy (enhancement by >80-1250 fold) of tetracycline antibiotics towards blaNDM-1 Klebsiella pneumonia and blaNDM-1 Escherichia coli clinical isolates. Organismic studies showed that bacteria had an increased and faster uptake of tetracycline in the presence of MAMs which is attributed to the mechanism of re-sensitization. Moreover, bacteria did not develop resistance to MAMs and MAMs stalled the development of bacterial resistance to tetracycline. MAMs displayed membrane-active properties such as dissipation of membrane potential and membrane-permeabilization that enabled higher uptake of tetracycline in bacteria. In-vivo toxicity studies displayed good safety profiles and preliminary in-vivo antibacterial efficacy studies showed that mice treated with MAMs in combination with antibiotics had significantly decreased bacterial burden compared to the untreated mice. This report of re-instating the efficacy of the antibiotics towards blaNDM-1 pathogens using membrane-active molecules advocates their potential for synergistic co-delivery of antibiotics to combat Gram-negative superbugs. JF - PloS one AU - Uppu, Divakara S S M AU - Manjunath, Goutham B AU - Yarlagadda, Venkateswarlu AU - Kaviyil, Jyothi E AU - Ravikumar, Raju AU - Paramanandham, Krishnamoorthy AU - Shome, Bibek R AU - Haldar, Jayanta AD - Chemical Biology & Medicinal Chemistry Laboratory, New Chemistry Unit, Jawaharlal Nehru Centre for Advanced Scientific Research (JNCASR), Jakkur, Bangalore, 560064, India. ; Department of Neuromicrobiology, National Institute of Mental Health and Neuro Sciences (NIMHANS), Hosur Road, Bangalore, 560029, India. ; National Institute of Veterinary Epidemiology and Disease Informatics (NIVEDI), Hebbal, Bengaluru, 560024, Karnataka, India. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 3 KW - Maleimides KW - 0 KW - beta-Lactamases KW - EC 3.5.2.6 KW - beta-lactamase NDM-1 KW - Tetracycline KW - F8VB5M810T KW - Index Medicus KW - Animals KW - Drug Resistance, Bacterial -- drug effects KW - Klebsiella pneumoniae -- drug effects KW - Cell Membrane -- drug effects KW - Humans KW - Mice KW - Membrane Potentials -- drug effects KW - beta-Lactamases -- metabolism KW - Tetracycline -- administration & dosage KW - Klebsiella Infections -- drug therapy KW - Maleimides -- chemistry KW - Maleimides -- administration & dosage KW - Drug Synergism KW - Klebsiella Infections -- microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665124375?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Membrane-active+macromolecules+resensitize+NDM-1+gram-negative+clinical+isolates+to+tetracycline+antibiotics.&rft.au=Uppu%2C+Divakara+S+S+M%3BManjunath%2C+Goutham+B%3BYarlagadda%2C+Venkateswarlu%3BKaviyil%2C+Jyothi+E%3BRavikumar%2C+Raju%3BParamanandham%2C+Krishnamoorthy%3BShome%2C+Bibek+R%3BHaldar%2C+Jayanta&rft.aulast=Uppu&rft.aufirst=Divakara+S+S&rft.date=2015-01-01&rft.volume=10&rft.issue=3&rft.spage=e0119422&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0119422 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-02-09 N1 - Date created - 2015-03-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Lancet Infect Dis. 2011 May;11(5):355-62 [21478057] Nat Chem Biol. 2011 Jun;7(6):348-50 [21516114] Indian J Med Microbiol. 2011 Jul-Sep;29(3):249-53 [21860104] Macromol Biosci. 2013 Oct;13(10):1285-99 [23832766] Adv Mater. 2013 Dec 10;25(46):6730-6 [24018824] Acc Chem Res. 2013 Dec 17;46(12):2977-87 [24007507] Antimicrob Agents Chemother. 2014;58(1):297-303 [24165187] ACS Chem Biol. 2014 Jan 17;9(1):122-7 [24131198] Antimicrob Agents Chemother. 2014;58(3):1494-500 [24366742] J Am Chem Soc. 2014 Mar 19;136(11):4410-8 [24601599] J Am Chem Soc. 2014 Apr 2;136(13):4873-6 [24628053] ACS Chem Biol. 2014 May 16;9(5):1172-7 [24601489] J Med Chem. 2014 May 22;57(10):4263-72 [24801877] J Med Chem. 2014 Jun 12;57(11):4558-68 [24846441] Nature. 2014 Jun 26;510(7506):503-6 [24965651] Chem Commun (Camb). 2013 Oct 21;49(82):9389-91 [23868724] Nature. 2000 Aug 17;406(6797):775-81 [10963607] J Antimicrob Chemother. 2003 Jul;52(1):1 [12805255] Proc Natl Acad Sci U S A. 1978 Mar;75(3):1319-23 [418409] Annu Rev Microbiol. 1985;39:219-42 [2998266] Antimicrob Agents Chemother. 1991 Jan;35(1):53-6 [2014981] Food Chem Toxicol. 1995 Mar;33(3):223-31 [7896233] Proc Natl Acad Sci U S A. 2009 Apr 28;106(17):6968-73 [19359494] Antimicrob Agents Chemother. 2012 Jun;56(6):3432-4 [22450982] J Med Chem. 2012 Apr 26;55(8):4003-9 [22475244] ACS Chem Biol. 2012 Sep 21;7(9):1547-55 [22698393] PLoS Biol. 2013;11(4):e1001540 [23630452] Sci Transl Med. 2013 Jun 19;5(190):190ra81 [23785037] FASEB J. 2013 Sep;27(9):3818-26 [23733749] Erratum In: PLoS One. 2015;10(4):e0126757 [25879927] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0119422 ER - TY - JOUR T1 - An AAVS1-Targeted Minigene Platform for Correction of iPSCs From All Five Types of Chronic Granulomatous Disease AN - 1664193671; PQ0001222705 AB - There are five genetic forms of chronic granulomatous disease (CGD), resulting from mutations in any of five subunits of phagocyte oxidase, an enzyme complex in neutrophils, monocytes, and macrophages that produces microbicidal reactive oxygen species. We generated induced pluripotent stem cells (iPSCs) from peripheral blood CD34 super(+) hematopoietic stem cells of patients with each of five CGD genotypes. We used zinc finger nuclease (ZFN) targeting the AAVS1 safe harbor site together with CGD genotype-specific minigene plasmids with flanking AAVS1 sequence to target correction of iPSC representing each form of CGD. We achieved targeted insertion with constitutive expression of desired oxidase subunit in 70-80% of selected iPSC clones. Neutrophils and macrophages differentiated from corrected CGD iPSCs demonstrated restored oxidase activity and antimicrobial function against CGD bacterial pathogens Staphylococcus aureus and Granulibacter bethesdensis. Using a standard platform that combines iPSC generation from peripheral blood CD34 super(+) cells and ZFN mediated AAVS1 safe harbor minigene targeting, we demonstrate efficient generation of genetically corrected iPSCs using an identical approach for all five genetic forms of CGD. This safe harbor minigene targeting platform is broadly applicable to a wide range of inherited single gene metabolic disorders. JF - Molecular Therapy AU - Merling, Randall K AU - Sweeney, Colin L AU - Chu, Jessica AU - Bodansky, Aaron AU - Choi, Uimook AU - Priel, Debra Long AU - Kuhns, Douglas B AU - Wang, Hongmei AU - Vasilevsky, Sam AU - Ravin, Suk See De AD - Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Maryland, USA Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 147 EP - 157 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 23 IS - 1 SN - 1525-0016, 1525-0016 KW - Biotechnology and Bioengineering Abstracts KW - Macrophages KW - Metabolic disorders KW - Inhibitory postsynaptic potentials KW - Leukocytes (neutrophilic) KW - Zinc finger proteins KW - Enzymes KW - Nuclease KW - CD34 antigen KW - Peripheral blood KW - Genotypes KW - Pathogens KW - Plasmids KW - Antimicrobial agents KW - Stem cells KW - Insertion KW - Monocytes KW - Staphylococcus aureus KW - Chronic granulomatous disease KW - Mutation KW - microbicides KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664193671?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Therapy&rft.atitle=An+AAVS1-Targeted+Minigene+Platform+for+Correction+of+iPSCs+From+All+Five+Types+of+Chronic+Granulomatous+Disease&rft.au=Merling%2C+Randall+K%3BSweeney%2C+Colin+L%3BChu%2C+Jessica%3BBodansky%2C+Aaron%3BChoi%2C+Uimook%3BPriel%2C+Debra+Long%3BKuhns%2C+Douglas+B%3BWang%2C+Hongmei%3BVasilevsky%2C+Sam%3BRavin%2C+Suk+See+De&rft.aulast=Merling&rft.aufirst=Randall&rft.date=2015-01-01&rft.volume=23&rft.issue=1&rft.spage=147&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2014.195 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Macrophages; Metabolic disorders; Inhibitory postsynaptic potentials; Leukocytes (neutrophilic); Nuclease; Enzymes; Zinc finger proteins; Peripheral blood; CD34 antigen; Pathogens; Genotypes; Plasmids; Antimicrobial agents; Stem cells; Insertion; Monocytes; Chronic granulomatous disease; Mutation; microbicides; Staphylococcus aureus DO - http://dx.doi.org/10.1038/mt.2014.195 ER - TY - JOUR T1 - Graft Versus Leukemia Response Without Graft-versus-host Disease Elicited By Adoptively Transferred Multivirus-specific T-cells AN - 1664190829; PQ0001222708 AB - A 12-year-old boy with refractory acute lymphoblastic leukemia received a haploidentical transplant from his mother. As prophylaxis for Epstein-Barr virus (EBV), cyto-megalovirus (CMV) and adenovirus, he received ex vivo expanded virus-specific donor T cells 3.5 months after transplant. Four weeks later leukemic blasts bearing the E2A deletion, identified by fluorescent in situ hybridization (FISH), appeared transiently in the blood followed by a FISH-negative hematological remission, which was sustained until a testicular relapse 3.5 months later. Clearance of the circulating leukemic cells coincided with a marked increase in circulating virus-specific T cells. The virus-specific cytotoxic T-cell (CTL) line showed strong polyfunctional reactivity with the patient's leukemic cells but not phytohemagglutinin (PHA) blasts, suggesting that virus-specific CTL lines may have clinically significant antileukemia activity. JF - Molecular Therapy AU - Melenhorst, Jan J AU - Castillo, Paul AU - Hanley, Patrick J AU - Keller, Michael D AU - Krance, Robert A AU - Margolin, Judith AU - Leen, Ann M AU - Heslop, Helen E AU - Barrett, A John AU - Rooney, Cliona M AU - Bollard, Catherine M AD - Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA; Translational Research Program, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA, cbollard@childrensnational.org Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 179 EP - 183 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 23 IS - 1 SN - 1525-0016, 1525-0016 KW - Immunology Abstracts; Biotechnology and Bioengineering Abstracts KW - Testes KW - Adenovirus KW - Remission KW - Graft-versus-host reaction KW - phytohemagglutinins KW - Cytomegalovirus KW - Blood KW - Epstein-Barr virus KW - Cytotoxicity KW - Acute lymphatic leukemia KW - Lymphocytes T KW - Prophylaxis KW - Blast KW - Fluorescence in situ hybridization KW - F 06960:Molecular Immunology KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1664190829?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Therapy&rft.atitle=Graft+Versus+Leukemia+Response+Without+Graft-versus-host+Disease+Elicited+By+Adoptively+Transferred+Multivirus-specific+T-cells&rft.au=Melenhorst%2C+Jan+J%3BCastillo%2C+Paul%3BHanley%2C+Patrick+J%3BKeller%2C+Michael+D%3BKrance%2C+Robert+A%3BMargolin%2C+Judith%3BLeen%2C+Ann+M%3BHeslop%2C+Helen+E%3BBarrett%2C+A+John%3BRooney%2C+Cliona+M%3BBollard%2C+Catherine+M&rft.aulast=Melenhorst&rft.aufirst=Jan&rft.date=2015-01-01&rft.volume=23&rft.issue=1&rft.spage=179&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2014.192 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Testes; Blood; Cytotoxicity; Acute lymphatic leukemia; Prophylaxis; Lymphocytes T; Remission; Graft-versus-host reaction; phytohemagglutinins; Blast; Fluorescence in situ hybridization; Epstein-Barr virus; Adenovirus; Cytomegalovirus DO - http://dx.doi.org/10.1038/mt.2014.192 ER - TY - JOUR T1 - Comparative Pathobiology of Environmentally Induced Lung Cancers in Humans and Rodents AN - 1660409634; PQ0001016674 AB - Lung cancer is the number one cause of cancer-related deaths in humans worldwide. Environmental factors play an important role in the epidemiology of these cancers. Rodents are the most common experimental model to study human lung cancers and are frequently used in bioassays to identify environmental exposure hazards associated with lung cancer. Lung tumors in rodents are common, particularly in certain strains of mice. Rodent lung tumors are predominantly bronchioloalveolar carcinomas and usually follow a progressive continuum of hyperplasia to adenoma to carcinoma. Human lung cancers are phenotypically more diverse and broadly constitute 2 types: small cell lung cancers and nonsmall cell lung cancers (NSCLCs). Rodent lung tumors resulting from exposure to environmental agents are comparable with certain adenocarcinomas that are a subset of human NSCLCs. Human pulmonary carcinomas differ from rodent lung tumors by exhibiting greater morphologic heterogeneity (encompassing squamous cell, neuroendocrine, mucinous, sarcomatoid, and multiple cell combinations), higher metastatic rate, higher stromal response, aggressive clinical behavior, and lack of a clear continuum of proliferative lesions. In spite of these differences, rodent lung tumors recapitulate several fundamental aspects of human lung tumor biology at the morphologic and molecular level, especially in lung cancers resulting from exposure to environmental carcinogens. JF - Toxicologic Pathology AU - Pandiri, Arun AD - Experimental Pathology Laboratories, Inc., Research Triangle Park, North Carolina, USA, pandiriak@niehs.nih.govapandiri@epl-inc.com Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 107 EP - 114 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 43 IS - 1 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - lung cancer KW - animal models KW - environmental carcinogens KW - comparative pathology. KW - Squamous cells KW - Animal models KW - Aggressive behavior KW - Carcinogens KW - Tumors KW - Environmental factors KW - Carcinoma KW - Metastases KW - Hyperplasia KW - Epidemiology KW - Adenocarcinoma KW - Adenoma KW - Lung cancer KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660409634?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Comparative+Pathobiology+of+Environmentally+Induced+Lung+Cancers+in+Humans+and+Rodents&rft.au=Pandiri%2C+Arun&rft.aulast=Pandiri&rft.aufirst=Arun&rft.date=2015-01-01&rft.volume=43&rft.issue=1&rft.spage=107&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623314556516 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Number of references - 86 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Squamous cells; Animal models; Aggressive behavior; Tumors; Carcinogens; Environmental factors; Carcinoma; Metastases; Hyperplasia; Epidemiology; Adenocarcinoma; Adenoma; Lung cancer DO - http://dx.doi.org/10.1177/0192623314556516 ER - TY - JOUR T1 - Proceedings of the 2014 National Toxicology Program Satellite Symposium AN - 1660409625; PQ0001016670 AB - The 2014 annual National Toxicology Program (NTP) Satellite Symposium, entitled "Pathology Potpourri" was held in Washington, D.C., in advance of the Society of Toxicologic Pathology's 33rd annual meeting. The goal of this annual NTP Symposium is to present current diagnostic pathology or nomenclature issues to the Toxicologic Pathology community. This article presents summaries of the speakers' presentations, including diagnostic or nomenclature issues that were presented, along with select images that were used for audience voting and discussion. Some lesions and topics covered during the symposium included a pulmonary mucinous adenocarcinoma in a male B6C3F1 mouse; plexiform vasculopathy in Wistar Han (Crl:WI[Han]) rats; staging of the estrous cycle in rats and mice; peri-islet fibrosis, hemorrhage, lobular atrophy and inflammation in male Sprague-Dawley (SD) rats; retinal dysplasia in Crl:WI[Han] rats and B6C3F1 mice; multicentric lymphoma with intravascular microemboli and tumor lysis syndrome, and 2 cases of myopathy and vascular anomaly in Tg.rasH2 mice; benign thymomas in Crl:WI[Han] rats; angiomatous lesions in the mesenteric lymph nodes of Crl:WI[Han] rats; an unusual foveal lesion in a cynomolgous monkey; and finally a series of nomenclatures challenges from the endocrine International Harmonization of Nomenclature and Diagnostic Criteria (INHAND) Organ Working Group (OWG). JF - Toxicologic Pathology AU - Elmore, Susan A AU - Cora, Michelle C AU - Gruebbel, Margarita M AU - Hayes, Schantel A AU - Hoane, Jessica S AU - Koizumi, Haruko AU - Peters, Rachel AU - Rosol, Thomas J AU - Singh, Bhanu P AU - Szabo, Kathleen A AD - National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA, elmore@niehs.nih.gov Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 10 EP - 40 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 43 IS - 1 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - NTP Satellite Symposium KW - mucinous adenoma KW - plexiform vasculopathy KW - vaginal cytology KW - chronic-active pancreatitis KW - retinal dysplasia KW - thymoma KW - mesenteric lymph node angiomatous lesion KW - fovea cyst KW - endocrine nomenclature KW - acute tumor lysis syndrome. KW - Nomenclature KW - Dysplasia KW - Retina KW - Fibrosis KW - Tumors KW - Hemorrhage KW - Vascular diseases KW - Satellites KW - Lymph nodes KW - Inflammation KW - Lung KW - Atrophy KW - Adenocarcinoma KW - Lymphoma KW - Estrus cycle KW - Myopathy KW - Benign KW - X 24500:Reviews, Legislation, Book & Conference Notices UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660409625?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Proceedings+of+the+2014+National+Toxicology+Program+Satellite+Symposium&rft.au=Elmore%2C+Susan+A%3BCora%2C+Michelle+C%3BGruebbel%2C+Margarita+M%3BHayes%2C+Schantel+A%3BHoane%2C+Jessica+S%3BKoizumi%2C+Haruko%3BPeters%2C+Rachel%3BRosol%2C+Thomas+J%3BSingh%2C+Bhanu+P%3BSzabo%2C+Kathleen+A&rft.aulast=Elmore&rft.aufirst=Susan&rft.date=2015-01-01&rft.volume=43&rft.issue=1&rft.spage=10&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623314555526 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Number of references - 126 N1 - Last updated - 2015-08-05 N1 - SubjectsTermNotLitGenreText - Nomenclature; Retina; Dysplasia; Fibrosis; Tumors; Hemorrhage; Satellites; Vascular diseases; Lymph nodes; Inflammation; Lung; Atrophy; Adenocarcinoma; Lymphoma; thymoma; Estrus cycle; Benign; Myopathy DO - http://dx.doi.org/10.1177/0192623314555526 ER - TY - JOUR T1 - Longitudinal study of symptom severity and language in minimally verbal children with autism AN - 1660012169; 201502524 AB - A significant minority of children with autism spectrum disorder (ASD) are considered 'minimally verbal' due to language development stagnating at a few words. Recent developments allow for the severity of ASD symptoms to be examined using Autism Diagnostic Observation Schedule (ADOS) Social Affect (SA) and Restricted and Repetitive Behaviors (RRB) domain severity scores. The aim of the current study was to explore language outcomes in a cohort of minimally verbal children with autism evaluated through the preschool years and determine if and how ASD symptom severity in core domains predicts the development of spoken language by age 5. The sample consisted of 70 children with autism aged 1-5 years at the first evaluation who were examined at least 1 year later, during their fifth year of age. The ADOS overall level of language item was used to categorize children as minimally verbal or having phrase speech, and the Mullen Scales of Early Learning was used as a continuous measure of expressive language. At Time 1, 65% (n = 47) of children in the sample were minimally verbal and by Time 2, 36% (n = 17 of 47) of them had developed phrase speech. While the Time 1 ADOS calibrated severity scores did not predict whether or not a child remained minimally verbal at Time 2, change in the SA calibrated severity score (but not RRB) was predictive of the continuous measure of expressive language. However, change in SA severity no longer predicted continuous expressive language when nonverbal cognitive ability was added to the model. Findings indicate that the severity of SA symptoms has some relationship with continuous language outcome, but not categorical. However, the omnipresent influence of nonverbal cognitive ability was confirmed in the current study, as the addition of it to the model rendered null the predictive utility of SA severity. Adapted from the source document JF - The Journal of Child Psychology and Psychiatry AU - Thurm, Audrey AU - Manwaring, Stacy S AU - Swineford, Lauren AU - Farmer, Cristan AD - National Institute of Mental Health Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 97 EP - 104 VL - 56 IS - 1 SN - 0021-9630, 0021-9630 KW - Language Impairment (42700) KW - Delayed Language Acquisition (17950) KW - Autism (06800) KW - Language Acquisition (41600) KW - Children (11850) KW - article KW - 6610: mental retardation and disorders; mental disorders/mental retardation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660012169?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Allba&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+Child+Psychology+and+Psychiatry&rft.atitle=Longitudinal+study+of+symptom+severity+and+language+in+minimally+verbal+children+with+autism&rft.au=Thurm%2C+Audrey%3BManwaring%2C+Stacy+S%3BSwineford%2C+Lauren%3BFarmer%2C+Cristan&rft.aulast=Thurm&rft.aufirst=Audrey&rft.date=2015-01-01&rft.volume=56&rft.issue=1&rft.spage=97&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Child+Psychology+and+Psychiatry&rft.issn=00219630&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2015-03-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JPPDAI N1 - SubjectsTermNotLitGenreText - Autism (06800); Children (11850); Delayed Language Acquisition (17950); Language Impairment (42700); Language Acquisition (41600) ER - TY - JOUR T1 - Gene expression in obliterative bronchiolitis-like lesions in 2,3-pentanedione-exposed rats. AN - 1659768440; 25710175 AB - Obliterative bronchiolitis (OB) is an irreversible lung disease characterized by progressive fibrosis in the small airways with eventual occlusion of the airway lumens. OB is most commonly associated with lung transplant rejection; however, OB has also been diagnosed in workers exposed to artificial butter flavoring (ABF) vapors. Research has been limited by the lack of an adequate animal model of OB, and as a result the mechanism(s) is unclear and there are no effective treatments for this condition. Exposure of rats to the ABF component, 2,3-pentanedione (PD) results in airway lesions that are histopathologically similar to those in human OB. We used this animal model to evaluate changes in gene expression in the distal bronchi of rats with PD-induced OB. Male Wistar Han rats were exposed to 200 ppm PD or air 6 h/d, 5 d/wk for 2-wks. Bronchial tissues were laser microdissected from serial sections of frozen lung. In exposed lungs, both fibrotic and non-fibrotic airways were collected. Following RNA extraction and microarray analysis, differential gene expression was evaluated. In non-fibrotic bronchi of exposed rats, 4683 genes were significantly altered relative to air-exposed controls with notable down-regulation of many inflammatory cytokines and chemokines. In contrast, in fibrotic bronchi, 3807 genes were significantly altered with a majority of genes being up-regulated in affected pathways. Tgf-β2 and downstream genes implicated in fibrosis were significantly up-regulated in fibrotic lesions. Genes for collagens and extracellular matrix proteins were highly up-regulated. In addition, expression of genes for peptidases and peptidase inhibitors were significantly altered, indicative of the tissue remodeling that occurs during airway fibrosis. Our data provide new insights into the molecular mechanisms of OB. This new information is of potential significance with regard to future therapeutic targets for treatment. JF - PloS one AU - Morgan, Daniel L AU - Merrick, B Alex AU - Gerrish, Kevin E AU - Stockton, Patricia S AU - Wang, Yu AU - Foley, Julie F AU - Gwinn, William M AU - Kelly, Francine L AU - Palmer, Scott M AU - Ton, Thai-Vu T AU - Flake, Gordon P AD - Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America. ; Division of Intramural Research, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, United States of America. ; Duke University Medical Center, Durham, North Carolina, United States of America. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 2 KW - Pentanones KW - 0 KW - Transforming Growth Factor beta2 KW - RNA KW - 63231-63-0 KW - 2,3-pentanedione KW - K4WBE45SCM KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Animals KW - Transforming Growth Factor beta2 -- genetics KW - Transforming Growth Factor beta2 -- metabolism KW - Principal Component Analysis KW - Disease Models, Animal KW - Rats KW - Fibrosis -- pathology KW - RNA -- metabolism KW - Inhalation Exposure KW - RNA -- isolation & purification KW - Rats, Wistar KW - Immunohistochemistry KW - Male KW - Bronchiolitis Obliterans -- chemically induced KW - Up-Regulation -- drug effects KW - Bronchiolitis Obliterans -- genetics KW - Bronchiolitis Obliterans -- pathology KW - Bronchi -- metabolism KW - Down-Regulation -- drug effects KW - Bronchi -- pathology KW - Pentanones -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1659768440?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Gene+expression+in+obliterative+bronchiolitis-like+lesions+in+2%2C3-pentanedione-exposed+rats.&rft.au=Morgan%2C+Daniel+L%3BMerrick%2C+B+Alex%3BGerrish%2C+Kevin+E%3BStockton%2C+Patricia+S%3BWang%2C+Yu%3BFoley%2C+Julie+F%3BGwinn%2C+William+M%3BKelly%2C+Francine+L%3BPalmer%2C+Scott+M%3BTon%2C+Thai-Vu+T%3BFlake%2C+Gordon+P&rft.aulast=Morgan&rft.aufirst=Daniel&rft.date=2015-01-01&rft.volume=10&rft.issue=2&rft.spage=e0118459&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0118459 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-11-17 N1 - Date created - 2015-02-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1778-83 [10677534] Bioinformatics. 2006 May 1;22(9):1111-21 [16522673] Transplantation. 2000 Jul 27;70(2):362-7 [10933164] Matrix Biol. 2000 Dec;19(7):557-68 [11102746] J Histochem Cytochem. 2001 Feb;49(2):237-46 [11156692] Virchows Arch. 2001 Jul;439(1):78-84 [11499844] J Heart Lung Transplant. 2001 Nov;20(11):1144-51 [11704473] Nucleic Acids Res. 2002 Jan 1;30(1):207-10 [11752295] Proc Natl Acad Sci U S A. 2002 Apr 30;99(9):6292-7 [11983918] N Engl J Med. 2002 Aug 1;347(5):330-8 [12151470] Nature. 2002 Dec 12;420(6916):636-42 [12478285] J Cell Sci. 2003 Jan 15;116(Pt 2):217-24 [12482908] Am J Respir Cell Mol Biol. 2003 Feb;28(2):142-9 [12540481] Oncol Rep. 2003 Jul-Aug;10(4):881-4 [12792739] Cytokine Growth Factor Rev. 2003 Dec;14(6):479-88 [14563350] Am J Respir Crit Care Med. 2003 Dec 1;168(11):1277-92 [14644923] J Heart Lung Transplant. 2004 Apr;23(4):446-55 [15063404] J Immunol. 1982 May;128(5):2177-82 [6460819] J Cell Biol. 1983 Dec;97(6):1925-32 [6358238] Arthritis Rheum. 1984 Sep;27(9):995-1001 [6332633] J Immunol. 1985 Feb;134(2):904-9 [3871221] Biochem J. 1987 Nov 1;247(3):597-604 [3501287] J Biol Chem. 1988 Apr 5;263(10):4586-92 [2965146] Crit Rev Oral Biol Med. 1997;8(2):217-36 [9167094] Am J Respir Crit Care Med. 1997 Sep;156(3 Pt 1):951-8 [9310019] Scand Cardiovasc J. 1998;32(2):97-103 [9636965] Am J Physiol. 1998 Jun;274(6 Pt 1):L1049-57 [9609745] Clin Cancer Res. 1998 Jul;4(7):1785-8 [9676856] Biochem Biophys Res Commun. 1998 Sep 8;250(1):119-24 [9735343] Br J Cancer. 1999 Jan;79(2):354-9 [9888480] J Heart Lung Transplant. 1999 Sep;18(9):828-37 [10528744] J Allergy Clin Immunol. 2005 Jan;115(1):110-7 [15637555] Am J Physiol Lung Cell Mol Physiol. 2006 Dec;291(6):L1277-85 [16891397] Crit Care. 2007;11(1):R8 [17241453] Int J Biochem Cell Biol. 2008;40(3):484-95 [17931953] J Heart Lung Transplant. 2008 Apr;27(4):400-7 [18374876] Biochim Biophys Acta. 2008 Sep;1781(9):513-8 [18621144] J Perinatol. 2008 Dec;28 Suppl 3:S127-35 [19057604] Int J Oncol. 2009 Jan;34(1):5-13 [19082472] Am J Clin Pathol. 2009 May;131(5):738-43 [19369636] Proc Natl Acad Sci U S A. 2009 Jun 2;106(22):9021-6 [19439663] Am J Transplant. 2009 Sep;9(9):1981-7 [19663891] Am J Respir Cell Mol Biol. 2009 Dec;41(6):661-70 [19265174] Biochem Biophys Res Commun. 2010 Feb 19;392(4):495-9 [20093106] Cytokine. 2011 Jan;53(1):19-28 [21050772] Am J Physiol Lung Cell Mol Physiol. 2010 Dec;299(6):L785-93 [20833777] Curr Opin Immunol. 2010 Dec;22(6):800-6 [21071194] PLoS One. 2011;6(3):e17644 [21464978] Respir Res. 2011;12:48 [21496259] Transpl Int. 2011 Oct;24(10):1027-39 [21797940] Growth Factors. 2011 Oct;29(5):196-202 [21740331] Cold Spring Harb Perspect Biol. 2011 Oct;3(10):a009712 [21875984] Am J Physiol Lung Cell Mol Physiol. 2012 Jan 15;302(2):L193-205 [22003091] Nat Commun. 2012;3:735 [22415826] J Interferon Cytokine Res. 2012 Oct;32(10):443-9 [22900713] Annu Rev Physiol. 2013;75:551-67 [23072447] Respirology. 2013 May;18(4):643-51 [23253121] Chest. 1992 Jun;101(6):1663-73 [1534744] Eur Respir J. 2005 Mar;25(3):494-501 [15738294] Am J Transplant. 2005 Apr;5(4 Pt 1):671-83 [15760390] Immunity. 2005 Nov;23(5):479-90 [16286016] FASEB J. 2000 Jul;14(10):1362-74 [10877829] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0118459 ER - TY - JOUR T1 - Development and validation of a high-performance liquid chromatography-tandem mass spectrometry method for the simultaneous determination of irinotecan and its main metabolites in human plasma and its application in a clinical pharmacokinetic study. AN - 1657328296; 25689738 AB - Irinotecan is currently used in several cancer regimens mainly in colorectal cancer (CRC). This drug has a narrow therapeutic range and treatment can lead to side effects, mainly neutropenia and diarrhea, frequently requiring discontinuing or lowering the drug dose. A wide inter-individual variability in irinotecan pharmacokinetic parameters and pharmacodynamics has been reported and associated to patients' genetic background. In particular, a polymorphism in the UGT1A1 gene (UGT1A1*28) has been linked to an impaired detoxification of SN-38 (irinotecan active metabolite) to SN-38 glucuronide (SN-38G) leading to increased toxicities. Therefore, therapeutic drug monitoring of irinotecan, SN-38 and SN-38G is recommended to personalize therapy. In order to quantify simultaneously irinotecan and its main metabolites in patients' plasma, we developed and validated a new, sensitive and specific HPLC-MS/MS method applicable to all irinotecan dosages used in clinic. This method required a small plasma volume, addition of camptothecin as internal standard and simple protein precipitation. Chromatographic separation was done on a Gemini C18 column (3 μM, 100 mm x 2.0 mm) using 0.1% acetic acid/bidistilled water and 0.1% acetic acid/acetonitrile as mobile phases. The mass spectrometer worked with electrospray ionization in positive ion mode and selected reaction monitoring. The standard curves were linear (R2 ≥0.9962) over the concentration ranges (10-10000 ng/mL for irinotecan, 1-500 ng/mL for SN-38 and SN-38G and 1-5000 ng/mL for APC) and had good back-calculated accuracy and precision. The intra- and inter-day precision and accuracy, determined on three quality control levels for all the analytes, were always <12.3% and between 89.4% and 113.0%, respectively. Moreover, we evaluated this bioanalytical method by re-analysis of incurred samples as an additional measure of assay reproducibility. This method was successfully applied to a pharmacokinetic study in metastatic CRC patients enrolled in a genotype-guided phase Ib study of irinotecan administered in combination with 5-fluorouracil/leucovorin and bevacizumab. JF - PloS one AU - Marangon, Elena AU - Posocco, Bianca AU - Mazzega, Elisa AU - Toffoli, Giuseppe AD - CRO, National Cancer Institute, Aviano (PN), Italy. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 2 KW - irinotecan KW - 0H43101T0J KW - Camptothecin KW - XT3Z54Z28A KW - Index Medicus KW - Humans KW - Drug Monitoring KW - Camptothecin -- pharmacokinetics KW - Camptothecin -- metabolism KW - Tandem Mass Spectrometry -- methods KW - Blood Chemical Analysis -- methods KW - Chromatography, High Pressure Liquid -- methods KW - Camptothecin -- analogs & derivatives KW - Camptothecin -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1657328296?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Development+and+validation+of+a+high-performance+liquid+chromatography-tandem+mass+spectrometry+method+for+the+simultaneous+determination+of+irinotecan+and+its+main+metabolites+in+human+plasma+and+its+application+in+a+clinical+pharmacokinetic+study.&rft.au=Marangon%2C+Elena%3BPosocco%2C+Bianca%3BMazzega%2C+Elisa%3BToffoli%2C+Giuseppe&rft.aulast=Marangon&rft.aufirst=Elena&rft.date=2015-01-01&rft.volume=10&rft.issue=2&rft.spage=e0118194&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0118194 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-08 N1 - Date created - 2015-02-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Biomed Chromatogr. 2002 May;16(3):209-18 [11920947] J Chromatogr B Analyt Technol Biomed Life Sci. 2003 May 5;788(1):65-74 [12668072] J Clin Oncol. 2004 Apr 15;22(8):1382-8 [15007088] Biol Mass Spectrom. 1992 Nov;21(11):585-9 [1360817] J Chromatogr B Biomed Sci Appl. 1998 Aug 7;712(1-2):225-35 [9698245] J Clin Oncol. 2006 Jul 1;24(19):3061-8 [16809730] AAPS J. 2009 Jun;11(2):238-41 [19381839] J Clin Oncol. 2010 Feb 10;28(5):866-71 [20038727] Ther Drug Monit. 2010 Oct;32(5):638-46 [20683392] Colorectal Dis. 2012 Jan;14(1):3-17 [21040359] PLoS One. 2013;8(3):e58489 [23516488] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0118194 ER - TY - JOUR T1 - Dilemmas in treating smoldering multiple myeloma. AN - 1657314675; 25422486 AB - Novel therapies hold promise for high-risk smoldering multiple myeloma (SMM). Recent studies suggest that modern combination approaches can be options for high-risk SMM to obtain deep molecular responses with favorable toxicity profiles. Although pioneering treatment trials based on small numbers of patients suggest progression-free and overall survival benefits, application of the data to real-life practice remains to be validated. Therapeutic modulation of disease tempo, disease burden, clonal evolution, and tumor microenvironment in SMM remains to be understood and calls for reliable biomarkers reflective of disease biology. Here, we review studies that open a new management platform for SMM, address ongoing dilemmas in practice and under investigation, and highlight emerging scientific questions in the era of SMM treatment. © 2014 by American Society of Clinical Oncology. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Ahn, Inhye E AU - Mailankody, Sham AU - Korde, Neha AU - Landgren, Ola AD - Inhye Ahn and Sham Mailankody, the National Cancer Institute, National Institutes of Health, Bethesda, MD; Neha Korde and Ola Landgren, Memorial Sloan Kettering Cancer Center, New York, NY. ; Inhye Ahn and Sham Mailankody, the National Cancer Institute, National Institutes of Health, Bethesda, MD; Neha Korde and Ola Landgren, Memorial Sloan Kettering Cancer Center, New York, NY. landgrec@mskcc.org. Y1 - 2015/01/01/ PY - 2015 DA - 2015 Jan 01 SP - 115 EP - 123 VL - 33 IS - 1 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Disease-Free Survival KW - Humans KW - Clonal Evolution -- drug effects KW - Treatment Outcome KW - Prognosis KW - Disease Progression KW - Multiple Myeloma -- diagnosis KW - Multiple Myeloma -- drug therapy KW - Antineoplastic Agents -- therapeutic use KW - Tumor Microenvironment -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1657314675?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Dilemmas+in+treating+smoldering+multiple+myeloma.&rft.au=Ahn%2C+Inhye+E%3BMailankody%2C+Sham%3BKorde%2C+Neha%3BLandgren%2C+Ola&rft.aulast=Ahn&rft.aufirst=Inhye&rft.date=2015-01-01&rft.volume=33&rft.issue=1&rft.spage=115&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=1527-7755&rft_id=info:doi/10.1200%2FJCO.2014.56.4351 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-20 N1 - Date created - 2014-12-31 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Haematologica. 2010 Nov;95(11):1973-6 [20634494] Blood. 2013 Jul 11;122(2):219-26 [23699600] N Engl J Med. 2013 Aug 1;369(5):438-47 [23902483] Leukemia. 2013 Aug;27(8):1738-44 [23515097] Leuk Lymphoma. 2013 Oct;54(10):2215-8 [23311294] N Engl J Med. 2013 Oct 31;369(18):1762-3 [24171527] J Clin Oncol. 2013 Dec 1;31(34):4325-32 [24145347] Blood. 2014 Jan 2;123(1):78-85 [24144643] Nat Commun. 2014;5:2997 [24429703] Cancer Cell. 2014 Jan 13;25(1):91-101 [24434212] Leukemia. 2014 Feb;28(2):384-90 [23817176] Leukemia. 2014 May;28(5):981-92 [24177258] Blood. 2014 May 15;123(20):3073-9 [24646471] Haematologica. 2014 Jun;99(6):e81-3 [24658821] J Clin Oncol. 2014 Jul 10;32(20):2173-80 [24888806] Leukemia. 2014 Jul;28(7):1548-52 [24496302] Leukemia. 2014 Sep;28(9):1902-8 [24535407] Am J Hematol. 2014 Dec;89(12):1159-60 [25132630] Br J Cancer. 2000 Apr;82(7):1254-60 [10755397] Leukemia. 2001 Aug;15(8):1274-6 [11480571] Blood. 2001 Nov 15;98(10):3082-6 [11698294] Blood. 2002 Nov 1;100(9):3095-100 [12384404] Leukemia. 2003 Apr;17(4):775-9 [12682636] Blood. 2003 Jun 1;101(11):4569-75 [12576322] Eur J Haematol. 1991 Nov;47(5):338-41 [1761119] Eur J Haematol. 1993 Feb;50(2):95-102 [8440364] Blood. 1993 Dec 15;82(12):3712-20 [8260708] JAMA. 2010 Dec 1;304(21):2397-404 [21119086] J Biomed Opt. 2011 Jan-Feb;16(1):011006 [21280893] Nature. 2011 Mar 24;471(7339):467-72 [21430775] Leuk Lymphoma. 2011 May;52(5):771-5 [21299465] Blood. 2011 May 5;117(18):4691-5 [21292775] Blood. 2011 Nov 24;118(22):5752-8; quiz 5982 [21849487] Nat Rev Cancer. 2012 May;12(5):335-48 [22495321] Eur J Haematol. 2012 Jul;89(1):28-36 [22620863] Blood. 2012 Jul 5;120(1):9-19 [22498745] Blood. 2012 Jul 5;120(1):20-30 [22535658] Blood. 2012 Aug 23;120(8):1589-96 [22791289] Cancer. 2012 Nov 15;118(22):5544-9 [22786730] Leukemia. 2012 Nov;26(11):2406-13 [22722715] Leukemia. 2012 Dec;26(12):2521-9 [22565645] Blood. 2012 Dec 13;120(25):4929-37 [23074271] Leukemia. 2013 Jan;27(1):220-5 [22902362] J Clin Oncol. 2013 Feb 1;31(4):448-55 [23233713] Cell. 2013 Feb 14;152(4):714-26 [23415222] J Clin Oncol. 2013 Jul 10;31(20):2540-7 [23733781] J Clin Oncol. 2013 Jul 10;31(20):2523-6 [23733782] J Clin Oncol. 1995 Jan;13(1):251-6 [7799027] Haematologica. 2005 Oct;90(10):1365-72 [16219573] J Interferon Cytokine Res. 2006 Feb;26(2):83-95 [16487028] Blood. 2007 Feb 15;109(4):1692-700 [17023574] Blood. 2007 Apr 15;109(8):3489-95 [17209057] N Engl J Med. 2007 Jun 21;356(25):2582-90 [17582068] Blood. 2007 Oct 1;110(7):2586-92 [17576818] Blood. 2008 Jan 15;111(2):785-9 [17942755] Leukemia. 2008 Feb;22(2):231-9 [17972944] Cancer. 2008 Oct 1;113(7):1588-95 [18683218] Blood. 2008 Oct 15;112(8):3122-5 [18669874] Expert Rev Anticancer Ther. 2008 Oct;8(10):1569-80 [18925849] Blood. 2008 Nov 15;112(10):4017-23 [18669875] Leukemia. 2008 Dec;22(12):2280-4 [18528420] Leukemia. 2009 Jan;23(1):10-24 [18843284] Mayo Clin Proc. 2009 Feb;84(2):114-22 [19181644] J Clin Oncol. 2009 Sep 20;27(27):4585-90 [19687334] Mayo Clin Proc. 2010 Mar;85(3):300 [20194156] J Clin Oncol. 2010 Mar 20;28(9):1606-10 [20177023] Br J Haematol. 2010 May;149(3):334-51 [20201947] Leukemia. 2010 Jun;24(6):1121-7 [20410922] Br J Haematol. 2003 Jun;121(5):749-57 [12780789] Leuk Lymphoma. 2003 Sep;44(9):1545-8 [14565658] Br J Haematol. 2004 Sep;126(5):686-9 [15327520] N Engl J Med. 1980 Jun 12;302(24):1347-9 [7374679] Arch Intern Med. 1988 Sep;148(9):1963-5 [2458080] J Clin Invest. 1989 Dec;84(6):2008-11 [2592570] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1200/JCO.2014.56.4351 ER - TY - JOUR T1 - Methamphetamine accelerates cellular senescence through stimulation of de novo ceramide biosynthesis. AN - 1655261062; 25671639 AB - Methamphetamine is a highly addictive psychostimulant that causes profound damage to the brain and other body organs. Post mortem studies of human tissues have linked the use of this drug to diseases associated with aging, such as coronary atherosclerosis and pulmonary fibrosis, but the molecular mechanism underlying these findings remains unknown. Here we used functional lipidomics and transcriptomics experiments to study abnormalities in lipid metabolism in select regions of the brain and, to a greater extent, peripheral organs and tissues of rats that self-administered methamphetamine. Experiments in various cellular models (primary mouse fibroblasts and myotubes) allowed us to investigate the molecular mechanisms of systemic inflammation and cellular aging related to methamphetamine abuse. We report now that methamphetamine accelerates cellular senescence and activates transcription of genes involved in cell-cycle control and inflammation by stimulating production of the sphingolipid messenger ceramide. This pathogenic cascade is triggered by reactive oxygen species, likely generated through methamphetamine metabolism via cytochrome P450, and involves the recruitment of nuclear factor-κB (NF-κB) to induce expression of enzymes in the de novo pathway of ceramide biosynthesis. Inhibitors of NF-κB signaling and ceramide formation prevent methamphetamine-induced senescence and systemic inflammation in rats self-administering the drug, attenuating their health deterioration. The results suggest new therapeutic strategies to reduce the adverse consequences of methamphetamine abuse and improve effectiveness of abstinence treatments. JF - PloS one AU - Astarita, Giuseppe AU - Avanesian, Agnesa AU - Grimaldi, Benedetto AU - Realini, Natalia AU - Justinova, Zuzana AU - Panlilio, Leight V AU - Basit, Abdul AU - Goldberg, Steven R AU - Piomelli, Daniele AD - Department of Pharmacology, University of California Irvine, Irvine, California, United States of America. ; Drug Discovery and Development, Italian Institute of Technology, Genoa, Italy. ; Preclinical Pharmacology Section, Behavioral Neuroscience Research Branch, National Institute on Drug Abuse, Baltimore, Maryland, United States of America; Departement of Psychiatry, MPRC, University of Maryland School of Medicine, Baltimore, Maryland, United States of America. ; Preclinical Pharmacology Section, Behavioral Neuroscience Research Branch, National Institute on Drug Abuse, Baltimore, Maryland, United States of America. ; Drug Discovery and Development, Italian Institute of Technology, Genoa, Italy; Department of Anatomy and Neurobiology, University of California Irvine, Irvine, California, United States of America. Y1 - 2015 PY - 2015 DA - 2015 SP - 1 VL - 10 IS - 2 KW - Central Nervous System Stimulants KW - 0 KW - Ceramides KW - NF-kappa B KW - Methamphetamine KW - 44RAL3456C KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - Index Medicus KW - Rats KW - Animals KW - Transcription, Genetic -- drug effects KW - Self Administration KW - Kinetics KW - Cytochrome P-450 Enzyme System -- metabolism KW - Mice KW - Male KW - Cell Line KW - NF-kappa B -- metabolism KW - Methamphetamine -- administration & dosage KW - Central Nervous System Stimulants -- toxicity KW - Ceramides -- metabolism KW - Central Nervous System Stimulants -- administration & dosage KW - Ceramides -- biosynthesis KW - Methamphetamine -- toxicity KW - Cell Aging -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1655261062?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Methamphetamine+accelerates+cellular+senescence+through+stimulation+of+de+novo+ceramide+biosynthesis.&rft.au=Astarita%2C+Giuseppe%3BAvanesian%2C+Agnesa%3BGrimaldi%2C+Benedetto%3BRealini%2C+Natalia%3BJustinova%2C+Zuzana%3BPanlilio%2C+Leight+V%3BBasit%2C+Abdul%3BGoldberg%2C+Steven+R%3BPiomelli%2C+Daniele&rft.aulast=Astarita&rft.aufirst=Giuseppe&rft.date=2015-01-01&rft.volume=10&rft.issue=2&rft.spage=e0116961&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0116961 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-05 N1 - Date created - 2015-02-12 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: PLoS One. 2010;5(1):e8790 [20098750] Ann N Y Acad Sci. 2010 Feb;1187:101-21 [20201848] Trends Mol Med. 2010 May;16(5):238-46 [20444648] Adv Exp Med Biol. 2010;688:1-23 [20919643] J Int Neuropsychol Soc. 2010 Sep;16(5):890-901 [20727252] Biochem J. 2012 Feb 1;441(3):789-802 [22248339] Anticancer Agents Med Chem. 2012 May;12(4):340-63 [21707511] Neurotoxicology. 2012 Jun;33(3):491-9 [22433442] J Cell Sci. 2000 Oct;113 ( Pt 20):3613-22 [11017877] Mech Ageing Dev. 2000 Feb 15;113(3):169-81 [10714936] Biochem Biophys Res Commun. 2012 Aug 24;425(2):478-84 [22877754] Brain Res. 2000 Dec 1;885(1):25-31 [11121526] J Gerontol A Biol Sci Med Sci. 2001 Jan;56(1):B8-19 [11193225] J Neurochem. 2001 Oct;79(1):152-60 [11595767] Am J Psychiatry. 2001 Dec;158(12):2015-21 [11729018] J Neurosci Res. 2001 Nov 15;66(4):583-91 [11746378] J Biol Chem. 2002 Jul 19;277(29):25847-50 [12011103] J Neurosci Res. 2002 Oct 1;70(1):82-9 [12237866] J Neurosci. 2004 Jun 30;24(26):6028-36 [15229250] J Addict Dis. 2004;23(3):39-53 [15256343] Neurochem Res. 1989 Mar;14(3):245-8 [2725825] EMBO J. 1991 Aug;10(8):2247-58 [2065663] J Biol Chem. 1993 Aug 25;268(24):17762-6 [8349660] J Neurochem. 1993 Sep;61(3):955-60 [8360694] J Biol Chem. 1993 Dec 25;268(36):27299-306 [8262970] Biochem Biophys Res Commun. 1995 Jun 15;211(2):396-403 [7794249] Proc Natl Acad Sci U S A. 1995 Sep 26;92(20):9363-7 [7568133] J Biol Chem. 1995 Dec 22;270(51):30701-8 [8530509] Biochem Pharmacol. 1997 Jun 1;53(11):1605-12 [9264312] Drug Metab Dispos. 1997 Sep;25(9):1059-64 [9311621] Brain Res Mol Brain Res. 1998 Oct 1;60(2):305-9 [9757070] Brain Res. 1998 Nov 30;813(1):200-2 [9824698] J Forensic Sci. 1999 Mar;44(2):359-68 [10097363] Nat Med. 2005 May;11(5):491-8 [15852018] Biotechniques. 2005 Nov;39(5):715-25 [16315372] Gen Dent. 2006 Mar-Apr;54(2):125-9; quiz 130 [16689071] AAPS J. 2006;8(2):E413-8 [16808044] Biochem Pharmacol. 2006 Nov 30;72(11):1493-505 [16723122] Lipids. 2006 Sep;41(9):859-63 [17152923] Annu Rev Pharmacol Toxicol. 2007;47:681-98 [17209801] Mech Ageing Dev. 2007 Jan;128(1):36-44 [17116315] Addiction. 2007 Aug;102(8):1204-11 [17565561] Diabetes. 2007 Aug;56(8):1960-8 [17620421] Nat Rev Mol Cell Biol. 2007 Sep;8(9):729-40 [17667954] Exp Neurol. 2007 Sep;207(1):42-51 [17603040] Methods Enzymol. 2007;434:233-41 [17954250] Curr Protoc Mol Biol. 2001 May;Chapter 23:Unit 23.2 [18265203] Addiction. 2008 Aug;103(8):1353-60 [18855825] Mol Cancer Res. 2009 Jun;7(6):890-6 [19531570] Biol Psychiatry. 2009 Jul 15;66(2):118-27 [19345341] Adicciones. 2009;21(2):99-104 [19578726] Methods Mol Biol. 2009;579:201-19 [19763477] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0116961 ER - TY - JOUR T1 - Interaction of paroxetine with mitochondrial proteins mediates neuroprotection. AN - 1654700168; 25404050 AB - There are severe neurological complications that arise from HIV infection, ranging from peripheral sensory neuropathy to cognitive decline and dementia for which no specific treatments are available. The HIV proteins secreted from infected macrophages, gp120 and Tat, are neurotoxic. The goal of this study was to screen, identify and develop neuroprotective compounds relevant to HIV-associated neurocognitive disorders (HAND). We screened more than 2000 compounds that included FDA approved drugs for protective efficacy against oxidative stress-mediated neurodegeneration and identified selective serotonin reuptake inhibitors (SSRIs) as potential neuroprotectants. Numerous SSRIs were then extensively evaluated as protectants against neurotoxicity as measured by changes in neuronal cell death, mitochondrial potential, and axodendritic degeneration elicited by HIV Tat and gp120 and other mitochondrial toxins. While many SSRIs demonstrated neuroprotective actions, paroxetine was potently neuroprotective (100 nM potency) against these toxins in vitro and in vivo following systemic administration in a gp120 neurotoxicity model. Interestingly, the inhibition of serotonin reuptake by paroxetine was not required for neuroprotection, since depletion of the serotonin transporter had no effect on its neuroprotective properties. We determined that paroxetine interacts selectively and preferentially with brain mitochondrial proteins and blocks calcium-dependent swelling but had less effect on liver mitochondria. Additionally, paroxetine induced proliferation of neural progenitor cells in vitro and in vivo in gp120 transgenic animals. Therefore, SSRIs such as paroxetine may provide a novel adjunctive neuroprotective and neuroregenerative therapy to treat HIV-infected individuals. JF - Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics AU - Steiner, Joseph P AU - Bachani, Muznabanu AU - Wolfson-Stofko, Brett AU - Lee, Myoung-Hwa AU - Wang, Tongguang AU - Wang, Tonguang AU - Li, Guanhan AU - Li, Wenxue AU - Strayer, David AU - Haughey, Norman J AU - Nath, Avindra AD - Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA, steinerjp@ninds.nih.gov. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 200 EP - 216 VL - 12 IS - 1 KW - Mitochondrial Proteins KW - 0 KW - Neuroprotective Agents KW - Paroxetine KW - 41VRH5220H KW - Index Medicus KW - Rats KW - In Situ Nick-End Labeling KW - Animals KW - Rats, Sprague-Dawley KW - Blotting, Western KW - Cells, Cultured KW - Humans KW - Mice KW - Immunohistochemistry KW - Mice, Knockout KW - AIDS Dementia Complex -- metabolism KW - Mitochondrial Proteins -- drug effects KW - Paroxetine -- pharmacology KW - Neuroprotective Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654700168?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotherapeutics+%3A+the+journal+of+the+American+Society+for+Experimental+NeuroTherapeutics&rft.atitle=Interaction+of+paroxetine+with+mitochondrial+proteins+mediates+neuroprotection.&rft.au=Steiner%2C+Joseph+P%3BBachani%2C+Muznabanu%3BWolfson-Stofko%2C+Brett%3BLee%2C+Myoung-Hwa%3BWang%2C+Tongguang%3BWang%2C+Tonguang%3BLi%2C+Guanhan%3BLi%2C+Wenxue%3BStrayer%2C+David%3BHaughey%2C+Norman+J%3BNath%2C+Avindra&rft.aulast=Steiner&rft.aufirst=Joseph&rft.date=2015-01-01&rft.volume=12&rft.issue=1&rft.spage=200&rft.isbn=&rft.btitle=&rft.title=Neurotherapeutics+%3A+the+journal+of+the+American+Society+for+Experimental+NeuroTherapeutics&rft.issn=1878-7479&rft_id=info:doi/10.1007%2Fs13311-014-0315-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-19 N1 - Date created - 2015-02-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Br J Pharmacol. 1999 Dec;128(7):1609-15 [10602343] J Neuropathol Exp Neurol. 2009 May;68(5):456-73 [19525894] Am J Pathol. 2010 Sep;177(3):1397-410 [20651230] AIDS Care. 2010 Sep;22(9):1159-70 [20824569] J Neurovirol. 2010 Oct;16(5):355-67 [20839920] Neurobiol Dis. 2011 Mar;41(3):678-87 [21146610] J Neurovirol. 2011 Feb;17(1):3-16 [21174240] PLoS One. 2011;6(3):e17837 [21448457] J Affect Disord. 2012 Feb;136(3):993-9 [21784531] PLoS One. 2012;7(8):e43950 [22952817] J Neurovirol. 2012 Dec;18(6):445-55 [22886603] J Pharmacol Exp Ther. 2001 Sep;298(3):1108-19 [11504808] Ann Neurol. 2000 Feb;47(2):186-94 [10665489] Am J Pathol. 2000 Apr;156(4):1441-53 [10751368] Neuropsychopharmacology. 2000 Oct;23(4):428-38 [10989270] J Neurosci. 2000 Dec 15;20(24):9104-10 [11124987] J Neuroimmunol. 2001 Apr 2;115(1-2):182-91 [11282169] Am J Psychiatry. 2001 May;158(5):725-30 [11329393] J Pharmacol Exp Ther. 2002 Feb;300(2):543-8 [11805215] J Gen Physiol. 2002 Jun;119(6):511-20 [12034759] Naunyn Schmiedebergs Arch Pharmacol. 2002 Aug;366(2):158-65 [12122503] J Biol Chem. 2002 Oct 18;277(42):39312-9 [12167619] J Acquir Immune Defic Syndr. 2002 Oct 1;31 Suppl 2:S55-61 [12394783] Science. 2003 Feb 7;299(5608):896-9 [12574632] Br J Pharmacol. 2003 Mar;138(6):1119-28 [12684268] Curr Med Chem. 2003 Aug;10(16):1507-25 [12871123] Science. 2003 Aug 8;301(5634):805-9 [12907793] Mol Cell Neurosci. 2003 Sep;24(1):224-37 [14550782] Neuroreport. 2003 Dec 19;14(18):2451-5 [14663209] Curr HIV Res. 2003 Oct;1(4):373-83 [15049424] Hepatology. 2004 Sep;40(3):565-73 [15349894] J Immunol Methods. 1983 Dec 16;65(1-2):55-63 [6606682] Psychopharmacol Ser. 1993;10:174-89 [8361975] Nature. 1994 Jan 13;367(6459):188-93 [8114918] Int Clin Psychopharmacol. 1994 Mar;9 Suppl 1:19-26 [8021435] Science. 1996 Dec 13;274(5294):1917-21 [8943206] Proc Natl Acad Sci U S A. 1998 Mar 17;95(6):3117-21 [9501225] J Clin Psychiatry. 1998 May;59(5):217-24 [9632030] Neuropsychopharmacology. 2009 Oct;34(11):2376-89 [19606083] Brain Struct Funct. 2010 Mar;214(2-3):219-34 [19888600] Ann Neurol. 2010 Jun;67(6):699-714 [20517932] J Neurosci. 1998 Jul 15;18(14):5151-9 [9651198] J Neuroimmunol. 1998 Jul 1;87(1-2):33-42 [9670843] Am J Psychiatry. 1999 Jan;156(1):101-7 [9892304] Depress Anxiety. 1999;9(2):70-4 [10207661] J Neurochem. 1999 Jun;72(6):2488-97 [10349859] J Pharmacol Exp Ther. 1999 Oct;291(1):1-6 [10490879] J Neuroimmunol. 2004 Dec;157(1-2):176-84 [15579295] Mol Genet Metab. 2005 Apr;84(4):378 [15781203] Biotechnol Prog. 2005 Mar-Apr;21(2):451-9 [15801785] Cell Death Differ. 2005 Aug;12 Suppl 1:893-904 [15761472] FEBS Lett. 2005 Sep 12;579(22):5105-10 [16139271] Neuropsychopharmacology. 2005 Aug;30(8):1576-83 [15886723] Nature. 2005 Oct 27;437(7063):1370-5 [16251967] Neurotox Res. 2005 Oct;8(1-2):119-34 [16260390] J Neurovirol. 2007 Jun;13(3):274-83 [17613718] AIDS. 2007 Sep 12;21(14):1877-86 [17721095] Front Biosci. 2008;13:2484-94 [17981728] J Infect Dis. 2007 Dec 15;196(12):1779-83 [18190258] Cell Stem Cell. 2007 Aug 16;1(2):230-6 [18371353] Neurology. 2008 May 6;70(19 Pt 2):1753-62 [18077799] Biol Psychiatry. 2008 Aug 15;64(4):293-301 [18406399] Biochim Biophys Acta. 2009 Nov;1787(11):1416-24 [19298790] Erratum In: Neurotherapeutics. 2016 Jan;13(1):237 [26692391] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s13311-014-0315-9 ER - TY - JOUR T1 - Global Transcriptional Start Site Mapping Using Differential RNA Sequencing Reveals Novel Antisense RNAs in Escherichia coli AN - 1654695285; 21328400 AB - While the model organism Escherichia coli has been the subject of intense study for decades, the full complement of its RNAs is only now being examined. Here we describe a survey of the E. coli transcriptome carried out using a differential RNA sequencing (dRNA-seq) approach, which can distinguish between primary and processed transcripts, and an automated prediction algorithm for transcriptional start sites (TSS). With the criterion of expression under at least one of three growth conditions examined, we predicted 14,868 TSS candidates, including 5,574 internal to annotated genes (iTSS) and 5,495 TSS corresponding to potential antisense RNAs (asRNAs). We examined expression of 14 candidate asRNAs by Northern analysis using RNA from wild-type E. coli and from strains defective for RNases III and E, two RNases reported to be involved in asRNA processing. Interestingly, nine asRNAs detected as distinct bands by Northern analysis were differentially affected by the rnc and rne mutations. We also compared our asRNA candidates with previously published asRNA annotations from RNA-seq data and discuss the challenges associated with these cross-comparisons. Our global transcriptional start site map represents a valuable resource for identification of transcription start sites, promoters, and novel transcripts in E. coli and is easily accessible, together with the cDNA coverage plots, in an online genome browser. JF - Journal of Bacteriology AU - Thomason, Maureen K AU - Bischler, Thorsten AU - Eisenbart, Sara K AU - Forstner, Konrad U AU - Zhang, Aixia AU - Herbig, Alexander AU - Nieselt, Kay AU - Sharma, Cynthia M AU - Storz, Gisela AD - Cell Biology and Metabolism Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA, storzg@mail.nih.gov. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 18 EP - 28 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 197 IS - 1 SN - 0021-9193, 0021-9193 KW - Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology KW - Genomes KW - Data processing KW - Growth conditions KW - Antisense RNA KW - Algorithms KW - Transcription KW - Gene expression KW - Promoters KW - RNA KW - Escherichia coli KW - Mutation KW - Internet KW - Gene mapping KW - J 02320:Cell Biology KW - N 14830:RNA UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654695285?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=Global+Transcriptional+Start+Site+Mapping+Using+Differential+RNA+Sequencing+Reveals+Novel+Antisense+RNAs+in+Escherichia+coli&rft.au=Thomason%2C+Maureen+K%3BBischler%2C+Thorsten%3BEisenbart%2C+Sara+K%3BForstner%2C+Konrad+U%3BZhang%2C+Aixia%3BHerbig%2C+Alexander%3BNieselt%2C+Kay%3BSharma%2C+Cynthia+M%3BStorz%2C+Gisela&rft.aulast=Thomason&rft.aufirst=Maureen&rft.date=2015-01-01&rft.volume=197&rft.issue=1&rft.spage=18&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/10.1128%2FJB.02096-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Number of references - 56 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Gene expression; Genomes; Promoters; Data processing; RNA; Growth conditions; Antisense RNA; Algorithms; Transcription; Mutation; Internet; Gene mapping; Escherichia coli DO - http://dx.doi.org/10.1128/JB.02096-14 ER - TY - JOUR T1 - Identifying novel targets of oncogenic EGF receptor signaling in lung cancer through global phosphoproteomics AN - 1654682175; 21335444 AB - Mutations in the epidermal growth factor receptor (EGFR) kinase domain occur in 10-30% of lung adenocarcinoma and are associated with tyrosine kinase inhibitor (TKI) sensitivity. We sought to identify the immediate direct and indirect phosphorylation targets of mutant EGFRs in lung adenocarcinoma. We undertook SILAC strategy, phosphopeptide enrichment, and quantitative MS to identify dynamic changes of phosphorylation downstream of mutant EGFRs in lung adenocarcinoma cells harboring EGFR super(L858R) and EGFR super(L858R/T790M), the TKI-sensitive, and TKI-resistant mutations, respectively. Top canonical pathways that were inhibited upon erlotinib treatment in sensitive cells, but not in the resistant cells include EGFR, insulin receptor, hepatocyte growth factor, mitogen-activated protein kinase, mechanistic target of rapamycin, ribosomal protein S6 kinase beta 1, and Janus kinase/signal transducer and activator of transcription signaling. We identified phosphosites in proteins of the autophagy network, such as ULK1 (S623) that is constitutively phosphorylated in these lung adenocarcinoma cells; phosphorylation is inhibited upon erlotinib treatment in sensitive cells, but not in resistant cells. Finally, kinase-substrate prediction analysis from our data indicated that substrates of basophilic kinases from, AGC and Calcium and calmodulin-dependent kinase groups, as well as STE group kinases were significantly enriched and those of proline-directed kinases from, CMGC and Casein kinase groups were significantly depleted among substrates that exhibited increased phosphorylation upon EGF stimulation and reduced phosphorylation upon TKI inhibition. This is the first study to date to examine global phosphorylation changes upon erlotinib treatment of lung adenocarcinoma cells and results from this study provide new insights into signaling downstream of mutant EGFRs in lung adenocarcinoma. All MS data have been deposited in the ProteomeXchange with identifier PXD001101 ( http://proteomecentral.proteomexchange.org/dataset/PXD001101 ). JF - Proteomics AU - Zhang, Xu AU - Belkina, Natalya AU - Jacob, Harrys Kishore Charles AU - Maity, Tapan AU - Biswas, Romi AU - Venugopalan, Abhilash AU - Shaw, Patrick G AU - Kim, Min-Sik AU - Chaerkady, Raghothama AU - Pandey, Akhilesh AU - Guha, Udayan AD - Thoracic and Gastrointestinal Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA. Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 340 EP - 355 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 15 IS - 2-3 SN - 1615-9853, 1615-9853 KW - Oncogenes & Growth Factors Abstracts; Biotechnology and Bioengineering Abstracts KW - MAP kinase KW - Calcium KW - Data processing KW - Transcription KW - Epidermal growth factor receptors KW - Insulin receptors KW - Casein KW - Janus kinase KW - Phosphorylation KW - Lung KW - Ribosomal protein S6 kinase KW - Protein-tyrosine kinase KW - proteomics KW - Phagocytosis KW - Epidermal growth factor KW - Adenocarcinoma KW - TOR protein KW - Mutation KW - Hepatocyte growth factor KW - Signal transduction KW - Lung cancer KW - B 26600:Tyrosine Kinase Activity KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1654682175?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proteomics&rft.atitle=Identifying+novel+targets+of+oncogenic+EGF+receptor+signaling+in+lung+cancer+through+global+phosphoproteomics&rft.au=Zhang%2C+Xu%3BBelkina%2C+Natalya%3BJacob%2C+Harrys+Kishore+Charles%3BMaity%2C+Tapan%3BBiswas%2C+Romi%3BVenugopalan%2C+Abhilash%3BShaw%2C+Patrick+G%3BKim%2C+Min-Sik%3BChaerkady%2C+Raghothama%3BPandey%2C+Akhilesh%3BGuha%2C+Udayan&rft.aulast=Zhang&rft.aufirst=Xu&rft.date=2015-01-01&rft.volume=15&rft.issue=2-3&rft.spage=340&rft.isbn=&rft.btitle=&rft.title=Proteomics&rft.issn=16159853&rft_id=info:doi/10.1002%2Fpmic.201400315 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-02-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - MAP kinase; Data processing; Calcium; Transcription; Epidermal growth factor receptors; Insulin receptors; Casein; Janus kinase; Phosphorylation; Lung; Ribosomal protein S6 kinase; Protein-tyrosine kinase; proteomics; TOR protein; Adenocarcinoma; Epidermal growth factor; Phagocytosis; Mutation; Hepatocyte growth factor; Lung cancer; Signal transduction DO - http://dx.doi.org/10.1002/pmic.201400315 ER - TY - JOUR T1 - Fundamentals of translational neuroscience in toxicologic pathology: optimizing the value of animal data for human risk assessment. AN - 1652442264; 25398755 AB - A half-day Society of Toxicologic Pathology continuing education course on "Fundamentals of Translational Neuroscience in Toxicologic Pathology" presented some current major issues faced when extrapolating animal data regarding potential neurological consequences to assess potential human outcomes. Two talks reviewed functional-structural correlates in rodent and nonrodent mammalian brains needed to predict behavioral consequences of morphologic changes in discrete neural cell populations. The third lecture described practical steps for ensuring that specimens from rodent developmental neurotoxicity tests will be processed correctly to produce highly homologous sections. The fourth talk detailed demographic factors (e.g., species, strain, sex, and age); physiological traits (body composition, brain circulation, pharmacokinetic/pharmacodynamic patterns, etc.); and husbandry influences (e.g., group housing) known to alter the effects of neuroactive agents. The last presentation discussed the appearance, unknown functional effects, and potential relevance to humans of polyethylene glycol (PEG)-associated vacuoles within the choroid plexus epithelium of animals. Speakers provided real-world examples of challenges with data extrapolation among species or with study design considerations that may impact the interpretability of results. Translational neuroscience will be bolstered in the future as less invasive and/or more quantitative techniques are devised for linking overt functional deficits to subtle anatomic and chemical lesions. © 2014 by The Author(s). JF - Toxicologic pathology AU - Morrison, James P AU - Sharma, Alok K AU - Rao, Deepa AU - Pardo, Ingrid D AU - Garman, Robert H AU - Kaufmann, Wolfgang AU - Bolon, Brad AD - Charles River Pathology Associates, Durham, North Carolina, USA. ; Covance Inc., Madison, Wisconsin, USA. ; National Toxicology Program, National Institute of Environmental Health Sciences and Integrated Laboratory Systems, Research Triangle Park, North Carolina, USA. ; Pfizer, Groton, Connecticut, USA. ; Consultants in Veterinary Pathology, Inc., Murrysville, Pennsylvania, USA. ; Merck KGaA, Darmstadt, Germany. ; The Ohio State University, College of Veterinary Medicine, Columbus, Ohio, USA bolon.15@osu.edu. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 132 EP - 139 VL - 43 IS - 1 KW - Index Medicus KW - neuroscience KW - translational medicine KW - nervous system KW - PEGylation. KW - neuropathology KW - neurotoxicity KW - neuroanatomy KW - Animals KW - Humans KW - Toxicity Tests KW - Neurosciences KW - Risk Assessment KW - Disease Models, Animal KW - Neurotoxicity Syndromes -- pathology KW - Translational Medical Research UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1652442264?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+pathology&rft.atitle=Fundamentals+of+translational+neuroscience+in+toxicologic+pathology%3A+optimizing+the+value+of+animal+data+for+human+risk+assessment.&rft.au=Morrison%2C+James+P%3BSharma%2C+Alok+K%3BRao%2C+Deepa%3BPardo%2C+Ingrid+D%3BGarman%2C+Robert+H%3BKaufmann%2C+Wolfgang%3BBolon%2C+Brad&rft.aulast=Morrison&rft.aufirst=James&rft.date=2015-01-01&rft.volume=43&rft.issue=1&rft.spage=132&rft.isbn=&rft.btitle=&rft.title=Toxicologic+pathology&rft.issn=1533-1601&rft_id=info:doi/10.1177%2F0192623314558306 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-12-30 N1 - Date created - 2015-01-28 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/0192623314558306 ER - TY - JOUR T1 - Incorporation of rician noise in the analysis of biexponential transverse relaxation in cartilage using a multiple gradient echo sequence at 3 and 7 tesla AN - 1647012653; 21215000 AB - Purpose Previous work has evaluated the quality of different analytic methods for extracting relaxation times from magnitude imaging data exhibiting Rician noise. However, biexponential analysis of relaxation in tissue, including cartilage, and materials is of increasing interest. We, therefore, analyzed biexponential transverse relaxation decay in the presence of Rician noise and assessed the accuracy and precision of several approaches to determining component fractions and apparent transverse relaxation times. Theory and Methods Comparisons of four different voxel-by-voxel fitting methods were performed using Monte Carlo simulations, and phantom and ex vivo bovine nasal cartilage (BNC) experiments. In each case, preclinical and clinical imaging field strengths of 7 Tesla (T) and 3T, respectively, and parameters, were investigated across a range of signal-to-noise ratios (SNR). Results were compared with Cramer-Rao lower bound calculations. Results As expected, at high SNR, all methods performed well. At lower SNR, fits explicitly incorporating the analytic form of the Rician noise maintained performance. The much more efficient correction scheme of Gudbjartsson and Patz performed almost as well in many cases. Ex vivo experiments on phantoms and BNC were consistent with simulation results. Conclusion Explicit incorporation of Rician noise greatly improves accuracy and precision in the analysis of biexponential transverse decay data. Magn Reson Med 73:352-366, 2015. copyright 2014 Wiley Periodicals, Inc. JF - Magnetic Resonance in Medicine AU - Bouhrara, Mustapha AU - Reiter, David A AU - Celik, Hasan AU - Bonny, Jean-Marie AU - Lukas, Vanessa AU - Fishbein, Kenneth W AU - Spencer, Richard G AD - Laboratory of Clinical Investigation, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, USA. Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 352 EP - 366 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 73 IS - 1 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Monte Carlo simulation KW - Data processing KW - Cartilage KW - N.M.R. KW - imaging KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647012653?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Magnetic+Resonance+in+Medicine&rft.atitle=Incorporation+of+rician+noise+in+the+analysis+of+biexponential+transverse+relaxation+in+cartilage+using+a+multiple+gradient+echo+sequence+at+3+and+7+tesla&rft.au=Bouhrara%2C+Mustapha%3BReiter%2C+David+A%3BCelik%2C+Hasan%3BBonny%2C+Jean-Marie%3BLukas%2C+Vanessa%3BFishbein%2C+Kenneth+W%3BSpencer%2C+Richard+G&rft.aulast=Bouhrara&rft.aufirst=Mustapha&rft.date=2015-01-01&rft.volume=73&rft.issue=1&rft.spage=352&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.25111 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Monte Carlo simulation; Data processing; Cartilage; N.M.R.; imaging DO - http://dx.doi.org/10.1002/mrm.25111 ER - TY - JOUR T1 - Elevated mutation rate during meiosis in Saccharomyces cerevisiae. AN - 1645778585; 25569256 AB - Mutations accumulate during all stages of growth, but only germ line mutations contribute to evolution. While meiosis contributes to evolution by reassortment of parental alleles, we show here that the process itself is inherently mutagenic. We have previously shown that the DNA synthesis associated with repair of a double-strand break is about 1000-fold less accurate than S-phase synthesis. Since the process of meiosis involves many programmed DSBs, we reasoned that this repair might also be mutagenic. Indeed, in the early 1960's Magni and Von Borstel observed elevated reversion of recessive alleles during meiosis, and found that the revertants were more likely to be associated with a crossover than non-revertants, a process that they called "the meiotic effect." Here we use a forward mutation reporter (CAN1 HIS3) placed at either a meiotic recombination coldspot or hotspot near the MAT locus on Chromosome III. We find that the increased mutation rate at CAN1 (6 to 21 -fold) correlates with the underlying recombination rate at the locus. Importantly, we show that the elevated mutation rate is fully dependent upon Spo11, the protein that introduces the meiosis specific DSBs. To examine associated recombination we selected for random spores with or without a mutation in CAN1. We find that the mutations isolated this way show an increased association with recombination (crossovers, loss of crossover interference and/or increased gene conversion tracts). Polζ appears to contribute about half of the mutations induced during meiosis, but is not the only source of mutations for the meiotic effect. We see no difference in either the spectrum or distribution of mutations between mitosis and meiosis. The correlation of hotspots with elevated mutagenesis provides a mechanism for organisms to control evolution rates in a gene specific manner. JF - PLoS genetics AU - Rattray, Alison AU - Santoyo, Gustavo AU - Shafer, Brenda AU - Strathern, Jeffrey N AD - Gene Regulation and Chromosome Biology Laboratory, NCI-Frederick, FNLCR, Frederick, Maryland, United States of America. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 1 VL - 11 IS - 1 KW - Amino Acid Transport Systems, Basic KW - 0 KW - CAN1 protein, S cerevisiae KW - Homeodomain Proteins KW - MATA1 protein, S cerevisiae KW - Repressor Proteins KW - Saccharomyces cerevisiae Proteins KW - Endodeoxyribonucleases KW - EC 3.1.- KW - Spo11 protein, S cerevisiae KW - Index Medicus KW - DNA Repair -- genetics KW - Homeodomain Proteins -- genetics KW - Saccharomyces cerevisiae Proteins -- genetics KW - Amino Acid Transport Systems, Basic -- genetics KW - Endodeoxyribonucleases -- genetics KW - Chromosomes -- metabolism KW - Repressor Proteins -- genetics KW - Mutation KW - Gene Conversion -- genetics KW - Saccharomyces cerevisiae KW - Mitosis -- genetics KW - Recombination, Genetic KW - Meiosis -- genetics KW - Mutation Rate UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1645778585?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+genetics&rft.atitle=Elevated+mutation+rate+during+meiosis+in+Saccharomyces+cerevisiae.&rft.au=Rattray%2C+Alison%3BSantoyo%2C+Gustavo%3BShafer%2C+Brenda%3BStrathern%2C+Jeffrey+N&rft.aulast=Rattray&rft.aufirst=Alison&rft.date=2015-01-01&rft.volume=11&rft.issue=1&rft.spage=e1004910&rft.isbn=&rft.btitle=&rft.title=PLoS+genetics&rft.issn=1553-7404&rft_id=info:doi/10.1371%2Fjournal.pgen.1004910 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-06-30 N1 - Date created - 2015-01-09 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Genetics. 1985 Jun;110(2):187-216 [3891509] Genetics. 1979 Jan;91(1):35-51 [372045] Genetics. 1989 Mar;121(3):445-62 [2653960] Methods Enzymol. 1991;194:281-301 [2005793] Genetica. 1992;85(2):173-9 [1624139] Genetics. 1993 Feb;133(2):159-69 [8436266] Genetics. 1993 Mar;133(3):489-98 [8454201] Nature. 1993 Apr 22;362(6422):709-15 [8469282] Yeast. 1994 Dec;10(13):1793-808 [7747518] Genetics. 1995 Jul;140(3):965-72 [7672595] Cell. 1997 Feb 7;88(3):375-84 [9039264] Genetics. 1997 Jul;146(3):781-95 [9215887] Genetics. 1997 Nov;147(3):1017-24 [9383049] Mol Cell. 1998 Jul;2(1):9-22 [9702187] Mol Cell Biol. 1999 Jul;19(7):4832-42 [10373533] Yeast. 1999 Oct;15(14):1541-53 [10514571] Arch Int Physiol Biochim. 1962 Dec;70:766-7 [14000449] Proc Natl Acad Sci U S A. 1963 Nov;50:975-80 [14082365] Mutat Res. 1964 May;106:2-9 [14195748] J Cell Physiol. 1964 Oct;64:SUPPL 1:165-71 [14218581] Curr Biol. 2004 Dec 29;14(24):R1036-7 [15620632] Genome Biol. 2006;7(3):R20 [16542486] Methods Enzymol. 2006;409:195-213 [16793403] Mol Cell Biol. 2006 Jul;26(14):5406-20 [16809776] Genetics. 2006 Sep;174(1):41-55 [16782999] Mol Cell Biol. 2006 Dec;26(24):9555-63 [17030609] Nature. 2007 May 3;447(7140):102-5 [17410126] Crit Rev Biochem Mol Biol. 2007 Jul-Aug;42(4):285-311 [17687670] Plasmid. 2007 Sep;58(2):148-58 [17434584] PLoS Biol. 2007 Dec;5(12):e324 [18076285] Genetics. 2008 Jan;178(1):67-82 [18202359] Proc Natl Acad Sci U S A. 2008 Jul 22;105(29):10051-6 [18621713] Nature. 2008 Jul 24;454(7203):479-85 [18615017] Mol Biol Evol. 2008 Nov;25(11):2439-44 [18723832] PLoS Genet. 2008 Nov;4(11):e1000264 [19023402] Am Nat. 2009 Jul;174 Suppl 1:S1-S14 [19441962] BMC Genomics. 2009;10:475 [19832984] Proc Natl Acad Sci U S A. 2010 Apr 27;107(17):7847-52 [20385822] Science. 2010 Jul 2;329(5987):82-5 [20595613] PLoS Genet. 2010 Aug;6(8). pii: e1001083. doi: 10.1371/journal.pgen.1001083 [20865162] PLoS Biol. 2010;8(10):e1000520 [20976044] PLoS Biol. 2011;9(2):e1000594 [21347245] Cell. 2011 Mar 4;144(5):719-31 [21376234] Cell Cycle. 2011 Apr 1;10(7):1073-85 [21406975] Genome Biol Evol. 2011;3:799-811 [21666225] Cell. 2011 Oct 14;147(2):267-70 [22000007] Annu Rev Genet. 2012;46:455-73 [23146099] PLoS Genet. 2013 Jun;9(6):e1003551 [23785298] Nat Rev Genet. 2013 Nov;14(11):794-806 [24136506] Philos Trans R Soc Lond B Biol Sci. 2001 Jan 29;356(1405):41-6 [11205328] Nat Rev Genet. 2001 May;2(5):360-9 [11331902] Genetics. 2001 May;158(1):109-22 [11333222] Nat Rev Genet. 2001 Jul;2(7):504-15 [11433357] Cell. 2001 Jul 13;106(1):47-57 [11461701] Cell. 2001 Jul 13;106(1):59-70 [11461702] Nature. 2002 Jul 25;418(6896):387-91 [12140549] Genetics. 2002 Nov;162(3):1063-77 [12454056] Nat Genet. 2003 Mar;33(3):392-5 [12577060] Cell. 2004 Apr 2;117(1):9-15 [15066278] Annu Rev Cell Dev Biol. 2004;20:525-58 [15473851] Genetics. 1968 May;59(1):33-6 [5683638] Nature. 1989 Mar 2;338(6210):87-90 [2645528] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pgen.1004910 ER - TY - JOUR T1 - Congenital anomalies and in utero antiretroviral exposure in human immunodeficiency virus-exposed uninfected infants. AN - 1643146607; 25383770 AB - Most studies examining the association of prenatal antiretroviral (ARV) exposures with congenital anomalies (CAs) in children born to human immunodeficiency virus (HIV)-infected women have been reassuring, but some evidence suggests an increased risk with specific ARV agents. To evaluate the association of in utero ARV exposures with CAs in HIV-exposed uninfected children. Prospective cohort study design. The Pediatric HIV/AIDS Cohort Study's Surveillance Monitoring of ART Toxicities (SMARTT) Study was performed at 22 US medical centers among 2580 HIV-exposed uninfected children enrolled in the SMARTT Study between March 23, 2007, and June 18, 2012. First-trimester exposure to any ARV and to specific ARV medications. The primary end point was a CA based on physician review of infant physical examinations according to the Antiretroviral Pregnancy Registry modification of the Metropolitan Atlanta Congenital Defects Program. Rates of CAs were estimated overall and by birth year. Logistic regression models were used to evaluate the association of CAs with first-trimester ARV exposures, adjusting for demographic and maternal characteristics. Congenital anomalies occurred in 175 of 2580 children, yielding a prevalence of 6.78% (95% CI, 5.85%-7.82%); 242 major CAs were confirmed, including 72 musculoskeletal and 55 cardiovascular CAs. The prevalence of CAs increased significantly among successive birth cohorts (3.8% for children born before 2002 and up to 8.3% for those born 2008-2010). In adjusted models, no association of first-trimester exposures with CAs was found for any ARV, for combination ARV regimens, or for any drug class. No individual ARV in the reverse transcriptase inhibitor drug classes was associated with an increased risk of CAs. Among protease inhibitors, higher odds of CAs were observed for atazanavir sulfate (adjusted odds ratio [aOR], 1.95; 95% CI, 1.24-3.05) and for ritonavir used as a booster (aOR, 1.56; 95% CI, 1.11-2.20). With first-trimester atazanavir exposure, risks were highest for skin (aOR, 5.23) and musculoskeletal (aOR, 2.55) CAs. Few individual ARVs and no drug classes were associated with an increased risk of CAs in HIV-exposed infants after adjustment for calendar year and maternal characteristics. While the overall risk remained low, a relative increase was observed in successive years and with atazanavir exposure. Given the low absolute CA risk, the benefits of recommended ARV therapy use during pregnancy still outweigh such risks, although further studies are warranted. JF - JAMA pediatrics AU - Williams, Paige L AU - Crain, Marilyn J AU - Yildirim, Cenk AU - Hazra, Rohan AU - Van Dyke, Russell B AU - Rich, Kenneth AU - Read, Jennifer S AU - Stuard, Emma AU - Rathore, Mobeen AU - Mendez, Hermann A AU - Watts, D Heather AU - Pediatric HIV/AIDS Cohort Study AD - Center for Biostatistics in AIDS Research, Harvard School of Public Health, Boston, Massachusetts2Departments of Biostatistics and Epidemiology, Harvard School of Public Health, Boston, Massachusetts. ; Departments of Pediatrics and Microbiology, University of Alabama at Birmingham. ; Center for Biostatistics in AIDS Research, Harvard School of Public Health, Boston, Massachusetts. ; Maternal and Pediatric Infectious Disease Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, Maryland. ; Department of Pediatrics, Tulane University School of Medicine, New Orleans, Louisiana. ; Department of Pediatrics, University of Illinois at Chicago. ; Division of Allergy, Immunology, and Transplantation, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland. ; Department of Pediatric Infectious Disease, Bronx-Lebanon Hospital, Bronx, New York. ; University of Florida Center for HIV/AIDS Research, Education and Service, Jacksonville. ; State University of New York Downstate Medical Center, Brooklyn. ; Office of the US Global AIDS Coordinator, US Department of State, Washington, DC. ; Pediatric HIV/AIDS Cohort Study Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 48 EP - 55 VL - 169 IS - 1 KW - Anti-Retroviral Agents KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Prospective Studies KW - Pregnancy Trimester, First KW - Georgia -- epidemiology KW - Risk Factors KW - Humans KW - Treatment Outcome KW - Infant, Newborn KW - Female KW - Prevalence KW - Pregnancy KW - Infectious Disease Transmission, Vertical -- prevention & control KW - Abnormalities, Drug-Induced -- epidemiology KW - HIV Infections -- transmission KW - Prenatal Exposure Delayed Effects -- chemically induced KW - HIV Infections -- drug therapy KW - Anti-Retroviral Agents -- adverse effects KW - Prenatal Exposure Delayed Effects -- epidemiology KW - Abnormalities, Drug-Induced -- etiology KW - Pregnancy Complications, Infectious -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1643146607?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=JAMA+pediatrics&rft.atitle=Congenital+anomalies+and+in+utero+antiretroviral+exposure+in+human+immunodeficiency+virus-exposed+uninfected+infants.&rft.au=Williams%2C+Paige+L%3BCrain%2C+Marilyn+J%3BYildirim%2C+Cenk%3BHazra%2C+Rohan%3BVan+Dyke%2C+Russell+B%3BRich%2C+Kenneth%3BRead%2C+Jennifer+S%3BStuard%2C+Emma%3BRathore%2C+Mobeen%3BMendez%2C+Hermann+A%3BWatts%2C+D+Heather%3BPediatric+HIV%2FAIDS+Cohort+Study&rft.aulast=Williams&rft.aufirst=Paige&rft.date=2015-01-01&rft.volume=169&rft.issue=1&rft.spage=48&rft.isbn=&rft.btitle=&rft.title=JAMA+pediatrics&rft.issn=2168-6211&rft_id=info:doi/10.1001%2Fjamapediatrics.2014.1889 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-16 N1 - Date created - 2015-01-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Perinatol. 2005 Aug;25(8):555-6 [16047034] Am J Med Genet A. 2014 Apr;164A(4):943-9 [24458943] AIDS Behav. 2010 Dec;14(6):1269-78 [20532607] J Perinat Med. 2011 Mar;39(2):163-70 [21142844] AIDS Patient Care STDS. 2011 Jul;25(7):385-94 [21992592] Am J Epidemiol. 2011 Nov 1;174(9):1062-8 [21946386] J Acquir Immune Defic Syndr. 2005 Sep 1;40(1):116-8 [16123696] Drug Saf. 2006;29(6):467-90 [16752931] J Acquir Immune Defic Syndr. 2007 Mar 1;44(3):299-305 [17159659] N Engl J Med. 2007 Jun 28;356(26):2675-83 [17596601] AIDS. 2008 May 11;22(8):973-81 [18453857] AIDS. 2009 Feb 20;23(4):519-24 [19165088] J Acquir Immune Defic Syndr. 2009 Aug 1;51(4):456-61 [19381099] Pediatr Infect Dis J. 2012 Feb;31(2):164-70 [21983213] AIDS. 2011 Nov 28;25(18):2301-4 [21918421] J Acquir Immune Defic Syndr. 2010 Feb;53(2):176-85 [20104119] Am J Epidemiol. 2012 May 1;175(9):950-61 [22491086] AIDS Patient Care STDS. 2012 Aug;26(8):439-43 [22663250] Pediatr Infect Dis J. 2014 Jul;33(7):741-6 [24445829] N Engl J Med. 2014 Jun 19;370(25):2397-407 [24941178] Am J Epidemiol. 2002 Jan 15;155(2):176-84 [11790682] Arch Intern Med. 2002 Feb 11;162(3):355 [11822930] Obstet Gynecol. 2004 Jun;103(6):1181-9 [15172850] Curr Drug Saf. 2013 Jul;8(3):153-61 [23845112] BJOG. 2013 Nov;120(12):1466-75 [23721372] Drug Saf. 2013 Nov;36(11):1069-78 [23828658] Hum Reprod. 2014 Jan;29(1):168-83 [24108217] AIDS Patient Care STDS. 2014 Feb;28(2):56-65 [24517538] BMJ Open. 2014;4(3):e004244 [24589823] PLoS One. 2014;9(3):e90991 [24604067] Pediatr Infect Dis J. 2010 Aug;29(8):721-7 [20539252] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1001/jamapediatrics.2014.1889 ER - TY - JOUR T1 - Anthropology, ethical dissonance, and the construction of the Object AN - 1642624775; 4630500 AB - In this article, I discuss certain questions relating to the ethical difficulties faced by anthropologists when dealing with two different social groups and when one group holds a position of dominance over the other. In the first example, I draw on my work on doctor-patient relationships in France; in the second, on a study on reproduction in immigrant African families from Mali and Senegal, living in polygynous households in France. I use these examples to explore questions of positionality, beneficence, and potential harm. I show the choices I made in order to construct an epistemologically ethical object. Reprinted by permission of Harwood Academic Publishers, Taylor and Francis Ltd JF - Medical anthropology AU - Fainzang, Sylvie AD - National Institutes of Health Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 11 EP - 23 VL - 34 IS - 1 SN - 0145-9740, 0145-9740 KW - Anthropology KW - France KW - Mali KW - Medical anthropology KW - Ethics KW - Polygyny KW - Power relations KW - Doctor-patient relationship KW - Epistemology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1642624775?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medical+anthropology&rft.atitle=Anthropology%2C+ethical+dissonance%2C+and+the+construction+of+the+Object&rft.au=Fainzang%2C+Sylvie&rft.aulast=Fainzang&rft.aufirst=Sylvie&rft.date=2015-01-01&rft.volume=34&rft.issue=1&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=Medical+anthropology&rft.issn=01459740&rft_id=info:doi/10.1080%2F01459740.2014.945080 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2015-01-07 N1 - Last updated - 2015-01-07 N1 - SubjectsTermNotLitGenreText - 3673 6823; 9829; 9975 9965; 7871 1077; 4362 9486; 4408 8282 8281 6085; 134 462 129; 233 456 2 DO - http://dx.doi.org/10.1080/01459740.2014.945080 ER - TY - JOUR T1 - Replication of live attenuated cold-adapted H2N2 influenza virus vaccine candidates in non human primates AN - 1642623269; 21143762 AB - The development of an H2N2 vaccine is a priority in pandemic preparedness planning. We previously showed that a single dose of a cold-adapted (ca) H2N2 live attenuated influenza vaccine (LAIV) based on the influenza A/Ann Arbor/6/60 (AA ca) virus was immunogenic and efficacious in mice and ferrets. However, in a Phase I clinical trial, viral replication was restricted and immunogenicity was poor. In this study, we compared the replication of four H2N2 LAIV candidate viruses, AA ca, A/Tecumseh/3/67 (TEC67 ca), and two variants of A/Japan/305/57 (JAP57 ca) in three non-human primate (NHP) species: African green monkeys (AGM), cynomolgus macaques (CM) and rhesus macaques (RM). One JAP57 ca virus had glutamine and glycine at HA amino acid positions 226 and 228 (Q-G) that binds to alpha 2-3 linked sialic acids, and one had leucine and serine that binds to alpha 2-3 and alpha 2-6 linked residues (L-S). The replication of all ca viruses was restricted, with low titers detected in the upper respiratory tract of all NHP species, however replication was detected in significantly more CMs than AGMs. The JAP57 ca Q-G and TEC67 ca viruses replicated in a significantly higher percentage of NHPs than the AA ca virus, with the TEC67 ca virus recovered from the greatest percentage of animals. Altering the receptor specificity of the JAP57 ca virus from alpha 2-3 to both alpha 2-3 and alpha 2-6 linked sialic acid residues did not significantly increase the number of animals infected or the titer to which the virus replicated. Taken together, our data show that in NHPs the AA ca virus more closely reflects the human experience than mice or ferret studies. We suggest that CMs and RMs may be the preferred species for evaluating H2N2 LAIV viruses, and the TEC67 ca virus may be the most promising H2N2 LAIV candidate for further evaluation. JF - Vaccine AU - Broadbent, Andrew J AU - Santos, Celia P AU - Paskel, Myeisha AU - Matsuoka, Yumiko AU - Lu, Janine AU - Chen, Zhongying AU - Jin, Hong AU - Subbarao, Kanta AD - Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 193 EP - 200 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 33 IS - 1 SN - 0264-410X, 0264-410X KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts; Immunology Abstracts KW - H2N2 KW - Influenza KW - Vaccine KW - LAIV KW - Non-human primate KW - Monkey KW - INW, Japan KW - Glutamine KW - Influenza A KW - Viruses KW - Clinical trials KW - pandemics KW - Mustela KW - Leucine KW - Cynomolgus KW - Macaca mulatta KW - Serine KW - Respiratory tract KW - Data processing KW - Amino acids KW - Residues KW - Glycine KW - Replication KW - Mice KW - Primates KW - Influenza virus KW - Immunogenicity KW - Africa KW - Priorities KW - Vaccines KW - Sialic acids KW - V 22350:Immunology KW - F 06905:Vaccines KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1642623269?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=Replication+of+live+attenuated+cold-adapted+H2N2+influenza+virus+vaccine+candidates+in+non+human+primates&rft.au=Broadbent%2C+Andrew+J%3BSantos%2C+Celia+P%3BPaskel%2C+Myeisha%3BMatsuoka%2C+Yumiko%3BLu%2C+Janine%3BChen%2C+Zhongying%3BJin%2C+Hong%3BSubbarao%2C+Kanta&rft.aulast=Broadbent&rft.aufirst=Andrew&rft.date=2015-01-01&rft.volume=33&rft.issue=1&rft.spage=193&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/10.1016%2Fj.vaccine.2014.10.065 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2015-08-05 N1 - SubjectsTermNotLitGenreText - Glutamine; Amino acids; Data processing; Replication; Glycine; Influenza A; Clinical trials; pandemics; Immunogenicity; Leucine; Vaccines; Sialic acids; Serine; Respiratory tract; Influenza; Residues; Viruses; Priorities; Mice; Primates; Influenza virus; Mustela; Macaca mulatta; Cynomolgus; INW, Japan; Africa DO - http://dx.doi.org/10.1016/j.vaccine.2014.10.065 ER - TY - JOUR T1 - Regulated Apoptosis of Genetically Modified Hematopoietic Stem and Progenitor Cells Via an Inducible Caspase-9 Suicide Gene in Rhesus Macaques AN - 1642620510; 21191463 AB - Abstract The high risk of insertional oncogenesis reported in clinical trials using integrating retroviral vectors to genetically modify hematopoietic stem and progenitor cells (HSPCs) requires the development of safety strategies to minimize risks associated with novel cell and gene therapies. The ability to ablate genetically modified cells in vivo is desirable, should an abnormal clone emerge. Inclusion of "suicide genes" in vectors to facilitate targeted ablation of vector-containing abnormal clones in vivo is one potential safety approach. We tested whether the inclusion of the "inducible Caspase-9" (iCasp9) suicide gene in a gamma-retroviral vector facilitated efficient elimination of vector-containing HSPCs and their hematopoietic progeny in vivo long-term, in an autologous non-human primate transplantation model. Following stable engraftment of iCasp9 expressing hematopoietic cells in rhesus macaques, administration of AP1903, a chemical inducer of dimerization able to activate iCasp9, specifically eliminated vector-containing cells in all hematopoietic lineages long-term, suggesting activity at the HSPC level. Between 75% and 94% of vector-containing cells were eliminated by well-tolerated AP1903 dosing, but lack of complete ablation was linked to lower iCasp9 expression in residual cells. Further investigation of resistance mechanisms demonstrated upregulation of Bcl-2 in hematopoietic cell lines transduced with the vector and resistant to AP1903 ablation. These results demonstrate both the potential and the limitations of safety approaches using iCasp9 to HSPC-targeted gene therapy settings, in a model with great relevance to clinical development. Stem Cells 2015; 33:91-100 JF - Stem Cells AU - Barese, Cecilia N AU - Felizardo, Tania C AU - Sellers, Stephanie E AU - Keyvanfar, Keyvan AU - Di Stasi, Antonio AU - Metzger, Mark E AU - Krouse, Allen E AU - Donahue, Robert E AU - Spencer, David M AU - Dunbar, Cynthia E AD - Hematology Branch, National Heart, Lung, and Blood Institute (NHLBI). Y1 - 2015/01// PY - 2015 DA - Jan 2015 SP - 91 EP - 100 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 33 IS - 1 SN - 1066-5099, 1066-5099 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Autografts KW - Caspase-9 KW - Apoptosis KW - Gene therapy KW - Tumorigenesis KW - Animal models KW - Primates KW - Clinical trials KW - Expression vectors KW - Stem cells KW - Risk factors KW - Hemopoiesis KW - Macaca mulatta KW - Progeny KW - Bcl-2 protein KW - suicide genes KW - W 30905:Medical Applications KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1642620510?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+Cells&rft.atitle=Regulated+Apoptosis+of+Genetically+Modified+Hematopoietic+Stem+and+Progenitor+Cells+Via+an+Inducible+Caspase-9+Suicide+Gene+in+Rhesus+Macaques&rft.au=Barese%2C+Cecilia+N%3BFelizardo%2C+Tania+C%3BSellers%2C+Stephanie+E%3BKeyvanfar%2C+Keyvan%3BDi+Stasi%2C+Antonio%3BMetzger%2C+Mark+E%3BKrouse%2C+Allen+E%3BDonahue%2C+Robert+E%3BSpencer%2C+David+M%3BDunbar%2C+Cynthia+E&rft.aulast=Barese&rft.aufirst=Cecilia&rft.date=2015-01-01&rft.volume=33&rft.issue=1&rft.spage=91&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.1869 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Autografts; Caspase-9; Apoptosis; Gene therapy; Tumorigenesis; Animal models; Clinical trials; Expression vectors; Stem cells; Risk factors; Hemopoiesis; Progeny; Bcl-2 protein; suicide genes; Macaca mulatta; Primates DO - http://dx.doi.org/10.1002/stem.1869 ER - TY - JOUR T1 - Meaningful prevention of breast cancer metastasis: candidate therapeutics, preclinical validation, and clinical trial concerns. AN - 1641858540; 25412774 AB - The development of drugs to treat breast and other cancers proceeds through phase I dose finding, phase II efficacy, and phase III comparative studies in the metastatic setting, only then asking if metastasis can be prevented in adjuvant trials. Compounds without overt cytotoxic activity, such as those developed to inhibit metastatic colonization, will likely fail to shrink established lesions in the metastatic setting and never be tested in a metastasis prevention scenario where they were preclinically validated. We and others have proposed phase II primary and secondary metastasis prevention studies to address this need. Herein, we have asked whether preclinical metastasis prevention data agrees with the positive adjuvant setting trials. The data are limited but complimentary. We also review fundamental pathways involved in metastasis, including Src, integrins, focal adhesion kinase (FAK), and fibrosis, for their clinical progress to date and potential for metastasis prevention. Issues of inadequate preclinical validation and clinical toxicity profiles are discussed. JF - Journal of molecular medicine (Berlin, Germany) AU - Zimmer, Alexandra S AU - Steeg, Patricia S AD - Women's Malignancies Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, 20892, USA, alexandra.zimmer@nih.gov. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 13 EP - 29 VL - 93 IS - 1 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Clinical Trials as Topic KW - Antineoplastic Agents -- therapeutic use KW - Female KW - Chemotherapy, Adjuvant KW - Breast Neoplasms -- drug therapy KW - Breast Neoplasms -- pathology KW - Neoplasm Metastasis -- drug therapy KW - Neoplasm Metastasis -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1641858540?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+molecular+medicine+%28Berlin%2C+Germany%29&rft.atitle=Meaningful+prevention+of+breast+cancer+metastasis%3A+candidate+therapeutics%2C+preclinical+validation%2C+and+clinical+trial+concerns.&rft.au=Zimmer%2C+Alexandra+S%3BSteeg%2C+Patricia+S&rft.aulast=Zimmer&rft.aufirst=Alexandra&rft.date=2015-01-01&rft.volume=93&rft.issue=1&rft.spage=13&rft.isbn=&rft.btitle=&rft.title=Journal+of+molecular+medicine+%28Berlin%2C+Germany%29&rft.issn=1432-1440&rft_id=info:doi/10.1007%2Fs00109-014-1226-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-08 N1 - Date created - 2015-01-01 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00109-014-1226-2 ER - TY - JOUR T1 - Redistribution, hyperproliferation, activation of natural killer cells and CD8 T cells, and cytokine production during first-in-human clinical trial of recombinant human interleukin-15 in patients with cancer. AN - 1641426587; 25403209 AB - Interleukin-15 (IL-15) has significant potential in cancer immunotherapy as an activator of antitumor CD8 T and natural killer (NK) cells. The primary objectives of this trial were to determine safety, adverse event profile, dose-limiting toxicity, and maximum-tolerated dose of recombinant human IL-15 (rhIL-15) administered as a daily intravenous bolus infusion for 12 consecutive days in patients with metastatic malignancy. We performed a first in-human trial of Escherichia coli-produced rhIL-15. Bolus infusions of 3.0, 1.0, and 0.3 μg/kg per day of IL-15 were administered for 12 consecutive days to patients with metastatic malignant melanoma or metastatic renal cell cancer. Flow cytometry of peripheral blood lymphocytes revealed dramatic efflux of NK and memory CD8 T cells from the circulating blood within minutes of IL-15 administration, followed by influx and hyperproliferation yielding 10-fold expansions of NK cells that ultimately returned to baseline. Up to 50-fold increases of serum levels of multiple inflammatory cytokines were observed. Dose-limiting toxicities observed in patients receiving 3.0 and 1.0 μg/kg per day were grade 3 hypotension, thrombocytopenia, and elevations of ALT and AST, resulting in 0.3 μg/kg per day being determined the maximum-tolerated dose. Indications of activity included clearance of lung lesions in two patients. IL-15 could be safely administered to patients with metastatic malignancy. IL-15 administration markedly altered homeostasis of lymphocyte subsets in blood, with NK cells and γδ cells most dramatically affected, followed by CD8 memory T cells. To reduce toxicity and increase efficacy, alternative dosing strategies have been initiated, including continuous intravenous infusions and subcutaneous IL-15 administration. © 2014 by American Society of Clinical Oncology. JF - Journal of clinical oncology : official journal of the American Society of Clinical Oncology AU - Conlon, Kevin C AU - Lugli, Enrico AU - Welles, Hugh C AU - Rosenberg, Steven A AU - Fojo, Antonio Tito AU - Morris, John C AU - Fleisher, Thomas A AU - Dubois, Sigrid P AU - Perera, Liyanage P AU - Stewart, Donn M AU - Goldman, Carolyn K AU - Bryant, Bonita R AU - Decker, Jean M AU - Chen, Jing AU - Worthy, Tat'Yana A AU - Figg, William D AU - Peer, Cody J AU - Sneller, Michael C AU - Lane, H Clifford AU - Yovandich, Jason L AU - Creekmore, Stephen P AU - Roederer, Mario AU - Waldmann, Thomas A AD - Kevin C. Conlon, Steven A. Rosenberg, Antonio Tito Fojo, John C. Morris, Thomas A. Fleisher, Sigrid P. Dubois, Liyanage P. Perera, Donn M. Stewart, Carolyn K. Goldman, Bonita R. Bryant, Jean M. Decker, Jing Chen, Tat'Yana A. Worthy, William D. Figg Sr, Cody J. Peer, and Thomas A. Waldmann, National Cancer Institute; Enrico Lugli, Hugh C. Welles, Michael C. Sneller, H. Clifford Lane, and Mario Roederer, National Institute of Allergy and Infectious Diseases, Bethesda; Jason L. Yovandich and Stephen P. Creekmore, National Cancer Institute, Frederick, MD; and Hugh C. Welles, Columbian College of Arts and Sciences, George Washington University, Washington, DC. ; Kevin C. Conlon, Steven A. Rosenberg, Antonio Tito Fojo, John C. Morris, Thomas A. Fleisher, Sigrid P. Dubois, Liyanage P. Perera, Donn M. Stewart, Carolyn K. Goldman, Bonita R. Bryant, Jean M. Decker, Jing Chen, Tat'Yana A. Worthy, William D. Figg Sr, Cody J. Peer, and Thomas A. Waldmann, National Cancer Institute; Enrico Lugli, Hugh C. Welles, Michael C. Sneller, H. Clifford Lane, and Mario Roederer, National Institute of Allergy and Infectious Diseases, Bethesda; Jason L. Yovandich and Stephen P. Creekmore, National Cancer Institute, Frederick, MD; and Hugh C. Welles, Columbian College of Arts and Sciences, George Washington University, Washington, DC. tawald@helix.nih.gov. Y1 - 2015/01/01/ PY - 2015 DA - 2015 Jan 01 SP - 74 EP - 82 VL - 33 IS - 1 KW - IL15 protein, human KW - 0 KW - Interleukin-15 KW - Recombinant Proteins KW - Index Medicus KW - Young Adult KW - Drug Administration Schedule KW - Area Under Curve KW - Infusions, Intravenous KW - Dose-Response Relationship, Drug KW - Humans KW - Recombinant Proteins -- pharmacokinetics KW - Neutropenia -- chemically induced KW - Metabolic Clearance Rate KW - Aged KW - Nausea -- chemically induced KW - Fever -- chemically induced KW - Lymphocyte Activation -- drug effects KW - Aged, 80 and over KW - Adult KW - Treatment Outcome KW - Neoplasm Metastasis KW - Middle Aged KW - Recombinant Proteins -- therapeutic use KW - Recombinant Proteins -- administration & dosage KW - Female KW - Male KW - Cell Proliferation -- drug effects KW - Neoplasms -- drug therapy KW - Interleukin-15 -- adverse effects KW - CD4-Positive T-Lymphocytes -- metabolism KW - Interleukin-15 -- therapeutic use KW - Interleukin-15 -- genetics KW - CD4-Positive T-Lymphocytes -- drug effects KW - Killer Cells, Natural -- metabolism KW - Killer Cells, Natural -- drug effects KW - Neoplasms -- metabolism KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1641426587?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.atitle=Redistribution%2C+hyperproliferation%2C+activation+of+natural+killer+cells+and+CD8+T+cells%2C+and+cytokine+production+during+first-in-human+clinical+trial+of+recombinant+human+interleukin-15+in+patients+with+cancer.&rft.au=Conlon%2C+Kevin+C%3BLugli%2C+Enrico%3BWelles%2C+Hugh+C%3BRosenberg%2C+Steven+A%3BFojo%2C+Antonio+Tito%3BMorris%2C+John+C%3BFleisher%2C+Thomas+A%3BDubois%2C+Sigrid+P%3BPerera%2C+Liyanage+P%3BStewart%2C+Donn+M%3BGoldman%2C+Carolyn+K%3BBryant%2C+Bonita+R%3BDecker%2C+Jean+M%3BChen%2C+Jing%3BWorthy%2C+Tat%27Yana+A%3BFigg%2C+William+D%3BPeer%2C+Cody+J%3BSneller%2C+Michael+C%3BLane%2C+H+Clifford%3BYovandich%2C+Jason+L%3BCreekmore%2C+Stephen+P%3BRoederer%2C+Mario%3BWaldmann%2C+Thomas+A&rft.aulast=Conlon&rft.aufirst=Kevin&rft.date=2015-01-01&rft.volume=33&rft.issue=1&rft.spage=74&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+oncology+%3A+official+journal+of+the+American+Society+of+Clinical+Oncology&rft.issn=1527-7755&rft_id=info:doi/10.1200%2FJCO.2014.57.3329 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-04-20 N1 - Date created - 2014-12-31 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT01021059; ClinicalTrials.gov N1 - SuppNotes - Cited By: Science. 1994 May 13;264(5161):965-8 [8178155] JAMA. 1994 Mar 23-30;271(12):907-13 [8120958] Proc Natl Acad Sci U S A. 1994 May 24;91(11):4940-4 [8197161] Eur J Immunol. 1994 Jan;24(1):281-4 [7517363] EMBO J. 1995 Aug 1;14(15):3654-63 [7641685] Cell Immunol. 1995 Oct 15;165(2):289-93 [7553894] Blood. 2013 Jun 27;121(26):5154-7 [23678006] J Clin Invest. 2014 Jan;124(1):99-110 [24292706] J Exp Med. 1996 Mar 1;183(3):721-4 [8642275] Annu Rev Immunol. 1996;14:179-205 [8717512] Cell Immunol. 1997 Jul 10;179(1):66-73 [9259773] Annu Rev Immunol. 1999;17:19-49 [10358752] J Immunol. 2004 Dec 1;173(11):6537-41 [15557143] J Exp Med. 2005 Jan 3;201(1):139-48 [15630141] Blood. 2005 Jan 15;105(2):721-7 [15367431] Nat Immunol. 2005 Nov;6(11):1071-2 [16239920] J Clin Oncol. 2006 Mar 1;24(7):1169-77 [16505437] Blood. 2006 Mar 15;107(6):2409-14 [16304057] Nat Rev Immunol. 2006 Aug;6(8):595-601 [16868550] Clin Cancer Res. 2007 Mar 15;13(6):1936-46 [17363550] Cancer Res. 2007 Aug 1;67(15):7487-94 [17671219] Blood. 2010 Oct 28;116(17):3238-48 [20631381] Cytometry A. 2011 Feb;79(2):167-74 [21265010] Blood. 2011 May 5;117(18):4787-95 [21385847] Blood. 2011 Dec 22;118(26):6845-8 [22067383] J Interferon Cytokine Res. 2012 Feb;32(2):60-5 [22136372] Proc Natl Acad Sci U S A. 2012 Apr 17;109(16):6187-92 [22474386] J Immunol. 2012 Jun 15;188(12):6156-64 [22593619] Sci Transl Med. 2013 Mar 20;5(177):177ra38 [23515080] N Engl J Med. 2013 Apr 18;368(16):1509-18 [23527958] J Exp Med. 2000 Mar 6;191(5):771-80 [10704459] Proc Natl Acad Sci U S A. 2000 Oct 10;97(21):11445-50 [11016962] Immunity. 2001 Feb;14(2):105-10 [11239443] Cytokine Growth Factor Rev. 2002 Apr;13(2):169-83 [11900992] J Exp Med. 2002 Jun 17;195(12):1541-8 [12070282] Immunity. 2002 Nov;17(5):537-47 [12433361] Proc Natl Acad Sci U S A. 2004 Feb 17;101(7):1969-74 [14762166] J Exp Med. 2004 Oct 4;200(7):825-34 [15452177] Science. 1993 Dec 17;262(5141):1877-80 [8266077] Proc Natl Acad Sci U S A. 1994 May 24;91(11):4935-9 [8197160] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1200/JCO.2014.57.3329 ER - TY - JOUR T1 - Schisandrol B protects against acetaminophen-induced hepatotoxicity by inhibition of CYP-mediated bioactivation and regulation of liver regeneration. AN - 1640483057; 25319358 AB - Acetaminophen (APAP) overdose is the most frequent cause of drug-induced acute liver failure. Schisandra sphenanthera is a traditional hepato-protective Chinese medicine and Schisandrol B (SolB) is one of its major active constituents. In this study, the protective effect of SolB against APAP-induced acute hepatotoxicity in mice and the involved mechanisms were investigated. Morphological and biochemical assessments clearly demonstrated a protective effect of SolB against APAP-induced liver injury. SolB pretreatment significantly attenuated the increases in alanine aminotransferase and aspartate aminotransferase activity, and prevented elevated hepatic malondialdehyde formation and the depletion of mitochondrial glutathione (GSH) in a dose-dependent manner. SolB also dramatically altered APAP metabolic activation by inhibiting the activities of CYP2E1 and CYP3A11, which was evidenced by significant inhibition of the formation of the oxidized APAP metabolite NAPQI-GSH. A molecular docking model also predicted that SolB had potential to interact with the CYP2E1 and CYP3A4 active sites. In addition, SolB abrogated APAP-induced activation of p53 and p21, and increased expression of liver regeneration and antiapoptotic-related proteins such as cyclin D1 (CCND1), PCNA, and BCL-2. This study demonstrated that SolB exhibited a significant protective effect toward APAP-induced liver injury, potentially through inhibition of CYP-mediated APAP bioactivation and regulation of the p53, p21, CCND1, PCNA, and BCL-2 to promote liver regeneration. © The Author 2014. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. JF - Toxicological sciences : an official journal of the Society of Toxicology AU - Jiang, Yiming AU - Fan, Xiaomei AU - Wang, Ying AU - Chen, Pan AU - Zeng, Hang AU - Tan, Huasen AU - Gonzalez, Frank J AU - Huang, Min AU - Bi, Huichang AD - *School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou 510006, China and Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892. ; *School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou 510006, China and Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 bihchang@mail.sysu.edu.cn. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 107 EP - 115 VL - 143 IS - 1 KW - Apoptosis Regulatory Proteins KW - 0 KW - Benzoquinones KW - Biomarkers KW - Cyclooctanes KW - Cytochrome P-450 CYP2E1 Inhibitors KW - Cytochrome P-450 CYP3A Inhibitors KW - Dioxoles KW - Drugs, Chinese Herbal KW - Imines KW - Lignans KW - Membrane Proteins KW - Acetaminophen KW - 362O9ITL9D KW - schizandrol B KW - 58546-54-6 KW - Cytochrome P-450 CYP2E1 KW - EC 1.14.13.- KW - Cyp3a11 protein, mouse KW - EC 1.14.14.1 KW - Cytochrome P-450 CYP3A KW - N-acetyl-4-benzoquinoneimine KW - G6S9BN13TI KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - liver injury KW - liver regeneration KW - acetaminophen KW - schisandrol B KW - bioactivation KW - Animals KW - Mitochondria, Liver -- enzymology KW - Dose-Response Relationship, Drug KW - Glutathione -- metabolism KW - Activation, Metabolic KW - Benzoquinones -- metabolism KW - Catalytic Domain KW - Cytoprotection KW - Disease Models, Animal KW - Mitochondria, Liver -- drug effects KW - Protein Binding KW - Binding Sites KW - Molecular Docking Simulation KW - Cytochrome P-450 CYP3A -- metabolism KW - Signal Transduction -- drug effects KW - Apoptosis Regulatory Proteins -- metabolism KW - Mice, Inbred C57BL KW - Biomarkers -- metabolism KW - Cytochrome P-450 CYP3A -- chemistry KW - Imines -- metabolism KW - Male KW - Protein Conformation KW - Liver Regeneration -- drug effects KW - Liver -- pathology KW - Liver -- enzymology KW - Chemical and Drug Induced Liver Injury -- pathology KW - Cytochrome P-450 CYP2E1 -- chemistry KW - Membrane Proteins -- chemistry KW - Membrane Proteins -- metabolism KW - Lignans -- pharmacology KW - Cytochrome P-450 CYP2E1 -- metabolism KW - Lignans -- chemistry KW - Drugs, Chinese Herbal -- pharmacology KW - Dioxoles -- pharmacology KW - Chemical and Drug Induced Liver Injury -- enzymology KW - Cytochrome P-450 CYP2E1 Inhibitors -- pharmacology KW - Chemical and Drug Induced Liver Injury -- prevention & control KW - Cyclooctanes -- pharmacology KW - Liver -- drug effects KW - Cytochrome P-450 CYP3A Inhibitors -- pharmacology KW - Cyclooctanes -- chemistry KW - Membrane Proteins -- antagonists & inhibitors KW - Dioxoles -- chemistry KW - Acetaminophen -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1640483057?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.atitle=Schisandrol+B+protects+against+acetaminophen-induced+hepatotoxicity+by+inhibition+of+CYP-mediated+bioactivation+and+regulation+of+liver+regeneration.&rft.au=Jiang%2C+Yiming%3BFan%2C+Xiaomei%3BWang%2C+Ying%3BChen%2C+Pan%3BZeng%2C+Hang%3BTan%2C+Huasen%3BGonzalez%2C+Frank+J%3BHuang%2C+Min%3BBi%2C+Huichang&rft.aulast=Jiang&rft.aufirst=Yiming&rft.date=2015-01-01&rft.volume=143&rft.issue=1&rft.spage=107&rft.isbn=&rft.btitle=&rft.title=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.issn=1096-0929&rft_id=info:doi/10.1093%2Ftoxsci%2Fkfu216 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2016-01-05 N1 - Date created - 2014-12-24 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Drug Metab Dispos. 2004 Dec;32(12):1351-8 [15342469] Toxicol Pathol. 2005;33(1):41-51 [15805055] Clin Pharmacol Ther. 2005 Jul;78(1):19-24 [16003288] Nat Genet. 2007 Jan;39(1):99-105 [17143283] Rapid Commun Mass Spectrom. 2007;21(5):635-43 [17279482] Br J Clin Pharmacol. 2008 Apr;65 Suppl 1:38-46 [18333864] J Hepatol. 2011 Apr;54(4):685-94 [21146511] Proc Natl Acad Sci U S A. 2010 Oct 26;107(43):18422-7 [20937904] Toxicol Appl Pharmacol. 2010 Jan 15;242(2):182-90 [19835899] J Ethnopharmacol. 2008 Jul 23;118(2):183-212 [18515024] Toxicol Lett. 2008 Aug 28;180(3):174-81 [18588957] J Biol Chem. 2008 Nov 28;283(48):33698-707 [18818195] Drug Metab Dispos. 2009 Dec;37(12):2399-407 [19741040] Life Sci. 2011 Apr 25;88(17-18):737-45 [21296090] Biol Pharm Bull. 2012;35(2):171-7 [22293346] J Clin Invest. 2012 Apr;122(4):1574-83 [22378043] Free Radic Biol Med. 2012 Aug 15;53(4):834-41 [22749810] Planta Med. 2012 Sep;78(13):1490-514 [22565299] Toxicol Lett. 2012 Oct 2;214(1):69-80 [22939915] Gastroenterology. 2012 Dec;143(6):1609-1619.e4 [22960658] J Mol Biol. 2013 Apr 12;425(7):1111-8 [23318952] JAMA. 2014 Feb 12;311(6):563 [24519283] J Gastroenterol Hepatol. 2014 Mar;29(3):640-7 [24219791] Drug Metab Dispos. 2014 May;42(5):844-52 [24510383] Expert Rev Clin Pharmacol. 2014 May;7(3):341-8 [24678654] Clin Pharmacol Ther. 2000 Mar;67(3):275-82 [10741631] Planta Med. 2000 Aug;66(6):521-5 [10985077] Nature. 2000 Nov 16;408(6810):307-10 [11099028] Pharmacol Toxicol. 2001 Mar;88(3):135-41 [11245408] Free Radic Biol Med. 2001 Aug 1;31(3):277-91 [11461765] J Pharmacol Exp Ther. 2003 Oct;307(1):67-73 [12954812] Toxicol Appl Pharmacol. 2003 Dec 1;193(2):218-27 [14644624] Hepatology. 2004 Jul;40(1):10-5 [15239079] Chin Med J (Engl). 1989 Oct;102(10):740-9 [2517053] Semin Liver Dis. 1990 Nov;10(4):267-78 [2281334] Toxicol Appl Pharmacol. 1996 Jan;136(1):146-54 [8560468] Oncogene. 1998 Apr 23;16(16):2141-50 [9572495] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/toxsci/kfu216 ER - TY - JOUR T1 - Transient receptor potential vanilloid 1 gene deficiency ameliorates hepatic injury in a mouse model of chronic binge alcohol-induced alcoholic liver disease. AN - 1639976308; 25447051 AB - Experimental alcohol-induced liver injury is exacerbated by a high polyunsaturated fat diet rich in linoleic acid. We postulated that bioactive oxidized linoleic acid metabolites (OXLAMs) play a critical role in the development/progression of alcohol-mediated hepatic inflammation and injury. OXLAMs are endogenous ligands for transient receptor potential vanilloid 1 (TRPV1). Herein, we evaluated the role of signaling through TRPV1 in an experimental animal model of alcoholic liver disease (ALD). Chronic binge alcohol administration increased plasma OXLAM levels, specifically 9- and 13-hydroxy-octadecadienoic acids. This effect was associated with up-regulation of hepatic TRPV1. Exposure of hepatocytes to these OXLAMs in vitro resulted in activation of TRPV1 signal transduction with increased intracellular Ca(2+) levels. Genetic depletion of TRPV1 did not blunt hepatic steatosis caused by ethanol, but prevented hepatic injury. TRPV1 deficiency protected from hepatocyte death and prevented the increase in proinflammatory cytokine and chemokine expression, including tumor necrosis factor-α, IL-6, macrophage inflammatory protein-2, and monocyte chemotactic protein 1. TRPV1 depletion markedly blunted ethanol-mediated induction of plasminogen activator inhibitor-1, an important alcohol-induced hepatic inflammation mediator, via fibrin accumulation. This study indicates, for the first time, that TRPV1 receptor pathway may be involved in hepatic inflammatory response in an experimental animal model of ALD. TRPV1-OXLAM interactions appear to play a significant role in hepatic inflammation/injury, further supporting an important role for dietary lipids in ALD. Copyright © 2015 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved. JF - The American journal of pathology AU - Liu, Huilin AU - Beier, Juliane I AU - Arteel, Gavin E AU - Ramsden, Christopher E AU - Feldstein, Ariel E AU - McClain, Craig J AU - Kirpich, Irina A AD - Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky; College of Food Science and Engineering, Jilin Agricultural University, Changchun, China. ; Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, Kentucky. ; National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland. ; Department of Pediatrics, University of California San Diego, San Diego, California. ; Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky; Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, Kentucky; Division of Gastroenterology, Department of Medicine, Robley Rex Veterans Medical Center, Louisville, Kentucky. ; Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, University of Louisville School of Medicine, Louisville, Kentucky; Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, Kentucky. Electronic address: i0kirp01@louisville.edu. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 43 EP - 54 VL - 185 IS - 1 KW - Ccl2 protein, mouse KW - 0 KW - Chemokine CCL2 KW - Chemokine CXCL2 KW - Cxcl2 protein, mouse KW - Interleukin-6 KW - Ligands KW - TRPV Cation Channels KW - TRPV1 protein, mouse KW - Tumor Necrosis Factor-alpha KW - interleukin-6, mouse KW - Ethanol KW - 3K9958V90M KW - Linoleic Acid KW - 9KJL21T0QJ KW - Casp3 protein, mouse KW - EC 3.4.22.- KW - Caspase 3 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Liver -- pathology KW - Linoleic Acid -- metabolism KW - Humans KW - Liver -- metabolism KW - Disease Models, Animal KW - Mice KW - Binge Drinking -- pathology KW - Mice, Knockout KW - Chemokine CCL2 -- blood KW - Interleukin-6 -- blood KW - Hep G2 Cells KW - Liver -- drug effects KW - Mice, Inbred C57BL KW - Tumor Necrosis Factor-alpha -- blood KW - Ethanol -- chemistry KW - Chemokine CXCL2 -- blood KW - Signal Transduction KW - Male KW - Caspase 3 -- metabolism KW - Inflammation -- pathology KW - TRPV Cation Channels -- physiology KW - Liver Diseases, Alcoholic -- genetics KW - TRPV Cation Channels -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1639976308?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+pathology&rft.atitle=Transient+receptor+potential+vanilloid+1+gene+deficiency+ameliorates+hepatic+injury+in+a+mouse+model+of+chronic+binge+alcohol-induced+alcoholic+liver+disease.&rft.au=Liu%2C+Huilin%3BBeier%2C+Juliane+I%3BArteel%2C+Gavin+E%3BRamsden%2C+Christopher+E%3BFeldstein%2C+Ariel+E%3BMcClain%2C+Craig+J%3BKirpich%2C+Irina+A&rft.aulast=Liu&rft.aufirst=Huilin&rft.date=2015-01-01&rft.volume=185&rft.issue=1&rft.spage=43&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+pathology&rft.issn=1525-2191&rft_id=info:doi/10.1016%2Fj.ajpath.2014.09.007 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-09-15 N1 - Date created - 2014-12-22 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Hypertension. 2013 Jan;61(1):246-52 [23150506] Sci Rep. 2013;3:1349 [23443229] Life Sci. 1989;44(3):223-7 [2915600] FEBS Lett. 1995 Mar 13;361(1):118-22 [7890029] Blood. 1996 Jan 1;87(1):162-73 [8547638] Hepatology. 1996 Aug;24(2):391-7 [8690410] J Lipid Res. 1997 May;38(5):860-9 [9186904] Nature. 1997 Oct 23;389(6653):816-24 [9349813] Nature. 1999 Apr 1;398(6726):436-41 [10201375] Blood. 2004 Dec 15;104(13):3993-4001 [15328163] Alcohol. 2004 Aug;34(1):21-5 [15670661] Eur J Endocrinol. 2005 Dec;153(6):963-9 [16322403] Gastroenterology. 2006 Jun;130(7):2099-112 [16762632] Mol Immunol. 2007 Feb;44(6):1429-35 [16777226] Nat Protoc. 2013 Mar;8(3):627-37 [23449255] Alcohol. 2013 May;47(3):257-64 [23453163] J Cell Sci. 2013 Jul 1;126(Pt 13):2903-13 [23613465] J Pharmacol Exp Ther. 2002 Sep;302(3):839-45 [12183638] Hepatology. 2002 Nov;36(5):1206-13 [12395331] Biochem J. 2003 May 1;371(Pt 3):1045-53 [12564954] J Nutr. 2004 Apr;134(4):904-12 [15051845] Cell Calcium. 2004 Jul;36(1):19-28 [15126053] J Invest Dermatol. 2004 Jun;122(6):1365-71 [15175025] Biochem Biophys Res Commun. 2004 Aug 13;321(1):219-25 [15358238] J Biol Chem. 2006 Oct 20;281(42):31337-47 [16923814] Eur J Neurosci. 2007 Jan;25(1):213-23 [17241282] Circ Res. 2007 Apr 13;100(7):1063-70 [17347480] J Cell Physiol. 2007 Dec;213(3):730-9 [17508360] FASEB J. 2007 Nov;21(13):3747-55 [17601984] J Pharmacol Exp Ther. 2008 Jun;325(3):801-8 [18339969] Mol Endocrinol. 2008 Jun;22(6):1416-26 [18292240] Natl Vital Stat Rep. 2008 Apr 24;56(10):1-120 [18512336] Invest Ophthalmol Vis Sci. 2008 Jul;49(7):3004-17 [18362111] Cancer Genet Cytogenet. 2008 Oct;186(1):25-32 [18786439] Am J Gastroenterol. 2008 Dec;103(12):3047-56 [19086956] Invest Ophthalmol Vis Sci. 2009 Feb;50(2):717-28 [18952924] Hepatology. 2009 May;49(5):1545-53 [19291788] Proc Natl Acad Sci U S A. 2009 Nov 3;106(44):18820-4 [19843694] Mediators Inflamm. 2013;2013:925171 [23878415] Pflugers Arch. 2013 Sep;465(9):1303-16 [23605066] J Clin Invest. 2013 Sep;123(9):3941-51 [23925292] Nat Immunol. 2013 Oct;14(10):1045-53 [23995233] Annu Rev Cell Dev Biol. 2013;29:355-84 [24099085] Hepatology. 2013 Nov;58(5):1814-23 [23532958] Br J Pharmacol. 2000 Jan;129(2):227-30 [10694225] Proc Natl Acad Sci U S A. 2000 May 23;97(11):6155-60 [10823958] Brain Res Bull. 2000 Nov 1;53(4):437-43 [11137001] Nat Neurosci. 2002 Jun;5(6):546-51 [11992116] Hepatology. 2002 Jul;36(1):227-42 [12085369] Pharmacol Ther. 2010 Feb;125(2):181-95 [19896501] J Clin Invest. 2010 May;120(5):1617-26 [20424317] J Biol Chem. 2010 Jul 16;285(29):22211-20 [20460374] J Lipid Res. 2010 Oct;51(10):3046-54 [20631297] J Nutr Biochem. 2011 Jan;22(1):38-45 [20303728] Adv Exp Med Biol. 2011;704:667-86 [21290321] PLoS One. 2011;6(4):e18281 [21483776] Exp Biol Med (Maywood). 2012 Jan;237(1):1-9 [22238286] Pflugers Arch. 2012 Apr;463(5):727-32 [22395410] Alcohol Clin Exp Res. 2012 May;36(5):835-46 [22150547] Proc Natl Acad Sci U S A. 2012 Jul 10;109(28):11282-7 [22733741] Nucleic Acids Res. 2012 Aug;40(15):e115 [22730293] Prostaglandins Other Lipid Mediat. 2012 Oct;99(1-2):51-6 [22706383] Am J Physiol Gastrointest Liver Physiol. 2012 Sep 1;303(5):G635-45 [22790593] J Clin Invest. 2012 Oct;122(10):3476-89 [22945633] Hepatology. 2012 Oct;56(4):1291-9 [22505276] Nature. 2012 Dec 6;492(7427):123-7 [23143333] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.ajpath.2014.09.007 ER - TY - JOUR T1 - Excess NF-κB induces ectopic odontogenesis in embryonic incisor epithelium. AN - 1639493008; 25376721 AB - Nuclear factor kappa B (NF-κB) signaling plays critical roles in many physiological and pathological processes, including regulating organogenesis. Down-regulation of NF-κB signaling during development results in hypohidrotic ectodermal dysplasia. The roles of NF-κB signaling in tooth development, however, are not fully understood. We examined mice overexpressing IKKβ, an essential component of the NF-κB pathway, under keratin 5 promoter (K5-Ikkβ). K5-Ikkβ mice showed supernumerary incisors whose formation was accompanied by up-regulation of canonical Wnt signaling. Apoptosis that is normally observed in wild-type incisor epithelium was reduced in K5-Ikkβ mice. The supernumerary incisors in K5-Ikkβ mice were found to phenocopy extra incisors in mice with mutations of Wnt inhibitor, Wise. Excess NF-κB activity thus induces an ectopic odontogenesis program that is usually suppressed under physiological conditions. © International & American Associations for Dental Research 2014. JF - Journal of dental research AU - Blackburn, J AU - Kawasaki, K AU - Porntaveetus, T AU - Kawasaki, M AU - Otsuka-Tanaka, Y AU - Miake, Y AU - Ota, M S AU - Watanabe, M AU - Hishinuma, M AU - Nomoto, T AU - Oommen, S AU - Ghafoor, S AU - Harada, F AU - Nozawa-Inoue, K AU - Maeda, T AU - Peterková, R AU - Lesot, H AU - Inoue, J AU - Akiyama, T AU - Schmidt-Ullrich, R AU - Liu, B AU - Hu, Y AU - Page, A AU - Ramírez, Á AU - Sharpe, P T AU - Ohazama, A AD - Craniofacial Development and Stem Cell Biology and Biomedical Research Centre, Kings College London, London, UK. ; Craniofacial Development and Stem Cell Biology and Biomedical Research Centre, Kings College London, London, UK Department of Pediatric Dentistry, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan. ; Craniofacial Development and Stem Cell Biology and Biomedical Research Centre, Kings College London, London, UK Department of Physiology, Faculty of Dentistry, Chulalongkorn University, Bangkok, Thailand. ; Craniofacial Development and Stem Cell Biology and Biomedical Research Centre, Kings College London, London, UK Division of Bio-Prosthodontics, Department of Oral Health Science, Course for Oral Life Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan. ; Craniofacial Development and Stem Cell Biology and Biomedical Research Centre, Kings College London, London, UK Department of Special Needs Dentistry, Nihon University School of Dentistry at Matsudo, Matsudo, Japan. ; Department of Ultrastructural Science, Tokyo Dental College, Chiyoda-ku, Tokyo, Japan. ; Laboratory of Food Biological Science, Department of Food and Nutrition, Japan Women's University, Bunkyō, Japan. ; Division of Oral Anatomy, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan. ; Department of Special Needs Dentistry, Nihon University School of Dentistry at Matsudo, Matsudo, Japan. ; Department of Teratology, Institute of Experimental Medicine, Academy of Sciences CR, Prague, Czech Republic. ; INSERM UMR_S1109, Team "Osteoarticular and Dental Regenerative NanoMedicine," FMTS, Faculté de Médecine, Faculté de Chirurgie Dentaire, Université de Strasbourg, Strasbourg, France. ; Division of Cellular and Molecular Biology, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo, Japan. ; Department of Signal Transduction in Tumor Cells, Max-Delbrück-Center for Molecular Medicine, Berlin, Germany. ; Department of Molecular Carcinogenesis, University of Texas MD Anderson Cancer Center, Smithville, TX, USA. ; Laboratory of Experimental Immunology, Inflammation and Tumorigenesis Section, National. Cancer Institute-Frederick, Frederick, MD, USA. ; Department of Epithelial Biomedicine, Centro de Investigaciones Energéticas, Medioambientales y Tecnológicas (CIEMAT), Madrid, Spain. ; Craniofacial Development and Stem Cell Biology and Biomedical Research Centre, Kings College London, London, UK paul.sharpe@kcl.ac.uk atsushiohazama@dent.niigata-u.ac.jp. ; Craniofacial Development and Stem Cell Biology and Biomedical Research Centre, Kings College London, London, UK Division of Oral Anatomy, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan paul.sharpe@kcl.ac.uk atsushiohazama@dent.niigata-u.ac.jp. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 121 EP - 128 VL - 94 IS - 1 KW - Amelogenin KW - 0 KW - Bone Morphogenetic Proteins KW - Hedgehog Proteins KW - Keratin-15 KW - Krt1-15 protein, mouse KW - NF-kappa B KW - Patched Receptors KW - Receptors, Cell Surface KW - Shh protein, mouse KW - Sostdc1 protein, mouse KW - Chuk protein, mouse KW - EC 2.7.11.10 KW - I-kappa B Kinase KW - Dentistry KW - Index Medicus KW - Wnt signaling KW - cervical loop KW - Ikkβ KW - wise KW - enamel KW - tooth development KW - Animals KW - X-Ray Microtomography -- methods KW - Keratin-15 -- genetics KW - I-kappa B Kinase -- physiology KW - Apoptosis -- physiology KW - Tooth, Supernumerary -- etiology KW - Hedgehog Proteins -- physiology KW - Amelogenin -- analysis KW - Mice KW - Tooth, Supernumerary -- genetics KW - Bone Morphogenetic Proteins -- genetics KW - Phenotype KW - Wnt Signaling Pathway -- physiology KW - Mice, Mutant Strains KW - Microradiography -- methods KW - Imaging, Three-Dimensional -- methods KW - Mutation -- genetics KW - Promoter Regions, Genetic -- genetics KW - Wnt Signaling Pathway -- genetics KW - Dental Enamel -- cytology KW - Receptors, Cell Surface -- physiology KW - Epithelium -- embryology KW - Ameloblasts -- cytology KW - Incisor -- abnormalities KW - Incisor -- embryology KW - Tooth Germ -- abnormalities KW - Tooth Germ -- embryology KW - NF-kappa B -- physiology KW - Odontogenesis -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1639493008?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+dental+research&rft.atitle=Excess+NF-%CE%BAB+induces+ectopic+odontogenesis+in+embryonic+incisor+epithelium.&rft.au=Blackburn%2C+J%3BKawasaki%2C+K%3BPorntaveetus%2C+T%3BKawasaki%2C+M%3BOtsuka-Tanaka%2C+Y%3BMiake%2C+Y%3BOta%2C+M+S%3BWatanabe%2C+M%3BHishinuma%2C+M%3BNomoto%2C+T%3BOommen%2C+S%3BGhafoor%2C+S%3BHarada%2C+F%3BNozawa-Inoue%2C+K%3BMaeda%2C+T%3BPeterkov%C3%A1%2C+R%3BLesot%2C+H%3BInoue%2C+J%3BAkiyama%2C+T%3BSchmidt-Ullrich%2C+R%3BLiu%2C+B%3BHu%2C+Y%3BPage%2C+A%3BRam%C3%ADrez%2C+%C3%81%3BSharpe%2C+P+T%3BOhazama%2C+A&rft.aulast=Blackburn&rft.aufirst=J&rft.date=2015-01-01&rft.volume=94&rft.issue=1&rft.spage=121&rft.isbn=&rft.btitle=&rft.title=Journal+of+dental+research&rft.issn=1544-0591&rft_id=info:doi/10.1177%2F0022034514556707 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-03-30 N1 - Date created - 2014-12-19 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1177/0022034514556707 ER - TY - JOUR T1 - Phase I clinical trial of ifosfamide, oxaliplatin, and etoposide (IOE) in pediatric patients with refractory solid tumors. AN - 1639490678; 24942022 AB - Oxaliplatin, although related to cisplatin and carboplatin, has a more favorable toxicity profile and may offer advantages in combination regimens. We combined oxaliplatin, ifosfamide, and etoposide (IOE) and estimated the regimen's maximum tolerated dose (MTD) in children with refractory solid tumors. Dose-limiting toxicity (DLT) and MTD were assessed at 3 dose levels in a 21-day regimen: day 1, oxaliplatin 130 mg/m (consistent dose); days 1 to 3, ifosfamide 1200 mg/m/d (level 0) or 1500 mg/m/d (levels 1 and 2) and etoposide 75 mg/m/d (levels 0 and 1) or 100 mg/m/d (level 2). Course 1 filgrastim/pegfilgrastim was permitted after initial DLT determination, if neutropenia was dose limiting. Seventeen patients received 59 courses. Without filgrastim (n=9), DLT was neutropenia in 2 patients at dose level 1. No DLT was observed after adding filgrastim (n=8). There was no ototoxicity, nephrotoxicity >grade 1, or neurotoxicity >grade 2. One patient experienced a partial response and 9 had stable disease after 2 courses. In conclusion, the IOE regimen was well tolerated. Without filgrastim, neutropenia was dose limiting with MTD at ifosfamide 1200 mg/m/d and etoposide 75 mg/m/d. The MTD with filgrastim was not defined due to early study closure. Filgrastim allowed ifosfamide and etoposide dose escalation and should be included in future studies. JF - Journal of pediatric hematology/oncology AU - Lam, Catherine G AU - Furman, Wayne L AU - Wang, Chong AU - Spunt, Sheri L AU - Wu, Jianrong AU - Ivy, Percy AU - Santana, Victor M AU - McGregor, Lisa M AD - Departments of *Oncology ‡Biostatistics, St Jude Children's Research Hospital, Memphis †Department of Pediatrics, University of Tennessee Health Sciences Center, Memphis, TN §Cancer Therapy Evaluation Program, National Cancer Institute, Rockville, MD ∥Department of Pediatric Hematology/Oncology, Penn State Hershey Children's Hospital, Hershey, PA. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - e13 EP - e18 VL - 37 IS - 1 KW - Organoplatinum Compounds KW - 0 KW - oxaliplatin KW - 04ZR38536J KW - Etoposide KW - 6PLQ3CP4P3 KW - Ifosfamide KW - UM20QQM95Y KW - Index Medicus KW - Organoplatinum Compounds -- administration & dosage KW - Humans KW - Ifosfamide -- adverse effects KW - Child KW - Child, Preschool KW - Infant KW - Organoplatinum Compounds -- adverse effects KW - Etoposide -- administration & dosage KW - Adult KW - Etoposide -- adverse effects KW - Maximum Tolerated Dose KW - Adolescent KW - Female KW - Male KW - Ifosfamide -- administration & dosage KW - Neoplasms -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1639490678?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+pediatric+hematology%2Foncology&rft.atitle=Phase+I+clinical+trial+of+ifosfamide%2C+oxaliplatin%2C+and+etoposide+%28IOE%29+in+pediatric+patients+with+refractory+solid+tumors.&rft.au=Lam%2C+Catherine+G%3BFurman%2C+Wayne+L%3BWang%2C+Chong%3BSpunt%2C+Sheri+L%3BWu%2C+Jianrong%3BIvy%2C+Percy%3BSantana%2C+Victor+M%3BMcGregor%2C+Lisa+M&rft.aulast=Lam&rft.aufirst=Catherine&rft.date=2015-01-01&rft.volume=37&rft.issue=1&rft.spage=e13&rft.isbn=&rft.btitle=&rft.title=Journal+of+pediatric+hematology%2Foncology&rft.issn=1536-3678&rft_id=info:doi/10.1097%2FMPH.0000000000000186 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-25 N1 - Date created - 2014-12-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer. 2009 Feb 1;115(3):655-64 [19117350] Br J Cancer. 2002 Mar 18;86(6):999-1005 [11953836] Eur J Cancer. 2009 Dec;45(18):3213-9 [19850470] Pediatr Blood Cancer. 2010 Sep;55(3):440-5 [20658614] Eur J Cancer. 2011 Jan;47(2):230-8 [20943374] J Clin Oncol. 2011 Feb 1;29(4):421-7 [21189381] N Engl J Med. 2011 May 12;364(19):1817-25 [21561347] J Pediatr Hematol Oncol. 2011 Jul;33(5):344-9 [21572345] Ann Oncol. 2012 Jan;23(1):200-5 [21427067] Mol Cancer Ther. 2002 Jan;1(3):227-35 [12467217] J Neurooncol. 2004 Mar-Apr;67(1-2):65-73 [15072449] N Engl J Med. 2004 Jun 3;350(23):2343-51 [15175436] Cancer. 1995 Jun 15;75(12):2966-70 [7773949] Semin Oncol. 1995 Jun;22(3 Suppl 7):23-7 [7610395] J Pediatr Hematol Oncol. 1995 Aug;17(3):265-9 [7620926] Biochem Pharmacol. 1996 Dec 24;52(12):1855-65 [8951344] Invest New Drugs. 1997;15(2):109-14 [9220289] Ann Oncol. 1998 Jan;9(1):105-8 [9541691] Cancer Res. 1998 Aug 15;58(16):3579-85 [9721864] Mol Pharmacol. 1998 Nov;54(5):770-7 [9804612] Eur J Cancer. 1999 Jan;35(1):86-90 [10211093] Clin Cancer Res. 2005 Jan 15;11(2 Pt 1):690-6 [15701857] Cancer. 2006 Nov 1;107(9):2291-7 [17019740] Ann Oncol. 2007 Mar;18(3):461-7 [17110590] J Clin Oncol. 2007 Jun 1;25(16):2274-80 [17538173] J Clin Oncol. 2008 Mar 20;26(9):1435-42 [18349393] Cancer. 2009 Apr 15;115(8):1765-75 [19170226] Lancet. 2012 Jan 28;379(9813):315-21 [22226517] Lancet Oncol. 2012 Feb;13(2):181-8 [22192731] Br J Haematol. 2011 Apr;153(2):191-8 [21385169] J Clin Oncol. 2012 May 20;30(15):1755-62 [22473155] J Clin Oncol. 2012 Jul 1;30(19):2408-17 [22547603] Pediatr Blood Cancer. 2013 Feb;60(2):230-6 [23024067] Pediatr Blood Cancer. 2013 Jul;60(7):1103-7 [23335436] J Natl Cancer Inst. 2000 Feb 2;92(3):205-16 [10655437] J Clin Oncol. 2000 Aug;18(16):2938-47 [10944126] Ann Oncol. 2000 Nov;11(11):1477-83 [11142489] Ann Oncol. 2001 Oct;12(10):1411-5 [11762813] J Clin Oncol. 2008 Sep 20;26(27):4394-400 [18802151] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1097/MPH.0000000000000186 ER - TY - JOUR T1 - The RASSF1A tumor suppressor regulates XPA-mediated DNA repair. AN - 1635005427; 25368379 AB - RASSF1A may be the most frequently inactivated tumor suppressor identified in human cancer so far. It is a proapoptotic Ras effector and plays an important role in the apoptotic DNA damage response (DDR). We now show that in addition to DDR regulation, RASSF1A also plays a key role in the DNA repair process itself. We show that RASSF1A forms a DNA damage-regulated complex with the key DNA repair protein xeroderma pigmentosum A (XPA). XPA requires RASSF1A to exert full repair activity, and RASSF1A-deficient cells exhibit an impaired ability to repair DNA. Moreover, a cancer-associated RASSF1A single-nucleotide polymorphism (SNP) variant exhibits differential XPA binding and inhibits DNA repair. The interaction of XPA with other components of the repair complex, such as replication protein A (RPA), is controlled in part by a dynamic acetylation/deacetylation cycle. We found that RASSF1A and its SNP variant differentially regulate XPA protein acetylation, and the SNP variant hyperstabilizes the XPA-RPA70 complex. Thus, we identify two novel functions for RASSF1A in the control of DNA repair and protein acetylation. As RASSF1A modulates both apoptotic DDR and DNA repair, it may play an important and unanticipated role in coordinating the balance between repair and death after DNA damage. Copyright © 2015, American Society for Microbiology. All Rights Reserved. JF - Molecular and cellular biology AU - Donninger, Howard AU - Clark, Jennifer AU - Rinaldo, Francesca AU - Nelson, Nicholas AU - Barnoud, Thibaut AU - Schmidt, M Lee AU - Hobbing, Katharine R AU - Vos, Michele D AU - Sils, Brian AU - Clark, Geoffrey J AD - Department of Medicine, J. G. Brown Cancer Center, Molecular Targets Program, University of Louisville, Louisville, Kentucky, USA. ; Department of Biochemistry and Molecular Biology, University of Louisville, Louisville, Kentucky, USA. ; Department of Pharmacology and Toxicology, University of Louisville, Louisville, Kentucky, USA. ; National Cancer Institute, NIH, Bethesda, Maryland, USA. ; Department of Pharmacology and Toxicology, University of Louisville, Louisville, Kentucky, USA gjclar01@louisville.edu. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 277 EP - 287 VL - 35 IS - 1 KW - RASSF1 protein, human KW - 0 KW - RASSF1 protein, mouse KW - Replication Protein A KW - Tumor Suppressor Proteins KW - XPA protein, human KW - Xeroderma Pigmentosum Group A Protein KW - Index Medicus KW - Comet Assay KW - Animals KW - Polymorphism, Single Nucleotide KW - Apoptosis KW - DNA Damage KW - Humans KW - HEK293 Cells KW - Mice KW - Cell Line, Tumor KW - Replication Protein A -- metabolism KW - Mice, Knockout KW - Gene Expression Regulation, Neoplastic KW - DNA Repair KW - Tumor Suppressor Proteins -- metabolism KW - Xeroderma Pigmentosum Group A Protein -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635005427?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biology&rft.atitle=The+RASSF1A+tumor+suppressor+regulates+XPA-mediated+DNA+repair.&rft.au=Donninger%2C+Howard%3BClark%2C+Jennifer%3BRinaldo%2C+Francesca%3BNelson%2C+Nicholas%3BBarnoud%2C+Thibaut%3BSchmidt%2C+M+Lee%3BHobbing%2C+Katharine+R%3BVos%2C+Michele+D%3BSils%2C+Brian%3BClark%2C+Geoffrey+J&rft.aulast=Donninger&rft.aufirst=Howard&rft.date=2015-01-01&rft.volume=35&rft.issue=1&rft.spage=277&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biology&rft.issn=1098-5549&rft_id=info:doi/10.1128%2FMCB.00202-14 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-12 N1 - Date created - 2014-12-10 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Genet. 2000 Jul;25(3):315-9 [10888881] J Biol Chem. 2011 Feb 18;286(7):5476-83 [21148310] Mol Cell Biol. 2002 Jun;22(12):4309-18 [12024041] J Biol Chem. 2002 May 31;277(22):19358-66 [11884408] Mutat Res. 2003 Jan 10;534(1-2):15-20 [12504751] Science. 2003 Jun 6;300(5625):1542-8 [12791985] Oncogene. 2003 Nov 6;22(50):8125-36 [14603253] Annu Rev Biochem. 2004;73:39-85 [15189136] Cancer Res. 2004 Jun 15;64(12):4112-6 [15205320] Cancer Res. 2004 Jun 15;64(12):4244-50 [15205337] Biochemistry. 1993 Nov 16;32(45):12096-104 [8218288] Mol Cell Biol. 1995 Oct;15(10):5396-402 [7565690] Cancer Res. 1997 Feb 15;57(4):581-4 [9044829] Semin Cancer Biol. 1996 Oct;7(5):229-40 [9110400] Genes Dev. 1999 Apr 1;13(7):768-85 [10197977] Cancer Res. 2005 Jan 1;65(1):92-8 [15665283] Histol Histopathol. 2005 Apr;20(2):645-63 [15736067] Nat Rev Cancer. 2005 Jul;5(7):564-73 [16069818] J Biol Chem. 2006 Feb 24;281(8):4557-63 [16344548] Cancer Res. 2006 Mar 15;66(6):2997-3005 [16540648] Health Aff (Millwood). 2007 Jan-Feb;26(1):38-48 [17211012] Curr Biol. 2007 Apr 17;17(8):700-5 [17379520] Biochim Biophys Acta. 2007 Sep;1776(1):58-85 [17692468] J Cell Sci. 2007 Sep 15;120(Pt 18):3163-72 [17878233] Cancer Res. 2008 Jan 1;68(1):22-5 [18172292] FASEB J. 2008 Feb;22(2):603-11 [17848622] Mol Cell. 2008 Jul 11;31(1):9-20 [18614043] Adv Exp Med Biol. 2008;637:28-38 [19181108] Cell Mol Life Sci. 2009 Mar;66(6):965-7 [19153660] J Biol Chem. 2009 Sep 4;284(36):24213-22 [19586908] Curr Biol. 2009 Dec 15;19(23):2020-5 [19962312] Mol Cell. 2010 Jul 30;39(2):247-58 [20670893] J Clin Invest. 2010 Oct;120(10):3555-67 [20890045] Oncogene. 2010 Oct 21;29(42):5729-40 [20697344] Biochim Biophys Acta. 2010 Oct-Dec;1799(10-12):702-16 [20965294] J Biol Chem. 2011 Mar 4;286(9):6940-5 [21212262] J Biol Chem. 2011 May 27;286(21):18483-91 [21489991] DNA Repair (Amst). 2011 Oct 10;10(10):1044-50 [21880556] Semin Cancer Biol. 2011 Dec;21(6):367-76 [22037160] Dev Cell. 2011 Dec 13;21(6):1077-91 [22137763] Mol Cell. 2011 Dec 23;44(6):893-906 [22195963] J Biol Chem. 2012 Feb 3;287(6):3908-18 [22179778] Trends Genet. 2012 Mar;28(3):128-36 [22265392] Cancer Res. 2012 May 1;72(9):2206-17 [22389451] PLoS One. 2012;7(11):e49199 [23152873] Cancer Lett. 2013 May 28;332(2):237-48 [22261329] Handb Clin Neurol. 2013;113:1637-50 [23622385] Oncotarget. 2013 Oct;4(10):1556-71 [24298606] Mol Cell. 2014 May 22;54(4):639-50 [24813943] J Biol Chem. 2000 Nov 17;275(46):35669-72 [10998413] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/MCB.00202-14 ER - TY - JOUR T1 - Performance of self-collected cervical samples in screening for future precancer using human papillomavirus DNA testing. AN - 1634727335; 25479804 AB - Self-collected human papillomavirus (HPV) testing could reduce barriers to cervical cancer screening, with performance comparable to clinician-collected specimens. The ability of self-collected specimens to cross-sectionally and prospectively detect precursor lesions was investigated in an HPV vaccine randomized trial in Costa Rica. In the trial, 7466 women age 18 to 25 years received an HPV16/18 or control vaccine and were followed at least annually for four years. In this secondary analysis, we included all women who provided a self-collected cervicovaginal specimen six months after enrollment (5109 women = full analytical cohort). A subset (615 women = restricted cohort) also had clinician-collected specimens at the six-month postenrollment visit. High-grade squamous intraepithelial lesion or repeat low-grade squamous intraepithelial lesion prompted colposcopic referral throughout the study. HPV testing was performed with SPF10PCR/DEIA/LiPA25. Cross-sectional and prospective sensitivity, specificity, and predictive values were estimated. In the full cohort, one-time HPV testing on self-collected samples detected prevalent CIN2+ with a sensitivity of 88.7% (95% confidence interval [CI] =77.0% to 95.7%) and a specificity of 68.9% (95% CI = 67.6% to 70.1%). For predicting incident CIN2+ in the subsequent four years, sensitivity was 73.9% (95% CI = 65.8% to 81.0%) and specificity 69.4% (95% CI = 68.1% to 70.7%). In the restricted cohort, for incident CIN2+, self-collected HPV was much more sensitive than cytology (80.0% vs 10.0%); relative sensitivity was 0.1 (95% CI = 0.03% to 0.5%). Furthermore, three times more women with normal baseline cytology developed incident CIN2+ than those with negative self-collected HPV. Self-collected and clinician-collected HPV testing had comparable performance. Agreement between self- and clinician-collected samples was 89.7% (kappa = 0.78, McNemar χ2 = 0.62) for carcinogenic HPV types. Self-collected specimens can be used for HPV-based screening, providing sensitivity and specificity comparable with clinician-collected specimens and detecting disease earlier than cytology. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com. JF - Journal of the National Cancer Institute AU - Porras, Carolina AU - Hildesheim, Allan AU - González, Paula AU - Schiffman, Mark AU - Rodríguez, Ana Cecilia AU - Wacholder, Sholom AU - Jiménez, Silvia AU - Quint, Wim AU - Guillen, Diego AU - Kreimer, Aimée R AU - Herrero, Rolando AU - CVT Vaccine Group AD - Affiliations of authors: Proyecto Epidemiológico Guanacaste, Fundación INCIENSA, San José, Costa Rica (CP, PG, ACR, SJ, DG); Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD (AH, MS, SW, ARK); DDL Diagnostic Laboratory, Rijswijk, the Netherlands (WQ); Prevention and Implementation Group, International Agency for Research on Cancer, World Health Organization, Lyon, France (PG, RH). cporras@proyectoguanacaste.org. ; Affiliations of authors: Proyecto Epidemiológico Guanacaste, Fundación INCIENSA, San José, Costa Rica (CP, PG, ACR, SJ, DG); Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD (AH, MS, SW, ARK); DDL Diagnostic Laboratory, Rijswijk, the Netherlands (WQ); Prevention and Implementation Group, International Agency for Research on Cancer, World Health Organization, Lyon, France (PG, RH). ; CVT Vaccine Group Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 400 VL - 107 IS - 1 KW - DNA, Viral KW - 0 KW - Papillomavirus Vaccines KW - Index Medicus KW - Sensitivity and Specificity KW - Cross-Sectional Studies KW - Prospective Studies KW - Humans KW - Costa Rica KW - Papillomavirus Vaccines -- administration & dosage KW - Cohort Studies KW - Adult KW - Aged KW - Middle Aged KW - Female KW - Colposcopy KW - Uterine Cervical Neoplasms -- prevention & control KW - Alphapapillomavirus -- isolation & purification KW - Cervical Intraepithelial Neoplasia -- prevention & control KW - Specimen Handling -- methods KW - Mass Screening -- methods KW - Precancerous Conditions -- virology KW - Alphapapillomavirus -- genetics KW - DNA, Viral -- analysis KW - Precancerous Conditions -- prevention & control KW - Vaginal Smears KW - Cervical Intraepithelial Neoplasia -- virology KW - Early Detection of Cancer -- methods KW - Uterine Cervical Neoplasms -- virology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1634727335?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=Performance+of+self-collected+cervical+samples+in+screening+for+future+precancer+using+human+papillomavirus+DNA+testing.&rft.au=Porras%2C+Carolina%3BHildesheim%2C+Allan%3BGonz%C3%A1lez%2C+Paula%3BSchiffman%2C+Mark%3BRodr%C3%ADguez%2C+Ana+Cecilia%3BWacholder%2C+Sholom%3BJim%C3%A9nez%2C+Silvia%3BQuint%2C+Wim%3BGuillen%2C+Diego%3BKreimer%2C+Aim%C3%A9e+R%3BHerrero%2C+Rolando%3BCVT+Vaccine+Group&rft.aulast=Porras&rft.aufirst=Carolina&rft.date=2015-01-01&rft.volume=107&rft.issue=1&rft.spage=400&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdju400 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-20 N1 - Date created - 2014-12-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Epidemiol Biomarkers Prev. 2001 Feb;10(2):95-100 [11219778] Ann Intern Med. 2000 May 16;132(10):810-9 [10819705] Med Care. 2006 Feb;44(2):132-40 [16434912] J Clin Microbiol. 2006 Sep;44(9):3292-8 [16954263] Cancer Res. 2006 Nov 1;66(21):10630-6 [17062559] Gynecol Oncol. 2007 May;105(2):530-5 [17335880] Lancet. 2007 Sep 8;370(9590):890-907 [17826171] N Engl J Med. 2007 Oct 18;357(16):1579-88 [17942871] N Engl J Med. 2007 Oct 18;357(16):1589-97 [17942872] Lancet. 2007 Nov 24;370(9601):1764-72 [17919718] Sex Transm Dis. 2007 Nov;34(11):849-55 [17621246] Vaccine. 2008 Sep 2;26(37):4795-808 [18640170] BMJ. 2008;337:a1754 [18852164] Cancer Epidemiol Biomarkers Prev. 2009 Mar;18(3):863-5 [19273486] N Engl J Med. 2009 Apr 2;360(14):1385-94 [19339719] Lancet Oncol. 2009 Apr;10(4):321-2 [19350698] Int J Cancer. 2009 Dec 1;125(11):2489-96 [19626591] J Natl Cancer Inst. 2010 Mar 3;102(5):315-24 [20157096] Lancet Oncol. 2010 Mar;11(3):249-57 [20089449] Int J Gynecol Cancer. 2010 Nov;20(8):1415-23 [21051987] J Natl Cancer Inst. 2011 Mar 2;103(5):368-83 [21282563] Lancet. 2011 Jun 18;377(9783):2085-92 [21684381] Lancet Oncol. 2011 Jul;12(7):663-72 [21684207] Int J Cancer. 2011 Aug 1;129(3):517-27 [21384341] Lancet Oncol. 2011 Sep;12(9):880-90 [21865084] Lancet. 2011 Nov 26;378(9806):1868-73 [22051739] Lancet Oncol. 2012 Jan;13(1):78-88 [22177579] Future Microbiol. 2012 Feb;7(2):193-9 [22324989] Int J Cancer. 2012 Apr 15;130(8):1855-60 [21630255] Am J Clin Pathol. 2012 Apr;137(4):516-42 [22431528] Arch Pathol Lab Med. 2012 Oct;136(10):1266-97 [22742517] Lancet Oncol. 2014 Feb;15(2):172-83 [24433684] Womens Health Issues. 2013 Mar-Apr;23(2):e123-30 [23410619] Vaccine. 2012 Nov 20;30 Suppl 5:F107-16 [23199953] Lancet Infect Dis. 2014 Oct;14(10):958-66 [25107680] Int J Cancer. 2013 May 15;132(10):2223-36 [22907569] J Clin Microbiol. 1999 Aug;37(8):2508-17 [10405393] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/jnci/dju400 ER - TY - JOUR T1 - (R)Evolutionary therapy: the potential of immunotherapy to fulfill the promise of personalized cancer treatment. AN - 1629584722; 25432410 AB - Since the millennium, personalized medicine has been at the forefront of therapeutic endeavors in medical oncology. The latest technology has given researchers the ability to define cancer at its molecular core. This has led to the development of "targeted therapies," designed to eliminate driver mutations while leaving healthy cells unscathed. Unfortunately, more than 10 years into the targeted molecular therapy era, successes have been infrequent, and toxicity remains largely unchanged compared with relatively indiscriminant, traditional chemotherapy. Emerging data suggests that the malignant clonal heterogeneity within solid tumors is so diverse that targeting one or even several mutations is likely to have minimal, transient impact. In recent years, new therapies have emerged that can effectively stimulate the immune system and improve survival in patients with metastatic disease. Through immune activation, there is the potential to target the cancer with a biologic diversity that can potentially rival the multiplicity of malignant mutations within tumors. Stimulating the immune system to become an evolving adversary against malignant cells may revolutionize cancer therapy in the years to come. Published by Oxford University Press 2014. JF - Journal of the National Cancer Institute AU - Madan, Ravi A AU - Gulley, James L AD - Genitourinary Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD. madanr@mail.nih.gov. ; Genitourinary Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD. Y1 - 2015/01// PY - 2015 DA - January 2015 SP - 347 VL - 107 IS - 1 KW - Index Medicus KW - Precision Medicine KW - Humans KW - Neoplasms -- drug therapy KW - Molecular Targeted Therapy -- methods KW - Neoplasms -- immunology KW - Immunotherapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1629584722?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+National+Cancer+Institute&rft.atitle=%28R%29Evolutionary+therapy%3A+the+potential+of+immunotherapy+to+fulfill+the+promise+of+personalized+cancer+treatment.&rft.au=Madan%2C+Ravi+A%3BGulley%2C+James+L&rft.aulast=Madan&rft.aufirst=Ravi&rft.date=2015-01-01&rft.volume=107&rft.issue=1&rft.spage=347&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdju347 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-20 N1 - Date created - 2014-11-29 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nature. 2010 Oct 28;467(7319):1114-7 [20981102] J Clin Oncol. 2011 Feb 20;29(6):610-8 [21245428] N Engl J Med. 2012 Feb 23;366(8):707-14 [22356324] Cancer Discov. 2011 Jun;1(1):44-53 [22586319] Cancer Immunol Immunother. 2013 Jan;62(1):137-47 [22865266] Ann N Y Acad Sci. 2013 May;1284:62-5 [23651195] Cancer Immunol Immunother. 2007 May;56(5):641-8 [16960692] N Engl J Med. 2002 Feb 28;346(9):645-52 [11870241] Leukemia. 2002 Nov;16(11):2190-6 [12399961] J Exp Med. 2005 Jan 17;201(2):249-57 [15657294] Cancer Discov. 2014 Jan;4(1):94-109 [24265153] Cancer Immunol Immunother. 2013 Sep;62(9):1453-61 [23771160] Immunity. 2013 Jul 25;39(1):1-10 [23890059] Int J Cancer. 2013 Aug 1;133(3):624-36 [23364915] J Clin Oncol. 2013 May 10;31(14):1767-74 [23569304] Int J Cancer. 2004 Mar 20;109(2):265-73 [14750179] Clin Cancer Res. 2005 Apr 1;11(7):2552-60 [15814633] Clin Cancer Res. 2005 May 1;11(9):3353-62 [15867235] J Immunol. 2008 Mar 1;180(5):3585-93 [18292586] Cancer Res. 2009 Mar 15;69(6):2514-22 [19276342] J Clin Oncol. 2009 Oct 1;27(28):4685-92 [19720923] Clin Cancer Res. 2010 Aug 1;16(15):4046-56 [20562209] N Engl J Med. 2010 Aug 19;363(8):711-23 [20525992] N Engl J Med. 2010 Jul 29;363(5):411-22 [20818862] Oncologist. 2010;15(9):969-75 [20798195] Nature. 2010 Oct 28;467(7319):1109-13 [20981101] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/jnci/dju347 ER - TY - JOUR T1 - Kidney biomarkers associated with blood lead, mercury, and cadmium in premenopausal women: a prospective cohort study. AN - 1628528906; 25424620 AB - Certain metals are harmful to the kidney and liver at high levels, but associations with functional biomarkers at low exposure levels among premenopausal women apparently has not been evaluated. Healthy, regularly menstruating women (n = 259) were followed for up to 2 menstrual cycles with up to 16 visits. Renal and liver biomarkers were measured in serum at each clinic visit. Cadmium (Cd), lead (Pb), and mercury (Hg) were measured in whole blood at baseline. Linear mixed models were adjusted for age, body mass index (BMI), race, average calories, alcohol intake, smoking, and cycle day. Median levels of Cd, Pb, and Hg were 0.31 μg/L, 0.88 μg/dl, and 1.1 μg/L, respectively. One-third of women had diminished glomerular filtration rate (eGFR) (<90 ml/min/1.73 m(2)). Each twofold increase in Cd was associated with a negative 4.9% change in blood urea nitrogen (BUN) and bilirubin. Each twofold rise in Pb was associated with decreased eGFR and increased creatinine. A twofold elevation in Hg was associated with higher protein and reduced alkaline phosphatase. In healthy, predominantly nonsmoking women, low levels of Cd, Pb, and Hg were associated with changes in select biomarkers of kidney and liver function. JF - Journal of toxicology and environmental health. Part A AU - Pollack, Anna Z AU - Mumford, Sunni L AU - Mendola, Pauline AU - Perkins, Neil J AU - Rotman, Yaron AU - Wactawski-Wende, Jean AU - Schisterman, Enrique F AD - a Epidemiology Branch, Division of Intramural Population Health Research , Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health , Bethesda , Maryland , USA. Y1 - 2015 PY - 2015 DA - 2015 SP - 119 EP - 131 VL - 78 IS - 2 SN - 1528-7394, 1528-7394 KW - Biomarkers KW - 0 KW - Cadmium KW - 00BH33GNGH KW - Lead KW - 2P299V784P KW - Creatinine KW - AYI8EX34EU KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - Alkaline Phosphatase KW - EC 3.1.3.1 KW - Mercury KW - FXS1BY2PGL KW - Bilirubin KW - RFM9X3LJ49 KW - Index Medicus KW - Young Adult KW - Glomerular Filtration Rate -- drug effects KW - Humans KW - Linear Models KW - Liver -- metabolism KW - Blood Urea Nitrogen KW - Body Mass Index KW - Alkaline Phosphatase -- blood KW - Aspartate Aminotransferases -- blood KW - Alanine Transaminase -- blood KW - Prospective Studies KW - Creatinine -- metabolism KW - Liver -- drug effects KW - Adult KW - Bilirubin -- blood KW - Adolescent KW - Female KW - Kidney -- metabolism KW - Mercury -- blood KW - Kidney -- drug effects KW - Premenopause -- blood KW - Cadmium -- blood KW - Biomarkers -- blood KW - Lead -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1628528906?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+toxicology+and+environmental+health.+Part+A&rft.atitle=Kidney+biomarkers+associated+with+blood+lead%2C+mercury%2C+and+cadmium+in+premenopausal+women%3A+a+prospective+cohort+study.&rft.au=Pollack%2C+Anna+Z%3BMumford%2C+Sunni+L%3BMendola%2C+Pauline%3BPerkins%2C+Neil+J%3BRotman%2C+Yaron%3BWactawski-Wende%2C+Jean%3BSchisterman%2C+Enrique+F&rft.aulast=Pollack&rft.aufirst=Anna&rft.date=2015-01-01&rft.volume=78&rft.issue=2&rft.spage=119&rft.isbn=&rft.btitle=&rft.title=Journal+of+toxicology+and+environmental+health.+Part+A&rft.issn=15287394&rft_id=info:doi/10.1080%2F15287394.2014.944680 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-01-20 N1 - Date created - 2014-11-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Paediatr Perinat Epidemiol. 2009 Mar;23(2):171-84 [19159403] Kidney Int. 2003 Mar;63(3):1044-50 [12631086] J Toxicol Environ Health A. 2014;77(1-3):133-42 [24555654] Occup Environ Med. 2000 Oct;57(10):668-72 [10984338] Scand J Work Environ Health. 2000 Oct;26(5):427-35 [11103842] Arch Intern Med. 2001 Jan 22;161(2):264-71 [11176742] Sci Total Environ. 2001 Nov 12;279(1-3):151-8 [11712592] Am J Kidney Dis. 2002 Feb;39(2 Suppl 1):S1-266 [11904577] Ann Intern Med. 2002 Jul 2;137(1):1-10 [12093239] Occup Environ Med. 2003 Aug;60(8):551-62 [12883015] Med Sci Monit. 2004 Mar;10(3):CR112-6 [14976454] Toxicol Lett. 2004 Mar 21;148(3):187-97 [15041069] Environ Health Perspect. 2004 Apr;112(5):562-70 [15064162] Br J Ind Med. 1974 Apr;31(2):113-27 [4830763] Ind Health. 1986;24(3):151-5 [3781894] Int Arch Occup Environ Health. 1988;61(1-2):65-9 [3264272] Br J Ind Med. 1992 Jun;49(6):394-401 [1606025] N Engl J Med. 1992 Jul 16;327(3):151-6 [1608406] JAMA. 1994 Jul 27;272(4):284-91 [8028141] JAMA. 1996 Apr 17;275(15):1177-81 [8609685] Biometals. 2004 Oct;17(5):505-9 [15688854] Environ Health Perspect. 2005 Nov;113(11):1627-31 [16263522] Am J Epidemiol. 2006 Feb 15;163(4):374-83 [16394206] Int J Environ Res Public Health. 2004 Mar;1(1):21-5 [16696177] J Toxicol Environ Health A. 2006 Oct;69(19):1781-96 [16905508] Environ Res. 2007 Feb;103(2):191-7 [16890218] Sci Total Environ. 2007 Sep 1;382(2-3):214-23 [17544058] Toxicol Ind Health. 2007 Apr;23(3):161-5 [18220158] Environ Res. 2008 Oct;108(2):224-32 [18684440] Environ Res. 2009 Jan;109(1):101-7 [19038382] Environ Health Perspect. 2009 Jan;117(1):47-53 [19165386] Environ Health Perspect. 2009 Feb;117(2):181-4 [19270785] Am J Epidemiol. 2009 Nov 1;170(9):1156-64 [19700501] J Toxicol Environ Health A. 2009;72(21-22):1493-8 [20077223] Environ Res. 2010 Jul;110(5):505-12 [20400068] Occup Environ Med. 2011 Apr;68(4):257-64 [20935291] J Nutr Sci Vitaminol (Tokyo). 2011;57(2):177-85 [21697638] Environ Health. 2011;10:77 [21888673] Environ Health Perspect. 2011 Dec;119(12):1800-5 [21835726] J Toxicol Environ Health A. 2012;75(7):374-90 [22524593] Pediatr Nephrol. 2012 Sep;27(9):1551-6 [22527529] Cancer Epidemiol Biomarkers Prev. 2013 Jan;22(1):102-8 [23150064] J Toxicol Environ Health A. 2013;76(2):86-97 [23294297] Epidemiology. 2013 May;24(3):421-9 [23514838] J Toxicol Environ Health A. 2014;77(1-3):69-79 [24555648] Med Lav. 2002 May-Jun;93(3):191-201 [12197269] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1080/15287394.2014.944680 ER - TY - JOUR T1 - Toxicoepigenomics and cancer: implications for screening. AN - 1628241318; 25421670 AB - Scientists have long considered genetics to be the key mechanism that alters gene expression because of exposure to the environment and toxic substances (toxicants). Recently, epigenetic mechanisms have emerged as an alternative explanation for alterations in gene expression resulting from such exposure. The fact that certain toxic substances that contribute to tumor development do not induce mutations probably results from underlying epigenetic mechanisms. The field of toxicoepigenomics emerged from the combination of epigenetics and classical toxicology. High-throughput technologies now enable evaluation of altered epigenomic profiling in response to toxins and environmental pollutants. Furthermore, differences in the epigenomic backgrounds of individuals may explain why, although whole populations are exposed to toxicants, only a few people in a population develop cancer. Metals in the environment and toxic substances not only alter DNA methylation patterns and histone modifications but also affect enzymes involved in posttranslational modifications of proteins and epigenetic regulation, and thereby contribute to carcinogenesis. This article describes different toxic substances and environmental pollutants that alter epigenetic profiling and discusses how this information can be used in screening populations at high risk of developing cancer. Research opportunities and challengers in the field also are discussed. JF - Methods in molecular biology (Clifton, N.J.) AU - Verma, Mukesh AD - Methods and Technologies Branch, Epidemiology and Genomics Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health (NIH), 9609 Medical Center Drive, Room 4E102, Rockville, MD, 20850, USA, vermam@mail.nih.gov. Y1 - 2015 PY - 2015 DA - 2015 SP - 355 EP - 367 VL - 1238 KW - Environmental Pollutants KW - 0 KW - Index Medicus KW - Animals KW - Environmental Pollutants -- toxicity KW - Humans KW - Neoplasms -- diagnosis KW - Neoplasms -- chemically induced KW - Epigenesis, Genetic -- drug effects KW - Toxicogenetics -- methods KW - Mass Screening -- methods KW - Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1628241318?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.atitle=Toxicoepigenomics+and+cancer%3A+implications+for+screening.&rft.au=Verma%2C+Mukesh&rft.aulast=Verma&rft.aufirst=Mukesh&rft.date=2015-01-01&rft.volume=1238&rft.issue=&rft.spage=355&rft.isbn=&rft.btitle=&rft.title=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.issn=1940-6029&rft_id=info:doi/10.1007%2F978-1-4939-1804-1_19 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-07-03 N1 - Date created - 2014-11-25 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/978-1-4939-1804-1_19 ER -