TY - JOUR T1 - The receptors that mediate the direct lethality of anthrax toxin. AN - 1273707041; 23271637 AB - Tumor endothelium marker-8 (TEM8) and capillary morphogenesis protein-2 (CMG2) are the two well-characterized anthrax toxin receptors, each containing a von Willebrand factor A (vWA) domain responsible for anthrax protective antigen (PA) binding. Recently, a cell-based analysis was used to implicate another vWA domain-containing protein, integrin β1 as a third anthrax toxin receptor. To explore whether proteins other than TEM8 and CMG2 function as anthrax toxin receptors in vivo, we challenged mice lacking TEM8 and/or CMG2. Specifically, we used as an effector protein the fusion protein FP59, a fusion between the PA-binding domain of anthrax lethal factor (LF) and the catalytic domain of Pseudomonas aeruginosa exotoxin A. FP59 is at least 50-fold more potent than LF in the presence of PA, with 2 μg PA + 2 μg FP59 being sufficient to kill a mouse. While TEM8(-/-) and wild type control mice succumbed to a 5 μg PA + 5 μg FP59 challenge, CMG2(-/-) mice were completely resistant to this dose, confirming that CMG2 is the major anthrax toxin receptor in vivo. To detect whether any toxic effects are mediated by TEM8 or other putative receptors such as integrin β1, CMG2(-/-)/TEM8(-/-) mice were challenged with as many as five doses of 50 μg PA + 50 μg FP59. Strikingly, the CMG2(-/-)/TEM8(-/-) mice were completely resistant to the 5-dose challenge. These results strongly suggest that TEM8 is the only minor anthrax toxin receptor mediating direct lethality in vivo and that other proteins implicated as receptors do not play this role. JF - Toxins AU - Liu, Shihui AU - Zhang, Yi AU - Hoover, Benjamin AU - Leppla, Stephen H AD - Laboratory of Parasitic Diseases, Microbial Pathogenesis Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. shliu@niaid.nih.gov Y1 - 2012/12/27/ PY - 2012 DA - 2012 Dec 27 SP - 1 EP - 8 VL - 5 IS - 1 KW - Antigens, Bacterial KW - 0 KW - Antigens, CD29 KW - Antxr1 protein, mouse KW - Antxr2 protein, mouse KW - Bacterial Toxins KW - Biomarkers, Tumor KW - Receptors, Peptide KW - anthrax toxin KW - Index Medicus KW - Animals KW - Humans KW - Longevity -- drug effects KW - Disease Models, Animal KW - Mice KW - Human Umbilical Vein Endothelial Cells KW - Anthrax -- metabolism KW - Mice, Knockout KW - Host-Pathogen Interactions KW - Cell Survival -- drug effects KW - Anthrax -- microbiology KW - Anthrax -- mortality KW - Female KW - Male KW - Biomarkers, Tumor -- metabolism KW - Antigens, Bacterial -- toxicity KW - Biomarkers, Tumor -- genetics KW - Receptors, Peptide -- metabolism KW - Bacterial Toxins -- metabolism KW - Antigens, Bacterial -- metabolism KW - Antigens, CD29 -- metabolism KW - Bacillus anthracis -- pathogenicity KW - Bacillus anthracis -- metabolism KW - Antigens, CD29 -- genetics KW - Receptors, Peptide -- genetics KW - Bacterial Toxins -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273707041?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxins&rft.atitle=The+receptors+that+mediate+the+direct+lethality+of+anthrax+toxin.&rft.au=Liu%2C+Shihui%3BZhang%2C+Yi%3BHoover%2C+Benjamin%3BLeppla%2C+Stephen+H&rft.aulast=Liu&rft.aufirst=Shihui&rft.date=2012-12-27&rft.volume=5&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Toxins&rft.issn=2072-6651&rft_id=info:doi/10.3390%2Ftoxins5010001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-06-04 N1 - Date created - 2012-12-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Expert Opin Biol Ther. 2003 Aug;3(5):843-53 [12880383] J Biol Chem. 2003 Feb 14;278(7):5227-34 [12468536] Mol Cell. 2003 Sep;12(3):603-13 [14527407] Proc Natl Acad Sci U S A. 1982 May;79(10):3162-6 [6285339] J Biol Chem. 1992 Aug 5;267(22):15542-8 [1639793] Science. 1998 May 1;280(5364):734-7 [9563949] Biochem Biophys Res Commun. 1998 Jul 30;248(3):706-11 [9703991] Am J Pathol. 2005 Nov;167(5):1309-20 [16251415] J Cell Biol. 2006 Jan 16;172(2):309-20 [16401723] Clin Cancer Res. 2006 Dec 15;12(24):7437-43 [17189417] Cell Microbiol. 2007 Apr;9(4):977-87 [17381430] J Biol Chem. 2008 Jan 4;283(1):529-40 [17974567] PLoS One. 2008;3(9):e3130 [18769623] Proc Natl Acad Sci U S A. 2009 Jul 28;106(30):12424-9 [19617532] Mol Aspects Med. 2009 Dec;30(6):439-55 [19638283] PLoS Pathog. 2010 May;6(5):e1000906 [20502689] Proc Natl Acad Sci U S A. 2010 Aug 31;107(35):15583-8 [20713715] Cell Host Microbe. 2010 Nov 18;8(5):455-62 [21075356] Protein Expr Purif. 2011 Nov;80(1):80-90 [21827967] PLoS Pathog. 2012;8(3):e1002638 [22479187] Proc Natl Acad Sci U S A. 2012 Aug 21;109(34):13817-22 [22869748] Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5170-4 [12700348] Biochem J. 2000 Dec 15;352 Pt 3:739-45 [11104681] Nature. 2001 Nov 8;414(6860):225-9 [11700562] Trends Microbiol. 2002 Jun;10(6):287-93 [12088665] J Cell Biol. 2003 Feb 3;160(3):321-8 [12551953] J Clin Invest. 2003 Sep;112(5):670-82 [12952916] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.3390/toxins5010001 ER - TY - JOUR T1 - Neurodevelopmental outcomes in the early CPAP and pulse oximetry trial. AN - 1273252910; 23268664 AB - Previous results from our trial of early treatment with continuous positive airway pressure (CPAP) versus early surfactant treatment in infants showed no significant difference in the outcome of death or bronchopulmonary dysplasia. A lower (vs. higher) target range of oxygen saturation was associated with a lower rate of severe retinopathy but higher mortality. We now report longer-term results from our prespecified hypotheses. Using a 2-by-2 factorial design, we randomly assigned infants born between 24 weeks 0 days and 27 weeks 6 days of gestation to early CPAP with a limited ventilation strategy or early surfactant administration and to lower or higher target ranges of oxygen saturation (85 to 89% or 91 to 95%). The primary composite outcome for the longer-term analysis was death before assessment at 18 to 22 months or neurodevelopmental impairment at 18 to 22 months of corrected age. The primary outcome was determined for 1234 of 1316 enrolled infants (93.8%); 990 of the 1058 surviving infants (93.6%) were evaluated at 18 to 22 months of corrected age. Death or neurodevelopmental impairment occurred in 27.9% of the infants in the CPAP group (173 of 621 infants), versus 29.9% of those in the surfactant group (183 of 613) (relative risk, 0.93; 95% confidence interval [CI], 0.78 to 1.10; P=0.38), and in 30.2% of the infants in the lower-oxygen-saturation group (185 of 612), versus 27.5% of those in the higher-oxygen-saturation group (171 of 622) (relative risk, 1.12; 95% CI, 0.94 to 1.32; P=0.21). Mortality was increased with the lower-oxygen-saturation target (22.1%, vs. 18.2% with the higher-oxygen-saturation target; relative risk, 1.25; 95% CI, 1.00 to 1.55; P=0.046). We found no significant differences in the composite outcome of death or neurodevelopmental impairment among extremely premature infants randomly assigned to early CPAP or early surfactant administration and to a lower or higher target range of oxygen saturation. (Funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development and the National Heart, Lung, and Blood Institute; SUPPORT ClinicalTrials.gov number, NCT00233324.). JF - The New England journal of medicine AU - Vaucher, Yvonne E AU - Peralta-Carcelen, Myriam AU - Finer, Neil N AU - Carlo, Waldemar A AU - Gantz, Marie G AU - Walsh, Michele C AU - Laptook, Abbot R AU - Yoder, Bradley A AU - Faix, Roger G AU - Das, Abhik AU - Schibler, Kurt AU - Rich, Wade AU - Newman, Nancy S AU - Vohr, Betty R AU - Yolton, Kimberly AU - Heyne, Roy J AU - Wilson-Costello, Deanne E AU - Evans, Patricia W AU - Goldstein, Ricki F AU - Acarregui, Michael J AU - Adams-Chapman, Ira AU - Pappas, Athina AU - Hintz, Susan R AU - Poindexter, Brenda AU - Dusick, Anna M AU - McGowan, Elisabeth C AU - Ehrenkranz, Richard A AU - Bodnar, Anna AU - Bauer, Charles R AU - Fuller, Janell AU - O'Shea, T Michael AU - Myers, Gary J AU - Higgins, Rosemary D AU - SUPPORT Study Group of the Eunice Kennedy Shriver NICHD Neonatal Research Network AD - Department of Pediatrics, University of California at San Diego, San Diego, California 92013, USA. ; SUPPORT Study Group of the Eunice Kennedy Shriver NICHD Neonatal Research Network Y1 - 2012/12/27/ PY - 2012 DA - 2012 Dec 27 SP - 2495 EP - 2504 VL - 367 IS - 26 KW - Pulmonary Surfactants KW - 0 KW - Oxygen KW - S88TT14065 KW - Abridged Index Medicus KW - Index Medicus KW - Oximetry KW - Humans KW - Infant, Newborn KW - Infant Mortality KW - Bronchopulmonary Dysplasia -- epidemiology KW - Outcome Assessment (Health Care) KW - Socioeconomic Factors KW - Retinopathy of Prematurity -- epidemiology KW - Infant KW - Oxygen -- blood KW - Infant, Extremely Low Birth Weight KW - Follow-Up Studies KW - Infant, Extremely Premature KW - Oxygen -- administration & dosage KW - Female KW - Pulmonary Surfactants -- adverse effects KW - Continuous Positive Airway Pressure -- adverse effects KW - Pulmonary Surfactants -- therapeutic use KW - Oxygen Inhalation Therapy -- adverse effects KW - Child Development KW - Developmental Disabilities -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273252910?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Neurodevelopmental+outcomes+in+the+early+CPAP+and+pulse+oximetry+trial.&rft.au=Vaucher%2C+Yvonne+E%3BPeralta-Carcelen%2C+Myriam%3BFiner%2C+Neil+N%3BCarlo%2C+Waldemar+A%3BGantz%2C+Marie+G%3BWalsh%2C+Michele+C%3BLaptook%2C+Abbot+R%3BYoder%2C+Bradley+A%3BFaix%2C+Roger+G%3BDas%2C+Abhik%3BSchibler%2C+Kurt%3BRich%2C+Wade%3BNewman%2C+Nancy+S%3BVohr%2C+Betty+R%3BYolton%2C+Kimberly%3BHeyne%2C+Roy+J%3BWilson-Costello%2C+Deanne+E%3BEvans%2C+Patricia+W%3BGoldstein%2C+Ricki+F%3BAcarregui%2C+Michael+J%3BAdams-Chapman%2C+Ira%3BPappas%2C+Athina%3BHintz%2C+Susan+R%3BPoindexter%2C+Brenda%3BDusick%2C+Anna+M%3BMcGowan%2C+Elisabeth+C%3BEhrenkranz%2C+Richard+A%3BBodnar%2C+Anna%3BBauer%2C+Charles+R%3BFuller%2C+Janell%3BO%27Shea%2C+T+Michael%3BMyers%2C+Gary+J%3BHiggins%2C+Rosemary+D%3BSUPPORT+Study+Group+of+the+Eunice+Kennedy+Shriver+NICHD+Neonatal+Research+Network&rft.aulast=Vaucher&rft.aufirst=Yvonne&rft.date=2012-12-27&rft.volume=367&rft.issue=26&rft.spage=2495&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=1533-4406&rft_id=info:doi/10.1056%2FNEJMoa1208506 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-07 N1 - Date created - 2012-12-27 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00233324; ClinicalTrials.gov N1 - SuppNotes - Cited By: J Pediatr. 2005 Jun;146(6):798-804 [15973322] Pediatrics. 2012 Mar;129(3):480-4 [22371462] Pediatrics. 2010 Jul;126(1):e215-21 [20587676] Childs Nerv Syst. 2010 Sep;26(9):1139-49 [20349187] Cochrane Database Syst Rev. 2010;(12):CD000509 [21154346] BMC Pediatr. 2011;11:6 [21235822] Pediatrics. 2011 Feb;127(2):e414-22 [21220391] Pediatrics. 2000 Jun;105(6):1216-26 [10835060] N Engl J Med. 2000 Aug 10;343(6):378-84 [10933736] Arch Dis Child Fetal Neonatal Ed. 2001 Mar;84(2):F106-10 [11207226] Pediatr Res. 2001 Dec;50(6):712-9 [11726729] J Paediatr Child Health. 2002 Dec;38(6):597-600 [12410874] J Neuropathol Exp Neurol. 2003 May;62(5):441-50 [12769184] J Matern Fetal Neonatal Med. 2003 Sep;14(3):145-6 [14694967] Dev Med Child Neurol. 1997 Apr;39(4):214-23 [9183258] Pediatrics. 2005 Mar;115(3):673-80 [15741371] Arch Ophthalmol. 2005 Mar;123(3):311-8 [15767472] J Pediatr. 2012 Aug;161(2):222-8.e3 [22421261] Pediatrics. 2005 Dec;116(6):1391-400 [16322163] Arch Dis Child Fetal Neonatal Ed. 2006 Sep;91(5):F320-6 [16690640] Dev Med Child Neurol Suppl. 2007 Feb;109:8-14 [17370477] Pediatrics. 2007 Apr;119(4):e860-5 [17339385] Arch Pediatr Adolesc Med. 2007 Jun;161(6):583-90 [17548764] Stat Methods Med Res. 2007 Jun;16(3):199-218 [17621468] Eur J Pediatr. 2008 Jan;167(1):87-95 [17333273] Pediatrics. 2008 Jan;121(1):73-81 [18166559] Pediatrics. 2009 Jan;123(1):313-8 [19117897] N Engl J Med. 2010 May 27;362(21):1959-69 [20472937] N Engl J Med. 2010 May 27;362(21):1970-9 [20472939] Dev Med Child Neurol. 2010 Jun;52(6):e119-25 [20163431] Curr Opin Pediatr. 2011 Apr;23(2):173-8 [21150442] N Engl J Med. 2011 Apr 28;364(17):1680-2 [21524227] Pediatrics. 2011 May;127(5):e1247-57 [21482612] Neonatology. 2011;100(1):1-8 [21150224] Comment In: Z Geburtshilfe Neonatol. 2013 Feb;217(1):5-6 [23556203] Natl Med J India. 2013 May-Jun;26(3):163-5 [24476165] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1056/NEJMoa1208506 ER - TY - JOUR T1 - Evolutionarily conserved protein ERH controls CENP-E mRNA splicing and is required for the survival of KRAS mutant cancer cells. AN - 1273338463; 23236152 AB - Cancers with Ras mutations represent a major therapeutic problem. Recent RNAi screens have uncovered multiple nononcogene addiction pathways that are necessary for the survival of Ras mutant cells. Here, we identify the evolutionarily conserved gene enhancer of rudimentary homolog (ERH), in which depletion causes greater toxicity in cancer cells with mutations in the small GTPase KRAS compared with KRAS WT cells. ERH interacts with the spliceosome protein SNRPD3 and is required for the mRNA splicing of the mitotic motor protein CENP-E. Loss of ERH leads to loss of CENP-E and consequently, chromosome congression defects. Gene expression profiling indicates that ERH is required for the expression of multiple cell cycle genes, and the gene expression signature resulting from ERH down-regulation inversely correlates with KRAS signatures. Clinically, tumor ERH expression is inversely associated with survival of colorectal cancer patients whose tumors harbor KRAS mutations. Together, these findings identify a role of ERH in mRNA splicing and mitosis, and they provide evidence that KRAS mutant cancer cells are dependent on ERH for their survival. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Weng, Meng-Tzu AU - Lee, Jih-Hsiang AU - Wei, Shu-Chen AU - Li, Qiuning AU - Shahamatdar, Sina AU - Hsu, Dennis AU - Schetter, Aaron J AU - Swatkoski, Stephen AU - Mannan, Poonam AU - Garfield, Susan AU - Gucek, Marjan AU - Kim, Marianne K H AU - Annunziata, Christina M AU - Creighton, Chad J AU - Emanuele, Michael J AU - Harris, Curtis C AU - Sheu, Jin-Chuan AU - Giaccone, Giuseppe AU - Luo, Ji AD - Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/12/26/ PY - 2012 DA - 2012 Dec 26 SP - E3659 EP - E3667 VL - 109 IS - 52 KW - Cell Cycle Proteins KW - 0 KW - Chromosomal Proteins, Non-Histone KW - ERH protein, human KW - KRAS protein, human KW - Proto-Oncogene Proteins KW - RNA, Messenger KW - SNRPD3 protein, human KW - Transcription Factors KW - centromere protein E KW - snRNP Core Proteins KW - Proto-Oncogene Proteins p21(ras) KW - EC 3.6.5.2 KW - ras Proteins KW - Index Medicus KW - Chromosomes, Human -- metabolism KW - Cell Survival -- genetics KW - Humans KW - Cell Line, Tumor KW - Colorectal Neoplasms -- genetics KW - RNA, Messenger -- genetics KW - Protein Binding KW - Gene Expression Regulation, Neoplastic KW - Oncogenes KW - RNA, Messenger -- metabolism KW - Colorectal Neoplasms -- pathology KW - Cell Cycle -- genetics KW - snRNP Core Proteins -- metabolism KW - Survival Analysis KW - ras Proteins -- genetics KW - RNA Splicing -- genetics KW - Chromosomal Proteins, Non-Histone -- genetics KW - Conserved Sequence KW - Transcription Factors -- metabolism KW - Mutation -- genetics KW - Proto-Oncogene Proteins -- genetics KW - Chromosomal Proteins, Non-Histone -- metabolism KW - Evolution, Molecular KW - Cell Cycle Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273338463?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Evolutionarily+conserved+protein+ERH+controls+CENP-E+mRNA+splicing+and+is+required+for+the+survival+of+KRAS+mutant+cancer+cells.&rft.au=Weng%2C+Meng-Tzu%3BLee%2C+Jih-Hsiang%3BWei%2C+Shu-Chen%3BLi%2C+Qiuning%3BShahamatdar%2C+Sina%3BHsu%2C+Dennis%3BSchetter%2C+Aaron+J%3BSwatkoski%2C+Stephen%3BMannan%2C+Poonam%3BGarfield%2C+Susan%3BGucek%2C+Marjan%3BKim%2C+Marianne+K+H%3BAnnunziata%2C+Christina+M%3BCreighton%2C+Chad+J%3BEmanuele%2C+Michael+J%3BHarris%2C+Curtis+C%3BSheu%2C+Jin-Chuan%3BGiaccone%2C+Giuseppe%3BLuo%2C+Ji&rft.aulast=Weng&rft.aufirst=Meng-Tzu&rft.date=2012-12-26&rft.volume=109&rft.issue=52&rft.spage=E3659&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.1207673110 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-02-21 N1 - Date created - 2012-12-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nat Rev Cancer. 2011 Nov;11(11):761-74 [21993244] Trends Genet. 2011 Nov;27(11):446-53 [21872963] Nature. 2012 Mar 29;483(7391):603-7 [22460905] Cell. 2012 Apr 27;149(3):642-55 [22541434] Nature. 2012 Jul 19;487(7407):330-7 [22810696] Nucleic Acids Res. 2000 Aug 15;28(16):3003-10 [10931913] Oncogene. 2000 Aug 10;19(34):3948-54 [10951588] J Cell Biol. 2001 Jun 11;153(6):1239-50 [11402067] Nat Biotechnol. 2001 Oct;19(10):940-5 [11581659] Biol Chem. 2001 Sep;382(9):1379-85 [11688721] Dev Cell. 2002 Sep;3(3):351-65 [12361599] J Cell Biol. 2003 Apr 28;161(2):267-80 [12719470] J Cell Biol. 2003 Aug 18;162(4):551-63 [12925705] Cancer Cell. 2003 Aug;4(2):111-20 [12957286] Mol Cell. 2003 Nov;12(5):1187-200 [14636577] J Cell Sci. 2004 Mar 15;117(Pt 8):1577-89 [15020684] Cancer Cell. 2004 Apr;5(4):375-87 [15093544] Nature. 1992 Oct 8;359(6395):536-9 [1406971] Science. 1993 Apr 2;260(5104):85-8 [8465203] Proc Natl Acad Sci U S A. 1994 May 24;91(11):5124-8 [8197195] Proc Natl Acad Sci U S A. 1994 Dec 6;91(25):12317-21 [7527560] Genetics. 1994 Dec;138(4):1163-70 [7896098] Science. 1997 Jul 25;277(5325):574-8 [9228009] J Cell Biol. 1997 Dec 15;139(6):1373-82 [9396744] FEBS Lett. 2005 Jan 31;579(3):683-9 [15670829] Cancer Cell. 2005 Jun;7(6):561-73 [15950905] FEBS J. 2006 Oct;273(20):4728-41 [16984396] Mol Cancer Ther. 2007 Jan;6(1):269-76 [17237286] Nat Rev Mol Cell Biol. 2007 May;8(5):379-93 [17426725] Mol Biol Cell. 2007 Jun;18(6):2216-25 [17409356] Clin Cancer Res. 2007 Jun 15;13(12):3682-8 [17575233] Proteins. 2007 Aug 1;68(2):427-37 [17444515] Nat Cell Biol. 2007 Dec;9(12):1401-12 [17994010] FEBS J. 2008 Jan;275(2):332-40 [18081865] Cancer Res. 2008 May 1;68(9):3077-80; discussion 3080 [18451130] Oncogene. 2008 May 15;27(22):3122-33 [18071315] Nat Rev Mol Cell Biol. 2008 Jul;9(7):517-31 [18568040] Curr Opin Genet Dev. 2009 Feb;19(1):74-81 [19195877] Cell. 2009 Mar 6;136(5):823-37 [19269363] Cancer Cell. 2009 Jun 2;15(6):489-500 [19477428] Cell. 2009 May 29;137(5):821-34 [19490892] Cell. 2009 May 29;137(5):835-48 [19490893] J Clin Oncol. 2009 Jun 10;27(17):2793-9 [19414676] Oncogene. 2009 Aug 6;28(31):2773-83 [19525976] Nature. 2009 Nov 5;462(7269):108-12 [19847166] J Proteome Res. 2010 Jan;9(1):556-63 [19928837] Nature. 2010 Apr 1;464(7289):721-7 [20360735] Cell Mol Life Sci. 2010 Jul;67(13):2145-61 [20232224] Nat Rev Genet. 2008 Sep;9(9):699-712 [18679436] Genes Dev. 2010 Jul 1;24(13):1434-47 [20595234] Cell. 2010 Aug 6;142(3):444-55 [20691903] J Clin Invest. 2010 Nov;120(11):3940-52 [20972333] Mol Cell. 2011 Apr 22;42(2):185-98 [21504830] Cold Spring Harb Perspect Biol. 2011 Jul;3(7). pii: a003707. doi: 10.1101/cshperspect.a003707 [21441581] Nucleus. 2010 Nov-Dec;1(6):447-59 [21327086] Proc Natl Acad Sci U S A. 2011 Oct 4;108(40):16759-64 [21940503] Cancer Res. 2012 Jan 1;72(1):100-11 [22080568] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1073/pnas.1207673110 ER - TY - JOUR T1 - Occupational trichloroethylene exposure and kidney cancer risk: a meta-analysis AN - 1551613814; 20363752 AB - ObjectivesInconsistent epidemiological findings, debate over interpretation, and extrapolation of findings from animal studies to humans have produced uncertainty surrounding the carcinogenicity of trichloroethylene (TCE) exposure in occupational settings. We updated meta-analyses of published case-control and cohort studies exploring occupational TCE exposure and kidney cancer risk, incorporating new analytical results from three recently published cohort studies and a case-control study.MethodsPubMed MEDLINE was searched for studies published from 1950 to 2011 assessing occupational exposure to chlorinated solvents, degreasers or TCE. All cohort (N=15) and case-control (N=13) studies included in analyses were stratified by assessment of occupational exposure to TCE specifically and to any chlorinated solvent.ResultsSignificantly elevated summary estimates were observed for cohort studies (relative risk (RR) 1.26, 95% CI 1.02 to 1.56; p heterogeneity=0.65), case-control studies (OR 1.35, 95% CI 1.17 to 1.57; p heterogeneity=0.41), and cohort and case-control studies combined (RR 1.32, 95% CI 1.17 to 1.50, p heterogeneity=0.63) that specifically assessed TCE exposure after excluding outlier studies that contributed to heterogeneity. Non-significantly elevated summary estimates were generally observed for studies of workers exposed to chlorinated solvents but who were not assessed for TCE specifically.ConclusionsRegardless of study design, significant and stronger estimates were only observed in studies specifically assessing occupational exposure to TCE. Estimates were lower in studies assessing occupational exposure to chlorinated solvents. This updated meta-analysis supports an association between occupational TCE exposure and kidney cancer and provides evidence that exposure misclassification may weaken estimates assessing exposure to the broader class of chlorinated solvents. JF - Occupational and Environmental Medicine AU - Karami, Sara AU - Lan, Qing AU - Rothman, Nathaniel AU - Stewart, Patricia A AU - Lee, Kyoung-Mu AU - Vermeulen, Roel AU - Moore, Lee E AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA Y1 - 2012/12/20/ PY - 2012 DA - 2012 Dec 20 SP - 858 EP - 867 PB - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom VL - 69 IS - 12 SN - 1351-0711, 1351-0711 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Risk assessment KW - Health risks KW - Carcinogenicity KW - Solvents KW - Kidney KW - Trichloroethylene KW - Occupational exposure KW - Cancer KW - R2 23060:Medical and environmental health KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551613814?accountid=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=Occupational+and+Environmental+Medicine&rft.atitle=Occupational+trichloroethylene+exposure+and+kidney+cancer+risk%3A+a+meta-analysis&rft.au=Karami%2C+Sara%3BLan%2C+Qing%3BRothman%2C+Nathaniel%3BStewart%2C+Patricia+A%3BLee%2C+Kyoung-Mu%3BVermeulen%2C+Roel%3BMoore%2C+Lee+E&rft.aulast=Karami&rft.aufirst=Sara&rft.date=2012-12-20&rft.volume=69&rft.issue=12&rft.spage=858&rft.isbn=&rft.btitle=&rft.title=Occupational+and+Environmental+Medicine&rft.issn=13510711&rft_id=info:doi/10.1136%2Foemed-2012-100932 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2015-03-20 N1 - SubjectsTermNotLitGenreText - Risk assessment; Health risks; Carcinogenicity; Kidney; Solvents; Trichloroethylene; Cancer; Occupational exposure DO - http://dx.doi.org/10.1136/oemed-2012-100932 ER - TY - JOUR T1 - Circulating Carotenoids and Risk of Breast Cancer: Pooled Analysis of Eight Prospective Studies AN - 1272707515; 17516024 AB - Background Carotenoids, micronutrients in fruits and vegetables, may reduce breast cancer risk. Most, but not all, past studies of circulating carotenoids and breast cancer have found an inverse association with at least one carotenoid, although the specific carotenoid has varied across studies. Methods We conducted a pooled analysis of eight cohort studies comprising more than 80% of the world's published prospective data on plasma or serum carotenoids and breast cancer, including 3055 case subjects and 3956 matched control subjects. To account for laboratory differences and examine population differences across studies, we recalibrated participant carotenoid levels to a common standard by reassaying 20 plasma or serum samples from each cohort together at the same laboratory. Using conditional logistic regression, adjusting for several breast cancer risk factors, we calculated relative risks (RRs) and 95% confidence intervals (CIs) using quintiles defined among the control subjects from all studies. All P values are two-sided. Results Statistically significant inverse associations with breast cancer were observed for alpha -carotene (top vs bottom quintile RR = 0.87, 95% CI = 0.71 to 1.05, Ptrend = .04), beta -carotene (RR = 0.83, 95% CI = 0.70 to 0.98, Ptrend = .02), lutein+zeaxanthin (RR = 0.84, 95% CI = 0.70 to 1.01, Ptrend = .05), lycopene (RR = 0.78, 95% CI = 0.62 to 0.99, Ptrend = .02), and total carotenoids (RR = 0.81, 95% CI = 0.68 to 0.96, Ptrend = .01). beta -Cryptoxanthin was not statistically significantly associated with risk. Tests for heterogeneity across studies were not statistically significant. For several carotenoids, associations appeared stronger for estrogen receptor negative (ER super(-)) than for ER super(+) tumors (eg, beta -carotene: ER super(-): top vs bottom quintile RR = 0.52, 95% CI = 0.36 to 0.77, Ptrend = .001; ER super(+): RR = 0.83, 95% CI = 0.66 to 1.04, Ptrend = .06; Pheterogeneity = .01). Conclusions This comprehensive prospective analysis suggests women with higher circulating levels of alpha -carotene, beta -carotene, lutein+zeaxanthin, lycopene, and total carotenoids may be at reduced risk of breast cancer. JF - Journal of the National Cancer Institute AU - Eliassen, AHeather AU - Hendrickson, Sara J AU - Brinton, Louise A AU - Buring, Julie E AU - Campos, Hannia AU - Dai, Qi AU - Dorgan, Joanne F AU - Franke, Adrian A AU - Gao, Yu-tang AU - Goodman, Marc T AU - Hallmans, Goran AU - Helzlsouer, Kathy J AU - Hoffman-Bolton, Judy AU - Hulten, Kerstin AU - Sesso, Howard D AU - Sowell, Anne L AU - Tamimi, Rulla M AU - Toniolo, Paolo AU - Wilkens, Lynne R AU - Winkvist, Anna AU - Zeleniuch-Jacquotte, Anne AU - Zheng, Wei AU - Hankinson, Susan E AD - Affiliations of authors: Channing Division of Network Medicine (AHE, RMT, SEH) and Division of Preventive Medicine (JEB, HDS), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA; Department of Epidemiology (AHE, SJH, RMT, SEH) and Department of Nutrition (SJH, HC), Harvard School of Public Health, Boston, MA; Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD (LAB); Vanderbilt University School of Medicine, Nashville, TN (QD, WZ); Fox Chase Cancer Center, Philadelphia, PA (JFD); University of Hawaii Cancer Center, Honolulu, HI (AAF, MTG, LRW); Shanghai Cancer Institute, Shanghai, China (Y-tG); Department of Public Health and Clinical Medicine, Umea University, Umea, Sweden (GH, KH); George W. Comstock Center for Public Health Research and Prevention, Johns Hopkins University, Bloomberg School of Public Health, Baltimore, MD (KJH, JH-B); The Prevention and R, heather.eliassen@channing.harvard.edu Y1 - 2012/12/19/ PY - 2012 DA - 2012 Dec 19 SP - 1905 EP - 1916 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 104 IS - 24 SN - 0027-8874, 0027-8874 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Breast cancer KW - Cancer KW - Estrogens KW - Fruits KW - Micronutrients KW - Risk factors KW - Risk reduction KW - Tumors 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/1272707515?accountid=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+the+National+Cancer+Institute&rft.atitle=Circulating+Carotenoids+and+Risk+of+Breast+Cancer%3A+Pooled+Analysis+of+Eight+Prospective+Studies&rft.au=Eliassen%2C+AHeather%3BHendrickson%2C+Sara+J%3BBrinton%2C+Louise+A%3BBuring%2C+Julie+E%3BCampos%2C+Hannia%3BDai%2C+Qi%3BDorgan%2C+Joanne+F%3BFranke%2C+Adrian+A%3BGao%2C+Yu-tang%3BGoodman%2C+Marc+T%3BHallmans%2C+Goran%3BHelzlsouer%2C+Kathy+J%3BHoffman-Bolton%2C+Judy%3BHulten%2C+Kerstin%3BSesso%2C+Howard+D%3BSowell%2C+Anne+L%3BTamimi%2C+Rulla+M%3BToniolo%2C+Paolo%3BWilkens%2C+Lynne+R%3BWinkvist%2C+Anna%3BZeleniuch-Jacquotte%2C+Anne%3BZheng%2C+Wei%3BHankinson%2C+Susan+E&rft.aulast=Eliassen&rft.aufirst=AHeather&rft.date=2012-12-19&rft.volume=104&rft.issue=24&rft.spage=1905&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/10.1093%2Fjnci%2Fdjs461 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-01-01 N1 - Last updated - 2013-02-22 N1 - SubjectsTermNotLitGenreText - Fruits; Estrogens; Risk factors; Breast cancer; Micronutrients; Tumors; Risk reduction; Cancer DO - http://dx.doi.org/10.1093/jnci/djs461 ER - TY - JOUR T1 - Significant variation in the concentration of carcinogenic polycyclic aromatic hydrocarbons in yerba maté samples by brand, batch, and processing method. AN - 1240903599; 23101992 AB - Drinking maté, common in southern South America, may increase the risk of esophageal squamous cell carcinoma (ESCC). In 2006, we found high but variable polycyclic aromatic hydrocarbon (PAH) content in commercial yerba maté samples from eight Brazilian brands. The PAH content of new samples from the same brands, purchased in 2008, and four brands from a single manufacturer processed in different ways, obtained in 2010, were quantified to determine whether PAH concentration was still high, whether PAH content variation was brand specific, and whether processing method affects PAH content of commercial yerba maté. Concentrations of individual PAHs were quantified using gas chromatography/mass spectrometry with deuterated PAHs as internal standards. Median total PAH concentration was 1500 ng/g (range: 625-3710 ng/g) and 1090 ng/g (621-1990 ng/g) in 2008 and 2010 samples, respectively. Comparing 2006 and 2008 samples, some brands had high PAH concentrations in both years, while PAH concentration changed considerably in others. Benzo[a]pyrene concentrations ranged from 11.9 to 99.3 ng/g and 5.11 to 21.0 ng/g in 2008 and 2010 samples, respectively. The 2010 sample processed without touching smoke had the lowest benzo[a]pyrene content. These results support previous findings of very high total and carcinogenic PAH concentrations in yerba maté, perhaps contributing to the high incidence of ESCC in southern South America. The large PAH content variation by brand, batch, and processing method suggests it may be possible to reduce the content of carcinogenic PAHs in commercial yerba maté, making it a healthier beverage. JF - Environmental science & technology AU - Golozar, Asieh AU - Fagundes, Renato B AU - Etemadi, Arash AU - Schantz, Michele M AU - Kamangar, Farin AU - Abnet, Christian C AU - Dawsey, Sanford M AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA. Y1 - 2012/12/18/ PY - 2012 DA - 2012 Dec 18 SP - 13488 EP - 13493 VL - 46 IS - 24 KW - Carcinogens KW - 0 KW - Polycyclic Aromatic Hydrocarbons KW - Benzo(a)pyrene KW - 3417WMA06D KW - Index Medicus KW - Brazil KW - Plant Leaves -- chemistry KW - Benzo(a)pyrene -- analysis KW - Polycyclic Aromatic Hydrocarbons -- analysis KW - Food Handling KW - Ilex paraguariensis -- chemistry KW - Carcinogens -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1240903599?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+science+%26+technology&rft.atitle=Significant+variation+in+the+concentration+of+carcinogenic+polycyclic+aromatic+hydrocarbons+in+yerba+mat%C3%A9+samples+by+brand%2C+batch%2C+and+processing+method.&rft.au=Golozar%2C+Asieh%3BFagundes%2C+Renato+B%3BEtemadi%2C+Arash%3BSchantz%2C+Michele+M%3BKamangar%2C+Farin%3BAbnet%2C+Christian+C%3BDawsey%2C+Sanford+M&rft.aulast=Golozar&rft.aufirst=Asieh&rft.date=2012-12-18&rft.volume=46&rft.issue=24&rft.spage=13488&rft.isbn=&rft.btitle=&rft.title=Environmental+science+%26+technology&rft.issn=1520-5851&rft_id=info:doi/10.1021%2Fes303494s LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-06-04 N1 - Date created - 2012-12-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Epidemiol Biomarkers Prev. 2003 Jun;12(6):508-13 [12814995] BMC Cancer. 2002 Dec 26;2:36 [12502433] Int J Cancer. 1987 Jun 15;39(6):710-6 [3583451] Carcinogenesis. 1990 Jul;11(7):1241-3 [2372884] Carcinogenesis. 1995 May;16(5):1079-85 [7767968] Eur J Cancer. 1998 Apr;34(5):757-8 [9713287] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078] Anticancer Res. 2005 Jan-Feb;25(1B):425-8 [15816606] Epidemiology. 2005 Nov;16(6):744-50 [16222163] BMC Cancer. 2006;6:139 [16729889] Arch Iran Med. 2007 Jan;10(1):70-82 [17198458] J Food Sci. 2007 Nov;72(9):R138-51 [18034743] Cancer Epidemiol Biomarkers Prev. 2008 May;17(5):1262-8 [18483349] Gastroenterol Clin North Am. 2009 Mar;38(1):27-57, vii [19327566] Int J Cancer. 2009 Aug 1;125(3):491-524 [19415743] Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2010 Jun;27(6):776-82 [20349373] J Ethnopharmacol. 2011 Jul 14;136(3):378-84 [20599603] Int J Cancer. 2000 Nov 15;88(4):658-64 [11058886] Regul Toxicol Pharmacol. 2002 Apr;35(2 Pt 1):142-56 [12052000] Mutat Res. 2003 Nov;544(2-3):365-73 [14644339] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1021/es303494s ER - TY - JOUR T1 - HER2-Associated Radioresistance of Breast Cancer Stem Cells Isolated from HER2-Negative Breast Cancer Cells AN - 1668252186; 20318798 AB - Purpose: To understand the role of HER2-associated signaling network in breast cancer stem cells (BCSC) using radioresistant breast cancer cells and clinical recurrent breast cancers to evaluate HER2-targeted therapy as a tumor eliminating strategy for recurrent HER2-/low breast cancers.Experimental Design: HER2-expressing BCSCs (HER2+/CD44+/CD24-/low) were isolated from radiation-treated breast cancer MCF7 cells and in vivo irradiated MCF7 xenograft tumors. Tumor aggressiveness and radioresistance were analyzed by gap filling, Matrigel invasion, tumor-sphere formation, and clonogenic survival assays. The HER2/CD44 feature was analyzed in 40 primary and recurrent breast cancer specimens. Protein expression profiling in HER2+/CD44+/CD24-/low versus HER2-/CD44+/CD24-/low BCSCs was conducted with two-dimensional difference gel electrophoresis (2-D DIGE) and high-performance liquid chromatography tandem mass spectrometry (HPLC/MS-MS) analysis and HER2-mediated signaling network was generated by MetaCore program.Results: Compared with HER2-negative BCSCs, HER2+/CD44+/CD24-/low cells showed elevated aldehyde dehydrogenase (ALDH) activity and aggressiveness tested by Matrigel invasion, tumor sphere formation, and in vivo tumorigenesis. The enhanced aggressive phenotype and radioresistance of the HER2+/CD44+/CD24-/low cells were markedly reduced by inhibition of HER2 via siRNA or Herceptin treatments. Clinical breast cancer specimens revealed that cells coexpressing HER2 and CD44 were more frequently detected in recurrent (84.6%) than primary tumors (57.1%). In addition, 2-D DIGE and HPLC/MS-MS of HER2+/CD44+/CD24-/low versus HER2-/CD44+/CD24-/low BCSCs reported a unique HER2-associated protein profile including effectors involved in tumor metastasis, apoptosis, mitochondrial function, and DNA repair. A specific feature of HER2-STAT3 network was identified.Conclusion: This study provides the evidence that HER2-mediated prosurvival signaling network is responsible for the aggressive phenotype of BCSCs that could be targeted to control the therapy-resistant HER2-/low breast cancer. Clin Cancer Res; 18(24); 6634-47. [copy2012 AACR. JF - Clinical Cancer Research AU - Duru, Nadire AU - Fan, Ming AU - Candas, Demet AU - Menaa, Cheikh AU - Liu, Hsin-Chen AU - Nantajit, Danupon AU - Wen, Yunfei AU - Xiao, Kai AU - Eldridge, Angela AU - Chromy, Brett A AU - Li, Shiyong AU - Spitz, Douglas R AU - Lam, Kit S AU - Wicha, Max S AU - Li, Jian Jian AD - Departments of Radiation Oncology, Biochemistry and Molecular Medicine, and Pathology and Laboratory Medicine, University of California Davis School of Medicine; NCI-Designated Comprehensive Cancer Center, University of California Davis, Sacramento; Physical and Life Sciences Directorate, Lawrence Livermore National Laboratory, Livermore, California; Department of Gynecologic Oncology, MD Anderson Cancer Center, University of Texas, Houston, Texas; Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia; Free Radical and Radiation Biology Program, Department of Radiation Oncology, Holden Comprehensive Cancer Center, The University of Iowa, Iowa City, Iowa; and University of Michigan Comprehensive Cancer Center, Ann Arbor, Michigan Y1 - 2012/12/15/ PY - 2012 DA - 2012 Dec 15 SP - 6634 EP - 6647 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 18 IS - 24 SN - 1078-0432, 1078-0432 KW - Biotechnology and Bioengineering Abstracts KW - High-performance liquid chromatography KW - ErbB-2 protein KW - Apoptosis KW - CD44 antigen KW - Tumorigenesis KW - Mitochondria KW - DNA repair KW - Gel electrophoresis KW - Mass spectroscopy KW - Metastases KW - Stem cells KW - siRNA KW - Breast cancer KW - Xenografts KW - Radioresistance KW - Aldehyde dehydrogenase KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668252186?accountid=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=HER2-Associated+Radioresistance+of+Breast+Cancer+Stem+Cells+Isolated+from+HER2-Negative+Breast+Cancer+Cells&rft.au=Duru%2C+Nadire%3BFan%2C+Ming%3BCandas%2C+Demet%3BMenaa%2C+Cheikh%3BLiu%2C+Hsin-Chen%3BNantajit%2C+Danupon%3BWen%2C+Yunfei%3BXiao%2C+Kai%3BEldridge%2C+Angela%3BChromy%2C+Brett+A%3BLi%2C+Shiyong%3BSpitz%2C+Douglas+R%3BLam%2C+Kit+S%3BWicha%2C+Max+S%3BLi%2C+Jian+Jian&rft.aulast=Duru&rft.aufirst=Nadire&rft.date=2012-12-15&rft.volume=18&rft.issue=24&rft.spage=6634&rft.isbn=&rft.btitle=&rft.title=Clinical+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-12-1436 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-04-02 N1 - SubjectsTermNotLitGenreText - High-performance liquid chromatography; Apoptosis; ErbB-2 protein; CD44 antigen; Tumorigenesis; Mitochondria; DNA repair; Mass spectroscopy; Gel electrophoresis; Metastases; Stem cells; siRNA; Breast cancer; Radioresistance; Xenografts; Aldehyde dehydrogenase DO - http://dx.doi.org/10.1158/1078-0432.CCR-12-1436 ER - TY - CPAPER T1 - Direct imaging of sterol-enriched micro-domains that segregate vacuolar membrane proteins T2 - 2012 Annual Meeting of the American Society for Cell Biology (ASCB 2012) AN - 1313114650; 6188265 JF - 2012 Annual Meeting of the American Society for Cell Biology (ASCB 2012) AU - Toulmay, A AU - Prinz, W Y1 - 2012/12/15/ PY - 2012 DA - 2012 Dec 15 KW - Membrane proteins KW - Imaging techniques UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313114650?accountid=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=2012+Annual+Meeting+of+the+American+Society+for+Cell+Biology+%28ASCB+2012%29&rft.atitle=Direct+imaging+of+sterol-enriched+micro-domains+that+segregate+vacuolar+membrane+proteins&rft.au=Toulmay%2C+A%3BPrinz%2C+W&rft.aulast=Toulmay&rft.aufirst=A&rft.date=2012-12-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Annual+Meeting+of+the+American+Society+for+Cell+Biology+%28ASCB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://ascb.org/meetings/files/program/2012-AM-Program-Web.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Is Translocation of Actin Filaments by Myosin Essential for Cytokinesis? T2 - 2012 Annual Meeting of the American Society for Cell Biology (ASCB 2012) AN - 1313111856; 6188080 JF - 2012 Annual Meeting of the American Society for Cell Biology (ASCB 2012) AU - Ma, Xuefei AU - Adelstein, Bob Y1 - 2012/12/15/ PY - 2012 DA - 2012 Dec 15 KW - Translocation KW - Myosin KW - Actin KW - Cytokinesis KW - Filaments UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313111856?accountid=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=article&rft.jtitle=PloS+one&rft.atitle=Development+and+validation+of+an+immunoassay+for+quantification+of+topoisomerase+I+in+solid+tumor+tissues.&rft.au=Pfister%2C+Thomas+D%3BHollingshead%2C+Melinda%3BKinders%2C+Robert+J%3BZhang%2C+Yiping%3BEvrard%2C+Yvonne+A%3BJi%2C+Jiuping%3BKhin%2C+Sonny+A%3BBorgel%2C+Suzanne%3BStotler%2C+Howard%3BCarter%2C+John%3BDivelbiss%2C+Raymond%3BKummar%2C+Shivaani%3BPommier%2C+Yves%3BParchment%2C+Ralph+E%3BTomaszewski%2C+Joseph+E%3BDoroshow%2C+James+H&rft.aulast=Pfister&rft.aufirst=Thomas&rft.date=2012-01-01&rft.volume=7&rft.issue=12&rft.spage=e50494&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0050494 L2 - http://ascb.org/meetings/files/program/2012-AM-Program-Web.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Causes and Consequences of Chromosomal Aneuploidy in Cancer Cells T2 - 2012 Annual Meeting of the American Society for Cell Biology (ASCB 2012) AN - 1313107488; 6187961 JF - 2012 Annual Meeting of the American Society for Cell Biology (ASCB 2012) AU - Ried, Thomas Y1 - 2012/12/15/ PY - 2012 DA - 2012 Dec 15 KW - Cancer KW - Chromosomes KW - Aneuploidy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313107488?accountid=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=2012+Annual+Meeting+of+the+American+Society+for+Cell+Biology+%28ASCB+2012%29&rft.atitle=Causes+and+Consequences+of+Chromosomal+Aneuploidy+in+Cancer+Cells&rft.au=Ried%2C+Thomas&rft.aulast=Ried&rft.aufirst=Thomas&rft.date=2012-12-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Annual+Meeting+of+the+American+Society+for+Cell+Biology+%28ASCB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://ascb.org/meetings/files/program/2012-AM-Program-Web.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Biochemical Reconstitution of the ESCRT Complex Assembly at HIV-1 Budding Sites T2 - 2012 Annual Meeting of the American Society for Cell Biology (ASCB 2012) AN - 1313107132; 6188071 JF - 2012 Annual Meeting of the American Society for Cell Biology (ASCB 2012) AU - Carlson, Lars-Anders Y1 - 2012/12/15/ PY - 2012 DA - 2012 Dec 15 KW - Biochemistry KW - Budding KW - Human immunodeficiency virus 1 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313107132?accountid=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=2012+Annual+Meeting+of+the+American+Society+for+Cell+Biology+%28ASCB+2012%29&rft.atitle=Biochemical+Reconstitution+of+the+ESCRT+Complex+Assembly+at+HIV-1+Budding+Sites&rft.au=Carlson%2C+Lars-Anders&rft.aulast=Carlson&rft.aufirst=Lars-Anders&rft.date=2012-12-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Annual+Meeting+of+the+American+Society+for+Cell+Biology+%28ASCB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://ascb.org/meetings/files/program/2012-AM-Program-Web.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Lysosomes as novel regulators of gene expression, organelle biogenesis, and autophagy induction T2 - 2012 Annual Meeting of the American Society for Cell Biology (ASCB 2012) AN - 1313106598; 6188163 JF - 2012 Annual Meeting of the American Society for Cell Biology (ASCB 2012) AU - Martina, J AU - Puertollano, R Y1 - 2012/12/15/ PY - 2012 DA - 2012 Dec 15 KW - Gene expression KW - Biogenesis KW - Lysosomes KW - Organelles KW - Phagocytosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313106598?accountid=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=2012+Annual+Meeting+of+the+American+Society+for+Cell+Biology+%28ASCB+2012%29&rft.atitle=Lysosomes+as+novel+regulators+of+gene+expression%2C+organelle+biogenesis%2C+and+autophagy+induction&rft.au=Martina%2C+J%3BPuertollano%2C+R&rft.aulast=Martina&rft.aufirst=J&rft.date=2012-12-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Annual+Meeting+of+the+American+Society+for+Cell+Biology+%28ASCB+2012%29&rft.issn=&rft_id=info:doi/10.1186%2F1743-8977-9-20 L2 - http://ascb.org/meetings/files/program/2012-AM-Program-Web.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Visualizing Cell Structure and Dynamics with Point-Localization Super-Resolution Microscopy T2 - 2012 Annual Meeting of the American Society for Cell Biology (ASCB 2012) AN - 1313077602; 6188011 JF - 2012 Annual Meeting of the American Society for Cell Biology (ASCB 2012) AU - Sengupta, Prabuddha AU - Lippincott-Schwartz, Jennifer Y1 - 2012/12/15/ PY - 2012 DA - 2012 Dec 15 KW - Microscopy KW - Cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313077602?accountid=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=2012+Annual+Meeting+of+the+American+Society+for+Cell+Biology+%28ASCB+2012%29&rft.atitle=Visualizing+Cell+Structure+and+Dynamics+with+Point-Localization+Super-Resolution+Microscopy&rft.au=Sengupta%2C+Prabuddha%3BLippincott-Schwartz%2C+Jennifer&rft.aulast=Sengupta&rft.aufirst=Prabuddha&rft.date=2012-12-15&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Annual+Meeting+of+the+American+Society+for+Cell+Biology+%28ASCB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://ascb.org/meetings/files/program/2012-AM-Program-Web.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Effectiveness of a simple rapid human papillomavirus DNA test in rural Nigeria. AN - 1114952317; 22473652 AB - Success of the new human papillomavirus (HPV) DNA test for low-resource settings (careHPV™ test; QIAGEN Gaithersburg Inc., Gaithersburg, MD) requires good test performance when operated by personnel with limited laboratory experience. We evaluated the transferability, reliability, and accuracy of the careHPV test nested within a cervical screening project in a large Nigerian village. CareHPV testing was performed on screen-positive (n = 345) and screen-negative (n = 42) women attending colposcopy (68.3% of referred). Biopsies of abnormal-appearing areas were processed and read in the U.S. CareHPV specimens taken immediately before colposcopy were processed up to four times (in the field) by two secondary school graduates without laboratory experience, trained for this study. Specifically, QIAGEN Gaithersburg trained a laboratory-inexperienced U.S. researcher, who trained the first local technician who, in turn, trained the second. Residual specimens were sent to the U.S. for MY09/MY11 PCR testing for 13 carcinogenic genotypes (HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68) plus HPV66 (included in careHPV). Intrarater agreement was 98.8% (κ = 0.97) and 98.9% (κ = 0.97) for Technicians 1 and 2, respectively, while inter-rater agreement was 96.3% (κ = 0.90). Agreement with MY09/MY11 PCR (virologic reference standard) was 89.3% (κ = 0.73) with 74.2% sensitivity and 95.7% specificity. The careHPV test detected 12 (80%) of 15 histologically confirmed cervical intraepithelial neoplasia Grade 2 (CIN2) or worse lesions, with an estimated 83.0% specificity to detect 98 %) than the bromo precursor (20-52 %). After intravenous administration of [ super(11)C]SP203 into three rhesus monkeys, radioactivity peaked early in brain (average 12.5 min) with a regional distribution in rank order of expected mGluR5 density. Peak uptake was followed by a steady decline. No radioactivity accumulated in the skull. In monkeys pretreated with MTEP before [ super(11)C]SP203 administration, radioactivity uptake in brain was again high but then declined more rapidly than in the baseline scan to a common low level. [ super(11)C]SP203 was unstable in monkey blood in vitro and in vivo, and gave predominantly less lipophilic radiometabolites. By contrast, [ super(11)C]SP203 was stable in human blood in vitro. Conclusion: [ super(11)C]SP203 emulates [ super(18)F]SP203 with regard to providing a sizeable mGluR5-specific signal in monkey brain, and advantageously avoids troublesome accumulation of radioactivity in bone. Although [ super(11)C]SP203 is unsuitable for mGluR5 quantification in monkey brain, its evaluation as a PET radioligand for studying human brain mGluR5 is nevertheless warranted. JF - European Journal of Nuclear Medicine and Molecular Imaging AU - Simeon, Fabrice G AU - Liow, Jeih-San AU - Zhang, Yi AU - Hong, Jinsoo AU - Gladding, Robert L AU - Zoghbi, Sami S AU - Innis, Robert B AU - Pike, Victor W AD - Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, Building 10, Rm. B3 C346A, 10 Center Drive, Bethesda, MD, 20892, USA, pikev@mail.nih.gov Y1 - 2012/12// PY - 2012 DA - Dec 2012 SP - 1949 EP - 1958 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 39 IS - 12 SN - 1619-7070, 1619-7070 KW - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts KW - High-performance liquid chromatography KW - Intravenous administration KW - Neuroimaging KW - Glutamic acid receptors (metabotropic) KW - Brain KW - Lipophilic KW - Bone KW - Blood KW - Skull KW - Scanning KW - Positron emission tomography KW - Radioisotopes KW - Nuclear medicine KW - Macaca mulatta KW - Radioactivity KW - Glutamic acid KW - Metabotropic receptors KW - W 30910:Imaging KW - N3 11145:Methodology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1257756692?accountid=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=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.atitle=Synthesis+and+characterization+in+monkey+of+%5B+super%2811%29C%5DSP203+as+a+radioligand+for+imaging+brain+metabotropic+glutamate+5+receptors&rft.au=Simeon%2C+Fabrice+G%3BLiow%2C+Jeih-San%3BZhang%2C+Yi%3BHong%2C+Jinsoo%3BGladding%2C+Robert+L%3BZoghbi%2C+Sami+S%3BInnis%2C+Robert+B%3BPike%2C+Victor+W&rft.aulast=Simeon&rft.aufirst=Fabrice&rft.date=2012-12-01&rft.volume=39&rft.issue=12&rft.spage=1949&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.issn=16197070&rft_id=info:doi/10.1007%2Fs00259-012-2205-x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-12-01 N1 - Last updated - 2013-08-12 N1 - SubjectsTermNotLitGenreText - High-performance liquid chromatography; Glutamic acid receptors (metabotropic); Neuroimaging; Intravenous administration; Brain; Lipophilic; Bone; Blood; Scanning; Skull; Radioisotopes; Positron emission tomography; Nuclear medicine; Glutamic acid; Radioactivity; Metabotropic receptors; Macaca mulatta DO - http://dx.doi.org/10.1007/s00259-012-2205-x ER - TY - JOUR T1 - Predicting Polyp Location on Optical Colonoscopy From CT Colonography by Minimal-Energy Curve Modeling of the Colonoscope Path AN - 1257747936; 17431067 AB - The ability to accurately locate a polyp found on computed tomographic colonography (CTC) at subsequent optical colonoscopy (OC) is an important task in colorectal cancer screening. We present a method to more accurately match polyp locations at CTC and OC. A colonoscope was modeled as a flexible tube with negligible stretch and minimal strain. The path of the colonoscope was estimated using a minimal-energy curve method. The energy function was defined and optimized by a subdivision scheme. The prediction of polyp locations at OC from CTC was converted to an optimization problem. The prediction performance was evaluated on 134 polyps by comparing the predicted with the true polyp locations at OC. The method can accurately predict polyp locations at OC to within plus or minus 0.5 colonoscope mark (5 cm) for more than 58% of polyps and to within plus or minus 1 colonoscope mark (10 cm) for more than 96% of polyps, significantly improving upon previously published methods. This method can be easily incorporated into routine OC practice and allow the colonoscopist to begin the examination by targeting locations of potential polyps found at CTC. JF - IEEE Transactions on Biomedical Engineering AU - Liu, Jiamin AU - Chang, Kevin W AU - Yao, Jianhua AU - Summers, Ronald M AD - Department of Radiology and Imaging Science, National Institutes of Health, Bethesda, MD, USA Y1 - 2012/12// PY - 2012 DA - Dec 2012 SP - 3531 EP - 3540 PB - Institute of Electrical and Electronics Engineers, Inc., 345 E. 47th St. NY NY 10017-2394 United States VL - 59 IS - 12 SN - 0018-9294, 0018-9294 KW - Biotechnology and Bioengineering Abstracts KW - Energy KW - Computed tomography KW - Colorectal cancer KW - Polyps KW - W 30905:Medical Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1257747936?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Comparison+of+the+cobas+Human+Papillomavirus+%28HPV%29+test+with+the+hybrid+capture+2+and+linear+array+HPV+DNA+tests.&rft.au=Gage%2C+Julia+C%3BSadorra%2C+Mark%3BLamere%2C+Brandon+J%3BKail%2C+Randi%3BAldrich%2C+Carrie%3BKinney%2C+Walter%3BFetterman%2C+Barbara%3BLorey%2C+Thomas%3BSchiffman%2C+Mark%3BCastle%2C+Philip+E%3BPaP+Cohort+Study+Group&rft.aulast=Gage&rft.aufirst=Julia&rft.date=2012-01-01&rft.volume=50&rft.issue=1&rft.spage=61&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+microbiology&rft.issn=1098-660X&rft_id=info:doi/10.1128%2FJCM.05989-11 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-12-01 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Energy; Computed tomography; Colorectal cancer; Polyps DO - http://dx.doi.org/10.1109/TBME.2012.2217960 ER - TY - JOUR T1 - Kyasanur forest disease AN - 1257737452; 17425597 AB - In the spring of 1957, an outbreak of severe disease was documented in people living near the Kyasanur forest in Karnataka state, India, which also affected wild nonhuman primates. Collection of samples from dead animals and the use of classical virological techniques led to the isolation of a previously unrecognized virus, named Kyasanur forest disease virus (KFDV), which was found to be related to the Russian spring-summer encephalitis (RSSE) complex of tick-borne viruses. Further evaluation found that KFD, which frequently took the form of a hemorrhagic syndrome, differed from most other RSSE virus infections, which were characterized by neurologic disease. Its association with illness in wild primates was also unique. Hemaphysalis spinigera was identified as the probable tick vector. Despite an estimated annual incidence in India of 400-500 cases, KFD is historically understudied. Most of what is known about the disease comes from studies in the late 1950s and early 1960s by the Virus Research Center in Pune, India and their collaborators at the Rockefeller Foundation. A report in ProMED in early 2012 indicated that the number of cases of KFD this year is possibly the largest since 2005, reminding us that there are significant gaps in our knowledge of the disease, including many aspects of its pathogenesis, the host response to infection and potential therapeutic options. A vaccine is currently in use in India, but efforts could be made to improve its long-term efficacy. JF - Antiviral Research AU - Holbrook, Michael R AD - NIAID Integrated Research Facility, 8200 Research Plaza, Ft. Detrick, Frederick, MD 21702, United States, michael.holbrook@nih.gov Y1 - 2012/12// PY - 2012 DA - Dec 2012 SP - 353 EP - 362 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 96 IS - 3 SN - 0166-3542, 0166-3542 KW - Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Encephalitis KW - Forests KW - Hemorrhage KW - Infection KW - Neurological diseases KW - Pest outbreaks KW - Vaccines KW - Vectors KW - Ixodidae KW - Kyasanur forest disease virus KW - Primates KW - A 01340:Antibiotics & Antimicrobials KW - V 22400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1257737452?accountid=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=Antiviral+Research&rft.atitle=Kyasanur+forest+disease&rft.au=Holbrook%2C+Michael+R&rft.aulast=Holbrook&rft.aufirst=Michael&rft.date=2012-12-01&rft.volume=96&rft.issue=3&rft.spage=353&rft.isbn=&rft.btitle=&rft.title=Antiviral+Research&rft.issn=01663542&rft_id=info:doi/10.1016%2Fj.antiviral.2012.10.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-12-01 N1 - Last updated - 2013-01-11 N1 - SubjectsTermNotLitGenreText - Neurological diseases; Vectors; Forests; Vaccines; Hemorrhage; Pest outbreaks; Infection; Encephalitis; Ixodidae; Primates; Kyasanur forest disease virus DO - http://dx.doi.org/10.1016/j.antiviral.2012.10.005 ER - TY - JOUR T1 - Prevention of liver carcinogenesis by amarogentin through modulation of G1/S cell cycle check point and induction of apoptosis. AN - 1221848618; 22948180 AB - Amarogentin, a secoiridoid glycoside, is an active component of the medicinal plant Swertia chirata. In this study, chemopreventive and chemotherapeutic actions of amarogentin were evaluated in a carbon tetrachloride (CCl(4))/N-nitrosodiethylamine (NDEA)-induced liver carcinogenesis mouse model system during continuous and posttreatment schedule. Better survival, no toxicity and increased body weight were noted in amarogentin-treated mice. Reduction in proliferation and increase in apoptosis frequency were evident in amarogentin-treated groups. In carcinogen control group moderate dysplasia, severe dysplasia and hepatocellular carcinoma were evident at 10th, 20th and 30th week, respectively. Amarogentin was found to prevent progression of liver carcinogenesis at mild dysplastic stage. Exposure to CCl(4)/NDEA resulted in upregulation of ppRb807/811, cyclinD1 and cdc25A at 10th week and additional activation of cMyc and mdm2 along with downregulation of LIMD1, p53 and p21 at 20th week. This was followed by activation of ppRb567 and downregulation of Rbsp3 at 30th week. Prevention of carcinogenesis by amarogentin in both groups might be due to cumulative upregulation of LIMD1, RBSP3, p16 and downregulation of cdc25A at 10th week along with activation of p53 and p21 and downregulation of ppRb807/811 and ppRb567 at 20th week, followed by downregulation of cyclinD1, cMyc and mdm2 at 30th week. During carcinogenesis reduction of apoptosis was evident since 20th week. However, amarogentin treatment could significantly induce apoptosis through upregulation of the Bax-Bcl2 ratio, activation of caspase-3 and poly ADP ribose polymerase cleavage. This is the first report of chemopreventive/therapeutic role of amarogentin during liver carcinogenesis through modulation of cell cycle and apoptosis. JF - Carcinogenesis AU - Pal, Debolina AU - Sur, Subhayan AU - Mandal, Suvra AU - Das, Ashes AU - Roy, Anup AU - Das, Sukta AU - Panda, Chinmay Kumar AD - Department of Oncogene Regulation, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata 700 026, India. Y1 - 2012/12// PY - 2012 DA - December 2012 SP - 2424 EP - 2431 VL - 33 IS - 12 KW - Iridoids KW - 0 KW - Retinoblastoma Protein KW - amarogentin KW - 5L82GT5I0W KW - Index Medicus KW - Animals KW - Liver -- pathology KW - Phosphorylation KW - Body Weight -- drug effects KW - Retinoblastoma Protein -- metabolism KW - Mice KW - Chemoprevention KW - Cell Proliferation KW - Female KW - S Phase -- drug effects KW - Liver Neoplasms, Experimental -- pathology KW - Liver Neoplasms, Experimental -- mortality KW - Apoptosis -- drug effects KW - Cell Cycle Checkpoints -- drug effects KW - G1 Phase -- drug effects KW - Liver Neoplasms, Experimental -- prevention & control KW - Iridoids -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1221848618?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Prevention+of+liver+carcinogenesis+by+amarogentin+through+modulation+of+G1%2FS+cell+cycle+check+point+and+induction+of+apoptosis.&rft.au=Pal%2C+Debolina%3BSur%2C+Subhayan%3BMandal%2C+Suvra%3BDas%2C+Ashes%3BRoy%2C+Anup%3BDas%2C+Sukta%3BPanda%2C+Chinmay+Kumar&rft.aulast=Pal&rft.aufirst=Debolina&rft.date=2012-12-01&rft.volume=33&rft.issue=12&rft.spage=2424&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgs276 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-03-08 N1 - Date created - 2012-12-03 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/carcin/bgs276 ER - TY - JOUR T1 - Distinct and overlapping genomic profiles and antiviral effects of Interferon- lambda and - alpha on HCV-infected and noninfected hepatoma cells AN - 1221140265; 17372431 AB - Summary. Recently, several SNPs in the region of the IL28B (IFN- lambda ) gene have been associated with spontaneous clearance of hepatitis C virus (HCV) and enhanced cure rates for IFN-alfa-based therapies, suggesting a potential correlation between IFN- lambda and the ability to clear HCV. To understand the mechanism of IFN- lambda 's as compared to IFN- alpha 's antiviral activity, we performed a comprehensive analysis of their anti-HCV effects, whole genome transcriptome profiling with validation, and signalling of IFN- alpha and IFN- lambda using J6/JFH-1 and Huh7.5 cells in vitro. IFN- lambda and IFN- alpha exhibited comparable anti-HCV activity and gene expression profiles in Huh7.5 cells. While the majority of genes induced by IFN- alpha and IFN- lambda were similar, IFN- lambda exhibits profound, but delayed kinetics of IFN-stimulated genes (ISG) induction, while IFN- alpha induced more rapid induction of ISGs. Furthermore, the increased induction of ISG expression by IFN- lambda correlated with up-regulation of IFN- lambda receptor (IL-28RA) expression and more prolonged activation of the Jak-STAT signalling pathway. The findings from our comparative analysis of IFN- alpha and IFN- lambda in HCV-infected and noninfected cells support the clinical use of IFN- lambda as a potential alternative to IFN- alpha in the treatment of chronic hepatitis C. JF - Journal of Viral Hepatitis AU - Kohli, A AU - Zhang, X AU - Yang, J AU - Russell, R S AU - Donnelly, R P AU - Sheikh, F AU - Sherman, A AU - Young, H AU - Imamichi, T AU - Lempicki, R A AU - Masur, H AU - Kottilil, S AD - Laboratory of Immunoregulation, NIAID, NIH, Bethesda, MD, USA Y1 - 2012/12// PY - 2012 DA - Dec 2012 SP - 843 EP - 853 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 19 IS - 12 SN - 1352-0504, 1352-0504 KW - Genetics Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - Gene expression KW - Genomes KW - Hepatoma KW - Hepatitis C virus KW - Single-nucleotide polymorphism KW - Kinetics KW - alpha -Interferon KW - genomics KW - Hepatitis C KW - Antiviral activity KW - Signal transduction KW - G 07720:Immunogenetics KW - A 01340:Antibiotics & Antimicrobials KW - V 22340:Antiviral Agents UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1221140265?accountid=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+Viral+Hepatitis&rft.atitle=Distinct+and+overlapping+genomic+profiles+and+antiviral+effects+of+Interferon-+lambda+and+-+alpha+on+HCV-infected+and+noninfected+hepatoma+cells&rft.au=Kohli%2C+A%3BZhang%2C+X%3BYang%2C+J%3BRussell%2C+R+S%3BDonnelly%2C+R+P%3BSheikh%2C+F%3BSherman%2C+A%3BYoung%2C+H%3BImamichi%2C+T%3BLempicki%2C+R+A%3BMasur%2C+H%3BKottilil%2C+S&rft.aulast=Kohli&rft.aufirst=A&rft.date=2012-12-01&rft.volume=19&rft.issue=12&rft.spage=843&rft.isbn=&rft.btitle=&rft.title=Journal+of+Viral+Hepatitis&rft.issn=13520504&rft_id=info:doi/10.1111%2Fj.1365-2893.2012.01610.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-11-01 N1 - Document feature - figure 5 N1 - Last updated - 2013-10-21 N1 - SubjectsTermNotLitGenreText - Genomes; Gene expression; Hepatoma; Single-nucleotide polymorphism; Kinetics; alpha -Interferon; Hepatitis C; genomics; Antiviral activity; Signal transduction; Hepatitis C virus DO - http://dx.doi.org/10.1111/j.1365-2893.2012.01610.x ER - TY - JOUR T1 - Cardiac complications of unwitting co-injection of quinine/quinidine with heroin in an intravenous drug user. AN - 1221129123; 22592353 AB - Adulterants "cut into" street heroin are common and often not detected by standard urine toxicology screening; however, their unwitting co-injection may have clinical consequences. We report a case of accelerated atrioventricular junctional arrhythmia that we determined to have been caused by quinine/quinidine cut into heroin. While identification and discontinuation of the offending agent helps confirm the diagnosis and is the treatment of choice, this is often complicated by the individual's dependence on the street drug in which the adulterant is mixed. This case highlights the need for clinicians to be aware of common adulterants, to know how to test for them, and to consider them as possible causes of medical complications in individuals who use drugs. JF - Journal of general internal medicine AU - Phillips, Karran A AU - Hirsch, Glenn A AU - Epstein, David H AU - Preston, Kenzie L AD - National Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, 251 Bayview Blvd, Bldg BRC, Suite 200, Baltimore, MD 21224, USA. phillipsk@nida.nih.gov Y1 - 2012/12// PY - 2012 DA - December 2012 SP - 1722 EP - 1725 VL - 27 IS - 12 KW - Quinine KW - A7V27PHC7A KW - Quinidine KW - ITX08688JL KW - Index Medicus KW - Drug Users KW - Drug Contamination KW - Humans KW - Adult KW - Follow-Up Studies KW - Male KW - Risk Assessment KW - Quinine -- adverse effects KW - Arrhythmias, Cardiac -- diagnosis KW - Arrhythmias, Cardiac -- chemically induced KW - Electrocardiography KW - Quinine -- administration & dosage KW - Quinidine -- administration & dosage KW - Substance Abuse, Intravenous -- complications KW - Heroin Dependence -- complications KW - Quinidine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1221129123?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+general+internal+medicine&rft.atitle=Cardiac+complications+of+unwitting+co-injection+of+quinine%2Fquinidine+with+heroin+in+an+intravenous+drug+user.&rft.au=Phillips%2C+Karran+A%3BHirsch%2C+Glenn+A%3BEpstein%2C+David+H%3BPreston%2C+Kenzie+L&rft.aulast=Phillips&rft.aufirst=Karran&rft.date=2012-12-01&rft.volume=27&rft.issue=12&rft.spage=1722&rft.isbn=&rft.btitle=&rft.title=Journal+of+general+internal+medicine&rft.issn=1525-1497&rft_id=info:doi/10.1007%2Fs11606-012-2089-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-06-04 N1 - Date created - 2012-11-29 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Toxicol Lett. 2000 Apr 3;114(1-3):47-53 [10713468] Dermatology. 2011;223(1):25-8 [21846960] J R Soc Med. 1980 Mar;73(3):208-11 [6453230] J Cardiovasc Pharmacol. 1983 Mar-Apr;5(2):173-5 [6188885] N Engl J Med. 1985 May 16;312(20):1273-8 [3887162] Br J Clin Pharmacol. 1993 Mar;35(3):265-71 [8471402] Ann Pharmacother. 1995 Jan;29(1):33-5 [7711344] Circulation. 1995 Nov 15;92(10):2944-50 [7586264] J Emerg Nurs. 1997 Oct;23(5):457-9 [9369611] N Engl J Med. 1998 Jan 1;338(1):35-45 [9414330] J Toxicol Clin Toxicol. 1999;37(4):491-6 [10465247] MMWR Morb Mortal Wkly Rep. 2005 Aug 19;54(32):793-6 [16107783] Lancet Infect Dis. 2007 Aug;7(8):549-58 [17646028] MMWR Morb Mortal Wkly Rep. 2009 Dec 18;58(49):1381-5 [20019655] Drug Test Anal. 2009 Aug;1(8):372-81 [20355217] Cardiovasc Ther. 2010 Aug;28(4):246-53 [20633025] Clin Pharmacol Ther. 2010 Sep;88(3):408-11 [20668440] Drug Test Anal. 2011 Feb;3(2):89-96 [21322119] Drug Alcohol Rev. 2011 Mar;30(2):173-80 [21355903] Drug Alcohol Rev. 2011 Jul;30(4):388-96 [21355918] J Toxicol Clin Toxicol. 2000;38(6):597-608 [11185966] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s11606-012-2089-2 ER - TY - JOUR T1 - Animal models used to examine the role of the environment in the development of autoimmune disease: findings from an NIEHS Expert Panel Workshop. AN - 1220364785; 22748431 AB - Autoimmunity is thought to result from a combination of genetics, environmental triggers, and stochastic events. Environmental factors, such as chemicals, drugs or infectious agents, have been implicated in the expression of autoimmune disease, yet human studies are extremely limited in their ability to test isolated exposures to demonstrate causation or to assess pathogenic mechanisms. In this review we examine the research literature on the ability of chemical, physical and biological agents to induce and/or exacerbate autoimmunity in a variety of animal models. There is no single animal model capable of mimicking the features of human autoimmune disease, particularly as related to environmental exposures. An objective, therefore, was to assess the types of information that can be gleaned from the use of animal models, and how well that information can be used to translate back to human health. Our review notes the importance of genetic background to the types and severity of the autoimmune response following exposure to environmental factors, and emphasizes literature where animal model studies have led to increased confidence about environmental factors that affect expression of autoimmunity. A high level of confidence was reached if there were multiple studies from different laboratories confirming the same findings. Examples include mercury, pristane, and infection with Streptococcus or Coxsackie B virus. A second level of consensus identified those exposures likely to influence autoimmunity but requiring further confirmation. To fit into this category, there needed to be significant supporting data, perhaps by multiple studies from a single laboratory, or repetition of some but not all findings in multiple laboratories. Examples include silica, gold, TCE, TCDD, UV radiation, and Theiler's murine encephalomyelitis virus. With the caveat that researchers must keep in mind the limitations and appropriate applications of the various approaches, animal models are shown to be extremely valuable tools for studying the induction or exacerbation of autoimmunity by environmental conditions and exposures. Copyright © 2012 Elsevier Ltd. All rights reserved. JF - Journal of autoimmunity AU - Germolec, Dori AU - Kono, Dwight H AU - Pfau, Jean C AU - Pollard, K Michael AD - National Toxicology Program, NIEHS, Morrisville, NC 27560, USA. Y1 - 2012/12// PY - 2012 DA - December 2012 SP - 285 EP - 293 VL - 39 IS - 4 KW - Biological Products KW - 0 KW - Environmental Pollutants KW - Index Medicus KW - Rats KW - Animals KW - Reproducibility of Results KW - Models, Immunological KW - Humans KW - Ultraviolet Rays -- adverse effects KW - Disease Models, Animal KW - Mice KW - Congresses as Topic KW - Species Specificity KW - Autoimmune Diseases -- genetics KW - Environmental Pollutants -- toxicity KW - Autoimmune Diseases -- etiology KW - Autoimmunity -- drug effects KW - Biological Products -- toxicity KW - Environmental Exposure -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1220364785?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+autoimmunity&rft.atitle=Animal+models+used+to+examine+the+role+of+the+environment+in+the+development+of+autoimmune+disease%3A+findings+from+an+NIEHS+Expert+Panel+Workshop.&rft.au=Germolec%2C+Dori%3BKono%2C+Dwight+H%3BPfau%2C+Jean+C%3BPollard%2C+K+Michael&rft.aulast=Germolec&rft.aufirst=Dori&rft.date=2012-12-01&rft.volume=39&rft.issue=4&rft.spage=285&rft.isbn=&rft.btitle=&rft.title=Journal+of+autoimmunity&rft.issn=1095-9157&rft_id=info:doi/10.1016%2Fj.jaut.2012.05.020 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-04-25 N1 - Date created - 2012-11-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Crit Rev Immunol. 2001;21(1-3):29-40 [11642611] Autoimmunity. 2001;34(3):193-7 [11908777] Immunol Rev. 2001 Dec;184:184-202 [12086312] J Exp Med. 2002 Jul 1;196(1):135-40 [12093878] Arthritis Rheum. 2002 Aug;46(8):2235-44 [12209530] Environ Health Perspect. 2002 Dec;110(12):1169-73 [12460794] Diabetes Metab Res Rev. 2003 Jan-Feb;19(1):8-31 [12592641] Clin Exp Immunol. 2003 Mar;131(3):415-21 [12605693] Immunol Lett. 2003 Apr 3;86(2):207-12 [12644324] Ind Health. 2003 Jul;41(3):158-66 [12916745] Clin Immunol. 2003 Oct;109(1):72-9 [14585278] Scand J Immunol. 2004 May;59(5):469-77 [15140057] Inhal Toxicol. 2004 Mar;16(3):133-9 [15204774] J Autoimmun. 2004 Nov;23(3):211-20 [15501392] Arch Immunol Ther Exp (Warsz). 2004 Sep-Oct;52(5):316-25 [15507872] Nature. 1982 Aug 12;298(5875):608 [7099259] J Invest Dermatol. 1985 Sep;85(3):181-6 [3897390] Semin Arthritis Rheum. 1985 May;14(4):238-46 [2934818] J Immunol. 1986 Mar 1;136(5):1846-52 [3005402] Br J Ind Med. 1988 Oct;45(10):701-4 [3264183] Arthritis Rheum. 1989 Aug;32(8):1022-30 [2765002] Int Arch Allergy Appl Immunol. 1989;90(1):47-53 [2509376] J Clin Invest. 1990 Nov;86(5):1757-63 [2243145] Clin Exp Immunol. 1991 Nov;86(2):291-8 [1657464] Clin Immunol Immunopathol. 1993 Aug;68(2):159-69 [7689428] Clin Immunol Immunopathol. 1993 Nov;69(2):189-98 [8403556] J Clin Invest. 1994 Apr;93(4):1473-80 [8163652] FASEB J. 1994 Nov;8(14):1183-90 [7958626] J Clin Invest. 1994 Nov;94(5):2125-9 [7962558] J Exp Med. 1995 Mar 1;181(3):1123-31 [7869033] Toxicol Appl Pharmacol. 1995 Jun;132(2):299-309 [7785057] Toxicol Appl Pharmacol. 1995 Sep;134(1):155-60 [7676450] Clin Immunol Immunopathol. 1995 Dec;77(3):291-7 [7586739] J Immunol. 1996 May 15;156(10):4050-8 [8621948] Eur J Immunol. 1996 Jul;26(7):1519-26 [8766555] Environ Health Perspect. 1996 Apr;104(4):422-6 [8732953] J Autoimmun. 1996 Apr;9(2):139-49 [8738957] J Rheumatol Suppl. 1996 Oct;46:93-7; discussion 92, 97-8 [8895185] Clin Immunol Immunopathol. 1996 Dec;81(3):287-92 [8938107] Clin Exp Immunol. 1997 Jun;108(3):438-45 [9182889] Toxicol Appl Pharmacol. 2008 Sep 15;231(3):344-53 [18579175] J Immunol. 2008 Nov 15;181(10):7367-79 [18981160] Ann N Y Acad Sci. 2008 Nov;1143:240-67 [19076354] Clin Exp Immunol. 2009 Jan;155(1):117-24 [19076835] Arch Dermatol Res. 2009 Jan;301(1):99-105 [18797892] Nat Immunol. 2009 Feb;10(2):129-32 [19148193] Nephrol Dial Transplant. 1991;6(9):621-30 [1745385] Arthritis Rheum. 1991 Dec;34(12):1594-9 [1684107] J Autoimmun. 1991 Dec;4(6):871-80 [1812893] J Immunol. 1992 Jun 1;148(11):3369-76 [1588038] Autoimmunity. 1992;13(3):209-14 [1472632] J Clin Invest. 1993 Mar;91(3):804-11 [8450062] Toxicol Appl Pharmacol. 1998 Feb;148(2):222-8 [9473529] J Immunol. 1998 Jul 1;161(1):234-40 [9647229] J Dent Res. 1998 Jun;77(6):1415-25 [9649170] Cell Immunol. 1999 Mar 15;192(2):113-21 [10087179] J Autoimmun. 1999 May;12(3):157-65 [10222025] Environ Health Perspect. 1999 Oct;107 Suppl 5:729-35 [10502538] J Exp Med. 1950 May 1;91(5):485-98 [15415504] Nat Rev Immunol. 2004 Dec;4(12):989-97 [15573133] Endocrinology. 2005 Jan;146(1):294-300 [15459116] Immunology. 2005 Mar;114(3):428-37 [15720444] Environ Health Perspect. 2005 Mar;113(3):323-8 [15743722] Toxicology. 2005 Apr 15;209(2):135-47 [15767026] J Exp Med. 2005 Mar 21;201(6):949-60 [15781585] Diabetologia. 2005 May;48(5):931-7 [15830185] Clin Exp Immunol. 2005 Aug;141(2):230-7 [15996187] Trends Parasitol. 2005 Nov;21(11):513-6 [16125464] Toxicology. 2006 Feb 1;218(2-3):81-9 [16309813] Autoimmunity. 2006 Feb;39(1):41-54 [16455581] Environ Res. 2006 Jul;101(3):419-28 [16445906] Eur J Immunol. 2006 Aug;36(8):2106-15 [16761311] Springer Semin Immunopathol. 2006 Oct;28(2):83-96 [16972052] J Immunol. 2006 Dec 1;177(11):8234-40 [17114501] Ann N Y Acad Sci. 2006 Oct;1079:138-46 [17130545] Toxicol Sci. 2007 Feb;95(2):401-11 [17077186] Bull NYU Hosp Jt Dis. 2007;65(3):200-4 [17922670] Methods Mol Med. 2007;136:255-68 [17983154] PLoS Med. 2007 Dec;4(12):e332 [18162039] Am J Physiol Gastrointest Liver Physiol. 2008 Jan;294(1):G217-25 [18006603] Annu Rev Pathol. 2008;3:127-55 [18039131] Clin Rev Allergy Immunol. 2008 Jun;34(3):283-99 [18231878] J Agric Food Chem. 2009 Feb 25;57(4):1219-25 [19170508] Clin Exp Med. 2009 Mar;9(1):51-9 [18953634] J Am Coll Cardiol. 2009 Apr 7;53(14):1219-26 [19341864] Infect Immun. 2009 May;77(5):2177-83 [19273562] J Immunol. 2009 May 15;182(10):6576-86 [19414813] Environ Health Perspect. 2009 May;117(5):696-702 [19479009] Curr Opin Rheumatol. 2009 Sep;21(5):547-51 [19593142] Trends Immunol. 2009 Sep;30(9):455-64 [19699150] Arthritis Rheum. 2009 Oct 15;61(10):1305-11 [19790128] J Clin Immunol. 2009 Nov;29(6):730-7 [19826933] Chem Res Toxicol. 2010 Mar 15;23(3):455-66 [20078109] Reprod Toxicol. 2011 Apr;31(3):312-8 [20728533] Rheumatol Int. 2011 May;31(5):611-5 [20049452] Toxicology. 2011 Dec 18;290(2-3):156-68 [21925233] Clin Exp Immunol. 2003 Mar;131(3):405-14 [12605692] Clin Exp Immunol. 2007 Oct;150(1):179-88 [17680821] Immunopharmacology. 2000 Feb;46(2):123-37 [10647871] Adv Exp Med Biol. 1999;467:507-16 [10721094] Am J Vet Res. 2000 Apr;61(4):462-8 [10772115] Toxicol Sci. 2000 Apr;54(2):384-9 [10774820] J Immunol. 2000 Jul 15;165(2):1036-43 [10878381] Clin Exp Immunol. 2000 Aug;121(2):399-405 [10931159] Infect Immun. 2000 Oct;68(10):5803-8 [10992488] Toxicol Sci. 2000 Oct;57(2):345-52 [11006364] Andrologia. 2000 Sep;32(4-5):263-70 [11021518] Arthritis Res. 2000;2(6):437-440 [11094455] Environ Health Perspect. 2001 Jan;109(1):27-33 [11171521] Lupus. 2001;10(4):272-83 [11341104] Infect Immun. 2001 Jun;69(6):4072-8 [11349078] Exp Biol Med (Maywood). 2001 Mar;226(3):177-84 [11361035] Scand J Immunol. 2001 Jul-Aug;54(1-2):190-7 [11439166] Eur J Immunol. 2001 Aug;31(8):2266-76 [11477538] Infect Immun. 2001 Sep;69(9):5643-9 [11500440] Clin Exp Immunol. 2001 Aug;125(2):202-10 [11529910] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.jaut.2012.05.020 ER - TY - JOUR T1 - Developing treatment for spinal and bulbar muscular atrophy. AN - 1197486436; 22668795 AB - Spinal and bulbar muscular atrophy is unique among the polyglutamine diseases in that the toxicity of the mutant protein, the androgen receptor, is ligand-dependent. In cell culture and animal models the mutant androgen receptor causes protein aggregation and alterations in transcriptional regulation, axonal transport, and mitochondrial function. Various therapeutic approaches have shown efficacy in mouse models, including androgen reduction and agents that alter the processing and degradation of the mutant androgen receptor protein, such as HSP90 inhibitors, IGF-1, and ASC-J9. Clinical trials of androgen-reducing agents have shown indications of efficacy but not proof of clinically meaningful benefit to date. This trial experience has set the stage for future clinical studies of other agents that have been found to be beneficial in transgenic animal models. Published by Elsevier Ltd. JF - Progress in neurobiology AU - Fischbeck, Kenneth H AD - Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35-2A1000, 35 Convent Dr., Bethesda, MD 20892, USA. kf@ninds.nih.gov Y1 - 2012/12// PY - 2012 DA - December 2012 SP - 257 EP - 261 VL - 99 IS - 3 KW - Peptides KW - 0 KW - Receptors, Androgen KW - polyglutamine KW - 26700-71-0 KW - Index Medicus KW - Animals KW - Muscular Disorders, Atrophic -- genetics KW - Muscular Disorders, Atrophic -- drug therapy KW - Receptors, Androgen -- genetics KW - Humans KW - Receptors, Androgen -- metabolism KW - Clinical Trials as Topic KW - Peptides -- metabolism KW - Disease Models, Animal KW - Muscular Disorders, Atrophic -- metabolism KW - Muscular Atrophy, Spinal -- metabolism KW - Muscular Atrophy, Spinal -- genetics KW - Muscular Atrophy, Spinal -- physiopathology KW - Muscular Atrophy, Spinal -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1197486436?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Science&rft.atitle=Impact+of+cellular+autophagy+on+viruses%3A+Insights+from+hepatitis+B+virus+and+human+retroviruses&rft.au=Tang%2C+Sai-Wen%3BDucroux%2C+Aurelie%3BJeang%2C+Kuan-Teh%3BNeuveut%2C+Christine&rft.aulast=Tang&rft.aufirst=Sai-Wen&rft.date=2012-01-01&rft.volume=19&rft.issue=1&rft.spage=92&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomedical+Science&rft.issn=14230127&rft_id=info:doi/10.1186%2F1423-0127-19-92 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-05-09 N1 - Date created - 2012-11-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nat Med. 2005 Oct;11(10):1088-95 [16155577] Nature. 1991 Jul 4;352(6330):77-9 [2062380] Nat Med. 2007 Mar;13(3):348-53 [17334372] Nature. 2007 Jun 14;447(7146):859-63 [17568747] Hum Mol Genet. 2007 Jul 1;16(13):1593-603 [17470458] Hum Mol Genet. 2009 Jan 1;18(1):27-42 [18824496] J Neurosci. 2009 Feb 18;29(7):1987-97 [19228953] Ann Neurol. 2009 Feb;65(2):140-50 [19259967] 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] Front Neuroendocrinol. 2011 Oct;32(4):416-25 [21745497] J Neurosci. 2011 Nov 30;31(48):17425-36 [22131404] Cell Tissue Res. 2012 Jul;349(1):313-20 [22476656] Brain. 2009 Dec;132(Pt 12):3242-51 [19846582] J Neurosci Res. 2010 Aug 1;88(10):2207-16 [20336775] Lancet Neurol. 2010 Sep;9(9):875-84 [20691641] Neuron. 2010 Sep 23;67(6):936-52 [20869592] Trends Pharmacol Sci. 2010 Nov;31(11):523-7 [20863580] Lancet Neurol. 2011 Feb;10(2):140-7 [21216197] Hum Mol Genet. 2000 Sep 1;9(14):2197-202 [10958659] Nat Genet. 2000 Sep;26(1):29-36 [10973244] Proc Natl Acad Sci U S A. 2001 Jun 19;98(13):7200-5 [11404460] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15179-84 [11742087] Trends Mol Med. 2002 May;8(5):195-7 [12067622] Hum Mol Genet. 2002 Aug 15;11(17):1967-76 [12165558] Neurology. 2002 Sep 10;59(5):770-2 [12221177] Neuron. 2002 Aug 29;35(5):843-54 [12372280] Neuron. 2002 Aug 29;35(5):855-64 [12372281] Nat Med. 2003 Jun;9(6):768-73 [12754502] J Neuroendocrinol. 2003 Sep;15(9):882-7 [12899683] Hum Mol Genet. 2004 Jun 1;13(11):1183-92 [15102712] J Neurosci. 2004 May 19;24(20):4778-86 [15152038] Proc Natl Acad Sci U S A. 2006 Mar 14;103(11):4246-51 [16537516] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.pneurobio.2012.05.012 ER - TY - JOUR T1 - Neuroprotective peptides influence cytokine and chemokine alterations in a model of fetal alcohol syndrome. AN - 1197484942; 23174390 AB - Fetal alcohol syndrome (FAS) is associated with intellectual disability and neurodevelopmental abnormalities. Neuroprotective peptides NAPVSIPQ (NAP) and SALLRSIPA (SAL) can prevent some of the alcohol-induced teratogenesis including fetal death, growth abnormalities, and learning impairment in part by preventing alcohol-induced alterations in N-methyl-D-aspartate receptor gene expression in a mouse model for FAS. We evaluated a panel of cytokines and chemokines to determine whether NAP plus SAL work through a cytokine/chemokine-mediated pathway in preventing these alterations. Using a well-characterized FAS model, timed, pregnant C57BL6/J mice were treated on gestational day (E) 8 with alcohol (0.03 mL/g), placebo, or alcohol plus peptides. Embryos were evaluated at 2 time points: after 6 hours and 10 days later at E18. A panel of cytokines/chemokines was measured using a microsphere-based multiplex immunoassay (Luminex xMAP; Millipore, Billerica, MA). Statistical analysis included Kruskal-Wallis, with P < .05 considered significant. Six hours after treatment, interleukin (IL)-6 and keratinocyte chemoattractant cytokine (KC) were not detectable in the control embryos. Alcohol treatment resulted in detectable levels and significant increases in IL-6 (median, 15.7; range, 10.1-45.9 pg/mL) and KC (median, 45.9; range, 32.5-99.1 pg/mL). Embryos exposed to alcohol plus NAP plus SAL had undetectable IL-6 and KC (both P < .003), similar to the controls. Alcohol exposure resulted in a significant increase of granulocyte colony-stimulating factor (G-CSF) (P < .003) as compared with controls, and treatment with NAP plus SAL prevented the alcohol-induced increase. IL-13 and IL-1β were decreased 6 hours after alcohol exposure, and exposure to alcohol plus NAP plus SAL did not completely ameliorate the decrease. At E18, 10 days after exposure, these alterations were no longer present. Several analytes (regulated upon activation, normal T cell expressed, and secreted, tumor necrosis factor-α, interferon-γ, and IL-4) were not detectable at either time point in any of the groups. Prenatal alcohol exposure acutely results in a significant elevation of IL-6, G-CSF and the KC, which are known to affect N-methyl-D-aspartate receptors. NAP plus SAL treatment prevented alcohol-induced increases. This provides additional insight into the mechanism of alcohol damage in FAS and NAP plus SAL prevention of neurodevelopmental anomalies. Copyright © 2012 Mosby, Inc. All rights reserved. JF - American journal of obstetrics and gynecology AU - Roberson, Robin AU - Kuddo, Thea AU - Benassou, Ines AU - Abebe, Daniel AU - Spong, Catherine Y AD - Unit on Perinatal and Developmental Neurobiology, Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA. robersor@mail.nih.gov Y1 - 2012/12// PY - 2012 DA - December 2012 SP - 499.e1 EP - 5 VL - 207 IS - 6 KW - Chemokines KW - 0 KW - Cytokines KW - Immunologic Factors KW - Interleukin-6 KW - Oligopeptides KW - seryl-alanyl-leucy-leucyl-arginyl-seryl-isoleucyl-prolyl-alanine KW - Granulocyte Colony-Stimulating Factor KW - 143011-72-7 KW - keratinocyte-derived chemokines KW - 147037-79-4 KW - Ethanol KW - 3K9958V90M KW - davunetide KW - GF00K3IIWE KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Granulocyte Colony-Stimulating Factor -- metabolism KW - Interleukin-6 -- metabolism KW - Mice, Inbred C57BL KW - Ethanol -- toxicity KW - Disease Models, Animal KW - Mice KW - Granulocyte Colony-Stimulating Factor -- drug effects KW - Immunologic Factors -- metabolism KW - Female KW - Pregnancy KW - Fetal Alcohol Spectrum Disorders -- drug therapy KW - Chemokines -- drug effects KW - Chemokines -- metabolism KW - Fetal Alcohol Spectrum Disorders -- metabolism KW - Oligopeptides -- pharmacology KW - Cytokines -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1197484942?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+obstetrics+and+gynecology&rft.atitle=Neuroprotective+peptides+influence+cytokine+and+chemokine+alterations+in+a+model+of+fetal+alcohol+syndrome.&rft.au=Roberson%2C+Robin%3BKuddo%2C+Thea%3BBenassou%2C+Ines%3BAbebe%2C+Daniel%3BSpong%2C+Catherine+Y&rft.aulast=Roberson&rft.aufirst=Robin&rft.date=2012-12-01&rft.volume=207&rft.issue=6&rft.spage=499.e1&rft.isbn=&rft.btitle=&rft.title=American+journal+of+obstetrics+and+gynecology&rft.issn=1097-6868&rft_id=info:doi/10.1016%2Fj.ajog.2012.10.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-02-05 N1 - Date created - 2012-11-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.ajog.2012.10.005 ER - TY - JOUR T1 - Bladder cancer and schistosomiasis. AN - 1178703812; 23159285 AB - Schistosoma-associated bladder cancer was believed, for several decades, to be a completely unique entity of disease, different from urothelial cancer. This was probably due to its distinct clinicopathologic and demographic features that varied from those of urothelial entity. The carcinogenesis is an extremely complex process resulting from the accumulation of many genetic and epigenetic changes leading to alterations in the cell proliferation regulation process. In bladder cancer, many of these carcinogenic cascades were not fully documented or somewhat conflicting. Inspite of the efforts performed, much is still needed to explore the presence or absence of the carcinogenic difference with a different etiology. The control of schistosomiasis in certain countries and the subsequent decrease in the intensity of infestation showed changing of features approaching that of urothelial tumors. However the schistosoma-associated bladder cancer presented in more advanced stages than schistosoma-non associated urothelial cancer. More recently, data are gathered that, upon applying the same treatment protocol and management care, stage by stage comparison of the treatment end-results were found to be similar in bladder cancer patients with a different etiology. All treatment options; including radical cystectomy with or without adjuvant or neoadjuvant chemo- or radiotherapy or trimodality bladder preserving treatment seem to lead to similar end-results regardless of etiologic factor(s) implicated in bladder cancer development. Copyright © 2012. Published by Elsevier B.V. JF - Journal of the Egyptian National Cancer Institute AU - Zaghloul, Mohamed S AD - Radiation Oncology Department, Children's Cancer Hospital and National Cancer Institute, Cairo University, Cairo, Egypt. mszagh@yahoo.com Y1 - 2012/12// PY - 2012 DA - December 2012 SP - 151 EP - 159 VL - 24 IS - 4 SN - 1110-0362, 1110-0362 KW - Index Medicus KW - Neoplasm Invasiveness KW - Radiotherapy, Adjuvant KW - Cystectomy KW - Humans KW - Neoadjuvant Therapy KW - Prognosis KW - Chemotherapy, Adjuvant KW - Urinary Bladder Neoplasms -- pathology KW - Schistosomiasis haematobia -- complications KW - Schistosomiasis haematobia -- pathology KW - Urinary Bladder Neoplasms -- therapy KW - Urinary Bladder Neoplasms -- mortality KW - Urinary Bladder Neoplasms -- parasitology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1178703812?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Bladder+cancer+and+schistosomiasis.&rft.au=Zaghloul%2C+Mohamed+S&rft.aulast=Zaghloul&rft.aufirst=Mohamed&rft.date=2012-12-01&rft.volume=24&rft.issue=4&rft.spage=151&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+Egyptian+National+Cancer+Institute&rft.issn=11100362&rft_id=info:doi/10.1016%2Fj.jnci.2012.08.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-09-09 N1 - Date created - 2012-11-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.jnci.2012.08.002 ER - TY - JOUR T1 - A phase I/II trial of vandetanib for patients with recurrent malignant glioma. AN - 1171874475; 23099652 AB - Vandetanib is a once-daily multitargeted tyrosine kinase inhibitor of vascular endothelial growth factor receptor-2, epidermal growth factor receptor, and the rearranged-during-transfection oncogene. A phase I trial was conducted to describe the pharmacokinetics of vandetanib in patients with recurrent glioma on enzyme-inducing anti-epileptic drugs (EIAEDs) and to identify the maximum tolerated dose (MTD) in this population. A phase II trial evaluated the efficacy of vandetanib in patients with recurrent malignant glioma not on EIAEDs as measured by 6-month progression-free survival (PFS6). In the phase I trial, 15 patients were treated with vandetanib at doses of 300, 400, and 500 mg/day, in a standard dose-escalation design. The MTD in patients on EIAEDs was 400 mg/day, and steady-state levels were similar to those measured in patients not on EIAEDs. Dose-limiting toxicities were prolonged QTc and thromboembolism. Thirty-two patients with recurrent glioblastoma multiforme (GBM) and 32 patients with recurrent anaplastic gliomas (AGs) were treated in the phase II trial, at a dosage of 300 mg/day on 28-day cycles. Six patients (4 GBM, 2 AG) had radiographic response. PFS6 was 6.5% in the GBM arm and 7.0% in the AG arm. Median overall survival was 6.3 months in the GBM arm and 7.6 months in the AG arm. Seizures were an unexpected toxicity of therapy. Vandetanib did not have significant activity in unselected patients with recurrent malignant glioma. JF - Neuro-oncology AU - Kreisl, Teri N AU - McNeill, Katharine A AU - Sul, Joohee AU - Iwamoto, Fabio M AU - Shih, Joanna AU - Fine, Howard A AD - Neuro-Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. kreislt@mail.nih.gov Y1 - 2012/12// PY - 2012 DA - December 2012 SP - 1519 EP - 1526 VL - 14 IS - 12 KW - Antineoplastic Agents KW - 0 KW - Piperidines KW - Quinazolines KW - N-(4-bromo-2-fluorophenyl)-6-methoxy-7-((1-methylpiperidin-4-yl)methoxy)quinazolin-4-amine KW - YO460OQ37K KW - Index Medicus KW - Kaplan-Meier Estimate KW - Young Adult KW - Disease-Free Survival KW - Dose-Response Relationship, Drug KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Maximum Tolerated Dose KW - Male KW - Female KW - Quinazolines -- pharmacokinetics KW - Brain Neoplasms -- pathology KW - Antineoplastic Agents -- administration & dosage KW - Brain Neoplasms -- mortality KW - Antineoplastic Agents -- pharmacokinetics KW - Piperidines -- pharmacokinetics KW - Glioma -- mortality KW - Piperidines -- adverse effects KW - Antineoplastic Agents -- adverse effects KW - Quinazolines -- administration & dosage KW - Glioma -- pathology KW - Brain Neoplasms -- drug therapy KW - Glioma -- drug therapy KW - Neoplasm Recurrence, Local -- drug therapy KW - Piperidines -- administration & dosage KW - Quinazolines -- adverse effects KW - Neoplasm Recurrence, Local -- mortality KW - Neoplasm Recurrence, Local -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1171874475?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+phase+I%2FII+trial+of+vandetanib+for+patients+with+recurrent+malignant+glioma.&rft.au=Kreisl%2C+Teri+N%3BMcNeill%2C+Katharine+A%3BSul%2C+Joohee%3BIwamoto%2C+Fabio+M%3BShih%2C+Joanna%3BFine%2C+Howard+A&rft.aulast=Kreisl&rft.aufirst=Teri&rft.date=2012-12-01&rft.volume=14&rft.issue=12&rft.spage=1519&rft.isbn=&rft.btitle=&rft.title=Neuro-oncology&rft.issn=1523-5866&rft_id=info:doi/10.1093%2Fneuonc%2Fnos265 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-06-26 N1 - Date created - 2012-11-16 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Clin Oncol. 2012 Jan 10;30(2):134-41 [22025146] N Engl J Med. 2005 Mar 10;352(10):997-1003 [15758010] J Pharm Biomed Anal. 2005 Sep 15;39(3-4):705-11 [15935603] Clin Cancer Res. 2005 Nov 15;11(22):8145-57 [16299247] Lung Cancer. 2006 Jan;51(1):89-96 [16290256] Neuro Oncol. 2006 Jan;8(1):67-78 [16443950] Cancer Treat Rev. 2006 Apr;32(2):74-89 [16488082] J Thorac Oncol. 2006 Nov;1(9):1002-9 [17409986] J Clin Oncol. 2007 Oct 10;25(29):4536-41 [17876014] J Clin Oncol. 2007 Oct 20;25(30):4743-50 [17909199] J Clin Oncol. 2007 Oct 20;25(30):4722-9 [17947719] J Clin Oncol. 2009 Feb 10;27(5):740-5 [19114704] Invest New Drugs. 2009 Jun;27(3):253-61 [19002384] J Clin Oncol. 2010 Apr 10;28(11):1963-72 [20231676] Neuro Oncol. 2010 Aug;12(8):855-61 [20200024] Neuro Oncol. 2010 Dec;12(12):1300-10 [20716591] Drugs R D. 2011;11(1):37-51 [21410294] J Neurooncol. 2011 Jul;103(3):491-501 [20872043] J Clin Oncol. 1999 Aug;17(8):2572-8 [10561324] J Neurooncol. 2001 Nov;55(2):91-100 [11817706] Cancer Res. 2002 Aug 1;62(15):4307-15 [12154034] Cancer Res. 2003 Oct 15;63(20):6962-70 [14583498] J Clin Oncol. 2004 Jan 1;22(1):133-42 [14638850] Oncogene. 2004 Jun 3;23(26):4594-602 [15077177] J Clin Oncol. 2004 Aug 15;22(16):3238-47 [15310767] Br J Cancer. 2004 Sep 13;91(6):1174-80 [15305185] J Clin Oncol. 1990 Jul;8(7):1277-80 [2358840] Cancer Res. 1991 Feb 15;51(4):1345-51 [1705174] J Neurosurg. 1992 May;76(5):792-8 [1564542] Crit Rev Oncol Hematol. 1995 Jul;19(3):183-232 [7612182] JAMA. 2005 Feb 2;293(5):557-64 [15687310] N Engl J Med. 2005 Mar 10;352(10):987-96 [15758009] J Clin Oncol. 2005 Apr 10;23(11):2544-55 [15753462] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1093/neuonc/nos265 ER - TY - JOUR T1 - A herpes simplex virus 2 glycoprotein D mutant generated by bacterial artificial chromosome mutagenesis is severely impaired for infecting neuronal cells and infects only Vero cells expressing exogenous HVEM. AN - 1126620437; 22993162 AB - We constructed a herpes simplex virus 2 (HSV-2) bacterial artificial chromosome (BAC) clone, bHSV2-BAC38, which contains full-length HSV-2 inserted into a BAC vector. Unlike previously reported HSV-2 BAC clones, the virus genome inserted into this BAC clone has no known gene disruptions. Virus derived from the BAC clone had a wild-type phenotype for growth in vitro and for acute infection, latency, and reactivation in mice. HVEM, expressed on epithelial cells and lymphocytes, and nectin-1, expressed on neurons and epithelial cells, are the two principal receptors used by HSV to enter cells. We used the HSV-2 BAC clone to construct an HSV-2 glycoprotein D mutant (HSV2-gD27) with point mutations in amino acids 215, 222, and 223, which are critical for the interaction of gD with nectin-1. HSV2-gD27 infected cells expressing HVEM, including a human epithelial cell line. However, the virus lost the ability to infect cells expressing only nectin-1, including neuronal cell lines, and did not infect ganglia in mice. Surprisingly, we found that HSV2-gD27 could not infect Vero cells unless we transduced the cells with a retrovirus expressing HVEM. High-level expression of HVEM in Vero cells also resulted in increased syncytia and enhanced cell-to-cell spread in cells infected with wild-type HSV-2. The inability of the HSV2-gD27 mutant to infect neuronal cells in vitro or sensory ganglia in mice after intramuscular inoculation suggests that this HSV-2 mutant might be an attractive candidate for a live attenuated HSV-2 vaccine. JF - Journal of virology AU - Wang, Kening AU - Kappel, Justin D AU - Canders, Caleb AU - Davila, Wilmer F AU - Sayre, Dean AU - Chavez, Mayra AU - Pesnicak, Lesley AU - Cohen, Jeffrey I AD - Medical Virology Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland, USA. kwang@niaid.nih.gov Y1 - 2012/12// PY - 2012 DA - December 2012 SP - 12891 EP - 12902 VL - 86 IS - 23 KW - Cell Adhesion Molecules KW - 0 KW - Oligonucleotides KW - Receptors, Tumor Necrosis Factor, Member 14 KW - Viral Envelope Proteins KW - nectins KW - Index Medicus KW - Point Mutation -- genetics KW - Animals KW - Humans KW - Mice KW - Mice, Inbred BALB C KW - Mutagenesis KW - Polymerase Chain Reaction KW - Receptors, Tumor Necrosis Factor, Member 14 -- metabolism KW - Cercopithecus aethiops KW - Chromosomes, Artificial, Bacterial -- genetics KW - Cell Adhesion Molecules -- metabolism KW - Cell Line KW - Oligonucleotides -- genetics KW - Herpesvirus 2, Human -- genetics KW - Vero Cells -- metabolism KW - Vero Cells -- virology KW - Virus Internalization KW - Neurons -- virology KW - Herpesvirus 2, Human -- metabolism KW - Viral Envelope Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1126620437?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+herpes+simplex+virus+2+glycoprotein+D+mutant+generated+by+bacterial+artificial+chromosome+mutagenesis+is+severely+impaired+for+infecting+neuronal+cells+and+infects+only+Vero+cells+expressing+exogenous+HVEM.&rft.au=Wang%2C+Kening%3BKappel%2C+Justin+D%3BCanders%2C+Caleb%3BDavila%2C+Wilmer+F%3BSayre%2C+Dean%3BChavez%2C+Mayra%3BPesnicak%2C+Lesley%3BCohen%2C+Jeffrey+I&rft.aulast=Wang&rft.aufirst=Kening&rft.date=2012-12-01&rft.volume=86&rft.issue=23&rft.spage=12891&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=1098-5514&rft_id=info:doi/10.1128%2FJVI.01055-12 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-14 N1 - Date created - 2012-11-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Virol. 2009 Apr;83(7):2951-61 [19129446] J Biol Chem. 2009 Jun 26;284(26):17370-82 [19386594] Proc Natl Acad Sci U S A. 2009 Oct 20;106(42):17916-20 [19805039] Proc Natl Acad Sci U S A. 2009 Nov 10;106(45):19138-43 [19858479] J Virol. 2010 Jan;84(2):1189-92 [19889786] J Virol. 2010 May;84(9):4659-72 [20181707] J Virol. 2010 May;84(10):5303-13 [20219902] Virology. 2010 Nov 25;407(2):360-7 [20863544] MMWR Recomm Rep. 2010 Dec 17;59(RR-12):1-110 [21160459] J Virol. 2011 May;85(9):4501-9 [21325410] Can J Public Health. 2011 May-Jun;102(3):225-9 [21714324] PLoS Pathog. 2011 Sep;7(9):e1002277 [21980294] Arch Virol. 2011 Dec;156(12):2267-72 [21894520] J Virol. 2012 Jun;86(11):6371-2 [22570244] Proc Natl Acad Sci U S A. 2004 Aug 24;101(34):12414-21 [15273289] Herpes. 2004 Apr;11 Suppl 1:2A-23A [15115626] Herpes. 2004 Apr;11 Suppl 1:24A-35A [15115627] Mol Ther. 2001 Feb;3(2):160-8 [11237672] J Virol. 2001 Jun;75(12):5692-6 [11356978] J Virol. 2001 Sep;75(17):8166-72 [11483762] Mol Cell. 2001 Jul;8(1):169-79 [11511370] Acta Crystallogr D Biol Crystallogr. 2002 May;58(Pt 5):836-8 [11976496] J Virol. 2002 Jun;76(12):6185-96 [12021352] J Virol. 2003 Jan;77(2):1382-91 [12502854] J Virol. 2003 May;77(9):5073-83 [12692210] J Virol. 2003 Aug;77(16):8962-72 [12885913] Virology. 2004 Jan 5;318(1):420-8 [14972567] Cell Microbiol. 2004 May;6(5):401-10 [15056211] Virology. 2004 May 1;322(2):286-99 [15110526] Vaccine. 2004 Sep 28;22(29-30):4069-74 [15364458] J Mol Biol. 1967 Jun 14;26(2):365-9 [4291934] Ann Intern Med. 1983 Jun;98(6):958-72 [6344712] J Mol Biol. 1985 Jan 5;181(1):1-13 [2984429] J Gen Virol. 1988 Jul;69 ( Pt 7):1531-74 [2839594] J Gen Virol. 1988 Nov;69 ( Pt 11):2831-46 [2846760] J Virol. 1990 Nov;64(11):5342-8 [2170675] Proc Natl Acad Sci U S A. 1992 Sep 15;89(18):8794-7 [1528894] J Exp Med. 1995 Jan 1;181(1):297-306 [7807009] Cell. 1996 Nov 1;87(3):427-36 [8898196] Int J Epidemiol. 1997 Aug;26(4):698-709 [9279600] J Virol. 1997 Oct;71(10):7903-10 [9311880] J Virol. 1998 Jan;72(1):873-5 [9420303] J Virol. 1998 Mar;72(3):2010-21 [9499055] Science. 1998 Jun 5;280(5369):1618-20 [9616127] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8245-50 [9653172] Virology. 1999 Jun 5;258(2):365-74 [10366573] J Virol. 1999 Aug;73(8):7056-60 [10400809] J Virol. 1999 Oct;73(10):8320-9 [10482582] J Virol. 2005 Jan;79(2):1282-95 [15613355] Nucleic Acids Res. 2005;33(4):e36 [15731329] J Virol. 2005 Jun;79(12):7827-37 [15919936] Curr Med Res Opin. 2005 Oct;21(10):1577-82 [16238897] AIDS. 2006 Jan 2;20(1):73-83 [16327322] Virology. 2006 Jan 5;344(1):17-24 [16364731] Hum Gene Ther. 2006 Jan;17(1):93-104 [16409128] J Virol Methods. 2006 Aug;135(2):197-206 [16647145] J Gene Med. 2006 Oct;8(10):1251-61 [16952195] J Virol. 2007 Feb;81(4):1872-8 [17151134] Vaccine. 2007 Jun 28;25(27):5006-12 [17540483] J Virol. 2007 Sep;81(17):9024-33 [17581997] J Virol. 2007 Dec;81(23):13200-8 [17913822] J Virol. 2008 Jan;82(2):700-9 [18032483] Virology. 2008 Mar 30;373(1):98-111 [18076965] Proc Natl Acad Sci U S A. 2008 Aug 5;105(31):10931-6 [18678906] Bull World Health Organ. 2008 Oct;86(10):805-12, A [18949218] J Virol. 2009 Feb;83(3):1433-42 [19019961] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1128/JVI.01055-12 ER - TY - JOUR T1 - MDM2 SNP285 does not antagonize the effect of SNP309 in lung cancer. AN - 1080882815; 22487911 AB - Conflicting reports exist regarding the contribution of SNP309 in MDM2 to cancer risk. Recently, SNP285 was shown to act as an antagonist to SNP309 by overriding the effect of SNP309 on SP1-mediated transcription. Moreover, SNP285 modified the relationship between SNP309 and risk of breast, ovarian and endometrial cancer. We assessed whether SNP285 confounded the effect of SNP309 in lung cancer in a cohort of 720 controls and 556 cases. Our cohort included both Caucasians and African Americans. Neither SNP309 nor SNP285 was associated with lung cancer risk or survival. In addition, removal of individuals who carried the variant C allele of SNP285 did not modify the association between SNP309 with either lung cancer risk or survival. Although an effect of SNP285 has been demonstrated in breast, ovarian and endometrial cancer, our findings do not support a role for this SNP in lung cancer and raise the possibility that the effect of SNP285 is restricted to cancers in women. Copyright © 2012 UICC. JF - International journal of cancer AU - Ryan, Bríd M AU - Calhoun, Kara M AU - Pine, Sharon R AU - Bowman, Elise D AU - Robles, Ana I AU - Ambs, Stefan AU - Harris, Curtis C AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4258, USA. Y1 - 2012/12/01/ PY - 2012 DA - 2012 Dec 01 SP - 2710 EP - 2716 VL - 131 IS - 11 KW - MDM2 protein, human KW - EC 2.3.2.27 KW - Proto-Oncogene Proteins c-mdm2 KW - Index Medicus KW - Polymorphism, Single Nucleotide KW - Alleles KW - Humans KW - Cohort Studies KW - Case-Control Studies KW - Aged KW - Genetic Predisposition to Disease KW - Male KW - Female KW - Proto-Oncogene Proteins c-mdm2 -- genetics KW - Lung Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1080882815?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=MDM2+SNP285+does+not+antagonize+the+effect+of+SNP309+in+lung+cancer.&rft.au=Ryan%2C+Br%C3%ADd+M%3BCalhoun%2C+Kara+M%3BPine%2C+Sharon+R%3BBowman%2C+Elise+D%3BRobles%2C+Ana+I%3BAmbs%2C+Stefan%3BHarris%2C+Curtis+C&rft.aulast=Ryan&rft.aufirst=Br%C3%ADd&rft.date=2012-12-01&rft.volume=131&rft.issue=11&rft.spage=2710&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.27573 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-03-08 N1 - Date created - 2012-09-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 2000 Feb 25;275(8):5379-87 [10681512] Eur J Cancer. 2012 Sep;48(13):1988-96 [22119201] Br J Cancer. 1997;75(9):1302-8 [9155050] Cell. 2004 Nov 24;119(5):591-602 [15550242] Int J Cancer. 2006 Mar 1;118(5):1275-8 [16152608] Int J Cancer. 2006 Apr 1;118(7):1790-7 [16217767] Int J Cancer. 2006 Aug 1;119(3):718-21 [16496380] Cancer Res. 2006 May 15;66(10):5104-10 [16707433] J Natl Cancer Inst. 2006 Jul 5;98(13):911-9 [16818855] Cancer Epidemiol Biomarkers Prev. 2006 Aug;15(8):1559-61 [16896050] Lung Cancer. 2006 Oct;54(1):19-24 [16876289] J Med Genet. 2006 Dec;43(12):950-2 [16825430] Mol Carcinog. 2007 Feb;46(2):100-5 [17013834] J Clin Oncol. 2007 Jun 1;25(16):2243-7 [17538168] Breast Cancer Res Treat. 2007 Aug;104(2):153-7 [17080308] Carcinogenesis. 2007 Nov;28(11):2262-7 [17827408] BMC Cancer. 2008;8:281 [18828900] BMC Cancer. 2010;10:88 [20219101] Trends Cell Biol. 2010 May;20(5):299-309 [20172729] Cancer Cell. 2011 Feb 15;19(2):273-82 [21316605] Oncotarget. 2011 Mar;2(3):251-8 [21436469] Mol Carcinog. 2011 Jun;50(6):433-8 [21268124] CA Cancer J Clin. 2012 Jan-Feb;62(1):10-29 [22237781] Nature. 1995 Nov 9;378(6553):206-8 [7477327] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/ijc.27573 ER - TY - JOUR T1 - Methylation of HPV18, HPV31, and HPV45 genomes and cervical intraepithelial neoplasia grade 3. AN - 1186929684; 23093560 AB - Persistent infections with carcinogenic human papillomavirus (HPV) types are the necessary cause of cervical cancer. We recently demonstrated that the HPV16 genome is strongly methylated in cervical precancer compared with transient infections. However, the extent of methylation in other HPV types and its role in progression to cancer is poorly understood. We analyzed whole-genome methylation patterns of the three next most carcinogenic HPV genotypes: HPV31 (closely related to HPV16), and two other closely related types, HPV18 and HPV45. DNA was extracted from cervical cytology specimens from 92 women with precancer and 96 women infected with HPV31, HPV18, or HPV45, but who had no cytological or histological abnormalities. After bisulfite modification, genome-wide pyrosequencing was performed covering 80-106 sites. We calculated differences in median methylation, odds ratios, areas under the curve, and Spearman rank correlation coefficients for methylation levels between different sites. All statistical tests were two-sided. For all three HPV types, we observed strongly elevated methylation levels at multiple CpG sites in the E2, L2, and L1 regions among women with cervical intraepithelial neoplasia grade 3 compared with women with transient infections. We observed high correlation of methylation patterns between phylogenetically related types. The highest areas under the curve were 0.81 for HPV31, 0.85 for HPV18, and 0.98 for HPV45. Differential methylation patterns in cervical intraepithelial neoplasia grade 3 patients with multiple infections suggest that methylation can clarify which of the infections is causal. Carcinogenic HPV DNA methylation indicates transforming HPV infections. Our findings show that methylation of carcinogenic HPV types is a general phenomenon that warrants development of diagnostic assays. JF - Journal of the National Cancer Institute AU - Wentzensen, Nicolas AU - Sun, Chang AU - Ghosh, Arpita AU - Kinney, Walter AU - Mirabello, Lisa AU - Wacholder, Sholom AU - Shaber, Ruth AU - LaMere, Brandon AU - Clarke, Megan AU - Lorincz, Attila T AU - Castle, Philip E AU - Schiffman, Mark AU - Burk, Robert D AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd, Room 5024, Rockville, MD 20852-7234, USA. wentzenn@mail.nih.gov Y1 - 2012/11/21/ PY - 2012 DA - 2012 Nov 21 SP - 1738 EP - 1749 VL - 104 IS - 22 KW - DNA, Viral KW - 0 KW - Index Medicus KW - Genotype KW - Logistic Models KW - Humans KW - Adult KW - Case-Control Studies KW - Vaginal Smears KW - Neoplasm Grading KW - Middle Aged KW - Sample Size KW - Female KW - Cervical Intraepithelial Neoplasia -- pathology KW - Alphapapillomavirus -- classification KW - Papillomavirus Infections -- complications KW - Papillomavirus Infections -- virology KW - Genome, Viral KW - Uterine Cervical Dysplasia -- virology KW - Precancerous Conditions -- virology KW - Precancerous Conditions -- pathology KW - Human papillomavirus 31 -- genetics KW - Uterine Cervical Dysplasia -- pathology KW - Human papillomavirus 18 -- genetics KW - Alphapapillomavirus -- genetics KW - DNA Methylation KW - Cervical Intraepithelial Neoplasia -- virology KW - Uterine Cervical Neoplasms -- pathology KW - Uterine Cervical Neoplasms -- virology KW - DNA, Viral -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1186929684?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Methylation+of+HPV18%2C+HPV31%2C+and+HPV45+genomes+and+cervical+intraepithelial+neoplasia+grade+3.&rft.au=Wentzensen%2C+Nicolas%3BSun%2C+Chang%3BGhosh%2C+Arpita%3BKinney%2C+Walter%3BMirabello%2C+Lisa%3BWacholder%2C+Sholom%3BShaber%2C+Ruth%3BLaMere%2C+Brandon%3BClarke%2C+Megan%3BLorincz%2C+Attila+T%3BCastle%2C+Philip+E%3BSchiffman%2C+Mark%3BBurk%2C+Robert+D&rft.aulast=Wentzensen&rft.aufirst=Nicolas&rft.date=2012-11-21&rft.volume=104&rft.issue=22&rft.spage=1738&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdjs425 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-14 N1 - Date created - 2012-11-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mol Cell Biol. 2002 May;22(9):3157-73 [11940673] J Natl Cancer Inst. 2012 Apr 4;104(7):556-65 [22448030] Virology. 2004 Jul 1;324(2):483-92 [15207633] Virology. 2006 May 25;349(1):175-83 [16472835] Dis Markers. 2007;23(4):297-313 [17627064] Dis Markers. 2007;23(4):315-30 [17627065] 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] Cancer Res. 2008 Jan 1;68(1):307-13 [18172324] Lancet Oncol. 2008 May;9(5):425-34 [18407790] J Virol. 2009 Feb;83(3):1443-55 [19036820] Gynecol Oncol. 2009 Feb;112(2):293-9 [19054549] Genome Res. 2009 Mar;19(3):438-51 [19208682] Int J Cancer. 2009 Nov 1;125(9):2151-8 [19585494] Eur J Obstet Gynecol Reprod Biol. 2009 Dec;147(2):215-20 [19819061] Int J Cancer. 2011 Feb 15;128(4):927-35 [20473886] J Natl Cancer Inst. 2011 Mar 2;103(5):368-83 [21282563] Gynecol Oncol. 2011 Apr;121(1):59-63 [21306759] Cancer Epidemiol Biomarkers Prev. 2011 May;20(5):946-53 [21415357] PLoS One. 2011;6(5):e20183 [21673791] PLoS One. 2011;6(8):e23897 [21887341] J Med Virol. 2002 Nov;68(3):417-23 [12226831] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/jnci/djs425 ER - TY - JOUR T1 - δ-Tocopherol reduces lipid accumulation in Niemann-Pick type C1 and Wolman cholesterol storage disorders. AN - 1178670551; 23035117 AB - Niemann-Pick disease type C (NPC) and Wolman disease are two members of a family of storage disorders caused by mutations of genes encoding lysosomal proteins. Deficiency in function of either the NPC1 or NPC2 protein in NPC disease or lysosomal acid lipase in Wolman disease results in defective cellular cholesterol trafficking. Lysosomal accumulation of cholesterol and enlarged lysosomes are shared phenotypic characteristics of both NPC and Wolman cells. Utilizing a phenotypic screen of an approved drug collection, we found that δ-tocopherol effectively reduced lysosomal cholesterol accumulation, decreased lysosomal volume, increased cholesterol efflux, and alleviated pathological phenotypes in both NPC1 and Wolman fibroblasts. Reduction of these abnormalities may be mediated by a δ-tocopherol-induced intracellular Ca(2+) response and subsequent enhancement of lysosomal exocytosis. Consistent with a general mechanism for reduction of lysosomal lipid accumulation, we also found that δ-tocopherol reduces pathological phenotypes in patient fibroblasts from other lysosomal storage diseases, including NPC2, Batten (ceroid lipofuscinosis, neuronal 2, CLN2), Fabry, Farber, Niemann-Pick disease type A, Sanfilippo type B (mucopolysaccharidosis type IIIB, MPSIIIB), and Tay-Sachs. Our data suggest that regulated exocytosis may represent a potential therapeutic target for reduction of lysosomal storage in this class of diseases. JF - The Journal of biological chemistry AU - Xu, Miao AU - Liu, Ke AU - Swaroop, Manju AU - Porter, Forbes D AU - Sidhu, Rohini AU - Firnkes, Sally AU - Finkes, Sally AU - Ory, Daniel S AU - Marugan, Juan J AU - Xiao, Jingbo AU - Southall, Noel AU - Pavan, William J AU - Davidson, Cristin AU - Walkley, Steven U AU - Remaley, Alan T AU - Baxa, Ulrich AU - Sun, Wei AU - McKew, John C AU - Austin, Christopher P AU - Zheng, Wei AD - National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, Maryland 20892, USA. Y1 - 2012/11/16/ PY - 2012 DA - 2012 Nov 16 SP - 39349 EP - 39360 VL - 287 IS - 47 KW - Tocopherols KW - 1406-66-2 KW - Cholesterol KW - 97C5T2UQ7J KW - delta-tocopherol KW - JU84X1II0N KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Exocytosis -- drug effects KW - Calcium -- metabolism KW - Animals KW - Humans KW - Cell Line KW - Cricetinae KW - Calcium Signaling -- drug effects KW - Lipid Metabolism -- drug effects KW - Tocopherols -- pharmacology KW - Niemann-Pick Disease, Type C -- pathology KW - Lysosomes -- pathology KW - Cholesterol -- metabolism KW - Wolman Disease -- metabolism KW - Niemann-Pick Disease, Type C -- metabolism KW - Lysosomes -- metabolism KW - Wolman Disease -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1178670551?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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%B4-Tocopherol+reduces+lipid+accumulation+in+Niemann-Pick+type+C1+and+Wolman+cholesterol+storage+disorders.&rft.au=Xu%2C+Miao%3BLiu%2C+Ke%3BSwaroop%2C+Manju%3BPorter%2C+Forbes+D%3BSidhu%2C+Rohini%3BFirnkes%2C+Sally%3BFinkes%2C+Sally%3BOry%2C+Daniel+S%3BMarugan%2C+Juan+J%3BXiao%2C+Jingbo%3BSouthall%2C+Noel%3BPavan%2C+William+J%3BDavidson%2C+Cristin%3BWalkley%2C+Steven+U%3BRemaley%2C+Alan+T%3BBaxa%2C+Ulrich%3BSun%2C+Wei%3BMcKew%2C+John+C%3BAustin%2C+Christopher+P%3BZheng%2C+Wei&rft.aulast=Xu&rft.aufirst=Miao&rft.date=2012-11-16&rft.volume=287&rft.issue=47&rft.spage=39349&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M112.357707 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-02-19 N1 - Date created - 2012-11-19 N1 - Date revised - 2017-01-24 N1 - SuppNotes - Cited By: Nat Rev Mol Cell Biol. 2008 Feb;9(2):125-38 [18216769] J Lipid Res. 1997 Aug;38(8):1503-21 [9300773] J Lipid Res. 2008 Aug;49(8):1646-57 [18413899] Nat Med. 2008 Nov;14(11):1247-55 [18953351] J Biol Chem. 2008 Nov 21;283(47):32273-82 [18805791] Proc Natl Acad Sci U S A. 2009 Feb 17;106(7):2377-82 [19171898] J Biol Chem. 2009 Jun 5;284(23):15826-34 [19351882] Cell. 2009 Jun 26;137(7):1213-24 [19563754] PLoS One. 2009;4(9):e6951 [19750228] Can J Biochem Physiol. 1959 Aug;37(8):911-7 [13671378] J Appl Genet. 2004;45(4):461-7 [15523158] Biochem Biophys Res Commun. 2005 Feb 18;327(3):663-7 [15649398] Life Sci. 2006 Mar 27;78(18):2088-98 [16458936] J Neurosci. 2006 Apr 26;26(17):4630-7 [16641243] Eur J Pediatr. 2006 Jul;165(7):429-34 [16491383] J Lipid Res. 2007 May;48(5):1090-8 [17284776] Vitam Horm. 2007;76:45-65 [17628171] J Cell Sci. 2007 Nov 1;120(Pt 21):3838-49 [17940064] Am J Clin Nutr. 2008 May;87(5):1306-13 [18469254] Biochim Biophys Acta. 2009 Dec;1791(12):1155-65 [19699313] J Alzheimers Dis. 2009;18(4):829-41 [19749436] Mol Nutr Food Res. 2010 May;54(5):641-51 [20166146] Mol Nutr Food Res. 2010 May;54(5):652-60 [20169586] Mol Nutr Food Res. 2010 May;54(5):693-709 [20187127] Methods Mol Biol. 2011;697:83-91 [21116956] PLoS One. 2010;5(11):e15054 [21124786] Proc Natl Acad Sci U S A. 2011 Apr 5;108(14):5620-5 [21436030] Sci Transl Med. 2011 Apr 27;3(80):80ps16 [21525397] Curr Pharm Biotechnol. 2011 Jun;12(6):897-901 [21235443] Cold Spring Harb Perspect Biol. 2011 Jun;3(6). pii: a004804. doi: 10.1101/cshperspect.a004804 [21502308] Cell Microbiol. 2011 Jul;13(7):943-54 [21501360] Trends Neurosci. 2011 Aug;34(8):401-10 [21723623] Dev Cell. 2011 Sep 13;21(3):421-30 [21889421] Proc Natl Acad Sci U S A. 2011 Nov 22;108(47):18932-6 [22065762] Nutrients. 2012 Jun;4(6):467-90 [22822447] Hum Gene Ther. 2001 Feb 10;12(3):279-89 [11177564] Cell. 2001 Jul 27;106(2):157-69 [11511344] J Biol Chem. 2002 Jul 12;277(28):25290-6 [11997390] Arterioscler Thromb Vasc Biol. 2003 May 1;23(5):712-9 [12615688] Clin Genet. 2003 Oct;64(4):269-81 [12974729] J Nutr. 2003 Oct;133(10):3137-40 [14519797] Trends Cardiovasc Med. 2004 Feb;14(2):66-72 [15030792] Anal Biochem. 2004 Jul 15;330(2):317-31 [15203339] J Biol Chem. 1972 Mar 25;247(6):1918-29 [5012767] J Biol Chem. 1986 Dec 15;261(35):16769-74 [3782141] Pediatr Neurol. 1990 May-Jun;6(3):177-83 [2360958] Biochim Biophys Acta. 1995 Apr 24;1270(2-3):103-36 [7727535] Clin Pediatr (Phila). 1995 Apr;34(4):207-12 [7789014] Erratum In: J Biol Chem. 2013 Jan 4;288(1):296 N1 - Last updated - 2017-01-25 DO - http://dx.doi.org/10.1074/jbc.M112.357707 ER - TY - JOUR T1 - Cutaneous retinoic acid levels determine hair follicle development and downgrowth. AN - 1178666224; 23007396 AB - Retinoic acid (RA) is essential during embryogenesis and for tissue homeostasis, whereas excess RA is well known as a teratogen. In humans, excess RA is associated with hair loss. In the present study, we demonstrate that specific levels of RA, regulated by Cyp26b1, one of the RA-degrading enzymes, are required for hair follicle (hf) morphogenesis. Mice with embryonic ablation of Cyp26b1 (Cyp26b1(-/-)) have excessive endogenous RA, resulting in arrest of hf growth at the hair germ stage. The altered hf development is rescued by grafting the mutant skin on immunodeficient mice. Our results show that normalization of RA levels is associated with reinitiation of hf development. Conditional deficiency of Cyp26b1 in the dermis (En1Cre;Cyp26b1f/-) results in decreased hair follicle density and specific effect on hair type, indicating that RA levels also influence regulators of hair bending. Our results support the model of RA-dependent dermal signals regulating hf downgrowth and bending. To elucidate target gene pathways of RA, we performed microarray and RNA-Seq profiling of genes differentially expressed in Cyp26b1(-/-) skin and En1Cre;Cyp26b1f/- tissues. We show specific effects on the Wnt-catenin pathway and on members of the Runx, Fox, and Sox transcription factor families, indicating that RA modulates pathways and factors implicated in hf downgrowth and bending. Our results establish that proper RA distribution is essential for morphogenesis, development, and differentiation of hfs. JF - The Journal of biological chemistry AU - Okano, Junko AU - Levy, Clara AU - Lichti, Ulrike AU - Sun, Hong-Wei AU - Yuspa, Stuart H AU - Sakai, Yasuo AU - Morasso, Maria I AD - Developmental Skin Biology Section, NIAMS, National Institutes of Health, Bethesda, Maryland 20892, USA. Y1 - 2012/11/16/ PY - 2012 DA - 2012 Nov 16 SP - 39304 EP - 39315 VL - 287 IS - 47 KW - Keratolytic Agents KW - 0 KW - Tretinoin KW - 5688UTC01R KW - Cytochrome P-450 Enzyme System KW - 9035-51-2 KW - CYP26B1 protein, human KW - EC 1.14.14.1 KW - Cyp26b1 protein, mouse KW - Retinoic Acid 4-Hydroxylase KW - Index Medicus KW - Animals KW - Humans KW - Skin Transplantation KW - Mice, Nude KW - Mice KW - Transplantation, Homologous KW - Mice, Knockout KW - Tretinoin -- pharmacology KW - Hair Follicle -- enzymology KW - Dermis -- cytology KW - Gene Expression Regulation, Enzymologic -- drug effects KW - Cytochrome P-450 Enzyme System -- genetics KW - Hair Follicle -- cytology KW - Keratolytic Agents -- pharmacology KW - Cytochrome P-450 Enzyme System -- biosynthesis KW - Wnt Signaling Pathway -- drug effects KW - Dermis -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1178666224?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cutaneous+retinoic+acid+levels+determine+hair+follicle+development+and+downgrowth.&rft.au=Okano%2C+Junko%3BLevy%2C+Clara%3BLichti%2C+Ulrike%3BSun%2C+Hong-Wei%3BYuspa%2C+Stuart+H%3BSakai%2C+Yasuo%3BMorasso%2C+Maria+I&rft.aulast=Okano&rft.aufirst=Junko&rft.date=2012-11-16&rft.volume=287&rft.issue=47&rft.spage=39304&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M112.397273 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-02-19 N1 - Date created - 2012-11-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochim Biophys Acta. 2012 Jan;1821(1):222-9 [21914489] Mol Cell Endocrinol. 2012 Jan 30;348(2):348-60 [21504779] Development. 2012 Mar;139(5):843-58 [22318625] Development. 2012 Apr;139(8):1522-33 [22434869] J Cell Sci. 2012 Apr 1;125(Pt 7):1827-36 [22366455] Nat Genet. 2000 Apr;24(4):434-7 [10742113] Mol Cell Biol. 2000 Dec;20(24):9331-6 [11094083] Mech Dev. 2001 Sep;107(1-2):69-82 [11520664] Mech Dev. 2002 Jan;110(1-2):173-7 [11744378] Hum Mol Genet. 2001 Dec 15;10(26):2973-81 [11751679] Nature. 2001 Dec 20-27;414(6866):913-6 [11780064] J Invest Dermatol. 2002 Feb;118(2):216-25 [11841536] Dev Biol. 2003 Jul 1;259(1):123-36 [12812793] Hum Mol Genet. 2003 Nov 15;12(22):2931-40 [14506134] Hum Mol Genet. 2004 Nov 1;13(21):2595-606 [15367491] Trends Genet. 1992 Feb;8(2):55-61 [1566372] J Invest Dermatol. 1992 Jun;98(6 Suppl):42S-49S [1375251] J Invest Dermatol. 1992 Dec;99(6):842-7 [1281867] J Dermatol. 1992 Nov;19(11):774-80 [1284070] J Cell Physiol. 1996 Jun;167(3):556-61 [8655609] Development. 1999 Oct;126(20):4557-68 [10498690] Differentiation. 2004 Dec;72(9-10):512-26 [15617562] J Invest Dermatol. 2005 Jun;124(6):1119-26 [15955085] Mech Dev. 2005 Sep;122(9):988-97 [16024235] PLoS Biol. 2005 Nov;3(11):e331 [16162033] J Invest Dermatol. 2005 Nov;125(5):873-82 [16297183] Proc Natl Acad Sci U S A. 2006 Jun 13;103(24):9142-7 [16738056] Dev Biol. 2006 Aug 1;296(1):164-76 [16730693] Mol Endocrinol. 2006 Sep;20(9):2173-86 [16675541] Mech Dev. 2006 Aug;123(8):641-8 [16875803] Mech Dev. 2006 Nov;123(11):842-50 [17011173] Dev Biol. 2007 May 1;305(1):246-61 [17376426] Semin Cell Dev Biol. 2007 Apr;18(2):225-36 [17317239] Semin Cell Dev Biol. 2007 Apr;18(2):267-73 [17324597] Development. 2008 Mar;135(6):1019-28 [18256193] Development. 2008 Sep;135(18):3149-59 [18684741] Curr Biol. 2009 Feb 10;19(3):R132-42 [19211055] PLoS One. 2009;4(3):e4794 [19277121] Bioinformatics. 2009 May 1;25(9):1105-11 [19289445] Development. 2009 Aug;136(16):2815-23 [19605494] Development. 2009 Oct;136(19):3205-14 [19736321] Birth Defects Res C Embryo Today. 2009 Sep;87(3):263-72 [19750518] Methods Mol Biol. 2010;585:253-60 [19908008] J Dermatol Sci. 2010 Jan;57(1):2-11 [20022473] PLoS One. 2010;5(4):e10009 [20386733] Dev Cell. 2010 Apr 20;18(4):633-42 [20412777] Nat Biotechnol. 2010 May;28(5):511-5 [20436464] Exp Cell Res. 2010 Jul 1;316(11):1763-72 [20138864] J Cell Sci. 2011 Apr 15;124(Pt 8):1179-82 [21444748] Annu Rev Nutr. 2011 Aug 21;31:65-87 [21529158] Am J Hum Genet. 2011 Nov 11;89(5):595-606 [22019272] Biochem Pharmacol. 2012 Jan 1;83(1):149-63 [22020119] Nutrients. 2011 Apr;3(4):385-428 [22254103] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1074/jbc.M112.397273 ER - TY - JOUR T1 - Associations of ABCB1 and IL-10 genetic polymorphisms with sirolimus-induced dyslipidemia in renal transplant recipients. AN - 1273490102; 23073467 AB - Hyperlipidemia is a common adverse effect of sirolimus (SRL). We previously showed significant associations of ABCB1 3435C>T and IL-10 -1082G>A with log-transformed SRL dose-adjusted weighted-normalized trough. We further examined to see whether these polymorphisms were also associated with SRL-induced dyslipidemia. Genotyping was performed for ABCB1 1236C>T, 2677 G>T/A, and 3435C>T; CYP3A4 -392A>G; CYP3A5 6986A>G and 14690G>A; IL-10 -1082G>A; TNF -308G>A; and ApoE ε2, ε3, and ε4 alleles. The longitudinal changes of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglyceride (TG) levels after SRL treatment before statin therapy were analyzed by a linear mixed-effects model, with adjustments for selected covariates for each lipid. Under the dominant genetic model, ABCB1 3435C>T was associated with TC (P=0.0001) and LDL-C (PT under the recessive model and IL-10 -1082G>A under the dominant model were associated with log-transformed TG values (P=0.0051 and 0.0436, respectively). Mean TG value was 25.1% higher in ABCB1 1236TT homozygotes compared with ABCB1 1236C carriers and was 12.4% higher in IL-10 -1082AA homozygotes than -1082G carriers. ABCB1 polymorphisms were found to be associated with lipid responses to SRL treatment, confirming the role of ABCB1 gene in SRL pharmacokinetics and pharmacodynamics. Further studies are necessary to define the role of ABCB1 and IL-10 polymorphisms on SRL-induced dyslipidemia in renal transplantation. JF - Transplantation AU - Sam, Wai-Johnn AU - Chamberlain, Christine E AU - Lee, Su-Jun AU - Goldstein, Joyce A AU - Hale, Douglas A AU - Mannon, Roslyn B AU - Kirk, Allan D AU - Hon, Yuen Yi AD - Clinical Center Pharmacy Department, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/11/15/ PY - 2012 DA - 2012 Nov 15 SP - 971 EP - 977 VL - 94 IS - 9 KW - ABCB1 protein, human KW - 0 KW - Cholesterol, LDL KW - Immunosuppressive Agents KW - P-Glycoprotein KW - P-Glycoproteins KW - Triglycerides KW - Interleukin-10 KW - 130068-27-8 KW - Sirolimus KW - W36ZG6FT64 KW - Index Medicus KW - Triglycerides -- blood KW - Cholesterol, LDL -- blood KW - Dose-Response Relationship, Drug KW - Humans KW - Linear Models KW - Retrospective Studies KW - Aged KW - Longitudinal Studies KW - Graft Rejection -- prevention & control KW - Pharmacogenetics KW - Genotype KW - Adult KW - Middle Aged KW - Graft Rejection -- immunology KW - Immunosuppressive Agents -- pharmacokinetics KW - Immunosuppressive Agents -- therapeutic use KW - Male KW - Female KW - Immunosuppressive Agents -- adverse effects KW - Sirolimus -- adverse effects KW - Dyslipidemias -- genetics KW - P-Glycoprotein -- genetics KW - Kidney Transplantation -- immunology KW - Interleukin-10 -- genetics KW - Dyslipidemias -- epidemiology KW - Sirolimus -- therapeutic use KW - Sirolimus -- pharmacokinetics KW - Polymorphism, Single Nucleotide -- genetics KW - Dyslipidemias -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273490102?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Transplantation&rft.atitle=Associations+of+ABCB1+and+IL-10+genetic+polymorphisms+with+sirolimus-induced+dyslipidemia+in+renal+transplant+recipients.&rft.au=Sam%2C+Wai-Johnn%3BChamberlain%2C+Christine+E%3BLee%2C+Su-Jun%3BGoldstein%2C+Joyce+A%3BHale%2C+Douglas+A%3BMannon%2C+Roslyn+B%3BKirk%2C+Allan+D%3BHon%2C+Yuen+Yi&rft.aulast=Sam&rft.aufirst=Wai-Johnn&rft.date=2012-11-15&rft.volume=94&rft.issue=9&rft.spage=971&rft.isbn=&rft.btitle=&rft.title=Transplantation&rft.issn=1534-6080&rft_id=info:doi/10.1097%2FTP.0b013e31826b55e2 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-14 N1 - Date created - 2012-11-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Arterioscler Thromb Vasc Biol. 2009 Sep;29(9):1310-5 [19667110] Clin Chim Acta. 2009 May;403(1-2):198-202 [19285054] Transplantation. 2010 Apr 27;89(8):1001-8 [20061995] Am J Transplant. 2010 Feb;10(2):338-53 [20415903] Diabetes. 2010 Jun;59(6):1338-48 [20299475] Pharmacogenomics. 2010 Aug;11(8):1065-76 [20712525] Transplant Proc. 2010 Sep;42(7):2513-7 [20832534] DNA Cell Biol. 2010 Oct;29(10):629-37 [20578904] J Clin Lipidol. 2011 Mar-Apr;5(2):91-6 [21392722] Transplantation. 2011 Jul 27;92(2):183-9 [21558986] PLoS One. 2011;6(9):e23614 [21949682] Lancet. 2011 Oct 15;378(9800):1419-27 [22000138] Transplantation. 2011 Dec 27;92(12):1342-7 [22094953] Nephrol Dial Transplant. 2012 Feb;27(2):850-7 [21617197] Pharmacogenomics. 2009 Nov;10(11):1743-51 [19891551] Nephrol Dial Transplant. 2000 Jun;15(6):928 [10831671] J Am Soc Nephrol. 2000 Sep;11(9):1735-43 [10966499] Transplant Proc. 2000 Dec;32(8):2783-4 [11134804] Transplantation. 2001 Oct 15;72(7):1244-50 [11602850] Diabetes. 2002 Apr;51(4):1088-92 [11916930] Am J Transplant. 2002 Jul;2(6):551-9 [12118900] Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10347-52 [12145328] J Lipid Res. 2002 Aug;43(8):1170-80 [12177161] Transplantation. 2003 Mar 15;75(5):711-7 [12640314] Transplantation. 2003 Jul 27;76(2):375-82 [12883196] J Biol Chem. 2003 Dec 5;278(49):48529-33 [14507923] Am J Cardiol. 2004 Apr 15;93(8):1046-50 [15081455] Ann Intern Med. 2004 Jul 20;141(2):137-47 [15262670] J Lipid Res. 1992 Apr;33(4):447-54 [1388198] J Biol Chem. 1996 Feb 2;271(5):2634-40 [8576233] Biochemistry. 1996 Apr 16;35(15):4820-7 [8664272] J Biol Chem. 1997 Jan 10;272(2):1026-31 [8995398] Transpl Int. 2005 Jun;18(6):681-9 [15910294] Braz J Med Biol Res. 2005 Sep;38(9):1389-97 [16138223] Am J Transplant. 2005 Dec;5(12):2929-36 [16303007] Pharmacogenomics J. 2005;5(6):352-8 [16103896] Clin Pharmacol Ther. 2005 Nov;78(5):551-8 [16321621] Transplantation. 2005 Dec 27;80(12):1705-11 [16378065] Atherosclerosis. 2006 Mar;185(1):97-107 [16002074] Transplantation. 2006 Sep 15;82(5):603-11 [16969281] J Lipid Res. 2007 Sep;48(9):2072-8 [17563401] Transplantation. 2007 Oct 27;84(8):1029-36 [17989609] Clin J Am Soc Nephrol. 2008 May;3(3):822-8 [18322053] Ann Transplant. 2008;13(2):46-53 [18566560] Pharmacogenet Genomics. 2008 Aug;18(8):677-82 [18622260] Curr Protoc Hum Genet. 2009 Jan;Chapter 2:Unit 2.12 [19170031] Clin Pharmacol Ther. 2008 Oct;84(4):457-61 [19238649] Int J Clin Pharmacol Ther. 2010 Jan;48(1):36-45 [20040338] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1097/TP.0b013e31826b55e2 ER - TY - JOUR T1 - Aryl hydrocarbon receptor-induced adrenomedullin mediates cigarette smoke carcinogenicity in humans and mice. AN - 1273242867; 22993405 AB - Cigarette smoking (CS) is a leading cause of death worldwide. The aryl hydrocarbon receptor (AHR) is partially responsible for tobacco-induced carcinogenesis although the underlying mechanisms involving early effector genes have yet to be determined. Here, we report that adrenomedullin (ADM) significantly contributes to the carcinogenicity of tobacco-activated AHR. CS and AHR activating ligands induced ADM in vitro and in vivo but not in AHR-deficient fibroblasts and mice. Ectopic transfection of AHR rescued ADM expression in AHR(-/-) fibroblasts whereas AHR blockage with siRNA in wild type cells significantly decreased ADM expression. AHR regulates ADM expression through two intronic xenobiotic response elements located close to the start codon in the ADM gene. Using tissue microarrays we showed that ADM and AHR were coupregulated in lung tumor biopsies from smoker patients. Microarray meta-analysis of 304 independent microarray experiments showed that ADM is elevated in smokers and smokers with cancer. In addition, ADM coassociated with a subset of AHR responsive genes and efficiently differentiated patients with lung cancer from nonsmokers. In a novel preclinical model of CS-induced tumor progression, host exposure to CS extracts significantly elevated tumor ADM although systemic treatment with the ADM antagonist NSC16311 efficiently blocked tobacco-induced tumor growth. In conclusion, ADM significantly contributes the carcinogenic effect of AHR and tobacco combustion products. We suggest that therapeutics targeting the AHR/ADM axis may be of clinical relevance in the treatment of tobacco-induced pulmonary malignancies. ©2012 AACR. JF - Cancer research AU - Portal-Nuñez, Sergio AU - Shankavaram, Uma T AU - Rao, Mahadev AU - Datrice, Nicole AU - Atay, Scott AU - Aparicio, Marta AU - Camphausen, Kevin A AU - Fernández-Salguero, Pedro M AU - Chang, Han AU - Lin, Pinpin AU - Schrump, David S AU - Garantziotis, Stavros AU - Cuttitta, Frank AU - Zudaire, Enrique AD - Angiogenesis Core Facility, Radiation Oncology Branch, Radiation Oncology Branch, Surgery Branch, National Cancer Institute, NIH, Bethesda, Maryland 21702-1201, USA. Y1 - 2012/11/15/ PY - 2012 DA - 2012 Nov 15 SP - 5790 EP - 5800 VL - 72 IS - 22 KW - Receptors, Aryl Hydrocarbon KW - 0 KW - Tobacco Smoke Pollution KW - Adrenomedullin KW - 148498-78-6 KW - Index Medicus KW - Animals KW - Hep G2 Cells KW - Humans KW - MCF-7 Cells KW - Mice KW - Up-Regulation KW - Lung -- pathology KW - Lung -- metabolism KW - Administration, Inhalation KW - Transcriptional Activation KW - Adrenomedullin -- biosynthesis KW - Lung Neoplasms -- etiology KW - Cell Transformation, Neoplastic -- pathology KW - Cell Transformation, Neoplastic -- metabolism KW - Adrenomedullin -- genetics KW - Tobacco Smoke Pollution -- adverse effects KW - Receptors, Aryl Hydrocarbon -- metabolism KW - Cell Transformation, Neoplastic -- genetics KW - Lung Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273242867?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Temporal+shifts+in+the+skin+microbiome+associated+with+disease+flares+and+treatment+in+children+with+atopic+dermatitis&rft.au=Kong%2C+Heidi+H%3BOh%2C+Julia%3BDeming%2C+Clay%3BConlan%2C+Sean%3BGrice%2C+Elizabeth+A%3BBeatson%2C+Melony+A%3BNomicos%2C+Effie%3BPolley%2C+Eric+C%3BKomarow%2C+Hirsh+D%3BMurray%2C+Patrick+R%3BTurner%2C+Maria+L%3BSegre%2C+Julia+A&rft.aulast=Kong&rft.aufirst=Heidi&rft.date=2012-01-01&rft.volume=22&rft.issue=5&rft.spage=850&rft.isbn=&rft.btitle=&rft.title=Genome+Research&rft.issn=10889051&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-03-05 N1 - Date created - 2012-11-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Toxicol Pathol. 2003 Jan-Feb;31(1):22-30 [12597446] Oncogene. 2001 May 24;20(23):2937-45 [11420706] Genome Biol. 2003;4(4):R28 [12702209] Cancer Cell. 2003 Sep;4(3):191-6 [14522253] J Natl Cancer Inst. 2004 Jan 21;96(2):99-106 [14734699] Cancer Res. 2004 Jul 15;64(14):4707-10 [15256435] Endocrinology. 2004 Aug;145(8):3858-65 [15107357] J Clin Exp Neuropsychol. 2004 May;26(3):320-31 [15512923] J Biol Chem. 1990 Jun 5;265(16):9251-8 [2160969] Biochemistry. 1992 Jun 2;31(21):5060-7 [1318077] Science. 1995 May 5;268(5211):722-6 [7732381] Annu Rev Pharmacol Toxicol. 1995;35:307-40 [7598497] Endocrinology. 1995 Sep;136(9):4099-105 [7649118] J Biol Chem. 1995 Nov 3;270(44):26292-302 [7592839] Endocrinology. 1997 Dec;138(12):5597-604 [9389548] J Natl Cancer Inst. 1999 Jul 21;91(14):1194-210 [10413421] Neuroreport. 1999 Sep 9;10(13):2829-33 [10511448] J Clin Oncol. 2005 May 10;23(14):3243-56 [15886312] J Biol Chem. 2005 Aug 5;280(31):28731-41 [15946950] Am J Physiol Lung Cell Mol Physiol. 2005 Sep;289(3):L391-9 [15863442] Am J Pathol. 2002 Apr;160(4):1279-92 [11943713] Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):9990-5 [12107286] Lancet Oncol. 2002 Aug;3(8):461-9 [12147432] Nat Med. 2002 Aug;8(8):816-24 [12118244] J Natl Cancer Inst. 2002 Aug 21;94(16):1226-37 [12189226] Horm Metab Res. 2005 Oct;37(10):585-8 [16278779] Am J Pathol. 2006 Jan;168(1):280-91 [16400030] Br J Cancer. 2006 Jan 16;94(1):1-7 [16251875] Cancer Res. 2006 Jul 15;66(14):7143-50 [16849560] Clin Cancer Res. 2007 Jan 1;13(1):38-45 [17200336] Cancer Lett. 2007 Jul 18;252(2):184-94 [17189671] Cancer Res. 2007 Sep 15;67(18):8966-72 [17875740] Am J Pathol. 2007 Nov;171(5):1538-48 [17823287] J Clin Invest. 2008 Jan;118(1):23-6 [18097477] J Clin Invest. 2008 Feb;118(2):640-50 [18172554] CA Cancer J Clin. 2008 Mar-Apr;58(2):71-96 [18287387] Physiol Genomics. 2008 Jun 12;34(1):34-41 [18430810] Cell Signal. 2009 Apr;21(4):597-608 [19166930] Environ Health Perspect. 2009 Jul;117(7):1139-46 [19654925] Nature. 2010 Jan 14;463(7278):184-90 [20016488] Cancer Cell. 2010 Jan 19;17(1):89-97 [20129250] Gynecol Oncol. 2012 Apr;125(1):214-9 [22178239] J Exp Clin Cancer Res. 2012;31:19 [22400488] Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):779-82 [10639156] Mol Endocrinol. 2000 Jun;14(6):848-62 [10847587] Carcinogenesis. 2001 Jan;22(1):171-7 [11159756] Regul Pept. 2003 Apr 15;112(1-3):175-83 [12667640] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1158/0008-5472.CAN-12-0818 ER - TY - JOUR T1 - Atrazine acts as an endocrine disrupter by inhibiting cAMP-specific phosphodiesterase-4 AN - 1171895426; 17359767 AB - Atrazine, one of the most commonly used herbicides worldwide, acts as an endocrine disruptor, but the mechanism of its action has not been characterized. In this study, we show that atrazine rapidly increases cAMP levels in cultured rat pituitary and testicular Leydig cells in a concentration-dependent manner, but less effectively than 3-isobutyl-1-methylxanthine, a competitive non-specific inhibitor of phosphodiesterases (PDEs). In forskolin (an activator of adenylyl cyclase)- and probenecid (an inhibitor of cyclic nucleotide transporters)-treated cells, but not in 3-isobutyl-1-methylxanthine-treated cells, atrazine further increased cAMP levels, indicating that inhibition of PDEs accounts for accumulation of cAMP. In contrast to cAMP, atrazine did not alter cGMP levels, further indicating that it inhibits cAMP-specific PDEs. Atrazine-induced changes in cAMP levels were sufficient to stimulate prolactin release in pituitary cells and androgen production in Leydig cells, indicating that it acts as an endocrine disrupter both in cells that secrete by exocytosis of prestored hormones and in cells that secrete by de novo hormone synthesis. Rolipram abolished the stimulatory effect of atrazine on cAMP release in both cell types, suggesting that it acts as an inhibitor of PDE4s, isoforms whose mRNA transcripts dominate in pituitary and Leydig cells together with mRNA for PDE8A. In contrast, immortalized lacto-somatotrophs showed low expression of these mRNA transcripts and several fold higher cAMP levels compared to normal pituitary cells, and atrazine was unable to further increase cAMP levels. These results indicate that atrazine acts as a general endocrine disrupter by inhibiting cAMP-specific PDE4s. JF - Toxicology and Applied Pharmacology AU - Kucka, Marek AU - Pogrmic-Majkic, Kristina AU - Fa, Svetlana AU - Stojilkovic, Stanko S AU - Kovacevic, Radmila AD - Section on Cellular Signaling, Program in Developmental Neuroscience, NICHD, NIH, Bethesda, MD, USA, radmila.kovacevic@dbe.uns.ac.rs Y1 - 2012/11/15/ PY - 2012 DA - 2012 Nov 15 SP - 19 EP - 26 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 265 IS - 1 SN - 0041-008X, 0041-008X KW - Toxicology Abstracts KW - Androgens KW - Atrazine KW - Cyclic AMP KW - Cyclic GMP KW - Cyclic nucleotides KW - Endocrine disruptors KW - Exocytosis KW - Forskolin KW - Gene expression KW - Herbicides KW - Hormones KW - Leydig cells KW - Pituitary KW - Prolactin KW - Testes KW - phosphodiesterase KW - rolipram KW - X 24330:Agrochemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1171895426?accountid=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+and+Applied+Pharmacology&rft.atitle=Atrazine+acts+as+an+endocrine+disrupter+by+inhibiting+cAMP-specific+phosphodiesterase-4&rft.au=Kucka%2C+Marek%3BPogrmic-Majkic%2C+Kristina%3BFa%2C+Svetlana%3BStojilkovic%2C+Stanko+S%3BKovacevic%2C+Radmila&rft.aulast=Kucka&rft.aufirst=Marek&rft.date=2012-11-15&rft.volume=265&rft.issue=1&rft.spage=19&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+Applied+Pharmacology&rft.issn=0041008X&rft_id=info:doi/10.1016%2Fj.taap.2012.09.019 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-11-01 N1 - Last updated - 2012-12-03 N1 - SubjectsTermNotLitGenreText - rolipram; Testes; Leydig cells; Endocrine disruptors; Cyclic AMP; Exocytosis; Cyclic nucleotides; Herbicides; Hormones; Prolactin; Cyclic GMP; Gene expression; Pituitary; Atrazine; phosphodiesterase; Androgens; Forskolin DO - http://dx.doi.org/10.1016/j.taap.2012.09.019 ER - TY - JOUR T1 - Inactivation of the Dlc1 gene cooperates with downregulation of p15INK4b and p16Ink4a, leading to neoplastic transformation and poor prognosis in human cancer. AN - 1171879037; 23010077 AB - The tumor suppressor gene deleted in liver cancer-1 (DLC1), which encodes a protein with strong RhoGAP (GTPase activating protein) activity and weak Cdc42GAP activity, is inactivated in various human malignancies. Following Dlc1 inactivation, mouse embryo fibroblasts (MEF) with a conditional Dlc1 knockout allele reproducibly underwent neoplastic transformation. In addition to inactivation of Dlc1 and increased activity of Rho and Cdc42, transformation depended on the subsequent decreased expression of the Cdk4/6 inhibitors p15(Ink4b) and p16(Ink4a) together with increased expression and activation of Cdk4/6. The level of expression of these cell-cycle regulatory genes was relevant to human tumors with low DLC1 expression. Analysis of publicly available annotated datasets of lung and colon cancer with gene expression microarray profiles indicated that, in pairwise comparisons, low DLC1 expression occurred frequently together (P < 0.01) with downregulation of p15(Ink4b) or p16(Ink4a) or upregulation of CDK4 or CDK6. In addition, an unfavorable prognosis (P < 0.05) was associated with low DLC1 and low p15(Ink4b) in lung cancer and colon cancer, low DLC1 and low p16(Ink4a) in lung cancer, low DLC1 and high CDK4 in lung cancer, and low DLC1 and high CDK6 in colon cancer. Thus, several genes and biochemical activities collaborate with the inactivation of DLC1 to give rise to cell transformation in MEFs, and the identified genes are relevant to human tumors with low DLC1 expression. ©2012 AACR. JF - Cancer research AU - Qian, Xiaolan AU - Durkin, Marian E AU - Wang, Dunrui AU - Tripathi, Brajendra K AU - Olson, Lyra AU - Yang, Xu-Yu AU - Vass, William C AU - Popescu, Nicholas C AU - Lowy, Douglas R AD - Laboratories of Cellular Oncology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. Y1 - 2012/11/15/ PY - 2012 DA - 2012 Nov 15 SP - 5900 EP - 5911 VL - 72 IS - 22 KW - Cyclin-Dependent Kinase Inhibitor p15 KW - 0 KW - Cyclin-Dependent Kinase Inhibitor p16 KW - DLC-1 (deleted in liver cancer) protein, mouse KW - DLC1 protein, human KW - GTPase-Activating Proteins KW - Tumor Suppressor Proteins KW - rho-Associated Kinases KW - EC 2.7.11.1 KW - Cyclin-Dependent Kinase 4 KW - EC 2.7.11.22 KW - Cyclin-Dependent Kinase 6 KW - MAP Kinase Kinase 4 KW - EC 2.7.12.2 KW - Index Medicus KW - Animals KW - Gene Silencing KW - Humans KW - Prognosis KW - Mice KW - Genes, p16 KW - Fibroblasts -- metabolism KW - Cyclin-Dependent Kinase 4 -- metabolism KW - Gene Expression Regulation, Neoplastic KW - Genes, ras KW - rho-Associated Kinases -- metabolism KW - Fibroblasts -- pathology KW - Down-Regulation KW - Mice, Inbred C57BL KW - Cyclin-Dependent Kinase 6 -- metabolism KW - MAP Kinase Kinase 4 -- metabolism KW - Cyclin-Dependent Kinase Inhibitor p16 -- genetics KW - Male KW - Female KW - Cyclin-Dependent Kinase Inhibitor p15 -- genetics KW - GTPase-Activating Proteins -- genetics KW - Neoplasms -- pathology KW - Tumor Suppressor Proteins -- genetics KW - Neoplasms -- genetics KW - Cell Transformation, Neoplastic -- genetics KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1171879037?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inactivation+of+the+Dlc1+gene+cooperates+with+downregulation+of+p15INK4b+and+p16Ink4a%2C+leading+to+neoplastic+transformation+and+poor+prognosis+in+human+cancer.&rft.au=Qian%2C+Xiaolan%3BDurkin%2C+Marian+E%3BWang%2C+Dunrui%3BTripathi%2C+Brajendra+K%3BOlson%2C+Lyra%3BYang%2C+Xu-Yu%3BVass%2C+William+C%3BPopescu%2C+Nicholas+C%3BLowy%2C+Douglas+R&rft.aulast=Qian&rft.aufirst=Xiaolan&rft.date=2012-11-15&rft.volume=72&rft.issue=22&rft.spage=5900&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-12-2368 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-03-05 N1 - Date created - 2012-11-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1158/0008-5472.CAN-12-2368 ER - TY - JOUR T1 - Targeted oxidation of Torpedo californica acetylcholinesterase by singlet oxygen: identification of N-formylkynurenine tryptophan derivatives within the active-site gorge of its complex with the photosensitizer methylene blue. AN - 1113981265; 22888904 AB - The principal role of AChE (acetylcholinesterase) is termination of impulse transmission at cholinergic synapses by rapid hydrolysis of the neurotransmitter acetylcholine. The active site of AChE is near the bottom of a long and narrow gorge lined with aromatic residues. It contains a CAS (catalytic 'anionic' subsite) and a second PAS (peripheral 'anionic' site), the gorge mouth, both of which bind acetylcholine via π-cation interactions, primarily with two conserved tryptophan residues. It was shown previously that generation of (1)O(2) by illumination of MB (Methylene Blue) causes irreversible inactivation of TcAChE (Torpedo californica AChE), and suggested that photo-oxidation of tryptophan residues might be responsible. In the present study, structural modification of the TcAChE tryptophan residues induced by MB-sensitized oxidation was investigated using anti-N-formylkynurenine antibodies and MS. From these analyses, we determined that N-formylkynurenine derivatives were specifically produced from Trp(84) and Trp(279), present at the CAS and PAS respectively. Peptides containing these two oxidized tryptophan residues were not detected when the competitive inhibitors, edrophonium and propidium (which should displace MB from the gorge) were present during illumination, in agreement with their efficient protection against the MB-induced photo-inactivation. Thus the bound MB elicited selective action of (1)O(2) on the tryptophan residues facing on to the water-filled active-site gorge. The findings of the present study thus demonstrate the localized action and high specificity of MB-sensitized photo-oxidation of TcAChE, as well as the value of this enzyme as a model system for studying the mechanism of action and specificity of photosensitizing agents. JF - The Biochemical journal AU - Triquigneaux, Mathilde M AU - Ehrenshaft, Marilyn AU - Roth, Esther AU - Silman, Israel AU - Ashani, Yakov AU - Mason, Ronald P AU - Weiner, Lev AU - Deterding, Leesa J AD - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, DHHS, PO Box 12233 MD F0-03, Research Triangle Park, NC 27709, USA. triquigneauxm@mail.nih.gov Y1 - 2012/11/15/ PY - 2012 DA - 2012 Nov 15 SP - 83 EP - 91 VL - 448 IS - 1 KW - Cholinesterase Inhibitors KW - 0 KW - Photosensitizing Agents KW - Water KW - 059QF0KO0R KW - N'-formylkynurenine KW - 1022-31-7 KW - Singlet Oxygen KW - 17778-80-2 KW - Kynurenine KW - 343-65-7 KW - Propidium KW - 36015-30-2 KW - Edrophonium KW - 70FP3JLY7N KW - Tryptophan KW - 8DUH1N11BX KW - Acetylcholinesterase KW - EC 3.1.1.7 KW - Methylene Blue KW - T42P99266K KW - Index Medicus KW - Photochemistry KW - Animals KW - Mass Spectrometry KW - Models, Molecular KW - Edrophonium -- metabolism KW - Catalytic Domain KW - Electric Organ -- enzymology KW - Tryptophan -- chemistry KW - Hydrolysis KW - Kynurenine -- analogs & derivatives KW - Kynurenine -- chemistry KW - Structure-Activity Relationship KW - Oxidation-Reduction KW - Binding, Competitive KW - Propidium -- metabolism KW - Edrophonium -- pharmacology KW - Substrate Specificity KW - Propidium -- pharmacology KW - Protein Conformation KW - Cholinesterase Inhibitors -- pharmacology KW - Torpedo -- metabolism KW - Photosensitizing Agents -- chemistry KW - Methylene Blue -- metabolism KW - Singlet Oxygen -- pharmacology KW - Methylene Blue -- chemistry KW - Cholinesterase Inhibitors -- chemistry KW - Photosensitizing Agents -- metabolism KW - Photosensitizing Agents -- radiation effects KW - Acetylcholinesterase -- chemistry KW - Methylene Blue -- radiation effects KW - Acetylcholinesterase -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1113981265?accountid=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=FASEB+Journal&rft.atitle=Systemic+SIRT1+insufficiency+results+in+disruption+of+energy+homeostasis+and+steroid+hormone+metabolism+upon+high-fat-diet+feeding&rft.au=Purushotham%2C+Aparna%3BXu%2C+Qing%3BLi%2C+Xiaoling&rft.aulast=Purushotham&rft.aufirst=Aparna&rft.date=2012-01-01&rft.volume=26&rft.issue=2&rft.spage=656&rft.isbn=&rft.btitle=&rft.title=FASEB+Journal&rft.issn=08926638&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-14 N1 - Date created - 2012-10-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Acc Chem Res. 2000 May;33(5):299-306 [10813874] Protein Sci. 2012 Aug;21(8):1138-52 [22674800] Proc Natl Acad Sci U S A. 1979 Jun;76(6):2546-50 [288044] Biochim Biophys Acta. 1982 May 21;704(1):52-8 [7093289] Biochem Cell Biol. 1986 Jun;64(6):515-22 [3017385] Methods Enzymol. 1990;193:455-79 [2074832] Science. 1991 Aug 23;253(5022):872-9 [1678899] Biochim Biophys Acta. 1991 Sep 2;1075(1):42-9 [1892865] Proc Natl Acad Sci U S A. 1993 Oct 1;90(19):9031-5 [8415649] Curr Opin Pharmacol. 2005 Jun;5(3):293-302 [15907917] Rapid Commun Mass Spectrom. 2006;20(13):1989-94 [16755610] EMBO J. 2006 Jun 21;25(12):2746-56 [16763558] Rapid Commun Mass Spectrom. 2007;21(5):730-44 [17279597] Free Radic Biol Med. 2009 May 1;46(9):1260-6 [19353782] Proteomics. 2010 Feb;10(4):634-49 [19953542] Chem Soc Rev. 2010 Aug;39(8):3181-209 [20571680] Chem Biol Interact. 2010 Sep 6;187(1-3):10-22 [20138030] Photochem Photobiol Sci. 2010 Oct 28;9(10):1342-50 [20820672] Biomed Chromatogr. 2011 Jan;25(1-2):278-99 [21154892] Photochem Photobiol. 2011 Mar-Apr;87(2):308-16 [21155827] Behav Brain Res. 2011 Aug 10;221(2):555-63 [21145918] J Mass Spectrom. 2011 Oct;46(10):1030-8 [22012669] Photochem Photobiol. 2011 Nov-Dec;87(6):1321-9 [21770952] Nat Rev Cancer. 2003 May;3(5):380-7 [12724736] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1042/BJ20120992 ER - TY - JOUR T1 - Repeated dose toxicity and relative potency of 1,2,3,4,6,7-hexachloronaphthalene (PCN 66) 1,2,3,5,6,7-hexachloronaphthalene (PCN 67) compared to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) for induction of CYP1A1, CYP1A2 and thymic atrophy in female Harlan Sprague-Dawley rats. AN - 1033159283; 22813907 AB - In this study we assessed the relative toxicity and potency of the chlorinated naphthalenes 1,2,3,4,6,7-hexachloronaphthalene (PCN 66) and 1,2,3,5,6,7-hexachloronaphthalene (PCN 67) relative to that of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Chemicals were administered in corn oil:acetone (99:1) by gavage to female Harlan Sprague-Dawley rats at dosages of 0 (vehicle), 500, 1500, 5000, 50,000 and 500,000 ng/kg (PCN 66 and PCN 67) and 1, 3, 10, 100, and 300 ng/kg (TCDD) for 2 weeks. Histopathologic changes were observed in the thymus, liver and lung of TCDD treated animals and in the liver and thymus of PCN treated animals. Significant increases in CYP1A1 and CYP1A2 associated enzyme activity were observed in all animals exposed to TCDD, PCN 66 and PCN 67. Dose response modeling of CYP1A1, CYP1A2 and thymic atrophy gave ranges of estimated relative potencies, as compared to TCDD, of 0.0015-0.0072, for PCN 66 and 0.00029-0.00067 for PCN 67. Given that PCN 66 and PCN 67 exposure resulted in biochemical and histopathologic changes similar to that seen with TCDD, this suggests that they should be included in the WHO toxic equivalency factor (TEF) scheme, although the estimated relative potencies indicate that these hexachlorinated naphthalenes should not contribute greatly to the overall human body burden of dioxin-like activity. Copyright © 2012. Published by Elsevier Ireland Ltd. JF - Toxicology AU - Hooth, Michelle J AU - Nyska, Abraham AU - Fomby, Laurene M AU - Vasconcelos, Daphne Y AU - Vallant, Molly AU - DeVito, Michael J AU - Walker, Nigel J AD - Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. hooth@niehs.nih.gov Y1 - 2012/11/15/ PY - 2012 DA - 2012 Nov 15 SP - 85 EP - 93 VL - 301 IS - 1-3 KW - 1,2,3,4,6,7-hexachlorinated naphthalene KW - 0 KW - 1,2,3,5,6,7-hexachloronaphthalene KW - Hydrocarbons, Chlorinated KW - Naphthalenes KW - Polychlorinated Dibenzodioxins KW - Cytochrome P-450 CYP1A1 KW - EC 1.14.14.1 KW - Cytochrome P-450 CYP1A2 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Sprague-Dawley KW - Enzyme Induction -- drug effects KW - Dose-Response Relationship, Drug KW - Thymus Gland -- pathology KW - Atrophy KW - Thymus Gland -- drug effects KW - Female KW - Hydrocarbons, Chlorinated -- toxicity KW - Naphthalenes -- administration & dosage KW - Polychlorinated Dibenzodioxins -- administration & dosage KW - Polychlorinated Dibenzodioxins -- toxicity KW - Hydrocarbons, Chlorinated -- administration & dosage KW - Naphthalenes -- toxicity KW - Cytochrome P-450 CYP1A2 -- biosynthesis KW - Cytochrome P-450 CYP1A1 -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1033159283?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Repeated+dose+toxicity+and+relative+potency+of+1%2C2%2C3%2C4%2C6%2C7-hexachloronaphthalene+%28PCN+66%29+1%2C2%2C3%2C5%2C6%2C7-hexachloronaphthalene+%28PCN+67%29+compared+to+2%2C3%2C7%2C8-tetrachlorodibenzo-p-dioxin+%28TCDD%29+for+induction+of+CYP1A1%2C+CYP1A2+and+thymic+atrophy+in+female+Harlan+Sprague-Dawley+rats.&rft.au=Hooth%2C+Michelle+J%3BNyska%2C+Abraham%3BFomby%2C+Laurene+M%3BVasconcelos%2C+Daphne+Y%3BVallant%2C+Molly%3BDeVito%2C+Michael+J%3BWalker%2C+Nigel+J&rft.aulast=Hooth&rft.aufirst=Michelle&rft.date=2012-11-15&rft.volume=301&rft.issue=1-3&rft.spage=85&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=1879-3185&rft_id=info:doi/10.1016%2Fj.tox.2012.07.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-16 N1 - Date created - 2012-08-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Environ Pollut. 2003;121(1):81-5 [12475064] Environ Pollut. 2002;119(1):69-78 [12125730] Environ Sci Technol. 2003 Mar 15;37(6):1075-82 [12680657] Environ Int. 2003 Sep;29(6):861-77 [12850102] Food Addit Contam. 2003 Nov;20(11):995-1014 [14668151] Toxicol Appl Pharmacol. 2004 Jan 15;194(2):156-68 [14736496] Sci Total Environ. 1978 Nov;10(3):219-30 [734441] Toxicology. 1983 Mar-Apr;26(3-4):193-205 [6857695] Pharmacol Toxicol. 1991 Dec;69(6):442-9 [1766920] Arch Toxicol. 1992;66(4):237-44 [1514921] Arch Toxicol. 1993;67(8):558-64 [8285855] Environ Health Perspect. 1994 Jan;102 Suppl 1:195-204 [8187709] Toxicol Appl Pharmacol. 1995 Jun;132(2):237-44 [7540335] Arch Biochem Biophys. 1996 Jul 15;331(2):145-69 [8660694] Rapid Commun Mass Spectrom. 1997;11(4):410-4 [9069644] J Toxicol Environ Health A. 1998 Feb 20;53(4):293-311 [9490327] Environ Res. 1998 Jan;76(1):1-18 [9466892] Arch Environ Contam Toxicol. 1998 May;34(4):414-23 [9543513] Toxicol Sci. 2006 Oct;93(2):223-41 [16829543] Toxicol Pathol. 2007 Dec;35(7):880-9 [18098034] Environ Pollut. 2009 Mar;157(3):910-5 [19084307] Chemosphere. 2009 Oct;77(5):640-51 [19733382] Environ Sci Technol. 2010 Jul 1;44(13):5188-94 [20455569] Toxicol Pathol. 2010 Dec;38(7 Suppl):5S-81S [21191096] Chemosphere. 2011 Oct;85(3):322-8 [21783225] Arch Environ Contam Toxicol. 2000 Oct;39(3):273-81 [10948276] Toxicol Pathol. 2000 Nov-Dec;28(6):761-9 [11127289] Environ Toxicol Chem. 2001 Sep;20(9):1878-89 [11521813] Toxicol Pathol. 2002 Jan-Feb;30(1):93-6 [11890482] Environ Pollut. 2003;122(1):75-89 [12535597] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.tox.2012.07.005 ER - TY - JOUR T1 - Persistent Environmental Pollutants and Couple Fecundity: The LIFE Study AN - 1318696140; 17758874 AB - Background: Evidence suggesting that persistent environmental pollutants may be reproductive toxicants underscores the need for prospective studies of couples for whom exposures are measured. Objectives: We examined the relationship between selected persistent pollutants and couple fecundity as measured by time to pregnancy. Methods: A cohort of 501 couples who discontinued contraception to become pregnant was prospectively followed for 12 months of trying to conceive or until a human chorionic gonadotrophin (hCG) test confirmed pregnancy. Couples completed daily journals on lifestyle and provided biospecimens for the quantification of 9 organochlorine pesticides, 1 polybrominated biphenyl, 10 polybrominated diphenyl ethers, 36 polychlorinated biphenyls (PCBs), and 7 perfluorochemicals (PFCs) in serum. Using Cox models for discrete time, we estimated fecundability odds ratios (FORs) and 95% CIs separately for each partner's concentrations adjusting for age, body mass index, serum cotinine, serum lipids (except for PFCs), and study site (Michigan or Texas); sensitivity models were further adjusted for left truncation or time off of contraception ( less than or equal to 2 months) before enrollment. Results: The adjusted reduction in fecundability associated with standard deviation increases in log-transformed serum concentrations ranged between 18% and 21% for PCB congeners 118, 167, 209, and perfluorooctane sulfonamide in females; and between 17% and 29% for p,p-DDE and PCB congeners 138, 156, 157, 167, 170, 172, and 209 in males. The strongest associations were observed for PCB 167 (FOR 0.79; 95% CI: 0.64, 0.97) in females and PCB 138 (FOR = 0.71; 95% CI: 0.52, 0.98) in males. Conclusions: In this couple-based prospective cohort study with preconception enrollment and quantification of exposures in both female and male partners, we observed that a subset of persistent environmental chemicals were associated with reduced fecundity. JF - Environmental Health Perspectives AU - Louis, Germaine MBuck AU - Sundaram, Rajeshwari AU - Schisterman, Enrique F AU - Sweeney, Anne M AU - Lynch, Courtney D AU - Gore-Langton, Robert E AU - Maisog, Jose AU - Kim, Sungduk AU - Chen, Zhen AU - Barr, Dana B AD - Division of Epidemiology, Statistics and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland, USA Y1 - 2012/11/14/ PY - 2012 DA - 2012 Nov 14 SP - 231 EP - 236 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 121 IS - 2 SN - 0091-6765, 0091-6765 KW - Pollution Abstracts; Environment Abstracts; Health & Safety Science Abstracts KW - conception KW - cotinine KW - fecundity KW - organochlorine pesticides KW - polybrominated diphenyl ethers KW - polychlorinated biphenyls KW - perfluorochemicals KW - time to pregnancy KW - Polybrominated diphenyl ethers KW - Chemicals KW - Sensitivity KW - Fecundity KW - Organochlorine pesticides KW - Toxicants KW - Lipids KW - USA, Texas KW - PCB compounds KW - Pregnancy KW - ENA 09:Land Use & Planning KW - H 4000:Food and Drugs KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1318696140?accountid=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=Environmental+Health+Perspectives&rft.atitle=Persistent+Environmental+Pollutants+and+Couple+Fecundity%3A+The+LIFE+Study&rft.au=Louis%2C+Germaine+MBuck%3BSundaram%2C+Rajeshwari%3BSchisterman%2C+Enrique+F%3BSweeney%2C+Anne+M%3BLynch%2C+Courtney+D%3BGore-Langton%2C+Robert+E%3BMaisog%2C+Jose%3BKim%2C+Sungduk%3BChen%2C+Zhen%3BBarr%2C+Dana+B&rft.aulast=Louis&rft.aufirst=Germaine&rft.date=2012-11-14&rft.volume=121&rft.issue=2&rft.spage=231&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1205301 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-03-01 N1 - Last updated - 2015-05-13 N1 - SubjectsTermNotLitGenreText - Chemicals; Polybrominated diphenyl ethers; Sensitivity; Organochlorine pesticides; Fecundity; Toxicants; Lipids; PCB compounds; Pregnancy; USA, Texas DO - http://dx.doi.org/10.1289/ehp.1205301 ER - TY - CPAPER T1 - Site-Specific Detection and Imaging of Free Radicals in DNA Induced by Cu(11)-H2O2 Oxidizing System and Its Repair Using ESR, Immuno-Spin Trapping, Confocal Microscopy, LC-MS and MS/MS T2 - 19th Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2012) AN - 1313116774; 6197226 JF - 19th Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2012) AU - Bhattacharjee, Suchandra Y1 - 2012/11/14/ PY - 2012 DA - 2012 Nov 14 KW - Confocal microscopy KW - Imaging techniques KW - Trapping KW - Free radicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313116774?accountid=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=19th+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2012%29&rft.atitle=Site-Specific+Detection+and+Imaging+of+Free+Radicals+in+DNA+Induced+by+Cu%2811%29-H2O2+Oxidizing+System+and+Its+Repair+Using+ESR%2C+Immuno-Spin+Trapping%2C+Confocal+Microscopy%2C+LC-MS+and+MS%2FMS&rft.au=Bhattacharjee%2C+Suchandra&rft.aulast=Bhattacharjee&rft.aufirst=Suchandra&rft.date=2012-11-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+therapeutic+patents&rft.issn=1744-7674&rft_id=info:doi/10.1517%2F13543776.2012.646261 L2 - http://www.sfrbm.org/events.php?id=1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Mechanism of Thiol Modification by Reactive Nitrogen Oxide Species in Signal Transduction Pathways T2 - 19th Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2012) AN - 1313110775; 6197207 JF - 19th Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2012) AU - Wink Jr, David Y1 - 2012/11/14/ PY - 2012 DA - 2012 Nov 14 KW - Nitrogen oxides KW - Photochemicals KW - Transduction KW - Signal transduction KW - oxides KW - Thiols KW - Nitrogen UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313110775?accountid=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=19th+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2012%29&rft.atitle=Mechanism+of+Thiol+Modification+by+Reactive+Nitrogen+Oxide+Species+in+Signal+Transduction+Pathways&rft.au=Wink+Jr%2C+David&rft.aulast=Wink+Jr&rft.aufirst=David&rft.date=2012-11-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=19th+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfrbm.org/events.php?id=1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Enhancement of the Efficacy of Hypoxia Dependent Cytotoxicity of the Bioreductively Activated Hypoxia-Activated Prodrug TH-302 T2 - 19th Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2012) AN - 1313100524; 6197217 JF - 19th Annual Meeting of the Society for Free Radical Biology and Medicine (SFRBM 2012) AU - Takakusagi, Yoichi Y1 - 2012/11/14/ PY - 2012 DA - 2012 Nov 14 KW - Hypoxia KW - Cytotoxicity KW - prodrugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313100524?accountid=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=19th+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2012%29&rft.atitle=Enhancement+of+the+Efficacy+of+Hypoxia+Dependent+Cytotoxicity+of+the+Bioreductively+Activated+Hypoxia-Activated+Prodrug+TH-302&rft.au=Takakusagi%2C+Yoichi&rft.aulast=Takakusagi&rft.aufirst=Yoichi&rft.date=2012-11-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=19th+Annual+Meeting+of+the+Society+for+Free+Radical+Biology+and+Medicine+%28SFRBM+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfrbm.org/events.php?id=1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - NRTI backbone in HIV treatment: will it remain relevant? AN - 1114700295; 23083109 AB - Nucleoside reverse transcriptase inhibitors (NRTIs) remain a critical component of therapy for HIV-infected patients. The drugs are effective, relatively inexpensive and an important component of antiretroviral therapy (ART), particularly in areas where the introduction of effective therapy has been delayed. They are an essential part of initial therapy for HIV and for prevention of mother-to-child transmission; however, toxicities and resistance may limit their use. The role for pre-exposure prophylaxis (PrEP) to reduce sexual transmission of HIV is still undefined, but this use may have a significant impact on NRTI resistance worldwide, most particularly in areas where subtype C predominates. With increasing prevalence of resistant HIV, the approval of new agents that are effective against resistant virus, and those that use novel cellular targets, are essential. Large studies are now in progress examining the safety and efficacy of NRTI-sparing regimens, but results are not currently available. NRTIs may lose relevance in the not distant future unless steps are put in place to reduce the development and spread of NRTI-resistant viruses, and new NRTIs with minimal toxicity are developed that have a novel resistance profile. This article describes the principal NRTIs, their mechanism of action, and resistance and selected toxicities of the class and of the individual drugs. JF - Drugs AU - Tressler, Randall AU - Godfrey, Catherine AD - HJF, Division of AIDS, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MA 20892, USA. Y1 - 2012/11/12/ PY - 2012 DA - 2012 Nov 12 SP - 2051 EP - 2062 VL - 72 IS - 16 KW - Anti-HIV Agents KW - 0 KW - Reverse Transcriptase Inhibitors KW - HIV Reverse Transcriptase KW - EC 2.7.7.49 KW - Index Medicus KW - Randomized Controlled Trials as Topic KW - Drug Resistance, Viral KW - Humans KW - HIV Reverse Transcriptase -- antagonists & inhibitors KW - Adult KW - Treatment Outcome KW - Child KW - HIV -- drug effects KW - Anti-HIV Agents -- therapeutic use KW - HIV Infections -- drug therapy KW - Reverse Transcriptase Inhibitors -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1114700295?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=EUMETSAT+Meteorological+Satellite+Conference&rft.atitle=Merged+satellite+information+and+ground+measurements+of+the+precipitation+for+hydrological+modeling&rft.au=Dimitrov%2C+Dobri%3BBalabanova%2C+Snezhanka%3BKoshinchanov%2C+Georgy&rft.aulast=Dimitrov&rft.aufirst=Dobri&rft.date=2012-01-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=EUMETSAT+Meteorological+Satellite+Conference&rft.issn=10113932&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-03-12 N1 - Date created - 2012-10-22 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.2165/11640830-000000000-00000 ER - TY - JOUR T1 - Selenoproteins reduce susceptibility to DMBA-induced mammary carcinogenesis AN - 1458539658; 16900266 AB - Selenium is an essential micronutrient in the diet of humans and other mammals. Based largely on animal studies and epidemiological evidence, selenium is purported to be a promising cancer chemopreventive agent. However, the biological mechanisms by which chemopreventive activity takes place are poorly understood. It remains unclear whether selenium acts in its elemental form, through incorporation into organic compounds, through selenoproteins or any combination of these. The purpose of this study was to determine whether selenoproteins mitigate the risk of developing chemically induced mammary cancer. Selenoprotein expression was ablated in mouse mammary epithelial cells through genetic deletion of the selenocysteine (Sec) tRNA gene (Trsp), whose product, designated selenocysteine tRNA, is required for selenoprotein translation. Trsp floxed and mouse mammary tumor virus (MMTV)-cre mice were crossed to achieve tissue-specific excision of Trsp in targeted mammary glands. Eight- to twelve-week-old second generation Trsp super(fl/+); wt, Trsp super(fl/+); MMTV-c re, Trsp super(fl/fl); wt and Trsp super(fl/fl); MMTV- cre female mice were administered standard doses of the carcinogen, 7,12-dimethylbenzylbenz[a]antracene. Our results revealed that heterozygous, Trsp super(fl/+); MMTV-c re mice showed no difference in tumor incidence, tumor rate and survival compared with the Trsp super(fl/+); wt mice. However, 54.8% of homozygous Trsp super(fl/fl); MMTV-cre mice developed mammary tumors and exhibited significantly shorter survival than the corresponding Trsp super(fl/fl); wt mice, where only 36.4% developed tumors. Loss of the homozygous Trsp alleles was associated with the reduction of selenoprotein expression. The results suggest that mice with reduced selenoprotein expression have increased susceptibility to developing carcinogen-induced mammary tumors and that a major protective mechanism against carcinogen-induced mammary cancer requires the expression of these selenoproteins. JF - Carcinogenesis AU - Hudson, Tamaro S AU - Carlson, Bradley A AU - Hoeneroff, Mark J AU - Young, Heather A AU - Sordillo, Lorraine AU - Muller, William J AU - Hatfield, Dolph L AU - Green, Jeffrey E AD - Transgenic Oncogenesis and Genomics Section, Laboratory of Cancer Biology and Genetics, jegreen@nih.gov Y1 - 2012/11/06/ PY - 2012 DA - 2012 Nov 06 SP - 1 EP - 6 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 33 IS - 6 SN - 0143-3334, 0143-3334 KW - Toxicology Abstracts KW - Diets KW - tRNA Sec KW - Epithelial cells KW - Translation KW - selenoproteins KW - Clonal deletion KW - Mammary gland KW - Selenocysteine KW - Survival KW - Carcinogens KW - Tumors KW - Cancer KW - Selenium KW - Mouse mammary tumor virus KW - Gene deletion KW - Carcinogenesis KW - chemopreventive agents KW - Micronutrients KW - Organic compounds KW - X 24360:Metals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1458539658?accountid=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=Carcinogenesis&rft.atitle=Selenoproteins+reduce+susceptibility+to+DMBA-induced+mammary+carcinogenesis&rft.au=Hudson%2C+Tamaro+S%3BCarlson%2C+Bradley+A%3BHoeneroff%2C+Mark+J%3BYoung%2C+Heather+A%3BSordillo%2C+Lorraine%3BMuller%2C+William+J%3BHatfield%2C+Dolph+L%3BGreen%2C+Jeffrey+E&rft.aulast=Hudson&rft.aufirst=Tamaro&rft.date=2012-11-06&rft.volume=33&rft.issue=6&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Drug+and+Alcohol+Dependence&rft.issn=03768716&rft_id=info:doi/10.1016%2Fj.drugalcdep.2011.07.007 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-11-01 N1 - Last updated - 2013-12-04 N1 - SubjectsTermNotLitGenreText - Diets; Translation; Epithelial cells; tRNA Sec; Clonal deletion; selenoproteins; Mammary gland; Selenocysteine; Survival; Tumors; Carcinogens; Cancer; Selenium; Gene deletion; Carcinogenesis; chemopreventive agents; Organic compounds; Micronutrients; Mouse mammary tumor virus DO - http://dx.doi.org/10.1093/carcin/bgs129 ER - TY - CPAPER T1 - Testing for rare variant associations in the presence of missing data T2 - 62nd Annual Meeting of the American Society of Human Genetics AN - 1313078634; 6140604 JF - 62nd Annual Meeting of the American Society of Human Genetics AU - Livermore Auer, P AU - Leal, S AU - Wang, G Y1 - 2012/11/06/ PY - 2012 DA - 2012 Nov 06 KW - Data processing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313078634?accountid=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=62nd+Annual+Meeting+of+the+American+Society+of+Human+Genetics&rft.atitle=Testing+for+rare+variant+associations+in+the+presence+of+missing+data&rft.au=Livermore+Auer%2C+P%3BLeal%2C+S%3BWang%2C+G&rft.aulast=Livermore+Auer&rft.aufirst=P&rft.date=2012-11-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=62nd+Annual+Meeting+of+the+American+Society+of+Human+Genetics&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/2012meeting/pages/sessionlisting.shtml#sess25 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Neurodegeneration and disorders of copper transport T2 - 62nd Annual Meeting of the American Society of Human Genetics AN - 1313044573; 6140590 JF - 62nd Annual Meeting of the American Society of Human Genetics AU - Kaler, S Y1 - 2012/11/06/ PY - 2012 DA - 2012 Nov 06 KW - Copper KW - Neurodegeneration UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313044573?accountid=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=62nd+Annual+Meeting+of+the+American+Society+of+Human+Genetics&rft.atitle=Neurodegeneration+and+disorders+of+copper+transport&rft.au=Sotto%2C+Albert%3BRichard%2C+Jean-Louis%3BMessad%2C+Nourredine%3BMolinari%2C+Nicolas%3BJourdan%2C+Nathalie%3BSchuldiner%2C+Sophie%3BSultan%2C+Ariane%3BCarriere%2C+Christian%3BCanivet%2C+Bertrand%3BLandraud%2C+Luce%3BLina%2C+Gerard%3BLavigne%2C+Jean-Philippe&rft.aulast=Sotto&rft.aufirst=Albert&rft.date=2012-01-01&rft.volume=35&rft.issue=3&rft.spage=617&rft.isbn=&rft.btitle=&rft.title=Diabetes+Care&rft.issn=01495992&rft_id=info:doi/ L2 - http://www.ashg.org/2012meeting/pages/sessionlisting.shtml#sess25 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Friedreich ataxia and diseases of iron sulfur cluster assembly T2 - 62nd Annual Meeting of the American Society of Human Genetics AN - 1313044545; 6140589 JF - 62nd Annual Meeting of the American Society of Human Genetics AU - Rouault, T Y1 - 2012/11/06/ PY - 2012 DA - 2012 Nov 06 KW - Sulfur KW - Iron KW - Friedreich's ataxia UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313044545?accountid=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=62nd+Annual+Meeting+of+the+American+Society+of+Human+Genetics&rft.atitle=Friedreich+ataxia+and+diseases+of+iron+sulfur+cluster+assembly&rft.au=Rouault%2C+T&rft.aulast=Rouault&rft.aufirst=T&rft.date=2012-11-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=62nd+Annual+Meeting+of+the+American+Society+of+Human+Genetics&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/2012meeting/pages/sessionlisting.shtml#sess25 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Lessons learned from the NHLBI-Exome Sequencing Project T2 - 62nd Annual Meeting of the American Society of Human Genetics AN - 1312992312; 6140554 JF - 62nd Annual Meeting of the American Society of Human Genetics AU - Leal, S Y1 - 2012/11/06/ PY - 2012 DA - 2012 Nov 06 KW - Genetics KW - Human physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312992312?accountid=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=62nd+Annual+Meeting+of+the+American+Society+of+Human+Genetics&rft.atitle=Lessons+learned+from+the+NHLBI-Exome+Sequencing+Project&rft.au=Leal%2C+S&rft.aulast=Leal&rft.aufirst=S&rft.date=2012-11-06&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=62nd+Annual+Meeting+of+the+American+Society+of+Human+Genetics&rft.issn=&rft_id=info:doi/ L2 - http://www.ashg.org/2012meeting/pages/sessionlisting.shtml#sess25 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Occupational exposure to chlorinated solvents and risks of glioma and meningioma in adults AN - 1551613931; 20363782 AB - ObjectivesChlorinated solvents are classified as probable or possible carcinogens. It is unknown whether exposure to these agents increases the risk of malignant or benign brain tumours. Our objective was to evaluate associations of brain tumour risk with occupational exposure to six chlorinated solvents (ie, dichloromethane, chloroform, carbon tetrachloride, 1,1,1-trichloroethane, trichloroethylene and perchloroethylene).Methods489 glioma cases, 197 meningioma cases and 799 controls were enrolled in a hospital-based case-control study conducted at three USA hospitals in Arizona, Massachusetts and Pennsylvania. Information about occupational history was obtained through a detailed inperson interview that included job-specific modules of questions such that the interview was tailored to each individual's particular work history. An industrial hygienist assessed potential solvent exposure based on this information and an exhaustive review of the relevant industrial hygiene literature. Unconditional logistic regression models were used to calculate OR and 95% CI for each solvent for ever/never, duration, cumulative, average weekly and highest exposure.ResultsOverall, we found no consistent evidence of an increased risk of glioma or meningioma related to occupational exposure to the six chlorinated solvents evaluated. There was some suggestion of an association between carbon tetrachloride and glioma in analyses restricted to exposed subjects, with average weekly exposure above the median associated with increased risk compared with below the median exposure (OR = 7.1, 95% CI 1.1 to 45.2).ConclusionsWe found no consistent evidence for increased brain tumour risk related to chlorinated solvents. JF - Occupational and Environmental Medicine AU - Neta, Gila AU - Stewart, Patricia A AU - Rajaraman, Preetha AU - Hein, Misty J AU - Waters, Martha A AU - Purdue, Mark P AU - Samanic, Claudine AU - Coble, Joseph B AU - Linet, Martha S AU - Inskip, Peter D AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA Y1 - 2012/11/03/ PY - 2012 DA - 2012 Nov 03 SP - 793 EP - 801 PB - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom VL - 69 IS - 11 SN - 1351-0711, 1351-0711 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Risk assessment KW - Historical account KW - USA, Massachusetts KW - Solvents KW - Carcinogens KW - Brain tumors KW - Chloroform KW - Reviews KW - USA, Pennsylvania KW - USA, Arizona KW - Glioma KW - Trichloroethylene KW - Hygiene KW - Occupational exposure KW - Hospitals KW - R2 23060:Medical and environmental health KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551613931?accountid=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=Occupational+and+Environmental+Medicine&rft.atitle=Occupational+exposure+to+chlorinated+solvents+and+risks+of+glioma+and+meningioma+in+adults&rft.au=Neta%2C+Gila%3BStewart%2C+Patricia+A%3BRajaraman%2C+Preetha%3BHein%2C+Misty+J%3BWaters%2C+Martha+A%3BPurdue%2C+Mark+P%3BSamanic%2C+Claudine%3BCoble%2C+Joseph+B%3BLinet%2C+Martha+S%3BInskip%2C+Peter+D&rft.aulast=Neta&rft.aufirst=Gila&rft.date=2012-11-03&rft.volume=69&rft.issue=11&rft.spage=793&rft.isbn=&rft.btitle=&rft.title=Occupational+and+Environmental+Medicine&rft.issn=13510711&rft_id=info:doi/10.1136%2Foemed-2012-100742 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2015-03-20 N1 - SubjectsTermNotLitGenreText - Brain tumors; Risk assessment; Chloroform; Historical account; Reviews; Solvents; Carcinogens; Trichloroethylene; Glioma; Hygiene; Occupational exposure; Hospitals; USA, Massachusetts; USA, Pennsylvania; USA, Arizona DO - http://dx.doi.org/10.1136/oemed-2012-100742 ER - TY - JOUR T1 - Metabolic map and bioactivation of the anti-tumour drug noscapine AN - 1780513376; PQ0002784790 AB - BACKGROUND AND PURPOSE Noscapine is a promising anti-tumour agent. The purpose of the present study was to describe the metabolic map and investigate the bioactivation of noscapine. EXPERIMENTAL APPROACH Ultra-performance liquid chromatography coupled with electrospray ionization quadrupole time-of-flight mass spectrometry-based metabolomics was used to analyse the in vitro incubation mixtures, urine and faeces samples from mice treated with noscapine. Recombinant drug-metabolizing enzymes were employed to identify those involved in noscapine metabolism. Hepatic GSH levels and serum biochemistry were also carried out to determine reactive metabolites of noscapine. KEY RESULTS Several novel phase I metabolites of noscapine were detected after oral gavage of mice, including an N-demethylated metabolite, two hydroxylated metabolites, one metabolite undergoing both demethylation and cleavage of the methylenedioxy group and a bis-demethylated metabolite. Additionally, several novel glucuronides were detected, and their structures were elucidated through MS/MS fragmentology. Recombinant enzymes screening showed the involvement of several cytochromes P450, flavin-containing mono-oxygenase 1 and the UDP-glucuronosyltransferases UGT1A1, UGT1A3, UGT1A9 and UGT2B7, in noscapine metabolism. In vitro glutathione trapping revealed the existence of an ortho-quinone reactive intermediate formed through further oxidation of a catechol metabolite. However, this bioactivation process of noscapine does not occur in vivo. Similar to this result, altered glutathione levels in liver and serum biochemistry revealed no evidence of hepatic damage, thus indicating that, at least in mice, noscapine does not induce hepatotoxicity through bioactivation. CONCLUSIONS AND IMPLICATIONS A comprehensive metabolic map and bioactivation evaluation provides important information for the development of noscapine as an anti-tumour drug. JF - British Journal of Pharmacology AU - Fang, Zhong-Ze AU - Krausz, Kristopher W AU - Li, Fei AU - Cheng, Jie AU - Tanaka, Naoki AU - Gonzalez, Frank J AD - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 1271 EP - 1286 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 167 IS - 6 SN - 0007-1188, 0007-1188 KW - Toxicology Abstracts KW - Glutathione KW - Dimethylaniline monooxygenase (N-oxide-forming) KW - UDP-glucuronosyltransferase KW - Enzymes KW - Metabolites KW - Drug development KW - Trapping KW - hepatotoxicity KW - Catechol KW - Demethylation KW - Liquid chromatography KW - Urine KW - Oxidation KW - Liver KW - Cytochrome P450 KW - Feces KW - Drugs KW - Ionization KW - metabolomics KW - X 24310:Pharmaceuticals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780513376?accountid=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=British+Journal+of+Pharmacology&rft.atitle=Metabolic+map+and+bioactivation+of+the+anti-tumour+drug+noscapine&rft.au=Fang%2C+Zhong-Ze%3BKrausz%2C+Kristopher+W%3BLi%2C+Fei%3BCheng%2C+Jie%3BTanaka%2C+Naoki%3BGonzalez%2C+Frank+J&rft.aulast=Fang&rft.aufirst=Zhong-Ze&rft.date=2012-11-01&rft.volume=167&rft.issue=6&rft.spage=1271&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Pharmacology&rft.issn=00071188&rft_id=info:doi/10.1111%2Fj.1476-5381.2012.02067.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Glutathione; UDP-glucuronosyltransferase; Dimethylaniline monooxygenase (N-oxide-forming); Enzymes; Drug development; Metabolites; Trapping; hepatotoxicity; Catechol; Demethylation; Urine; Liquid chromatography; Oxidation; Liver; Cytochrome P450; Feces; Ionization; Drugs; metabolomics DO - http://dx.doi.org/10.1111/j.1476-5381.2012.02067.x ER - TY - JOUR T1 - Overcoming Limitations in Nanoparticle Drug Delivery: Triggered, Intravascular Release to Improve Drug Penetration into Tumors AN - 1668264803; 20331911 AB - This article suggests a straightforward and widely applicable solution to one of the core problems in nanoparticle-based therapeutic approaches, which is the pharmacologic problem of how to specifically and efficiently deliver cargo to tumor cells. JF - Cancer Research AU - Manzoor, Ashley A AU - Lindner, Lars H AU - Landon, Chelsea D AU - Park, Ji-Young AU - Simnick, Andrew J AU - Dreher, Matthew R AU - Das, Shiva AU - Hanna, Gabi AU - Park, Won AU - Chilkoti, Ashutosh AU - Koning, Gerben A AU - ten Hagen, Timo LM AU - Needham, David AU - Dewhirst, Mark W AD - Medical Physics Program, Department of Biomedical Engineering, Duke University; Department of Radiation Oncology, Duke University Medical Center, Durham, North Carolina; Laboratory Experimental Surgical Oncology, Section Surgical Oncology, Department of Surgery, Erasmus Medical Center, Rotterdam, The Netherlands; Department of Internal Medicine III, University Hospital Grosshadern, Ludwig-Maximilians University; CCG Hyperthermia, Helmholtz Zentrum Munchen, German Research Center for Environmental Health, Munich, Germany; and Radiology and Imaging Sciences, Clinical Center, National Institutes of Health, Bethesda, Maryland Y1 - 2012/11/01/ PY - 2012 DA - 2012 Nov 01 SP - 5566 EP - 5575 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 72 IS - 21 SN - 0008-5472, 0008-5472 KW - Biotechnology and Bioengineering Abstracts KW - Drug delivery KW - Tumors KW - Tumor cells KW - nanoparticles KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668264803?accountid=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=Cancer+Research&rft.atitle=Overcoming+Limitations+in+Nanoparticle+Drug+Delivery%3A+Triggered%2C+Intravascular+Release+to+Improve+Drug+Penetration+into+Tumors&rft.au=Manzoor%2C+Ashley+A%3BLindner%2C+Lars+H%3BLandon%2C+Chelsea+D%3BPark%2C+Ji-Young%3BSimnick%2C+Andrew+J%3BDreher%2C+Matthew+R%3BDas%2C+Shiva%3BHanna%2C+Gabi%3BPark%2C+Won%3BChilkoti%2C+Ashutosh%3BKoning%2C+Gerben+A%3Bten+Hagen%2C+Timo+LM%3BNeedham%2C+David%3BDewhirst%2C+Mark+W&rft.aulast=Manzoor&rft.aufirst=Ashley&rft.date=2012-11-01&rft.volume=72&rft.issue=21&rft.spage=5566&rft.isbn=&rft.btitle=&rft.title=Cancer+Research&rft.issn=00085472&rft_id=info:doi/10.1158%2F0008-5472.CAN-12-1683 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-04-02 N1 - SubjectsTermNotLitGenreText - Drug delivery; Tumors; nanoparticles; Tumor cells DO - http://dx.doi.org/10.1158/0008-5472.CAN-12-1683 ER - TY - JOUR T1 - Now What? Toward an Integrated Research and Practice Agenda in Distress Screening AN - 1567030707; 201433335 AB - Significant gains have been made in the detection and treatment of cancer, contributing to increased survival, but a cancer diagnosis and treatment may be accompanied by physical and psychosocial after-effects. Distress screening has been championed as a mechanism to identify patients with high levels of psychosocial morbidity for subsequent assessment and psychosocial care delivery. However, implementation of distress screening has been variable, in scope and in the consistency and quality of metrics and methods used. This capstone article identifies challenges in the measurement and implementation of distress screening and examines future opportunities for research and implementation. Adapted from the source document. JF - Journal of Psychosocial Oncology AU - Parry, Carla AU - Padgett, Lynne S AU - Zebrack, Brad AD - Office of Cancer Survivorship, National Cancer Institute, Bethesda, MD, USA Carla.parry@nih.gov Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 715 EP - 727 PB - Taylor & Francis, Philadelphia PA VL - 30 IS - 6 SN - 0734-7332, 0734-7332 KW - Screening KW - Care delivery KW - Psychological distress KW - Psychosocial factors KW - Morbidity KW - Cancer KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1567030707?accountid=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+Psychosocial+Oncology&rft.atitle=Now+What%3F+Toward+an+Integrated+Research+and+Practice+Agenda+in+Distress+Screening&rft.au=Parry%2C+Carla%3BPadgett%2C+Lynne+S%3BZebrack%2C+Brad&rft.aulast=Parry&rft.aufirst=Carla&rft.date=2012-11-01&rft.volume=30&rft.issue=6&rft.spage=715&rft.isbn=&rft.btitle=&rft.title=Journal+of+Psychosocial+Oncology&rft.issn=07347332&rft_id=info:doi/10.1080%2F07347332.2012.721486 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-10-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JPONED N1 - SubjectsTermNotLitGenreText - Screening; Psychological distress; Psychosocial factors; Cancer; Care delivery; Morbidity DO - http://dx.doi.org/10.1080/07347332.2012.721486 ER - TY - JOUR T1 - Leiomyosarcoma and sarcoma with myogenic differentiation AN - 1562675420; 19420601 AB - BACKGROUND: The objective of this study was to evaluate whether the distinction between leiomyosarcomas (LMS) and sarcomas with myogenic differentiation (SMD), based on the expression of muscular markers, has any clinical implications. METHODS: Patients with localized LMS (excluding any gynecologic subtype) or SMD who underwent surgery at the authors' institution from 1994 to 2010 were analyzed. Overall survival (OS) and the crude cumulative incidence of local recurrence and distant metastasis (DM) were calculated, and multivariable analyses for DM and OS were carried out. RESULTS: In total, 327 patients were studied (71% LMS, 29% SMD). The median follow-up was 58 months (interquartile range, 31-97 months). The 5-year overall survival rate was 72.9% (95% confidence interval, 66.3%-80.2%) for the patients with LMS and 64.4% (95% confidence interval, 53.7%-77.1%) for the patients with SMD. The 5-year crude cumulative incidence of distant metastasis was 36.2% (95% confidence interval, 30.1%-43.5%) in the LMS group and 32.6% (95% confidence interval, 24%-44.2%) in the SMD group. Although tumor grade in LMS identified 3 distinct classes of risk, patients with grade 2 and grade 3 SMD had a similar course. The median postmetastasis survival was longer in patients with grade 3 LMS compared versus patients with grade 3 SMD (31 months vs 15 months, respectively). In patients who had grade 3 lesions, adjuvant chemotherapy yielded a better outcome in the SMD group compared with the LMS group (hazard ratio, 0.38). Patients who had superficial LMS had better outcomes compared with patients who had superficial SMD. CONCLUSIONS: The current results indicated that LMS and SMD do not share the same natural history. A limited prognostic impact of grade was observed in patients with SMD. Differences in response to chemotherapy should be taken into account in planning the therapeutic approach for patients with these tumors. The current clinical observations may correspond to the biology of a different disease and deserve further study. Cancer 2012. copyright 2012 American Cancer Society. Sarcoma with myogenic differentiation and leiomyosarcoma have different natural histories and sensitivity to therapies. These entities should be considered different diseases, and patients with such tumors should receive different therapies. JF - Cancer AU - Colombo, Chiara AU - Miceli, Rosalba AU - Collini, Paola AU - Radaelli, Stefano AU - Palassini, Elena AU - Stacchiotti, Silvia AU - Fiore, Marco AU - Mariani, Luigi AU - Casali, Paolo G AU - Gronchi, Alessandro AD - Department of Surgery-Sarcoma Service, Scientific Institutes for Recovery and Cure (IRCCS) Foundation, National Cancer Institute, Milan, Italy. Y1 - 2012/11// PY - 2012 DA - Nov 2012 SP - 5349 EP - 5357 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 118 IS - 21 SN - 0008-543X, 0008-543X KW - Risk Abstracts KW - sarcoma KW - leiomyosarcoma KW - myogenic differentiation KW - survival KW - metastasis KW - prognostic factors KW - Health risks KW - Historical account KW - Sensitivity KW - Chemotherapy KW - Surgery KW - Sarcoma KW - Survival KW - Lesions KW - Tumors KW - Cancer KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562675420?accountid=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=Leiomyosarcoma+and+sarcoma+with+myogenic+differentiation&rft.au=Colombo%2C+Chiara%3BMiceli%2C+Rosalba%3BCollini%2C+Paola%3BRadaelli%2C+Stefano%3BPalassini%2C+Elena%3BStacchiotti%2C+Silvia%3BFiore%2C+Marco%3BMariani%2C+Luigi%3BCasali%2C+Paolo+G%3BGronchi%2C+Alessandro&rft.aulast=Colombo&rft.aufirst=Chiara&rft.date=2012-11-01&rft.volume=118&rft.issue=21&rft.spage=5349&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=0008543X&rft_id=info:doi/10.1002%2Fcncr.27569 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2014-10-02 N1 - SubjectsTermNotLitGenreText - Sensitivity; Historical account; Health risks; Surgery; Chemotherapy; Sarcoma; Lesions; Survival; Tumors; Cancer DO - http://dx.doi.org/10.1002/cncr.27569 ER - TY - JOUR T1 - Depressive symptoms are associated with weight gain among women AN - 1541983978; 201423148 AB - Many studies have linked depression and obesity; few have more than two assessments of depressive symptoms and adiposity to address the potential bidirectional relationship between adiposity and depressive symptoms from young adulthood through old age. We tested whether baseline depressive symptoms are associated with changes in weight, whether baseline adiposity is associated with changes in depressive symptoms, and whether these associations vary by sex. Participants (n=2251; 47% female) were from the Baltimore Longitudinal Study of Aging (BLSA). Using hierarchical linear modeling (HLM) on 30 years of data, the trajectory of adiposity and depressive symptoms over adulthood was estimated from >10 000 observations (mean=4.5 assessments per participant) of body mass index (BMI; kg/m2), waist circumference and hip circumference and >10 000 observations (mean=4.5 assessments per participant) of the Center for Epidemiological Studies Depression Scale (CES-D). Baseline depressive symptoms and adiposity were then tested as predictors of the trajectory of adiposity and depressive symptoms respectively. Additional analyses tested for sex-specific associations. Sex moderated the association between depressive symptoms and weight gain such that women who experienced depressed affect had greater increases in BMI (b interaction=0.12, s.e.=0.04), waist (b interaction=0.22, s.e.=0.10) and hip circumference (b interaction=0.20, s.e.=0.07) across the adult lifespan, controlling for relevant demographic and behavioral covariates. Baseline adiposity was unrelated to the trajectory of depressive symptoms (median b=0.00) for both sexes. Women who experience symptoms of depression tend to gain more weight across adulthood than men who experience such symptoms. Whether an individual was normal weight or overweight was unrelated to changes in depressive symptoms across adulthood. Adapted from the source document. JF - Psychological Medicine AU - Sutin, A R AU - Zonderman, A B AD - National Institute on Aging, NIH, DHHS, Baltimore, MD, USA sutina@mail.nih.gov Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 2351 EP - 2360 PB - Cambridge University Press, UK VL - 42 IS - 11 SN - 0033-2917, 0033-2917 KW - Assessment KW - Symptoms KW - Depression KW - Adulthood KW - Women KW - Body Mass Index KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541983978?accountid=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=Depressive+symptoms+are+associated+with+weight+gain+among+women&rft.au=Sutin%2C+A+R%3BZonderman%2C+A+B&rft.aulast=Sutin&rft.aufirst=A&rft.date=2012-11-01&rft.volume=42&rft.issue=11&rft.spage=2351&rft.isbn=&rft.btitle=&rft.title=Psychological+Medicine&rft.issn=00332917&rft_id=info:doi/10.1017%2FS0033291712000566 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-07-01 N1 - Number of references - 70 N1 - Last updated - 2016-09-27 N1 - CODEN - PSMDCO N1 - SubjectsTermNotLitGenreText - Depression; Adulthood; Body Mass Index; Assessment; Women; Symptoms DO - http://dx.doi.org/10.1017/S0033291712000566 ER - TY - JOUR T1 - The Effectiveness of Training to Improve Person Perception Accuracy: A Meta-Analysis AN - 1541977360; 201415227 AB - Making accurate perceptions of others is a valuable skill. This meta-analysis examines whether accurate person perception is a skill amenable to training in nonclinical adult populations and, if training can increase accuracy, what are the most effective training methods. Across person perception domains, training interventions significantly increased accuracy. Training approach mattered more than length of training. Practice and feedback were more effective approaches than instruction alone; however, a combination of training approaches was the most effective intervention. Results of this meta-analysis advance person perception theory and offer practical advice for future development of trainings to increase person perception accuracy. Adapted from the source document. JF - Basic and Applied Social Psychology AU - Blanch-Hartigan, Danielle AU - Andrzejewski, Susan A AU - Hill, Krista M AD - National Cancer Institute danielleblanch@gmail.com Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 483 EP - 498 PB - Taylor & Francis, Philadelphia PA VL - 34 IS - 6 SN - 0197-3533, 0197-3533 KW - Perceptions KW - Interventions KW - Person perception KW - Accuracy KW - Feedback KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1541977360?accountid=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=Basic+and+Applied+Social+Psychology&rft.atitle=The+Effectiveness+of+Training+to+Improve+Person+Perception+Accuracy%3A+A+Meta-Analysis&rft.au=Blanch-Hartigan%2C+Danielle%3BAndrzejewski%2C+Susan+A%3BHill%2C+Krista+M&rft.aulast=Blanch-Hartigan&rft.aufirst=Danielle&rft.date=2012-11-01&rft.volume=34&rft.issue=6&rft.spage=483&rft.isbn=&rft.btitle=&rft.title=Basic+and+Applied+Social+Psychology&rft.issn=01973533&rft_id=info:doi/10.1080%2F01973533.2012.728122 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-07-01 N1 - Last updated - 2016-09-27 N1 - CODEN - BASPEG N1 - SubjectsTermNotLitGenreText - Person perception; Accuracy; Interventions; Feedback; Perceptions DO - http://dx.doi.org/10.1080/01973533.2012.728122 ER - TY - JOUR T1 - Zoonotic Infections Among Employees from Great Smoky Mountains and Rocky Mountain National Parks, 2008-2009 AN - 1516754261; 17718361 AB - U.S. National Park Service employees may have prolonged exposure to wildlife and arthropods, placing them at increased risk of infection with endemic zoonoses. To evaluate possible zoonotic risks present at both Great Smoky Mountains (GRSM) and Rocky Mountain (ROMO) National Parks, we assessed park employees for baseline seroprevalence to specific zoonotic pathogens, followed by evaluation of incident infections over a 1-year study period. Park personnel showed evidence of prior infection with a variety of zoonotic agents, including California serogroup bunyaviruses (31.9%), Bartonella henselae (26.7%), spotted fever group rickettsiae (22.2%), Toxoplasma gondii (11.1%), Anaplasma phagocytophilum (8.1%), Brucella spp. (8.9%), flaviviruses (2.2%), and Bacillus anthracis (1.5%). Over a 1-year study period, we detected incident infections with leptospirosis (5.7%), B. henselae (5.7%), spotted fever group rickettsiae (1.5%), T. gondii (1.5%), B. anthracis (1.5%), and La Crosse virus (1.5%) in staff members at GRSM, and with spotted fever group rickettsiae (8.5%) and B. henselae (4.3%) in staff at ROMO. The risk of any incident infection was greater for employees who worked as resource managers (OR 7.4; 95% CI 1.4, 37.5; p=0.02), and as law enforcement rangers/rescue crew (OR 6.5; 95% CI 1.1, 36.5; p=0.03), relative to those who worked primarily in administration or management. The results of this study increase our understanding of the pathogens circulating within both parks, and can be used to inform the development of effective guidelines and interventions to increase visitor and staff awareness and help prevent exposure to zoonotic agents. JF - Vector Borne and Zoonotic Diseases AU - Adjemian, J AU - Weber, IB AU - McQuiston, J AU - Griffith, K S AU - Mead, P S AU - Nicholson, W AU - Roche, A AU - Schriefer, M AU - Fischer, M AU - Kosoy, O AU - Laven, J J AU - Stoddard, R A AU - Hoffmaster, A R AU - Smith, T AD - National Institute of Allergy and Infectious Diseases, Epidemic Intelligence Service, Laboratory of Clinical Infectious Diseases, Quarters 15 B-1, 8 West Drive MSC 2665, Bethesda, MD 20892, USA, Jennifer.adjemian@nih.gov Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 922 EP - 931 VL - 12 IS - 11 SN - 1530-3667, 1530-3667 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources KW - La Crosse virus KW - Resource management KW - USA, Colorado, Rocky Mountain Natl. Park KW - Anaplasma phagocytophilum KW - Leptospira KW - Surveillance and enforcement KW - Brucella KW - Pathogens KW - Hosts KW - Bacillus anthracis KW - Disease transmission KW - North America, Rocky Mts. KW - Endemic species KW - Arthropoda KW - Personnel KW - Toxoplasma gondii KW - Bartonella henselae KW - USA, California 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/1516754261?accountid=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=Vector+Borne+and+Zoonotic+Diseases&rft.atitle=Zoonotic+Infections+Among+Employees+from+Great+Smoky+Mountains+and+Rocky+Mountain+National+Parks%2C+2008-2009&rft.au=Adjemian%2C+J%3BWeber%2C+IB%3BMcQuiston%2C+J%3BGriffith%2C+K+S%3BMead%2C+P+S%3BNicholson%2C+W%3BRoche%2C+A%3BSchriefer%2C+M%3BFischer%2C+M%3BKosoy%2C+O%3BLaven%2C+J+J%3BStoddard%2C+R+A%3BHoffmaster%2C+A+R%3BSmith%2C+T&rft.aulast=Adjemian&rft.aufirst=J&rft.date=2012-11-01&rft.volume=12&rft.issue=11&rft.spage=922&rft.isbn=&rft.btitle=&rft.title=Vector+Borne+and+Zoonotic+Diseases&rft.issn=15303667&rft_id=info:doi/10.1089%2Fvbz.2011.0917 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2016-10-12 N1 - SubjectsTermNotLitGenreText - Endemic species; Resource management; Personnel; Surveillance and enforcement; Hosts; Pathogens; Disease transmission; La Crosse virus; Arthropoda; Toxoplasma gondii; Leptospira; Anaplasma phagocytophilum; Brucella; Bartonella henselae; Bacillus anthracis; North America, Rocky Mts.; USA, Colorado, Rocky Mountain Natl. Park; USA, California DO - http://dx.doi.org/10.1089/vbz.2011.0917 ER - TY - JOUR T1 - Sex Differences in Prevalence and Comorbidity of Alcohol and Drug Use Disorders: Results From Wave 2 of the National Epidemiologic Survey on Alcohol and Related Conditions AN - 1463069471; 201325876 AB - Objective: The present study examined sex differences in lifetime Axis I and II psychiatric comorbidity of DSM-IV alcohol use disorders (AUDs) and drug use disorders (DUDs) among general population U.S. adults. Method: Using data from Waves 1 and 2 of the National Epidemiologic Survey on Alcohol and Related Conditions, Wave 2 lifetime prevalences of each disorder comorbid with alcohol abuse, alcohol dependence, drug abuse, and drug dependence were compared between men and women. Sex-specific associations of alcohol, any drug, and cannabis- and cocaine-specific abuse and dependence with each comorbid disorder were examined using logistic regression, first with adjustment for sociodemographic variables and then with additional adjustment for all other psychiatric disorders. Results: Prevalences of most comorbid disorders differed significantly by sex among respondents with each AUD and DUD. However, after adjustment for sociodemographic characteristics and additional co-occurring psychiatric diagnoses, there were few sex differences in unique comorbid associations of specific AUDs and DUDs with specific psychiatric disorders. Conclusions: Rates of psychiatric disorders comorbid with AUDs and DUDs indicate large burdens of morbidity in both sexes, highlighting the need for careful assessment and appropriate treatment of both substance use and mental health disorders. The unique comorbid associations with AUDs and DUDs identified in this study further indicate the need for prospective etiological research to characterize these associations, their underlying mechanisms, and the possible sex specificity of those mechanisms. Adapted from the source document. JF - Journal of Studies on Alcohol and Drugs AU - Goldstein, Rise B AU - Dawson, Deborah A AU - Chou, S Patricia AU - Grant, Bridget F AD - 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 - 2012/11// PY - 2012 DA - November 2012 SP - 938 EP - 950 PB - Center of Alcohol Studies, Rutgers, The State University of New Jersey, Piscataway VL - 73 IS - 6 SN - 1937-1888, 1937-1888 KW - Psychiatric disorders KW - Drug abuse KW - Gender differences KW - Adjustment KW - Substance abuse KW - Comorbidity KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1463069471?accountid=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=Sex+Differences+in+Prevalence+and+Comorbidity+of+Alcohol+and+Drug+Use+Disorders%3A+Results+From+Wave+2+of+the+National+Epidemiologic+Survey+on+Alcohol+and+Related+Conditions&rft.au=Goldstein%2C+Rise+B%3BDawson%2C+Deborah+A%3BChou%2C+S+Patricia%3BGrant%2C+Bridget+F&rft.aulast=Goldstein&rft.aufirst=Rise&rft.date=2012-11-01&rft.volume=73&rft.issue=6&rft.spage=938&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 - 2013-12-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Comorbidity; Gender differences; Psychiatric disorders; Drug abuse; Adjustment; Substance abuse ER - TY - JOUR T1 - Drugs that target pathogen public goods are robust against evolved drug resistance AN - 1448223103; 18676313 AB - Pathogen drug resistance is a central problem in medicine and public health. It arises through somatic evolution, by mutation and selection among pathogen cells within a host. Here, we examine the hypothesis that evolution of drug resistance could be reduced by developing drugs that target the secreted metabolites produced by pathogen cells instead of directly targeting the cells themselves. Using an agent-based computational model of an evolving population of pathogen cells, we test this hypothesis and find support for it. We also use our model to explain this effect within the framework of standard evolutionary theory. We find that in our model, the drugs most robust against evolved drug resistance are those that target the most widely shared external products, or 'public goods', of pathogen cells. We also show that these drugs exert a weak selective pressure for resistance because they create only a weak correlation between drug resistance and cell fitness. The same principles apply to design of vaccines that are robust against vaccine escape. Because our theoretical results have crucial practical implications, they should be tested by empirical experiments. JF - Evolutionary Applications AU - Pepper, John W AD - Division of Cancer Prevention, National Cancer Institute, Bethesda, MD, USA. Y1 - 2012/11// PY - 2012 DA - Nov 2012 SP - 757 EP - 761 PB - John Wiley & Sons, Ltd., Baffins Lane Chichester W. Sussex PO19 1UD United Kingdom VL - 5 IS - 7 SN - 1752-4571, 1752-4571 KW - Ecology Abstracts; Environment Abstracts; Health & Safety Science Abstracts KW - Fitness KW - Mathematical models KW - Drug resistance KW - Metabolites KW - Pathogens KW - Public health KW - Vaccines KW - Drugs KW - Mutation KW - Evolution KW - D 04040:Ecosystem and Ecology Studies KW - H 4000:Food and Drugs KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1448223103?accountid=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=Evolutionary+Applications&rft.atitle=Drugs+that+target+pathogen+public+goods+are+robust+against+evolved+drug+resistance&rft.au=Pepper%2C+John+W&rft.aulast=Pepper&rft.aufirst=John&rft.date=2012-11-01&rft.volume=5&rft.issue=7&rft.spage=757&rft.isbn=&rft.btitle=&rft.title=Evolutionary+Applications&rft.issn=17524571&rft_id=info:doi/10.1111%2Fj.1752-4571.2012.00254.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-10-01 N1 - Last updated - 2014-05-15 N1 - SubjectsTermNotLitGenreText - Fitness; Mathematical models; Drug resistance; Metabolites; Vaccines; Pathogens; Mutation; Evolution; Public health; Drugs DO - http://dx.doi.org/10.1111/j.1752-4571.2012.00254.x ER - TY - JOUR T1 - Dichlorodiphenyltrichloroethane and risk of hepatocellular carcinoma AN - 1443373407; 18611590 AB - Dichlorodiphenyltrichloroethane (p,p'-DDT), an organochlorine pesticide known to have deleterious health effects in humans, has been linked to hepatocellular carcinoma (HCC) in rodents. A recent study has reported that p,p'-DDT and its most persistent metabolite, dichlorodiphenyldichloroethylene (p,p'-DDE), may also be associated with HCC in humans. To examine whether there is an association between p,p'-DDT and/or p,p'-DDE in a population at high-risk of developing HCC, a nested case-control study was conducted within the 83,794 person Haimen City Cohort in China. Sera and questionnaire data were collected from all participants between 1992 and 1993. This study included 473 persons who developed HCC and 492 who did not, frequency matched on sex, age and area of residence. p,p'-DDT and p,p'-DDE levels were determined by mass spectrometry. Hepatitis B viral infection status (based on hepatitis B virus surface antigen; HBsAg) was also determined. p,p'-DDT and/or p,p'-DDE serum levels were significantly associated with sex, area of residence, occupation, alcohol consumption and cigarette smoking. Adjusting for age, sex, area of residence, HBsAg, family history of HCC, history of acute hepatitis, smoking, alcohol, occupation (farmer vs. other) and levels of p,p'-DDT or p,p'-DDE, odds ratios (OR) and 95% confidence intervals (CI) were calculated via unconditional logistic regression. Overall, the highest quintile of p,p'-DDT was associated with an increased risk of HCC, OR = 2.96 95% CI; 1.19-7.40. There were no statistically significant associations with p,p'-DDE. Overall, these results suggest that recent exposure to p,p'-DDT may increase risk of HCC. JF - International Journal of Cancer AU - Persson, EChristina AU - Graubard, Barry I AU - Evans, Alison A AU - London, WThomas AU - Weber, Jean-Philippe AU - LeBlanc, Alain AU - Chen, Gang AU - Lin, Wenyao AU - McGlynn, Katherine A AD - Drexel School of Public Health, Philadelphia, PA., christina.persson@nih.gov Y1 - 2012/11// PY - 2012 DA - Nov 2012 SP - 2078 EP - 2084 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 131 IS - 9 SN - 0020-7136, 0020-7136 KW - Risk Abstracts KW - Hepatitis KW - Alcohol KW - Genetics KW - Age KW - Organochlorine pesticides KW - Hepatitis B virus KW - Cigarettes KW - Hepatitis B KW - Mass spectrometry KW - China, People's Rep. KW - Rodents KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443373407?accountid=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=Dichlorodiphenyltrichloroethane+and+risk+of+hepatocellular+carcinoma&rft.au=Persson%2C+EChristina%3BGraubard%2C+Barry+I%3BEvans%2C+Alison+A%3BLondon%2C+WThomas%3BWeber%2C+Jean-Philippe%3BLeBlanc%2C+Alain%3BChen%2C+Gang%3BLin%2C+Wenyao%3BMcGlynn%2C+Katherine+A&rft.aulast=Persson&rft.aufirst=EChristina&rft.date=2012-11-01&rft.volume=131&rft.issue=9&rft.spage=2078&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.27459 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-10-01 N1 - Last updated - 2013-10-21 N1 - SubjectsTermNotLitGenreText - Hepatitis; Genetics; Alcohol; Age; Organochlorine pesticides; Cigarettes; Hepatitis B; Mass spectrometry; Rodents; Hepatitis B virus; China, People's Rep. DO - http://dx.doi.org/10.1002/ijc.27459 ER - TY - JOUR T1 - Benzo[a]pyrene (BP) DNA adduct formation in DNA repair-deficient p53 haploinsufficient [Xpa(-/-)p53(+/-)] and wild-type mice fed BP and BP plus chlorophyllin for 28 days AN - 1439220674; 18514277 AB - We have evaluated DNA damage (DNA adduct formation) after feeding benzo[a]pyrene (BP) to wild-type (WT) and cancer-susceptible Xpa(-/-)p53 (+/-) mice deficient in nucleotide excision repair and haploinsufficient for the tumor suppressor p53. DNA damage was evaluated by high-performance liquid chromatography/electrospray ionization tandem mass spectrometry (HPLC/ES-MS/MS), which measures r7,t8,t9-trihydroxy-c-10-(N super(2)-deoxyguanosyl)-7,8,9,10-tetrah ydrobenzo[a]pyr ene (BPdG), and a chemiluminescence immunoassay (CIA), using anti-r7,t8-dihydroxy-t-9,10-epoxy-7,8,9,10-tetrahydrobenzo[ a]pyrene (BPDE)-DNA antiserum, which measures both BPdG and the other stable BP-DNA adducts. When mice were fed 100 ppm BP for 28 days, BP-induced DNA damage measured in esophagus, liver and lung was typically higher in Xpa(-/-)p53 (+/-) mice, compared with WT mice. This result is consistent with the previously observed tumor susceptibility of Xpa(-/-)p53 (+/-) mice. BPdG, the major DNA adduct associated with tumorigenicity, was the primary DNA adduct formed in esophagus (a target tissue in the mouse), whereas total BP-DNA adducts predominated in higher levels in the liver (a non-target tissue in the mouse). In an attempt to lower BP-induced DNA damage, we fed the WT and Xpa(-/-)p53 (+/-) mice 0.3% chlorophyllin (CHL) in the BP-containing diet for 28 days. The addition of CHL resulted in an increase of BP-DNA adducts in esophagus, liver and lung of WT mice, a lowering of BPdG in esophagi of WT mice and livers of Xpa(-/-)p53 (+/-) mice and an increase of BPdG in livers of WT mice. Therefore, the addition of CHL to a BP-containing diet showed a lack of consistent chemoprotective effect, indicating that oral CHL administration may not reduce PAH-DNA adduct levels consistently in human organs. JF - Carcinogenesis AU - John, Kaarthik AU - Pratt, MMargaret AU - Beland, Frederick A AU - Churchwell, Mona I AU - McMullen, Gail AU - Olivero, Ofelia A AU - Pogribny, Igor P AU - Poirier, Miriam C AD - Carcinogen-DNA Interactions Section, LCBG, CCR, National Cancer Institute, NIH, Bethesda, MD 20892-4255, USA, poirierm@exchange.nih.gov Y1 - 2012/11// PY - 2012 DA - Nov 2012 SP - 2236 EP - 2241 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 33 IS - 11 SN - 0143-3334, 0143-3334 KW - Toxicology Abstracts; Oncogenes & Growth Factors Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - High-performance liquid chromatography KW - Diets KW - Esophagus KW - DNA adducts KW - Tumor suppressor genes KW - Feeding KW - Tumorigenicity KW - Tumors KW - Mass spectroscopy KW - p53 protein KW - DNA damage KW - Nucleotide excision repair KW - Lung KW - Carcinogenesis KW - Liver KW - Benzo(a)pyrene KW - chlorophyllin KW - Chemiluminescence KW - Immunoassays KW - N 14820:DNA Metabolism & Structure KW - B 26670:Tumor Suppressors KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1439220674?accountid=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=Carcinogenesis&rft.atitle=Benzo%5Ba%5Dpyrene+%28BP%29+DNA+adduct+formation+in+DNA+repair-deficient+p53+haploinsufficient+%5BXpa%28-%2F-%29p53%28%2B%2F-%29%5D+and+wild-type+mice+fed+BP+and+BP+plus+chlorophyllin+for+28+days&rft.au=John%2C+Kaarthik%3BPratt%2C+MMargaret%3BBeland%2C+Frederick+A%3BChurchwell%2C+Mona+I%3BMcMullen%2C+Gail%3BOlivero%2C+Ofelia+A%3BPogribny%2C+Igor+P%3BPoirier%2C+Miriam+C&rft.aulast=John&rft.aufirst=Kaarthik&rft.date=2012-11-01&rft.volume=33&rft.issue=11&rft.spage=2236&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/10.1093%2Fcarcin%2Fbgs247 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-10-01 N1 - Last updated - 2014-11-12 N1 - SubjectsTermNotLitGenreText - Esophagus; Diets; High-performance liquid chromatography; Feeding; Tumor suppressor genes; DNA adducts; Tumorigenicity; Tumors; Mass spectroscopy; p53 protein; DNA damage; Nucleotide excision repair; Lung; Carcinogenesis; Liver; chlorophyllin; Benzo(a)pyrene; Chemiluminescence; Immunoassays DO - http://dx.doi.org/10.1093/carcin/bgs247 ER - TY - JOUR T1 - Attachment style is associated with perceived spouse responses and pain-related outcomes AN - 1438671726; 201320905 AB - Purpose/Objective: Attachment theory can provide a heuristic model for examining factors that may influence the relationship of social context to adjustment in chronic pain. This study examined the associations of attachment style with self-reported pain behavior, pain intensity, disability, depression, and perceived spouse responses to pain behavior. We also examined whether attachment style moderates associations between perceived spouse responses and self-reported pain behavior and depressive symptoms, as well as perceived spouse responses as a mediator of these associations. Method: Individuals with chronic pain (N = 182) completed measures of self-reported attachment style, perceived spouse responses, and pain-related criterion variables. Results: Secure attachment was inversely associated with self-reported pain behaviors, pain intensity, disability, depressive symptoms, and perceived negative spouse responses; preoccupied and fearful attachment scores were positively associated with these variables. In multivariable regression models, both attachment style and perceived spouse responses were uniquely associated with self-reported pain behavior and depressive symptoms. Attachment style did not moderate associations between perceived spouse responses to self-reported pain behavior and pain criterion variables, but negative spouse responses partially mediated some relationships between attachment styles and pain outcomes. Conclusions/Implications: Findings suggest that attachment style is associated with pain-related outcomes and perceptions of spouse responses. The hypothesized moderation effects for attachment were not found; however, mediation analyses showed that perceived spouse responses may partially explain associations between attachment and adjustment to pain. Future research is needed to clarify how attachment style and the social environment affect the pain experience. [Copyright The American Psychological Association.] JF - Rehabilitation Psychology AU - Forsythe, Laura P AU - Romano, Joan M AU - Jensen, Mark P AU - Thorn, Beverly E AD - Department of Psychology, The University of Alabama laura.forsythe@nih.gov Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 290 EP - 300 PB - Educational Publishing Foundation/American Psychological Association, Washington DC VL - 57 IS - 4 SN - 0090-5550, 0090-5550 KW - attachment KW - chronic pain KW - depression KW - pain behavior KW - spouse responses KW - Attachment style KW - Depression KW - Attachment KW - Chronic pain KW - Disability KW - Spouses KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1438671726?accountid=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=Rehabilitation+Psychology&rft.atitle=Attachment+style+is+associated+with+perceived+spouse+responses+and+pain-related+outcomes&rft.au=Forsythe%2C+Laura+P%3BRomano%2C+Joan+M%3BJensen%2C+Mark+P%3BThorn%2C+Beverly+E&rft.aulast=Forsythe&rft.aufirst=Laura&rft.date=2012-11-01&rft.volume=57&rft.issue=4&rft.spage=290&rft.isbn=&rft.btitle=&rft.title=Rehabilitation+Psychology&rft.issn=00905550&rft_id=info:doi/10.1037%2Fa0030083 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-10-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Chronic pain; Spouses; Attachment style; Attachment; Depression; Disability DO - http://dx.doi.org/10.1037/a0030083 ER - TY - JOUR T1 - FSelector: a Ruby gem for feature selection AN - 1434023985; 18513703 AB - Summary: The FSelector package contains a comprehensive list of feature selection algorithms for supporting bioinformatics and machine learning research. FSelector primarily collects and implements the filter type of feature selection techniques, which are computationally efficient for mining large datasets. In particular, FSelector allows ensemble feature selection that takes advantage of multiple feature selection algorithms to yield more robust results. FSelector also provides many useful auxiliary tools, including normalization, discretization and missing data imputation.Availability: FSelector, written in the Ruby programming language, is free and open-source software that runs on all Ruby supporting platforms, including Windows, Linux and Mac OS X. FSelector is available from https://rubygems.org/gems/fselector and can be installed like a breeze via the command gem install fselector. The source code is available (https://github.com/need47/fselector) and is fully documented (http://rubydoc.info/gems/fselector/frames). JF - Bioinformatics AU - Cheng, Tiejun AU - Wang, Yanli AU - Bryant, Stephen H AD - Computational Biology Branch, National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, 8600 Rockville Pike, Bethesda, MD 20894, USA Y1 - 2012/11/01/ PY - 2012 DA - 2012 Nov 01 SP - 2851 EP - 2852 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 28 IS - 21 SN - 1367-4803, 1367-4803 KW - Biotechnology and Bioengineering Abstracts KW - Computer programs KW - software KW - Data processing KW - Algorithms KW - Language KW - Bioinformatics KW - Learning algorithms KW - Internet KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434023985?accountid=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=FSelector%3A+a+Ruby+gem+for+feature+selection&rft.au=Cheng%2C+Tiejun%3BWang%2C+Yanli%3BBryant%2C+Stephen+H&rft.aulast=Cheng&rft.aufirst=Tiejun&rft.date=2012-11-01&rft.volume=28&rft.issue=21&rft.spage=2851&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbts528 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2015-03-20 N1 - SubjectsTermNotLitGenreText - Computer programs; software; Data processing; Algorithms; Language; Learning algorithms; Bioinformatics; Internet DO - http://dx.doi.org/10.1093/bioinformatics/bts528 ER - TY - JOUR T1 - Unrealistic optimism is associated with subclinical atherosclerosis AN - 1373490341; 201312854 AB - Objective: Unrealistic optimism -- typically conceptualized as underestimation of comparative risk -- has been previously associated with poorer health behaviors and outcomes, but no research to date has examined the association between unrealistic optimism and subclinical or clinical disease endpoints. Here, cross-sectional data from one time point in the Pittsburgh Healthy Heart study are used to examine whether unrealistic optimism about risk of heart disease is associated with carotid artery intima-media thickness (IMT), a subclinical marker of atherosclerosis. Methods: Participants were 148 adults aged 57-77. Objective risk score was calculated using the Framingham calculator, and IMT was regressed on risk score and perceived risk. Controlling for the Framingham risk score effectively equated risk across the sample, meaning that lower risk perceptions represented unrealistic optimism. Results: When controlling for the risk score, risk perceptions were negatively associated with IMT (beta = -.21, p < .01, t = -2.79, d = .46), a finding that was not moderated by gender. The risk score was also associated with IMT (beta = .42, p < .001, t = 5.55, d = .91). Conclusions: Unrealistic optimism was associated with subclinical atherosclerosis. Future longitudinal research is necessary to evaluate the temporal sequence as well as to examine putative explanatory mechanisms. [Copyright The American Psychological Association.] JF - Health Psychology AU - Ferrer, Rebecca A AU - Klein, William M P AU - Zajac, Laura E AU - Sutton-Tyrrell, Kim AU - Muldoon, Matthew F AU - Kamarck, Thomas W AD - Basic Biobehavioral and Psychological Sciences Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Rockville, MD, US ferrerra@mail.nih.gov Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 815 EP - 820 PB - American Psychological Association, Washington DC VL - 31 IS - 6 SN - 0278-6133, 0278-6133 KW - cardiovascular disease KW - risk perceptions KW - subclinical atherosclerosis KW - unrealistic optimism KW - Atherosclerosis KW - Health problems KW - Health status KW - Optimism KW - Risk perception KW - Heart diseases KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1373490341?accountid=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+Psychology&rft.atitle=Unrealistic+optimism+is+associated+with+subclinical+atherosclerosis&rft.au=Ferrer%2C+Rebecca+A%3BKlein%2C+William+M+P%3BZajac%2C+Laura+E%3BSutton-Tyrrell%2C+Kim%3BMuldoon%2C+Matthew+F%3BKamarck%2C+Thomas+W&rft.aulast=Ferrer&rft.aufirst=Rebecca&rft.date=2012-11-01&rft.volume=31&rft.issue=6&rft.spage=815&rft.isbn=&rft.btitle=&rft.title=Health+Psychology&rft.issn=02786133&rft_id=info:doi/10.1037%2Fa0027675 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-07-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Optimism; Risk perception; Atherosclerosis; Heart diseases; Health status; Health problems DO - http://dx.doi.org/10.1037/a0027675 ER - TY - JOUR T1 - Observations on the Preparation of beta -Lactose Octaacetate AN - 1348482588; 17881523 AB - Attempts to substantially increase the relative proportion of beta -lactose octaacetate in products of acetylation of alpha -lactose monohydrate using various acetylation protocols failed. Nevertheless, the revised protocol for isolation and crystallization, based on the classical work by Hudson and Johnson, rendered preparation of beta -lactose octaacetate less labor intensive. It is proposed that the melting point and [ alpha ] sub(D) value are not reliable criteria of purity of beta -lactose octaacetate, which can be confidently determined by 1H NMR spectroscopy. JF - Journal of Carbohydrate Chemistry AU - Xu, Peng AU - Yang, Jacqueline Y AU - Kovac, Pavol AD - NIDDK, LBC, National Institutes of Health, Bethesda, MD, 20892-0815, USA, kpn@hlix.nih.gov Y1 - 2012/11/01/ PY - 2012 DA - 2012 Nov 01 SP - 711 EP - 720 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 31 IS - 9 SN - 0732-8303, 0732-8303 KW - Biotechnology and Bioengineering Abstracts KW - Melting KW - Crystallization KW - Acetylation KW - Magnetic resonance spectroscopy KW - Carbohydrates KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1348482588?accountid=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+Carbohydrate+Chemistry&rft.atitle=Observations+on+the+Preparation+of+beta+-Lactose+Octaacetate&rft.au=Xu%2C+Peng%3BYang%2C+Jacqueline+Y%3BKovac%2C+Pavol&rft.aulast=Xu&rft.aufirst=Peng&rft.date=2012-11-01&rft.volume=31&rft.issue=9&rft.spage=711&rft.isbn=&rft.btitle=&rft.title=Journal+of+Carbohydrate+Chemistry&rft.issn=07328303&rft_id=info:doi/10.1080%2F07328303.2012.739230 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-05-01 N1 - Last updated - 2013-05-31 N1 - SubjectsTermNotLitGenreText - Crystallization; Melting; Acetylation; Magnetic resonance spectroscopy; Carbohydrates DO - http://dx.doi.org/10.1080/07328303.2012.739230 ER - TY - JOUR T1 - miRNA pharmacogenomics: the new frontier for personalized medicine in cancer? AN - 1328513209; 17402302 AB - In recent years pharmacogenomic research has highlighted several genetic biomarkers of treatment toxicity and efficacy, dealing with drug metabolism, transport and mechanism of action. More recently, polymorphisms in miRNA encoding genes, their targets or factors involved in their maturation are rising as new pharmacogenomic markers in cancer. miRNAs are brief ncRNAs involved in DNA translational control, with an effect on mRNA and protein-expression levels. The study of genetic polymorphisms in genes involved in miRNA translational control machinery could give innovative insights in pharmacogenomics. This review summarizes the most recent and promising results in the field and gives an overview of the future perspective of personalized cancer therapy. JF - Pharmacogenomics AU - Dreussi, Eva AU - Biason, Paola AU - Toffoli, Giuseppe AU - Cecchin, Erika AD - super(1)Experimental & Clinical Pharmacology Unit, Centro di Riferimento Oncologico - National Cancer Institute, Via Franco Gallini, 2, 33081 Aviano, Italy, gtoffoli@cro.it Y1 - 2012/11// PY - 2012 DA - Nov 2012 SP - 1635 EP - 1650 PB - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom VL - 13 IS - 14 SN - 1462-2416, 1462-2416 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Translation KW - pharmacogenomics KW - Gene polymorphism KW - Drug metabolism KW - miRNA KW - non-coding RNA KW - Toxicity KW - biomarkers KW - Cancer KW - mRNA KW - Reviews KW - DNA KW - W 30940:Products KW - N 14830:RNA KW - G 07700:Molecular Genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1328513209?accountid=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&rft.atitle=miRNA+pharmacogenomics%3A+the+new+frontier+for+personalized+medicine+in+cancer%3F&rft.au=Dreussi%2C+Eva%3BBiason%2C+Paola%3BToffoli%2C+Giuseppe%3BCecchin%2C+Erika&rft.aulast=Dreussi&rft.aufirst=Eva&rft.date=2012-11-01&rft.volume=13&rft.issue=14&rft.spage=1635&rft.isbn=&rft.btitle=&rft.title=Pharmacogenomics&rft.issn=14622416&rft_id=info:doi/10.2217%2Fpgs.12.147 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-04-01 N1 - Number of references - 107 N1 - Last updated - 2013-08-23 N1 - SubjectsTermNotLitGenreText - Translation; pharmacogenomics; Drug metabolism; Reviews; Gene polymorphism; miRNA; DNA; non-coding RNA; Toxicity; biomarkers; Cancer; mRNA DO - http://dx.doi.org/10.2217/pgs.12.147 ER - TY - JOUR T1 - Modalities of Infant-Mother Interaction in Japanese, Japanese American Immigrant, and European American Dyads AN - 1283740173; 201300800 AB - Cultural variation in relations and moment-to-moment contingencies of infant-mother person-oriented and object-oriented interactions were compared in 118 Japanese, Japanese American immigrant, and European American dyads with 5.5-month-olds. Infant and mother person-oriented behaviors were related in all cultural groups, but infant and mother object-oriented behaviors were related only among European Americans. Infant and mother behaviors within each modality were mutually contingent in all groups. Culture moderated lead-lag relations: Japanese infants were more likely than their mothers to respond in object-oriented interactions; European American mothers were more likely than their infants to respond in person-oriented interactions. Japanese American dyads behaved like European American dyads. Interactions, infant effects, and parent socialization findings are set in cultural and accultural models of infant-mother transactions. Adapted from the source document. JF - Child Development AU - Bornstein, Marc H AU - Cote, Linda R AU - Haynes, O Maurice AU - Suwalsky, Joan T D AU - Bakeman, Roger AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 2073 EP - 2088 PB - Wiley-Blackwell, Oxford UK VL - 83 IS - 6 SN - 0009-3920, 0009-3920 KW - Mother-Infant interactions KW - Immigrants KW - Transactions KW - Parents KW - Japan KW - Infants KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1283740173?accountid=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=Modalities+of+Infant-Mother+Interaction+in+Japanese%2C+Japanese+American+Immigrant%2C+and+European+American+Dyads&rft.au=Bornstein%2C+Marc+H%3BCote%2C+Linda+R%3BHaynes%2C+O+Maurice%3BSuwalsky%2C+Joan+T+D%3BBakeman%2C+Roger&rft.aulast=Bornstein&rft.aufirst=Marc&rft.date=2012-11-01&rft.volume=83&rft.issue=6&rft.spage=2073&rft.isbn=&rft.btitle=&rft.title=Child+Development&rft.issn=00093920&rft_id=info:doi/10.1111%2Fj.1467-8624.2012.01822.x LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-02-01 N1 - Last updated - 2016-09-27 N1 - CODEN - CHDEAW N1 - SubjectsTermNotLitGenreText - Japan; Infants; Immigrants; Mother-Infant interactions; Parents; Transactions DO - http://dx.doi.org/10.1111/j.1467-8624.2012.01822.x ER - TY - JOUR T1 - Cross-sectional and longitudinal abnormalities in brain structure in children with severe mood dysregulation or bipolar disorder AN - 1266173236; 201300004 AB - Background: There is debate as to whether chronic irritability (operationalized as severe mood dysregulation, SMD) is a developmental form of bipolar disorder (BD). Although structural brain abnormalities in BD have been demonstrated, no study compares neuroanatomy among SMD, BD, and healthy volunteers (HV) either cross-sectionally or over time. Furthermore, the developmental trajectories of structural abnormalities in BD or SMD are unknown. This study provides such data in BD, SMD, and HV. Methods: An optimized, modulated voxel-based morphometry (VBM) analysis was conducted on structural MRI scans from 201 children (78 SMD, 55 BD, and 68 HV). In addition, 92 children (31 SMD, 34 BD, and 27 HV) were rescanned after 2 years (mean interval 1.99+/-0.94 years), to compare time-related changes among the three groups. Results: Cross-sectionally, the groups differed in gray matter (GM) volume in presupplementary motor area (pre-SMA), dorsolateral prefrontal cortex (DLPFC), insula, and globus pallidus. The cortical differences were driven mainly by increased GM volume in HV compared with BD and SMD. In globus pallidus, there was increased GM in BD compared with HV and SMD. Longitudinally, group-by-time interactions were evident in two clusters in the superior/inferior parietal lobule (R SPL/IPL) and in the precuneus. In both clusters, the interactions were driven by an abnormal increase in volume in BD. Conclusions: Cross-sectionally, both BD and SMD are associated with structural abnormalities in frontal cortex, insula, and basal ganglia. Although some of these deficits overlap (insula and DLPFC), others differentiate SMD and BD (pre-SMA and globus pallidus). Abnormal developmental trajectories in lateral parietal cortex and precuneus are present in, and unique to, BD. Because of the high proportion of co-occurring ADHD in the SMD subjects, we could not separate effects of ADHD from those of SMD, and future research including a nonirritable ADHD group must address this issue. Adapted from the source document. JF - The Journal of Child Psychology and Psychiatry AU - Adleman, Nancy E AU - Fromm, Stephen J AU - Razdan, Varun AU - Kayser, Reilly AU - Dickstein, Daniel P AU - Brotman, Melissa A AU - Pine, Daniel S AU - Leibenluft, Ellen AD - Emotion and Development Branch, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 1149 EP - 1156 PB - Blackwell Publishing, Oxford UK VL - 53 IS - 11 SN - 0021-9630, 0021-9630 KW - Cortex KW - Bipolar affective disorder KW - Genetic engineering KW - Attention deficit hyperactivity disorder KW - Moods KW - Children KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1266173236?accountid=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+Child+Psychology+and+Psychiatry&rft.atitle=Cross-sectional+and+longitudinal+abnormalities+in+brain+structure+in+children+with+severe+mood+dysregulation+or+bipolar+disorder&rft.au=Adleman%2C+Nancy+E%3BFromm%2C+Stephen+J%3BRazdan%2C+Varun%3BKayser%2C+Reilly%3BDickstein%2C+Daniel+P%3BBrotman%2C+Melissa+A%3BPine%2C+Daniel+S%3BLeibenluft%2C+Ellen&rft.aulast=Adleman&rft.aufirst=Nancy&rft.date=2012-11-01&rft.volume=53&rft.issue=11&rft.spage=1149&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Child+Psychology+and+Psychiatry&rft.issn=00219630&rft_id=info:doi/10.1111%2Fj.1469-7610.2012.02568.x LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-01-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JPPDAI N1 - SubjectsTermNotLitGenreText - Genetic engineering; Attention deficit hyperactivity disorder; Cortex; Children; Moods; Bipolar affective disorder DO - http://dx.doi.org/10.1111/j.1469-7610.2012.02568.x ER - TY - JOUR T1 - Lifetime organophosphorous insecticide use among private pesticide applicators in the Agricultural Health Study AN - 1257746552; 17410891 AB - Organophosphorous insecticides (OPs) are the most commonly used insecticides in US agriculture, but little information is available regarding specific OP use by individual farmers. We describe OP use for licensed private pesticide applicators from Iowa and North Carolina in the Agricultural Health Study (AHS) using lifetime pesticide use data from 701 randomly selected male participants collected at three time periods. Of 27 OPs studied, 20 were used by >1%. Overall, 95% had ever applied at least one OP. The median number of different OPs used was 4 (maximum=13). Malathion was the most commonly used OP (74%) followed by chlorpyrifos (54%). OP use declined over time. At the first interview (1993-1997), 68% of participants had applied OPs in the past year; by the last interview (2005-2007), only 42% had. Similarly, median annual application days of OPs declined from 13.5 to 6 days. Although OP use was common, the specific OPs used varied by state, time period, and individual. Much of the variability in OP use was associated with the choice of OP, rather than the frequency or duration of application. Information on farmers' OP use enhances our ability to characterize and understand the potential health effects of multiple OP exposures. JF - Journal of Exposure Science and Environmental Epidemiology AU - Hoppin, Jane A AU - Long, Stuart AU - Umbach, David M AU - Lubin, Jay H AU - Starks, Sarah E AU - Gerr, Fred AU - Thomas, Kent AU - Hines, Cynthia J AU - Weichenthal, Scott AU - Kamel, Freya AU - Koutros, Stella AU - Alavanja, Michael AU - Beane Freeman, Laura E AU - Sandler, Dale P AD - Epidemiology Branch, NIEHS, NIH, DHHS, Research Triangle Park, North Carolina, USA Y1 - 2012/11// PY - 2012 DA - Nov 2012 SP - 584 EP - 592 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 22 IS - 6 SN - 1559-0631, 1559-0631 KW - Toxicology Abstracts; Health & Safety Science Abstracts KW - Agriculture KW - USA, North Carolina KW - Data processing KW - Malathion KW - Chlorpyrifos KW - Insecticides KW - USA, Iowa KW - Pesticides KW - H 5000:Pesticides KW - X 24330:Agrochemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1257746552?accountid=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+immunology%2C+immunotherapy+%3A+CII&rft.atitle=Endpoints%2C+patient+selection%2C+and+biomarkers+in+the+design+of+clinical+trials+for+cancer+vaccines.&rft.au=Bilusic%2C+Marijo%3BGulley%2C+James+L&rft.aulast=Bilusic&rft.aufirst=Marijo&rft.date=2012-01-01&rft.volume=61&rft.issue=1&rft.spage=109&rft.isbn=&rft.btitle=&rft.title=Cancer+immunology%2C+immunotherapy+%3A+CII&rft.issn=1432-0851&rft_id=info:doi/10.1007%2Fs00262-011-1141-0 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-12-01 N1 - Last updated - 2013-06-28 N1 - SubjectsTermNotLitGenreText - Chlorpyrifos; Agriculture; Data processing; Insecticides; Pesticides; Malathion; USA, North Carolina; USA, Iowa DO - http://dx.doi.org/10.1038/jes.2012.79 ER - TY - JOUR T1 - A complex network of small non-coding RNAs regulate motility in Escherichia coli AN - 1171898539; 17338159 AB - Small Hfq-dependent non-coding regulatory RNAs (sRNAs) that alter mRNA stability and expression by pairing with target mRNAs have increasingly been shown to be important in influencing the behaviour of bacteria. In Escherichia coli, flhD and flhC, which encode the master regulator of flagellar synthesis, are co-transcribed from a promoter that is regulated by multiple transcription factors that respond to different environmental cues. Here, we show that the 5' untranslated region (5' UTR) of the flhDC mRNA also serves as a hub to integrate additional environmental cues into the decision to make flagella. Four sRNAs, ArcZ, OmrA, OmrB and OxyS, negatively regulated and one sRNA, McaS, positively regulated motility and flhDC expression by base-pairing with the 5' UTR of this mRNA. Another sRNA, MicA, positively regulated motility independent of regulation of flhDC. Furthermore, we demonstrate that the regulation of motility by the ArcB/A two component system is in part due to its regulation of ArcZ. flhDC is the first mRNA that has been shown to be both positively and negatively regulated by direct pairing to sRNAs. Moreover, both positive regulation by McaS and negative regulation by ArcZ require the same binding site in the flhDC mRNA. JF - Molecular Microbiology AU - De Lay, Nicholas AU - Gottesman, Susan AD - Laboratory of Molecular Biology. Center for Cancer Research, National Cancer Institute Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 524 EP - 538 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 86 IS - 3 SN - 0950-382X, 0950-382X KW - Microbiology Abstracts B: Bacteriology KW - Promoters KW - Decision making KW - Motility KW - mRNA stability KW - Transcription factors KW - Escherichia coli KW - non-coding RNA KW - Flagella KW - J 02320:Cell Biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1171898539?accountid=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=Molecular+Microbiology&rft.atitle=A+complex+network+of+small+non-coding+RNAs+regulate+motility+in+Escherichia+coli&rft.au=De+Lay%2C+Nicholas%3BGottesman%2C+Susan&rft.aulast=De+Lay&rft.aufirst=Nicholas&rft.date=2012-11-01&rft.volume=86&rft.issue=3&rft.spage=524&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/10.1111%2Fj.1365-2958.2012.08209.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-11-01 N1 - Last updated - 2016-04-29 N1 - SubjectsTermNotLitGenreText - Decision making; Promoters; mRNA stability; Motility; Transcription factors; non-coding RNA; Flagella; Escherichia coli DO - http://dx.doi.org/10.1111/j.1365-2958.2012.08209.x ER - TY - JOUR T1 - Surfing biological surfaces: exploiting the nucleoid for partition and transport in bacteria AN - 1171898493; 17338152 AB - The ParA family of ATPases is responsible for transporting bacterial chromosomes, plasmids and large protein machineries. ParAs pattern the nucleoid in vivo, but how patterning functions or is exploited in transport is of considerable debate. Here we discuss the process of self-organization into patterns on the bacterial nucleoid and explore how it relates to the molecular mechanism of ParA action. We review ParA-mediated DNA partition as a general mechanism of how ATP-driven protein gradients on biological surfaces can result in spatial organization on a mesoscale. We also discuss how the nucleoid acts as a formidable diffusion barrier for large bodies in the cell, and make the case that the ParA family evolved to overcome the barrier by exploiting the nucleoid as a matrix for movement. JF - Molecular Microbiology AU - Vecchiarelli, Anthony G AU - Mizuuchi, Kiyoshi AU - Funnell, Barbara E AD - Laboratory of Molecular Biology National Institute of Diabetes, and Digestive and Kidney Diseases. National Institutes of Health Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 513 EP - 523 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 86 IS - 3 SN - 0950-382X, 0950-382X KW - Microbiology Abstracts B: Bacteriology KW - Molecular modelling KW - Chromosomes KW - Adenosinetriphosphatase KW - Reviews KW - DNA KW - Nucleoids KW - Diffusion KW - Plasmids KW - J 02410:Animal Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1171898493?accountid=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=Molecular+Microbiology&rft.atitle=Surfing+biological+surfaces%3A+exploiting+the+nucleoid+for+partition+and+transport+in+bacteria&rft.au=Vecchiarelli%2C+Anthony+G%3BMizuuchi%2C+Kiyoshi%3BFunnell%2C+Barbara+E&rft.aulast=Vecchiarelli&rft.aufirst=Anthony&rft.date=2012-11-01&rft.volume=21&rft.issue=2&rft.spage=253&rft.isbn=&rft.btitle=&rft.title=Cancer+Epidemiology%2C+Biomarkers+%26+Prevention&rft.issn=10559965&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-11-01 N1 - Last updated - 2016-04-29 N1 - SubjectsTermNotLitGenreText - Molecular modelling; Chromosomes; Adenosinetriphosphatase; Reviews; DNA; Diffusion; Nucleoids; Plasmids DO - http://dx.doi.org/10.1111/mmi.12017 ER - TY - JOUR T1 - Genomic determinants of sporulation in Bacilli and Clostridia: towards the minimal set of sporulation-specific genes AN - 1171885295; 17337754 AB - Three classes of low-G+C Gram-positive bacteria (Firmicutes), Bacilli, Clostridia and Negativicutes, include numerous members that are capable of producing heat-resistant endospores. Spore-forming firmicutes include many environmentally important organisms, such as insect pathogens and cellulose-degrading industrial strains, as well as human pathogens responsible for such diseases as anthrax, botulism, gas gangrene and tetanus. In the best-studied model organism Bacillus subtilis, sporulation involves over 500 genes, many of which are conserved among other bacilli and clostridia. This work aimed to define the genomic requirements for sporulation through an analysis of the presence of sporulation genes in various firmicutes, including those with smaller genomes than B.subtilis. Cultivable spore-formers were found to have genomes larger than 2300kb and encompass over 2150 protein-coding genes of which 60 are orthologues of genes that are apparently essential for sporulation in B.subtilis. Clostridial spore-formers lack, among others, spoIIB, sda, spoVID and safA genes and have non-orthologous displacements of spoIIQ and spoIVFA, suggesting substantial differences between bacilli and clostridia in the engulfment and spore coat formation steps. Many B.subtilis sporulation genes, particularly those encoding small acid-soluble spore proteins and spore coat proteins, were found only in the family Bacillaceae, or even in a subset of Bacillus spp. Phylogenetic profiles of sporulation genes, compiled in this work, confirm the presence of a common sporulation gene core, but also illuminate the diversity of the sporulation processes within various lineages. These profiles should help further experimental studies of uncharacterized widespread sporulation genes, which would ultimately allow delineation of the minimal set(s) of sporulation-specific genes in Bacilli and Clostridia. JF - Environmental Microbiology AU - Galperin, Michael Y AU - Mekhedov, Sergei L AU - Puigbo, Pere AU - Smirnov, Sergey AU - Wolf, Yuri I AU - Rigden, Daniel J AD - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD 20894, USA. Y1 - 2012/11// PY - 2012 DA - Nov 2012 SP - 2870 EP - 2890 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 14 IS - 11 SN - 1462-2912, 1462-2912 KW - Microbiology Abstracts B: Bacteriology KW - Phylogeny KW - Genomes KW - Bacilli KW - Gas gangrene KW - Bacillus subtilis KW - small acid-soluble spore proteins KW - Botulism KW - Bacillaceae KW - Gram-positive bacteria KW - Industrial strains KW - Spore coats KW - Sporulation KW - Firmicutes KW - Pathogens KW - Tetanus KW - Anthrax KW - genomics KW - Bacillus KW - J 02410:Animal Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1171885295?accountid=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=Environmental+Microbiology&rft.atitle=Genomic+determinants+of+sporulation+in+Bacilli+and+Clostridia%3A+towards+the+minimal+set+of+sporulation-specific+genes&rft.au=Galperin%2C+Michael+Y%3BMekhedov%2C+Sergei+L%3BPuigbo%2C+Pere%3BSmirnov%2C+Sergey%3BWolf%2C+Yuri+I%3BRigden%2C+Daniel+J&rft.aulast=Galperin&rft.aufirst=Michael&rft.date=2012-11-01&rft.volume=14&rft.issue=11&rft.spage=2870&rft.isbn=&rft.btitle=&rft.title=Environmental+Microbiology&rft.issn=14622912&rft_id=info:doi/10.1111%2Fj.1462-2920.2012.02841.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-11-01 N1 - Document feature - figure 1 N1 - Last updated - 2013-07-26 N1 - SubjectsTermNotLitGenreText - Genomes; Phylogeny; Bacilli; Gas gangrene; Botulism; small acid-soluble spore proteins; Spore coats; Industrial strains; Gram-positive bacteria; Sporulation; Pathogens; Tetanus; Anthrax; genomics; Bacillus subtilis; Bacillaceae; Firmicutes; Bacillus DO - http://dx.doi.org/10.1111/j.1462-2920.2012.02841.x ER - TY - JOUR T1 - Iron in relation to gastric cancer in the Alpha-tocopherol, Beta-carotene Cancer Prevention Study. AN - 1151031274; 23001240 AB - Iron is an essential micronutrient that can have carcinogenic effects when at high or low concentrations. Previous studies of iron in relation to gastric cancer have not assessed subtype-specific relationships. We used the prospective Alpha-Tocopherol, Beta-Carotene (ATBC) Cancer Prevention Study to assess whether iron metrics were associated with gastric cardia cancer (GCC) and gastric noncardia cancer (GNCC). We selected 341 incident gastric cancer cases (86 cardia, 172 noncardia, and 83 nonspecified), accrued during 22 years of follow-up, and 341 individually matched controls. We measured prediagnostic serum iron, ferritin, unsaturated iron binding capacity, and C-reactive protein. Total iron-binding capacity (TIBC) and transferrin saturation were estimated from these metrics. Dietary iron exposures were estimated from a food frequency questionnaire. Multivariable logistic regression was used for analysis. Serum iron metrics were not associated with GCC, except for a potential "n"-shaped relationship with TIBC (global P = 0.038). GNCC was inversely associated with serum ferritin (global P = 0.024), serum iron (global P = 0.060) and, possibly, transferrin saturation. TIBC appeared to share a "u"-shaped relationship with GNCC (global P = 0.033). Dietary iron exposures were not associated with either subsite. Adjustment for Helicobacter pylori and gastric atrophy had little effect on observed associations. We found little evidence for the involvement of iron exposure in the pathogenesis of GCC. GNCC was associated with an iron profile similar to that of iron deficiency. Our findings indicate that inverse associations between iron metrics and gastric cancer are driven by associations with GNCC. Further elucidation of potential mechanisms is warranted. ©2012 AACR. JF - Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology AU - Cook, Michael B AU - Kamangar, Farin AU - Weinstein, Stephanie J AU - Albanes, Demetrius AU - Virtamo, Jarmo AU - Taylor, Philip R AU - Abnet, Christian C AU - Wood, Richard J AU - Petty, Gayle AU - Cross, Amanda J AU - Dawsey, Sanford M AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, 6120 Executive Blvd, EPS/Suite 550/Room 5014, Bethesda, MD 20852-7234, USA. michael.cook@nih.gov Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 2033 EP - 2042 VL - 21 IS - 11 KW - Placebos KW - 0 KW - Transferrin KW - beta Carotene KW - 01YAE03M7J KW - Ferritins KW - 9007-73-2 KW - Iron KW - E1UOL152H7 KW - alpha-Tocopherol KW - H4N855PNZ1 KW - Index Medicus KW - Transferrin -- metabolism KW - Ferritins -- blood KW - Double-Blind Method KW - Risk Factors KW - Humans KW - Case-Control Studies KW - Aged KW - Middle Aged KW - Finland -- epidemiology KW - Male KW - beta Carotene -- administration & dosage KW - Stomach Neoplasms -- pathology KW - alpha-Tocopherol -- administration & dosage KW - Stomach Neoplasms -- blood KW - Iron -- blood KW - Stomach Neoplasms -- prevention & control KW - Stomach Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1151031274?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.atitle=Iron+in+relation+to+gastric+cancer+in+the+Alpha-tocopherol%2C+Beta-carotene+Cancer+Prevention+Study.&rft.au=Cook%2C+Michael+B%3BKamangar%2C+Farin%3BWeinstein%2C+Stephanie+J%3BAlbanes%2C+Demetrius%3BVirtamo%2C+Jarmo%3BTaylor%2C+Philip+R%3BAbnet%2C+Christian+C%3BWood%2C+Richard+J%3BPetty%2C+Gayle%3BCross%2C+Amanda+J%3BDawsey%2C+Sanford+M&rft.aulast=Cook&rft.aufirst=Michael&rft.date=2012-11-01&rft.volume=21&rft.issue=11&rft.spage=2033&rft.isbn=&rft.btitle=&rft.title=Cancer+epidemiology%2C+biomarkers+%26+prevention+%3A+a+publication+of+the+American+Association+for+Cancer+Research%2C+cosponsored+by+the+American+Society+of+Preventive+Oncology&rft.issn=1538-7755&rft_id=info:doi/10.1158%2F1055-9965.EPI-12-0799 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-07-10 N1 - Date created - 2012-11-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Epidemiol. 2009 Nov;33(5):368-73 [19800305] Gut. 2010 Mar;59(3):282-4 [20207629] Am J Gastroenterol. 2011 Mar;106(3):432-42 [20978481] Int J Cancer. 2012 Jun 1;130(11):2654-63 [21717452] Mutat Res. 2012 May 1;733(1-2):92-9 [22349350] J Nutr. 2000 Mar;130(3):621-8 [10702595] Scand J Gastroenterol. 2000 Sep;35(9):950-6 [11063155] Proc Natl Acad Sci U S A. 2002 Feb 19;99(4):2264-9 [11854522] Eur J Gastroenterol Hepatol. 2002 Feb;14(2):107-13 [11981333] Acta Oncol. 2002;41(4):381-8 [12234031] Int J Clin Pract. 2002 Sep;56(7):505-8 [12296612] Helicobacter. 2004 Aug;9(4):335-41 [15270748] J Nutr. 2004 Nov;134(11):3171S-3172S [15514292] Am J Epidemiol. 1988 Sep;128(3):655-66 [2458036] N Engl J Med. 1988 Oct 20;319(16):1047-52 [3173433] Med Oncol Tumor Pharmacother. 1990;7(2-3):177-81 [2146450] Cancer. 1991 Mar 15;67(6):1707-12 [2001562] Cancer Res. 1992 Dec 15;52(24):6735-40 [1458460] Cancer Epidemiol Biomarkers Prev. 1992 Nov-Dec;1(7):547-50 [1302566] Int J Cancer. 1994 Feb 1;56(3):364-9 [8314323] Int J Cancer. 1994 Feb 1;56(3):379-82 [8314326] N Engl J Med. 1994 Apr 14;330(15):1029-35 [8127329] Ann Epidemiol. 1994 Jan;4(1):1-10 [8205268] Am J Epidemiol. 1995 Oct 1;142(7):692-8 [7572938] Jpn J Cancer Res. 1995 Oct;86(10):916-23 [7493909] Eur J Epidemiol. 1995 Feb;11(1):55-65 [7489774] Cancer. 1997 Sep 15;80(6):1021-8 [9305701] J Natl Cancer Inst. 1998 Jan 21;90(2):150-5 [9450576] Scand J Gastroenterol. 1999 Apr;34(4):353-60 [10365894] Indian J Gastroenterol. 2005 Jul-Aug;24(4):147-50 [16204900] Am J Clin Nutr. 2005 Oct;82(4):813-20 [16210711] J Natl Cancer Inst. 2006 Oct 18;98(20):1445-52 [17047193] BMC Gastroenterol. 2006;6:41 [17144908] Gut. 2007 Jul;56(7):918-25 [17317788] Scand J Gastroenterol. 2007 Aug;42(8):933-40 [17613922] Ann Oncol. 2009 Jan;20(1):160-5 [18669867] Helicobacter. 2008 Oct;13(5):323-40 [19250507] Nutr Cancer. 2009;61(4):415-26 [19838913] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1158/1055-9965.EPI-12-0799 ER - TY - JOUR T1 - Research opportunities for cancer associated with indoor air pollution from solid-fuel combustion. AN - 1126619292; 22846419 AB - Indoor air pollution (IAP) derived largely from the use of solid fuels for cooking and heating affects about 3 billion people worldwide, resulting in substantial adverse health outcomes, including cancer. Women and children from developing countries are the most exposed populations. A workshop was held in Arlington, Virginia, 9-11 May 2011, to better understand women's and children's potential health effects from IAP in developing countries. Workshop participants included international scientists, manufacturers, policy and regulatory officials, community leaders, and advocates who held extensive discussions to help identify future research needs. Our objective was to identify research opportunities regarding IAP and cancer, including research questions that could be incorporated into studies of interventions to reduce IAP exposure. In this commentary, we describe the state of the science in understanding IAP and its associations with cancer and suggest research opportunities for improving our understanding of the issues. Opportunities for research on IAP and cancer include studies of the effect of IAP on cancers other than lung cancer; studies of genetic factors that modify susceptibility; studies to determine whether the effects of IAP are mediated via germline, somatic, and/or epigenetic changes; and studies of the effects of IAP exposure via dermal and/or oral routes. IAP from indoor coal use increases the risk of lung cancer. Installing chimneys can reduce risk, and some genotypes, including GSTM1-null, can increase risk. Additional research is needed regarding the effects of IAP on other cancers and the effects of different types of solid fuels, oral and dermal routes of IAP exposure, genetic and epigenetic mechanisms, and genetic susceptibility. JF - Environmental health perspectives AU - Reid, Britt C AU - Ghazarian, Armen A AU - DeMarini, David M AU - Sapkota, Amir AU - Jack, Darby AU - Lan, Qing AU - Winn, Deborah M AU - Birnbaum, Linda S AD - Modifiable Risk Factors Branch, Epidemiology and Genomics Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland 20892, USA. reidbr@mail.nih.gov Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 1495 EP - 1498 VL - 120 IS - 11 KW - Coal KW - 0 KW - Charcoal KW - 16291-96-6 KW - Index Medicus KW - Coal -- toxicity KW - Humans KW - Wood -- toxicity KW - Neoplasms -- epidemiology KW - Neoplasms -- genetics KW - Genetic Predisposition to Disease -- etiology KW - Heating KW - Risk Factors KW - Cooking KW - Neoplasms -- chemically induced KW - Charcoal -- toxicity KW - Genetic Predisposition to Disease -- epidemiology KW - Feces KW - Air Pollution, Indoor -- adverse effects KW - Lung Neoplasms -- epidemiology KW - Lung Neoplasms -- genetics KW - Developing Countries KW - Lung Neoplasms -- chemically induced KW - Air Pollution, Indoor -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1126619292?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Research+opportunities+for+cancer+associated+with+indoor+air+pollution+from+solid-fuel+combustion.&rft.au=Reid%2C+Britt+C%3BGhazarian%2C+Armen+A%3BDeMarini%2C+David+M%3BSapkota%2C+Amir%3BJack%2C+Darby%3BLan%2C+Qing%3BWinn%2C+Deborah+M%3BBirnbaum%2C+Linda+S&rft.aulast=Reid&rft.aufirst=Britt&rft.date=2012-11-01&rft.volume=120&rft.issue=11&rft.spage=1495&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1204962 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-07-08 N1 - Date created - 2012-11-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Br J Cancer. 1990 Dec;62(6):982-7 [2257230] J Environ Monit. 2011 Aug;13(8):2165-71 [21687840] Lung Cancer. 1996 Mar;14 Suppl 1:S85-91 [8785670] Int J Epidemiol. 1997 Feb;26(1):24-31 [9126500] J Assoc Physicians India. 2005 Mar;53:190-2 [15926600] Int J Cancer. 2005 Sep 20;116(5):768-73 [15849729] Am J Epidemiol. 2005 Aug 15;162(4):326-33 [16014775] Environ Health Perspect. 2006 Mar;114(3):373-8 [16507460] Environ Mol Mutagen. 2012 Apr;53(3):166-72 [22351488] IARC Monogr Eval Carcinog Risks Hum. 2012;100(Pt E):1-538 [23193840] Cancer Epidemiol Biomarkers Prev. 2000 Jun;9(6):605-8 [10868696] Cancer Causes Control. 2001 May;12(4):289-300 [11456224] Cancer Res. 2001 Sep 15;61(18):6679-81 [11559534] Int J Cancer. 2002 Feb 1;97(4):536-41 [11802219] J Natl Cancer Inst. 2002 Jun 5;94(11):826-35 [12048270] Int J Tuberc Lung Dis. 2004 Mar;8(3):377-83 [15139478] Lung Cancer. 2004 Aug;45(2):155-60 [15246186] IARC Monogr Eval Carcinog Risks Hum. 2004;83:1-1438 [15285078] Int J Toxicol. 2004;23(5):301-33 [15513831] J Natl Cancer Inst. 1989 Dec 6;81(23):1800-6 [2555531] Am J Epidemiol. 2007 Mar 15;165(6):634-42 [17189590] Cancer Res. 2007 Jun 1;67(11):5103-6 [17545587] Int Arch Occup Environ Health. 2007 Oct;81(1):9-17 [17387503] Mutat Res. 2007 Nov-Dec;636(1-3):134-43 [17428724] J Toxicol Environ Health A. 2007 Dec;70(24):2080-8 [18049997] Proc Natl Acad Sci U S A. 2008 Jan 15;105(2):605-10 [18195365] Int J Epidemiol. 2008 Apr;37(2):321-8 [18234740] Nat Genet. 2008 May;40(5):616-22 [18385676] Eur J Cancer Prev. 2008 Oct;17(5):473-8 [18714191] Environ Sci Technol. 2008 Jul 15;42(14):5074-80 [18754350] Int J Cancer. 2008 Nov 1;123(9):2164-9 [18712724] Nat Genet. 2008 Dec;40(12):1407-9 [18978787] Nat Genet. 2008 Dec;40(12):1404-6 [18978790] Br J Cancer. 2008 Dec 2;99(11):1934-9 [19034286] Mutat Res. 2009 Mar 31;674(1-2):116-22 [19041418] Am J Hum Genet. 2009 Nov;85(5):679-91 [19836008] Int J Cancer. 2010 Aug 15;127(4):932-41 [20013811] PLoS Genet. 2010 Aug;6(8). pii: e1001051. doi: 10.1371/journal.pgen.1001051 [20700438] Environ Mol Mutagen. 2006 Aug;47(7):553-61 [16795085] J Environ Monit. 2007 Jan;9(1):23-32 [17213939] IARC Monogr Eval Carcinog Risks Hum. 2010;95:1-430 [20701241] Br J Cancer. 2010 Aug 24;103(5):727-9 [20648014] Environ Health Perspect. 2010 Dec;118(12):1743-7 [20846923] Syst Biol Reprod Med. 2011 Feb;57(1-2):63-71 [21208146] Toxicol Pathol. 2010 Dec;38(7):1085-98 [20924080] Asian Pac J Cancer Prev. 2010;11(6):1789-93 [21338234] Proc Natl Acad Sci U S A. 2011 Aug 2;108(31):12811-4 [21768363] Int J Epidemiol. 1990;19 Suppl 1:S62-6 [2258278] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1289/ehp.1204962 ER - TY - JOUR T1 - Transcriptomic profiling reveals hepatic stem-like gene signatures and interplay of miR-200c and epithelial-mesenchymal transition in intrahepatic cholangiocarcinoma. AN - 1126577252; 22707408 AB - Intrahepatic cholangiocellular carcinoma (ICC) is the second most common type of primary liver cancer. However, its tumor heterogeneity and molecular characteristics are largely unknown. In this study, we conducted transcriptomic profiling of 23 ICC and combined hepatocellular cholangiocarcinoma tumor specimens from Asian patients using Affymetrix messenger RNA (mRNA) and NanoString microRNA microarrays to search for unique gene signatures linked to tumor subtypes and patient prognosis. We validated the signatures in an additional 68 ICC cases derived from Caucasian patients. We found that both mRNA and microRNA expression profiles could independently classify Asian ICC cases into two main subgroups, one of which shared gene expression signatures with previously identified hepatocellular carcinoma (HCC) with stem cell gene expression traits. ICC-specific gene signatures could predict survival in Asian HCC cases and independently in Caucasian ICC cases. Integrative analyses of the ICC-specific mRNA and microRNA expression profiles revealed that a common signaling pathway linking miR-200c signaling to epithelial-mesenchymal transition (EMT) was preferentially activated in ICC with stem cell gene expression traits. Inactivation of miR-200c resulted in an induction of EMT, whereas activation of miR-200c led to a reduction of EMT including a reduced cell migration and invasion in ICC cells. We also found that miR-200c and neural cell adhesion molecule 1 (NCAM1) expression were negatively correlated and their expression levels were predictive of survival in ICC samples. NCAM1, a known hepatic stem/progenitor cell marker, was experimentally demonstrated to be a direct target of miR-200c. Our results indicate that ICC and HCC share common stem-like molecular characteristics and poor prognosis. We suggest that the specific components of EMT may be exploited as critical biomarkers and clinically relevant therapeutic targets for an aggressive form of stem cell-like ICC. Copyright © 2012 American Association for the Study of Liver Diseases. JF - Hepatology (Baltimore, Md.) AU - Oishi, Naoki AU - Kumar, Mia R AU - Roessler, Stephanie AU - Ji, Junfang AU - Forgues, Marshonna AU - Budhu, Anuradha AU - Zhao, Xuelian AU - Andersen, Jesper B AU - Ye, Qing-Hai AU - Jia, Hu-Liang AU - Qin, Lun-Xiu AU - Yamashita, Taro AU - Woo, Hyun Goo AU - Kim, Yoon Jun AU - Kaneko, Shuichi AU - Tang, Zhao-You AU - Thorgeirsson, Snorri S AU - Wang, Xin Wei AD - National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 1792 EP - 1803 VL - 56 IS - 5 KW - Antigens, CD56 KW - 0 KW - MIRN200 microRNA, human KW - MicroRNAs KW - NCAM1 protein, human KW - RNA, Messenger KW - Index Medicus KW - Kaplan-Meier Estimate KW - Gene Expression Profiling KW - Neoplastic Stem Cells KW - Antigens, CD56 -- genetics KW - Humans KW - Carcinoma, Hepatocellular -- genetics KW - Signal Transduction -- genetics KW - Cell Line, Tumor KW - European Continental Ancestry Group -- genetics KW - Asian Continental Ancestry Group -- genetics KW - Liver Neoplasms -- genetics KW - Cholangiocarcinoma -- genetics KW - Bile Duct Neoplasms -- genetics KW - Bile Ducts, Intrahepatic KW - MicroRNAs -- genetics KW - Epithelial-Mesenchymal Transition -- genetics KW - RNA, Messenger -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1126577252?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Transcriptomic+profiling+reveals+hepatic+stem-like+gene+signatures+and+interplay+of+miR-200c+and+epithelial-mesenchymal+transition+in+intrahepatic+cholangiocarcinoma.&rft.au=Oishi%2C+Naoki%3BKumar%2C+Mia+R%3BRoessler%2C+Stephanie%3BJi%2C+Junfang%3BForgues%2C+Marshonna%3BBudhu%2C+Anuradha%3BZhao%2C+Xuelian%3BAndersen%2C+Jesper+B%3BYe%2C+Qing-Hai%3BJia%2C+Hu-Liang%3BQin%2C+Lun-Xiu%3BYamashita%2C+Taro%3BWoo%2C+Hyun+Goo%3BKim%2C+Yoon+Jun%3BKaneko%2C+Shuichi%3BTang%2C+Zhao-You%3BThorgeirsson%2C+Snorri+S%3BWang%2C+Xin+Wei&rft.aulast=Oishi&rft.aufirst=Naoki&rft.date=2012-11-01&rft.volume=56&rft.issue=5&rft.spage=1792&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.25890 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-15 N1 - Date created - 2012-11-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Curr Biol. 1998 Nov 19;8(23):1243-52 [9822576] J Hepatol. 1997 Jun;26(6):1313-23 [9210619] Cells Tissues Organs. 2005;179(1-2):11-23 [15942189] Gastroenterology. 2005 Nov;129(5):1375-83 [16285938] Nat Med. 2006 Apr;12(4):410-6 [16532004] Gastroenterology. 2006 Jun;130(7):2113-29 [16762633] Cancer Cell. 2006 Aug;10(2):99-111 [16904609] Clin Cancer Res. 2006 Sep 15;12(18):5369-76 [17000670] Biochim Biophys Acta. 2007 Jan;1775(1):21-62 [16904831] Gastroenterology. 2007 Jun;132(7):2542-56 [17570225] Oncogene. 2007 Sep 13;26(42):6133-40 [17404574] Am J Pathol. 1949 Jul;25(4):647-55 [18152860] Cancer Cell. 2008 Feb;13(2):153-66 [18242515] 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] Genes Dev. 2008 Apr 1;22(7):894-907 [18381893] Hepatology. 2008 May;47(5):1544-56 [18393293] EMBO Rep. 2008 Jun;9(6):582-9 [18483486] Dev Cell. 2008 Oct;15(4):494-6 [18854134] Gastroenterology. 2009 Mar;136(3):1012-24 [19150350] Curr Opin Cell Biol. 2009 Apr;21(2):166-76 [19237272] Cancer Res. 2009 May 1;69(9):4059-66 [19366792] J Clin Invest. 2009 Jun;119(6):1420-8 [19487818] Hepatology. 2009 Aug;50(2):472-80 [19585654] N Engl J Med. 2009 Oct 8;361(15):1437-47 [19812400] Nat Cell Biol. 2009 Dec;11(12):1487-95 [19935649] Eur J Cancer. 2010 Apr;46(6):1056-61 [20202823] J Clin Invest. 2010 Apr;120(4):1031-4 [20335655] Cancer Res. 2010 Apr 15;70(8):3034-41 [20395200] Cancer Lett. 2010 Aug 1;294(1):25-34 [20149523] J Cell Sci. 2010 Jul 15;123(Pt 14):2357-68 [20592182] Proc Natl Acad Sci U S A. 2010 Nov 23;107(47):20471-6 [21059911] Cancer Res. 2010 Dec 15;70(24):10202-12 [21159642] Hepatology. 2011 Mar;53(3):1035-45 [21374667] Gastroenterology. 2011 Mar;140(3):1063-70 [21094160] Nat Med. 2011 Mar;17(3):313-9 [21386835] CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855] Int J Biol Sci. 2011;7(5):517-35 [21552419] Biochem Biophys Res Commun. 2011 Dec 9;416(1-2):135-9 [22100809] J Cell Mol Med. 2012 Jan;16(1):160-73 [21352471] Gastroenterology. 2012 Apr;142(4):1021-1031.e15 [22178589] Hepatology. 2012 Jun;55(6):1776-86 [22234953] J Clin Invest. 2010 Sep;120(9):3326-39 [20697159] Nat Med. 2003 Apr;9(4):416-23 [12640447] Minerva Chir. 2003 Aug;58(4):469-78 [14603159] Semin Liver Dis. 2004 May;24(2):115-25 [15192785] Semin Liver Dis. 2004 May;24(2):127-37 [15192786] Cell. 2004 Jun 25;117(7):927-39 [15210113] Am J Physiol. 1992 Aug;263(2 Pt 1):G139-48 [1325126] Hepatology. 1999 Apr;29(4):1037-43 [10094943] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/hep.25890 ER - TY - JOUR T1 - Non-steroidal anti-inflammatory drug use and ovarian cancer risk: findings from the NIH-AARP Diet and Health Study and systematic review AN - 1125229307; 17272436 AB - Background: Chronic inflammation has been proposed as a risk factor for ovarian cancer. Some data suggest that anti-inflammatory medications may be protective against ovarian cancer; however, results have been inconsistent. Methods: We evaluated the risk of epithelial ovarian cancer with regular use of NSAIDs prospectively in the NIH-AARP Diet and Health Study, using Cox proportional hazard models. We also examined the risk of common subtypes of epithelial ovarian cancer (serous, mucinous, endometrioid, clear cell, and other epithelial) with regular use of NSAIDs. In addition, we performed meta-analyses summarizing the risk of ovarian cancer with "regular use" of NSAIDs in previously published studies. Results: We did not observe a significant association between regular use of NSAIDs with ovarian cancer risk in the AARP cohort (aspirin: RR 1.06, 95 % CI 0.87-1.29; non-aspirin NSAIDs: RR 0.93, 95 % CI 0.74-1.15); however, summary estimates from prospective cohort studies demonstrated that use of non-aspirin NSAIDs may reduce the risk of ovarian cancer (RR 0.88, 95 % CI 0.77-1.01). Although not significant, we found that mucinous tumors were inversely associated with non-aspirin NSAID use (RR 0.69, 95 % CI 0.23-2.10) in the AARP cohort, which was supported by the meta-analysis (RR 0.69, CI 0.50-0.94.) Conclusion: Although results from the NIH-AARP cohort study were not statistically significant, our meta-analysis suggests that non-aspirin NSAIDs may be protective against ovarian cancer. Additional analyses, focusing on dose, duration, and frequency of NSAID use and accounting for ovarian cancer heterogeneity are necessary to further elucidate the association between NSAID use and ovarian cancer risk. JF - Cancer Causes & Control AU - Murphy, Megan A AU - Trabert, Britton AU - Yang, Hannah P AU - Park, Yikyung AU - Brinton, Louise A AU - Hartge, Patricia AU - Sherman, Mark E AU - Hollenbeck, Albert AU - Wentzensen, Nicolas AD - Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA, wentzenn@mail.nih.gov Y1 - 2012/11// PY - 2012 DA - Nov 2012 SP - 1839 EP - 1852 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 23 IS - 11 SN - 0957-5243, 0957-5243 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Antiinflammatory agents KW - Aspirin KW - Cancer KW - Diets KW - Ovarian carcinoma KW - Reviews KW - Risk factors KW - Risk reduction KW - Tumors 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/1125229307?accountid=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+Causes+%26+Control&rft.atitle=Non-steroidal+anti-inflammatory+drug+use+and+ovarian+cancer+risk%3A+findings+from+the+NIH-AARP+Diet+and+Health+Study+and+systematic+review&rft.au=Murphy%2C+Megan+A%3BTrabert%2C+Britton%3BYang%2C+Hannah+P%3BPark%2C+Yikyung%3BBrinton%2C+Louise+A%3BHartge%2C+Patricia%3BSherman%2C+Mark+E%3BHollenbeck%2C+Albert%3BWentzensen%2C+Nicolas&rft.aulast=Murphy&rft.aufirst=Megan&rft.date=2012-11-01&rft.volume=23&rft.issue=11&rft.spage=1839&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-0063-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2013-02-22 N1 - SubjectsTermNotLitGenreText - Diets; Aspirin; Risk factors; Reviews; Ovarian carcinoma; Tumors; Risk reduction; Antiinflammatory agents; Cancer DO - http://dx.doi.org/10.1007/s10552-012-0063-2 ER - TY - JOUR T1 - Genetic ablation of cyclooxygenase-2 in keratinocytes produces a cell-autonomous defect in tumor formation. AN - 1124752102; 22902545 AB - Using a mouse skin tumor model, we reported previously that cyclooxygenase-2 (COX-2) deficiency reduced papilloma formation. However, this model did not differentiate between the effects of systemic COX-2-deficiency and keratinocyte-specific COX-2 deficiency on tumor formation. To determine whether keratinocyte-specific COX-2 deficiency reduced papilloma formation, v-H-ras-transformed COX-2+/+ and COX-2-/- keratinocytes were grafted onto nude mice and tumor development was compared. Transformed COX-2+/+ and COX-2-/- keratinocytes expressed similar levels of H-ras, epidermal growth factor receptor and phospho-extracellular signal-regulated kinase 1/2 in vitro; and COX-2-deficiency did not reduce uninfected or v-H-ras infected keratinocyte replication. In contrast, tumors arising from grafted transformed COX-2+/+ and COX-2-/- keratinocytes expressed similar levels of H-ras, but COX-2 deficiency reduced phospho-extracellular signal-regulated kinase 1/2 and epidermal growth factor receptor levels 50-60% and tumor volume by 80% at 3 weeks. Two factors appeared to account for the reduced papilloma size. First, papillomas derived from COX-2-/- keratinocytes showed about 70% decreased proliferation, as measured by bromodeoxyuridine incorporation, compared with papillomas derived from COX-2+/+ keratinocytes. Second, keratin 1 immunostaining of papillomas indicated that COX-2-/- keratinocytes prematurely initiated terminal differentiation. Differences in the levels of apoptosis and vascularization did not appear to be contributing factors as their levels were similar in tumors derived from COX-2-/- and COX-2+/+ keratinocytes. Overall, the data are in agreement with our previous observations that decreased papilloma number and size on COX-2-/- mice resulted from reduced keratinocyte proliferation and accelerated keratinocyte differentiation. Furthermore, the data indicate that deficiency/inhibition of COX-2 in the initiated keratinocyte is an important determinant of papilloma forming ability. JF - Carcinogenesis AU - Lao, Huei-Chen AU - Akunda, Jacqueline K AU - Chun, Kyung-Soo AU - Flake, Gordon P AU - Yuspa, Stuart H AU - Langenbach, Robert AD - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 2293 EP - 2300 VL - 33 IS - 11 KW - Ptgs2 protein, mouse KW - EC 1.14.99.- KW - Cyclooxygenase 2 KW - EC 1.14.99.1 KW - Index Medicus KW - Animals KW - Blotting, Western KW - Apoptosis KW - Cells, Cultured KW - Mice, Inbred C57BL KW - Mice, Nude KW - Mice KW - Immunoenzyme Techniques KW - Mice, Knockout KW - Cyclooxygenase 2 -- physiology KW - Skin Neoplasms -- enzymology KW - Papilloma -- enzymology KW - Cell Transformation, Neoplastic -- pathology KW - Papilloma -- pathology KW - Papilloma -- etiology KW - Skin Neoplasms -- etiology KW - Skin Neoplasms -- pathology KW - Keratinocytes -- pathology KW - Keratinocytes -- metabolism KW - Neovascularization, Pathologic KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1124752102?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Genetic+ablation+of+cyclooxygenase-2+in+keratinocytes+produces+a+cell-autonomous+defect+in+tumor+formation.&rft.au=Lao%2C+Huei-Chen%3BAkunda%2C+Jacqueline+K%3BChun%2C+Kyung-Soo%3BFlake%2C+Gordon+P%3BYuspa%2C+Stuart+H%3BLangenbach%2C+Robert&rft.aulast=Lao&rft.aufirst=Huei-Chen&rft.date=2012-11-01&rft.volume=33&rft.issue=11&rft.spage=2293&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgs267 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-17 N1 - Date created - 2012-10-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Ann N Y Acad Sci. 1999;889:84-6 [10668485] J Gastroenterol. 2012 Feb;47(2):97-106 [22218775] Cancer Res. 2000 Jul 1;60(13):3328-32 [10910032] Cancer Metastasis Rev. 2000;19(1-2):19-27 [11191059] Proc Natl Acad Sci U S A. 2001 Jan 30;98(3):1059-64 [11158594] Semin Oncol. 2001 Dec;28(6):543-50 [11740807] Cancer Res. 2002 Jan 15;62(2):506-11 [11809702] Cancer Res. 2002 Jun 15;62(12):3395-401 [12067981] J Environ Pathol Toxicol Oncol. 2002;21(2):183-91 [12086405] Proc Natl Acad Sci U S A. 2002 Sep 17;99(19):12483-8 [12221288] J Biol Chem. 2003 May 23;278(21):19352-7 [12637551] Mol Carcinog. 2003 Oct;38(2):49-58 [14502644] Cancer Cell. 2003 Dec;4(6):431-6 [14706335] Proc Natl Acad Sci U S A. 2004 Jan 13;101(2):591-6 [14688410] Nature. 1986 Oct 30-Nov 5;323(6091):822-4 [2430189] Cancer Res. 1994 Mar 1;54(5):1178-89 [8118803] Methods Enzymol. 1995;254:3-20 [8531694] Cell. 1995 Nov 3;83(3):473-82 [8521477] Cancer Res. 1997 Aug 1;57(15):3180-8 [9242447] Mol Carcinog. 1999 Aug;25(4):231-40 [10449029] Mol Cell Biol. 1999 Oct;19(10):7181-90 [10490653] Carcinogenesis. 1999 Oct;20(10):1939-44 [10506108] Cancer Res. 2005 May 1;65(9):3958-65 [15867397] Eur J Cancer. 2005 Sep;41(13):1854-63 [16002278] Oncol Rep. 2006 Feb;15(2):471-7 [16391871] Gene. 2006 Jan 17;366(1):2-16 [16377102] Cancer Res. 2006 Jul 15;66(14):7059-66 [16849551] Cancer. 2007 Feb 1;109(3):588-97 [17177201] Mol Carcinog. 2007 May;46(5):363-71 [17219415] Oncogene. 2007 May 14;26(22):3291-310 [17496923] Mol Carcinog. 2007 Aug;46(8):692-8 [17443745] Mol Carcinog. 2007 Aug;46(8):705-10 [17546626] Cancer. 2007 Aug 15;110(4):791-800 [17582802] Cell Physiol Biochem. 2007;20(5):607-16 [17762187] J Invest Dermatol. 2008 Jun;128(6):1365-74 [18049451] Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3372-7 [19218449] Hepatology. 2009 Sep;50(3):834-43 [19585617] Exp Dermatol. 2009 Nov;18(11):939-46 [19558494] Cancer Prev Res (Phila). 2010 Jan;3(1):25-34 [20051370] Vet Pathol. 2011 Jan;48(1):254-65 [20876365] Carcinogenesis. 2011 Mar;32(3):417-26 [21156970] Cell. 2011 Mar 4;144(5):646-74 [21376230] Semin Cutan Med Surg. 2011 Mar;30(1):3-5 [21540015] Carcinogenesis. 2011 Oct;32(10):1441-9 [21771729] Cancer Metastasis Rev. 2011 Dec;30(3-4):343-61 [22038018] J Clin Invest. 2000 Jun;105(11):1589-94 [10841517] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/carcin/bgs267 ER - TY - JOUR T1 - Chrnb3 is more strongly associated with fagerström test for cigarette dependence-based nicotine dependence than cigarettes per day: phenotype definition changes genome-wide association studies results AN - 1124749852; 4357361 AB - Nicotine dependence is a highly heritable disorder associated with severe medical morbidity and mortality. Recent meta-analyses have found novel genetic loci associated with cigarettes per day (CPD), a proxy for nicotine dependence. The aim of this paper is to evaluate the importance of phenotype definition (i.e. CPD versus Fagerström Test for Cigarette Dependence (FTCD) score as a measure of nicotine dependence) on genome-wide association studies of nicotine dependence. Genome-wide association study. Community sample. A total of 3365 subjects who had smoked at least one cigarette were selected from the Study of Addiction: Genetics and Environment (SAGE). Of the participants, 2267 were European Americans, 999 were African Americans. Nicotine dependence defined by FTCD score #>4, CPD. The genetic locus most strongly associated with nicotine dependence was rs1451240 on chromosome 8 in the region of CHRNB3 [odds ratio (OR) =  ;0.65, P = 2.4   10−8]. This association was further strengthened in a meta-analysis with a previously published data set (combined P = 6.7  ;  10−16, total n = 4200). When CPD was used as an alternate phenotype, the association no longer reached genome-wide significance (β = −0.08, P = 0.0004). Daily cigarette consumption and the Fagerstrom Test for Cigarette Dependence show different associations with polymorphisms in genetic loci. Reprinted by permission of Blackwell Publishing JF - Addiction AU - Laurie, Cathy AU - Manolio, Teri A AU - Neuman, Rosalind J AU - Nurnberger, John I AU - Porjesz, Bernice AU - Pugh, Elizabeth AU - Ramos, Erin M AU - Saccone, Nancy AU - Saccone, Scott AU - Schuckit, Marc AU - Bierut, Laura J AU - Rice, John P AU - Hartz, Sarah M AU - Agrawal, Arpana AU - Almasy, Laura AU - Bennett, Siiri AU - Breslau, Naomi AU - Bucholz, Kathleen K AU - Doheny, Kimberly F AU - Edenberg, Howard J AU - Goate, Alison M AU - Hesselbrock, Victor AU - Howells, William B AU - Johnson, Eric O AU - Kramer, John AU - Krueger, Robert F AU - Kuperman, Samuel AD - University of Washington ; Texas Biomedical Research Institute ; Michigan State University ; Johns Hopkins University ; Indiana University ; University of Connecticut ; Research Triangle Institute International ; University of Iowa ; National Human Genome Research Institute ; State University of New York ; University of California, San Diego ; University of Minnesota Y1 - 2012/11// PY - 2012 DA - Nov 2012 SP - 2019 EP - 2028 VL - 107 IS - 11 SN - 0965-2140, 0965-2140 KW - Sociology KW - Smoking KW - Genetics KW - Community studies KW - Tobacco KW - Africa KW - Europe KW - Addiction KW - U.S.A. KW - Community care UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1124749852?accountid=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=Addiction&rft.atitle=Chrnb3+is+more+strongly+associated+with+fagerstr%C3%B6m+test+for+cigarette+dependence-based+nicotine+dependence+than+cigarettes+per+day%3A+phenotype+definition+changes+genome-wide+association+studies+results&rft.au=Laurie%2C+Cathy%3BManolio%2C+Teri+A%3BNeuman%2C+Rosalind+J%3BNurnberger%2C+John+I%3BPorjesz%2C+Bernice%3BPugh%2C+Elizabeth%3BRamos%2C+Erin+M%3BSaccone%2C+Nancy%3BSaccone%2C+Scott%3BSchuckit%2C+Marc%3BBierut%2C+Laura+J%3BRice%2C+John+P%3BHartz%2C+Sarah+M%3BAgrawal%2C+Arpana%3BAlmasy%2C+Laura%3BBennett%2C+Siiri%3BBreslau%2C+Naomi%3BBucholz%2C+Kathleen+K%3BDoheny%2C+Kimberly+F%3BEdenberg%2C+Howard+J%3BGoate%2C+Alison+M%3BHesselbrock%2C+Victor%3BHowells%2C+William+B%3BJohnson%2C+Eric+O%3BKramer%2C+John%3BKrueger%2C+Robert+F%3BKuperman%2C+Samuel&rft.aulast=Laurie&rft.aufirst=Cathy&rft.date=2012-11-01&rft.volume=107&rft.issue=11&rft.spage=2019&rft.isbn=&rft.btitle=&rft.title=Addiction&rft.issn=09652140&rft_id=info:doi/10.1111%2Fj.1360-0443.2012.03922.x LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2013-06-12 N1 - Last updated - 2013-09-16 N1 - SubjectsTermNotLitGenreText - 561 6220; 5460 1615 8573 11325; 2604 11949 13521; 2619 10733 10738 12092 1247; 11755 5707 6071 1542 11325; 12766 3055 798 10286; 2; 129; 433 293 14 DO - http://dx.doi.org/10.1111/j.1360-0443.2012.03922.x ER - TY - JOUR T1 - Anxioselective anxiolytics: on a quest for the Holy Grail. AN - 1115529125; 22981367 AB - The discovery of benzodiazepine receptors provided the impetus to discover and develop anxioselective anxiolytics ('Valium without the side effects'). The market potential for an anxioselective based on the γ-aminobutyric acid A (GABA(A)) receptor resulted in clinical trials of multiple compounds. In contrast to the anxioselective profile displayed in preclinical models, compounds such as bretazenil, TPA023, and MRK 409 produced benzodiazepine-like side effects (sedation, dizziness) in Phase I studies, whereas alpidem and ocinaplon exhibited many of the characteristics of an anxioselective in the clinic. Alpidem was briefly marketed for the treatment of anxiety, but was withdrawn because of liver toxicity. Reversible elevations in liver enzymes halted development of ocinaplon in Phase III. The clinical profiles of these two molecules demonstrate that it is possible to develop GABA(A) receptor-based anxioselectives. However, despite the formidable molecular toolbox at our disposal, we are no better informed about the GABA(A) receptors responsible for an anxioselective profile in the clinic. Here, I discuss the evolution of a quest, spanning four decades, for molecules that retain the rapid and robust anti-anxiety actions of benzodiazepines without the side effects that limit their usefulness. Published by Elsevier Ltd. JF - Trends in pharmacological sciences AU - Skolnick, Phil AD - Division of Pharmacotherapies and Medical Consequences of Drug Abuse, National Institute on Drug Abuse, National Institutes of Health, 6001 Executive Boulevard, Suite 4123, Bethesda, MD 20892, USA. phil.skolnick@nih.gov Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 611 EP - 620 VL - 33 IS - 11 KW - Anti-Anxiety Agents KW - 0 KW - GABA-A Receptor Agonists KW - Receptors, GABA-A KW - Index Medicus KW - GABA-A Receptor Agonists -- pharmacology KW - Animals KW - Humans KW - Receptors, GABA-A -- metabolism KW - Receptors, GABA-A -- drug effects KW - Anti-Anxiety Agents -- pharmacology KW - Anxiety Disorders -- drug therapy KW - Anti-Anxiety Agents -- therapeutic use KW - Anxiety Disorders -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1115529125?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Anxioselective+anxiolytics%3A+on+a+quest+for+the+Holy+Grail.&rft.au=Skolnick%2C+Phil&rft.aulast=Skolnick&rft.aufirst=Phil&rft.date=2012-11-01&rft.volume=33&rft.issue=11&rft.spage=611&rft.isbn=&rft.btitle=&rft.title=Trends+in+pharmacological+sciences&rft.issn=1873-3735&rft_id=info:doi/10.1016%2Fj.tips.2012.08.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-02-18 N1 - Date created - 2012-10-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 2011 Dec 8;480(7376):161-2 [22158218] J Psychopharmacol. 2011 Mar;25(3):329-44 [20156926] Nature. 1999 Oct 21;401(6755):796-800 [10548105] Nat Neurosci. 2000 Jun;3(6):587-92 [10816315] Behav Pharmacol. 2000 Apr;11(2):125-31 [10877117] Science. 2000 Oct 6;290(5489):131-4 [11021797] Mol Pharmacol. 2001 Mar;59(3):442-5 [11179437] Mol Pharmacol. 2001 May;59(5):1108-18 [11306694] Proc Natl Acad Sci U S A. 2001 May 22;98(11):6464-9 [11353839] J Clin Psychiatry. 2001 May;62(5):350-7 [11411817] J Clin Psychiatry. 2001;62 Suppl 11:15-9; discussion 20-1 [11414546] J Pharmacol Exp Ther. 2002 Jan;300(1):2-8 [11752090] J Clin Psychiatry. 2002 Sep;63(9):756-7 [12363113] Am J Psychiatry. 2003 Mar;160(3):533-40 [12611835] Proc Natl Acad Sci U S A. 2004 Mar 9;101(10):3674-9 [14990800] Proc Natl Acad Sci U S A. 2004 May 18;101(20):7769-74 [15136735] J Biol Chem. 2004 Oct 15;279(42):43654-60 [15304513] Psychopharmacologia. 1971;21(1):1-7 [5105868] Nature. 1977 Apr 21;266(5604):732-4 [876354] Nature. 1977 Sep 22;269(5626):342-4 [561893] Science. 1977 Nov 25;198(4319):849-51 [918669] Nat Chem Biol. 2012 May;8(5):455-64 [22446838] Psychopharmacology (Berl). 1994 Mar;114(2):191-9 [7838907] Gastroenterol Clin Biol. 1994;18(12):1129-31 [7750686] Trends Neurosci. 1996 Apr;19(4):139-43 [8658597] Eur Neuropsychopharmacol. 1996 May;6(2):119-25 [8791037] Br J Clin Pharmacol. 1996 Jun;41(6):565-73 [8799523] Pharmacol Biochem Behav. 1997 Feb;56(2):317-24 [9050091] J Clin Psychiatry. 1997;58 Suppl 11:19-23 [9363044] Pharmacol Rev. 1998 Jun;50(2):291-313 [9647870] Br J Psychiatry Suppl. 1998;(34):55-63 [9829018] Pharmacol Biochem Behav. 1978 Dec;9(6):853-6 [34175] Pharmacol Biochem Behav. 1979 May;10(5):831-43 [40258] Pharmacol Biochem Behav. 1979 Jul;11(1):99-106 [40260] Science. 1980 Jan 18;207(4428):274-81 [6101294] Life Sci. 1982 Oct 4;31(14):1409-17 [6292638] Life Sci. 1984 Nov 26;35(22):2227-36 [6094935] Nature. 1987 Jul 16-22;328(6127):221-7 [3037384] Pharmacol Biochem Behav. 1988 Apr;29(4):803-6 [2901120] J Pharmacol Exp Ther. 1990 Apr;253(1):334-43 [1970361] Pharmacopsychiatry. 1990 May;23 Suppl 3:108-13 [1974069] Pharmacopsychiatry. 1990 May;23 Suppl 3:120-3 [1974071] Neuron. 1989 Sep;3(3):327-37 [2561970] Trends Pharmacol Sci. 1990 Nov;11(11):452-6 [1980040] Adv Biochem Psychopharmacol. 1990;46:61-72 [1981304] J Biol Chem. 1992 Jan 25;267(3):1426-9 [1346133] J Neurosci. 1992 Mar;12(3):1040-62 [1312131] Eur J Pharmacol. 1993 Jan 4;244(1):29-35 [8380558] Br J Clin Pharmacol. 1993 Apr;35(4):386-94 [8097921] Mol Pharmacol. 1993 Aug;44(2):437-42 [8102787] Eur J Pharmacol. 1993 Aug 15;246(3):283-7 [8223951] Mol Pharmacol. 1993 Oct;44(4):866-70 [7901754] Neuropharmacology. 1993 Sep;32(9):855-63 [7901790] Psychopharmacol Ser. 1993;11:50-61 [7908433] Neurosci Biobehav Rev. 1994 Fall;18(3):355-72 [7984354] Proc Natl Acad Sci U S A. 2005 May 17;102(20):7380-5 [15870187] J Neurosci. 2005 Nov 16;25(46):10682-8 [16291941] J Psychopharmacol. 2008 Jan;22(1):24-32 [18187530] Adv Pharmacol. 2009;57:137-85 [20230761] CNS Neurosci Ther. 2010 Apr;16(2):63-75 [20041911] J Psychopharmacol. 2011 Mar;25(3):314-28 [20147571] Comment In: Trends Pharmacol Sci. 2013 Mar;34(3):145-6 [23394682] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.tips.2012.08.003 ER - TY - JOUR T1 - Characteristics, procedural differences, and costs of inpatients with drug poisoning in acute care hospitals in Japan. AN - 1114952489; 22902257 AB - This study aimed to describe the clinical and procedural characteristics of drug poisoning, to examine procedural differences between drug poisoning repeaters and non-repeaters, and to estimate the costs of drug poisoning. A retrospective cohort study of a nationally representative sample of 6585 inpatients with drug poisoning was conducted, using the administrative database of the Diagnosis Procedure Combination/Per-Diem Payment System in 2008. Although only 3% of patients required surgery and 65% were discharged from the hospitals within 3 days, greater than 30% were admitted to tertiary emergency care (i.e., high-level emergency care) centers that provide care to severely ill and trauma patients who require intensive care. Only 30% of patients received psychiatric consultation during hospitalization. In addition, repeaters were less likely to be admitted to hospitals by ambulance (67% vs. 76%) and more likely to be discharged within 3 days (77% vs. 65%) than non-repeaters. The annual economic burden of drug poisoning in Japan was $66 million (¥7.7 billion), with the population aged 20-39 years accounting for 50% of these costs. This study highlights the need for optimally allocating resources and improving prevention strategies. Copyright © 2012 Elsevier Inc. All rights reserved. JF - General hospital psychiatry AU - Okumura, Yasuyuki AU - Shimizu, Sayuri AU - Ishikawa, Koichi B AU - Matsuda, Shinya AU - Fushimi, Kiyohide AU - Ito, Hiroto AD - Department of Social Psychiatry, National Institute of Mental Health, National Center of Neurology and Psychiatry, Kodaira 187-8553, Tokyo, Japan. yokumura@ncnp.go.jp PY - 2012 SP - 681 EP - 685 VL - 34 IS - 6 KW - Index Medicus KW - Humans KW - Hospitalization -- economics KW - Retrospective Studies KW - Child KW - Japan -- epidemiology KW - Length of Stay -- statistics & numerical data KW - Adult KW - Cohort Studies KW - Length of Stay -- economics KW - Middle Aged KW - Adolescent KW - Hospitalization -- statistics & numerical data KW - Female KW - Male KW - Drug Overdose -- physiopathology KW - Health Care Costs -- statistics & numerical data KW - Drug Overdose -- economics KW - Accidents -- economics KW - Suicide, Attempted -- statistics & numerical data KW - Suicide, Attempted -- economics KW - Drug Overdose -- epidemiology KW - Accidents -- statistics & numerical data UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1114952489?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=General+hospital+psychiatry&rft.atitle=Characteristics%2C+procedural+differences%2C+and+costs+of+inpatients+with+drug+poisoning+in+acute+care+hospitals+in+Japan.&rft.au=Okumura%2C+Yasuyuki%3BShimizu%2C+Sayuri%3BIshikawa%2C+Koichi+B%3BMatsuda%2C+Shinya%3BFushimi%2C+Kiyohide%3BIto%2C+Hiroto&rft.aulast=Okumura&rft.aufirst=Yasuyuki&rft.date=2012-11-01&rft.volume=34&rft.issue=6&rft.spage=681&rft.isbn=&rft.btitle=&rft.title=General+hospital+psychiatry&rft.issn=1873-7714&rft_id=info:doi/10.1016%2Fj.genhosppsych.2012.07.009 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-05-03 N1 - Date created - 2012-10-23 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.genhosppsych.2012.07.009 ER - TY - JOUR T1 - P6981, an arylstibonic acid, is a novel low nanomolar inhibitor of cAMP response element-binding protein binding to DNA. AN - 1114699701; 22851716 AB - Several basic leucine zipper (B-ZIP) transcription factors have been implicated in cancer, substance abuse, and other pathological conditions. We previously identified arylstibonic acids that bind to B-ZIP proteins and inhibit their interaction with DNA. In this study, we used electrophoretic mobility shift assay to analyze 46 arylstibonic acids for their activity to disrupt the DNA binding of three B-ZIP [CCAAT/enhancer-binding protein α, cyclic AMP-response element-binding protein (CREB), and vitellogenin gene-binding protein (VBP)] and two basic helix-loop-helix leucine zipper (B-HLH-ZIP) [USF (upstream stimulating factor) and Mitf] proteins. Twenty-five arylstibonic acids showed activity at micromolar concentrations. The most active compound, P6981 [2-(3-stibonophenyl)malonic acid], had half-maximal inhibition at ~5 nM for CREB. Circular dichroism thermal denaturation studies indicated that P6981 binds both the B-ZIP domain and the leucine zipper. The crystal structure of an arylstibonic acid, NSC13778, bound to the VBP leucine zipper identified electrostatic interactions between both the stibonic and carboxylic acid groups of NSC13778 [(E)-3-(3-stibonophenyl)acrylic acid] and arginine side chains of VBP, which is also involved in interhelical salt bridges in the leucine zipper. P6981 induced GFP-B-ZIP chimeric proteins to partially localize to the cytoplasm, demonstrating that it is active in cells. P6981 inhibited the growth of a patient-derived clear cell sarcoma cell line whose oncogenic potential is driven by a chimeric protein EWS-ATF1 (Ewing's sarcoma protein-activating transcription factor 1), which contains the DNA binding domain of ATF1, a B-ZIP protein. NSC13778 inhibited the growth of xenografted clear cell sarcoma, and no toxicity was observed. These experiments suggest that antimony containing arylstibonic acids are promising leads for suppression of DNA binding activities of B-ZIP and B-HLH-ZIP transcription factors. JF - Molecular pharmacology AU - Zhao, Jianfei AU - Stagno, Jason R AU - Varticovski, Lyuba AU - Nimako, Eric AU - Rishi, Vikas AU - McKinnon, Kathy AU - Akee, Rhone AU - Shoemaker, Robert H AU - Ji, Xinhua AU - Vinson, Charles AD - Laboratory of Metabolism, National Cancer Institute, Bethesda, Maryland 20892, USA. Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 814 EP - 823 VL - 82 IS - 5 KW - 2-(3-stibonophenyl)malonic acid KW - 0 KW - Acids, Noncarboxylic KW - Basic-Leucine Zipper Transcription Factors KW - CCAAT-Enhancer-Binding Protein-alpha KW - Cinnamates KW - Cyclic AMP Response Element-Binding Protein KW - NSC 13778 KW - Organometallic Compounds KW - Vitellogenins KW - DNA KW - 9007-49-2 KW - Antimony KW - 9IT35J3UV3 KW - Index Medicus KW - Molecular Structure KW - Cinnamates -- chemistry KW - Drug Screening Assays, Antitumor KW - Animals KW - Models, Molecular KW - Humans KW - Cell Cycle Checkpoints KW - Electrophoretic Mobility Shift Assay KW - Protein Denaturation KW - Circular Dichroism KW - Mice KW - Cell Line, Tumor KW - Antimony -- chemistry KW - Vitellogenins -- genetics KW - Leucine Zippers KW - CCAAT-Enhancer-Binding Protein-alpha -- antagonists & inhibitors KW - Basic-Leucine Zipper Transcription Factors -- antagonists & inhibitors KW - Cell Survival -- drug effects KW - Basic-Leucine Zipper Transcription Factors -- metabolism KW - Transplantation, Heterologous KW - Crystallography, X-Ray KW - Mice, SCID KW - Cell Line KW - Acids, Noncarboxylic -- chemistry KW - Organometallic Compounds -- pharmacology KW - DNA -- metabolism KW - Cyclic AMP Response Element-Binding Protein -- antagonists & inhibitors KW - Acids, Noncarboxylic -- pharmacology KW - Organometallic Compounds -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1114699701?accountid=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=BMC+Neuroscience&rft.atitle=Dose-dependent+changes+in+neuroinflammatory+and+arachidonic+acid+cascade+markers+with+synaptic+marker+loss+in+rat+lipopolysaccharide+infusion+model+of+neuroinflammation&rft.au=Kellom%2C+Matthew%3BBasselin%2C+Mireille%3BKeleshian%2C+Vasken+L%3BChen%2C+Mei%3BRapoport%2C+Stanley+I%3BRao%2C+Jagadeesh+S&rft.aulast=Kellom&rft.aufirst=Matthew&rft.date=2012-01-01&rft.volume=13&rft.issue=1&rft.spage=50&rft.isbn=&rft.btitle=&rft.title=BMC+Neuroscience&rft.issn=14712202&rft_id=info:doi/10.1186%2F1471-2202-13-50 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-02-12 N1 - Date created - 2012-10-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Cell. 2006 Jun;9(6):473-84 [16766266] Pharmacol Ther. 2005 Oct;108(1):65-75 [16095714] Cancer Res. 2007 Feb 15;67(4):1867-76 [17308129] Mol Pharmacol. 2008 Mar;73(3):669-77 [18042731] Curr Opin Cell Biol. 2008 Apr;20(2):180-5 [18358708] Bioorg Chem. 2008 Aug;36(4):190-7 [18508107] Mol Cancer Res. 2009 May;7(5):654-64 [19435810] J Biomol Screen. 2009 Jul;14(6):700-7 [19470714] Am J Pathol. 2009 Nov;175(5):2197-206 [19815709] Acta Crystallogr D Biol Crystallogr. 2010 Jan;66(Pt 1):12-21 [20057044] Nat Rev Cancer. 2010 Feb;10(2):130-7 [20094047] Acta Crystallogr D Biol Crystallogr. 2010 Feb;66(Pt 2):125-32 [20124692] J Struct Biol. 2010 May;170(2):216-25 [20176111] Eur J Cell Biol. 2010 Jul;89(7):564-73 [20362353] Cancer Res. 2010 May 1;70(9):3813-22 [20388797] Curr Cancer Drug Targets. 2010 Jun;10(4):384-91 [20370681] Nature. 2010 May 20;465(7296):311-5 [20485428] Am J Surg Pathol. 2012 Jul;36(7):e1-e11 [22510762] Nature. 2012 Jun 7;486(7401):80-4 [22678283] Mol Cell Biol. 2000 Jan;20(2):429-40 [10611221] J Biol Chem. 2000 Nov 3;275(44):34826-32 [10942764] Nat Rev Mol Cell Biol. 2001 Aug;2(8):599-609 [11483993] Int J Cancer. 2002 Jun 1;99(4):560-7 [11992546] Mol Cell Biol. 2002 Sep;22(18):6321-35 [12192032] Acta Crystallogr D Biol Crystallogr. 2002 Nov;58(Pt 11):1948-54 [12393927] Oncogene. 2003 May 19;22(20):3035-41 [12789278] Science. 2003 Jun 27;300(5628):2097-101 [12805554] Cell Microbiol. 2003 Nov;5(11):821-34 [14531897] J Biol Chem. 2004 Mar 19;279(12):11863-74 [14702347] Cancer Res. 2004 May 15;64(10):3395-405 [15150091] Science. 1989 Nov 17;246(4932):911-6 [2683088] Science. 1991 Oct 25;254(5031):539-44 [1948029] Mol Endocrinol. 1992 Apr;6(4):647-55 [1350057] New Biol. 1992 Apr;4(4):396-403 [1622934] Nat Genet. 1993 Aug;4(4):341-5 [8401579] EMBO J. 1994 Jun 15;13(12):2849-61 [8026470] EMBO J. 1995 Nov 1;14(21):5329-37 [7489722] Oncogene. 1996 Jan 4;12(1):159-67 [8552387] J Biol Chem. 1997 Jul 25;272(30):18586-94 [9228025] Biochemistry. 1997 Oct 14;36(41):12567-73 [9376362] Oncogene. 1997 Oct 23;15(17):2069-75 [9366524] Mol Cell Biol. 1998 Feb;18(2):967-77 [9447994] J Biol Chem. 1998 Apr 17;273(16):9357-60 [9545256] J Mol Biol. 1998 Jun 19;279(4):959-72 [9642074] N Engl J Med. 1999 Apr 29;340(17):1330-40 [10219069] J Mol Biol. 1999 May 14;288(4):743-52 [10329176] Cancer Cell. 2005 Apr;7(4):351-62 [15837624] Anal Biochem. 2005 May 15;340(2):259-71 [15840499] J Virol. 2005 May;79(10):6122-33 [15857997] Pigment Cell Res. 2005 Oct;18(5):337-48 [16162174] Cancer Res. 2006 Aug 1;66(15):7578-88 [16885357] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1124/mol.112.080820 ER - TY - JOUR T1 - Up-regulation of human prostaglandin reductase 1 improves the efficacy of hydroxymethylacylfulvene, an antitumor chemotherapeutic agent. AN - 1112674055; 22895897 AB - Prostaglandin reductase 1 (PTGR1) is a highly inducible enzyme with enone reductase activity. Previous studies demonstrated the role of rat PTGR1 in the activation of acylfulvene analogs, a class of antitumor natural product derivatives. Of these, hydroxymethylacylfulvene (HMAF) was in advanced clinical development for the treatment of advanced solid tumors, including prostate, ovarian, and pancreatic cancers. However, the efficiency of human PTGR1 in activating acylfulvenes and its potential to enhance therapeutic efficacy have remained uncharacterized. In this study, human PTGR1 was polymerase chain reaction-cloned and purified. Conversion of HMAF to its cellular metabolite by the purified enzyme proceeded at a 20-fold higher rate than with the rat variant of the enzyme. The Km was 4.9 μM, which was 40-fold lower than for the rat variant and similar to the therapeutic dose. Human cell lines, including colon cancer lines, were transfected with a vector containing rat PTGR1 or human PTGR1, and cell viability was examined after dosing with HMAF. New data obtained in this study suggest that transfection with human PTGR1, or its induction in colon and liver cancer cell lines with 1,2-dithiol-3-thione, enhances susceptibility to the cytotoxic influences of HMAF by 2- to 10-fold. Furthermore, similar or enhanced enzyme induction and HMAF toxicity results from preconditioning cancer cells with the bioactive food components curcumin and resveratrol. The functional impact of PTGR1 induction in human cells and chemical-based strategies for its activation can provide important knowledge for the design of clinical strategies involving reductively activated cytotoxic chemotherapeutics. JF - The Journal of pharmacology and experimental therapeutics AU - Yu, Xiang AU - Erzinger, Melanie M AU - Pietsch, Kathryn E AU - Cervoni-Curet, Frances N AU - Whang, John AU - Niederhuber, John AU - Sturla, Shana J AD - Cancer Cell and Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. xshawnyu@gmail.com Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 426 EP - 433 VL - 343 IS - 2 KW - Antineoplastic Agents, Alkylating KW - 0 KW - Antioxidants KW - Indicators and Reagents KW - NF-E2-Related Factor 2 KW - NFE2L2 protein, human KW - Recombinant Proteins KW - Sesquiterpenes KW - irofulven KW - 6B799IH05A KW - 15-Oxoprostaglandin 13-Reductase KW - EC 1.3.1.48 KW - Index Medicus KW - Animals KW - Recombinant Proteins -- biosynthesis KW - Plasmids -- genetics KW - Humans KW - NF-E2-Related Factor 2 -- genetics KW - Antioxidant Response Elements KW - Cell Line, Tumor KW - Recombinant Proteins -- genetics KW - Biotransformation -- physiology KW - NF-E2-Related Factor 2 -- metabolism KW - Cloning, Molecular KW - Up-Regulation -- physiology KW - Rats KW - Polymerase Chain Reaction KW - Blotting, Western KW - Promoter Regions, Genetic -- drug effects KW - Antioxidants -- pharmacology KW - Cell Survival -- drug effects KW - Enzyme Induction -- drug effects KW - Kinetics KW - Antineoplastic Agents, Alkylating -- pharmacology KW - 15-Oxoprostaglandin 13-Reductase -- genetics KW - Sesquiterpenes -- pharmacology KW - 15-Oxoprostaglandin 13-Reductase -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1112674055?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Up-regulation+of+human+prostaglandin+reductase+1+improves+the+efficacy+of+hydroxymethylacylfulvene%2C+an+antitumor+chemotherapeutic+agent.&rft.au=Yu%2C+Xiang%3BErzinger%2C+Melanie+M%3BPietsch%2C+Kathryn+E%3BCervoni-Curet%2C+Frances+N%3BWhang%2C+John%3BNiederhuber%2C+John%3BSturla%2C+Shana+J&rft.aulast=Yu&rft.aufirst=Xiang&rft.date=2012-11-01&rft.volume=343&rft.issue=2&rft.spage=426&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=1521-0103&rft_id=info:doi/10.1124%2Fjpet.112.195768 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-12-31 N1 - Date created - 2012-10-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Drug Metab Rev. 1983;14(6):1145-63 [6373208] Mutat Res. 1983 Nov;111(3):405-17 [6646150] Nucleic Acids Res. 1988 Sep 12;16(17):8207-11 [3138659] J Natl Cancer Inst. 1990 Oct 3;82(19):1562-5 [2402017] J Biol Chem. 1993 Aug 25;268(24):18128-35 [8394361] Br J Cancer. 1995 Nov;72(5):1144-50 [7577460] J Nat Prod. 1996 Sep;59(9):896-9 [8864242] Invest New Drugs. 1996;14(2):161-7 [8913837] Carcinogenesis. 1996 Nov;17(11):2297-303 [8968041] Cancer Res. 1997 Jan 15;57(2):279-83 [9000568] Cancer Chemother Pharmacol. 1997;40(1):65-71 [9137532] Br J Cancer. 1998 Apr;77(8):1241-52 [9579829] Br J Cancer. 1999 Jun;80(8):1223-30 [10376975] Cancer Epidemiol Biomarkers Prev. 2005 Jan;14(1):120-5 [15668484] Cancer Chemother Pharmacol. 2005 Sep;56(3):307-16 [15877230] Toxicol In Vitro. 2006 Mar;20(2):176-86 [16293390] J Med Chem. 2006 Apr 20;49(8):2593-9 [16610802] J Biol Chem. 2006 Sep 8;281(36):26245-52 [16857669] Neurotoxicology. 2006 Dec;27(6):1094-100 [16959318] J Am Chem Soc. 2007 Feb 21;129(7):2101-11 [17256933] Cancer Epidemiol Biomarkers Prev. 2007 Jun;16(6):1246-52 [17548692] Int J Cancer. 2007 Nov 1;121(9):1883-91 [17631644] Chem Res Toxicol. 2007 Oct;20(10):1513-9 [17900171] Cancer Res. 2007 Dec 15;67(24):12007-17 [18089832] Cancer Res. 2010 Feb 15;70(4):1573-84 [20145130] Pharm Res. 2011 Nov;28(11):2680-94 [21818712] Chem Rev. 2012 Jun 13;112(6):3578-610 [22482429] Br J Cancer. 1995 Sep;72(3):669-75 [7669579] Biochem Pharmacol. 2000 May 15;59(10):1217-26 [10736422] Free Radic Biol Med. 2000 Mar 15;28(6):944-52 [10802226] Proc Natl Acad Sci U S A. 2001 Mar 13;98(6):3410-5 [11248092] Mol Med. 2001 Feb;7(2):135-45 [11471548] J Biol Chem. 2001 Nov 2;276(44):40803-10 [11524419] Prostaglandins Other Lipid Mediat. 2002 Aug;68-69:483-93 [12432938] J Biol Chem. 2003 Mar 7;278(10):8135-45 [12506115] Clin Cancer Res. 2004 Feb 15;10(4):1492-9 [14977853] J Biol Chem. 2004 Apr 23;279(17):17269-77 [14966122] J Biol Chem. 2004 May 21;279(21):22615-23 [15007077] Mutat Res. 2004 Nov 2;555(1-2):133-48 [15476857] Br J Cancer. 2004 Oct 18;91(8):1624-31 [15467770] Cancer Res. 1987 Jun 15;47(12):3186-9 [3472654] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1124/jpet.112.195768 ER - TY - JOUR T1 - Efficacy of anti-insulin-like growth factor I receptor monoclonal antibody cixutumumab in mesothelioma is highly correlated with insulin growth factor-I receptor sites/cell. AN - 1036882305; 22323052 AB - Insulin growth factor-I receptor (IGF-IR) is expressed in mesothelioma and therefore an attractive target for therapy. The antitumor activity of cixutumumab, a humanized monoclonal antibody to IGF-IR, in mesothelioma and relationship to IGF-IR expression was investigated using eight early passage tumor cells obtained from patients, nine established cell lines and an in vivo human mesothelioma tumor xenograft model. Although IGF-IR expression at the mRNA and protein level was present in all mesothelioma cells, using a quantitative ELISA immunoassay, there was considerable variability of IGF-IR expression ranging from 1 to 14 ng/mg of lysate. Using flow cytometry, the number of IGF-IR surface receptors varied from ≈ 2,000 to 50,000 sites/cell. Cells expressing >10,000 sites/cell had greater than 10% growth inhibition when treated with cixutumumab (100 μg/ml). Cixutumumab also induced antibody-dependent cell-mediated toxicity (>10% specific lysis) in cell lines, which had >20,000 IGF-IR sites/cell. Treatment with cixutumumab decreased phosphorylation of IGF-IR, Akt and Erk in cell lines, H226 and H28 having 24,000 and 51,000 IGF-IR sites/cell, respectively, but not in the cell line H2052 with 3,000 IGF-IR sites/cell. In vivo, cixutumumab treatment delayed growth of H226 mesothelioma tumor xenografts in mice and improved the overall survival of these mice compared to mice treated with saline (p < 0.004). Our results demonstrate that the antitumor efficacy of cixutumumab including inhibition of IGF-IR downstream signaling is highly correlated with IGF-IR sites/cell. A phase II clinical trial of cixutumumab is currently ongoing for the treatment of patients with mesothelioma. Copyright © 2012 UICC. JF - International journal of cancer AU - Kalra, Neetu AU - Zhang, Jingli AU - Yu, Yunkai AU - Ho, Mitchell AU - Merino, Maria AU - Cao, Liang AU - Hassan, Raffit AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4264, USA. Y1 - 2012/11/01/ PY - 2012 DA - 2012 Nov 01 SP - 2143 EP - 2152 VL - 131 IS - 9 KW - Antibodies, Monoclonal KW - 0 KW - Intercellular Signaling Peptides and Proteins KW - RNA, Messenger KW - RNA, Small Interfering KW - anti-IGF-1R antibody A12 KW - Insulin-Like Growth Factor I KW - 67763-96-6 KW - Receptor, IGF Type 1 KW - EC 2.7.10.1 KW - Proto-Oncogene Proteins c-akt KW - EC 2.7.11.1 KW - Index Medicus KW - Cell Proliferation -- drug effects KW - Animals KW - Proto-Oncogene Proteins c-akt -- metabolism KW - Humans KW - Insulin-Like Growth Factor I -- metabolism KW - Cell Line, Tumor KW - Mice KW - RNA, Messenger -- genetics KW - Binding Sites KW - Tumor Cells, Cultured KW - RNA, Messenger -- metabolism KW - Phosphorylation KW - Xenograft Model Antitumor Assays KW - Transplantation, Heterologous KW - RNA Interference KW - Intercellular Signaling Peptides and Proteins -- metabolism KW - Mesothelioma -- drug therapy KW - Receptor, IGF Type 1 -- immunology KW - Receptor, IGF Type 1 -- metabolism KW - Receptor, IGF Type 1 -- antagonists & inhibitors KW - Receptor, IGF Type 1 -- genetics KW - Antibodies, Monoclonal -- pharmacology KW - Mesothelioma -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1036882305?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Efficacy+of+anti-insulin-like+growth+factor+I+receptor+monoclonal+antibody+cixutumumab+in+mesothelioma+is+highly+correlated+with+insulin+growth+factor-I+receptor+sites%2Fcell.&rft.au=Kalra%2C+Neetu%3BZhang%2C+Jingli%3BYu%2C+Yunkai%3BHo%2C+Mitchell%3BMerino%2C+Maria%3BCao%2C+Liang%3BHassan%2C+Raffit&rft.aulast=Kalra&rft.aufirst=Neetu&rft.date=2012-11-01&rft.volume=131&rft.issue=9&rft.spage=2143&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.27471 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-11-08 N1 - Date created - 2012-08-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Clin Oncol. 2003 Jul 15;21(14):2636-44 [12860938] Curr Treat Options Oncol. 2011 Jun;12(2):201-16 [21465419] Cancer Res. 2004 Oct 15;64(20):7479-85 [15492273] Cancer Res. 1993 Jun 15;53(12):2858-64 [7684950] Cancer Res. 1996 Sep 1;56(17):4044-8 [8752177] Exp Cell Res. 1997 Feb 1;230(2):284-92 [9024787] N Engl J Med. 2005 Oct 13;353(15):1591-603 [16221782] Ann Thorac Surg. 2006 Sep;82(3):996-1001; discussion 1001-2 [16928523] Cancer Sci. 2007 Aug;98(8):1275-80 [17498200] Clin Cancer Res. 2007 Sep 15;13(18 Pt 2):5549s-5555s [17875788] Mol Cancer Ther. 2008 Sep;7(9):2575-88 [18790742] Cancer Res. 2008 Oct 1;68(19):8039-48 [18829562] Nat Rev Cancer. 2008 Dec;8(12):915-28 [19029956] Cancer Lett. 2009 Jun 8;278(1):49-55 [19178995] J Clin Oncol. 2009 May 20;27(15):2516-22 [19380445] Oncogene. 2009 Aug 27;28(34):3009-21 [19581933] PLoS One. 2009;4(10):e7273 [19806209] Lancet Oncol. 2010 Feb;11(2):129-35 [20036194] Clin Cancer Res. 2010 May 1;16(9):2512-7 [20388853] Cancer J. 2010 May-Jun;16(3):183-94 [20526094] J Clin Oncol. 2010 Sep 20;28(27):4240-6 [20713879] Br J Cancer. 2011 Jan 4;104(1):68-74 [21102589] Br J Cancer. 2011 Jan 4;104(1):1-3 [21206496] Cancer Res. 2003 Dec 15;63(24):8912-21 [14695208] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/ijc.27471 ER - TY - JOUR T1 - Angiotensin II AT(1) receptor blockers as treatments for inflammatory brain disorders. AN - 1028016611; 22827472 AB - The effects of brain AngII (angiotensin II) depend on AT(1) receptor (AngII type 1 receptor) stimulation and include regulation of cerebrovascular flow, autonomic and hormonal systems, stress, innate immune response and behaviour. Excessive brain AT(1) receptor activity associates with hypertension and heart failure, brain ischaemia, abnormal stress responses, blood-brain barrier breakdown and inflammation. These are risk factors leading to neuronal injury, the incidence and progression of neurodegerative, mood and traumatic brain disorders, and cognitive decline. In rodents, ARBs (AT(1) receptor blockers) ameliorate stress-induced disorders, anxiety and depression, protect cerebral blood flow during stroke, decrease brain inflammation and amyloid-β neurotoxicity and reduce traumatic brain injury. Direct anti-inflammatory protective effects, demonstrated in cultured microglia, cerebrovascular endothelial cells, neurons and human circulating monocytes, may result not only in AT(1) receptor blockade, but also from PPARγ (peroxisome-proliferator-activated receptor γ) stimulation. Controlled clinical studies indicate that ARBs protect cognition after stroke and during aging, and cohort analyses reveal that these compounds significantly reduce the incidence and progression of Alzheimer's disease. ARBs are commonly used for the therapy of hypertension, diabetes and stroke, but have not been studied in the context of neurodegenerative, mood or traumatic brain disorders, conditions lacking effective therapy. These compounds are well-tolerated pleiotropic neuroprotective agents with additional beneficial cardiovascular and metabolic profiles, and their use in central nervous system disorders offers a novel therapeutic approach of immediate translational value. ARBs should be tested for the prevention and therapy of neurodegenerative disorders, in particular Alzheimer's disease, affective disorders, such as co-morbid cardiovascular disease and depression, and traumatic brain injury. JF - Clinical science (London, England : 1979) AU - Saavedra, Juan M AD - Section on Pharmacology, Division of Intramural Research Programs, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, Bethesda, MD 20892, USA. Saavedrj@mail.nih.gov Y1 - 2012/11// PY - 2012 DA - November 2012 SP - 567 EP - 590 VL - 123 IS - 10 KW - Angiotensin II Type 1 Receptor Blockers KW - 0 KW - Biomarkers KW - Neuroprotective Agents KW - Receptor, Angiotensin, Type 1 KW - Angiotensin II KW - 11128-99-7 KW - Index Medicus KW - Inflammation -- physiopathology KW - Brain -- drug effects KW - Humans KW - Brain Injuries -- prevention & control KW - Brain Injuries -- etiology KW - Brain -- metabolism KW - Mood Disorders -- prevention & control KW - Brain -- physiopathology KW - Stroke -- drug therapy KW - Angiotensin II -- metabolism KW - Brain Ischemia -- drug therapy KW - Aging -- drug effects KW - Biomarkers -- metabolism KW - Mood Disorders -- drug therapy KW - Renin-Angiotensin System -- drug effects KW - Stroke -- complications KW - Brain Ischemia -- prevention & control KW - Brain -- blood supply KW - Inflammation -- drug therapy KW - Mood Disorders -- etiology KW - Neurodegenerative Diseases -- prevention & control KW - Neurodegenerative Diseases -- drug therapy KW - Brain Ischemia -- complications KW - Brain Injuries -- drug therapy KW - Risk Factors KW - Renin-Angiotensin System -- physiology KW - Inflammation -- metabolism KW - Neurodegenerative Diseases -- etiology KW - Stroke -- prevention & control KW - Receptor, Angiotensin, Type 1 -- metabolism KW - Stress, Physiological KW - Angiotensin II Type 1 Receptor Blockers -- therapeutic use KW - Brain Diseases -- prevention & control KW - Brain Diseases -- drug therapy KW - Neuroprotective Agents -- therapeutic use KW - Angiotensin II Type 1 Receptor Blockers -- pharmacology KW - Brain Diseases -- etiology KW - Neuroprotective Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028016611?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+science+%28London%2C+England+%3A+1979%29&rft.atitle=Angiotensin+II+AT%281%29+receptor+blockers+as+treatments+for+inflammatory+brain+disorders.&rft.au=Saavedra%2C+Juan+M&rft.aulast=Saavedra&rft.aufirst=Juan&rft.date=2012-11-01&rft.volume=123&rft.issue=10&rft.spage=567&rft.isbn=&rft.btitle=&rft.title=Clinical+science+%28London%2C+England+%3A+1979%29&rft.issn=1470-8736&rft_id=info:doi/10.1186%2F1471-2350-13-62 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-01 N1 - Date created - 2012-07-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Stress. 2008 Jan;11(1):62-72 [17853061] Lancet. 2008 Oct 18;372(9647):1394-402 [18823656] Neuroimmunomodulation. 2008;15(4-6):323-30 [19047808] Eur J Clin Pharmacol. 2004 Feb;59(12):863-8 [14747881] 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[19925528] Nat Immunol. 2010 Feb;11(2):155-61 [20037584] Pharmacol Ther. 2010 Jan;125(1):27-38 [19723538] J Med Chem. 2010 Feb 11;53(3):1076-85 [20073471] Neurotherapeutics. 2010 Jan;7(1):115-26 [20129503] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1042/CS20120078 ER - TY - JOUR T1 - Ter-dependent stress response systems: novel pathways related to metal sensing, production of a nucleoside-like metabolite, and DNA-processing. AN - 1124755290; 23044854 AB - The mode of action of the bacterial ter cluster and TelA genes, implicated in natural resistance to tellurite and other xenobiotic toxic compounds, pore-forming colicins and several bacteriophages, has remained enigmatic for almost two decades. Using comparative genomics, sequence-profile searches and structural analysis we present evidence that the ter gene products and their functional partners constitute previously underappreciated, chemical stress response and anti-viral defense systems of bacteria. Based on contextual information from conserved gene neighborhoods and domain architectures, we show that the ter gene products and TelA lie at the center of membrane-linked metal recognition complexes with regulatory ramifications encompassing phosphorylation-dependent signal transduction, RNA-dependent regulation, biosynthesis of nucleoside-like metabolites and DNA processing. Our analysis suggests that the multiple metal-binding and non-binding TerD paralogs and TerC are likely to constitute a membrane-associated complex, which might also include TerB and TerY, and feature several, distinct metal-binding sites. Versions of the TerB domain might also bind small molecule ligands and link the TerD paralog-TerC complex to biosynthetic modules comprising phosphoribosyltransferases (PRTases), ATP grasp amidoligases, TIM-barrel carbon-carbon lyases, and HAD phosphoesterases, which are predicted to synthesize novel nucleoside-like molecules. One of the PRTases is also likely to interact with RNA by means of its Pelota/Ribosomal protein L7AE-like domain. The von Willebrand factor A domain protein, TerY, is predicted to be part of a distinct phosphorylation switch, coupling a protein kinase and a PP2C phosphatase. We show, based on the evidence from numerous conserved gene neighborhoods and domain architectures, that both the TerB and TelA domains have been linked to diverse lipid-interaction domains, such as two novel PH-like and the Coq4 domains, in different bacteria, and are likely to comprise membrane-associated sensory complexes that might additionally contain periplasmic binding-protein-II and OmpA domains. We also show that the TerD and TerB domains and the TerY-associated phosphorylation system are functionally linked to many distinct DNA-processing complexes, which feature proteins with SWI2/SNF2 and RecQ-like helicases, multiple AAA+ ATPases, McrC-N-terminal domain proteins, several restriction endonuclease fold DNases, DNA-binding domains and a type-VII/Esx-like system, which is at the center of a predicted DNA transfer apparatus. These DNA-processing modules and associated genes are predicted to be involved in restriction or suicidal action in response to phages and possibly repairing xenobiotic-induced DNA damage. In some eukaryotes, certain components of the ter system appear to be recruited to function in conjunction with the ubiquitin system and calcium-signaling pathways. JF - Molecular bioSystems AU - Anantharaman, Vivek AU - Iyer, Lakshminarayan M AU - Aravind, L AD - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, Maryland 20894, USA. Y1 - 2012/10/30/ PY - 2012 DA - 2012 Oct 30 SP - 3142 EP - 3165 VL - 8 IS - 12 KW - Colicins KW - 0 KW - DNA replication terminus site-binding protein, E coli KW - DNA, Bacterial KW - DNA-Binding Proteins KW - Escherichia coli Proteins KW - Lipids KW - Membrane Proteins KW - Metals KW - KlaA protein, E coli KW - 134944-10-8 KW - Adenosine Triphosphatases KW - EC 3.6.1.- KW - tellurous acid KW - IVA6SGP6QM KW - Tellurium KW - NQA0O090ZJ KW - Index Medicus KW - DNA Repair KW - Drug Resistance, Bacterial KW - Membrane Proteins -- metabolism KW - Operon KW - Principal Component Analysis KW - Virus Inactivation KW - Colicins -- metabolism KW - Phosphorylation KW - Lipids -- chemistry KW - Coliphages -- physiology KW - Crystallography, X-Ray KW - Tellurium -- pharmacology KW - Protein Structure, Tertiary KW - Protein Interaction Domains and Motifs KW - Signal Transduction KW - Stress, Physiological KW - Escherichia coli Proteins -- chemistry KW - Escherichia coli Proteins -- metabolism KW - Escherichia coli -- metabolism KW - DNA-Binding Proteins -- chemistry KW - Escherichia coli -- drug effects KW - DNA-Binding Proteins -- genetics KW - Adenosine Triphosphatases -- metabolism KW - DNA, Bacterial -- metabolism KW - Metals -- metabolism KW - Adenosine Triphosphatases -- genetics KW - Escherichia coli Proteins -- genetics KW - DNA-Binding Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1124755290?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+bioSystems&rft.atitle=Ter-dependent+stress+response+systems%3A+novel+pathways+related+to+metal+sensing%2C+production+of+a+nucleoside-like+metabolite%2C+and+DNA-processing.&rft.au=Anantharaman%2C+Vivek%3BIyer%2C+Lakshminarayan+M%3BAravind%2C+L&rft.aulast=Anantharaman&rft.aufirst=Vivek&rft.date=2012-10-30&rft.volume=8&rft.issue=12&rft.spage=3142&rft.isbn=&rft.btitle=&rft.title=Molecular+bioSystems&rft.issn=1742-2051&rft_id=info:doi/10.1039%2Fc2mb25239b LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-05-02 N1 - Date created - 2012-10-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Folia Microbiol (Praha). 1998;43(6):589-99 [10069007] Trends Microbiol. 1999 Mar;7(3):111-5 [10203839] J Mol Biol. 1999 Jul 2;290(1):49-60 [10388557] 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[9348106] J Mol Biol. 1998 Nov 6;283(4):707-25 [9790834] Nucleic Acids Res. 1999 Mar 1;27(5):1223-42 [9973609] Mol Biosyst. 2010 Aug;6(8):1475-91 [20517567] Neuron. 2010 Sep 23;67(6):915-28 [20869590] Antimicrob Agents Chemother. 2010 Nov;54(11):4658-63 [20713661] Gene. 2010 Dec 1;469(1-2):18-30 [20713135] Annu Rev Genet. 2010;44:393-417 [21047263] J Mol Biol. 2011 Jan 28;405(4):939-55 [21093452] J Mol Biol. 2011 Feb 4;405(5):1188-201 [21112337] Curr Opin Chem Biol. 2011 Feb;15(1):66-78 [21093351] Biochem J. 2011 Apr 1;435(1):85-91 [21244361] Gene. 2011 Apr 15;475(2):63-78 [21182906] Vet Microbiol. 2011 May 12;150(1-2):146-51 [21295415] Mol Biosyst. 2011 Jul;7(7):2261-77 [21547297] Nucleic Acids Res. 2011 Jun;39(11):4532-52 [21306995] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1039/c2mb25239b ER - TY - CPAPER T1 - Alcohol Modulation of Receptor Signaling: An Overview T2 - 45th Annual Meeting of the Society for Leukocyte Biology AN - 1313119909; 6161861 JF - 45th Annual 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T2 - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AN - 1313032707; 6157215 JF - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AU - Dionne, Raymond AU - Hafner-Eaton, Chris Y1 - 2012/10/27/ PY - 2012 DA - 2012 Oct 27 KW - Pain UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313032707?accountid=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=article&rft.jtitle=BMC+Bioinformatics&rft.atitle=Primer-BLAST%3A+A+tool+to+design+target-specific+primers+for+polymerase+chain+reaction&rft.au=Ye%2C+Jian%3BCoulouris%2C+George%3BZaretskaya%2C+Irena%3BCutcutache%2C+Ioana%3BRozen%2C+Steve%3BMadden%2C+Thomas+L&rft.aulast=Ye&rft.aufirst=Jian&rft.date=2012-01-01&rft.volume=13&rft.issue=1&rft.spage=134&rft.isbn=&rft.btitle=&rft.title=BMC+Bioinformatics&rft.issn=14712105&rft_id=info:doi/10.1186%2F1471-2105-13-134 L2 - https://apha.confex.com/apha/140am/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Planning NextGen health systems for health equity: Using complex determinants of health across the life-course T2 - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AN - 1313032681; 6157214 JF - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AU - Kaplan, Robert AU - Hafner-Eaton, Chris Y1 - 2012/10/27/ PY - 2012 DA - 2012 Oct 27 KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313032681?accountid=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=140th+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2012%29&rft.atitle=Planning+NextGen+health+systems+for+health+equity%3A+Using+complex+determinants+of+health+across+the+life-course&rft.au=Kaplan%2C+Robert%3BHafner-Eaton%2C+Chris&rft.aulast=Kaplan&rft.aufirst=Robert&rft.date=2012-10-27&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=140th+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2012%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/140am/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Translating Interdisciplinary Team Science into Health Equity T2 - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AN - 1313032651; 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6158931 JF - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AU - Okamoto, Janet AU - Breslau, Erica Y1 - 2012/10/27/ PY - 2012 DA - 2012 Oct 27 KW - USA KW - Cancer KW - Mortality KW - Financing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313029286?accountid=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=140th+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2012%29&rft.atitle=State+funding+and+health+system+factors+associated+with+cancer+mortality+in+older+adult+in+the+United+States%3A+1999-2008&rft.au=Okamoto%2C+Janet%3BBreslau%2C+Erica&rft.aulast=Okamoto&rft.aufirst=Janet&rft.date=2012-10-27&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=140th+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2012%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/140am/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - NIH Grants and review processes T2 - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AN - 1313027105; 6155331 JF - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AU - Chollette, Veronica Y1 - 2012/10/27/ PY - 2012 DA - 2012 Oct 27 KW - Reviews KW - Grants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313027105?accountid=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=140th+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2012%29&rft.atitle=NIH+Grants+and+review+processes&rft.au=Chollette%2C+Veronica&rft.aulast=Chollette&rft.aufirst=Veronica&rft.date=2012-10-27&rft.volume=13&rft.issue=1&rft.spage=74&rft.isbn=&rft.btitle=&rft.title=Biostatistics+%28Oxford%2C+England%29&rft.issn=1468-4357&rft_id=info:doi/10.1093%2Fbiostatistics%2Fkxr024 L2 - https://apha.confex.com/apha/140am/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - National Cancer Institute's Behavioral Research Program: Funding priorities, portfolio, and opportunities T2 - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AN - 1313027047; 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6158250 JF - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AU - Webb, Candace AU - Winston, Stefanie AU - Patrick, Ryan Y1 - 2012/10/27/ PY - 2012 DA - 2012 Oct 27 KW - USA KW - Human immunodeficiency virus KW - Prisons KW - Acquired immune deficiency syndrome UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313026792?accountid=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=140th+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2012%29&rft.atitle=Women+on+the+Inside%3A+Incarcerated+U.S.+Women+and+HIV%2FAIDS&rft.au=Webb%2C+Candace%3BWinston%2C+Stefanie%3BPatrick%2C+Ryan&rft.aulast=Webb&rft.aufirst=Candace&rft.date=2012-10-27&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=140th+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2012%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/140am/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Classification of Laws Associated with School Students (C.L.A.S.S.): Examples of state level physical education and school nutrition policy evaluation T2 - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AN - 1313025563; 6155264 JF - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AU - Oh, April Y1 - 2012/10/27/ PY - 2012 DA - 2012 Oct 27 KW - Schools KW - Classification KW - Nutrition KW - Education KW - Policies UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313025563?accountid=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=140th+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2012%29&rft.atitle=Classification+of+Laws+Associated+with+School+Students+%28C.L.A.S.S.%29%3A+Examples+of+state+level+physical+education+and+school+nutrition+policy+evaluation&rft.au=Oh%2C+April&rft.aulast=Oh&rft.aufirst=April&rft.date=2012-10-27&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=140th+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2012%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/140am/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Linking vulnerable drug using populations to quality care and services T2 - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AN - 1313003045; 6158406 JF - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AU - Jones, Dionne AU - Wechsberg, Wendee AU - Surratt, Hilary AU - Milburn, Norweeta Y1 - 2012/10/27/ PY - 2012 DA - 2012 Oct 27 KW - Drugs KW - Vulnerability UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313003045?accountid=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=article&rft.jtitle=Biostatistics+%28Oxford%2C+England%29&rft.atitle=A+survival+analysis+approach+to+modeling+human+fecundity.&rft.au=Sundaram%2C+Rajeshwari%3BMcLain%2C+Alexander+C%3BBuck+Louis%2C+Germaine+M&rft.aulast=Sundaram&rft.aufirst=Rajeshwari&rft.date=2012-01-01&rft.volume=13&rft.issue=1&rft.spage=4&rft.isbn=&rft.btitle=&rft.title=Biostatistics+%28Oxford%2C+England%29&rft.issn=1468-4357&rft_id=info:doi/10.1093%2Fbiostatistics%2Fkxr015 L2 - https://apha.confex.com/apha/140am/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Painting a Conceptual Picture of Disability: Using the International Classification of Functioning, Disability and Health (ICF) to examine disability measures and programs T2 - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AN - 1313000626; 6157258 JF - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AU - Brandt, Diane AU - Ho, Pei-Shu AU - Rasch, Elizabeth AU - Chan, Leighton Y1 - 2012/10/27/ PY - 2012 DA - 2012 Oct 27 KW - Disabilities KW - Classification UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313000626?accountid=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=140th+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2012%29&rft.atitle=Painting+a+Conceptual+Picture+of+Disability%3A+Using+the+International+Classification+of+Functioning%2C+Disability+and+Health+%28ICF%29+to+examine+disability+measures+and+programs&rft.au=Brandt%2C+Diane%3BHo%2C+Pei-Shu%3BRasch%2C+Elizabeth%3BChan%2C+Leighton&rft.aulast=Brandt&rft.aufirst=Diane&rft.date=2012-10-27&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=140th+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2012%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/140am/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - A Solution in Sight: A Global Partnership to Improve Access to Ophthalmic Information in Developing Countries T2 - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AN - 1313000567; 6157779 JF - 140th American Public Health Association Annual Meeting and Exposition (APHA 2012) AU - Sieving, Pamela AU - Gilbert, Suzanne AU - Anton, Bette AU - Judson, Katherine Y1 - 2012/10/27/ PY - 2012 DA - 2012 Oct 27 KW - Developing countries UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313000567?accountid=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=140th+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2012%29&rft.atitle=A+Solution+in+Sight%3A+A+Global+Partnership+to+Improve+Access+to+Ophthalmic+Information+in+Developing+Countries&rft.au=Sieving%2C+Pamela%3BGilbert%2C+Suzanne%3BAnton%2C+Bette%3BJudson%2C+Katherine&rft.aulast=Sieving&rft.aufirst=Pamela&rft.date=2012-10-27&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=140th+American+Public+Health+Association+Annual+Meeting+and+Exposition+%28APHA+2012%29&rft.issn=&rft_id=info:doi/ L2 - https://apha.confex.com/apha/140am/webprogram/start.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Influence of vitamin D binding protein on the association between circulating vitamin D and risk of bladder cancer AN - 1125236818; 17323104 AB - Background: There is little research investigating the role of vitamin D binding protein (DBP) in the association between 25-hydroxyvitamin D (25(OH)D) and disease risk. Methods: Within the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study, 250 bladder cancer cases were randomly sampled and matched 1:1 to controls on age and date of blood collection. Odds ratios (OR) and 95% confidence intervals (CI) of bladder cancer were estimated by quartiles of DBP (measured by ELISA), 25(OH)D and the molar ratio of 25(OH)D:DBP, a proxy for free circulating 25(OH)D. Analyses were also conducted stratifying 25(OH)D by DBP (median split) and vice versa. Results: We found no direct association between circulating DBP levels and bladder cancer risk (P-trend=0.83). The inverse association between 25(OH)D and bladder cancer risk was unchanged after adjustment for DBP (Q4 vs Q1 OR=0.61, 95% CI=0.36-1.05; P-trend=0.04), and was stronger among men with lower DBP (low DBP: 25(OH)D Q4 vs Q1 OR=0.47, 95% CI=0.23-1.00; high DBP: 25(OH)D Q4 vs Q1 OR=0.83, 95% CI=0.40-1.75; P for interaction=0.11). Conclusion: Our findings provide additional support for an aetiologic role for vitamin D in bladder cancer and suggest that free, rather than total, circulating vitamin D may be a more relevant exposure when examining bladder and, perhaps, other cancers. JF - British Journal of Cancer AU - Mondul, A M AU - Weinstein, S J AU - Virtamo, J AU - Albanes, D AD - Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services, 6120 Executive Boulevard, Suite 320, Rockville, MD, USA Y1 - 2012/10/23/ PY - 2012 DA - 2012 Oct 23 SP - 1589 EP - 1594 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 107 IS - 9 SN - 0007-0920, 0007-0920 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Age KW - Prevention KW - Vitamin D KW - Urinary bladder KW - Vitamins KW - Proteins 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/1125236818?accountid=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=Bioorganic+and+Medicinal+Chemistry&rft.atitle=Bisubstrate+analogue+inhibitors+of+6-hydroxymethyl-7%2C8-dihydropterin+pyrophosphokinase%3A+New+design+with+improved+properties&rft.au=Shi%2C+Genbin%3BShaw%2C+Gary%3BLiang%2C+Yu-He%3BSubburaman%2C+Priadarsini%3BLi%2C+Yue%3BWu%2C+Yan%3BYan%2C+Honggao%3BJi%2C+Xinhua&rft.aulast=Shi&rft.aufirst=Genbin&rft.date=2012-01-01&rft.volume=20&rft.issue=1&rft.spage=47&rft.isbn=&rft.btitle=&rft.title=Bioorganic+and+Medicinal+Chemistry&rft.issn=09680896&rft_id=info:doi/10.1016%2Fj.bmc.2011.11.032 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Prevention; Age; Vitamin D; Urinary bladder; Vitamins; Proteins; Cancer DO - http://dx.doi.org/10.1038/bjc.2012.417 ER - TY - JOUR T1 - Selective Inhibition of HER2-Positive Breast Cancer Cells by the HIV Protease Inhibitor Nelfinavir AN - 1125235555; 17317677 AB - Background Human epidermal growth factor receptor 2 (HER2)-positive breast cancer is highly aggressive and has higher risk of recurrence than HER2-negative cancer. With few treatment options available, new drug targets specific for HER2-positive breast cancer are needed. Methods We conducted a pharmacological profiling of seven genotypically distinct breast cancer cell lines using a subset of inhibitors of breast cancer cells from a screen of the Johns Hopkins Drug Library. To identify molecular targets of nelfinavir, identified in the screen as a selective inhibitor of HER2-positive cells, we conducted a genome-wide screen of a haploinsufficiency yeast mutant collection. We evaluated antitumor activity of nelfinavir with xenografts in athymic nude mouse models (n = 4-6 per group) of human breast cancer and repeated mixed-effects regression analysis. All statistical tests were two-sided. Results Pharmacological profiling showed that nelfinavir, an anti-HIV drug, selectively inhibited the growth of HER2-positive breast cancer cells in vitro. A genome-wide screening of haploinsufficiency yeast mutants revealed that nelfinavir inhibited heat shock protein 90 (HSP90) function. Further characterization using proteolytic footprinting experiments indicated that nelfinavir inhibited HSP90 in breast cancer cells through a novel mechanism. In vivo, nelfinavir selectively inhibited the growth of HER2-positive breast cancer cells (tumor volume index of HCC1954 cells on day 29, vehicle vs nelfinavir, mean = 14.42 vs 5.16, difference = 9.25, 95% confidence interval [CI] = 5.93 to 12.56, P < .001; tumor volume index of BT474 cells on day 26, vehicle vs nelfinavir, mean = 2.21 vs 0.90, difference = 1.31, 95% CI = 0.83 to 1.78, P < .001). Moreover, nelfinavir inhibited the growth of trastuzumab- and/or lapatinib-resistant, HER2-positive breast cancer cells in vitro at clinically achievable concentrations. Conclusion Nelfinavir was found to be a new class of HSP90 inhibitor and can be brought to HER2-breast cancer treatment trials with the same dosage regimen as that used among HIV patients. JF - Journal of the National Cancer Institute AU - Shim, Joong Sup AU - Rao, Rajini AU - Beebe, Kristin AU - Neckers, Len AU - Han, Inkyu AU - Nahta, Rita AU - Liu, Jun O AD - Affiliations of authors: Department of Pharmacology and Molecular Sciences (JSS, JOL), Department of Oncology (JOL), and Department of Physiology (RR), Johns Hopkins School of Medicine, and Department of Environmental Health Sciences (IH), Johns Hopkins Bloomberg School of Public Health, Baltimore, MD; Urologic Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD (KB, LN); Department of Pharmacology, Emory University School of Medicine, Atlanta, GA (RN)., joliu@jhu.edu Y1 - 2012/10/17/ PY - 2012 DA - 2012 Oct 17 SP - 1576 EP - 1590 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 104 IS - 20 SN - 0027-8874, 0027-8874 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Yeasts KW - proteinase inhibitors KW - Human immunodeficiency virus KW - Breast cancer KW - New classes KW - Tumors KW - Drugs KW - Cancer KW - Mutants KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - R2 23110:Psychological aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1125235555?accountid=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+the+National+Cancer+Institute&rft.atitle=Selective+Inhibition+of+HER2-Positive+Breast+Cancer+Cells+by+the+HIV+Protease+Inhibitor+Nelfinavir&rft.au=Shim%2C+Joong+Sup%3BRao%2C+Rajini%3BBeebe%2C+Kristin%3BNeckers%2C+Len%3BHan%2C+Inkyu%3BNahta%2C+Rita%3BLiu%2C+Jun+O&rft.aulast=Shim&rft.aufirst=Joong&rft.date=2012-10-17&rft.volume=104&rft.issue=20&rft.spage=1576&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/10.1093%2Fjnci%2Fdjs396 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2013-09-09 N1 - SubjectsTermNotLitGenreText - Yeasts; proteinase inhibitors; Human immunodeficiency virus; New classes; Breast cancer; Tumors; Drugs; Cancer; Mutants DO - http://dx.doi.org/10.1093/jnci/djs396 ER - TY - JOUR T1 - Impact of the HIV Epidemic on the Incidence Rates of Anal Cancer in the United States AN - 1125235538; 17317676 AB - Background The risk of anal cancer is substantially increased in HIV-infected individuals. Thus, the HIV epidemic may have influenced the increasing anal cancer trends in the United States. We estimated the impact of the HIV epidemic on trends in anal cancer incidence in the United States during 1980-2005. Methods Data on anal cancer cases with and without AIDS were obtained from the HIV/AIDS Cancer Match Study. The number of HIV-infected anal cancer cases without AIDS was estimated from the number of anal cancers occurring before diagnosis of AIDS. The proportion of anal cancer cases with HIV infection in the general population was calculated. We estimated temporal trends in the incidence rates of anal cancer in the general population overall and after exclusion of HIV-infected cancer cases by calculating annual percent changes and 95% confidence intervals (CIs) using a Joinpoint log-linear model. All incidence rates were standardized to the 2000 US population by age, sex, and race. Results During 1980-2005, of the 20 533 estimated anal cancer cases, 1665 (8.1%) were HIV-infected. During 2001-2005, the proportion of anal cancer cases with HIV infection was the highest-1.2% (95% CI = 0.93 to 1.4%) among females and 28.4% (95% CI = 26.6 to 29.4%) among males. During 1980-2005, HIV infection did not have an impact on the trends in anal cancer among females (incidence rates increased by 3.3% [95% CI = 3.0 to 3.7%] annually overall, and by 3.3% [95% CI = 2.9 to 3.6%] annually without HIV-infected anal cancer cases) but had a strong impact on the trends in anal cancer among males (incidence rates increased by 3.4% [95% CI = 2.9 to 3.9%] annually overall, and by 1.7% [95% CI = 1.2 to 2.3%] annually without HIV infection). Conclusion During 1980-2005, the increasing anal cancer incidence rates in the United States were strongly influenced by the HIV epidemic in males but were independent of HIV infection in females. JF - Journal of the National Cancer Institute AU - Shiels, Meredith S AU - Pfeiffer, Ruth M AU - Chaturvedi, Anil K AU - Kreimer, Aimee R AU - Engels, Eric A AD - Affiliation of authors: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD., shielsms@mail.nih.gov Y1 - 2012/10/17/ PY - 2012 DA - 2012 Oct 17 SP - 1591 EP - 1598 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 104 IS - 20 SN - 0027-8874, 0027-8874 KW - Risk Abstracts; Health & Safety Science Abstracts KW - USA KW - Acquired immune deficiency syndrome KW - Age KW - Human immunodeficiency virus KW - Standards KW - Infection 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/1125235538?accountid=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+the+National+Cancer+Institute&rft.atitle=Impact+of+the+HIV+Epidemic+on+the+Incidence+Rates+of+Anal+Cancer+in+the+United+States&rft.au=Shiels%2C+Meredith+S%3BPfeiffer%2C+Ruth+M%3BChaturvedi%2C+Anil+K%3BKreimer%2C+Aimee+R%3BEngels%2C+Eric+A&rft.aulast=Shiels&rft.aufirst=Meredith&rft.date=2012-10-17&rft.volume=104&rft.issue=20&rft.spage=1591&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/10.1093%2Fjnci%2Fdjs371 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2013-09-09 N1 - SubjectsTermNotLitGenreText - Age; Acquired immune deficiency syndrome; Human immunodeficiency virus; Standards; Infection; Cancer; USA DO - http://dx.doi.org/10.1093/jnci/djs371 ER - TY - CPAPER T1 - Neuroimaging and cortical histology in murine x-monosomy T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313123583; 6176599 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Raznahan, A AU - Probst, F AU - Lalonde, F AU - Germann, J AU - Giedd, J AU - Lerch, J Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Histology KW - Neuroimaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313123583?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=Neuroimaging+and+cortical+histology+in+murine+x-monosomy&rft.au=Raznahan%2C+A%3BProbst%2C+F%3BLalonde%2C+F%3BGermann%2C+J%3BGiedd%2C+J%3BLerch%2C+J&rft.aulast=Raznahan&rft.aufirst=A&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Nucleus accumbens, thalamus and insula functional connectivity during incentive anticipation in typical adults and adolescents T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313122137; 6176127 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Ernst, M AU - Cho, Y AU - Fromm, S AU - Pine, D AU - Fudge, J Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Adolescents KW - Incentives KW - Thalamus KW - Nucleus accumbens UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313122137?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=Nucleus+accumbens%2C+thalamus+and+insula+functional+connectivity+during+incentive+anticipation+in+typical+adults+and+adolescents&rft.au=Ernst%2C+M%3BCho%2C+Y%3BFromm%2C+S%3BPine%2C+D%3BFudge%2C+J&rft.aulast=Ernst&rft.aufirst=M&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - The role of serotonin in the neurocircuitry of anxiety: Serotonergic inhibition of the dorsal medial prefrontal-amygdala 'aversive amplification' circuit? T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313122052; 6176895 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Robinson, O AU - Overstreet, C AU - Allen, P AU - Vytal, K AU - Pine, D AU - Grillon, C Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Circuits KW - Anxiety KW - Serotonin UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313122052?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=The+role+of+serotonin+in+the+neurocircuitry+of+anxiety%3A+Serotonergic+inhibition+of+the+dorsal+medial+prefrontal-amygdala+%27aversive+amplification%27+circuit%3F&rft.au=Robinson%2C+O%3BOverstreet%2C+C%3BAllen%2C+P%3BVytal%2C+K%3BPine%2C+D%3BGrillon%2C+C&rft.aulast=Robinson&rft.aufirst=O&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Anticipatory anxiety enhances stimulus-driven actions T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313122044; 6176893 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Cornwell, B AU - Mueller, S AU - Ernst, M Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Anxiety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313122044?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=Anticipatory+anxiety+enhances+stimulus-driven+actions&rft.au=Cornwell%2C+B%3BMueller%2C+S%3BErnst%2C+M&rft.aulast=Cornwell&rft.aufirst=B&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Conditional expression of Parkinson's disease related mutant alpha-synuclein in the midbrain dopaminergic neurons causes progressive neurodegeneration and degradation of transcription factor Nuclear Receptor Related 1 T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313118810; 6176364 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Cai, H AU - Lin, X AU - Parisiadou, L AU - Sgobio, C AU - Yu, J. Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Degradation KW - Parkinson's disease KW - Mutants KW - Transcription factors KW - Neurons KW - Nuclear receptors KW - Mesencephalon KW - Movement disorders KW - Neurodegenerative diseases KW - Neurodegeneration KW - Synuclein UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313118810?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=Conditional+expression+of+Parkinson%27s+disease+related+mutant+alpha-synuclein+in+the+midbrain+dopaminergic+neurons+causes+progressive+neurodegeneration+and+degradation+of+transcription+factor+Nuclear+Receptor+Related+1&rft.au=Cai%2C+H%3BLin%2C+X%3BParisiadou%2C+L%3BSgobio%2C+C%3BYu%2C+J.&rft.aulast=Cai&rft.aufirst=H&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Opioid peptides induce long-term depression at glutamatergic synapses in the dorsal striatum T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313118800; 6176206 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Atwood, B AU - Lovinger, D Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Depression KW - Peptides KW - Synapses KW - Long-term depression KW - opioid peptides KW - Neostriatum KW - synaptic depression KW - Glutamatergic transmission UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313118800?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=Opioid+peptides+induce+long-term+depression+at+glutamatergic+synapses+in+the+dorsal+striatum&rft.au=Atwood%2C+B%3BLovinger%2C+D&rft.aulast=Atwood&rft.aufirst=B&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Down-scaling of synaptic strength by antidromic action potentials associated with sharp-wave ripple complex T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313109102; 6176207 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Bukalo, O AU - Fields, D Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Action potential KW - Synaptic strength UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313109102?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=Down-scaling+of+synaptic+strength+by+antidromic+action+potentials+associated+with+sharp-wave+ripple+complex&rft.au=Bukalo%2C+O%3BFields%2C+D&rft.aulast=Bukalo&rft.aufirst=O&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - RNA-Seq analysis of DRG neuronal subpopulation: Insights into the "nociceptome" and axotomy induced gene expression T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313090768; 6177316 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Clokie, S AU - Goswami, S AU - Gonnella, G AU - Kominsky, H AU - Kaszas, K AU - Mishra, S AU - Lebovitz, E AU - Hoon, M AU - Iadarola, M Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Subpopulations KW - Gene expression KW - Axotomy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313090768?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=RNA-Seq+analysis+of+DRG+neuronal+subpopulation%3A+Insights+into+the+%22nociceptome%22+and+axotomy+induced+gene+expression&rft.au=Clokie%2C+S%3BGoswami%2C+S%3BGonnella%2C+G%3BKominsky%2C+H%3BKaszas%2C+K%3BMishra%2C+S%3BLebovitz%2C+E%3BHoon%2C+M%3BIadarola%2C+M&rft.aulast=Clokie&rft.aufirst=S&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Speed of human visual-associative face learning predicted by structural properties ofthe uncinate fasciculus T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313089728; 6176428 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Thomas, C AU - Walker, L AU - Pierpaoli, C AU - Baker, C Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Learning UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313089728?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=Speed+of+human+visual-associative+face+learning+predicted+by+structural+properties+ofthe+uncinate+fasciculus&rft.au=Thomas%2C+C%3BWalker%2C+L%3BPierpaoli%2C+C%3BBaker%2C+C&rft.aulast=Thomas&rft.aufirst=C&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Effect of tractography methods on tract volume T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313089393; 6176916 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Marenco, S AU - Chandramohan, D AU - Dejong, K AU - Kippenhan, J AU - Roe, K AU - Mervis, C AU - Pani, A AU - Morris, C AU - Weinberger, D AU - Berman, K Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Neuroscience UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313089393?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=Effect+of+tractography+methods+on+tract+volume&rft.au=Marenco%2C+S%3BChandramohan%2C+D%3BDejong%2C+K%3BKippenhan%2C+J%3BRoe%2C+K%3BMervis%2C+C%3BPani%2C+A%3BMorris%2C+C%3BWeinberger%2C+D%3BBerman%2C+K&rft.aulast=Marenco&rft.aufirst=S&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Escalated alcohol self-administration in alcohol preferring P rats is associated with upregulated neurokinin-1 receptors in the central amygdala T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313087343; 6176095 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Schank, J AU - Tapocik, J AU - Barbier, E AU - Damadzic, R AU - Eskay, R AU - Sun, H AU - Rowe, K AU - King, C AU - Yao, M AU - Karlsson, C AU - Cheng, K AU - Rice, K AU - Heilig, M Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - alcohols KW - Rats KW - Ethanol KW - Amygdala KW - Neurokinin NK1 receptors KW - Drug self-administration UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313087343?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=Escalated+alcohol+self-administration+in+alcohol+preferring+P+rats+is+associated+with+upregulated+neurokinin-1+receptors+in+the+central+amygdala&rft.au=Schank%2C+J%3BTapocik%2C+J%3BBarbier%2C+E%3BDamadzic%2C+R%3BEskay%2C+R%3BSun%2C+H%3BRowe%2C+K%3BKing%2C+C%3BYao%2C+M%3BKarlsson%2C+C%3BCheng%2C+K%3BRice%2C+K%3BHeilig%2C+M&rft.aulast=Schank&rft.aufirst=J&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - A mechanism for rapid immediate-early gene transcription in neurons T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313086945; 6175825 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Dudek, S Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Transcription KW - Neurons KW - Immediate-early proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313086945?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=A+mechanism+for+rapid+immediate-early+gene+transcription+in+neurons&rft.au=Dudek%2C+S&rft.aulast=Dudek&rft.aufirst=S&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Hand representations in the dorsal and ventral pathways: seeing you touching me? T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313045176; 6175937 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Chan, A AU - Truong, S AU - Baker, C Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Hand UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313045176?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=Hand+representations+in+the+dorsal+and+ventral+pathways%3A+seeing+you+touching+me%3F&rft.au=Chan%2C+A%3BTruong%2C+S%3BBaker%2C+C&rft.aulast=Chan&rft.aufirst=A&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Mechanisms of impaired cortical synchrony in an NMDA receptor hypofunction mouse model for schizophrenia T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313043633; 6176312 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Zsiros, V AU - Elkahloun, A AU - Nakazawa, K Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Mental disorders KW - Schizophrenia KW - Animal models KW - N-Methyl-D-aspartic acid receptors KW - Cortex KW - Glutamic acid receptors (ionotropic) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313043633?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=Mechanisms+of+impaired+cortical+synchrony+in+an+NMDA+receptor+hypofunction+mouse+model+for+schizophrenia&rft.au=Zsiros%2C+V%3BElkahloun%2C+A%3BNakazawa%2C+K&rft.aulast=Zsiros&rft.aufirst=V&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Modulation of neural structures underlying motor function after stroke T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313042671; 6176639 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Cohen, L Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Stroke KW - Structure-function relationships UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313042671?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=Modulation+of+neural+structures+underlying+motor+function+after+stroke&rft.au=Cohen%2C+L&rft.aulast=Cohen&rft.aufirst=L&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - How perceptual is perceptual expertise? Neural and behavioral evidence for the involvement of top-down factors in visual expertise T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313041779; 6176438 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Harel, A AU - Gilaie-Dotan, S AU - Bentin, S Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Neuroscience UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313041779?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=How+perceptual+is+perceptual+expertise%3F+Neural+and+behavioral+evidence+for+the+involvement+of+top-down+factors+in+visual+expertise&rft.au=Harel%2C+A%3BGilaie-Dotan%2C+S%3BBentin%2C+S&rft.aulast=Harel&rft.aufirst=A&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Propensity score as a means for studying the combined impact of multiple risk genes for schizophrenia using imaging genetics T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313041678; 6176615 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Callicott, III, J. AU - Zheutlin, A AU - Dickinson, D AU - Zhang, F AU - Straub, R AU - Kolachana, B AU - Mattay, V AU - Weinberger, D Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Genetics KW - Mental disorders KW - Imaging techniques KW - Schizophrenia UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313041678?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=Propensity+score+as+a+means+for+studying+the+combined+impact+of+multiple+risk+genes+for+schizophrenia+using+imaging+genetics&rft.au=Callicott%2C+III%2C+J.%3BZheutlin%2C+A%3BDickinson%2C+D%3BZhang%2C+F%3BStraub%2C+R%3BKolachana%2C+B%3BMattay%2C+V%3BWeinberger%2C+D&rft.aulast=Callicott&rft.aufirst=III&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Sustained anxiety alters amygdala-prefrontal coupling: A mechanism for cognitive disruption and adaptive defensive preparations T2 - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AN - 1313014686; 6176897 JF - 42nd Annual Meeting of the Society for Neuroscience (Neuroscience 2012) AU - Vytal, K AU - Overstreet, C AU - Robinson, O AU - Grillon, C Y1 - 2012/10/13/ PY - 2012 DA - 2012 Oct 13 KW - Anxiety KW - Cognitive ability UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313014686?accountid=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=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.atitle=Sustained+anxiety+alters+amygdala-prefrontal+coupling%3A+A+mechanism+for+cognitive+disruption+and+adaptive+defensive+preparations&rft.au=Vytal%2C+K%3BOverstreet%2C+C%3BRobinson%2C+O%3BGrillon%2C+C&rft.aulast=Vytal&rft.aufirst=K&rft.date=2012-10-13&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=42nd+Annual+Meeting+of+the+Society+for+Neuroscience+%28Neuroscience+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.sfn.org/am2012/index.aspx?pagename=final_program LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - High-efficiency Transduction of Rhesus Hematopoietic Repopulating Cells by a Modified HIV1-based Lentiviral Vector AN - 1668268093; PQ0001270063 AB - Human immunodeficiency virus type 1 (HIV1) vectors poorly transduce rhesus hematopoietic cells due to species-specific restriction factors, including the tripartite motif-containing 5 isoform alpha (TRIM5 alpha ) which targets the HIV1 capsid. We previously developed a chimeric HIV1 ( chi HIV) vector system wherein the vector genome is packaged with the simian immunodeficiency virus (SIV) capsid for efficient transduction of both rhesus and human CD34 super(+) cells. To evaluate whether chi HIV vectors could efficiently transduce rhesus hematopoietic repopulating cells, we performed a competitive repopulation assay in rhesus macaques, in which half of the CD34 super(+) cells were transduced with standard SIV vectors and the other half with chi HIV vectors. As compared with SIV vectors, chi HIV vectors achieved higher vector integration, and the transgene expression rates were two- to threefold higher in granulocytes and red blood cells and equivalent in lymphocytes and platelets for 2 years. A recipient of chi HIV vector-only transduced cells reached up to 40% of transgene expression rates in granulocytes and lymphocytes and 20% in red blood cells. Similar to HIV1 and SIV vectors, chi HIV vector frequently integrated into gene regions, especially into introns. In summary, our chi HIV vector demonstrated efficient transduction for rhesus long-term repopulating cells, comparable with SIV vectors. This chi HIV vector should allow preclinical testing of HIV1-based therapeutic vectors in large animal models. JF - Molecular Therapy AU - Uchida, Naoya AU - Hargrove, Phillip W AU - Lap, Coen J AU - Evans, Molly E AU - Phang, Oswald AU - Bonifacino, Aylin C AU - Krouse, Allen E AU - Metzger, Mark E AU - Nguyen, Anh-Dao AU - Hsieh, Matthew M AU - Wolfsberg, Tyra G AU - Donahue, Robert E AU - Persons, Derek A AU - Tisdale, John F AD - Molecular and Clinical Hematology Branch, National Heart Lung and Blood Institutes (NHLBI)/National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH), Bethesda, Maryland, USA, johntis@mail.nih.gov Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 1882 EP - 1892 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 20 IS - 10 SN - 1525-0016, 1525-0016 KW - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts KW - Genomes KW - Capsids KW - Transgenes KW - Erythrocytes KW - Animal models KW - CD34 antigen KW - Lymphocytes KW - Expression vectors KW - Integration KW - Leukocytes (granulocytic) KW - Human immunodeficiency virus KW - Human immunodeficiency virus 1 KW - Platelets KW - Introns KW - Hemopoiesis KW - Macaca mulatta KW - Simian immunodeficiency virus KW - W 30905:Medical Applications KW - V 22360:AIDS and HIV UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668268093?accountid=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=High-efficiency+Transduction+of+Rhesus+Hematopoietic+Repopulating+Cells+by+a+Modified+HIV1-based+Lentiviral+Vector&rft.au=Uchida%2C+Naoya%3BHargrove%2C+Phillip+W%3BLap%2C+Coen+J%3BEvans%2C+Molly+E%3BPhang%2C+Oswald%3BBonifacino%2C+Aylin+C%3BKrouse%2C+Allen+E%3BMetzger%2C+Mark+E%3BNguyen%2C+Anh-Dao%3BHsieh%2C+Matthew+M%3BWolfsberg%2C+Tyra+G%3BDonahue%2C+Robert+E%3BPersons%2C+Derek+A%3BTisdale%2C+John+F&rft.aulast=Uchida&rft.aufirst=Naoya&rft.date=2012-10-01&rft.volume=20&rft.issue=10&rft.spage=1882&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2012.193 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Capsids; Genomes; Erythrocytes; Transgenes; Animal models; CD34 antigen; Lymphocytes; Expression vectors; Leukocytes (granulocytic); Integration; Introns; Platelets; Hemopoiesis; Human immunodeficiency virus; Human immunodeficiency virus 1; Macaca mulatta; Simian immunodeficiency virus DO - http://dx.doi.org/10.1038/mt.2012.193 ER - TY - JOUR T1 - Thymidine Kinase Suicide Gene-mediated Ganciclovir Ablation of Autologous Gene-modified Rhesus Hematopoiesis AN - 1668248602; PQ0001270068 AB - Despite the genotoxic complications encountered in clinical gene therapy trials for primary immunodeficiency diseases targeting hematopoietic cells with integrating vectors; this strategy holds promise for the cure of several monogenic blood, metabolic and neurodegenerative diseases. In this study, we asked whether the inclusion of a suicide gene in a standard retrovirus vector would allow elimination of vector-containing stem and progenitor cells and their progeny in vivo following transplantation, using our rhesus macaque transplantation model. Following stable engraftment with autologous CD34 super(+) cells transduced with a retrovirus vector encoding a highly sensitive modified Herpes simplex virus thymidine kinase SR39, the administration of the antiviral prodrug ganciclovir (GCV) was effective in completely eliminating vector-containing cells in all hematopoietic lineages in vivo. The sustained absence of vector-containing cells over time, without additional GCV administration, suggests that the ablation of TkSR39 GCV-sensitive cells occurred in the most primitive hematopoietic long-term repopulating stem or progenitor cell compartment. These results are a proof-of-concept that the inclusion of a suicide gene in integrating vectors, in addition to a therapeutic gene, can provide a mechanism for later elimination of vector-containing cells, thereby increasing the safety of gene transfer. JF - Molecular Therapy AU - Barese, Cecilia N AU - Krouse, Allen E AU - Metzger, Mark E AU - King, Connor A AU - Traversari, Catia AU - Marini, Frank C AU - Donahue, Robert E AU - Dunbar, Cynthia E AD - Hematology Branch, The National Heart, Lung, and Blood Institute (NHLBI), National Institutes of Health (NIH), Bethesda, Maryland, USA, dunbarc@nhlbi.nih.gov Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 1932 EP - 1943 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 20 IS - 10 SN - 1525-0016, 1525-0016 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Autografts KW - Transplantation KW - Gene therapy KW - Genotoxicity KW - Immunodeficiency KW - Suicide KW - Ganciclovir KW - Thymidine kinase KW - CD34 antigen KW - Clinical trials KW - Expression vectors KW - Neurodegenerative diseases KW - Blood KW - Stem cells KW - Retrovirus KW - prodrugs KW - Hemopoiesis KW - Macaca mulatta KW - Progeny KW - Herpes simplex virus 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/1668248602?accountid=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=Thymidine+Kinase+Suicide+Gene-mediated+Ganciclovir+Ablation+of+Autologous+Gene-modified+Rhesus+Hematopoiesis&rft.au=Barese%2C+Cecilia+N%3BKrouse%2C+Allen+E%3BMetzger%2C+Mark+E%3BKing%2C+Connor+A%3BTraversari%2C+Catia%3BMarini%2C+Frank+C%3BDonahue%2C+Robert+E%3BDunbar%2C+Cynthia+E&rft.aulast=Barese&rft.aufirst=Cecilia&rft.date=2012-10-01&rft.volume=20&rft.issue=10&rft.spage=1932&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2012.159 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Autografts; Transplantation; Gene therapy; Genotoxicity; Immunodeficiency; Suicide; CD34 antigen; Thymidine kinase; Ganciclovir; Clinical trials; Expression vectors; Blood; Neurodegenerative diseases; Stem cells; Retrovirus; prodrugs; Hemopoiesis; Progeny; suicide genes; Macaca mulatta; Herpes simplex virus DO - http://dx.doi.org/10.1038/mt.2012.159 ER - TY - JOUR T1 - Dengue Research Opportunities in the Americas AN - 1622611331; 20900042 AB - Dengue is a systemic arthropod-borne viral disease of major global public health importance. At least 2.5 billion people who live in areas of the world where dengue occurs are at risk of developing dengue fever (DF) and its severe complications, dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Repeated reemergences of dengue in sudden explosive epidemics often cause public alarm and seriously stress healthcare systems. The control of dengue is further challenged by the lack of effective therapies, vaccines, and point-of-care diagnostics. Despite years of study, even its pathogenic mechanisms are poorly understood. This article discusses recent advances in dengue research and identifies challenging gaps in research on dengue clinical evaluation, diagnostics, epidemiology, immunology, therapeutics, vaccinology/clinical trials research, vector biology, and vector ecology. Although dengue is a major global tropical pathogen, epidemiologic and disease control considerations in this article emphasize dengue in the Americas. JF - Journal of Infectious Diseases AU - Laughlin, Catherine A AU - Morens, David M AU - Cassetti, M Cristina AU - Denis, Adriana Costero-Saint AU - San Martin, Jose-Luis AU - Whitehead, Stephen S AU - Fauci, Anthony S AD - Virology Branch, Division of Microbiology and Infectious Disease, NIAID, NIH, 6610 Rockledge Drive MSC 6603, Bethesda, MD 20892-6603, claughlin@niaid.nih.gov Y1 - 2012/10/01/ PY - 2012 DA - 2012 Oct 01 SP - 1121 EP - 1127 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 206 IS - 7 SN - 0022-1899, 0022-1899 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Virology & AIDS Abstracts; Health & Safety Science Abstracts KW - Symptoms KW - Human diseases KW - Disease control KW - Hosts KW - Clinical trials KW - Public health KW - Disease transmission KW - Ecology KW - Infectious diseases KW - Dengue KW - Epidemics KW - Complications KW - Immunology KW - Stress KW - Vectors KW - Pathogens KW - Dengue hemorrhagic fever KW - Health care KW - Shock KW - Epidemiology KW - Viral diseases KW - Explosives KW - Vaccines KW - Q1 08485:Species interactions: pests and control KW - Q5 08524:Public health, medicines, dangerous organisms KW - V 22400:Human Diseases KW - H 4000:Food and Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1622611331?accountid=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=Dengue+Research+Opportunities+in+the+Americas&rft.au=Laughlin%2C+Catherine+A%3BMorens%2C+David+M%3BCassetti%2C+M+Cristina%3BDenis%2C+Adriana+Costero-Saint%3BSan+Martin%2C+Jose-Luis%3BWhitehead%2C+Stephen+S%3BFauci%2C+Anthony+S&rft.aulast=Laughlin&rft.aufirst=Catherine&rft.date=2012-10-01&rft.volume=206&rft.issue=7&rft.spage=1121&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjis351 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Symptoms; Human diseases; Viral diseases; Disease control; Vaccines; Pathogens; Hosts; Disease transmission; Public health; Epidemics; Vectors; Stress; Clinical trials; Dengue hemorrhagic fever; Epidemiology; Shock; Dengue; Explosives; Complications; Immunology; Ecology; Health care; Infectious diseases DO - http://dx.doi.org/10.1093/infdis/jis351 ER - TY - JOUR T1 - Contributing to the formation and harmonisation of injury data collection in the Philippines AN - 1551635270; 20347711 AB - BackgroundData on injury has been sporadically collected by different agencies in the Philippines. No policy assigned any particular office or agency to harmonise data from different government and non-government organisations. There were problems on data duplication, increased cost of maintaining the systems and difficulty of sharing.Aims/Objectives/PurposeNeed for baseline data to drive its programmes brought Safe Kids Philippines (SKP) to closely work with the different agencies who could supply reliable data.MethodsSKP aligned itself with the Department of Health (DOH) as part of the Technical Working and Steering Committees for injury data collection and contributed to the formation and development of the Online Electronic Injury Surveillance System. SKP helped to bridge access among DOH, Department of Public Works and Highways (DPWH), and the Metro Manila Development Authority (MMDA) exposing these agencies to existing but overlapping complementary data systems. Issues of ownership, proprietorship and being the principal agency for road crash data slowly eroded as a collegial setting and better communication among the agencies lead to better interaction.ResultsToday, the data bases of DOH and DPWH form the base of the Philippine Network on Injury Data Management System (PNIDMS) initiative. MMDA data is currently being integrated. SKP will contribute data analysis to PNIDMS. Other agencies are lined up for inclusion into the PNIDMS.SignificanceSynchronised data collection efforts were formalised through a Memorandum of Agreement among DOH, WHO, Department of Transportation and Communications, UNICEF, MMDA, Land Transportation Office, DPWH with the Philippine National Police, and SKP. JF - Injury Prevention AU - Perez, M AU - Consunji, R AU - Rolloque, A AU - Alcantara, M AD - Study Group for Injury Prevention, National Institutes of Health, Philippines Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - A237 PB - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom VL - 18 IS - Suppl 1 SN - 1353-8047, 1353-8047 KW - Health & Safety Science Abstracts KW - Philippines KW - Data collection KW - Injuries KW - Philippines, Luzon I., Manila KW - Data management KW - Prevention KW - Communications KW - Transportation KW - Committees KW - Police KW - Highways KW - Data bases KW - H 2000:Transportation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551635270?accountid=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=Contributing+to+the+formation+and+harmonisation+of+injury+data+collection+in+the+Philippines&rft.au=Perez%2C+M%3BConsunji%2C+R%3BRolloque%2C+A%3BAlcantara%2C+M&rft.aulast=Perez&rft.aufirst=M&rft.date=2012-10-01&rft.volume=18&rft.issue=Suppl+1&rft.spage=A237&rft.isbn=&rft.btitle=&rft.title=Injury+Prevention&rft.issn=13538047&rft_id=info:doi/10.1136%2Finjuryprev-2012-040590w.45 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2014-08-21 N1 - SubjectsTermNotLitGenreText - Prevention; Data collection; Transportation; Communications; Injuries; Committees; Police; Highways; Data management; Data bases; Philippines; Philippines, Luzon I., Manila DO - http://dx.doi.org/10.1136/injuryprev-2012-040590w.45 ER - TY - JOUR T1 - WOMEN'S SAFETY ISSUES IN EXPORT ZONES IN DEVELOPING COUNTRIES IN THE CONTEXT OF A GLOBALISED ECONOMY AN - 1551630690; 20347929 AB - BackgroundWomen dominate the labourforce in export zones which are multinational enclaves in the country. In this type of work, there are reports of safety issues that affect their health.ObjectivesThis study tried to look into the occupational safety issues of women workers.MethodsThis investigated 630 women workers in 31 industries in export zones in the Philippines. Tools included work investigation, industrial hygiene and interviews.ResultsThe study showed that technology has intensified work. The new work arrangements were seen to produce new hazards. The characteristics now of the new workplace are: information technology intensive work, fast pace of work, the need for upskilling, burnout, chronic sleep debt, and superspeed communications. Accidents were a common sight in factories. The women reported the following accidents in the workplace for the past one-year: eye infection due to dust and wounds due to sharp objects. The more severe forms of accidents were falling (14%), electrical accidents (6.3%) and being caught in the machine (17.3%). The latter was the most common form of amputation of any body part.SignificanceThe contribution of this study to the field is to show that with the growing internationalisation of work and economies of nation states, women's involvement in the labour market has increased their vulnerability to hazards and injuries where consequent safety programmes are not implemented. JF - Injury Prevention AU - Lu, J L AD - National Institutes of Health, University of the Philippine Manila Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - A12 PB - B M J Publishing Group, B.M.A. House London WC1H 9JR United Kingdom VL - 18 IS - Suppl 1 SN - 1353-8047, 1353-8047 KW - Health & Safety Science Abstracts KW - Philippines KW - Eye KW - Injuries KW - Occupational safety KW - Safety KW - Infection KW - Burnout KW - Accidents KW - Prevention KW - Communications KW - Exports KW - Economics KW - Vulnerability KW - Developing countries KW - Technology KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551630690?accountid=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=WOMEN%27S+SAFETY+ISSUES+IN+EXPORT+ZONES+IN+DEVELOPING+COUNTRIES+IN+THE+CONTEXT+OF+A+GLOBALISED+ECONOMY&rft.au=Lu%2C+J+L&rft.aulast=Lu&rft.aufirst=J&rft.date=2012-10-01&rft.volume=18&rft.issue=Suppl+1&rft.spage=A12&rft.isbn=&rft.btitle=&rft.title=Injury+Prevention&rft.issn=13538047&rft_id=info:doi/10.1136%2Finjuryprev-2012-040580a.37 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2014-08-21 N1 - SubjectsTermNotLitGenreText - Injuries; Eye; Safety; Occupational safety; Infection; Burnout; Prevention; Accidents; Communications; Exports; Economics; Vulnerability; Developing countries; Technology; Philippines DO - http://dx.doi.org/10.1136/injuryprev-2012-040580a.37 ER - TY - JOUR T1 - Global transmission of influenza viruses from humans to swine AN - 1551623566; 20329205 AB - To determine the extent to which influenza viruses jump between human and swine hosts, we undertook a large-scale phylogenetic analysis of pandemic A/H1N1/09 (H1N1pdm09) influenza virus genome sequence data. From this, we identified at least 49 human-to-swine transmission events that occurred globally during 2009-2011, thereby highlighting the ability of the H1N1pdm09 virus to transmit repeatedly from humans to swine, even following adaptive evolution in humans. Similarly, we identified at least 23 separate introductions of human seasonal (non-pandemic) H1 and H3 influenza viruses into swine globally since 1990. Overall, these results reveal the frequency with which swine are exposed to human influenza viruses, indicate that humans make a substantial contribution to the genetic diversity of influenza viruses in swine, and emphasize the need to improve biosecurity measures at the human-swine interface, including influenza vaccination of swine workers. JF - Journal of General Virology AU - Nelson, Martha I AU - Gramer, Marie R AU - Vincent, Amy L AU - Holmes, Edward C AD - Fogarty International Center, National Institutes of Health, Bethesda, MD 20892, USA Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 2195 EP - 2203 PB - Society for General Microbiology, Marlborough House, Basingstoke Road Reading RG7 1AG United Kingdom VL - 93 IS - Pt 10 SN - 1465-2099, 1465-2099 KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Genomes KW - Phylogeny KW - Data processing KW - Nucleotide sequence KW - Viruses KW - Genetic diversity KW - Vaccination KW - Influenza KW - pandemics KW - Influenza virus KW - Sulfur dioxide KW - Vaccines 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/1551623566?accountid=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+General+Virology&rft.atitle=Global+transmission+of+influenza+viruses+from+humans+to+swine&rft.au=Nelson%2C+Martha+I%3BGramer%2C+Marie+R%3BVincent%2C+Amy+L%3BHolmes%2C+Edward+C&rft.aulast=Nelson&rft.aufirst=Martha&rft.date=2012-10-01&rft.volume=93&rft.issue=Pt+10&rft.spage=2195&rft.isbn=&rft.btitle=&rft.title=Journal+of+General+Virology&rft.issn=14652099&rft_id=info:doi/10.1099%2Fvir.0.044974-0 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2015-04-02 N1 - SubjectsTermNotLitGenreText - Phylogeny; Genomes; Influenza; pandemics; Data processing; Nucleotide sequence; Genetic diversity; Vaccination; Evolution; Sulfur dioxide; Viruses; Vaccines; Seasonal variations; Influenza virus DO - http://dx.doi.org/10.1099/vir.0.044974-0 ER - TY - JOUR T1 - The Frontera Collaboration: A Preliminary Report of Health Sciences Librarians Promoting Evidence-Based Practice in U.S.-Mexico Border Communities AN - 1512200706; 201403503 AB - This article reviews the formation of the Frontera Collaboration, a coalition of health sciences librarians serving clinicians and public health personnel in the U.S.-Mexico border region. Based on findings from an assessment of the target populations' learning needs, the Frontera Collaboration participants developed a shared set of training materials that have been used in pilot training sessions. The Frontera Collaboration's participants learned several lessons related to collaborative health information outreach and increased their understanding of the concerns and needs of clinicians and public health personnel serving border communities. Adapted from the source document. JF - Medical Reference Services Quarterly AU - Cogdill, Keith W AU - Ambriz, Lorely AU - Billman, Brooke L AU - Carter, Kathleen V AU - Nail-Chiwetalu, Barbara AU - Trumble, Julie M AU - El-Khayat, Yamila M AU - Nunez, Annabelle V AD - National Institutes of Health Library, Bethesda, Maryland, USA keith.cogdill@nih.gov. Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 400 EP - 413 PB - Taylor & Francis, Philadelphia PA VL - 31 IS - 4 SN - 0276-3869, 0276-3869 KW - community outreach KW - evidence-based practice KW - Frontera Collaboration KW - health care disparities KW - health sciences libraries KW - health status disparities KW - Hispanic Americans KW - minority health KW - U.S.-Mexico border KW - USA KW - Mexico KW - Librarians KW - Library consortia KW - Health care libraries KW - article KW - 6.1: COOPERATION UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1512200706?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Alisa&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medical+Reference+Services+Quarterly&rft.atitle=The+Frontera+Collaboration%3A+A+Preliminary+Report+of+Health+Sciences+Librarians+Promoting+Evidence-Based+Practice+in+U.S.-Mexico+Border+Communities&rft.au=Cogdill%2C+Keith+W%3BAmbriz%2C+Lorely%3BBillman%2C+Brooke+L%3BCarter%2C+Kathleen+V%3BNail-Chiwetalu%2C+Barbara%3BTrumble%2C+Julie+M%3BEl-Khayat%2C+Yamila+M%3BNunez%2C+Annabelle+V&rft.aulast=Cogdill&rft.aufirst=Keith&rft.date=2012-10-01&rft.volume=31&rft.issue=4&rft.spage=400&rft.isbn=&rft.btitle=&rft.title=Medical+Reference+Services+Quarterly&rft.issn=02763869&rft_id=info:doi/10.1080%2F02763869.2012.724285 LA - English DB - Library & Information Science Abstracts (LISA) N1 - Date revised - 2014-04-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Health care libraries; Librarians; Mexico; Library consortia; USA DO - http://dx.doi.org/10.1080/02763869.2012.724285 ER - TY - JOUR T1 - Toenail trace element status and risk of Barrett's oesophagus and oesophageal adenocarcinoma: Results from the FINBAR study AN - 1439225892; 18611548 AB - Trace elements have been cited as both inhibitory and causative agents of cancer but importantly exposure to them is potentially modifiable. Our study aimed to examine toenail trace element status and risk of Barrett's oesophagus (BO) and oesophageal adenocarcinoma (OAC). Toenail clippings from each hallux were obtained from 638 participants of the FINBAR (Factors Influencing the Barrett's Adenocarcinoma Relationship) study comprising 221 healthy controls, 98 reflux oesophagitis, 182 BO and 137 OAC cases. The concentrations of eight toenail trace elements were determined using instrumental neutron activation analysis. Using multivariable adjusted logistic regression analysis, odds ratios (OR) and 95% confidence intervals (CIs) were calculated within tertiles of trace element concentrations. A twofold increased risk of BO was observed, but not OAC, among individuals in the highest tertile of toenail zinc status OR 2.21 (95% CI, 1.11-4.40). A higher toenail selenium status was not associated with risk of OAC OR 0.94 (95% CI, 0.44-2.04) or BO OR 0.89 (95% CI, 0.37-2.12). A borderline significant increased risk of BO was detected with a higher toenail cobalt concentration, OR 1.97 (95% CI, 1.01-3.85). No association was found between toenail levels of chromium, cerium, mercury and OAC or BO risk. This is the first case-control study to investigate a variety of trace elements in relation to OAC and BO risk. Despite antioxidant and proapoptotic properties, no associations were found with selenium. Higher concentrations of toenail zinc and cobalt were associated with an increased BO risk, but not OAC. These findings need confirmation in prospective analysis. JF - International Journal of Cancer AU - O'Rorke, Michael A AU - Cantwell, Marie M AU - Abnet, Christian C AU - Brockman, John D AU - Murray, Liam J AD - Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD., m.ororke@qub.ac.uk Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 1882 EP - 1891 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 131 IS - 8 SN - 0020-7136, 0020-7136 KW - Risk Abstracts; Toxicology Abstracts KW - Esophagus KW - Toenail KW - Apoptosis KW - Antioxidants KW - Chromium KW - Cerium KW - Cancer KW - Trace elements KW - Health risks KW - Selenium KW - Cobalt KW - Zinc KW - Regression analysis KW - Mercury KW - Adenocarcinoma KW - Neutron activation analysis KW - X 24360:Metals KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1439225892?accountid=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=Toenail+trace+element+status+and+risk+of+Barrett%27s+oesophagus+and+oesophageal+adenocarcinoma%3A+Results+from+the+FINBAR+study&rft.au=O%27Rorke%2C+Michael+A%3BCantwell%2C+Marie+M%3BAbnet%2C+Christian+C%3BBrockman%2C+John+D%3BMurray%2C+Liam+J&rft.aulast=O%27Rorke&rft.aufirst=Michael&rft.date=2012-10-01&rft.volume=131&rft.issue=8&rft.spage=1882&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.27434 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-10-01 N1 - Last updated - 2013-10-21 N1 - SubjectsTermNotLitGenreText - Toenail; Esophagus; Antioxidants; Apoptosis; Chromium; Trace elements; Selenium; Cobalt; Zinc; Regression analysis; Mercury; Adenocarcinoma; Neutron activation analysis; Health risks; Cerium; Cancer DO - http://dx.doi.org/10.1002/ijc.27434 ER - TY - JOUR T1 - Chronic alcohol remodels prefrontal neurons and disrupts NMDAR-mediated fear extinction encoding AN - 1434026619; 18477066 AB - Alcoholism is frequently co-morbid with post-traumatic stress disorder, but it is unclear how alcohol affects the neural circuits mediating recovery from trauma. We found that chronic intermittent ethanol (CIE) impaired fear extinction and remodeled the dendritic arbor of medial prefrontal cortical (mPFC) neurons in mice. CIE impaired extinction encoding by infralimbic mPFC neurons in vivo and functionally downregulated burst-mediating NMDA GluN1 receptors. These findings suggest that alcohol may increase risk for trauma-related anxiety disorders by disrupting mPFC-mediated extinction of fear. JF - Nature Neuroscience AU - Holmes, Andrew AU - Fitzgerald, Paul J AU - MacPherson, Kathryn P AU - DeBrouse, Lauren AU - Colacicco, Giovanni AU - Flynn, Shaun M AU - Masneuf, Sophie AU - Pleil, Kristen E AU - Li, Chia AU - Marcinkiewcz, Catherine A AU - Kash, Thomas L AU - Gunduz-Cinar, Ozge AU - Camp, Marguerite AD - Laboratory of Behavioral and Genomic Neuroscience, National Institute on Alcohol Abuse and Alcoholism, US National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 1359 EP - 1361 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 15 IS - 10 SN - 1097-6256, 1097-6256 KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - Alcoholism 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/1434026619?accountid=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=Nature+Neuroscience&rft.atitle=Chronic+alcohol+remodels+prefrontal+neurons+and+disrupts+NMDAR-mediated+fear+extinction+encoding&rft.au=Holmes%2C+Andrew%3BFitzgerald%2C+Paul+J%3BMacPherson%2C+Kathryn+P%3BDeBrouse%2C+Lauren%3BColacicco%2C+Giovanni%3BFlynn%2C+Shaun+M%3BMasneuf%2C+Sophie%3BPleil%2C+Kristen+E%3BLi%2C+Chia%3BMarcinkiewcz%2C+Catherine+A%3BKash%2C+Thomas+L%3BGunduz-Cinar%2C+Ozge%3BCamp%2C+Marguerite&rft.aulast=Holmes&rft.aufirst=Andrew&rft.date=2012-10-01&rft.volume=15&rft.issue=10&rft.spage=1359&rft.isbn=&rft.btitle=&rft.title=Nature+Neuroscience&rft.issn=10976256&rft_id=info:doi/10.1038%2Fnn.3204 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2014-04-03 N1 - SubjectsTermNotLitGenreText - Ethanol DO - http://dx.doi.org/10.1038/nn.3204 ER - TY - JOUR T1 - Regulation and Expression of the ATP-Binding Cassette Transporter ABCG2 in Human Embryonic Stem Cells AN - 1434024194; 18540508 AB - The expression and function of several multidrug transporters (including ABCB1 and ABCG2) have been studied in human cancer cells and in mouse and human adult stem cells. However, the expression of ABCG2 in human embryonic stem cells (hESCs) remains unclear. Limited and contradictory results in the literature from two research groups have raised questions regarding its expression and function. In this study, we used quantitative real-time PCR, Northern blots, whole genome RNA sequencing, Western blots, and immunofluorescence microscopy to study ABCG2 expression in hESCs. We found that full-length ABCG2 mRNA transcripts are expressed in undifferentiated hESC lines. However, ABCG2 protein was undetectable even under embryoid body differentiation or cytotoxic drug induction. Moreover, surface ABCG2 protein was coexpressed with the differentiation marker stage-specific embryonic antigen-1 of hESCs, following constant BMP-4 signaling at days 4 and 6. This expression was tightly correlated with the downregulation of two microRNAs (miRNAs) (i.e., hsa-miR-519c and hsa-miR-520h). Transfection of miRNA mimics and inhibitors of these two miRNAs confirmed their direct involvement in the regulation ABCG2 translation. Our findings clarify the controversy regarding the expression of the ABCG2 gene and also provide new insights into translational control of the expression of membrane transporter mRNAs by miRNAs in hESCs. STEM Cells2012; 30:2175-2187 JF - Stem Cells AU - Padmanabhan, Raji AU - Chen, Kevin G AU - Gillet, Jean-Pierre AU - Handley, Misty AU - Mallon, Barbara S AU - Hamilton, Rebecca S AU - Park, Kyeyoon AU - Varma, Sudhir AU - Mehaffey, Michele G AU - Robey, Pamela G AU - McKay, Ronald DG AU - Gottesman, Michael M AD - NIH Stem Cell Unit, National Institute of Neurological Disorders and Stroke,National Institutes of Health, Bethesda, Maryland, USA., mgottesman@nih.gov Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 2175 EP - 2187 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 30 IS - 10 SN - 1066-5099, 1066-5099 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Genomes KW - Western blotting KW - Translation KW - miRNA KW - Immunofluorescence KW - Cancer KW - Differentiation KW - ABCG2 gene KW - Stem cells KW - Cytotoxicity KW - Embryo cells KW - Transfection KW - ATP-binding protein KW - Microscopy KW - Polymerase chain reaction KW - Bone morphogenetic protein 4 KW - Drugs KW - G 07720:Immunogenetics KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434024194?accountid=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=Regulation+and+Expression+of+the+ATP-Binding+Cassette+Transporter+ABCG2+in+Human+Embryonic+Stem+Cells&rft.au=Padmanabhan%2C+Raji%3BChen%2C+Kevin+G%3BGillet%2C+Jean-Pierre%3BHandley%2C+Misty%3BMallon%2C+Barbara+S%3BHamilton%2C+Rebecca+S%3BPark%2C+Kyeyoon%3BVarma%2C+Sudhir%3BMehaffey%2C+Michele+G%3BRobey%2C+Pamela+G%3BMcKay%2C+Ronald+DG%3BGottesman%2C+Michael+M&rft.aulast=Padmanabhan&rft.aufirst=Raji&rft.date=2012-10-01&rft.volume=30&rft.issue=10&rft.spage=2175&rft.isbn=&rft.btitle=&rft.title=Stem+Cells&rft.issn=10665099&rft_id=info:doi/10.1002%2Fstem.1195 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2013-10-21 N1 - SubjectsTermNotLitGenreText - Genomes; Translation; Western blotting; miRNA; Immunofluorescence; Cancer; Differentiation; Cytotoxicity; Stem cells; ABCG2 gene; Embryo cells; Transfection; ATP-binding protein; Microscopy; Polymerase chain reaction; Drugs; Bone morphogenetic protein 4 DO - http://dx.doi.org/10.1002/stem.1195 ER - TY - JOUR T1 - Quantitative proteomics of parotid saliva in primary Sjogren's syndrome AN - 1434024029; 18539857 AB - The diagnosis of primary Sjogren's syndrome (pSS) is difficult due to the lack of specific laboratory and clinical tests. As an initial step for the global discovery of changes in the abundance of parotid salivary proteins in pSS, a pooled sample was compared to that from healthy control subjects by multidimensional protein identification technology (MudPIT). A total of 1246 proteins were identified by MudPIT. The abundance of 477 of these proteins did not change, 529 were only detected in either the pSS or HC sample, while 206 of these proteins were significantly upregulated greater than or equal to twofold and 34 were downregulated less than or equal to 0.5. Ingenuity Pathway Analyses of differentially expressed proteins identified by MudPIT resulted in the identification of 100 significant pathways. The same samples were quantified in parallel using RP MS. Fifty-eight of 71 proteins identified by RP overlapped with MudPIT results. Five proteins were further analyzed by targeted label-free quantification to confirm the similar relative differential expression observed by RP and MudPIT approaches. The present study supports the use of MS for global discovery and validation of marker proteins for improved and early diagnosis of pSS. JF - Proteomics AU - Ambatipudi, Kiran S AU - Swatkoski, Stephen AU - Moresco, James J AU - Tu, Patricia G AU - Coca, Andreea AU - Anolik, Jennifer H AU - Gucek, Marjan AU - Sanz, Ignacio AU - Yates, John R AU - Melvin, James E AD - Secretory Mechanisms and Dysfunction Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA. Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 3113 EP - 3120 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 12 IS - 19-20 SN - 1615-9853, 1615-9853 KW - Biotechnology and Bioengineering Abstracts KW - Sjogren's syndrome KW - proteomics KW - Saliva KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434024029?accountid=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=Quantitative+proteomics+of+parotid+saliva+in+primary+Sjogren%27s+syndrome&rft.au=Ambatipudi%2C+Kiran+S%3BSwatkoski%2C+Stephen%3BMoresco%2C+James+J%3BTu%2C+Patricia+G%3BCoca%2C+Andreea%3BAnolik%2C+Jennifer+H%3BGucek%2C+Marjan%3BSanz%2C+Ignacio%3BYates%2C+John+R%3BMelvin%2C+James+E&rft.aulast=Ambatipudi&rft.aufirst=Kiran&rft.date=2012-10-01&rft.volume=12&rft.issue=19-20&rft.spage=3113&rft.isbn=&rft.btitle=&rft.title=Proteomics&rft.issn=16159853&rft_id=info:doi/10.1002%2Fpmic.201200208 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2013-09-20 N1 - SubjectsTermNotLitGenreText - Sjogren's syndrome; Saliva; proteomics DO - http://dx.doi.org/10.1002/pmic.201200208 ER - TY - JOUR T1 - Dissociating neural correlates of meaningful emblems from meaningless gestures in deaf signers and hearing non-signers AN - 1417555214; 201311042 AB - Emblems are meaningful, culturally-specific hand gestures that are analogous to words. In this fMRI study, we contrasted the processing of emblematic gestures with meaningless gestures by pre-lingually Deaf and hearing participants. Deaf participants, who used American Sign Language, activated bilateral auditory processing and associative areas in the temporal cortex to a greater extent than the hearing participants while processing both types of gestures relative to rest. The hearing non-signers activated a diverse set of regions, including those implicated in the mirror neuron system, such as premotor cortex (BA 6) and inferior parietal lobule (BA 40) for the same contrast. Further, when contrasting the processing of meaningful to meaningless gestures (both relative to rest), the Deaf participants, but not the hearing, showed greater response in the left angular and supramarginal gyri, regions that play important roles in linguistic processing. These results suggest that whereas the signers interpreted emblems to be comparable to words, the non-signers treated emblems as similar to pictorial descriptions of the world and engaged the mirror neuron system. [Copyright Elsevier B.V.] JF - Brain Research AU - Husain, Fatima T AU - Patkin, Debra J AU - Kim, Jieun AU - Braun, Allen R AU - Horwitz, Barry AD - Brain Imaging and Modeling Section, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD, USA husainf@illinois.edu Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 24 EP - 35 VL - 1478 IS - Oct 10 SN - 0006-8993, 0006-8993 KW - Functional Magnetic Resonance Imaging (fMRI) (26525) KW - Mirror Neurons (54280) KW - Meaning (52200) KW - Gestures (27950) KW - Auditory Processing (05920) KW - Language Processing (43550) KW - American Sign Language (02350) KW - Deafness (17420) KW - article KW - 4017: psycholinguistics; psychoacoustics/speech perception UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1417555214?accountid=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=Brain+Research&rft.atitle=Dissociating+neural+correlates+of+meaningful+emblems+from+meaningless+gestures+in+deaf+signers+and+hearing+non-signers&rft.au=Husain%2C+Fatima+T%3BPatkin%2C+Debra+J%3BKim%2C+Jieun%3BBraun%2C+Allen+R%3BHorwitz%2C+Barry&rft.aulast=Husain&rft.aufirst=Fatima&rft.date=2012-10-01&rft.volume=1478&rft.issue=Oct+10&rft.spage=24&rft.isbn=&rft.btitle=&rft.title=Brain+Research&rft.issn=00068993&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2013-08-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Gestures (27950); Functional Magnetic Resonance Imaging (fMRI) (26525); Deafness (17420); American Sign Language (02350); Auditory Processing (05920); Language Processing (43550); Meaning (52200); Mirror Neurons (54280) ER - TY - JOUR T1 - Stability and transitions of depressive subtypes over a 2-year follow-up AN - 1417548398; 201315849 AB - Identifying depressive subtypes is an important tool in reducing the heterogeneity of major depressive disorder. However, few studies have examined the stability of putative subtypes of depression over time. The sample included 488 persons from the Netherlands Study of Depression and Anxiety (NESDA) who had major depressive disorder at baseline and at the 2-year follow-up assessment. A latent transition analysis (LTA) was applied to examine the stability of depressive subtypes across time-points. Differences in demographic, clinical, psychosocial and health correlates between subtypes were evaluated in a subsample of persons with stable subtypes. Three subtypes were identified at each time-point: a moderate subtype (prevalence T0 39%, T1 42%), a severe typical subtype (T0 30%, T1 25%), and a severe atypical subtype (T0 31%, T1 34%). The LTA showed 76% stability across the 2-year follow-up, with the greatest stability in the severe atypical class (79%). Analyses of correlates in the stable subtypes showed a predominance of women and more overweight and obesity in the severe atypical subtype, and a greater number of negative life events and higher neuroticism and functioning scores in the severe typical subtype. Subtypes of major depressive disorder were found to be stable across a 2-year follow-up and to have distinct determinants, supporting the notion that the identified subtypes are clinically meaningful. Adapted from the source document. JF - Psychological Medicine AU - Lamers, F AU - Rhebergen, D AU - Merikangas, K R AU - de Jonge, P AU - Beekman, A T F AU - Penninx, B. W. J. H. AD - Genetic Epidemiology Research Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA lamersf@mail.nih.gov Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 2083 EP - 2093 PB - Cambridge University Press, UK VL - 42 IS - 10 SN - 0033-2917, 0033-2917 KW - Depressive personality disorders KW - Depression KW - Subtypes KW - Neuroticism KW - Obese women KW - Anxiety-Depression KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1417548398?accountid=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=Stability+and+transitions+of+depressive+subtypes+over+a+2-year+follow-up&rft.au=Lamers%2C+F%3BRhebergen%2C+D%3BMerikangas%2C+K+R%3Bde+Jonge%2C+P%3BBeekman%2C+A+T+F%3BPenninx%2C+B.+W.+J.+H.&rft.aulast=Lamers&rft.aufirst=F&rft.date=2012-10-01&rft.volume=42&rft.issue=10&rft.spage=2083&rft.isbn=&rft.btitle=&rft.title=Psychological+Medicine&rft.issn=00332917&rft_id=info:doi/10.1017%2FS0033291712000141 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-08-01 N1 - Last updated - 2016-09-27 N1 - CODEN - PSMDCO N1 - SubjectsTermNotLitGenreText - Subtypes; Depression; Anxiety-Depression; Depressive personality disorders; Obese women; Neuroticism DO - http://dx.doi.org/10.1017/S0033291712000141 ER - TY - JOUR T1 - A modular fuzzy inference system approach in integrating qualitative and quantitative analysis of store image AN - 1347784696; 201317851 AB - The image situation in a store includes various stimuli, such as color, sound, scent, taste, layout and space, which are important clues for buyers. This paper describes store image response and a fuzzy logic model developed by comprehensive literature studies on image measurements (including atmospheric factors) and perceptual measures. Here, a fuzzy inference system is proposed as an alternative approach to handle effectively the impreciseness and uncertainty that are normally found in store image selection processes. This paper also shows that the proposed decision-making model is application to modified stimulus-organism-response (S-O-R) framework for integrating qualitative and quantitative analysis. The result of the simulation indicates a numerical and linguistic change in the store image perception after analyzing three input parameters. This finding is able to provide a solid foundation on which retailers and decision makers can base suitable strategies for ensuring the efficiency and stability of store image management system. Adapted from the source document. JF - Quality and Quantity AU - Lin, Ling-Zhong AU - Hsu, Tsuen-Ho AD - Department of Marketing Management, Shih Chien University, Kaohsiung Campus, 200 University Road, Nei-Men Hsiang, Kaohsiung Hsien, 845, Taiwan ling@mail.kh.usc.edu.tw Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 1847 EP - 1864 PB - Springer, Dordrecht The Netherlands VL - 46 IS - 6 SN - 0033-5177, 0033-5177 KW - Logic KW - Certainty KW - Management KW - Alternative Approaches KW - Stimuli KW - Linguistics KW - Decision Making KW - article KW - 0104: methodology and research technology; research methods/tools UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1347784696?accountid=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=Quality+and+Quantity&rft.atitle=A+modular+fuzzy+inference+system+approach+in+integrating+qualitative+and+quantitative+analysis+of+store+image&rft.au=Lin%2C+Ling-Zhong%3BHsu%2C+Tsuen-Ho&rft.aulast=Lin&rft.aufirst=Ling-Zhong&rft.date=2012-10-01&rft.volume=46&rft.issue=6&rft.spage=1847&rft.isbn=&rft.btitle=&rft.title=Quality+and+Quantity&rft.issn=00335177&rft_id=info:doi/10.1007%2Fs11135-011-9561-7 LA - English DB - Sociological Abstracts N1 - Date revised - 2013-05-01 N1 - Last updated - 2016-09-28 N1 - CODEN - QQEJAV N1 - SubjectsTermNotLitGenreText - Decision Making; Alternative Approaches; Linguistics; Certainty; Management; Logic; Stimuli DO - http://dx.doi.org/10.1007/s11135-011-9561-7 ER - TY - JOUR T1 - The Association of Beliefs About Heredity with Preventive and Interpersonal Behaviors in Communities Affected by Podoconiosis in Rural Ethiopia AN - 1257732582; 17411327 AB - Little is known about how beliefs about heredity as a cause of health conditions might influence preventive and interpersonal behaviors among those individuals with low genetic and health literacy. We explored causal beliefs about podoconiosis, a neglected tropical disease (NTD) endemic in Ethiopia. Podoconiosis clusters in families but can be prevented if individuals at genetically high risk wear shoes consistently. Adults (/V = 242) from four rural Ethiopian communities participated in qualitative assessments of beliefs about the causes of podoconiosis. Heredity was commonly mentioned, with heredity being perceived as (1) the sole cause of podoconiosis, (2) not a causal factor, or (3) one of multiple causes. These beliefs influenced the perceived controllability of podoconiosis and in turn, whether individuals endorsed preventive and interpersonal stigmatizing behaviors. Culturally informed education programs that increase the perceived controllability of stigmatized hereditary health conditions like podoconiosis have promise for increasing preventive behaviors and reducing interpersonal stigma. JF - American Journal of Tropical Medicine and Hygiene AU - Ayode, D AU - McBride, C M AU - de Heer, H AU - Watanabe, E AU - Gebreyesus, T AU - Tadele, G AU - Tora, A AU - Davey, G AD - Social and Behavioral Research Branch, National Human Genome Research Institute, Building 31, MSC 2073, 31 Center Drive, Room B1B54, Bethesda, MD 20892, USA, cmcbride@mail.nih.gov Y1 - 2012/10// PY - 2012 DA - October 2012 VL - 87 IS - 4 SN - 0002-9637, 0002-9637 KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Risk Abstracts KW - Education KW - Ethiopia KW - Behavior KW - Heredity KW - Perception KW - Risk factors KW - Stigma KW - Clothing KW - Rural areas KW - K 03400:Human Diseases KW - J 02400:Human Diseases KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1257732582?accountid=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=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=The+Association+of+Beliefs+About+Heredity+with+Preventive+and+Interpersonal+Behaviors+in+Communities+Affected+by+Podoconiosis+in+Rural+Ethiopia&rft.au=Ayode%2C+D%3BMcBride%2C+C+M%3Bde+Heer%2C+H%3BWatanabe%2C+E%3BGebreyesus%2C+T%3BTadele%2C+G%3BTora%2C+A%3BDavey%2C+G&rft.aulast=Ayode&rft.aufirst=D&rft.date=2012-10-01&rft.volume=87&rft.issue=4&rft.spage=&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-12-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Heredity; Risk factors; Stigma; Clothing; Education; Behavior; Perception; Rural areas; Ethiopia ER - TY - JOUR T1 - Erwinia asparaginase in pediatric acute lymphoblastic leukemia AN - 1221145863; 17366373 AB - Introduction: Asparaginase is a major a component of therapy for acute lymphoblastic leukemia (ALL) and has been used for over 40 years. Hypersensitivity reactions limit the use and efficacy of asparaginase products. However, Erwinia asparaginase gained the Food and Drug Administration (FDA) approval in November 2011, for use in patients with allergic reactions to Escherichia coli-derived asparaginase. Areas covered: Erwinia asparaginase is an enzyme that hydrolyzes the amino acid asparagine. This review examines the properties of Erwinia asparaginase compared to the two other preparations of asparaginase available for use in the United States. Results of selected clinical trials involving Erwinia asparaginase, including the pivotal study resulting in FDA approval, are presented. Expert opinion: Erwinia asparaginase is well tolerated, and it is effective in achieving asparaginase levels associated with efficacy in the treatment of ALL. With FDA approval of Erwinia asparagainse, oncologists now have an alternative for ALL patients who become hypersensitive to E. coli-derived asparaginase. Future studies will be needed to establish optimal dosing of Erwinia asparaginase (e.g., intravenous vs. intramuscular) and to better define the most appropriate indications for its use in patients previously treated with E. coli-derived asparaginase. JF - Expert Opinion in Biological Therapy AU - Salzer, Wanda AU - Seibel, Nita AU - Smith, Malcolm AD - NCI, Bethesda, USA, wanda.salzer@us.army.mil Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 1407 EP - 1414 PB - Ashley Publications Ltd., Unitec House, 3rd Floor London, N3 1QB United Kingdom VL - 12 IS - 10 SN - 1471-2598, 1471-2598 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Acute lymphatic leukemia KW - Amino acids KW - Asparaginase KW - Asparagine KW - Clinical trials KW - Enzymes KW - Food hypersensitivity KW - Hypersensitivity KW - Intravenous administration KW - Pediatrics KW - Reviews KW - Escherichia KW - Erwinia KW - F 06925:Hypersensitivity KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1221145863?accountid=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=Expert+Opinion+in+Biological+Therapy&rft.atitle=Erwinia+asparaginase+in+pediatric+acute+lymphoblastic+leukemia&rft.au=Salzer%2C+Wanda%3BSeibel%2C+Nita%3BSmith%2C+Malcolm&rft.aulast=Salzer&rft.aufirst=Wanda&rft.date=2012-10-01&rft.volume=12&rft.issue=10&rft.spage=1407&rft.isbn=&rft.btitle=&rft.title=Expert+Opinion+in+Biological+Therapy&rft.issn=14712598&rft_id=info:doi/http%3A%2F%2Fdx.doi.org%2F10.1517%2F14712598.2012.718327 L2 - http://www.ingentaconnect.com/content/apl/ebt/2012/00000012/00000010/art00011 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-11-01 N1 - Last updated - 2013-01-25 N1 - SubjectsTermNotLitGenreText - Asparaginase; Intravenous administration; Hypersensitivity; Amino acids; Food hypersensitivity; Pediatrics; Reviews; Acute lymphatic leukemia; Enzymes; Asparagine; Clinical trials; Escherichia; Erwinia DO - http://dx.doi.org/10.1517/14712598.2012.718327 ER - TY - JOUR T1 - Recognition of Glioma Stem Cells by Genetically Modified T Cells Targeting EGFRvIII and Development of Adoptive Cell Therapy for Glioma AN - 1221142878; 17398392 AB - No curative treatment exists for glioblastoma, with median survival times of less than 2 years from diagnosis. As an approach to develop immune-based therapies for glioblastoma, we sought to target antigens expressed in glioma stem cells (GSCs). GSCs have multiple properties that make them significantly more representative of glioma tumors than established glioma cell lines. Epidermal growth factor receptor variant III (EGFRvIII) is the result of a novel tumor-specific gene rearrangement that produces a unique protein expressed in approximately 30% of gliomas, and is an ideal target for immunotherapy. Using PCR primers spanning the EGFRvIII-specific deletion, we found that this tumor-specific gene is expressed in three of three GCS lines. Based on the sequence information of seven EGFRvIII-specific monoclonal antibodies (mAbs), we assembled chimeric antigen receptors (CARs) and evaluated the ability of CAR-engineered T cells to recognize EGFRvIII. Three of these anti-EGFRvIII CAR-engineered T cells produced the effector cytokine, interferon- gamma , and lysed antigen-expressing target cells. We concentrated development on a CAR produced from human mAb 139, which specifically recognized GSC lines and glioma cell lines expressing mutant EGFRvIII, but not wild-type EGFR and did not recognize any normal human cell tested. Using the 139-based CAR, T cells from glioblastoma patients could be genetically engineered to recognize EGFRvIII-expressing tumors and could be expanded ex vivo to large numbers, and maintained their antitumor activity. Based on these observations, a gamma -retroviral vector expressing this EGFRvIII CAR was produced for clinical application. JF - Human Gene Therapy AU - Morgan, R A AU - Johnson, LA AU - Davis, J L AU - Zheng, Z AU - Woolard, K D AU - Reap, E A AU - Feldman, SA AU - Chinnasamy, N AU - Kuan, C-T AU - Song, H AU - Zhang, W AU - Fine, HA AU - Rosenberg, SA AD - Surgery Branch/NCI, Building 10 CRC, Room 3W5940, 10 Center Drive, Bethesda, MD 20892, USA, rmorgan@mail.nih.gov Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 1043 EP - 1053 VL - 23 IS - 10 SN - 1043-0342, 1043-0342 KW - Genetics Abstracts; CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts KW - Antitumor activity KW - Brain tumors KW - Cytokines KW - Epidermal growth factor receptors KW - Gene deletion KW - Gene therapy KW - Genetic engineering KW - Glioblastoma KW - Glioma KW - Glioma cells KW - Immunotherapy KW - Lymphocytes T KW - Monoclonal antibodies KW - Polymerase chain reaction KW - Primers KW - Stem cells KW - Tumors KW - gamma -Interferon KW - gene rearrangement KW - W 30905:Medical Applications KW - N3 11023:Neurogenetics KW - G 07880:Human Genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1221142878?accountid=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=Recognition+of+Glioma+Stem+Cells+by+Genetically+Modified+T+Cells+Targeting+EGFRvIII+and+Development+of+Adoptive+Cell+Therapy+for+Glioma&rft.au=Morgan%2C+R+A%3BJohnson%2C+LA%3BDavis%2C+J+L%3BZheng%2C+Z%3BWoolard%2C+K+D%3BReap%2C+E+A%3BFeldman%2C+SA%3BChinnasamy%2C+N%3BKuan%2C+C-T%3BSong%2C+H%3BZhang%2C+W%3BFine%2C+HA%3BRosenberg%2C+SA&rft.aulast=Morgan&rft.aufirst=R&rft.date=2012-10-01&rft.volume=23&rft.issue=10&rft.spage=1043&rft.isbn=&rft.btitle=&rft.title=Human+Gene+Therapy&rft.issn=10430342&rft_id=info:doi/10.1089%2Fhum.2012.041 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-11-01 N1 - Last updated - 2013-02-08 N1 - SubjectsTermNotLitGenreText - Glioblastoma; gamma -Interferon; Gene therapy; Monoclonal antibodies; Immunotherapy; Epidermal growth factor receptors; Tumors; Brain tumors; Gene deletion; Stem cells; gene rearrangement; Genetic engineering; Glioma cells; Lymphocytes T; Polymerase chain reaction; Cytokines; Primers; Glioma; Antitumor activity DO - http://dx.doi.org/10.1089/hum.2012.041 ER - TY - JOUR T1 - Dosage effects of X and Y chromosomes on language and social functioning in children with supernumerary sex chromosome aneuploidies: implications for idiopathic language impairment and autism spectrum disorders AN - 1125282973; 201226745 AB - Background: Supernumerary sex chromosome aneuploidies (X/Y-aneuploidies), the presence of extra X and/or Y chromosomes, are associated with heightened rates of language impairments and social difficulties. However, no single study has examined different language domains and social functioning in the same sample of children with tri-, tetra-, and pentasomy X/Y-aneuploidy. The current research sought to fill this gap in the literature and to examine dosage effects of X and Y chromosomes on language and social functioning. Methods: Participants included 110 youth with X/Y-aneuploidies (32 female) and 52 with typical development (25 female) matched on age (mean ~12 years; range 4-22) and maternal education. Participants completed the Wechsler intelligence scales, and parents completed the Children's Communication Checklist-2 and the Social Responsiveness Scale to assess language skills and autistic traits, respectively. Results: Both supernumerary X and Y chromosomes were related to depressed structural and pragmatic language skills and increased autistic traits. The addition of a Y chromosome had a disproportionately greater impact on pragmatic language; the addition of one or more X chromosomes had a disproportionately greater impact on structural language. Conclusions: Given that we link extra X chromosomes with structural language impairments and an extra Y chromosome with pragmatic language impairments, X/Y-aneuploidies may provide clues to genetic mechanisms contributing to idiopathic language impairment and autism spectrum disorders. Adapted from the source document. JF - The Journal of Child Psychology and Psychiatry AU - Lee, Nancy Raitano AU - Wallace, Gregory L AU - Adeyemi, Elizabeth I AU - Lopez, Katherine C AU - Blumenthal, Jonathan D AU - Clasen, Liv S AU - Giedd, Jay N AD - Child Psychiatry Branch, National Institute of Mental Health, NIH, Bethesda, MD, USA Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 1072 EP - 1081 PB - Blackwell Publishing, Oxford UK VL - 53 IS - 10 SN - 0021-9630, 0021-9630 KW - Chromosomes KW - Social functioning KW - Y chromosomes KW - Language disorders KW - Pragmatics KW - Autistic spectrum disorders KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1125282973?accountid=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+Child+Psychology+and+Psychiatry&rft.atitle=Dosage+effects+of+X+and+Y+chromosomes+on+language+and+social+functioning+in+children+with+supernumerary+sex+chromosome+aneuploidies%3A+implications+for+idiopathic+language+impairment+and+autism+spectrum+disorders&rft.au=Lee%2C+Nancy+Raitano%3BWallace%2C+Gregory+L%3BAdeyemi%2C+Elizabeth+I%3BLopez%2C+Katherine+C%3BBlumenthal%2C+Jonathan+D%3BClasen%2C+Liv+S%3BGiedd%2C+Jay+N&rft.aulast=Lee&rft.aufirst=Nancy&rft.date=2012-10-01&rft.volume=53&rft.issue=10&rft.spage=1072&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Child+Psychology+and+Psychiatry&rft.issn=00219630&rft_id=info:doi/10.1111%2Fj.1469-7610.2012.02573.x LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-11-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JPPDAI N1 - SubjectsTermNotLitGenreText - Y chromosomes; Language disorders; Chromosomes; Social functioning; Pragmatics; Autistic spectrum disorders DO - http://dx.doi.org/10.1111/j.1469-7610.2012.02573.x ER - TY - JOUR T1 - Crystallization and preliminary X-ray diffraction analysis of PsaA, the adhesive pilin subunit that forms the pH 6 antigen on the surface of Yersinia pestis AN - 1125239642; 17251935 AB - Yersinia pestis has been responsible for a number of high-mortality epidemics throughout human history. Like all other bacterial infections, the pathogenesis of Y. pestis begins with the attachment of bacteria to the surface of host cells. At least five surface proteins from Y. pestis have been shown to interact with host cells. Psa, the pH 6 antigen, is one of them and is deployed on the surface of bacteria as thin flexible fibrils that are the result of the polymerization of a single PsaA pilin subunit. Here, the crystallization of recombinant donor-strand complemented PsaA by the hanging-drop vapor-diffusion method is reported. X-ray diffraction data sets were collected to 1.9Aa resolution from a native crystal and to 1.5Aa resolution from a bromide-derivatized crystal. These crystals displayed the symmetry of the orthorhombic space group P2221, with unit-cell parameters a = 26.3, b = 54.6, c = 102.1Aa. Initial phases were derived from single isomorphous replacement with anomalous scattering experiments, resulting in an electron-density map that showed a single molecule in the crystallographic asymmetric unit. Sequence assignment was aided by residues binding to bromide ions of the heavy-atom derivative. JF - Acta Crystallographica Section F AU - Bao, Rui AU - Esser, Lothar AU - Sadhukhan, Annapurna AU - Nair, Manoj KM AU - Schifferli, Dieter M AU - Xia, Di AD - Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD 20892-4256, USA Y1 - 2012/10/01/ PY - 2012 DA - 2012 Oct 01 SP - 1243 EP - 1246 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 68 IS - 10 SN - 1744-3091, 1744-3091 KW - Microbiology Abstracts B: Bacteriology KW - Crystallization KW - Ions KW - Epidemics KW - Data processing KW - Polymerization KW - pilin KW - Yersinia pestis KW - Crystals KW - Infection KW - bromides KW - X-ray diffraction KW - Antigens KW - Adhesives KW - pH effects KW - Fibrils KW - J 02330:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1125239642?accountid=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=Acta+Crystallographica+Section+F&rft.atitle=Crystallization+and+preliminary+X-ray+diffraction+analysis+of+PsaA%2C+the+adhesive+pilin+subunit+that+forms+the+pH+6+antigen+on+the+surface+of+Yersinia+pestis&rft.au=Bao%2C+Rui%3BEsser%2C+Lothar%3BSadhukhan%2C+Annapurna%3BNair%2C+Manoj+KM%3BSchifferli%2C+Dieter+M%3BXia%2C+Di&rft.aulast=Bao&rft.aufirst=Rui&rft.date=2012-10-01&rft.volume=68&rft.issue=10&rft.spage=1243&rft.isbn=&rft.btitle=&rft.title=Acta+Crystallographica+Section+F&rft.issn=17443091&rft_id=info:doi/10.1107%2FS1744309112033076 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Document feature - figure 0 N1 - Last updated - 2015-04-09 N1 - SubjectsTermNotLitGenreText - Crystallization; Ions; Polymerization; Data processing; Epidemics; pilin; Crystals; X-ray diffraction; bromides; Infection; Antigens; Adhesives; pH effects; Fibrils; Yersinia pestis DO - http://dx.doi.org/10.1107/S1744309112033076 ER - TY - JOUR T1 - Clinical equipoise and risk-benefit assessment AN - 1125229111; 17287496 AB - Clinical equipoise is widely regarded as an ethical requirement for the design and conduct of randomized controlled trials (RCTs). Underlying clinical equipoise is the norm that no patient should be randomized to treatment known (or believed by the expert clinical community) to be inferior to the established standard of care. This implies that patient-subjects should not be exposed to net risks in control groups of randomized trials - risks that are not compensated by the prospect of direct medical benefits from the control intervention. However, proponents of clinical equipoise have no moral objections to permitting net risks for 'nontherapeutic' research procedures employed in Clinical Trials. This differential assessment makes risk-benefit assessment of randomized trials incoherent. In this article, I examine critically four arguments in defense of clinical equipoise as a requirement for risk-benefit assessment. Each of these arguments fails to support clinical equipoise, leading to the conclusion that we should dispense with this principle in risk-benefit assessment of RCTs. JF - Clinical Trials AU - Miller, Franklin G AD - Department of Bioethics, National Institutes of Health, Bethesda, MD, USA Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 621 EP - 627 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 9 IS - 5 SN - 1740-7745, 1740-7745 KW - Risk Abstracts KW - Ethics KW - Intervention KW - Clinical trials KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1125229111?accountid=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=Clinical+Trials&rft.atitle=Clinical+equipoise+and+risk-benefit+assessment&rft.au=Miller%2C+Franklin+G&rft.aulast=Miller&rft.aufirst=Franklin&rft.date=2012-10-01&rft.volume=9&rft.issue=5&rft.spage=621&rft.isbn=&rft.btitle=&rft.title=Clinical+Trials&rft.issn=17407745&rft_id=info:doi/10.1177%2F1740774512450952 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Number of references - 23 N1 - Last updated - 2013-07-26 N1 - SubjectsTermNotLitGenreText - Ethics; Intervention; Clinical trials DO - http://dx.doi.org/10.1177/1740774512450952 ER - TY - JOUR T1 - Cigarette smoking, alcohol intake, and thyroid cancer risk: a pooled analysis of five prospective studies in the United States AN - 1113240895; 17196808 AB - Objective: We examined the associations between cigarette smoking, alcohol intake, and thyroid cancer risk in a pooled analysis of five prospective studies. Methods: Data from five prospective U.S. studies were standardized and then combined into one aggregate dataset (384,433 men and 361,664 women). Pooled hazard ratios (HR) and 95 % confidence intervals (CI) for thyroid cancer were estimated from mutually adjusted models of cigarette smoking and alcohol intake, which were additionally adjusted for age, sex, education, race, marital status, body mass index, and cohort. Results: Over follow-up, 1,003 incident thyroid cancer cases (335 men and 668 women) were identified. Compared to never smokers, current smoking was associated with reduced risk of thyroid cancer (HR = 0.68, 95 % CI 0.55-0.85); this association was slightly stronger among non-drinkers (HR = 0.46, 95 % CI 0.29-0.74). No reduction in risk was observed for former, compared to never, smokers. Greater smoking intensity, duration, and pack-years were associated with further reductions in risk among former and current smokers. Alcohol intake was also inversely associated with thyroid cancer risk ( greater than or equal to 7 drinks/week versus 0, HR = 0.72, 95 % CI 0.58-0.90, p trend = 0.002). Inverse associations with smoking and alcohol were more pronounced for papillary versus follicular tumors. Conclusion: The results of this pooled analysis suggest that both cigarette smoking and alcohol consumption are associated with reduced risks of papillary thyroid cancer and, possibly, follicular thyroid cancer. JF - Cancer Causes & Control AU - Kitahara, Cari M AU - Linet, Martha S AU - Beane Freeman, Laura E AU - Check, David P AU - Church, Timothy R AU - Park, Yikyung AU - Purdue, Mark P AU - Schairer, Catherine AU - Berrington de Gonzalez, Amy AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, EPS 7056, 6120 Executive Blvd, Rockville, MD, 20852, USA, kitaharac@mail.nih.gov Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 1615 EP - 1624 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 23 IS - 10 SN - 0957-5243, 0957-5243 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Alcohol KW - Cancer KW - Cigarettes KW - Education KW - Marriage KW - Risk reduction KW - Standards KW - Thyroid KW - Tumors KW - USA 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/1113240895?accountid=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+Causes+%26+Control&rft.atitle=Cigarette+smoking%2C+alcohol+intake%2C+and+thyroid+cancer+risk%3A+a+pooled+analysis+of+five+prospective+studies+in+the+United+States&rft.au=Kitahara%2C+Cari+M%3BLinet%2C+Martha+S%3BBeane+Freeman%2C+Laura+E%3BCheck%2C+David+P%3BChurch%2C+Timothy+R%3BPark%2C+Yikyung%3BPurdue%2C+Mark+P%3BSchairer%2C+Catherine%3BBerrington+de+Gonzalez%2C+Amy&rft.aulast=Kitahara&rft.aufirst=Cari&rft.date=2012-10-01&rft.volume=23&rft.issue=10&rft.spage=1615&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-0039-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2012-11-20 N1 - SubjectsTermNotLitGenreText - Alcohol; Education; Cigarettes; Thyroid; Marriage; Standards; Tumors; Risk reduction; Cancer; USA DO - http://dx.doi.org/10.1007/s10552-012-0039-2 ER - TY - JOUR T1 - The risk of a second primary lung cancer after a first invasive breast cancer according to estrogen receptor status AN - 1113227030; 17196807 AB - Purpose: Lung cancers account for 5 % of second primary cancers after breast cancer. The low overall 5-year relative survival rate of lung cancer makes it a particularly concerning new malignancy for breast cancer survivors. It is unknown whether second lung cancer risk varies by estrogen receptor (ER) expression of the first breast cancer. Methods: We evaluated second primary lung cancer risks using standardized incidence ratios (SIRs) (95 % confidence intervals (CIs)) among 222,148 one-year breast cancer survivors in the NCI-SEER Program registry database (1992-2008). Relative risks (RRs) and 95 % CIs for lung cancer following ER super(-) compared with ER super(+) breast cancer were estimated using Poisson regression, adjusted for age, year, and stage of breast cancer diagnosis, attained age, latency, and radiotherapy. We also examined the reciprocal association of second ER super(-) and ER super(+) breast cancers among 28,107 1-year lung cancer survivors. Results: There were 418 and 1,444 second lung cancers diagnosed following 50,781 ER super(-) and 171,367 ER super(+) breast cancers. Second lung cancer rates were significantly elevated after ER super(-) (SIR = 1.20 (1.09-1.33)), but not ER super(+) (SIR = 0.96 (0.91-1.01)) breast cancer. The adjusted RR for a second lung cancer following ER super(-) compared with ER super(+) breast cancer was 1.22 (1.10-1.37). The reciprocal adjusted RR for a second ER super(-) compared with ER super(+) breast cancer following lung cancer was 1.29 (0.98-1.70). Conclusion: The parallel increase for a second lung cancer following an ER super(-) first breast cancer and for a second ER super(-) breast cancer after a first lung cancer suggests that there may be shared etiologic factors for these cancers. Further evaluation of lung cancer risk after ER super(-) breast cancer may identify women at high risk for this fatal malignancy. JF - Cancer Causes & Control AU - Schonfeld, Sara J AU - Curtis, Rochelle E AU - Anderson, William F AU - Berrington de Gonzalez, Amy AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA, schonfelds@fellows.iarc.fr Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 1721 EP - 1728 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 23 IS - 10 SN - 0957-5243, 0957-5243 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Estrogens KW - Age KW - Breast cancer KW - Survival KW - Standards KW - radiotherapy 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/1113227030?accountid=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+Causes+%26+Control&rft.atitle=The+risk+of+a+second+primary+lung+cancer+after+a+first+invasive+breast+cancer+according+to+estrogen+receptor+status&rft.au=Schonfeld%2C+Sara+J%3BCurtis%2C+Rochelle+E%3BAnderson%2C+William+F%3BBerrington+de+Gonzalez%2C+Amy&rft.aulast=Schonfeld&rft.aufirst=Sara&rft.date=2012-10-01&rft.volume=23&rft.issue=10&rft.spage=1721&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-0054-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2014-05-29 N1 - SubjectsTermNotLitGenreText - Age; Estrogens; Survival; Breast cancer; Standards; radiotherapy; Lung cancer DO - http://dx.doi.org/10.1007/s10552-012-0054-3 ER - TY - JOUR T1 - Sharing Heterogeneous Data: The National Database for Autism Research AN - 1113220117; 17257557 AB - The National Database for Autism Research (NDAR) is a secure research data repository designed to promote scientific data sharing and collaboration among autism spectrum disorder investigators. The goal of the project is to accelerate scientific discovery through data sharing, data harmonization, and the reporting of research results. Data from over 25,000 research participants are available to qualified investigators through the NDAR portal. Summary information about the available data is available to everyone through that portal. JF - Neuroinformatics AU - Hall, Dan AU - Huerta, Michael F AU - McAuliffe, Matthew J AU - Farber, Gregory K AD - OMNITEC Solutions, Inc., 6001 Executive Boulevard, Suite 7161, Rockville, MD, 20892-9640, USA, farberg@mail.nih.gov Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 331 EP - 339 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 10 IS - 4 SN - 1539-2791, 1539-2791 KW - Biotechnology and Bioengineering Abstracts; CSA Neurosciences Abstracts KW - Autism KW - Bioinformatics KW - Data processing KW - Databases KW - N3 11001:Behavioral and Cognitive Neuroscience KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1113220117?accountid=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=Neuroinformatics&rft.atitle=Sharing+Heterogeneous+Data%3A+The+National+Database+for+Autism+Research&rft.au=Hall%2C+Dan%3BHuerta%2C+Michael+F%3BMcAuliffe%2C+Matthew+J%3BFarber%2C+Gregory+K&rft.aulast=Hall&rft.aufirst=Dan&rft.date=2012-10-01&rft.volume=10&rft.issue=4&rft.spage=331&rft.isbn=&rft.btitle=&rft.title=Neuroinformatics&rft.issn=15392791&rft_id=info:doi/10.1007%2Fs12021-012-9151-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2012-11-20 N1 - SubjectsTermNotLitGenreText - Databases; Data processing; Bioinformatics; Autism DO - http://dx.doi.org/10.1007/s12021-012-9151-4 ER - TY - JOUR T1 - Chronic inflammation, immune escape, and oncogenesis in the liver: a unique neighborhood for novel intersections. AN - 1093525117; 22378061 AB - Sustained hepatic inflammation, driven by alcohol consumption, nonalcoholic fatty liver disease, and/or chronic viral hepatitis (hepatitis B and C), results in damage to parenchyma, oxidative stress, and compensatory regeneration/proliferation. There is substantial evidence linking these inflammation-associated events with the increased incidence of hepatocellular carcinogenesis. Although acute liver inflammation can play a vital and beneficial role in response to liver damage or acute infection, the effects of chronic liver inflammation, including liver fibrosis and cirrhosis, are sufficient in a fraction of individuals to initiate the process of transformation and the development of hepatocellular carcinoma. This review highlights immune-dependent mechanisms that may be associated with hepatocellular oncogenesis, including critical transformative events/pathways in the context of chronic inflammation and subverted tolerogenesis. Copyright © 2012 American Association for the Study of Liver Diseases. JF - Hepatology (Baltimore, Md.) AU - Stauffer, Jimmy K AU - Scarzello, Anthony J AU - Jiang, Qun AU - Wiltrout, Robert H AD - Cancer and Inflammation Program, NCI, Frederick, MD 21702, USA. Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 1567 EP - 1574 VL - 56 IS - 4 KW - Index Medicus KW - Liver Cirrhosis -- pathology KW - Hepatitis C, Chronic -- immunology KW - Humans KW - Prognosis KW - Hepatitis B, Chronic -- immunology KW - Non-alcoholic Fatty Liver Disease KW - Precancerous Conditions -- pathology KW - Hepatitis, Chronic -- immunology KW - Fatty Liver -- immunology KW - Oxidative Stress -- physiology KW - Hepatitis, Chronic -- pathology KW - Hepatitis B, Chronic -- pathology KW - Fatty Liver -- pathology KW - Liver Cirrhosis -- immunology KW - Oxidative Stress -- immunology KW - Hepatitis C, Chronic -- pathology KW - Liver Neoplasms -- pathology KW - Cell Transformation, Neoplastic -- pathology KW - Carcinoma, Hepatocellular -- pathology KW - Hepatitis, Viral, Human -- pathology KW - Hepatitis, Viral, Human -- immunology KW - Cell Transformation, Neoplastic -- immunology KW - Carcinoma, Hepatocellular -- immunology KW - Liver Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1093525117?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Chronic+inflammation%2C+immune+escape%2C+and+oncogenesis+in+the+liver%3A+a+unique+neighborhood+for+novel+intersections.&rft.au=Stauffer%2C+Jimmy+K%3BScarzello%2C+Anthony+J%3BJiang%2C+Qun%3BWiltrout%2C+Robert+H&rft.aulast=Stauffer&rft.aufirst=Jimmy&rft.date=2012-10-01&rft.volume=56&rft.issue=4&rft.spage=1567&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.25674 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-17 N1 - Date created - 2012-10-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Gastroenterology. 2001 Feb;120(2):512-24 [11159892] Carcinogenesis. 2011 Oct;32(10):1434-40 [21771728] Hepatology. 2006 Feb;43(2 Suppl 1):S54-62 [16447271] Immunol Rev. 2006 Aug;212:28-50 [16903904] Eur J Immunol. 2006 Sep;36(9):2483-93 [16917958] Int J Biochem Cell Biol. 2007;39(1):44-84 [16978905] J Immunol. 2006 Nov 15;177(10):6758-68 [17082589] J Leukoc Biol. 2006 Dec;80(6):1197-213 [16946019] Nature. 2007 Feb 8;445(7128):656-60 [17251933] J Exp Med. 2007 Feb 19;204(2):239-43 [17296790] J Clin Oncol. 2007 Jun 20;25(18):2586-93 [17577038] Hepatology. 2007 Aug;46(2):590-7 [17661407] J Leukoc Biol. 2007 Dec;82(6):1407-19 [17881511] Hepatology. 2008 Feb;47(2):729-36 [18167066] J Hepatol. 2008 Apr;48(4):666-75 [18280000] Annu Rev Immunol. 2008;26:677-704 [18173375] PLoS One. 2008;3(6):e2493 [18560566] Gastroenterology. 2008 Jul;135(1):234-43 [18485901] Cancer Cell. 2008 Aug 12;14(2):156-65 [18691550] J Immunol. 2009 Jan 1;182(1):240-9 [19109155] Gastroenterology. 2009 Feb;136(2):694-704.e4 [18952083] Hepatology. 2009 Feb;49(2):471-81 [19105207] J Clin Invest. 2009 Mar;119(3):551-64 [19229109] Cancer Res. 2009 Mar 1;69(5):2000-9 [19244125] Annu Rev Immunol. 2009;27:147-63 [19302037] Cancer Res. 2009 Apr 1;69(7):2775-82 [19276364] Curr Opin Gastroenterol. 2009 May;25(3):223-9 [19396960] Cancer Res. 2009 Jul 1;69(13):5514-21 [19549903] J Leukoc Biol. 2009 Sep;86(3):513-28 [19542050] Clin Exp Immunol. 2009 Oct;158(1):115-24 [19737238] Cancer Cell. 2009 Oct 6;16(4):295-308 [19800575] Immunity. 2011 Sep 23;35(3):400-12 [21943489] Immunotherapy. 2011 Oct;3(10):1167-84 [21995570] Nature. 2011 Nov 24;479(7374):547-51 [22080947] Hepatology. 2012 Jan;55(1):121-31 [21898503] Cell Tissue Res. 2012 Jan;347(1):225-43 [21626291] Surgery. 2012 Feb;151(2):213-22 [21975289] Hepatology. 2012 Feb;55(2):343-53 [21953144] Hepatology. 2012 Mar;55(3):709-19 [21932384] Liver Int. 2012 Apr;32(4):644-55 [22118340] Cell. 2009 Nov 13;139(4):693-706 [19878981] Cold Spring Harb Perspect Biol. 2009 Nov;1(5):a000141 [20066113] J Clin Invest. 2010 Jul;120(7):2508-15 [20551512] Eur J Clin Invest. 2010 Sep;40(9):851-63 [20597961] Nat Rev Immunol. 2010 Nov;10(11):753-66 [20972472] Cancer Cell. 2010 Nov 16;18(5):485-98 [21035406] Int J Cancer. 2011 Feb 15;128(4):887-96 [20473887] Cell Res. 2011 Jan;21(1):159-68 [21187858] PLoS One. 2011;6(1):e15324 [21246041] Annu Rev Immunol. 2011;29:235-71 [21219185] Cancer Biol Ther. 2011 Apr 1;11(7):615-26 [21278493] Cancer Res. 2011 Apr 1;71(7):2718-27 [21324921] Oncogene. 2011 Apr 7;30(14):1615-30 [21170083] Hepatology. 2011 Apr;53(4):1342-51 [21480338] Swiss Med Wkly. 2011;141:w13197 [21557112] Proc Natl Acad Sci U S A. 2011 Jun 28;108(26):10662-7 [21670304] J Exp Med. 2011 Jul 4;208(7):1359-66 [21690253] PLoS One. 2011;6(9):e24671 [21935436] Cancer Cell. 2005 May;7(5):411-23 [15894262] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/hep.25674 ER - TY - JOUR T1 - Estrogen receptors and human disease: an update AN - 1093470701; 17175368 AB - A myriad of physiological processes in mammals are influenced by estrogens and the estrogen receptors (ERs), ER alpha and ER beta . As we reviewed previously, given the widespread role for estrogen in normal human physiology, it is not surprising that estrogen is implicated in the development or progression of a number of diseases. In this review, we are giving a 5-year update of the literature regarding the influence of estrogens on a number of human cancers (breast, ovarian, colorectal, prostate, and endometrial), endometriosis, fibroids, and cardiovascular disease. A large number of sophisticated experimental studies have provided insights into human disease, but for this review, the literature citations were limited to articles published after our previous review (Deroo and Korach in J Clin Invest 116(3):561-570, 2006) and will focus in most cases on human data and clinical trials. We will describe the influence in which estrogen's action, through one of or both of the ERs, mediates the aforementioned human disease states. JF - Archives of Toxicology AU - Burns, Katherine A AU - Korach, Kenneth S AD - Receptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health (NIH), B3-02, PO Box 12233, Research Triangle Park, NC, 27709, USA, korach@niehs.nih.gov Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 1491 EP - 1504 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 86 IS - 10 SN - 0340-5761, 0340-5761 KW - Toxicology Abstracts KW - Ovarian cancer KW - Endometrium KW - Data processing KW - Colorectal cancer KW - Endometriosis KW - Clinical trials KW - Cancer KW - Reviews KW - Breast cancer KW - Cardiovascular diseases KW - Estrogen receptors KW - Prostate KW - X 24500:Reviews, Legislation, Book & Conference Notices UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1093470701?accountid=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=Estrogen+receptors+and+human+disease%3A+an+update&rft.au=Burns%2C+Katherine+A%3BKorach%2C+Kenneth+S&rft.aulast=Burns&rft.aufirst=Katherine&rft.date=2012-10-01&rft.volume=86&rft.issue=10&rft.spage=1491&rft.isbn=&rft.btitle=&rft.title=Archives+of+Toxicology&rft.issn=03405761&rft_id=info:doi/10.1007%2Fs00204-012-0868-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2013-11-04 N1 - SubjectsTermNotLitGenreText - Ovarian cancer; Endometrium; Data processing; Reviews; Colorectal cancer; Breast cancer; Endometriosis; Cardiovascular diseases; Prostate; Clinical trials; Estrogen receptors; Cancer DO - http://dx.doi.org/10.1007/s00204-012-0868-5 ER - TY - JOUR T1 - A 1536-Well Quantitative High-Throughput Screen to Identify Compounds Targeting Cancer Stem Cells AN - 1093468226; 17169004 AB - Tumor cell subpopulations called cancer stem cells (CSCs) or tumor-initiating cells (TICs) have self-renewal potential and are thought to drive metastasis and tumor formation. Data suggest that these cells are resistant to current chemotherapy and radiation therapy treatments, leading to cancer recurrence. Therefore, finding new drugs and/or drug combinations that cause death of both the differentiated tumor cells as well as CSC populations is a critical unmet medical need. Here, we describe how cancer-derived CSCs are generated from cancer cell lines using stem cell growth media and nonadherent conditions in quantities that enable high-throughput screening (HTS). A cell growth assay in a 1536-well microplate format was developed with these CSCs and used to screen a focused collection of oncology drugs and clinical candidates to find compounds that are cytotoxic against these highly aggressive cells. A hit selection process that included potency and efficacy measurements during the primary screen allowed us to efficiently identify compounds with potent cytotoxic effects against spheroid-derived CSCs. Overall, this research demonstrates one of the first miniaturized HTS assays using CSCs. The procedures described here should enable further testing of the effect of compounds on CSCs and help determine which pathways need to be targeted to kill them. JF - Journal of Biomolecular Screening AU - Mathews, Lesley A AU - Keller, Jonathan M AU - Goodwin, Bonnie L AU - Guha, Rajarshi AU - Shinn, Paul AU - Mull, Rebecca AU - Thomas, Craig J AU - de Kluyver, Rachel L AU - Sayers, Thomas J AU - Ferrer, Marc AD - Division of Preclinical Innovation, National Center for Advancing Translational Sciences (NCATS), National Institutes of Health, Rockville, MD, USA Y1 - 2012/10// PY - 2012 DA - Oct 2012 SP - 1231 EP - 1242 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 17 IS - 9 SN - 1087-0571, 1087-0571 KW - Biotechnology and Bioengineering Abstracts KW - Cancer KW - Chemotherapy KW - Cytotoxicity KW - Data processing KW - Drug development KW - Media (selective) KW - Metastases KW - Oncology KW - Radiation KW - Stem cells KW - Tumor cell lines KW - Tumor cells KW - Tumors KW - high-throughput screening KW - W 30935:Food Biotechnology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1093468226?accountid=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+Biomolecular+Screening&rft.atitle=A+1536-Well+Quantitative+High-Throughput+Screen+to+Identify+Compounds+Targeting+Cancer+Stem+Cells&rft.au=Mathews%2C+Lesley+A%3BKeller%2C+Jonathan+M%3BGoodwin%2C+Bonnie+L%3BGuha%2C+Rajarshi%3BShinn%2C+Paul%3BMull%2C+Rebecca%3BThomas%2C+Craig+J%3Bde+Kluyver%2C+Rachel+L%3BSayers%2C+Thomas+J%3BFerrer%2C+Marc&rft.aulast=Mathews&rft.aufirst=Lesley&rft.date=2012-10-01&rft.volume=17&rft.issue=9&rft.spage=1231&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomolecular+Screening&rft.issn=10870571&rft_id=info:doi/10.1177%2F1087057112458152 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Number of references - 35 N1 - Last updated - 2012-10-19 N1 - SubjectsTermNotLitGenreText - Data processing; Chemotherapy; Drug development; Oncology; Tumors; Tumor cells; Media (selective); Cancer; Metastases; Stem cells; Cytotoxicity; Tumor cell lines; Radiation; high-throughput screening DO - http://dx.doi.org/10.1177/1087057112458152 ER - TY - JOUR T1 - Engineering of an elastic scaffolding polyprotein based on an SH3-binding intrinsically disordered titin PEVK module. AN - 1082237924; 22910563 AB - Titin is a large elastic protein found in muscle that maintains the elasticity and structural integrity of the sarcomere. The PEVK region of titin is intrinsically disordered, highly elastic and serves as a hub to bind signaling proteins. Systematic investigation of the structure and affinity profile of the PEVK region will provide important information about the functions of titin. Since PEVK is highly heterogeneous due to extensive differential splicing from more than one hundred exons, we engineered and expressed polyproteins that consist of a defined number of identical single exon modules. These customized polyproteins reduce heterogeneity, amplify interactions of less dominant modules, and most importantly, provide tags for atomic force microscopy and allow more readily interpretable data from single-molecule techniques. Expression and purification of recombinant polyprotein with repeat regions presented many technical challenges: recombination events in tandem repeats of identical DNA sequences exacerbated by high GC content, toxicity of polymer plasmid and expressed protein to the bacteria; early truncation of proteins expressed with different numbers of modules; and extreme sensitivity to proteolysis. We have investigated a number of in vitro and in vivo bacterial and yeast expression systems, as well as baculoviral systems as potential solutions to these problems. We successfully expressed and purified in gram quantities a polyprotein derived from human titin exon 172 using Pichia pastoris yeast. This study provides valuable insights into the technical challenges regarding the engineering and purification of a tandem repeat sequence of an intrinsically disordered biopolymer. Copyright © 2012 Elsevier Inc. All rights reserved. JF - Protein expression and purification AU - Tsai, Wanxia Li AU - Forbes, Jeffrey G AU - Wang, Kuan AD - Muscle Proteomics and Nanotechnology Section, Laboratory of Muscle Biology, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH/DHHS, Bethesda, MD 20892-8024, USA. liwan@mail.nih.gov Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 187 EP - 199 VL - 85 IS - 2 KW - Connectin KW - 0 KW - Muscle Proteins KW - Polyproteins KW - Recombinant Proteins KW - TTN protein, human KW - Protein Kinases KW - EC 2.7.- KW - Glucose KW - IY9XDZ35W2 KW - Index Medicus KW - Baculoviridae -- genetics KW - Blotting, Western KW - Protein Engineering KW - Pichia -- genetics KW - Models, Molecular KW - Humans KW - Glucose -- metabolism KW - Escherichia coli -- genetics KW - Plasmids KW - Tandem Repeat Sequences KW - src Homology Domains KW - Muscle Proteins -- metabolism KW - Muscle Proteins -- genetics KW - Recombinant Proteins -- isolation & purification KW - Protein Kinases -- metabolism KW - Polyproteins -- chemistry KW - Recombinant Proteins -- metabolism KW - Muscle Proteins -- chemistry KW - Protein Kinases -- genetics KW - Recombinant Proteins -- chemistry KW - Polyproteins -- genetics KW - Recombinant Proteins -- genetics KW - Polyproteins -- metabolism KW - Protein Kinases -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1082237924?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+expression+and+purification&rft.atitle=Engineering+of+an+elastic+scaffolding+polyprotein+based+on+an+SH3-binding+intrinsically+disordered+titin+PEVK+module.&rft.au=Tsai%2C+Wanxia+Li%3BForbes%2C+Jeffrey+G%3BWang%2C+Kuan&rft.aulast=Tsai&rft.aufirst=Wanxia&rft.date=2012-10-01&rft.volume=85&rft.issue=2&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=Protein+expression+and+purification&rft.issn=1096-0279&rft_id=info:doi/10.1016%2Fj.pep.2012.08.003 LA - 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Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.pep.2012.08.003 ER - TY - JOUR T1 - RAP80 is critical in maintaining genomic stability and suppressing tumor development. AN - 1082237813; 22896338 AB - The ubiquitin interaction motif-containing protein RAP80 was recently found to play a key role in DNA damage response (DDR) signaling by facilitating the translocation of several DDR mediators, including BRCA1, to ionizing irradiation (IR)-induced foci. In this study, we examine the effect of the loss of RAP80 on genomic stability and the susceptibility to cancer development in RAP80 null (RAP80(-/-)) mice. RAP80(-/-) mice are viable and did not exhibit any apparent developmental defects. Mouse embryonic fibroblasts (MEF) derived from RAP80(-/-) mice underwent premature senescence compared with wild-type (WT) MEFs, were more sensitive to IR, and exhibited a higher level of spontaneous and IR-induced genomic instability. RAP80(-/-) thymocytes were more sensitive to IR-induced cell death than WT thymocytes. RAP80(-/-) mice were more susceptible to spontaneous lymphoma development and the development of 7,12-dimethylbenz(a)anthracene-induced mammary gland tumors. Moreover, the loss of RAP80 accelerated tumor formation in both p53(-/-) and p53(+/-) mice. Our data indicate that RAP80-deficiency promotes genomic instability and causes an increase in cancer risk consistent with the concept that RAP80 exhibits a tumor suppressor function. ©2012 AACR. JF - Cancer research AU - Yin, Zhengyu AU - Menendez, Daniel AU - Resnick, Michael A AU - French, John E AU - Janardhan, Kyathanahalli S AU - Jetten, Anton M AD - Laboratory of Respiratory Biology, National Institute of Environmental Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA. Y1 - 2012/10/01/ PY - 2012 DA - 2012 Oct 01 SP - 5080 EP - 5090 VL - 72 IS - 19 KW - Benz(a)Anthracenes KW - 0 KW - Cell Cycle Proteins KW - Rap80 protein, mouse KW - Transcription Factors KW - Tumor Suppressor Protein p53 KW - Tumor Suppressor Proteins KW - 7,12-dihydroxymethylbenz(a)anthracene KW - 2564-65-0 KW - Index Medicus KW - Thymocytes -- metabolism KW - Animals KW - Thymocytes -- radiation effects KW - Mammary Neoplasms, Experimental -- genetics KW - Mice KW - Reverse Transcriptase Polymerase Chain Reaction KW - Cell Aging -- genetics KW - Fibroblasts -- metabolism KW - Mice, Knockout KW - Mammary Neoplasms, Experimental -- pathology KW - Gene Expression Regulation, Neoplastic KW - Kaplan-Meier Estimate KW - Mammary Neoplasms, Experimental -- chemically induced KW - Cells, Cultured KW - Lymphoma -- genetics KW - Embryo, Mammalian -- cytology KW - Mice, Inbred C57BL KW - Fibroblasts -- radiation effects KW - Tumor Suppressor Protein p53 -- genetics KW - Lymphoma -- pathology KW - Male KW - Female KW - Cell Aging -- radiation effects KW - Genomic Instability -- radiation effects KW - Cell Cycle Proteins -- genetics KW - Tumor Suppressor Proteins -- genetics KW - Genomic Instability -- genetics KW - Transcription Factors -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1082237813?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=RAP80+is+critical+in+maintaining+genomic+stability+and+suppressing+tumor+development.&rft.au=Yin%2C+Zhengyu%3BMenendez%2C+Daniel%3BResnick%2C+Michael+A%3BFrench%2C+John+E%3BJanardhan%2C+Kyathanahalli+S%3BJetten%2C+Anton+M&rft.aulast=Yin&rft.aufirst=Zhengyu&rft.date=2012-10-01&rft.volume=72&rft.issue=19&rft.spage=5080&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-12-1484 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-12-21 N1 - Date created - 2012-10-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nat Cell Biol. 2011 Oct;13(10):1161-9 [21968989] Cancer Res. 2011 Sep 1;71(17):5792-805 [21799032] Front Biosci (Landmark Ed). 2012;17:1362-88 [22201809] J Biol Chem. 2012 Jun 29;287(27):22919-26 [22539352] FEBS Lett. 2011 Sep 16;585(18):2883-90 [21621538] Cancer Res. 2001 Sep 1;61(17):6577-82 [11522657] Science. 2002 May 3;296(5569):922-7 [11934988] Genes Dev. 2003 Jan 15;17(2):201-13 [12533509] Nat Rev Cancer. 2004 Sep;4(9):665-76 [15343273] Cancer Res. 1980 Feb;40(2):368-73 [6243251] Int J Cancer. 1981 Dec;28(6):739-46 [6800966] Br J Cancer. 1993 Oct;68(4):653-61 [8398688] Prog Clin Biol Res. 1996;395:1-11 [8895979] Proc Natl Acad Sci U S A. 1997 Dec 23;94(26):14590-5 [9405657] J Biol Chem. 1998 Mar 6;273(10):5858-68 [9488723] Nature. 2004 Nov 18;432(7015):316-23 [15549093] Toxicol Pathol. 2006;34(2):187-98 [16546942] Nat Rev Cancer. 2006 Dec;6(12):909-23 [17128209] Nucleic Acids Res. 2007;35(5):1673-86 [17311814] Science. 2007 May 25;316(5828):1194-8 [17525340] Science. 2007 May 25;316(5828):1198-202 [17525341] Science. 2007 May 25;316(5828):1202-5 [17525342] Cancer Res. 2007 Jul 15;67(14):6647-56 [17621610] Nat Struct Mol Biol. 2007 Aug;14(8):716-20 [17643121] Annu Rev Genomics Hum Genet. 2007;8:37-55 [17887919] Cell Res. 2008 Jan;18(1):8-16 [18087291] Cancer Res. 2008 Jun 1;68(11):4269-76 [18519686] Cancer Lett. 2008 Nov 28;271(2):179-90 [18550271] Breast Cancer Res Treat. 2009 Jan;113(2):371-6 [18270812] Breast Cancer Res Treat. 2009 Jan;113(2):377-81 [18306035] Proc Natl Acad Sci U S A. 2009 Mar 3;106(9):3166-71 [19202061] Oncogene. 2009 Apr 23;28(16):1843-52 [19305427] J Biol Chem. 2009 Jul 17;284(29):19280-9 [19433585] Breast Cancer Res Treat. 2009 Sep;117(2):453-9 [18695986] Nat Rev Cancer. 2009 Oct;9(10):749-58 [19776744] Dev Cell. 2010 Mar 16;18(3):371-84 [20153262] J Exp Med. 2010 May 10;207(5):973-81 [20385748] Curr Opin Genet Dev. 2010 Jun;20(3):268-76 [20346647] DNA Repair (Amst). 2010 Dec 10;9(12):1219-28 [21035408] Genes Dev. 2011 Mar 1;25(5):409-33 [21363960] Genes Dev. 2011 Apr 1;25(7):685-700 [21406551] J Biol Chem. 2011 Apr 15;286(15):13669-80 [21335604] PLoS Genet. 2011 Apr;7(4):e1001381 [21552324] Nucleic Acids Res. 2011 Jun;39(11):4769-82 [21317191] DNA Repair (Amst). 2011 Aug 15;10(8):806-14 [21622030] Nat Rev Cancer. 2012 Jan;12(1):68-78 [22193408] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1158/0008-5472.CAN-12-1484 ER - TY - JOUR T1 - 450K epigenome-wide scan identifies differential DNA methylation in newborns related to maternal smoking during pregnancy. AN - 1082235522; 22851337 AB - Epigenetic modifications, such as DNA methylation, due to in utero exposures may play a critical role in early programming for childhood and adult illness. Maternal smoking is a major risk factor for multiple adverse health outcomes in children, but the underlying mechanisms are unclear. We investigated epigenome-wide methylation in cord blood of newborns in relation to maternal smoking during pregnancy. We examined maternal plasma cotinine (an objective biomarker of smoking) measured during pregnancy in relation to DNA methylation at 473,844 CpG sites (CpGs) in 1,062 newborn cord blood samples from the Norwegian Mother and Child Cohort Study (MoBa) using the Infinium HumanMethylation450 BeadChip (450K). We found differential DNA methylation at epigenome-wide statistical significance (p-value < 1.06 × 10-7) for 26 CpGs mapped to 10 genes. We replicated findings for CpGs in AHRR, CYP1A1, and GFI1 at strict Bonferroni-corrected statistical significance in a U.S. birth cohort. AHRR and CYP1A1 play a key role in the aryl hydrocarbon receptor signaling pathway, which mediates the detoxification of the components of tobacco smoke. GFI1 is involved in diverse developmental processes but has not previously been implicated in responses to tobacco smoke. We identified a set of genes with methylation changes present at birth in children whose mothers smoked during pregnancy. This is the first study of differential methylation across the genome in relation to maternal smoking during pregnancy using the 450K platform. Our findings implicate epigenetic mechanisms in the pathogenesis of the adverse health outcomes associated with this important in utero exposure. JF - Environmental health perspectives AU - Joubert, Bonnie R AU - Håberg, Siri E AU - Nilsen, Roy M AU - Wang, Xuting AU - Vollset, Stein E AU - Murphy, Susan K AU - Huang, Zhiqing AU - Hoyo, Cathrine AU - Midttun, Øivind AU - Cupul-Uicab, Lea A AU - Ueland, Per M AU - Wu, Michael C AU - Nystad, Wenche AU - Bell, Douglas A AU - Peddada, Shyamal D AU - London, Stephanie J AD - Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina 27709, USA. Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 1425 EP - 1431 VL - 120 IS - 10 KW - AHRR protein, human KW - 0 KW - Basic Helix-Loop-Helix Transcription Factors KW - Biomarkers KW - DNA-Binding Proteins KW - GFI1 protein, human KW - Repressor Proteins KW - Tobacco Smoke Pollution KW - Transcription Factors KW - CYP1A1 protein, human KW - EC 1.14.14.1 KW - Cytochrome P-450 CYP1A1 KW - Cotinine KW - K5161X06LL KW - Index Medicus KW - Cytochrome P-450 CYP1A1 -- genetics KW - Norway -- epidemiology KW - Transcription Factors -- metabolism KW - Humans KW - Repressor Proteins -- metabolism KW - Infant, Newborn KW - DNA-Binding Proteins -- genetics KW - Cytochrome P-450 CYP1A1 -- metabolism KW - Tandem Mass Spectrometry KW - Basic Helix-Loop-Helix Transcription Factors -- genetics KW - Transcription Factors -- genetics KW - Repressor Proteins -- genetics KW - Pregnancy KW - Fetal Blood KW - Adult KW - Basic Helix-Loop-Helix Transcription Factors -- metabolism KW - Cohort Studies KW - Chromatography, Liquid KW - United States -- epidemiology KW - Biomarkers -- blood KW - Male KW - Female KW - DNA-Binding Proteins -- metabolism KW - DNA Methylation KW - Prenatal Exposure Delayed Effects -- chemically induced KW - Tobacco Smoke Pollution -- adverse effects KW - Cotinine -- blood KW - Prenatal Exposure Delayed Effects -- epidemiology KW - Epigenesis, Genetic KW - Maternal Exposure KW - Prenatal Exposure Delayed Effects -- genetics KW - Genome-Wide Association Study UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1082235522?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=450K+epigenome-wide+scan+identifies+differential+DNA+methylation+in+newborns+related+to+maternal+smoking+during+pregnancy.&rft.au=Joubert%2C+Bonnie+R%3BH%C3%A5berg%2C+Siri+E%3BNilsen%2C+Roy+M%3BWang%2C+Xuting%3BVollset%2C+Stein+E%3BMurphy%2C+Susan+K%3BHuang%2C+Zhiqing%3BHoyo%2C+Cathrine%3BMidttun%2C+%C3%98ivind%3BCupul-Uicab%2C+Lea+A%3BUeland%2C+Per+M%3BWu%2C+Michael+C%3BNystad%2C+Wenche%3BBell%2C+Douglas+A%3BPeddada%2C+Shyamal+D%3BLondon%2C+Stephanie+J&rft.aulast=Joubert&rft.aufirst=Bonnie&rft.date=2012-10-01&rft.volume=120&rft.issue=10&rft.spage=1425&rft.isbn=&rft.btitle=&rft.title=Environmental+health+perspectives&rft.issn=1552-9924&rft_id=info:doi/10.1289%2Fehp.1205412 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-07-08 N1 - Date created - 2012-10-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Epigenetics. 2011 Nov;6(11):1284-94 [21937876] Genomics. 2011 Oct;98(4):288-95 [21839163] Environ Health Perspect. 2012 Mar;120(3):355-60 [22128036] Mol Cell Biol. 2004 Oct;24(20):8803-12 [15456856] Genome Biol. 2004;5(10):R80 [15461798] Mol Cell Biol. 2005 Dec;25(23):10338-51 [16287849] Biochem Pharmacol. 2006 Jul 28;72(3):267-79 [16488401] Eur J Epidemiol. 2006;21(8):619-25 [17031521] Int J Epidemiol. 2006 Oct;35(5):1146-50 [16926217] Nature. 2007 May 24;447(7143):425-32 [17522676] Proc Natl Acad Sci U S A. 2007 Aug 7;104(32):13056-61 [17670942] Arch Biochem Biophys. 2007 Aug 15;464(2):207-12 [17481570] Chem Res Toxicol. 2008 Jan;21(1):102-16 [18076143] Pediatr Res. 2008 Jun;63(6):593-8 [18317238] Cancer Epidemiol Biomarkers Prev. 2008 Sep;17(9):2306-10 [18768498] J Clin Invest. 2008 Oct;118(10):3462-9 [18802477] Semin Immunol. 2011 Oct;23(5):368-78 [21920773] J Biol Chem. 2011 Dec 16;286(50):43214-28 [21984831] Am J Med Genet B Neuropsychiatr Genet. 2012 Mar;159B(2):141-51 [22232023] Nat Immunol. 2012 Feb;13(2):117-9 [22261961] Gene. 2012 Feb 15;494(1):36-43 [22202639] Environ Health Perspect. 2012 Feb;120(2):296-302 [22005006] Hum Mol Genet. 2012 Jul 1;21(13):3073-82 [22492999] Nat Rev Genet. 2011 Aug;12(8):529-41 [21747404] J Pediatr. 2009 Jan;154(1):17-9 [18990410] Rapid Commun Mass Spectrom. 2009 May;23(9):1371-9 [19337982] Genome Res. 2009 Jul;19(7):1165-74 [19494038] Am J Respir Crit Care Med. 2009 Sep 1;180(5):462-7 [19498054] J Cell Physiol. 2010 Feb;222(2):282-5 [19847803] Virchows Arch. 2010 Jan;456(1):13-21 [19844740] Science. 2010 Sep 10;329(5997):1345-8 [20688981] J Allergy Clin Immunol. 2011 Jan;127(1):262-4, 264.e1 [21094522] Am J Epidemiol. 2011 Feb 1;173(3):355-9 [21178103] BMC Public Health. 2011;11(1):46 [21255390] Am J Hum Genet. 2011 Apr 8;88(4):450-7 [21457905] Blood. 2011 Apr 14;117(15):e142-50 [21343615] Epigenetics. 2011 Jun;6(6):692-702 [21593595] Stem Cells. 2011 Feb;29(2):376-85 [21732494] Comment In: Environ Health Perspect. 2012 Oct;120(10):a402 [23026408] Erratum In: Environ Health Perspect. 2012 Dec;120(12):A455 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1289/ehp.1205412 ER - TY - JOUR T1 - A pooled analysis of thyroid cancer incidence following radiotherapy for childhood cancer. AN - 1082235224; 22857014 AB - Childhood cancer five-year survival now exceeds 70-80%. Childhood exposure to radiation is a known thyroid carcinogen; however, data are limited for the evaluation of radiation dose-response at high doses, modifiers of the dose-response relationship and joint effects of radiotherapy and chemotherapy. To address these issues, we pooled two cohort and two nested case-control studies of childhood cancer survivors including 16,757 patients, with 187 developing primary thyroid cancer. Relative risks (RR) with 95% confidence intervals (CI) for thyroid cancer by treatment with alkylating agents, anthracyclines or bleomycin were 3.25 (0.9-14.9), 4.5 (1.4-17.8) and 3.2 (0.8-10.4), respectively, in patients without radiotherapy, and declined with greater radiation dose (RR trends, P = 0.02, 0.12 and 0.01, respectively). Radiation dose-related RRs increased approximately linearly for 50 Gy. The fitted RR at 10 Gy was 13.7 (95% CI: 8.0-24.0). Dose-related excess RRs increased with decreasing age at exposure (P < 0.01), but did not vary with attained age or time-since-exposure, remaining elevated 25+ years after exposure. Gender and number of treatments did not modify radiation effects. Thyroid cancer risks remained elevated many decades following radiotherapy, highlighting the need for continued follow up of childhood cancer survivors. JF - Radiation research AU - Veiga, Lene H S AU - Lubin, Jay H AU - Anderson, Harald AU - de Vathaire, Florent AU - Tucker, Margaret AU - Bhatti, Parveen AU - Schneider, Arthur AU - Johansson, Robert AU - Inskip, Peter AU - Kleinerman, Ruth AU - Shore, Roy AU - Pottern, Linda AU - Holmberg, Erik AU - Hawkins, Michael M AU - Adams, M Jacob AU - Sadetzki, Siegal AU - Lundell, Marie AU - Sakata, Ritsu AU - Damber, Lena AU - Neta, Gila AU - Ron, Elaine AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, Maryland 20892, USA. Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 365 EP - 376 VL - 178 IS - 4 KW - Index Medicus KW - Space life sciences KW - Infant KW - Humans KW - Adult KW - Case-Control Studies KW - Incidence KW - Child KW - Dose-Response Relationship, Radiation KW - Adolescent KW - Male KW - Female KW - Radiotherapy -- adverse effects KW - Child, Preschool KW - Thyroid Neoplasms -- epidemiology KW - Neoplasms, Second Primary -- epidemiology KW - Neoplasms -- radiotherapy KW - Neoplasms, Radiation-Induced -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1082235224?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+pooled+analysis+of+thyroid+cancer+incidence+following+radiotherapy+for+childhood+cancer.&rft.au=Veiga%2C+Lene+H+S%3BLubin%2C+Jay+H%3BAnderson%2C+Harald%3Bde+Vathaire%2C+Florent%3BTucker%2C+Margaret%3BBhatti%2C+Parveen%3BSchneider%2C+Arthur%3BJohansson%2C+Robert%3BInskip%2C+Peter%3BKleinerman%2C+Ruth%3BShore%2C+Roy%3BPottern%2C+Linda%3BHolmberg%2C+Erik%3BHawkins%2C+Michael+M%3BAdams%2C+M+Jacob%3BSadetzki%2C+Siegal%3BLundell%2C+Marie%3BSakata%2C+Ritsu%3BDamber%2C+Lena%3BNeta%2C+Gila%3BRon%2C+Elaine&rft.aulast=Veiga&rft.aufirst=Lene+H&rft.date=2012-10-01&rft.volume=178&rft.issue=4&rft.spage=365&rft.isbn=&rft.btitle=&rft.title=Radiation+research&rft.issn=1938-5404&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-12-07 N1 - Date created - 2012-10-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 1991 Jun 1;51(11):2885-8 [1851664] Cancer Epidemiol Biomarkers Prev. 2012 Jan;21(1):92-101 [22028399] Int J Radiat Oncol Biol Phys. 1997 Jan 1;37(1):163-9 [9054892] J Clin Endocrinol Metab. 1950 Oct;10(10):1296-1308 [14794754] N Engl J Med. 1963 Feb 21;268:406-10 [13989805] Environ Health Perspect. 2004 Dec;112(17):1691-6 [15579415] Proc Natl Acad Sci U S A. 2005 Sep 13;102(37):13040-5 [16150705] Am J Epidemiol. 2006 Feb 15;163(4):374-83 [16394206] Acta Oncol. 2006;45(4):438-48 [16760180] Radiat Res. 2007 Jul;168(1):1-64 [17722996] Health Phys. 2007 Nov;93(5):502-11 [18049226] Eur J Cancer. 2008 Jan;44(2):205-15 [18077152] Oncologist. 2008 Nov;13(11):1181-92 [18987046] Cancer Epidemiol Biomarkers Prev. 2009 Apr;18(4):1033-40 [19336557] J Radiol Prot. 2009 Jun;29(2A):A171-84 [19454800] Int J Cancer. 2009 Nov 15;125(10):2400-5 [19610069] Eur J Cancer. 2010 Jan;46(2):384-94 [19818600] Cancer Sci. 2010 Mar;101(3):787-92 [20132215] JAMA. 2010 Jul 14;304(2):172-9 [20628130] Cancer. 2010 Oct 15;116(20):4882-91 [20597129] Br J Cancer. 2010 Nov 23;103(11):1663-70 [21063404] Radiat Res. 2010 Dec;174(6):741-52 [21128798] Radiat Res. 1995 Mar;141(3):259-77 [7871153] Arch Intern Med. 1999 Dec 13-27;159(22):2713-9 [10597762] Erratum In: Radiat Res. 2013 Dec;180(6):e41 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Cancer mortality following radiotherapy for benign gynecologic disorders. AN - 1082235211; 22856888 AB - The purpose of this study is to quantify cancer mortality in relationship to organ-specific radiation dose among women irradiated for benign gynecologic disorders. Included in this study are 12,955 women treated for benign gynecologic disorders at hospitals in the Northeastern U.S. between 1925 and 1965; 9,770 women treated by radiation and 3,186 women treated by other methods. The average age at treatment was 45.9 years (range, 13-88 years), and the average follow-up period was 30.1 years (maximum, 69.9 years). Radiation doses to organs and active bone marrow were reconstructed by medical physicists using original radiotherapy records. The highest doses were received by the uterine cervix (median, 120 Gy) and uterine corpus (median, 34 Gy), followed by the bladder, rectum and colon (median, 1.7-7.2 Gy), with other abdominal organs receiving median doses ≤1 Gy and organs in the chest and head receiving doses <0.1 Gy. Standardized mortality rate ratios relative to the general U.S. population were calculated. Radiation-related risks were estimated in internal analyses using Poisson regression models. Mortality was significantly elevated among irradiated women for cancers of the uterine corpus, ovary, bladder, rectum, colon and brain, as well as for leukemia (exclusive of chronic lymphocytic leukemia) but not for cancer of the cervix, Hodgkin or non-Hodgkin lymphoma, multiple myeloma, or chronic lymphocytic leukemia. Evidence of a dose-response was seen for cancers of the ovary [excess relative risk (ERR) = 0.31/Gy, P < 0.001], bladder (ERR = 0.21/Gy, P = 0.02) and rectum (ERR = 0.23/Gy, P = 0.05) and suggested for colon (ERR = 0.09/Gy, P = 0.10), but not for cancers of the uterine corpus or brain nor for non-chronic lymphocytic leukemia. Relative risks of mortality due to cancers of the stomach, pancreas, liver and kidney were close to 1.0, with no evidence of dose-response over the range of 0-1.5 Gy. Breast cancer was not significantly associated with dose to the breast or ovary. Mortality due to cancers of heavily irradiated organs remained elevated up to 40 years after irradiation. Significantly elevated radiation-related risk was seen for cancers of organs proximal to the radiation source or fields (bladder, rectum and ovary), as well as for non-chronic lymphocytic leukemia. Our results corroborate those from previous studies that suggest that cells of the uterine cervix and lymphopoietic system are relatively resistant to the carcinogenic effects of radiation. Studies of women irradiated for benign gynecologic disorders, together with studies of women treated with higher doses of radiation for uterine cancers, provide quantitative information on cancer risks associated with a broad range of pelvic radiation exposures. JF - Radiation research AU - Sakata, Ritsu AU - Kleinerman, Ruth A AU - Mabuchi, Kiyohiko AU - Stovall, Marilyn AU - Smith, Susan A AU - Weathers, Rita AU - Wactawski-Wende, Jean AU - Cookfair, Diane L AU - Boice, John D AU - Inskip, Peter D AD - Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. rsakata@rerf.or.jp Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 266 EP - 279 VL - 178 IS - 4 KW - Index Medicus KW - Space life sciences KW - Aged, 80 and over KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Adolescent KW - Female KW - Genital Neoplasms, Female -- pathology KW - Genital Neoplasms, Female -- radiotherapy KW - Genital Neoplasms, Female -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1082235211?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Cancer+mortality+following+radiotherapy+for+benign+gynecologic+disorders.&rft.au=Sakata%2C+Ritsu%3BKleinerman%2C+Ruth+A%3BMabuchi%2C+Kiyohiko%3BStovall%2C+Marilyn%3BSmith%2C+Susan+A%3BWeathers%2C+Rita%3BWactawski-Wende%2C+Jean%3BCookfair%2C+Diane+L%3BBoice%2C+John+D%3BInskip%2C+Peter+D&rft.aulast=Sakata&rft.aufirst=Ritsu&rft.date=2012-10-01&rft.volume=178&rft.issue=4&rft.spage=266&rft.isbn=&rft.btitle=&rft.title=Radiation+research&rft.issn=1938-5404&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-12-07 N1 - Date created - 2012-10-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Epidemiol Biomarkers Prev. 2010 Feb;19(2):464-74 [20142245] J Clin Oncol. 2009 Aug 20;27(24):3901-7 [19620485] J Natl Cancer Inst. 1968 May;40(5):951-82 [5648139] Br J Radiol. 1969 Jul;42(499):519-21 [5788062] Br J Radiol. 1971 Apr;44(520):295-8 [4994676] Phys Med Biol. 1981 May;26(3):389-400 [7243876] Am J Epidemiol. 1985 Feb;121(2):309-23 [3839345] J Natl Cancer Inst. 1987 Dec;79(6):1295-311 [3480381] Radiat Res. 1988 Oct;116(1):3-55 [3186929] Int J Cancer. 1989 Jul 15;44(1):7-16 [2744900] Med Phys. 1989 Sep-Oct;16(5):726-33 [2509867] Acta Oncol. 1990;29(5):563-7 [2206566] Radiat Res. 1990 Sep;123(3):275-84 [2217725] Radiat Res. 1990 Sep;123(3):331-44 [2217730] Radiat Res. 1993 Jul;135(1):108-24 [8327655] Int J Cancer. 1994 Mar 15;56(6):793-801 [8119768] Radiat Res. 1994 Feb;137(2 Suppl):S68-97 [8127953] J Natl Cancer Inst. 1994 Sep 7;86(17):1315-24 [8064889] Int J Cancer. 1994 Nov 1;59(3):327-38 [7927937] Cancer Causes Control. 1994 Sep;5(5):471-8 [7999969] Acta Oncol. 1995;34(6):713-9 [7576736] Cancer. 1995 Aug 1;76(3):442-52 [8625126] Radiat Res. 1996 Jul;146(1):1-27 [8677290] Am J Obstet Gynecol. 1954 Jan;67(1):121-9 [13114295] Trans N Engl Obstet Gynecol Soc. 1960;14:163-77 [13729717] Am J Obstet Gynecol. 1956 Sep;72(3):497-505 [13354658] Int J Cancer. 2005 May 1;114(5):797-805 [15609304] Epidemiology. 2006 Jul;17(4):469-72 [16755263] Radiat Res. 2006 Jul;166(1 Pt 2):141-57 [16808603] Radiat Res. 2007 Jul;168(1):1-64 [17722996] Cancer. 2008 Oct 1;113(7 Suppl):1980-93 [18798536] Am J Epidemiol. 2009 Apr 15;169(8):969-76 [19270049] Br J Cancer. 2000 Dec;83(11):1565-72 [11076670] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - L-asparaginase inhibits invasive and angiogenic activity and induces autophagy in ovarian cancer. AN - 1081431257; 22333033 AB - Recent work identified L-asparaginase (L-ASP) as a putative therapeutic target for ovarian cancer. We suggest that L-ASP, a dysregulator of glycosylation, would interrupt the local microenvironment, affecting the ovarian cancer cell-endothelial cell interaction and thus angiogenesis without cytotoxic effects. Ovarian cancer cell lines and human microvascular endothelial cells (HMVEC) were exposed to L-ASP at physiologically attainable concentrations and subjected to analyses of endothelial tube formation, invasion, adhesion and the assessment of sialylated proteins involved in matrix-associated and heterotypic cell adhesion. Marked reduction in HMVEC tube formation in vitro, HMVEC and ovarian cancer cell invasion, and heterotypic cell-cell and cell-matrix adhesion was observed (P < 0.05-0.0001). These effects were associated with reduced binding to ß1integrin, activation of FAK, and cell surface sialyl Lewis(X) (sLe(x)) expression. No reduction in HMVEC E-selectin expression was seen consistent with the unidirectional inhibitory actions observed. L-ASP concentrations were non-toxic to either ovarian cancer or HMVEC lines in the time frame of the assays. However, early changes of autophagy were observed in both cell types with induction of ATG12, beclin-1, and cleavage of LC-3, indicating cell injury did occur. These data and the known mechanism of action of L-ASP on glycosylation of nascent proteins suggest that L-ASP reduces of ovarian cancer dissemination and progression through modification of its microenvironment. The reduction of ovarian cancer cell surface sLe(x) inhibits interaction with HMVEC and thus HMVEC differentiation into tubes, inhibits interaction with the local matrix reducing invasive behaviour, and causes cell injury initiating autophagy in tumour and vascular cells. © 2012 The Authors Journal of Cellular and Molecular Medicine © 2012 Foundation for Cellular and Molecular Medicine/Blackwell Publishing Ltd. JF - Journal of cellular and molecular medicine AU - Yu, Minshu AU - Henning, Ryan AU - Walker, Amanda AU - Kim, Geoffrey AU - Perroy, Alyssa AU - Alessandro, Riccardo AU - Virador, Victoria AU - Kohn, Elise C AD - Molecular Signaling Section, Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA. Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 2369 EP - 2378 VL - 16 IS - 10 KW - 5-acetylneuraminyl-(2-3)-galactosyl-(1-4)-(fucopyranosyl-(1-3))-N-acetylglucosamine KW - 0 KW - Angiogenesis Inhibitors KW - Antigens, CD29 KW - E-Selectin KW - Oligosaccharides KW - Asparaginase KW - EC 3.5.1.1 KW - Index Medicus KW - Cell-Matrix Junctions KW - E-Selectin -- metabolism KW - Humans KW - Cell Line, Tumor KW - Neovascularization, Pathologic -- enzymology KW - Neovascularization, Pathologic -- pathology KW - Oligosaccharides -- metabolism KW - Oligosaccharides -- genetics KW - Antigens, CD29 -- metabolism KW - Glycosylation -- drug effects KW - Cell Adhesion -- drug effects KW - E-Selectin -- genetics KW - Female KW - Endothelial Cells -- metabolism KW - Autophagy -- drug effects KW - Ovarian Neoplasms -- metabolism KW - Angiogenesis Inhibitors -- pharmacology KW - Ovarian Neoplasms -- pathology KW - Asparaginase -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1081431257?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+and+molecular+medicine&rft.atitle=L-asparaginase+inhibits+invasive+and+angiogenic+activity+and+induces+autophagy+in+ovarian+cancer.&rft.au=Yu%2C+Minshu%3BHenning%2C+Ryan%3BWalker%2C+Amanda%3BKim%2C+Geoffrey%3BPerroy%2C+Alyssa%3BAlessandro%2C+Riccardo%3BVirador%2C+Victoria%3BKohn%2C+Elise+C&rft.aulast=Yu&rft.aufirst=Minshu&rft.date=2012-10-01&rft.volume=16&rft.issue=10&rft.spage=2369&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+and+molecular+medicine&rft.issn=1582-4934&rft_id=info:doi/10.1111%2Fj.1582-4934.2012.01547.x LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-03-26 N1 - Date created - 2012-09-27 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nature. 2001 May 17;411(6835):375-9 [11357145] Science. 2000 Dec 1;290(5497):1717-21 [11099404] Biochem Biophys Res Commun. 2002 May 10;293(3):1099-106 [12051773] J Clin Invest. 2002 Oct;110(7):913-4 [12370267] Biochem Biophys Res Commun. 2003 Feb 21;301(4):907-14 [12589798] Nat Rev Cancer. 2002 Feb;2(2):91-100 [12635172] Oncogene. 2003 Oct 16;22(46):7137-45 [14562042] J Clin Oncol. 2003 Dec 1;21(23):4356-63 [14645425] Biochim Biophys Acta. 2003 Dec 7;1643(1-3):113-23 [14654234] Leuk Res. 2004 Apr;28(4):321-4 [15109528] Nature. 1970 May 30;226(5248):850-1 [5444625] Biochem Biophys Res Commun. 1972 Jul 11;48(1):35-40 [4557511] Adv Cancer Res. 1985;43:1-73 [2581423] J Biol Chem. 1988 Jun 5;263(16):7591-603 [3372501] Lab Invest. 1989 Dec;61(6):629-34 [2481152] Biochem Biophys Res Commun. 1990 Sep 14;171(2):860-6 [2119581] Exp Cell Res. 1991 Sep;196(1):20-5 [1679016] Blood. 1991 Sep 15;78(6):1452-60 [1679356] Biochem Biophys Res Commun. 1992 Feb 14;182(3):1376-82 [1371681] Gut. 1993 Jun;34(6):829-36 [8314518] Nature. 1993 Sep 16;365(6443):267-9 [7690465] Mol Cell Biol. 1994 Mar;14(3):1680-8 [7509446] J Biol Chem. 1994 Aug 26;269(34):21505-11 [8063786] Proc Natl Acad Sci U S A. 1995 Feb 28;92(5):1307-11 [7533291] J Cell Biol. 1996 Aug;134(3):793-9 [8707856] Cancer Res. 2005 Jun 1;65(11):4645-52 [15930282] J Cell Biol. 2005 Jun 20;169(6):941-52 [15967814] Eur J Cell Biol. 2006 Jan;85(1):47-57 [16373174] Curr Opin Cell Biol. 2006 Oct;18(5):516-23 [16919435] Mol Cancer Ther. 2006 Nov;5(11):2613-23 [17088436] J Clin Invest. 2007 Apr;117(4):1049-57 [17380207] Nature. 2007 Apr 12;446(7137):745-7 [17429391] Autophagy. 2007 Sep-Oct;3(5):512-5 [17643071] Cancer Sci. 2007 Oct;98(10):1586-91 [17711507] J Clin Oncol. 2007 Nov 20;25(33):5180-6 [18024865] Cell. 2008 Jan 11;132(1):27-42 [18191218] Cancer Res. 2008 Jan 15;68(2):388-94 [18199532] Autophagy. 2008 Apr;4(3):351-3 [18196957] J Clin Oncol. 2008 Aug 1;26(22):3709-14 [18669456] Curr Opin Cell Biol. 2008 Oct;20(5):583-8 [18573652] Mol Cancer Ther. 2008 Oct;7(10):3123-8 [18852115] Nat Chem Biol. 2008 Dec;4(12):751-7 [18953356] Cell Death Differ. 2009 Jan;16(1):1-2 [19079285] J Biol Chem. 2009 Feb 6;284(6):3739-49 [19075018] Cancer Metastasis Rev. 2009 Jun;28(1-2):35-49 [19169797] PLoS One. 2009;4(4):e5136 [19352495] Curr Mol Med. 2009 May;9(4):417-24 [19519399] Acta Biochim Pol. 2010;57(1):55-61 [20066177] Biochim Biophys Acta. 2010 Jun;1800(6):545-55 [20332015] Nature. 2011 Jun 30;474(7353):609-15 [21720365] Oncogene. 2011 Sep 1;30(35):3766-83 [21478904] Exp Cell Res. 2002 May 15;276(1):101-10 [11978012] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/j.1582-4934.2012.01547.x ER - TY - JOUR T1 - Stress and gene expression of individuals with chronic abdominal pain. AN - 1080613061; 23007871 AB - Research examining the role of stress in gastrointestinal (GI) symptoms such as chronic abdominal pain (CAP) is controversial. The purpose of this study was to examine the expression of genes involved in metabolic stress and toxicity in men and women with high and low levels of perceived stress with and without CAP. Data and samples were collected and the expression of genes involved in metabolic stress and toxicity was analyzed in 26 individuals who had consented to participate in a natural history protocol. Subjects completed the 10-item Perceived Stress scale (PSS). Fasting participants' peripheral whole blood was collected for proteomic and genomic studies. Polymerase chain reaction (PCR) array was used to analyze the expression of 84 key genes involved in human stress and toxicity plus 5 housekeeping genes. Plasma interleukin-1 alpha (IL-1α) protein was quantified via enzyme-linked immunosorbent assay (ELISA). Interleukin-1 alpha gene (IL1A) was upregulated in females with high stress versus females with low stress by 2.58-fold (95% CI [0.88, 4.28]). IL1A was upregulated in participants with high stress and CAP versus those with low stress and CAP by 3.47-fold (95% CI [1.14, 5.80]). An upregulation of the gene coding the pro-inflammatory cytokine IL-1α suggests that the mechanism behind stress-related changes in GI symptoms is pro-inflammatory in nature. The results of this study contribute to the knowledge of the mechanism behind stress-related CAP symptoms and gender differences associated with these disorders. JF - Biological research for nursing AU - Peace, Ralph Michael AU - Majors, Benjamin L AU - Patel, Nayan S AU - Wang, Dan AU - Valle-Pinero, Arseima Y Del AU - Martino, Angela C AU - Henderson, Wendy A AD - Howard Hughes Medical Institute-National Institutes of Health Research Scholar, Chevy Chase, MD, USA. Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 405 EP - 411 VL - 14 IS - 4 KW - Index Medicus KW - Nursing KW - Cross-Sectional Studies KW - Humans KW - Adult KW - Chronic Disease KW - Male KW - Female KW - Abdominal Pain -- genetics KW - Gene Expression KW - Stress, Psychological -- psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1080613061?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biological+research+for+nursing&rft.atitle=Stress+and+gene+expression+of+individuals+with+chronic+abdominal+pain.&rft.au=Peace%2C+Ralph+Michael%3BMajors%2C+Benjamin+L%3BPatel%2C+Nayan+S%3BWang%2C+Dan%3BValle-Pinero%2C+Arseima+Y+Del%3BMartino%2C+Angela+C%3BHenderson%2C+Wendy+A&rft.aulast=Peace&rft.aufirst=Ralph&rft.date=2012-10-01&rft.volume=14&rft.issue=4&rft.spage=405&rft.isbn=&rft.btitle=&rft.title=Biological+research+for+nursing&rft.issn=1552-4175&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-02-06 N1 - Date created - 2012-09-25 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Am J Gastroenterol. 2006 Jun;101(6):1295-8 [16771952] Nat Rev Drug Discov. 2006 Feb;5(2):99-100 [16521327] Brain Behav Immun. 2007 Oct;21(7):901-12 [17475444] Arthritis Rheum. 2008 Feb;58(2):376-83 [18240230] J Psychosom Res. 2008 Jun;64(6):583-7 [18501258] Nutr Clin Pract. 2008 Jun-Jul;23(3):275-83 [18595860] Curr Gastroenterol Rep. 2008 Aug;10(4):385-90 [18627650] Bioinformatics. 2009 Mar 15;25(6):765-71 [19176553] Gastroenterology. 2009 May;136(6):1979-88 [19457422] Dig Dis Sci. 2009 Jul;54(7):1542-9 [18979200] Brain Behav Immun. 2009 Jul;23(5):622-8 [19070658] Arthritis Res Ther. 2009;11(3):R61 [19413909] Psychoneuroendocrinology. 2010 Apr;35(3):442-50 [19766403] Annu Rev Med. 2011;62:381-96 [21090962] Biol Res Nurs. 2011 Jul;13(3):235-42 [21586496] Biol Res Nurs. 2011 Oct;13(4):391-8 [21112918] J Physiol Pharmacol. 2011 Dec;62(6):591-9 [22314561] Biol Res Nurs. 2013 Jan;15(1):26-36 [21765120] Gut. 1999 Sep;45 Suppl 2:II43-7 [10457044] J Clin Gastroenterol. 1999 Dec;29(4):339-43 [10599638] Eur J Gastroenterol Hepatol. 2000 Jan;12(1):39-43 [10656208] Am J Gastroenterol. 2000 Apr;95(4):974-80 [10763947] J Rheumatol. 2001 Mar;28(3):490-5 [11296947] Ann Intern Med. 2001 May 1;134(9 Pt 2):860-8 [11346322] J Invest Dermatol. 2001 Aug;117(2):309-17 [11511309] Gut. 2002 Jul;51 Suppl 1:i41-4 [12077063] Cytokine Growth Factor Rev. 2002 Aug-Oct;13(4-5):323-40 [12220547] Gut. 2002 Oct;51(4):507-13 [12235072] N Engl J Med. 2003 Nov 27;349(22):2136-46 [14645642] Lab Invest. 1971 Sep;25(3):220-9 [4106224] Best Pract Res Clin Gastroenterol. 2004 Aug;18(4):641-61 [15324705] Neurogastroenterol Motil. 2004 Apr;16 Suppl 1:137-42 [15066020] J Health Soc Behav. 1983 Dec;24(4):385-96 [6668417] J Immunol. 1986 May 1;136(9):3317-23 [3007615] Ann N Y Acad Sci. 1990;597:81-91 [2201245] Behav Med. 1991 Fall;17(3):101-10 [1932843] Dig Dis Sci. 1993 Sep;38(9):1569-80 [8359066] Psychosom Med. 1998 May-Jun;60(3):362-5 [9625226] Am J Physiol. 1998 Nov;275(5 Pt 1):G1037-44 [9815034] Am J Physiol. 1999 Aug;277(2 Pt 1):G391-9 [10444454] Curr Gastroenterol Rep. 2005 Aug;7(4):257-63 [16042908] Gut. 2005 Oct;54(10):1481-91 [16162953] Clin Drug Investig. 2007;27(1):15-33 [17177577] N1 - Last updated - 2017-01-19 ER - TY - JOUR T1 - Role of TSH in the spontaneous development of asymmetrical thyroid carcinoma in mice with a targeted mutation in a single allele of the thyroid hormone-β receptor. AN - 1074763912; 22919057 AB - Mutations of the thyroid hormone receptor-β gene (THRB) cause resistance to thyroid hormone (RTH). A mouse model of RTH harboring a homozygous thyroid hormone receptor (TR)-β mutation known as PV (Thrb(PV/PV) mouse) spontaneously develops follicular thyroid cancer (FTC). Similar to RTH patients with mutations of two alleles of the THRB gene, the Thrb(PV/PV) mouse exhibits elevated thyroid hormones accompanied by highly nonsuppressible TSH. However, the heterozygous Thrb(PV/+) mouse with mildly elevated TSH (~2-fold) does not develop FTC. The present study examined whether the mutation of a single allele of the Thrb gene is sufficient to induce FTC in Thrb(PV/+) mice under stimulation by high TSH. Thrb(PV/+) mice and wild-type siblings were treated with propylthiouracil (PTU) to elevate serum TSH. Thrb(PV/+)mice treated with PTU (Thrb(PV/+)-PTU) spontaneously developed FTC similar to human thyroid cancer, but wild-type siblings treated with PTU did not. Interestingly, approximately 33% of Thrb(PV/+)-PTU mice developed asymmetrical thyroid tumors, as is frequently observed in human thyroid cancer. Molecular analyses showed activation of the cyclin 1-cyclin-dependent kinase-4-transcription factor E2F1 pathway to increase thyroid tumor cell proliferation of Thrb(PV/+)-PTU mice. Moreover, via extranuclear signaling, the PV also activated the integrin-Src-focal adhesion kinase-AKT-metalloproteinase pathway to increase migration and invasion of tumor cells. Therefore, mutation of a single allele of the Thrb gene is sufficient to drive the TSH-simulated hyperplastic thyroid follicular cells to undergo carcinogenesis. The present study suggests that the Thrb(PV/+)-PTU mouse model potentially could be used to gain insights into the molecular basis underlying the association between thyroid cancer and RTH seen in some affected patients. JF - Endocrinology AU - Zhao, Li AU - Zhu, Xuguang AU - Won Park, Jeong AU - Fozzatti, Laura AU - Willingham, Mark AU - Cheng, Sheue-yann AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892-4264, USA. Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 5090 EP - 5100 VL - 153 IS - 10 KW - Thyroid Hormone Receptors beta KW - 0 KW - Thyroid Hormones KW - Thyrotropin KW - 9002-71-5 KW - Cyclin-Dependent Kinases KW - EC 2.7.11.22 KW - Abridged Index Medicus KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Cyclin-Dependent Kinases -- genetics KW - Animals KW - Alleles KW - Signal Transduction -- genetics KW - Mice KW - Cell Proliferation KW - Thyroid Hormones -- blood KW - Mutation KW - Thyrotropin -- genetics KW - Thyroid Neoplasms -- genetics KW - Carcinoma -- pathology KW - Thyroid Gland -- pathology KW - Thyroid Neoplasms -- pathology KW - Thyroid Hormone Receptors beta -- genetics KW - Carcinoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1074763912?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Role+of+TSH+in+the+spontaneous+development+of+asymmetrical+thyroid+carcinoma+in+mice+with+a+targeted+mutation+in+a+single+allele+of+the+thyroid+hormone-%CE%B2+receptor.&rft.au=Zhao%2C+Li%3BZhu%2C+Xuguang%3BWon+Park%2C+Jeong%3BFozzatti%2C+Laura%3BWillingham%2C+Mark%3BCheng%2C+Sheue-yann&rft.aulast=Zhao&rft.aufirst=Li&rft.date=2012-10-01&rft.volume=153&rft.issue=10&rft.spage=5090&rft.isbn=&rft.btitle=&rft.title=Endocrinology&rft.issn=1945-7170&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-12-11 N1 - Date created - 2012-09-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2006 Feb 7;103(6):1780-5 [16446424] Mol Cell Biol. 2005 Jan;25(1):124-35 [15601836] J Clin Invest. 2006 Nov;116(11):2972-84 [17039256] Biochim Biophys Acta. 2007 Jan;1775(1):163-80 [17084981] Carcinogenesis. 2007 May;28(5):932-9 [17127711] Histol Histopathol. 2008 May;23(5):629-50 [18283648] Mol Cell Biol. 2008 Jul;28(14):4598-608 [18474620] Curr Opin Pharmacol. 2008 Aug;8(4):427-32 [18625340] Clin Endocrinol (Oxf). 2009 Sep;71(3):434-9 [19067720] Nat Rev Clin Oncol. 2009 Oct;6(10):587-95 [19787002] Endocr Relat Cancer. 2009 Dec;16(4):1251-60 [19528244] Endocr Relat Cancer. 2009 Dec;16(4):1065-72 [19620248] Endocrinology. 2010 Apr;151(4):1929-39 [20133453] IUBMB Life. 2010 Apr;62(4):268-76 [20101634] Oncogene. 2010 Apr 1;29(13):1909-19 [20062085] J Korean Med Sci. 2010 Sep;25(9):1368-71 [20808683] Thyroid. 2011 Jul;21(7):793-7 [21649470] Steroids. 2011 Aug;76(9):885-91 [21473875] Adv Drug Deliv Rev. 2011 Jul 18;63(8):610-5 [21118706] Arq Bras Endocrinol Metabol. 2012 Feb;56(1):67-71 [22460197] J Clin Endocrinol Metab. 2012 Apr;97(4):1134-45 [22278420] J Clin Endocrinol Metab. 2012 Apr;97(4):1328-36 [22319036] Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13209-14 [11069286] Cancer Res. 2001 Aug 15;61(16):6105-11 [11507060] Science. 2001 Nov 23;294(5547):1708-12 [11721053] Thyroid. 2002 Nov;12(11):963-9 [12490073] EMBO J. 2003 Jun 16;22(12):3102-12 [12805224] Carcinogenesis. 2003 Sep;24(9):1467-79 [12869418] Cancer Res. 2003 Sep 1;63(17):5274-80 [14500358] Endocrinology. 1991 May;128(5):2601-9 [1708338] Mol Endocrinol. 1991 Mar;5(3):327-35 [1653889] J Clin Endocrinol Metab. 1991 Nov;73(5):990-4 [1682340] J Clin Invest. 1991 Dec;88(6):2123-30 [1661299] Endocr Rev. 1993 Jun;14(3):348-99 [8319599] Mol Endocrinol. 1994 Nov;8(11):1450-4 [7877614] Ann Intern Med. 1995 Oct 15;123(8):572-83 [7677297] Mol Cell Biol. 1996 Oct;16(10):5623-33 [8816475] Int J Biochem Cell Biol. 1997 Jul;29(7):929-34 [9375372] Oncogene. 2006 May 4;25(19):2736-47 [16314832] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Prevalence of α1-antitrypsin deficiency alleles PI*S and PI*Z worldwide and effective screening for each of the five phenotypic classes PI*MS, PI*MZ, PI*SS, PI*SZ, and PI*ZZ: a comprehensive review. AN - 1069209608; 22933512 AB - Genetic epidemiological studies on the prevalence and numbers of individuals with α1-antitrypsin deficiency in each of 97 countries worldwide were used to estimate the numbers in each of the five following phenotypic classes: PI*MS, PI*MZ, PI*SS, PI*SZ, and PI*ZZ. These 97 countries were then grouped into 10 major geographic regions to make it possible to compare the numbers in each of these five phenotypic classes in immediately adjacent countries. Such groupings also make it possible to review the spread of the PI*S and PI*Z alleles from one major geographic grouping to another in the world as well as the spread of these two deficiency alleles within a major geographic region. The data in the 10 tables on the numbers in each of the five phenotypic classes in the countries in the same geographic region as well as the prevalence of the PI*S and PI*Z alleles in countries in the same geographic region provide a novel database for the identification of large numbers of individuals in a given phenotypic class. The database also provides useful information for the identification of countries with high numbers of PI*ZZ individuals for augmentation therapy within a given geographic region. JF - Therapeutic advances in respiratory disease AU - de Serres, Frederick J AU - Blanco, Ignacio AD - Center for Evaluation of Risks to Human Reproduction, National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709-2233, USA. deserres@bellsouth.net Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 277 EP - 295 VL - 6 IS - 5 KW - SERPINA1 protein, human KW - 0 KW - alpha 1-Antitrypsin KW - Index Medicus KW - Phenotype KW - Global Health KW - Alleles KW - Gene Frequency KW - Molecular Epidemiology KW - Humans KW - Prevalence KW - alpha 1-Antitrypsin -- genetics KW - Databases, Genetic KW - alpha 1-Antitrypsin Deficiency -- genetics KW - alpha 1-Antitrypsin Deficiency -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1069209608?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+advances+in+respiratory+disease&rft.atitle=Prevalence+of+%CE%B11-antitrypsin+deficiency+alleles+PI*S+and+PI*Z+worldwide+and+effective+screening+for+each+of+the+five+phenotypic+classes+PI*MS%2C+PI*MZ%2C+PI*SS%2C+PI*SZ%2C+and+PI*ZZ%3A+a+comprehensive+review.&rft.au=de+Serres%2C+Frederick+J%3BBlanco%2C+Ignacio&rft.aulast=de+Serres&rft.aufirst=Frederick&rft.date=2012-10-01&rft.volume=6&rft.issue=5&rft.spage=277&rft.isbn=&rft.btitle=&rft.title=Therapeutic+advances+in+respiratory+disease&rft.issn=1753-4666&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-02-20 N1 - Date created - 2012-09-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Ceruloplasmin (ferroxidase) oxidizes hydroxylamine probes: deceptive implications for free radical detection. AN - 1069205619; 22824865 AB - Ceruloplasmin (ferroxidase) is a copper-binding protein known to promote Fe(2+) oxidation in plasma of mammals. In addition to its classical ferroxidase activity, ceruloplasmin is known to catalyze the oxidation of various substrates, such as amines and catechols. Assays based on cyclic hydroxylamine oxidation are used to quantify and detect free radicals in biological samples ex vivo and in vitro. We show here that human ceruloplasmin promotes the oxidation of the cyclic hydroxylamine 1-hydroxy-3-carboxy-2,2,5,5-tetramethylpyrrolidine hydrochloride (CPH) and related probes in Chelex-treated phosphate buffer and rat serum. The reaction is suppressed by the metal chelators DTPA, EDTA, and desferal, whereas heparin and bathocuproine have no effect. Catalase or superoxide dismutase additions do not interfere with the CPH-oxidation yield, demonstrating that oxygen-derived free radicals are not involved in the CPH oxidation mediated by ceruloplasmin. Plasma samples immunodepleted of ceruloplasmin have lower levels of CPH oxidation, which confirms the role of ceruloplasmin (ferroxidase) as a biological oxidizing agent of cyclic hydroxylamines. In conclusion, we show that the ferroxidase activity of ceruloplasmin is a possible biological source of artifacts in the cyclic hydroxylamine-oxidation assay used for reactive oxygen species detection and quantification. Published by Elsevier Inc. JF - Free radical biology & medicine AU - Ganini, Douglas AU - Canistro, Donatella AU - Jiang, JinJie AU - Jang, JinJie AU - Stadler, Krisztian AU - Mason, Ronald P AU - Kadiiska, Maria B AD - Free Radical Metabolism Section, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Y1 - 2012/10/01/ PY - 2012 DA - 2012 Oct 01 SP - 1514 EP - 1521 VL - 53 IS - 7 KW - Chelating Agents KW - 0 KW - Free Radicals KW - Hydroxylamines KW - Oxidants KW - Phenanthrolines KW - Pentetic Acid KW - 7A314HQM0I KW - Heparin KW - 9005-49-6 KW - Edetic Acid KW - 9G34HU7RV0 KW - bathocuproine KW - 9THP2V94FX KW - Catalase KW - EC 1.11.1.6 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Ceruloplasmin KW - EC 1.16.3.1 KW - Deferoxamine KW - J06Y7MXW4D KW - Index Medicus KW - Animals KW - Artifacts KW - Humans KW - Pentetic Acid -- chemistry KW - Heparin -- chemistry KW - Oxidation-Reduction KW - Rats KW - Chelating Agents -- chemistry KW - Phenanthrolines -- chemistry KW - Deferoxamine -- chemistry KW - Superoxide Dismutase -- chemistry KW - Catalase -- chemistry KW - Edetic Acid -- chemistry KW - Ceruloplasmin -- chemistry KW - Hydroxylamines -- chemistry KW - Oxidants -- chemistry KW - Biological Assay KW - Free Radicals -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1069205619?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Ceruloplasmin+%28ferroxidase%29+oxidizes+hydroxylamine+probes%3A+deceptive+implications+for+free+radical+detection.&rft.au=Ganini%2C+Douglas%3BCanistro%2C+Donatella%3BJiang%2C+JinJie%3BJang%2C+JinJie%3BStadler%2C+Krisztian%3BMason%2C+Ronald+P%3BKadiiska%2C+Maria+B&rft.aulast=Ganini&rft.aufirst=Douglas&rft.date=2012-10-01&rft.volume=53&rft.issue=7&rft.spage=1514&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2012.07.013 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-03-11 N1 - Date created - 2012-09-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Clin Rheumatol. 2005 Aug;24(4):331-5 [15583971] J Zhejiang Univ Sci B. 2005 Nov;6(11):1045-56 [16252337] Clin Biochem. 2005 Dec;38(12):1103-11 [16214125] Clin Chim Acta. 2006 Mar;365(1-2):330-6 [16274685] Biometals. 2006 Feb;19(1):1-5 [16502325] Clin Chim Acta. 2006 Jun;368(1-2):53-76 [16483560] Circulation. 2006 Jun 20;113(24):2818-25 [16769910] Nat Chem Biol. 2006 Sep;2(9):486-93 [16906150] Schizophr Res. 2006 Sep;86(1-3):167-71 [16842975] Chest. 2006 Oct;130(4):1276; 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AN - 1041324598; 22988867 AB - Mutations in LRRK2 (leucine-rich repeat kinase 2) are a relatively common cause of inherited PD (Parkinson's disease), but the mechanism(s) by which mutations lead to disease are poorly understood. In the present paper, I discuss what is known about LRRK2 in cellular models, focusing specifically on assays that have been used to tease apart the effects of LRRK2 mutations on cellular phenotypes. LRRK2 expression has been suggested to cause loss of neuronal viability, although because it also has a strong effect on the length of neurites on these cells, whether this is true toxicity or not is unclear. Also, LRRK2 mutants can promote the redistribution of LRRK2 from diffuse cytosolic staining to more discrete structures, at least at high expression levels achieved in transfection experiments. The relevance of these phenotypes for PD is not yet clear, and a great deal of work is needed to understand them in more depth. JF - Biochemical Society transactions AU - Cookson, Mark R AD - Cell Biology and Gene Expression Unit, Laboratory of Neurogenetics, National Institute on Aging, 35 Convent Drive, Bethesda, MD 20892-3707, USA. cookson@mail.nih.gov Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 1070 EP - 1073 VL - 40 IS - 5 KW - LRRK2 protein, human KW - EC 2.7.11.1 KW - Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 KW - Protein-Serine-Threonine Kinases KW - Index Medicus KW - Phenotype KW - Humans KW - Protein-Serine-Threonine Kinases -- metabolism KW - Parkinson Disease -- metabolism KW - Protein-Serine-Threonine Kinases -- genetics KW - Mutation KW - Parkinson Disease -- pathology KW - Parkinson Disease -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1041324598?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Society+transactions&rft.atitle=Cellular+effects+of+LRRK2+mutations.&rft.au=Cookson%2C+Mark+R&rft.aulast=Cookson&rft.aufirst=Mark&rft.date=2012-10-01&rft.volume=40&rft.issue=5&rft.spage=1070&rft.isbn=&rft.btitle=&rft.title=Biochemical+Society+transactions&rft.issn=1470-8752&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-02-26 N1 - Date created - 2012-09-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Physiol Rev. 2011 Oct;91(4):1161-218 [22013209] J Neuropathol Exp Neurol. 2009 Jul;68(7):785-96 [19535993] Hum Mol Genet. 2012 Feb 1;21(3):511-25 [22012985] Hum Mol Genet. 2012 Feb 15;21(4):890-9 [22080837] PLoS One. 2012;7(1):e30834 [22303461] Hum Mol Genet. 2012 Mar 15;21(6):1350-63 [22171073] PLoS Genet. 2012;8(2):e1002526 [22363216] Mol Neurodegener. 2012;7:2 [22230652] J Neurosci. 2012 Mar 14;32(11):3877-86 [22423108] Neurodegener Dis. 2012;10(1-4):238-41 [22204929] EMBO Mol Med. 2012 May;4(5):380-95 [22407749] Nat Rev Mol Cell Biol. 2012 Jul;13(7):463-70 [22722608] Biochem J. 2012 Aug 15;446(1):99-111 [22612223] Parkinsonism Relat Disord. 2012 Aug;18(7):819-23 [22525366] Ann Neurol. 2005 Jun;57(6):918-21 [15880653] Neurobiol Dis. 2006 Aug;23(2):329-41 [16750377] Nat Neurosci. 2006 Oct;9(10):1231-3 [16980962] Neuron. 2006 Nov 22;52(4):587-93 [17114044] Ann Neurol. 2006 Nov;60(5):557-69 [17120249] Hum Mol Genet. 2007 Jan 15;16(2):223-32 [17200152] Hum Mol Genet. 2007 Jun 1;16(11):1319-26 [17409193] J Neurochem. 2008 May;105(3):1048-56 [18182054] J Neurosci Res. 2008 Jun;86(8):1711-20 [18214993] Exp Cell Res. 2008 Jun 10;314(10):2055-65 [18445495] Neuron. 2004 Nov 18;44(4):595-600 [15541308] Trends Cell Biol. 2000 Dec;10(12):524-30 [11121744] Proc Natl Acad Sci U S A. 2009 Feb 24;106(8):2897-902 [19196961] Neuron. 2004 Nov 18;44(4):601-7 [15541309] Biol Rev Camb Philos Soc. 2009 Aug;84(3):431-48 [19659885] Proc Natl Acad Sci U S A. 2009 Aug 25;106(34):14622-7 [19667187] J Neurochem. 2009 Sep;110(5):1514-22 [19545277] J Neuropathol Exp Neurol. 2009 Sep;68(9):994-1005 [19680143] Neuroscience. 2009 Oct 6;163(2):533-9 [19559761] Hum Mol Genet. 2009 Nov 1;18(21):4022-34 [19640926] Biochim Biophys Acta. 2009 Dec;1792(12):1194-7 [19781641] PLoS One. 2009;4(12):e8463 [20041156] Curr Opin Cell Biol. 2010 Apr;22(2):150-6 [20036114] Proc Natl Acad Sci U S A. 2010 May 25;107(21):9879-84 [20457918] Biochem J. 2010 Sep 15;430(3):405-13 [20659021] Nat Med. 2010 Sep;16(9):998-1000 [20729864] Nat Rev Neurosci. 2010 Dec;11(12):791-7 [21088684] Parkinsonism Relat Disord. 2010 Dec;16(10):650-5 [20850369] J Neurosci. 2011 Jan 19;31(3):907-12 [21248115] PLoS One. 2011;6(4):e18568 [21494637] J Biol Chem. 2011 May 6;286(18):16140-9 [21454543] J Neural Transm (Vienna). 2011 May;118(5):795-808 [21552986] Hum Mol Genet. 2011 Nov 1;20(21):4209-23 [21828077] Parkinsonism Relat Disord. 2012 Jan;18 Suppl 1:S186-9 [22166430] N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Promoter-proximal pausing of RNA polymerase II: emerging roles in metazoans. AN - 1041142836; 22986266 AB - Recent years have witnessed a sea change in our understanding of transcription regulation: whereas traditional models focused solely on the events that brought RNA polymerase II (Pol II) to a gene promoter to initiate RNA synthesis, emerging evidence points to the pausing of Pol II during early elongation as a widespread regulatory mechanism in higher eukaryotes. Current data indicate that pausing is particularly enriched at genes in signal-responsive pathways. Here the evidence for pausing of Pol II from recent high-throughput studies will be discussed, as well as the potential interconnected functions of promoter-proximally paused Pol II. JF - Nature reviews. Genetics AU - Adelman, Karen AU - Lis, John T AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA. adelmank@niehs.nih.gov Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 720 EP - 731 VL - 13 IS - 10 KW - RNA Polymerase II KW - EC 2.7.7.- KW - Index Medicus KW - Regulatory Sequences, Nucleic Acid -- genetics KW - Protein Binding -- physiology KW - Animals KW - Humans KW - Regulatory Sequences, Nucleic Acid -- physiology KW - Models, Biological KW - Transcription, Genetic -- physiology KW - Gene Expression Regulation -- genetics KW - Binding Sites KW - RNA Polymerase II -- physiology KW - RNA Polymerase II -- metabolism KW - Promoter Regions, Genetic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1041142836?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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.+Genetics&rft.atitle=Promoter-proximal+pausing+of+RNA+polymerase+II%3A+emerging+roles+in+metazoans.&rft.au=Adelman%2C+Karen%3BLis%2C+John+T&rft.aulast=Adelman&rft.aufirst=Karen&rft.date=2012-10-01&rft.volume=13&rft.issue=10&rft.spage=720&rft.isbn=&rft.btitle=&rft.title=Nature+reviews.+Genetics&rft.issn=1471-0064&rft_id=info:doi/10.1038%2Fnrg3293 LA - 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Last updated - 2017-01-18 DO - http://dx.doi.org/10.1038/nrg3293 ER - TY - JOUR T1 - Parameterizing dose-response models to estimate relative potency functions directly. AN - 1041139877; 22700543 AB - Many comparative analyses of toxicity assume that the potency of a test chemical relative to a reference chemical is constant, but employing such a restrictive assumption uncritically may generate misleading conclusions. Recent efforts to characterize non-constant relative potency rely on relative potency functions and estimate them secondarily after fitting dose-response models for the test and reference chemicals. We study an alternative approach of specifying a relative potency model a priori and estimating it directly using the dose-response data from both chemicals. We consider a power function in dose as a relative potency model and find that it keeps the two chemicals' dose-response functions within the same family of models for families typically used in toxicology. When differences in the response limits for the test and reference chemicals are attributable to the chemicals themselves, the older two-stage approach is the more convenient. When differences in response limits are attributable to other features of the experimental protocol or when response limits do not differ, the direct approach is straightforward to apply with nonlinear regression methods and simplifies calculation of simultaneous confidence bands. We illustrate the proposed approach using Hill models with dose-response data from U.S. National Toxicology Program bioassays. Though not universally applicable, this method of estimating relative potency functions directly can be profitably applied to a broad family of dose-response models commonly used in toxicology. JF - Toxicological sciences : an official journal of the Society of Toxicology AU - Dinse, Gregg E AU - Umbach, David M AD - Biostatistics Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA. dinse@niehs.nih.gov Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 447 EP - 455 VL - 129 IS - 2 KW - Index Medicus KW - Dose-Response Relationship, Drug KW - Toxicity Tests KW - Models, Theoretical UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1041139877?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Parameterizing+dose-response+models+to+estimate+relative+potency+functions+directly.&rft.au=Dinse%2C+Gregg+E%3BUmbach%2C+David+M&rft.aulast=Dinse&rft.aufirst=Gregg&rft.date=2012-10-01&rft.volume=129&rft.issue=2&rft.spage=447&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%2Fkfs209 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-02-14 N1 - Date created - 2012-09-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biometrics. 1965 Dec;21(4):785-98 [5857228] Am J Physiol. 1978 Aug;235(2):E97-102 [686171] Toxicol Appl Pharmacol. 2000 Sep 15;167(3):157-72 [10986007] J Pharmacol Exp Ther. 1964 May;144:143-9 [14183424] Regul Toxicol Pharmacol. 2011 Aug;60(3):342-53 [21601607] FASEB J. 1988 Mar 1;2(3):209-15 [3350235] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/toxsci/kfs209 ER - TY - JOUR T1 - Three murine leukemia virus integration regions within 100 kilobases upstream of c-myb are proximal to the 5' regulatory region of the gene through DNA looping. AN - 1039203691; 22811527 AB - Retroviruses integrated into genomic DNA participate in long-range gene activation from as far away as several hundred kilobases. Hypotheses have been put forth to account for these phenomena, but data have not been provided to support a physical mechanism that explains long-range activation. In murine leukemia virus-induced myeloid leukemia in mice, integrated proviruses have been found upstream of c-myb in three regions, named Mml1, Mml2, and Mml3 (25, 50, and 70 kb upstream, respectively). The transcription factor c-Myb is an oncogene whose dysregulation and/or mutation can lead to human leukemia. We hypothesized that the murine c-myb upstream region contains regulatory elements accessed by the retrovirus. To identify regulatory sites in the murine c-myb upstream region, we looked by chromatin immunoprecipitation with microarray technology (ChIP-on-chip) for histone modifications implicating gene activation in normal cells. H3K4me3, H3K4me1, and H3K9/14ac were enriched at Mml1 and/or Mml2 in the myeloblastic cell line M1, which expresses c-myb. The enrichment of all of these histone marks decreased with differentiation-induced downregulation of the gene in M1 cells but increased and spread in tumor cells containing integrated provirus. Importantly, using chromosome conformation capture (3C)-quantitative PCR assays, interactions between the 5' region, including the promoter and all Mml sites (Mml1, Mml2, and Mml3), were detected due to DNA looping in M1 cells and tumor cells with provirus in Mml1, Mml2, or Mml3. Therefore, our study provides a new mechanism of retrovirus insertional mutagenesis whereby spatial chromatin organization allows distally located provirus, with its own enhancer elements, to access the 5' regulatory region of the gene. JF - Journal of virology AU - Zhang, Junfang AU - Markus, Jan AU - Bies, Juraj AU - Paul, Thomas AU - Wolff, Linda AD - Laboratory of Cellular Oncology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland, USA. Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 10524 EP - 10532 VL - 86 IS - 19 KW - Chromatin KW - 0 KW - Histones KW - Proto-Oncogene Proteins c-myb KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Retroviridae -- metabolism KW - 3T3 Cells KW - Animals KW - Chromatin -- metabolism KW - Genes, myb KW - DNA -- metabolism KW - Cell Differentiation KW - Cell Line, Tumor KW - Mice KW - Models, Biological KW - Mutagenesis KW - Enhancer Elements, Genetic KW - Histones -- metabolism KW - Polymerase Chain Reaction -- methods KW - Chromatin Immunoprecipitation KW - Leukemia Virus, Murine -- genetics KW - Proto-Oncogene Proteins c-myb -- genetics KW - Gene Expression Regulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1039203691?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Three+murine+leukemia+virus+integration+regions+within+100+kilobases+upstream+of+c-myb+are+proximal+to+the+5%27+regulatory+region+of+the+gene+through+DNA+looping.&rft.au=Zhang%2C+Junfang%3BMarkus%2C+Jan%3BBies%2C+Juraj%3BPaul%2C+Thomas%3BWolff%2C+Linda&rft.aulast=Zhang&rft.aufirst=Junfang&rft.date=2012-10-01&rft.volume=86&rft.issue=19&rft.spage=10524&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=1098-5514&rft_id=info:doi/10.1128%2FJVI.01077-12 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-11-29 N1 - Date created - 2012-09-11 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - GSE34770; GEO N1 - SuppNotes - Cited By: J Virol. 1987 Dec;61(12):3721-5 [2824810] Science. 1987 Sep 18;237(4821):1473-6 [3498214] Oncogene. 1989 May;4(5):583-92 [2471131] Proc Natl Acad Sci U S A. 1989 Oct;86(19):7326-30 [2678098] J Virol. 1991 Jul;65(7):3607-16 [1645785] Proc Natl Acad Sci U S A. 1993 Feb 15;90(4):1619-23 [7679511] Virology. 1996 Oct 1;224(1):224-34 [8862417] Oncogene. 1997 Apr 10;14(14):1715-23 [9135073] Crit Rev Oncog. 1996;7(3-4):245-60 [9258605] PLoS Pathog. 2006 Jun;2(6):e60 [16789841] Genes Dev. 2006 Sep 1;20(17):2349-54 [16951251] Genes Chromosomes Cancer. 2006 Dec;45(12):1143-54 [16977606] Mol Cell Biol. 2006 Nov;26(21):7953-65 [16940183] Nat Genet. 2007 Mar;39(3):311-8 [17277777] Nat Genet. 2007 May;39(5):593-5 [17435759] Cell. 2007 May 18;129(4):823-37 [17512414] Cancer Res. 2007 Jun 1;67(11):5148-55 [17545593] Genome Res. 2007 Jun;17(6):691-707 [17567990] Nat Protoc. 2007;2(7):1722-33 [17641637] Blood. 2007 Aug 15;110(4):1251-61 [17452517] Proc Natl Acad Sci U S A. 2007 Aug 21;104(34):13762-7 [17690249] Nat Rev Cancer. 2008 Jul;8(7):523-34 [18574464] Hum Gene Ther. 2008 Jun;19(6):557-68 [18533894] Semin Immunol. 2008 Aug;20(4):247-56 [18585056] Rev Med Virol. 2008 Nov-Dec;18(6):387-405 [18729235] Proc Natl Acad Sci U S A. 2008 Dec 23;105(51):20398-403 [19074263] Nature. 2009 May 7;459(7243):108-12 [19295514] Cell. 2009 Jun 26;137(7):1194-211 [19563753] Blood. 2009 Aug 6;114(6):1254-62 [19528534] Cell. 2009 Sep 4;138(5):1019-31 [19698979] Proc Natl Acad Sci U S A. 2009 Dec 22;106(51):21689-94 [19955420] Nat Genet. 2010 Apr;42(4):282-4 [20348962] Blood. 2010 Apr 15;115(15):3098-108 [20190193] Nature. 2010 Sep 23;467(7314):430-5 [20720539] EMBO J. 2012 Feb 15;31(4):986-99 [22157820] Cell. 2007 Feb 23;128(4):693-705 [17320507] Mol Cell Biol. 2000 Mar;20(6):1970-81 [10688644] Science. 2002 Feb 15;295(5558):1306-11 [11847345] J Gen Virol. 2002 Apr;83(Pt 4):819-27 [11907331] Cell. 1981 Feb;23(2):323-34 [6258798] Cell. 1984 Nov;39(1):223-32 [6091913] J Immunol. 1988 Jul 15;141(2):681-9 [2838552] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1128/JVI.01077-12 ER - TY - JOUR T1 - Alcohol consumption and premotor corpus callosum in older adults. AN - 1036881906; 22401959 AB - Heavy alcohol consumption is toxic to the brain, especially to the frontal white matter (WM), but whether lesser amounts of alcohol negatively impact the brain WM is unclear. In this study, we examined the relationship between self-reported alcohol consumption and regional WM and grey matter (GM) volume in fifty-six men and thirty-seven women (70+- 7years) cognitively intact participants of the Baltimore Longitudinal Study of Aging (BLSA) with no history of alcohol abuse. We used regional analysis of volumes examined in normalized space (RAVENS) maps methodology for WM and GM segmentation and normalization followed by voxel based morphometry (VBM) implemented in SPM8 to examine the cross-sectional association between alcohol consumption and regional WM (and, separately, GM) volume controlling for age, sex, smoking, blood pressure and dietary thiamine intake. WM VBM revealed that in men, but not in women, higher alcohol consumption was associated with lower volume in premotor frontal corpus callosum. This finding suggests that even moderate amounts of alcohol may be detrimental to corpus callosum and white matter integrity. Published by Elsevier B.V. JF - European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology AU - Kapogiannis, Dimitrios AU - Kisser, Jason AU - Davatzikos, Christos AU - Ferrucci, Luigi AU - Metter, Jeffrey AU - Resnick, Susan M AD - National Institute on Aging/National Institutes of Health (NIA/NIH), Clinical Research Branch, 3001 South Hanover St., Baltimore, MD 21225, USA. kapogiannisd@mail.nih.gov Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 704 EP - 710 VL - 22 IS - 10 KW - Index Medicus KW - Severity of Illness Index KW - Magnetic Resonance Imaging KW - Neuroimaging KW - Sex Characteristics KW - Humans KW - Aged KW - Organ Specificity KW - Longitudinal Studies KW - Organ Size KW - Self Report KW - Baltimore KW - Imaging, Three-Dimensional KW - Cohort Studies KW - Middle Aged KW - Female KW - Male KW - Alcohol-Related Disorders -- physiopathology KW - Corpus Callosum -- pathology KW - Alcohol Drinking -- pathology KW - Aging KW - Alcohol Drinking -- adverse effects KW - Alcohol-Related Disorders -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1036881906?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neuropsychopharmacology+%3A+the+journal+of+the+European+College+of+Neuropsychopharmacology&rft.atitle=Alcohol+consumption+and+premotor+corpus+callosum+in+older+adults.&rft.au=Kapogiannis%2C+Dimitrios%3BKisser%2C+Jason%3BDavatzikos%2C+Christos%3BFerrucci%2C+Luigi%3BMetter%2C+Jeffrey%3BResnick%2C+Susan+M&rft.aulast=Kapogiannis&rft.aufirst=Dimitrios&rft.date=2012-10-01&rft.volume=22&rft.issue=10&rft.spage=704&rft.isbn=&rft.btitle=&rft.title=European+neuropsychopharmacology+%3A+the+journal+of+the+European+College+of+Neuropsychopharmacology&rft.issn=1873-7862&rft_id=info:doi/10.1016%2Fj.euroneuro.2012.02.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-18 N1 - Date created - 2012-08-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Comput Assist Tomogr. 1998 Sep-Oct;22(5):827-37 [9754125] J Neuropathol Exp Neurol. 1998 Feb;57(2):101-10 [9600202] Neuropsychopharmacology. 2005 Feb;30(2):423-32 [15562292] Curr Opin Pharmacol. 2005 Feb;5(1):73-8 [15661629] Alcohol Clin Exp Res. 2005 Apr;29(4):656-63 [15834232] Neuroreport. 2005 May 31;16(8):795-8 [15891572] Alcohol Clin Exp Res. 2005 May;29(5):896-901 [15897736] Neuroimage. 2005 Jun;26(2):536-45 [15907310] Cereb Cortex. 2005 Sep;15(9):1384-92 [15635059] Alcohol Clin Exp Res. 2005 Sep;29(9):1698-705 [16205370] Neurology. 2005 Oct 25;65(8):1210-7 [16247047] J Neuroimaging. 2005 Oct;15(4):367-72 [16254403] Neurology. 2006 Apr 25;66(8):1286; author reply 1286 [16636264] Neurobiol Aging. 2006 Jul;27(7):994-1009 [15964101] Alcohol Clin Exp Res. 2006 Jun;30(6):1045-50 [16737464] Neuroimage. 2006 Sep;32(3):989-94 [16854598] Brain. 2007 Jan;130(Pt 1):36-47 [17178742] Neuropsychopharmacology. 2007 Feb;32(2):429-38 [17047671] Dement Geriatr Cogn Disord. 2007;23(3):140-9 [17170526] Neuropsychopharmacology. 2007 Oct;32(10):2207-16 [17299515] Cereb Cortex. 2008 Jan;18(1):136-44 [17443018] Neuroimage. 2008 Aug 1;42(1):60-9 [18502665] Neuroimage. 2009 Feb 15;44(4):1415-22 [19027862] Alcohol Alcohol. 2009 Mar-Apr;44(2):136-40 [19147798] Rev Neurosci. 2008;19(6):451-66 [19317183] Am J Drug Alcohol Abuse. 2009;35(2):55-8 [19322728] Biol Psychiatry. 2009 Apr 15;65(8):680-90 [19103436] Neuroimage. 2009 Jun;46(2):505-10 [19233298] J Alzheimers Dis. 2009;17(1):7-31 [19494429] Am J Geriatr Psychiatry. 2009 Jul;17(7):542-55 [19546653] Neuroimage. 2011 Sep 1;58(1):16-25 [21704711] IEEE Trans Med Imaging. 1999 Sep;18(9):737-52 [10571379] J Stud Alcohol. 2000 Jan;61(1):55-63 [10627097] Neuropsychiatry Neuropsychol Behav Neurol. 2000 Jan;13(1):67-76 [10645739] J Neurol Neurosurg Psychiatry. 2000 Jun;68(6):731-7 [10811696] Cereb Cortex. 2000 May;10(5):464-72 [10847596] Neuroimage. 2000 Jun;11(6 Pt 1):805-21 [10860804] Am J Psychiatry. 2001 Feb;158(2):188-97 [11156800] Am J Psychiatry. 2001 Feb;158(2):198-204 [11156801] Alcohol Alcohol. 2001 Sep-Oct;36(5):357-68 [11524299] Stroke. 2001 Sep;32(9):1939-46 [11546878] Neuroimage. 2001 Dec;14(6):1361-9 [11707092] AJNR Am J Neuroradiol. 2001 Nov-Dec;22(10):1926-32 [11733327] IEEE Trans Med Imaging. 2002 Nov;21(11):1421-39 [12575879] JAMA. 2003 Mar 19;289(11):1405-13 [12636463] Neuropsychologia. 2004;42(2):257-71 [14644111] Stroke. 2004 Jan;35(1):16-21 [14657449] BMJ. 2004 Sep 4;329(7465):539 [15304383] J Neurol. 2004 Sep;251(9):1050-9 [15372245] Br J Addict. 1988 May;83(5):577-80 [3382816] Arch Neurol. 1988 Sep;45(9):990-2 [3415529] Arch Neurol. 1991 Sep;48(9):939-42 [1953418] Alcohol Clin Exp Res. 1993 Feb;17(1):2-11 [8452204] Metab Brain Dis. 1995 Mar;10(1):9-16 [7596332] Folia Neuropathol. 1995;33(1):25-9 [8673416] J Neurol Sci. 1997 Mar 10;146(2):145-51 [9077511] Neuroscience. 1997 Aug;79(4):983-98 [9219961] Cereb Cortex. 1998 Oct-Nov;8(7):635-40 [9823484] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.euroneuro.2012.02.003 ER - TY - JOUR T1 - The molecular basis for high affinity of a universal ligand for human bombesin receptor (BnR) family members. AN - 1036880080; 22828605 AB - There is increased interest in the Bn-receptor family because they are frequently over/ectopically expressed by tumors and thus useful as targets for imaging or receptor-targeted-cytotoxicity. The synthetic Bn-analog, [D-Tyr(6), β-Ala(11), Phe(13), Nle(14)]Bn(6-14) [Univ.Lig] has the unique property of having high affinity for all three human BNRs (GRPR, NMBR, BRS-3), and thus could be especially useful for this approach. However, the molecular basis of this property is unclear and is the subject of this study. To accomplish this, site-directed mutagenesis was used after identifying potentially important amino acids using sequence homology analysis of all BnRs with high affinity for Univ.Lig compared to the Cholecystokinin-receptor (CCK(A)R), which has low affinity. Using various criteria 74 amino acids were identified and 101 mutations made in GRPR by changing each to those of CCK(A)R or to alanine. 22 GRPR mutations showed a significant decrease in affinity for Univ.Lig (>2-fold) with 2 in EC2[D97N, G112V], 1 in UTM6[Y284A], 2 in EC4[R287N, H300S] showing >10-fold decrease in Univ.Lig affinity. Additional mutations were made to explore the molecular basis for these changes. Our results show that high affinity for Univ.Lig by human Bn-receptors requires positively charged amino acids in extracellular (EC)-domain 4 and to a lesser extent EC2 and EC3 suggesting charge-charge interactions may be particularly important for determining the general high affinity of this ligand. Furthermore, transmembrane amino acids particularly in UTM6 are important contributing both charge-charge interactions as well as interaction with a tyrosine residue in close proximity suggesting possible receptor-peptide cation-π or H-bonding interactions are also important for determining its high affinity. Published by Elsevier Inc. JF - Biochemical pharmacology AU - Uehara, Hirotsugu AU - Hocart, Simon J AU - González, Nieves AU - Mantey, Samuel A AU - Nakagawa, Tomoo AU - Katsuno, Tatsuro AU - Coy, David H AU - Jensen, Robert T AD - Digestive Diseases Branch, NIDDK, National Institutes of Health, Bethesda, MD 20892-1804, USA. Y1 - 2012/10/01/ PY - 2012 DA - 2012 Oct 01 SP - 936 EP - 948 VL - 84 IS - 7 KW - Ligands KW - 0 KW - Peptides KW - Receptors, Bombesin KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Animals KW - Humans KW - Molecular Sequence Data KW - Cell Membrane KW - Amino Acid Sequence KW - Cell Line KW - Protein Conformation KW - Cricetinae KW - Binding Sites KW - Peptides -- chemistry KW - Receptors, Bombesin -- metabolism KW - Receptors, Bombesin -- antagonists & inhibitors KW - Peptides -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1036880080?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+molecular+basis+for+high+affinity+of+a+universal+ligand+for+human+bombesin+receptor+%28BnR%29+family+members.&rft.au=Uehara%2C+Hirotsugu%3BHocart%2C+Simon+J%3BGonz%C3%A1lez%2C+Nieves%3BMantey%2C+Samuel+A%3BNakagawa%2C+Tomoo%3BKatsuno%2C+Tatsuro%3BCoy%2C+David+H%3BJensen%2C+Robert+T&rft.aulast=Uehara&rft.aufirst=Hirotsugu&rft.date=2012-10-01&rft.volume=84&rft.issue=7&rft.spage=936&rft.isbn=&rft.btitle=&rft.title=Biochemical+pharmacology&rft.issn=1873-2968&rft_id=info:doi/10.1016%2Fj.bcp.2012.07.010 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-11-01 N1 - Date created - 2012-08-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Science. 1996 Jan 12;271(5246):163-8 [8539615] J Biol Chem. 1996 Jan 26;271(4):1950-6 [8567643] Eur J Pharmacol. 1995 Dec 27;294(1):55-69 [8788416] J Cell Biochem Suppl. 1996;24:237-46 [8806106] Proc Natl Acad Sci U S A. 1996 Oct 1;93(20):10566-71 [8855218] J Biol Chem. 1996 Dec 13;271(50):32016-20 [8943250] Protein Eng. 1997 Feb;10(2):109-17 [9089810] Mol Pharmacol. 1997 May;51(5):721-32 [9145910] J Biol Chem. 1997 Jul 11;272(28):17405-9 [9211882] J Biol Chem. 1997 Oct 10;272(41):26062-71 [9325344] Nature. 1997 Nov 13;390(6656):165-9 [9367152] Mol Endocrinol. 1997 Dec;11(13):2048-53 [9415408] Mol Pharmacol. 1997 Dec;52(6):1087-94 [9415719] Electrophoresis. 1997 Dec;18(15):2714-23 [9504803] Eur J Pharmacol. 1998 Feb 19;343(2-3):275-87 [9570477] J Biol Chem. 1998 May 29;273(22):13613-24 [9593699] J Biol Chem. 1998 Jun 26;273(26):15927-32 [9632639] Mol Pharmacol. 1998 Aug;54(2):364-71 [9687578] Biochemistry. 1999 Jun 1;38(22):7307-20 [10353842] J Biol Chem. 1999 Jul 16;274(29):20457-64 [10400673] Proc Natl Acad Sci U S A. 1999 Aug 17;96(17):9459-64 [10449714] J Pharmacol Exp Ther. 1999 Sep;290(3):1202-11 [10454496] Biochem Pharmacol. 2005 Feb 15;69(4):579-93 [15670577] Cell Tissue Res. 2005 Apr;320(1):21-31 [15726424] J Pharmacol Exp Ther. 2006 Nov;319(2):980-9 [16943256] Biochemistry. 2006 Dec 5;45(48):14355-61 [17128974] Curr Opin Endocrinol Diabetes Obes. 2008 Feb;15(1):58-64 [18185064] J Pharmacol Exp Ther. 2008 Feb;324(2):463-74 [18006692] Pharmacol Rev. 2008 Mar;60(1):1-42 [18055507] Curr Opin Endocrinol Diabetes Obes. 2009 Feb;16(1):66-71 [19115523] Peptides. 2009 Aug;30(8):1473-86 [19463875] J Med Chem. 2009 Aug 13;52(15):4923-35 [19606869] J Pharmacol Exp Ther. 2009 Oct;331(1):265-76 [19628633] Endocr Relat Cancer. 2010 Mar;17(1):R53-73 [19995807] Peptides. 2010 Jan;31(1):130-8 [19874863] Cell Metab. 2010 Feb 3;11(2):101-12 [20096642] J Pharmacol Exp Ther. 2010 Apr;333(1):51-9 [20065020] Peptides. 2010 Aug;31(8):1569-78 [20438784] Curr Drug Deliv. 2011 Jan;8(1):79-134 [21034419] Nature. 2011 Jan 13;469(7329):241-4 [21228877] J Pharmacol Exp Ther. 2011 Feb;336(2):356-64 [21036912] Peptides. 2011 Aug;32(8):1685-99 [21729729] Endocrinology. 2011 Nov;152(11):4106-15 [21878513] Curr Opin Endocrinol Diabetes Obes. 2012 Feb;19(1):3-7 [22157398] Endocrinology. 2000 Mar;141(3):1236-44 [10698201] J Biol Chem. 2001 Jan 5;276(1):495-504 [11013243] J Biol Chem. 2001 Mar 23;276(12):9219-29 [11112777] Peptides. 2001 Apr;22(4):689-99 [11311741] J Biol Chem. 2001 Sep 28;276(39):36652-63 [11463790] Clin Cancer Res. 2002 Apr;8(4):1139-46 [11948125] Mol Pharmacol. 2002 Jun;61(6):1435-43 [12021405] Biochemistry. 2002 Jul 16;41(28):8954-60 [12102638] J Biol Chem. 2004 May 28;279(22):23580-9 [15016826] Genomics. 2004 Jul;84(1):139-46 [15203211] Br J Pharmacol. 1975 Oct;55(2):221-7 [1201380] Mol Pharmacol. 1989 Dec;36(6):840-7 [2557534] J Biol Chem. 1990 Sep 15;265(26):15695-703 [1697594] Am J Physiol. 1990 Sep;259(3 Pt 1):G468-73 [2169207] Neuron. 1991 Mar;6(3):421-30 [1848080] Trends Pharmacol Sci. 1991 Jan;12(1):13-9 [1706545] J Mol Biol. 1991 Mar 20;218(2):465-75 [2010920] J Biol Chem. 1992 Dec 25;267(36):25668-71 [1281470] Mol Pharmacol. 1992 Dec;42(6):1058-68 [1336112] J Biol Chem. 1993 Mar 15;268(8):5979-84 [8383682] J Biol Chem. 1993 Jul 15;268(20):14622-6 [8392057] J Biol Chem. 1993 Sep 25;268(27):20285-90 [8397203] Mol Pharmacol. 1993 Nov;44(5):934-9 [8246916] J Biol Chem. 1994 Jan 21;269(3):1610-3 [8294406] J Biol Chem. 1994 Apr 29;269(17):12383-6 [8175640] Biochem Biophys Res Commun. 1994 Jun 15;201(2):523-30 [8002982] Mol Pharmacol. 1994 Aug;46(2):235-45 [8078487] Mol Pharmacol. 1995 Jan;47(1):10-20 [7838118] Mol Pharmacol. 1995 Apr;47(4):660-5 [7536886] J Biol Chem. 1995 Apr 28;270(17):9702-5 [7730346] Proc Natl Acad Sci U S A. 1995 Jun 20;92(13):6205-9 [7597102] Eur J Biochem. 1995 Jul 1;231(1):266-70 [7628480] J Biol Chem. 1995 Jul 28;270(30):17884-91 [7629092] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.bcp.2012.07.010 ER - TY - JOUR T1 - Long-term toxicology and carcinogenicity of 2,4,6-trichlorophenol. AN - 1032608631; 22748215 AB - Carcinogenesis bioassays were conducted by giving 2,4,6-trichlorophenol [2,4,6-TCP] in feed to groups of 50 male and female Fischer rats and male B6C3F1 mice for two years. Dietary concentrations were 0 [20/group], 5000 [0.5%], or 10,000 [1%] ppm. Female mice began with 10,000 and 20,000 ppm but after 38 weeks were lowered due to reduced body weights to 2500 and 5000 ppm for 67 weeks; exposures averaged 5200 and 10,400 ppm. Adverse effects at two years were leukocytosis and monocytosis of peripheral blood and hyperplasia of bone marrow in both sexes of rats. In mice, liver toxicity, including individual liver cell abnormalities, focal areas of cellular alteration, and focal and nodular areas of hyperplasia were commonly present. Regarding carcinogenic activity, TCP caused leukemias/lymphomas in male rats, and possibly in female rats and female mice as well, and induced liver tumors in male and female mice. Using NTP categories of evidence indicates 'clear evidence of carcinogenicity' for male rats [hematopoietic system tumors]; 'equivocal evidence of carcinogenicity' for female rats [hematopoietic system tumors]; 'clear evidence of carcinogenicity' for male and female mice [liver tumors]. Published by Elsevier Ltd. JF - Chemosphere AU - Huff, James AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. huff1@niehs.nih.gov Y1 - 2012/10// PY - 2012 DA - October 2012 SP - 521 EP - 525 VL - 89 IS - 5 KW - Carcinogens KW - 0 KW - Chlorophenols KW - 2,4,6-trichlorophenol KW - MHS8C5BAUZ KW - Index Medicus KW - Animals KW - Humans KW - Neoplasms -- chemically induced KW - Time Factors KW - Biological Assay -- methods KW - Chlorophenols -- toxicity KW - Carcinogens -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1032608631?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Long-term+toxicology+and+carcinogenicity+of+2%2C4%2C6-trichlorophenol.&rft.au=Huff%2C+James&rft.aulast=Huff&rft.aufirst=James&rft.date=2012-10-01&rft.volume=89&rft.issue=5&rft.spage=521&rft.isbn=&rft.btitle=&rft.title=Chemosphere&rft.issn=1879-1298&rft_id=info:doi/10.1016%2Fj.chemosphere.2012.05.015 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-12-14 N1 - Date created - 2012-08-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.chemosphere.2012.05.015 ER - TY - JOUR T1 - Consortium-Based Science: The NIEHS's Multipronged, Collaborative Approach to Assessing the Health Effects of Bisphenol A AN - 1291617249; 17649937 AB - Background: Bisphenol A (BPA) is a high production volume chemical used to make polycarbonate plastic and is found in many consumer products. Some studies using animal models have suggested that BPA exposures may have adverse health effects. However, research gaps have precluded a full understanding of the effects of BPA in humans and engendered controversies surrounding the chemical's potential toxicity. Objectives: The National Institute of Environmental Health Sciences (NIEHS) and National Toxicology Program (NTP) have developed an integrated, multipronged, consortium-based approach to optimize BPA-focused research investments to more effectively address data gaps and inform decision making. Discussion: NIEHS/NTP BPA research investments made over the past 4 years include extramural research grants, establishment of a BPA Grantee Consortium, intramural research activities on BPA's mechanisms of action, the launch of two clinical studies and an occupational study, development of a round-robin experiment to validate BPA measurements in human serum, and, in collaboration with the Food and Drug Administration (FDA), formation of a consortium to design and execute a chronic toxicity study of BPA in rats. The NIEHS's new consortium-based approach has led to more integrated, collaborative efforts and should improve our ability to resolve controversies over the potential human health effects of exposures to low levels of endocrine-active agents. JF - Environmental Health Perspectives AU - Birnbaum, Linda S AU - Bucher, John R AU - Collman, Gwen W AU - Zeldin, Darryl C AU - Johnson, Anne F AU - Schug, Thaddeus T AU - Heindel, Jerrold J AD - 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 - 2012/09/25/ PY - 2012 DA - 2012 Sep 25 SP - 1640 EP - 1644 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 120 IS - 2 SN - 0091-6765, 0091-6765 KW - Environment Abstracts; Health & Safety Science Abstracts KW - bisphenol A KW - consortium-based research KW - endocrine disruptor KW - low dose KW - NIEHS KW - Bisphenol A KW - Rats KW - Decision making KW - Consumer products KW - Chronic toxicity KW - Animal models KW - FDA KW - Environmental health KW - Toxicity KW - Toxicology 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/1291617249?accountid=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=Environmental+Health+Perspectives&rft.atitle=Consortium-Based+Science%3A+The+NIEHS%27s+Multipronged%2C+Collaborative+Approach+to+Assessing+the+Health+Effects+of+Bisphenol+A&rft.au=Birnbaum%2C+Linda+S%3BBucher%2C+John+R%3BCollman%2C+Gwen+W%3BZeldin%2C+Darryl+C%3BJohnson%2C+Anne+F%3BSchug%2C+Thaddeus+T%3BHeindel%2C+Jerrold+J&rft.aulast=Birnbaum&rft.aufirst=Linda&rft.date=2012-09-25&rft.volume=120&rft.issue=2&rft.spage=1640&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1205330 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-01 N1 - Last updated - 2015-05-13 N1 - SubjectsTermNotLitGenreText - Rats; Bisphenol A; Decision making; Consumer products; Chronic toxicity; FDA; Animal models; Environmental health; Toxicity; Toxicology DO - http://dx.doi.org/10.1289/ehp.1205330 ER - TY - JOUR T1 - Ovarian cancer and menopausal hormone therapy in the NIH-AARP diet and health study AN - 1113242439; 17212722 AB - Background: Women using unopposed estrogens during menopause are at increased risk of ovarian cancer. It is uncertain whether oestrogen plus progestin therapy exerts similar effects. Methods: We evaluated menopausal hormone use and incident ovarian cancer (n=426) in 92 601 post-menopausal women enrolled in the National Institutes of Health-AARP (NIH-AARP) Diet and Health Study. Participants were administered questionnaires in 1996-1997 and followed through 2006. Hazard rate ratios (RR) and 95% confidence intervals (CIs) were estimated using Cox regression. Results: Increased risks were associated with long duration (10+ years) use of unopposed oestrogen (RR 2.15, 95% CI: 1.30-3.57 among women with a hysterectomy) and oestrogen plus progestin (RR 1.68, 95% CI: 1.13-2.49 among women with intact uteri) therapy. Similar risks were associated with progestins that were used sequentially (25 days progestin per month) (RR 1.43, 95% CI: 1.032-2.01; P-value for heterogeneity=0.63). Conclusion: Our findings suggest that long duration use of both unopposed estrogens and oestrogen plus progestins are associated with increased risks of ovarian cancer, and that risk associated with oestrogen plus progestin use does not vary by regimen (sequential or continuous). JF - British Journal of Cancer AU - Trabert, B AU - Wentzensen, N AU - Yang, H P AU - Sherman, M E AU - Hollenbeck, A AU - Danforth, K N AU - Park, Y AU - Brinton, L A AD - Department of Health and Human Services, Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 6120 Executive Boulevard, Suite 550, Rockville, MD 20852, USA Y1 - 2012/09/25/ PY - 2012 DA - 2012 Sep 25 SP - 1181 EP - 1187 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 107 IS - 7 SN - 0007-0920, 0007-0920 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Cancer KW - Diets KW - Estrogens KW - Hormones KW - Menopause KW - Ovarian carcinoma 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/1113242439?accountid=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=Ovarian+cancer+and+menopausal+hormone+therapy+in+the+NIH-AARP+diet+and+health+study&rft.au=Trabert%2C+B%3BWentzensen%2C+N%3BYang%2C+H+P%3BSherman%2C+M+E%3BHollenbeck%2C+A%3BDanforth%2C+K+N%3BPark%2C+Y%3BBrinton%2C+L+A&rft.aulast=Trabert&rft.aufirst=B&rft.date=2012-09-25&rft.volume=107&rft.issue=7&rft.spage=1181&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2012.397 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2013-02-22 N1 - SubjectsTermNotLitGenreText - Diets; Estrogens; Ovarian carcinoma; Hormones; Menopause; Cancer DO - http://dx.doi.org/10.1038/bjc.2012.397 ER - TY - JOUR T1 - Acute Gastrointestinal Infection Induces Long-Lived Microbiota-Specific T Cell Responses AN - 1566852028; 20372333 AB - Recognizing Escaped CommensalsIn order to coexist peacefully, the billions of bacteria in our gut and our immune system have reached a detente. An intestinal mucosal firewall exists, so bacteria remain localized to the gut, where the immune system is tightly regulated so that these bacteria are tolerated. Enteric infections, however, lead to a breach in this mucosal firewall, resulting in exposure of the peripheral immune system to the intestinal bacterial contents. What is the result? Using oral Toxoplasma gondii infection in mice, Hand et al. (p. 1553, published online 23 August) show that, besides the T. gondii-specific T cell response, a commensal bacteria-specific T cell response is elicited. The CD4+ T cell-specific response was tracked to a commensal-derived flagellin, and these T cells expanded after T. gondii infection and formed long-lived memory cells able to respond to subsequent challenges. Thus, enteric infections can lead to the formation of commensal bacteria-specific, long-lived memory T cells that reside throughout the body-which may play a role in intestinal pathologies such as inflammatory bowel disease. JF - Science AU - Hand, Timothy W AU - Dos Santos, Liliane M AU - Bouladoux, Nicolas AU - Molloy, Michael J AU - Pagan, Antonio J AU - Pepper, Marion AU - Maynard, Craig L AU - Elson, Charles O AU - Belkaid, Yasmine AD - Mucosal Immunology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health (NIH), Bethesda, MD 20892, USA, ybelkaid@niaid.nih.gov Y1 - 2012/09/21/ PY - 2012 DA - 2012 Sep 21 SP - 1553 EP - 1556 PB - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States VL - 337 IS - 6101 SN - 0036-8075, 0036-8075 KW - Microbiology Abstracts A: Industrial & Applied Microbiology KW - Immune system KW - Mucosa KW - Immunological memory KW - Memory cells KW - Commensals KW - Hand KW - Infection KW - CD4 antigen KW - Digestive tract KW - Inflammatory bowel diseases KW - Toxoplasma gondii KW - Intestine KW - Lymphocytes T KW - Flagellin KW - Internet KW - A 01490:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566852028?accountid=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=Acute+Gastrointestinal+Infection+Induces+Long-Lived+Microbiota-Specific+T+Cell+Responses&rft.au=Hand%2C+Timothy+W%3BDos+Santos%2C+Liliane+M%3BBouladoux%2C+Nicolas%3BMolloy%2C+Michael+J%3BPagan%2C+Antonio+J%3BPepper%2C+Marion%3BMaynard%2C+Craig+L%3BElson%2C+Charles+O%3BBelkaid%2C+Yasmine&rft.aulast=Hand&rft.aufirst=Timothy&rft.date=2012-09-21&rft.volume=337&rft.issue=6101&rft.spage=1553&rft.isbn=&rft.btitle=&rft.title=Science&rft.issn=00368075&rft_id=info:doi/10.1126%2Fscience.1220961 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Immune system; Mucosa; Commensals; Memory cells; Immunological memory; Hand; Infection; CD4 antigen; Digestive tract; Inflammatory bowel diseases; Lymphocytes T; Intestine; Flagellin; Internet; Toxoplasma gondii DO - http://dx.doi.org/10.1126/science.1220961 ER - TY - JOUR T1 - Further characterization of the immune response in mice to inactivated and live rabies vaccines expressing Ebola virus glycoprotein. AN - 1038227529; 22884661 AB - We have previously developed (a) replication-competent, (b) replication-deficient, and (c) chemically inactivated rabies virus (RABV) vaccines expressing Ebola virus (EBOV) glycoprotein (GP) that induce humoral immunity against each virus and confer protection from both lethal RABV and mouse-adapted EBOV challenge in mice. Here, we expand our investigation of the immunogenic properties of these bivalent vaccines in mice. Both live and killed vaccines induced primary EBOV GP-specific T-cells and a robust recall response as measured by interferon-γ ELISPOT assay. In addition to cellular immunity, an effective filovirus vaccine will likely require a multivalent humoral immune response against multiple virus species. As a proof-of-principle experiment, we demonstrated that inactivated RV-GP could be formulated with another inactivated RABV vaccine expressing the nontoxic fragment of botulinum neurotoxin A heavy chain (HC50) without a reduction in immunity to each component. Finally, we demonstrated that humoral immunity to GP could be induced by immunization of mice with inactivated RV-GP in the presence of pre-existing immunity to RABV. The ability of these novel vaccines to induce strong humoral and cellular immunity indicates that they should be further evaluated in additional animal models of infection. Published by Elsevier Ltd. JF - Vaccine AU - Papaneri, Amy B AU - Wirblich, Christoph AU - Cooper, Kurt AU - Jahrling, Peter B AU - Schnell, Matthias J AU - Blaney, Joseph E AD - Emerging Viral Pathogens Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Fort Detrick, MD 21702, USA. Y1 - 2012/09/21/ PY - 2012 DA - 2012 Sep 21 SP - 6136 EP - 6141 VL - 30 IS - 43 KW - Antibodies, Viral KW - 0 KW - Ebola Vaccines KW - Membrane Glycoproteins KW - Rabies Vaccines KW - Vaccines, Inactivated KW - Viral Matrix Proteins KW - transmembrane glycoprotein, Ebola virus KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - Antibodies, Viral -- blood KW - Animals KW - Vaccines, Inactivated -- immunology KW - Immunity, Cellular KW - Mice KW - Interferon-gamma -- immunology KW - Mice, Inbred BALB C KW - Ebolavirus -- immunology KW - T-Lymphocytes -- immunology KW - Immunity, Humoral KW - Ebola Vaccines -- immunology KW - Antibody Specificity KW - Hemorrhagic Fever, Ebola -- prevention & control KW - Membrane Glycoproteins -- immunology KW - Viral Matrix Proteins -- immunology KW - Rabies Vaccines -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1038227529?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=Further+characterization+of+the+immune+response+in+mice+to+inactivated+and+live+rabies+vaccines+expressing+Ebola+virus+glycoprotein.&rft.au=Papaneri%2C+Amy+B%3BWirblich%2C+Christoph%3BCooper%2C+Kurt%3BJahrling%2C+Peter+B%3BSchnell%2C+Matthias+J%3BBlaney%2C+Joseph+E&rft.aulast=Papaneri&rft.aufirst=Amy&rft.date=2012-09-21&rft.volume=30&rft.issue=43&rft.spage=6136&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=1873-2518&rft_id=info:doi/10.1016%2Fj.vaccine.2012.07.073 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-10 N1 - Date created - 2012-09-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Virol. 2011 Oct;85(20):10605-16 [21849459] Nat Med. 2011 Sep;17(9):1128-31 [21857654] Viruses. 2011 Jul;3(7):982-1000 [21994766] Biosecur Bioterror. 2011 Dec;9(4):361-71 [22070137] J Biomed Biotechnol. 2011;2011:984241 [22253531] Proc Natl Acad Sci U S A. 2012 Mar 27;109(13):5034-9 [22411795] Vaccine. 2011 Jun 20;29(28):4638-45 [21549784] Nature. 2000 Nov 30;408(6812):605-9 [11117750] Virology. 2002 Jan 5;292(1):24-34 [11878905] Bull World Health Organ. 2002;80(4):304-10 [12075367] J Virol. 2003 Jan;77(1):237-44 [12477829] Nature. 2003 Aug 7;424(6949):681-4 [12904795] Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15889-94 [14673108] Science. 2004 Jan 16;303(5656):387-90 [14726594] Gene. 1995 Jun 9;158(2):157-62 [7607536] J Gen Virol. 2005 May;86(Pt 5):1435-40 [15831955] J Immunol. 2005 Jul 15;175(2):1184-91 [16002721] Science. 2006 Dec 8;314(5805):1564 [17158318] J Infect Dis. 2007 Nov 15;196 Suppl 2:S404-12 [17940977] J Infect Dis. 2007 Nov 15;196 Suppl 2:S430-7 [17940980] Virology. 2009 Jan 5;383(1):12-21 [18986663] Virology. 2009 Jan 20;383(2):348-61 [19010509] Nat Rev Microbiol. 2009 May;7(5):393-400 [19369954] J Virol. 2009 Jul;83(14):7296-304 [19386702] Vaccine. 2009 Dec 11;28(2):299-308 [19879223] Nat Rev Microbiol. 2010 Jan;8(1):51-61 [19946287] J Virol. 2010 Mar;84(6):2820-31 [20053743] Virology. 2010 Apr 10;399(2):290-8 [20129638] PLoS Pathog. 2010 May;6(5):e1000904 [20502688] Rev Med Virol. 2010 Nov;20(6):344-57 [20658513] Vaccine. 2010 Dec 10;29(1):17-25 [21034822] Hum Vaccin. 2011 Jun;7(6):701-11 [21519188] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.vaccine.2012.07.073 ER - TY - JOUR T1 - Contribution of Behavioral Risk Factors and Obesity to Socioeconomic Differences in Colorectal Cancer Incidence AN - 1113226744; 17188529 AB - Background Health behaviors are known risk factors for colorectal cancer and are more common in low socioeconomic status (SES) populations. We evaluated the extent to which behavioral risk factors and body mass index (BMI) explain SES disparities in colorectal cancer incidence, overall and by tumor location. Methods We analyzed prospective National Institutes of Health-AARP Diet and Health Study data on 506 488 participants who were recruited in 1995-1996 from six US states and two metropolitan areas and followed through 2006. Detailed baseline data on risk factors for colorectal cancer, including health behaviors, were obtained using questionnaires. SES was measured by self-reported education and census-tract data. The outcome was primary incident invasive colorectal adenocarcinoma. Poisson regression was used to estimate the association between SES and risk of incident colorectal cancer, with adjustment for age, sex, race and ethnicity, family history, and state of residence. The model estimates were used to derive percentage mediation by behavioral risk factors; bias-corrected 95% confidence intervals were obtained through bootstrap techniques. Results Seven-thousand six-hundred seventy-six participants developed colorectal cancer during follow-up. SES differences in prevalence of physical inactivity, unhealthy diet, smoking, and unhealthy weight each explained between 11.3% (BMI) and 21.6% (diet) of the association between education and risk of colorectal cancer and between 8.6% (smoking) and 15.3% (diet) of the association between neighborhood SES and risk of colorectal cancer. Health behaviors and BMI combined explained approximately 43.9% (95% CI = 35.1% to 57.9%) of the association of education and 36.2% (95% CI = 28.0% to 51.2%) of the association of neighborhood SES with risk of colorectal cancer. The percentage explained by all factors and BMI combined was largest for right colon cancers and smallest for rectal cancers. Conclusion A substantial proportion of the socioeconomic disparity in risk of new-onset colorectal cancer, and particularly of right colon cancers, may be attributable to the higher prevalence of adverse health behaviors in low-SES populations. JF - Journal of the National Cancer Institute AU - Doubeni, Chyke A AU - Major, Jacqueline M AU - Laiyemo, Adeyinka O AU - Schootman, Mario AU - Zauber, Ann G AU - Hollenbeck, Albert R AU - Sinha, Rashmi AU - Allison, Jeroan AD - Affiliations of authors: Department of Family Medicine and Community Health (CAD) and Quantitative Health Sciences, University of Massachusetts Medical School, Worcester, MA (CAD, JA); Department of Family Medicine and Community Health, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA (CAD); Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD (JMM, RS); Department of Medicine, Howard University, Washington, DC (AOL); Division of Health Behavior Research, Department of Medicine, Washington University School of Medicine, St. Louis, MO (MS); Department of Epidemiology and Biostatistics, Memorial Sloan-Kettering Cancer Center, New York, NY (AGZ); AARP, Washington, DC (ARH)., Chyke.Doubeni@uphs.upenn.edu Y1 - 2012/09/19/ PY - 2012 DA - 2012 Sep 19 SP - 1353 EP - 1362 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 104 IS - 18 SN - 0027-8874, 0027-8874 KW - Risk Abstracts KW - Diets KW - Smoking KW - Genetics KW - Education KW - Risk factors KW - Colorectal carcinoma KW - Socioeconomics KW - Cancer KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1113226744?accountid=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+the+National+Cancer+Institute&rft.atitle=Contribution+of+Behavioral+Risk+Factors+and+Obesity+to+Socioeconomic+Differences+in+Colorectal+Cancer+Incidence&rft.au=Doubeni%2C+Chyke+A%3BMajor%2C+Jacqueline+M%3BLaiyemo%2C+Adeyinka+O%3BSchootman%2C+Mario%3BZauber%2C+Ann+G%3BHollenbeck%2C+Albert+R%3BSinha%2C+Rashmi%3BAllison%2C+Jeroan&rft.aulast=Doubeni&rft.aufirst=Chyke&rft.date=2012-09-19&rft.volume=104&rft.issue=18&rft.spage=1353&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/10.1093%2Fjnci%2Fdjs346 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2016-08-03 N1 - SubjectsTermNotLitGenreText - Diets; Genetics; Smoking; Education; Risk factors; Socioeconomics; Colorectal carcinoma; Cancer DO - http://dx.doi.org/10.1093/jnci/djs346 ER - TY - JOUR T1 - Myelin Basic Protein-Specific TCR/HLA-DRB5*01:01 Transgenic Mice Support the Etiologic Role of DRB5*01:01 in Multiple Sclerosis AN - 1551623346; 20355218 AB - Genetic susceptibility to multiple sclerosis (MS) has been linked to the HLA-DR15 haplotype consisting of DRB1*15:01(DR2b) and DRB5*01:01(DR2a) alleles. Given almost complete linkage disequilibrium of the two alleles, recent studies suggested differential roles in susceptibility (DR2b) or protection from MS (DR2a). Our objective was to assess the potential contribution of DR2a to disease etiology in MS using a humanized model of autoimmunity. To assess the potential contribution of DR2a to disease etiology, we created DR2a humanized transgenic (Tg) mice and subsequently crossed them to Tg mice expressing TL3A6, an MS patient-derived myelin basic protein 83-99-specific TCR. In TL3A6/DR2a Tg mice, CD4 Tg T cells escape thymic and peripheral deletion and initiate spontaneous experimental autoimmune encephalomyelitis (EAE) at low rates, depending on the level of DR2a expression. The ability to induce active EAE was also increased in animals expressing higher levels of DR2a. Inflammatory infiltrates and neuronal damage were present throughout the spinal cord, consistent with a classical ascending EAE phenotype with minor involvement of the cerebellum, brainstem, and peripheral nerve roots in spontaneous, as well as actively induced, disease. These studies emphasize the pathologic contribution of the DR2a allele to the development of autoimmunity when expressed as the sole MHC class II molecule, as well as strongly argue for DR2a as a contributor to the CNS autoimmunity in MS. JF - Journal of Immunology AU - Quandt, Jacqueline A AU - Huh, Jaebong AU - Baig, Mirza AU - Yao, Karen AU - Ito, Naoko AU - Bryant, Mark AU - Kawamura, Kazuyuki AU - Pinilla, Clemencia AU - McFarland, Henry F AU - Martin, Roland AU - Ito, Kouichi AD - Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892 Y1 - 2012/09/15/ PY - 2012 DA - 2012 Sep 15 SP - 2897 EP - 2908 PB - American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 United States VL - 189 IS - 6 SN - 0022-1767, 0022-1767 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts; CSA Neurosciences Abstracts; Immunology Abstracts KW - Histocompatibility antigen HLA KW - Central nervous system KW - Etiology KW - T-cell receptor KW - Myelin KW - Multiple sclerosis KW - Spinal cord KW - Thymus KW - Autoimmune diseases KW - Brain stem KW - Cerebellum KW - Animal models KW - Autoimmunity KW - Major histocompatibility complex KW - Transgenic mice KW - Inflammation KW - Linkage disequilibrium KW - CD4 antigen KW - Haplotypes KW - Lymphocytes T KW - Experimental allergic encephalomyelitis KW - Peripheral nerves KW - Myelin basic protein KW - W 30925:Genetic Engineering KW - F 06930:Autoimmunity KW - G 07730:Development & Cell Cycle KW - N3 11024:Neuroimmunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551623346?accountid=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+Immunology&rft.atitle=Myelin+Basic+Protein-Specific+TCR%2FHLA-DRB5*01%3A01+Transgenic+Mice+Support+the+Etiologic+Role+of+DRB5*01%3A01+in+Multiple+Sclerosis&rft.au=Quandt%2C+Jacqueline+A%3BHuh%2C+Jaebong%3BBaig%2C+Mirza%3BYao%2C+Karen%3BIto%2C+Naoko%3BBryant%2C+Mark%3BKawamura%2C+Kazuyuki%3BPinilla%2C+Clemencia%3BMcFarland%2C+Henry+F%3BMartin%2C+Roland%3BIto%2C+Kouichi&rft.aulast=Quandt&rft.aufirst=Jacqueline&rft.date=2012-09-15&rft.volume=189&rft.issue=6&rft.spage=2897&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunology&rft.issn=00221767&rft_id=info:doi/10.4049%2Fjimmunol.1103087 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Histocompatibility antigen HLA; Central nervous system; T-cell receptor; Etiology; Myelin; Spinal cord; Multiple sclerosis; Brain stem; Autoimmune diseases; Thymus; Animal models; Cerebellum; Major histocompatibility complex; Autoimmunity; Transgenic mice; Inflammation; Linkage disequilibrium; CD4 antigen; Haplotypes; Lymphocytes T; Experimental allergic encephalomyelitis; Myelin basic protein; Peripheral nerves DO - http://dx.doi.org/10.4049/jimmunol.1103087 ER - TY - JOUR T1 - A population-based study of therapy and survival for patients with head and neck cancer treated in the community. AN - 1038593639; 22252676 AB - The objective of this study was to examine patterns of care and survival in a population-based sample of patients with head and neck cancer (HNC) who were treated in the community or in hospitals that had residency training programs. Data from the National Cancer Institute's Surveillance, Epidemiology, and End Results Program were used to sample 1317 patients aged ≥20 years with invasive squamous HNC who were diagnosed during 2004 and who had vital status available through 2008. Treatment and survival were influenced by tumor site and disease stage. Patients who had stage I/II cancer of the oral cavity generally underwent surgery; patients with stage III oral cavity disease underwent surgery and received radiation; and patients with stage IV oral cavity disease underwent surgery and received chemoradiation. Patients with early stage cancer of the oropharynx either underwent surgery or received radiation and chemotherapy, and patients with late/unstaged oropharyngeal disease primarily received radiation and chemotherapy. Patients with early stage cancer of the larynx mainly received radiation alone, and patients with late stage laryngeal disease generally received chemoradiation. Cisplatin-based regimens were used most frequently. Overall, taxanes were used in 32% of regimens, and cetuximab was used in <3% of regimens. Patients aged ≥50 years, those with a Charlson comorbidity score ≥1, those with stage IV disease, and those with cancer located in the oral cavity or larynx had poorer survival. Although facilities with residency training programs treated more black patients and more patients with late stage disease, when adjusted for other factors, survival rates were similar to those reported in facilities with no such programs. Therapy generally followed accepted standards for 2004. Findings in particular tumor sites and stages may reflect the variability that still exists for the treatment of HNC. The use of taxanes and cetuximab is expected to increase based on new evidence of benefit. Reducing treatment-related toxicities and long-term functional deficits will be critical and especially important with the increase in human papillomavirus-related cancers. In addition, further attempts to improve survival for older patients are needed. Copyright © 2011 American Cancer Society. JF - Cancer AU - Dansky Ullmann, Claudio AU - Harlan, Linda C AU - Shavers, Vickie L AU - Stevens, Jennifer L AD - Cancer Therapy Evaluation Program, National Cancer Institute, Bethesda, MD, USA. danskyullc@mail.nih.gov Y1 - 2012/09/15/ PY - 2012 DA - 2012 Sep 15 SP - 4452 EP - 4461 VL - 118 IS - 18 KW - Antibodies, Monoclonal KW - 0 KW - Antibodies, Monoclonal, Humanized KW - Antineoplastic Agents KW - Taxoids KW - Cetuximab KW - PQX0D8J21J KW - Cisplatin KW - Q20Q21Q62J KW - Abridged Index Medicus KW - Index Medicus KW - Young Adult KW - Hospitals, Community KW - Mouth Neoplasms -- mortality KW - Laryngeal Neoplasms -- therapy KW - Mouth Neoplasms -- therapy KW - Humans KW - Prognosis KW - Aged KW - Taxoids -- therapeutic use KW - Oropharyngeal Neoplasms -- mortality KW - Antibodies, Monoclonal -- therapeutic use KW - Cisplatin -- therapeutic use KW - Laryngeal Neoplasms -- mortality KW - Oropharyngeal Neoplasms -- therapy KW - Adult KW - Middle Aged KW - Antineoplastic Agents -- therapeutic use KW - Male KW - Female KW - Head and Neck Neoplasms -- therapy KW - Head and Neck Neoplasms -- mortality KW - SEER Program -- statistics & numerical data UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1038593639?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=A+population-based+study+of+therapy+and+survival+for+patients+with+head+and+neck+cancer+treated+in+the+community.&rft.au=Dansky+Ullmann%2C+Claudio%3BHarlan%2C+Linda+C%3BShavers%2C+Vickie+L%3BStevens%2C+Jennifer+L&rft.aulast=Dansky+Ullmann&rft.aufirst=Claudio&rft.date=2012-09-15&rft.volume=118&rft.issue=18&rft.spage=4452&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=1097-0142&rft_id=info:doi/10.1002%2Fcncr.27419 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-11-19 N1 - Date created - 2012-09-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/cncr.27419 ER - TY - JOUR T1 - Accumulation of pre-let-7g and downregulation of mature let-7g with the depletion of EWS AN - 1238120205; 17160972 AB - EWS functions in RNA splicing and transcription by encoding an RNA binding protein, which results in the chromosomal translocation t(11; 22)(q24; q12) found in Ewing sarcoma. EWS interacts with the microprocessor complex involving Drosha and DGCR8, which play roles as the cofactors of primary microRNA processing. However, the role of EWS in microRNA biogenesis has not been investigated. Here, we show that endogenous EWS interacts with endogenous Drosha by IP-western blotting. In addition, EWS knockout mouse decreased the expression of Drosha. The depletion of EWS results in the accumulation of precursor let-7g but down-regulates mature let-7g in U2OS cells. Consistently, mature let 7g was suppressed in both Ewing sarcoma cell and primary Ewing sarcoma. Also, expression levels of Dicer and CCND1 (Cyclin D1), which are known target genes of the let-7 family were upregulated. Our findings suggest that EWS mediates generation of mature let-7g from pre-let-7g. JF - Biochemical and Biophysical Research Communications AU - Sohn, Eun Jung AU - Park, Junhong AU - Kang, Soo-im AU - Wu, Yun-Ping AD - Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20871, USA, eunjungs93@gmail.com Y1 - 2012/09/14/ PY - 2012 DA - 2012 Sep 14 SP - 89 EP - 93 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 426 IS - 1 SN - 0006-291X, 0006-291X KW - Toxicology Abstracts KW - Chromosome translocations KW - Cofactors KW - Ewing's sarcoma KW - RNA KW - RNA-binding protein KW - Splicing KW - Transcription KW - cyclin D1 KW - miRNA KW - X 24390:Radioactive Materials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1238120205?accountid=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=Biochemical+and+Biophysical+Research+Communications&rft.atitle=Accumulation+of+pre-let-7g+and+downregulation+of+mature+let-7g+with+the+depletion+of+EWS&rft.au=Sohn%2C+Eun+Jung%3BPark%2C+Junhong%3BKang%2C+Soo-im%3BWu%2C+Yun-Ping&rft.aulast=Sohn&rft.aufirst=Eun&rft.date=2012-09-14&rft.volume=426&rft.issue=1&rft.spage=89&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+Biophysical+Research+Communications&rft.issn=0006291X&rft_id=info:doi/10.1016%2Fj.bbrc.2012.08.041 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-12-01 N1 - Last updated - 2012-12-14 N1 - SubjectsTermNotLitGenreText - Splicing; Ewing's sarcoma; Cofactors; RNA-binding protein; RNA; Chromosome translocations; miRNA; Transcription; cyclin D1 DO - http://dx.doi.org/10.1016/j.bbrc.2012.08.041 ER - TY - CPAPER T1 - The Serologic Assessment of Filarial Infections T2 - 52nd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2012) AN - 1313121281; 6195474 JF - 52nd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2012) AU - Nutman, Thomas Y1 - 2012/09/09/ PY - 2012 DA - 2012 Sep 09 KW - Infection UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313121281?accountid=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=52nd+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2012%29&rft.atitle=The+Serologic+Assessment+of+Filarial+Infections&rft.au=Nutman%2C+Thomas&rft.aulast=Nutman&rft.aufirst=Thomas&rft.date=2012-09-09&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.icaac.org/images/icaac_2012_finalprogram_web4a.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Emerging Artemisinin Resistance in Plasmodium falciparum Malaria T2 - 52nd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2012) AN - 1313120113; 6195380 JF - 52nd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2012) AU - Fairhurst, Rick Y1 - 2012/09/09/ PY - 2012 DA - 2012 Sep 09 KW - Malaria KW - Parasites KW - Public health KW - artemisinin KW - Plasmodium falciparum UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313120113?accountid=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=52nd+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2012%29&rft.atitle=Emerging+Artemisinin+Resistance+in+Plasmodium+falciparum+Malaria&rft.au=Fairhurst%2C+Rick&rft.aulast=Fairhurst&rft.aufirst=Rick&rft.date=2012-09-09&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.icaac.org/images/icaac_2012_finalprogram_web4a.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - What the Site of a Fungal Infection Means for Outcome T2 - 52nd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2012) AN - 1313102398; 6185650 JF - 52nd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2012) AU - Lionakis, Michail Y1 - 2012/09/09/ PY - 2012 DA - 2012 Sep 09 KW - Infection UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313102398?accountid=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=52nd+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2012%29&rft.atitle=What+the+Site+of+a+Fungal+Infection+Means+for+Outcome&rft.au=Lionakis%2C+Michail&rft.aulast=Lionakis&rft.aufirst=Michail&rft.date=2012-09-09&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.icaac.org/images/icaac_2012_finalprogram_web4a.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - What Can We Learn from the History of Resistance to Anti- Malarial Drugs? T2 - 52nd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2012) AN - 1313073932; 6185742 JF - 52nd Interscience Conference on Antimicrobial Agents and Chemotherapy (ICAAC 2012) AU - Wellems, Thomas Y1 - 2012/09/09/ PY - 2012 DA - 2012 Sep 09 KW - Historical account KW - Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313073932?accountid=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=52nd+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2012%29&rft.atitle=What+Can+We+Learn+from+the+History+of+Resistance+to+Anti-+Malarial+Drugs%3F&rft.au=Wellems%2C+Thomas&rft.aulast=Wellems&rft.aufirst=Thomas&rft.date=2012-09-09&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=52nd+Interscience+Conference+on+Antimicrobial+Agents+and+Chemotherapy+%28ICAAC+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.icaac.org/images/icaac_2012_finalprogram_web4a.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Radiation Metabolomics. 5. Identification of Urinary Biomarkers of Ionizing Radiation Exposure in Nonhuman Primates by Mass Spectrometry-Based Metabolomics AN - 1136542377; 17234944 AB - Mass spectrometry-based metabolomics has previously demonstrated utility for identifying biomarkers of ionizing radiation exposure in cellular, mouse and rat in vivo radiation models. To provide a valuable link from small laboratory rodents to humans, gamma -radiation-induced urinary biomarkers were investigated using a nonhuman primate total-body-irradiation model. Mass spectrometry-based metabolomics approaches were applied to determine whether biomarkers could be identified, as well as the previously discovered rodent biomarkers of gamma radiation. Ultra-performance liquid chromatography-electrospray ionization quadrupole time-of-flight mass spectrometry analysis was carried out on a time course of clean-catch urine samples collected from nonhuman primates (n = 6 per cohort) exposed to sham, 1.0, 3.5, 6.5 or 8.5 Gy doses of 60Co gamma ray ( similar to 0.55 Gy/min) ionizing radiation. By multivariate data analysis, 13 biomarkers of radiation were discovered: N-acetyltaurine, isethionic acid, taurine, xanthine, hypoxanthine, uric acid, creatine, creatinine, tyrosol sulfate, 3-hydroxytyrosol sulfate, tyramine sulfate, N-acetylserotonin sulfate, and adipic acid. N-Acetyltaurine, isethionic acid, and taurine had previously been identified in rats, and taurine and xanthine in mice after ionizing radiation exposure. Mass spectrometry-based metabolomics has thus successfully revealed and verified urinary biomarkers of ionizing radiation exposure in the nonhuman primate for the first time, which indicates possible mechanisms for ionizing radiation injury. JF - Radiation Research AU - Johnson, Caroline H AU - Patterson, Andrew D AU - Krausz, Kristopher W AU - Kalinich, John F AU - Tyburski, John B AU - Kang, Dong Wook AU - Luecke, Hans AU - Gonzalez, Frank J AU - Blakely, William F AU - Idle, Jeffrey R AD - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, jeff.idle@ikp.unibe.ch Y1 - 2012/09/06/ PY - 2012 DA - 2012 Sep 06 SP - 328 EP - 340 PB - Radiation Research Society VL - 178 IS - 4 SN - 0033-7587, 0033-7587 KW - Toxicology Abstracts KW - Data processing KW - Injuries KW - Xanthine KW - Creatine KW - Primates KW - biomarkers KW - Mass spectroscopy KW - Sulfate KW - Taurine KW - Creatinine KW - Urine KW - Ionizing radiation KW - adipic acid KW - Hypoxanthine KW - N-Acetylserotonin KW - gamma Radiation KW - tyramine KW - tyrosol KW - metabolomics KW - Uric acid KW - X 24390:Radioactive Materials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1136542377?accountid=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=Radiation+Research&rft.atitle=Radiation+Metabolomics.+5.+Identification+of+Urinary+Biomarkers+of+Ionizing+Radiation+Exposure+in+Nonhuman+Primates+by+Mass+Spectrometry-Based+Metabolomics&rft.au=Johnson%2C+Caroline+H%3BPatterson%2C+Andrew+D%3BKrausz%2C+Kristopher+W%3BKalinich%2C+John+F%3BTyburski%2C+John+B%3BKang%2C+Dong+Wook%3BLuecke%2C+Hans%3BGonzalez%2C+Frank+J%3BBlakely%2C+William+F%3BIdle%2C+Jeffrey+R&rft.aulast=Johnson&rft.aufirst=Caroline&rft.date=2012-09-06&rft.volume=178&rft.issue=4&rft.spage=328&rft.isbn=&rft.btitle=&rft.title=Radiation+Research&rft.issn=00337587&rft_id=info:doi/10.1667%2FRR2950.1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-12-01 N1 - Number of references - 34 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Data processing; Injuries; Xanthine; Creatine; biomarkers; Mass spectroscopy; Sulfate; Taurine; Creatinine; Urine; Ionizing radiation; adipic acid; gamma Radiation; N-Acetylserotonin; Hypoxanthine; tyramine; metabolomics; tyrosol; Uric acid; Primates DO - http://dx.doi.org/10.1667/RR2950.1 ER - TY - JOUR T1 - Risk of Heart Failure in Breast Cancer Patients After Anthracycline and Trastuzumab Treatment: A Retrospective Cohort Study AN - 1125233832; 17317730 AB - Background Clinical trials demonstrated that women treated for breast cancer with anthracycline or trastuzumab are at increased risk for heart failure and/or cardiomyopathy (HF/CM), but the generalizability of these findings is unknown. We estimated real-world adjuvant anthracycline and trastuzumab use and their associations with incident HF/CM. Methods We conducted a population-based, retrospective cohort study of 12 500 women diagnosed with incident, invasive breast cancer from January 1, 1999 through December 31, 2007, at eight integrated Cancer Research Network health systems. Using administrative procedure and pharmacy codes, we identified anthracycline, trastuzumab, and other chemotherapy use. We identified incident HF/CM following chemotherapy initiation and assessed risk of HF/CM with time-varying chemotherapy exposures vs no chemotherapy. Multivariable Cox proportional hazards regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) with adjustment for age at diagnosis, stage, Cancer Research Network site, year of diagnosis, radiation therapy, and comorbidities. Results Among 12 500 women (mean age = 60 years, range = 22-99 years), 29.6% received anthracycline alone, 0.9% received trastuzumab alone, 3.5% received anthracycline plus trastuzumab, 19.5% received other chemotherapy, and 46.5% received no chemotherapy. Anthracycline and trastuzumab recipients were younger, with fewer comorbidities than recipients of other chemotherapy or none. Compared with no chemotherapy, the risk of HF/CM was higher in patients treated with anthracycline alone (adjusted HR = 1.40, 95% CI = 1.11 to 1.76), although the increased risk was similar to other chemotherapy (adjusted HR = 1.49, 95% CI = 1.25 to 1.77); the risk was highly increased in patients treated with trastuzumab alone (adjusted HR = 4.12, 95% CI = 2.30 to 7.42) or anthracycline plus trastuzumab (adjusted HR = 7.19, 95% CI = 5.00 to 10.35). Conclusions Anthracycline and trastuzumab were primarily used in younger, healthier women and associated with increased HF/CM risk compared with no chemotherapy. This population-based observational study complements findings from clinical trials on cancer treatment safety. JF - Journal of the National Cancer Institute AU - Bowles, Erin JAiello AU - Wellman, Robert AU - Feigelson, Heather Spencer AU - Onitilo, Adedayo A AU - Freedman, Andrew N AU - Delate, Thomas AU - Allen, Larry A AU - Nekhlyudov, Larissa AU - Goddard, Katrina AB AU - Davis, Robert L AU - Habel, Laurel A AU - Yood, Marianne Ulcickas AU - Mccarty, Catherine AU - Magid, David J AU - Wagner, Edward H AD - Affiliations of authors: Group Health Research Institute, Group Health Cooperative, Seattle, WA (EJAB, RW, EHW); Institute for Health Research, Kaiser Permanente Colorado, Denver, CO (HSF, TD, DJM); Department of Hematology/Oncology, Marshfield Clinic Weston Center, Weston, WI (AAO, CM); Marshfield Clinic Research Foundation, Marshfield, WI (AAO); National Cancer Institute, Bethesda, MD (ANF); Division of Cardiology, University of Colorado, Aurora, CO (LAA); Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston, MA, and Department of Medicine, Harvard Vanguard Medical Associates, Boston, MA (LN); Center for Health Research, Kaiser Permanente Northwest, Portland, OR (KABG); Center for Health Research-Southeast, Kaiser Permanente Georgia, Atlanta, GA (RLD); Division of Research, Kaiser Permanente Northern California, Oakland, CA (LAH); Department of Research, Henry Ford Hospital and Health System, Detroit, MI (MUY); Essentia Institute of Rural Hea, bowles.e@ghc.org Y1 - 2012/09/05/ PY - 2012 DA - 2012 Sep 05 SP - 1293 EP - 1305 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 104 IS - 17 SN - 0027-8874, 0027-8874 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Age KW - Breast cancer KW - Cancer KW - Chemotherapy KW - Clinical trials KW - Morbidity KW - Radiation therapy 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/1125233832?accountid=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+the+National+Cancer+Institute&rft.atitle=Risk+of+Heart+Failure+in+Breast+Cancer+Patients+After+Anthracycline+and+Trastuzumab+Treatment%3A+A+Retrospective+Cohort+Study&rft.au=Bowles%2C+Erin+JAiello%3BWellman%2C+Robert%3BFeigelson%2C+Heather+Spencer%3BOnitilo%2C+Adedayo+A%3BFreedman%2C+Andrew+N%3BDelate%2C+Thomas%3BAllen%2C+Larry+A%3BNekhlyudov%2C+Larissa%3BGoddard%2C+Katrina+AB%3BDavis%2C+Robert+L%3BHabel%2C+Laurel+A%3BYood%2C+Marianne+Ulcickas%3BMccarty%2C+Catherine%3BMagid%2C+David+J%3BWagner%2C+Edward+H&rft.aulast=Bowles&rft.aufirst=Erin&rft.date=2012-09-05&rft.volume=104&rft.issue=17&rft.spage=1293&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=00278874&rft_id=info:doi/10.1093%2Fjnci%2Fdjs317 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2013-02-22 N1 - SubjectsTermNotLitGenreText - Radiation therapy; Age; Chemotherapy; Breast cancer; Clinical trials; Morbidity; Cancer DO - http://dx.doi.org/10.1093/jnci/djs317 ER - TY - JOUR T1 - Impact of caloric restriction on health and survival in rhesus monkeys from the NIA study AN - 1439235226; 18476812 AB - Calorie restriction (CR), a reduction of 10-40% in intake of a nutritious diet, is often reported as the most robust non-genetic mechanism to extend lifespan and healthspan. CR is frequently used as a tool to understand mechanisms behind ageing and age-associated diseases. In addition to and independently of increasing lifespan, CR has been reported to delay or prevent the occurrence of many chronic diseases in a variety of animals. Beneficial effects of CR on outcomes such as immune function, motor coordination and resistance to sarcopenia in rhesus monkeys have recently been reported. We report here that a CR regimen implemented in young and older age rhesus monkeys at the National Institute on Aging (NIA) has not improved survival outcomes. Our findings contrast with an ongoing study at the Wisconsin National Primate Research Center (WNPRC), which reported improved survival associated with 30% CR initiated in adult rhesus monkeys (7-14years) and a preliminary report with a small number of CR monkeys. Over the years, both NIA and WNPRC have extensively documented beneficial health effects of CR in these two apparently parallel studies. The implications of the WNPRC findings were important as they extended CR findings beyond the laboratory rodent and to a long-lived primate. Our study suggests a separation between health effects, morbidity and mortality, and similar to what has been shown in rodents, study design, husbandry and diet composition may strongly affect the life-prolonging effect of CR in a long-lived nonhuman primate. JF - Nature AU - Mattison, Julie A AU - Roth, George S AU - Beasley, TMark AU - Tilmont, Edward M AU - Handy, April M AU - Herbert, Richard L AU - Longo, Dan L AU - Allison, David B AU - Young, Jennifer E AU - Bryant, Mark AU - Barnard, Dennis AU - Ward, Walter F AU - Qi, Wenbo AU - Ingram, Donald K AU - de Cabo, Rafael AD - Laboratory of Experimental Gerontology, National Institute on Aging, NIH Animal Center, 16701 Elmer School Road Building 103, Dickerson, Maryland 20842, USA PY - 2012 SP - 318 EP - 321 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 489 IS - 7415 SN - 0028-0836, 0028-0836 KW - Ecology Abstracts KW - Diets KW - Mortality KW - Dietary restrictions KW - Life span KW - Aging KW - Survival KW - sarcopenia KW - Primates KW - Morbidity KW - Nutrient deficiency KW - Geriatrics KW - Macaca mulatta KW - Immune response KW - Husbandry KW - D 04040:Ecosystem and Ecology Studies UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1439235226?accountid=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=Impact+of+caloric+restriction+on+health+and+survival+in+rhesus+monkeys+from+the+NIA+study&rft.au=Mattison%2C+Julie+A%3BRoth%2C+George+S%3BBeasley%2C+TMark%3BTilmont%2C+Edward+M%3BHandy%2C+April+M%3BHerbert%2C+Richard+L%3BLongo%2C+Dan+L%3BAllison%2C+David+B%3BYoung%2C+Jennifer+E%3BBryant%2C+Mark%3BBarnard%2C+Dennis%3BWard%2C+Walter+F%3BQi%2C+Wenbo%3BIngram%2C+Donald+K%3Bde+Cabo%2C+Rafael&rft.aulast=Mattison&rft.aufirst=Julie&rft.date=2012-09-03&rft.volume=489&rft.issue=7415&rft.spage=318&rft.isbn=&rft.btitle=&rft.title=Nature&rft.issn=00280836&rft_id=info:doi/10.1038%2Fnature11432 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-10-01 N1 - Last updated - 2015-12-23 N1 - SubjectsTermNotLitGenreText - Diets; Mortality; Nutrient deficiency; Dietary restrictions; Aging; Life span; Geriatrics; sarcopenia; Survival; Immune response; Husbandry; Morbidity; Macaca mulatta; Primates DO - http://dx.doi.org/10.1038/nature11432 ER - TY - JOUR T1 - A strategic plan to accelerate development of acute stroke treatments AN - 1780517201; PQ0002829361 AB - In order to reenergize acute stroke research and accelerate the development of new treatments, we need to transform the usual design and conduct of clinical trials to test for small but significant improvements in effectiveness, and treat patients as soon as possible after stroke onset when treatment effects are most detectable. This requires trials that include thousands of acute stroke patients. A plan to make these trials possible is proposed. There are four components: (1) free access to the electronic medical record; (2) a large stroke emergency network and clinical trial coordinating center connected in real time to hundreds of emergency departments; (3) a clinical trial technology development center; and (4) strategic leadership to raise funds, motivate clinicians to participate, and interact with politicians, insurers, legislators, and other national and international organizations working to advance the quality of stroke care. JF - Annals of the New York Academy of Sciences AU - Marler, John R AD - National Institute of Neurological Disorders and Stroke Acute Stroke Study Group, National Institutes of Health, Rockville, Maryland. Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 152 EP - 156 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 1268 IS - 1 SN - 0077-8923, 0077-8923 KW - Environment Abstracts KW - Funds KW - Stroke KW - International organizations KW - Clinical trials KW - Emergency medical services KW - Technology KW - ENA 08:International UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780517201?accountid=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=A+strategic+plan+to+accelerate+development+of+acute+stroke+treatments&rft.au=Marler%2C+John+R&rft.aulast=Marler&rft.aufirst=John&rft.date=2012-09-01&rft.volume=1268&rft.issue=1&rft.spage=152&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/10.1111%2Fj.1749-6632.2012.06714.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-04-29 N1 - SubjectsTermNotLitGenreText - Funds; International organizations; Stroke; Clinical trials; Technology; Emergency medical services DO - http://dx.doi.org/10.1111/j.1749-6632.2012.06714.x ER - TY - JOUR T1 - Down regulating HIV latency by transcription activation AN - 1673398549; PQ0001372708 AB - One difficulty in curing HIV/AIDS is the tendency of the virus to enter into latency, where minimal or no viral gene expression occurs. The sequestered virus is thus immune to chemotherapy. One way to subject the virus to therapy again would be to activate viral gene expression. Latency could be due to blockade both of transcriptional initiation and transcript elongation. We have tested this idea in a cell culture model of latency where lymphocytic Jurkat cells harbor latent env- and GFP+ provirus. We subjected these cells to treatment, singly and in combination, with inducers of initiation - NFkB activation with prostratin (5 uM), chromatin remodeling with hydroxamic acid (SAHA) (5uM), and promoter demethylation with Aza-deoxycytidine (AzaCdR) (1 uM)- and also deblocking of elongation by transactivation with Tat-1 by way of lentiviral vector (50 ul) transduction. The results (see Table) support the idea that latent virus expression can be activated and in some case it is advantageous to activate both transcriptional initiation and elongation. JF - Molecular Therapy AU - Arya, Suresh K AU - Holczbauer, Agnes AD - National Cancer Institute, National Institutes of Health, Bethesda, MD, USA Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 43 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 20 IS - 9 SN - 1525-0016, 1525-0016 KW - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts KW - Acquired immune deficiency syndrome KW - Chromatin remodeling KW - Chemotherapy KW - Transcription KW - Cell culture KW - Hydroxamic acid KW - NF- Kappa B protein KW - Transcription initiation KW - Gene expression KW - Promoters KW - Elongation KW - Demethylation KW - Human immunodeficiency virus KW - Transcription elongation KW - W 30905:Medical Applications KW - V 22360:AIDS and HIV UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673398549?accountid=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=Down+regulating+HIV+latency+by+transcription+activation&rft.au=Arya%2C+Suresh+K%3BHolczbauer%2C+Agnes&rft.aulast=Arya&rft.aufirst=Suresh&rft.date=2012-09-01&rft.volume=20&rft.issue=9&rft.spage=43&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Acquired immune deficiency syndrome; Chromatin remodeling; Chemotherapy; Transcription; Cell culture; Hydroxamic acid; Transcription initiation; NF- Kappa B protein; Gene expression; Elongation; Promoters; Demethylation; Transcription elongation; Human immunodeficiency virus ER - TY - JOUR T1 - Characterization of Surface Markers, Clonogenicity and Gene Expression during Neutrophil Differentiation from Human Induced Pluripotent Stem Cells AN - 1673397779; PQ0001372664 AB - We derived neutrophils from human induced pluripotent stem cells (iPSCs) through discontinuous culture over 32 days (18 days of embryoid body (EB) formation in hematopoietic stem cell (HSC) cytokines; EB dissociation and 7 days co-culture with OP9 stromal cells in HSC cytokines; transfer of non-adherent cells for final 7 days OP9 co-culture in G-CSF). The CD45 hematopoietic surface marker appeared gradually during the EB stage, but rose rapidly upon OP9 co-culture. The CD34 surface marker exhibited biphasic expression, with ~11% CD34+ but CD45- at day 10, likely representing hemangioblast precursors of both hematopoietic and endothelial cells, correlating with increased microRNA-126 expression. Our study provides the first detailed characterization of surface markers correlated with functional assay and transcription factor expression during neutrophil differentiation from human iPSCs. This begins to define complete myeloid differentiation from human iPSCs, and will help to identify stages for further manipulating this process. JF - Molecular Therapy AU - Wang, Hongmei AU - Sweeney, Colin AU - Malech, Harry L AD - Laboratory of Host Defenses, NIAID, NIH, Bethesda, MD Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 18 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 20 IS - 9 SN - 1525-0016, 1525-0016 KW - Genetics Abstracts; Immunology Abstracts; Biotechnology and Bioengineering Abstracts KW - CD45 antigen KW - stromal cells KW - Inhibitory postsynaptic potentials KW - miRNA KW - Leukocytes (neutrophilic) KW - CD34 antigen KW - Cell culture KW - Granulocyte colony-stimulating factor KW - Endothelial cells KW - Gene expression KW - Differentiation KW - Stem cells KW - Hemangioblasts KW - Transcription factors KW - Cytokines KW - Hemopoiesis KW - Surface markers KW - W 30940:Products KW - F 06960:Molecular Immunology KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673397779?accountid=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=Characterization+of+Surface+Markers%2C+Clonogenicity+and+Gene+Expression+during+Neutrophil+Differentiation+from+Human+Induced+Pluripotent+Stem+Cells&rft.au=Wang%2C+Hongmei%3BSweeney%2C+Colin%3BMalech%2C+Harry+L&rft.aulast=Wang&rft.aufirst=Hongmei&rft.date=2012-09-01&rft.volume=20&rft.issue=9&rft.spage=18&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - stromal cells; CD45 antigen; miRNA; Inhibitory postsynaptic potentials; Leukocytes (neutrophilic); Cell culture; CD34 antigen; Granulocyte colony-stimulating factor; Gene expression; Endothelial cells; Differentiation; Stem cells; Hemangioblasts; Transcription factors; Hemopoiesis; Cytokines; Surface markers ER - TY - JOUR T1 - Pentostatin-based Host Conditioning and Syngeneic Th1/Tc1 Cell Transfer Each Contribute to the Regression of Established Murine Prostate Carcinoma Tumors AN - 1673391702; PQ0001372689 AB - Host conditioning is often used to enhance adoptive T cell therapy, yet the independent (direct) effect of conditioning on anti-tumor responses remains an important therapeutic consideration. Here, we have evaluated whether this PC regimen might also directly mediate anti-tumor responses in a murine model of established prostate carcinoma; of note, there are no reports in the literature to indicate that pentostatin mediates anti-tumor responses against solid tumors. We hypothesized that (1) because solid tumors reportedly have elevated levels of ADA, anti-tumor effects may be attained using a PC conditioning regimen; and (2) T1.R cells may induce an anti-tumor effect that is enhanced by the PC regimen. We have made the novel observation that PC chemotherapy directly mediates anti-tumor effects against non-hematopoietic tumor cells. Host immune depletion using PC thus offers the additional benefit of controlling aggressive solid tumor growth prior to adoptive T cell therapy. Subsequent adoptive transfer of rapamycinresistant Th1/Tc1 cells further induces significant tumor volume reduction. In conclusion, syngeneic T1.R cell therapy after P/C conditioning represents a new immune therapy approach. JF - Molecular Therapy AU - Mossoba, Miriam AU - Felizardo, Tania AU - Foley, Jason AU - Medin, Jeffrey A AU - Fowler, Daniel H AD - Experimental Transplantation and Immunology Branch, National Cancer Institute (NCI), Bethesda, MD, United States Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 31 EP - 32 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 20 IS - 9 SN - 1525-0016, 1525-0016 KW - Immunology Abstracts; Biotechnology and Bioengineering Abstracts KW - prostate carcinoma KW - Solid tumors KW - Helper cells KW - Chemotherapy KW - Lymphocytes T KW - Adoptive transfer KW - Animal models KW - Tumors KW - Tumor cells KW - F 06960:Molecular Immunology KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673391702?accountid=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=Pentostatin-based+Host+Conditioning+and+Syngeneic+Th1%2FTc1+Cell+Transfer+Each+Contribute+to+the+Regression+of+Established+Murine+Prostate+Carcinoma+Tumors&rft.au=Mossoba%2C+Miriam%3BFelizardo%2C+Tania%3BFoley%2C+Jason%3BMedin%2C+Jeffrey+A%3BFowler%2C+Daniel+H&rft.aulast=Mossoba&rft.aufirst=Miriam&rft.date=2012-09-01&rft.volume=20&rft.issue=9&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - prostate carcinoma; Solid tumors; Chemotherapy; Helper cells; Animal models; Adoptive transfer; Lymphocytes T; Tumors; Tumor cells ER - TY - JOUR T1 - Expression of the Transcriptional Co-Activator PGC1 alpha by a Lentiviral Vector in Human Neural Progenitor Cells Arrests Cell Proliferation, Induces beta -tubulin III Expression and Causes a Microtubule Catastrophe - Balancing ATP Production with Microtubule Stability AN - 1673391588; PQ0001372730 AB - The transcriptional co-activator PGC1 alpha , in conjunction with several transcription factors, plays an important regulatory role in mitochondrial biosynthesis and metabolic homeostasis. It also provides neuroprotection under oxidative and metabolic stress. Here we describe for the first time that the overexpression of PGC1 alpha in neural cells impacts microtubule stability, which may contribute to neurodegeneration. To examine whether PGC1 alpha plays a role at early stages during neural differentiation, proliferating human neural progenitor cells (hNPCs) were infected with a PGC1 alpha -encoding vector or control vectors. The induction of [Beta]-tubulin III by PGC1 alpha will be discussed with respect to its potential effect on microtubule stability during neurodegeneration and the switch from oxidative phosphorylation to glycolysis in cancer cells. JF - Molecular Therapy AU - Schubert, Manfred AU - Fishman, Paul S AD - National Institute of Neurological Disorders and Stroke, NIH, Bethesda MD Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 55 EP - 56 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 20 IS - 9 SN - 1525-0016, 1525-0016 KW - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts KW - Microtubules KW - Oxidative phosphorylation KW - Stress KW - Mitochondria KW - ATP KW - Neuroprotection KW - Homeostasis KW - Neurodegeneration KW - Cancer KW - Expression vectors KW - Differentiation KW - Transcription factors KW - Tubulin KW - Cell proliferation KW - Glycolysis KW - Neural stem cells KW - W 30905:Medical Applications KW - V 22310:Genetics, Taxonomy & Structure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673391588?accountid=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=Expression+of+the+Transcriptional+Co-Activator+PGC1+alpha+by+a+Lentiviral+Vector+in+Human+Neural+Progenitor+Cells+Arrests+Cell+Proliferation%2C+Induces+beta+-tubulin+III+Expression+and+Causes+a+Microtubule+Catastrophe+-+Balancing+ATP+Production+with+Microtubule+Stability&rft.au=Schubert%2C+Manfred%3BFishman%2C+Paul+S&rft.aulast=Schubert&rft.aufirst=Manfred&rft.date=2012-09-01&rft.volume=20&rft.issue=9&rft.spage=55&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Microtubules; Oxidative phosphorylation; ATP; Mitochondria; Stress; Neuroprotection; Homeostasis; Neurodegeneration; Cancer; Expression vectors; Differentiation; Transcription factors; Cell proliferation; Tubulin; Neural stem cells; Glycolysis ER - TY - JOUR T1 - Enrichment of melanoma-reactive cells from the fresh tumor digest through selection of CD8 T cells expressing PD-1, LAG-3, Tim-3 and 41 BB AN - 1673391585; PQ0001372638 AB - Due to the unknown antigen specificities of melanoma-derived TIL, enrichment of tumor-reactive cells from the fresh tumor digest remains a challenge. The identification of a specific phenotype within the fresh tumor digest that would include the tumor-reactive cells and separate them from the non-reactive ones would enable us to enrich the tumor-reactive cells without the need for screening for tumor-reactivity. The main objective of our work was to characterize the phenotype of TIL in fresh melanoma tumor digests and to assess the usefulness of the markers studied to enrich for tumor-specific cells. In order to do this, we studied the expression of PD-1, Tim-3, LAG-3 and 41BB on CD8 T cells in the fresh melanoma digest, as well as their differentiation stage (CD62L, CCR7, CD45RO, CD27, CD28 and CD57). Our results suggest that tumor-reactive T cells in the fresh melanoma digest express PD-1, LAG-3, Tim-3 and 41BB and thus, these markers can be used to enrich for melanoma-reactive cells. JF - Molecular Therapy AU - Gros, Alena AU - Turcotte, Simon AU - Tran, Eric AU - Inozume, Takashi AU - Hanada, Ken-ichi AU - Wang, Qiong AU - Dudley, Mark E AU - Wunderlich, John R AU - Yang, James C AU - Rosenberg, Steven A AD - Surgery Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 2 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 20 IS - 9 SN - 1525-0016, 1525-0016 KW - Immunology Abstracts; Biotechnology and Bioengineering Abstracts KW - CD223 antigen KW - CD28 antigen KW - CD8 antigen KW - Tumors KW - Melanoma KW - Differentiation KW - PD-1 protein KW - CC chemokine receptors KW - CD57 antigen KW - CD27 antigen KW - Lymphocytes T KW - CCR7 protein KW - CD62L protein KW - F 06960:Molecular Immunology KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1673391585?accountid=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=Enrichment+of+melanoma-reactive+cells+from+the+fresh+tumor+digest+through+selection+of+CD8+T+cells+expressing+PD-1%2C+LAG-3%2C+Tim-3+and+41+BB&rft.au=Gros%2C+Alena%3BTurcotte%2C+Simon%3BTran%2C+Eric%3BInozume%2C+Takashi%3BHanada%2C+Ken-ichi%3BWang%2C+Qiong%3BDudley%2C+Mark+E%3BWunderlich%2C+John+R%3BYang%2C+James+C%3BRosenberg%2C+Steven+A&rft.aulast=Gros&rft.aufirst=Alena&rft.date=2012-09-01&rft.volume=20&rft.issue=9&rft.spage=2&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-04-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - CD223 antigen; Tumors; CD8 antigen; CD28 antigen; Melanoma; PD-1 protein; Differentiation; CC chemokine receptors; CD27 antigen; CD57 antigen; Lymphocytes T; CCR7 protein; CD62L protein ER - TY - JOUR T1 - Regular black tea habit could reduce tobacco associated ROS generation and DNA damage in oral mucosa of normal population AN - 1642610525; 21138031 AB - Tobacco and tea habit are very common in world wide. In the present study, an attempt was made to evaluate the effect of regular drinking of black tea on reactive oxygen species (ROS) generation and DNA damage in buccal cells of normal subjects with or without tobacco habit. Expression of ROS associated proteins I Kappa B, NF- Kappa B as well as DNA repair associated proteins p53, MLH1 were also analyzed. Exfoliated buccal cells were collected from 308 healthy individuals and classified according to age, tobacco and tea habits. In all age groups, comparatively high ROS level and significantly high DNA damage frequency were seen in individuals with tobacco habit than the subjects without tea and tobacco habits. Tea habit effectively lowered ROS level and restrict DNA damage in tobacco users irrespective of ages. The DNA damage seen in the subjects was not associated with apoptosis. Moreover, tea habit effectively lowered the expression of I Kappa B, NF- Kappa B, p53 and MLH1 in tobacco users in all age groups. It seems that regular black tea habit could have anti-genotoxic effect as revealed by reduced tobacco associated ROS generation and DNA damage in buccal cells. JF - Food and Chemical Toxicology AU - Pal, Debolina AU - Sur, Subhayan AU - Mandal, Shyamsundar AU - Das, Sukta AU - Panda, Chinmay Kumar AD - Department of Oncogene Regulation, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata 700 026, India Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 2996 EP - 3003 PB - Elsevier B.V., P.O. Box 800 Kidlington Oxford OX5 1DX United Kingdom VL - 50 IS - 9 SN - 0278-6915, 0278-6915 KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - Exfoliated buccal cells KW - Black tea KW - Reactive oxygen species (ROS) KW - DNA damage KW - Drinking KW - MLH1 protein KW - Age KW - Apoptosis KW - Mucosa KW - DNA repair KW - p53 protein KW - NF- Kappa B protein KW - Reactive oxygen species KW - Tea KW - Tobacco KW - X 24380:Social Poisons & Drug Abuse KW - N 14820:DNA Metabolism & Structure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1642610525?accountid=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=Food+and+Chemical+Toxicology&rft.atitle=Regular+black+tea+habit+could+reduce+tobacco+associated+ROS+generation+and+DNA+damage+in+oral+mucosa+of+normal+population&rft.au=Pal%2C+Debolina%3BSur%2C+Subhayan%3BMandal%2C+Shyamsundar%3BDas%2C+Sukta%3BPanda%2C+Chinmay+Kumar&rft.aulast=Pal&rft.aufirst=Debolina&rft.date=2012-09-01&rft.volume=50&rft.issue=9&rft.spage=2996&rft.isbn=&rft.btitle=&rft.title=Food+and+Chemical+Toxicology&rft.issn=02786915&rft_id=info:doi/10.1016%2Fj.fct.2012.06.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-01-01 N1 - Last updated - 2016-06-22 N1 - SubjectsTermNotLitGenreText - Drinking; MLH1 protein; DNA damage; Age; Apoptosis; Reactive oxygen species; Tea; Mucosa; Tobacco; DNA repair; NF- Kappa B protein; p53 protein DO - http://dx.doi.org/10.1016/j.fct.2012.06.005 ER - TY - JOUR T1 - Olfactomedin 4 Inhibits Cathepsin C-Mediated Protease Activities, Thereby Modulating Neutrophil Killing of Staphylococcus aureus and Escherichia coli in Mice AN - 1551627268; 20354992 AB - Neutrophils kill bacteria generally through oxidative and nonoxidative mechanisms. Whereas much research has focused on the enzymes essential for neutrophil killing, little is known about the regulatory molecules responsible for such killing. In this study, we investigated the role of olfactomedin 4 (OLFM4), an olfactomedin-related glycoprotein, in neutrophil bactericidal capability and host innate immunity. Neutrophils from OLFM4-/- mice have increased intracellular killing of Staphylococcus aureus and Escherichia coli in vitro. The OLFM4-/- mice have enhanced in vivo bacterial clearance and are more resistant to sepsis when challenged with S. aureus or E. coli by i.p. injection. OLFM4 was found to interact with cathepsin C, a cysteine protease that plays an important role in bacterial killing and immune regulation. We demonstrated that OLFM4 inhibited cathepsin C activity in vitro and in vivo. The cathepsin C activity in neutrophils from OLFM4-/- mice was significantly higher than that in neutrophils from wild-type littermate mice. The activities of three serine proteases (neutrophil elastase, cathepsin G, and proteinase 3), which require cathepsin C activity for processing and maturity, were also significantly higher in OLFM4-/- neutrophils. The bacterial killing and clearance capabilities observed in OLFM4-/- mice that were enhanced relative to wild-type mice were significantly compromised by the additional loss of cathepsin C in mice with OLFM4 and cathepsin C double deficiency. These results indicate that OLFM4 is an important negative regulator of neutrophil bactericidal activity by restricting cathepsin C activity and its downstream granule-associated serine proteases. JF - Journal of Immunology AU - Liu, Wenli AU - Yan, Ming AU - Liu, Yueqin AU - McLeish, Kenneth R AU - Coleman, William G AU - Rodgers, Griffin P AD - Molecular and Clinical Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda, MD 20892 Y1 - 2012/09/01/ PY - 2012 DA - 2012 Sep 01 SP - 2460 EP - 2467 PB - American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 United States VL - 189 IS - 5 SN - 0022-1767, 0022-1767 KW - CSA Neurosciences Abstracts; Microbiology Abstracts B: Bacteriology; Chemoreception Abstracts; Immunology Abstracts KW - Immunoregulation KW - Dipeptidyl-peptidase I KW - Serine proteinase KW - Elastase KW - Leukocytes (neutrophilic) KW - Enzymes KW - Immunity KW - Intracellular killing KW - Sepsis KW - proteinase 3 KW - Cathepsin G KW - Escherichia coli KW - cathepsins KW - Maturity KW - Glycoproteins KW - Staphylococcus aureus KW - Bactericidal activity KW - Olfactomedin KW - Cysteine proteinase KW - F 06910:Microorganisms & Parasites KW - N3 11024:Neuroimmunology KW - J 02340:Antibiotics & Antimicrobials KW - R 18160:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551627268?accountid=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=Olfactomedin+4+Inhibits+Cathepsin+C-Mediated+Protease+Activities%2C+Thereby+Modulating+Neutrophil+Killing+of+Staphylococcus+aureus+and+Escherichia+coli+in+Mice&rft.au=Liu%2C+Wenli%3BYan%2C+Ming%3BLiu%2C+Yueqin%3BMcLeish%2C+Kenneth+R%3BColeman%2C+William+G%3BRodgers%2C+Griffin+P&rft.aulast=Liu&rft.aufirst=Wenli&rft.date=2012-09-01&rft.volume=189&rft.issue=5&rft.spage=2460&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunology&rft.issn=00221767&rft_id=info:doi/10.4049%2Fjimmunol.1103179 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Dipeptidyl-peptidase I; Immunoregulation; Serine proteinase; Elastase; Leukocytes (neutrophilic); Enzymes; Immunity; Intracellular killing; Sepsis; proteinase 3; Cathepsin G; cathepsins; Glycoproteins; Maturity; Bactericidal activity; Olfactomedin; Cysteine proteinase; Escherichia coli; Staphylococcus aureus DO - http://dx.doi.org/10.4049/jimmunol.1103179 ER - TY - JOUR T1 - Automatic segmentation and supervised learning-based selection of nuclei in cancer tissue images AN - 1492651124; 18967543 AB - Analysis of preferential localization of certain genes within the cell nuclei is emerging as a new technique for the diagnosis of breast cancer. Quantitation requires accurate segmentation of 100-200 cell nuclei in each tissue section to draw a statistically significant result. Thus, for large-scale analysis, manual processing is too time consuming and subjective. Fortuitously, acquired images generally contain many more nuclei than are needed for analysis. Therefore, we developed an integrated workflow that selects, following automatic segmentation, a subpopulation of accurately delineated nuclei for positioning of fluorescence in situ hybridization-labeled genes of interest. Segmentation was performed by a multistage watershed-based algorithm and screening by an artificial neural network-based pattern recognition engine. The performance of the workflow was quantified in terms of the fraction of automatically selected nuclei that were visually confirmed as well segmented and by the boundary accuracy of the well-segmented nuclei relative to a 2D dynamic programming-based reference segmentation method. Application of the method was demonstrated for discriminating normal and cancerous breast tissue sections based on the differential positioning of the HES5 gene. Automatic results agreed with manual analysis in 11 out of 14 cancers, all four normal cases, and all five noncancerous breast disease cases, thus showing the accuracy and robustness of the proposed approach. copyright Published 2012 Wiley Periodicals, Inc. JF - Cytometry Part A AU - Nandy, Kaustav AU - Gudla, Prabhakar R AU - Amundsen, Ryan AU - Meaburn, Karen J AU - Misteli, Tom AU - Lockett, Stephen J AD - Department of Assymetric Operations, Johns Hopkins University Applied Physics Laboratory, Laurel, Maryland 20723-6099., nandyk@mail.nih.gov Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 743 EP - 754 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 81A IS - 9 SN - 1552-4922, 1552-4922 KW - Biotechnology and Bioengineering Abstracts KW - Algorithms KW - Nuclei KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492651124?accountid=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=Automatic+segmentation+and+supervised+learning-based+selection+of+nuclei+in+cancer+tissue+images&rft.au=Nandy%2C+Kaustav%3BGudla%2C+Prabhakar+R%3BAmundsen%2C+Ryan%3BMeaburn%2C+Karen+J%3BMisteli%2C+Tom%3BLockett%2C+Stephen+J&rft.aulast=Nandy&rft.aufirst=Kaustav&rft.date=2012-09-01&rft.volume=81A&rft.issue=9&rft.spage=743&rft.isbn=&rft.btitle=&rft.title=Cytometry+Part+A&rft.issn=15524922&rft_id=info:doi/10.1002%2Fcyto.a.22097 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-01-01 N1 - Last updated - 2014-02-11 N1 - SubjectsTermNotLitGenreText - Nuclei DO - http://dx.doi.org/10.1002/cyto.a.22097 ER - TY - JOUR T1 - Synthesis and cytotoxicity evaluation of novel pyrido[3,4-d]pyrimidine derivatives as potential anticancer agents AN - 1468359119; 18517812 AB - A new series of 4-substituted 2-amino pyrido[3,4-d]pyrimidine derivatives has been designed and synthesized as potential anticancer agents. These compounds were prepared from a common intermediate, 4-chloro-8-methoxy pyrido[3,4-d]pyrimidin-2-amine, followed by palladium catalyzed cross-coupling reactions or nucleophilic aromatic substitutions at the C-4 position. Evaluation of the representative analogs using the US National Cancer Institute's 60 human cancer cell line (NCI 60) panel identified some of these compounds as exhibiting highly selective activities against breast cancer and renal cancer cell lines. A structure-activity relationship (SAR) study was explored to facilitate further development of this new class of compounds. JF - MedChemComm AU - Wei, Linyi AU - Malhotra, Sanjay V AD - Laboratory of Synthetic Chemistry; SAIC-Frederick, Inc.; Frederick National Laboratory for Cancer Research; Frederick; MD 21702; USA; , malhotrasa@mail.nih.gov Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 1250 EP - 1257 PB - RSC Publishing, Thomas Graham House Cambridge, CB4 OWF United Kingdom VL - 3 IS - 10 SN - 2040-2503, 2040-2503 KW - Biotechnology and Bioengineering Abstracts KW - Tumor cell lines KW - Cytotoxicity KW - palladium KW - Kidney KW - Breast cancer KW - Antitumor agents KW - Structure-activity relationships KW - Aromatics KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1468359119?accountid=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=MedChemComm&rft.atitle=Synthesis+and+cytotoxicity+evaluation+of+novel+pyrido%5B3%2C4-d%5Dpyrimidine+derivatives+as+potential+anticancer+agents&rft.au=Wei%2C+Linyi%3BMalhotra%2C+Sanjay+V&rft.aulast=Wei&rft.aufirst=Linyi&rft.date=2012-09-01&rft.volume=3&rft.issue=10&rft.spage=1250&rft.isbn=&rft.btitle=&rft.title=MedChemComm&rft.issn=20402503&rft_id=info:doi/10.1039%2Fc2md20097j LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-12-01 N1 - Number of references - 25 N1 - Last updated - 2013-12-16 N1 - SubjectsTermNotLitGenreText - palladium; Cytotoxicity; Tumor cell lines; Kidney; Breast cancer; Structure-activity relationships; Antitumor agents; Aromatics DO - http://dx.doi.org/10.1039/c2md20097j ER - TY - JOUR T1 - Measures of Substance Consumption Among Substance Users, DSM-IV Abusers, and Those With DSM-IV Dependence Disorders in a Nationally Representative Sample AN - 1463067011; 201326255 AB - Objective: Neither the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised (DSM-III-R), nor the DSM-IV uses measures of substance consumption as part of the diagnostic criteria for substance use disorders. Therefore, this report examined the extent to which frequency and/or quantity of consumption across a broad spectrum of substances are associated with DSM-IV diagnoses of specific substance use disorders and whether there are informative hierarchical levels of consumption among users, abusers, and those who are substance dependent in the U.S. general population. Method: The analyses focused on consumption data from respondents of the 2001-2002 National Epidemiologic Survey of Alcohol and Related Disorders. Multinomial logistic regression was used to predict DSM-IV diagnoses of dependence or abuse based on the continuous consumption measures. Results: Among individuals who used substances, the substances with the greatest liability for dependence were nicotine first and cocaine second. For nearly all substances investigated, users without specific substance use disorders demonstrated lower levels of quantity and frequency of consumption relative to those with DSM-IV abuse and dependence disorders. Dose-response curves for the log odds of abuse and dependence suggested unidimensionality of abuse and dependence for frequency of alcohol drinking; frequency of cannabis use; frequency of opioid use; frequency of hallucinogen use; and, to a lesser extent, frequency of amphetamine use. However, the dose-response curves for the quantity of alcohol consumed demonstrated differential patterns for abuse and dependence such that alcohol dependence has a distinctly greater "quantity of use" relationship than that found among alcohol-abusing individuals. Conclusions: These results confirm the findings of others concerning the unidimensionality of abuse and dependence diagnoses when consumption variables alone are examined and suggest that consumption measures may be useful metrics gauging severity. Adapted from the source document. JF - Journal of Studies on Alcohol and Drugs AU - Moss, Howard B AU - Chen, Chiung M AU - Yi, Hsiao-Ye AD - National Institute on Alcohol Abuse and Alcoholism, National Institues of Health, MSC 9304. 5635 Fishers Lane. Bethesda, MD 20892-9304 mossh@mail.nih.gov Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 820 EP - 828 PB - Center of Alcohol Studies, Rutgers, The State University of New Jersey, Piscataway VL - 73 IS - 5 SN - 1937-1888, 1937-1888 KW - Abusers KW - Alcohol dependence KW - Substance abuse disorders KW - Cannabis KW - Consumption KW - Substance abuse KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1463067011?accountid=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=Measures+of+Substance+Consumption+Among+Substance+Users%2C+DSM-IV+Abusers%2C+and+Those+With+DSM-IV+Dependence+Disorders+in+a+Nationally+Representative+Sample&rft.au=Moss%2C+Howard+B%3BChen%2C+Chiung+M%3BYi%2C+Hsiao-Ye&rft.aulast=Moss&rft.aufirst=Howard&rft.date=2012-09-01&rft.volume=73&rft.issue=5&rft.spage=820&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 - 2013-12-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Consumption; Substance abuse disorders; Abusers; Alcohol dependence; Cannabis; Substance abuse ER - TY - JOUR T1 - Prospective study of ultraviolet radiation exposure and risk of cancer in the United States AN - 1443373473; 18611478 AB - Ecologic studies have reported that solar ultraviolet radiation (UVR) exposure is associated with cancer; however, little evidence is available from prospective studies. We aimed to assess the association between an objective measure of ambient UVR exposure and risk of total and site-specific cancer in a large, regionally diverse cohort [450,934 white, non-Hispanic subjects (50-71 years) in the prospective National Institutes of Health (NIH)-AARP Diet and Health Study] after accounting for individual-level confounding risk factors. Estimated erythemal UVR exposure from satellite Total Ozone Mapping Spectrometer (TOMS) data from NASA was linked to the US Census Bureau 2000 census tract (centroid) of baseline residence for each subject. We used Cox proportional hazards models adjusted for multiple potential confounders to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for quartiles of UVR exposure. Restricted cubic splines examined nonlinear relationships. Over 9 years of follow-up, UVR exposure was inversely associated with total cancer risk (N = 75,917; highest versus lowest quartile; HR = 0.97, 95% CI = 0.95-0.99; p-trend < 0.001). In site-specific cancer analyses, UVR exposure was associated with increased melanoma risk (highest versus lowest quartile; HR = 1.22, 95% CI = 1.13-1.32; p-trend < 0.001) and decreased risk of non-Hodgkin's lymphoma (HR = 0.82, 95% CI = 0.74-0.92) and colon (HR = 0.88, 95% CI = 0.82-0.96), squamous cell lung (HR = 0.86, 95% CI = 0.75-0.98), pleural (HR = 0.57, 95% CI = 0.38-0.84), prostate (HR = 0.91, 95% CI = 0.88-0.95), kidney (HR = 0.83, 95% CI = 0.73-0.94) and bladder (HR = 0.88, 95% CI = 0.81-0.96) cancers (all p-trend < 0.05). We also found nonlinear associations for some cancer sites, including the thyroid and pancreas. Our results add to mounting evidence for the influential role of UVR exposure on cancer. JF - International Journal of Cancer AU - Lin, Shih-Wen AU - Wheeler, David C AU - Park, Yikyung AU - Cahoon, Elizabeth K AU - Hollenbeck, Albert R AU - Freedman, DMichal AU - Abnet, Christian C AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD., lins4@mail.nih.gov Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - E1015 EP - E1023 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 131 IS - 6 SN - 0020-7136, 0020-7136 KW - Risk Abstracts KW - Risk assessment KW - Health risks KW - USA KW - Urinary bladder KW - Lung KW - Kidney KW - Thyroid KW - Census KW - Cancer KW - Melanoma KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443373473?accountid=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=Prospective+study+of+ultraviolet+radiation+exposure+and+risk+of+cancer+in+the+United+States&rft.au=Lin%2C+Shih-Wen%3BWheeler%2C+David+C%3BPark%2C+Yikyung%3BCahoon%2C+Elizabeth+K%3BHollenbeck%2C+Albert+R%3BFreedman%2C+DMichal%3BAbnet%2C+Christian+C&rft.aulast=Lin&rft.aufirst=Shih-Wen&rft.date=2012-09-01&rft.volume=131&rft.issue=6&rft.spage=E1015&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.27619 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-10-01 N1 - Last updated - 2013-10-21 N1 - SubjectsTermNotLitGenreText - Risk assessment; Health risks; Lung; Urinary bladder; Thyroid; Kidney; Census; Cancer; Melanoma; USA DO - http://dx.doi.org/10.1002/ijc.27619 ER - TY - JOUR T1 - Exposure to oral bisphosphonates and risk of cancer AN - 1443373368; 18611462 AB - Recently, oral bisphosphonate use has increased markedly in the United States and elsewhere. Little is known about cancer risks associated with these drugs. A few studies have observed associations between bisphosphonates and the risk of breast, colorectal and esophageal cancer. However, the risk of all cancer and the risk of other cancers have not been investigated. In our study, we examined the risk of all cancer and site specific cancers in individuals taking bisphosphonates. Data were extracted from the UK General Practice Research Database to compare site-specific cancer incidence in a cohort of oral bisphosphonate users and a control cohort. Hazard ratios (HRs) were calculated using Cox regression modeling. The bisphosphonate and control cohort contained 41,826 participants (mean age 70, 81% female). Overall, the bisphosphonate cohort compared with the control cohort had a reduced risk of all cancer after any bisphosphonate usage [HR = 0.87, 95% confidence interval (CI) 0.82, 0.92]. In the bisphosphonate cohort, compared with the control cohort, there was no evidence of a difference in the risk of lung (HR = 1.03, 95% CI 0.88, 1.20) or prostate cancer (HR = 0.86, 95% CI 0.67, 1.09) but breast (HR = 0.71, 95% CI 0.62, 0.81) and colorectal cancer (HR = 0.74, 95% CI, 0.60-0.91) were both reduced. Our findings indicate that bisphosphonates do not appear to increase cancer risk. Although reductions in breast and colorectal cancer incidence were observed in bisphosphonate users it is unclear, particularly for breast cancer, to what extent confounding by low bone density may explain the association. JF - International Journal of Cancer AU - Cardwell, Chris R AU - Abnet, Christian C AU - Veal, Philip AU - Hughes, Carmel M AU - Cantwell, Marie M AU - Murray, Liam J AD - Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD., c.cardwell@qub.ac.uk Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - E717 EP - E725 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 131 IS - 5 SN - 0020-7136, 0020-7136 KW - Health & Safety Science Abstracts; Risk Abstracts KW - British Isles KW - Health risks KW - USA KW - Prostate cancer KW - Bisphosphonates KW - Lung KW - Bone density KW - Breast cancer KW - Colorectal carcinoma KW - Risk reduction KW - Cancer 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/1443373368?accountid=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=Exposure+to+oral+bisphosphonates+and+risk+of+cancer&rft.au=Cardwell%2C+Chris+R%3BAbnet%2C+Christian+C%3BVeal%2C+Philip%3BHughes%2C+Carmel+M%3BCantwell%2C+Marie+M%3BMurray%2C+Liam+J&rft.aulast=Cardwell&rft.aufirst=Chris&rft.date=2012-09-01&rft.volume=131&rft.issue=5&rft.spage=E717&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.27389 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-10-01 N1 - Last updated - 2013-11-15 N1 - SubjectsTermNotLitGenreText - Health risks; Prostate cancer; Bisphosphonates; Lung; Bone density; Colorectal carcinoma; Breast cancer; Risk reduction; Cancer; British Isles; USA DO - http://dx.doi.org/10.1002/ijc.27389 ER - TY - JOUR T1 - Association of dietary fat intakes with risk of esophageal and gastric cancer in the NIH-AARP diet and health study AN - 1443370347; 18611473 AB - The aim of our study was to investigate whether intakes of total fat and fat subtypes were associated with esophageal adenocarcinoma (EAC), esophageal squamous cell carcinoma (ESCC), gastric cardia or gastric noncardia adenocarcinoma. From 1995-1996, dietary intake data was reported by 494,978 participants of the NIH-AARP cohort. The 630 EAC, 215 ESCC, 454 gastric cardia and 501 gastric noncardia adenocarcinomas accrued to the cohort. Cox proportional hazards regression was used to examine the association between the dietary fat intakes, whilst adjusting for potential confounders. Although apparent associations were observed in energy-adjusted models, multivariate adjustment attenuated results to null [e.g., EAC energy adjusted hazard ratio (HR) and 95% confidence interval (95% CI) 1.66 (1.27-2.18) p for trend <0.01; EAC multivariate adjusted HR (95% CI) 1.17 (0.84-1.64) p for trend = 0.58]. Similar patterns were also observed for fat subtypes [e.g., EAC saturated fat, energy adjusted HR (95% CI) 1.79 (1.37-2.33) p for trend <0.01; EAC saturated fat, multivariate adjusted HR (95% CI) 1.27 (0.91-1.78) p for trend = 0.28]. However, in multivariate models an inverse association for polyunsaturated fat (continuous) was seen for EAC in subjects with a body mass index (BMI) in the normal range (18.5-<25 kg/m super(2)) [HR (95% CI) 0.76 (0.63-0.92)], that was not present in overweight subjects [HR (95% CI) 1.04 (0.96-1.14)], or in unstratified analysis [HR (95% CI) 0.97 (0.90-1.05)]. p for interaction = 0.02. Overall, we found null associations between the dietary fat intakes with esophageal or gastric cancer risk; although a protective effect of polyunsaturated fat intake was seen for EAC in subjects with a normal BMI. JF - International Journal of Cancer AU - O'Doherty, Mark G AU - Freedman, Neal D AU - Hollenbeck, Albert R AU - Schatzkin, Arthur AU - Murray, Liam J AU - Cantwell, Marie M AU - Abnet, Christian C AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, MD., m.odoherty@qub.ac.uk Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 1376 EP - 1387 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 131 IS - 6 SN - 0020-7136, 0020-7136 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Diets KW - Health risks KW - Obesity KW - Energy KW - Body mass KW - Ingestion 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/1443370347?accountid=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=Association+of+dietary+fat+intakes+with+risk+of+esophageal+and+gastric+cancer+in+the+NIH-AARP+diet+and+health+study&rft.au=O%27Doherty%2C+Mark+G%3BFreedman%2C+Neal+D%3BHollenbeck%2C+Albert+R%3BSchatzkin%2C+Arthur%3BMurray%2C+Liam+J%3BCantwell%2C+Marie+M%3BAbnet%2C+Christian+C&rft.aulast=O%27Doherty&rft.aufirst=Mark&rft.date=2012-09-01&rft.volume=131&rft.issue=6&rft.spage=1376&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.27366 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-10-01 N1 - Last updated - 2013-12-04 N1 - SubjectsTermNotLitGenreText - Diets; Obesity; Health risks; Body mass; Energy; Ingestion; Cancer DO - http://dx.doi.org/10.1002/ijc.27366 ER - TY - JOUR T1 - Differential trajectories of age-related changes in components of executive and memory processes AN - 1438671985; 201321007 AB - Several studies have demonstrated age-related declines in general executive function and memory. In this study, we examined cross-sectional and longitudinal age effects in more specific cognitive processes that constitute executive function and memory. We postulated that, whereas some components of executive and memory functions would show age differences and longitudinal declines, other specific abilities would be maintained or even improve with repeated testing. In a sample of individuals =55 years old from the Baltimore Longitudinal Study of Aging, we found longitudinal declines in inhibition, manipulation, semantic retrieval, phonological retrieval, switching, and long-term memory over a maximum of 14 years follow-up. In contrast, abstraction, capacity, chunking, discrimination, and short-term memory were maintained or even improved longitudinally, probably due in part to repeated testing. Moreover, whereas several different abilities were correlated across participants' cross-sectional performance, longitudinal changes in performance showed more heterogeneous trajectories. Finally, compared with cross-sectional performance, longitudinal trajectories showed better distinction between participants with and those without later cognitive impairment. These results show that longitudinal cognitive aging of executive and memory functions is not a uniform process but a heterogeneous one and suggest that certain executive and memory functions remain stable despite age-related declines in other component processes. [Copyright American Psychological Association] JF - Psychology and Aging AU - Goh, Joshua O AU - An, Yang AU - Resnick, Susan M Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 707 EP - 719 PB - American Psychological Association, Washington DC VL - 27 IS - 3 SN - 0882-7974, 0882-7974 KW - aging KW - cross-sectional KW - executive function KW - longitudinal KW - memory KW - Short term KW - Ageing KW - Memory KW - Retrieval KW - Age differences KW - Executive function KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1438671985?accountid=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=Psychology+and+Aging&rft.atitle=Differential+trajectories+of+age-related+changes+in+components+of+executive+and+memory+processes&rft.au=Goh%2C+Joshua+O%3BAn%2C+Yang%3BResnick%2C+Susan+M&rft.aulast=Goh&rft.aufirst=Joshua&rft.date=2012-09-01&rft.volume=27&rft.issue=3&rft.spage=707&rft.isbn=&rft.btitle=&rft.title=Psychology+and+Aging&rft.issn=08827974&rft_id=info:doi/10.1037%2Fa0026715 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-10-01 N1 - Last updated - 2016-09-27 N1 - CODEN - PAGIEL N1 - SubjectsTermNotLitGenreText - Memory; Ageing; Age differences; Executive function; Retrieval; Short term DO - http://dx.doi.org/10.1037/a0026715 ER - TY - JOUR T1 - Computational prediction of N-linked glycosylation incorporating structural properties and patterns AN - 1434026141; 18513622 AB - Motivation: N-linked glycosylation occurs predominantly at the N-X-T/S motif, where X is any amino acid except proline. Not all N-X-T/S sequons are glycosylated, and a number of web servers for predicting N-linked glycan occupancy using sequence and/or residue pattern information have been developed. None of the currently available servers, however, utilizes protein structural information for the prediction of N-glycan occupancy.Results: Here, we describe a novel classifier algorithm, NGlycPred, for the prediction of glycan occupancy at the N-X-T/S sequons. The algorithm utilizes both structural as well as residue pattern information and was trained on a set of glycosylated protein structures using the Random Forest algorithm. The best predictor achieved a balanced accuracy of 0.687 under 10-fold cross-validation on a curated dataset of 479 N-X-T/S sequons and outperformed sequence-based predictors when evaluated on the same dataset. The incorporation of structural information, including local contact order, surface accessibility/composition and secondary structure thus improves the prediction accuracy of glycan occupancy at the N-X-T/S consensus sequon. Availability and Implementation: NGlycPred is freely available to non-commercial users as a web-based server at http://exon.niaid.nih.gov/nglycpred/. JF - Bioinformatics AU - Chuang, Gwo-Yu AU - Boyington, Jeffrey C AU - Joyce, M Gordon AU - Zhu, Jiang AU - Nabel, Gary J AU - Kwong, Peter D AU - Georgiev, Ivelin AD - Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MA 20892, USA Y1 - 2012/09/01/ PY - 2012 DA - 2012 Sep 01 SP - 2249 EP - 2255 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 28 IS - 17 SN - 1367-4803, 1367-4803 KW - Biotechnology and Bioengineering Abstracts KW - Proline KW - Data processing KW - Amino acids KW - Secondary structure KW - Algorithms KW - Forests KW - Glycosylation KW - Polysaccharides KW - Computer applications KW - Protein structure KW - N-linked glycans KW - Information processing KW - N-glycans KW - Bioinformatics KW - Internet KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434026141?accountid=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=Computational+prediction+of+N-linked+glycosylation+incorporating+structural+properties+and+patterns&rft.au=Chuang%2C+Gwo-Yu%3BBoyington%2C+Jeffrey+C%3BJoyce%2C+M+Gordon%3BZhu%2C+Jiang%3BNabel%2C+Gary+J%3BKwong%2C+Peter+D%3BGeorgiev%2C+Ivelin&rft.aulast=Chuang&rft.aufirst=Gwo-Yu&rft.date=2012-09-01&rft.volume=28&rft.issue=17&rft.spage=2249&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbts426 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2015-04-09 N1 - SubjectsTermNotLitGenreText - Proline; Amino acids; Data processing; Secondary structure; Algorithms; Forests; Glycosylation; Computer applications; Polysaccharides; Protein structure; N-linked glycans; N-glycans; Information processing; Bioinformatics; Internet DO - http://dx.doi.org/10.1093/bioinformatics/bts426 ER - TY - JOUR T1 - Sensitivity enhancement of remotely coupled NMR detectors using wirelessly powered parametric amplification AN - 1434025914; 18539684 AB - A completely wireless detection coil with an integrated parametric amplifier has been constructed to provide local amplification and transmission of MR signals. The sample coil is one element of a parametric amplifier using a zero-bias diode that mixes the weak MR signal with a strong pump signal that is obtained from an inductively coupled external loop. The NMR sample coil develops current gain via reduction in the effective coil resistance. Higher gain can be obtained by adjusting the level of the pumping power closer to the oscillation threshold, but the gain is ultimately constrained by the bandwidth requirement of MRI experiments. A feasibility study here shows that on a NaCl/D sub(2)O phantom, super(23)Na signals with 20 dB of gain can be readily obtained with a concomitant bandwidth of 144 kHz. This gain is high enough that the integrated coil with parametric amplifier, which is coupled inductively to external loops, can provide sensitivity approaching that of direct wire connection. Magn Reson Med, 2012. [copy 2012 Wiley Periodicals, Inc. JF - Magnetic Resonance in Medicine AU - Qian, Chunqi AU - Murphy-Boesch, Joseph AU - Dodd, Stephen AU - Koretsky, Alan AD - 10 Center Drive Room 3D17, National Institutes of Health, Bethesda, MD 20892., qianc2@ninds.nih.gov Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 989 EP - 996 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 68 IS - 3 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Oscillations KW - Magnetic resonance imaging KW - N.M.R. KW - Sodium chloride KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434025914?accountid=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=Sensitivity+enhancement+of+remotely+coupled+NMR+detectors+using+wirelessly+powered+parametric+amplification&rft.au=Qian%2C+Chunqi%3BMurphy-Boesch%2C+Joseph%3BDodd%2C+Stephen%3BKoretsky%2C+Alan&rft.aulast=Qian&rft.aufirst=Chunqi&rft.date=2012-09-01&rft.volume=68&rft.issue=3&rft.spage=989&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.23274 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2013-09-20 N1 - SubjectsTermNotLitGenreText - Oscillations; Magnetic resonance imaging; N.M.R.; Sodium chloride DO - http://dx.doi.org/10.1002/mrm.23274 ER - TY - JOUR T1 - Retrospective reconstruction of high temporal resolution cine images from real-time MRI using iterative motion correction AN - 1434025842; 18539658 AB - Cardiac function has traditionally been evaluated using breath-hold cine acquisitions. However, there is a great need for free breathing techniques in patients who have difficulty in holding their breath. Real-time cardiac MRI is a valuable alternative to the traditional breath-hold imaging approach, but the real-time images are often inferior in spatial and temporal resolution. This article presents a general method for reconstruction of high spatial and temporal resolution cine images from a real-time acquisition acquired over multiple cardiac cycles. The method combines parallel imaging and motion correction based on nonrigid registration and can be applied to arbitrary k-space trajectories. The method is demonstrated with real-time Cartesian imaging and Golden Angle radial acquisitions, and the motion-corrected acquisitions are compared with raw real-time images and breath-hold cine acquisitions in 10 (N = 10) subjects. Acceptable image quality was obtained in all motion-corrected reconstructions, and the resulting mean image quality score was (a) Cartesian real-time: 2.48, (b) Golden Angle real-time: 1.90 (1.00-2.50), (c) Cartesian motion correction: 3.92, (d) Radial motion correction: 4.58, and (e) Breath-hold cine: 5.00. The proposed method provides a flexible way to obtain high-quality, high-resolution cine images in patients with difficulty holding their breath. Magn Reson Med, 2012. [copy 2011 Wiley Periodicals, Inc. JF - Magnetic Resonance in Medicine AU - Hansen, Michael S AU - Soerensen, Thomas S AU - Arai, Andrew E AU - Kellman, Peter AD - Department of Computer Science and Institute of Clinical Medicine, Aarhus University, Aarhus, Denmark., michael.hansen@nih.gov Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 741 EP - 750 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 68 IS - 3 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Heart KW - Respiration KW - Magnetic resonance imaging KW - N.M.R. KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434025842?accountid=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=Retrospective+reconstruction+of+high+temporal+resolution+cine+images+from+real-time+MRI+using+iterative+motion+correction&rft.au=Hansen%2C+Michael+S%3BSoerensen%2C+Thomas+S%3BArai%2C+Andrew+E%3BKellman%2C+Peter&rft.aulast=Hansen&rft.aufirst=Michael&rft.date=2012-09-01&rft.volume=68&rft.issue=3&rft.spage=741&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.23284 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2013-10-21 N1 - SubjectsTermNotLitGenreText - Heart; Respiration; Magnetic resonance imaging; N.M.R. DO - http://dx.doi.org/10.1002/mrm.23284 ER - TY - JOUR T1 - Free-breathing inner-volume black-blood imaging of the human heart using two-dimensionally selective local excitation at 3 T AN - 1434023594; 18539672 AB - Black-blood fast spin-echo imaging is a powerful technique for the evaluation of cardiac anatomy. To avoid fold-over artifacts, using a sufficiently large field of view in phase-encoding direction is mandatory. The related oversampling affects scanning time and respiratory chest motion artifacts are commonly observed. The excitation of a volume that exclusively includes the heart without its surrounding structures may help to improve scan efficiency and minimize motion artifacts. Therefore, and by building on previously reported inner-volume approach, the combination of a black-blood fast spin-echo sequence with a two-dimensionally selective radiofrequency pulse is proposed for selective "local excitation" small field of view imaging of the heart. This local excitation technique has been developed, implemented, and tested in phantoms and in vivo. With this method, small field of view imaging of a user-specified region in the human thorax is feasible, scanning becomes more time efficient, motion artifacts can be minimized, and additional flexibility in the choice of imaging parameters can be exploited. Magn Reson Med, 2012. [copy 2011 Wiley Periodicals, Inc. JF - Magnetic Resonance in Medicine AU - Abd-Elmoniem, Khaled Z AU - Barmet, Christoph AU - Stuber, Matthias AD - Institute for Biomedical Engineering, University and ETH Zurich, Switzerland., abdelmoniemkz@mail.nih.gov Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 822 EP - 829 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 68 IS - 3 SN - 0740-3194, 0740-3194 KW - Biotechnology and Bioengineering Abstracts KW - Heart KW - Scanning KW - Thorax KW - N.M.R. KW - Chest KW - imaging KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434023594?accountid=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=Free-breathing+inner-volume+black-blood+imaging+of+the+human+heart+using+two-dimensionally+selective+local+excitation+at+3+T&rft.au=Abd-Elmoniem%2C+Khaled+Z%3BBarmet%2C+Christoph%3BStuber%2C+Matthias&rft.aulast=Abd-Elmoniem&rft.aufirst=Khaled&rft.date=2012-09-01&rft.volume=68&rft.issue=3&rft.spage=822&rft.isbn=&rft.btitle=&rft.title=Magnetic+Resonance+in+Medicine&rft.issn=07403194&rft_id=info:doi/10.1002%2Fmrm.23305 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2013-09-20 N1 - SubjectsTermNotLitGenreText - Heart; Scanning; Thorax; N.M.R.; Chest; imaging DO - http://dx.doi.org/10.1002/mrm.23305 ER - TY - JOUR T1 - A Longitudinal Process Analysis of Mother-Child Emotional Relationships in a Rural Appalachian European American Community AN - 1417525078; 201306913 AB - This prospective longitudinal study examines emotional relationships in 58 Appalachian mother-child dyads observed at home at 5 and 20 months. Between infancy and toddlerhood, 3 of 4 dimensions of dyadic emotional relationships were stable, and three remained continuous in their mean level. Increasing maternal age was associated with greater maternal sensitivity and structuring and with more responsive and involving children. Marital status and father presence in the home as well as maternal openness, parenting knowledge, investment, and satisfaction accounted for effects of maternal age on dyadic emotional relationships. This longitudinal process analysis provides unique insights into temporal dynamics of mother-child emotional relationships and their determinants in an underserved and underresearched US community. Implications for community-specific interventions are discussed. Adapted from the source document. JF - American Journal of Community Psychology AU - Bornstein, Marc H AU - Putnick, Diane L AU - Suwalsky, Joan T D AD - Child and Family Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Public Health Service Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 89 EP - 100 PB - Springer, Dordrecht The Netherlands VL - 50 IS - 1-2 SN - 0091-0562, 0091-0562 KW - Marital Status KW - Mothers KW - United States of America KW - Intervention KW - Europe KW - Childrearing Practices KW - Fathers KW - Rural Areas KW - Knowledge KW - article KW - 6152: community development/organizing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1417525078?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Asocialservices&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Community+Psychology&rft.atitle=A+Longitudinal+Process+Analysis+of+Mother-Child+Emotional+Relationships+in+a+Rural+Appalachian+European+American+Community&rft.au=Bornstein%2C+Marc+H%3BPutnick%2C+Diane+L%3BSuwalsky%2C+Joan+T+D&rft.aulast=Bornstein&rft.aufirst=Marc&rft.date=2012-09-01&rft.volume=50&rft.issue=1-2&rft.spage=89&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Community+Psychology&rft.issn=00910562&rft_id=info:doi/10.1007%2Fs10464-011-9479-1 LA - English DB - Social Services Abstracts N1 - Date revised - 2013-08-01 N1 - Last updated - 2016-09-28 N1 - CODEN - AJCPCK N1 - SubjectsTermNotLitGenreText - Mothers; Marital Status; Knowledge; Intervention; Childrearing Practices; Rural Areas; United States of America; Fathers; Europe DO - http://dx.doi.org/10.1007/s10464-011-9479-1 ER - TY - JOUR T1 - A nanoscale graphene oxide-peptide biosensor for real-time specific biomarker detection on the cell surface AN - 1399905873; 17144126 AB - A nanoscale RGD-pyrene-graphene oxide (GO) biosensor was prepared for real-time in situdetection of a cancer cell surface marker, integrin alpha v beta 3. This nanoscale GO-based biosensor is simple, robust, sensitive and of high selectivity. It can also be adapted to other cancer cell surface marker evaluation systems. JF - Chemical Communications: Chem Comm AU - Wang, Zhe AU - Huang, Peng AU - Bhirde, Ashwinkumar AU - Jin, Albert AU - Ma, Ying AU - Niu, Gang AU - Neamati, Nouri AU - Chen, Xiaoyuan AD - Center for Molecular Imaging and Translational Medicine; School of Public Health; Xiamen University; Xiamen; China; 361005; , shawn.chen@nih.gov Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 9768 EP - 9770 PB - Royal Society of Chemistry VL - 48 IS - 78 SN - 1359-7345, 1359-7345 KW - Biotechnology and Bioengineering Abstracts KW - Biosensors KW - W 30955:Biosensors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399905873?accountid=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=Chemical+Communications%3A+Chem+Comm&rft.atitle=A+nanoscale+graphene+oxide-peptide+biosensor+for+real-time+specific+biomarker+detection+on+the+cell+surface&rft.au=Wang%2C+Zhe%3BHuang%2C+Peng%3BBhirde%2C+Ashwinkumar%3BJin%2C+Albert%3BMa%2C+Ying%3BNiu%2C+Gang%3BNeamati%2C+Nouri%3BChen%2C+Xiaoyuan&rft.aulast=Wang&rft.aufirst=Zhe&rft.date=2012-09-01&rft.volume=48&rft.issue=78&rft.spage=9768&rft.isbn=&rft.btitle=&rft.title=Chemical+Communications%3A+Chem+Comm&rft.issn=13597345&rft_id=info:doi/10.1039%2Fc2cc31974h LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-07-01 N1 - Number of references - 1 N1 - Last updated - 2014-02-21 N1 - SubjectsTermNotLitGenreText - Biosensors DO - http://dx.doi.org/10.1039/c2cc31974h ER - TY - JOUR T1 - Fractionation of social brain circuits in autism spectrum disorders AN - 1323347037; 201305463 AB - Autism spectrum disorders are developmental disorders characterized by impairments in social and communication abilities and repetitive behaviours. Converging neuroscientific evidence has suggested that the neuropathology of autism spectrum disorders is widely distributed, involving impaired connectivity throughout the brain. Here, we evaluate the hypothesis that decreased connectivity in high-functioning adolescents with an autism spectrum disorder relative to typically developing adolescents is concentrated within domain-specific circuits that are specialized for social processing. Using a novel whole-brain connectivity approach in functional magnetic resonance imaging, we found that not only are decreases in connectivity most pronounced between regions of the social brain but also they are selective to connections between limbic-related brain regions involved in affective aspects of social processing from other parts of the social brain that support language and sensorimotor processes. This selective pattern was independently obtained for correlations with measures of social symptom severity, implying a fractionation of the social brain in autism spectrum disorders at the level of whole circuits. Adapted from the source document JF - Brain AU - Gotts, Stephen J AU - Simmons, W Kyle AU - Milbury, Lydia A AU - Wallace, Gregory L AU - Cox, Robert W AU - Martin, Alex AD - Section on Cognitive Neuropsychology, Laboratory of Brain and Cognition, National Institute of Mental Health (NIMH), National Institutes of Health, Bethesda, MD 20892, USA gottss@mail.nih.gov Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 2711 EP - 2725 VL - 135 IS - 9 SN - 0006-8950, 0006-8950 KW - Autism (06800) KW - Developmental Disabilities (18450) KW - Communication Disorders (13625) KW - Magnetic Resonance Imaging (MRI) (50620) KW - Brain (09350) KW - Social Factors (79910) 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/1323347037?accountid=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=Brain&rft.atitle=Fractionation+of+social+brain+circuits+in+autism+spectrum+disorders&rft.au=Gotts%2C+Stephen+J%3BSimmons%2C+W+Kyle%3BMilbury%2C+Lydia+A%3BWallace%2C+Gregory+L%3BCox%2C+Robert+W%3BMartin%2C+Alex&rft.aulast=Gotts&rft.aufirst=Stephen&rft.date=2012-09-01&rft.volume=135&rft.issue=9&rft.spage=2711&rft.isbn=&rft.btitle=&rft.title=Brain&rft.issn=00068950&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2013-04-01 N1 - Last updated - 2016-09-27 N1 - CODEN - BRAIAK N1 - SubjectsTermNotLitGenreText - Magnetic Resonance Imaging (MRI) (50620); Autism (06800); Communication Disorders (13625); Social Factors (79910); Brain (09350); Developmental Disabilities (18450) ER - TY - JOUR T1 - Modeling individual vulnerability to communicable diseases: a framework and design AN - 1312418508; 4409737 AB - Reports on dangerous communicable diseases, such as severe acute respiratory syndrome (SARS) and H1N1 flu, have repeatedly stressed the importance of individuals in disease transmission. Still in its infancy, individual-based modeling faces many challenges. From the perspective of modeling approaches, this article explores (1) the framework of a three-population (daytime, nighttime, and pastime population) and two-scale (local and societal scale) social network; (2) a design that can represent heterogeneous, mobile, interacting individuals and their individualized vulnerability to infection; and (3) a simulation of individuals' vulnerability to influenza in an urban area in the Northeastern United States to illustrate the proposed framework and design. Simulation results correspond well to the reported epidemic information. The findings offer a valuable platform to devise much-needed spatially and temporally oriented control and intervention strategies for communicable diseases. JF - Annals of the Association of American Geographers AU - Wilson, Deborah AU - Bian, Ling AU - Huang, Yuxia AU - Mao, Liang AU - Lim, Eunjung AU - Lee, Gyoungju AU - Yang, Yan AU - Cohen, Murray AD - State University of New York, Buffalo ; Texas A&M University ; University of Florida ; University of Maryland ; Korea National University ; National Institutes of Health Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 1016 EP - 1025 VL - 102 IS - 5 SN - 0004-5608, 0004-5608 KW - Sociology KW - Social networks KW - Epidemics KW - Down's syndrome KW - Diseases KW - U.S.A. KW - Urban areas KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312418508?accountid=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=Annals+of+the+Association+of+American+Geographers&rft.atitle=Modeling+individual+vulnerability+to+communicable+diseases%3A+a+framework+and+design&rft.au=Wilson%2C+Deborah%3BBian%2C+Ling%3BHuang%2C+Yuxia%3BMao%2C+Liang%3BLim%2C+Eunjung%3BLee%2C+Gyoungju%3BYang%2C+Yan%3BCohen%2C+Murray&rft.aulast=Wilson&rft.aufirst=Deborah&rft.date=2012-09-01&rft.volume=102&rft.issue=5&rft.spage=1016&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+Association+of+American+Geographers&rft.issn=00045608&rft_id=info:doi/10.1080%2F00045608.2012.674844 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2013-06-12 N1 - Last updated - 2013-09-16 N1 - SubjectsTermNotLitGenreText - 3617 6220; 11873 8634; 4356 3617 6220; 3718 6220; 10449 5772; 13161 1247; 433 293 14 DO - http://dx.doi.org/10.1080/00045608.2012.674844 ER - TY - JOUR T1 - Diagnosis disclosure, medication hiding, and medical functioning among perinatally infected, HIV-positive children and adolescents AN - 1283738922; 201300841 AB - Little is known about the immunological and virological impact of diagnosis disclosure among HIV-positive children and adolescents. The current cross-sectional study examined medication hiding as a mediator of the relationship between disclosure to friends and three medical outcomes: CD4+ absolute count, CD4+ percentage, and viral load. Participants included 25 perinatally infected, HIV-positive children and adolescents ages 11-18 years from the US. Diagnosis disclosure and medication hiding were self-reported by participants and medical markers were derived from blood samples drawn during the same clinic visit. Bootstrapping analyses revealed that disclosure to at least one friend (versus no friends) was associated with less medication hiding, which was associated with higher CD4+ absolute counts and percentages but not viral load. Further, among the subset of participants who had disclosed to at least one friend (n = 19), those who reported disclosing to 11 or more versus 1-10 friends were less likely to hide medication taking, which was associated with higher CD4+ absolute counts. Findings suggest HIV-positive children and adolescents' diagnosis disclosure to friends corresponds to less medication hiding, ultimately yielding better immune functioning. Health care providers should be cognizant of these potential medical benefits associated with disclosure when offering support around disclosure decision-making. Adapted from the source document. JF - AIDS Care AU - Calabrese, Sarah K AU - Martin, Staci AU - Wolters, Pamela L AU - Toledo-Tamula, Mary A AU - Brennan, Tara L AU - Wood, Lauren V AD - Center for Interdisciplinary Research on AIDS, Yale University, New Haven, CT, USA Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 1092 EP - 1096 PB - Taylor & Francis, Abingdon UK VL - 24 IS - 9 SN - 0954-0121, 0954-0121 KW - pediatric HIV disclosure HAART medical functioning KW - Diagnosis KW - Children KW - HIV KW - Friends KW - Disclosure KW - Adolescents KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1283738922?accountid=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=AIDS+Care&rft.atitle=Diagnosis+disclosure%2C+medication+hiding%2C+and+medical+functioning+among+perinatally+infected%2C+HIV-positive+children+and+adolescents&rft.au=Calabrese%2C+Sarah+K%3BMartin%2C+Staci%3BWolters%2C+Pamela+L%3BToledo-Tamula%2C+Mary+A%3BBrennan%2C+Tara+L%3BWood%2C+Lauren+V&rft.aulast=Calabrese&rft.aufirst=Sarah&rft.date=2012-09-01&rft.volume=24&rft.issue=9&rft.spage=1092&rft.isbn=&rft.btitle=&rft.title=AIDS+Care&rft.issn=09540121&rft_id=info:doi/10.1080%2F09540121.2012.699670 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-02-01 N1 - Last updated - 2016-09-27 N1 - CODEN - AIDCEF N1 - SubjectsTermNotLitGenreText - Disclosure; Friends; Adolescents; HIV; Diagnosis; Children DO - http://dx.doi.org/10.1080/09540121.2012.699670 ER - TY - JOUR T1 - Using collaborative web technology to construct the health information national trends survey AN - 1272075835; 4386017 AB - Scientists are taking advantage of web-based technology to work in new collaborative environments, a phenomenon known as Science 2.0 . The National Cancer Institute created a web-based tool called HINTS-GEM, which allows a diverse group of stakeholders to collaborate in a virtual environment by providing input on content for the Health Information National Trends Survey (HINTS). This involved stakeholders providing new suggested content and commenting and rating on existing content. HINTS is a nationally representative survey of the US noninstitutionalized adult population. This article describes the conceptual development of HINTS-GEM and provides results of its use by stakeholders in creating an improved survey instrument. Reprinted by permission of Taylor & Francis Ltd. JF - Journal of health communication AU - Moser, Richard P AU - Beckjord, Ellen Burke AU - Finney Rutten, Lila J AU - Blake, Kelly AU - Hesse, Bradford W AD - National Cancer Institute ; University of Pittsburgh ; SAIC-Frederick, Inc. Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 990 EP - 1000 VL - 17 IS - 8 SN - 1081-0730, 1081-0730 KW - Sociology KW - Health Information National Trends Survey (HINTS) KW - Scientific communities KW - Stakeholder KW - Collaboration KW - Surveys KW - U.S.A. KW - Information and communication technologies KW - Internet KW - Health promotion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1272075835?accountid=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=Using+collaborative+web+technology+to+construct+the+health+information+national+trends+survey&rft.au=Moser%2C+Richard+P%3BBeckjord%2C+Ellen+Burke%3BFinney+Rutten%2C+Lila+J%3BBlake%2C+Kelly%3BHesse%2C+Bradford+W&rft.aulast=Moser&rft.aufirst=Richard&rft.date=2012-09-01&rft.volume=17&rft.issue=8&rft.spage=990&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/ LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2013-06-12 N1 - Last updated - 2013-09-16 N1 - SubjectsTermNotLitGenreText - 12429; 11338 2603; 2464 2859; 6813 6518; 5790 5772; 12158; 6518; 433 293 14 ER - TY - JOUR T1 - Picking up the pace: changes in method and frame for the Health Information National Trends Survey (2011-2014) AN - 1272075814; 4386016 AB - Health communication and health information technology influence the ways in which health care professionals and the public seek, use, and comprehend health information. The Health Information National Trends Survey (HINTS) program was developed to assess the effect of health communication and health information technology on health-related attitudes, knowledge, and behavior. HINTS has fielded 3 national data collections with the fourth (HINTS 4) currently underway. Throughout this time, the Journal of Health Communication has been a dedicated partner in disseminating research based on HINTS data. Thus, the authors thought it the perfect venue to provide an historical overview of the HINTS program and to introduce the most recent HINTS data collection effort. This commentary describes the rationale for and structure of HINTS 4, summarizes the methodological approach applied in Cycle 1 of HINTS 4, describes the timeline for the HINTS 4 data collection, and identifies priorities for research using HINTS 4 data. Reprinted by permission of Taylor & Francis Ltd. JF - Journal of health communication AU - Finney Rutten, Lila J AU - Davis, Terisa AU - Beckjord, Ellen Burke AU - Blake, Kelly AU - Moser, Richard P AU - Hesse, Bradford W AD - SAIC-Frederick, Inc. ; Westat ; University of Pittsburgh ; National Cancer Institute Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 979 EP - 989 VL - 17 IS - 8 SN - 1081-0730, 1081-0730 KW - Sociology KW - Health Information National Trends Survey (HINTS) KW - Information KW - Research trends KW - Data collection KW - Communication KW - Surveys KW - Health KW - U.S.A. KW - Information and communication technologies KW - Methodology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1272075814?accountid=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=Picking+up+the+pace%3A+changes+in+method+and+frame+for+the+Health+Information+National+Trends+Survey+%282011-2014%29&rft.au=Finney+Rutten%2C+Lila+J%3BDavis%2C+Terisa%3BBeckjord%2C+Ellen+Burke%3BBlake%2C+Kelly%3BMoser%2C+Richard+P%3BHesse%2C+Bradford+W&rft.aulast=Finney+Rutten&rft.aufirst=Lila&rft.date=2012-09-01&rft.volume=17&rft.issue=8&rft.spage=979&rft.isbn=&rft.btitle=&rft.title=Journal+of+health+communication&rft.issn=10810730&rft_id=info:doi/ LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2013-06-12 N1 - Last updated - 2013-09-16 N1 - SubjectsTermNotLitGenreText - 5772; 6515; 2572; 6518; 3286; 10932 10902; 7994; 12429; 433 293 14 ER - TY - JOUR T1 - Basic language comprehension and production in >100,000 young children from sixteen developing nations AN - 1221439062; 201215614 AB - Using the Multiple Indicator Cluster Survey, language comprehension and production were compared in a sample of 101,250 children aged 2 ; 00 to 9 ; 11 and a focus subsample of 38,845 children aged 2 ; 00 to 4 ; 11 from sixteen under-researched developing nations. In the whole sample, comprehension slightly exceeded production; correlations between comprehension and production by country were positive and significant, but varied in size, and the average correlation was positive, significant, and small to medium. Mean comprehension and production varied with child age, reaching an asymptote at 5 ; 00, and correlations between comprehension and production by age were positive, significant, and similar at each age. In the focus subsample, comprehension exceeded production; correlations between comprehension and production by country were positive and significant, but varied in size, and the average correlation was positive, significant, and medium in size. Children in countries with lower standards of living were less likely to demonstrate basic language comprehension or production. Adapted from the source document JF - Journal of Child Language AU - Bornstein, Marc H AU - Hendricks, Charlene AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development Marc_H_Bornstein@nih.gov Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 899 EP - 918 VL - 39 IS - 4 SN - 0305-0009, 0305-0009 KW - Native Language Acquisition (56394) KW - Comprehension (13950) KW - Language Processing (43550) KW - Children (11850) KW - article KW - 4015: psycholinguistics; child language acquisition UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1221439062?accountid=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=Journal+of+Child+Language&rft.atitle=Basic+language+comprehension+and+production+in+%26gt%3B100%2C000+young+children+from+sixteen+developing+nations&rft.au=Bornstein%2C+Marc+H%3BHendricks%2C+Charlene&rft.aulast=Bornstein&rft.aufirst=Marc&rft.date=2012-09-01&rft.volume=39&rft.issue=4&rft.spage=899&rft.isbn=&rft.btitle=&rft.title=Journal+of+Child+Language&rft.issn=03050009&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2012-12-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JCLGBJ N1 - SubjectsTermNotLitGenreText - Language Processing (43550); Comprehension (13950); Children (11850); Native Language Acquisition (56394) ER - TY - JOUR T1 - Sustainable management strategies for an urban-type and low dissolved oxygen stream using measured biochemical coefficients AN - 1171873414; 17344455 AB - A water quality model, QUAL2K, with the measured biological coefficients was employed to develop sustainable management strategies for an urban-type stream. To master the data of hydrological and receiving water quality, three surveys were conducted at 20 sampling stations along the Wan-Nian stream in the Pingtung city of southern Taiwan. Then the biochemical coefficients including deoxygenation, nitrification, and reaeration rate coefficients, and sediment oxygen demand were measured and incorporated with influent pollutant loadings and boundary conditions to calibrate and verify the developed model. Simulation evaluated with the mean absolute percentage error method fits reasonably well except for a suspended solid sampled on 16 January 2011. The improvement goal for attaining the water quality of the Wan-Nian stream was set at Class C regulated by the Taiwan EPA. The assimilative capacity of the stream studied to Carbonaceous Biochemical Oxygen Demand (CBOD) and NH sub(3)-N was estimated to be around 1,399 and 79 kg day super(-1), but the collected sewage was about 5,831 and 189 kg day super(-1), respectively, far exceeded its self-purification capacity. After reducing the pollutant loadings, the model results revealed that the water quality could reach the minimum Class C criteria. Water quality management strategies such as wastewater interception and diversion to the treatment plant as well as installation of contact aeration treatment units were drafted according to the model results after pollutant reduction. The present study demonstrates that the simulation analysis using QUAL2K is promising to frame the water quality management strategies of an urban-type river. JF - Desalination and Water Treatment AU - Tang, P-K AU - Huang, Y-C AU - Lin, Y-J AD - Department of Environmental Science and Engineering, National Pingtung University of Science and Technology, 1 Hseuh Fu Rd., Nei Pu Township, Pingtung 91201, Taiwan, ych@mail.npust.edu.tw Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 69 EP - 77 PB - European Desalination Society, Tosti 28 1-67100 L'Aquila Italy VL - 47 IS - 1-3 SN - 1944-3994, 1944-3994 KW - Pollution Abstracts; Meteorological & Geoastrophysical Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; Sustainability Science Abstracts; Water Resources Abstracts; Aqualine Abstracts; Environment Abstracts KW - Assimilative Capacity KW - Taiwan KW - Biochemistry KW - Sustainable development KW - Water quality models KW - Water quality KW - Streams KW - Boundary conditions KW - Dissolved oxygen KW - Hydrologic Models KW - Pollutants KW - Oxygen demand KW - Water Quality Management KW - Stream Pollution KW - Urban areas KW - Sediment pollution KW - Deoxygenation KW - Hydrologic analysis KW - Water Quality KW - Pollution Load KW - Simulation KW - Water pollution KW - EPA KW - Numerical simulations KW - Nitrification KW - Water management KW - Stream KW - Capacity KW - Biochemical oxygen demand KW - SW 3040:Wastewater treatment processes KW - AQ 00006:Sewage KW - ENA 09:Land Use & Planning KW - P 2000:FRESHWATER POLLUTION KW - M3 1010:Issues in Sustainable Development KW - Q5 08502:Methods and instruments KW - M2 551.5:General (551.5) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1171873414?accountid=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=Desalination+and+Water+Treatment&rft.atitle=Sustainable+management+strategies+for+an+urban-type+and+low+dissolved+oxygen+stream+using+measured+biochemical+coefficients&rft.au=Tang%2C+P-K%3BHuang%2C+Y-C%3BLin%2C+Y-J&rft.aulast=Tang&rft.aufirst=P-K&rft.date=2012-09-01&rft.volume=47&rft.issue=1-3&rft.spage=69&rft.isbn=&rft.btitle=&rft.title=Desalination+and+Water+Treatment&rft.issn=19443994&rft_id=info:doi/10.1080%2F19443994.2012.696793 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-11-01 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Sediment pollution; Deoxygenation; Nitrification; Oxygen demand; Water management; Stream; Water quality; Dissolved oxygen; Water pollution; Hydrologic analysis; Numerical simulations; Water quality models; Boundary conditions; EPA; Biochemistry; Sustainable development; Simulation; Biochemical oxygen demand; Streams; Urban areas; Assimilative Capacity; Hydrologic Models; Pollutants; Water Quality Management; Water Quality; Pollution Load; Stream Pollution; Capacity; Taiwan DO - http://dx.doi.org/10.1080/19443994.2012.696793 ER - TY - JOUR T1 - Cancer Mortality Following In Utero Exposure Among Offspring of Female Mayak Worker Cohort Members AN - 1136531132; 17226326 AB - Little is known about long-term cancer risks following in utero radiation exposure. We evaluated the association between in utero radiation exposure and risk of solid cancer and leukemia mortality among 8,000 offspring, born from 1948-1988, of female workers at the Mayak Nuclear Facility in Ozyorsk, Russia. Mother's cumulative gamma radiation uterine dose during pregnancy served as a surrogate for fetal dose. We used Poisson regression methods to estimate relative risks (RRs) and 95% confidence intervals (CIs) of solid cancer and leukemia mortality associated with in utero radiation exposure and to quantify excess relative risks (ERRs) as a function of dose. Using currently available dosimetry information, 3,226 (40%) offspring were exposed in utero (mean dose = 54.5 mGy). Based on 75 deaths from solid cancers (28 exposed) and 12 (6 exposed) deaths from leukemia, in utero exposure status was not significantly associated with solid cancer: RR = 0.94, 95% CI 0.58 to 1.49; ERR/Gy = -0.1 (95% CI < -0.1 to 4.1), or leukemia mortality; RR = 1.65, 95% CI 0.52 to 5.27; ERR/Gy = -0.8 (95% CI < -0.8 to 46.9). These initial results provide no evidence that low-dose gamma in utero radiation exposure increases solid cancer or leukemia mortality risk, but the data are not inconsistent with such an increase. As the offspring cohort is relatively young, subsequent analyses based on larger case numbers are expected to provide more precise estimates of adult cancer mortality risk following in utero exposure to ionizing radiation. JF - Radiation Research AU - Schonfeld, S J AU - Tsareva, Y V AU - Preston, D L AU - Okatenko, P V AU - Gilbert, E S AU - Ron, E AU - Sokolnikov, ME AU - Koshurnikova, NA AD - Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, schonfes@mail.nih.gov Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 160 EP - 165 PB - Radiation Research Society VL - 178 IS - 3 SN - 0033-7587, 0033-7587 KW - Risk Abstracts; Health & Safety Science Abstracts; Toxicology Abstracts KW - Risk assessment KW - Prenatal experience KW - Offspring KW - Leukemia KW - gamma Radiation KW - Occupational exposure KW - Mortality KW - Uterus KW - Data processing KW - Dosimetry KW - Intrauterine exposure KW - Fetuses KW - Cancer KW - Pregnancy KW - Ionizing radiation KW - Progeny KW - Russia KW - Females KW - X 24390:Radioactive Materials KW - R2 23060:Medical and environmental health KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1136531132?accountid=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=Radiation+Research&rft.atitle=Cancer+Mortality+Following+In+Utero+Exposure+Among+Offspring+of+Female+Mayak+Worker+Cohort+Members&rft.au=Schonfeld%2C+S+J%3BTsareva%2C+Y+V%3BPreston%2C+D+L%3BOkatenko%2C+P+V%3BGilbert%2C+E+S%3BRon%2C+E%3BSokolnikov%2C+ME%3BKoshurnikova%2C+NA&rft.aulast=Schonfeld&rft.aufirst=S&rft.date=2012-09-01&rft.volume=178&rft.issue=3&rft.spage=160&rft.isbn=&rft.btitle=&rft.title=Radiation+Research&rft.issn=00337587&rft_id=info:doi/10.1667%2FRR2848.1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-12-01 N1 - Number of references - 22 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Risk assessment; Mortality; Uterus; Data processing; Dosimetry; Intrauterine exposure; Cancer; Fetuses; Pregnancy; Leukemia; Ionizing radiation; gamma Radiation; Progeny; Occupational exposure; Prenatal experience; Females; Offspring; Russia DO - http://dx.doi.org/10.1667/RR2848.1 ER - TY - JOUR T1 - Advancing American Indian/Alaska Native Substance Abuse Research AN - 1125284986; 201227791 AB - American Indians and Alaska Natives (AI/AN) have disproportionately high rates of substance abuse yet there is little empirical research addressing this significant public health problem. This paper is an introduction to a special issue that includes cutting edge science in this research area. Adapted from the source document. JF - The American Journal of Drug and Alcohol Abuse AU - Volkow, Nora D AU - Warren, Kenneth R AD - National Institute on Drug Abuse, National Institutes of Health, Bethesda, MD, USA nvolkow@nida.nih.gov Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 371 PB - Taylor & Francis Inc., Philadelphia, PA VL - 38 IS - 5 SN - 0095-2990, 0095-2990 KW - American Indian people KW - Medical research KW - Alaska Native people KW - Substance abuse KW - Public health KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1125284986?accountid=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+of+Drug+and+Alcohol+Abuse&rft.atitle=Advancing+American+Indian%2FAlaska+Native+Substance+Abuse+Research&rft.au=Volkow%2C+Nora+D%3BWarren%2C+Kenneth+R&rft.aulast=Volkow&rft.aufirst=Nora&rft.date=2012-09-01&rft.volume=38&rft.issue=5&rft.spage=371&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+of+Drug+and+Alcohol+Abuse&rft.issn=00952990&rft_id=info:doi/10.3109%2F00952990.2012.712174 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-11-01 N1 - Last updated - 2016-09-27 N1 - CODEN - AJDABD N1 - SubjectsTermNotLitGenreText - Substance abuse; American Indian people; Alaska Native people; Public health; Medical research DO - http://dx.doi.org/10.3109/00952990.2012.712174 ER - TY - JOUR T1 - Advancing American Indian and Alaska Native Substance Abuse Research: Current Science and Future Directions AN - 1125282962; 201226093 AB - American Indians and Alaska Natives (AI/AN) have disproportionately high rates of substance abuse yet there is little empirical research addressing this significant public health problem. This paper is an introduction to a special issue that includes cutting edge science in this research area. We identify several areas that require consideration in this field and indicate how the papers in the special issue address these gaps. These overarching areas of need, which should be considered in any substantive research, include attention to heterogeneity within the population, research that has tangible health benefits, continued work on research methods and strategies, increased focus on strength based and community oriented approaches, and the need for strong research partnerships. The special issue marks a major step forward for AI/AN substance abuse research. However, articles also highlight where more work is need to improve public health in AI/AN communities by addressing identified gap areas. Adapted from the source document. JF - The American Journal of Drug and Alcohol Abuse AU - Etz, Kathleen E AU - Arroyo, Judith A AU - Crump, Aria D AU - Rosa, Carmen L AU - Scott, Marcia S AD - National Institute on Drug Abuse, National Institutes of Health, Bethesda, MD, USA ketz@nida.nih.gov Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 372 EP - 375 PB - Taylor & Francis Inc., Philadelphia, PA VL - 38 IS - 5 SN - 0095-2990, 0095-2990 KW - substance abuse, American Indian, Alaska Native, drug abuse, alcohol abuse KW - American Indian people KW - Medical research KW - Heterogeneity KW - Alaska Native people KW - Substance abuse KW - Public health KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1125282962?accountid=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+of+Drug+and+Alcohol+Abuse&rft.atitle=Advancing+American+Indian+and+Alaska+Native+Substance+Abuse+Research%3A+Current+Science+and+Future+Directions&rft.au=Etz%2C+Kathleen+E%3BArroyo%2C+Judith+A%3BCrump%2C+Aria+D%3BRosa%2C+Carmen+L%3BScott%2C+Marcia+S&rft.aulast=Etz&rft.aufirst=Kathleen&rft.date=2012-09-01&rft.volume=38&rft.issue=5&rft.spage=372&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+of+Drug+and+Alcohol+Abuse&rft.issn=00952990&rft_id=info:doi/10.3109%2F00952990.2012.712173 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-11-01 N1 - Last updated - 2016-09-27 N1 - CODEN - AJDABD N1 - SubjectsTermNotLitGenreText - Substance abuse; Medical research; Public health; Alaska Native people; American Indian people; Heterogeneity DO - http://dx.doi.org/10.3109/00952990.2012.712173 ER - TY - JOUR T1 - Fractionated Radiation Alters Oncomir and Tumor Suppressor miRNAs in Human Prostate Cancer Cells AN - 1125231520; 17226261 AB - We have previously demonstrated that prostate carcinoma cells exposed to fractionated radiation differentially expressed more genes compared to single-dose radiation. To understand the role of miRNA in regulation of radiation-induced gene expression, we analyzed miRNA expression in LNCaP, PC3 and DU145 prostate cancer cells treated with single-dose radiation and fractionated radiation by microarray. Selected miRNAs were studied in RWPE-1 normal prostate epithelial cells by RT-PCR. Fractionated radiation significantly altered more miRNAs as compared to single-dose radiation. Downregulation of oncomiR-17-92 cluster was observed only in the p53 positive LNCaP and RWPE-1 cells treated with single-dose radiation and fractionated radiation. Comparison of miRNA and mRNA data by IPA target filter analysis revealed an inverse correlation between miR-17-92 cluster and several targets including TP53INP1 in p53 signaling pathway. The base level expressions of these miRNAs were significantly different among the cell lines and did not predict the radiation outcome. Tumor suppressor miR-34a and let-7 miRNAs were upregulated by fractionated radiation in radiosensitive LNCaP (p53 positive) and PC3 (p53-null) cells indicating that radiation-induced miRNA expression may not be regulated by p53 alone. Our data support the potential for using fractionated radiation to induce molecular targets and radiation-induced miRNAs may have a significant role in predicting radiosensitivity. JF - Radiation Research AU - John-Aryankalayil, Molykutty AU - Palayoor, Sanjeewani T AU - Makinde, Adeola Y AU - Cerna, David AU - Simone, Charles B AU - Falduto, Michael T AU - Magnuson, Scott R AU - Coleman, CNorman AD - Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland; and, aryankalayilm@mail.nih.gov Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 105 EP - 117 PB - Radiation Research Society VL - 178 IS - 3 SN - 0033-7587, 0033-7587 KW - Toxicology Abstracts; Oncogenes & Growth Factors Abstracts KW - Data processing KW - Radiation KW - X:24390 KW - B:26670 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1125231520?accountid=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=Radiation+Research&rft.atitle=Fractionated+Radiation+Alters+Oncomir+and+Tumor+Suppressor+miRNAs+in+Human+Prostate+Cancer+Cells&rft.au=John-Aryankalayil%2C+Molykutty%3BPalayoor%2C+Sanjeewani+T%3BMakinde%2C+Adeola+Y%3BCerna%2C+David%3BSimone%2C+Charles+B%3BFalduto%2C+Michael+T%3BMagnuson%2C+Scott+R%3BColeman%2C+CNorman&rft.aulast=John-Aryankalayil&rft.aufirst=Molykutty&rft.date=2012-09-01&rft.volume=178&rft.issue=3&rft.spage=105&rft.isbn=&rft.btitle=&rft.title=Radiation+Research&rft.issn=00337587&rft_id=info:doi/10.1667%2FRR2703.1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Number of references - 1 N1 - Last updated - 2014-02-21 N1 - SubjectsTermNotLitGenreText - Radiation DO - http://dx.doi.org/10.1667/RR2703.1 ER - TY - JOUR T1 - Targeting iron assimilation to develop new antibacterials AN - 1125224625; 17183403 AB - Introduction: Since the first application of antibiotics to treat bacterial infections, the development and spread of resistance has been a persistent threat. An ever evolving pipeline of next-generation therapeutics is required for modern medicine to remain one step ahead of pathogens. Areas covered: This review describes recent efforts to develop drugs that interrupt the assimilation of iron by bacteria: a process that is vital to cellular homeostasis and is not currently targeted by antibiotics used in the clinic. This review also covers the mechanisms by which bacteria acquire iron for their environment, and details efforts to intervene in these processes, using small molecule inhibitors that target key steps in these pathways, with a special emphasis on recent advances published during the 2010 - 2012 period. Expert opinion: For decades, the routes used by bacteria to assimilate iron from host and environmental settings have been the subject of intense study. While numerous investigations have identified inhibitors of these pathways, many have stopped short of translating the in vitro results to in vivo proof of concept experiments. The extension of preliminary findings in this manner will significantly increase the impact of the field. JF - Expert Opinion on Drug Discovery AU - Foley, Timothy L AU - Simeonov, Anton AD - National Institutes of Health, National Center for Advancing Translational Sciences, Division of Preclinical Innovation, 9800 Medical Center Drive, Bethesda, MD 20892-3370, USA +1 301 217 5721; +1 301 217 5736, asimeono@mail.nih.gov Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 831 EP - 847 PB - Informa Healthcare VL - 7 IS - 9 SN - 1746-0441, 1746-0441 KW - Biotechnology and Bioengineering Abstracts; Microbiology Abstracts B: Bacteriology KW - Antibiotics KW - Pathogens KW - Homeostasis KW - Infection KW - Iron KW - W 30915:Pharmaceuticals & Vaccines KW - J 02340:Antibiotics & Antimicrobials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1125224625?accountid=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=Expert+Opinion+on+Drug+Discovery&rft.atitle=Targeting+iron+assimilation+to+develop+new+antibacterials&rft.au=Foley%2C+Timothy+L%3BSimeonov%2C+Anton&rft.aulast=Foley&rft.aufirst=Timothy&rft.date=2012-09-01&rft.volume=7&rft.issue=9&rft.spage=831&rft.isbn=&rft.btitle=&rft.title=Expert+Opinion+on+Drug+Discovery&rft.issn=17460441&rft_id=info:doi/http%3A%2F%2Fdx.doi.org%2F10.1517%2F17460441.2012.708335 L2 - http://www.ingentaconnect.com/content/apl/edc/2012/00000007/00000009/art00008 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2013-07-15 N1 - SubjectsTermNotLitGenreText - Antibiotics; Homeostasis; Pathogens; Infection; Iron DO - http://dx.doi.org/10.1517/17460441.2012.708335 ER - TY - JOUR T1 - Information borrowing methods for covariate-adjusted ROC curve AN - 1112142179; 4349356 AB - // ABSTRACT IN ENGLISH: In medical diagnostic testing problems, the covariate adjusted receiver operating characteristic (ROC) curves have been discussed recently for achieving the best separation between disease and control. Due to various restrictions such as cost, the availability of patients, and ethical issues quite frequently only limited information is available. As a result, we are unlikely to have a large enough overall sample size to support reliable direct estimations of ROCs for all the underlying covariates of interest. For example, some genetic factors are less commonly observable compared with others. To get an accurate covariate adjusted ROC estimation, novel statistical methods are needed to effectively utilize the limited information. Therefore, it is desirable to use indirect estimates that borrow strength by employing values of the variables of interest from neighbouring covariates. In this paper we discuss two semiparametric exponential tilting models, where the density functions from different covariate levels share a common baseline density, and the parameters in the exponential tilting component reflect the difference among the covariates. With the proposed models, the estimated covariate adjusted ROC is much smoother and more efficient than the nonparametric counterpart without borrowing information from neighbouring covariates. A simulation study and a real data application are reported. // ABSTRACT IN FRENCH: Pour les problèmes de diagnostics médicaux, il a été montré récemment que la courbe d'efficacité du récepteur (ROC) ajustée pour les covariables permet d'obtenir la meilleure séparation entre la maladie et le contrôle. Ë cause de différentes restrictions telles que le coût, la disponibilité des patients et des raisons éthiques, seule une information partielle est disponible. Conséquemment, il y a peu de chance d'avoir suffisamment d'observations pour estimer la ROC directement pour toutes les covariables d'intérêt. Par exemple, certains facteurs génétiques sont moins fréquemment observés que d'autres. Pour obtenir une estimation précise de la ROC ajustée pour les covariables, plusieurs nouvelles méthodes statistiques sont nécessaires afin d'utiliser efficacement l'information partielle. Il est donc souhaitable d'utiliser des estimateurs indirects qui utilisent l'information contenue dans les variables d'intérêt des covariables avoisinantes. Dans cet article, nous présentons deux modèles semi-paramétriques de nivellement exponentiel. Pour ces modèles, les fonctions de densités des différents niveaux des covariables partagent la même densité de base et les paramètres des composantes du nivellement exponentiel représentent la différence entre les covariables. Avec les modèles proposés, la ROC ajustée pour les covariables estimées est beaucoup plus lisse et plus efficace que sa contrepartie non paramétrique qui n'utilise pas l'information des covariables avoisinantes. Une étude de simulation et une application de vraies données sont aussi discutées. JF - Canadian journal of statistics AU - Guan, Zhong AU - Qin, Jing AU - Zhang, Biao AD - Indiana University, South Bend ; National Institute of Allergy and Infectious Diseases, USA ; University of Toledo Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 569 EP - 587 VL - 40 IS - 3 SN - 0319-5724, 0319-5724 KW - Economics KW - ROC curves KW - Statistical models KW - Medical ethics KW - Simulation KW - Estimation KW - Data analysis KW - Covariance KW - Public health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1112142179?accountid=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=Information+borrowing+methods+for+covariate-adjusted+ROC+curve&rft.au=Guan%2C+Zhong%3BQin%2C+Jing%3BZhang%2C+Biao&rft.aulast=Guan&rft.aufirst=Zhong&rft.date=2012-09-01&rft.volume=40&rft.issue=3&rft.spage=569&rft.isbn=&rft.btitle=&rft.title=Canadian+journal+of+statistics&rft.issn=03195724&rft_id=info:doi/10.1002%2Fcjs.11145 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2013-06-12 N1 - Last updated - 2013-09-16 N1 - SubjectsTermNotLitGenreText - 10449 5772; 12230 8163; 2977 13249 10214 12224 971; 4403 7854; 11670; 7879 4408 8282 8281 6085; 3279 971 3286 DO - http://dx.doi.org/10.1002/cjs.11145 ER - TY - JOUR T1 - The clinical relevance of persistent recombinant immunoblot assay-indeterminate reactions: insights into the natural history of hepatitis C virus infection and implications for donor counseling AN - 1093467571; 17143130 AB - BACKGROUND: Recombinant immunoblot assay (RIBA) is used to determine the specificity of antibody to hepatitisC virus (anti-HCV). The RIBA result is recorded as positive, negative, or indeterminate. The interpretation and significance of RIBA-indeterminate reactions are unclear. We addressed the clinical relevance of these reactions in the context of the natural history of HCV infection in a prospectively followed cohort of anti-HCV-positive blood donors. STUDY DESIGN AND METHODS: Donor demographics, exposure history, and humoral and cell-mediated immunity (CMI) were compared in 15 RIBA-indeterminate subjects, nine chronic HCV carriers, and eight spontaneously recovered subjects. Serum samples were tested for anti-HCV by a quantitative, liquid luciferase immunoprecipitation system (LIPS). CMI was assessed by interferon- gamma enzyme-linked immunosorbent spot assay. RESULTS: In the LIPS assay, the sum of antibody responses to six HCV antigens showed significant (p<0.001) stepwise diminution progressing from chronic carriers to spontaneously recovered to RIBA-indeterminate subjects. CMI responses in RIBA-indeterminate subjects were similar to spontaneously recovered subjects and greater than chronic carriers and controls (p<0.008). A parenteral risk factor was identified in only 13% of RIBA-indeterminate subjects compared to 89% of chronic carriers and 87% of spontaneously recovered subjects. RIBA-indeterminate donors were older than the other groups. CONCLUSION: The CMI and LIPS results suggest that persistent RIBA-indeterminate reactions represent waning anti-HCV responses in persons who have recovered from a remote HCV infection. In such cases, detectable antibody may ultimately disappear leaving no residual serologic evidence of prior HCV infection, as reported in a minority of long-term HCV-recovered subjects. JF - Transfusion AU - Makuria, Addisalem T AU - Raghuraman, Sukanya AU - Burbelo, Peter D AU - Cantilena, Cathy C AU - Allison, Robert D AU - Gibble, Joan AU - Rehermann, Barbara AU - Alter, Harvey J AD - From the Infectious Disease Section, Department of Transfusion Medicine; Immunology Section, National Institute for Diabetes and Digestive and Kidney Diseases; Neurobiology and Pain Therapeutics Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, Department of Health and Human Services, Bethesda, Maryland; and The Greater Chesapeake and Potomac Region American Red Cross, Baltimore, Maryland. Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 1940 EP - 1948 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 52 IS - 9 SN - 0041-1132, 0041-1132 KW - Virology & AIDS Abstracts; Risk Abstracts KW - Antibodies KW - Blood donors KW - Demography KW - Hepatitis KW - Historical account KW - Immunity (cell-mediated) KW - Immunity (humoral) KW - Immunoprecipitation KW - Immunosorbents KW - Infection KW - Risk factors KW - gamma -Interferon KW - Hepatitis C virus KW - V 22350:Immunology KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1093467571?accountid=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=Transfusion&rft.atitle=The+clinical+relevance+of+persistent+recombinant+immunoblot+assay-indeterminate+reactions%3A+insights+into+the+natural+history+of+hepatitis+C+virus+infection+and+implications+for+donor+counseling&rft.au=Makuria%2C+Addisalem+T%3BRaghuraman%2C+Sukanya%3BBurbelo%2C+Peter+D%3BCantilena%2C+Cathy+C%3BAllison%2C+Robert+D%3BGibble%2C+Joan%3BRehermann%2C+Barbara%3BAlter%2C+Harvey+J&rft.aulast=Makuria&rft.aufirst=Addisalem&rft.date=2012-09-01&rft.volume=52&rft.issue=9&rft.spage=1940&rft.isbn=&rft.btitle=&rft.title=Transfusion&rft.issn=00411132&rft_id=info:doi/10.1111%2Fj.1537-2995.2011.03524.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Document feature - figure 3 N1 - Last updated - 2012-10-19 N1 - SubjectsTermNotLitGenreText - Immunity (humoral); Demography; Blood donors; gamma -Interferon; Antibodies; Immunity (cell-mediated); Risk factors; Immunoprecipitation; Immunosorbents; Hepatitis; Historical account; Infection; Hepatitis C virus DO - http://dx.doi.org/10.1111/j.1537-2995.2011.03524.x ER - TY - JOUR T1 - Tridimensional acculturation and adaptation among Jamaican adolescent-mother dyads in the United States AN - 1082145582; 4344929 AB - A bidimensional acculturation framework cannot account for multiple destination cultures within contemporary settlement societies. A tridimensional model is proposed and tested among Jamaican adolescent-mother dyads in the United States compared to Jamaican Islander, European American, African American, and other Black and non-Black U.S. immigrant dyads (473 dyads, M adolescent age=14years). Jamaican immigrants evidence tridimensional acculturation, orienting toward Jamaican, African American, and European American cultures. Integration is favored (70%), particularly tricultural integration; moreover, Jamaican and other Black U.S. immigrants are more oriented toward African American than European American culture. Jamaican immigrant youth adapt at least as well as nonimmigrant peers in Jamaica and the United States. However, assimilated adolescents, particularly first generation immigrants, have worse sociocultural adaptation than integrated and separated adolescents. Reprinted by permission of the University of Chicago Press. © All rights reserved JF - Child development AU - Ferguson, Gail M AU - Bornstein, Marc H AU - Pottinger, Audrey M AD - Knox College ; National Institute of Child Health and Human Development ; University of the West Indies Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 1486 EP - 1493 VL - 83 IS - 5 SN - 0009-3920, 0009-3920 KW - Sociology KW - Immigrant adaptation KW - Immigrant acculturation KW - Cultural integration KW - Immigrant assimilation KW - Jamaica KW - U.S.A. KW - Child development KW - Adolescents UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1082145582?accountid=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=Tridimensional+acculturation+and+adaptation+among+Jamaican+adolescent-mother+dyads+in+the+United+States&rft.au=Ferguson%2C+Gail+M%3BBornstein%2C+Marc+H%3BPottinger%2C+Audrey+M&rft.aulast=Ferguson&rft.aufirst=Gail&rft.date=2012-09-01&rft.volume=83&rft.issue=5&rft.spage=1486&rft.isbn=&rft.btitle=&rft.title=Child+development&rft.issn=00093920&rft_id=info:doi/10.1111%2Fj.1467-8624.2012.01787.x LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2013-06-12 N1 - Last updated - 2013-09-16 N1 - SubjectsTermNotLitGenreText - 2197 2212 6075 3483; 6229 539 3105 3198; 593; 6230 6232 8037 559 3087 3105 3198; 6231 3095 3105 3198 6232 8037; 3153 3178 3121 3198 3549 2688 2449 10404; 433 293 14; 189 77 14 DO - http://dx.doi.org/10.1111/j.1467-8624.2012.01787.x ER - TY - JOUR T1 - Comprehensive evaluation of cortical structure abnormalities in drug-naive, adult patients with obsessive-compulsive disorder: A surface-based morphometry study AN - 1081897057; 201225300 AB - The study objective was to comprehensively evaluate drug-naive, adult patients with Obsessive Compulsive Disorder (OCD) for cortical structure abnormalities in comparison with healthy controls. In this cross-sectional study of case-control design, Magnetic Resonance Imaging (1-mm) was performed in drug-naive OCD patients (N = 50) & age- sex-, education- and handedness-matched healthy controls (N = 40). We examined cortical volume, thickness, surface area & local Gyrification Index (LGI) through a completely automated surface-based morphometric analysis using FreeSurfer software. OCD symptoms and insight were assessed using Yale-Brown Obsessive Compulsive Symptom (Y-BOCS) check-list and severity scale. Illness severity was assessed using Clinical Global Impression Severity (CGI-S) Scale. OCD patients had significantly deficient volume, thickness and surface area of right anterior cingulate gyrus (ACG). Right lingual gyrus surface area was found to be significantly decreased in patients. Y-BOCS obsession score had significant negative correlation with left frontal pole volume. Y-BOCS compulsion score had significant negative correlations with right ACG volume and surface area and right lateral orbitofrontal cortex LGI. CGI-Severity score had significant negative correlations with right lingual gyrus volume, thickness and surface area as well as right lateral orbitofrontal area. Y-BOCS insight score showed a significant negative correlation with LGI of left medial OFC and left rostral ACG. Identification of novel deficits involving occipital brain regions and first-time observations of relevant correlations between various illness characteristics and cortical measures in OCD patients supports a network involving anterior cingulate, orbitofrontal and occipital brain regions in the pathogenesis of OCD. [Copyright Elsevier Ltd.] JF - Journal of Psychiatric Research AU - Venkatasubramanian, Ganesan AU - Zutshi, Amit AU - Jindal, Sachin AU - Srikanth, Subbamma G AU - Kovoor, Jerry M.E. AU - Kumar, J Keshav AU - Reddy, Y.C. Janardhan AD - Department of Psychiatry, National Institute of Mental Health & Neurosciences, Bangalore 560029, India. Tel.: +91 80 26995256; Fax: +91 80 26564830 Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 1161 EP - 1168 PB - Elsevier Ltd, Oxford UK VL - 46 IS - 9 SN - 0022-3956, 0022-3956 KW - Obsessive-compulsive disorder, Cingulate gyrus, Cortical thickness, Gyrification KW - Symptoms KW - Cortex KW - Severity KW - Cross-sectional studies KW - Impressions KW - Obsessive-Compulsive neuroses KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1081897057?accountid=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+Psychiatric+Research&rft.atitle=Comprehensive+evaluation+of+cortical+structure+abnormalities+in+drug-naive%2C+adult+patients+with+obsessive-compulsive+disorder%3A+A+surface-based+morphometry+study&rft.au=Venkatasubramanian%2C+Ganesan%3BZutshi%2C+Amit%3BJindal%2C+Sachin%3BSrikanth%2C+Subbamma+G%3BKovoor%2C+Jerry+M.E.%3BKumar%2C+J+Keshav%3BReddy%2C+Y.C.+Janardhan&rft.aulast=Venkatasubramanian&rft.aufirst=Ganesan&rft.date=2012-09-01&rft.volume=46&rft.issue=9&rft.spage=1161&rft.isbn=&rft.btitle=&rft.title=Journal+of+Psychiatric+Research&rft.issn=00223956&rft_id=info:doi/10.1016%2Fj.jpsychires.2012.06.003 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-10-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JPYRA3 N1 - SubjectsTermNotLitGenreText - Obsessive-Compulsive neuroses; Severity; Cortex; Symptoms; Cross-sectional studies; Impressions DO - http://dx.doi.org/10.1016/j.jpsychires.2012.06.003 ER - TY - JOUR T1 - Identification of clinical isolates of anaerobic bacteria using matrix-assisted laser desorption ionization-time of flight mass spectrometry AN - 1069195811; 17135090 AB - We evaluated the use of matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF) for the rapid identification of anaerobic bacteria that had been isolated from clinical specimens and previously identified by 16s rRNA sequencing. The Bruker Microflex MALDI-TOF instrument with the Biotyper Software was used. We tested 152 isolates of anaerobic bacteria from 24 different genera and 75 different species. A total of 125 isolates (82%) had Biotyper software scores greater than 2.0 and the correct identification to genus and species was made by MALDI-TOF for 120 (79%) of isolates. Of the 12 isolates with a score between 1.8 and 2.0, 2 (17%) organisms were incorrectly identified by MALDI-TOF. Only 15 (10%) isolates had a score less than 1.8 and MALDI-TOF gave the wrong genus and species for four isolates, the correct genus for two isolates, and the correct genus and species for nine isolates. Therefore, we found the Bruker MALDI-TOF MicroFlex LT with an expanded database and the use of bacteria extracts rather than whole organisms correctly identified 130 of 152 (86%) isolates to genus and species when the cut-off for an acceptable identification was a spectrum score greater than or equal to 1.8. JF - European Journal of Clinical Microbiology & Infectious Diseases AU - Fedorko, D P AU - Drake, S K AU - Stock, F AU - Murray, PR AD - Department of Laboratory Medicine, Clinical Center, Nationals Institutes of Health, Microbiology Service, Bldg 10/Rm 2C385, 10 Center Drive MSC 1508, Bethesda, MD, 20892-1508, USA, dfedorko@nih.gov Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 2257 EP - 2262 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 31 IS - 9 SN - 0934-9723, 0934-9723 KW - Microbiology Abstracts B: Bacteriology KW - Anaerobic bacteria KW - Clinical isolates KW - Computer programs KW - Databases KW - Lasers KW - Mass spectroscopy KW - rRNA 16S KW - software KW - J 02300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1069195811?accountid=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=European+Journal+of+Clinical+Microbiology+%26+Infectious+Diseases&rft.atitle=Identification+of+clinical+isolates+of+anaerobic+bacteria+using+matrix-assisted+laser+desorption+ionization-time+of+flight+mass+spectrometry&rft.au=Fedorko%2C+D+P%3BDrake%2C+S+K%3BStock%2C+F%3BMurray%2C+PR&rft.aulast=Fedorko&rft.aufirst=D&rft.date=2012-09-01&rft.volume=31&rft.issue=9&rft.spage=2257&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Clinical+Microbiology+%26+Infectious+Diseases&rft.issn=09349723&rft_id=info:doi/10.1007%2Fs10096-012-1563-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-09-01 N1 - Last updated - 2012-10-08 N1 - SubjectsTermNotLitGenreText - Clinical isolates; Databases; Computer programs; software; Lasers; rRNA 16S; Mass spectroscopy; Anaerobic bacteria DO - http://dx.doi.org/10.1007/s10096-012-1563-4 ER - TY - JOUR T1 - Expression of calmodulin in germ cells is associated with fenvalerate-induced male reproductive toxicity AN - 1069195236; 17128452 AB - Exposure to fenvalerate was demonstrated to be toxic to the male reproductive system. Our previous data revealed that intracellular calcium plays an important role in regulating the above toxicity, through actions on both T-type calcium channels and endoplasmic reticulum calcium signals. The present study explored the effects of fenvalerate on the expression of calmodulin in mouse testis and GC-2spd(ts) cells, and its association with fenvalerate-induced male reproductive toxicity. Male mice were subjected to different doses (3.71, 18.56, 37.12, 92.81 mg/kg bw) of fenvalerate or vehicle control for 4 weeks. Expression of calmodulin was determined by real-time polymerase chain reaction (PCR) and Western blot analysis in mouse testis. Similar approaches were utilized in GC-2spd(ts) cells cultured with 5 mu M fenvalerate at different time points. In the in vivo study, all mice survived through the entire 4 weeks. Administration of fenvalerate resulted in a dose-dependent reduction in testis weight/body weight, sperm motility, and increased head abnormality rate. By histological staining, mice treated with fenvalerate at higher doses showed dilated seminiferous tubules and disturbed arrangement of spermatogenic cells. Meanwhile, both mRNA and protein expression of calmodulin were significantly increased in the testes of mice exposed to fenvalerate compared to control mice. Moreover, in the in vitro study, 5 mu M fenvalerate significantly increased the expression of calmodulin at the mRNA and protein levels in GC-2spd(ts) cells after 8 h of incubation and sustained these levels for at least 24 h. Collectively, these data suggested that enhanced expression of calmodulin correlates with male reproductive damage induced by fenvalerate. JF - Archives of Toxicology AU - Gao, Xiaohua AU - Wang, Qiang AU - Wang, Jun AU - Wang, Changsong AU - Lu, Liang AU - Gao, Rong AU - Huan, Fei AU - Dixon, Darlene AU - Xiao, Hang AD - Department of Toxicology and Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University, 140 Hanzhong Road, Nanjing, 210029, Jiangsu, People's Republic of China, dixon@niehs.nih.gov Y1 - 2012/09// PY - 2012 DA - Sep 2012 SP - 1443 EP - 1451 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 86 IS - 9 SN - 0340-5761, 0340-5761 KW - Toxicology Abstracts KW - Testes KW - Western blotting KW - Data processing KW - Fenvalerate KW - Head KW - Germ cells KW - Sperm KW - Toxicity KW - Reproductive system KW - mRNA KW - Calcium (intracellular) KW - Gene expression KW - Endoplasmic reticulum KW - Calcium channels (T-type) KW - Polymerase chain reaction KW - Calmodulin KW - Calcium signalling KW - Calcium-binding protein KW - Calcium (reticular) KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1069195236?accountid=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=Expression+of+calmodulin+in+germ+cells+is+associated+with+fenvalerate-induced+male+reproductive+toxicity&rft.au=Gao%2C+Xiaohua%3BWang%2C+Qiang%3BWang%2C+Jun%3BWang%2C+Changsong%3BLu%2C+Liang%3BGao%2C+Rong%3BHuan%2C+Fei%3BDixon%2C+Darlene%3BXiao%2C+Hang&rft.aulast=Gao&rft.aufirst=Xiaohua&rft.date=2012-09-01&rft.volume=86&rft.issue=9&rft.spage=1443&rft.isbn=&rft.btitle=&rft.title=Archives+of+Toxicology&rft.issn=03405761&rft_id=info:doi/10.1007%2Fs00204-012-0825-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-09-01 N1 - Last updated - 2013-11-04 N1 - SubjectsTermNotLitGenreText - Testes; Western blotting; Fenvalerate; Data processing; Head; Germ cells; Toxicity; Sperm; Reproductive system; Calcium (intracellular); mRNA; Gene expression; Endoplasmic reticulum; Calcium channels (T-type); Calmodulin; Polymerase chain reaction; Calcium signalling; Calcium (reticular); Calcium-binding protein DO - http://dx.doi.org/10.1007/s00204-012-0825-3 ER - TY - CONF T1 - 2nd PEGS Annual Symposium on Antibodies for Cancer Therapy: April 30-May 1, 2012, Boston, USA. AN - 1038615916; 22864478 AB - The 2nd Annual Antibodies for Cancer Therapy symposium, organized again by Cambridge Healthtech Institute as part of the Protein Engineering Summit, was held in Boston, USA from April 30th to May 1st, 2012. Since the approval of the first cancer antibody therapeutic, rituximab, fifteen years ago, eleven have been approved for cancer therapy, although one, gemtuzumab ozogamicin, was withdrawn from the market. The first day of the symposium started with a historical review of early work for lymphomas and leukemias and the evolution from murine to human antibodies. The symposium discussed the current status and future perspectives of therapeutic antibodies in the biology of immunoglobulin, emerging research on biosimilars and biobetters, and engineering bispecific antibodies and antibody-drug conjugates. The tumor penetration session was focused on the understanding of antibody therapy using ex vivo tumor spheroids and the development of novel agents targeting epithelial junctions in solid tumors. The second day of the symposium discussed the development of new generation recombinant immunotoxins with low immunogenicity, construction of chimeric antigen receptors, and the proof-of-concept of 'photoimmunotherapy'. The preclinical and clinical session presented antibodies targeting Notch signaling and chemokine receptors. Finally, the symposium discussed emerging technologies and platforms for therapeutic antibody discovery. JF - mAbs AU - Ho, Mitchell AU - Royston, Ivor AU - Beck, Alain Y1 - 2012 PY - 2012 DA - 2012 SP - 562 EP - 570 VL - 4 IS - 5 KW - Antibodies, Bispecific KW - 0 KW - Antibodies, Monoclonal KW - Antibodies, Neoplasm KW - Immunotoxins KW - Index Medicus KW - Antibodies, Bispecific -- immunology KW - Humans KW - Immunotoxins -- therapeutic use KW - Antibodies, Bispecific -- therapeutic use KW - Antibodies, Neoplasm -- therapeutic use KW - Antibodies, Neoplasm -- immunology KW - Neoplasms -- therapy KW - Immunotherapy -- trends KW - Neoplasms -- immunology KW - Antibodies, Monoclonal -- therapeutic use KW - Antibodies, Monoclonal -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1038615916?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=mAbs&rft.atitle=2nd+PEGS+Annual+Symposium+on+Antibodies+for+Cancer+Therapy%3A+April+30-May+1%2C+2012%2C+Boston%2C+USA.&rft.au=Ho%2C+Mitchell%3BRoyston%2C+Ivor%3BBeck%2C+Alain&rft.aulast=Ho&rft.aufirst=Mitchell&rft.date=2012-09-01&rft.volume=4&rft.issue=5&rft.spage=562&rft.isbn=&rft.btitle=&rft.title=mAbs&rft.issn=1942-0870&rft_id=info:doi/10.4161%2Fmabs.21521 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-17 N1 - Date created - 2012-09-07 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Blood. 2012 Mar 22;119(12):2709-20 [22160384] Nat Biotechnol. 2012 Feb;30(2):184-9 [22267010] PLoS One. 2012;7(6):e39556 [22737246] Anal Chem. 2012 Jun 5;84(11):4637-46 [22510259] Drug Discov Today. 2012 Sep;17(17-18):954-63 [22561895] MAbs. 2012 Sep-Oct;4(5):600-13 [22864384] PLoS One. 2013;8(12):e83232 [24349470] Tissue Eng Part C Methods. 2011 Jan;17(1):61-7 [20673133] Nat Med. 2000 Apr;6(4):443-6 [10742152] Cancer Immunol Immunother. 2000 Mar;48(12):673-83 [10752475] Blood. 2000 Jun 15;95(12):3900-8 [10845926] N Engl J Med. 2001 Jul 26;345(4):241-7 [11474661] Nat Rev Cancer. 2003 Jan;3(1):35-45 [12509765] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218] Cancer Cell. 2004 Apr;5(4):317-28 [15093539] Nature. 1975 Aug 7;256(5517):495-7 [1172191] Blood. 1982 Jan;59(1):1-11 [7032624] N Engl J Med. 1982 Mar 4;306(9):517-22 [6173751] Blood. 1982 May;59(5):1036-45 [6896161] Proc Natl Acad Sci U S A. 1983 Oct;80(20):6327-31 [6604917] J Clin Oncol. 1984 Aug;2(8):881-91 [6379121] Cancer Invest. 1987;5(5):449-57 [3501329] Semin Oncol. 1989 Jun;16(3):199-210 [2658083] Proc Natl Acad Sci U S A. 1989 Dec;86(24):10024-8 [2513569] Blood. 1994 Jan 15;83(2):435-45 [7506951] Protein Eng. 1996 Jul;9(7):617-21 [8844834] Biochem Soc Trans. 1997 May;25(2):705-8 [9191187] Nat Med. 1997 Jul;3(7):730-7 [9212098] Cancer Cell. 2005 Apr;7(4):301-11 [15837620] J Clin Oncol. 2005 Sep 20;23(27):6719-29 [16061911] J Immunol. 2006 Dec 15;177(12):8822-34 [17142785] Annu Rev Med. 2007;58:221-37 [17059365] Clin Cancer Res. 2007 Sep 1;13(17):5144-9 [17785569] Eur J Cancer. 2008 Jan;44(1):46-53 [17945478] Structure. 2008 Feb;16(2):216-27 [18275813] Proc Natl Acad Sci U S A. 2008 Aug 12;105(32):11311-6 [18678888] Proc Natl Acad Sci U S A. 2008 Aug 26;105(34):12451-6 [18719095] Curr Pharm Biotechnol. 2008 Dec;9(6):482-501 [19075687] Nat Med. 2009 Jan;15(1):104-9 [19029979] Cancer Res. 2009 Feb 15;69(4):1268-72 [19176373] Blood. 2009 Apr 16;113(16):3792-800 [18988862] Cell Stem Cell. 2009 Aug 7;5(2):168-77 [19664991] Clin Cancer Res. 2009 Aug 15;15(16):5274-9 [19671873] J Exp Med. 2009 Nov 23;206(12):2779-93 [19858324] Nat Rev Immunol. 2010 May;10(5):345-52 [20414207] Curr Opin Mol Ther. 2010 Jun;12(3):350-60 [20521224] Blood. 2010 Aug 19;116(7):1035-44 [20439624] Discov Med. 2010 Oct;10(53):329-39 [21034674] Analyst. 2011 Feb 7;136(3):473-8 [20967331] MAbs. 2011 Jan-Feb;3(1):67-75 [21051930] PLoS One. 2011;6(1):e14640 [21305058] Acc Chem Res. 2011 Feb 15;44(2):83-90 [21062101] Cancer Res. 2011 Mar 1;71(5):1520-5 [21193546] Int J Cancer. 2011 May 1;128(9):2020-30 [20635390] MAbs. 2011 Mar-Apr;3(2):161-72 [21441786] Proc Natl Acad Sci U S A. 2011 Apr 5;108(14):5742-7 [21436054] Leuk Lymphoma. 2011 Jun;52 Suppl 2:87-90 [21504287] MAbs. 2011 Jul-Aug;3(4):331-7 [21691144] J Immunol. 2011 Oct 15;187(8):4040-50 [21908732] Cancer Res. 2011 Nov 15;71(22):7080-90 [21990319] Nat Med. 2011 Dec;17(12):1685-91 [22057348] N Engl J Med. 2012 Jan 12;366(2):109-19 [22149875] J Clin Oncol. 2012 May 20;30(15):1822-8 [22355053] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.4161/mabs.21521 ER - TY - JOUR T1 - Photooxidation of Amplex Red to resorufin: implications of exposing the Amplex Red assay to light. AN - 1037655608; 22765927 AB - The Amplex Red assay, a fluorescent assay for the detection of H(2)O(2), relies on the reaction of H(2)O(2) and colorless, nonfluorescent Amplex Red with a 1:1 stoichiometry to form colored, fluorescent resorufin, catalyzed by horseradish peroxidase (HRP). We have found that resorufin is artifactually formed when Amplex Red is exposed to light. In the absence of H(2)O(2) and HRP, the absorption and fluorescence spectra of Amplex Red changed during exposure to ambient room light or instrumental excitation light, clearly indicating that the fluorescent product resorufin had formed. This photochemistry was initiated by trace amounts of resorufin that are present in Amplex Red stock solutions. ESR spin-trapping studies demonstrated that superoxide radical was an intermediate in this process. Oxygen consumption measurements further confirmed that superoxide and H(2)O(2) were artifactually produced by the photooxidation of Amplex Red. The artifactual formation of resorufin was also significantly increased by the presence of superoxide dismutase or HRP. This photooxidation process will result in a less sensitive assay for H(2)O(2) under ambient light exposure and potentially invalid measurements under high energy exposure such as UVA irradiation. In general, precautions should be taken to minimize exposure to light during measurement of oxidative stress with Amplex Red. Published by Elsevier Inc. JF - Free radical biology & medicine AU - Zhao, Baozhong AU - Summers, Fiona A AU - Mason, Ronald P AD - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA. Y1 - 2012/09/01/ PY - 2012 DA - 2012 Sep 01 SP - 1080 EP - 1087 VL - 53 IS - 5 KW - Oxazines KW - 0 KW - amplex red reagent KW - 119171-73-2 KW - resorufin KW - 635-78-9 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Index Medicus KW - Oxidation-Reduction KW - Oxidative Stress KW - Photochemical Processes KW - Hydrogen Peroxide -- analysis KW - Oxazines -- chemistry KW - Ultraviolet Rays UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1037655608?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Photooxidation+of+Amplex+Red+to+resorufin%3A+implications+of+exposing+the+Amplex+Red+assay+to+light.&rft.au=Zhao%2C+Baozhong%3BSummers%2C+Fiona+A%3BMason%2C+Ronald+P&rft.aulast=Zhao&rft.aufirst=Baozhong&rft.date=2012-09-01&rft.volume=53&rft.issue=5&rft.spage=1080&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2012.06.034 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-06-07 N1 - Date created - 2012-08-31 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Free Radic Biol Med. 2012 Jan 1;52(1):1-6 [22027063] Free Radic Biol Med. 1999 Dec;27(11-12):1197-202 [10641711] J Neurosci. 2004 Sep 8;24(36):7779-88 [15356189] Arch Biochem Biophys. 2004 Nov 1;431(1):138-44 [15464736] Anal Biochem. 2004 Nov 15;334(2):290-6 [15494136] Biochim Biophys Acta. 1980 Jun 5;630(1):119-30 [6248123] Arch Biochem Biophys. 1989 Feb 1;268(2):605-16 [2464338] Chem Res Toxicol. 1992 Mar-Apr;5(2):268-73 [1643257] J Immunol Methods. 1997 Mar 28;202(2):133-41 [9107302] Anal Biochem. 1997 Nov 15;253(2):162-8 [9367498] J Invest Dermatol. 1998 Jun;110(6):966-71 [9620307] Free Radic Biol Med. 1999 Jan;26(1-2):148-61 [9890650] J Mol Cell Cardiol. 2004 Dec;37(6):1119-36 [15572043] J Appl Physiol (1985). 2005 Jan;98(1):404-14 [15591310] Proc Natl Acad Sci U S A. 2005 Apr 5;102(14):5044-9 [15795385] Anal Biochem. 2005 Jul 15;342(2):327-37 [15913534] J Biol Chem. 2005 Dec 23;280(51):42026-35 [16243845] Methods Cell Biol. 2007;80:355-77 [17445704] Free Radic Biol Med. 2007 Oct 1;43(7):995-1022 [17761297] Chest. 2008 Jun;133(6):1410-4 [18339777] Circ Res. 2008 Oct 10;103(8):873-80 [18776040] J Biol Chem. 2009 Jan 2;284(1):46-55 [19001413] J Am Chem Soc. 2009 May 6;131(17):6277-82 [19338338] Free Radic Biol Med. 2010 Jun 1;48(11):1485-91 [20188819] Free Radic Biol Med. 2010 Jul 1;49(1):61-6 [20332022] Free Radic Biol Med. 2011 Jul 1;51(1):153-9 [21419845] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.freeradbiomed.2012.06.034 ER - TY - JOUR T1 - Epstein-Barr virus and breast cancer: epidemiological and molecular study on Egyptian and Iraqi women. AN - 1037242841; 22929918 AB - The role of Epstein-Barr virus (EBV) in breast carcinogenesis is still controversial. Unraveling this relationship is potentially important for better understanding of breast cancer etiology, early detection and possibly prevention of breast cancer. The aim of the current study is to unravel the association between EBV and primary invasive breast cancer (PIBC) in two different Arab populations (Egyptian and Iraqi women). The study was done on paraffin-embedded tissues of 40 Egyptian and 50 Iraqi patients with PIBC in addition to 20 normal breast tissues as controls for each group. Both controls and neoplastic tissues were assessed for the expression of EBV genes and proteins (EBNA-1, LMP-1, and EBER) as well as CD21 marker by immunohistochemistry (IHC), in situ hybridization (ISH) and PCR techniques. Our gold standard for EBV reactivity in breast cancer cases was positivity of both EBNA1 by PCR and EBER by in situ hybridization. EBV was detected in 18/40 (45%) and 14/50 (28%) of Egyptian and Iraqi women; respectively where p=0.073, compared to 0/20 (0%) of their control groups (p<0.05). Regarding the association between EBV positivity and tumor grade, there was not any statistical significant difference between EBV presence and tumor grade in both populations where p=0.860 and p=0.976 and the calculated rank biserial correlation coefficient was 0.114 and 0.269 for Egyptian and Iraqi women respectively. Our findings show that EBV might act as a promoter for the development of PIBC and it might contribute to increased tumor aggressiveness in Egyptian and Iraqi patients. Copyright © 2012. Published by Elsevier B.V. JF - Journal of the Egyptian National Cancer Institute AU - Zekri, Abdel-Rahman N AU - Bahnassy, Abeer A AU - Mohamed, Waleed S AU - El-Kassem, Fatma A AU - El-Khalidi, Saja J AU - Hafez, Mohamed M AU - Hassan, Zeinab K AD - Virology and Immunology Unit, Cancer Biology Department, National Cancer Institute, Cairo University, Cairo 11976, Egypt. ncizekri@yahoo.com Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 123 EP - 131 VL - 24 IS - 3 SN - 1110-0362, 1110-0362 KW - Biomarkers, Tumor KW - 0 KW - Receptors, Complement 3d KW - Viral Proteins KW - Index Medicus KW - Viral Proteins -- genetics KW - Biomarkers, Tumor -- genetics KW - Humans KW - Gene Expression KW - Aged KW - Biomarkers, Tumor -- metabolism KW - Molecular Epidemiology KW - Receptors, Complement 3d -- metabolism KW - Egypt -- epidemiology KW - Adult KW - Viral Proteins -- metabolism KW - Middle Aged KW - Female KW - Iraq -- epidemiology KW - Herpesvirus 4, Human -- metabolism KW - Epstein-Barr Virus Infections -- metabolism KW - Epstein-Barr Virus Infections -- epidemiology KW - Breast Neoplasms -- metabolism KW - Breast Neoplasms -- epidemiology KW - Carcinoma, Lobular -- virology KW - Epstein-Barr Virus Infections -- complications KW - Carcinoma, Ductal, Breast -- epidemiology KW - Carcinoma, Lobular -- epidemiology KW - Herpesvirus 4, Human -- genetics KW - Carcinoma, Lobular -- metabolism KW - Carcinoma, Ductal, Breast -- metabolism KW - Breast Neoplasms -- virology KW - Carcinoma, Ductal, Breast -- virology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1037242841?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Epstein-Barr+virus+and+breast+cancer%3A+epidemiological+and+molecular+study+on+Egyptian+and+Iraqi+women.&rft.au=Zekri%2C+Abdel-Rahman+N%3BBahnassy%2C+Abeer+A%3BMohamed%2C+Waleed+S%3BEl-Kassem%2C+Fatma+A%3BEl-Khalidi%2C+Saja+J%3BHafez%2C+Mohamed+M%3BHassan%2C+Zeinab+K&rft.aulast=Zekri&rft.aufirst=Abdel-Rahman&rft.date=2012-09-01&rft.volume=24&rft.issue=3&rft.spage=123&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+Egyptian+National+Cancer+Institute&rft.issn=11100362&rft_id=info:doi/10.1016%2Fj.jnci.2012.06.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-09-09 N1 - Date created - 2012-08-29 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.jnci.2012.06.001 ER - TY - JOUR T1 - Thioredoxin reductase 1 protects against chemically induced hepatocarcinogenesis via control of cellular redox homeostasis. AN - 1035107255; 22791808 AB - Thioredoxin reductase 1 (TR1) controls the redox state of protein thiols in mammalian cells and has been shown to have roles in both preventing and promoting cancer. To define the role of this selenoenzyme in hepatocellular carcinoma development, we examined tumor incidence in the liver of mice with tissue-specific knockout of mouse TR1 subjected to the liver carcinogen, diethylnitrosamine (DEN). TR1-deficient livers manifested ~90% tumor incidence compared with ~16% in control livers. The TR1-dependent effect was observed independent of sex, and, in control mice, tumorigenesis did not affect the expression of TR1. On the other hand, we observed upregulation of another selenoenzyme, glutathione peroxidase 2 (GPx2), and components of the glutathione (GSH) system, including those that generate reduced GSH. Overall, this study shows that TR1 protects against chemically induced hepatocarcinogenesis via the control of the cellular redox state, whereas its role in promoting this type of cancer is minimal. JF - Carcinogenesis AU - Carlson, Bradley A AU - Yoo, Min-Hyuk AU - Tobe, Ryuta AU - Mueller, Charles AU - Naranjo-Suarez, Salvador AU - Hoffmann, Victoria J AU - Gladyshev, Vadim N AU - Hatfield, Dolph L AD - Molecular Biology of Selenium Section, Laboratory of Cancer Prevention, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 1806 EP - 1813 VL - 33 IS - 9 KW - glutathione peroxidase GPX1 KW - EC 1.11.1.- KW - Glutathione Peroxidase KW - EC 1.11.1.9 KW - Thioredoxin Reductase 1 KW - EC 1.8.1.9 KW - Txnrd1 protein, mouse KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Oxidation-Reduction KW - Body Weight KW - Animals KW - Glutathione -- metabolism KW - Mice, Inbred C57BL KW - Mice KW - Homeostasis KW - Organ Size KW - Male KW - Glutathione Peroxidase -- analysis KW - Female KW - Liver Neoplasms -- prevention & control KW - Liver Neoplasms -- chemically induced KW - Thioredoxin Reductase 1 -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1035107255?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Thioredoxin+reductase+1+protects+against+chemically+induced+hepatocarcinogenesis+via+control+of+cellular+redox+homeostasis.&rft.au=Carlson%2C+Bradley+A%3BYoo%2C+Min-Hyuk%3BTobe%2C+Ryuta%3BMueller%2C+Charles%3BNaranjo-Suarez%2C+Salvador%3BHoffmann%2C+Victoria+J%3BGladyshev%2C+Vadim+N%3BHatfield%2C+Dolph+L&rft.aulast=Carlson&rft.aufirst=Bradley&rft.date=2012-09-01&rft.volume=33&rft.issue=9&rft.spage=1806&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgs230 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-31 N1 - Date created - 2012-08-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochem Biophys Res Commun. 2006 Jan 6;339(1):79-88 [16293230] Cancer Biol Ther. 2005 Jan;4(1):6-13 [15684606] Cell Mol Life Sci. 2005 Nov;62(21):2414-37 [16231092] Crit Rev Clin Lab Sci. 2006;43(2):143-81 [16517421] J Biol Chem. 2006 May 12;281(19):13005-8 [16565519] Semin Cancer Biol. 2006 Dec;16(6):452-65 [17056271] Semin Cancer Biol. 2006 Dec;16(6):427-35 [17081769] Semin Cancer Biol. 2006 Dec;16(6):420-6 [17092741] Annu Rev Pharmacol Toxicol. 2007;47:89-116 [16968214] Free Radic Biol Med. 2007 Sep 15;43(6):911-23 [17697936] Cancer Res. 2007 Dec 1;67(23):11141-6 [18056438] PLoS One. 2009;4(7):e6158 [19584930] Cell Death Differ. 2009 Oct;16(10):1303-14 [19662025] Biochim Biophys Acta. 2009 Nov;1790(11):1541-5 [19272412] Biochim Biophys Acta. 2009 Nov;1790(11):1555-68 [19289149] Antioxid Redox Signal. 2010 Apr 1;12(7):867-80 [19769465] Anticancer Res. 2010 Apr;30(4):1169-81 [20530424] J Cell Sci. 2010 Jul 15;123(Pt 14):2402-12 [20571049] Biochem J. 2010 Sep 1;430(2):285-93 [20536427] Cancer Res. 2010 Nov 15;70(22):9505-14 [21045148] Arch Toxicol. 2011 Apr;85(4):273-84 [21369766] Drugs. 2011 Jul 30;71(11):1385-96 [21812504] Clin Cancer Res. 2011 Oct 1;17(19):6206-17 [21844013] Free Radic Biol Med. 2012 Jan 15;52(2):436-43 [22100505] Free Radic Biol Med. 2012 Feb 15;52(4):803-10 [22198266] EMBO J. 2000 Jan 17;19(2):306-14 [10637234] Eur J Biochem. 2000 Oct;267(20):6102-9 [11012661] EMBO J. 2000 Dec 15;19(24):6882-90 [11118223] J Biol Chem. 2003 Jan 10;278(2):745-50 [12424231] J Biol Chem. 2004 Feb 27;279(9):8011-7 [14660662] Antioxid Redox Signal. 2004 Feb;6(1):41-52 [14980055] Cancer Res. 2004 Apr 15;64(8):2910-7 [15087411] Biochem Biophys Res Commun. 1998 Oct 20;251(2):488-93 [9792801] Cancer Res. 1999 Jul 1;59(13):3175-9 [10397262] Mol Cell Biol. 2005 Mar;25(5):1980-8 [15713651] Oncogene. 2005 Dec 1;24(54):8003-11 [16170372] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/carcin/bgs230 ER - TY - JOUR T1 - Opportunistic intestinal infections and risk of colorectal cancer among people with AIDS. AN - 1034801854; 22149090 AB - Because mucosal inflammation contributes to colorectal carcinogenesis, we studied the impact of intestinal infections on risk of this malignancy among people with AIDS (PWA). Using the population-based HIV/AIDS Cancer Match, which includes approximately half of all PWA in the United States, the cancer registries ascertained colorectal cancers (ICD-O3 codes C180-C189, C199, C209, and C260). During 4-120 months after AIDS onset, risk of cancer occurring after AIDS-defining intestinal infections (considered as time-dependent exposures) was estimated with hazard ratios (HR) and 95% confidence intervals (CI) calculated by Cox regression. Analyses included cancers overall and by histology and anatomic site. After excluding 118 squamous cell rectal cancers (possible anal cancers), we analyzed 320 incident colorectal cancer cases that occurred among 471,909 PWA. Colorectal cancer risk was marginally elevated following cryptosporidiosis (HR=2.08, 95% CI=0.93-4.70, p=0.08) and mucocutaneous herpes (HR=1.69, 95% CI=0.97-2.95, p=0.07) but not with Pneumocystis pneumonia (HR=0.79, 95% CI=0.57-1.10). Cryptosporidiosis was associated with rare colon squamous cell carcinoma [N=8, HR=13, 95% CI=1.5-110] and uncommon histologies [HR=4.4, 95% CI=1.1-18, p=0.04], but it was not associated with colorectal adenocarcinoma (N=269, HR=1.3, 95% CI=0.4-3.9, p=0.70). Mucocutaneous herpes was associated with colon squamous cell carcinoma (HR=13, 95% CI=2.4-67, p=0.003) but not with colorectal adenocarcinoma (HR=1.3, 95% CI=0.6-2.6, p=0.52) or uncommon histologies (HR=2.5, 95% CI=0.8-8.2, p=0.13). Colon squamous cell carcinoma risk was significantly elevated among PWA who had cryptosporidiosis or mucocutaneous herpes. These findings might suggest that HPV or inflammation from other infection may contribute to carcinogenesis. JF - AIDS research and human retroviruses AU - Shebl, Fatma M AU - Engels, Eric A AU - Goedert, James J AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland, USA. sheblf@mail.nih.gov Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 994 EP - 999 VL - 28 IS - 9 KW - Index Medicus KW - AIDS/HIV KW - Inflammation -- virology KW - Risk Factors KW - Humans KW - Adult KW - Inflammation -- etiology KW - Middle Aged KW - Immunocompromised Host KW - CD4 Lymphocyte Count KW - United States -- epidemiology KW - Male KW - Female KW - Inflammation -- epidemiology KW - Acquired Immunodeficiency Syndrome -- complications KW - AIDS-Related Opportunistic Infections -- complications KW - Carcinoma, Squamous Cell -- etiology KW - Carcinoma, Squamous Cell -- epidemiology KW - Intestinal Mucosa -- immunology KW - Cryptosporidiosis -- epidemiology KW - AIDS-Related Opportunistic Infections -- epidemiology KW - Herpes Simplex -- complications KW - Carcinoma, Squamous Cell -- virology KW - AIDS-Related Opportunistic Infections -- immunology KW - Acquired Immunodeficiency Syndrome -- epidemiology KW - Acquired Immunodeficiency Syndrome -- immunology KW - Herpes Simplex -- epidemiology KW - Colorectal Neoplasms -- etiology KW - Cryptosporidiosis -- complications KW - Colorectal Neoplasms -- virology KW - Colorectal Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1034801854?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Opportunistic+intestinal+infections+and+risk+of+colorectal+cancer+among+people+with+AIDS.&rft.au=Shebl%2C+Fatma+M%3BEngels%2C+Eric+A%3BGoedert%2C+James+J&rft.aulast=Shebl&rft.aufirst=Fatma&rft.date=2012-09-01&rft.volume=28&rft.issue=9&rft.spage=994&rft.isbn=&rft.btitle=&rft.title=AIDS+research+and+human+retroviruses&rft.issn=1931-8405&rft_id=info:doi/10.1089%2FAID.2011.0185 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-12-27 N1 - Date created - 2012-08-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Indian J Cancer. 1999 Mar;36(1):38-42 [10810553] Gastroenterology. 2001 Mar;120(4):988-94 [11231953] JAMA. 2001 Apr 4;285(13):1736-45 [11277828] Arch Pathol Lab Med. 2001 Aug;125(8):1042-6 [11473454] J Acquir Immune Defic Syndr. 2002 Sep 1;31(1):90-7 [12352155] J Natl Cancer Inst. 2002 Nov 6;94(21):1604-13 [12419786] Lancet. 2002 Nov 16;360(9345):1557-63 [12443594] J Infect Chemother. 2003 Sep;9(3):278-81 [14513402] J Clin Oncol. 2004 Jul 1;22(13):2730-9 [15226341] N Engl J Med. 1981 Dec 10;305(24):1439-44 [6272110] N Engl J Med. 1983 Apr 14;308(15):868-71 [6300674] N Engl J Med. 1987 Oct 15;317(16):973-7 [2821396] Ann Intern Med. 1988 Mar;108(3):328-33 [2829677] Cancer. 1988 Aug 1;62(3):616-9 [3390798] Contrib Gynecol Obstet. 1991;18:54-70 [1657523] Ann Intern Med. 1992 Jan 1;116(1):63-77 [1463471] Am J Gastroenterol. 1994 Feb;89(2):254-6 [8304313] J Gastroenterol Hepatol. 1994 May-Jun;9(3):291-303 [8054532] AIDS. 1994 Oct;8(10):1489-93 [7818822] Gastroenterol Clin North Am. 1996 Sep;25(3):691-707 [8863046] Am J Epidemiol. 1996 Nov 1;144(9):807-16 [8890659] J Diarrhoeal Dis Res. 1997 Jun;15(2):71-4 [9360344] Lancet. 1998 Jun 20;351(9119):1833-9 [9652666] Clin Infect Dis. 2005 Dec 1;41(11):1621-7 [16267735] J Ayub Med Coll Abbottabad. 2005 Jul-Sep;17(3):38-40 [16320794] Cancer Res. 2006 Jan 15;66(2):828-38 [16424015] AIDS. 2006 Aug 1;20(12):1645-54 [16868446] Curr Opin Oncol. 2006 Sep;18(5):469-78 [16894295] Cancer. 2006 Sep 1;107(5 Suppl):1128-41 [16802325] Can J Gastroenterol. 2007 Jan;21(1):47-50 [17225882] Am J Surg Pathol. 2007 Jun;31(6):919-25 [17527081] Lancet. 2007 Jul 7;370(9581):59-67 [17617273] J Parasitol. 2007 Jun;93(3):722-4 [17626376] Ann Intern Med. 2008 May 20;148(10):728-36 [18490686] J Infect. 2008 Jun;56(6):413-22 [18474400] Gut. 2009 Aug;58(8):1129-34 [19293177] World J Gastroenterol. 2009 Sep 21;15(35):4380-6 [19764088] Int J Clin Oncol. 2009 Dec;14(6):551-4 [19967495] Am J Trop Med Hyg. 2010 Feb;82(2):257-65 [20134002] Arch Iran Med. 2010 Jul;13(4):282-7 [20597560] Pathol Oncol Res. 2010 Sep;16(3):461-8 [20232185] Genome Res. 2012 Feb;22(2):299-306 [22009989] Genome Res. 2012 Feb;22(2):292-8 [22009990] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1089/AID.2011.0185 ER - TY - JOUR T1 - Human CYP2C8 is post-transcriptionally regulated by microRNAs 103 and 107 in human liver. AN - 1034517498; 22723340 AB - The CYP2C genes are extensively regulated at the transcriptional stage. The present study shows for the first time that CYP2Cs are also regulated post-transcriptionally by microRNAs (miRNAs). By using online search engines, we found potential miRNA response elements (MREs) in the 3'-untranslated region (3'-UTR) of the CYP2C mRNAs. Among these were a MRE for the miRNAs miR-103 and miR-107 in the 3'-UTR of human CYP2C8. CYP2C8 protein levels (measured through immunoblot analyses) did not correlate with CYP2C8 mRNA levels (measured through quantitative polymerase chain reaction analyses) in human liver samples. The translation efficiency (protein/mRNA ratio) for CYP2C8 was inversely correlated with the expression of miR-103 and miR-107. When three copies of the putative MRE from CYP2C8 were inserted downstream from a luciferase expression reporter, transfection with precursors for miR-103 or miR-107 decreased luciferase activity in primary hepatocytes, whereas transfection with antisense oligonucleotides (AsOs) for miR-103/miR-107 increased luciferase activity. As expected, there was no effect of the precursors or AsOs when three copies of the putative MRE were inserted in the reverse orientation. When precursors for miR-103/miR-107 were transfected into primary human hepatocytes, CYP2C8 protein levels were decreased, whereas AsOs increased CYP2C8 protein levels. Neither precursors nor AsOs affected CYP2C8 mRNA levels, which indicated that the effect was post-transcriptional. Putative MRE motifs were also found in the 3'-UTRs of CYP2C9 and CYP2C19, which suggested that the same miRNAs could regulate translation of other members of the CYP2C family, although to a lesser degree than CYP2C8. These results clearly show that CYP2Cs are regulated post-transcriptionally by miR-103 and miR-107. JF - Molecular pharmacology AU - Zhang, Shu-Yun AU - Surapureddi, Sailesh AU - Coulter, Sherry AU - Ferguson, Stephen S AU - Goldstein, Joyce A AD - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 529 EP - 540 VL - 82 IS - 3 KW - 3' Untranslated Regions KW - 0 KW - HNF4A protein, human KW - Hepatocyte Nuclear Factor 4 KW - MIRN107 microRNA, human KW - MicroRNAs KW - Oligonucleotides, Antisense KW - RNA, Messenger KW - Receptors, Glucocorticoid KW - Luciferases KW - EC 1.13.12.- KW - Aryl Hydrocarbon Hydroxylases KW - EC 1.14.14.1 KW - CYP2C8 protein, human KW - Cytochrome P-450 CYP2C8 KW - Index Medicus KW - Protein Biosynthesis KW - Cell Survival -- genetics KW - Humans KW - Oligonucleotides, Antisense -- genetics KW - Luciferases -- metabolism KW - Hepatocyte Nuclear Factor 4 -- genetics KW - RNA, Messenger -- genetics KW - Hepatocyte Nuclear Factor 4 -- metabolism KW - Hepatocytes -- enzymology KW - Receptors, Glucocorticoid -- metabolism KW - Transfection -- methods KW - Gene Expression Regulation, Enzymologic KW - Hep G2 Cells KW - Cells, Cultured KW - Oligonucleotides, Antisense -- metabolism KW - Hepatocytes -- physiology KW - Receptors, Glucocorticoid -- genetics KW - Hepatocytes -- metabolism KW - Liver -- enzymology KW - Aryl Hydrocarbon Hydroxylases -- metabolism KW - MicroRNAs -- metabolism KW - MicroRNAs -- genetics KW - Liver -- metabolism KW - Aryl Hydrocarbon Hydroxylases -- genetics KW - RNA Processing, Post-Transcriptional KW - Liver -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1034517498?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+CYP2C8+is+post-transcriptionally+regulated+by+microRNAs+103+and+107+in+human+liver.&rft.au=Zhang%2C+Shu-Yun%3BSurapureddi%2C+Sailesh%3BCoulter%2C+Sherry%3BFerguson%2C+Stephen+S%3BGoldstein%2C+Joyce+A&rft.aulast=Zhang&rft.aufirst=Shu-Yun&rft.date=2012-09-01&rft.volume=82&rft.issue=3&rft.spage=529&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=1521-0111&rft_id=info:doi/10.1124%2Fmol.112.078386 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-17 N1 - Date created - 2012-08-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Pharmacol Res. 2011 May;63(5):405-13 [21292004] Expert Opin Ther Targets. 2011 Mar;15(3):265-79 [21208133] Nature. 2011 Jun 30;474(7353):649-53 [21654750] Pharmacol Ther. 2011 Sep;131(3):330-7 [21565218] FASEB J. 2011 Oct;25(10):3436-47 [21697548] Nat Rev Genet. 2004 Jul;5(7):522-31 [15211354] Arch Biochem Biophys. 1992 Nov 15;299(1):110-5 [1444443] Cancer Res. 1994 Nov 1;54(21):5543-6 [7923194] Jpn J Hum Genet. 1994 Sep;39(3):337-43 [7841444] Pharmacogenetics. 1994 Dec;4(6):285-99 [7704034] Drug Metab Dispos. 1999 Nov;27(11):1260-6 [10534310] Mol Pharmacol. 2000 Aug;58(2):361-72 [10908304] Drug Metab Dispos. 2000 Nov;28(11):1303-10 [11038157] Mol Pharmacol. 2000 Dec;58(6):1441-50 [11093784] Drug Metab Dispos. 2001 Mar;29(3):242-51 [11181490] Pharmacogenetics. 2001 Oct;11(7):597-607 [11668219] Br J Clin Pharmacol. 2001 Oct;52(4):349-55 [11678778] J Pharmacol Exp Ther. 2002 Feb;300(2):399-407 [11805197] Drug Metab Dispos. 2002 Apr;30(4):438-45 [11901098] Mol Pharmacol. 2002 Sep;62(3):737-46 [12181452] J Pharmacol Exp Ther. 2002 Oct;303(1):412-23 [12235278] Drug Metab Dispos. 2002 Dec;30(12):1352-6 [12433802] Yakugaku Zasshi. 2003 May;123(5):369-75 [12772594] Cell. 2003 Jun 13;113(6):673-6 [12809598] Dev Biol. 2003 Jul 1;259(1):9-18 [12812784] Drug Metab Dispos. 2003 Jul;31(7):908-15 [12814968] Mol Pharmacol. 2003 Aug;64(2):316-24 [12869636] Science. 2003 Jul 18;301(5631):336-8 [12869753] Pharmacogenetics. 2003 Dec;13(12):715-20 [14646690] Nucleic Acids Res. 2004 Jan 1;32(Database issue):D109-11 [14681370] Cell. 2004 Jan 23;116(2):281-97 [14744438] J Pharmacol Exp Ther. 2004 Feb;308(2):495-501 [14600250] Drug Metabol Drug Interact. 2003;19(4):257-85 [14768974] Cancer Res. 2004 May 1;64(9):3119-25 [15126349] Biochem Pharmacol. 1998 Mar 15;55(6):825-30 [9586955] Br J Clin Pharmacol. 1999 May;47(5):545-52 [10336579] J Biochem Mol Toxicol. 1999;13(6):289-95 [10487415] Br J Clin Pharmacol. 1999 Sep;48(3):424-32 [10510156] Cell. 2005 Jan 14;120(1):15-20 [15652477] Nature. 2005 Mar 17;434(7031):338-45 [15735639] 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):191-7 [16299161] Cancer Res. 2006 Sep 15;66(18):9090-8 [16982751] Drug Metab Dispos. 2007 Apr;35(4):682-8 [17220242] Pharmacol Ther. 2007 Dec;116(3):496-526 [18001838] Drug Metab Dispos. 2009 Oct;37(10):2112-7 [19581388] Carcinogenesis. 2008 Dec;29(12):2394-9 [18780894] J Biol Chem. 2008 Apr 11;283(15):9674-80 [18268015] Mol Pharmacol. 2009 Oct;76(4):702-9 [19570947] Curr Drug Metab. 2009 Jul;10(6):567-78 [19702536] Biochem Pharmacol. 2010 Apr 1;79(7):1045-52 [19945440] J Biol Chem. 2010 Feb 12;285(7):4415-22 [20018894] Gut. 2010 Feb;59(2):236-46 [19671543] Drug Metab Dispos. 2010 Apr;38(4):591-9 [20086032] J Lipid Res. 2010 Aug;51(8):2223-33 [20351063] J Mol Biol. 2010 Sep 24;402(3):491-509 [20678503] Mol Cell Biol. 2011 Feb;31(3):466-81 [21135126] FASEB J. 2011 Feb;25(2):703-13 [21059750] PLoS One. 2011;6(5):e20038 [21625387] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1124/mol.112.078386 ER - TY - JOUR T1 - New insights for drug design from the X-ray crystallographic structures of G-protein-coupled receptors. AN - 1034517450; 22695719 AB - Methodological advances in X-ray crystallography have made possible the recent solution of X-ray structures of pharmaceutically important G protein-coupled receptors (GPCRs), including receptors for biogenic amines, peptides, a nucleoside, and a sphingolipid. These high-resolution structures have greatly increased our understanding of ligand recognition and receptor activation. Conformational changes associated with activation common to several receptors entail outward movements of the intracellular side of transmembrane helix 6 (TM6) and movements of TM5 toward TM6. Movements associated with specific agonists or receptors have also been described [e.g., extracellular loop (EL) 3 in the A(2A) adenosine receptor]. The binding sites of different receptors partly overlap but differ significantly in ligand orientation, depth, and breadth of contact areas in TM regions and the involvement of the ELs. A current challenge is how to use this structural information for the rational design of novel potent and selective ligands. For example, new chemotypes were discovered as antagonists of various GPCRs by subjecting chemical libraries to in silico docking in the X-ray structures. The vast majority of GPCR structures and their ligand complexes are still unsolved, and no structures are known outside of family A GPCRs. Molecular modeling, informed by supporting information from site-directed mutagenesis and structure-activity relationships, has been validated as a useful tool to extend structural insights to related GPCRs and to analyze docking of other ligands in already crystallized GPCRs. JF - Molecular pharmacology AU - Jacobson, Kenneth A AU - Costanzi, Stefano AD - Molecular Recognition Section, Laboratory of Bioorganic Chemistry, National Institutes of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-0810, USA. kajacobs@helix.nih.gov Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 361 EP - 371 VL - 82 IS - 3 KW - Ligands KW - 0 KW - Receptors, G-Protein-Coupled KW - Index Medicus KW - Humans KW - Crystallography, X-Ray -- methods KW - Binding Sites KW - Receptors, G-Protein-Coupled -- chemistry KW - Receptors, G-Protein-Coupled -- metabolism KW - Drug Design UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1034517450?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=New+insights+for+drug+design+from+the+X-ray+crystallographic+structures+of+G-protein-coupled+receptors.&rft.au=Jacobson%2C+Kenneth+A%3BCostanzi%2C+Stefano&rft.aulast=Jacobson&rft.aufirst=Kenneth&rft.date=2012-09-01&rft.volume=82&rft.issue=3&rft.spage=361&rft.isbn=&rft.btitle=&rft.title=Molecular+pharmacology&rft.issn=1521-0111&rft_id=info:doi/10.1124%2Fmol.112.079335 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-17 N1 - Date created - 2012-08-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Curr Top Med Chem. 2011;11(12):1528-34 [21510834] Science. 2000 Aug 4;289(5480):739-45 [10926528] J Med Chem. 2011 Jul 14;54(13):4283-311 [21615150] J Med Chem. 2011 Jul 14;54(13):4312-23 [21661720] Nature. 2011 Jul 7;475(7354):65-70 [21697825] Curr Opin Chem Biol. 2011 Aug;15(4):553-9 [21723773] Structure. 2011 Aug 10;19(8):1108-26 [21827947] Curr Opin Struct Biol. 2011 Aug;21(4):559-66 [21775127] Structure. 2011 Sep 7;19(9):1283-93 [21885291] Nat Chem Biol. 2011 Oct;7(10):692-700 [21857662] Nature. 2011 Sep 29;477(7366):549-55 [21772288] Pharmacol Rev. 2011 Dec;63(4):901-37 [21969326] J Mol Biol. 2011 Oct 28;413(3):615-27 [21906602] Nat Chem Biol. 2011 Nov;7(11):769-78 [21926995] J Med Chem. 2011 Dec 8;54(23):8195-206 [22007643] ChemMedChem. 2011 Dec 9;6(12):2302-11 [22021213] J Med Chem. 2012 Jan 12;55(1):538-52 [22104008] PLoS One. 2012;7(1):e29817 [22238661] J Comput Chem. 2012 Feb 15;33(5):561-72 [22170280] Nature. 2012 Feb 9;482(7384):237-40 [22286059] Methods Mol Biol. 2012;857:259-79 [22323225] Science. 2012 Feb 17;335(6070):851-5 [22344443] Br J Pharmacol. 2012 Mar;165(