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 - 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Last updated - 2017-01-18 DO - http://dx.doi.org/10.1124/mol.112.079335 ER - TY - JOUR T1 - Comparative dermal toxicity of dicyclohexylcarbodiimide and diisopropylcarbodiimide in rodents. AN - 1034516081; 22060820 AB - Dicyclohexylcarbodiimide (DCC) and Diisopropylcarbodiimide (DIC) are two representative chemicals in the carbodiimide class of chemicals used in industry as stabilizing agents. There is a potential of dermal exposure to these agents in chemical, pharmaceutical and recombinant DNA industries. The National Toxicology Program conducted a number of animal studies to characterize toxicity and carcinogenicity of DIC and DCC. Dermal administration of DCC and DIC in F344/N rats and B6C3F1 mice for 90-days induced skin irritation at the site of application in a dose-dependent manner. Microscopically, dose-dependent increases in epidermal hyperplasia and chronic inflammation were observed. We further evaluated the effects of dermal exposure of DCC and DIC in p53 haploinsufficient and Tg.AC mouse models. Results revealed the skin as the primary target of DCC and DIC exposure as indicated by dose - dependent skin lesions (hyperplasia, inflammation and necrosis). DCC induced squamous cell papillomas in Tg.AC mice but did not induce any neoplastic lesions in p53 haploinsufficient mice. Dermal application of DIC did not induce any neoplastic lesions in Tg.AC mice and p53 haploinsufficient mice. Based on these studies, it was predicted that DIC would be negative and DCC positive for carcinogenic activity in the traditional two-year bioassay. In the subsequent studies, the carcinogenic potential of DIC only in F344 rats and B6C3F1 mice in a traditional 2-year chronic carcinogenicity bioassay was evaluated by the dermal route. Findings revealed the skin as the major target organ of toxicity in both sexes in rats and in male mice. There were no neoplastic lesions observed in rats or mice with the administration of DIC. In rats, there were clinical signs of toxicity in the highest dose-group which included ataxia, excitability, impaired gait, low muscle tone, abnormal breathing, lethargy, and seizures. This was accompanied by non-neoplastic lesions in the brain and lung only at the highest dose level. In conclusion, both DIC and DCC are dermal toxicants. DIC did not have any carcinogenic activity in transgenic mouse models or in the traditional NTP two-year carcinogenicity studies in F344 rats and B6C3F1 mice. DCC was positive in the Tg.AC mouse model and likely to be carcinogenic in the 2-year bioassay as well. JF - Cutaneous and ocular toxicology AU - Surh, Inok AU - Behl, Mamta AU - Elmore, Susan A AU - Chhabra, Rajendra S AD - Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC 22709, USA. Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 177 EP - 187 VL - 31 IS - 3 KW - Carbodiimides KW - 0 KW - Dicyclohexylcarbodiimide KW - 538-75-0 KW - 1,3-diisopropylcarbodiimide KW - 693-13-0 KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Mice KW - Male KW - Female KW - Dicyclohexylcarbodiimide -- toxicity KW - Skin -- drug effects KW - Carbodiimides -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1034516081?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cutaneous+and+ocular+toxicology&rft.atitle=Comparative+dermal+toxicity+of+dicyclohexylcarbodiimide+and+diisopropylcarbodiimide+in+rodents.&rft.au=Surh%2C+Inok%3BBehl%2C+Mamta%3BElmore%2C+Susan+A%3BChhabra%2C+Rajendra+S&rft.aulast=Surh&rft.aufirst=Inok&rft.date=2012-09-01&rft.volume=31&rft.issue=3&rft.spage=177&rft.isbn=&rft.btitle=&rft.title=Cutaneous+and+ocular+toxicology&rft.issn=1556-9535&rft_id=info:doi/10.3109%2F15569527.2011.629384 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-12-26 N1 - Date created - 2012-08-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Erratum In: Cutan Ocul Toxicol. 2012 Sep;31(3):187 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.3109/15569527.2011.629384 ER - TY - JOUR T1 - Combination of N-methylisatin-β-thiosemicarbazone derivative (SCH16) with ribavirin and mycophenolic acid potentiates the antiviral activity of SCH16 against Japanese encephalitis virus in vitro. AN - 1034201935; 22738253 AB -  To investigate the drug to drug interaction of N-methylisatin-β-thiosemicarbazone (MIBT) derivative (SCH16) with ribavirin, mycophenolic acid and pentoxifylline against Japanese encephalitis virus in vitro. Our earlier studies have reported significant antiviral activity of these compounds against Japanese encephalitis virus in vitro and in vivo.  An in vitro drug to drug combination analysis was carried out to investigate whether or not the direct antiviral effect shown by the individual MIBT derivative could be effectively increased when lower concentrations of two compounds in combination were used. The results of this study showed that the combination of MIBT derivative (SCH16) with ribavirin or mycophenolic acid significantly enhanced the antiviral activity of SCH16 against JEV in vitro. In contrast, the combination of SCH16 and pentoxifylline resulted in antagonism.  The antiviral activity showed by SCH16 was enhanced in the presence of ribavirin and mycophenolic acid.  Studying the synergistic/additive interaction of the compounds in combination would help in lowering the effective concentration so as to overcome the concern of toxicity. © 2012 The Authors. Letters in Applied Microbiology © 2012 The Society for Applied Microbiology. JF - Letters in applied microbiology AU - Sebastian, L AU - Desai, A AU - Yogeeswari, P AU - Sriram, D AU - Madhusudana, S N AU - Ravi, V AD - Department of Neurovirology, National Institute of Mental Health and Neurosciences, Bangalore, India. Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 234 EP - 239 VL - 55 IS - 3 KW - Antiviral Agents KW - 0 KW - Indoles KW - Thiosemicarbazones KW - N-methylisatin KW - 2058-74-4 KW - Ribavirin KW - 49717AWG6K KW - Mycophenolic Acid KW - HU9DX48N0T KW - Pentoxifylline KW - SD6QCT3TSU KW - Index Medicus KW - Swine KW - Animals KW - Pentoxifylline -- pharmacology KW - Cells, Cultured KW - Indoles -- pharmacology KW - Drug Synergism KW - Mycophenolic Acid -- pharmacology KW - Ribavirin -- pharmacology KW - Antiviral Agents -- pharmacology KW - Encephalitis Virus, Japanese -- drug effects KW - Thiosemicarbazones -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1034201935?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Letters+in+applied+microbiology&rft.atitle=Combination+of+N-methylisatin-%CE%B2-thiosemicarbazone+derivative+%28SCH16%29+with+ribavirin+and+mycophenolic+acid+potentiates+the+antiviral+activity+of+SCH16+against+Japanese+encephalitis+virus+in+vitro.&rft.au=Sebastian%2C+L%3BDesai%2C+A%3BYogeeswari%2C+P%3BSriram%2C+D%3BMadhusudana%2C+S+N%3BRavi%2C+V&rft.aulast=Sebastian&rft.aufirst=L&rft.date=2012-09-01&rft.volume=55&rft.issue=3&rft.spage=234&rft.isbn=&rft.btitle=&rft.title=Letters+in+applied+microbiology&rft.issn=1472-765X&rft_id=info:doi/10.1111%2Fj.1472-765X.2012.03282.x LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-05-30 N1 - Date created - 2012-08-17 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1111/j.1472-765X.2012.03282.x ER - TY - JOUR T1 - An ethanolic extract of black cohosh causes hematological changes but not estrogenic effects in female rodents. AN - 1034198823; 22687605 AB - Black cohosh rhizome (Actaea racemosa) is used as a remedy for pain and gynecological ailments; modern preparations are commonly sold as ethanolic extracts available as dietary supplements. Black cohosh was nominated to the National Toxicology Program (NTP) for toxicity testing due to its widespread use and lack of safety data. Several commercially available black cohosh extracts (BCE) were characterized by the NTP, and one with chemical composition closest to formulations available to consumers was used for all studies. Female B6C3F1/N mice and Wistar Han rats were given 0, 15 (rats only), 62.5 (mice only), 125, 250, 500, or 1000 mg/kg/day BCE by gavage for 90 days starting at weaning. BCE induced dose-dependent hematological changes consistent with a non-regenerative macrocytic anemia and increased frequencies of peripheral micronucleated red blood cells (RBC) in both species. Effects were more severe in mice, which had decreased RBC counts in all treatment groups and increased micronucleated RBC at doses above 125 mg/kg. Dose-dependent thymus and liver toxicity was observed in rats but not mice. No biologically significant effects were observed in other organs. Puberty was delayed 2.9 days at the highest treatment dose in rats; a similar magnitude delay in mice occurred in the 125 and 250 mg/kg groups but not at the higher doses. An additional uterotrophic assay conducted in mice exposed for 3 days to 0.001, 0.01, 0.1, 1, 10, 100 and 500 mg/kg found no estrogenic or anti-estrogenic activity. These are the first studies to observe adverse effects of BCE in rodents. Copyright © 2012 Elsevier Inc. All rights reserved. JF - Toxicology and applied pharmacology AU - Mercado-Feliciano, Minerva AU - Cora, Michelle C AU - Witt, Kristine L AU - Granville, Courtney A AU - Hejtmancik, Milton R AU - Fomby, Laurene AU - Knostman, Katherine A AU - Ryan, Michael J AU - Newbold, Retha AU - Smith, Cynthia AU - Foster, Paul M AU - Vallant, Molly K AU - Stout, Matthew D AD - National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, 111 Alexander Drive, Research Triangle Park, NC, USA. Y1 - 2012/09/01/ PY - 2012 DA - 2012 Sep 01 SP - 138 EP - 147 VL - 263 IS - 2 KW - Estrogens KW - 0 KW - Plant Extracts KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Severity of Illness Index KW - Animals KW - Erythrocytes -- drug effects KW - Liver -- pathology KW - Anemia, Macrocytic -- chemically induced KW - Estrogens -- metabolism KW - Dose-Response Relationship, Drug KW - Thymus Gland -- pathology KW - Mice KW - Thymus Gland -- drug effects KW - Rats KW - Liver -- drug effects KW - Toxicity Tests KW - Rats, Wistar KW - Ethanol -- chemistry KW - Species Specificity KW - Erythrocytes -- pathology KW - Female KW - Sexual Maturation -- drug effects KW - Hematologic Diseases -- chemically induced KW - Cimicifuga -- chemistry KW - Plant Extracts -- toxicity KW - Hematologic Diseases -- pathology KW - Plant Extracts -- administration & dosage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1034198823?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+and+applied+pharmacology&rft.atitle=An+ethanolic+extract+of+black+cohosh+causes+hematological+changes+but+not+estrogenic+effects+in+female+rodents.&rft.au=Mercado-Feliciano%2C+Minerva%3BCora%2C+Michelle+C%3BWitt%2C+Kristine+L%3BGranville%2C+Courtney+A%3BHejtmancik%2C+Milton+R%3BFomby%2C+Laurene%3BKnostman%2C+Katherine+A%3BRyan%2C+Michael+J%3BNewbold%2C+Retha%3BSmith%2C+Cynthia%3BFoster%2C+Paul+M%3BVallant%2C+Molly+K%3BStout%2C+Matthew+D&rft.aulast=Mercado-Feliciano&rft.aufirst=Minerva&rft.date=2012-09-01&rft.volume=263&rft.issue=2&rft.spage=138&rft.isbn=&rft.btitle=&rft.title=Toxicology+and+applied+pharmacology&rft.issn=1096-0333&rft_id=info:doi/10.1016%2Fj.taap.2012.05.022 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-22 N1 - Date created - 2012-08-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Annu Rev Nutr. 2004;24:105-31 [15189115] Environ Mol Mutagen. 2004;43(1):3-9 [14743340] Am J Pathol. 1983 Nov;113(2):198-206 [6638150] Toxicol Appl Pharmacol. 1986 Mar 30;83(1):95-100 [3952753] Toxicol Appl Pharmacol. 1986 Sep 30;85(3):450-5 [3020740] Biometrics. 1987 Mar;43(1):225-34 [3567307] Environ Mutagen. 1987;9(3):235-50 [3569168] Biol Reprod. 1991 Oct;45(4):523-32 [1661182] Blood. 1992 May 1;79(9):2273-80 [1571542] Gynecol Endocrinol. 2005 Jan;20(1):30-5 [15969244] Mol Cell Endocrinol. 2005 Jul 15;239(1-2):27-36 [15950373] Toxicol Sci. 2006 Nov;94(1):92-107 [16888079] Blood Rev. 2006 Nov;20(6):299-318 [16716475] Can J Clin Pharmacol. 2006 Fall;13(3):e257-61 [17085773] J Agric Food Chem. 2006 Dec 27;54(26):9852-7 [17177511] Carcinogenesis. 2007 Mar;28(3):625-31 [16973674] Environ Mol Mutagen. 2007 Apr-May;48(3-4):322-9 [17358032] Yonsei Med J. 2007 Apr 30;48(2):289-94 [17461529] Birth Defects Res B Dev Reprod Toxicol. 2007 Apr;80(2):84-97 [17342777] Mutat Res. 2007 Dec 1;634(1-2):235-40 [17851117] Mutat Res. 2008 Jan 8;649(1-2):101-13 [17869571] Menopause. 2008 Sep-Oct;15(5):832-40 [18521048] J Agric Food Chem. 2008 Dec 24;56(24):11718-26 [19049296] Phytomedicine. 2009 Jan;16(1):72-84 [19010650] Eur J Gastroenterol Hepatol. 2009 Aug;21(8):941-5 [19404202] Climacteric. 2010 Apr;13(2):187-91 [19657787] Med J Aust. 2010 Oct 18;193(8):479-81 [20955128] Phytochem Anal. 2011 Jul-Aug;22(4):339-51 [21337649] Toxicol Sci. 1999 Dec;52(2):269-77 [10630580] Maturitas. 2008 Jul-Aug;60(3-4):209-15 [18691839] Menopause. 2011 Apr;18(4):366-75 [21228727] Environ Mol Mutagen. 2000;36(3):163-94 [11044899] J Clin Oncol. 2001 May 15;19(10):2739-45 [11352967] Reprod Toxicol. 2001 May-Jun;15(3):245-52 [11390168] Maturitas. 2003 Mar 14;44 Suppl 1:S31-8 [12609557] Eur J Endocrinol. 2003 Oct;149(4):351-62 [14514351] Environ Mol Mutagen. 2004;44(4):321-8 [15476197] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.taap.2012.05.022 ER - TY - JOUR T1 - Escherichia coli UmuC active site mutants: effects on translesion DNA synthesis, mutagenesis and cell survival. AN - 1033536894; 22784977 AB - Escherichia coli polymerase V (pol V/UmuD(2)'C) is a low-fidelity DNA polymerase that has recently been shown to avidly incorporate ribonucleotides (rNTPs) into undamaged DNA. The fidelity and sugar selectivity of pol V can be modified by missense mutations around the "steric gate" of UmuC. Here, we analyze the ability of three steric gate mutants of UmuC to facilitate translesion DNA synthesis (TLS) of a cyclobutane pyrimidine dimer (CPD) in vitro, and to promote UV-induced mutagenesis and cell survival in vivo. The pol V (UmuC_F10L) mutant discriminates against rNTP and incorrect dNTP incorporation much better than wild-type pol V and although exhibiting a reduced ability to bypass a CPD in vitro, does so with high-fidelity and consequently produces minimal UV-induced mutagenesis in vivo. In contrast, pol V (UmuC_Y11A) readily misincorporates both rNTPs and dNTPs during efficient TLS of the CPD in vitro. However, cells expressing umuD'C(Y11A) were considerably more UV-sensitive and exhibited lower levels of UV-induced mutagenesis than cells expressing wild-type umuD'C or umuD'C(Y11F). We propose that the increased UV-sensitivity and reduced UV-mutability of umuD'C(Y11A) is due to excessive incorporation of rNTPs during TLS that are subsequently targeted for repair, rather than an inability to traverse UV-induced lesions. Published by Elsevier B.V. JF - DNA repair AU - Kuban, Wojciech AU - Vaisman, Alexandra AU - McDonald, John P AU - Karata, Kiyonobu AU - Yang, Wei AU - Goodman, Myron F AU - Woodgate, Roger AD - Laboratory of Genomic Integrity, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-3371, USA. Y1 - 2012/09/01/ PY - 2012 DA - 2012 Sep 01 SP - 726 EP - 732 VL - 11 IS - 9 KW - DNA, Bacterial KW - 0 KW - Deoxyribonucleotides KW - Escherichia coli Proteins KW - Pyrimidine Dimers KW - Ribonucleotides KW - UmuC protein, E coli KW - 98059-80-4 KW - DNA polymerase V, E coli KW - EC 2.7.7.7 KW - DNA-Directed DNA Polymerase KW - Index Medicus KW - Ultraviolet Rays KW - DNA Repair KW - Pyrimidine Dimers -- metabolism KW - Ribonucleotides -- metabolism KW - Deoxyribonucleotides -- metabolism KW - DNA Damage KW - Mutagenesis -- genetics KW - DNA, Bacterial -- radiation effects KW - Escherichia coli K12 -- genetics KW - Escherichia coli Proteins -- metabolism KW - DNA, Bacterial -- genetics KW - Escherichia coli K12 -- radiation effects KW - DNA, Bacterial -- biosynthesis KW - Catalytic Domain -- genetics KW - DNA-Directed DNA Polymerase -- genetics KW - DNA-Directed DNA Polymerase -- metabolism KW - Escherichia coli K12 -- enzymology KW - Escherichia coli Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1033536894?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=DNA+repair&rft.atitle=Escherichia+coli+UmuC+active+site+mutants%3A+effects+on+translesion+DNA+synthesis%2C+mutagenesis+and+cell+survival.&rft.au=Kuban%2C+Wojciech%3BVaisman%2C+Alexandra%3BMcDonald%2C+John+P%3BKarata%2C+Kiyonobu%3BYang%2C+Wei%3BGoodman%2C+Myron+F%3BWoodgate%2C+Roger&rft.aulast=Kuban&rft.aufirst=Wojciech&rft.date=2012-09-01&rft.volume=11&rft.issue=9&rft.spage=726&rft.isbn=&rft.btitle=&rft.title=DNA+repair&rft.issn=1568-7856&rft_id=info:doi/10.1016%2Fj.dnarep.2012.06.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-12-07 N1 - Date created - 2012-08-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Bacteriol. 2000 Feb;182(4):1127-35 [10648540] Nucleic Acids Res. 2012 Jul;40(13):6144-57 [22422840] Mol Microbiol. 2000 Mar;35(6):1443-53 [10760145] Mol Microbiol. 2000 Mar;35(6):1560-72 [10760155] EMBO J. 2000 Oct 2;19(19):5251-8 [11013227] J Bacteriol. 2001 Feb;183(4):1215-24 [11157933] Genetics. 2001 May;158(1):41-64 [11333217] Mutat Res. 2002 Jan 29;499(1):85-95 [11804607] Nucleic Acids Res. 2003 Jul 15;31(14):4129-37 [12853630] DNA Repair (Amst). 2003 Dec 9;2(12):1361-9 [14642565] Mol Cell Biol. 2004 Apr;24(7):2734-46 [15024063] Mol Gen Genet. 1972;119(2):93-102 [4565757] Mol Gen Genet. 1977 Nov 14;156(2):121-31 [340898] Mol Gen Genet. 1978 Sep 20;165(1):87-93 [362169] Proc Natl Acad Sci U S A. 1981 Sep;78(9):5749-53 [7029544] Gene. 1984 Nov;31(1-3):165-71 [6098521] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1806-10 [3126496] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1811-5 [3279417] Proc Natl Acad Sci U S A. 1988 Mar;85(6):1816-20 [3279418] J Bacteriol. 1990 Jun;172(6):3030-6 [2188949] Proc Natl Acad Sci U S A. 1990 Sep;87(18):7190-4 [2205854] Proc Natl Acad Sci U S A. 1990 Oct;87(19):7663-7 [2217198] Mol Gen Genet. 1991 Sep;229(1):10-6 [1654503] Mol Gen Genet. 1993 May;239(1-2):137-44 [8510643] Mol Microbiol. 1993 Dec;10(5):963-71 [7934872] J Bacteriol. 1996 May;178(9):2559-63 [8626322] J Bacteriol. 1996 Aug;178(15):4400-11 [8755866] Proc Natl Acad Sci U S A. 1996 Sep 17;93(19):10291-6 [8816793] J Mol Biol. 1997 Jul 11;270(2):201-11 [9236122] Proc Natl Acad Sci U S A. 1998 Mar 31;95(7):3402-7 [9520378] Mol Microbiol. 1998 Apr;28(2):281-91 [9622353] J Biol Chem. 1998 Dec 4;273(49):32384-7 [9829966] Genes Dev. 1998 Dec 15;12(24):3889-99 [9869642] EMBO J. 1999 Jun 15;18(12):3491-501 [10369688] Nature. 1999 Jun 17;399(6737):700-4 [10385124] Proc Natl Acad Sci U S A. 1999 Aug 3;96(16):8919-24 [10430871] Proc Natl Acad Sci U S A. 1999 Aug 3;96(16):9218-23 [10430923] Mol Cell. 1999 Aug;4(2):281-6 [10488344] J Bacteriol. 1950 Jul;60(1):17-28 [15436457] Nature. 2006 Jan 12;439(7073):225-8 [16407906] Nature. 2006 Aug 24;442(7105):883-7 [16929290] J Biol Chem. 2006 Sep 15;281(37):27286-91 [16831866] Proc Natl Acad Sci U S A. 2008 Jun 24;105(25):8679-84 [18562283] Biochemistry. 2009 May 26;48(20):4239-46 [19341290] DNA Repair (Amst). 2009 Jul 4;8(7):852-6 [19386556] J Bacteriol. 2009 Aug;191(15):4815-23 [19482923] Nature. 2009 Jul 16;460(7253):359-63 [19606142] Nature. 2010 Jun 24;465(7301):1044-8 [20577208] Biochemistry. 2011 Feb 22;50(7):1135-42 [21226515] DNA Repair (Amst). 2012 Apr 1;11(4):431-40 [22341652] J Mol Biol. 2000 Mar 31;297(3):585-97 [10731413] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.dnarep.2012.06.005 ER - TY - JOUR T1 - Determinants of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans in house dust samples from four areas of the United States. AN - 1033534569; 22832089 AB - Determinants of levels of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/F) in dust in U.S. homes are not well characterized. We conducted a pilot study to evaluate the relationship between concentrations of PCDD/F in house dust and residential proximity to known sources, including industrial facilities and traffic. Samples from vacuum bag dust from homes of 40 residents of Detroit, Los Angeles, Seattle, or Iowa who participated in a population-based case-control study of non-Hodgkin lymphoma conducted in 1998-2000 were analyzed using high resolution gas chromatography/high resolution mass spectrometry for 7 PCDD and 10 PCDF congeners considered toxic by the U.S. Environmental Protection Agency (EPA). Locations of 10 types of PCDD/F-emitting facilities were obtained from the EPA; however only 4 types were located near study homes (non-hazardous waste cement kilns, coal-fired power plants, sewage sludge incinerators, and medical waste incinerators). Relationships between concentrations of each PCDD/F and proximity to industrial facilities, freight routes, and major roads were evaluated using separate multivariate regression models for each congener. The median (inter-quartile range [IQR]) toxic equivalence (TEQ) concentration of these congeners in the house dust was 20.3 pg/g (IQR=14.3, 32.7). Homes within 3 or 5 km of a cement kiln had 2 to 9-fold higher concentrations of 5 PCDD and 5 PCDF (p<0.1 in each model). Proximity to freight routes and major roads was associated with elevated concentrations of 1 PCDD and 8 PCDF. Higher concentrations of certain PCDD/F in homes near cement kilns, freight routes, and major roads suggest that these outdoor sources are contributing to indoor environmental exposures. Further study of the contribution of these sources and other facility types to total PCDD/F exposure in a larger number of homes is warranted. Published by Elsevier B.V. JF - The Science of the total environment AU - Deziel, N C AU - Nuckols, J R AU - Colt, J S AU - De Roos, A J AU - Pronk, A AU - Gourley, C AU - Severson, R K AU - Cozen, W AU - Cerhan, J R AU - Hartge, P AU - Ward, M H AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Department of Health and Human Services, Rockville, MD, United States. dezielnc@mail.nih.gov Y1 - 2012/09/01/ PY - 2012 DA - 2012 Sep 01 SP - 516 EP - 522 VL - 433 KW - Dust KW - 0 KW - Polychlorinated Dibenzodioxins KW - Index Medicus KW - United States KW - Polychlorinated Dibenzodioxins -- analysis KW - Dust -- analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1033534569?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Science+of+the+total+environment&rft.atitle=Determinants+of+polychlorinated+dibenzo-p-dioxins+and+polychlorinated+dibenzofurans+in+house+dust+samples+from+four+areas+of+the+United+States.&rft.au=Deziel%2C+N+C%3BNuckols%2C+J+R%3BColt%2C+J+S%3BDe+Roos%2C+A+J%3BPronk%2C+A%3BGourley%2C+C%3BSeverson%2C+R+K%3BCozen%2C+W%3BCerhan%2C+J+R%3BHartge%2C+P%3BWard%2C+M+H&rft.aulast=Deziel&rft.aufirst=N&rft.date=2012-09-01&rft.volume=433&rft.issue=&rft.spage=516&rft.isbn=&rft.btitle=&rft.title=The+Science+of+the+total+environment&rft.issn=1879-1026&rft_id=info:doi/10.1016%2Fj.scitotenv.2012.06.098 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-12-26 N1 - Date created - 2012-08-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Stat Med. 1991 Apr;10(4):585-98 [2057657] Bull Environ Contam Toxicol. 1992 Jun;48(6):789-94 [1568054] Br J Cancer. 1996 Mar;73(5):702-10 [8605111] Zentralbl Hyg Umweltmed. 1997 Apr;199(6):537-50 [9376066] Chemosphere. 1998 Oct-Nov;37(9-12):2173-97 [9828336] Environ Health Perspect. 2004 Dec;112(17):1691-6 [15579415] Epidemiology. 2005 Jul;16(4):516-25 [15951670] Cancer Res. 2005 Dec 1;65(23):11214-26 [16322272] Toxicol Sci. 2006 Oct;93(2):223-41 [16829543] Chemosphere. 2007 Apr;67(9):S279-85 [17234249] Cancer Epidemiol Biomarkers Prev. 2007 Mar;16(3):373-6 [17337641] Environ Sci Technol. 2009 Feb 15;43(4):1036-41 [19320154] Arch Environ Contam Toxicol. 2009 Nov;57(4):639-50 [19488800] Lancet Oncol. 2009 Dec;10(12):1143-4 [19998521] Environ Res. 2010 Jan;110(1):70-8 [19840879] Environ Int. 2011 Feb;37(2):449-53 [21167603] J Environ Health. 2011 Jan-Feb;73(6):34-46 [21306093] Crit Rev Toxicol. 2011 Aug;41(7):622-36 [21718216] Environ Health Perspect. 2011 Dec;119(12):1700-5 [21810551] Sci Total Environ. 2012 Mar 1;419:37-43 [22285082] Environ Health. 2013;12:20 [23433489] Environ Health. 2009;8:39 [19754930] Environ Sci Technol. 2007 Mar 1;41(5):1537-44 [17396638] Environ Res. 2007 Oct;105(2):194-9 [17517389] Int J Health Geogr. 2008;7:4 [18226215] Food Chem Toxicol. 2008 May;46(5):1721-33 [18289758] Environ Health. 2008;7:51 [18959776] J Occup Environ Hyg. 2009 Mar;6(3):188-99 [19152164] J Hazard Mater. 2000 Aug 28;76(1):1-12 [10863010] Food Addit Contam. 2000 Apr;17(4):241-59 [10912239] Rev Environ Contam Toxicol. 2002;175:1-46 [12206053] Epidemiology. 2003 Jul;14(4):392-8 [12843761] Environ Res. 2003 Jun;92(2):99-109 [12854689] Chemosphere. 2003 Oct;53(2):137-42 [12892676] J Expo Anal Environ Epidemiol. 2004 Jan;14(1):74-83 [14726946] J Med Dent Sci. 2003 Dec;50(4):249-55 [15074352] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.scitotenv.2012.06.098 ER - TY - JOUR T1 - Oxaliplatin-based chemotherapy in the treatment of elderly patients with metastatic colorectal cancer (CRC). AN - 1033456369; 21937127 AB - Elderly patients constitute a subpopulation with special clinical features that differ from those of the general population and are under-represented in clinical trials. We retrospectively analyzed the toxicity and efficacy of oxaliplatin-based chemotherapy in the treatment of elderly patients affected by metastatic (m) CRC. Seventy-five consecutive patients aged 65-75 years (median age 71 years), 51 males and 24 females, with mCRC and measurable disease, were analyzed. The primary site of metastases was the liver (38.6% of patients). The majority of patients had a performance status (PS) according to the Eastern Cooperative Oncology Group (ECOG) PS before treatment of 0-1 (96%). The overall response rate was 57.3%, median progression-free survival was 7 months and median overall survival was 27 months. The main hematological and extra-hematological toxicities (grade 3 or 4) were neutropenia (20.0%), and neurological toxicity or diarrhea (6.7%), respectively. No toxic death occurred. Oxaliplatin-based chemotherapy maintains its efficacy, and safety in elderly patients with mCRC and good PS. This regimen should be considered in the treatment of this particular setting of patients. Copyright © 2011 Elsevier Ireland Ltd. All rights reserved. JF - Archives of gerontology and geriatrics AU - Berretta, Massimiliano AU - Zanet, Ernesto AU - Nasti, Guglielmo AU - Lleshi, Arben AU - Frustaci, Sergio AU - Fiorica, Francesco AU - Bearz, Alessandra AU - Talamini, Renato AU - Lestuzzi, Chiara AU - Lazzarini, Renzo AU - Fisichella, Rossella AU - Cannizzaro, Renato AU - Iaffaioli, Rosario Vincenzo AU - Berretta, Salvatore AU - Tirelli, Umberto AD - Department of Medical Oncology, National Cancer Institute, IRCCS, Via Franco Gallini 2, I-33081 Aviano (PN), Italy. mberretta@cro.it PY - 2012 SP - 271 EP - 275 VL - 55 IS - 2 KW - Antineoplastic Agents KW - 0 KW - Organoplatinum Compounds KW - oxaliplatin KW - 04ZR38536J KW - Index Medicus KW - Disease-Free Survival KW - Diarrhea -- chemically induced KW - Humans KW - Treatment Outcome KW - Retrospective Studies KW - Neutropenia -- chemically induced KW - Aged KW - Male KW - Female KW - Organoplatinum Compounds -- adverse effects KW - Colorectal Neoplasms -- pathology KW - Liver Neoplasms -- drug therapy KW - Organoplatinum Compounds -- therapeutic use KW - Adenocarcinoma -- secondary KW - Liver Neoplasms -- secondary KW - Antineoplastic Agents -- therapeutic use KW - Adenocarcinoma -- drug therapy KW - Colorectal Neoplasms -- drug therapy KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1033456369?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+gerontology+and+geriatrics&rft.atitle=Oxaliplatin-based+chemotherapy+in+the+treatment+of+elderly+patients+with+metastatic+colorectal+cancer+%28CRC%29.&rft.au=Berretta%2C+Massimiliano%3BZanet%2C+Ernesto%3BNasti%2C+Guglielmo%3BLleshi%2C+Arben%3BFrustaci%2C+Sergio%3BFiorica%2C+Francesco%3BBearz%2C+Alessandra%3BTalamini%2C+Renato%3BLestuzzi%2C+Chiara%3BLazzarini%2C+Renzo%3BFisichella%2C+Rossella%3BCannizzaro%2C+Renato%3BIaffaioli%2C+Rosario+Vincenzo%3BBerretta%2C+Salvatore%3BTirelli%2C+Umberto&rft.aulast=Berretta&rft.aufirst=Massimiliano&rft.date=2012-09-01&rft.volume=55&rft.issue=2&rft.spage=271&rft.isbn=&rft.btitle=&rft.title=Archives+of+gerontology+and+geriatrics&rft.issn=1872-6976&rft_id=info:doi/10.1016%2Fj.archger.2011.08.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-28 N1 - Date created - 2012-08-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.archger.2011.08.016 ER - TY - JOUR T1 - Sleep disturbances in Alzheimer's and Parkinson's diseases. AN - 1033454242; 22552887 AB - Alzheimer's disease (AD) and Parkinson's disease (PD) are the two most common neurodegenerative disorders and exact a burden on our society greater than cardiovascular disease and cancer combined. While cognitive and motor symptoms are used to define AD and PD, respectively, patients with both disorders exhibit sleep disturbances including insomnia, hypersomnia and excessive daytime napping. The molecular basis of perturbed sleep in AD and PD may involve damage to hypothalamic and brainstem nuclei that control sleep-wake cycles. Perturbations in neurotransmitter and hormone signaling (e.g., serotonin, norepinephrine and melatonin) and the neurotrophic factor BDNF likely contribute to the disease process. Abnormal accumulations of neurotoxic forms of amyloid β-peptide, tau and α-synuclein occur in brain regions involved in the regulation of sleep in AD and PD patients, and are sufficient to cause sleep disturbances in animal models of these neurodegenerative disorders. Disturbed regulation of sleep often occurs early in the course of AD and PD, and may contribute to the cognitive and motor symptoms. Treatments that target signaling pathways that control sleep have been shown to retard the disease process in animal models of AD and PD, suggesting a potential for such interventions in humans at risk for or in the early stages of these disorders. JF - Neuromolecular medicine AU - Rothman, Sarah M AU - Mattson, Mark P AD - Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224, USA. rothmansm@mail.nih.gov Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 194 EP - 204 VL - 14 IS - 3 KW - Index Medicus KW - Animals KW - Humans KW - Disease Models, Animal KW - Brain -- physiopathology KW - Alzheimer Disease -- complications KW - Alzheimer Disease -- physiopathology KW - Brain -- anatomy & histology KW - Sleep Wake Disorders -- etiology KW - Parkinson Disease -- complications KW - Parkinson Disease -- physiopathology KW - Sleep Wake Disorders -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1033454242?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neuromolecular+medicine&rft.atitle=Sleep+disturbances+in+Alzheimer%27s+and+Parkinson%27s+diseases.&rft.au=Rothman%2C+Sarah+M%3BMattson%2C+Mark+P&rft.aulast=Rothman&rft.aufirst=Sarah&rft.date=2012-09-01&rft.volume=14&rft.issue=3&rft.spage=194&rft.isbn=&rft.btitle=&rft.title=Neuromolecular+medicine&rft.issn=1559-1174&rft_id=info:doi/10.1007%2Fs12017-012-8181-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-06-03 N1 - Date created - 2012-08-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mov Disord. 1990;5(4):280-5 [2259351] Prog Brain Res. 1991;88:307-21 [1687619] J Neural Transm Gen Sect. 1993;91(2-3):135-59 [8099796] Mov Disord. 1993 Jul;8(3):315-20 [8341295] Ann N Y Acad Sci. 1993 Sep 24;695:1-9 [7902053] Sleep. 1995 Apr;18(3):145-8 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[3475716] Neuroscience. 1988 May;25(2):401-17 [3399052] Biol Psychiatry. 1989 Feb 1;25(3):320-8 [2914155] Clin Neuropharmacol. 1988 Dec;11(6):512-9 [3233589] J Gerontol. 1990 Jul;45(4):M131-8 [2365965] Psychiatry Res. 1990 Aug;33(2):113-9 [2243887] Biol Psychiatry. 1999 Feb 15;45(4):417-21 [10071710] Biol Psychiatry. 1999 Jun 15;45(12):1646-52 [10376127] J Neurosci Res. 1999 Jul 15;57(2):195-206 [10398297] J Geriatr Psychiatry Neurol. 1999 Summer;12(2):53-9 [10483925] Proc Natl Acad Sci U S A. 2004 Dec 28;101(52):18171-6 [15604149] Neuroscience. 2005;131(2):375-85 [15708480] FASEB J. 2005 Apr;19(6):659-61 [15650008] J Neurosci. 2005 Apr 27;25(17):4217-21 [15858047] Sleep Med. 2005 Jul;6(4):347-52 [15978517] Curr Biol. 2005 Jul 12;15(13):1165-75 [16005288] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s12017-012-8181-2 ER - TY - JOUR T1 - Alterations of RASSF1A in premalignant cervical lesions: clinical and prognostic significance. AN - 1027373500; 21809394 AB - This study aimed to understand the importance of RASSF1A and CACNA2D2, located in chromosomal 3p21.31 region, in the development of uterine cervical carcinoma (CACX). To this end, firstly the expression (RNA) profiles of RASSF1A and CACNA2D2 were screened in primary cervical carcinoma (CACX) samples which indicated highly reduced expression for both genes. Thereafter alterations (deletion/methylation) of these genes were analyzed in 23 cervical intraepithelial neoplasia (CIN) and 110 CACX samples. In CIN, deletion was observed only for RASSF1A (26%), whereas methylation was in the following order: RASSF1A (35%) > CACNA2D2 (9%). However, in CACX their deletion frequencies were the same (50%) and methylation frequencies were comparable RASSF1A (33%), CACNA2D2 (27%). The reduced expression and molecular alterations of these genes were concordant. Overall alterations of RASSF1A showed association with CIN lesions and CACNA2D2 with disease progression from CIN → stage I/II. Interestingly, alterations of these genes showed significant association in CACX suggesting possible functional synergism during tumor progression. Alterations of RASSF1A and CACNA2D2 predicted poor prognosis for the patients. Moreover, RASSF1A alterations along with multiparity (≥5 yr) and early sexual debut (<19 yr) were determinants of worse prognosis. Our data suggests the association of RASSF1A and CACNA2D2 in cervical carcinogenesis and its importance in early diagnosis and prognosis of the tumor. Copyright © 2011 Wiley Periodicals, Inc. JF - Molecular carcinogenesis AU - Mitra, Sraboni AU - Mazumder Indra, Dipanjana AU - Basu, Partha S AU - Mondal, Ranajit K AU - Roy, Anup AU - Roychoudhury, Susanta AU - Panda, Chinmay K AD - Department of Oncogene Regulation, Chittaranjan National Cancer Institute, Kolkata, West Bengal, India. Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 723 EP - 733 VL - 51 IS - 9 KW - CACNA2D2 protein, human KW - 0 KW - Calcium Channels KW - RASSF1 protein, human KW - RNA, Messenger KW - Tumor Suppressor Proteins KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Parity KW - Cervix Uteri -- pathology KW - Neoplasm Invasiveness KW - Neoplasm Staging KW - Carcinoma, Squamous Cell -- mortality KW - Humans KW - Cervix Uteri -- metabolism KW - Prognosis KW - Chromosomes, Human, Pair 3 -- genetics KW - Disease Progression KW - Calcium Channels -- genetics KW - Reverse Transcriptase Polymerase Chain Reaction KW - RNA, Messenger -- genetics KW - Gene Expression Regulation, Neoplastic KW - Survival Rate KW - Carcinoma, Squamous Cell -- pathology KW - Adult KW - Carcinoma, Squamous Cell -- genetics KW - Promoter Regions, Genetic -- genetics KW - Middle Aged KW - Female KW - Precancerous Conditions -- genetics KW - Precancerous Conditions -- mortality KW - Cervical Intraepithelial Neoplasia -- pathology KW - DNA Methylation KW - Cervical Intraepithelial Neoplasia -- genetics KW - Uterine Cervical Neoplasms -- mortality KW - Tumor Suppressor Proteins -- genetics KW - Uterine Cervical Neoplasms -- genetics KW - Cervical Intraepithelial Neoplasia -- mortality KW - Uterine Cervical Neoplasms -- pathology KW - Precancerous Conditions -- pathology KW - Gene Deletion UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1027373500?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+carcinogenesis&rft.atitle=Alterations+of+RASSF1A+in+premalignant+cervical+lesions%3A+clinical+and+prognostic+significance.&rft.au=Mitra%2C+Sraboni%3BMazumder+Indra%2C+Dipanjana%3BBasu%2C+Partha+S%3BMondal%2C+Ranajit+K%3BRoy%2C+Anup%3BRoychoudhury%2C+Susanta%3BPanda%2C+Chinmay+K&rft.aulast=Mitra&rft.aufirst=Sraboni&rft.date=2012-09-01&rft.volume=51&rft.issue=9&rft.spage=723&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=1098-2744&rft_id=info:doi/10.1002%2Fmc.20837 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-27 N1 - Date created - 2012-07-19 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/mc.20837 ER - TY - JOUR T1 - Paradigm shift in toxicity testing and modeling. AN - 1021978309; 22528508 AB - The limitations of traditional toxicity testing characterized by high-cost animal models with low-throughput readouts, inconsistent responses, ethical issues, and extrapolability to humans call for alternative strategies for chemical risk assessment. A new strategy using in vitro human cell-based assays has been designed to identify key toxicity pathways and molecular mechanisms leading to the prediction of an in vivo response. The emergence of quantitative high-throughput screening (qHTS) technology has proved to be an efficient way to decompose complex toxicological end points to specific pathways of targeted organs. In addition, qHTS has made a significant impact on computational toxicology in two aspects. First, the ease of mechanism of action identification brought about by in vitro assays has enhanced the simplicity and effectiveness of machine learning, and second, the high-throughput nature and high reproducibility of qHTS have greatly improved the data quality and increased the quantity of training datasets available for predictive model construction. In this review, the benefits of qHTS routinely used in the US Tox21 program will be highlighted. Quantitative structure-activity relationships models built on traditional in vivo data and new qHTS data will be compared and analyzed. In conjunction with the transition from the pilot phase to the production phase of the Tox21 program, more qHTS data will be made available that will enrich the data pool for predictive toxicology. It is perceivable that new in silico toxicity models based on high-quality qHTS data will achieve unprecedented reliability and robustness, thus becoming a valuable tool for risk assessment and drug discovery. JF - The AAPS journal AU - Sun, Hongmao AU - Xia, Menghang AU - Austin, Christopher P AU - Huang, Ruili AD - Department of Health and Human Services, NIH Chemical Genomics Center, National Institutes of Health, Bethesda, Maryland 20892-3370, USA. hongmao.sun@nih.gov Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 473 EP - 480 VL - 14 IS - 3 KW - Index Medicus KW - Toxicity Tests KW - Models, Theoretical UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1021978309?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+AAPS+journal&rft.atitle=Paradigm+shift+in+toxicity+testing+and+modeling.&rft.au=Sun%2C+Hongmao%3BXia%2C+Menghang%3BAustin%2C+Christopher+P%3BHuang%2C+Ruili&rft.aulast=Sun&rft.aufirst=Hongmao&rft.date=2012-09-01&rft.volume=14&rft.issue=3&rft.spage=473&rft.isbn=&rft.btitle=&rft.title=The+AAPS+journal&rft.issn=1550-7416&rft_id=info:doi/10.1208%2Fs12248-012-9358-1 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-26 N1 - Date created - 2012-06-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Investig Dermatol Symp Proc. 2009 Aug;14(1):63-6 [19675557] Anal Biochem. 2009 Nov 1;394(1):30-8 [19583963] Toxicol Sci. 2009 Oct;111(2):202-25 [19567883] Toxicol Sci. 2009 Nov;112(1):153-63 [19502547] Nat Biotechnol. 2009 Nov;27(11):1050-5 [19855396] J Biomol Screen. 2009 Oct;14(9):1054-66 [19773588] Curr Top Med Chem. 2009;9(13):1181-93 [19807664] J Comput Aided Mol Des. 2003 Feb-Apr;17(2-4):83-92 [13677477] J Chronic Dis. 1984;37(9-10):721-31 [6501544] Environ Health Perspect. 1985 Sep;61:5-10 [2998750] Mutagenesis. 1990 Jan;5(1):3-14 [2184307] Mutat Res. 1991 May;257(3):229-306 [1707500] Environ Health Perspect. 1991 Dec;96:23-31 [1820269] Mutagenesis. 1994 Jan;9(1):3-5 [7911554] Mutagenesis. 1994 Jan;9(1):7-15 [8208133] Environ Health Perspect. 1996 Oct;104 Suppl 5:1001-10 [8933048] Environ Health Perspect. 1996 Oct;104 Suppl 5:1031-40 [8933051] J Med Chem. 2010 Jan 14;53(1):37-51 [19908840] Drug Discov Today. 2010 Jan;15(1-2):16-22 [19835978] Biochem Pharmacol. 2010 May 1;79(9):1272-80 [20067776] ChemMedChem. 2010 Jun 7;5(6):847-58 [20414918] J Chem Inf Model. 2010 Jun 28;50(6):1034-41 [20578727] Ophthalmic Res. 2010;44(2):82-104 [20484950] Gene Ther. 2010 Aug;17(8):939-48 [20428209] Environ Health Perspect. 1996 Oct;104 Suppl 5:1041-4 [8933052] Environ Health Perspect. 1996 Oct;104 Suppl 5:1059-63 [8933055] Toxicology. 1997 Apr 11;119(1):29-35 [9129192] Toxicology. 1997 May 16;119(3):213-25 [9152017] Environ Health Perspect. 1997 Jul;105(7):688 [9294709] J Natl Cancer Inst. 1998 Nov 18;90(22):1702-9 [9827524] Environ Health Perspect. 1998 Dec;106 Suppl 6:1385-93 [9860897] Drug Discov Today. 2005 Jan 1;10(1):17-22 [15676295] Drug Discov Today. 2005 Jan 15;10(2):139-47 [15718163] Curr Opin Drug Discov Devel. 2005 Jul;8(4):495-504 [16022186] Altern Lab Anim. 2005 Oct;33(5):445-59 [16268757] Chem Rev. 2006 Feb;106(2):302-23 [16464007] Chem Rev. 2006 Feb;106(2):474-88 [16464015] Nat Biotechnol. 2006 Feb;24(2):167-75 [16465162] Drug Discov Today. 2006 Apr;11(7-8):277-9 [16580969] Proc Natl Acad Sci U S A. 2006 Aug 1;103(31):11473-8 [16864780] Curr Top Med Chem. 2006;6(15):1579-91 [16918470] Toxicol Sci. 2010 Nov;118(1):251-65 [20702588] Drug Discov Today. 2010 Dec;15(23-24):997-1007 [20708096] Drug Discov Today. 2010 Dec;15(23-24):1052-7 [20970519] Drug Metab Dispos. 2011 Jan;39(1):151-9 [20966043] J Chem Inf Model. 2010 Dec 27;50(12):2094-111 [21033656] Environ Health Perspect. 2011 Mar;119(3):364-70 [20980217] Chem Rev. 2011 Apr 13;111(4):2507-36 [21265518] Toxicol Appl Pharmacol. 2011 May 1;252(3):250-8 [21362439] Chem Res Toxicol. 2011 Jun 20;24(6):934-49 [21504223] J Chem Inf Model. 2011 Jun 27;51(6):1271-80 [21598906] Environ Health Perspect. 2011 Aug;119(8):1142-8 [21543282] Environ Mol Mutagen. 2011 Aug;52(7):547-61 [21538559] J Chem Inf Model. 2011 Oct 24;51(10):2474-81 [21905670] J Chem Inf Model. 2011 May 23;51(5):996-1011 [21491913] Environ Health Perspect. 2001 May;109(5):509-14 [11401763] Toxicology. 2003 Apr 1;185(3):221-7 [12581697] Int J Hyg Environ Health. 2003 Aug;206(4-5):437-45 [12971699] Nat Biotechnol. 2006 Dec;24(12):1565-7 [17160063] Eur J Pharm Sci. 2007 Jul;31(3-4):190-201 [17481865] Nat Chem Biol. 2007 Aug;3(8):466-79 [17637779] Mol Pharm. 2007 Jul-Aug;4(4):524-38 [17637064] Environ Health Perspect. 2008 Mar;116(3):284-91 [18335092] Chem Res Toxicol. 2008 Mar;21(3):659-67 [18281954] Toxicol Sci. 2008 May;103(1):14-27 [18065772] Drug Discov Today. 2008 Apr;13(7-8):303-10 [18405842] Environ Health Perspect. 2008 Apr;116(4):506-13 [18414635] Toxicol In Vitro. 2008 Jun;22(4):1099-106 [18400464] J Mol Graph Model. 2008 Jun;26(8):1315-26 [18328754] BMC Bioinformatics. 2008;9:241 [18489778] J Chem Inf Model. 2008 Sep;48(9):1733-46 [18729318] Curr Top Med Chem. 2008;8(18):1628-55 [19075771] Toxicol Sci. 2009 Feb;107(2):324-30 [19074763] Doc Ophthalmol. 2009 Feb;118(1):3-28 [18998183] Proc Natl Acad Sci U S A. 2009 Feb 17;106(7):2412-7 [19196967] Expert Opin Drug Metab Toxicol. 2009 Jan;5(1):1-14 [19236225] Risk Anal. 2009 Apr;29(4):485-7; discussion 492-7 [19076321] Environ Health Perspect. 2009 May;117(5):685-95 [19479008] Nucleic Acids Res. 2009 Jul;37(Web Server issue):W623-33 [19498078] Mol Biosyst. 2009 Sep;5(9):1039-50 [19668870] Environ Health Perspect. 2009 Aug;117(8):A348-53 [19672388] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1208/s12248-012-9358-1 ER - TY - JOUR T1 - Mutational analysis of residues involved in nucleotide and divalent cation stabilization in the rotavirus RNA-dependent RNA polymerase catalytic pocket. AN - 1021260893; 22664357 AB - The rotavirus RNA-dependent RNA polymerase (RdRp), VP1, contains canonical RdRp motifs and a priming loop that is hypothesized to undergo conformational rearrangements during RNA synthesis. In the absence of viral core shell protein VP2, VP1 fails to interact stably with divalent cations or nucleotides and has a retracted priming loop. To identify residues of potential import to nucleotide and divalent cation stabilization, we aligned VP1 of divergent rotaviruses and the structural homolog reovirus λ3. VP1 mutants were engineered and characterized for RNA synthetic capacity in vitro. Conserved aspartic acids in RdRp motifs A and C and arginines in motif F that likely stabilize divalent cations and nucleotides were required for efficient RNA synthesis. Mutation of individual priming loop residues diminished or enhanced RNA synthesis efficiency without obviating the need for VP2, which suggests that this structure serves as a dynamic regulatory element that links RdRp activity to particle assembly. Published by Elsevier Inc. JF - Virology AU - Ogden, Kristen M AU - Ramanathan, Harish N AU - Patton, John T AD - Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8026, USA. PY - 2012 SP - 12 EP - 20 VL - 431 IS - 1-2 KW - Cations, Divalent KW - 0 KW - Nucleotides KW - VP1 protein, Rotavirus KW - Viral Core Proteins KW - RNA KW - 63231-63-0 KW - RNA Replicase KW - EC 2.7.7.48 KW - Index Medicus KW - Mutagenesis, Site-Directed KW - Sequence Alignment KW - RNA -- metabolism KW - Models, Molecular KW - Molecular Sequence Data KW - Amino Acid Sequence KW - Mammalian orthoreovirus 3 -- genetics KW - Protein Conformation KW - Viral Core Proteins -- chemistry KW - Nucleotides -- metabolism KW - Rotavirus -- chemistry KW - Cations, Divalent -- metabolism KW - RNA Replicase -- metabolism KW - Viral Core Proteins -- genetics KW - Rotavirus -- genetics KW - Rotavirus -- enzymology KW - Viral Core Proteins -- metabolism KW - RNA Replicase -- genetics KW - RNA Replicase -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1021260893?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=Mutational+analysis+of+residues+involved+in+nucleotide+and+divalent+cation+stabilization+in+the+rotavirus+RNA-dependent+RNA+polymerase+catalytic+pocket.&rft.au=Ogden%2C+Kristen+M%3BRamanathan%2C+Harish+N%3BPatton%2C+John+T&rft.aulast=Ogden&rft.aufirst=Kristen&rft.date=2012-09-01&rft.volume=431&rft.issue=1-2&rft.spage=12&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=1096-0341&rft_id=info:doi/10.1016%2Fj.virol.2012.05.009 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-29 N1 - Date created - 2012-06-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mol Cell. 2006 Apr 7;22(1):5-13 [16600865] Curr Top Microbiol Immunol. 2006;309:189-219 [16913048] Virology. 2007 Mar 15;359(2):415-24 [17059839] Curr Top Microbiol Immunol. 2008;320:137-56 [18268843] RNA. 2000 Oct;6(10):1455-67 [11073221] Structure. 2008 Nov 12;16(11):1678-88 [19000820] J Virol. 2009 Feb;83(4):1754-66 [19036817] J Virol. 2009 Jun;83(12):6135-48 [19357162] J Infect Dis. 2009 Nov 1;200 Suppl 1:S9-S15 [19817620] Curr Opin Struct Biol. 2009 Dec;19(6):775-82 [19914820] J Mol Biol. 2010 Mar 26;397(2):587-99 [20122940] J Virol. 2010 Oct;84(19):10254-65 [20631147] J Struct Biol. 2010 Dec;172(3):253-60 [20599509] J Virol. 2011 Mar;85(5):1958-69 [21147920] J Virol. 2011 Apr;85(7):3095-105 [21248043] Virology. 2011 Apr 10;412(2):384-91 [21329955] Nucleic Acids Res. 2003 Apr 1;31(7):1821-9 [12654997] J Mol Biol. 2003 Feb 28;326(4):1025-35 [12589751] Cell. 2002 Nov 27;111(5):733-45 [12464184] J Virol. 2002 Apr;76(7):3482-92 [11884572] Virus Res. 2002 Feb 26;83(1-2):179-87 [11864750] Virology. 2001 Sep 1;287(2):251-60 [11531403] Nature. 2001 Mar 8;410(6825):235-40 [11242087] Virology. 2012 Sep 15-30;431(1-2):50-7 [22687427] Curr Opin Struct Biol. 2006 Feb;16(1):27-34 [16364629] Virology. 1998 Dec 20;252(2):287-303 [9878607] Nature. 1998 Jan 15;391(6664):231-2 [9440683] J Virol. 1997 Oct;71(10):7353-60 [9311813] J Virol. 1996 Nov;70(11):7940-7 [8892917] J Comput Chem. 2004 Oct;25(13):1605-12 [15264254] J Gen Virol. 2004 May;85(Pt 5):1077-93 [15105525] J Biol Chem. 2003 Aug 29;278(35):32673-82 [12788926] J Gen Virol. 2008 Oct;89(Pt 10):2622-9 [18796732] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.virol.2012.05.009 ER - TY - JOUR T1 - Artichoke polyphenols induce apoptosis and decrease the invasive potential of the human breast cancer cell line MDA-MB231. AN - 1015248478; 22170094 AB - The human breast cancer cell line, estrogen receptor negative, MDA-MB231, was used to evaluate the antitumor effect of polyphenolic extracts from the edible part of artichokes (AEs). Treatment of cancer cells reduced cell viability and inhibited cell growth in a dose-dependent manner. Importantly, AEs did not have any effect on normal breast epithelial cell line, MCF10A. Chlorogenic acid (ChA), the most representative component of the polyphenolic fraction of artichoke, had no prominent effects on the cell death rate of MDA-MB231 cells. The addition of AEs to the cells, rather than ChA, triggered apoptosis via a mitochondrial and a death-receptor pathway, as shown by the activation of caspase-9 and caspase-8, respectively. Furthermore, an increase of the Bax:Bcl2 ratio and up-regulation of cyclin-dependent kinase inhibitor, p21(WAF1), crucial apoptotic players, were documented. According to our data on activation of caspase-9, a loss of mitochondrial transmembrane potential (Ψ(m)) was shown. Cell motility and invasion capabilities were remarkably inhibited by AEs-treatment in highly invasive MDA-MB231 cells. In addition, a significant decrease of proteolytic activity of metalloproteinase-2 protein (MMP-2), involved in degrading components of the extracellular matrix, was detected. Our findings indicate that AEs reduced cell viability, inhibited cell growth, triggered apoptotic mechanisms, and showed inhibitory properties against the invasive behavior of MDA-MB231 cancer cell line. Altogether, these data indicate the potential chemopreventive activity of artichoke polyphenolic extracts. Copyright © 2011 Wiley Periodicals, Inc. JF - Journal of cellular physiology AU - Mileo, Anna Maria AU - Di Venere, Donato AU - Linsalata, Vito AU - Fraioli, Rocco AU - Miccadei, Stefania AD - Department of Development of Therapeutic Programs, Regina Elena National Cancer Institute, Rome, Italy. Y1 - 2012/09// PY - 2012 DA - September 2012 SP - 3301 EP - 3309 VL - 227 IS - 9 KW - CDKN1A protein, human KW - 0 KW - Cyclin-Dependent Kinase Inhibitor p21 KW - Plant Extracts KW - Polyphenols KW - Proto-Oncogene Proteins c-bcl-2 KW - bcl-2-Associated X Protein KW - Chlorogenic Acid KW - 318ADP12RI KW - Caspase 8 KW - EC 3.4.22.- KW - Caspase 9 KW - Matrix Metalloproteinase 2 KW - EC 3.4.24.24 KW - Index Medicus KW - Caspase 8 -- metabolism KW - Humans KW - Cyclin-Dependent Kinase Inhibitor p21 -- genetics KW - Caspase 8 -- genetics KW - Breast Neoplasms -- metabolism KW - Cell Line, Tumor KW - Matrix Metalloproteinase 2 -- metabolism KW - bcl-2-Associated X Protein -- metabolism KW - bcl-2-Associated X Protein -- genetics KW - Chlorogenic Acid -- pharmacology KW - Membrane Potential, Mitochondrial -- drug effects KW - Caspase 9 -- genetics KW - Breast Neoplasms -- pathology KW - Caspase 9 -- metabolism KW - Cell Survival -- drug effects KW - Neoplasm Invasiveness -- pathology KW - Proto-Oncogene Proteins c-bcl-2 -- metabolism KW - Matrix Metalloproteinase 2 -- genetics KW - Cell Movement -- drug effects KW - Cyclin-Dependent Kinase Inhibitor p21 -- metabolism KW - Proto-Oncogene Proteins c-bcl-2 -- genetics KW - Female KW - Neoplasm Invasiveness -- prevention & control KW - Plant Extracts -- pharmacology KW - Apoptosis -- drug effects KW - Cynara scolymus -- chemistry KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Polyphenols -- pharmacology KW - Polyphenols -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1015248478?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+physiology&rft.atitle=Artichoke+polyphenols+induce+apoptosis+and+decrease+the+invasive+potential+of+the+human+breast+cancer+cell+line+MDA-MB231.&rft.au=Mileo%2C+Anna+Maria%3BDi+Venere%2C+Donato%3BLinsalata%2C+Vito%3BFraioli%2C+Rocco%3BMiccadei%2C+Stefania&rft.aulast=Mileo&rft.aufirst=Anna&rft.date=2012-09-01&rft.volume=227&rft.issue=9&rft.spage=3301&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+physiology&rft.issn=1097-4652&rft_id=info:doi/10.1002%2Fjcp.24029 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-25 N1 - Date created - 2012-05-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/jcp.24029 ER - TY - JOUR T1 - Compartmentalized Control of Skin Immunity by Resident Commensals AN - 1566852395; 20372162 AB - Skin SpecificsMuch of the recent attention paid to the trillions of bacteria that colonize our bodies has been given to the bacteria that reside in the gut. Naik et al. (p. 1115, published online 26 July) report that colonization of the skin with commensal bacteria is important for tuning effector T cell responses in the skin and for protective immunity against cutaneous infection with the parasite Leishmania major in mice. In contrast, selective depletion of the gut microbiota, which plays an important role in modulating immune responses in the gut, had no impact on T cell responses in the skin. JF - Science AU - Naik, Shruti AU - Bouladoux, Nicolas AU - Wilhelm, Christoph AU - Molloy, Michael J AU - Salcedo, Rosalba AU - Kastenmuller, Wolfgang AU - Deming, Clayton AU - Quinones, Mariam AU - Koo, Lily AU - Conlan, Sean AU - Spencer, Sean AU - Hall, Jason A AU - Dzutsev, Amiran AU - Kong, Heidi AU - Campbell, Daniel J AU - Trinchieri, Giorgio AU - Segre, Julia A AU - Belkaid, Yasmine AD - Immunology Graduate Group, University of Pennsylvania, Philadelphia, PA 19104, USA, ybelkaid@niaid.nih.gov Y1 - 2012/08/31/ PY - 2012 DA - 2012 Aug 31 SP - 1115 EP - 1119 PB - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States VL - 337 IS - 6098 SN - 0036-8075, 0036-8075 KW - Ecology Abstracts KW - Colonization KW - Parasites KW - Skin KW - Digestive tract KW - Commensals KW - Lymphocytes T KW - Immunity KW - Infection KW - Leishmania major KW - Internet KW - D 04040:Ecosystem and Ecology Studies UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1566852395?accountid=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=Science&rft.atitle=Compartmentalized+Control+of+Skin+Immunity+by+Resident+Commensals&rft.au=Naik%2C+Shruti%3BBouladoux%2C+Nicolas%3BWilhelm%2C+Christoph%3BMolloy%2C+Michael+J%3BSalcedo%2C+Rosalba%3BKastenmuller%2C+Wolfgang%3BDeming%2C+Clayton%3BQuinones%2C+Mariam%3BKoo%2C+Lily%3BConlan%2C+Sean%3BSpencer%2C+Sean%3BHall%2C+Jason+A%3BDzutsev%2C+Amiran%3BKong%2C+Heidi%3BCampbell%2C+Daniel+J%3BTrinchieri%2C+Giorgio%3BSegre%2C+Julia+A%3BBelkaid%2C+Yasmine&rft.aulast=Naik&rft.aufirst=Shruti&rft.date=2012-08-31&rft.volume=337&rft.issue=6098&rft.spage=1115&rft.isbn=&rft.btitle=&rft.title=Science&rft.issn=00368075&rft_id=info:doi/10.1126%2Fscience.1225152 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2015-03-20 N1 - SubjectsTermNotLitGenreText - Parasites; Colonization; Digestive tract; Skin; Lymphocytes T; Commensals; Immunity; Infection; Internet; Leishmania major DO - http://dx.doi.org/10.1126/science.1225152 ER - TY - JOUR T1 - IL-1R-MyD88 signaling in keratinocyte transformation and carcinogenesis. AN - 1036875943; 22908325 AB - Constitutively active RAS plays a central role in the development of human cancer and is sufficient to induce tumors in two-stage skin carcinogenesis. RAS-mediated tumor formation is commonly associated with up-regulation of cytokines and chemokines that mediate an inflammatory response considered relevant to oncogenesis. In this study, we report that mice lacking IL-1R or MyD88 are less sensitive to topical skin carcinogenesis than their respective wild-type (WT) controls. MyD88(-/-) or IL-1R(-/-) keratinocytes expressing oncogenic RAS are hyperproliferative and fail to up-regulate proinflammatory genes or down-regulate differentiation markers characteristic of RAS-expressing WT keratinocytes. Although RAS-expressing MyD88(-/-) keratinocytes form only a few small tumors in orthotopic grafts, IL-1R-deficient RAS-expressing keratinocytes retain the ability to form tumors in orthotopic grafts. Using both genetic and pharmacological approaches, we find that the differentiation and proinflammatory effects of oncogenic RAS in keratinocytes require the establishment of an autocrine loop through IL-1α, IL-1R, and MyD88 leading to phosphorylation of IκBα and NF-κB activation. Blocking IL-1α-mediated NF-κB activation in RAS-expressing WT keratinocytes reverses the differentiation defect and inhibits proinflammatory gene expression. Collectively, these results demonstrate that MyD88 exerts a cell-intrinsic function in RAS-mediated transformation of keratinocytes. JF - The Journal of experimental medicine AU - Cataisson, Christophe AU - Salcedo, Rosalba AU - Hakim, Shakeeb AU - Moffitt, B Andrea AU - Wright, Lisa AU - Yi, Ming AU - Stephens, Robert AU - Dai, Ren-Ming AU - Lyakh, Lyudmila AU - Schenten, Dominik AU - Yuspa, H Stuart AU - Trinchieri, Giorgio AD - Laboratory of Cancer Biology and Genetics, National Cancer Institute, Bethesda, MD 20892, USA. Y1 - 2012/08/27/ PY - 2012 DA - 2012 Aug 27 SP - 1689 EP - 1702 VL - 209 IS - 9 KW - I-kappa B Proteins KW - 0 KW - Interleukin-1alpha KW - Myd88 protein, mouse KW - Myeloid Differentiation Factor 88 KW - NF-kappa B KW - Receptors, Interleukin-1 KW - 9,10-Dimethyl-1,2-benzanthracene KW - 57-97-6 KW - EGFR protein, mouse KW - EC 2.7.10.1 KW - Receptor, Epidermal Growth Factor KW - Index Medicus KW - Animals KW - Receptor, Epidermal Growth Factor -- metabolism KW - I-kappa B Proteins -- metabolism KW - Interleukin-1alpha -- metabolism KW - Cell Differentiation -- genetics KW - Inflammation -- genetics KW - Mice KW - Skin Neoplasms -- metabolism KW - Genes, ras KW - Mice, Mutant Strains KW - Phosphorylation KW - 9,10-Dimethyl-1,2-benzanthracene -- toxicity KW - Skin Neoplasms -- chemically induced KW - Mice, Inbred C57BL KW - Inflammation -- metabolism KW - Signal Transduction KW - Cell Transformation, Neoplastic -- genetics KW - NF-kappa B -- metabolism KW - Myeloid Differentiation Factor 88 -- metabolism KW - Receptors, Interleukin-1 -- genetics KW - Myeloid Differentiation Factor 88 -- genetics KW - Keratinocytes -- pathology KW - Keratinocytes -- metabolism KW - Receptors, Interleukin-1 -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1036875943?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+experimental+medicine&rft.atitle=IL-1R-MyD88+signaling+in+keratinocyte+transformation+and+carcinogenesis.&rft.au=Cataisson%2C+Christophe%3BSalcedo%2C+Rosalba%3BHakim%2C+Shakeeb%3BMoffitt%2C+B+Andrea%3BWright%2C+Lisa%3BYi%2C+Ming%3BStephens%2C+Robert%3BDai%2C+Ren-Ming%3BLyakh%2C+Lyudmila%3BSchenten%2C+Dominik%3BYuspa%2C+H+Stuart%3BTrinchieri%2C+Giorgio&rft.aulast=Cataisson&rft.aufirst=Christophe&rft.date=2012-08-27&rft.volume=209&rft.issue=9&rft.spage=1689&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+experimental+medicine&rft.issn=1540-9538&rft_id=info:doi/10.1084%2Fjem.20101355 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-11-09 N1 - Date created - 2012-08-28 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - GSE22777; GEO N1 - SuppNotes - Cited By: Carcinogenesis. 2009 Nov;30(11):1841-7 [19805574] EMBO J. 2010 Jul 7;29(13):2242-52 [20526283] J Clin Invest. 2010 Oct;120(10):3663-7 [20941850] Proc Natl Acad Sci U S A. 2010 Nov 16;107(46):19903-8 [21041641] Nature. 2011 Feb 3;470(7332):115-9 [21179087] Nat Rev Cancer. 2011 Nov;11(11):761-74 [21993244] Blood. 2011 Nov 24;118(22):5813-23 [21860022] Oncogene. 2000 Jul 20;19(31):3477-86 [10918606] Cell. 2000 Oct 27;103(3):481-90 [11081634] Proc Natl Acad Sci U S A. 2001 Apr 24;98(9):5116-21 [11309499] Int J Cancer. 2001 Sep15;93(6):781-5 [11519037] J Biol Chem. 2002 Apr 5;277(14):12318-23 [11812791] J Immunol. 2002 Jul 1;169(1):469-75 [12077278] J Investig Dermatol Symp Proc. 2002 Dec;7(1):17-26 [12518788] Nature. 2003 Feb 6;421(6923):639-43 [12571598] Eur J Immunol. 2003 Feb;33(2):314-25 [12548562] J Immunol. 2003 Sep 1;171(5):2703-13 [12928424] FASEB J. 2004 Jan;18(1):161-3 [14597552] J Immunol. 2004 Mar 1;172(5):2853-60 [14978086] Genesis. 2004 May;39(1):52-7 [15124227] Cancer Res. 2004 Sep 15;64(18):6511-23 [15374962] Nature. 1986 Oct 30-Nov 5;323(6091):822-4 [2430189] J Exp Med. 1986 Dec 1;164(6):2095-100 [2431094] Differentiation. 1987;35(2):143-50 [2450799] Mol Carcinog. 1990;3(6):363-73 [1703765] Mol Carcinog. 1991;4(3):196-202 [2064725] Carcinogenesis. 1991 Nov;12(11):2063-7 [1718620] J Cell Biol. 1993 Jan;120(1):217-25 [7678013] Mol Carcinog. 1993;7(1):26-35 [8435107] EMBO J. 1993 Dec;12(12):4685-95 [8223478] Cancer Res. 1994 Mar 1;54(5):1344-51 [7509717] FASEB J. 1994 Oct;8(13):1081-7 [7926375] Cancer Res. 1994 Dec 15;54(24):6413-20 [7987836] Mol Cell Biol. 1995 Feb;15(2):872-82 [7823953] Cancer Res. 1995 May 1;55(9):1883-93 [7728756] Arch Dermatol. 1995 Jul;131(7):796-800 [7611795] Science. 1995 Jul 14;269(5221):230-4 [7618084] J Biol Chem. 1996 Mar 8;271(10):5325-31 [8621384] EMBO J. 1997 Mar 17;16(6):1413-26 [9135156] Cancer Res. 1997 Aug 1;57(15):3180-8 [9242447] Nat Med. 1999 Jul;5(7):828-31 [10395330] Cancer Res. 2004 Nov 1;64(21):7801-12 [15520186] Cancer Cell. 2004 Nov;6(5):447-58 [15542429] J Immunol. 2005 Feb 1;174(3):1686-92 [15661932] Cancer Cell. 2005 Mar;7(3):219-26 [15766660] J Clin Invest. 2005 Nov;115(11):2979-91 [16239969] Lancet Oncol. 2006 Feb;7(2):167-74 [16455481] Clin Cancer Res. 2006 Feb 15;12(4):1088-96 [16489061] BMC Bioinformatics. 2006;7:30 [16423281] Nat Rev Cancer. 2006 Apr;6(4):270-80 [16541145] Eur J Cancer. 2006 Apr;42(6):735-44 [16527478] Cancer Res. 2006 Apr 15;66(8):4198-207 [16618742] Cancer Res. 2006 Apr 15;66(8):4279-84 [16618752] J Exp Med. 2006 Apr 17;203(4):941-51 [16567391] J Clin Invest. 2006 Oct;116(10):2757-66 [16964312] Cancer Metastasis Rev. 2006 Sep;25(3):387-408 [17043764] Clin Cancer Res. 2007 Feb 15;13(4):1076-82 [17317814] Expert Rev Anticancer Ther. 2007 Mar;7(3):351-60 [17338654] Nat Rev Cancer. 2007 Apr;7(4):295-308 [17384584] Cell. 2007 Jun 1;129(5):957-68 [17540175] Curr Biol. 2007 Jul 3;17(13):1140-5 [17600714] Mol Cancer Res. 2007 Aug;5(8):847-61 [17670913] Cancer Res. 2007 Oct 15;67(20):9791-9 [17942909] J Exp Med. 2007 Oct 29;204(11):2603-14 [17908936] Proc Natl Acad Sci U S A. 2008 Jan 15;105(2):652-6 [18178624] Nat Protoc. 2008;3(5):799-810 [18451788] Curr Opin Genet Dev. 2008 Feb;18(1):19-26 [18440219] Cancer Lett. 2008 Aug 28;267(2):262-70 [18502035] Lancet Oncol. 2008 Aug;9(8):713-20 [18617440] Cancer Cell. 2008 Aug 12;14(2):156-65 [18691550] Cancer Res. 2009 Jan 1;69(1):319-28 [19118017] Annu Rev Immunol. 2009;27:519-50 [19302047] BMC Bioinformatics. 2009;10:200 [19563622] Cancer Cell. 2009 Aug 4;16(2):149-60 [19647225] Immunobiology. 2009;214(9-10):761-77 [19616341] Nat Protoc. 2009;4(9):1350-62 [19713956] Cell Metab. 2009 Oct;10(4):249-59 [19808018] Cancer Res. 2009 Nov 15;69(22):8579-84 [19887608] Comment In: Nat Rev Immunol. 2012 Oct;12(10):681 [22955844] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1084/jem.20101355 ER - TY - JOUR T1 - The Head-off Environmental Asthma in Louisiana (HEAL) Study-Methods and Study Population AN - 1660052966; 17649945 AB - Background: In the city of New Orleans, Louisiana, and surrounding parishes (NOLA), children with asthma were perilously impacted by Hurricane Katrina as a result of disrupted health care, high home mold and allergen levels, and high stress. Objectives: The Head-off Environmental Asthma in Louisiana (HEAL) study was conducted to examine relationships between the post-Katrina environment and childhood asthma in NOLA and assess a novel asthma counselor intervention that provided case management and guidance for reducing home mold and allergen levels. Methods: Children (4-12 years old) with moderate-to-severe asthma were recruited from NOLA schools. Over 1 year, they received two clinical evaluations, three home environmental evaluations, and the asthma intervention. Quarterly end points included symptom days, medication use, and unscheduled emergency department or clinic visits. A community advisory group was assembled and informed HEAL at all phases. Results: Of the children (n = 182) enrolled in HEAL, 67% were African American, and 25% came from households with annual incomes < $15,000. HEAL children were symptomatic, averaging 6.6 symptom days in the 2 weeks before baseline, and had frequent unscheduled visits to clinics or emergency departments (76% had at least one unscheduled visit in the preceding 3 months). In this report, we describe study design and baseline characteristics of HEAL children. Conclusions: Despite numerous challenges faced by investigators, study staff, and participants, including destroyed infrastructure, disrupted lives, and lost jobs, HEAL was successful in terms of recruitment and retention, the high quality of data collected that will provide insight into asthma-allergen relationships, and the asthma intervention. This success was attributable to using an adaptive approach and refining processes as needed. JF - Environmental Health Perspectives AU - Chulada, Patricia C AU - Kennedy, Suzanne AU - Mvula, Mosanda M AU - Jaffee, Katy AU - Wildfire, Jeremy AU - Thornton, Eleanor AU - Cohn, Richard D AU - Grimsley, LFaye AU - Mitchell, Herman AU - El-Dahr, Jane AU - Sterling, Yvonne AU - Martin, William J AU - White, LuAnn AU - Stephens, Kevin U AU - Lichtveld, Maureen AD - Clinical Research Program, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA Y1 - 2012/08/15/ PY - 2012 DA - 2012 Aug 15 SP - 1592 EP - 1599 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 120 IS - 1 SN - 0091-6765, 0091-6765 KW - Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE) KW - asthma KW - asthma case management KW - asthma counselor KW - environmental intervention KW - Hurricane Katrina KW - indoor allergens KW - mold KW - Communities KW - Phases KW - Recruitment KW - Molds KW - Emergencies KW - Asthma KW - Children KW - Emergency medical services UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660052966?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvironmentalengabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=The+Head-off+Environmental+Asthma+in+Louisiana+%28HEAL%29+Study-Methods+and+Study+Population&rft.au=Chulada%2C+Patricia+C%3BKennedy%2C+Suzanne%3BMvula%2C+Mosanda+M%3BJaffee%2C+Katy%3BWildfire%2C+Jeremy%3BThornton%2C+Eleanor%3BCohn%2C+Richard+D%3BGrimsley%2C+LFaye%3BMitchell%2C+Herman%3BEl-Dahr%2C+Jane%3BSterling%2C+Yvonne%3BMartin%2C+William+J%3BWhite%2C+LuAnn%3BStephens%2C+Kevin+U%3BLichtveld%2C+Maureen&rft.aulast=Chulada&rft.aufirst=Patricia&rft.date=2012-08-15&rft.volume=120&rft.issue=1&rft.spage=1592&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1104239 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-03-01 N1 - Last updated - 2015-10-05 DO - http://dx.doi.org/10.1289/ehp.1104239 ER - TY - JOUR T1 - Effects of NH+4 on Ce(IV) electro-regeneration in simulated and real spent TFT-LCD Cr-etching solutions AN - 1020855960; 16790617 AB - This investigation studies the electro-regeneration of Ce(IV) from Ce(III) in 4 M HNO3 in the presence/absence of NH 4 + and real spent thin-film transistor liquid-crystal display (TFT-LCD) Cr-etching solutions. On Pt, at 2 A and 70 degree C for 100 min, the Ce(IV) yield and apparent rate constant of Ce(III) oxidation in 4 M HNO3 without NH 4 + were 100% and 5.54 10-4 s-1, respectively (and the activation energy was 13.1 kJ mol-1). Cyclic voltammetric and electrolytic measurements consistently support the noticeable inhibition by NH 4 + of Ce(III) oxidation and lowering of the Ce(IV) yield, respectively. The apparent diffusion coefficients for 0.2 and 0.02 M Ce(III) oxidation in 4 M HNO3 that contained 0-0.6 M NH 4 + were (0.38-0.25) 10-5 and (1.6-0.9) 10-5 cm2 s-1 , respectively. Because of combined effects of NH 4 + and anion impurities, the 100 min Ce(IV) yield of a real spent TFT-LCD Cr-etching solution (with [ NH 4 + ] / [ Ce ( III ) ] = 0.74 M/0.39 M) was 82%, lower than that of 4 M HNO3 without NH 4 + , but higher than those of 4 M HNO3 that contained anion impurities with/without 0.4 M NH 4 + . JF - Journal of Environmental Management AU - Chen, Te-San AU - Huang, Kuo-Lin AU - Lai, Yu-Chan AU - Kuo, Yi-Ming AD - Department of Environmental Engineering and Science, National Pingtung University of Science and Technology, 1 Hseuh Fu Road, Nei Pu Hsiang, Pingtung 91201, Taiwan, huangkL@mail.npust.edu.tw Y1 - 2012/08/15/ PY - 2012 DA - 2012 Aug 15 SP - 85 EP - 90 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 104 SN - 0301-4797, 0301-4797 KW - Environment Abstracts; Sustainability Science Abstracts; Ecology Abstracts KW - Spent TFT-LCD Cr-etching solution KW - Electro-regeneration KW - Ce(IV) yield KW - NH+ 4 KW - Rate constant KW - Anions KW - Oxidation KW - Impurities KW - Diffusion KW - Diffusion coefficient KW - M3 1010:Issues in Sustainable Development KW - D 04060:Management and Conservation KW - ENA 07:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020855960?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Environmental+Management&rft.atitle=Effects+of+NH%2B4+on+Ce%28IV%29+electro-regeneration+in+simulated+and+real+spent+TFT-LCD+Cr-etching+solutions&rft.au=Chen%2C+Te-San%3BHuang%2C+Kuo-Lin%3BLai%2C+Yu-Chan%3BKuo%2C+Yi-Ming&rft.aulast=Chen&rft.aufirst=Te-San&rft.date=2012-08-15&rft.volume=104&rft.issue=&rft.spage=85&rft.isbn=&rft.btitle=&rft.title=Journal+of+Environmental+Management&rft.issn=03014797&rft_id=info:doi/10.1016%2Fj.jenvman.2012.03.026 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Anions; Impurities; Oxidation; Diffusion coefficient; Diffusion DO - http://dx.doi.org/10.1016/j.jenvman.2012.03.026 ER - TY - JOUR T1 - Evaluation of the Association between Arsenic and Diabetes: A National Toxicology Program Workshop Review AN - 1291611355; 17649921 AB - Background: Diabetes affects an estimated 346 million persons globally, and total deaths from diabetes are projected to increase > 50% in the next decade. Understanding the role of environmental chemicals in the development or progression of diabetes is an emerging issue in environmental health. In 2011, the National Toxicology Program (NTP) organized a workshop to assess the literature for evidence of associations between certain chemicals, including inorganic arsenic, and diabetes and/or obesity to help develop a focused research agenda. This review is derived from discussions at that workshop. Objectives: Our objectives were to assess the consistency, strength/weaknesses, and biological plausibility of findings in the scientific literature regarding arsenic and diabetes and to identify data gaps and areas for future evaluation or research. The extent of the existing literature was insufficient to consider obesity as an outcome. Data Sources, Extraction, and Synthesis: Studies related to arsenic and diabetes or obesity were identified through PubMed and supplemented with relevant studies identified by reviewing the reference lists in the primary literature or review articles. Conclusions: Existing human data provide limited to sufficient support for an association between arsenic and diabetes in populations with relatively high exposure levels ( greater than or equal to 150 mu g arsenic/L in drinking water). The evidence is insufficient to conclude that arsenic is associated with diabetes in lower exposure (< 150 mu g arsenic/L drinking water), although recent studies with better measures of outcome and exposure support an association. The animal literature as a whole was inconclusive; however, studies using better measures of diabetes-relevant end points support a link between arsenic and diabetes. JF - Environmental Health Perspectives AU - Maull, Elizabeth A AU - Ahsan, Habibul AU - Edwards, Joshua AU - Longnecker, Matthew P AU - Navas-Acien, Ana AU - Pi, Jingbo AU - Silbergeld, Ellen K AU - Styblo, Miroslav AU - Tseng, Chin-Hsiao AU - Thayer, Kristina A AU - Loomis, Dana AD - Biomolecular Screening Branch, Division of the National Toxicology Program, National Institute of Environmental Sciences (NIEHS), National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Research Triangle Park, North Carolina, USA Y1 - 2012/08/10/ PY - 2012 DA - 2012 Aug 10 SP - 1658 EP - 1670 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 - Toxicology Abstracts; Environment Abstracts; Health & Safety Science Abstracts; Water Resources Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; Aqualine Abstracts KW - animal KW - arsenic toxicity KW - cell line KW - chemically induced/epidemiology KW - cultured cell KW - diabetes KW - environmental epidemiology KW - glucose KW - insulin KW - metabolism KW - obesity KW - Chemicals KW - Environmental health KW - Evaluation KW - Drinking Water KW - Exposure KW - Synthesis KW - Toxicology KW - Mortality KW - Obesity KW - Arsenic KW - Data processing KW - Conferences KW - Diabetes mellitus KW - Strength KW - Reviews KW - Drinking water KW - Q5 08503:Characteristics, behavior and fate KW - H 3000:Environment and Ecology KW - SW 5080:Evaluation, processing and publication KW - AQ 00008:Effects of Pollution KW - X 24360:Metals KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1291611355?accountid=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=Environmental+Health+Perspectives&rft.atitle=Evaluation+of+the+Association+between+Arsenic+and+Diabetes%3A+A+National+Toxicology+Program+Workshop+Review&rft.au=Maull%2C+Elizabeth+A%3BAhsan%2C+Habibul%3BEdwards%2C+Joshua%3BLongnecker%2C+Matthew+P%3BNavas-Acien%2C+Ana%3BPi%2C+Jingbo%3BSilbergeld%2C+Ellen+K%3BStyblo%2C+Miroslav%3BTseng%2C+Chin-Hsiao%3BThayer%2C+Kristina+A%3BLoomis%2C+Dana&rft.aulast=Maull&rft.aufirst=Elizabeth&rft.date=2012-08-10&rft.volume=120&rft.issue=2&rft.spage=1658&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1104579 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-01 N1 - Last updated - 2015-05-13 N1 - SubjectsTermNotLitGenreText - Arsenic; Drinking Water; Conferences; Toxicology; Diabetes mellitus; Obesity; Data processing; Reviews; Drinking water; Chemicals; Mortality; Environmental health; Evaluation; Strength; Exposure; Synthesis DO - http://dx.doi.org/10.1289/ehp.1104579 ER - TY - JOUR T1 - Suppression of Tumorigenicity-14, encoding matriptase, is a critical suppressor of colitis and colitis-associated colon carcinogenesis. AN - 1033154402; 22139080 AB - Colitis-associated colorectal cancers are an etiologically distinct subgroup of colon cancers that occur in individuals suffering from inflammatory bowel disease and arise as a consequence of persistent exposure of hyperproliferative epithelial stem cells to an inflammatory microenvironment. An intrinsic defect in the intestinal epithelial barrier has been proposed to be one of several factors that contribute to the inappropriate immune response to the commensal microbiota that underlies inflammatory bowel disease. Matriptase is a membrane-anchored serine protease encoded by Suppression of Tumorigenicity-14 (ST14) that strengthens the intestinal epithelial barrier by promoting tight junction formation. Here, we show that intestinal epithelial-specific ablation of St14 in mice causes formation of colon adenocarcinoma with very early onset and high penetrance. Neoplastic progression is preceded by a chronic inflammation of the colon that resembles human inflammatory bowel disease and is promoted by the commensal microbiota. This study demonstrates that inflammation-associated colon carcinogenesis can be initiated and promoted solely by an intrinsic intestinal permeability barrier perturbation, establishes St14 as a critical tumor-suppressor gene in the mouse gastrointestinal tract and adds matriptase to the expanding list of pericellular proteases with tumor-suppressive functions. JF - Oncogene AU - Kosa, P AU - Szabo, R AU - Molinolo, A A AU - Bugge, T H AD - Oral and Pharyngeal Cancer Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/08/09/ PY - 2012 DA - 2012 Aug 09 SP - 3679 EP - 3695 VL - 31 IS - 32 KW - Anti-Bacterial Agents KW - 0 KW - Membrane Proteins KW - beta Catenin KW - Serine Endopeptidases KW - EC 3.4.21.- KW - St14 protein, mouse KW - EC 3.4.21.109 KW - Index Medicus KW - Neoplasm Invasiveness KW - Animals KW - Precancerous Conditions KW - Inflammatory Bowel Diseases -- enzymology KW - Colon -- pathology KW - Humans KW - Cell Transformation, Neoplastic -- metabolism KW - Metagenome -- drug effects KW - Anti-Bacterial Agents -- pharmacology KW - Epithelium -- enzymology KW - Mice KW - Intestinal Absorption KW - Cell Proliferation KW - Mice, Knockout KW - Gene Expression Regulation, Neoplastic KW - Mice, 129 Strain KW - Basement Membrane -- enzymology KW - Inflammatory Bowel Diseases -- microbiology KW - Gene Expression Regulation, Enzymologic KW - Adenoma -- enzymology KW - Basement Membrane -- metabolism KW - beta Catenin -- metabolism KW - Mice, Inbred C57BL KW - Epithelium -- metabolism KW - Inflammatory Bowel Diseases -- pathology KW - Signal Transduction KW - Adenocarcinoma -- enzymology KW - Serine Endopeptidases -- metabolism KW - Serine Endopeptidases -- genetics KW - Genes, Tumor Suppressor KW - Colitis -- pathology KW - Colitis -- enzymology KW - Colonic Neoplasms -- pathology KW - Colonic Neoplasms -- enzymology KW - Colitis -- microbiology KW - Adenocarcinoma -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1033154402?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Suppression+of+Tumorigenicity-14%2C+encoding+matriptase%2C+is+a+critical+suppressor+of+colitis+and+colitis-associated+colon+carcinogenesis.&rft.au=Kosa%2C+P%3BSzabo%2C+R%3BMolinolo%2C+A+A%3BBugge%2C+T+H&rft.aulast=Kosa&rft.aufirst=P&rft.date=2012-08-09&rft.volume=31&rft.issue=32&rft.spage=3679&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2011.545 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-16 N1 - Date created - 2012-08-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Annu Rev Cell Dev Biol. 2011;27:213-35 [21721945] Neoplasia. 2004 Jan-Feb;6(1):1-6 [15068665] Cell. 2004 Jul 23;118(2):229-41 [15260992] Cancer Res. 2004 Oct 1;64(19):6965-72 [15466188] Nat Genet. 1995 Jun;10(2):143-50 [7663509] J Clin Microbiol. 1996 Apr;34(4):942-6 [8815113] J Clin Invest. 1996 Aug 15;98(4):1010-20 [8770874] Gut. 1996 Jul;39(1):87-92 [8881816] Oncogene. 2000 Feb 21;19(8):1102-13 [10713697] Cell Mol Life Sci. 2000 Jan 20;57(1):25-40 [10949579] J Biol Chem. 2000 Aug 25;275(34):26333-42 [10831593] J Biol Chem. 2000 Nov 24;275(47):36720-5 [10962009] Tumour Biol. 2001 Mar-Apr;22(2):104-14 [11125283] J Infect Dis. 2001 Jul 15;184(2):227-30 [11424022] Science. 2002 Mar 1;295(5560):1726-9 [11872843] J Biol Chem. 2002 May 10;277(19):16960-7 [11864986] Oncogene. 2002 May 23;21(23):3765-79 [12032844] J Gastroenterol Hepatol. 2002 Oct;17(10):1078-83 [12201867] J Biol Chem. 2002 Sep 6;277(36):33275-83 [12065599] Cancer Res. 2002 Nov 15;62(22):6362-6 [12438215] Am J Pathol. 2003 Feb;162(2):691-702 [12547727] Cancer Metastasis Rev. 2003 Jun-Sep;22(2-3):237-58 [12784999] J Biol Chem. 2003 Jul 18;278(29):26773-9 [12738778] Nat Genet. 2003 Nov;35(3):252-7 [14517555] J Biol Chem. 2004 Apr 9;279(15):14899-908 [14747469] Inflamm Bowel Dis. 1998 Aug;4(3):196-202 [9741021] Cytogenet Cell Genet. 1998;83(1-2):56-7 [9925927] Immunogenetics. 1999 May;49(5):420-8 [10199918] J Biol Chem. 1999 Jun 25;274(26):18231-6 [10373424] Cell. 1999 Jul 23;98(2):137-46 [10428026] Proc Natl Acad Sci U S A. 1999 Sep 28;96(20):11054-61 [10500122] Nat Rev Cancer. 2004 Nov;4(11):876-90 [15516960] Clin Diagn Lab Immunol. 2005 Apr;12(4):531-6 [15817762] Nat Rev Genet. 2005 May;6(5):376-88 [15861209] J Cell Sci. 2005 Aug 1;118(Pt 15):3387-95 [16079282] Genes Dev. 2005 Aug 15;19(16):1934-50 [16103220] Int J Oncol. 2005 Oct;27(4):1061-70 [16142324] Cancer Res. 2006 Jan 15;66(2):828-38 [16424015] Nat Genet. 2006 Mar;38(3):337-42 [16444271] Cancer Res. 2006 Aug 15;66(16):7968-75 [16912171] Nat Rev Cancer. 2006 Oct;6(10):764-75 [16990854] Blood. 2006 Oct 15;108(8):2616-23 [16794252] J Biol Chem. 2006 Nov 3;281(44):32941-5 [16980306] Cancer Sci. 2006 Dec;97(12):1327-34 [16999819] Front Biosci. 2007;12:471-91 [17127311] Proc Natl Acad Sci U S A. 2007 Apr 3;104(14):5771-6 [17389401] Nature. 2007 Jul 26;448(7152):427-34 [17653185] Nat Rev Cancer. 2007 Oct;7(10):800-8 [17851543] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15823-8 [17895374] Helicobacter. 2007 Dec;12(6):598-604 [18001399] Genome Biol. 2007;8(7):R131 [17615082] Am J Pathol. 2008 May;172(5):1363-80 [18403596] Nat Rev Cancer. 2008 Oct;8(10):806-12 [18756288] Am J Pathol. 2008 Nov;173(5):1528-39 [18832569] Gastroenterology. 2009 Feb;136(2):551-63 [19027740] Cancer Res. 2009 Mar 1;69(5):1828-35 [19223533] J Cell Sci. 2009 May 1;122(Pt 9):1285-94 [19386895] Nat Genet. 2009 May;41(5):518-20 [19330028] J Biol Chem. 2009 Aug 28;284(35):23177-81 [19487698] Annu Rev Genomics Hum Genet. 2009;10:89-116 [19453248] Cancer Cell. 2009 Sep 8;16(3):208-19 [19732721] Am J Pathol. 2009 Oct;175(4):1453-63 [19717635] Cell Cycle. 2009 Nov 15;8(22):3657-62 [19844170] Am J Pathol. 2010 Feb;176(2):952-67 [20042677] Biochem J. 2010 Mar 1;426(2):219-28 [20015050] Proc Natl Acad Sci U S A. 2010 Mar 2;107(9):4200-5 [20142489] Annu Rev Immunol. 2010;28:573-621 [20192811] Cell. 2010 Apr 2;141(1):52-67 [20371345] Oncogene. 2010 Jun 10;29(23):3313-23 [20400974] Nat Genet. 2010 Aug;42(8):676-83 [20657595] Cancer Res. 2010 Dec 1;70(23):9631-40 [21098708] Nat Rev Immunol. 2011 Jan;11(1):9-20 [21151034] Nat Rev Gastroenterol Hepatol. 2011 Feb;8(2):90-100 [21293509] Oncogene. 2011 Apr 28;30(17):2003-16 [21217780] Nature. 2011 Jun 16;474(7351):318-26 [21677748] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1038/onc.2011.545 ER - TY - JOUR T1 - A Pooled Analysis of Thyroid Cancer Incidence Following Radiotherapy for Childhood Cancer AN - 1136525536; 17234942 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 HS 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, MJacob 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, lubinj@mail.nih.gov Y1 - 2012/08/02/ PY - 2012 DA - 2012 Aug 02 SP - 365 EP - 376 PB - Radiation Research Society VL - 178 IS - 4 SN - 0033-7587, 0033-7587 KW - Toxicology Abstracts KW - Alkylating agents KW - Risk assessment KW - Age KW - Data processing KW - Chemotherapy KW - Survival KW - Radiotherapy KW - Carcinogens KW - Children KW - Bleomycin KW - Radiation KW - Dose-response effects KW - thyroid cancer KW - Anthracycline KW - X 24390:Radioactive Materials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1136525536?accountid=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=A+Pooled+Analysis+of+Thyroid+Cancer+Incidence+Following+Radiotherapy+for+Childhood+Cancer&rft.au=Veiga%2C+Lene+HS%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+MJacob%3BSadetzki%2C+Siegal%3BLundell%2C+Marie%3BSakata%2C+Ritsu%3BDamber%2C+Lena%3BNeta%2C+Gila%3BRon%2C+Elaine&rft.aulast=Veiga&rft.aufirst=Lene&rft.date=2012-08-02&rft.volume=178&rft.issue=4&rft.spage=365&rft.isbn=&rft.btitle=&rft.title=Radiation+Research&rft.issn=00337587&rft_id=info:doi/10.1667%2FRR2889.1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-12-01 N1 - Number of references - 28 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Risk assessment; Alkylating agents; Age; Data processing; Chemotherapy; Radiotherapy; Survival; Carcinogens; Children; Bleomycin; Radiation; Dose-response effects; thyroid cancer; Anthracycline DO - http://dx.doi.org/10.1667/RR2889.1 ER - TY - JOUR T1 - Two-Photon Imaging of Microbial Immunity in Living Tissues AN - 1694973985; 18961523 AB - The immune system is highly evolved and can respond to infection throughout the body. Pathogen-specific immune cells are usually generated in secondary lymphoid tissues (e.g., spleen, lymph nodes) and then migrate to sites of infection where their functionality is shaped by the local milieu. Because immune cells are so heavily influenced by the infected tissue in which they reside, it is important that their interactions and dynamics be studied in vivo. Two-photon microscopy is a powerful approach to study host-immune interactions in living tissues, and recent technical advances in the field have enabled researchers to capture movies of immune cells and infectious agents operating in real time. These studies have shed light on pathogen entry and spread through intact tissues as well as the mechanisms by which innate and adaptive immune cells participate in thwarting infections. This review focuses on how two-photon microscopy can be used to study tissue-specific immune responses in vivo, and how this approach has advanced our understanding of host-immune interactions following infection. JF - Microscopy and Microanalysis AU - Herz, Jasmin AU - Zinselmeyer, Bernd H AU - McGavern, Dorian B AD - National Institute of Neurological Disorders and Stroke, The National Institutes of Health, Bethesda, MD 20892, USA, mcgavernd@mail.nih.gov Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - 730 EP - 741 PB - Cambridge University Press, The Edinburgh Building, Cambridge CB2 2RU United Kingdom VL - 18 IS - 4 SN - 1431-9276, 1431-9276 KW - Microbiology Abstracts A: Industrial & Applied Microbiology KW - Immune system KW - Microscopy KW - Spleen KW - Pathogens KW - Cell migration KW - Immune response KW - Immunity KW - Infection KW - imaging KW - Lymphoid tissue KW - Lymph nodes KW - A 01300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1694973985?accountid=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=Microscopy+and+Microanalysis&rft.atitle=Two-Photon+Imaging+of+Microbial+Immunity+in+Living+Tissues&rft.au=Herz%2C+Jasmin%3BZinselmeyer%2C+Bernd+H%3BMcGavern%2C+Dorian+B&rft.aulast=Herz&rft.aufirst=Jasmin&rft.date=2012-08-01&rft.volume=18&rft.issue=4&rft.spage=730&rft.isbn=&rft.btitle=&rft.title=Microscopy+and+Microanalysis&rft.issn=14319276&rft_id=info:doi/10.1017%2FS1431927612000281 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-07-01 N1 - Number of references - 77 N1 - Last updated - 2015-07-23 N1 - SubjectsTermNotLitGenreText - Immune system; Microscopy; Spleen; Immunity; Immune response; Cell migration; Pathogens; Infection; imaging; Lymph nodes; Lymphoid tissue DO - http://dx.doi.org/10.1017/S1431927612000281 ER - TY - JOUR T1 - T-Cell Therapy for Viral Infections Following Transplantation: Why Stop at Three Viruses? AN - 1668268158; PQ0001244614 AB - The prolonged recovery phase of cell-mediated immunity after allogeneic hematopoietic stem cell transplantation (SCT) brings serious and often fatal risks from opportunistic reactivation or acquisition of common viruses.1 Post-transplant immunodeficiency particularly involves defective T-cell function, and it is now established that adoptive transfer of viral-specific T cells can prevent and treat viral complications.2-5 In this issue, Gerdemann and colleagues describe a technique to generate clinical-grade virus-specific T-cell lines targeting seven viruses that commonly cause morbidity and mortality after SCT.6 JF - Molecular Therapy AU - Barrett, John A AD - Stem Cell Transplantation Section, Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892, USA, barrettj@nhlbi.nih.gov Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - 1487 EP - 1488 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 20 IS - 8 SN - 1525-0016, 1525-0016 KW - Virology & AIDS Abstracts; Immunology Abstracts; Biotechnology and Bioengineering Abstracts KW - Mortality KW - Immunity (cell-mediated) KW - stem cell transplantation KW - Lymphocytes T KW - Immunodeficiency KW - Adoptive transfer KW - Infection KW - Morbidity KW - V 22350:Immunology KW - F 06960:Molecular Immunology KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668268158?accountid=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=T-Cell+Therapy+for+Viral+Infections+Following+Transplantation%3A+Why+Stop+at+Three+Viruses%3F&rft.au=Barrett%2C+John+A&rft.aulast=Barrett&rft.aufirst=John&rft.date=2012-08-01&rft.volume=20&rft.issue=8&rft.spage=1487&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2012.138 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Mortality; Immunity (cell-mediated); stem cell transplantation; Adoptive transfer; Immunodeficiency; Lymphocytes T; Infection; Morbidity DO - http://dx.doi.org/10.1038/mt.2012.138 ER - TY - JOUR T1 - Sublytic concentrations of Staphylococcus aureus Panton-Valentine leukocidin alter human PMN gene expression and enhance bactericidal capacity AN - 1551624088; 20356002 AB - PVL-mediated priming of PMNs enhances the host innate immune response. JF - Journal of Leukocyte Biology AU - Graves, Shawna F AU - Kobayashi, Scott D AU - Braughton, Kevin R AU - Whitney, Adeline R AU - Sturdevant, Daniel E AU - Rasmussen, Devon L AU - Kirpotina, Liliya N AU - Quinn, Mark T AU - DeLeo, Frank R AD - Division of Biological Sciences, Department of Biochemistry and Biophysics, University of Montana, Missoula, Montana, USA; and, fdeleo@niaid.nih.gov Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - 361 EP - 374 PB - Federation of American Societies for Experimental Biology, 9650 Rockville Pike Bethesda MD 20814 United States VL - 92 IS - 2 SN - 0741-5400, 0741-5400 KW - Genetics Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - MRSA KW - priming KW - neutrophil KW - leukocidin KW - Leukocytes KW - pmn gene KW - Immune response KW - Staphylococcus aureus KW - G 07720:Immunogenetics KW - A 01340:Antibiotics & Antimicrobials KW - F 06910:Microorganisms & Parasites KW - J 02340:Antibiotics & Antimicrobials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551624088?accountid=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+Leukocyte+Biology&rft.atitle=Sublytic+concentrations+of+Staphylococcus+aureus+Panton-Valentine+leukocidin+alter+human+PMN+gene+expression+and+enhance+bactericidal+capacity&rft.au=Graves%2C+Shawna+F%3BKobayashi%2C+Scott+D%3BBraughton%2C+Kevin+R%3BWhitney%2C+Adeline+R%3BSturdevant%2C+Daniel+E%3BRasmussen%2C+Devon+L%3BKirpotina%2C+Liliya+N%3BQuinn%2C+Mark+T%3BDeLeo%2C+Frank+R&rft.aulast=Graves&rft.aufirst=Shawna&rft.date=2012-08-01&rft.volume=92&rft.issue=2&rft.spage=361&rft.isbn=&rft.btitle=&rft.title=Journal+of+Leukocyte+Biology&rft.issn=07415400&rft_id=info:doi/10.1189%2Fjlb.1111575 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2014-11-12 N1 - SubjectsTermNotLitGenreText - leukocidin; Leukocytes; pmn gene; Immune response; Staphylococcus aureus DO - http://dx.doi.org/10.1189/jlb.1111575 ER - TY - JOUR T1 - Land use inventory as framework for environmental accounting: an application in Italy AN - 1540229261; 20097578 AB - Land use inventories are sound measures to provide information on the area occupied by different land use or land cover types and their changes, although less widespread than traditional mapping; as such, they are distinctively well established tools for generating statistics on the state and the dynamics of land use in the European Union. Italy has recently set up a land use inventory system (IUTI) as a key instrument for accounting removals and emissions of greenhouse gases (GHG) associated to land use, land use change and forestry (LULUCF) activities elected by Italy under the Kyoto Protocol. IUTI adopts a statistical sampling procedure to estimate the area covered by LULUCF land use categories in Italy, and associated uncertainty estimates. In a broader perspective, IUTI methodology, by providing reliable estimates and well-defined levels of statistical uncertainty for assessing stocks and flows of land use at national level, can be further implemented to frame other key questions for sustainable development policies, like the set up of environmental-economic accounting systems. JF - iForest: Biogeosciences & Forestry AU - Corona, Piermaria AU - Barbati, Anna AU - Tomao, Antonio AU - Bertani, Remo AU - Valentini, Riccardo AU - Marchetti, Marco AU - Fattorini, Lorenzo AU - Perugini, Lucia AD - Dipartimento per l'Innovazione nei sistemi Biologici, Agroalimentari e Forestali (DIBAF), Universita della Tuscia, v. San Camillo de Lellis, s.n.c., I-01100 Viterbo (Italy), perugini@unitus.it Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - 204 EP - 209 PB - Italian Society of Silviculture and Forest Ecology, Dipartimento di Produzione Vegetale Potenza 85100 Italy VL - 5 KW - Pollution Abstracts; Sustainability Science Abstracts; Ecology Abstracts KW - Land Use Survey KW - Land Use Change KW - Statistical Sampling KW - Forest KW - Environmental Accounting KW - Statistics KW - International cooperation KW - Statistical sampling KW - Sustainable development KW - Air pollution control KW - Italy KW - Kyoto Protocol KW - Emissions KW - Sound KW - Sampling KW - Mapping KW - Forestry KW - Inventories KW - Emission control KW - Environmental policy KW - Accounting KW - Land use KW - European Union KW - Environmental accounting KW - Greenhouse gases KW - P 0000:AIR POLLUTION KW - M3 1010:Issues in Sustainable Development KW - D 04060:Management and Conservation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1540229261?accountid=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=iForest%3A+Biogeosciences+%26+Forestry&rft.atitle=Land+use+inventory+as+framework+for+environmental+accounting%3A+an+application+in+Italy&rft.au=Corona%2C+Piermaria%3BBarbati%2C+Anna%3BTomao%2C+Antonio%3BBertani%2C+Remo%3BValentini%2C+Riccardo%3BMarchetti%2C+Marco%3BFattorini%2C+Lorenzo%3BPerugini%2C+Lucia&rft.aulast=Corona&rft.aufirst=Piermaria&rft.date=2012-08-01&rft.volume=5&rft.issue=&rft.spage=204&rft.isbn=&rft.btitle=&rft.title=iForest%3A+Biogeosciences+%26+Forestry&rft.issn=1971-7458&rft_id=info:doi/10.3832%2Fifor0625-005 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2015-05-27 N1 - SubjectsTermNotLitGenreText - Inventories; Statistics; Sound; Sustainable development; Mapping; Sampling; Greenhouse gases; Land use; Forestry; International cooperation; Statistical sampling; Air pollution control; Emission control; Accounting; Environmental policy; Kyoto Protocol; European Union; Environmental accounting; Emissions; Italy DO - http://dx.doi.org/10.3832/ifor0625-005 ER - TY - JOUR T1 - Ovarian cancer risk factors by histologic subtypes in the NIH-AARP diet and health study AN - 1443372831; 18611381 AB - Data suggest that risk factors for ovarian carcinoma vary by histologic type, but findings are inconsistent. We prospectively evaluated risk factors by histological subtypes of incident ovarian cancer (n = 849) in a cohort of 169,391 women in the NIH-AARP Diet and Health Study. We constructed Cox models of individual exposures by comparing case subtypes to the entire non-case group and assessed p-heterogeneity in case-case comparisons using serous as the reference category. Substantial risk differences between histologic subtypes were observed for menopausal hormone therapy (MHT) use, oral contraceptive (OC) use, parity and body mass index (p-heterogeneity = 0.01, 0.03, 0.05, 0.03, respectively). MHT users were at increased risk for all histologic subtypes except for mucinous carcinomas, where risk was reduced (relative risk (RR) = 0.37; 95% confidence interval (CI): 0.18, 0.80). OC users were only at significantly decreased risk for serous cancers (RR = 0.69; 95% CI: 0.55, 0.85). Although parity was inversely associated with risk of all subtypes, the RRs ranged from 0.28 (clear cell) to 0.83 (serous). Obesity was a significant risk factor only for endometrioid cancers (RR = 1.64; 95% CI: 1.00, 2.70). Our findings support a link between etiological factors and histological heterogeneity in ovarian carcinoma. JF - International Journal of Cancer AU - Yang, Hannah P AU - Trabert, Britton AU - Murphy, Megan A AU - Sherman, Mark E AU - Sampson, Joshua N AU - Brinton, Louise A AU - Hartge, Patricia AU - Hollenbeck, Albert AU - Park, Yikyung AU - Wentzensen, Nicolas AD - Biostatistics Branch, Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, Bethesda, MD., yanghan@mail.nih.gov Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - 938 EP - 948 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 131 IS - 4 SN - 0020-7136, 0020-7136 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Risk assessment KW - Diets KW - Parity KW - Health risks KW - Obesity KW - Risk factors KW - Body mass KW - Ovarian carcinoma KW - Hormones KW - Cancer KW - Contraceptives 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/1443372831?accountid=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=Ovarian+cancer+risk+factors+by+histologic+subtypes+in+the+NIH-AARP+diet+and+health+study&rft.au=Yang%2C+Hannah+P%3BTrabert%2C+Britton%3BMurphy%2C+Megan+A%3BSherman%2C+Mark+E%3BSampson%2C+Joshua+N%3BBrinton%2C+Louise+A%3BHartge%2C+Patricia%3BHollenbeck%2C+Albert%3BPark%2C+Yikyung%3BWentzensen%2C+Nicolas&rft.aulast=Yang&rft.aufirst=Hannah&rft.date=2012-08-01&rft.volume=131&rft.issue=4&rft.spage=938&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.26469 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-10-01 N1 - Last updated - 2013-12-04 N1 - SubjectsTermNotLitGenreText - Parity; Diets; Risk assessment; Obesity; Health risks; Body mass; Risk factors; Ovarian carcinoma; Hormones; Contraceptives; Cancer DO - http://dx.doi.org/10.1002/ijc.26469 ER - TY - JOUR T1 - Community-Responsive Interventions to Reduce Cardiovascular Risk in American Indians AN - 1438556483; 201308076 AB - American Indian and Alaska Native (AI/AN) populations bear a heavy burden of cardiovascular disease (CVD), and they have the highest rates of risk factors for CVD, such as cigarette smoking, obesity, and diabetes, of any U.S. population group. Yet, few randomized controlled trials have been launched to test potential preventive interventions in Indian Country. Five randomized controlled trials were initiated recently in AI/AN communities to test the effectiveness of interventions targeting adults and/or children to promote healthy behaviors that are known to impact biological CVD risk factors. This article provides a context for and an overview of these five trials. The high burden of CVD among AI/AN populations will worsen unless behaviors and lifestyles affecting CVD risk can be modified. These five trials, if successful, represent a starting point in addressing these significant health disparities. Adapted from the source document. JF - The Journal of Primary Prevention AU - Jobe, Jared B AU - Adams, Alexandra K AU - Henderson, Jeffrey A AU - Karanja, Njeri AU - Lee, Elisa T AU - Walters, Karina L AD - Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, MD, USA jobej@mail.nih.gov Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 153 EP - 159 PB - Springer Science+Business Media, Dordrecht, The Netherlands VL - 33 IS - 4 SN - 0278-095X, 0278-095X KW - Risk KW - Heart Diseases KW - Risk Factors KW - Health Behavior KW - Medical Research KW - Intervention KW - American Indians KW - Trials KW - Lifestyle KW - article KW - 6121: therapeutic interventions UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1438556483?accountid=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=The+Journal+of+Primary+Prevention&rft.atitle=Community-Responsive+Interventions+to+Reduce+Cardiovascular+Risk+in+American+Indians&rft.au=Jobe%2C+Jared+B%3BAdams%2C+Alexandra+K%3BHenderson%2C+Jeffrey+A%3BKaranja%2C+Njeri%3BLee%2C+Elisa+T%3BWalters%2C+Karina+L&rft.aulast=Jobe&rft.aufirst=Jared&rft.date=2012-08-01&rft.volume=33&rft.issue=4&rft.spage=153&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Primary+Prevention&rft.issn=0278095X&rft_id=info:doi/10.1007%2Fs10935-012-0277-9 LA - English DB - Social Services Abstracts N1 - Date revised - 2013-10-01 N1 - Last updated - 2016-09-28 N1 - CODEN - JPPRDT N1 - SubjectsTermNotLitGenreText - Intervention; Trials; Medical Research; American Indians; Risk; Heart Diseases; Risk Factors; Health Behavior; Lifestyle DO - http://dx.doi.org/10.1007/s10935-012-0277-9 ER - TY - JOUR T1 - Software support for SBGN maps: SBGN-ML and LibSBGN AN - 1434026282; 18513571 AB - Motivation: LibSBGN is a software library for reading, writing and manipulating Systems Biology Graphical Notation (SBGN) maps stored using the recently developed SBGN-ML file format. The library (available in C++ and Java) makes it easy for developers to add SBGN support to their tools, whereas the file format facilitates the exchange of maps between compatible software applications. The library also supports validation of maps, which simplifies the task of ensuring compliance with the detailed SBGN specifications. With this effort we hope to increase the adoption of SBGN in bioinformatics tools, ultimately enabling more researchers to visualize biological knowledge in a precise and unambiguous manner. JF - Bioinformatics AU - van Iersel, Martijn P AU - Villeger, Alice C AU - Czauderna, Tobias AU - Boyd, Sarah E AU - Bergmann, Frank T AU - Luna, Augustin AU - Demir, Emek AU - Sorokin, Anatoly AU - Dogrusoz, Ugur AU - Matsuoka, Yukiko AU - Funahashi, Akira AU - Aladjem, Mirit I AU - Mi, Huaiyu AU - Moodie, Stuart L AU - Kitano, Hiroaki AU - Le Novere, Nicolas AU - Schreiber, Falk AD - super(1)EMBL European Bioinformatics Institute, Hinxton, UK, super(2)Netherlands Consortium for Systems Biology (NCSB), Amsterdam, super(3)Department of Bioinformatics - BiGCaT, University of Maastricht, Maastricht, The Netherlands, super(4)School of Computer Science, Faculty of Engineering and Physical Sciences, University of Manchester, Manchester, UK, super(5)Leibniz Institute of Plant Genetics and Crop Plant Research (IPK), Gatersleben, Germany, super(6)School of Mathematical Sciences, Faculty of Science, Monash University, Melbourne, Australia, super(7)Control and Dynamical Systems, California Institute of Technology, Pasadena, CA, super(8)National Cancer Institute, Bethesda, MD, super(9)Bioinformatics Program, Boston University, Boston, MA, super(10)Computational Biology, Memorial Sloan Kettering Y1 - 2012/08/01/ PY - 2012 DA - 2012 Aug 01 SP - 2016 EP - 2021 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 28 IS - 15 SN - 1367-4803, 1367-4803 KW - Biotechnology and Bioengineering Abstracts KW - Computer programs KW - software KW - Computer graphics KW - Language KW - Adoption KW - Bioinformatics KW - Maps KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434026282?accountid=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=Software+support+for+SBGN+maps%3A+SBGN-ML+and+LibSBGN&rft.au=van+Iersel%2C+Martijn+P%3BVilleger%2C+Alice+C%3BCzauderna%2C+Tobias%3BBoyd%2C+Sarah+E%3BBergmann%2C+Frank+T%3BLuna%2C+Augustin%3BDemir%2C+Emek%3BSorokin%2C+Anatoly%3BDogrusoz%2C+Ugur%3BMatsuoka%2C+Yukiko%3BFunahashi%2C+Akira%3BAladjem%2C+Mirit+I%3BMi%2C+Huaiyu%3BMoodie%2C+Stuart+L%3BKitano%2C+Hiroaki%3BLe+Novere%2C+Nicolas%3BSchreiber%2C+Falk&rft.aulast=van+Iersel&rft.aufirst=Martijn&rft.date=2012-08-01&rft.volume=28&rft.issue=15&rft.spage=2016&rft.isbn=&rft.btitle=&rft.title=Bioinformatics&rft.issn=13674803&rft_id=info:doi/10.1093%2Fbioinformatics%2Fbts270 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2015-03-20 N1 - SubjectsTermNotLitGenreText - Computer programs; software; Computer graphics; Adoption; Language; Bioinformatics; Maps DO - http://dx.doi.org/10.1093/bioinformatics/bts270 ER - TY - JOUR T1 - Recruiting Substance-Using Men Who Have Sex With Men into HIV Prevention Research: Current Status and Future Directions AN - 1373429616; 201305467 AB - Research investigators have identified increasing challenges to the recruitment of men who have sex with men (MSM) for observational and intervention HIV/AIDS studies. To address these issues, program staff from the National Institute on Drug Abuse convened a meeting on April 28th to 29th, 2009 to discuss issues in MSM recruitment. The panel indicated that there was decreased community identification with HIV research, although altruistic, community-oriented motives continued to be important. Substance use adds to recruitment challenges, particularly recruitment of MSM who use stigmatized substances. Relatively new recruitment methods such as respondent driven sampling, venue-data-time sampling, and internet sampling have helped advance knowledge about the recruitment process; however, they have not mitigated the challenges to MSM recruitment. Recruitment of youth and members of racial/ethnic minority populations present additional considerations. This report summarizes the meeting's proceedings, key points of discussion, and areas for further research consideration. Adapted from the source document. JF - AIDS and Behavior AU - Jenkins, Richard A AD - Prevention Research Branch, National Institute on Drug Abuse, 6001 Executive Blvd., Rm. 5185 MSC 9589, Bethesda, MD, 20892-9589, USA jenkinsri@mail.nih.gov Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 1411 EP - 1419 PB - Springer, Dordrecht, The Netherlands VL - 16 IS - 6 SN - 1090-7165, 1090-7165 KW - Prevention KW - Minority Groups KW - Ethnicity KW - Acquired Immune Deficiency Syndrome KW - Recruitment KW - Intervention KW - Homosexuality KW - Knowledge KW - Drug Abuse KW - article KW - 6126: acquired immune deficiency syndrome (AIDS) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1373429616?accountid=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=AIDS+and+Behavior&rft.atitle=Recruiting+Substance-Using+Men+Who+Have+Sex+With+Men+into+HIV+Prevention+Research%3A+Current+Status+and+Future+Directions&rft.au=Jenkins%2C+Richard+A&rft.aulast=Jenkins&rft.aufirst=Richard&rft.date=2012-08-01&rft.volume=16&rft.issue=6&rft.spage=1411&rft.isbn=&rft.btitle=&rft.title=AIDS+and+Behavior&rft.issn=10907165&rft_id=info:doi/10.1007%2Fs10461-011-0037-5 LA - English DB - Social Services Abstracts N1 - Date revised - 2013-07-01 N1 - Last updated - 2016-09-28 N1 - CODEN - AIBEFC N1 - SubjectsTermNotLitGenreText - Recruitment; Homosexuality; Acquired Immune Deficiency Syndrome; Intervention; Prevention; Knowledge; Ethnicity; Minority Groups; Drug Abuse DO - http://dx.doi.org/10.1007/s10461-011-0037-5 ER - TY - JOUR T1 - Mental Health and Family Functioning as Correlates of a Sedentary Lifestyle Among Low-Income Women with Young Children AN - 1347782435; 201321685 AB - The authors in this cross-sectional study examined mental health and family environmental factors related to a sedentary lifestyle, including lack of leisure-time physical activity and high levels of television viewing, among low-income mothers/female guardians of preschool-aged children. A self-administered questionnaire was completed by 131 mothers in 2010. Primary outcome measures included television viewing time (minutes/day) and leisure-time physical activity (=150 minutes per week). Independent variables included depressive symptoms, perceived stress, and family functioning. Demographic factors (age, marriage, work status, education, number of children in the household, and race/ethnicity) were examined as potential covariates. Participating women watched television on average 186.1 minutes/day (i.e., >3 hours). Additionally, 36% of women engaged in less than the recommended 150-minute leisure-time physical activity per week. Hierarchical multiple regression analyses indicated that greater depressive symptoms (B = 76.4, p < 0.01) and lower family functioning (B = 33.0, p < 0.05) were independently related to greater television viewing when controlling for other variables. No independent factors were identified for lack of leisure-time physical activity when controlling for other covariates. Findings suggest that health promotion efforts to promote an active lifestyle among low-income women with young children should address mental health and family functioning factors, especially depressive symptoms. Adapted from the source document. JF - Women & Health AU - Li, Kaigang AU - Davison, Kirsten K AU - Jurkowski, Janine M AD - Department of Health Policy, Management and Behavior, University at Albany (SUNY), Albany, New York, USA lik2@mail.nih.gov Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 606 EP - 619 PB - Taylor & Francis, Philadelphia PA VL - 52 IS - 6 SN - 0363-0242, 0363-0242 KW - Low Income Groups KW - Television Viewing KW - Family Relations KW - Depression (Psychology) KW - Physical Fitness KW - Mental Health KW - Females KW - Children KW - Lifestyle KW - article KW - 2045: sociology of health and medicine; sociology of medicine & health care UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1347782435?accountid=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=Women+%26+Health&rft.atitle=Mental+Health+and+Family+Functioning+as+Correlates+of+a+Sedentary+Lifestyle+Among+Low-Income+Women+with+Young+Children&rft.au=Li%2C+Kaigang%3BDavison%2C+Kirsten+K%3BJurkowski%2C+Janine+M&rft.aulast=Li&rft.aufirst=Kaigang&rft.date=2012-08-01&rft.volume=52&rft.issue=6&rft.spage=606&rft.isbn=&rft.btitle=&rft.title=Women+%26+Health&rft.issn=03630242&rft_id=info:doi/10.1080%2F03630242.2012.705243 LA - English DB - Sociological Abstracts N1 - Date revised - 2013-05-01 N1 - Last updated - 2016-09-28 N1 - CODEN - WOHEDI N1 - SubjectsTermNotLitGenreText - Females; Family Relations; Physical Fitness; Television Viewing; Depression (Psychology); Children; Low Income Groups; Mental Health; Lifestyle DO - http://dx.doi.org/10.1080/03630242.2012.705243 ER - TY - JOUR T1 - A continuous simulation model for design-hydrograph estimation in small and ungauged watersheds AN - 1323806842; 17796917 AB - The estimation of design hydrographs for small and ungauged watersheds is a key topic in hydrology. In this context, event-based procedures, which transform design storms deduced from intensity-duration-frequency curves by lumped rainfall-runoff models, are commonly applied. This study introduces a continuous simulation model that involves a two-stage rainfall generator, a geomorphological rainfall-runoff model and a flood frequency analysis applied to simulated runoff time series. The resulting design hydrograph with an assigned return period preserves peak and volume information. The case study results indicate that the continuous model is able to return a range of flood scenarios corresponding to a wide range of possible watershed physical conditions. Moreover, the rainfall-runoff model applied using empirical calibration without observations appears to be as accurate as other models based on regionalized information. Editor D. Koutsoyiannis Citation Grimaldi, S., Petroselli, A., and Serinaldi, F., 2012. A continuous simulation model for design-hydrograph estimation in small and ungauged watersheds. Hydrological Sciences Journal, 57 (6), 1035-1051. JF - Hydrological Sciences Journal/Journal des Sciences Hydrologiques AU - Grimaldi, S AU - Petroselli, A AU - Serinaldi, F AD - Dipartimento per l'Innovazione nei Sistemi Biologici, Agroalimentari e Forestali (DIBAF), University of Tuscia, Via San Camillo De Lellis snc, I-01100, Viterbo, Italy, salvatore.grimaldi@unitus.it Y1 - 2012/08/01/ PY - 2012 DA - 2012 Aug 01 SP - 1035 EP - 1051 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 57 IS - 6 SN - 0262-6667, 0262-6667 KW - Water Resources Abstracts; Aqualine Abstracts KW - Indexing in process UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323806842?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hydrological+Sciences+Journal%2FJournal+des+Sciences+Hydrologiques&rft.atitle=A+continuous+simulation+model+for+design-hydrograph+estimation+in+small+and+ungauged+watersheds&rft.au=Grimaldi%2C+S%3BPetroselli%2C+A%3BSerinaldi%2C+F&rft.aulast=Grimaldi&rft.aufirst=S&rft.date=2012-08-01&rft.volume=57&rft.issue=6&rft.spage=1035&rft.isbn=&rft.btitle=&rft.title=Hydrological+Sciences+Journal%2FJournal+des+Sciences+Hydrologiques&rft.issn=02626667&rft_id=info:doi/10.1080%2F02626667.2012.702214 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-04-01 N1 - Last updated - 2013-05-06 DO - http://dx.doi.org/10.1080/02626667.2012.702214 ER - TY - JOUR T1 - Age-Related Differences in Biomedical and Folk Beliefs as Causes for Diabetes and Heart Disease Among Mexican Origin Adults AN - 1323338985; 201304706 AB - An understanding of health beliefs is key to creating culturally appropriate health services for Hispanic populations in the US. In this study we explore age-based variations in causal beliefs for heart disease and diabetes among Mexican origin adults in Houston, TX. This cross-sectional study included 497 adults of Mexican origin. Participants were asked to indicate the importance of biomedically defined and folk illness-related risk factors as causes for heart disease and diabetes. Biomedical risk factors were ranked highest as causes of diabetes and heart disease among all participants. Folk illness-related factors were ranked below biomedical factors as causes of heart disease among all age groups. Susto was ranked above the median as a risk factor for diabetes among older participants. Age-related differences in causal beliefs may have implications for designing culturally appropriate health services, such as tailored diabetes interventions for older Mexican origin adults. Adapted from the source document. JF - Journal of Immigrant and Minority Health AU - Palmquist, Aunchalee E L AU - Wilkinson, Anna V AU - Sandoval, Juan-Miguel AU - Koehly, Laura M AD - National Institutes of Health, National Human Genome Research Institute, Social and Behavioral Research Branch, Bethesda, MD, USA apalmquist@elon.edu Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 596 EP - 601 PB - Springer, Dordrecht The Netherlands VL - 14 IS - 4 SN - 1557-1912, 1557-1912 KW - Risk factors KW - Health services KW - Age differences KW - Mexican people KW - Heart diseases KW - Diabetes KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323338985?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Immigrant+and+Minority+Health&rft.atitle=Age-Related+Differences+in+Biomedical+and+Folk+Beliefs+as+Causes+for+Diabetes+and+Heart+Disease+Among+Mexican+Origin+Adults&rft.au=Palmquist%2C+Aunchalee+E+L%3BWilkinson%2C+Anna+V%3BSandoval%2C+Juan-Miguel%3BKoehly%2C+Laura+M&rft.aulast=Palmquist&rft.aufirst=Aunchalee+E&rft.date=2012-08-01&rft.volume=14&rft.issue=4&rft.spage=596&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immigrant+and+Minority+Health&rft.issn=15571912&rft_id=info:doi/10.1007%2Fs10903-011-9522-1 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-04-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Diabetes; Heart diseases; Mexican people; Risk factors; Age differences; Health services DO - http://dx.doi.org/10.1007/s10903-011-9522-1 ER - TY - JOUR T1 - An affective booster moderates the effect of gain- and loss-framed messages on behavioral intentions for colorectal cancer screening AN - 1323338820; 201303839 AB - Previous research has demonstrated that loss-framed messages are more effective than gain-framed messages in motivating detection behaviors such as screening. The present study examined whether affective context moderates the degree to which message frame is associated with behavioral intentions to engage in colorectal cancer screening. In particular, we buttressed a framing manipulation with an "affective booster" to increase anticipated and anticipatory emotions associated with the framed messages. Consistent with previous research, we found that loss-framed messages are more effective in increasing intentions to screen. However, we found that among individuals who received gain-framed messages (but not loss-framed messages), the affective booster increased message persuasiveness. This effect on intentions was partially mediated by self-efficacy for engaging in screening. This study indicates that in the presence of emotional boosters, loss-framed messages may lose their advantage over gain-framed messages in motivating detection behaviors, and that self-efficacy may partially explain these effects. Adapted from the source document. JF - Journal of Behavioral Medicine AU - Ferrer, Rebecca A AU - Klein, William M P AU - Zajac, Laura E AU - Land, Stephanie R AU - Ling, Bruce S AD - Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, 6130 Executive Blvd., Room 4083, Rockville, MD, 20852, USA ferrerra@mail.nih.gov Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 452 EP - 461 PB - Springer Science+Business Media, Inc., Dordrecht, The Netherlands VL - 35 IS - 4 SN - 0160-7715, 0160-7715 KW - Selfefficacy KW - Screening KW - Emotions KW - Detection KW - Colorectal cancer KW - Framing KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323338820?accountid=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+Behavioral+Medicine&rft.atitle=An+affective+booster+moderates+the+effect+of+gain-+and+loss-framed+messages+on+behavioral+intentions+for+colorectal+cancer+screening&rft.au=Ferrer%2C+Rebecca+A%3BKlein%2C+William+M+P%3BZajac%2C+Laura+E%3BLand%2C+Stephanie+R%3BLing%2C+Bruce+S&rft.aulast=Ferrer&rft.aufirst=Rebecca&rft.date=2012-08-01&rft.volume=35&rft.issue=4&rft.spage=452&rft.isbn=&rft.btitle=&rft.title=Journal+of+Behavioral+Medicine&rft.issn=01607715&rft_id=info:doi/10.1007%2Fs10865-011-9371-3 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-04-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JBMEDD N1 - SubjectsTermNotLitGenreText - Screening; Colorectal cancer; Detection; Selfefficacy; Framing; Emotions DO - http://dx.doi.org/10.1007/s10865-011-9371-3 ER - TY - JOUR T1 - Agreement in Mother and Father Acceptance-Rejection, Warmth, and Hostility/Rejection/ Neglect of Children Across Nine Countries AN - 1283639632; 201303649 AB - The authors assessed whether mothers' and fathers' self-reports of acceptance-rejection, warmth, and hostility/rejection/neglect (HRN) of their preadolescent children differ cross-nationally and relative to the gender of the parent and child in 10 communities in 9 countries, including China, Colombia, Italy, Jordan, Kenya, the Philippines, Sweden, Thailand, and the United States (N = 998 families). Mothers and fathers in all countries reported a high degree of acceptance and warmth, and a low degree of HRN, but countries also varied. Mothers reported greater acceptance of children than fathers in China, Italy, Sweden, and the United States, and these effects were accounted for by greater self-reported warmth in mothers than in fathers in China, Italy, the Philippines, Sweden, and Thailand and less HRN in mothers than in fathers in Sweden. Fathers reported greater warmth than mothers in Kenya. Mother and father acceptance-rejection were moderately correlated. Relative levels of mother and father acceptance and rejection appear to be country specific. [Reprinted by permission of Sage Publications Inc., copyright holder.] JF - Cross-Cultural Research AU - Putnick, Diane L AU - Bornstein, Marc H AU - Lansford, Jennifer E AU - Chang, Lei AU - Deater-Deckard, Kirby AU - Di Giunta, Laura AU - Gurdal, Sevtap AU - Dodge, Kenneth A AU - Malone, Patrick S AU - Oburu, Paul O AU - Pastorelli, Concetta AU - Skinner, Ann T AU - Sorbring, Emma AU - Tapanya, Sombat AU - Tirado, Liliana Maria Uribe AU - Zelli, Arnaldo AU - Alampay, Liane Pena AU - Al-Hassan, Suha M AU - Bacchini, Dario AU - Bombi, Anna Silvia AD - Child and Family Research, National Institute of Child Health and Human Development, National Institutes of Health, Public Health Service, Bethesda, MD, USA Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 191 EP - 223 PB - Sage Publications, Thousand Oaks CA VL - 46 IS - 3 SN - 1069-3971, 1069-3971 KW - parenting acceptance rejection culture KW - Peoples Republic of China KW - Kenya KW - Thailand KW - Mothers KW - Child Neglect KW - Children KW - Fathers KW - Italy KW - Sweden KW - article KW - 0513: culture and social structure; culture (kinship, forms of social organization, social cohesion & integration, & social representations) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1283639632?accountid=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=Cross-Cultural+Research&rft.atitle=Agreement+in+Mother+and+Father+Acceptance-Rejection%2C+Warmth%2C+and+Hostility%2FRejection%2F+Neglect+of+Children+Across+Nine+Countries&rft.au=Putnick%2C+Diane+L%3BBornstein%2C+Marc+H%3BLansford%2C+Jennifer+E%3BChang%2C+Lei%3BDeater-Deckard%2C+Kirby%3BDi+Giunta%2C+Laura%3BGurdal%2C+Sevtap%3BDodge%2C+Kenneth+A%3BMalone%2C+Patrick+S%3BOburu%2C+Paul+O%3BPastorelli%2C+Concetta%3BSkinner%2C+Ann+T%3BSorbring%2C+Emma%3BTapanya%2C+Sombat%3BTirado%2C+Liliana+Maria+Uribe%3BZelli%2C+Arnaldo%3BAlampay%2C+Liane+Pena%3BAl-Hassan%2C+Suha+M%3BBacchini%2C+Dario%3BBombi%2C+Anna+Silvia&rft.aulast=Putnick&rft.aufirst=Diane&rft.date=2012-08-01&rft.volume=46&rft.issue=3&rft.spage=191&rft.isbn=&rft.btitle=&rft.title=Cross-Cultural+Research&rft.issn=10693971&rft_id=info:doi/10.1177%2F1069397112440931 LA - English DB - Sociological Abstracts N1 - Date revised - 2013-02-01 N1 - Last updated - 2016-09-28 N1 - CODEN - CRCRE4 N1 - SubjectsTermNotLitGenreText - Mothers; Sweden; Peoples Republic of China; Fathers; Italy; Child Neglect; Children; Kenya; Thailand DO - http://dx.doi.org/10.1177/1069397112440931 ER - TY - JOUR T1 - Comparability and repeatability of methods for estimating the dietary intake of the heterocyclic amine contaminant 2-amino-1-methyl-6-phenylimidazo[4,5b]pyridine (PhIP) AN - 1268653915; 17485824 AB - Inconsistent risk estimates for dietary heterocyclic amine (HCA) exposure and cancers may be due to differences in exposure assessment methods and the associated measurement error. We evaluated repeatability and comparability of intake estimates of the HCA 2-amino-1-methyl-6-phenylimidazo[4,5b]pyridine (PhIP) among two food frequency questionnaire (FFQ) collections, three diary collections, and three measurements of urinary PhIP and its metabolites in 36 non-smokers in Baltimore, Maryland, during 2004-2005. Collections spanned similar to 9 months. Method repeatability was characterised with intraclass correlation coefficients (ICCs). Comparability among methods was assessed with Spearman correlation coefficients. Within-subject variability in PhIP intake was comparably high across all methods (ICCs of 0.20, 0.30, and 0.15 for FFQ, diary, and creatinine-adjusted urinary PhIP, respectively). Mean diary-based PhIP intake and mean urinary PhIP concentration were strongly correlated when restricting the analysis to participants with at least one non-zero diary-based estimate of PhIP intake (n = 15, r = 0.75, p = 0.001), but not in the full study population (n = 36, r = 0.18, p = 0.28). Mean PhIP intake from the FFQ was not associated with that either based on the diary or urinary PhIP separately, but was modestly correlated with a metric that combined the diary- and biomarker-based approaches (r = 0.30, p = 0.08). The high within-subject variability will result in significantly attenuated associations if a single measure is used to estimate exposure within an epidemiologic study. Improved HCA assessment tools, such as a combination of methods or validated biomarkers that capture long term exposure, are needed. JF - Food Additives & Contaminants: Part A - Chemistry, Analysis, Control, Exposure & Risk Assessment AU - Deziel, Nicole C AU - Buckley, Timothy J AU - Sinha, Rashmi AU - Abubaker, Salahaddhin AU - Platz, Elizabeth A AU - Strickland, Paul T AD - Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe St., Baltimore, MD, USA, dezielnc@mail.nih.gov Y1 - 2012/08/01/ PY - 2012 DA - 2012 Aug 01 SP - 1202 EP - 1211 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 29 IS - 8 SN - 1944-0049, 1944-0049 KW - Pollution Abstracts; Risk Abstracts; Health & Safety Science Abstracts KW - Amines KW - Bioindicators KW - Cancer KW - Contaminants KW - Diets KW - Food additives KW - Metabolites KW - Risk assessment KW - Urine KW - USA, Maryland, Baltimore KW - P 9999:GENERAL POLLUTION KW - R2 23060:Medical and environmental health KW - H 12000:Epidemiology and Public Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1268653915?accountid=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=Food+Additives+%26+Contaminants%3A+Part+A+-+Chemistry%2C+Analysis%2C+Control%2C+Exposure+%26+Risk+Assessment&rft.atitle=Comparability+and+repeatability+of+methods+for+estimating+the+dietary+intake+of+the+heterocyclic+amine+contaminant+2-amino-1-methyl-6-phenylimidazo%5B4%2C5b%5Dpyridine+%28PhIP%29&rft.au=Deziel%2C+Nicole+C%3BBuckley%2C+Timothy+J%3BSinha%2C+Rashmi%3BAbubaker%2C+Salahaddhin%3BPlatz%2C+Elizabeth+A%3BStrickland%2C+Paul+T&rft.aulast=Deziel&rft.aufirst=Nicole&rft.date=2012-08-01&rft.volume=29&rft.issue=8&rft.spage=1202&rft.isbn=&rft.btitle=&rft.title=Food+Additives+%26+Contaminants%3A+Part+A+-+Chemistry%2C+Analysis%2C+Control%2C+Exposure+%26+Risk+Assessment&rft.issn=19440049&rft_id=info:doi/10.1080%2F19440049.2012.682657 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-01-01 N1 - Last updated - 2013-02-08 N1 - SubjectsTermNotLitGenreText - Risk assessment; Diets; Bioindicators; Food additives; Urine; Metabolites; Contaminants; Amines; Cancer; USA, Maryland, Baltimore DO - http://dx.doi.org/10.1080/19440049.2012.682657 ER - TY - JOUR T1 - Accelerometer-based measures of active and sedentary behavior in relation to breast cancer risk AN - 1113239924; 17187157 AB - Epidemiologic studies suggest that physical activity reduces breast cancer risk by 20-40 %. However, prior studies have relied on measures of self-report. In a population-based case-control study, we evaluated accelerometer measures of active and sedentary behavior in relation to breast cancer among 996 incident cases and 1,164 controls, residents of Warsaw, Poland (2000-2003), who were asked to wear an accelerometer for 7 days. Accelerometer values were averaged across valid wear days and summarized as overall activity (counts [ct]/min/day); in minutes spent in sedentary behavior (0-99 ct/min); and light (100-759 ct/min) and moderate-to-vigorous (760+ ct/min) activity. Odds ratios (OR) and 95 % confidence intervals (CI) were estimated using unconditional logistic regression. Comparing women in the highest quartile (Q4) of activity to those in the lowest (Q1), time spent in moderate-to-vigorous activity was inversely associated with breast cancer odds after adjustment for known risk factors, sedentary behavior and wear time (OR sub(Q4vsQ1) 0.39, 95 % CI 0.27-0.56; P-trend < .0001). Sedentary time was positively associated with breast cancer, independent of moderate-to-vigorous activity (OR sub(Q4vsQ1) 1.81, 95 % CI 1.26-2.60; P-trend = 0.001). Light activity was not associated with breast cancer in multivariable models including both moderate-to-vigorous activity and sedentary behavior. Our findings support an inverse association between accelerometer-based measures of moderate-to-vigorous physical activity and breast cancer while also suggesting potential increases in risk with sedentary time. JF - Breast Cancer Research and Treatment AU - Dallal, Cher M AU - Brinton, Louise A AU - Matthews, Charles E AU - Lissowska, Jolanta AU - Peplonska, Beata AU - Hartman, Terryl J AU - Gierach, Gretchen L AD - Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA, cher.dallal@nih.gov Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - 1279 EP - 1290 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 134 IS - 3 SN - 0167-6806, 0167-6806 KW - Health & Safety Science Abstracts KW - Behavior KW - Breast cancer KW - Cancer KW - Physical activity KW - Risk factors KW - Wear KW - accelerometers KW - Poland KW - H 11000:Diseases/Injuries/Trauma UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1113239924?accountid=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=Breast+Cancer+Research+and+Treatment&rft.atitle=Accelerometer-based+measures+of+active+and+sedentary+behavior+in+relation+to+breast+cancer+risk&rft.au=Dallal%2C+Cher+M%3BBrinton%2C+Louise+A%3BMatthews%2C+Charles+E%3BLissowska%2C+Jolanta%3BPeplonska%2C+Beata%3BHartman%2C+Terryl+J%3BGierach%2C+Gretchen+L&rft.aulast=Dallal&rft.aufirst=Cher&rft.date=2012-08-01&rft.volume=134&rft.issue=3&rft.spage=1279&rft.isbn=&rft.btitle=&rft.title=Breast+Cancer+Research+and+Treatment&rft.issn=01676806&rft_id=info:doi/10.1007%2Fs10549-012-2129-y LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2012-11-20 N1 - SubjectsTermNotLitGenreText - Behavior; Risk factors; Physical activity; accelerometers; Breast cancer; Wear; Cancer; Poland DO - http://dx.doi.org/10.1007/s10549-012-2129-y ER - TY - JOUR T1 - The policy impact on clean technology diffusion AN - 1113221933; 17216599 AB - We employ a logistic model to examine the impacts of environmental policy (emission standards and economic instruments) and plant characteristics on clean technology diffusion by using the amount of total suspended particulate (TSP), sulfur oxide (SO sub(x)), and nitric oxide (NO sub(x)) emissions in 14 power plants provided by Taiwan Power Company covering the period of 1989-2006. The concentration of the pollutants emitted to air from fossil-fired power plants is modeled as the performance of technology development. The objective of this study is to investigate the determinants of technology diffusion to help generate strategic insights on environmental policy. The results show that the environmental policy by regulating emission standard provides a negative effect on technology diffusion while the 'mixed policy' (an integration of environmental standards and economic instruments) has a significantly positive effect on technology diffusion for NO sub(x) but insignificantly for TSP and SO sub(x). JF - Clean Technologies and Environmental Policy AU - Chen, Yi-Tui AU - Chang, Dong-Shang AU - Chen, Chia-Yon AU - Chen, Chu-Chieh AD - Department of Health Care Management, National Taipei University of Nursing and Health Sciences, 89, Nei-Chiang St., Wan-Hua Dist., Taipei, Taiwan, ROC, yitui@ntunhs.edu.tw Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - 699 EP - 708 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 14 IS - 4 SN - 1618-954X, 1618-954X KW - Sustainability Science Abstracts KW - Sulfur oxides KW - Taiwan KW - Economics KW - Emission standards KW - Power plants KW - Emissions KW - Diffusion KW - Suspended particulate matter KW - Environmental policy KW - Technology KW - M3 1010:Issues in Sustainable Development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1113221933?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Assamodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clean+Technologies+and+Environmental+Policy&rft.atitle=The+policy+impact+on+clean+technology+diffusion&rft.au=Chen%2C+Yi-Tui%3BChang%2C+Dong-Shang%3BChen%2C+Chia-Yon%3BChen%2C+Chu-Chieh&rft.aulast=Chen&rft.aufirst=Yi-Tui&rft.date=2012-08-01&rft.volume=14&rft.issue=4&rft.spage=699&rft.isbn=&rft.btitle=&rft.title=Clean+Technologies+and+Environmental+Policy&rft.issn=1618954X&rft_id=info:doi/10.1007%2Fs10098-011-0435-4 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Sulfur oxides; Economics; Emissions; Power plants; Emission standards; Diffusion; Suspended particulate matter; Environmental policy; Technology; Taiwan DO - http://dx.doi.org/10.1007/s10098-011-0435-4 ER - TY - JOUR T1 - Interacting epidemics? Sleep curtailment, insulin resistance, and obesity AN - 1082215183; 17084036 AB - In the last 50 years, the average self-reported sleep duration in the United States has decreased by 1.5-2 hours in parallel with an increasing prevalence of obesity and diabetes. Epidemiological studies and meta-analyses report a strong relationship between short or disturbed sleep, obesity, and abnormalities in glucose metabolism. This relationship is likely to be bidirectional and causal in nature, but many aspects remain to be elucidated. Sleep and the internal circadian clock influence a host of endocrine parameters. Sleep curtailment in humans alters multiple metabolic pathways, leading to more insulin resistance, possibly decreased energy expenditure, increased appetite, and immunological changes. On the other hand, psychological, endocrine, and anatomical abnormalities in individuals with obesity and/or diabetes can interfere with sleep duration and quality, thus creating a vicious cycle. In this review, we address mechanisms linking sleep with metabolism, highlight the need for studies conducted in real-life settings, and explore therapeutic interventions to improve sleep, with a potential beneficial effect on obesity and its comorbidities. JF - Annals of the New York Academy of Sciences AU - Lucassen, Eliane A AU - Rother, Kristina I AU - Cizza, Giovanni AD - Immunogenetics Section, Clinical Center, National Institutes of Health, Bethesda, Maryland. Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - 110 EP - 134 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 1264 IS - 1 SN - 0077-8923, 0077-8923 KW - Solid State and Superconductivity Abstracts (SO); Environmental Engineering Abstracts (EN); Electronics and Communications Abstracts (EA) KW - Abnormalities KW - Diabetes KW - Expenditures KW - Glucose KW - Insulin KW - Metabolism KW - Obesity KW - Sleep UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1082215183?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvironmentalengabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+the+New+York+Academy+of+Sciences&rft.atitle=Interacting+epidemics%3F+Sleep+curtailment%2C+insulin+resistance%2C+and+obesity&rft.au=Lucassen%2C+Eliane+A%3BRother%2C+Kristina+I%3BCizza%2C+Giovanni&rft.aulast=Lucassen&rft.aufirst=Eliane&rft.date=2012-08-01&rft.volume=1264&rft.issue=1&rft.spage=110&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/10.1111%2Fj.1749-6632.2012.06655.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Document feature - figure 3 N1 - Last updated - 2012-10-04 DO - http://dx.doi.org/10.1111/j.1749-6632.2012.06655.x ER - TY - JOUR T1 - Structure of major depressive disorder in adolescents and adults in the US general population AN - 1081895595; 201224643 AB - Background: Although techniques such as latent class analysis have been used to derive empirically based subtypes of depression in adult samples, there is limited information on subtypes of depression in youth. Aims: To identify empirically based subtypes of depression in a nationally representative sample of US adolescents, and to test the comparability of subtypes of depression in adolescents with those derived from a nationally representative sample of adults. Method: Respondents included 912 adolescents and 805 adults with a 12-month major depressive disorder, selected from the National Comorbidity Survey Adolescent Supplement and the National Comorbidity Survey Replication samples respectively. Latent class analysis was used to identify subtypes of depression across samples. Sociodemographic and clinical correlates of derived subtypes were also examined to establish their validity. Results: Three subtypes of depression were identified among adolescents, whereas four subtypes were identified among adults. Two of these subtypes displayed similar diagnostic profiles across adolescent and adult samples (P = 0.43); these subtypes were labelled 'severe typical' (adults 45%, adolescents 35%) and 'atypical' (adults 16%, adolescents 26%). The latter subtype was characterised by increased appetite and weight gain. Conclusions: The structure of depression observed in adolescents is highly similar to the structure observed in adults. Longitudinal research is necessary to evaluate the stability of these subtypes of depression across development. Declaration of interest: None. Adapted from the source document. JF - The British Journal of Psychiatry AU - Lamers, Femke AU - Burstein, Marcy AU - He, Jian-ping AU - Avenevoli, Shelli AU - Angst, Jules AU - Merikangas, Kathleen R AD - National Institutes of Health, National Institute of Mental Health, 35 Convent Drive, MSC 3720. Bethesda, MD 20892-3720, USA Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 143 EP - 150 PB - Royal College of Psychiatrists, London UK VL - 201 IS - 2 SN - 0007-1250, 0007-1250 KW - Depressive personality disorders KW - Depression KW - Latent class analysis KW - Subtypes KW - Weight gain KW - Declarations KW - Eating behaviour KW - Comorbidity KW - Adolescents KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1081895595?accountid=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+British+Journal+of+Psychiatry&rft.atitle=Structure+of+major+depressive+disorder+in+adolescents+and+adults+in+the+US+general+population&rft.au=Lamers%2C+Femke%3BBurstein%2C+Marcy%3BHe%2C+Jian-ping%3BAvenevoli%2C+Shelli%3BAngst%2C+Jules%3BMerikangas%2C+Kathleen+R&rft.aulast=Lamers&rft.aufirst=Femke&rft.date=2012-08-01&rft.volume=201&rft.issue=2&rft.spage=143&rft.isbn=&rft.btitle=&rft.title=The+British+Journal+of+Psychiatry&rft.issn=00071250&rft_id=info:doi/10.1192%2Fbjp.bp.111.098079 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-10-01 N1 - Last updated - 2016-09-27 N1 - CODEN - BJPYAJ N1 - SubjectsTermNotLitGenreText - Subtypes; Adolescents; Depression; Latent class analysis; Comorbidity; Depressive personality disorders; Eating behaviour; Declarations; Weight gain DO - http://dx.doi.org/10.1192/bjp.bp.111.098079 ER - TY - JOUR T1 - Cooking with biomass increases the risk of depression in pre-menopausal women in India AN - 1074665536; 4338290 AB - Cooking with biomass fuel, a common practice in rural India, is associated with a high level of indoor air pollution (IAP). The aim of this study was to investigate whether IAP from biomass burning increases the risk of depression. For this cross-sectional study, we enrolled a group of 952 women (median age 37 years) who cooked regularly with biomass and a control group of 804 age-matched women who cooked with cleaner fuel (liquefied petroleum gas). Depression was assessed using the second edition of Beck's depression inventory (BDI-II). Platelet P-selectin expression was assessed by flow cytometry and platelet serotonin was measured by ELISA. Particulate matter having diameter of less than 10 and 2.5 @mm (PM'1'0 and PM'2'.'5, respectively) in indoor air was measured by real-time aerosol monitor. Carbon monoxide (CO) in exhaled breath was measured by CO monitor. Compared with the control group, women who cooked with biomass had a higher prevalence of depression and depleted platelet serotonin, suggesting altered serotonergic activity in the brain. In addition, P-selectin expression on platelet surface was up-regulated implying platelet hyperactivity and consequent risk of cardiovascular disease. Biomass-using households had increased levels of PM'1'0 and PM'2'.'5, and biomass users had elevated levels of CO in expired air. Controlling potential confounders, cooking with biomass was found to be an independent and strong risk factor for depression. IAP from cooking with biomass is a risk for depression among rural women in their child-bearing age. All rights reserved, Elsevier JF - Social science and medicine AU - Banerjee, M AU - Siddique, S AU - Dutta, A AU - Mukherjee, B AU - Ray, Manas Ranjan AD - Chittaranjan National Cancer Institute Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - 565 EP - 572 VL - 75 IS - 3 SN - 0277-9536, 0277-9536 KW - Sociology KW - Anthropology KW - Depression KW - Women's health KW - Cooking KW - Mental health KW - Biofuels KW - India UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1074665536?accountid=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=Social+science+and+medicine&rft.atitle=Cooking+with+biomass+increases+the+risk+of+depression+in+pre-menopausal+women+in+India&rft.au=Banerjee%2C+M%3BSiddique%2C+S%3BDutta%2C+A%3BMukherjee%2C+B%3BRay%2C+Manas+Ranjan&rft.aulast=Banerjee&rft.aufirst=M&rft.date=2012-08-01&rft.volume=75&rft.issue=3&rft.spage=565&rft.isbn=&rft.btitle=&rft.title=Social+science+and+medicine&rft.issn=02779536&rft_id=info:doi/10.1016%2Fj.socscimed.2012.03.021 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2013-06-12 N1 - Last updated - 2013-09-16 N1 - SubjectsTermNotLitGenreText - 2854 5129; 3439 4196 7951 6220 7954; Biofuels; 13609 5772; 7947 5772 7954; 175 387 30 DO - http://dx.doi.org/10.1016/j.socscimed.2012.03.021 ER - TY - JOUR T1 - The electronic scientific portfolio assistant: integrating scientific knowledge databases to support program impact assessment AN - 1074653610; 4341853 AB - The US National Institutes of Health (NIH) supports basic and applied biomedical research by funding grants and contracts. To measure the outcomes and impact of their programs, NIH staff conduct program evaluations and undertake targeted investigations of research portfolios. Recently, the NIH launched the electronic scientific portfolio assistant (eSPA), a web-based analytics system based on linked scientific databases that provides quantitative information for program officers and planning and evaluation officials managing research portfolios. This system has improved the ability to create and collaboratively refine research portfolios, has reduced the time needed to collect and link outcomes data such as publications and patents, and is providing information used to support research management decisions. After describing the eSPA system, we provide examples of three eSPA evaluation projects that illustrate the impact of this system on NIH evaluation objectives. Reproduced by permission of Bibliothèque de Sciences Po JF - Problèmes d'Amérique latine AU - Haak, Laurel L AU - Ferriss, Will AU - Wright, Kevin AU - Pollard, Michael E AU - Barden, Kirk AU - Probus, Matt A AU - Tartakovsky, Michael AU - Hackett, Charles J AD - National Institutes of Health Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - 464 EP - 475 VL - 39 IS - 4 SN - 0765-1333, 0765-1333 KW - Economics KW - Databases KW - Medical research KW - Biomedicine KW - Planning methods KW - U.S.A. KW - Information and communication technologies KW - Science and technology KW - Programme evaluation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1074653610?accountid=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=Probl%C3%A8mes+d%27Am%C3%A9rique+latine&rft.atitle=The+electronic+scientific+portfolio+assistant%3A+integrating+scientific+knowledge+databases+to+support+program+impact+assessment&rft.au=Haak%2C+Laurel+L%3BFerriss%2C+Will%3BWright%2C+Kevin%3BPollard%2C+Michael+E%3BBarden%2C+Kirk%3BProbus%2C+Matt+A%3BTartakovsky%2C+Michael%3BHackett%2C+Charles+J&rft.aulast=Haak&rft.aufirst=Laurel&rft.date=2012-08-01&rft.volume=39&rft.issue=4&rft.spage=464&rft.isbn=&rft.btitle=&rft.title=Probl%C3%A8mes+d%27Am%C3%A9rique+latine&rft.issn=07651333&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 - 11326 11325 12622; 3291 3286; 1618 7894; 7886 10902; 10319 4551; 6518; 9560; 433 293 14 ER - TY - JOUR T1 - Leiomyoma: genetics, assisted reproduction, pregnancy and therapeutic advances AN - 1069202949; 17156898 AB - Purpose: Uterine leiomyomas are common, benign, reproductive tract tumors affecting a majority of reproductive aged women. They are associated with gynecologic morbidity and detrimentally affect reproductive potential. The etiology of leiomyomas is poorly understood and their diagnosis prior to treatment with Assisted Reproductive Technologies (ART) represents a management dilemma. The purpose of this paper is to review known genetic and molecular contributions to the etiologies of leiomyomas, describe their impact on ART outcomes and reproductive potential, and review alternative therapies and future directions in management. Methods: A critical review of the literature pertaining to genetic component of uterine leiomyomas, their impact on ART and pregnancy and leiomyoma therapeutics was performed. Results: Uterine leiomyomas are characterized by complex molecular mechanisms. Their location and size determines their potential detriment to ART and reproductive function and novel therapeutic modalities are being developed. Conclusion: The high prevalence of uterine leiomyomas and their potential detrimental influence on ART and reproductive function warrants continued well-designed studies to ascertain their etiology, optimal treatment and novel less morbid therapies. JF - Journal of Assisted Reproduction and Genetics AU - Levy, Gary AU - Hill, Micah J AU - Beall, Stephanie AU - Zarek, Shvetha M AU - Segars, James H AU - Catherino, William H AD - Program in Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institute of Health, Bethesda, MD, USA, gary.levy@nih.gov Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - 703 EP - 712 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 29 IS - 8 SN - 1058-0468, 1058-0468 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Molecular modelling KW - Uterus KW - Etiology KW - Literature reviews KW - Reviews KW - Reproduction KW - Tumors KW - Morbidity KW - Reproductive system KW - Pregnancy KW - Benign KW - W 30900:Methods KW - G 07700:Molecular Genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1069202949?accountid=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+Assisted+Reproduction+and+Genetics&rft.atitle=Leiomyoma%3A+genetics%2C+assisted+reproduction%2C+pregnancy+and+therapeutic+advances&rft.au=Levy%2C+Gary%3BHill%2C+Micah+J%3BBeall%2C+Stephanie%3BZarek%2C+Shvetha+M%3BSegars%2C+James+H%3BCatherino%2C+William+H&rft.aulast=Levy&rft.aufirst=Gary&rft.date=2012-08-01&rft.volume=29&rft.issue=8&rft.spage=703&rft.isbn=&rft.btitle=&rft.title=Journal+of+Assisted+Reproduction+and+Genetics&rft.issn=10580468&rft_id=info:doi/10.1007%2Fs10815-012-9784-0 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-09-01 N1 - Last updated - 2013-05-31 N1 - SubjectsTermNotLitGenreText - Molecular modelling; Etiology; Uterus; Literature reviews; Reviews; Reproduction; Tumors; Reproductive system; Morbidity; Benign; Pregnancy DO - http://dx.doi.org/10.1007/s10815-012-9784-0 ER - TY - JOUR T1 - Sedentary behavior and health: A view from the National Institutes of Health-American Association of Retired Persons diet and health study AN - 1038615885; 17069725 AB - Older adults in Western countries routinely spend 60 to 70 hours or more each week in sedentary behaviors (i.e., sitting), and it appears that a few hours of exercise each week may not be sufficient to provide complete protection against the adverse health effects associated with so much sitting. However, our understanding of the full range of health/disease outcomes associated with prolonged sitting remains incomplete. In the mid-1990's The National Institutes of Health American Association of Retired Persons (NIH-AARP) Diet and Health Study enrolled more than 500,000 US adults aged 50 to 71 years into the study and it has followed their health since that time. It is among the largest prospective studies investigating the relation between time spent in sedentary behaviors and health in older adults. New results from the NIH-AARP Study will be presented evaluating the role of sedentary behaviors and all-cause, cardiovascular, and cancer mortality. In addition, study results for several incident cancers will be examined. The findings from our study and others continue to provide new insight into the range of disease outcomes that have been linked to large amounts of sedentary behavior in older adults, but many questions remain unresolved. At what level (or amount) of sedentary behavior does the risk for chronic disease increase? How much, what type, and what patterns of physical activity are effective in minimizing risks associated with too much sitting? The opportunities for answering these etiologic questions and addressing future measurement challenges will be discussed. JF - Journal of Aging and Physical Activity AU - Matthews, CE AD - Division of Cancer Epidemiology and Genetics, Nutritional Epidemiology Branch, National Cancer Institute, United States Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - S300 EP - S301 VL - 20 SN - 1063-8652, 1063-8652 KW - Physical Education Index KW - Adults KW - Behavior KW - Cancer KW - Diseases KW - Exercise KW - Gerontology KW - Health KW - Health (behavior) KW - Sitting KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1038615885?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Aging+and+Physical+Activity&rft.atitle=Sedentary+behavior+and+health%3A+A+view+from+the+National+Institutes+of+Health-American+Association+of+Retired+Persons+diet+and+health+study&rft.au=Matthews%2C+CE&rft.aulast=Matthews&rft.aufirst=CE&rft.date=2012-08-01&rft.volume=20&rft.issue=&rft.spage=S300&rft.isbn=&rft.btitle=&rft.title=Journal+of+Aging+and+Physical+Activity&rft.issn=10638652&rft_id=info:doi/ LA - English DB - Physical Education Index N1 - Date revised - 2012-09-01 N1 - Last updated - 2012-10-08 N1 - SubjectsTermNotLitGenreText - Behavior; Gerontology; Health (behavior); Health; Diseases; Exercise; Sitting; Adults; Cancer ER - TY - JOUR T1 - Patterns of adolescent bullying behaviors: Physical, verbal, exclusion, rumor, and cyber AN - 1038112491; 201223731 AB - Patterns of engagement in cyber bullying and four types of traditional bullying were examined using latent class analysis (LCA). Demographic differences and externalizing problems were evaluated across latent class membership. Data were obtained from the 2005-2006 Health Behavior in School-aged Survey and the analytic sample included 7,508 U.S. adolescents in grades 6 through 10. LCA models were tested on physical bullying, verbal bullying, social exclusion, spreading rumors, and cyber bullying behaviors. Three latent classes were identified for each gender: All-Types Bullies (10.5% for boys and 4.0% for girls), Verbal/Social Bullies (29.3% for boys and 29.4% for girls), and a Non-Involved class (60.2% for boys and 66.6% for girls). Boys were more likely to be All-Types Bullies than girls. The prevalence rates of All-Types and Verbal/Social Bullies peaked during grades 6 to 8 and grades 7 and 8, respectively. Pairwise comparisons across the three latent classes on externalizing problems were conducted. Overall, the All-Types Bullies were at highest risk of using substances and carrying weapons, the Non-Involved were at lowest risk, and the Verbal/Social Bullies were in the middle. Results also suggest that most cyber bullies belong to a group of highly aggressive adolescents who conduct all types of bullying. This finding does not only improve our understanding of the relation between cyber bullying and traditional bullying, but it also suggests that prevention and intervention efforts could target cyber bullies as a high-risk group for elevated externalizing problems. [Copyright the Society for the Study of School Psychology; published by Elsevier Ltd.] JF - Journal of School Psychology AU - Wang, Jing AU - Iannotti, Ronald J AU - Luk, Jeremy W AD - Glotech, Inc., Division of Epidemiology, Statistics & Prevention Research, Eunice Kennedy Shriver National Institute of Child Health & Human Development, 6100 Building Room 7B13 MSC 7510, Bethesda, MD 20892-7510, United States, Tel: + 1 301 451 3420, Fax: + 1 301 402 2084 wangji2@mail.nih.gov Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 521 EP - 534 PB - Elsevier Science, Amsterdam The Netherlands VL - 50 IS - 4 SN - 0022-4405, 0022-4405 KW - Bullying, Cyber bullying, Demographic differences, Externalizing problems, Latent class analysis KW - Latent class analysis KW - Aggression KW - Externalizing problems KW - Adolescents KW - Bullying KW - Prevalence KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1038112491?accountid=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+School+Psychology&rft.atitle=Patterns+of+adolescent+bullying+behaviors%3A+Physical%2C+verbal%2C+exclusion%2C+rumor%2C+and+cyber&rft.au=Wang%2C+Jing%3BIannotti%2C+Ronald+J%3BLuk%2C+Jeremy+W&rft.aulast=Wang&rft.aufirst=Jing&rft.date=2012-08-01&rft.volume=50&rft.issue=4&rft.spage=521&rft.isbn=&rft.btitle=&rft.title=Journal+of+School+Psychology&rft.issn=00224405&rft_id=info:doi/10.1016%2Fj.jsp.2012.03.004 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-09-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JSCPAA N1 - SubjectsTermNotLitGenreText - Bullying; Externalizing problems; Adolescents; Aggression; Latent class analysis; Prevalence DO - http://dx.doi.org/10.1016/j.jsp.2012.03.004 ER - TY - JOUR T1 - The influence of emotional stimuli on attention orienting and inhibitory control in pediatric anxiety AN - 1038111216; 201223126 AB - Background: Anxiety disorders are highly prevalent in children and adolescents, and are associated with aberrant emotion-related attention orienting and inhibitory control. While recent studies conducted with high-trait anxious adults have employed novel emotion-modified antisaccade tasks to examine the influence of emotional information on orienting and inhibition, similar studies have yet to be conducted in youths. Methods: Participants were 22 children/adolescents diagnosed with an anxiety disorder, and 22 age-matched healthy comparison youths. Participants completed an emotion-modified antisaccade task that was similar to those used in studies of high-trait anxious adults. This task probed the influence of abruptly appearing neutral, happy, angry, or fear stimuli on orienting (prosaccade) or inhibitory (antisaccade) responses. Results: Anxious compared to healthy children showed facilitated orienting toward angry stimuli. With respect to inhibitory processes, threat-related information improved antisaccade accuracy in healthy but not anxious youth. These findings were not linked to individual levels of reported anxiety or specific anxiety disorders. Conclusions: Findings suggest that anxious relative to healthy children manifest enhanced orienting toward threat-related stimuli. In addition, the current findings suggest that threat may modulate inhibitory control during adolescent development. Adapted from the source document. JF - The Journal of Child Psychology and Psychiatry AU - Mueller, Sven C AU - Hardin, Michael G AU - Mogg, Karin AU - Benson, Valerie AU - Bradley, Brendan P AU - Reinholdt-Dunne, Marie Louise AU - Liversedge, Simon P AU - Pine, Daniel S AU - Ernst, Monique AD - Section of Developmental and Affective Neuroscience, National Institute of Mental Health, Bethesda, MD, USA Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 856 EP - 863 PB - Blackwell Publishing, Oxford UK VL - 53 IS - 8 SN - 0021-9630, 0021-9630 KW - Anxiety disorders KW - Inhibitory processes KW - Antisaccade task KW - Children KW - Anger KW - Adolescents KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1038111216?accountid=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=The+influence+of+emotional+stimuli+on+attention+orienting+and+inhibitory+control+in+pediatric+anxiety&rft.au=Mueller%2C+Sven+C%3BHardin%2C+Michael+G%3BMogg%2C+Karin%3BBenson%2C+Valerie%3BBradley%2C+Brendan+P%3BReinholdt-Dunne%2C+Marie+Louise%3BLiversedge%2C+Simon+P%3BPine%2C+Daniel+S%3BErnst%2C+Monique&rft.aulast=Mueller&rft.aufirst=Sven&rft.date=2012-08-01&rft.volume=53&rft.issue=8&rft.spage=856&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Child+Psychology+and+Psychiatry&rft.issn=00219630&rft_id=info:doi/10.1111%2Fj.1469-7610.2012.02541.x LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-09-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JPPDAI N1 - SubjectsTermNotLitGenreText - Anxiety disorders; Inhibitory processes; Children; Adolescents; Antisaccade task; Anger DO - http://dx.doi.org/10.1111/j.1469-7610.2012.02541.x ER - TY - JOUR T1 - RECONSTRUCTION OF OCCUPATIONAL EXPOSURE FROM HISTORICAL NUCLEAR MEDICINE PROCEDURES AN - 1032892775; 16966735 AB - A long-term follow-up and cancer risk analysis of a cohort of about 130,000 U.S. radiologic technologists (USRT) is underway at the National Cancer Institute. To evaluate cancer risk in the USRT cohort due to radiation exposure, occupational doses need to be reconstructed for the technologists who worked throughout the 20th century beginning as early as the 1920's. One component of occupational exposure is from conducting radioisotope procedures. An extensive literature review was conducted to evaluate doses from the 1950's onwards. Very limited information was found on occupational exposure from conducting radioisotope procedures from the 1950's until the mid-1970's. To collect historical data needed to reconstruct doses to personnel, a focus-group meeting was conducted with experts who began using radioisotopes in medicine in the 1950's and the 1960's. The focus group discussed the typical protocols most frequently used diagnostic radioisotope procedures including radiopharmaceuticals used for each examination, administered activities, mode of administration, and time spent either in close contact or at different distances from patients. Standard protocols were used to reconstruct occupational doses received by personnel from diagnostic radioisotopes procedures conducted in the 1950's to 1960's and from the same procedures conducted starting the mid-1960's with super(99m)Tc. Air kerma rates as a function of distance from a hybrid phantom simulating a reference patient who was administered radiopharmaceuticals were estimated by Monte Carlo radiation transport calculations. The radioisotope activities in the organs of the reference patient were calculated using the biokinetic models described in ICRP Publication 53. Doses per procedure on the surface of technologist's body in the abdomen area were found to vary from less than 0.05 mu Gy (thyroid scan with 1.85 MBq of administered super(131)I iodide) to 0.3 mu Gy (brain scan with 26 MBq of super(203)Hg). Comparison with doses calculated for the same procedures conducted with super(99m)Tc shows that the introduction of super(99m)Tc in the mid-1960's resulted in an increase in occupational doses per procedure. The results of this study are being used in the USRT study to supplement the occupational doses resulting from radiographic and fluoroscopic procedures, which are estimated in a parallel study. JF - Health Physics AU - Drozdovitch, V AU - Lee, C AU - Bouville, A AU - Linet, M AU - Melo, D AU - Simon, S AD - National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - S32 EP - S33 PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States VL - 103 IS - 2 SN - 0017-9078, 0017-9078 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Historical account KW - Iodides KW - USA KW - Risk analysis KW - Literature reviews KW - Radioisotopes KW - Brain KW - Organs KW - Cancer KW - Occupational exposure KW - H 1000:Occupational Safety and Health KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1032892775?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Physics&rft.atitle=RECONSTRUCTION+OF+OCCUPATIONAL+EXPOSURE+FROM+HISTORICAL+NUCLEAR+MEDICINE+PROCEDURES&rft.au=Drozdovitch%2C+V%3BLee%2C+C%3BBouville%2C+A%3BLinet%2C+M%3BMelo%2C+D%3BSimon%2C+S&rft.aulast=Drozdovitch&rft.aufirst=V&rft.date=2012-08-01&rft.volume=103&rft.issue=2&rft.spage=S32&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-08-01 N1 - Last updated - 2013-08-12 N1 - SubjectsTermNotLitGenreText - Iodides; Historical account; Risk analysis; Literature reviews; Brain; Radioisotopes; Organs; Occupational exposure; Cancer; USA ER - TY - JOUR T1 - RISK OF THYROID CANCER AFTER ADULT RADIATION EXPOSURE: TIME TO REASSESS? AN - 1032892743; 16966732 AB - The recent disaster at the Fukushima Daiichi nuclear power plant complex re-alerted the world to the possibility that large groups of people can be exposed to super(131)I. Additionally, that accident has reminded us that it is important to understand the effect of age at exposure on cancer risk in order to develop effective radiation protection policies as well as to appropriately plan for responses to future nuclear accidents or terrorist events involving release of radioactivity. It is widely accepted that the thyroid gland is an organ at considerable risk for developing cancer after radiation exposure, particularly when exposure occurs during childhood. Moreover, the thyroid has been established as one of the most sensitive organs to radiation exposure, with convincing evidence for cancer risk at as low as about 0.10 Gy. However, it is widely believed that the risk of thyroid cancer following radiation exposure is markedly decreased among those exposed as an adult. Contradictory to this view regarding the risk from adult exposure, there are findings from several published health risk studies that suggest that the risk of thyroid cancer following adult exposure may not be as small as many believe. The purpose of this presentation is to bring to light the accumulated evidence from eight studies published over the last 24 years that suggest substantial risk following exposure as an adult. These studies include cohorts exposed in occupational, medical, and public settings in a dose range from 0.07 to 0.6 Gy, a range very relevant to many radiation protection situations and activities. When viewed alone, none of those studies are completely convincing and, when viewed together, there is an extremely wide range of the risk, both which suggest that a better understanding is needed about cancer risks associated with adult compared to childhood exposure. The overall outcome of our review is that it is timely to conduct new focused studies, including acquiring new data for an independent assessment, to re-appraise the widely accepted assumptions of negligible thyroid cancer risk following adult exposure. JF - Health Physics AU - Simon, S AU - Mabuchi, K AD - National Cancer Institute, Bethesda, MD 20892, USA Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - 1 PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States VL - 103 IS - 2 SN - 0017-9078, 0017-9078 KW - Risk Abstracts; Pollution Abstracts; Health & Safety Science Abstracts KW - Risk assessment KW - Nuclear power plants KW - Accidents KW - Reviews KW - Thyroid KW - Radioactivity KW - Children KW - Organs KW - Cancer KW - H 1000:Occupational Safety and Health KW - R2 23060:Medical and environmental health KW - P 6000:TOXICOLOGY AND HEALTH UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1032892743?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Physics&rft.atitle=RISK+OF+THYROID+CANCER+AFTER+ADULT+RADIATION+EXPOSURE%3A+TIME+TO+REASSESS%3F&rft.au=Simon%2C+S%3BMabuchi%2C+K&rft.aulast=Simon&rft.aufirst=S&rft.date=2012-08-01&rft.volume=103&rft.issue=2&rft.spage=S31&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-08-01 N1 - Last updated - 2013-08-12 N1 - SubjectsTermNotLitGenreText - Risk assessment; Nuclear power plants; Accidents; Reviews; Thyroid; Radioactivity; Children; Organs; Cancer ER - TY - JOUR T1 - ABC transporter function and regulation at the blood-spinal cord barrier. AN - 1031159332; 22472606 AB - We present here an initial characterization of ATP binding cassette (ABC) transporter function and regulation at the blood-spinal cord barrier. We isolated capillaries from rat spinal cords and studied transport function using a confocal microscopy-based assay and protein expression using western blots. These capillaries exhibited transport function and protein expression of P-glycoprotein (Abcb1), multidrug resistance protein 2 (Mrp2, Abcc2), and breast cancer-related protein (Bcrp, Abcg2). Exposing isolated capillaries to dioxin (activates aryl hydrocarbon receptor) increased transport mediated by all three transporters. Brain and spinal cord capillaries from dioxin-dosed rats exhibited increased P-glycoprotein-mediated transport and increased protein expression for all three ABC transporters. These findings indicate similar ABC transporter expression, function, and regulation at the blood-spinal cord and blood-brain barriers. JF - Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism AU - Campos, Christopher R AU - Schröter, Christian AU - Wang, Xueqian AU - Miller, David S AD - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA. Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 1559 EP - 1566 VL - 32 IS - 8 KW - ATP Binding Cassette Transporter, Sub-Family G, Member 2 KW - 0 KW - Abcc2 protein, rat KW - Abcg2 protein, rat KW - Ligands KW - P-Glycoproteins KW - Polychlorinated Dibenzodioxins KW - Xenobiotics KW - multidrug resistance protein 3 KW - Index Medicus KW - Microscopy, Confocal KW - Animals KW - Electrophoretic Mobility Shift Assay KW - Biological Transport KW - Mice KW - Mice, Knockout KW - Rats KW - Xenobiotics -- pharmacokinetics KW - Rats, Sprague-Dawley KW - Blotting, Western KW - Polychlorinated Dibenzodioxins -- pharmacokinetics KW - Cell Membrane -- metabolism KW - Capillaries -- metabolism KW - Male KW - P-Glycoproteins -- genetics KW - Spinal Cord -- metabolism KW - ATP-Binding Cassette Transporters -- metabolism KW - Blood-Brain Barrier -- metabolism KW - ATP-Binding Cassette Transporters -- genetics KW - P-Glycoproteins -- metabolism KW - Spinal Cord -- blood supply UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1031159332?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+cerebral+blood+flow+and+metabolism+%3A+official+journal+of+the+International+Society+of+Cerebral+Blood+Flow+and+Metabolism&rft.atitle=ABC+transporter+function+and+regulation+at+the+blood-spinal+cord+barrier.&rft.au=Campos%2C+Christopher+R%3BSchr%C3%B6ter%2C+Christian%3BWang%2C+Xueqian%3BMiller%2C+David+S&rft.aulast=Campos&rft.aufirst=Christopher&rft.date=2012-08-01&rft.volume=32&rft.issue=8&rft.spage=1559&rft.isbn=&rft.btitle=&rft.title=Journal+of+cerebral+blood+flow+and+metabolism+%3A+official+journal+of+the+International+Society+of+Cerebral+Blood+Flow+and+Metabolism&rft.issn=1559-7016&rft_id=info:doi/10.1038%2Fjcbfm.2012.47 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-15 N1 - Date created - 2012-08-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mol Pharmacol. 2000 Dec;58(6):1357-67 [11093774] Nat Rev Neurosci. 2011 Dec;12(12):723-38 [22048062] FEBS Lett. 2003 Jul 31;548(1-3):17-20 [12885400] Mol Pharmacol. 2004 Sep;66(3):387-94 [15322229] Jpn J Cancer Res. 1990 Aug;81(8):727-30 [1975805] Am J Physiol. 1995 Jan;268(1 Pt 2):F46-52 [7840247] Mol Cell Biol. 1999 Sep;19(9):6318-22 [10454578] Life Sci. 2005 Oct 21;77(23):2911-26 [15964599] J Neuroimmunol. 2006 Aug;177(1-2):209-14 [16806499] Steroids. 2007 Mar;72(3):231-46 [17284330] Neuron. 2008 Jan 24;57(2):178-201 [18215617] J Cereb Blood Flow Metab. 2008 Jun;28(6):1222-34 [18349876] Exp Neurol. 2008 Sep;213(1):229-37 [18625223] Neurobiol Dis. 2010 Jan;37(1):13-25 [19664713] Neurosci Lett. 2010 Mar 26;472(3):166-70 [20138122] Trends Pharmacol Sci. 2010 Jun;31(6):246-54 [20417575] Mol Pharmacol. 2010 Sep;78(3):376-83 [20547735] J Cereb Blood Flow Metab. 2010 Oct;30(10):1742-55 [20216549] FASEB J. 2011 Feb;25(2):644-52 [21048045] Ann Neurol. 2011 Aug;70(2):194-206 [21674586] J Neurochem. 2002 Oct;83(2):241-8 [12423235] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1038/jcbfm.2012.47 ER - TY - JOUR T1 - Molecular pathways: targeting phosphoinositide 3-kinase p110-delta in chronic lymphocytic leukemia. AN - 1030871313; 22711705 AB - The advent of targeted therapy, specifically to the B-cell receptor (BCR), has changed the convention for the treatment of chronic lymphocytic leukemia (CLL). The phosphoinositide 3-kinase (PI3K) pathway, activated upstream by the BCR, receptor tyrosine kinases, and cytokine receptors, has been a potential target for a multitude of cancers, but until the recent introduction of isoform-specific inhibitors has not been widely used. In this review, we focus on describing the intricate upstream and downstream signaling, leading to cell survival mediated by PI3K in B cells with a specific focus on the impact and importance of the p110δ isoform (which is localized to hematopoietic cells and regulates distinct cellular functions in B cells). In addition, the clinical advances from targeting p110δ are described, with a focus on clinical outcome, toxicities, and rational combination therapies. The experiences with p110δ in CLL have led to a more fundamental understanding of CLL signaling defects and may be predictive of other BCR-directed therapeutics. JF - Clinical cancer research : an official journal of the American Association for Cancer Research AU - Herman, Sarah E M AU - Johnson, Amy J AD - Hematology Branch, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, USA. Y1 - 2012/08/01/ PY - 2012 DA - 2012 Aug 01 SP - 4013 EP - 4018 VL - 18 IS - 15 SN - 1078-0432, 1078-0432 KW - Antineoplastic Agents KW - 0 KW - Purines KW - Quinazolinones KW - Class Ia Phosphatidylinositol 3-Kinase KW - EC 2.7.1.137 KW - idelalisib KW - YG57I8T5M0 KW - Index Medicus KW - Drug Screening Assays, Antitumor KW - Cell Survival -- drug effects KW - Humans KW - Clinical Trials as Topic KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- pharmacology KW - Class Ia Phosphatidylinositol 3-Kinase -- antagonists & inhibitors KW - Quinazolinones -- therapeutic use KW - Leukemia, Lymphocytic, Chronic, B-Cell -- drug therapy KW - Signal Transduction -- drug effects KW - Purines -- pharmacology KW - Purines -- therapeutic use KW - Leukemia, Lymphocytic, Chronic, B-Cell -- pathology KW - Class Ia Phosphatidylinositol 3-Kinase -- metabolism KW - Quinazolinones -- pharmacology KW - Leukemia, Lymphocytic, Chronic, B-Cell -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1030871313?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.atitle=Molecular+pathways%3A+targeting+phosphoinositide+3-kinase+p110-delta+in+chronic+lymphocytic+leukemia.&rft.au=Herman%2C+Sarah+E+M%3BJohnson%2C+Amy+J&rft.aulast=Herman&rft.aufirst=Sarah+E&rft.date=2012-08-01&rft.volume=18&rft.issue=15&rft.spage=4013&rft.isbn=&rft.btitle=&rft.title=Clinical+cancer+research+%3A+an+official+journal+of+the+American+Association+for+Cancer+Research&rft.issn=10780432&rft_id=info:doi/10.1158%2F1078-0432.CCR-11-1402 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-12-21 N1 - Date created - 2012-08-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochem Soc Trans. 2006 Nov;34(Pt 5):647-62 [17052169] Nat Rev Genet. 2006 Aug;7(8):606-19 [16847462] Cell. 2007 Jun 29;129(7):1261-74 [17604717] Eur J Immunol. 2008 Dec;38(12):3543-8 [19016531] J Cell Sci. 2008 Dec 15;121(Pt 24):4124-33 [19033389] Biochem J. 2009 Oct 1;423(1):e5-8 [19740077] Blood. 2010 Sep 23;116(12):2078-88 [20522708] Blood. 2011 Jan 13;117(2):591-4 [20959606] Blood. 2011 Sep 29;118(13):3603-12 [21803855] Immunol Rev. 2000 Aug;176:30-46 [11043766] J Cell Sci. 2001 Apr;114(Pt 8):1439-45 [11282020] Trends Biochem Sci. 2001 Nov;26(11):657-64 [11701324] J Exp Med. 2002 Jan 7;195(1):143-9 [11781373] Mol Cell Biol. 2002 Jun;22(12):4062-72 [12024020] J Exp Med. 2002 Sep 16;196(6):753-63 [12235209] Mol Cell Biol. 2002 Dec;22(24):8580-91 [12446777] Nat Rev Immunol. 2002 Dec;2(12):945-56 [12461567] Biochem Soc Trans. 2003 Feb;31(Pt 1):270-4 [12546700] Nat Immunol. 2003 Apr;4(4):313-9 [12660731] Nat Rev Immunol. 2003 Apr;3(4):317-30 [12669022] Trends Pharmacol Sci. 2003 Jul;24(7):366-76 [12871670] Zhejiang Da Xue Xue Bao Yi Xue Ban. 2003 Aug;32(4):335-8 [12970938] Cancer Cell. 2003 Oct;4(4):257-62 [14585353] J Biol Chem. 2004 Jan 9;279(2):1010-9 [14581487] Annu Rev Immunol. 2004;22:563-98 [15032589] Biochem Soc Trans. 2004 Apr;32(Pt 2):315-9 [15046598] Mol Immunol. 2004 Jul;41(6-7):599-613 [15219998] J Biol Chem. 1997 Aug 1;272(31):19236-41 [9235916] Trends Biochem Sci. 2005 Apr;30(4):194-204 [15817396] J Biochem Mol Biol. 2002 Jan 31;35(1):106-15 [16248975] Blood. 2006 Jan 15;107(2):642-50 [16179367] Proc Natl Acad Sci U S A. 2006 Jan 31;103(5):1289-94 [16432180] Blood. 2006 Mar 1;107(5):2090-3 [16322480] Biochem Soc Trans. 2007 Apr;35(Pt 2):199-203 [17371237] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1158/1078-0432.CCR-11-1402 ER - TY - JOUR T1 - Achaete-scute homologue-1 (ASH1) stimulates migration of lung cancer cells through Cdk5/p35 pathway. AN - 1030502682; 22696682 AB - Our previous data suggested that the human basic helix-loop-helix transcription factor achaete-scute homologue-1 (hASH1) may stimulate both proliferation and migration in the lung. In the CNS, cyclin-dependent kinase 5 (Cdk5) and its activator p35 are important for neuronal migration that is regulated by basic helix-loop-helix transcription factors. Cdk5/p35 may also play a role in carcinogenesis. In this study, we found that the neuronal activator p35 was commonly expressed in primary human lung cancers. Cdk5 and p35 were also expressed by several human lung cancer cell lines and coupled with migration and invasion. When the kinase activity was inhibited by the Cdk5 inhibitor roscovitine or dominant-negative (dn) Cdk5, the migration of lung cancer cells was reduced. In neuroendocrine cells expressing hASH1, such as a pulmonary carcinoid cell line, knocking down the gene expression by short hairpin RNA reduced the levels of Cdk5/p35, nuclear p35 protein, and migration. Furthermore, expression of hASH1 in lung adenocarcinoma cells normally lacking hASH1 increased p35/Cdk5 activity and enhanced cellular migration. We were also able to show that p35 was a direct target for hASH1. In conclusion, induction of Cdk5 activity is a novel mechanism through which hASH1 may regulate migration in lung carcinogenesis. JF - Molecular biology of the cell AU - Demelash, Abeba AU - Rudrabhatla, Parvathi AU - Pant, Harish C AU - Wang, Xiaoyang AU - Amin, Niranjana D AU - McWhite, Claire D AU - Naizhen, Xu AU - Linnoila, R Ilona AD - Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 2856 EP - 2866 VL - 23 IS - 15 KW - ASH1L protein, human KW - 0 KW - DNA-Binding Proteins KW - Nerve Tissue Proteins KW - Purines KW - Transcription Factors KW - neuronal Cdk5 activator (p25-p35) KW - roscovitine KW - 0ES1C2KQ94 KW - Cyclin-Dependent Kinase 5 KW - EC 2.7.11.1 KW - CDK5 protein, human KW - EC 2.7.11.22 KW - Index Medicus KW - Cell Proliferation -- drug effects KW - Neoplasm Invasiveness KW - Humans KW - HEK293 Cells KW - Cell Movement -- drug effects KW - Purines -- pharmacology KW - Cell Line, Tumor KW - Gene Expression Regulation, Neoplastic -- drug effects KW - Signal Transduction KW - Gene Expression Regulation, Neoplastic -- genetics KW - Adenocarcinoma -- metabolism KW - Transcription Factors -- metabolism KW - DNA-Binding Proteins -- genetics KW - Nerve Tissue Proteins -- metabolism KW - Cyclin-Dependent Kinase 5 -- antagonists & inhibitors KW - Nerve Tissue Proteins -- genetics KW - Cyclin-Dependent Kinase 5 -- metabolism KW - Cyclin-Dependent Kinase 5 -- genetics KW - Transcription Factors -- genetics KW - Lung Neoplasms -- pathology KW - Lung Neoplasms -- metabolism KW - DNA-Binding Proteins -- metabolism KW - Adenocarcinoma -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1030502682?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+biology+of+the+cell&rft.atitle=Achaete-scute+homologue-1+%28ASH1%29+stimulates+migration+of+lung+cancer+cells+through+Cdk5%2Fp35+pathway.&rft.au=Demelash%2C+Abeba%3BRudrabhatla%2C+Parvathi%3BPant%2C+Harish+C%3BWang%2C+Xiaoyang%3BAmin%2C+Niranjana+D%3BMcWhite%2C+Claire+D%3BNaizhen%2C+Xu%3BLinnoila%2C+R+Ilona&rft.aulast=Demelash&rft.aufirst=Abeba&rft.date=2012-08-01&rft.volume=23&rft.issue=15&rft.spage=2856&rft.isbn=&rft.btitle=&rft.title=Molecular+biology+of+the+cell&rft.issn=1939-4586&rft_id=info:doi/10.1091%2Fmbc.E10-12-1010 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-04-03 N1 - Date created - 2012-07-31 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 2000 Aug 1;60(15):4005-9 [10945598] Mol Cancer. 2010;9:221 [20727204] Nat Rev Mol Cell Biol. 2001 Oct;2(10):749-59 [11584302] J Neurosci Res. 2002 Feb 1;67(3):354-62 [11813240] Thorac Cardiovasc Surg. 2002 Feb;50(1):45-8 [11847604] Mol Cell Biol. 2002 May;22(9):3129-39 [11940670] Lung Cancer. 2002 May;36(2):115-24 [11955645] Nat Rev Cancer. 2002 Aug;2(8):563-72 [12154349] J Invest Dermatol. 2002 Dec;119(6):1304-9 [12485432] Mol Cancer Res. 2002 Nov;1(1):12-24 [12496365] Cancer Cell. 2003 Sep;4(3):181-9 [14522252] Cell Cycle. 2004 Feb;3(2):108-10 [14712065] Endocrinology. 2004 Jun;145(6):3023-31 [14976144] J Biol Chem. 2004 Jul 9;279(28):29302-7 [15123618] Cell. 1993 Nov 5;75(3):463-76 [8221886] Nature. 1994 Sep 29;371(6496):419-23 [8090221] Nature. 1994 Sep 29;371(6496):423-6 [8090222] Genes Dev. 1996 Apr 1;10(7):816-25 [8846918] J Cell Biochem Suppl. 1996;24:92-106 [8806093] Nature. 1997 Apr 24;386(6627):852-5 [9126746] Int J Cancer. 1998 Feb 9;75(4):489-96 [9466646] Int J Dev Biol. 2004;48(8-9):857-65 [15558477] EMBO J. 2005 Jan 12;24(1):209-20 [15592431] Proc Natl Acad Sci U S A. 2006 Jan 31;103(5):1319-24 [16432194] Cancer Res. 2006 Aug 1;66(15):7509-15 [16885348] J Biol Chem. 2006 Dec 22;281(51):39014-21 [17060323] Exp Mol Pathol. 2007 Feb;82(1):25-32 [17081516] J Biol Chem. 2007 Feb 2;282(5):2776-84 [17145757] Lab Invest. 2007 Jun;87(6):527-39 [17507989] Cancer Res. 2008 Mar 15;68(6):1647-55 [18339843] Proc Natl Acad Sci U S A. 2008 Jun 24;105(25):8772-7 [18550843] Proc Natl Acad Sci U S A. 2008 Nov 25;105(47):18567-71 [19017796] Cancer Res. 2009 Feb 1;69(3):845-54 [19176379] Cancer Sci. 2009 Mar;100(3):441-8 [19154401] Nat Cell Biol. 2009 May;11(5):624-30 [19363486] Am J Pathol. 2009 Aug;175(2):592-604 [19608871] Chin J Physiol. 2009 Feb 28;52(1):23-30 [19764350] Mol Cell Biol. 2009 Dec;29(24):6488-99 [19822667] Cancer Res. 2010 Jun 1;70(11):4460-9 [20484029] Toxicol Sci. 2010 Sep;117(1):238-48 [20554700] Cell Adh Migr. 2010 Jul-Sep;4(3):333-6 [20190570] J Biol Chem. 2010 Nov 12;285(46):35932-43 [20826806] J Neurol Sci. 2010 Dec 15;299(1-2):101-7 [20926102] Genes Dev. 2011 May 1;25(9):930-45 [21536733] Med Oncol. 2011 Sep;28(3):673-8 [20354813] Cancer Res. 2011 Oct 1;71(19):6165-73 [21856745] Clin Cancer Res. 2011 Oct 1;17(19):6140-50 [21825040] Lung Cancer. 2012 Jan;75(1):58-65 [21684625] J Biol Chem. 2001 Sep 7;276(36):34199-205 [11443123] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1091/mbc.E10-12-1010 ER - TY - JOUR T1 - Clinical implications of cancer stem cell biology in hepatocellular carcinoma. AN - 1030502364; 22846863 AB - Solid tumors are thought to contain cancer stem cells (CSCs) as a distinct population responsible for tumor relapse and metastasis due to their abilities to self-renew, differentiate, and give rise to a new tumor in local or distant organs. CSCs have been identified in many tumor types, including hepatocellular carcinoma (HCC), the fifth most common and third most deadly malignancy with observable heterogeneity. Numerous studies have shown that hepatic CSCs could be enriched via different cell surface markers, eg, CD13, CD24, CD44, CD90, CD133, EpCAM (CD326), and OV6. They also could be identified through functional assays such as isolating the side population cells by Hoechst dye staining or screening cells with a high activity of aldehyde dehydrogenase. Functional characterization of hepatic CSCs has revealed several deregulated signaling pathways, such as Wnt/β-catenin, AKT, transforming growth factor-beta (TGF-β), interleukin (IL)-6/STAT3 pathways to be critical in inducing "stemness" of HCC and in promoting self-renewal, tumorigenicity, and chemoresistance. An increased understanding of hepatic CSC biology facilitated the development of new diagnostic, prognostic, and therapeutic strategies for improving HCC clinical management. In this review, we summarize recent evidence including the identification of the hepatic CSC and its underlying biological mechanisms, and discuss the potential clinical implications in HCC. Published by Elsevier Inc. JF - Seminars in oncology AU - Ji, Junfang AU - Wang, Xin Wei AD - Liver Carcinogenesis Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 461 EP - 472 VL - 39 IS - 4 KW - AC133 Antigen KW - 0 KW - Antigens, CD KW - Antigens, CD24 KW - Antigens, CD44 KW - Antigens, Neoplasm KW - CD24 protein, human KW - CD44 protein, human KW - Cell Adhesion Molecules KW - Epithelial Cell Adhesion Molecule KW - Glycoproteins KW - PROM1 protein, human KW - Peptides KW - Index Medicus KW - Antigens, CD -- analysis KW - Glycoproteins -- analysis KW - Humans KW - Prognosis KW - Peptides -- analysis KW - Antigens, Neoplasm -- analysis KW - Antigens, CD44 -- analysis KW - Antigens, CD24 -- analysis KW - Drug Resistance, Neoplasm KW - Cell Adhesion Molecules -- analysis KW - Liver Neoplasms -- pathology KW - Carcinoma, Hepatocellular -- diagnosis KW - Neoplastic Stem Cells -- pathology KW - Carcinoma, Hepatocellular -- pathology KW - Liver Neoplasms -- diagnosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1030502364?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+oncology&rft.atitle=Clinical+implications+of+cancer+stem+cell+biology+in+hepatocellular+carcinoma.&rft.au=Ji%2C+Junfang%3BWang%2C+Xin+Wei&rft.aulast=Ji&rft.aufirst=Junfang&rft.date=2012-08-01&rft.volume=39&rft.issue=4&rft.spage=461&rft.isbn=&rft.btitle=&rft.title=Seminars+in+oncology&rft.issn=1532-8708&rft_id=info:doi/10.1053%2Fj.seminoncol.2012.05.011 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-04 N1 - Date created - 2012-07-31 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochem Biophys Res Commun. 2006 Dec 29;351(4):820-4 [17097610] Mol Cancer. 2006;5:67 [17140455] Nature. 2007 Jan 4;445(7123):111-5 [17122771] Nature. 2007 Jan 4;445(7123):106-10 [17122772] Am J Pathol. 2007 May;170(5):1750-62 [17456779] Gastroenterology. 2007 Jun;132(7):2542-56 [17570225] Gastroenterology. 2007 Jun;132(7):2557-76 [17570226] Blood. 2007 Jul 1;110(1):142-50 [17363739] J Exp Med. 2007 Aug 6;204(8):1973-87 [17664288] Cancer Res. 2007 Oct 1;67(19):8980-4 [17908997] Front Biosci. 2008;13:3096-100 [17981779] Cancer Res. 2007 Nov 15;67(22):10831-9 [18006828] Cancer Cell. 2008 Feb;13(2):153-66 [18242515] Stem Cells. 2008 Feb;26(2):364-71 [17975224] 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] Hepatology. 2008 Mar;47(3):919-28 [18275073] Oncogene. 2008 Mar 13;27(12):1749-58 [17891174] Cancer Res. 2008 Jun 1;68(11):4287-95 [18519688] Mol Cancer Res. 2008 Jul;6(7):1146-53 [18644979] N Engl J Med. 2008 Jul 24;359(4):366-77 [18596266] Int J Clin Pract. 2008 Aug;62(8):1212-8 [18479363] Cancer Res. 2008 Oct 1;68(19):7742-9 [18829528] J Cancer Res Clin Oncol. 2008 Nov;134(11):1155-63 [18470535] Future Oncol. 2008 Oct;4(5):647-60 [18922122] Cell Stem Cell. 2007 Nov;1(5):555-67 [18371393] Hepatology. 2008 Nov;48(5):1528-39 [18925631] Carcinogenesis. 2008 Dec;29(12):2289-97 [18820285] Gastroenterology. 2009 Mar;136(3):1012-24 [19150350] Clin Cancer Res. 2009 May 15;15(10):3462-71 [19447872] Hepatology. 2009 Aug;50(2):472-80 [19585654] Clin Cancer Res. 2009 Sep 1;15(17):5518-27 [19706825] Nat Med. 2009 Sep;15(9):1010-2 [19734877] BMC Cancer. 2009;9:324 [19744348] N Engl J Med. 2009 Oct 8;361(15):1437-47 [19812400] World J Gastroenterol. 2009 Oct 21;15(39):4896-906 [19842219] Cancer Biol Ther. 2009 Sep;8(18):1686-93 [19901517] Cancer Res. 2010 Jan 15;70(2):719-29 [20068153] Int J Cancer. 2010 May 1;126(9):2067-78 [19711346] Hepatology. 2010 May;51(5):1635-44 [20196115] Cancer Res. 2010 Jun 1;70(11):4687-97 [20484035] Gut. 2010 Jul;59(7):953-62 [20442200] Oncol Rep. 2010 Aug;24(2):537-46 [20596644] Semin Liver Dis. 2010 Aug;30(3):258-70 [20665378] J Clin Invest. 2010 Sep;120(9):3326-39 [20697159] Cell Stem Cell. 2010 Dec 3;7(6):694-707 [21112564] Gastroenterology. 2011 Jan;140(1):344-55 [20682318] Hepatology. 2011 Jan;53(1):160-70 [20979057] Cell Stem Cell. 2011 Jul 8;9(1):50-63 [21726833] Hematol Oncol Stem Cell Ther. 2011;4(2):60-6 [21727766] Acta Histochem. 2011 Dec;113(8):833-8 [21272924] Int J Oncol. 2012 Mar;40(3):747-56 [22025269] Int J Cancer. 2007 Apr 1;120(7):1444-50 [17205516] Cell. 2000 Jan 7;100(1):57-70 [10647931] J Hepatol. 2000 Jan;32(1):78-84 [10673070] Clin Liver Dis. 2001 Feb;5(1):145-59 [11218912] Gastroenterology. 2002 Feb;122(2):376-86 [11832452] Nat Genet. 2002 Aug;31(4):339-46 [12149612] Toxicology. 2002 Dec 27;181-182:43-7 [12505283] Lancet. 2003 Mar 15;361(9361):923-9 [12648972] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218] Nat Med. 2003 Apr;9(4):416-23 [12640447] Hepatology. 2004 Feb;39(2):518-27 [14768006] Hepatology. 2004 Jun;39(6):1477-87 [15185286] Hepatogastroenterology. 2004 Jul-Aug;51(58):1121-3 [15239258] Nat Med. 2004 Aug;10(8):789-99 [15286780] Hepatology. 2004 Sep;40(3):667-76 [15349906] Gastroenterology. 2004 Nov;127(5 Suppl 1):S5-S16 [15508102] Hepatology. 1992 Dec;16(6):1327-33 [1280243] Nature. 1994 Feb 17;367(6464):645-8 [7509044] Nat Med. 1997 Jul;3(7):730-7 [9212098] Histopathology. 1997 Oct;31(4):324-9 [9363447] N Engl J Med. 1999 Mar 11;340(10):745-50 [10072408] Nature. 2004 Nov 18;432(7015):396-401 [15549107] CA Cancer J Clin. 2005 Mar-Apr;55(2):74-108 [15761078] Nat Rev Cancer. 2005 Apr;5(4):275-84 [15803154] Stem Cells. 2005 Jun-Jul;23(6):752-60 [15917471] Hepatology. 2006 Mar;43(3):515-24 [16496320] Stem Cells. 2006 Mar;24(3):506-13 [16239320] Am J Physiol Gastrointest Liver Physiol. 2006 Jul;291(1):G45-54 [16769813] FASEB J. 2006 Jun;20(8):1045-54 [16770003] Proc Natl Acad Sci U S A. 2006 Jun 27;103(26):9912-7 [16782807] Hepatology. 2006 Jul;44(1):240-51 [16799977] Cancer Res. 2006 Oct 1;66(19):9339-44 [16990346] Cell. 2006 Nov 3;127(3):469-80 [17081971] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1053/j.seminoncol.2012.05.011 ER - TY - JOUR T1 - Kinetics of the oxidation of reduced Cu,Zn-superoxide dismutase by peroxymonocarbonate. AN - 1030348783; 22569304 AB - Kinetic evidence is reported for the role of the peroxymonocarbonate, HOOCO(2)(-), as an oxidant for reduced Cu,Zn-superoxide dismutase-Cu(I) (SOD1) during the peroxidase activity of the enzyme. The formation of this reactive oxygen species results from the equilibrium between hydrogen peroxide and bicarbonate. Recently, peroxymonocarbonate has been proposed to be a key substrate for reduced SOD1 and has been shown to oxidize SOD1-Cu(I) to SOD1-Cu(II) much faster than H(2)O(2). We have reinvestigated the kinetics of the reaction between SOD1-Cu(I) and HOOCO(2)(-) by using conventional stopped-flow spectrophotometry and obtained a second-order rate constant of k=1600±100M(-1)s(-1) for SOD1-Cu(I) oxidation by HOOCO(2)(-). Our results demonstrate that peroxymonocarbonate oxidizes SOD1-Cu(I) to SOD1-Cu(II) and is in turn reduced to the carbonate anion radical. It is proposed that the dissociation of His61 from the active site Cu(I) in SOD-Cu(I) contributes to this chemistry by facilitating the binding of larger anions, such as peroxymonocarbonate. Published by Elsevier Inc. JF - Free radical biology & medicine AU - Ranguelova, Kalina AU - Ganini, Douglas AU - Bonini, Marcelo G AU - London, Robert E AU - Mason, Ronald P AD - Laboratory of Pharmacology and Toxicology, NIEHS, National Institutes of Health, Research Triangle Park, NC 27709, USA. Y1 - 2012/08/01/ PY - 2012 DA - 2012 Aug 01 SP - 589 EP - 594 VL - 53 IS - 3 KW - Carbonates KW - 0 KW - Oxidants KW - Reactive Oxygen Species KW - peroxycarbonic acid KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Superoxide Dismutase-1 KW - Index Medicus KW - Oxidation-Reduction KW - Animals KW - Cattle KW - Models, Molecular KW - Kinetics KW - Catalytic Domain KW - Reactive Oxygen Species -- chemistry KW - Carbonates -- chemistry KW - Oxidants -- chemistry KW - Superoxide Dismutase -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1030348783?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Kinetics+of+the+oxidation+of+reduced+Cu%2CZn-superoxide+dismutase+by+peroxymonocarbonate.&rft.au=Ranguelova%2C+Kalina%3BGanini%2C+Douglas%3BBonini%2C+Marcelo+G%3BLondon%2C+Robert+E%3BMason%2C+Ronald+P&rft.aulast=Ranguelova&rft.aufirst=Kalina&rft.date=2012-08-01&rft.volume=53&rft.issue=3&rft.spage=589&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2012.04.029 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-17 N1 - Date created - 2012-07-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Free Radic Biol Med. 2003 Dec 15;35(12):1538-50 [14680677] J Biol Chem. 2003 Jun 6;278(23):21032-9 [12649272] Proc Natl Acad Sci U S A. 2004 Jan 20;101(3):743-4 [14711995] Biochem J. 2004 Mar 1;378(Pt 2):435-47 [14640973] Arch Biochem Biophys. 2004 Jan 15;421(2):255-9 [14984205] Free Radic Biol Med. 2004 Jun 1;36(11):1355-65 [15135171] Free Radic Biol Med. 2004 Jun 1;36(11):1444-7 [15135181] J Biol Chem. 1969 Nov 25;244(22):6049-55 [5389100] J Inorg Biochem. 1988 Jun;33(2):91-7 [3411318] Biochemistry. 1992 Dec 15;31(49):12410-5 [1463727] Arch Biochem Biophys. 1993 Aug 1;304(2):429-33 [8394057] J Biol Chem. 1994 Jan 28;269(4):2405-10 [8300566] Biochemistry. 1997 Jun 10;36(23):7109-13 [9188710] Arch Biochem Biophys. 1998 Apr 15;352(2):237-9 [9587411] Proc Natl Acad Sci U S A. 1998 Oct 27;95(22):12912-7 [9789014] J Biol Chem. 1999 Jan 15;274(3):1226-32 [9880490] Free Radic Biol Med. 2005 Jan 15;38(2):201-14 [15607903] Inorg Chem. 2005 May 2;44(9):3311-20 [15847441] Annu Rev Biochem. 2005;74:563-93 [15952898] J Biol Chem. 2005 Jul 22;280(29):27402-11 [15905164] Chem Res Toxicol. 2006 Nov;19(11):1475-82 [17112235] IUBMB Life. 2007 Apr-May;59(4-5):255-62 [17505962] Biochem J. 2009 Jan 1;417(1):341-53 [18764780] Chem Res Toxicol. 2009 Apr;22(4):639-48 [19243126] J Biol Chem. 2009 May 22;284(21):14618-27 [19286663] Free Radic Biol Med. 2010 Jun 15;48(12):1565-9 [20211248] Environ Health Perspect. 2010 Jul;118(7):970-5 [20348042] Biochemistry. 2010 Dec 21;49(50):10616-22 [21038859] Inorg Chem. 2010 Dec 20;49(24):11287-96 [21077618] J Biol Chem. 1999 Dec 3;274(49):34576-83 [10574920] Science. 1999 Dec 24;286(5449):2498-500 [10617463] Free Radic Biol Med. 1999 Dec;27(11-12):1444-7 [10641739] J Biol Chem. 2000 May 12;275(19):14038-45 [10799477] Free Radic Biol Med. 2002 May 1;32(9):841-59 [11978486] J Biol Chem. 2002 Sep 20;277(38):34674-8 [12107177] Biochemistry. 2004 Jan 20;43(2):344-51 [14717588] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.freeradbiomed.2012.04.029 ER - TY - JOUR T1 - A Novel STAT1 Mutation Associated with Disseminated Mycobacterial Disease AN - 1028036676; 16898052 AB - STAT1 is a key component of Interferon (IFN)- gamma and IFN- alpha signaling and mediates protection against mycobacteria, fungal, viral infections, and cancer. Dominant negative inhibitory as well as gain of function heterozygous STAT1 mutations demonstrate that IFN- gamma driven cellular responses need to be tightly regulated to control infections. We describe an autosomal dominant mutation in the SH2 domain of STAT1 that disrupts protein phosphorylation, c.1961T>A (M654K). The mutant allele does not permit STAT1 phosphorylation, and impairs STAT1 phosphorylation of the wild type allele. Protein dimerization is preserved but DNA binding activity, IFN- gamma driven GAS-luciferase activity, and expression of IFN- gamma target genes are reduced. IFN- alpha driven ISRE response, but not IFN- alpha driven GAS response, are preserved when cells are co-transfected with wild type and the mutant STAT1 constructs. M654K exerts a dominant negative effect on IFN- gamma related immunity and is recessive for IFN- alpha induced immune function. JF - Journal of Clinical Immunology AU - Sampaio, Elizabeth P AU - Bax, Hannelore I AU - Hsu, Amy P AU - Kristosturyan, Ervand AU - Pechacek, Joseph AU - Chandrasekaran, Prabha AU - Paulson, Michelle L AU - Dias, Dalton L AU - Spalding, Christine AU - Uzel, Gulbu AU - Ding, Li AU - McFarland, Elizabeth AU - Holland, Steven M AD - Laboratory of Clinical Infectious Diseases, NIAID, NIH, Bethesda, MD, USA, smh@nih.gov Y1 - 2012/08// PY - 2012 DA - Aug 2012 SP - 681 EP - 689 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 32 IS - 4 SN - 0271-9142, 0271-9142 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Cancer KW - DNA KW - Immune response KW - Immunity KW - Infection KW - Mutation KW - Phosphorylation KW - Stat1 protein KW - alpha -Interferon KW - gamma -Interferon KW - Mycobacterium UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028036676?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Clinical+Immunology&rft.atitle=A+Novel+STAT1+Mutation+Associated+with+Disseminated+Mycobacterial+Disease&rft.au=Sampaio%2C+Elizabeth+P%3BBax%2C+Hannelore+I%3BHsu%2C+Amy+P%3BKristosturyan%2C+Ervand%3BPechacek%2C+Joseph%3BChandrasekaran%2C+Prabha%3BPaulson%2C+Michelle+L%3BDias%2C+Dalton+L%3BSpalding%2C+Christine%3BUzel%2C+Gulbu%3BDing%2C+Li%3BMcFarland%2C+Elizabeth%3BHolland%2C+Steven+M&rft.aulast=Sampaio&rft.aufirst=Elizabeth&rft.date=2012-08-01&rft.volume=32&rft.issue=4&rft.spage=681&rft.isbn=&rft.btitle=&rft.title=Journal+of+Clinical+Immunology&rft.issn=02719142&rft_id=info:doi/10.1007%2Fs10875-012-9659-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2012-09-24 N1 - SubjectsTermNotLitGenreText - gamma -Interferon; Phosphorylation; Stat1 protein; alpha -Interferon; DNA; Immunity; Immune response; Infection; Mutation; Cancer; Mycobacterium DO - http://dx.doi.org/10.1007/s10875-012-9659-2 ER - TY - JOUR T1 - Thioredoxin reductase 1 deficiency enhances selenite toxicity in cancer cells via a thioredoxin-independent mechanism. AN - 1024932652; 22594686 AB - Selenium is an essential trace element in mammals, but is toxic at high levels. It is best known for its cancer prevention activity, but cancer cells are more sensitive to selenite toxicity than normal cells. Since selenite treatment leads to oxidative stress, and the Trx (thioredoxin) system is a major antioxidative system, we examined the interplay between TR1 (Trx reductase 1) and Trx1 deficiencies and selenite toxicity in DT cells, a malignant mouse cell line, and the corresponding parental NIH 3T3 cells. TR1-deficient cells were far more sensitive to selenite toxicity than Trx1-deficient or control cells. In contrast, this effect was not seen in cells treated with hydrogen peroxide, suggesting that the increased sensitivity of TR1 deficiency to selenite was not due to oxidative stress caused by this compound. Further analyses revealed that only TR1-deficient cells manifested strongly enhanced production and secretion of glutathione, which was associated with increased sensitivity of the cells to selenite. The results suggest a new role for TR1 in cancer that is independent of Trx reduction and compensated for by the glutathione system. The results also suggest that the enhanced selenite toxicity of cancer cells and simultaneous inhibition of TR1 can provide a new avenue for cancer therapy. JF - The Biochemical journal AU - Tobe, Ryuta AU - Yoo, Min-Hyuk AU - Fradejas, Noelia AU - Carlson, Bradley A AU - Calvo, Soledad AU - Gladyshev, Vadim N AU - Hatfield, Dolph L AD - Molecular Biology of Selenium Section, Laboratory of Cancer Prevention, Center for Cancer Research, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/08/01/ PY - 2012 DA - 2012 Aug 01 SP - 423 EP - 430 VL - 445 IS - 3 KW - Anticarcinogenic Agents KW - 0 KW - RNA, Small Interfering KW - Thioredoxins KW - 52500-60-4 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Thioredoxin Reductase 1 KW - EC 1.8.1.9 KW - Txnrd1 protein, mouse KW - Glutathione KW - GAN16C9B8O KW - Sodium Selenite KW - HIW548RQ3W KW - Index Medicus KW - Animals KW - Gene Knockdown Techniques KW - Base Sequence KW - Glutathione -- metabolism KW - Hydrogen Peroxide -- pharmacology KW - Anticarcinogenic Agents -- pharmacology KW - Oxidative Stress -- drug effects KW - Thioredoxins -- metabolism KW - Mice KW - Cell Line, Tumor KW - RNA, Small Interfering -- metabolism KW - NIH 3T3 Cells KW - Thioredoxin Reductase 1 -- genetics KW - Thioredoxin Reductase 1 -- antagonists & inhibitors KW - Thioredoxin Reductase 1 -- metabolism KW - Sodium Selenite -- pharmacology KW - Neoplasms, Experimental -- metabolism KW - Neoplasms, Experimental -- drug therapy KW - Thioredoxin Reductase 1 -- deficiency UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1024932652?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Biochemical+journal&rft.atitle=Thioredoxin+reductase+1+deficiency+enhances+selenite+toxicity+in+cancer+cells+via+a+thioredoxin-independent+mechanism.&rft.au=Tobe%2C+Ryuta%3BYoo%2C+Min-Hyuk%3BFradejas%2C+Noelia%3BCarlson%2C+Bradley+A%3BCalvo%2C+Soledad%3BGladyshev%2C+Vadim+N%3BHatfield%2C+Dolph+L&rft.aulast=Tobe&rft.aufirst=Ryuta&rft.date=2012-08-01&rft.volume=445&rft.issue=3&rft.spage=423&rft.isbn=&rft.btitle=&rft.title=The+Biochemical+journal&rft.issn=1470-8728&rft_id=info:doi/10.1042%2FBJ20120618 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-26 N1 - Date created - 2012-07-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Annu Rev Pharmacol Toxicol. 2007;47:89-116 [16968214] FEBS J. 2011 Nov;278(21):4112-21 [21880115] Nat Protoc. 2006;1(6):3159-65 [17406579] Biol Chem. 2007 Oct;388(10):1091-7 [17937623] PLoS One. 2007;2(10):e1112 [17971875] Chem Biodivers. 2008 Mar;5(3):389-95 [18357548] J Biol Chem. 2008 Nov 28;283(48):33183-90 [18835810] Mol Interv. 2009 Feb;9(1):18-21 [19299660] Mol Pharmacol. 2009 Jul;76(1):163-72 [19364812] PLoS One. 2009;4(7):e6158 [19584930] Proc Natl Acad Sci U S A. 2009 Jul 7;106(27):11400-5 [19549867] Biochem J. 2009 Aug 15;422(1):11-22 [19627257] Biochim Biophys Acta. 2009 Nov;1790(11):1541-5 [19272412] Biochem Pharmacol. 2010 Jan 15;79(2):90-101 [19665452] Antioxid Redox Signal. 2010 Apr 1;12(7):867-80 [19769465] Biofactors. 2010 Mar-Apr;36(2):153-8 [20333751] Cell. 2000 Jan 7;100(1):57-70 [10647931] J Biol Chem. 2000 Nov 10;275(45):35540-7 [10945981] Cancer Epidemiol Biomarkers Prev. 2000 Nov;9(11):1171-82 [11097224] Cancer Epidemiol Biomarkers Prev. 2001 Apr;10(4):385-90 [11319180] Nutr Cancer. 2001;40(1):42-9 [11799922] Biochem Pharmacol. 2002 May 15;63(10):1875-84 [12034372] J Biol Chem. 2003 Jan 10;278(2):745-50 [12424231] Anticancer Res. 2003 May-Jun;23(3B):2425-33 [12894524] Biochem Pharmacol. 2004 Feb 1;67(3):513-22 [15037203] Cancer Prev Res (Phila). 2010 May;3(5):630-9 [20388823] Biochem Biophys Res Commun. 2010 May 21;396(1):120-4 [20494123] Anticancer Res. 2010 Apr;30(4):1169-81 [20530424] Biochem J. 2010 Sep 1;430(2):285-93 [20536427] Cancer Res. 2010 Nov 15;70(22):9505-14 [21045148] Biochem Pharmacol. 2011 Jan 15;81(2):211-21 [20920480] Drugs. 2011 Jul 30;71(11):1385-96 [21812504] Anal Biochem. 1976 Jul;74(1):214-26 [962076] Proc Natl Acad Sci U S A. 1983 Sep;80(18):5602-6 [6604274] J Biol Chem. 1992 Apr 25;267(12):8030-4 [1569062] Eur J Biochem. 1992 Jul 15;207(2):435-39 [1321713] Proc Natl Acad Sci U S A. 1996 Jun 11;93(12):6146-51 [8650234] Cancer Res. 1999 Jul 1;59(13):3175-9 [10397262] Cancer Biol Ther. 2005 Jan;4(1):6-13 [15684606] Annu Rev Nutr. 2005;25:261-95 [16011468] Proc Nutr Soc. 2005 Nov;64(4):527-42 [16313696] Prostate. 2006 Feb 1;66(2):218-25 [16173037] Antioxid Redox Signal. 2005 Nov-Dec;7(11-12):1715-27 [16356132] J Nutr. 2006 May;136(5):1311-7 [16614422] J Biol Chem. 2006 May 12;281(19):13005-8 [16565519] Cancer Lett. 2006 May 18;236(2):164-74 [15955621] Proc Natl Acad Sci U S A. 2006 May 23;103(21):8179-84 [16690748] Free Radic Biol Med. 2006 Sep 15;41(6):874-85 [16934670] Semin Cancer Biol. 2006 Dec;16(6):452-65 [17056271] Semin Cancer Biol. 2006 Dec;16(6):420-6 [17092741] Biochem J. 2007 Jan 1;401(1):1-11 [17150040] J Nutr Biochem. 2011 Oct;22(10):945-55 [21190829] Free Radic Biol Med. 2007 Mar 15;42(6):872-81 [17320769] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1042/BJ20120618 ER - TY - JOUR T1 - A new model for predicting acute mucosal toxicity in head-and-neck cancer patients undergoing radiotherapy with altered schedules. AN - 1024351178; 22578541 AB - One of the worst radiation-induced acute effects in treating head-and-neck (HN) cancer is grade 3 or higher acute (oral and pharyngeal) mucosal toxicity (AMT), caused by the killing/depletion of mucosa cells. Here we aim to testing a predictive model of the AMT in HN cancer patients receiving different radiotherapy schedules. Various radiotherapeutic schedules have been reviewed and classified as tolerable or intolerable based on AMT severity. A modified normal tissue complication probability (NTCP) model has been investigated to describe AMT data in radiotherapy regimens, both conventional and altered in dose and overall treatment time (OTT). We tested the hypothesis that such a model could also be applied to identify intolerable treatment and to predict AMT. This AMT NTCP model has been compared with other published predictive models to identify schedules that are either tolerable or intolerable. The area under the curve (AUC) was calculated for all models, assuming treatment tolerance as the gold standard. The correlation between AMT and the predicted toxicity rate was assessed by a Pearson correlation test. The AMT NTCP model was able to distinguish between acceptable and intolerable schedules among the data available for the study (AUC = 0.84, 95% confidence interval = 0.75-0.92). In the equivalent dose at 2 Gy/fraction (EQD2) vs OTT space, the proposed model shows a trend similar to that of models proposed by other authors, but was superior in detecting some intolerable schedules. Moreover, it was able to predict the incidence of ≥G3 AMT. The proposed model is able to predict ≥G3 AMT after HN cancer radiotherapy, and could be useful for designing altered/hypofractionated schedules to reduce the incidence of AMT. Copyright © 2012 Elsevier Inc. All rights reserved. JF - International journal of radiation oncology, biology, physics AU - Strigari, Lidia AU - Pedicini, Piernicola AU - D'Andrea, Marco AU - Pinnarò, Paola AU - Marucci, Laura AU - Giordano, Carolina AU - Benassi, Marcello AD - Laboratory of Medical Physics and Expert Systems, Regina Elena National Cancer Institute, Rome, Italy. strigari@ifo.it Y1 - 2012/08/01/ PY - 2012 DA - 2012 Aug 01 SP - e697 EP - e702 VL - 83 IS - 5 KW - Index Medicus KW - Organs at Risk -- radiation effects KW - Acute Disease KW - Pharynx -- radiation effects KW - Mucositis -- etiology KW - Area Under Curve KW - Dose Fractionation KW - Humans KW - Mouth Mucosa -- radiation effects KW - Radiation Tolerance KW - Head and Neck Neoplasms -- radiotherapy KW - Models, Biological KW - Radiation Injuries -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1024351178?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.atitle=A+new+model+for+predicting+acute+mucosal+toxicity+in+head-and-neck+cancer+patients+undergoing+radiotherapy+with+altered+schedules.&rft.au=Strigari%2C+Lidia%3BPedicini%2C+Piernicola%3BD%27Andrea%2C+Marco%3BPinnar%C3%B2%2C+Paola%3BMarucci%2C+Laura%3BGiordano%2C+Carolina%3BBenassi%2C+Marcello&rft.aulast=Strigari&rft.aufirst=Lidia&rft.date=2012-08-01&rft.volume=83&rft.issue=5&rft.spage=e697&rft.isbn=&rft.btitle=&rft.title=International+journal+of+radiation+oncology%2C+biology%2C+physics&rft.issn=1879-355X&rft_id=info:doi/10.1016%2Fj.ijrobp.2012.02.004 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-17 N1 - Date created - 2012-07-09 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.ijrobp.2012.02.004 ER - TY - JOUR T1 - The central role of the c-Met pathway in rebuilding the liver. AN - 1023534051; 22387525 JF - Gut AU - Thorgeirsson, S S AD - Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892-4262, USA. snorri_thorgeirsson@nih.gov Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 1105 EP - 1106 VL - 61 IS - 8 KW - RNA, Messenger KW - 0 KW - Hepatocyte Growth Factor KW - 67256-21-7 KW - RON protein KW - EC 2.7.10.1 KW - Receptor Protein-Tyrosine Kinases KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Male KW - Female KW - Receptor Protein-Tyrosine Kinases -- genetics KW - Hepatocyte Growth Factor -- genetics KW - Hepatocytes -- transplantation KW - Gene Expression Regulation KW - Liver Transplantation -- methods KW - RNA, Messenger -- genetics KW - Liver Regeneration UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1023534051?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gut&rft.atitle=The+central+role+of+the+c-Met+pathway+in+rebuilding+the+liver.&rft.au=Thorgeirsson%2C+S+S&rft.aulast=Thorgeirsson&rft.aufirst=S&rft.date=2012-08-01&rft.volume=61&rft.issue=8&rft.spage=1105&rft.isbn=&rft.btitle=&rft.title=Gut&rft.issn=1468-3288&rft_id=info:doi/10.1136%2Fgutjnl-2012-302234 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-02 N1 - Date created - 2012-07-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment On: Gut. 2012 Aug;61(8):1209-18 [22287599] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1136/gutjnl-2012-302234 ER - TY - JOUR T1 - Directed therapy for patients with myelodysplastic syndromes (MDS) by suppression of cyclin D1 with ON 01910.Na. AN - 1021982573; 22524974 AB - We previously demonstrated upregulation of c-myc, survivin, and cyclin D1 in CD34+ bone marrow mononuclear cells (BMMNCs) of patients with trisomy 8 and monosomy 7 myelodysplastic syndromes (MDS). "Knockdown" of cyclin D1 by RNA interference decreased trisomy 8 cell growth, suggesting that this might be a therapeutic target in MDS. We performed preclinical studies using BMMNCs from patients with MDS and AML to examine the effects of the styryl sulfone ON 01910.Na on cyclin D1 accumulation, aneuploidy, and CD34+ blast percentage. We next treated twelve patients with higher risk MDS and two trisomy 8 AML patients with ON 01910.Na on a phase I clinical protocol (NCT00533416). ON 01910.Na inhibited cyclin D1 expression, and was selectively toxic to trisomy 8 cells in vitro. Flow cytometry studies demonstrated increased mature CD15+ myeloid cells and decreased CD34+ blasts. Three patients treated with ON 01910.Na on a clinical had decreased bone marrow blasts by ≥ 50%, and three patients had hematologic improvements, one of which was sustained for 33 months. Patients with hematologic responses to ON 01910.Na had decreased cyclin D1 expression in their CD34+ cells. The preclinical results and responses of patients on a clinical trial warrant further investigation of ON 01910.Na as a potential novel targeted therapy for higher risk MDS patients. Published by Elsevier Ltd. JF - Leukemia research AU - Olnes, Matthew J AU - Shenoy, Aarthie AU - Weinstein, Barbara AU - Pfannes, Loretta AU - Loeliger, Kelsey AU - Tucker, Zachary AU - Tian, Xin AU - Kwak, Minjung AU - Wilhelm, Francois AU - Yong, Agnes S M AU - Maric, Irina AU - Maniar, Manoj AU - Scheinberg, Phillip AU - Groopman, Jerome AU - Young, Neal S AU - Sloand, Elaine M AD - Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. olnesmj@nhlbi.nih.gov Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 982 EP - 989 VL - 36 IS - 8 KW - Antineoplastic Agents KW - 0 KW - ON 01910 KW - Sulfones KW - Cyclin D1 KW - 136601-57-5 KW - Glycine KW - TE7660XO1C KW - Index Medicus KW - Bone Marrow Cells -- drug effects KW - Antineoplastic Agents -- administration & dosage KW - Dose-Response Relationship, Drug KW - Humans KW - Algorithms KW - Aged KW - Chromosomes, Human, Pair 8 KW - Antineoplastic Agents -- adverse effects KW - Tumor Cells, Cultured KW - Aged, 80 and over KW - Bone Marrow Cells -- pathology KW - Trisomy -- pathology KW - Middle Aged KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- pharmacology KW - Male KW - Female KW - Cyclin D1 -- antagonists & inhibitors KW - Glycine -- analogs & derivatives KW - Myelodysplastic Syndromes -- pathology KW - Glycine -- administration & dosage KW - Myelodysplastic Syndromes -- genetics KW - Sulfones -- administration & dosage KW - Sulfones -- adverse effects KW - Sulfones -- pharmacology KW - Glycine -- pharmacology KW - Sulfones -- therapeutic use KW - Glycine -- therapeutic use KW - Myelodysplastic Syndromes -- drug therapy KW - Glycine -- adverse effects KW - Molecular Targeted Therapy -- methods KW - Molecular Targeted Therapy -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1021982573?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Leukemia+research&rft.atitle=Directed+therapy+for+patients+with+myelodysplastic+syndromes+%28MDS%29+by+suppression+of+cyclin+D1+with+ON+01910.Na.&rft.au=Olnes%2C+Matthew+J%3BShenoy%2C+Aarthie%3BWeinstein%2C+Barbara%3BPfannes%2C+Loretta%3BLoeliger%2C+Kelsey%3BTucker%2C+Zachary%3BTian%2C+Xin%3BKwak%2C+Minjung%3BWilhelm%2C+Francois%3BYong%2C+Agnes+S+M%3BMaric%2C+Irina%3BManiar%2C+Manoj%3BScheinberg%2C+Phillip%3BGroopman%2C+Jerome%3BYoung%2C+Neal+S%3BSloand%2C+Elaine+M&rft.aulast=Olnes&rft.aufirst=Matthew&rft.date=2012-08-01&rft.volume=36&rft.issue=8&rft.spage=982&rft.isbn=&rft.btitle=&rft.title=Leukemia+research&rft.issn=1873-5835&rft_id=info:doi/10.1016%2Fj.leukres.2012.04.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-05 N1 - Date created - 2012-06-22 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00533416; ClinicalTrials.gov N1 - SuppNotes - Cited By: Leukemia. 2003 Feb;17(2):379-89 [12592338] Leuk Res. 2012 Jan;36(1):98-103 [21924492] J Hematother Stem Cell Res. 2003 Aug;12(4):443-50 [12965081] Br J Haematol. 2003 Oct;123(1):173-6 [14510962] Blood. 2003 Nov 15;102(10):3786-92 [12893759] Leukemia. 2003 Dec;17(12):2474-86 [14562124] Biometrics. 1989 Sep;45(3):925-37 [2790129] Blood. 1997 Mar 15;89(6):2079-88 [9058730] Blood. 2004 Dec 15;104(13):4210-8 [15315976] N Engl J Med. 2005 Feb 10;352(6):549-57 [15703420] Blood. 2005 Aug 1;106(3):841-51 [15827127] Leukemia. 2005 Jul;19(7):1224-8 [15902281] Leuk Lymphoma. 2005 Nov;46(11):1605-1612 [16334487] Blood. 2006 Jan 1;107(1):205-12 [16144796] Blood. 2006 Jul 15;108(2):419-25 [16609072] Proc Natl Acad Sci U S A. 2006 Sep 26;103(39):14483-8 [16980411] Blood. 2007 Mar 15;109(6):2399-405 [17090657] Cancer. 2007 Apr 15;109(8):1536-42 [17345612] J Clin Oncol. 2007 Aug 10;25(23):3503-10 [17687155] J Chromatogr B Analyt Technol Biomed Life Sci. 2007 Sep 1;856(1-2):198-204 [17588831] Blood. 2007 Dec 15;110(13):4385-95 [17726160] Blood. 2008 May 15;111(10):4841-51 [18467609] J Clin Oncol. 2008 Dec 1;26(34):5504-10 [18955447] Science. 2008 Dec 19;322(5909):1861-5 [19095944] Lancet Oncol. 2009 Mar;10(3):223-32 [19230772] Oncogene. 2009 Mar 26;28(12):1518-28 [19198627] Blood. 2009 Apr 23;113(17):3947-52 [18987358] Cancer Chemother Pharmacol. 2009 Dec;65(1):177-86 [19466411] Ann Hematol. 2010 Apr;89(4):349-58 [19813013] JAMA. 2011 Feb 23;305(8):814-9 [21343581] Comment In: Leuk Res. 2012 Aug;36(8):964-5 [22607960] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.leukres.2012.04.002 ER - TY - JOUR T1 - Role of DLC1 tumor suppressor gene and MYC oncogene in pathogenesis of human hepatocellular carcinoma: potential prospects for combined targeted therapeutics (review). AN - 1020510850; 22580498 AB - Hepatocellular carcinoma (HCC) is the third leading cause of cancer death, and its incidence is increasing worldwide in an alarming manner. The development of curative therapy for advanced and metastatic HCC is a high clinical priority. The HCC genome is complex and heterogeneous; therefore, the identification of recurrent genomic and related gene alterations is critical for developing clinical applications for diagnosis, prognosis and targeted therapy of the disease. This article focuses on recent research progress and our contribution in identifying and deciphering the role of defined genetic alterations in the pathogenesis of HCC. A significant number of genes that promote or suppress HCC cell growth have been identified at the sites of genomic reorganization. Notwithstanding the accumulation of multiple genetic alterations, highly recurrent changes on a single chromosome can alter the expression of oncogenes and tumor suppressor genes (TSGs) whose deregulation may be sufficient to drive the progression of normal hepatocytes to malignancy. A distinct and highly recurrent pattern of genomic imbalances in HCC includes the loss of DNA copy number (associated with loss of heterozygosity) of TSG-containing chromosome 8p and gain of DNA copy number or regional amplification of protooncogenes on chromosome 8q. Even though 8p is relatively small, it carries an unusually large number of TSGs, while, on the other side, several oncogenes are dispersed along 8q. Compelling evidence demonstrates that DLC1, a potent TSG on 8p, and MYC oncogene on 8q play a critical role in the pathogenesis of human HCC. Direct evidence for their role in the genesis of HCC has been obtained in a mosaic mouse model. Knockdown of DLC1 helps MYC in the induction of hepatoblast transformation in vitro, and in the development of HCC in vivo. Therapeutic interventions, which would simultaneously target signaling pathways governing both DLC1 and MYC functions in hepatocarcinogenesis, could result in progress in the treatment of liver cancer. JF - International journal of oncology AU - Zimonjic, Drazen B AU - Popescu, Nicholas C AD - Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 393 EP - 406 VL - 41 IS - 2 KW - DLC1 protein, human KW - 0 KW - GTPase-Activating Proteins KW - Tumor Suppressor Proteins KW - Index Medicus KW - Gene Expression Regulation, Neoplastic KW - Animals KW - Humans KW - Cell Transformation, Neoplastic -- metabolism KW - Molecular Targeted Therapy KW - Mutation KW - Cell Transformation, Neoplastic -- genetics KW - Liver Neoplasms -- pathology KW - GTPase-Activating Proteins -- genetics KW - Tumor Suppressor Proteins -- physiology KW - Genes, myc KW - Carcinoma, Hepatocellular -- drug therapy KW - Liver Neoplasms -- drug therapy KW - Carcinoma, Hepatocellular -- genetics KW - GTPase-Activating Proteins -- physiology KW - Tumor Suppressor Proteins -- genetics KW - Carcinoma, Hepatocellular -- pathology KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Liver Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020510850?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+oncology&rft.atitle=Role+of+DLC1+tumor+suppressor+gene+and+MYC+oncogene+in+pathogenesis+of+human+hepatocellular+carcinoma%3A+potential+prospects+for+combined+targeted+therapeutics+%28review%29.&rft.au=Zimonjic%2C+Drazen+B%3BPopescu%2C+Nicholas+C&rft.aulast=Zimonjic&rft.aufirst=Drazen&rft.date=2012-08-01&rft.volume=41&rft.issue=2&rft.spage=393&rft.isbn=&rft.btitle=&rft.title=International+journal+of+oncology&rft.issn=1791-2423&rft_id=info:doi/10.3892%2Fijo.2012.1474 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-19 N1 - Date created - 2012-06-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 2009 Oct 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Dec;32(Pt 6):1107-9 [15506980] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.3892/ijo.2012.1474 ER - TY - JOUR T1 - Inflammation regulates microRNA expression in cooperation with p53 and nitric oxide. AN - 1017616914; 22042537 AB - microRNA (miRNA) are small non-coding RNA targeting mRNAs leading to their instability and diminished translation. Altered expression of miRNA is associated with cancer. Inflammation and nitric oxide modulates the development of lymphomas in p53 knockout mice and there exists a negative feedback loop between p53 and NOS2. Using a genetic strategy, we tested the hypothesis that inflammation-induced oxidative and nitrosative stress modulates miRNA expression in mouse model deficient in either p53 or NOS2. Mice treated with Corynebacterium parvum (C. parvum), to induce inflammation, clearly separated from controls by their miRNA profiles in wild-type, p53- and NOS2-knockout genetic backgrounds. C. parvum-induced inflammation significantly (p < 0.005) increased miR-21, miR-29b and miR-34a/b/c and decreased (p < 0.005) mir-29c and mir-181a/c expression in the spleen of C57BL mice. However, p53-knockout C57BL mice did not show a significant increase in the mir-34b/c or a decrease in mir-29c expression following C. parvum-induced inflammation. Expression of mir-21, mir-29b and mir-181a was independent of p53-status. NOS2-knockout C57BL mice showed a significant increase in miR-21 and miR-34a/b/c and decrease in miR-181a similar to the wild-type (WT) mice following C. parvum-induced inflammation. However, in contrast to the WT mice, miR-29b/c expression was not affected following C. parvum-induced inflammation in NOS2 knockout mice. N-acetyl cysteine, an anti-oxidant, reduced the expression of miR-21 and miR-29b in C. parvum-treated WT mice (p < 0.005) as compared with control C. parvum-treated mice. These data are consistent with the hypothesis that inflammation modulates miRNA expression in vivo and the alteration in specific miRNA under an inflammatory microenvironment, can be influenced by p53 (miR-34b/c) and NO(•) (29b/c). Copyright © 2011 UICC. JF - International journal of cancer AU - Mathé, Ewy AU - Nguyen, Giang H AU - Funamizu, Naotake AU - He, Peijun AU - Moake, Matthew AU - Croce, Carlo M AU - Hussain, S Perwez AD - Inflammation and Cancer Section, Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/08/01/ PY - 2012 DA - 2012 Aug 01 SP - 760 EP - 765 VL - 131 IS - 3 KW - MicroRNAs KW - 0 KW - Tumor Suppressor Protein p53 KW - Nitric Oxide KW - 31C4KY9ESH KW - Nitric Oxide Synthase Type II KW - EC 1.14.13.39 KW - Index Medicus KW - Animals KW - Nitric Oxide Synthase Type II -- deficiency KW - Mice, Inbred C57BL KW - Propionibacterium acnes -- immunology KW - Nitric Oxide Synthase Type II -- metabolism KW - Mice KW - Lymphoma -- immunology KW - Nitrosation KW - Nitric Oxide Synthase Type II -- genetics KW - Mice, Knockout KW - MicroRNAs -- metabolism KW - MicroRNAs -- genetics KW - Oxidative Stress KW - Nitric Oxide -- metabolism KW - Inflammation -- genetics KW - Tumor Suppressor Protein p53 -- genetics KW - Tumor Suppressor Protein p53 -- metabolism KW - Tumor Suppressor Protein p53 -- deficiency UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1017616914?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Inflammation+regulates+microRNA+expression+in+cooperation+with+p53+and+nitric+oxide.&rft.au=Math%C3%A9%2C+Ewy%3BNguyen%2C+Giang+H%3BFunamizu%2C+Naotake%3BHe%2C+Peijun%3BMoake%2C+Matthew%3BCroce%2C+Carlo+M%3BHussain%2C+S+Perwez&rft.aulast=Math%C3%A9&rft.aufirst=Ewy&rft.date=2012-08-01&rft.volume=131&rft.issue=3&rft.spage=760&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.26403 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-30 N1 - Date created - 2012-05-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nature. 2007 Jun 28;447(7148):1130-4 [17554337] Blood. 2007 Aug 15;110(4):1330-3 [17496199] Int J Cancer. 2007 Dec 1;121(11):2373-80 [17893866] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15805-10 [17890317] Cancer Cell. 2007 Nov;12(5):414-8 [17996645] Annu Rev Pathol. 2006;1:119-50 [18039110] Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3903-8 [18308936] Cancer Res. 2008 Sep 1;68(17):7130-6 [18757428] Gastroenterology. 2008 Nov;135(5):1624-1635.e24 [18835392] J Biol Chem. 2009 Mar 20;284(12):7903-13 [19158092] Proc Natl Acad Sci U S A. 2009 Jul 21;106(29):12085-90 [19597153] Nat Cell Biol. 2009 Sep;11(9):1135-42 [19701195] Clin Cancer Res. 2009 Sep 15;15(18):5878-87 [19737943] Nat Rev Genet. 2009 Oct;10(10):704-14 [19763153] Carcinogenesis. 2010 Jan;31(1):37-49 [19955394] Cell Death Differ. 2010 Feb;17(2):236-45 [19696787] J Exp Med. 2010 Mar 15;207(3):475-89 [20212066] Nat Rev Cancer. 2010 Jun;10(6):389-402 [20495573] Nature. 2010 Sep 2;467(7311):86-90 [20693987] Nat Rev Cancer. 2003 Apr;3(4):276-85 [12671666] Proc Natl Acad Sci U S A. 1998 Jul 21;95(15):8823-8 [9671763] Cancer Res. 2005 Nov 15;65(22):10255-64 [16288013] Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 [16461460] Proc Natl Acad Sci U S A. 2006 May 2;103(18):7024-9 [16641092] Proc Natl Acad Sci U S A. 2006 Aug 15;103(33):12481-6 [16885212] JAMA. 2007 May 2;297(17):1901-8 [17473300] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/ijc.26403 ER - TY - JOUR T1 - Challenges and opportunities of metabolomics. AN - 1011175300; 22034100 AB - The metabolome is a data-rich source of information concerning all the low-molecular-weight metabolites in a biofluid, which can indicate early biological changes to the host due to perturbations in metabolic pathways. Major changes can be seen after minor stimuli, which make it a valuable target for analysis. Due to the diverse and sensitive nature of the metabolome, studies must be designed in a manner to maintain consistency, reduce variation between subjects, and optimize information recovery. Technological advancements in experimental design, mouse models and instrumentation have aided in this effort. Metabolomics has the ultimate potential to be valuable in a clinical setting where it could be used for early diagnosis of a disease and as a predictor of treatment response and survival. During drug treatment, the metabolic status of an individual could be monitored and used to indicate possible toxic effects. Metabolomics therefore has great potential for improving diagnosis, treatment and aftercare of disease. Published in 2011 Wiley-Liss, Inc. This article is a U.S. Government work and is in the public domain in the USA. JF - Journal of cellular physiology AU - Johnson, Caroline H AU - Gonzalez, Frank J AD - Laboratory of Metabolism, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/08// PY - 2012 DA - August 2012 SP - 2975 EP - 2981 VL - 227 IS - 8 KW - Biomarkers KW - 0 KW - Index Medicus KW - Animals KW - Precision Medicine KW - Humans KW - Biomarkers -- analysis KW - Mice KW - Body Fluids -- metabolism KW - Metabolomics -- methods KW - Metabolome KW - Metabolic Networks and Pathways UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1011175300?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+physiology&rft.atitle=Challenges+and+opportunities+of+metabolomics.&rft.au=Johnson%2C+Caroline+H%3BGonzalez%2C+Frank+J&rft.aulast=Johnson&rft.aufirst=Caroline&rft.date=2012-08-01&rft.volume=227&rft.issue=8&rft.spage=2975&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+physiology&rft.issn=1097-4652&rft_id=info:doi/10.1002%2Fjcp.24002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-03 N1 - Date created - 2012-05-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/jcp.24002 ER - TY - JOUR T1 - That recognised risk factors can explain past and present international differences in breast cancer incidence: misconceptions 5 AN - 1093473398; 16969148 AB - Recent discussions on research priorities in the United States have revealed a widespread assumption that known risk factors entirely explain the historic international differences in rates of breast cancer. In fact, formal investigations of this question, both by modelling between-country differences and studies of migrants, indicate that an appreciable amount of the international differences in this disease remains unexplained. If this is not recognised, opportunities for research on breast cancer aetiology may be lost. JF - British Journal of Cancer AU - Hoover, R N AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA Y1 - 2012/07/24/ PY - 2012 DA - 2012 Jul 24 SP - 408 EP - 410 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 107 IS - 3 SN - 0007-0920, 0007-0920 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Breast cancer KW - Cancer KW - Historical account KW - Migrants KW - Risk factors 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/1093473398?accountid=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=That+recognised+risk+factors+can+explain+past+and+present+international+differences+in+breast+cancer+incidence%3A+misconceptions+5&rft.au=Hoover%2C+R+N&rft.aulast=Hoover&rft.aufirst=R&rft.date=2012-07-24&rft.volume=107&rft.issue=3&rft.spage=408&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2012.134 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2012-10-19 N1 - SubjectsTermNotLitGenreText - Historical account; Risk factors; Breast cancer; Migrants; Cancer; USA DO - http://dx.doi.org/10.1038/bjc.2012.134 ER - TY - JOUR T1 - Cerium dioxide nanoparticles induce apoptosis and autophagy in human peripheral blood monocytes. AN - 1027835419; 22717232 AB - Cerium dioxide nanoparticles (CeO(2) NPs) have diversified industrial uses, and novel therapeutic applications are actively being pursued. There is a lack of mechanistic data concerning the effects of CeO(2) NPs on primary human cells. We aimed at characterizing the cytotoxic effects of CeO(2) NPs in human peripheral blood monocytes. CeO(2) NPs and their suspensions were thoroughly characterized, including using transmission electron microscopy (TEM), dynamic light scattering, and zeta potential analysis. Blood from healthy human volunteers was drawn through phlebotomy, and CD14+ cells were isolated. Cells were exposed to CeO(2) NPs (0.5-10 μg/mL) for 20 or 40 h, and mechanisms of cell injury were studied. TEM revealed that CeO(2) NPs are internalized by monocytes and are found either in vesicles or free in the cytoplasm. CeO(2) NP exposure leads to decrease in cell viability, and treated cells exhibit characteristic hallmarks of apoptosis (activation of Bax, loss of mitochondrial membrane potential, DNA fragmentation). CeO(2) NP toxicity is caused by mitochondrial damage and overexpression of apoptosis inducing factor, but is not due to caspase activation or reactive oxygen species production. Moreover, CeO(2) NP exposure leads to autophagy, which is further increased after pharmacological inhibition of tumor suppressor protein p53. Inhibition of autophagy partially reverses cell death by CeO(2) NPs. It is concluded that CeO(2) NPs are toxic to primary human monocytes at relatively low doses. JF - ACS nano AU - Hussain, Salik AU - Al-Nsour, Faris AU - Rice, Annette B AU - Marshburn, Jamie AU - Yingling, Brenda AU - Ji, Zhaoxia AU - Zink, Jeffrey I AU - Walker, Nigel J AU - Garantziotis, Stavros AD - Clinical Research Unit, National Institute of Environmental Health Sciences/National Institute of Health, Research Triangle Park 27709, North Carolina, United States. salik.hussain@nih.gov Y1 - 2012/07/24/ PY - 2012 DA - 2012 Jul 24 SP - 5820 EP - 5829 VL - 6 IS - 7 KW - BAX protein, human KW - 0 KW - Reactive Oxygen Species KW - TP53 protein, human KW - Tumor Suppressor Protein p53 KW - bcl-2-Associated X Protein KW - Cerium KW - 30K4522N6T KW - ceric oxide KW - 619G5K328Y KW - Index Medicus KW - Autophagy -- drug effects KW - Reactive Oxygen Species -- metabolism KW - Microscopy, Electron, Transmission KW - Tumor Suppressor Protein p53 -- antagonists & inhibitors KW - Membrane Potential, Mitochondrial -- drug effects KW - Humans KW - In Vitro Techniques KW - Apoptosis -- drug effects KW - Tumor Suppressor Protein p53 -- metabolism KW - bcl-2-Associated X Protein -- metabolism KW - Nanotechnology KW - Metal Nanoparticles -- toxicity KW - Monocytes -- metabolism KW - Metal Nanoparticles -- ultrastructure KW - Monocytes -- pathology KW - Monocytes -- drug effects KW - Cerium -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1027835419?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=ACS+nano&rft.atitle=Cerium+dioxide+nanoparticles+induce+apoptosis+and+autophagy+in+human+peripheral+blood+monocytes.&rft.au=Hussain%2C+Salik%3BAl-Nsour%2C+Faris%3BRice%2C+Annette+B%3BMarshburn%2C+Jamie%3BYingling%2C+Brenda%3BJi%2C+Zhaoxia%3BZink%2C+Jeffrey+I%3BWalker%2C+Nigel+J%3BGarantziotis%2C+Stavros&rft.aulast=Hussain&rft.aufirst=Salik&rft.date=2012-07-24&rft.volume=6&rft.issue=7&rft.spage=5820&rft.isbn=&rft.btitle=&rft.title=ACS+nano&rft.issn=1936-086X&rft_id=info:doi/10.1021%2Fnn302235u LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-11-13 N1 - Date created - 2012-07-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Inhal Toxicol. 2008 Apr;20(6):547-66 [18444008] Toxicology. 2008 Mar 12;245(1-2):90-100 [18243471] Autophagy. 2008 Aug;4(6):810-4 [18604159] Toxicol Sci. 2008 Nov;106(1):140-52 [18632727] ACS Nano. 2008 Oct 28;2(10):2121-34 [19206459] Toxicology. 2009 Jun 16;260(1-3):142-9 [19464580] Nano Lett. 2009 Jun;9(6):2280-4 [19408924] Inhal Toxicol. 2009 Jul;21 Suppl 1:123-30 [19558244] Inhal Toxicol. 2009 Sep;21(11):943-51 [19552530] Small. 2009 Dec;5(24):2848-56 [19802857] Autophagy. 2009 Nov;5(8):1107-17 [19786831] J Mol Cell Biol. 2009 Oct;1(1):37-45 [19516051] Curr Opin Cell Biol. 2010 Apr;22(2):181-5 [20044243] Autophagy. 2010 Feb;6(2):310-1 [20104026] Part Fibre Toxicol. 2010;7:10 [20398356] Methods Mol Biol. 2011;697:207-12 [21116970] Environ Health Perspect. 2010 Dec;118(12):1699-706 [20729176] Crit Rev Toxicol. 2011 Mar;41(3):213-29 [21244219] Sci Total Environ. 2011 Jul 1;409(15):2987-92 [21570707] ACS Nano. 2011 Jun 28;5(6):4504-11 [21526848] ACS Nano. 2011 Jun 28;5(6):4537-49 [21612305] Nanotoxicology. 2011 Sep;5(3):312-25 [20925443] Autophagy. 2011 Oct;7(10):1251-3 [21743300] J Exp Med. 2011 Dec 19;208(13):2625-32 [22162830] Carcinogenesis. 2000 Mar;21(3):485-95 [10688869] Nat Rev Mol Cell Biol. 2000 Nov;1(2):120-9 [11253364] Am J Respir Crit Care Med. 2001 Aug 1;164(3):389-95 [11500338] J Cell Sci. 2002 Dec 15;115(Pt 24):4727-34 [12432061] Oncogene. 2004 Apr 12;23(16):2891-906 [15077152] Proc Natl Acad Sci U S A. 1991 May 1;88(9):3671-5 [2023917] Occup Environ Med. 1994 Mar;51(3):195-9 [8130849] Science. 1998 Aug 28;281(5381):1309-12 [9721092] Eur Cytokine Netw. 2004 Oct-Dec;15(4):339-46 [15627643] Nano Lett. 2005 Dec;5(12):2573-7 [16351218] Biomaterials. 2007 Apr;28(10):1918-25 [17222903] Chem Commun (Camb). 2007 Mar 14;(10):1056-8 [17325804] Nanomedicine (Lond). 2006 Dec;1(4):399-412 [17716143] J Immunol. 2007 Oct 1;179(7):4367-75 [17878331] Nat Nanotechnol. 2006 Nov;1(2):142-50 [18654167] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1021/nn302235u ER - TY - CPAPER T1 - Some Assembly Required: Mechanism of Rotavirus Genome Packaging and Replication T2 - 31st Annual Meeting of the American Society for Virology AN - 1313106933; 6187363 JF - 31st Annual Meeting of the American Society for Virology AU - Patton, John Y1 - 2012/07/21/ PY - 2012 DA - 2012 Jul 21 KW - Packaging KW - Replication KW - Genomes KW - Rotavirus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313106933?accountid=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=31st+Annual+Meeting+of+the+American+Society+for+Virology&rft.atitle=Some+Assembly+Required%3A+Mechanism+of+Rotavirus+Genome+Packaging+and+Replication&rft.au=Patton%2C+John&rft.aulast=Patton&rft.aufirst=John&rft.date=2012-07-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=31st+Annual+Meeting+of+the+American+Society+for+Virology&rft.issn=&rft_id=info:doi/ L2 - http://conferencing.uwex.edu/conferences/asv2012/conference.cfm LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Interferon-Induced TRIMming of Flavivirus Replication T2 - 31st Annual Meeting of the American Society for Virology AN - 1313106806; 6187350 JF - 31st Annual Meeting of the American Society for Virology AU - Best, Sonja Y1 - 2012/07/21/ PY - 2012 DA - 2012 Jul 21 KW - Replication KW - Flavivirus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313106806?accountid=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=31st+Annual+Meeting+of+the+American+Society+for+Virology&rft.atitle=Interferon-Induced+TRIMming+of+Flavivirus+Replication&rft.au=Best%2C+Sonja&rft.aulast=Best&rft.aufirst=Sonja&rft.date=2012-07-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=31st+Annual+Meeting+of+the+American+Society+for+Virology&rft.issn=&rft_id=info:doi/ L2 - http://conferencing.uwex.edu/conferences/asv2012/conference.cfm LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Exposure to Tobacco Smoke in Utero and Subsequent Plasma Lipids, ApoB, and CRP among Adult Women in the MoBa Cohort AN - 1660053044; 17649948 AB - Background: Recent findings suggest that maternal smoking during pregnancy may play a role in the development of metabolic alterations in offspring during childhood. However, whether such exposure increases the risk of developing similar metabolic alterations during adulthood is uncertain. Objective: We evaluated the association of in utero exposure to maternal tobacco smoke with plasma lipids, apolipoprotein B (apoB), and C-reactive protein (CRP) in adulthood. Methods: The study was based on a subsample of the Norwegian Mother and Child Cohort Study (MoBa) and included 479 pregnant women with plasma lipids, apoB, and CRP measurements. Information on in utero exposure to tobacco smoke, personal smoking, and other factors were obtained from the women by a self-completed questionnaire at enrollment, at approximately 17 weeks of gestation. Results: Women exposed to tobacco smoke in utero had higher triglycerides [10.7% higher; 95% confidence interval (CI): 3.9, 17.9] and lower high-density lipoprotein cholesterol (HDL) (-1.9 mg/dL; 95% CI: -4.3, 0.5) compared with unexposed women, after adjusting for age, physical activity, education, personal smoking, and current body mass index (BMI). Exposed women were also more likely to have triglycerides greater than or equal to 200 mg/dL [adjusted odds ratio (aOR) = 2.5; 95% CI: 1.3, 5.1] and HDL < 50 mg/dL (aOR = 2.3; 95% CI: 1.1, 5.0). Low-density lipoprotein cholesterol, total cholesterol, and apoB were not associated with the exposure. CRP was increased among exposed women; however, after adjustment for BMI, the association was completely attenuated. Conclusions: In this population, in utero exposure to tobacco smoke was associated with high triglycerides and low HDL in adulthood, 18-44 years after exposure. JF - Environmental Health Perspectives AU - Cupul-Uicab, Lea A AU - Skjaerven, Rolv AU - Haug, Kjell AU - Travlos, Gregory S AU - Wilson, Ralph E AU - Eggesboe, Merete AU - Hoppin, Jane A AU - Whitworth, Kristina W AU - Longnecker, Matthew P AD - Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA Y1 - 2012/07/19/ PY - 2012 DA - 2012 Jul 19 SP - 1532 EP - 1537 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 120 IS - 1 SN - 0091-6765, 0091-6765 KW - Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE) KW - clinical chemistry KW - C-reactive protein KW - metabolic syndrome KW - plasma lipids KW - prenatal exposure delayed effects KW - smoking KW - women KW - Smoke KW - Smoking KW - Triglycerides KW - Lipids KW - Exposure KW - Gestation KW - Tobacco KW - Cholesterol UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660053044?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvironmentalengabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Exposure+to+Tobacco+Smoke+in+Utero+and+Subsequent+Plasma+Lipids%2C+ApoB%2C+and+CRP+among+Adult+Women+in+the+MoBa+Cohort&rft.au=Cupul-Uicab%2C+Lea+A%3BSkjaerven%2C+Rolv%3BHaug%2C+Kjell%3BTravlos%2C+Gregory+S%3BWilson%2C+Ralph+E%3BEggesboe%2C+Merete%3BHoppin%2C+Jane+A%3BWhitworth%2C+Kristina+W%3BLongnecker%2C+Matthew+P&rft.aulast=Cupul-Uicab&rft.aufirst=Lea&rft.date=2012-07-19&rft.volume=120&rft.issue=1&rft.spage=1532&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1104563 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-03-01 N1 - Last updated - 2015-05-04 DO - http://dx.doi.org/10.1289/ehp.1104563 ER - TY - JOUR T1 - Recombinant immunotoxin engineered for low immunogenicity and antigenicity by identifying and silencing human B-cell epitopes. AN - 1027042253; 22753489 AB - Recombinant immunotoxins (RITs) are hybrid proteins used to treat cancer. These proteins are composed of an Fv that reacts with cancer cells joined to a portion of Pseudomonas exotoxin A, which kills the cell. Because the toxin is a foreign protein, it can induce neutralizing antibodies and thereby limit the number of doses a patient can receive. We previously identified seven major mouse B-cell epitopes in the toxin, and subsequently silenced them using point mutations that converted large hydrophilic amino acids to alanine, yet retained full antitumor activity. Here we present results in which we identify and silence human B-cell epitopes in the RIT HA22. We obtained B cells from patients with antibodies to RITs, isolated the corresponding variable fragments (Fvs), and constructed a phage-display library containing Fvs that bind to the RITs. We then used alanine scanning mutagenesis to locate the epitopes. We found that human and mouse epitopes frequently overlap but are not identical. Most mutations that remove mouse epitopes did not remove human epitopes. Using the epitope information, we constructed a variant immunotoxin, HA22-LR-LO10, which has low reactivity with human antisera, yet has high cytotoxic and antitumor activity and can be given to mice at high doses without excess toxicity. The toxin portion of this RIT (LR-LO10) can be used with Fvs targeting other cancer antigens and is suitable for clinical development. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Liu, Wenhai AU - Onda, Masanori AU - Lee, Byungkook AU - Kreitman, Robert J AU - Hassan, Raffit AU - Xiang, Laiman AU - Pastan, Ira AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/07/17/ PY - 2012 DA - 2012 Jul 17 SP - 11782 EP - 11787 VL - 109 IS - 29 KW - Antineoplastic Agents KW - 0 KW - Epitopes, B-Lymphocyte KW - Immunotoxins KW - Peptide Library KW - Recombinant Proteins KW - Single-Chain Antibodies KW - Index Medicus KW - Animals KW - Single-Chain Antibodies -- immunology KW - Humans KW - Protein Engineering -- methods KW - Molecular Sequence Data KW - Enzyme-Linked Immunosorbent Assay KW - Mice KW - Amino Acid Sequence KW - Statistics, Nonparametric KW - Mutagenesis KW - Immunotoxins -- pharmacokinetics KW - Immunotoxins -- chemistry KW - Neoplasms -- drug therapy KW - Antineoplastic Agents -- immunology KW - Models, Molecular KW - Immunotoxins -- immunology KW - Recombinant Proteins -- immunology KW - Recombinant Proteins -- pharmacokinetics KW - Immunotoxins -- genetics KW - Recombinant Proteins -- chemistry KW - Recombinant Proteins -- genetics KW - Epitopes, B-Lymphocyte -- immunology KW - Neoplasms -- immunology KW - Immunotherapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1027042253?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Recombinant+immunotoxin+engineered+for+low+immunogenicity+and+antigenicity+by+identifying+and+silencing+human+B-cell+epitopes.&rft.au=Liu%2C+Wenhai%3BOnda%2C+Masanori%3BLee%2C+Byungkook%3BKreitman%2C+Robert+J%3BHassan%2C+Raffit%3BXiang%2C+Laiman%3BPastan%2C+Ira&rft.aulast=Liu&rft.aufirst=Wenhai&rft.date=2012-07-17&rft.volume=109&rft.issue=29&rft.spage=11782&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.1209292109 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-11 N1 - Date created - 2012-07-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 2011 Oct 15;71(20):6300-9 [21998010] Proc Natl Acad Sci U S A. 2011 Apr 5;108(14):5742-7 [21436054] J Clin Oncol. 2012 May 20;30(15):1822-8 [22355053] J Clin Oncol. 2000 Apr;18(8):1622-36 [10764422] Protein J. 2004 Jan;23(1):39-52 [15115181] J Mol Biol. 1971 Feb 14;55(3):379-400 [5551392] Eur J Immunol. 1991 Apr;21(4):985-91 [2019291] J Mol Biol. 1991 Dec 5;222(3):581-97 [1748994] Int J Cancer. 1995 Jul 28;62(3):351-5 [7628878] J Protein Chem. 1996 Oct;15(7):691-700 [8968960] Int J Cancer. 1999 Mar 31;81(1):148-55 [10077166] Clin Cancer Res. 2005 Feb 15;11(4):1545-50 [15746059] Clin Cancer Res. 2005 Aug 15;11(16):5840-6 [16115924] Nat Rev Cancer. 2006 Jul;6(7):559-65 [16794638] J Immunol. 2006 Dec 15;177(12):8822-34 [17142785] Clin Cancer Res. 2007 Sep 1;13(17):5144-9 [17785569] Proc Natl Acad Sci U S A. 2008 Aug 12;105(32):11311-6 [18678888] Blood. 2009 Apr 16;113(16):3792-800 [18988862] Clin Cancer Res. 2009 Aug 15;15(16):5274-9 [19671873] Clin Cancer Res. 2010 Mar 15;16(6):1894-903 [20215554] Clin Cancer Res. 2011 Oct 15;17(20):6398-405 [22003067] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1073/pnas.1209292109 ER - TY - JOUR T1 - The Rates of HIV Superinfection and Primary HIV Incidence in a General Population in Rakai, Uganda AN - 1622601793; 20899982 AB - Background. Human immunodeficiency virus (HIV) superinfection has been documented in high-risk individuals; however, the rate of superinfection among HIV-infected individuals within a general population remains unknown. Methods. A novel next-generation ultra-deep sequencing technique was utilized to determine the rate of HIV superinfection in a heterosexual population by examining two regions of the viral genome in longitudinal samples from recent HIV seroconverters (n = 149) in Rakai District, Uganda. Results. The rate of superinfection was 1.44 per 100 person years (PYs) (95% confidence interval [CI], .4-2.5) and consisted of both inter- and intrasubtype superinfections. This was compared to primary HIV incidence in 20 220 initially HIV-negative individuals in the general population in Rakai (1.15 per 100 PYs; 95% CI, 1.1-1.2; P = .26). Propensity score matching (PS) was used to control for differences in sociodemographic and behavioral characteristics between the HIV-positive individuals at risk for superinfection and the HIV-negative population at baseline and follow-up. After PS matching, the estimated rate of primary incidence was 3.28 per 100 PYs (95% CI, 2.0-5.3; P = .07) controlling for baseline differences and 2.51 per 100 PYs (95% CI, 1.5-4.3; P = .24) controlling for follow-up differences. Conclusions. This suggests that the rate of HIV superinfection in a general population is substantial, which could have a significant impact on future public health and HIV vaccine strategies. JF - Journal of Infectious Diseases AU - Redd, Andrew D AU - Mullis, Caroline E AU - Serwadda, David AU - Kong, Xiangrong AU - Martens, Craig AU - Ricklefs, Stacy M AU - Tobian, Aaron A R AU - Xiao, Changchang AU - Grabowski, Mary K AU - Nalugoda, Fred AD - Laboratory of Immunoregulation, Division of Intramural Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health; National Institute of Allergy and Infectious Diseases, Rangos Bldg, Rm 527, 855 N Wolfe St, Baltimore, MD 21205, aredd2@jhmi.edu Y1 - 2012/07/15/ PY - 2012 DA - 2012 Jul 15 SP - 267 EP - 274 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 206 IS - 2 SN - 0022-1899, 0022-1899 KW - Virology & AIDS Abstracts; Risk Abstracts; Health & Safety Science Abstracts KW - Genomes KW - Risk taking KW - Uganda KW - Superinfection KW - Public health KW - Infectious diseases KW - Human immunodeficiency virus KW - Risk factors KW - Risk groups KW - Vaccines KW - V 22360:AIDS and HIV 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/1622601793?accountid=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+Infectious+Diseases&rft.atitle=The+Rates+of+HIV+Superinfection+and+Primary+HIV+Incidence+in+a+General+Population+in+Rakai%2C+Uganda&rft.au=Redd%2C+Andrew+D%3BMullis%2C+Caroline+E%3BSerwadda%2C+David%3BKong%2C+Xiangrong%3BMartens%2C+Craig%3BRicklefs%2C+Stacy+M%3BTobian%2C+Aaron+A+R%3BXiao%2C+Changchang%3BGrabowski%2C+Mary+K%3BNalugoda%2C+Fred&rft.aulast=Redd&rft.aufirst=Andrew&rft.date=2012-07-15&rft.volume=206&rft.issue=2&rft.spage=267&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjis325 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Genomes; Risk factors; Risk groups; Vaccines; Superinfection; Public health; Infectious diseases; Human immunodeficiency virus; Risk taking; Uganda DO - http://dx.doi.org/10.1093/infdis/jis325 ER - TY - JOUR T1 - Histone deacetylase inhibitors influence chemotherapy transport by modulating expression and trafficking of a common polymorphic variant of the ABCG2 efflux transporter. AN - 1026865073; 22472121 AB - Histone deacetylase inhibitors (HDI) have exhibited some efficacy in clinical trials, but it is clear that their most effective applications have yet to be fully determined. In this study, we show that HDIs influence the expression of a common polymorphic variant of the chemotherapy drug efflux transporter ABCG2, which contributes to normal tissue protection. As one of the most frequent variants in human ABCG2, the polymorphism Q141K impairs expression, localization, and function, thereby reducing drug clearance and increasing chemotherapy toxicity. Mechanistic investigations revealed that the ABCG2 Q141K variant was fully processed but retained in the aggresome, a perinuclear structure, where misfolded proteins aggregate. In screening for compounds that could correct its expression, localization, and function, we found that the microtubule-disrupting agent colchicine could induce relocalization of the variant from the aggresome to the cell surface. More strikingly, we found that HDIs could produce a similar effect but also restore protein expression to wild-type levels, yielding a restoration of ABCG2-mediated specific drug efflux activity. Notably, HDIs did not modify aggresome structures but instead rescued newly synthesized protein and prevented aggresome targeting, suggesting that HDIs disturbed trafficking along microtubules by eliciting changes in motor protein expression. Together, these results showed how HDIs are able to restore wild-type functions of the common Q141K polymorphic isoform of ABCG2. More broadly, our findings expand the potential uses of HDIs in the clinic. JF - Cancer research AU - Basseville, Agnes AU - Tamaki, Akina AU - Ierano, Caterina AU - Trostel, Shana AU - Ward, Yvona AU - Robey, Robert W AU - Hegde, Ramanujan S AU - Bates, Susan E AD - Medical Oncology Branch, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA. Y1 - 2012/07/15/ PY - 2012 DA - 2012 Jul 15 SP - 3642 EP - 3651 VL - 72 IS - 14 KW - ABCG2 protein, human KW - 0 KW - ATP Binding Cassette Transporter, Sub-Family G, Member 2 KW - Histone Deacetylase Inhibitors KW - Neoplasm Proteins KW - RNA, Small Interfering KW - Mitoxantrone KW - BZ114NVM5P KW - Index Medicus KW - Gene Expression -- drug effects KW - Humans KW - RNA, Small Interfering -- pharmacology KW - Mitoxantrone -- pharmacology KW - Cell Line KW - Biological Transport -- drug effects KW - Neoplasm Proteins -- drug effects KW - ATP-Binding Cassette Transporters -- drug effects KW - Histone Deacetylase Inhibitors -- pharmacology KW - Polymorphism, Genetic KW - ATP-Binding Cassette Transporters -- metabolism KW - Neoplasm Proteins -- genetics KW - ATP-Binding Cassette Transporters -- genetics KW - Neoplasm Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1026865073?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Histone+deacetylase+inhibitors+influence+chemotherapy+transport+by+modulating+expression+and+trafficking+of+a+common+polymorphic+variant+of+the+ABCG2+efflux+transporter.&rft.au=Basseville%2C+Agnes%3BTamaki%2C+Akina%3BIerano%2C+Caterina%3BTrostel%2C+Shana%3BWard%2C+Yvona%3BRobey%2C+Robert+W%3BHegde%2C+Ramanujan+S%3BBates%2C+Susan+E&rft.aulast=Basseville&rft.aufirst=Agnes&rft.date=2012-07-15&rft.volume=72&rft.issue=14&rft.spage=3642&rft.isbn=&rft.btitle=&rft.title=Cancer+research&rft.issn=1538-7445&rft_id=info:doi/10.1158%2F0008-5472.CAN-11-2008 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-25 N1 - Date created - 2012-07-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Anticancer Drugs. 2000 Jul;11(6):445-54 [11001385] N Engl J Med. 2011 Nov 3;365(18):1663-72 [22047557] Biochem Biophys Res Commun. 2001 Jul 6;285(1):111-7 [11437380] J Lipid Res. 2001 Jul;42(7):1007-17 [11441126] Nature. 2002 May 23;417(6887):455-8 [12024216] Cell Motil Cytoskeleton. 2002 Sep;53(1):26-38 [12211113] Exp Mol Pathol. 2003 Apr;74(2):173-9 [12710949] Cancer Res. 2003 Oct 1;63(19):6447-52 [14559835] J Neurosci. 2003 Nov 19;23(33):10672-80 [14627652] Cell. 2003 Dec 12;115(6):727-38 [14675537] Int J Cancer. 2004 Mar 20;109(2):238-46 [14750175] Curr Biol. 2004 Mar 23;14(6):488-92 [15043813] Cell. 1991 May 31;65(5):817-23 [1904010] J Biol Chem. 1994 Oct 14;269(41):25710-8 [7523390] J Biol Chem. 1994 Nov 18;269(46):28683-9 [7961819] EMBO J. 1994 Dec 15;13(24):6076-86 [7529176] Eur J Cell Biol. 1997 Mar;72(3):238-46 [9084986] J Cell Biol. 1998 Dec 28;143(7):1883-98 [9864362] Biochemistry. 2005 Apr 12;44(14):5420-9 [15807535] Mol Pharmacol. 2005 May;67(5):1797-807 [15722457] Cancer Chemother Pharmacol. 2005 Aug;56(2):161-72 [15838659] Proc Natl Acad Sci U S A. 2005 Sep 13;102(37):13135-40 [16141322] Carcinogenesis. 2006 Jan;27(1):123-30 [16000399] Cancer Res. 2006 Apr 1;66(7):3773-81 [16585204] J Bioenerg Biomembr. 2005 Dec;37(6):501-7 [16691490] Nat Rev Drug Discov. 2006 Sep;5(9):769-84 [16955068] Mol Pharmacol. 2007 Mar;71(3):751-8 [17132688] BMC Biochem. 2007;8 Suppl 1:S11 [18047735] Mol Cancer Res. 2008 Jan;6(1):151-64 [18234970] Biochem J. 2008 Jul 1;413(1):29-36 [18361776] Lancet. 2008 Dec 6;372(9654):1953-61 [18834626] Pharm Res. 2009 Feb;26(2):469-79 [18958403] Adv Drug Deliv Rev. 2009 Jan 31;61(1):3-13 [19135109] Drugs. 2009 Oct 1;69(14):1911-34 [19747008] Nat Chem Biol. 2010 Jan;6(1):25-33 [19966789] Biochem Soc Trans. 2010 Feb;38(Pt 1):144-9 [20074049] Nat Neurosci. 2010 Feb;13(2):180-9 [20037577] Biochemistry. 2010 Mar 16;49(10):2235-45 [20088606] Curr Drug Metab. 2010 Sep;11(7):603-17 [20812902] Mol Cancer Res. 2011 Apr;9(4):516-27 [21357443] Trends Cell Biol. 2000 Dec;10(12):524-30 [11121744] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1158/0008-5472.CAN-11-2008 ER - TY - JOUR T1 - Coffee intake and breast cancer risk in the NIH-AARP diet and health study cohort. AN - 1015756142; 22020403 AB - There are several biologic mechanisms whereby coffee might reduce breast cancer risk. Caffeine and caffeic acid, major coffee constituents, have been shown to suppress mammary tumor formation in animal models and to inhibit DNA methylation in human breast cancer cells, respectively. Coffee may also reduce risk through decreasing inflammation and influencing estrogen metabolism. However, epidemiologic studies have been inconsistent and few studies have examined the association by estrogen and progesterone receptor (ER/PR) status. We evaluated coffee intake for its effect on incident breast cancer in the National Institutes of Health-AARP Diet and Health Study cohort, which included 198,404 women aged 50-71 with no history of cancer, who in 1995-1996 completed a questionnaire capturing usual coffee intake over the past year. State cancer registry and mortality index linkage identified 9,915 primary incident breast carcinomas through December 2006; available information on hormone receptor (HR) status identified 2,051 ER+/PR+ and 453 ER-/PR- cancers. In multivariable proportional hazards models, coffee intake was not associated with breast cancer risk (p-value for trend = 0.38; relative risk = 0.98, 95% confidence interval: 0.91-1.07, for four or more cups per day as compared to women who never drank coffee), and results did not vary by body mass index or history of benign breast biopsy (p-value for interaction > 0.10). We found no evidence of a relationship with either caffeinated or decaffeinated coffee. Null findings persisted for risk of both HR-positive and -negative breast cancers. These findings from a large prospective cohort do not support a role of coffee intake in breast carcinogenesis. Copyright © 2011 UICC. JF - International journal of cancer AU - Gierach, Gretchen L AU - Freedman, Neal D AU - Andaya, Abegail AU - Hollenbeck, Albert R AU - Park, Yikyung AU - Schatzkin, Arthur AU - Brinton, Louise A AD - Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 6120 Executive Blvd, Suite 550, Rockville, MD, USA. gierachg@mail.nih.gov Y1 - 2012/07/15/ PY - 2012 DA - 2012 Jul 15 SP - 452 EP - 460 VL - 131 IS - 2 KW - Coffee KW - 0 KW - Receptors, Estrogen KW - Receptors, Progesterone KW - Caffeine KW - 3G6A5W338E KW - Index Medicus KW - Humans KW - Aged KW - Receptors, Estrogen -- analysis KW - Multivariate Analysis KW - Receptors, Progesterone -- analysis KW - Risk Assessment KW - DNA Methylation KW - Risk Factors KW - Cohort Studies KW - National Institutes of Health (U.S.) KW - Middle Aged KW - United States -- epidemiology KW - Female KW - Proportional Hazards Models KW - Caffeine -- administration & dosage KW - Breast Neoplasms -- chemistry KW - Diet KW - Breast Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1015756142?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Coffee+intake+and+breast+cancer+risk+in+the+NIH-AARP+diet+and+health+study+cohort.&rft.au=Gierach%2C+Gretchen+L%3BFreedman%2C+Neal+D%3BAndaya%2C+Abegail%3BHollenbeck%2C+Albert+R%3BPark%2C+Yikyung%3BSchatzkin%2C+Arthur%3BBrinton%2C+Louise+A&rft.aulast=Gierach&rft.aufirst=Gretchen&rft.date=2012-07-15&rft.volume=131&rft.issue=2&rft.spage=452&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.26372 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-30 N1 - Date created - 2012-05-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Clin Exp Metastasis. 2004;21(8):719-35 [16035617] Surgery. 1979 Jul;86(1):105-9 [222001] Am J Epidemiol. 1993 Sep 15;138(6):380-3 [8213743] Int J Cancer. 1992 Oct 21;52(4):511-6 [1399128] Am J Clin Nutr. 1991 Jan;53(1):166-71 [1845789] Br J Cancer. 1990 Aug;62(2):267-70 [2386741] Am J Obstet Gynecol. 1979 Sep 1;135(1):157-8 [224703] Carcinogenesis. 2006 Feb;27(2):269-77 [16081510] Carcinogenesis. 2003 May;24(5):991-1005 [12771045] J Clin Oncol. 2003 Jan 1;21(1):28-34 [12506166] J Obstet Gynaecol Can. 2002 Oct;24(10):783-90, 793-802 [12399806] Am J Epidemiol. 2001 Dec 15;154(12):1119-25 [11744517] Eur J Cancer Prev. 2000 Aug;9(4):241-56 [10958327] Cancer Causes Control. 2009 Dec;20(10):2039-44 [19597749] Cancer Causes Control. 2010 Nov;21(11):1941-8 [20680436] Cancer Causes Control. 2010 Oct;21(10):1533-44 [20512657] Breast Cancer Res Treat. 2010 Jun;121(2):461-7 [19847643] Am J Obstet Gynecol. 2009 Mar;200(3):290.e1-9 [19114275] Arch Intern Med. 2008 Oct 13;168(18):2022-31 [18852405] Int J Cancer. 2008 May 1;122(9):2071-6 [18183588] Breast Cancer Res. 2007;9(4):210 [17640394] Am J Clin Nutr. 2006 Oct;84(4):888-93 [17023717] Diabetes Care. 2005 Jun;28(6):1390-6 [15920057] Stat Med. 2004 Dec 30;23(24):3803-20 [15580597] Nutr Cancer. 1998;30(1):21-4 [9507508] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/ijc.26372 ER - TY - JOUR T1 - An Overlapping Protein-Coding Region in Influenza A Virus Segment 3 Modulates the Host Response AN - 1551631619; 20371855 AB - Influenza's Cryptic ConstraintBecause of the well-known pandemic potential of influenza viruses, it is important to understand the range of molecular interactions between the virus and its host. Despite years of intensive research on the virus, Jagger et al. (p. 199, published online 28 June; see the Perspective by Yewdell and Ince) have found that the influenza A virus has been hiding a gene in its small negative-sense RNA genome. An overlapping open reading frame was found contained in the PA viral RNA polymerase gene, which is accessed by ribosomal frameshifting to produce a fusion protein containing the N-terminal messenger RNA (mRNA) endonuclease domain of PA and an alternative C-terminal X domain. The resulting polypeptide, PA-X, selectively degrades host mRNAs and, in a mouse model of infection, modulated cellular immune responses, thus limiting viral pathogenesis. JF - Science AU - Jagger, B W AU - Wise, H M AU - Kash, J C AU - Walters, K-A AU - Wills, N M AU - Xiao, Y-L AU - Dunfee, R L AU - Schwartzman, L M AU - Ozinsky, A AU - Bell, G L AU - Dalton, R M AU - Lo, A AU - Efstathiou, S AU - Atkins, J F AU - Firth, A E AU - Taubenberger, J K AU - Digard, P AD - Viral Pathogenesis and Evolution Section, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA, aef24@cam.ac.uk Y1 - 2012/07/13/ PY - 2012 DA - 2012 Jul 13 SP - 199 EP - 204 PB - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States VL - 337 IS - 6091 SN - 0036-8075, 0036-8075 KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Genomes KW - Viruses KW - Animal models KW - Infection KW - mRNA KW - Influenza KW - DNA-directed RNA polymerase KW - pandemics KW - Influenza A virus KW - Proteins KW - Fusion protein KW - Immune response KW - Endonuclease KW - Internet KW - Open reading frames KW - V 22350:Immunology KW - H 0500:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551631619?accountid=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=Science&rft.atitle=An+Overlapping+Protein-Coding+Region+in+Influenza+A+Virus+Segment+3+Modulates+the+Host+Response&rft.au=Jagger%2C+B+W%3BWise%2C+H+M%3BKash%2C+J+C%3BWalters%2C+K-A%3BWills%2C+N+M%3BXiao%2C+Y-L%3BDunfee%2C+R+L%3BSchwartzman%2C+L+M%3BOzinsky%2C+A%3BBell%2C+G+L%3BDalton%2C+R+M%3BLo%2C+A%3BEfstathiou%2C+S%3BAtkins%2C+J+F%3BFirth%2C+A+E%3BTaubenberger%2C+J+K%3BDigard%2C+P&rft.aulast=Jagger&rft.aufirst=B&rft.date=2012-07-13&rft.volume=337&rft.issue=6091&rft.spage=199&rft.isbn=&rft.btitle=&rft.title=Science&rft.issn=00368075&rft_id=info:doi/10.1126%2Fscience.1222213 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Genomes; pandemics; DNA-directed RNA polymerase; Animal models; Immune response; Fusion protein; Infection; Endonuclease; Open reading frames; Internet; mRNA; Influenza; Viruses; Proteins; Influenza A virus DO - http://dx.doi.org/10.1126/science.1222213 ER - TY - JOUR T1 - Eltrombopag and improved hematopoiesis in refractory aplastic anemia. AN - 1024095157; 22762314 AB - Severe aplastic anemia, which is characterized by immune-mediated bone marrow hypoplasia and pancytopenia, can be treated effectively with immunosuppressive therapy or allogeneic transplantation. One third of patients have disease that is refractory to immunosuppression, with persistent, severe cytopenia and a profound deficit in hematopoietic stem cells and progenitor cells. Thrombopoietin may increase the number of hematopoietic stem cells and progenitor cells. We conducted a phase 2 study involving patients with aplastic anemia that was refractory to immunosuppression to determine whether the oral thrombopoietin mimetic eltrombopag (Promacta) can improve blood counts. Twenty-five patients received eltrombopag at a dose of 50 mg, which could be increased, as needed, to a maximum dose of 150 mg daily, for a total of 12 weeks. Primary end points were clinically significant changes in blood counts or transfusion independence. Patients with a response continued to receive eltrombopag. Eleven of 25 patients (44%) had a hematologic response in at least one lineage at 12 weeks, with minimal toxic effects. Nine patients no longer needed platelet transfusions (median increase in platelet count, 44,000 per cubic millimeter). Six patients had improved hemoglobin levels (median increase, 4.4 g per deciliter); 3 of them were previously dependent on red-cell transfusions and no longer needed transfusions. Nine patients had increased neutrophil counts (median increase, 1350 per cubic millimeter). Serial bone marrow biopsies showed normalization of trilineage hematopoiesis in patients who had a response, without increased fibrosis. Monitoring of immune function revealed no consistent changes. Treatment with eltrombopag was associated with multilineage clinical responses in some patients with refractory severe aplastic anemia. (Funded by the National Heart, Lung, and Blood Institute; ClinicalTrials.gov number, NCT00922883.). JF - The New England journal of medicine AU - Olnes, Matthew J AU - Scheinberg, Phillip AU - Calvo, Katherine R AU - Desmond, Ronan AU - Tang, Yong AU - Dumitriu, Bogdan AU - Parikh, Ankur R AU - Soto, Susan AU - Biancotto, Angelique AU - Feng, Xingmin AU - Lozier, Jay AU - Wu, Colin O AU - Young, Neal S AU - Dunbar, Cynthia E AD - Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/07/05/ PY - 2012 DA - 2012 Jul 05 SP - 11 EP - 19 VL - 367 IS - 1 KW - Benzoates KW - 0 KW - Hydrazines KW - Pyrazoles KW - eltrombopag KW - S56D65XJ9G KW - Abridged Index Medicus KW - Index Medicus KW - Young Adult KW - Humans KW - Adult KW - Drug Resistance KW - Aged KW - Middle Aged KW - Chronic Disease KW - Bone Marrow Cells -- cytology KW - Adolescent KW - Recurrence KW - Male KW - Female KW - Pyrazoles -- administration & dosage KW - Hydrazines -- administration & dosage KW - Hydrazines -- therapeutic use KW - Anemia, Aplastic -- pathology KW - Anemia, Aplastic -- drug therapy KW - Benzoates -- adverse effects KW - Pyrazoles -- adverse effects KW - Benzoates -- administration & dosage KW - Pyrazoles -- therapeutic use KW - Hydrazines -- adverse effects KW - Benzoates -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1024095157?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Eltrombopag+and+improved+hematopoiesis+in+refractory+aplastic+anemia.&rft.au=Olnes%2C+Matthew+J%3BScheinberg%2C+Phillip%3BCalvo%2C+Katherine+R%3BDesmond%2C+Ronan%3BTang%2C+Yong%3BDumitriu%2C+Bogdan%3BParikh%2C+Ankur+R%3BSoto%2C+Susan%3BBiancotto%2C+Angelique%3BFeng%2C+Xingmin%3BLozier%2C+Jay%3BWu%2C+Colin+O%3BYoung%2C+Neal+S%3BDunbar%2C+Cynthia+E&rft.aulast=Olnes&rft.aufirst=Matthew&rft.date=2012-07-05&rft.volume=367&rft.issue=1&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=1533-4406&rft_id=info:doi/10.1056%2FNEJMoa1200931 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-11 N1 - Date created - 2012-07-05 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00922883; ClinicalTrials.gov N1 - SuppNotes - Cited By: Br J Haematol. 1979 Oct;43(2):185-90 [508627] Ann Hematol. 2005 Jan;84(1):47-55 [15340760] Blood. 2007 Apr 1;109(7):2794-6 [17110459] N Engl J Med. 2007 Nov 29;357(22):2237-47 [18046028] Blood. 2008 Feb 1;111(3):981-6 [18223171] Cell Stem Cell. 2007 Dec 13;1(6):671-84 [18371408] Br J Haematol. 2009 Jan;144(2):206-16 [19036108] Haematologica. 2009 May;94(5):712-9 [19336743] Stem Cells. 2009 Feb;27(2):424-30 [19038790] Annu Rev Med. 2009;60:193-206 [19642221] Blood. 2009 Oct 29;114(18):3748-56 [19671919] JAMA. 2010 Sep 22;304(12):1358-64 [20858879] Br J Haematol. 1999 Nov;107(2):330-4 [10583220] Semin Hematol. 2000 Jan;37(1):91-101 [10676914] JAMA. 2003 Mar 5;289(9):1130-5 [12622583] Clin Infect Dis. 2011 Mar 15;52(6):726-35 [21367725] Haematologica. 2011 Apr;96(4):602-6 [21160069] Pediatr Blood Cancer. 2011 Aug;57(2):199-203 [21337678] N Engl J Med. 2011 Aug 4;365(5):430-8 [21812672] Leukemia. 2012 Apr;26(4):700-7 [22005790] Blood. 2006 Oct 15;108(8):2509-19 [16778145] Proc Natl Acad Sci U S A. 1998 Feb 3;95(3):1195-200 [9448308] Blood. 1996 Sep 15;88(6):1983-91 [8822917] Blood. 1996 May 15;87(10):4068-71 [8639762] Control Clin Trials. 1989 Mar;10(1):1-10 [2702835] Blood. 1994 Dec 15;84(12):4045-52 [7527664] Blood. 1996 Mar 15;87(6):2162-70 [8630375] Comment In: N Engl J Med. 2012 Sep 20;367(12):1162; author reply 1163 [22992084] N Engl J Med. 2012 Sep 20;367(12):1162-3; author reply 1163 [22992085] N Engl J Med. 2012 Jul 5;367(1):74-5 [22762322] Erratum In: N Engl J Med. 2012 Jul 19;367(3):284 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1056/NEJMoa1200931 ER - TY - JOUR T1 - Moving toward multimedia electronic health records: how do we get there? AN - 1551620076; 20322173 AB - This report, based on a workshop jointly sponsored the National Institute of Biomedical Imaging and Biomedical Engineering and the Office of the National Coordinator for Health Information Technology, examines the role and value of images as multimedia data in electronic health records (EHRs). The workshop, attended by a wide range of stakeholders, was motivated in part by the absence of image data from discussions of meaningful use of health information technology. Collectively, the workshop presenters and participants argued that images are not ancillary data and should be central to health information systems to facilitate clinical decisions and higher quality, efficiency, and safety of care. They emphasized that the imaging community has already developed standards that form the basis of interoperability. Despite the apparent value of images, workshop participants also identified challenges and barriers to their implementation within EHRs. Weighing the opportunities and challenges, workshop participants provided their perspectives on possible paths forward toward fully multimedia EHRs. JF - Journal of the American Medical Informatics Association AU - Seto, Belinda AU - Friedman, Charles AD - NIBIB, NIH, Bethesda, Maryland, USA Y1 - 2012/07/04/ PY - 2012 DA - 2012 Jul 04 SP - 503 EP - 505 PB - American Medical Informatics Association, 4915 St. Elmo Ave. Bethesda MD 20814 United States VL - 19 IS - 4 SN - 1067-5027, 1067-5027 KW - Biotechnology and Bioengineering Abstracts KW - Data processing KW - Conferences KW - Informatics KW - imaging KW - Information systems KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551620076?accountid=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+the+American+Medical+Informatics+Association&rft.atitle=Moving+toward+multimedia+electronic+health+records%3A+how+do+we+get+there%3F&rft.au=Seto%2C+Belinda%3BFriedman%2C+Charles&rft.aulast=Seto&rft.aufirst=Belinda&rft.date=2012-07-04&rft.volume=19&rft.issue=4&rft.spage=503&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+American+Medical+Informatics+Association&rft.issn=10675027&rft_id=info:doi/10.1136%2Famiajnl-2011-000660 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2014-08-07 N1 - SubjectsTermNotLitGenreText - Data processing; Conferences; Informatics; imaging; Information systems DO - http://dx.doi.org/10.1136/amiajnl-2011-000660 ER - TY - JOUR T1 - Pharmaco-metabolomics: an emerging "omics" tool for the personalization of anticancer treatments and identification of new valuable therapeutic targets. AN - 934256983; 22105661 AB - In the post-genomics era, metabolomics represents a new "omics" approach that in the last decade has received increased attention in the field of oncology. Metabolomics is based on the holistic study of the metabolic profile that characterizes a specific phenotype in a biological system. The metabolic profile provides a readout of the metabolic state of an individual that cannot be obtained directly from DNA genotyping, gene expression, or proteomic profiling analyses. The translational value of metabonomics in the oncology field has been demonstrated by the identification of diagnostic and prognostic biomarkers. The so-called pharmaco-metabolomic approach that is currently emerging aims to identify the individual metabolomic characteristics able to predict drug effectiveness and/or toxicity. This review presents the potential role of pharmaco-metabolomics in the future of anticancer pharmacology to achieve customized anticancer treatments and new, targeted therapeutic approaches. Copyright © 2011 Wiley Periodicals, Inc. JF - Journal of cellular physiology AU - Corona, Giuseppe AU - Rizzolio, Flavio AU - Giordano, Antonio AU - Toffoli, Giuseppe AD - Experimental and Clinical Pharmacology Division, IRCCS, National Cancer Institute, Aviano, Pordenone, Italy. Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 2827 EP - 2831 VL - 227 IS - 7 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Molecular Targeted Therapy KW - Neoplasms -- drug therapy KW - Metabolomics -- methods KW - Metabolome -- drug effects KW - Precision Medicine -- methods KW - Antineoplastic Agents -- therapeutic use KW - Antineoplastic Agents -- pharmacology KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/934256983?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+cellular+physiology&rft.atitle=Pharmaco-metabolomics%3A+an+emerging+%22omics%22+tool+for+the+personalization+of+anticancer+treatments+and+identification+of+new+valuable+therapeutic+targets.&rft.au=Corona%2C+Giuseppe%3BRizzolio%2C+Flavio%3BGiordano%2C+Antonio%3BToffoli%2C+Giuseppe&rft.aulast=Corona&rft.aufirst=Giuseppe&rft.date=2012-07-01&rft.volume=227&rft.issue=7&rft.spage=2827&rft.isbn=&rft.btitle=&rft.title=Journal+of+cellular+physiology&rft.issn=1097-4652&rft_id=info:doi/10.1002%2Fjcp.24003 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-19 N1 - Date created - 2012-03-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/jcp.24003 ER - TY - JOUR T1 - Glucocorticoid regulation of inflammation and its functional correlates: from HPA axis to glucocorticoid receptor dysfunction AN - 1780514505; PQ0002829269 AB - Enhanced susceptibility to inflammatory and autoimmune disease can be related to impairments in HPA axis activity and associated hypocortisolism, or to glucocorticoid resistance resulting from impairments in local factors affecting glucocorticoid availability and function, including the glucocorticoid receptor (GR). The enhanced inflammation and hypercortisolism that typically characterize stress-related illnesses, such as depression, metabolic syndrome, cardiovascular disease, or osteoporosis, may also be related to increased glucocorticoid resistance. This review focuses on impaired GR function as a molecular mechanism of glucocorticoid resistance. Both genetic and environmental factors can contribute to impaired GR function. The evidence that glucocorticoid resistance can be environmentally induced has important implications for management of stress-related inflammatory illnesses and underscores the importance of prevention and management of chronic stress. The simultaneous assessment of neural, endocrine, and immune biomarkers through various noninvasive methods will also be discussed. JF - Annals of the New York Academy of Sciences AU - Silverman, Marni N AU - Sternberg, Esther M AD - Section on Neuroendocrine Immunology and Behavior, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland. Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 55 EP - 63 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 1261 IS - 1 SN - 0077-8923, 0077-8923 KW - Environment Abstracts KW - Bioindicators KW - Prevention KW - Depression KW - Reviews KW - Metabolic disorders KW - Autoimmune diseases KW - Osteoporosis KW - Stress KW - Cardiovascular diseases KW - Environmental factors KW - ENA 07:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780514505?accountid=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=Glucocorticoid+regulation+of+inflammation+and+its+functional+correlates%3A+from+HPA+axis+to+glucocorticoid+receptor+dysfunction&rft.au=Silverman%2C+Marni+N%3BSternberg%2C+Esther+M&rft.aulast=Silverman&rft.aufirst=Marni&rft.date=2012-07-01&rft.volume=1261&rft.issue=1&rft.spage=55&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/10.1111%2Fj.1749-6632.2012.06633.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-04-29 N1 - SubjectsTermNotLitGenreText - Bioindicators; Prevention; Depression; Metabolic disorders; Reviews; Autoimmune diseases; Stress; Osteoporosis; Cardiovascular diseases; Environmental factors DO - http://dx.doi.org/10.1111/j.1749-6632.2012.06633.x ER - TY - JOUR T1 - Persister-promoting bacterial toxin TisB produces anion-selective pores in planar lipid bilayers AN - 1668257428; PQ0001195434 AB - We studied membrane activity of the bacterial peptide TisB involved in persister cell formation. TisB and its analogs form multi-state ion-conductive pores in planar lipid bilayers with all states displaying similar anionic selectivity. TisB analogs differing by plus or minus 1 elementary charges show corresponding changes in selectivity. Probing TisB pores with poly-(ethylene glycol)s reveals only restricted partitioning even for the smallest polymers, suggesting that the pores are characterized by a relatively small diameter. These findings allow us to suggest that TisB forms clusters of narrow pores that are essential for its mechanism of action. JF - FEBS Letters AU - Gurnev, Philip A AU - Ortenberg, Ron AU - Dorr, Tobias AU - Lewis, Kim AU - Bezrukov, Sergey M AD - Program in Physical Biology, National Institute of Child Health and Human Development, Bethesda, MD 20892, United States Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 2529 EP - 2534 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 586 IS - 16 SN - 0014-5793, 0014-5793 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology KW - Bacteria multi-drug tolerance KW - Toxin/antitoxin system KW - Biofilms KW - Cluster pore structure KW - Bacteria KW - Pores KW - Lipid bilayers KW - Toxins KW - A 01490:Miscellaneous KW - J 02330:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668257428?accountid=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=FEBS+Letters&rft.atitle=Persister-promoting+bacterial+toxin+TisB+produces+anion-selective+pores+in+planar+lipid+bilayers&rft.au=Gurnev%2C+Philip+A%3BOrtenberg%2C+Ron%3BDorr%2C+Tobias%3BLewis%2C+Kim%3BBezrukov%2C+Sergey+M&rft.aulast=Gurnev&rft.aufirst=Philip&rft.date=2012-07-01&rft.volume=586&rft.issue=16&rft.spage=2529&rft.isbn=&rft.btitle=&rft.title=FEBS+Letters&rft.issn=00145793&rft_id=info:doi/10.1016%2Fj.febslet.2012.06.021 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2016-08-17 N1 - SubjectsTermNotLitGenreText - Lipid bilayers; Pores; Toxins; Bacteria DO - http://dx.doi.org/10.1016/j.febslet.2012.06.021 ER - TY - JOUR T1 - Common Factors and Causal Networks AN - 1665156103 AB - The target article touches upon some of the most difficult and essential questions in personality psychology. Questioning the notion of a common factor as an as-yet-unobserved common cause of a behaviour domainʼs exemplars, the authors propose using graphical representations to inspire hypotheses of more complex causal structures. I do not find the case for the de-emphasis of the common factor model to be compelling for those behaviour domains (cognitive abilities) with which I am most familiar. It behoves all personality psychologists, however, to question the foundations of their favoured tools. Copyright © 2012 John Wiley & Sons, Ltd. JF - European Journal of Personality AU - Lee, James J AD - Vision Lab, Department of Psychology, Harvard University, Cambridge, MA, USA., Laboratory of Biological Modeling, NIDDK, NIH, Bethesda, MD, USA., Cognitive Genomics Lab, BGI-Shenzhen, Yantian District, Shenzhen, China. ; Vision Lab, Department of Psychology, Harvard University, Cambridge, MA, USA.; Laboratory of Biological Modeling, NIDDK, NIH, Bethesda, MD, USA.; Cognitive Genomics Lab, BGI-Shenzhen, Yantian District, Shenzhen, China. Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 441 EP - 442 CY - Bognor Regis PB - Wiley Subscription Services, Inc. VL - 26 IS - 4 SN - 0890-2070 KW - Psychology KW - Behaviour KW - Cognitive-Behavioural factors KW - Cognitive abilities KW - Personality KW - Psychologists UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665156103?accountid=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=European+Journal+of+Personality&rft.atitle=Common+Factors+and+Causal+Networks&rft.au=Lee%2C+James+J&rft.aulast=Lee&rft.aufirst=James&rft.date=2012-07-01&rft.volume=26&rft.issue=4&rft.spage=441&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Personality&rft.issn=08902070&rft_id=info:doi/10.1002%2Fper.1873 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-08-16 DO - http://dx.doi.org/10.1002/per.1873 ER - TY - JOUR T1 - Why Do (Some) Birds Flock? Causality and the Structure of Characteristic Adaptations AN - 1665152533 AB - Characteristic adaptations often cluster in mutually reinforcing networks. Evidence of stability and heritability suggests that the development of such networks is due in part to the causal influence of enduring dispositions or traits. Many different genetic models are consistent with this hypothesis, and the quest for genes can be pursued at many levels; of these, the intermediate level of specific facets may be the most promising. Published 2012. This article is a U. S. Government work and is in the public domain in the USA. JF - European Journal of Personality AU - Terracciano, Antonio AU - McCrae, Robert R AD - National Institute on Aging, NIH, DHHS, Baltimore, MD, USA. ; National Institute on Aging, NIH, DHHS, Baltimore, MD, USA. Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 449 EP - 450 CY - Bognor Regis PB - Wiley Subscription Services, Inc. VL - 26 IS - 4 SN - 0890-2070 KW - Psychology KW - Birds KW - Causality KW - Genes KW - Heritability KW - Public domain KW - Sentences UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665152533?accountid=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=European+Journal+of+Personality&rft.atitle=Why+Do+%28Some%29+Birds+Flock%3F+Causality+and+the+Structure+of+Characteristic+Adaptations&rft.au=Terracciano%2C+Antonio%3BMcCrae%2C+Robert+R&rft.aulast=Terracciano&rft.aufirst=Antonio&rft.date=2012-07-01&rft.volume=26&rft.issue=4&rft.spage=449&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Personality&rft.issn=08902070&rft_id=info:doi/10.1002%2Fper.1878 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-05-13 DO - http://dx.doi.org/10.1002/per.1878 ER - TY - JOUR T1 - A Prospective Study of the Association Between Vigorous Physical Activity During Pregnancy and Length of Gestation and Birthweight AN - 1458539222; 17186751 AB - Current US pregnancy-related physical activity recommendations do not provide specific guidance for vigorous intensity activity. We examined the associations between vigorous physical activity during pregnancy and length of gestation and birthweight. Methods: Women were recruited before 10 weeks gestation. At 13-16 weeks gestation, participants reported the type, frequency, and duration of their typical weekly vigorous physical activities. Activity domains included recreational, occupational, household, and child/adult care. Infant birth date was obtained from medical or vital records; if unavailable, self-report was used. Birthweight (from vital records) was studied among term births. We analyzed gestational age among 1,647 births using discrete-time survival analysis. We used logistic and linear regression to analyze preterm birth (birth at <37 weeks) and birthweight, respectively. Vigorous recreational activity was associated with longer gestation (any vs. none, hazard ratio (HR) [95% CI]: 0.85 [0.70, 1.05]) and we did not detect any dose-response association. Higher frequency of vigorous recreational activity sessions (adjusted for total volume of activity) was associated with a decreased odds of preterm birth ( greater than or equal to 4 sessions/week vs. 0 or 1, OR [95% CI]: 0.08 (0.006, 1.0). Birthweight was not associated with physical activity measures. In summary, vigorous physical activity does not appear to be detrimental to the timing of birth or birthweight. Our data support a reduced risk of preterm birth with vigorous recreational activity, particularly with increased frequency of recreational activity sessions. Future studies should investigate the components of physical activity (i.e., intensity, duration, and frequency) in relation to birth outcomes. JF - Maternal and Child Health Journal AU - Jukic, Anne Marie Z AU - Evenson, Kelly R AU - Daniels, Julie L AU - Herring, Amy H AU - Wilcox, Allen J AU - Hartmann, Katherine E AD - Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA, jukica@niehs.nih.gov Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 1031 EP - 1044 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 16 IS - 5 SN - 1092-7875, 1092-7875 KW - Physical Education Index KW - Coordination KW - Analysis KW - Women KW - Health KW - Exercise KW - Adults KW - Counseling KW - Pregnancy KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1458539222?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Maternal+and+Child+Health+Journal&rft.atitle=A+Prospective+Study+of+the+Association+Between+Vigorous+Physical+Activity+During+Pregnancy+and+Length+of+Gestation+and+Birthweight&rft.au=Jukic%2C+Anne+Marie+Z%3BEvenson%2C+Kelly+R%3BDaniels%2C+Julie+L%3BHerring%2C+Amy+H%3BWilcox%2C+Allen+J%3BHartmann%2C+Katherine+E&rft.aulast=Jukic&rft.aufirst=Anne+Marie&rft.date=2012-07-01&rft.volume=16&rft.issue=5&rft.spage=1031&rft.isbn=&rft.btitle=&rft.title=Maternal+and+Child+Health+Journal&rft.issn=10927875&rft_id=info:doi/10.1007%2Fs10995-011-0831-8 LA - English DB - Physical Education Index N1 - Date revised - 2013-11-01 N1 - Last updated - 2013-11-15 N1 - SubjectsTermNotLitGenreText - Coordination; Analysis; Women; Health; Adults; Exercise; Counseling; Pregnancy DO - http://dx.doi.org/10.1007/s10995-011-0831-8 ER - TY - JOUR T1 - Survival outcomes in endometrial cancer patients are associated with CXCL12 and estrogen receptor expression AN - 1443366819; 18611297 AB - CXCL12 is a chemotactic cytokine that has pro-metastatic functions in several malignancies through interactions with its receptor, CXCR4. CXCL12 is an estrogen-regulated gene, and notably, estrogen is a major risk factor for endometrial cancer (EC) development. As few studies examine concurrent CXCL12, CXCR4, and estrogen receptor (ER) expression in EC patients, we examined this pathway in 199 EC patients with data from the University of Pittsburgh Medical Center Cancer Registry. Immunohistochemistry (IHC) was used to detect CXCR4, CXCL12 and ER protein expression. As CXCR4 expression was positive in all cases, this investigation focused on associations between CXCL12 and ER expression, clinicopathologic factors and survival outcomes using chi-square tests, Kaplan-Meier graphs, and log-rank tests. CXCL12 expression was negative in 63 cases (32%) and positive in 136 cases (68%). Negative CXCL12 expression was borderline significantly associated with metastasis ( chi super(2) p = 0.07). ER expression was negative in 75 cases (38%) and positive in 124 cases (62%). Positive ER expression was significantly associated with low grade and early stage tumors ( chi super(2) p < 0.001). CXCL12 and ER were not significantly associated ( chi super(2) p = 0.11). Positive CXCL12 expression was associated with longer overall survival (OS) (log-rank p = 0.006) and longer recurrence-free survival (RFS) (log-rank p = 0.01) in ER negative patients, but not in ER positive patients. We identified a unique molecular signature associated with better OS and RFS in EC patients. In addition to pathological characteristics of the tumor, expression of CXCL12 and ER may be clinically useful for assigning adjuvant treatment to EC cases. JF - International Journal of Cancer AU - Felix, Ashley S AU - Stone, Roslyn A AU - Chivukula, Mamatha AU - Bowser, Robert AU - Parwani, Anil V AU - Linkov, Faina AU - Edwards, Robert P AU - Weissfeld, Joel L AD - Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, Rockville, MD., ashley.felix@gmail.com Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - E114 EP - E121 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 131 IS - 2 SN - 0020-7136, 0020-7136 KW - Risk Abstracts KW - Health risks KW - Estrogens KW - Risk factors KW - Survival KW - Proteins KW - Tumors KW - Cancer KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1443366819?accountid=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=Survival+outcomes+in+endometrial+cancer+patients+are+associated+with+CXCL12+and+estrogen+receptor+expression&rft.au=Felix%2C+Ashley+S%3BStone%2C+Roslyn+A%3BChivukula%2C+Mamatha%3BBowser%2C+Robert%3BParwani%2C+Anil+V%3BLinkov%2C+Faina%3BEdwards%2C+Robert+P%3BWeissfeld%2C+Joel+L&rft.aulast=Felix&rft.aufirst=Ashley&rft.date=2012-07-01&rft.volume=131&rft.issue=2&rft.spage=E114&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.27317 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-10-01 N1 - Last updated - 2013-10-21 N1 - SubjectsTermNotLitGenreText - Health risks; Estrogens; Risk factors; Proteins; Survival; Tumors; Cancer DO - http://dx.doi.org/10.1002/ijc.27317 ER - TY - JOUR T1 - An overview of anthrax infection including the recently identified form of disease in injection drug users AN - 1439229752; 16839256 AB - Purpose: Bacillus anthracis infection (anthrax) can be highly lethal. Two recent outbreaks related to contaminated mail in the USA and heroin in the UK and Europe and its potential as a bioterrorist weapon have greatly increased concerns over anthrax in the developed world. Methods: This review summarizes the microbiology, pathogenesis, diagnosis, and management of anthrax. Results and conclusions: Anthrax, a gram-positive bacterium, has typically been associated with three forms of infection: cutaneous, gastrointestinal, and inhalational. However, the anthrax outbreak among injection drug users has emphasized the importance of what is now considered a fourth disease form (i.e., injectional anthrax) that is characterized by severe soft tissue infection. While cutaneous anthrax is most common, its early stages are distinct and prompt appropriate treatment commonly produces a good outcome. However, early symptoms with the other three disease forms can be nonspecific and mistaken for less lethal conditions. As a result, patients with gastrointestinal, inhalational, or injectional anthrax may have advanced infection at presentation that can be highly lethal. Once anthrax is suspected, the diagnosis can usually be made with gram stain and culture from blood or tissue followed by confirmatory testing (e.g., PCR). While antibiotics are the mainstay of anthrax treatment, use of adjunctive therapies such as anthrax toxin antagonists are a consideration. Prompt surgical therapy appears to be important for successful management of injectional anthrax. JF - Intensive Care Medicine AU - Hicks, Caitlin W AU - Sweeney, Daniel A AU - Cui, Xizhong AU - Li, Yan AU - Eichacker, Peter Q AD - Cleveland Clinic Lerner College of Medicine, Cleveland, OH, 44122, USA, peichacker@cc.nih.gov Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 1092 EP - 1104 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 38 IS - 7 SN - 0342-4642, 0342-4642 KW - Toxicology Abstracts KW - Heroin KW - Antibiotics KW - Bacillus anthracis KW - Infection KW - Drug abuse KW - Toxins KW - Antagonists KW - Blood KW - Gram stain KW - Reviews KW - Anthrax KW - Polymerase chain reaction KW - Soft tissues KW - X 24380:Social Poisons & Drug Abuse UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1439229752?accountid=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=Intensive+Care+Medicine&rft.atitle=An+overview+of+anthrax+infection+including+the+recently+identified+form+of+disease+in+injection+drug+users&rft.au=Hicks%2C+Caitlin+W%3BSweeney%2C+Daniel+A%3BCui%2C+Xizhong%3BLi%2C+Yan%3BEichacker%2C+Peter+Q&rft.aulast=Hicks&rft.aufirst=Caitlin&rft.date=2012-07-01&rft.volume=38&rft.issue=7&rft.spage=1092&rft.isbn=&rft.btitle=&rft.title=Intensive+Care+Medicine&rft.issn=03424642&rft_id=info:doi/10.1007%2Fs00134-012-2541-0 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-10-01 N1 - Last updated - 2013-10-21 N1 - SubjectsTermNotLitGenreText - Blood; Gram stain; Heroin; Reviews; Polymerase chain reaction; Anthrax; Antibiotics; Drug abuse; Infection; Soft tissues; Antagonists; Toxins; Bacillus anthracis DO - http://dx.doi.org/10.1007/s00134-012-2541-0 ER - TY - JOUR T1 - Meat-related mutagen exposure, xenobiotic metabolizing gene polymorphisms and the risk of advanced colorectal adenoma and cancer AN - 1439222284; 18514359 AB - Meat mutagens, including heterocyclic amines (HCAs), polycyclic aromatic hydrocarbons (PAHs) and N-nitroso compounds (NOCs), may be involved in colorectal carcinogenesis depending on their activation or detoxification by phase I and II xenobiotic metabolizing enzymes (XME). Using unconditional logistic regression to estimate odds ratios (OR) and 95% confidence intervals (CI), we examined the intake of five meat mutagens and >300 single nucleotide polymorphisms (SNPs) in 18 XME genes in relation to advanced colorectal adenoma (1205 cases and 1387 controls) and colorectal cancer (370 cases and 401 controls) within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Dietary intake of meat mutagens was assessed using a food frequency questionnaire with a detailed meat-cooking module. An interaction was observed between 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) intake and the NAT1 polymorphism rs6586714 in the adenoma study (P sub(interaction) = 0.001). Among individuals carrying a GG genotype, high MeIQx intake was associated with a 43% increased risk of adenoma (95% CI 1.11-1.85, P sub(trend) = 0.07), whereas the reverse was observed among carriers of the A variant (OR = 0.50, 95% CI 0.30-0.84, P sub(trend) = 0.01). In addition, we observed some suggestive (P < 0.05) modifying effects for SNPs in other XME genes (UGT1A, CYP2E1, EPHX1, AHR and GSTM3), but these were not significant after adjustment for multiple testing. This large and comprehensive study of XME genes, meat mutagens and the risk of colorectal tumours found that a NAT1 polymorphism modified the association between MeIQx intake and colorectal adenoma risk. JF - Carcinogenesis AU - Gilsing, Anne MJ AU - Berndt, Sonja I AU - Ruder, Elizabeth H AU - Graubard, Barry I AU - Ferrucci, Leah M AU - Burdett, Laura AU - Weissfeld, Joel L AU - Cross, Amanda J AU - Sinha, Rashmi AD - super(1)Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human ServicesBethesda, MD, USA,, sinhar@nih.gov Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 1332 EP - 1339 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 33 IS - 7 SN - 0143-3334, 0143-3334 KW - Toxicology Abstracts; Oncogenes & Growth Factors Abstracts; Genetics Abstracts KW - Adenoma KW - Mutagens KW - B 26660:Miscellaneous Oncogenes & Growth Factors KW - G 07710:Chemical Mutagenesis & Radiation KW - X 24320:Food Additives & Contaminants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1439222284?accountid=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=Meat-related+mutagen+exposure%2C+xenobiotic+metabolizing+gene+polymorphisms+and+the+risk+of+advanced+colorectal+adenoma+and+cancer&rft.au=Gilsing%2C+Anne+MJ%3BBerndt%2C+Sonja+I%3BRuder%2C+Elizabeth+H%3BGraubard%2C+Barry+I%3BFerrucci%2C+Leah+M%3BBurdett%2C+Laura%3BWeissfeld%2C+Joel+L%3BCross%2C+Amanda+J%3BSinha%2C+Rashmi&rft.aulast=Gilsing&rft.aufirst=Anne&rft.date=2012-07-01&rft.volume=33&rft.issue=7&rft.spage=1332&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=01433334&rft_id=info:doi/10.1093%2Fcarcin%2Fbgs158 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-10-01 N1 - Last updated - 2014-03-20 N1 - SubjectsTermNotLitGenreText - Mutagens DO - http://dx.doi.org/10.1093/carcin/bgs158 ER - TY - JOUR T1 - Well being of female sex workers AN - 1418121723; 4463370 AB - Background: Subjective well being among female sex workers is less explored and only few studies talked about this complex issue. Aim: To study the subjective well being of female sex workers. Method: Based on the informed consent, seventy female sex workers were randomly selected from the study population. The PGI - General Well Being scale (Verma et al., 1983) and a semi structured socio demographic schedule were used to collect the data. Results: Major findings of the study were that half of the female sex workers fall under the age group of 27 to 36, having studied up to high school (50%), majority (90%) of them being married and were using one or other substance (72.9%). Their perception of subjective well being shows that 38.6% had good positive mental health, 35.7% had moderate mental health and about one quarter (25.7%) of the respondents had low positive mental health. High subjective well being among Pre University Course (PUC) and above educated female sex workers (M=16.88, ±4.52) was noted, whereas less was noted among the group of illiterate female sex workers (M-8.96, ±5.53). Conclusion: There is a need to address female sex workers issues beyond HIV/AIDS. The current findings open up the need for appropriate interventions. Reprinted by permission of World Scientific Publishing JF - Hong Kong journal of social work AU - Lakshmana, G AU - Pandian, Dhanasekara AD - Central University of Karnataka ; National Institute of Mental Health and Neuro Sciences Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 31 EP - 42 VL - 46 IS - 1-2 SN - 0219-2462, 0219-2462 KW - Sociology KW - Sex workers KW - Marital status KW - Level of education KW - AIDS KW - Well-being KW - Mental health KW - Prostitution KW - HIV KW - Substance use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1418121723?accountid=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=Hong+Kong+journal+of+social+work&rft.atitle=Well+being+of+female+sex+workers&rft.au=Lakshmana%2C+G%3BPandian%2C+Dhanasekara&rft.aulast=Lakshmana&rft.aufirst=G&rft.date=2012-07-01&rft.volume=46&rft.issue=1-2&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Hong+Kong+journal+of+social+work&rft.issn=02192462&rft_id=info:doi/10.1142%2FS0219246212000058 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2013-07-22 N1 - Last updated - 2013-09-16 N1 - SubjectsTermNotLitGenreText - 5703 3617 6220; 482 3617 6220; 11556 13682; 10359 11556 13682; 13530 13521; 7353 4049; 7699 7748 6823; 7947 5772 7954; 12357 DO - http://dx.doi.org/10.1142/S0219246212000058 ER - TY - JOUR T1 - Recovery-Oriented Community-Based Mental Health Service in Japan: The Development of Outreach Services AN - 1347818801; 201307979 AB - To promote the recovery of people with mental illness, outreach services in psychiatric rehabilitation is an effective treatment. In Japan, deinstitutionalization has been delayed, and outreach services were not developed until recently. However, Japan's Ministry of Health, Labor and Welfare announced in its 2004 report Mental Health and Medical Welfare Vision of Reform that the national policy of mental health must shift from hospital-oriented treatments to community-oriented treatments. As a result, many pioneering outreach activities are beginning to appear In this article, we review outreach services in Japan of assertive community treatment (ACT), psychiatric home-visit nursing (PHVN), and the welfare-based outreach program known as home-visit life skills coaching. To provide outreach services of all types to people with mental illness, the separate roles of ACT PHVN, and home-visit life skills coaching must be clearly defined. However few agencies provide outreach services to people with mental illness in the Japanese psychiatric system. Thus, we must promote studies and activities that demonstrate the effectiveness of such services and change the culture of psychiatric services from hospital oriented to community oriented. Adapted from the source document. JF - International Journal of Mental Health AU - Yoshida, Koji AU - Ito, Junichiro AD - Department of Psychiatric Rehabilitation, National Institute of Mental Health, National Center of Neurology and Psychiatry, Tokyo, Japan Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 29 EP - 37 PB - M.E. Sharpe, Armonk NY VL - 41 IS - 2 SN - 0020-7411, 0020-7411 KW - Mentally ill people KW - Coaching KW - Mental health KW - Japan KW - Life skills KW - Outreach programmes KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1347818801?accountid=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=International+Journal+of+Mental+Health&rft.atitle=Recovery-Oriented+Community-Based+Mental+Health+Service+in+Japan%3A+The+Development+of+Outreach+Services&rft.au=Yoshida%2C+Koji%3BIto%2C+Junichiro&rft.aulast=Yoshida&rft.aufirst=Koji&rft.date=2012-07-01&rft.volume=41&rft.issue=2&rft.spage=29&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Mental+Health&rft.issn=00207411&rft_id=info:doi/10.2753%2FIMH0020-7411410203 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-05-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Outreach programmes; Japan; Mentally ill people; Coaching; Mental health; Life skills DO - http://dx.doi.org/10.2753/IMH0020-7411410203 ER - TY - JOUR T1 - Overview of the Japanese Mental Health System AN - 1347818324; 201307491 AB - In the past decade, the Japanese government has instituted numerous mental health policies and laws relevant to mental health. This mental health system reform is aimed at deinstitutionalization and the improvement of community mental health, as Japan has one of the highest numbers of psychiatric beds per capita in the world, with 345,696 psychiatric beds in 2008. This article describes the current situation of mental health services, the mental health system reform process and its achievements, and the future challenges. Adapted from the source document. JF - International Journal of Mental Health AU - Setoya, Yutaro AD - Honorary researcher, National Institute of Mental Health, National Center of Neurology and Psychiatry, Tokyo, Japan Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 3 EP - 18 PB - M.E. Sharpe, Armonk NY VL - 41 IS - 2 SN - 0020-7411, 0020-7411 KW - Deinstitutionalization KW - Mental health policy KW - Mental health services KW - Psychiatric hospitals KW - Reforms KW - Japan KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1347818324?accountid=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=International+Journal+of+Mental+Health&rft.atitle=Overview+of+the+Japanese+Mental+Health+System&rft.au=Setoya%2C+Yutaro&rft.aulast=Setoya&rft.aufirst=Yutaro&rft.date=2012-07-01&rft.volume=41&rft.issue=2&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Mental+Health&rft.issn=00207411&rft_id=info:doi/10.2753%2FIMH0020-7411410201 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-05-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Mental health services; Japan; Reforms; Psychiatric hospitals; Deinstitutionalization; Mental health policy DO - http://dx.doi.org/10.2753/IMH0020-7411410201 ER - TY - JOUR T1 - Essential parameters to consider for the characterization of optical imaging probes AN - 1328510537; 17397581 AB - The Molecular Imaging and Contrast Agents Database (MICAD) was launched in 2005 to promote the development and application of imaging and contrast agents (probes) to advance the field of molecular imaging. As of March 2012, there are approximately 1170 agents available in MICAD. Based on the modality used for imaging, the largest category of probes described in MICAD are those used for PET (41.6%), followed by agents used for single-photon emission computed tomography (30.3%), optical imaging (12.0%), MRI (9.3%), multimodality imaging (3.4%), ultrasound (2.4%) and x-ray/computed tomography (1.0%). This article is intended to be a guideline for new investigators and students who wish to characterize an optical imaging probe that will be used to perform in vivo molecular imaging studies. It is necessary, however, to ensure that these agents meet certain quality control parameters before they are used in various in vitro and in vivo applications. JF - Nanomedicine AU - Leung, Kam AU - Chopra, Arvind AU - Shan, Liang AU - Eckelman, William C AU - Menkens, Anne E AD - super(1)Molecular Imaging & Contrast Agents Database, National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD 20894, USA., leung@ncbi.nlm.nih.gov Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 1101 EP - 1107 PB - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom VL - 7 IS - 7 SN - 1743-5889, 1743-5889 KW - Biotechnology and Bioengineering Abstracts KW - Computed tomography KW - Contrast media KW - Databases KW - Ionizing radiation KW - Magnetic resonance imaging KW - Probes KW - Quality control KW - Ultrasound KW - nanotechnology KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1328510537?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nanomedicine&rft.atitle=Essential+parameters+to+consider+for+the+characterization+of+optical+imaging+probes&rft.au=Leung%2C+Kam%3BChopra%2C+Arvind%3BShan%2C+Liang%3BEckelman%2C+William+C%3BMenkens%2C+Anne+E&rft.aulast=Leung&rft.aufirst=Kam&rft.date=2012-07-01&rft.volume=7&rft.issue=7&rft.spage=1101&rft.isbn=&rft.btitle=&rft.title=Nanomedicine&rft.issn=17435889&rft_id=info:doi/10.2217%2Fnnm.12.79 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-04-01 N1 - Number of references - 46 N1 - Last updated - 2013-04-19 N1 - SubjectsTermNotLitGenreText - Databases; Quality control; Ionizing radiation; Magnetic resonance imaging; Computed tomography; Contrast media; Probes; Ultrasound; nanotechnology DO - http://dx.doi.org/10.2217/nnm.12.79 ER - TY - JOUR T1 - Partnerships in Drug Abuse Prevention Services Research: Perspectives from the National Institute on Drug Abuse AN - 1323340249; 201304856 AB - Provides remarks for a special journal issue on Forging and Sustaining Partnerships to Support Child Mental Health Prevention and Services Research. Adapted from the source document. JF - Administration and Policy in Mental Health AND Mental Health Services Research AU - Robertson, Elizabeth B AU - Sims, Belinda E AU - Reider, Eve E AD - Prevention Research Branch (PRB), Division of Epidemiology Services and Prevention Research (DESPR), National Institute on Drug Abuse (NIDA), 6001 Executive Boulevard, Bethesda, MD, 20892, USA Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 327 EP - 330 PB - Springer, Dordrecht The Netherlands VL - 39 IS - 4 SN - 0894-587X, 0894-587X KW - Drug education KW - Mental health KW - Partnerships KW - Social services KW - Preventive mental health care KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323340249?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Administration+and+Policy+in+Mental+Health+AND+Mental+Health+Services+Research&rft.atitle=Partnerships+in+Drug+Abuse+Prevention+Services+Research%3A+Perspectives+from+the+National+Institute+on+Drug+Abuse&rft.au=Robertson%2C+Elizabeth+B%3BSims%2C+Belinda+E%3BReider%2C+Eve+E&rft.aulast=Robertson&rft.aufirst=Elizabeth&rft.date=2012-07-01&rft.volume=39&rft.issue=4&rft.spage=327&rft.isbn=&rft.btitle=&rft.title=Administration+and+Policy+in+Mental+Health+AND+Mental+Health+Services+Research&rft.issn=0894587X&rft_id=info:doi/10.1007%2Fs10488-011-0400-x LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-06-01 N1 - Last updated - 2016-09-27 N1 - CODEN - APMHEM N1 - SubjectsTermNotLitGenreText - Partnerships; Social services; Preventive mental health care; Drug education; Mental health DO - http://dx.doi.org/10.1007/s10488-011-0400-x ER - TY - JOUR T1 - Connecting Science and Practice in Child and Adolescent Mental Health Services Research AN - 1323339832; 201303562 AB - Collaboration between researchers and stakeholder groups is a potentially powerful mechanism for strengthening the quality of mental health research and for amplifying its public health impact. For stakeholders, collaboration offers opportunities to help shape research questions; participate in data collection and interpretation; and improve local capacity to access and use research findings. For researchers, collaboration can build understanding of what stakeholders want and need from research; enhance capacity to frame research questions and findings in language and metrics of value to stakeholders; and provide opportunities to contribute science-backed knowledge to decision-making processes in real world settings. Key stakeholder groups can include the recipients and providers of care, public and private care systems, health plans, schools, family service and faith-based organizations, correctional systems, and employers providing mental health benefits. This commentary reflects on the path that NIMH has taken in fostering researcher-stakeholder collaboration, particularly regarding child and adolescent mental health research. It describes the goals that NIMH set out to achieve, steps taken to realize those goals, lessons learned from those efforts, and possible next steps. Adapted from the source document. JF - Administration and Policy in Mental Health AND Mental Health Services Research AU - Chambers, David A AU - Pringle, Beverly AU - Juliano-Bult, Denise AD - Division of Services and Intervention Research, National Institute of Mental Health, 6001 Executive Blvd, Room 7164, Bethesda, MD, 20892-9631, USA Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 321 EP - 326 PB - Springer, Dordrecht The Netherlands VL - 39 IS - 4 SN - 0894-587X, 0894-587X KW - Goals KW - Stakeholders KW - Medical research KW - Mental health KW - Children KW - Adolescents KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323339832?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Administration+and+Policy+in+Mental+Health+AND+Mental+Health+Services+Research&rft.atitle=Connecting+Science+and+Practice+in+Child+and+Adolescent+Mental+Health+Services+Research&rft.au=Chambers%2C+David+A%3BPringle%2C+Beverly%3BJuliano-Bult%2C+Denise&rft.aulast=Chambers&rft.aufirst=David&rft.date=2012-07-01&rft.volume=39&rft.issue=4&rft.spage=321&rft.isbn=&rft.btitle=&rft.title=Administration+and+Policy+in+Mental+Health+AND+Mental+Health+Services+Research&rft.issn=0894587X&rft_id=info:doi/10.1007%2Fs10488-011-0399-z LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-04-01 N1 - Last updated - 2016-09-27 N1 - CODEN - APMHEM N1 - SubjectsTermNotLitGenreText - Stakeholders; Mental health; Medical research; Goals; Adolescents; Children DO - http://dx.doi.org/10.1007/s10488-011-0399-z ER - TY - JOUR T1 - Super-resolution microscopy reveals mechanistic details of bacterial cell division AN - 1285088633; 17480299 AB - Extended abstract of a paper presented at Microscopy and Microanalysis 2012 in Phoenix, Arizona, USA, July 29 - August 2, 2012. JF - Microscopy and Microanalysis AU - Eswara Moorthy, P AU - Ramamurthi, K S AU - Erb, M L AU - Gregory, JA AU - Pogliano, K AU - Pogliano, J AU - Silverman, J AD - National Cancer Institute, National Institutes of Health, Bethesda, MD Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 672 EP - 673 PB - Cambridge University Press, The Edinburgh Building, Cambridge CB2 2RU United Kingdom VL - 18 IS - S2 SN - 1431-9276, 1431-9276 KW - Microbiology Abstracts B: Bacteriology KW - Cell division KW - Microscopy KW - Bacteria KW - J 02320:Cell Biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285088633?accountid=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=Microscopy+and+Microanalysis&rft.atitle=Super-resolution+microscopy+reveals+mechanistic+details+of+bacterial+cell+division&rft.au=Eswara+Moorthy%2C+P%3BRamamurthi%2C+K+S%3BErb%2C+M+L%3BGregory%2C+JA%3BPogliano%2C+K%3BPogliano%2C+J%3BSilverman%2C+J&rft.aulast=Eswara+Moorthy&rft.aufirst=P&rft.date=2012-07-01&rft.volume=18&rft.issue=S2&rft.spage=672&rft.isbn=&rft.btitle=&rft.title=Microscopy+and+Microanalysis&rft.issn=14319276&rft_id=info:doi/10.1017%2FS1431927612005211 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-01 N1 - Last updated - 2013-02-22 N1 - SubjectsTermNotLitGenreText - Cell division; Microscopy; Bacteria DO - http://dx.doi.org/10.1017/S1431927612005211 ER - TY - JOUR T1 - Socioeconomic and Geographic Disparities in Health Information Seeking and Internet Use in Puerto Rico AN - 1266146823; 201300622 AB - Background: Geographically isolated Hispanic populations, such as those living in Puerto Rico, may face unique barriers to health information access. However, little is known about health information access and health information-seeking behaviors of this population. Objective: To examine differences in health and cancer information seeking among survey respondents who ever used the Internet and those who did not, and to explore sociodemographic and geographic trends. Methods: Data for our analyses were from a special implementation of the Health Information National Trends Survey conducted in Puerto Rico in 2009. We collected data through random digit dialing, computer-assisted telephone interviews (N = 639). The sample was drawn from the eight geographic regions of the Puerto Rico Department of Health. To account for complex survey design and perform weighted analyses to obtain population estimates, we analyzed the data using SUDAAN. Frequencies, cross-tabulation with chi-square, and logistic regression analyses were conducted. Geographic information system maps were developed to examine geographic distributions of Internet use and information seeking. Results: Of 639 participants, 142 (weighted percentage 32.7%) indicated that they had ever gone online to access the Internet or World Wide Web; this proportion was substantially lower than that of US mainland Hispanics who reported using the Internet (49%). While 101 of 142 (weighted percentage 59.6%) respondents who used the Web had ever sought health information, only 118 of 497 (weighted percentage 20.0%) of those who did not use the Web had sought health information. The pattern was similar for cancer information: 76 of 142 respondents (weighted percentage 47.2%) who used the Web had ever sought cancer information compared with 105 of 497 (weighted percentage 18.8%) of those who had not used the Web. These results were slightly lower but generally consistent with US mainland Hispanics' health (50.9%) and cancer (26.4%) information seeking. Results of separate logistic regression models controlling for sociodemographic characteristics demonstrated that, compared with individuals who did not seek health or cancer information, those who did were over 5 times as likely to have used the Internet (odds ratio 5.11, P< .001). Those who sought cancer information were over twice as likely to have used the Internet (odds ratio 2.5, P < .05). The frequency of Internet use and health and cancer information seeking was higher in the San Juan metro region than in more rural areas. Conclusions: Our results contribute to the evidence base for health and cancer communication planning for Puerto Rico, and suggest that health education and outreach efforts should explore the use of available and trusted methods of dissemination such as radio and television, as well as community-based health care providers and organizations, to supplement and encourage use of the Internet as a source of health information. Adapted from the source document. JF - Journal of Medical Internet Research AU - Rutten, Lila J. Finney AU - Hesse, Bradford W AU - Moser, Richard P AU - Ortiz Martinez, Ana Patricia AU - Kornfeld, Julie AU - Vanderpool, Robin C AU - Byrne, Margaret AU - Tortolero Luna, Guillermo AD - Clinical Monitoring Research Program, SAIC-Frederick, Inc, National Cancer Institute at Frederick, Frederick, MD, United States Y1 - 2012/07// PY - 2012 DA - July 2012 PB - Gunther Eysenbach MD MPH, Associate Professor, University of Toronto Senior Scientist, Centre for Global eHealth Innovation, Toronto, Canada VL - 14 IS - 4 SN - 1438-8871, 1438-8871 KW - Health information seeking KW - cancer information seeking KW - Internet use KW - disparities KW - special populations KW - geographic trends KW - Puerto Rico KW - Diseases KW - Information seeking behaviour KW - Consumer health information KW - Access to information KW - article KW - 12.22: SEARCHING UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1266146823?accountid=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=Journal+of+Medical+Internet+Research&rft.atitle=Socioeconomic+and+Geographic+Disparities+in+Health+Information+Seeking+and+Internet+Use+in+Puerto+Rico&rft.au=Rutten%2C+Lila+J.+Finney%3BHesse%2C+Bradford+W%3BMoser%2C+Richard+P%3BOrtiz+Martinez%2C+Ana+Patricia%3BKornfeld%2C+Julie%3BVanderpool%2C+Robin+C%3BByrne%2C+Margaret%3BTortolero+Luna%2C+Guillermo&rft.aulast=Rutten&rft.aufirst=Lila+J.&rft.date=2012-07-01&rft.volume=14&rft.issue=4&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Journal+of+Medical+Internet+Research&rft.issn=14388871&rft_id=info:doi/10.2196%2Fjmir.2007 L2 - http://www.jmir.org/ LA - English DB - Library & Information Science Abstracts (LISA) N1 - Date revised - 2013-01-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Consumer health information; Information seeking behaviour; Diseases; Puerto Rico; Access to information DO - http://dx.doi.org/10.2196/jmir.2007 ER - TY - JOUR T1 - Depressed mood enhances anxiety to unpredictable threat AN - 1038112223; 201223392 AB - Depression and anxiety disorders (ADs) are highly co-morbid, but the reason for this co-morbidity is unclear. One possibility is that they predispose one another. An informative way to examine interactions between disorders without the confounds present in patient populations is to manipulate the psychological processes thought to underlie the pathological states in healthy individuals. In this study we therefore asked whether a model of the sad mood in depression can enhance psychophysiological responses (startle) to a model of the anxiety in ADs. We predicted that sad mood would increase anxious anxiety-potentiated startle responses. In a between-subjects design, participants (n=36) completed either a sad mood induction procedure (MIP; n=18) or a neutral MIP (n=18). Startle responses were assessed during short-duration predictable electric shock conditions (fear-potentiated startle) or long-duration unpredictable threat of shock conditions (anxiety-potentiated startle). Induced sadness enhanced anxiety- but not fear-potentiated startle. This study provides support for the hypothesis that sadness can increase anxious responding measured by the affective startle response. This, taken together with prior evidence that ADs can contribute to depression, provides initial experimental support for the proposition that ADs and depression are frequently co-morbid because they may be mutually reinforcing. Adapted from the source document. JF - Psychological Medicine AU - Robinson, O J AU - Overstreet, C AU - Letkiewicz, A AU - Grillon, C AD - Section on Neurobiology of Fear and Anxiety, National Institute of Mental Health, NIH, Bethesda, MD, USA oliver.j.robinson@gmail.com Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 1397 EP - 1407 PB - Cambridge University Press, UK VL - 42 IS - 7 SN - 0033-2917, 0033-2917 KW - Sadness KW - Depression KW - Moods KW - Unpredictable KW - Comorbidity KW - Anxiety-Depression KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1038112223?accountid=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=Depressed+mood+enhances+anxiety+to+unpredictable+threat&rft.au=Robinson%2C+O+J%3BOverstreet%2C+C%3BLetkiewicz%2C+A%3BGrillon%2C+C&rft.aulast=Robinson&rft.aufirst=O&rft.date=2012-07-01&rft.volume=42&rft.issue=7&rft.spage=1397&rft.isbn=&rft.btitle=&rft.title=Psychological+Medicine&rft.issn=00332917&rft_id=info:doi/10.1017%2FS0033291711002583 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-09-01 N1 - Last updated - 2016-09-27 N1 - CODEN - PSMDCO N1 - SubjectsTermNotLitGenreText - Anxiety-Depression; Moods; Comorbidity; Sadness; Unpredictable; Depression DO - http://dx.doi.org/10.1017/S0033291711002583 ER - TY - JOUR T1 - Integrating information on substance use disorders into electronic health record systems AN - 1038111311; 201223596 AB - For reasons of safety and effectiveness, many forces in health care, especially the Affordable Care Act of 2010, are pressing for improved identification and management of substance use disorders within mainstream health care. Thus, standard information about patient substance use will have to be collected and used by providers within electronic health record systems (EHRS). Although there are many important technical, legal, and patient confidentiality issues that must be dealt with to achieve integration, this article focuses upon efforts by the National Institute on Drug Abuse and other federal agencies to develop a common set of core questions to screen, diagnose, and initiate treatment for substance use disorders as part of national EHRS. This article discusses the background and rationale for these efforts and presents the work to date to identify the questions and to promote information sharing among health care providers. [Copyright Elsevier Inc.] JF - Journal of Substance Abuse Treatment AU - Tai, Betty AU - McLellan, A Thomas AD - Clinical Trials Network, National Institute on Drug Abuse, National Institutes of Health, Bethesda, MD, USA btai@nida.nih.gov Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 12 EP - 19 PB - Elsevier, New York NY VL - 43 IS - 1 SN - 0740-5472, 0740-5472 KW - Substance abuse, Health information, Electronic health record system, Patient confidentiality, Patient safety KW - Health care KW - Information sharing KW - Computerized medical records KW - Substance abuse disorders KW - Federal agencies KW - Substance abuse KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1038111311?accountid=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+Substance+Abuse+Treatment&rft.atitle=Integrating+information+on+substance+use+disorders+into+electronic+health+record+systems&rft.au=Tai%2C+Betty%3BMcLellan%2C+A+Thomas&rft.aulast=Tai&rft.aufirst=Betty&rft.date=2012-07-01&rft.volume=43&rft.issue=1&rft.spage=12&rft.isbn=&rft.btitle=&rft.title=Journal+of+Substance+Abuse+Treatment&rft.issn=07405472&rft_id=info:doi/10.1016%2Fj.jsat.2011.10.010 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-09-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JSATEG N1 - SubjectsTermNotLitGenreText - Health care; Substance abuse disorders; Substance abuse; Computerized medical records; Information sharing; Federal agencies DO - http://dx.doi.org/10.1016/j.jsat.2011.10.010 ER - TY - JOUR T1 - Determinants of High Pesticide Exposure Events in the Agricultural Health Cohort Study from Enrollment (1993-1997) through Phase II (1999-2003) AN - 1034830773; 17062763 AB - We conducted an analysis of the determinants of high pesticide exposure events (HPEEs), which are defined as self-reported incidents of high exposure to pesticides, fertilizers, or other chemicals in the Agricultural Health Study, a cohort of private applicators and their spouses residing in North Carolina or Iowa, and commercial applicators residing in Iowa. We examined the risk of HPEEs occurring between enrollment (Phase I: 1993-1997) and follow-up (Phase II: 1999-2003) among participants who completed the Phase II questionnaire (n = 43,149) by calculating hazard rate ratios and 95% confidence intervals using Cox proportional-hazard regression. During the follow-up period, 1,582 HPEEs were reported (3.8%). HPEE risk was significantly higher among Iowa residents, younger participants, those with a hearing deficit, a risk-taking personality, and an HPEE prior to enrollment. Among private applicators (n = 30,102), larger farm size, higher frequency and duration of pesticide use, spraying pesticides with open cab windows, using a tractor cab without a charcoal filter, repairing spray equipment, wearing work clothing more than two days without changing, not removing work boots before entering the home, and storing pesticides in the home were associated with significantly higher HPEE risk. Among commercial applicators (n = 2,326), higher frequency of pesticide use was associated with a significantly higher HPEE risk. Among spouses (n = 10,721), higher frequency of pesticide use, using an application vehicle with a cab, and storing pesticides in the home were associated with a significantly higher HPEE risk. Our findings indicate that HPEEs were associated with several modifiable pesticide handling procedures that can be targeted in safety training and education. JF - Journal of Agricultural Safety and Health AU - Payne, K AU - Andreotti, G AU - Bell, E AU - Blair, A AU - Coble, J AU - Alavanja, M AD - NCI, DCEG, 6120 Executive Blvd., Rockville, MD 20852, USA, andreotg@mail.nih.gov Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 167 EP - 179 VL - 18 IS - 3 SN - 1074-7583, 1074-7583 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Charcoal KW - Chemicals KW - USA, North Carolina KW - Fertilizers KW - Education KW - Farms KW - USA, Iowa KW - Training KW - Pesticides KW - Sprays KW - Agricultural equipment KW - H 5000:Pesticides KW - R2 23110:Psychological aspects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1034830773?accountid=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+Agricultural+Safety+and+Health&rft.atitle=Determinants+of+High+Pesticide+Exposure+Events+in+the+Agricultural+Health+Cohort+Study+from+Enrollment+%281993-1997%29+through+Phase+II+%281999-2003%29&rft.au=Payne%2C+K%3BAndreotti%2C+G%3BBell%2C+E%3BBlair%2C+A%3BCoble%2C+J%3BAlavanja%2C+M&rft.aulast=Payne&rft.aufirst=K&rft.date=2012-07-01&rft.volume=18&rft.issue=3&rft.spage=167&rft.isbn=&rft.btitle=&rft.title=Journal+of+Agricultural+Safety+and+Health&rft.issn=10747583&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-08-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Chemicals; Charcoal; Education; Fertilizers; Farms; Training; Sprays; Pesticides; Agricultural equipment; USA, North Carolina; USA, Iowa ER - TY - JOUR T1 - Influence of Plasminogen Activator Inhibitor-1 (SERPINE1) 4G/5G Polymorphism on Circulating SERPINE-1 Antigen Expression in HCC Associated with Viral Infection AN - 1032894717; 16979752 AB - Hepatocarcinogenesis is heavily influenced by chronic hepatitis B (HBV) and C (HCV) infection. Elevated levels of plasminogen activator inhibitor-I (SERPINE1/IPAI-1) have been reported in patients with hepatocellular carcinoma (HCC) associated with viral infection. The gene encoding SERPINE1 is highly polymorphic and the frequently associated 415 guanosine (4G/5G) polymorphism in the gene promoter may influence its expression. Here, we investigated the distribution of genotypes and the frequency ofalleles of the 4G/5G polymorphism in patients with HCC, the influence of the 4G/5G polymorphism on plasma SERPINE1 levels and its association with viral infection. A total of 75 patients with HCC were enrolled: 32 (42.6%) were HBV sub(+)/HCV sub(+), 11 (14.6%) were only HCV sub(+), and 32 (42.6%) were negative for both viruses. A control group of healthy donors was also enrolled (n=50). SERPINE1 plasma concentrations were determined by ELISA and the detection of the promoter 4G/5G polymorphism was performed by an allele-specific PCR analysis. We found that the frequency of both the 4G/4G genotype (p=0.02) and the 4G allele (p=0.006) were significantly higher in patients with HCC compared to the control group, and particularly higher in patients with HCC co-infected with HBV sub(+)/HCV sub(+) than in those with no viral infection. We also found that patients with the 4G/4G genotype had significantly higher plasma SERPINE1 protein levels when compared with patients with the 4G/5G or 5GI5G genotype (p<0.001). Differences in frequency of 4G allele and genetic variability of 4GI5G SERPINE1 polymorphism with a higher level of SERPINE1 protein in patients with HCC with HBV sub(+)/HCV sub(+) than those without infection, suggest the presence of two distinct pathogenic mechanisms in hepatocarcinogenesis, depending on the etiology. JF - Cancer Genomics & Proteomics AU - Divella, R AU - Mazzocca, A AU - Gadaleta, C AU - Simone, G AU - Paradiso, A AU - Quaranta, M AU - Daniele, A AD - Department of Experimantal Oncology, Clinical Pathology Laboratory National Cancer Institute Giovanni Paolo II, Viale Orazio Flacco, 65, 70100, Bari, Italy, rosadive@inwind.it Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 193 EP - 198 VL - 9 IS - 4 SN - 1109-6535, 1109-6535 KW - Biochemistry Abstracts 2: Nucleic Acids; Oncogenes & Growth Factors Abstracts; Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts; Genetics Abstracts KW - Etiology KW - Enzyme-linked immunosorbent assay KW - Hepatitis B virus KW - Gene polymorphism KW - Infection KW - Promoters KW - Hepatitis C virus KW - Chronic infection KW - Hepatitis B KW - Polymerase chain reaction KW - Gene frequency KW - proteomics KW - Guanosine KW - plasminogen KW - Hepatocellular carcinoma KW - B 26660:Miscellaneous Oncogenes & Growth Factors KW - G 07880:Human Genetics KW - N 14845:Miscellaneous KW - W 30960:Bioinformatics & Computer Applications KW - V 22370:Oncology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1032894717?accountid=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+Genomics+%26+Proteomics&rft.atitle=Influence+of+Plasminogen+Activator+Inhibitor-1+%28SERPINE1%29+4G%2F5G+Polymorphism+on+Circulating+SERPINE-1+Antigen+Expression+in+HCC+Associated+with+Viral+Infection&rft.au=Divella%2C+R%3BMazzocca%2C+A%3BGadaleta%2C+C%3BSimone%2C+G%3BParadiso%2C+A%3BQuaranta%2C+M%3BDaniele%2C+A&rft.aulast=Divella&rft.aufirst=R&rft.date=2012-07-01&rft.volume=9&rft.issue=4&rft.spage=193&rft.isbn=&rft.btitle=&rft.title=Cancer+Genomics+%26+Proteomics&rft.issn=11096535&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-08-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Enzyme-linked immunosorbent assay; Etiology; Gene polymorphism; Infection; Promoters; Chronic infection; Hepatitis B; Polymerase chain reaction; Gene frequency; Guanosine; proteomics; plasminogen; Hepatocellular carcinoma; Hepatitis C virus; Hepatitis B virus ER - TY - JOUR T1 - Frequency of adverse reactions to first- and second-line anti-tuberculosis chemotherapy in a Korean cohort AN - 1032891471; 16910254 AB - OBJECTIVE: To determine the frequency of and risk factors for major adverse drug reactions (MADRs) associated with anti-tuberculosis treatment at a tuberculosis (TB) referral hospital in the Republic of Korea. METHODS: Data from an ongoing natural history cohort study were analyzed for permanent regimen changes due to adverse drug reactions and confirmed by chart review. RESULTS: Among 655 subjects, there were 132 MADRs in 112 (17%) subjects. The most common MADRs were gastrointestinal (n = 53), musculoskeletal (n = 22), psychiatric (n = 10), visual (n = 9) and peripheral neuropathic (n = 8). MADRs were more frequent in subjects being treated with second-line regimens (16%) compared to first-line regimens (2.5%). Drugs frequently associated with MADRs were amikacin (3/10, 30%), linezolid (8/29, 28%), para-aminosalicylic acid (47/192, 24%), pyrazinamide (31/528, 5.8%), macrolides (2/44, 4.5%) and cycloserine (12/272, 4.4%). Fluoroquinolones accounted for a single MADR (1/377, 0.003%), despite widespread usage. In multivariate analysis, infection with multi- or extensively drug-resistant disease and previous history of anti-tuberculosis treatment were risk factors for MADR, with adjusted hazard ratios of respectively 2.2 (P = 0.02) and 1.6 (P = 0.04). CONCLUSION: MADRs are common during anti-tuberculosis chemotherapy in this population, occurring in more than one in six subjects. New and less toxic agents to treat drug-resistant TB are urgently needed. JF - International Journal of Tuberculosis and Lung Disease AU - Carroll, M W AU - Lee, M AU - Cai, Y AU - Hallahan, C W AU - Shaw, P A AU - Min, J H AU - Goldfeder, L C AU - Alekseyev, V AU - Grinkrug, S AU - Kang, H S AU - Hwang, S AU - Park, H-M AU - Kang, E AU - Barry, CE III AD - Room 2W20D, Building 33, Tuberculosis Research Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 33 North Drive, Bethesda, MD 20892, USA, cbarry@mail.niaid.gov Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 961 EP - 966 PB - International Union Against Tuberculosis and Lung Disease VL - 16 IS - 7 SN - 1027-3719, 1027-3719 KW - Microbiology Abstracts B: Bacteriology; Risk Abstracts KW - Historical account KW - Amikacin KW - Mycobacterium KW - Chemotherapy KW - Drug resistance KW - Infection KW - Multivariate analysis KW - Risk factors KW - Tuberculosis KW - Korea, Rep. KW - Drugs KW - Linezolid KW - Cycloserine KW - Data processing KW - Fluoroquinolones KW - Lung diseases KW - Musculoskeletal system KW - Reviews KW - pyrazinamide KW - Side effects KW - Hospitals 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/1032891471?accountid=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=International+Journal+of+Tuberculosis+and+Lung+Disease&rft.atitle=Frequency+of+adverse+reactions+to+first-+and+second-line+anti-tuberculosis+chemotherapy+in+a+Korean+cohort&rft.au=Carroll%2C+M+W%3BLee%2C+M%3BCai%2C+Y%3BHallahan%2C+C+W%3BShaw%2C+P+A%3BMin%2C+J+H%3BGoldfeder%2C+L+C%3BAlekseyev%2C+V%3BGrinkrug%2C+S%3BKang%2C+H+S%3BHwang%2C+S%3BPark%2C+H-M%3BKang%2C+E%3BBarry%2C+CE+III&rft.aulast=Carroll&rft.aufirst=M&rft.date=2012-07-01&rft.volume=16&rft.issue=7&rft.spage=961&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Tuberculosis+and+Lung+Disease&rft.issn=10273719&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-08-01 N1 - Last updated - 2013-09-20 N1 - SubjectsTermNotLitGenreText - Cycloserine; Data processing; Fluoroquinolones; Amikacin; Drug resistance; Chemotherapy; Lung diseases; Infection; Multivariate analysis; Risk factors; Reviews; pyrazinamide; Tuberculosis; Linezolid; Drugs; Side effects; Hospitals; Historical account; Musculoskeletal system; Mycobacterium; Korea, Rep. ER - TY - JOUR T1 - Phylogeography and Demographic History of the Neotropical Otter (Lontra longicaudis) AN - 1032890837; 16958536 AB - The Neotropical otter (Lontra longicaudis) is a medium-sized semiaquatic carnivore with a broad distribution in the Neotropical region. Despite being apparently common in many areas, it is one of the least known otters, and genetic studies on this species are scarce. Here, we have investigated its genetic diversity, population structure, and demographic history across a large portion of its geographic range by analyzing 1471 base pairs (bp) of mitochondrial DNA from 52 individuals. Our results indicate that L. longicaudis presents high levels of genetic diversity and a consistent phylogeographic pattern, suggesting the existence of at least 4 distinct evolutionary lineages in South America. The observed phylogeographic partitions are partially congruent with the subspecies classification previously proposed for this species. Coalescence-based analyses indicate that Neotropical otter mitochondrial DNA lineages have shared a rather recent common ancestor, approximately 0.5 Ma, and have subsequently diversified into the observed phylogroups. A consistent scenario of recent population expansion was identified in Eastern South America based on several complementary analyses of historical demography. The results obtained here provide novel insights on the evolutionary history of this largely unknown Neotropical mustelid and should be useful to design conservation and management policies on behalf of this species and its habitats. JF - Journal of Heredity AU - Trinca, Cristine S AU - de Thoisy, Benoit AU - Rosas, Fernando CW AU - Waldemarin, Helen F AU - Koepfli, Klaus-Peter AU - Vianna, Juliana A AU - Eizirik, Eduardo AD - From the Departamento de Genetica, Universidade Federal do Rio Grande do Sul, Avenida Bento Goncalves, 9500, predio 43323, Porto Alegre, Rio Grande do Sul, Brazil (Trinca); Faculdade de Biociencias, PUCRS, Avenida Ipiranga, 6681, predio 12C, sala 172, Porto Alegre, Rio Grande do Sul, Brazil (Trinca and Eizirik); Kwata NGO, 16 Avenue Pasteur, F-97300, Cayenne, French Guiana (Thoisy); Laboratoire des Interactions Virus-Hotes, Institut Pasteur de la Guyane, 23 Avenue Pasteur, F-97300, Cayenne, French Guiana (Thoisy); Instituto Nacional de Pesquisas da Amazonia-INPA, Avenida Andre Araujo, 2936, Manaus, Amazonas, Brazil (Rosas); Projeto Ecolontras/Associacao Ecologica Ecomarapendi, Rua Paissandu 362, Rio de Janeiro, Rio de Janeiro, Brazil (Waldemarin); Laboratory of Genomic Diversity, National Cancer Institute, Frederick, MD (Koepfli); Departamento de Ecosistemas y Medio Ambiente, Pontificia Universidad Cató, eduardo.eizirik@pucrs.br Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 479 EP - 492 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 103 IS - 4 SN - 0022-1503, 0022-1503 KW - Ecology Abstracts; ASFA 1: Biological Sciences & Living Resources; Genetics Abstracts KW - Neotropical Region KW - Carnivores KW - Lontra KW - Genetic diversity KW - Habitat KW - Demography KW - Population genetics KW - Genetics KW - South America KW - Mitochondrial DNA KW - Classification KW - DNA KW - Conservation KW - Population structure KW - Evolution KW - Base pairs KW - G 07740:Evolution KW - D 04040:Ecosystem and Ecology Studies KW - Q1 08383:Biogeography and biogeographic regions UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1032890837?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Heredity&rft.atitle=Phylogeography+and+Demographic+History+of+the+Neotropical+Otter+%28Lontra+longicaudis%29&rft.au=Trinca%2C+Cristine+S%3Bde+Thoisy%2C+Benoit%3BRosas%2C+Fernando+CW%3BWaldemarin%2C+Helen+F%3BKoepfli%2C+Klaus-Peter%3BVianna%2C+Juliana+A%3BEizirik%2C+Eduardo&rft.aulast=Trinca&rft.aufirst=Cristine&rft.date=2012-07-01&rft.volume=103&rft.issue=4&rft.spage=479&rft.isbn=&rft.btitle=&rft.title=Journal+of+Heredity&rft.issn=00221503&rft_id=info:doi/10.1093%2Fjhered%2Fess001 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-08-01 N1 - Last updated - 2014-05-05 N1 - SubjectsTermNotLitGenreText - Genetics; Population genetics; Classification; Carnivores; DNA; Genetic diversity; Population structure; Evolution; Demography; Mitochondrial DNA; Conservation; Habitat; Base pairs; Lontra; South America; Neotropical Region DO - http://dx.doi.org/10.1093/jhered/ess001 ER - TY - JOUR T1 - New National Heart, Lung, and Blood Institute Integrated Cardiovascular Guidelines: Management of Pediatric Obesity AN - 1032613480; 22765030 AB - Despite efforts during the past decade to prevent and control overweight and obesity, 2007--2008 reports from the National Health and Nutrition Examination Survey show sustained high prevalence, with 16.9% of children and adolescents with a body mass index above the 95th percentile for age and gender.1 There are persistent differences in obesity prevalence by region, racial/ethnic group and socio-economic status exemplified in a recent report from the Bogalusa Heart Study, which began in the 1970s.2 Screening of 5- to 17-year-old school children revealed that the prevalence of obesity has increased more than fivefold, from 5.6% in 1973--1974 to 30.8% in 2008--2009.2 The evidence review performed by the expert panel for the new National Heart, Lung, and Blood Institute (NHLBI) Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents (Integrated CV Guidelines) identified substantial evidence that atherosclerosis in childhood and adolescence is associated with the presence of obesity.3 Two major postmortem studies have demonstrated that obesity in childhood and adolescence is associated with increased evidence of atherosclerosis at autopsy, especially in males.4 Obesity strongly correlates with elevated blood pressure, dyslipidemia, and insulin resistance, all factors shown to be associated with the presence and severity of atherosclerosis in major epidemiologic studies in children and adolescents.5--7 Because of these associations, obesity is even more powerfully correlated with the development of atherosclerosis. Longitudinal studies have demonstrated strong and consistent tracking of elevated body mass index (BMI) and increased adiposity in childhood to the presence of obesity in adulthood.8 Improvement in weight status and decrease in body fatness has been shown to be associated with a decrease in systolic and diastolic blood pressures and a decrease in total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and/or triglycerides (TG).9 Decreased obesity also results in decreases in insulin resistance and in inflammatory markers.9 From the accumulated evidence, obesity in childhood can be seen to be an important predictor of increased risk for cardiovascular disease in adult life and a decrease in obesity to be an important modifier of that risk. JF - Pediatric Annals AU - Washington, Reginald L, MD Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 1 EP - 7 CY - Thorofare PB - SLACK INCORPORATED VL - 41 IS - 7 SN - 00904481 KW - Medical Sciences--Pediatrics KW - Obesity KW - Weight control KW - Teenagers KW - Body mass index KW - Diet KW - Children & youth KW - United States KW - National Heart, Lung, & Blood Institute (U.S.) KW - Humans KW - Child KW - Adolescent KW - Obesity -- therapy KW - Cardiovascular Diseases -- etiology KW - Cardiovascular Diseases -- prevention & control KW - Obesity -- complications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1032613480?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthcompleteshell&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pediatric+Annals&rft.atitle=New+National+Heart%2C+Lung%2C+and+Blood+Institute+Integrated+Cardiovascular+Guidelines%3A+Management+of+Pediatric+Obesity&rft.au=Washington%2C+Reginald+L%2C+MD&rft.aulast=Washington&rft.aufirst=Reginald&rft.date=2012-07-01&rft.volume=41&rft.issue=7&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Pediatric+Annals&rft.issn=00904481&rft_id=info:doi/10.3928%2F00904481-20120625-07 LA - English DB - ProQuest Central N1 - Copyright - Copyright 2012, SLACK Incorporated N1 - Last updated - 2017-01-21 DO - http://dx.doi.org/10.3928/00904481-20120625-07 ER - TY - JOUR T1 - A preliminary study on the attitude of the Japanese public towards creative artwork by people with mental illness AN - 1030905679; 201221883 AB - Background: Although researchers have suggested that consumer art can help reduce the stigma of mental illness, there is little evidence of the attitudes of the Japanese public towards such artwork. Material: A total of 277 Japanese visitors attending an exhibition of visual arts by people with mental illness completed a short questionnaire. Discussion: After their visit, approximately 87% of the participants reported being strongly or fairly impressed by the creative art. Word frequency analysis implied generally positive attitudes towards the works. Conclusions: The Japanese public might generally have positive and empathetic attitudes towards artwork by people with mental illness. [Reprinted by permission of Sage Publications Ltd., copyright holder.] JF - International Journal of Social Psychiatry AU - Yamauchi, Takashi AU - Takeshima, Tadashi AU - Koh, Eugen AU - Chiba, Hisomu AU - Nakagawa, Ryuji AU - Sudo, Anju AU - Ono, Sayaka AU - Okazaki, Yuji AU - Kikkawa, Takehiko AD - Centre for Suicide Prevention, National Institute of Mental Health, National Centre of Neurology and Psychiatry, Tokyo, Japan Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 350 EP - 354 PB - Sage Publications, London UK VL - 58 IS - 4 SN - 0020-7640, 0020-7640 KW - arts attitudes general population mental illness qualitative study word frequency analysis KW - Mentally ill people KW - Attitudes KW - Stigmatization KW - Exhibitions KW - Positive thought KW - Japan KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1030905679?accountid=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=International+Journal+of+Social+Psychiatry&rft.atitle=A+preliminary+study+on+the+attitude+of+the+Japanese+public+towards+creative+artwork+by+people+with+mental+illness&rft.au=Yamauchi%2C+Takashi%3BTakeshima%2C+Tadashi%3BKoh%2C+Eugen%3BChiba%2C+Hisomu%3BNakagawa%2C+Ryuji%3BSudo%2C+Anju%3BOno%2C+Sayaka%3BOkazaki%2C+Yuji%3BKikkawa%2C+Takehiko&rft.aulast=Yamauchi&rft.aufirst=Takashi&rft.date=2012-07-01&rft.volume=58&rft.issue=4&rft.spage=350&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Social+Psychiatry&rft.issn=00207640&rft_id=info:doi/10.1177%2F0020764010397584 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-08-01 N1 - Last updated - 2016-09-27 N1 - CODEN - IJSPAG N1 - SubjectsTermNotLitGenreText - Japan; Mentally ill people; Positive thought; Attitudes; Exhibitions; Stigmatization DO - http://dx.doi.org/10.1177/0020764010397584 ER - TY - JOUR T1 - Validation of prostate cancer risk-related loci identified from genome-wide association studies using family-based association analysis: evidence from the International Consortium for Prostate Cancer Genetics (ICPCG) AN - 1028031724; 16835822 AB - Multiple prostate cancer (PCa) risk-related loci have been discovered by genome-wide association studies (GWAS) based on case-control designs. However, GWAS findings may be confounded by population stratification if cases and controls are inadvertently drawn from different genetic backgrounds. In addition, since these loci were identified in cases with predominantly sporadic disease, little is known about their relationships with hereditary prostate cancer (HPC). The association between seventeen reported PCa susceptibility loci was evaluated with a family-based association test using 1,979 hereditary PCa families of European descent collected by members of the International Consortium for Prostate Cancer Genetics, with a total of 5,730 affected men. The risk alleles for 8 of the 17 loci were significantly over-transmitted from parents to affected offspring, including SNPs residing in 8q24 (regions 1, 2 and 3), 10q11, 11q13, 17q12 (region 1), 17q24 and Xp11. In subgroup analyses, three loci, at 8q24 (regions 1 and 2) plus 17q12, were significantly over-transmitted in hereditary PCa families with five or more affected members, while loci at 3p12, 8q24 (region 2), 11q13, 17q12 (region 1), 17q24 and Xp11 were significantly over-transmitted in HPC families with an average age of diagnosis at 65 years or less. Our results indicate that at least a subset of PCa risk-related loci identified by case-control GWAS are also associated with disease risk in HPC families. JF - Human Genetics AU - Jin, Guangfu AU - Lu, Lingyi AU - Cooney, Kathleen A AU - Ray, Anna M AU - Zuhlke, Kimberly A AU - Lange, Ethan M AU - Cannon-Albright, Lisa A AU - Camp, Nicola J AU - Teerlink, Craig C AU - FitzGerald, Liesel M AU - Stanford, Janet L AU - Wiley, Kathleen E AU - Isaacs, Sarah D AU - Walsh, Patrick C AU - Foulkes, William D AU - Giles, Graham G AU - Hopper, John L AU - Severi, Gianluca AU - Eeles, Ros AU - Easton, Doug AU - Kote-Jarai, Zsofia AU - Guy, Michelle AU - Rinckleb, Antje AU - Maier, Christiane AU - Vogel, Walther AU - Cancel-Tassin, Geraldine AU - Egrot, Christophe AU - Cussenot, Olivier AU - Thibodeau, Stephen N AU - McDonnell, Shannon K AU - Schaid, Daniel J AU - Wiklund, Fredrik AU - Gronberg, Henrik AU - Emanuelsson, Monica AU - Whittemore, Alice S AU - Oakley-Girvan, Ingrid AU - Hsieh, Chih-Lin AU - Wahlfors, Tiina AU - Tammela, Teuvo AU - Schleutker, Johanna AU - Catalona, William J AU - Zheng, SLilly AU - Ostrander, Elaine A AU - Isaacs, William B AU - Xu, Jianfeng AD - Data Coordinating Center for the ICPCG and Center for Cancer Genomics, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA, eostrand@mail.nih.gov Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 1095 EP - 1103 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 131 IS - 7 SN - 0340-6717, 0340-6717 KW - Risk Abstracts; Health & Safety Science Abstracts; Genetics Abstracts KW - Age KW - Association analysis KW - Genetics KW - Offspring KW - Progeny KW - Prostate cancer KW - Single-nucleotide polymorphism KW - Stratification KW - chromosome 3 KW - chromosome 8 KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - G 07880:Human Genetics KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028031724?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+Genetics&rft.atitle=Validation+of+prostate+cancer+risk-related+loci+identified+from+genome-wide+association+studies+using+family-based+association+analysis%3A+evidence+from+the+International+Consortium+for+Prostate+Cancer+Genetics+%28ICPCG%29&rft.au=Jin%2C+Guangfu%3BLu%2C+Lingyi%3BCooney%2C+Kathleen+A%3BRay%2C+Anna+M%3BZuhlke%2C+Kimberly+A%3BLange%2C+Ethan+M%3BCannon-Albright%2C+Lisa+A%3BCamp%2C+Nicola+J%3BTeerlink%2C+Craig+C%3BFitzGerald%2C+Liesel+M%3BStanford%2C+Janet+L%3BWiley%2C+Kathleen+E%3BIsaacs%2C+Sarah+D%3BWalsh%2C+Patrick+C%3BFoulkes%2C+William+D%3BGiles%2C+Graham+G%3BHopper%2C+John+L%3BSeveri%2C+Gianluca%3BEeles%2C+Ros%3BEaston%2C+Doug%3BKote-Jarai%2C+Zsofia%3BGuy%2C+Michelle%3BRinckleb%2C+Antje%3BMaier%2C+Christiane%3BVogel%2C+Walther%3BCancel-Tassin%2C+Geraldine%3BEgrot%2C+Christophe%3BCussenot%2C+Olivier%3BThibodeau%2C+Stephen+N%3BMcDonnell%2C+Shannon+K%3BSchaid%2C+Daniel+J%3BWiklund%2C+Fredrik%3BGronberg%2C+Henrik%3BEmanuelsson%2C+Monica%3BWhittemore%2C+Alice+S%3BOakley-Girvan%2C+Ingrid%3BHsieh%2C+Chih-Lin%3BWahlfors%2C+Tiina%3BTammela%2C+Teuvo%3BSchleutker%2C+Johanna%3BCatalona%2C+William+J%3BZheng%2C+SLilly%3BOstrander%2C+Elaine+A%3BIsaacs%2C+William+B%3BXu%2C+Jianfeng&rft.aulast=Jin&rft.aufirst=Guangfu&rft.date=2012-07-01&rft.volume=131&rft.issue=7&rft.spage=1095&rft.isbn=&rft.btitle=&rft.title=Human+Genetics&rft.issn=03406717&rft_id=info:doi/10.1007%2Fs00439-011-1136-0 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2012-10-19 N1 - SubjectsTermNotLitGenreText - chromosome 8; Age; Association analysis; Prostate cancer; Single-nucleotide polymorphism; Progeny; chromosome 3; Genetics; Stratification; Offspring DO - http://dx.doi.org/10.1007/s00439-011-1136-0 ER - TY - JOUR T1 - Matching 3-D Prone and Supine CT Colonography Scans Using Graphs AN - 1028031177; 16888540 AB - In this paper, we propose a new registration method for prone and supine computed tomographic colonography scans using graph matching. We formulate 3-D colon registration as a graph matching problem and propose a new graph matching algorithm based on mean field theory. In the proposed algorithm, we solve the matching problem in an iterative way. In each step, we use mean field theory to find the matched pair of nodes with highest probability. During iterative optimization, one-to-one matching constraints are added to the system in a step-by-step approach. Prominent matching pairs found in previous iterations are used to guide subsequent mean field calculations. The proposed method was found to have the best performance with smallest standard deviation compared with two other baseline algorithms called the normalized distance along the colon centerline (NDACC) ( p = 0.17) with manual colon centerline correction and spectral matching ( p <1e-5). A major advantage of the proposed method is that it is fully automatic and does not require defining a colon centerline for registration. For the latter NDACC method, user interaction is almost always needed for identifying the colon centerlines. JF - IEEE Transactions on Information Technology in Biomedicine AU - Wang, Shijun AU - Petrick, Nicholas AU - Van Uitert, Robert L AU - Periaswamy, Senthil AU - Wei, Zhuoshi AU - Summers, Ronald M AD - Imaging Biomarkers and Computer-Aided Diagnosis Laboratory, Radiology and Imaging Sciences, National Institutes of Health Clinical Center, Bethesda, USA Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 676 EP - 682 PB - Institute of Electrical and Electronics Engineers, Inc., 3 Park Avenue, 17th Fl New York NY 10016-5997 United States VL - 16 IS - 4 SN - 1089-7771, 1089-7771 KW - Biotechnology and Bioengineering Abstracts KW - Standard deviation KW - Colon KW - Computed tomography KW - Algorithms KW - Nodes KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028031177?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IEEE+Transactions+on+Information+Technology+in+Biomedicine&rft.atitle=Matching+3-D+Prone+and+Supine+CT+Colonography+Scans+Using+Graphs&rft.au=Wang%2C+Shijun%3BPetrick%2C+Nicholas%3BVan+Uitert%2C+Robert+L%3BPeriaswamy%2C+Senthil%3BWei%2C+Zhuoshi%3BSummers%2C+Ronald+M&rft.aulast=Wang&rft.aufirst=Shijun&rft.date=2012-07-01&rft.volume=16&rft.issue=4&rft.spage=676&rft.isbn=&rft.btitle=&rft.title=IEEE+Transactions+on+Information+Technology+in+Biomedicine&rft.issn=10897771&rft_id=info:doi/10.1109%2FTITB.2012.2194297 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Standard deviation; Colon; Computed tomography; Algorithms; Nodes DO - http://dx.doi.org/10.1109/TITB.2012.2194297 ER - TY - JOUR T1 - Requirements for Borrelia burgdorferi plasmid maintenance AN - 1028026996; 16815538 AB - Borrelia burgdorferi has multiple linear and circular plasmids that are faithfully replicated and partitioned as the bacterium grows and divides. The low copy number of these replicons implies that active partitioning contributes to plasmid stability. Analyzing the requirements for plasmid replication and partition in B. burgdorferi is complicated by the complexity of the genome and the possibility that products may act in trans. Consequently, we have studied the replication-partition region (bbb10-13) of the B. burgdorferi 26kb circular plasmid (cp26) in Escherichia coli, by fusion with a partition-defective miniF plasmid. Our analysis demonstrated that bbb10, bbb11, and bbb13 are required for stable miniF maintenance, whereas bbb12 is dispensable. To validate these results, we attempted to inactivate two of these genes in B. burgdorferi. bbb12 mutants were obtained at a typical frequency, suggesting that the bbb12 product is dispensable for cp26 maintenance as well. We could not directly measure cp26 stability in the bbb12 mutant, because cp26 carries essential genes, and bacteria that have lost cp26 are inviable. Conversely, we were unable to inactivate bbb10 on cp26 of B. burgdorferi. Our results suggest that bbb12 is dispensable for cp26 maintenance, whereas bbb10, bbb11, and bbb13 play crucial roles in that process. JF - Plasmid AU - Tilly, Kit AU - Checroun, Claire AU - Rosa, Patricia A AD - Laboratory of Zoonotic Pathogens, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rocky Mountain Laboratories, Hamilton, MT 59840, United States, ktilly@niaid.nih.gov Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 1 EP - 12 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 68 IS - 1 SN - 0147-619X, 0147-619X KW - Microbiology Abstracts B: Bacteriology; Genetics Abstracts KW - Genomes KW - Plasmids KW - Replication KW - copy number KW - Borrelia burgdorferi KW - Escherichia coli UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028026996?accountid=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=Plasmid&rft.atitle=Requirements+for+Borrelia+burgdorferi+plasmid+maintenance&rft.au=Tilly%2C+Kit%3BChecroun%2C+Claire%3BRosa%2C+Patricia+A&rft.aulast=Tilly&rft.aufirst=Kit&rft.date=2012-07-01&rft.volume=68&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Plasmid&rft.issn=0147619X&rft_id=info:doi/10.1016%2Fj.plasmid.2012.01.009 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2012-09-24 N1 - SubjectsTermNotLitGenreText - Genomes; Replication; Plasmids; copy number; Borrelia burgdorferi; Escherichia coli DO - http://dx.doi.org/10.1016/j.plasmid.2012.01.009 ER - TY - JOUR T1 - The emerging medical ecology of the human gut microbiome AN - 1028026754; 16834189 AB - It is increasingly clear that the human gut microbiome has great medical importance, and researchers are beginning to investigate its basic biology and to appreciate the challenges that it presents to medical science. Several striking new empirical results in this area are perplexing within the standard conceptual framework of biomedicine, and this highlights the need for new perspectives from ecology and from dynamical systems theory. Here, we discuss recent results concerning sources of individual variation, temporal variation within individuals, long-term changes after transient perturbations and individualized responses to perturbation within the human gut microbiome. JF - Trends in Ecology & Evolution AU - Pepper, John W AU - Rosenfeld, Simon AD - Division of Cancer Prevention, National Cancer Institute, Bethesda, MD 20892-7354, USA, pepperjw@mail.nih.gov PY - 2012 SP - 381 EP - 384 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 27 IS - 7 SN - 0169-5347, 0169-5347 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Sustainability Science Abstracts; Ecology Abstracts KW - Ecology KW - Digestive tract KW - Temporal variations KW - Reviews KW - Medical importance KW - M3 1010:Issues in Sustainable Development KW - D 04040:Ecosystem and Ecology Studies KW - A 01490:Miscellaneous UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028026754?accountid=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=Trends+in+Ecology+%26+Evolution&rft.atitle=The+emerging+medical+ecology+of+the+human+gut+microbiome&rft.au=Pepper%2C+John+W%3BRosenfeld%2C+Simon&rft.aulast=Pepper&rft.aufirst=John&rft.date=2012-07-01&rft.volume=27&rft.issue=7&rft.spage=381&rft.isbn=&rft.btitle=&rft.title=Trends+in+Ecology+%26+Evolution&rft.issn=01695347&rft_id=info:doi/10.1016%2Fj.tree.2012.03.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Digestive tract; Temporal variations; Reviews; Medical importance; Ecology DO - http://dx.doi.org/10.1016/j.tree.2012.03.002 ER - TY - JOUR T1 - Ion and nutrient uptake by malaria parasite-infected erythrocytes AN - 1028025852; 16854114 AB - Erythrocytes infected with malaria parasites have increased permeability to diverse organic and inorganic solutes. While these permeability changes have been known for decades, the molecular basis of transport was unknown and intensively debated. CLAG3, a parasite protein previously thought to function in cytoadherence, has recently been implicated in formation of the plasmodial surface anion channel (PSAC), an unusual small conductance ion channel that mediates uptake of most solutes. Consistent with transport studies, the clag genes are conserved in all plasmodia but are absent from other genera. The encoded protein is integral to the host membrane, as also predicted by electrophysiology. An important question is whether functional channels are formed by CLAG3 alone or through interactions with other proteins. In either case, gene identification should advance our understanding of parasite biology and may lead to new therapeutics. JF - Cellular Microbiology AU - Desai, Sanjay A AD - The Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20894, USA. Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 1003 EP - 1009 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 14 IS - 7 SN - 1462-5814, 1462-5814 KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - Parasites KW - Human diseases KW - Conductance KW - Erythrocytes KW - Malaria KW - Electrophysiology KW - Solutes KW - Permeability KW - Ion channels KW - Microbiology KW - Anion channels KW - Uptake KW - Plasmodia KW - Nutrient uptake KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08524:Public health, medicines, dangerous organisms KW - K 03320:Cell Biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028025852?accountid=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=Cellular+Microbiology&rft.atitle=Ion+and+nutrient+uptake+by+malaria+parasite-infected+erythrocytes&rft.au=Desai%2C+Sanjay+A&rft.aulast=Desai&rft.aufirst=Sanjay&rft.date=2012-07-01&rft.volume=14&rft.issue=7&rft.spage=1003&rft.isbn=&rft.btitle=&rft.title=Cellular+Microbiology&rft.issn=14625814&rft_id=info:doi/10.1111%2Fj.1462-5822.2012.01790.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Document feature - figure 1 N1 - Last updated - 2015-10-28 N1 - SubjectsTermNotLitGenreText - Permeability; Parasites; Solutes; Human diseases; Microbiology; Erythrocytes; Uptake; Malaria; Electrophysiology; Conductance; Ion channels; Anion channels; Nutrient uptake; Plasmodia DO - http://dx.doi.org/10.1111/j.1462-5822.2012.01790.x ER - TY - JOUR T1 - Activity of Human Immunodeficiency Virus Type 1 Protease Inhibitors against the Initial Autocleavage in Gag-Pol Polyprotein Processing AN - 1028025468; 16873896 AB - Inhibitors of HIV protease have proven to be important drugs in combination anti-HIV therapy. These inhibitors were designed to target mature protease and prevent viral particle maturation by blocking Gag and Gag-Pol processing by mature protease. Currently there are few data assessing the ability of these protease inhibitors to block the initial step in autoproteolytic processing of Gag-Pol. This unique step involves the dimerization of two Gag-Pol polyproteins and autocleavage of the Gag-Pol polyprotein by the embedded dimeric protease. We developed a plasmid encoding a modified form of Gag-Pol that can undergo autoprocessing only at the initial cleavage site between p2 and nucleocapsid. Using an in vitro transcription/translation system, we assessed the ability of six different approved protease inhibitors (darunavir, indinavir, nelfinavir, ritonavir, saquinavir, and tipranavir) to block this initial autocleavage step. Of these inhibitors, darunavir and saquinavir were the most effective. Darunavir and saquinavir were also the most effective at blocking the initial autoprocessing of full-length Gag-Pol in HIV-1-infected T cells. Thus, we have identified at least two HIV-1 protease inhibitors that have activity against the primary autocatalytic step of the embedded HIV-1 protease in Gag-Pol at concentrations that may be attained in HIV-1-infected patients. Due to unique aspects of the initial processing step, it may be possible to develop inhibitors with greater potency against this step, thus halting viral maturation at the earliest stages. The transcription/translation assay could be used to develop more potent inhibitors of this essential first step in viral maturation. JF - Antimicrobial Agents & Chemotherapy AU - Davis, David A AU - Yarchoan, Robert AD - HIV and AIDS Malignancy Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, USA, DavidA.Davis,dadavis{at}helix.nih.gov. Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 3620 EP - 3628 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 56 IS - 7 SN - 0066-4804, 0066-4804 KW - Immunology Abstracts; Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Data processing KW - Drugs KW - Gag protein KW - Indinavir KW - Lymphocytes T KW - Nelfinavir KW - Nucleocapsids KW - Plasmids KW - Proteinase inhibitors KW - Ritonavir KW - Saquinavir KW - Transcription KW - Translation KW - polyproteins KW - Human immunodeficiency virus KW - Human immunodeficiency virus 1 KW - A 01340:Antibiotics & Antimicrobials KW - V 22360:AIDS and HIV KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028025468?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Activity+of+Human+Immunodeficiency+Virus+Type+1+Protease+Inhibitors+against+the+Initial+Autocleavage+in+Gag-Pol+Polyprotein+Processing&rft.au=Davis%2C+David+A%3BYarchoan%2C+Robert&rft.aulast=Davis&rft.aufirst=David&rft.date=2012-07-01&rft.volume=56&rft.issue=7&rft.spage=3620&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.00055-12 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Number of references - 26 N1 - Last updated - 2012-10-19 N1 - SubjectsTermNotLitGenreText - Translation; polyproteins; Data processing; Indinavir; Saquinavir; Proteinase inhibitors; Transcription; Plasmids; Gag protein; Ritonavir; Nucleocapsids; Lymphocytes T; Nelfinavir; Drugs; Human immunodeficiency virus; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1128/AAC.00055-12 ER - TY - JOUR T1 - Socioeconomic status, healthcare density, and risk of prostate cancer among African American and Caucasian men in a large prospective study AN - 1028024167; 16828890 AB - Objectives: The purpose of this study was to separately examine the impact of neighborhood socioeconomic deprivation and availability of healthcare resources on prostate cancer risk among African American and Caucasian men. Methods: In the large, prospective NIH-AARP Diet and Health Study, we analyzed baseline (1995-1996) data from adult men, aged 50-71 years. Incident prostate cancer cases (n = 22,523; 1,089 among African Americans) were identified through December 2006. Lifestyle and health risk information was ascertained by questionnaires administered at baseline. Area-level socioeconomic indicators were ascertained by linkage to the US Census and the Area Resource File. Multilevel Cox models were used to estimate hazard ratios (HRs) and 95 % confidence intervals (CIs). Results: A differential effect among African Americans and Caucasians was observed for neighborhood deprivation (p-interaction = 0.04), percent uninsured (p-interaction = 0.02), and urologist density (p-interaction = 0.01). Compared to men living in counties with the highest density of urologists, those with fewer had a substantially increased risk of developing advanced prostate cancer (HR = 2.68, 95 % CI = 1.31, 5.47) among African American. Conclusions: Certain socioeconomic indicators were associated with an increased risk of prostate cancer among African American men compared to Caucasians. Minimizing differences in healthcare availability may be a potentially important pathway to minimizing disparities in prostate cancer risk. JF - Cancer Causes & Control AU - Major, Jacqueline M AU - Norman Oliver, M AU - Doubeni, Chyke A AU - Hollenbeck, Albert R AU - Graubard, Barry I AU - Sinha, Rashmi AD - Division of Cancer Epidemiology and Genetics, Department of Health and Human Services, National Cancer Institute, National Institutes of Health, 6120 Executive Boulevard, Bethesda, MD, 20852, USA, Jacqueline.major@nih.gov Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 1185 EP - 1191 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 23 IS - 7 SN - 0957-5243, 0957-5243 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Diets KW - Risk assessment KW - Health care KW - Males KW - Socioeconomics KW - Census KW - prostate cancer KW - Ethnic groups 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/1028024167?accountid=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=Socioeconomic+status%2C+healthcare+density%2C+and+risk+of+prostate+cancer+among+African+American+and+Caucasian+men+in+a+large+prospective+study&rft.au=Major%2C+Jacqueline+M%3BNorman+Oliver%2C+M%3BDoubeni%2C+Chyke+A%3BHollenbeck%2C+Albert+R%3BGraubard%2C+Barry+I%3BSinha%2C+Rashmi&rft.aulast=Major&rft.aufirst=Jacqueline&rft.date=2012-07-01&rft.volume=23&rft.issue=7&rft.spage=1185&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-9988-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2013-09-09 N1 - SubjectsTermNotLitGenreText - Risk assessment; Diets; Health care; Males; Socioeconomics; Census; prostate cancer; Cancer; Ethnic groups DO - http://dx.doi.org/10.1007/s10552-012-9988-8 ER - TY - JOUR T1 - Evolution of Cancer Control P.L.A.N.E.T.: moving research into practice AN - 1028024153; 16828889 AB - Evidence-based interventions (EBIs) are not broadly implemented, despite widespread availability of programs, policies, and guidelines. Systematic processes for integrating EBIs with community preference remain challenging for cancer control and prevention, as well as other areas. The Cancer Control P.L.A.N.E.T. (P.L.A.N.E.T) Web portal provides a platform to access data, EBIs, and resources to foster local partnerships and assist public health researchers and practitioners design, implement, and evaluate evidence-based cancer control programs. This article summarizes the evolution of P.L.A.N.E.T. and describes effective and innovative Web 2.0 strategies to increase Web visits, create more interactive platforms for researchers and practitioners to integrate evidence-based resources, community preferences, and the complex context in which programs and policies are implemented. Lessons learned could benefit public health settings and reach low-income, high-risk communities. Researchers, community practitioners, and government partnerships should continue to develop and test innovative ways to address pressing issues in cancer control, health disparities, and health delivery. JF - Cancer Causes & Control AU - Sanchez, Michael A AU - Vinson, Cynthia A AU - Porta, Madeline La AU - Viswanath, Kasisomayajula AU - Kerner, Jon F AU - Glasgow, Russell E AD - National Cancer Institute, 6130 Executive Blvd, EPN, Room 6131A, Rockville, MD, 20852-7338, USA, sanchezgarciama@mail.nih.gov Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 1205 EP - 1212 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 23 IS - 7 SN - 0957-5243, 0957-5243 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Cancer KW - Guidelines KW - Innovations KW - Intervention KW - Prevention KW - Public health KW - Socioeconomics 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/1028024153?accountid=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=Evolution+of+Cancer+Control+P.L.A.N.E.T.%3A+moving+research+into+practice&rft.au=Sanchez%2C+Michael+A%3BVinson%2C+Cynthia+A%3BPorta%2C+Madeline+La%3BViswanath%2C+Kasisomayajula%3BKerner%2C+Jon+F%3BGlasgow%2C+Russell+E&rft.aulast=Sanchez&rft.aufirst=Michael&rft.date=2012-07-01&rft.volume=23&rft.issue=7&rft.spage=1205&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-9987-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2012-08-10 N1 - SubjectsTermNotLitGenreText - Prevention; Guidelines; Intervention; Socioeconomics; Cancer; Public health; Innovations DO - http://dx.doi.org/10.1007/s10552-012-9987-9 ER - TY - JOUR T1 - Adverse effects in risk assessment: Modeling polychlorinated biphenyls and thyroid hormone disruption outcomes in animals and humans AN - 1028023908; 16816050 AB - There is a growing need for quantitative approaches to extrapolate relationships between chemical exposures and early biological perturbations from animals to humans given increasing use of biological assays to evaluate toxicity pathways. We have developed such an approach using polychlorinated biphenyls (PCBs) and thyroid hormone (TH) disruption as a case study. We reviewed and identified experimental animal literature from which we developed a low-dose, linear model of PCB body burdens and decrements in free thyroxine (FT4) and total thyroxine (TT4), accounting for 33 PCB congeners; extrapolated the dose-response from animals to humans; and compared the animal dose-response to the dose-response of PCB body burdens and TH changes from eleven human epidemiological studies. We estimated a range of potencies for PCB congeners (over 4 orders of magnitude), with the strongest for PCB 126. Our approach to developing toxic equivalency models produced relative potencies similar to the toxicity equivalency factors (TEFs) from the World Health Organization (WHO). We generally found that the dose-response extrapolated from the animal studies tends to under-predict the dose-response estimated from human epidemiological studies. A quantitative approach to evaluating the relationship between chemical exposures and TH perturbations, based on animal data can be used to assess human health consequences of thyroid toxicity and inform decision-making. JF - Environmental Research AU - Parham, Fred AU - Wise, Amber AU - Axelrad, Daniel A AU - Guyton, Kathryn Z AU - Portier, Christopher AU - Zeise, Lauren AU - Thomas Zoeller, R AU - Woodruff, Tracey J AD - National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA, woodrufft@obgyn.ucsf.edu Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 74 EP - 84 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 116 SN - 0013-9351, 0013-9351 KW - Toxicology Abstracts; Risk Abstracts; Health & Safety Science Abstracts; Environment Abstracts KW - AhR KW - FT4 KW - g KW - LOD KW - max. KW - mu g/dL KW - mu g/kg KW - ml KW - NAS KW - ng/dL KW - ng/g KW - ng/kg KW - ng/L KW - NHANES KW - NIEHS KW - NTP KW - OCDF KW - PBPK KW - PCBs KW - PCDD KW - PCDF KW - pg/g KW - pg/mL KW - T3 KW - T4 KW - TCDD KW - TCDF KW - TEF KW - TEQ KW - TH KW - TSH KW - TT4 KW - USEPA KW - WHO KW - (5-10):polychlorinated biphenyls KW - Thyroid hormones KW - Adverse health outcomes KW - Biological perturbations KW - Risk assessment KW - Body burden KW - Data processing KW - Thyroid KW - Toxicity KW - Hormones KW - Models KW - Decision making KW - polychlorinated biphenyls KW - Dose-response effects KW - Reviews KW - Thyroxine KW - Congeners KW - PCB compounds KW - PCB KW - Side effects KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - X 24350:Industrial Chemicals KW - R2 23050:Environment KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028023908?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Research&rft.atitle=Adverse+effects+in+risk+assessment%3A+Modeling+polychlorinated+biphenyls+and+thyroid+hormone+disruption+outcomes+in+animals+and+humans&rft.au=Parham%2C+Fred%3BWise%2C+Amber%3BAxelrad%2C+Daniel+A%3BGuyton%2C+Kathryn+Z%3BPortier%2C+Christopher%3BZeise%2C+Lauren%3BThomas+Zoeller%2C+R%3BWoodruff%2C+Tracey+J&rft.aulast=Parham&rft.aufirst=Fred&rft.date=2012-07-01&rft.volume=116&rft.issue=&rft.spage=74&rft.isbn=&rft.btitle=&rft.title=Environmental+Research&rft.issn=00139351&rft_id=info:doi/10.1016%2Fj.envres.2012.04.003 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Risk assessment; Decision making; Thyroid hormones; Data processing; polychlorinated biphenyls; Reviews; Thyroxine; Congeners; Toxicity; Side effects; PCB; Models; Body burden; Dose-response effects; Thyroid; Hormones; PCB compounds DO - http://dx.doi.org/10.1016/j.envres.2012.04.003 ER - TY - JOUR T1 - Metalworking fluid exposure and cancer risk in a retrospective cohort of female autoworkers AN - 1028023149; 16828879 AB - Objectives: Metalworking fluids (MWFs) have been associated with cancer of several sites, but the risks have been primarily examined in men or in studies that adjusted for gender in analyses. To evaluate whether risks were similar in women, we report cancer mortality risk among 4,825 female autoworkers within the united autoworkers-general motors autoworkers cohort. Methods: Standardized mortality rates (SMRs) were calculated based on Michigan death rates (1980-2004). Internal comparisons (1941-2004) were examined using Cox regression for straight, soluble, and synthetic MWFs, and their corresponding oil- and water-based fractions. Results: MWF exposure levels in the female cohort were generally less than two-third the MWF levels in the male cohort. Female autoworkers had an excess of cancer from all sites (SMR, 1.10; 95 % confidence interval (CI), 0.98-1.22) and lung cancer (SMR, 2.08; 95 % CI, 1.71-2.52). Colon cancer risk increased with straight (mineral oil) MWF exposure (exposure > median; hazard ratio = 3.1; 95 % CI, 1.2-8.0). A protective effect was observed for ovarian cancer with the soluble MWFs and water-based MWF metrics. Although bladder, rectal, and laryngeal cancers and malignant melanoma have been associated with straight MWF exposure and pancreatic cancer with synthetic MWF in men, there were too few deaths in this female subcohort to examine exposure-response relations for these sites. Results were null for lung and breast cancer. Conclusions: Our findings support an association between colon cancer and straight MWFs, but we found limited evidence of risk for other tumor sites at the lower exposure levels experienced by the female autoworkers. JF - Cancer Causes & Control AU - Friesen, Melissa C AU - Betenia, Nicole AU - Costello, Sadie AU - Eisen, Ellen A AD - Occupational and Environmental Epidemiology Branch, National Cancer Institute, 6120 Executive Blvd, North Bethesda, MD, 20892, USA, friesenmc@mail.nih.gov Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 1075 EP - 1082 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 23 IS - 7 SN - 0957-5243, 0957-5243 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Breast cancer KW - Dose-response effects KW - Females KW - Lung cancer KW - Metal-working fluids KW - Mortality KW - Standards KW - Tumors KW - pancreatic 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/1028023149?accountid=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=Metalworking+fluid+exposure+and+cancer+risk+in+a+retrospective+cohort+of+female+autoworkers&rft.au=Friesen%2C+Melissa+C%3BBetenia%2C+Nicole%3BCostello%2C+Sadie%3BEisen%2C+Ellen+A&rft.aulast=Friesen&rft.aufirst=Melissa&rft.date=2012-07-01&rft.volume=23&rft.issue=7&rft.spage=1075&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-9976-z LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2012-08-10 N1 - SubjectsTermNotLitGenreText - Mortality; pancreatic cancer; Dose-response effects; Breast cancer; Standards; Tumors; Females; Metal-working fluids; Lung cancer DO - http://dx.doi.org/10.1007/s10552-012-9976-z ER - TY - JOUR T1 - Breast cancer incidence in Mongolia AN - 1028023112; 16828876 AB - Purpose: Data on international variation in breast cancer incidence may help to identify additional risk factors. Substantially lower breast cancer rates in Asia than in North America and Western Europe are established, but differences within Asia have been largely ignored despite heterogeneity in lifestyles and environments. Mongolia's breast cancer experience is of interest because of its shared genetics but vastly different diet compared with other parts of Asia. Methods: Age-standardized breast cancer incidence and mortality rates obtained from the International Association of Cancer Registries are presented for several Asian countries. Mongolian incidence rates obtained from its cancer registry describe incidence within the country. Results: Breast cancer incidence in Mongolia (age standardized 8.0/100,000) is almost a third of rates in China (21.6/100,000), and over five times that of Japan (42.7/100,000) and Russia (43.2/100,000). Rates within Mongolia appear to have increased slightly over the last decade and are higher in urban than rural areas (annual percentage increase of age-standardized rates from 1998 to 2005 was 3.60 and 2.57 %, respectively). The increase in breast cancer incidence with age plateaus at menopause, as in other Asian populations. Conclusions: Mongolia's low breast cancer incidence is of particular interest because of their unusual diet (primarily red meat and dairy) compared with other Asian countries. More intensive study of potential dietary, reproductive and lifestyle factors in Mongolia with comparison to other Asian populations may provide more clarity in what drives the international breast cancer rate differences. JF - Cancer Causes & Control AU - Troisi, Rebecca AU - Altantsetseg, Dalkhjav AU - Davaasambuu, Ganmaa AU - Rich-Edwards, Janet AU - Davaalkham, Dambadarjaa AU - Tretli, Steinar AU - Hoover, Robert N AU - Frazier, ALindsay AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA, troisir@mail.nih.gov Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 1047 EP - 1053 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 23 IS - 7 SN - 0957-5243, 0957-5243 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Age KW - Breast cancer KW - Cancer KW - Dairies KW - Diets KW - Genetics KW - Meat KW - Mortality KW - Standards KW - plateaus KW - Europe KW - North America KW - Mongolia KW - China, People's Rep. KW - Russia KW - Japan UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028023112?accountid=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=Breast+cancer+incidence+in+Mongolia&rft.au=Troisi%2C+Rebecca%3BAltantsetseg%2C+Dalkhjav%3BDavaasambuu%2C+Ganmaa%3BRich-Edwards%2C+Janet%3BDavaalkham%2C+Dambadarjaa%3BTretli%2C+Steinar%3BHoover%2C+Robert+N%3BFrazier%2C+ALindsay&rft.aulast=Troisi&rft.aufirst=Rebecca&rft.date=2012-07-01&rft.volume=23&rft.issue=7&rft.spage=1047&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-9973-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2012-09-24 N1 - SubjectsTermNotLitGenreText - Meat; Diets; Mortality; plateaus; Genetics; Dairies; Age; Breast cancer; Standards; Cancer; North America; Mongolia; Europe; Russia; China, People's Rep.; Japan DO - http://dx.doi.org/10.1007/s10552-012-9973-2 ER - TY - JOUR T1 - Immunohistochemical Investigation of F344/N Rat Islet Cell Tumors from National Toxicology Program Studies AN - 1024665531; 16856952 AB - In this study, we have investigated the immunoexpression of peptide hormones and mediators associated with human islet cell tumors in a group of proliferative islet cell lesions in F344 rats including islet cell hyperplasias, adenomas, and carcinomas, as defined by conventional histopathologic criteria. All proliferative islets expressed synaptophysin, although decreased expression intensity was observed in hyperplasias and adenomas. Most of the proliferative lesions expressed insulin, which generally decreased as lesions progressed toward malignancy. The distribution of glucagon, somatostatin, and gastrin-expressing cells was altered in proliferative islet lesions but did not comprise a large proportion of cells. Islet cell tumors were associated with increased nuclear expression of cyclin-dependent kinase 4 as well as increased proliferating cell nuclear antigen and decreased beta -catenin expression. c-Myelocytomatosis oncogene expression was variable. This is the first study to describe the immunophenotype of islet cell tumors in the F344 rat and to show that islet cell tumors in the F344 rat exhibit similarities in protein expression to the human counterpart. JF - Toxicologic Pathology AU - Koivisto, Christopher AU - Flake, Gordon P AU - Kolenda-Roberts, Holly AU - Masinde, Tiwanda AU - Kissling, Grace E AU - Sills, Robert C AU - Hoenerhoff, Mark J AD - Cellular and Molecular Pathology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA, hoenerhm@niehs.nih.gov Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 751 EP - 763 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 40 IS - 5 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - Adenoma KW - Carcinoma KW - Cyclin-dependent kinase 4 KW - Glucagon KW - Hyperplasia KW - Insulin KW - Islet cells KW - Islets of Langerhans KW - Malignancy KW - Oncogenes KW - Peptide hormones KW - Proliferating cell nuclear antigen KW - Somatostatin KW - Synaptophysin KW - Tumors KW - catenin KW - X 24490:Other UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1024665531?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Immunohistochemical+Investigation+of+F344%2FN+Rat+Islet+Cell+Tumors+from+National+Toxicology+Program+Studies&rft.au=Koivisto%2C+Christopher%3BFlake%2C+Gordon+P%3BKolenda-Roberts%2C+Holly%3BMasinde%2C+Tiwanda%3BKissling%2C+Grace+E%3BSills%2C+Robert+C%3BHoenerhoff%2C+Mark+J&rft.aulast=Koivisto&rft.aufirst=Christopher&rft.date=2012-07-01&rft.volume=40&rft.issue=5&rft.spage=751&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623312441407 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Number of references - 50 N1 - Last updated - 2012-07-27 N1 - SubjectsTermNotLitGenreText - Glucagon; Islet cells; Islets of Langerhans; Tumors; Cyclin-dependent kinase 4; Proliferating cell nuclear antigen; Insulin; Somatostatin; Carcinoma; Hyperplasia; Malignancy; Synaptophysin; catenin; Oncogenes; Adenoma; Peptide hormones DO - http://dx.doi.org/10.1177/0192623312441407 ER - TY - JOUR T1 - Using multiple imputation to assign pesticide use for non-responders in the follow-up questionnaire in the Agricultural Health Study AN - 1024662957; 16841568 AB - The Agricultural Health Study (AHS), a large prospective cohort, was designed to elucidate associations between pesticide use and other agricultural exposures and health outcomes. The cohort includes 57,310 pesticide applicators who were enrolled between 1993 and 1997 in Iowa and North Carolina. A follow-up questionnaire administered 5 years later was completed by 36,342 (63%) of the original participants. Missing pesticide use information from participants who did not complete the second questionnaire impedes both long-term pesticide exposure estimation and statistical inference of risk for health outcomes. Logistic regression and stratified sampling were used to impute key variables related to the use of specific pesticides for 20,968 applicators who did not complete the second questionnaire. To assess the imputation procedure, a 20% random sample of participants was withheld for comparison. The observed and imputed prevalence of any pesticide use in the holdout dataset were 85.7% and 85.3%, respectively. The distribution of prevalence and days/year of use for specific pesticides were similar across observed and imputed in the holdout sample. When appropriately implemented, multiple imputation can reduce bias and increase precision and can be more valid than other missing data approaches. JF - Journal of Exposure Science and Environmental Epidemiology AU - Heltshe, Sonya L AU - Lubin, Jay H AU - Koutros, Stella AU - Coble, Joseph B AU - Ji, Bu-Tian AU - Alavanja, Michael C R AU - Blair, Aaron AU - Sandler, Dale P AU - Hines, Cynthia J AU - Thomas, Kent W AU - Barker, Joseph AU - Andreotti, Gabriella AU - Hoppin, Jane A AU - Beane Freeman, Laura E AD - 1] Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland, USA [2] Department of Pediatrics, School of Medicine, University of Washington, Seattle, Washington, USA Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 409 EP - 416 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 22 IS - 4 SN - 1559-0631, 1559-0631 KW - Health & Safety Science Abstracts; Risk Abstracts; Toxicology Abstracts KW - Data processing KW - Inventories KW - Pesticides KW - Sampling KW - Statistics KW - USA, North Carolina KW - USA, Iowa KW - H 5000:Pesticides KW - R2 23060:Medical and environmental health KW - X 24330:Agrochemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1024662957?accountid=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+Exposure+Science+and+Environmental+Epidemiology&rft.atitle=Using+multiple+imputation+to+assign+pesticide+use+for+non-responders+in+the+follow-up+questionnaire+in+the+Agricultural+Health+Study&rft.au=Heltshe%2C+Sonya+L%3BLubin%2C+Jay+H%3BKoutros%2C+Stella%3BCoble%2C+Joseph+B%3BJi%2C+Bu-Tian%3BAlavanja%2C+Michael+C+R%3BBlair%2C+Aaron%3BSandler%2C+Dale+P%3BHines%2C+Cynthia+J%3BThomas%2C+Kent+W%3BBarker%2C+Joseph%3BAndreotti%2C+Gabriella%3BHoppin%2C+Jane+A%3BBeane+Freeman%2C+Laura+E&rft.aulast=Heltshe&rft.aufirst=Sonya&rft.date=2012-07-01&rft.volume=22&rft.issue=4&rft.spage=409&rft.isbn=&rft.btitle=&rft.title=Journal+of+Exposure+Science+and+Environmental+Epidemiology&rft.issn=15590631&rft_id=info:doi/10.1038%2Fjes.2012.31 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2012-12-28 N1 - SubjectsTermNotLitGenreText - Inventories; Statistics; Data processing; Pesticides; Sampling; USA, North Carolina; USA, Iowa DO - http://dx.doi.org/10.1038/jes.2012.31 ER - TY - JOUR T1 - Two Systems for Targeted Gene Deletion in Coxiella burnetii AN - 1024656666; 16837898 AB - Coxiella burnetii is a ubiquitous zoonotic bacterial pathogen and the cause of human acute Q fever, a disabling influenza-like illness. C. burnetii's former obligate intracellular nature significantly impeded the genetic characterization of putative virulence factors. However, recent host cell-free (axenic) growth of the organism has enabled development of shuttle vector, transposon, and inducible gene expression technologies, with targeted gene inactivation remaining an important challenge. In the present study, we describe two methods for generating targeted gene deletions in C. burnetii that exploit pUC/ColE1 ori-based suicide plasmids encoding sacB for positive selection of mutants. As proof of concept, C. burnetii dotA and dotB, encoding structural components of the type IVB secretion system (T4BSS), were selected for deletion. The first method exploited Cre-lox-mediated recombination. Two suicide plasmids carrying different antibiotic resistance markers and a loxP site were integrated into 5' and 3' flanking regions of dotA. Transformation of this strain with a third suicide plasmid encoding Cre recombinase resulted in the deletion of dotA under sucrose counterselection. The second method utilized a loop-in/loop-out strategy to delete dotA and dotB. A single suicide plasmid was first integrated into 5' or 3' target gene flanking regions. Resolution of the plasmid cointegrant by a second crossover event under sucrose counterselection resulted in gene deletion that was confirmed by PCR and Southern blot. Delta dotA and Delta dotB mutants failed to secrete T4BSS substrates and to productively infect host cells. The repertoire of C. burnetii genetic tools now allows ready fulfillment of molecular Koch's postulates for suspected virulence genes. JF - Applied and Environmental Microbiology AU - Beare, Paul A AU - Larson, Charles L AU - Gilk, Stacey D AU - Heinzen, Robert A AD - Coxiella Pathogenesis Section, Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana, USA, rheinzen@niaid.nih.gov Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 4580 EP - 4589 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 78 IS - 13 SN - 0099-2240, 0099-2240 KW - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Antibiotic resistance KW - Coxiella burnetii KW - Plasmids KW - A:01340 KW - J:02320 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1024656666?accountid=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=Applied+and+Environmental+Microbiology&rft.atitle=Two+Systems+for+Targeted+Gene+Deletion+in+Coxiella+burnetii&rft.au=Beare%2C+Paul+A%3BLarson%2C+Charles+L%3BGilk%2C+Stacey+D%3BHeinzen%2C+Robert+A&rft.aulast=Beare&rft.aufirst=Paul&rft.date=2012-07-01&rft.volume=78&rft.issue=13&rft.spage=4580&rft.isbn=&rft.btitle=&rft.title=Applied+and+Environmental+Microbiology&rft.issn=00992240&rft_id=info:doi/10.1128%2FAEM.00881-12 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Number of references - 1 N1 - Last updated - 2014-02-21 N1 - SubjectsTermNotLitGenreText - Plasmids; Coxiella burnetii DO - http://dx.doi.org/10.1128/AEM.00881-12 ER - TY - JOUR T1 - Peroxisome proliferator-activated receptor alpha induction of uncoupling protein 2 protects against acetaminophen-induced liver toxicity. AN - 1023533049; 22318764 AB - Acetaminophen (APAP) overdose causes acute liver failure in humans and rodents due in part to the destruction of mitochondria as a result of increased oxidative stress followed by hepatocellular necrosis. Activation of the peroxisome proliferator-activated receptor alpha (PPARα), a member of the nuclear receptor superfamily that controls the expression of genes encoding peroxisomal and mitochondrial fatty acid β-oxidation enzymes, with the experimental ligand Wy-14,643 or the clinically used fibrate drug fenofibrate, fully protects mice from APAP-induced hepatotoxicity. PPARα-humanized mice were also protected, whereas Ppara-null mice were not, thus indicating that the protection extends to human PPARα and is PPARα-dependent. This protection is due in part to induction of the PPARα target gene encoding mitochondrial uncoupling protein 2 (UCP2). Forced overexpression of UCP2 protected wildtype mice against APAP-induced hepatotoxicity in the absence of PPARα activation. Ucp2-null mice, however, were sensitive to APAP-induced hepatotoxicity despite activation of PPARα with Wy-14,643. Protection against hepatotoxicity by UCP2-induction through activation of PPARα is associated with decreased APAP-induced c-jun and c-fos expression, decreased phosphorylation of JNK and c-jun, lower mitochondrial H(2)O(2) levels, increased mitochondrial glutathione in liver, and decreased levels of circulating fatty acyl-carnitines. These studies indicate that the PPARα target gene UCP2 protects against elevated reactive oxygen species generated during drug-induced hepatotoxicity and suggest that induction of UCP2 may also be a general mechanism for protection of mitochondria during fatty acid β-oxidation. Copyright © 2012 American Association for the Study of Liver Diseases. JF - Hepatology (Baltimore, Md.) AU - Patterson, Andrew D AU - Shah, Yatrik M AU - Matsubara, Tsutomu AU - Krausz, Kristopher W AU - Gonzalez, Frank J AD - Laboratory of Metabolism, National Cancer Institute, National Institutes of Health, Bethesda, MD 20814, USA. Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 281 EP - 290 VL - 56 IS - 1 KW - Ion Channels KW - 0 KW - Mitochondrial Proteins KW - PPAR alpha KW - Pyrimidines KW - UCP2 protein, human KW - Ucp2 protein, mouse KW - Uncoupling Protein 2 KW - Acetaminophen KW - 362O9ITL9D KW - pirinixic acid KW - 86C4MRT55A KW - Index Medicus KW - Injections, Intraperitoneal KW - Animals KW - Reference Values KW - Analysis of Variance KW - Random Allocation KW - Dose-Response Relationship, Drug KW - Disease Models, Animal KW - Mice KW - Mice, Knockout KW - Oxidative Stress -- physiology KW - Blotting, Western KW - Liver -- drug effects KW - Oxidative Stress -- drug effects KW - Mice, Inbred C57BL KW - Immunohistochemistry KW - Male KW - Chemical and Drug Induced Liver Injury -- prevention & control KW - PPAR alpha -- drug effects KW - Chemical and Drug Induced Liver Injury -- etiology KW - Chemical and Drug Induced Liver Injury -- pathology KW - Ion Channels -- drug effects KW - Pyrimidines -- pharmacology KW - PPAR alpha -- metabolism KW - Mitochondrial Proteins -- metabolism KW - Mitochondrial Proteins -- drug effects KW - Acetaminophen -- toxicity KW - Ion Channels -- metabolism KW - Acetaminophen -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1023533049?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Peroxisome+proliferator-activated+receptor+alpha+induction+of+uncoupling+protein+2+protects+against+acetaminophen-induced+liver+toxicity.&rft.au=Patterson%2C+Andrew+D%3BShah%2C+Yatrik+M%3BMatsubara%2C+Tsutomu%3BKrausz%2C+Kristopher+W%3BGonzalez%2C+Frank+J&rft.aulast=Patterson&rft.aufirst=Andrew&rft.date=2012-07-01&rft.volume=56&rft.issue=1&rft.spage=281&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.25645 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-17 N1 - Date created - 2012-07-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Toxicol Sci. 2000 Oct;57(2):338-44 [11006363] Nature. 2011 Aug 4;476(7358):109-13 [21785437] J Biol Chem. 2002 Mar 15;277(11):9562-9 [11782473] Exp Physiol. 2003 Jan;88(1):65-84 [12525856] Cell Mol Life Sci. 2004 Feb;61(4):393-416 [14999402] Toxicol Appl Pharmacol. 1994 Dec;129(2):252-63 [7992315] Mol Cell Biol. 1995 Jun;15(6):3012-22 [7539101] Toxicol Appl Pharmacol. 1996 Sep;140(1):30-8 [8806867] Adverse Drug React Toxicol Rev. 1997 Mar;16(1):9-14 [9192054] Carcinogenesis. 1997 Nov;18(11):2029-33 [9395198] J Biol Chem. 1998 Mar 6;273(10):5678-84 [9488698] Toxicol Appl Pharmacol. 1998 Sep;152(1):193-9 [9772215] J Clin Invest. 1999 Jun;103(11):1489-98 [10359558] Cell Metab. 2005 Aug;2(2):85-93 [16098826] Biochim Biophys Acta. 2006 May-Jun;1757(5-6):480-5 [16597432] Drug Metab Dispos. 2007 Jan;35(1):1-8 [17020953] Mol Cell Biol. 2007 Jun;27(12):4238-47 [17438130] Gut. 2007 Jul;56(7):982-90 [17185352] Toxicol Sci. 2008 Jan;101(1):132-9 [17690133] FASEB J. 2008 Jan;22(1):9-18 [17855623] J Biol Chem. 2008 Feb 22;283(8):4543-59 [18093979] Toxicology. 2008 Apr 3;246(1):2-8 [18006136] J Med Toxicol. 2008 Mar;4(1):2-6 [18338302] J Biol Chem. 2008 May 16;283(20):13565-77 [18337250] Chem Res Toxicol. 2009 Apr;22(4):699-707 [19256530] Free Radic Biol Med. 2009 Sep 15;47(6):767-78 [19539749] IUBMB Life. 2009 Dec;61(12):1123-31 [19946892] Lab Invest. 2010 Aug;90(8):1189-98 [20368701] J Biol Chem. 2011 Jun 17;286(24):21865-75 [21515686] J Biol Chem. 2011 Oct 7;286(40):35071-8 [21844199] Endocrinology. 2001 Jan;142(1):249-56 [11145588] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/hep.25645 ER - TY - JOUR T1 - Detection and imaging of the free radical DNA in cells--site-specific radical formation induced by Fenton chemistry and its repair in cellular DNA as seen by electron spin resonance, immuno-spin trapping and confocal microscopy. AN - 1022858928; 22387463 AB - Oxidative stress-related damage to the DNA macromolecule produces lesions that are implicated in various diseases. To understand damage to DNA, it is important to study the free radical reactions causing the damage. Measurement of DNA damage has been a matter of debate as most of the available methods measure the end product of a sequence of events and provide limited information on the initial free radical formation. We report a measurement of free radical damage in DNA induced by a Cu(II)-H(2)O(2) oxidizing system using immuno-spin trapping supplemented with electron paramagnetic resonance. In this investigation, the short-lived radical generated is trapped by the spin trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO) immediately upon formation. The DMPO adduct formed is initially electron paramagnetic resonance active, but is subsequently oxidized to the stable nitrone adduct, which can be detected and visualized by immuno-spin trapping and has the potential to be further characterized by other analytical techniques. The radical was found to be located on the 2'-deoxyadenosine (dAdo) moiety of DNA. The nitrone adduct was repaired on a time scale consistent with DNA repair. In vivo experiments for the purpose of detecting DMPO-DNA nitrone adducts should be conducted over a range of time in order to avoid missing adducts due to the repair processes. JF - Nucleic acids research AU - Bhattacharjee, Suchandra AU - Chatterjee, Saurabh AU - Jiang, Jinjie AU - Sinha, Birandra Kumar AU - Mason, Ronald P AD - Laboratory of Toxicology and Chemistry, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA. bhattac1@niehs.nih.gov Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 5477 EP - 5486 VL - 40 IS - 12 KW - Cyclic N-Oxides KW - 0 KW - DNA Adducts KW - Fenton's reagent KW - Free Radicals KW - Nitrogen Oxides KW - Nucleosides KW - Spin Labels KW - nitrones KW - 5,5-dimethyl-1-pyrroline-1-oxide KW - 7170JZ1QF3 KW - Hydrogen Peroxide KW - BBX060AN9V KW - Iron KW - E1UOL152H7 KW - Index Medicus KW - Microscopy, Confocal KW - Free Radicals -- analysis KW - Animals KW - Electron Spin Resonance Spectroscopy KW - Nitrogen Oxides -- chemistry KW - Enzyme-Linked Immunosorbent Assay KW - Mice KW - Nucleosides -- chemistry KW - Cyclic N-Oxides -- chemistry KW - Cell Line KW - DNA Repair KW - DNA Adducts -- analysis KW - DNA Damage KW - DNA Adducts -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1022858928?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=Detection+and+imaging+of+the+free+radical+DNA+in+cells--site-specific+radical+formation+induced+by+Fenton+chemistry+and+its+repair+in+cellular+DNA+as+seen+by+electron+spin+resonance%2C+immuno-spin+trapping+and+confocal+microscopy.&rft.au=Bhattacharjee%2C+Suchandra%3BChatterjee%2C+Saurabh%3BJiang%2C+Jinjie%3BSinha%2C+Birandra+Kumar%3BMason%2C+Ronald+P&rft.aulast=Bhattacharjee&rft.aufirst=Suchandra&rft.date=2012-07-01&rft.volume=40&rft.issue=12&rft.spage=5477&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=1362-4962&rft_id=info:doi/10.1093%2Fnar%2Fgks180 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-01 N1 - Date created - 2012-06-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Am Chem Soc. 2001 Dec 19;123(50):12556-67 [11741420] Free Radic Biol Med. 2002 Aug 15;33(4):441-9 [12160926] Cancer Res. 2003 Feb 15;63(4):838-46 [12591735] Free Radic Biol Med. 2003 Apr 1;34(7):830-9 [12654471] J Am Chem Soc. 2003 Aug 27;125(34):10154-5 [12926921] Mutat Res. 2003 Oct 29;531(1-2):5-23 [14637244] Carcinogenesis. 2004 Mar;25(3):455-62 [14604891] J Biol Chem. 2004 Mar 19;279(12):11600-7 [14699100] Free Radic Biol Med. 2004 May 15;36(10):1214-23 [15110386] Arch Biochem Biophys. 1992 May 15;295(1):205-13 [1315504] Nature. 1993 Apr 22;362(6422):709-15 [8469282] Environ Health Perspect. 1993 Dec;101 Suppl 5:35-44 [8013423] Carcinogenesis. 1994 Sep;15(9):2037-43 [7923599] Lab Invest. 1997 Mar;76(3):365-74 [9121119] J Biol Chem. 1997 Aug 8;272(32):19633-6 [9289489] Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8353-8 [10411879] Nat Methods. 2006 Feb;3(2):123-7 [16432522] Free Radic Biol Med. 2006 Aug 1;41(3):422-30 [16843823] Free Radic Biol Med. 2007 Feb 15;42(4):530-40 [17275685] DNA Repair (Amst). 2007 Apr 1;6(4):530-43 [17113833] Free Radic Biol Med. 2007 Apr 1;42(7):985-92 [17349926] Nat Protoc. 2007;2(3):512-22 [17406615] J Am Chem Soc. 2007 Nov 7;129(44):13493-501 [17939657] Radiat Res. 2008 Mar;169(3):355-63 [18302484] J Neurosci. 2008 Apr 16;28(16):4115-22 [18417691] Hepatology. 2008 Jun;47(6):2089-111 [18506894] Biochemistry. 2008 Oct 28;47(43):11377-85 [18831539] J Phys Chem B. 2009 Jan 8;113(1):389-94 [19072618] Cancer Treat Rev. 2009 Feb;35(1):32-46 [18774652] Free Radic Biol Med. 2009 Feb 15;46(4):454-61 [19049863] J Biol Chem. 2009 Feb 27;284(9):5546-56 [19106092] Free Radic Biol Med. 2009 Jul 1;47(1):30-1 [19362140] J Natl Cancer Inst. 2009 Dec 16;101(24):1670-81 [19933942] Med Res Rev. 2010 Jul;30(4):708-49 [19626597] J Biol Chem. 2010 Jun 25;285(26):20062-71 [20406811] Curr Med Chem. 2010;17(25):2685-98 [20586723] Chemistry. 2010 Oct 18;16(39):11848-58 [20878802] Free Radic Biol Med. 2011 Apr 15;50(8):988-99 [21215311] Free Radic Biol Med. 2011 Jun 1;50(11):1536-45 [21382477] Free Radic Biol Med. 2002 Aug 1;33(3):364-9 [12126758] Annu Rev Biochem. 2002;71:51-70 [12045090] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/nar/gks180 ER - TY - JOUR T1 - Endogenous erythropoietin signaling facilitates skeletal muscle repair and recovery following pharmacologically induced damage. AN - 1022843257; 22490927 AB - Erythropoietin acts by binding to its cell surface receptor on erythroid progenitor cells to stimulate erythrocyte production. Erythropoietin receptor expression in nonhematopoietic tissue, including skeletal muscle progenitor cells, raises the possibility of a role for erythropoietin beyond erythropoiesis. Mice with erythropoietin receptor restricted to hematopoietic tissue were used to assess contributions of endogenous erythropoietin to promote skeletal myoblast proliferation and survival and wound healing in a mouse model of cardiotoxin induced muscle injury. Compared with wild-type controls, these mice had fewer skeletal muscle Pax-7(+) satellite cells and myoblasts that do not proliferate in culture, were more susceptible to skeletal muscle injury and reduced maximum load tolerated by isolated muscle. In contrast, mice with chronic elevated circulating erythropoietin had more Pax-7(+) satellite cells and myoblasts with increased proliferation and survival in culture, decreased muscle injury, and accelerated recovery of maximum load tolerated by isolated muscle. Skeletal muscle myoblasts also produced endogenous erythropoietin that increased at low O(2). Erythropoietin promoted proliferation, survival, and wound recovery in myoblasts via the phosphoinositide 3-kinase/AKT pathway. Therefore, endogenous and exogenous erythropoietin contribute to increasing satellite cell number following muscle injury, improve myoblast proliferation and survival, and promote repair and regeneration in this mouse induced muscle injury model independent of its effect on erythrocyte production. JF - FASEB journal : official publication of the Federation of American Societies for Experimental Biology AU - Jia, Yi AU - Suzuki, Norio AU - Yamamoto, Masayuki AU - Gassmann, Max AU - Noguchi, Constance Tom AD - Molecular Medicine Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-1822, USA. Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 2847 EP - 2858 VL - 26 IS - 7 KW - EPO protein, human KW - 0 KW - GATA3 Transcription Factor KW - Gata3 protein, mouse KW - PAX7 Transcription Factor KW - Pax7 protein, mouse KW - Receptors, Erythropoietin KW - Recombinant Proteins KW - Erythropoietin KW - 11096-26-7 KW - Proto-Oncogene Proteins c-akt KW - EC 2.7.11.1 KW - Index Medicus KW - Animals KW - Apoptosis KW - PAX7 Transcription Factor -- physiology KW - Humans KW - GATA3 Transcription Factor -- biosynthesis KW - Mice, Transgenic KW - Mice, Knockout KW - Recombinant Proteins -- metabolism KW - Receptors, Erythropoietin -- genetics KW - Myoblasts, Skeletal -- cytology KW - Receptors, Erythropoietin -- deficiency KW - Satellite Cells, Skeletal Muscle -- physiology KW - Proto-Oncogene Proteins c-akt -- metabolism KW - Wound Healing -- drug effects KW - Mice KW - Wound Healing -- physiology KW - Cell Hypoxia KW - Recombinant Proteins -- genetics KW - Satellite Cells, Skeletal Muscle -- cytology KW - Receptors, Erythropoietin -- physiology KW - Cells, Cultured KW - Signal Transduction -- drug effects KW - Mice, Inbred C57BL KW - Female KW - Myoblasts, Skeletal -- physiology KW - Muscle, Skeletal -- injuries KW - Erythropoietin -- administration & dosage KW - Muscle, Skeletal -- physiopathology KW - Erythropoietin -- genetics KW - Muscle, Skeletal -- drug effects KW - Erythropoietin -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1022843257?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.atitle=Endogenous+erythropoietin+signaling+facilitates+skeletal+muscle+repair+and+recovery+following+pharmacologically+induced+damage.&rft.au=Jia%2C+Yi%3BSuzuki%2C+Norio%3BYamamoto%2C+Masayuki%3BGassmann%2C+Max%3BNoguchi%2C+Constance+Tom&rft.aulast=Jia&rft.aufirst=Yi&rft.date=2012-07-01&rft.volume=26&rft.issue=7&rft.spage=2847&rft.isbn=&rft.btitle=&rft.title=FASEB+journal+%3A+official+publication+of+the+Federation+of+American+Societies+for+Experimental+Biology&rft.issn=1530-6860&rft_id=info:doi/10.1096%2Ffj.11-196618 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-20 N1 - Date created - 2012-06-29 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: FASEB J. 2009 Sep;23(9):3089-99 [19417086] Nat Commun. 2011;2:520 [22044999] J Clin Invest. 2010 Jan;120(1):11-9 [20051632] Proc Natl Acad Sci U S A. 2010 Jan 5;107(1):419-23 [19966291] Proc Natl Acad Sci U S A. 1991 Dec 1;88(23):10638-41 [1660143] Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):3974-8 [8171022] Nucleic Acids Res. 1995 Aug 11;23(15):3041-9 [7659529] J Biol Chem. 1998 Sep 25;273(39):25381-7 [9738005] Nat Cell Biol. 2005 Mar;7(3):286-94 [15723049] FASEB J. 2005 Jun;19(8):1009-11 [15811877] Blood. 2006 Feb 1;107(3):907-15 [16204311] J Neurosci. 2006 Jan 25;26(4):1269-74 [16436614] Am J Physiol Regul Integr Comp Physiol. 2006 Oct;291(4):R947-56 [16690772] Mol Cell Biol. 2006 Nov;26(22):8527-38 [16982687] Cell Signal. 2007 Mar;19(3):634-45 [17045782] Biochem Biophys Res Commun. 2007 Mar 9;354(2):372-8 [17250809] Circ Res. 2007 Mar 16;100(5):662-9 [17293480] Cell. 2007 Jun 1;129(5):999-1010 [17540178] J Biol Chem. 2007 Aug 31;282(35):25875-83 [17604282] Br J Haematol. 2007 Sep;138(6):792-801 [17672885] Exp Cell Res. 2008 Jan 1;314(1):193-203 [17963748] Proc Natl Acad Sci U S A. 2000 Oct 10;97(21):11609-13 [11027359] J Biol Chem. 2000 Dec 15;275(50):39754-61 [10995753] Nature. 2001 Aug 9;412(6847):641-7 [11493922] Development. 2002 Jan;129(2):505-16 [11807041] J Anat. 2002 Jan;200(Pt 1):69-79 [11837252] Blood. 2002 Oct 1;100(7):2279-88 [12239135] FASEB J. 2003 Feb;17(2):259-61 [12490547] J Appl Physiol (1985). 2008 Apr;104(4):1154-60 [18218911] Biol Reprod. 2008 Jun;78(6):1049-57 [18256329] Cardiovasc Drugs Ther. 2008 Aug;22(4):265-74 [18327705] J Mol Cell Cardiol. 2008 Aug;45(2):250-60 [18586265] J Orthop Res. 2008 Dec;26(12):1618-26 [18634017] J Biol Chem. 2008 Dec 5;283(49):34029-36 [18835816] Anesthesiology. 2009 Mar;110(3):648-59 [19212263] Nature. 2009 Jul 30;460(7255):627-31 [19554048] Eur J Endocrinol. 2009 Sep;161(3):427-34 [19515792] J Endocrinol. 2010 Apr;205(1):87-95 [20061512] Proc Natl Acad Sci U S A. 2010 Mar 30;107(13):5857-62 [20231451] J Biomed Biotechnol. 2010;2010:137817 [20414335] Am J Physiol Heart Circ Physiol. 2010 Aug;299(2):H372-8 [20495150] Int J Biochem Cell Biol. 2011 Mar;43(3):409-15 [21095239] Basic Res Cardiol. 2011 May;106(3):343-54 [21347618] Differentiation. 2009 Sep-Oct;78(2-3):185-94 [19751902] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1096/fj.11-196618 ER - TY - JOUR T1 - Proteomic analysis of covalent modifications of tubulins by isothiocyanates. AN - 1021983063; 22649267 AB - Although isothiocyanates (ITC), which are found in cruciferous vegetables, have been shown to inhibit carcinogenesis in animal models and induce apoptosis and cell cycle arrest in tumor cells, the biochemical mechanisms of cell growth inhibition by these compounds are not fully understood. Studies have reported that ITC binding to intracellular proteins may be an important event for initiating apoptosis. Specific protein target(s) and molecular mechanisms for ITC have been investigated in human lung cancer A549 cells using proteomic tools. Cells were treated with various amounts (1-100 μmol/L) of radiolabeled phenethyl-ITC (PEITC) and sulforaphane (SFN) and the extracted proteins resolved using 2-dimensional gel electrophoresis. The results of mass spectrometric analyses suggested that tubulin may be an in vivo binding target for ITC. The binding of ITC to tubulin was associated with growth arrest. The proliferation of A549 cells was significantly reduced by ITC, with benzyl-ITC (BITC) having a greater relative activity than PEITC or SFN. Mitotic arrest and apoptosis as well as disruption of microtubule polymerization were induced in the order: BITC > PEITC > SFN. An analysis of tubulins isolated from BITC-treated A549 cells showed that Cys(347), a conserved cysteine in all α-tubulin isoforms, was covalently modified by BITC. Taken together, these results suggest that tubulin is a binding target of ITC and that this interaction can lead to growth inhibition and apoptosis. JF - The Journal of nutrition AU - Xiao, Zhen AU - Mi, Lixin AU - Chung, Fung-Lung AU - Veenstra, Timothy D AD - Laboratory of Proteomics and Analytical Technologies, Advanced Technology Program, SAIC-Frederick, Inc., National Cancer Institute at Frederick, Frederick, MD, USA. Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 1377S EP - 81S VL - 142 IS - 7 KW - Antineoplastic Agents, Phytogenic KW - 0 KW - Isothiocyanates KW - Plant Extracts KW - Protein Isoforms KW - Tubulin KW - phenethyl isothiocyanate KW - 6U7TFK75KV KW - benzyl isothiocyanate KW - 871J6YOR8Q KW - Cysteine KW - K848JZ4886 KW - Index Medicus KW - Cell Proliferation -- drug effects KW - Mass Spectrometry KW - Cysteine -- metabolism KW - Humans KW - Cell Line, Tumor KW - Microtubules -- drug effects KW - Protein Binding KW - Plant Extracts -- pharmacology KW - Proteomics KW - Plant Extracts -- therapeutic use KW - Apoptosis -- drug effects KW - Electrophoresis, Gel, Two-Dimensional KW - Cell Cycle Checkpoints -- drug effects KW - Mitosis -- drug effects KW - Diet KW - Phytotherapy KW - Isothiocyanates -- pharmacology KW - Isothiocyanates -- therapeutic use KW - Antineoplastic Agents, Phytogenic -- therapeutic use KW - Lung Neoplasms -- drug therapy KW - Antineoplastic Agents, Phytogenic -- pharmacology KW - Tubulin -- metabolism KW - Lung Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1021983063?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+nutrition&rft.atitle=Proteomic+analysis+of+covalent+modifications+of+tubulins+by+isothiocyanates.&rft.au=Xiao%2C+Zhen%3BMi%2C+Lixin%3BChung%2C+Fung-Lung%3BVeenstra%2C+Timothy+D&rft.aulast=Xiao&rft.aufirst=Zhen&rft.date=2012-07-01&rft.volume=142&rft.issue=7&rft.spage=1377S&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+nutrition&rft.issn=1541-6100&rft_id=info:doi/10.3945%2Fjn.111.152041 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-30 N1 - Date created - 2012-06-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Phytochemistry. 2001 Jan;56(1):5-51 [11198818] Nutr J. 2011;10:11 [21272319] Cancer Res. 2001 Aug 15;61(16):6120-30 [11507062] J Mol Biol. 2001 Nov 9;313(5):1045-57 [11700061] Cancer Res. 2002 Jan 1;62(1):2-7 [11782348] Curr Drug Metab. 2002 Jun;3(3):233-55 [12083319] Carcinogenesis. 2002 Sep;23(9):1433-9 [12189184] Cancer Res. 2007 Jul 1;67(13):6409-16 [17616701] J Biol Chem. 2008 Aug 8;283(32):22136-46 [18524779] Forum Nutr. 2009;61:170-81 [19367121] Nat Chem Biol. 2009 Sep;5(9):616-24 [19690537] Biochem J. 2009 Nov 1;423(3):315-21 [19723024] Proteomics. 2009 Oct;9(20):4632-41 [19743430] Proc Natl Acad Sci U S A. 2002 Sep 3;99(18):11908-13 [12193649] Carcinogenesis. 2002 Dec;23(12):2055-61 [12507929] Cancer Res. 2003 Jul 15;63(14):3980-6 [12873994] Mol Cancer Ther. 2003 Oct;2(10):1045-52 [14578469] Curr Drug Metab. 2004 Apr;5(2):193-201 [15078196] J Nutr. 2004 Aug;134(8):2004-10 [15284390] Exp Biol Med (Maywood). 2004 Sep;229(8):835-42 [15337839] Mutat Res. 2004 Nov 2;555(1-2):191-202 [15476860] Crit Rev Food Sci Nutr. 1983;18(2):123-201 [6337782] Oxf Surv Eukaryot Genes. 1984;1:36-60 [6400775] Carcinogenesis. 1997 Nov;18(11):2143-7 [9395214] Cancer Res. 1998 Oct 15;58(20):4632-9 [9788615] Cancer Epidemiol Biomarkers Prev. 1998 Dec;7(12):1091-100 [9865427] Drug Metab Dispos. 1999 Jan;27(1):13-20 [9884304] Cancer Epidemiol Biomarkers Prev. 1999 May;8(5):447-51 [10350441] J Biol Chem. 2005 May 20;280(20):19911-24 [15764812] Mol Carcinog. 2005 Jul;43(3):130-40 [15880419] Biochem J. 2005 Jul 15;389(Pt 2):549-58 [15743274] Proc Natl Acad Sci U S A. 2005 Jul 19;102(29):10070-5 [16006525] Mol Cancer Ther. 2005 Aug;4(8):1250-9 [16093441] Anticancer Res. 2005 Sep-Oct;25(5):3375-86 [16101152] Cancer Res. 2005 Sep 15;65(18):8538-47 [16166335] Chem Res Toxicol. 2005 Dec;18(12):1917-26 [16359182] Carcinogenesis. 2006 Apr;27(4):782-90 [16364922] Biochim Biophys Acta. 2010 Feb;1804(2):318-25 [19837190] Am J Clin Nutr. 2010 Mar;91(3):704-11 [20042523] Br J Cancer. 2001 Mar 2;84(5):670-3 [11237388] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.3945/jn.111.152041 ER - TY - JOUR T1 - Histopathologic changes in the uterus, cervix and vagina of immature CD-1 mice exposed to low doses of perfluorooctanoic acid (PFOA) in a uterotrophic assay AN - 1020843073; 16793289 AB - The estrogenic and antiestrogenic potential of perfluorooctanoic acid (PFOA) was assessed using an immature mouse uterotrophic assay and by histologic evaluation of the uterus, cervix and vagina following treatment. Female offspring of CD-1 dams were weaned at 18days old and assigned to groups of equal weight, and received 0, 0.01, 0.1, or 1mg PFOA/kg BW/d by gavage with or without 17- beta estradiol (E2, 500 mu g/kg/d) from PND 18-20 (n=8/treatment/block). At 24h after the third dose (PND 21), uteri were removed and weighed. Absolute and relative uterine weights were significantly increased in the 0.01mg/kg PFOA only group. Characteristic estrogenic changes were present in all E2-treated mice; however, they were minimally visible in the 0.01 PFOA only mice. These data suggest that at a low dose PFOA produces minimal histopathologic changes in the reproductive tract of immature female mice, and does not antagonize the histopathologic effects of E2. JF - Reproductive Toxicology AU - Dixon, Darlene AU - Reed, Casey E AU - Moore, Alicia B AU - Gibbs-Flournoy, Eugene A AU - Hines, Erin P AU - Wallace, Elizabeth A AU - Stanko, Jason P AU - Lu, Yi AU - Jefferson, Wendy N AU - Newbold, Retha R AU - Fenton, Suzanne E AD - National Toxicology Program (NTP) Laboratories Branch, Division of the NTP, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC 27709, USA, dixon@niehs.nih.gov Y1 - 2012/07// PY - 2012 DA - Jul 2012 SP - 506 EP - 512 PB - Elsevier B.V., Box 882 New York NY 10159 United States VL - 33 IS - 4 SN - 0890-6238, 0890-6238 KW - Toxicology Abstracts KW - Cervix KW - Data processing KW - Estradiol KW - Progeny KW - Reproductive system KW - Uterus KW - Vagina KW - perfluorooctanoic acid KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020843073?accountid=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=Reproductive+Toxicology&rft.atitle=Histopathologic+changes+in+the+uterus%2C+cervix+and+vagina+of+immature+CD-1+mice+exposed+to+low+doses+of+perfluorooctanoic+acid+%28PFOA%29+in+a+uterotrophic+assay&rft.au=Dixon%2C+Darlene%3BReed%2C+Casey+E%3BMoore%2C+Alicia+B%3BGibbs-Flournoy%2C+Eugene+A%3BHines%2C+Erin+P%3BWallace%2C+Elizabeth+A%3BStanko%2C+Jason+P%3BLu%2C+Yi%3BJefferson%2C+Wendy+N%3BNewbold%2C+Retha+R%3BFenton%2C+Suzanne+E&rft.aulast=Dixon&rft.aufirst=Darlene&rft.date=2012-07-01&rft.volume=33&rft.issue=4&rft.spage=506&rft.isbn=&rft.btitle=&rft.title=Reproductive+Toxicology&rft.issn=08906238&rft_id=info:doi/10.1016%2Fj.reprotox.2011.10.011 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Last updated - 2012-06-29 N1 - SubjectsTermNotLitGenreText - Uterus; Data processing; Vagina; Progeny; perfluorooctanoic acid; Cervix; Reproductive system; Estradiol DO - http://dx.doi.org/10.1016/j.reprotox.2011.10.011 ER - TY - JOUR T1 - Expanding surgical treatment of pancreatic cancer: the role of regional chemotherapy. AN - 1020833706; 22695088 AB - Pancreatic cancer is a lethal disease that offers little chance of long-term survival for patients with unresectable tumors. Surgery remains the most effective means of attaining prolonged survival, yet its role remains limited. Regional chemotherapy has been described for patients with pancreatic cancer, including reports of objective tumor regression allowing for tumor resection in previously unresectable cases. However, comprehensive data have not been reviewed to date. A review of the literature from 1995 to 2010 was performed to analyze the results of regional chemotherapy administered to patients with advanced pancreatic cancer. Reports of individual cases, postoperative regional therapy, and treatment of mixed tumor types were excluded. Twenty-one reports of 895 total patients with pancreatic cancer were reviewed. Greater than 95% of the patients had stage III or IV adenocarcinoma. Objective response rates ranged from nil to 58%, with associated median survivals of 4 to 22 months. Low-grade gastrointestinal and hematologic toxicities were not uncommon. Regional chemotherapy can be administered safely to patients with pancreatic cancer but with unclear benefit. Advanced pancreatic tumors converted to resectable status by the use of regional chemotherapy may improve patient survival. JF - Pancreas AU - Davis, Jeremy L AU - Pandalai, Prakash K AU - Ripley, R Taylor AU - Langan, Russell C AU - Avital, Itzhak AD - Surgery Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 678 EP - 684 VL - 41 IS - 5 KW - Index Medicus KW - Combined Modality Therapy KW - Humans KW - Treatment Outcome KW - Aged KW - Middle Aged KW - Male KW - Female KW - Pancreatic Neoplasms -- radiotherapy KW - Pancreatic Neoplasms -- drug therapy KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Adenocarcinoma -- drug therapy KW - Adenocarcinoma -- surgery KW - Adenocarcinoma -- radiotherapy KW - Pancreatic Neoplasms -- surgery UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020833706?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Pancreas&rft.atitle=Expanding+surgical+treatment+of+pancreatic+cancer%3A+the+role+of+regional+chemotherapy.&rft.au=Davis%2C+Jeremy+L%3BPandalai%2C+Prakash+K%3BRipley%2C+R+Taylor%3BLangan%2C+Russell+C%3BAvital%2C+Itzhak&rft.aulast=Davis&rft.aufirst=Jeremy&rft.date=2012-07-01&rft.volume=41&rft.issue=5&rft.spage=678&rft.isbn=&rft.btitle=&rft.title=Pancreas&rft.issn=1536-4828&rft_id=info:doi/10.1097%2FMPA.0b013e318249955a LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-25 N1 - Date created - 2012-06-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Am Coll Surg. 1999 Jul;189(1):1-7 [10401733] Anticancer Res. 1999 Jul-Aug;19(4A):2459-69 [10470175] Ann Surg Oncol. 1999 Sep;6(6):582-90 [10493628] Ann Surg. 1958 Oct;148(4):616-32 [13583933] Pancreas. 2005 Apr;30(3):223-6 [15782098] J Clin Oncol. 2005 Jul 10;23(20):4538-44 [16002845] Front Biosci. 2006;11:782-7 [16146770] Anticancer Res. 2005 Nov-Dec;25(6C):4407-12 [16334117] Surg Today. 2006;36(2):155-61 [16440163] Ann Surg Oncol. 2006 May;13(5):635-44 [16523363] J Clin Oncol. 2006 Aug 20;24(24):4011-9 [16921055] J Clin Oncol. 2006 Sep 1;24(25):4196-201 [16943537] Ann Surg Oncol. 2006 Aug;13(8):1035-46 [16865597] In Vivo. 2006 Nov-Dec;20(6A):751-5 [17203761] JAMA. 2007 Jan 17;297(3):267-77 [17227978] Eur J Surg Oncol. 2007 Feb;33(1):72-8 [17166688] J Clin Oncol. 2007 May 20;25(15):1960-6 [17452677] Cardiovasc Intervent Radiol. 2007 Sep-Oct;30(5):912-21 [17710478] Pancreas. 2008 Jan;36(1):56-60 [18192882] Ann Surg. 2008 Feb;247(2):300-9 [18216537] Hepatogastroenterology. 2007 Dec;54(80):2373-7 [18265668] Hepatogastroenterology. 2007 Dec;54(80):2378-82 [18265669] Am J Clin Oncol. 2008 Feb;31(1):71-8 [18376231] J Gastrointestin Liver Dis. 2008 Sep;17(3):285-90 [18836621] Ann Surg Oncol. 2009 Apr;16(4):836-47 [19194760] Ann Surg Oncol. 2009 Jul;16(7):1727-33 [19396496] J Clin Oncol. 2009 Aug 10;27(23):3778-85 [19581537] Cochrane Database Syst Rev. 2006;(3):CD002093 [16855985] J Clin Oncol. 2009 Sep 1;27(25):4096-102 [19636002] Ann Surg Oncol. 2010 Jan;17(1):194-205 [19856029] CA Cancer J Clin. 2010 Sep-Oct;60(5):277-300 [20610543] N Engl J Med. 2011 May 12;364(19):1817-25 [21561347] JOP. 2011 Jul;12(4):316-21 [21737886] Cancer. 2000 Jul 15;89(2):303-13 [10918160] J Clin Oncol. 2001 Feb 15;19(4):1001-7 [11181662] Hepatogastroenterology. 2003 Mar-Apr;50(50):550-2 [12749270] Ann Surg Oncol. 2003 Oct;10(8):927-34 [14527913] Eur J Surg Oncol. 2004 Aug;30(6):671-80 [15256243] J Clin Oncol. 1984 May;2(5):498-504 [6547166] Abdom Imaging. 1996 May-Jun;21(3):202-6 [8661548] Cancer. 1996 Aug 1;78(3 Suppl):664-73 [8681305] AJR Am J Roentgenol. 1997 Jun;168(6):1439-43 [9168704] J Clin Oncol. 1997 Jun;15(6):2403-13 [9196156] Eur J Surg Oncol. 1997 Oct;23(5):409-14 [9393568] Int J Pancreatol. 1998 Jun;23(3):181-6 [9629517] Eur J Surg Oncol. 1998 Dec;24(6):542-7 [9870731] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1097/MPA.0b013e318249955a ER - TY - JOUR T1 - Chromatin changes in the development and pathology of the Fragile X-associated disorders and Friedreich ataxia. AN - 1019620429; 22245581 AB - The Fragile X-associated disorders (FXDs) and Friedreich ataxia (FRDA) are genetic conditions resulting from expansion of a trinucleotide repeat in a region of the affected gene that is transcribed but not translated. In the case of the FXDs, pathology results from expansion of CGG•CCG-repeat tract in the 5' UTR of the FMR1 gene, while pathology in FRDA results from expansion of a GAA•TTC-repeat in intron 1 of the FXN gene. Expansion occurs during gametogenesis or early embryogenesis by a mechanism that is not well understood. Associated Expansion then produces disease pathology in various ways that are not completely understood either. In the case of the FXDs, alleles with 55-200 repeats express higher than normal levels of a transcript that is thought to be toxic, while alleles with >200 repeats are silenced. In addition, alleles with >200 repeats are associated with a cytogenetic abnormality known as a fragile site, which is apparent as a constriction or gap in the chromatin that is seen when cells are grown in presence of inhibitors of thymidylate synthase. FRDA alleles show a deficit of the FXN transcript. This review will address the role of repeat-mediated chromatin changes in these aspects of FXD and FRDA disease pathology. This article is part of a Special Issue entitled: Chromatin in time and space. Published by Elsevier B.V. JF - Biochimica et biophysica acta AU - Kumari, Daman AU - Lokanga, Rachel AU - Yudkin, Dmitry AU - Zhao, Xiao-Nan AU - Usdin, Karen AD - Section on Gene Structure and Disease, Laboratory of Cell and Molecular Biology, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892-0830, USA. Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 802 EP - 810 VL - 1819 IS - 7 SN - 0006-3002, 0006-3002 KW - Chromatin KW - 0 KW - FMR1 protein, human KW - Fragile X Mental Retardation Protein KW - 139135-51-6 KW - Index Medicus KW - Animals KW - Gene Silencing KW - Humans KW - Heterozygote KW - Fragile X Mental Retardation Protein -- metabolism KW - Chromosome Fragility KW - Fragile X Mental Retardation Protein -- genetics KW - Tandem Repeat Sequences KW - DNA Repeat Expansion KW - Fragile X Syndrome -- metabolism KW - Chromatin -- metabolism KW - Fragile X Syndrome -- genetics KW - Friedreich Ataxia -- genetics KW - Mutation KW - Friedreich Ataxia -- metabolism KW - Chromatin -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1019620429?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Chromatin+changes+in+the+development+and+pathology+of+the+Fragile+X-associated+disorders+and+Friedreich+ataxia.&rft.au=Kumari%2C+Daman%3BLokanga%2C+Rachel%3BYudkin%2C+Dmitry%3BZhao%2C+Xiao-Nan%3BUsdin%2C+Karen&rft.aulast=Kumari&rft.aufirst=Daman&rft.date=2012-07-01&rft.volume=1819&rft.issue=7&rft.spage=802&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbagrm.2011.12.009 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-04-02 N1 - Date created - 2012-06-08 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Med Genet A. 2009 Oct;149A(10):2152-7 [19764037] Nat Genet. 1999 Dec;23(4):471-3 [10581038] Am J Hum Genet. 2000 Jan;66(1):6-15 [10631132] Hum 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2008 Apr 3;27(15):2109-17 [17934520] Hum Mol Genet. 2008 May 1;17(9):1306-17 [18252747] PLoS One. 2008;3(4):e1958 [18463734] Genome Res. 2008 Jul;18(7):1011-9 [18593815] Am J Hum Genet. 2008 Jul;83(1):77-88 [18597733] PLoS Genet. 2008;4(8):e1000155 [18704159] Cerebellum. 2008;7(2):150-8 [18418692] Cell Stem Cell. 2007 Nov;1(5):568-77 [18371394] Mol Cell. 2008 Oct 24;32(2):232-46 [18951091] PLoS Genet. 2008 Nov;4(11):e1000257 [19008940] Eur J Hum Genet. 2008 Dec;16(12):1487-98 [18628788] J Med Genet. 2008 Dec;45(12):808-12 [18697824] Neurobiol Dis. 2009 Jan;33(1):37-47 [18930147] Nat Struct Mol Biol. 2009 Feb;16(2):226-8 [19136957] J Neurol. 2009 Mar;256 Suppl 1:3-8 [19283344] Nucleic Acids Res. 2009 Apr;37(5):1363-77 [19139074] Hum Mol Genet. 2009 Jul 1;18(13):2443-51 [19377084] Nucleic Acids Res. 2002 Jul 15;30(14):3278-85 [12136110] Science. 2002 Sep 13;297(5588):1833-7 [12193640] Mol Cell. 2002 Nov;10(5):1223-33 [12453428] Hum Mol Genet. 2003 Jan 1;12(1):41-50 [12490531] Cell. 2002 Dec 13;111(6):779-89 [12526805] J Biol Chem. 2003 Jan 24;278(4):2425-31 [12441336] EMBO J. 2003 May 1;22(9):2264-73 [12727892] Science. 2003 Aug 8;301(5634):798-802 [12907790] J Mol Biol. 1996 Nov 8;263(4):511-6 [8918933] Nat Genet. 1997 Feb;15(2):190-2 [9020847] Cell. 1997 Feb 7;88(3):367-74 [9039263] Biochemistry. 1997 Mar 25;36(12):3687-99 [9132022] Hum Mol Genet. 1998 Jan;7(1):109-13 [9384610] J Med Genet. 1998 Feb;35(2):103-11 [9507388] Hum Reprod. 1998 May;13(5):1184-7 [9647544] Mol Cell. 1998 Mar;1(4):583-93 [9660942] Mol Cell. 1998 May;1(6):773-81 [9660961] Hum Mol Genet. 1998 Aug;7(8):1285-91 [9668171] Hum Mol Genet. 1999 Jan;8(1):99-106 [9887337] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.bbagrm.2011.12.009 ER - TY - JOUR T1 - Isolation and characterization of transcription fidelity mutants. AN - 1019614968; 22366339 AB - Accurate transcription is an essential step in maintaining genetic information. Error-prone transcription has been proposed to contribute to cancer, aging, adaptive mutagenesis, and mutagenic evolution of retroviruses and retrotransposons. The mechanisms controlling transcription fidelity and the biological consequences of transcription errors are poorly understood. Because of the transient nature of mRNAs and the lack of reliable experimental systems, the identification and characterization of defects that increase transcription errors have been particularly challenging. In this review we describe novel genetic screens for the isolation of fidelity mutants in both Saccharomyces cerevisiae and Escherichia coli RNA polymerases. We obtained and characterized two distinct classes of mutants altering NTP misincorporation and transcription slippage both in vivo and in vitro. Our study not only validates the genetic schemes for the isolation of RNA polymerase mutants that alter fidelity, but also sheds light on the mechanism of transcription accuracy. This article is part of a Special Issue entitled: Chromatin in time and space. Published by Elsevier B.V. JF - Biochimica et biophysica acta AU - Strathern, Jeffrey N AU - Jin, Ding Jun AU - Court, Donald L AU - Kashlev, Mikhail AD - Gene Regulation and Chromosome Biology Laboratory, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702, USA. strathej@mail.nih.gov Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 694 EP - 699 VL - 1819 IS - 7 SN - 0006-3002, 0006-3002 KW - Escherichia coli Proteins KW - 0 KW - RNA, Messenger KW - Saccharomyces cerevisiae Proteins KW - RNA Polymerase II KW - EC 2.7.7.- KW - Index Medicus KW - Base Sequence KW - Amino Acid Motifs KW - Humans KW - RNA, Messenger -- genetics KW - RNA, Messenger -- biosynthesis KW - Saccharomyces cerevisiae Proteins -- physiology KW - Saccharomyces cerevisiae Proteins -- metabolism KW - RNA Polymerase II -- physiology KW - RNA Polymerase II -- metabolism KW - Escherichia coli Proteins -- metabolism KW - RNA Polymerase II -- genetics KW - Saccharomyces cerevisiae Proteins -- genetics KW - Transcription, Genetic KW - Escherichia coli Proteins -- physiology KW - Mutation KW - Escherichia coli Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1019614968?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Isolation+and+characterization+of+transcription+fidelity+mutants.&rft.au=Strathern%2C+Jeffrey+N%3BJin%2C+Ding+Jun%3BCourt%2C+Donald+L%3BKashlev%2C+Mikhail&rft.aulast=Strathern&rft.aufirst=Jeffrey&rft.date=2012-07-01&rft.volume=1819&rft.issue=7&rft.spage=694&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbagrm.2012.02.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-04-02 N1 - Date created - 2012-06-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.bbagrm.2012.02.005 ER - TY - JOUR T1 - A molecular carrier to transport and deliver cisplatin into endometrial cancer cells. AN - 1019613096; 22260094 AB - The leader peptide of a recombinant manganese superoxide dismutase (rMnSOD-Lp) acts as a molecular carrier. Clonogenic tests on normal (MRC-5) and endometrial adenocarcinoma cells (HTB-112) were carried out in the presence of rMnSOD-Lp, cisplatin alone (CC) or cisplatin conjugated to the rMnSOD-Lp (rMnSOD-Lp-CC). The platinum delivered into the cells was measured by atomic spectrophotometric absorbance. The treatments on tumor and normal cells were finally evaluated by LM and TM microscopy. Tumor cell death in the case of 0.5 μM cisplatin on its own was minimal, while in the presence of 0.5 μM rMnSOD-Lp-CC, no tumor cells survived. Atomic absorbance analysis showed that rMnSOD-Lp-CC delivered approximately four times more cisplatin into HTB-112 cells than the amount delivered using cisplatin alone. By LM observation, the cells treated with rMnSOD-Lp-CC showed signs of nuclear and cytoplasmic fragmentation, that is, apoptosis induced by the treatment. The therapeutic effect of rMnSOD-Lp-CC on endometrial cancer cells was significant, while on the normal cells it showed only a minimal toxicity. We believe that rMnSOD-Lp deserves to be considered as a molecular carrier to deliver cisplatin directly into tumor cells, thus transforming its antireplicative activity into a specific and selective antitumor agent. © 2012 John Wiley & Sons A/S. JF - Chemical biology & drug design AU - Borrelli, Antonella AU - Schiattarella, Antonietta AU - Musella, Alessandra AU - Mancini, Roberto AU - Capasso, Clemente AU - De Luca, Viviana AU - Carginale, Vincenzo AU - Sanseverino, Marina AU - Tornesello, Anna Lucia AU - Gori, Enrico AU - Pica, Alessandra AU - Di Santi, Annalisa AU - Basile, Filomena AU - Iacobellis, Francesca AU - Colacurci, Nicola AU - Cobellis, Luigi AU - Mancini, Aldo AD - NCI of Naples Pascale Foundation, Molecular Biology and Viral Oncogenesis, Naples, Italy. Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 9 EP - 16 VL - 80 IS - 1 KW - Antineoplastic Agents KW - 0 KW - Drug Carriers KW - Recombinant Proteins KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - superoxide dismutase 2 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Humans KW - Endometrial Neoplasms -- pathology KW - Endometrial Neoplasms -- drug therapy KW - Superoxide Dismutase -- metabolism KW - Cell Line, Tumor KW - Spectrophotometry, Atomic KW - Recombinant Proteins -- genetics KW - Cell Survival -- drug effects KW - Recombinant Proteins -- metabolism KW - Drug Carriers -- chemistry KW - Superoxide Dismutase -- genetics KW - Immunohistochemistry KW - Female KW - Cisplatin -- therapeutic use KW - Cisplatin -- toxicity KW - Antineoplastic Agents -- toxicity KW - Antineoplastic Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1019613096?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+biology+%26+drug+design&rft.atitle=A+molecular+carrier+to+transport+and+deliver+cisplatin+into+endometrial+cancer+cells.&rft.au=Borrelli%2C+Antonella%3BSchiattarella%2C+Antonietta%3BMusella%2C+Alessandra%3BMancini%2C+Roberto%3BCapasso%2C+Clemente%3BDe+Luca%2C+Viviana%3BCarginale%2C+Vincenzo%3BSanseverino%2C+Marina%3BTornesello%2C+Anna+Lucia%3BGori%2C+Enrico%3BPica%2C+Alessandra%3BDi+Santi%2C+Annalisa%3BBasile%2C+Filomena%3BIacobellis%2C+Francesca%3BColacurci%2C+Nicola%3BCobellis%2C+Luigi%3BMancini%2C+Aldo&rft.aulast=Borrelli&rft.aufirst=Antonella&rft.date=2012-07-01&rft.volume=80&rft.issue=1&rft.spage=9&rft.isbn=&rft.btitle=&rft.title=Chemical+biology+%26+drug+design&rft.issn=1747-0285&rft_id=info:doi/10.1111%2Fj.1747-0285.2012.01337.x LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-27 N1 - Date created - 2012-06-08 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1111/j.1747-0285.2012.01337.x ER - TY - JOUR T1 - Supportive care in cancer unit at the National Cancer Institute of Milan: a new integrated model of medicine in oncology. AN - 1018862328; 22476190 AB - To present the model of the Supportive Care in Cancer Unit (SCCU) of the National Cancer Institute (NCI) of Milan. In the last few years, there has been a debate on different models of integration of palliative care in oncology, on early palliative care, supportive care, supportive and palliative care, continuous care, end-of life care and pain management in the trajectory of cancer. The aims of the SCCU of the NCI of Milan are mainly four: to collaborate with the individual specialists of NCI through integrated and ancillary activities while implementing a supportive therapy to treat the side effects, toxicities of oncological therapies, and comorbidities in the patients from the time of diagnosis and throughout the oncology treatment period; to assess all patients' needs through Italian validated versions of assessment tools, in order to ensure early care of the patient in a holistic approach; to support family members, survivors and healthcare professionals; and to promote research (pharmacological and non-pharmacological) and educational programs.Our integrated model of medicine in oncology, which we define 'supportive care', is part of the clinical history of the patients, from the time of diagnosis and during oncological treatments, to facilitate their psychological well being and improve adherence to treatment protocols. JF - Current opinion in oncology AU - Ida, Ripamonti Carla AU - Adelaide, Pessi Maria AU - Stefania, Boldini AD - Supportive Care in the Cancer Unit, IRCCS Foundation, National Cancer Institute, Milan, Italy. carla.ripamonti@istitutotumori.mi.it Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 391 EP - 396 VL - 24 IS - 4 KW - Index Medicus KW - Humans KW - Italy KW - Delivery of Health Care, Integrated -- organization & administration KW - Medical Oncology -- organization & administration KW - Palliative Care -- organization & administration KW - Neoplasms -- therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1018862328?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+oncology&rft.atitle=Supportive+care+in+cancer+unit+at+the+National+Cancer+Institute+of+Milan%3A+a+new+integrated+model+of+medicine+in+oncology.&rft.au=Ida%2C+Ripamonti+Carla%3BAdelaide%2C+Pessi+Maria%3BStefania%2C+Boldini&rft.aulast=Ida&rft.aufirst=Ripamonti&rft.date=2012-07-01&rft.volume=24&rft.issue=4&rft.spage=391&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+oncology&rft.issn=1531-703X&rft_id=info:doi/10.1097%2FCCO.0b013e328352eabc LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-10 N1 - Date created - 2012-06-05 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1097/CCO.0b013e328352eabc ER - TY - JOUR T1 - Discovering cytokines as targets for chemotherapy-induced painful peripheral neuropathy. AN - 1018634601; 22537849 AB - Chemotherapy-induced peripheral neuropathy (CIPN), a dose-limiting neurotoxic effect of chemotherapy, is the most common reason for early cessation of cancer treatment. This can result in an increased risk of recurrence and decreased survival rate. Inflammatory cascade activation, proinflammatory cytokine upregulation, and neuro-immune communication pathways play essential roles in the initiation and progression of CIPN. Most notably, TNF-α, IL-1β, IL-6, and CCL2 are involved in neuropathic pain. Further elucidation of the role of these cytokines could lead to their development and use as biomarkers for predicting the onset of painful peripheral neuropathy and early axonal damage. In this review, we provide evidence for the involvement of cytokines in CIPN, the possible underlying mechanisms, and their use as potential therapeutic targets and biomarkers to prevent and improve the painful peripheral neuropathy related to chemotherapeutic agents. Published by Elsevier Ltd. JF - Cytokine AU - Wang, Xiao-Min AU - Lehky, Tanya J AU - Brell, Joanna M AU - Dorsey, Susan G AD - National Institute of Nursing Research, National Institutes of Health, Bethesda, MD, USA. xmwang@mail.nih.gov Y1 - 2012/07// PY - 2012 DA - July 2012 SP - 3 EP - 9 VL - 59 IS - 1 KW - Antineoplastic Agents KW - 0 KW - Cytokines KW - Index Medicus KW - Animals KW - Humans KW - Nociceptors -- metabolism KW - Neuralgia -- complications KW - Peripheral Nervous System Diseases -- enzymology KW - Neuralgia -- enzymology KW - Molecular Targeted Therapy KW - Neuralgia -- chemically induced KW - Cytokines -- metabolism KW - Cytokines -- antagonists & inhibitors KW - Peripheral Nervous System Diseases -- chemically induced KW - Peripheral Nervous System Diseases -- complications KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1018634601?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cytokine&rft.atitle=Discovering+cytokines+as+targets+for+chemotherapy-induced+painful+peripheral+neuropathy.&rft.au=Wang%2C+Xiao-Min%3BLehky%2C+Tanya+J%3BBrell%2C+Joanna+M%3BDorsey%2C+Susan+G&rft.aulast=Wang&rft.aufirst=Xiao-Min&rft.date=2012-07-01&rft.volume=59&rft.issue=1&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=Cytokine&rft.issn=1096-0023&rft_id=info:doi/10.1016%2Fj.cyto.2012.03.027 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-05 N1 - Date created - 2012-06-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Comp Neurol. 1998 Jun 15;395(4):481-92 [9619501] Invest New Drugs. 1998;16(1):29-36 [9740541] Neuropathol Appl Neurobiol. 1999 Feb;25(1):29-40 [10194773] Support Care Cancer. 1999 Sep;7(5):354-61 [10483822] Cytokine. 2005 Jan 7;29(1):31-41 [15579376] Proc Natl Acad Sci U S A. 2005 Feb 1;102(5):1755-60 [15665080] Nat Rev Neurosci. 2005 Jul;6(7):521-32 [15995723] Joint Bone Spine. 2005 Oct;72(5):359-71 [16214069] J Neurol. 2005 Dec;252(12):1459-64 [16284715] Eur J Cancer. 2006 Jan;42(1):24-30 [16293411] J Neurochem. 2006 Jan;96(2):314-23 [16336636] Mol Cell Neurosci. 2006 Mar;31(3):407-15 [16297636] Neurosci Lett. 2006 Jun 12;400(3):258-61 [16530953] Pain. 2006 Jun;122(3):245-57 [16530964] Neurosci Lett. 2006 Sep 11;405(1-2):62-7 [16854522] Exp Neurol. 2006 Oct;201(2):507-14 [16797537] Exp Neurol. 2007 Jan;203(1):42-54 [17005179] Eur J Pharmacol. 2007 Apr 10;560(2-3):142-9 [17307159] Brain Behav Immun. 2007 Jul;21(5):686-98 [17174526] Brain Behav Immun. 2007 Jul;21(5):522-7 [17321718] Expert Opin Investig Drugs. 2007 Jul;16(7):935-50 [17594181] Brain Res. 2007 Sep 7;1168:46-59 [17698044] Cancer J. 2007 Nov-Dec;13(6):399-403 [18032978] Nat Neurosci. 2007 Nov;10(11):1361-8 [17965656] Pharmacology. 2008;81(2):158-63 [17989505] Nat Med. 2008 Mar;14(3):331-6 [18264108] Pain. 2008 Apr;135(3):262-70 [17659836] J Peripher Nerv Syst. 2008 Mar;13(1):27-46 [18346229] Neurosci Lett. 2008 Jun 6;437(3):188-93 [18420346] Exp Neurol. 2008 Jul;212(1):189-200 [18501894] Pharmacol Rep. 2008 May-Jun;60(3):297-307 [18622054] Brain. 2008 Jul;131(Pt 7):1903-11 [18515869] Brain Res. 2008 Sep 10;1229:100-10 [18652810] Cancer Sci. 2008 Aug;99(8):1618-25 [18754875] Mol Cell Neurosci. 2008 Dec;39(4):619-27 [18817874] Pharmacol Rep. 2008 Sep-Oct;60(5):735-41 [19066421] J Neurosci. 2008 Dec 24;28(52):14062-73 [19109489] PLoS Med. 2008 Dec 9;5(12):e239 [19071955] Pain. 2009 Apr;142(3):275-83 [19233564] Neuro Endocrinol Lett. 2009 Mar;30(1):144-52 [19300402] Pain. 2009 Sep;145(1-2):237-45 [19665302] Proc Natl Acad Sci U S A. 2009 Sep 22;106(38):16451-6 [19805319] Neurology. 2010 Jun 1;74(22):1806-13 [20513817] Proc Natl Acad Sci U S A. 2010 Jun 22;107(25):11313-8 [20534506] Lancet Oncol. 2010 Nov;11(11):1057-65 [20864405] Mol Pain. 2010;6:76 [21050491] Nat Rev Neurol. 2010 Dec;6(12):657-66 [21060341] Pain. 2011 Feb;152(2):308-13 [21145656] J Pineal Res. 2011 Mar;50(2):124-31 [21062351] J Neurosci. 2011 Feb 16;31(7):2688-99 [21325537] J Clin Oncol. 2011 Apr 10;29(11):1472-8 [21383290] Eur J Neurosci. 2011 May;33(9):1667-76 [21395870] Cell Res. 2011 Jun;21(6):944-56 [21321603] J Neurosci. 2011 Jul 13;31(28):10128-40 [21752989] Clin Pharmacol Ther. 2011 Sep;90(3):377-87 [21814197] Neurology. 2011 Sep 6;77(10):980-6 [21865571] Am J Clin Oncol. 1999 Dec;22(6):559-67 [10597739] Neurotoxicology. 2000 Jun;21(3):389-93 [10894128] J Comp Neurol. 2000 Sep 4;424(4):563-76 [10931481] Neurosci Lett. 2001 Sep 14;310(2-3):113-6 [11585580] Pain. 2001 Dec;94(3):293-304 [11731066] Neuroscience. 2001;108(3):507-15 [11738263] J Neurosci. 2002 Aug 1;22(15):6696-703 [12151548] Glia. 2002 Sep;39(3):279-91 [12203394] Physiol Rev. 2002 Oct;82(4):981-1011 [12270950] Curr Neurol Neurosci Rep. 2003 Jan;3(1):86-92 [12507417] Anticancer Res. 2002 Nov-Dec;22(6B):3465-72 [12552940] J Pharmacol Exp Ther. 2003 Aug;306(2):624-30 [12734393] Drugs. 2003;63(15):1549-63 [12887262] Ann Neurol. 2003 Sep;54(3):287-96 [12953261] J Pain Symptom Manage. 2004 Jan;27(1):72-8 [14711471] Neuropharmacology. 2004 Mar;46(3):404-11 [14975696] Neuroscience. 2004;124(4):945-52 [15026134] J Neurosci. 2004 May 5;24(18):4444-52 [15128858] Neurosci Lett. 2004 May 6;361(1-3):184-7 [15135924] Pain. 2004 Jul;110(1-2):56-63 [15275752] Mult Scler. 2004 Oct;10(5):494-8 [15471363] Environ Health Perspect. 1978 Oct;26:107-16 [363411] Acta Neuropathol. 1990;81(2):148-54 [2082654] J Neurol Neurosurg Psychiatry. 1991 Sep;54(9):768-74 [1659615] Ann Oncol. 1995 May;6(5):489-94 [7669713] Support Care Cancer. 1997 Mar;5(2):126-9 [9069612] Eur J Cancer. 1997 Aug;33(9):1393-9 [9337680] J Pineal Res. 1997 Aug;23(1):15-9 [9379341] J Clin Oncol. 1998 May;16(5):1852-60 [9586901] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.cyto.2012.03.027 ER - TY - JOUR T1 - Long-term risk of recurrent cervical human papillomavirus infection and precancer and cancer following excisional treatment. AN - 1009128592; 21823117 AB - Risk of recurrent CIN2+ (including cervical intraepithelial neoplasia grade 2 [CIN2], CIN3, carcinoma and in situ, adenocarcinoma in situ or cancer) remains elevated for years following treatment. The role of long-term post-treatment human papillomavirus (HPV) presence on subsequent risk of CIN2+ was evaluated in the 10,049-women Guanacaste cohort. Six hundred eighty-one women were referred to colposcopy because of high-grade cytology, positive cervicography and/or suspicion of cancer based on visual assessment; 486 were judged to require treatment. After excluding women with <12 months of follow-up (N = 88), prior cancer or hysterectomy (N = 37) or other reasons (N = 14), 347 were included in the analysis. Infections were categorized as persistent if present at both pre- and post-treatment visits and new if detected only post-treatment. Median time between the treatment and post-treatment visits was 6.7 years (interquartile range 3.8-7.8). At the post-treatment visit, 8 (2.4%), 2 (0.6%) and 8 (2.4%) of the 347 treated women had persistent HPV16, HPV18 or other carcinogenic HPV, respectively. Two (0.8%), 3 (1.0%) and 13 (4.0%) had new HPV16, HPV18 and other carcinogenic HPV, respectively. Six CIN2+ cases were identified at the post-treatment visit, all with persistent infections (three HPV16, one HPV18 and two other carcinogenic HPV). No recurrent disease was observed among women with new HPV infections during the follow-up period. Thus, persistence of HPV infection a median of six years after treatment was uncommon but, when present, posed a substantial risk of subsequent CIN2+. Serial follow-up data from other studies would further strengthen these conclusions. Copyright © 2011 UICC. JF - International journal of cancer AU - Kreimer, Aimée R AU - Schiffman, Mark AU - Herrero, Rolando AU - Hildesheim, Allan AU - González, Paula AU - Burk, Robert D AU - Porras, Carolina AU - Sherman, Mark E AU - Demuth, Franklin AU - Cheung, Li AU - Bratti, Concepción AU - Cecilia Rodríguez, Ana AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, DHHS, Rockville, MD, USA. Y1 - 2012/07/01/ PY - 2012 DA - 2012 Jul 01 SP - 211 EP - 218 VL - 131 IS - 1 KW - Index Medicus KW - Human papillomavirus 16 -- isolation & purification KW - Humans KW - Cohort Studies KW - Adult KW - Human papillomavirus 18 -- isolation & purification KW - Middle Aged KW - Neoplasm Recurrence, Local KW - Female KW - Colposcopy KW - Cervical Intraepithelial Neoplasia -- pathology KW - Cervical Intraepithelial Neoplasia -- surgery KW - Papillomavirus Infections -- virology KW - Precancerous Conditions -- surgery KW - Cervix Uteri -- virology KW - Cervical Intraepithelial Neoplasia -- virology KW - Uterine Cervical Neoplasms -- surgery KW - Uterine Cervical Neoplasms -- pathology KW - Precancerous Conditions -- virology KW - Precancerous Conditions -- pathology KW - Cervix Uteri -- surgery KW - Uterine Cervical Neoplasms -- virology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1009128592?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Long-term+risk+of+recurrent+cervical+human+papillomavirus+infection+and+precancer+and+cancer+following+excisional+treatment.&rft.au=Kreimer%2C+Aim%C3%A9e+R%3BSchiffman%2C+Mark%3BHerrero%2C+Rolando%3BHildesheim%2C+Allan%3BGonz%C3%A1lez%2C+Paula%3BBurk%2C+Robert+D%3BPorras%2C+Carolina%3BSherman%2C+Mark+E%3BDemuth%2C+Franklin%3BCheung%2C+Li%3BBratti%2C+Concepci%C3%B3n%3BCecilia+Rodr%C3%ADguez%2C+Ana&rft.aulast=Kreimer&rft.aufirst=Aim%C3%A9e&rft.date=2012-07-01&rft.volume=131&rft.issue=1&rft.spage=211&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.26349 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-14 N1 - Date created - 2012-04-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Rev Panam Salud Publica. 2004 Feb;15(2):75-89 [15030652] Oncol Rep. 2004 Aug;12(2):375-9 [15254705] N Engl J Med. 2003 Feb 6;348(6):518-27 [12571259] Obstet Gynecol. 2002 Nov;100(5 Pt 1):965-71 [12423862] J Med Virol. 2002 Nov;68(3):417-23 [12226831] Int J Cancer. 2002 Mar 20;98(3):435-9 [11920596] JAMA. 2001 Mar 21;285(11):1500-5 [11255427] Am J Obstet Gynecol. 2000 Nov;183(5):1238-42 [11084572] Rev Panam Salud Publica. 1997 May;1(5):362-75 [9180057] Obstet Gynecol. 1996 Mar;87(3):332-7 [8598950] J Low Genit Tract Dis. 2009 Jul;13(3):137-44 [19550210] Lancet Oncol. 2009 Apr;10(4):321-2 [19350698] Am J Obstet Gynecol. 2009 Apr;200(4):422.e1-9 [19167697] Cytopathology. 2009 Feb;20(1):5-16 [19133067] Int J Cancer. 2009 Feb 15;124(4):889-95 [19048594] JAMA. 2007 Aug 15;298(7):743-53 [17699008] BJOG. 2006 Nov;113(11):1303-7 [16978225] Vaccine. 2006 Aug 31;24 Suppl 3:S3/78-89 [16950021] Cancer Epidemiol Biomarkers Prev. 2006 May;15(5):908-14 [16702369] Int J Cancer. 2006 Apr 15;118(8):2048-55 [16284947] Gynecol Oncol. 2005 Dec;99(3 Suppl 1):S7-11 [16154623] J Infect Dis. 2005 Jun 1;191(11):1796-807 [15871111] Lancet. 1999 Jul 3;354(9172):20-5 [10406360] Cancer. 1999 Apr 25;87(2):48-55 [10227593] Am J Obstet Gynecol. 1999 Feb;180(2 Pt 1):290-8 [9988789] Obstet Gynecol. 1998 Nov;92(5):737-44 [9794661] Gynecol Oncol. 2003 Sep;90(3):587-92 [13678729] Gynecol Oncol. 1994 Feb;52(2):175-9 [8314135] JAMA. 1989 Aug 18;262(7):931-4 [2754794] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/ijc.26349 ER - TY - JOUR T1 - Aspirin but not ibuprofen use is associated with reduced risk of prostate cancer: a PLCO Study AN - 1028033018; 16859106 AB - Background: Although most epidemiological studies suggest that non-steroidal anti-inflammatory drug use is inversely associated with prostate cancer risk, the magnitude and specificity of this association remain unclear. Methods: We examined self-reported aspirin and ibuprofen use in relation to prostate cancer risk among 29 450 men ages 55-74 who were initially screened for prostate cancer from 1993 to 2001 in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Men were followed from their first screening exam until 31 December 2009, during which 3575 cases of prostate cancer were identified. Results: After adjusting for potential confounders, the hazard ratios (HRs) of prostate cancer associated with <1 and greater than or equal to 1 pill of aspirin daily were 0.98 (95% confidence interval (CI), 0.90-1.07) and 0.92 (95% CI: 0.85-0.99), respectively, compared with never use (P for trend 0.04). The effect of taking at least one aspirin daily was more pronounced when restricting the analyses to men older than age 65 or men who had a history of cardiovascular-related diseases or arthritis (HR (95% CI); 0.87 (0.78-0.97), 0.89 (0.80-0.99), and 0.88 (0.78-1.00), respectively). The data did not support an association between ibuprofen use and prostate cancer risk. Conclusion: Daily aspirin use, but not ibuprofen use, was associated with lower risk of prostate cancer risk. JF - British Journal of Cancer AU - Shebl, F M AU - Sakoda, L C AU - Black, A AU - Koshiol, J AU - Andriole, G L AU - Grubb, R AU - Church, T R AU - Chia, D AU - Zhou, C AU - Chu, L W AU - Huang, W-Y AU - Peters, U AU - Kirsh, V A AU - Chatterjee, N AU - Leitzmann, M F AU - Hayes, R B AU - Hsing, A W AD - 1] Department of Human Health and Services, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Rockville, MD, USA [2] Division of Chronic Disease Epidemiology, Yale School of Public Health, 60 College St., PO Box 208034, New Haven, CN, USA Y1 - 2012/06/26/ PY - 2012 DA - 2012 Jun 26 SP - 207 EP - 214 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 107 IS - 1 SN - 0007-0920, 0007-0920 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Age KW - Antiinflammatory agents KW - Aspirin KW - Cancer KW - Historical account KW - Lung KW - Ovarian carcinoma KW - Prostate cancer KW - Risk reduction KW - antiinflammatory agents KW - aspirin KW - ovarian carcinoma KW - prostate cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028033018?accountid=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=Aspirin+but+not+ibuprofen+use+is+associated+with+reduced+risk+of+prostate+cancer%3A+a+PLCO+Study&rft.au=Shebl%2C+F+M%3BSakoda%2C+L+C%3BBlack%2C+A%3BKoshiol%2C+J%3BAndriole%2C+G+L%3BGrubb%2C+R%3BChurch%2C+T+R%3BChia%2C+D%3BZhou%2C+C%3BChu%2C+L+W%3BHuang%2C+W-Y%3BPeters%2C+U%3BKirsh%2C+V+A%3BChatterjee%2C+N%3BLeitzmann%2C+M+F%3BHayes%2C+R+B%3BHsing%2C+A+W&rft.aulast=Shebl&rft.aufirst=F&rft.date=2012-06-26&rft.volume=107&rft.issue=1&rft.spage=207&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2012.227 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2012-09-24 N1 - SubjectsTermNotLitGenreText - aspirin; Historical account; Age; ovarian carcinoma; Risk reduction; Cancer; Prostate cancer; Aspirin; Lung; antiinflammatory agents; Ovarian carcinoma; prostate cancer; Antiinflammatory agents DO - http://dx.doi.org/10.1038/bjc.2012.227 ER - TY - JOUR T1 - Risk of liver cancer among US male veterans with cirrhosis, 1969-1996 AN - 1028029328; 16859090 AB - Background: Liver cancer incidence rates in the United States have increased for several decades for reasons that are not entirely clear. Regardless of aetiology, cirrhosis is a strong risk factor for liver cancer. As mortality from cirrhosis has been declining in recent decades, it is possible that the risk of liver cancer among persons with cirrhosis has been affected. Methods: Data from the US Veterans Affairs medical records database were analysed after adjustment for attained age, race, number of hospital visits, obesity, diabetes, and chronic obstructive pulmonary disease. Hazard ratio (HR) and 95% confidence interval (95% CI) were calculated using Cox proportional hazards modelling. Survival analyses were conducted using age as the time metric and incidence of cirrhosis as a time-dependent covariate. Results: Among 103 257 men with incident cirrhosis, 788 liver cancers developed. The HR of liver cancer was highest among men with viral-related cirrhosis (HR=37.59, 95% CI: 22.57-62.61), lowest among men with alcohol-related cirrhosis (HR=8.20, 95% CI: 7.55-8.91) and intermediate among men with idiopathic cirrhosis (HR=10.45, 95% CI: 8.52-12.81), when compared with those without cirrhosis. Regardless of cirrhosis type, white men had higher HRs than black men. The HR of developing liver cancer increased from 6.40 (95% CI: 4.40-9.33) in 1969-1973 to 34.71 (95% CI: 23.10-52.16) in 1992-1996 for those with cirrhosis compared with those without. Conclusion: In conclusion, the significantly increased HR of developing liver cancer among men with cirrhosis compared with men without cirrhosis in the United States may be contributing to the increasing incidence of liver cancer. JF - British Journal of Cancer AU - Persson, E C AU - Quraishi, S M AU - Welzel, T M AU - Carreon, J D AU - Gridley, G AU - Graubard, B I AU - McGlynn, K A AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD 20852-7234 USA Y1 - 2012/06/26/ PY - 2012 DA - 2012 Jun 26 SP - 195 EP - 200 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 107 IS - 1 SN - 0007-0920, 0007-0920 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Age KW - Cancer KW - Hospitals KW - Liver KW - Mortality KW - Obesity KW - Risk factors KW - Survival KW - males 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/1028029328?accountid=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=Risk+of+liver+cancer+among+US+male+veterans+with+cirrhosis%2C+1969-1996&rft.au=Persson%2C+E+C%3BQuraishi%2C+S+M%3BWelzel%2C+T+M%3BCarreon%2C+J+D%3BGridley%2C+G%3BGraubard%2C+B+I%3BMcGlynn%2C+K+A&rft.aulast=Persson&rft.aufirst=E&rft.date=2012-06-26&rft.volume=107&rft.issue=1&rft.spage=195&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2012.193 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2012-07-27 N1 - SubjectsTermNotLitGenreText - Obesity; Mortality; Age; Risk factors; Liver; males; Survival; Cancer; Hospitals; USA DO - http://dx.doi.org/10.1038/bjc.2012.193 ER - TY - JOUR T1 - Systematic Review and Meta-analysis of Circulatory Disease from Exposure to Low-Level Ionizing Radiation and Estimates of Potential Population Mortality Risks AN - 1660052557; 17649951 AB - Background: Although high doses of ionizing radiation have long been linked to circulatory disease, evidence for an association at lower exposures remains controversial. However, recent analyses suggest excess relative risks at occupational exposure levels. Objectives: We performed a systematic review and meta-analysis to summarize information on circulatory disease risks associated with moderate- and low-level whole-body ionizing radiation exposures. Methods: We conducted PubMed/ISI Thomson searches of peer-reviewed papers published since 1990 using the terms "radiation" AND "heart" AND "disease," OR "radiation" AND "stroke," OR "radiation" AND "circulatory" AND "disease." Radiation exposures had to be whole-body, with a cumulative mean dose of 0.5 Sv) generally driving the observed trends. If confirmed, our findings suggest that overall radiation-related mortality is about twice that currently estimated based on estimates for cancer end points alone (which range from 4.2% to 5.6%/Sv for these populations). JF - Environmental Health Perspectives AU - Little, Mark P AU - Azizova, Tamara V AU - Bazyka, Dimitry AU - Bouffler, Simon D AU - Cardis, Elisabeth AU - Chekin, Sergey AU - Chumak, Vadim V AU - Cucinotta, Francis A AU - de Vathaire, Florent AU - Hall, Per AU - Harrison, John D AU - Hildebrandt, Guido AU - Ivanov, Victor AU - Kashcheev, Valeriy V AU - Klymenko, Sergiy V AU - Kreuzer, Michaela AU - Laurent, Olivier AU - Ozasa, Kotaro AU - Schneider, Thierry AU - Tapio, Soile AU - Taylor, Andrew M AU - Tzoulaki, Ioanna AU - Vandoolaeghe, Wendy L AU - Wakeford, Richard AU - Zablotska, Lydia B AU - Zhang, Wei AU - Lipshultz, Steven E AD - Radiation Epidemiology Branch, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland, USA Y1 - 2012/06/22/ PY - 2012 DA - 2012 Jun 22 SP - 1503 EP - 1511 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 120 IS - 1 SN - 0091-6765, 0091-6765 KW - Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE) KW - cancer KW - circulatory disease KW - heart disease KW - radiation KW - stroke KW - Risk KW - Mortality KW - Estimates KW - Occupational KW - Ionizing radiation KW - Dosage KW - Circulation KW - Searching UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1660052557?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvironmentalengabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Systematic+Review+and+Meta-analysis+of+Circulatory+Disease+from+Exposure+to+Low-Level+Ionizing+Radiation+and+Estimates+of+Potential+Population+Mortality+Risks&rft.au=Little%2C+Mark+P%3BAzizova%2C+Tamara+V%3BBazyka%2C+Dimitry%3BBouffler%2C+Simon+D%3BCardis%2C+Elisabeth%3BChekin%2C+Sergey%3BChumak%2C+Vadim+V%3BCucinotta%2C+Francis+A%3Bde+Vathaire%2C+Florent%3BHall%2C+Per%3BHarrison%2C+John+D%3BHildebrandt%2C+Guido%3BIvanov%2C+Victor%3BKashcheev%2C+Valeriy+V%3BKlymenko%2C+Sergiy+V%3BKreuzer%2C+Michaela%3BLaurent%2C+Olivier%3BOzasa%2C+Kotaro%3BSchneider%2C+Thierry%3BTapio%2C+Soile%3BTaylor%2C+Andrew+M%3BTzoulaki%2C+Ioanna%3BVandoolaeghe%2C+Wendy+L%3BWakeford%2C+Richard%3BZablotska%2C+Lydia+B%3BZhang%2C+Wei%3BLipshultz%2C+Steven+E&rft.aulast=Little&rft.aufirst=Mark&rft.date=2012-06-22&rft.volume=120&rft.issue=1&rft.spage=1503&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1204982 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-03-01 N1 - Last updated - 2015-05-04 DO - http://dx.doi.org/10.1289/ehp.1204982 ER - TY - JOUR T1 - The Potential for Respiratory Droplet-Transmissible A/H5N1 Influenza Virus to Evolve in a Mammalian Host AN - 1551628258; 20371694 AB - Avian A/H5N1 influenza viruses pose a pandemic threat. As few as five amino acid substitutions, or four with reassortment, might be sufficient for mammal-to-mammal transmission through respiratory droplets. From surveillance data, we found that two of these substitutions are common in A/H5N1 viruses, and thus, some viruses might require only three additional substitutions to become transmissible via respiratory droplets between mammals. We used a mathematical model of within-host virus evolution to study factors that could increase and decrease the probability of the remaining substitutions evolving after the virus has infected a mammalian host. These factors, combined with the presence of some of these substitutions in circulating strains, make a virus evolving in nature a potentially serious threat. These results highlight critical areas in which more data are needed for assessing, and potentially averting, this threat. JF - Science AU - Russell, Colin A AU - Fonville, Judith M AU - Brown, Andre EX AU - Burke, David F AU - Smith, David L AU - James, Sarah L AU - Herfst, Sander AU - van Boheemen, Sander AU - Linster, Martin AU - Schrauwen, Eefje J AU - Katzelnick, Leah AU - Mosterin, Ana AU - Kuiken, Thijs AU - Maher, Eileen AU - Neumann, Gabriele AU - Osterhaus, Albert DME AU - Kawaoka, Yoshihiro AU - Fouchier, Ron AM AU - Smith, Derek J AD - Fogarty International Center, National Institutes of Health, Bethesda, MD 20892, USA, dsmith@zoo.cam.ac.uk Y1 - 2012/06/22/ PY - 2012 DA - 2012 Jun 22 SP - 1541 EP - 1547 PB - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States VL - 336 IS - 6088 SN - 0036-8075, 0036-8075 KW - Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Amino acids KW - Data processing KW - Mathematical models KW - Amino acid substitution KW - Mammals KW - Viruses KW - Influenza KW - pandemics KW - Influenza virus KW - Evolution KW - V 22410:Animal Diseases KW - H 1000:Occupational Safety and Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1551628258?accountid=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=Science&rft.atitle=The+Potential+for+Respiratory+Droplet-Transmissible+A%2FH5N1+Influenza+Virus+to+Evolve+in+a+Mammalian+Host&rft.au=Russell%2C+Colin+A%3BFonville%2C+Judith+M%3BBrown%2C+Andre+EX%3BBurke%2C+David+F%3BSmith%2C+David+L%3BJames%2C+Sarah+L%3BHerfst%2C+Sander%3Bvan+Boheemen%2C+Sander%3BLinster%2C+Martin%3BSchrauwen%2C+Eefje+J%3BKatzelnick%2C+Leah%3BMosterin%2C+Ana%3BKuiken%2C+Thijs%3BMaher%2C+Eileen%3BNeumann%2C+Gabriele%3BOsterhaus%2C+Albert+DME%3BKawaoka%2C+Yoshihiro%3BFouchier%2C+Ron+AM%3BSmith%2C+Derek+J&rft.aulast=Russell&rft.aufirst=Colin&rft.date=2012-06-22&rft.volume=336&rft.issue=6088&rft.spage=1541&rft.isbn=&rft.btitle=&rft.title=Science&rft.issn=00368075&rft_id=info:doi/10.1126%2Fscience.1222526 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-08-01 N1 - Last updated - 2014-10-30 N1 - SubjectsTermNotLitGenreText - Influenza; pandemics; Amino acid substitution; Mathematical models; Data processing; Evolution; Amino acids; Mammals; Viruses; Influenza virus DO - http://dx.doi.org/10.1126/science.1222526 ER - TY - JOUR T1 - Three postpartum antiretroviral regimens to prevent intrapartum HIV infection. AN - 1021979652; 22716975 AB - The safety and efficacy of adding antiretroviral drugs to standard zidovudine prophylaxis in infants of mothers with human immunodeficiency virus (HIV) infection who did not receive antenatal antiretroviral therapy (ART) because of late identification are unclear. We evaluated three ART regimens in such infants. Within 48 hours after their birth, we randomly assigned formula-fed infants born to women with a peripartum diagnosis of HIV type 1 (HIV-1) infection to one of three regimens: zidovudine for 6 weeks (zidovudine-alone group), zidovudine for 6 weeks plus three doses of nevirapine during the first 8 days of life (two-drug group), or zidovudine for 6 weeks plus nelfinavir and lamivudine for 2 weeks (three-drug group). The primary outcome was HIV-1 infection at 3 months in infants uninfected at birth. A total of 1684 infants were enrolled in the Americas and South Africa (566 in the zidovudine-alone group, 562 in the two-drug group, and 556 in the three-drug group). The overall rate of in utero transmission of HIV-1 on the basis of Kaplan-Meier estimates was 5.7% (93 infants), with no significant differences among the groups. Intrapartum transmission occurred in 24 infants in the zidovudine-alone group (4.8%; 95% confidence interval [CI], 3.2 to 7.1), as compared with 11 infants in the two-drug group (2.2%; 95% CI, 1.2 to 3.9; P=0.046) and 12 in the three-drug group (2.4%; 95% CI, 1.4 to 4.3; P=0.046). The overall transmission rate was 8.5% (140 infants), with an increased rate in the zidovudine-alone group (P=0.03 for the comparisons with the two- and three-drug groups). On multivariate analysis, zidovudine monotherapy, a higher maternal viral load, and maternal use of illegal substances were significantly associated with transmission. The rate of neutropenia was significantly increased in the three-drug group (P<0.001 for both comparisons with the other groups). In neonates whose mothers did not receive ART during pregnancy, prophylaxis with a two- or three-drug ART regimen is superior to zidovudine alone for the prevention of intrapartum HIV transmission; the two-drug regimen has less toxicity than the three-drug regimen. (Funded by the Eunice Kennedy Shriver National Institute of Child Health and Human Development [NICHD] and others; ClinicalTrials.gov number, NCT00099359.). JF - The New England journal of medicine AU - Nielsen-Saines, Karin AU - Watts, D Heather AU - Veloso, Valdilea G AU - Bryson, Yvonne J AU - Joao, Esau C AU - Pilotto, Jose Henrique AU - Gray, Glenda AU - Theron, Gerhard AU - Santos, Breno AU - Fonseca, Rosana AU - Kreitchmann, Regis AU - Pinto, Jorge AU - Mussi-Pinhata, Marisa M AU - Ceriotto, Mariana AU - Machado, Daisy AU - Bethel, James AU - Morgado, Marisa G AU - Dickover, Ruth AU - Camarca, Margaret AU - Mirochnick, Mark AU - Siberry, George AU - Grinsztejn, Beatriz AU - Moreira, Ronaldo I AU - Bastos, Francisco I AU - Xu, Jiahong AU - Moye, Jack AU - Mofenson, Lynne M AU - NICHD HPTN 040/PACTG 1043 Protocol Team AD - Division of Infectious Diseases, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA. knielsen@mednet.ucla.edu ; NICHD HPTN 040/PACTG 1043 Protocol Team Y1 - 2012/06/21/ PY - 2012 DA - 2012 Jun 21 SP - 2368 EP - 2379 VL - 366 IS - 25 KW - Anti-Retroviral Agents KW - 0 KW - Lamivudine KW - 2T8Q726O95 KW - Zidovudine KW - 4B9XT59T7S KW - Nevirapine KW - 99DK7FVK1H KW - Nelfinavir KW - HO3OGH5D7I KW - Abridged Index Medicus KW - Index Medicus KW - Kaplan-Meier Estimate KW - Drug Therapy, Combination -- adverse effects KW - Infant Formula KW - Drug Resistance, Viral KW - Humans KW - Pregnancy Complications, Infectious KW - Infant, Newborn KW - Postpartum Period KW - Male KW - Female KW - Pregnancy KW - Zidovudine -- therapeutic use KW - Infectious Disease Transmission, Vertical -- prevention & control KW - Nevirapine -- adverse effects KW - HIV Infections -- transmission KW - Nevirapine -- therapeutic use KW - Lamivudine -- adverse effects KW - HIV Infections -- mortality KW - Lamivudine -- therapeutic use KW - HIV-1 KW - Nelfinavir -- therapeutic use KW - Anti-Retroviral Agents -- therapeutic use KW - Nelfinavir -- adverse effects KW - Zidovudine -- adverse effects KW - Anti-Retroviral Agents -- adverse effects KW - HIV Infections -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1021979652?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Three+postpartum+antiretroviral+regimens+to+prevent+intrapartum+HIV+infection.&rft.au=Nielsen-Saines%2C+Karin%3BWatts%2C+D+Heather%3BVeloso%2C+Valdilea+G%3BBryson%2C+Yvonne+J%3BJoao%2C+Esau+C%3BPilotto%2C+Jose+Henrique%3BGray%2C+Glenda%3BTheron%2C+Gerhard%3BSantos%2C+Breno%3BFonseca%2C+Rosana%3BKreitchmann%2C+Regis%3BPinto%2C+Jorge%3BMussi-Pinhata%2C+Marisa+M%3BCeriotto%2C+Mariana%3BMachado%2C+Daisy%3BBethel%2C+James%3BMorgado%2C+Marisa+G%3BDickover%2C+Ruth%3BCamarca%2C+Margaret%3BMirochnick%2C+Mark%3BSiberry%2C+George%3BGrinsztejn%2C+Beatriz%3BMoreira%2C+Ronaldo+I%3BBastos%2C+Francisco+I%3BXu%2C+Jiahong%3BMoye%2C+Jack%3BMofenson%2C+Lynne+M%3BNICHD+HPTN+040%2FPACTG+1043+Protocol+Team&rft.aulast=Nielsen-Saines&rft.aufirst=Karin&rft.date=2012-06-21&rft.volume=366&rft.issue=25&rft.spage=2368&rft.isbn=&rft.btitle=&rft.title=The+New+England+journal+of+medicine&rft.issn=1533-4406&rft_id=info:doi/10.1056%2FNEJMoa1108275 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-26 N1 - Date created - 2012-06-21 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00099359; ClinicalTrials.gov N1 - SuppNotes - Cited By: Clin Infect Dis. 2002 Apr 1;34(7):991-1001 [11880966] Braz J Infect Dis. 2001 Apr;5(2):78-86 [11493413] Sex Transm Infect. 2003 Dec;79(6):448-52 [14663118] J Infect Dis. 2003 Dec 15;188(12):1820-6 [14673760] JAMA. 2004 Jul 14;292(2):202-9 [15249569] JAMA. 2004 Jul 14;292(2):219-23 [15249571] N Engl J Med. 1994 Nov 3;331(18):1173-80 [7935654] JAMA. 1996 Feb 28;275(8):599-605 [8594240] N Engl J Med. 1996 Nov 28;335(22):1621-9 [8965861] N Engl J Med. 1998 Nov 12;339(20):1409-14 [9811915] J Infect Dis. 1999 Jul;180(1):99-105 [10353867] Clin Infect Dis. 1999 May;28(5):1109-18 [10452644] AIDS. 2005 Aug 12;19(12):1289-97 [16052084] J Infect Dis. 2006 Feb 15;193(4):479-81 [16425125] Eur J Obstet Gynecol Reprod Biol. 2006 Sep-Oct;128(1-2):59-63 [16876310] J Acquir Immune Defic Syndr. 2007 Jun 1;45(2):251-3 [17527096] J Acquir Immune Defic Syndr. 2008 Mar 1;47(3):334-7 [18398973] AIDS Res Hum Retroviruses. 2009 Sep;25(9):861-7 [19689190] N Engl J Med. 2010 Jun 17;362(24):2271-81 [20554982] Rev Saude Publica. 2010 Oct;44(5):803-11 [20835495] J Neuroimmune Pharmacol. 2010 Dec;5(4):507-15 [20838913] AIDS. 2010 Nov 27;24(18):2819-26 [20885282] AIDS Patient Care STDS. 2011 Jan;25(1):1-4 [21162689] Int J Gynaecol Obstet. 2011 Apr;113(1):44-9 [21251654] HIV Med. 2011 Aug;12(7):422-7 [21251184] JAMA. 2011 Jul 6;306(1):70-8 [21730243] Pediatr Infect Dis J. 2011 Sep;30(9):769-72 [21666540] Lancet. 1999 Sep 4;354(9181):795-802 [10485720] JAMA. 2001 Apr 25;285(16):2083-93 [11311097] Lancet. 2003 Oct 11;362(9391):1171-7 [14568737] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1056/NEJMoa1108275 ER - TY - JOUR T1 - Mutation in the platelet-derived growth factor receptor alpha inhibits adeno-associated virus type 5 transduction. AN - 1012748251; 22520943 AB - Due to its non-pathogenic lifecycle, little is known about the cellular determinants of infection by adeno-associated virus (AAV). To identify these critical cellular factors, we took advantage of the gene transfer abilities of AAV in combination with a forward genetic selection to identify proteins critical for transduction by this virus. AAV serotype 5 (AAV5) vectors encoding the furin gene were used to transduce furin-deficient cells followed by selection with furin-dependent toxins. A population of cells specifically resistant to AAV5 transduction was identified and sequence analysis suggested all had a single amino acid mutation in the leader sequence of the platelet-derived growth factor receptor alpha (PDGFRα) gene. Characterization of this mutation suggested it inhibited PDGFRα trafficking resulting in limited expression on the plasma membrane. Mutagenesis and transfection experiments confirmed the effect of this mutation on PDGFRα trafficking, and the AAV5 resistant phenotype could be rescued by transfection with wild type PDGFRα. Published by Elsevier Inc. JF - Virology AU - Pilz, Ingo H AU - Di Pasquale, Giovanni AU - Rzadzinska, Agnieszka AU - Leppla, Stephen H AU - Chiorini, John A AD - Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA. ingo.hinrich.pilz@uniklinik-freiburg.de Y1 - 2012/06/20/ PY - 2012 DA - 2012 Jun 20 SP - 58 EP - 63 VL - 428 IS - 1 KW - Receptor, Platelet-Derived Growth Factor alpha KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Down-Regulation KW - Humans KW - CHO Cells KW - Cell Line KW - Cricetinae KW - Dependovirus -- physiology KW - Receptor, Platelet-Derived Growth Factor alpha -- metabolism KW - Parvoviridae Infections -- metabolism KW - Transduction, Genetic KW - Parvoviridae Infections -- virology KW - Dependovirus -- genetics KW - Mutation KW - Receptor, Platelet-Derived Growth Factor alpha -- genetics KW - Parvoviridae Infections -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1012748251?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Virology&rft.atitle=Mutation+in+the+platelet-derived+growth+factor+receptor+alpha+inhibits+adeno-associated+virus+type+5+transduction.&rft.au=Pilz%2C+Ingo+H%3BDi+Pasquale%2C+Giovanni%3BRzadzinska%2C+Agnieszka%3BLeppla%2C+Stephen+H%3BChiorini%2C+John+A&rft.aulast=Pilz&rft.aufirst=Ingo&rft.date=2012-06-20&rft.volume=428&rft.issue=1&rft.spage=58&rft.isbn=&rft.btitle=&rft.title=Virology&rft.issn=1096-0341&rft_id=info:doi/10.1016%2Fj.virol.2012.03.004 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-16 N1 - Date created - 2012-05-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2001 Apr 10;98(8):4443-8 [11296287] Neuroreport. 2000 Aug 21;11(12):2669-73 [10976941] Nat Med. 2010 Jun;16(6):662-4 [20473307] Proc Natl Acad Sci U S A. 2011 May 17;108(20):8426-31 [21536871] Virology. 2011 Jul 5;415(2):83-94 [21529875] Nat Med. 2003 Oct;9(10):1306-12 [14502277] Mol Cell. 2003 Sep;12(3):603-13 [14527407] J Biol Chem. 1987 Jul 15;262(20):9778-84 [3036871] J Biol Chem. 1990 Dec 25;265(36):22075-8 [2266110] Cell. 1992 Jul 24;70(2):313-22 [1386289] Proc Natl Acad Sci U S A. 1992 Nov 1;89(21):10277-81 [1438214] Infect Immun. 1995 Jan;63(1):82-7 [7806387] J Biol Chem. 1995 Nov 17;270(46):27876-9 [7499261] Science. 1997 Nov 28;278(5343):1630-2 [9374464] Hum Mol Genet. 2005 Jun 15;14(12):1679-90 [15879434] J Virol. 2006 Mar;80(6):2621-30 [16501072] Int Arch Allergy Immunol. 2006;141(1):37-46 [16804324] Nat Med. 2007 Jun;13(6):685-7 [17515894] Eur J Hum Genet. 2007 Sep;15(9):950-8 [17568391] Proteins. 2008 Feb 1;70(2):394-403 [17680692] Am J Physiol Renal Physiol. 2009 Mar;296(3):F459-69 [18971212] J Virol. 2009 Oct;83(19):10176-86 [19625394] Science. 2009 Nov 27;326(5957):1231-5 [19965467] J Virol. 2000 Apr;74(8):3852-8 [10729159] Ann Neurol. 2000 Apr;47(4):514-6 [10762164] J Virol. 2001 Aug;75(15):6884-93 [11435568] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.virol.2012.03.004 ER - TY - JOUR T1 - The counter regulatory response induced by CpG oligonucleotides prevents bleomycin induced pneumopathy. AN - 1034659594; 22708497 AB - Bleomycin (BLM) induces life-threatening pneumonitis and pulmonary fibrosis in 20% of patients, limiting its use as a chemotherapeutic agent. Oligonucleotides expressing immunostimulatory CpG motifs (CpG ODN) stimulate cells that express Toll-like receptor 9 to initiate an inflammatory response. This short-lived inflammation is physiologically suppressed by a counter-regulatory process that peaks five days later. Using a murine model of BLM-induced lung injury, the effect of CpG ODN treatment on pulmonary inflammation, fibrosis and mortality was examined. Administering CpG ODN 5 days before BLM (so that the peak of the counter-regulatory process induced by CpG ODN coincided with BLM delivery) resulted in a dose-dependent reduction in pulmonary toxicity (p < 0.005). Delaying the initiation of therapy until the day of or after BLM administration worsened the inflammatory process, consistent with the counter-regulatory process rather than initial pro-inflammatory response being critical to CpG induced protection. The protection afforded by CpG ODN correlated with reduced leukocyte accumulation and inflammatory cytokine/chemokine production in the lungs. These changes were associated with the increased production of IL-10, a critical element of the counter-regulatory process triggered by CpG ODN, and the concomitant down-regulation of BLM-induced IL-17A and TGF-β1 (which promote pulmonary toxicity). This work represents the first example of the physiologic counter-regulation of TLR induced immune activation being harnessed to block an unrelated inflammatory response. JF - Respiratory research AU - Kinjo, Takeshi AU - Tomaru, Koji AU - Haines, Diana C AU - Klinman, Dennis M AD - Cancer and Inflammation Program, National Cancer Institute, Frederick, MD 21702, USA. Y1 - 2012/06/18/ PY - 2012 DA - 2012 Jun 18 SP - 47 VL - 13 KW - CPG-oligonucleotide KW - 0 KW - Oligodeoxyribonucleotides KW - Bleomycin KW - 11056-06-7 KW - Index Medicus KW - Animals KW - Mice, Inbred C57BL KW - Mice KW - Female KW - Pneumonia -- prevention & control KW - Pneumonia -- chemically induced KW - Oligodeoxyribonucleotides -- therapeutic use KW - Bleomycin -- contraindications KW - Pulmonary Fibrosis -- pathology KW - Pulmonary Fibrosis -- chemically induced KW - Pulmonary Fibrosis -- prevention & control KW - Bleomycin -- toxicity KW - Bleomycin -- antagonists & inhibitors KW - Pneumonia -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1034659594?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Respiratory+research&rft.atitle=The+counter+regulatory+response+induced+by+CpG+oligonucleotides+prevents+bleomycin+induced+pneumopathy.&rft.au=Kinjo%2C+Takeshi%3BTomaru%2C+Koji%3BHaines%2C+Diana+C%3BKlinman%2C+Dennis+M&rft.aulast=Kinjo&rft.aufirst=Takeshi&rft.date=2012-06-18&rft.volume=13&rft.issue=&rft.spage=47&rft.isbn=&rft.btitle=&rft.title=Respiratory+research&rft.issn=1465-993X&rft_id=info:doi/10.1186%2F1465-9921-13-47 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-06-10 N1 - Date created - 2012-08-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Infect Immun. 2001 Apr;69(4):2123-9 [11254566] Nature. 2000 Dec 7;408(6813):740-5 [11130078] Chest. 2001 Aug;120(2):617-24 [11502668] J Immunol. 2002 May 1;168(9):4711-20 [11971021] J Chemother. 2003 Aug;15(4):394-9 [12962369] Nat Rev Immunol. 2004 Apr;4(4):249-58 [15057783] Exp Mol Pathol. 2004 Jun;76(3):205-11 [15126102] Expert Opin Biol Ther. 2004 Jun;4(6):937-46 [15174975] Ann Intern Med. 1978 Jan;88(1):47-9 [74226] Biochemistry. 1978 Jul 11;17(14):2740-6 [80226] Biochemistry. 1978 Jul 11;17(14):2746-54 [80227] JAMA. 1980 Jan 25;243(4):347-51 [6153225] J Biol Chem. 1981 Nov 25;256(22):11636-44 [6170635] Cancer. 1989 Aug 15;64(4):806-11 [2472865] Thorax. 1993 Oct;48(10):959-66 [7504843] Nature. 1995 Apr 6;374(6522):546-9 [7700380] Proc Natl Acad Sci U S A. 1996 Apr 2;93(7):2879-83 [8610135] J Immunol. 1999 May 15;162(10):6284-93 [10229876] J Immunol. 1999 Jul 1;163(1):224-31 [10384120] Semin Hematol. 2004 Oct;41(4 Suppl 7):26-31 [15768476] J Clin Oncol. 2005 Oct 20;23(30):7614-20 [16186594] Proc Am Thorac Soc. 2007 Jul;4(3):289-94 [17607015] J Clin Invest. 2007 Dec;117(12):3786-99 [17992263] Respir Res. 2007;8:72 [17925007] J Cereb Blood Flow Metab. 2008 May;28(5):1040-7 [18183029] Stroke. 2009 Mar;40(3 Suppl):S34-7 [19064776] J Leukoc Biol. 2009 May;85(5):788-95 [19179452] Am J Respir Crit Care Med. 2009 May 15;179(10):903-13 [19218193] Mol Immunol. 2010 Mar;47(6):1317-24 [20005572] J Exp Med. 2010 Mar 15;207(3):535-52 [20176803] J Exp Med. 2011 Jul 4;208(7):1339-50 [21727191] J Clin Oncol. 2011 Aug 20;29(24):e691-3 [21709191] PLoS One. 2011;6(8):e23185 [21858022] Br J Cancer. 2011 Sep 6;105(6):766-72 [21847130] J Immunol. 2011 Sep 15;187(6):3003-14 [21841134] Am J Physiol Lung Cell Mol Physiol. 2001 Jul;281(1):L92-7 [11404251] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1186/1465-9921-13-47 ER - TY - CPAPER T1 - The USG Policy for Oversight of Life Sciences Dual Use Research of Concern--Implementation Issues T2 - 112th General Meeting of the American Society for Microbiology (ASM 2012) AN - 1313011093; 6136607 JF - 112th General Meeting of the American Society for Microbiology (ASM 2012) AU - Dixon, Dennis Y1 - 2012/06/16/ PY - 2012 DA - 2012 Jun 16 KW - Policies UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313011093?accountid=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=112th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2012%29&rft.atitle=The+USG+Policy+for+Oversight+of+Life+Sciences+Dual+Use+Research+of+Concern--Implementation+Issues&rft.au=Dixon%2C+Dennis&rft.aulast=Dixon&rft.aufirst=Dennis&rft.date=2012-06-16&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=112th+General+Meeting+of+the+American+Society+for+Microbiology+%28ASM+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.asm.org/images/asm2012_finalprogram_webv.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Perfluorinated Compounds in Relation to Birth Weight in the Norwegian Mother and Child Cohort Study AN - 1257732828; 16838118 AB - Perfluorooctane sulfonate and perfluorooctanoic acid are perfluorinated compounds (PFCs) widely distributed in the environment. Previous studies of PFCs and birth weight are equivocal. The authors examined this association in the Norwegian Mother and Child Cohort Study (MoBa), using data from 901 women enrolled from 2003 to 2004 and selected for a prior case-based study of PFCs and subfecundity. Maternal plasma samples were obtained around 17 weeks of gestation. Outcomes included birth weight z scores, preterm birth, small for gestational age, and large for gestational age. The adjusted birth weight z scores were slightly lower among infants born to mothers in the highest quartiles of PFCs compared with infants born to mothers in the lowest quartiles: for perfluorooctane sulfonate, beta = -0.18 (95% confidence interval: -0.41, 0.05) and, for perfluorooctanoic acid, beta = -0.21 (95% confidence interval: -0.45, 0.04). No clear evidence of an association with small for gestational age or large for gestational age was observed. Perfluorooctane sulfonate and perfluorooctanoic acid were each associated with decreased adjusted odds of preterm birth, although the cell counts were small. Whether some of the associations suggested by these findings may be due to a noncausal pharmacokinetic mechanism remains unclear. JF - American Journal of Epidemiology AU - Whitworth, Kristina W AU - Haug, Line S AU - Baird, Donna D AU - Becher, Georg AU - Hoppin, Jane A AU - Skjaerven, Rolv AU - Thomsen, Cathrine AU - Eggesbo, Merete AU - Travlos, Gregory AU - Wilson, Ralph AU - Cupul-Uicab, Lea A AU - Brantsaeter, Anne Lise AU - Longnecker, Matthew P Y1 - 2012/06/15/ PY - 2012 DA - 2012 Jun 15 SP - 1209 EP - 1216 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 175 IS - 12 SN - 0002-9262, 0002-9262 KW - Health & Safety Science Abstracts KW - Birth weight KW - Age KW - Low-birth-weight KW - Sulfonates KW - Norway KW - Pharmacokinetics KW - Pregnancy KW - Infants KW - H 12000:Epidemiology and Public Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1257732828?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ahealthsafetyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Perfluorinated+Compounds+in+Relation+to+Birth+Weight+in+the+Norwegian+Mother+and+Child+Cohort+Study&rft.au=Whitworth%2C+Kristina+W%3BHaug%2C+Line+S%3BBaird%2C+Donna+D%3BBecher%2C+Georg%3BHoppin%2C+Jane+A%3BSkjaerven%2C+Rolv%3BThomsen%2C+Cathrine%3BEggesbo%2C+Merete%3BTravlos%2C+Gregory%3BWilson%2C+Ralph%3BCupul-Uicab%2C+Lea+A%3BBrantsaeter%2C+Anne+Lise%3BLongnecker%2C+Matthew+P&rft.aulast=Whitworth&rft.aufirst=Kristina&rft.date=2012-06-15&rft.volume=175&rft.issue=12&rft.spage=1209&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwr459 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-12-01 N1 - Last updated - 2013-11-04 N1 - SubjectsTermNotLitGenreText - Birth weight; Age; Low-birth-weight; Sulfonates; Pharmacokinetics; Infants; Pregnancy; Norway DO - http://dx.doi.org/10.1093/aje/kwr459 ER - TY - JOUR T1 - Selective blockade of tumor angiogenesis. AN - 1023199608; 22617387 AB - Blocking tumor angiogenesis is an important goal of cancer therapy, but clinically approved anti-angiogenic agents suffer from limited efficacy and adverse side effects, fueling the need to identify alternative angiogenesis regulators. Tumor endothelial marker 8 (TEM8) is a highly conserved cell surface receptor overexpressed on human tumor vasculature. Genetic disruption of Tem8 in mice revealed that TEM8 is important for promoting tumor angiogenesis and tumor growth but dispensable for normal development and wound healing. The induction of TEM8 in cultured endothelial cells by nutrient or growth factor deprivation suggests that TEM8 may be part of a survival response pathway that is activated by tumor microenvironmental stress. In preclinical studies, antibodies targeted against the extracellular domain of TEM8 inhibited tumor angiogenesis and blocked the growth of multiple human tumor xenografts. Anti-TEM8 antibodies augmented the activity of other anti-angiogenic agents, vascular targeting agents and conventional chemotherapeutic agents and displayed no detectable toxicity. Thus, anti-TEM8 antibodies provide a promising new tool for selective blockade of neovascularization associated with cancer and possibly other angiogenesis-dependent diseases. JF - Cell cycle (Georgetown, Tex.) AU - Chaudhary, Amit AU - St Croix, Brad AD - Tumor Angiogenesis Section, Mouse Cancer Genetics Program, National Cancer Institute, National Institutes of Health, Frederick, MD, USA. Y1 - 2012/06/15/ PY - 2012 DA - 2012 Jun 15 SP - 2253 EP - 2259 VL - 11 IS - 12 KW - ANTXR1 protein, human KW - 0 KW - Antibodies KW - Antxr1 protein, mouse KW - Antxr2 protein, mouse KW - Biomarkers, Tumor KW - Neoplasm Proteins KW - Receptors, Cell Surface KW - Receptors, Peptide KW - Index Medicus KW - Neoplasms -- drug therapy KW - Animals KW - Antibodies -- immunology KW - Biomarkers, Tumor -- genetics KW - Receptors, Peptide -- metabolism KW - Biomarkers, Tumor -- deficiency KW - HEK293 Cells KW - Humans KW - Mice KW - Mice, Knockout KW - Biomarkers, Tumor -- metabolism KW - Neoplasms -- pathology KW - Antibodies -- therapeutic use KW - Transfection KW - Cells, Cultured KW - Receptors, Peptide -- deficiency KW - Transplantation, Heterologous KW - Receptors, Peptide -- genetics KW - Neoplasms -- metabolism KW - Endothelial Cells -- metabolism KW - Receptors, Cell Surface -- metabolism KW - Neoplasm Proteins -- genetics KW - Receptors, Cell Surface -- genetics KW - Neovascularization, Pathologic KW - Neoplasm Proteins -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1023199608?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+cycle+%28Georgetown%2C+Tex.%29&rft.atitle=Selective+blockade+of+tumor+angiogenesis.&rft.au=Chaudhary%2C+Amit%3BSt+Croix%2C+Brad&rft.aulast=Chaudhary&rft.aufirst=Amit&rft.date=2012-06-15&rft.volume=11&rft.issue=12&rft.spage=2253&rft.isbn=&rft.btitle=&rft.title=Cell+cycle+%28Georgetown%2C+Tex.%29&rft.issn=1551-4005&rft_id=info:doi/10.4161%2Fcc.20374 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-10-17 N1 - Date created - 2012-06-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Trends Cardiovasc Med. 2006 Apr;16(3):80-8 [16546688] J Am Soc Nephrol. 2006 Mar;17(3):724-35 [16436493] Cancer Sci. 2007 Mar;98(3):405-10 [17214745] J Biol Chem. 2007 Mar 30;282(13):9834-45 [17251181] Nat Rev Cancer. 2007 Jun;7(6):475-85 [17522716] Cancer Cell. 2007 Jun;11(6):539-54 [17560335] Cell. 2007 Aug 24;130(4):691-703 [17719546] Neuro Oncol. 2007 Oct;9(4):384-92 [17704359] Cancer Metastasis Rev. 2007 Dec;26(3-4):433-41 [17786539] N Engl J Med. 2008 May 8;358(19):2039-49 [18463380] Cell Cycle. 2009 Feb 15;8(4):580-8 [19182515] J Dermatol Sci. 2009 Sep;55(3):197-200 [19592224] Cancer Res. 2009 Aug 1;69(15):6021-6 [19622764] Nat Rev Clin Oncol. 2009 Aug;6(8):465-77 [19581909] Proc Natl Acad Sci U S A. 2009 Jul 28;106(30):12424-9 [19617532] J Am Acad Dermatol. 2009 Oct;61(4):629-38 [19559501] Cell Cycle. 2010 Jan 1;9(1):64-68 [20016271] Curr Opin Hematol. 2010 May;17(3):206-12 [20216210] Cell Cycle. 2010 Mar 1;9(5):913-7 [20160500] J Proteomics. 2010 Oct 10;73(11):2219-29 [20541635] Mol Cell. 2010 Oct 22;40(2):280-93 [20965422] Cell Host Microbe. 2010 Nov 18;8(5):455-62 [21075356] Biochim Biophys Acta. 2011 Jan;1813(1):39-49 [21129411] Cell Cycle. 2011 Jan 1;10(1):10-2 [21191182] Oncotarget. 2010 Nov;1(7):662-73 [21317461] Nat Rev Clin Oncol. 2011 Apr;8(4):210-21 [21364524] Oncotarget. 2011 Mar;2(3):122-34 [21399234] EMBO J. 2012 Jan 4;31(1):3-13 [22215446] Cancer Cell. 2012 Feb 14;21(2):212-26 [22340594] Nature. 2001 Nov 8;414(6860):225-9 [11700562] Cancer Res. 2000 Mar 1;60(5):1388-93 [10728704] Science. 2000 Aug 18;289(5482):1197-202 [10947988] Am J Med Genet. 2001 Apr 22;100(2):122-9 [11298373] Blood. 2001 Sep 15;98(6):1904-13 [11535528] J Cell Sci. 2001 Aug;114(Pt 15):2755-73 [11683410] Clin Cancer Res. 2003 Apr;9(4):1399-405 [12684411] Proc Natl Acad Sci U S A. 2003 Apr 29;100(9):5170-4 [12700348] Am J Hum Genet. 2003 Oct;73(4):957-66 [12973667] Am J Hum Genet. 2003 Oct;73(4):791-800 [14508707] Cancer Res. 2004 Feb 1;64(3):817-20 [14871805] Nature. 2004 Jun 10;429(6992):629-35 [15190345] Am J Pathol. 2004 Aug;165(2):601-8 [15277233] Arch Dermatol Res. 1980;267(2):115-21 [6157366] Biochem Biophys Res Commun. 1987 Aug 31;147(1):275-81 [3632670] Pediatrics. 1991 Feb;87(2):228-34 [1702887] Biochem Biophys Res Commun. 1995 Dec 26;217(3):721-7 [8554590] J Dermatol Sci. 1996 Oct;13(1):37-48 [8902652] J Biol Chem. 1997 Sep 19;272(38):23659-67 [9295307] Cancer Res. 2004 Nov 1;64(21):7857-66 [15520192] Cell. 2005 Jan 28;120(2):237-48 [15680329] Exp Cell Res. 2005 Apr 15;305(1):133-44 [15777794] Am J Physiol Cell Physiol. 2005 Jun;288(6):C1402-10 [15689409] Nat Rev Cancer. 2005 Jun;5(6):436-46 [15928674] Semin Cancer Biol. 2005 Aug;15(4):254-66 [15916903] J Neurooncol. 2007 Feb;81(3):241-8 [17031559] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.4161/cc.20374 ER - TY - JOUR T1 - Human CCR4+ CCR6+ Th17 cells suppress autologous CD8+ T cell responses. AN - 1019615904; 22615204 AB - The role of Th17 cells in cancer patients remains unclear and controversial. In this study, we have analyzed the phenotype of in vitro primed Th17 cells and further characterized their function on the basis of CCR4 and CCR6 expression. We show a novel function for a subset of IL-17-secreting CD4(+) T cells, namely, CCR4(+)CCR6(+)Th17 cells. When cultured together, CCR4(+)CCR6(+)Th17 cells suppressed the lytic function, proliferation, and cytokine secretion of both Ag-specific and CD3/CD28/CD2-stimulated autologous CD8(+) T cells. In contrast, CCR4(-)CCR6(+) CD4(+) T cells, which also secrete IL-17, did not affect the CD8(+) T cells. Suppression of CD8(+) T cells by CCR4(+)CCR6(+)Th17 cells was partially dependent on TGF-β, because neutralization of TGF-β in cocultures reversed their suppressor function. In addition, we also found an increase in the frequency of CCR4(+)CCR6(+), but not CCR4(-)CCR6(+) Th17 cells in peripheral blood of hepatocellular carcinoma patients. Our study not only underlies the importance of analysis of subsets within Th17 cells to understand their function, but also suggests Th17 cells as yet another immune evasion mechanism in hepatocellular carcinoma. This has important implications when studying the mechanisms of carcinogenesis, as well as designing effective immunotherapy protocols for patients with cancer. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Zhao, Fei AU - Hoechst, Bastian AU - Gamrekelashvili, Jaba AU - Ormandy, Lars A AU - Voigtländer, Torsten AU - Wedemeyer, Heiner AU - Ylaya, Kris AU - Wang, Xin Wei AU - Hewitt, Stephen M AU - Manns, Michael P AU - Korangy, Firouzeh AU - Greten, Tim F AD - Gastrointestinal Malignancy Section, Medical Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/06/15/ PY - 2012 DA - 2012 Jun 15 SP - 6055 EP - 6062 VL - 188 IS - 12 KW - CCR4 protein, human KW - 0 KW - CCR6 protein, human KW - Cytokines KW - Receptors, CCR4 KW - Receptors, CCR6 KW - Abridged Index Medicus KW - Index Medicus KW - Receptors, CCR6 -- immunology KW - Coculture Techniques KW - Receptors, CCR4 -- immunology KW - Humans KW - Cytokines -- biosynthesis KW - Receptors, CCR4 -- metabolism KW - Cytokines -- immunology KW - Enzyme-Linked Immunosorbent Assay KW - Flow Cytometry KW - Receptors, CCR6 -- metabolism KW - Immunohistochemistry KW - Tumor Escape -- immunology KW - T-Lymphocyte Subsets -- metabolism KW - CD8-Positive T-Lymphocytes -- metabolism KW - CD8-Positive T-Lymphocytes -- immunology KW - T-Lymphocyte Subsets -- immunology KW - Th17 Cells -- immunology KW - Th17 Cells -- metabolism KW - Carcinoma, Hepatocellular -- immunology KW - Liver Neoplasms -- immunology KW - Cell Communication -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1019615904?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Human+CCR4%2B+CCR6%2B+Th17+cells+suppress+autologous+CD8%2B+T+cell+responses.&rft.au=Zhao%2C+Fei%3BHoechst%2C+Bastian%3BGamrekelashvili%2C+Jaba%3BOrmandy%2C+Lars+A%3BVoigtl%C3%A4nder%2C+Torsten%3BWedemeyer%2C+Heiner%3BYlaya%2C+Kris%3BWang%2C+Xin+Wei%3BHewitt%2C+Stephen+M%3BManns%2C+Michael+P%3BKorangy%2C+Firouzeh%3BGreten%2C+Tim+F&rft.aulast=Zhao&rft.aufirst=Fei&rft.date=2012-06-15&rft.volume=188&rft.issue=12&rft.spage=6055&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=1550-6606&rft_id=info:doi/10.4049%2Fjimmunol.1102918 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-14 N1 - Date created - 2012-06-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Exp Med. 2001 Aug 20;194(4):519-27 [11514607] N Engl J Med. 2011 Sep 22;365(12):1118-27 [21992124] Respir Med. 2003 Jun;97(6):726-33 [12814161] Proc Natl Acad Sci U S A. 2005 Jan 11;102(2):419-24 [15623559] J Immunol. 2005 May 1;174(9):5215-23 [15843517] Br J Cancer. 2005 May 23;92(10):1862-8 [15870713] J Immunol. 2005 Nov 1;175(9):6177-89 [16237115] Inflamm Bowel Dis. 2006 May;12(5):382-8 [16670527] Arthritis Rheum. 2006 Apr;54(4):1122-31 [16572447] J Exp Med. 2006 Jul 10;203(7):1701-11 [16818678] Cancer Cell. 2006 Aug;10(2):99-111 [16904609] J Immunol. 2006 Oct 1;177(7):4488-94 [16982885] J Hepatol. 2006 Dec;45(6):868-78 [17046096] Science. 2006 Dec 1;314(5804):1461-3 [17068223] Annu Rev Immunol. 2007;25:821-52 [17201677] Int Immunol. 2007 Apr;19(4):345-54 [17329235] J Immunol. 2007 Jun 1;178(11):6730-3 [17513719] Nat Immunol. 2007 Jun;8(6):639-46 [17486092] J Exp Med. 2007 Aug 6;204(8):1849-61 [17635957] Immunology. 2007 Sep;122(1):90-7 [17472719] J Invest Dermatol. 2008 May;128(5):1207-11 [18200064] Blood. 2008 Jul 15;112(2):362-73 [18354038] J Exp Med. 2008 Aug 4;205(8):1903-16 [18663128] Biochem Biophys Res Commun. 2008 Sep 26;374(3):533-7 [18655770] Proc Natl Acad Sci U S A. 2008 Oct 7;105(40):15505-10 [18832156] J Exp Med. 2009 Feb 16;206(2):313-28 [19204109] J Exp Med. 2009 Mar 16;206(3):525-34 [19273624] J Hepatol. 2009 May;50(5):980-9 [19329213] Annu Rev Immunol. 2009;27:485-517 [19132915] Curr Opin Investig Drugs. 2009 Jun;10(6):543-9 [19513943] Microbes Infect. 2009 Apr;11(5):620-4 [19371794] J Exp Med. 2009 Jul 6;206(7):1457-64 [19564351] Blood. 2009 Jul 9;114(2):357-9 [19289853] Blood. 2009 Jul 16;114(3):596-9 [19471017] Blood. 2009 Aug 6;114(6):1141-9 [19470694] Expert Rev Gastroenterol Hepatol. 2010 Jun;4(3):345-53 [20528121] J Hepatol. 2011 May;54(5):948-55 [21145847] Blood. 2011 Jun 16;117(24):6532-41 [21493801] Blood. 2002 Mar 15;99(6):2114-21 [11877287] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.4049/jimmunol.1102918 ER - TY - JOUR T1 - Use of nonsteroidal anti-inflammatory drugs and risk of basal cell carcinoma in the United States Radiologic Technologists study. AN - 1001958189; 21780102 AB - Nonsteroidal anti-inflammatory drugs (NSAIDs) have been associated with reduced risk of colorectal and other cancers, but the association with basal cell carcinoma (BCC) is unclear. Previous epidemiological studies have been small in size, conducted in especially vulnerable populations, or have not accounted for solar ultraviolet exposure, a major risk factor for BCC. In the United States Radiologic Technologists cohort, we followed subjects to assess NSAID use on risk of first incident BCC. We included Caucasian participants who responded to both second and third questionnaires (administered from 1994 to 1998 and 2003 to 2005, respectively), and who reported no cancer at the time of the second questionnaire, N = 58,213. BCC, constituent risk factors (e.g., eye color, complexion, hair color) and sun exposure history were assessed through self-administered survey. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazards models. Of the 58,213 people in the study population, 2,291 went on to develop BCC. Any NSAID use was not associated with subsequent incidence of BCC (HR = 1.04, 95% CI: 0.92-1.16) after adjusting for age, sex and estimated lifetime summer sun exposure. Neither association was observed when stratified by NSAID type (aspirin and other NSAIDs), nor did dose-response patterns emerge by frequency of use (average days per month). Further analyses did not reveal interaction with sex, birth cohort, smoking, alcohol consumption, sun exposure, occupational radiation exposure or personal risk factors for BCC. In this large nationwide study, we observed no association between NSAID use and subsequent BCC risk. Copyright © 2011 UICC. JF - International journal of cancer AU - Cahoon, Elizabeth K AU - Rajaraman, Preetha AU - Alexander, Bruce H AU - Doody, Michele M AU - Linet, Martha S AU - Freedman, D Michal AD - Department of Health and Human Services, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD 20892-7238, USA. khaykine@mail.nih.gov Y1 - 2012/06/15/ PY - 2012 DA - 2012 Jun 15 SP - 2939 EP - 2948 VL - 130 IS - 12 KW - Anti-Inflammatory Agents, Non-Steroidal KW - 0 KW - Pyrazoles KW - Sulfonamides KW - Celecoxib KW - JCX84Q7J1L KW - Index Medicus KW - Young Adult KW - Sunlight -- adverse effects KW - Humans KW - Aged KW - Pyrazoles -- therapeutic use KW - Sulfonamides -- therapeutic use KW - Aged, 80 and over KW - Risk Factors KW - Adult KW - Cohort Studies KW - Surveys and Questionnaires KW - Environmental Exposure KW - Middle Aged KW - United States -- epidemiology KW - Female KW - Male KW - Proportional Hazards Models KW - Anti-Inflammatory Agents, Non-Steroidal -- therapeutic use KW - Skin Neoplasms -- epidemiology KW - Carcinoma, Basal Cell -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1001958189?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Use+of+nonsteroidal+anti-inflammatory+drugs+and+risk+of+basal+cell+carcinoma+in+the+United+States+Radiologic+Technologists+study.&rft.au=Cahoon%2C+Elizabeth+K%3BRajaraman%2C+Preetha%3BAlexander%2C+Bruce+H%3BDoody%2C+Michele+M%3BLinet%2C+Martha+S%3BFreedman%2C+D+Michal&rft.aulast=Cahoon&rft.aufirst=Elizabeth&rft.date=2012-06-15&rft.volume=130&rft.issue=12&rft.spage=2939&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.26286 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-05 N1 - Date created - 2012-04-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mol Carcinog. 2003 Sep;38(1):33-9 [12949841] Recent Results Cancer Res. 2003;163:46-57; discussion 264-6 [12903842] Br J Dermatol. 2003 Jul;149(1):115-23 [12890204] Cancer Epidemiol Biomarkers Prev. 2002 Dec;11(12):1645-52 [12496056] BMJ. 2003 Oct 4;327(7418):794-8 [14525881] Cancer Res. 2004 Sep 1;64(17):6207-13 [15342406] Cancer. 1974 Jul;34(1):230-5 [4135144] Cancer. 1992 Jan 15;69(2):586-98 [1728391] Cancer Lett. 1995 Aug 16;95(1-2):213-9 [7656233] Am J Epidemiol. 1995 Nov 15;142(10):1103-12 [7485055] Am J Epidemiol. 1997 Jan 1;145(1):72-80 [8982025] Cancer Causes Control. 1998 Jan;9(1):67-75 [9486465] Mol Carcinog. 1999 Aug;25(4):231-40 [10449029] JAMA. 2005 Aug 10;294(6):681-90 [16091570] Int J Epidemiol. 2006 Apr;35(2):495-7 [16330477] Aust N Z J Public Health. 2007 Feb;31(1):87 [17333615] Mutat Res. 2007 Apr 1;617(1-2):138-46 [17307204] Mol Carcinog. 2007 Aug;46(8):692-8 [17443745] Br J Cancer. 2008 Jan 15;98(1):232-7 [18087276] Health Technol Assess. 2010 Jun;14(32):1-206 [20594533] Arch Dermatol. 2010 Mar;146(3):283-7 [20231499] Cancer Prev Res (Phila). 2010 Jan;3(1):25-34 [20051370] Pharmacoepidemiol Drug Saf. 2009 Apr;18(4):276-83 [19226541] J Photochem Photobiol B. 2010 Dec 2;101(3):321-5 [20826094] Int J Cancer. 2010 Nov 1;127(9):2190-8 [20473901] Int J Cancer. 2010 Oct 1;127(7):1680-91 [20091856] Biochem Pharmacol. 2010 Dec 15;80(12):2042-9 [20599768] J Natl Cancer Inst. 2010 Dec 15;102(24):1835-44 [21115882] Int J Cancer. 2006 Aug 1;119(3):682-6 [16496410] Photochem Photobiol. 2002 Jul;76(1):73-80 [12126310] Am J Ther. 2002 May-Jun;9(3):199-205 [11941379] Lancet Oncol. 2000 Nov;1:181-8 [11905657] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/ijc.26286 ER - TY - JOUR T1 - Infusion of hemolyzed red blood cells within peripheral blood stem cell grafts in patients with and without sickle cell disease. AN - 1020834224; 22547579 AB - Peripheral blood stem cell (PBSC) infusions are associated with complications such as elevated blood pressure and decreased creatinine clearance. Patients with sickle cell disease experience similar manifestations, and some have postulated release of plasma-free hemoglobin with subsequent nitric oxide consumption as causative. We sought to evaluate whether the infusion of PBSC grafts containing lysed red blood cells (RBCs) leads to the toxicity observed in transplant subjects. We report a prospective cohort study of 60 subjects divided into 4 groups based on whether their infusions contained dimethyl sulfoxide (DMSO) and lysed RBCs, no DMSO and fresh RBCs, DMSO and no RBCs, or saline. Our primary end point, change in maximum blood pressure compared with baseline, was not significantly different among groups. Tricuspid regurgitant velocity and creatinine levels also did not differ significantly among groups. Our data do not support free hemoglobin as a significant contributor to toxicity associated with PBSC infusions. This study was registered at clinicaltrials.gov (NCT00631787). JF - Blood AU - Fitzhugh, Courtney D AU - Unno, Hayato AU - Hathaway, Vincent AU - Coles, Wynona A AU - Link, Mary E AU - Weitzel, R Patrick AU - Zhao, Xiongce AU - Wright, Elizabeth C AU - Stroncek, David F AU - Kato, Gregory J AU - Hsieh, Matthew M AU - Tisdale, John F AD - Molecular and Clinical Hematology Branch, National Heart, Lung, and Blood Institute (NHLBI)/National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), National Institutes of Health (NIH), Bethesda, MD 20892, USA. Y1 - 2012/06/14/ PY - 2012 DA - 2012 Jun 14 SP - 5671 EP - 5673 VL - 119 IS - 24 KW - Haptoglobins KW - 0 KW - L-Lactate Dehydrogenase KW - EC 1.1.1.27 KW - Abridged Index Medicus KW - Index Medicus KW - Blood Pressure -- physiology KW - Infusions, Intravenous KW - Humans KW - Heart Rate -- physiology KW - Haptoglobins -- metabolism KW - L-Lactate Dehydrogenase -- metabolism KW - Peripheral Blood Stem Cell Transplantation KW - Hemolysis -- physiology KW - Anemia, Sickle Cell -- therapy KW - Erythrocytes -- physiology KW - Anemia, Sickle Cell -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020834224?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Blood&rft.atitle=Infusion+of+hemolyzed+red+blood+cells+within+peripheral+blood+stem+cell+grafts+in+patients+with+and+without+sickle+cell+disease.&rft.au=Fitzhugh%2C+Courtney+D%3BUnno%2C+Hayato%3BHathaway%2C+Vincent%3BColes%2C+Wynona+A%3BLink%2C+Mary+E%3BWeitzel%2C+R+Patrick%3BZhao%2C+Xiongce%3BWright%2C+Elizabeth+C%3BStroncek%2C+David+F%3BKato%2C+Gregory+J%3BHsieh%2C+Matthew+M%3BTisdale%2C+John+F&rft.aulast=Fitzhugh&rft.aufirst=Courtney&rft.date=2012-06-14&rft.volume=119&rft.issue=24&rft.spage=5671&rft.isbn=&rft.btitle=&rft.title=Blood&rft.issn=1528-0020&rft_id=info:doi/10.1182%2Fblood-2011-11-392654 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-24 N1 - Date created - 2012-06-15 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00631787; ClinicalTrials.gov N1 - SuppNotes - Cited By: Ann Hematol. 2000 Sep;79(9):523-6 [11043425] Cytotherapy. 1999;1(6):439-46 [20426544] Biol Blood Marrow Transplant. 2004 Feb;10(2):135-41 [14750079] Arch Int Pharmacodyn Ther. 1976 May;221(1):21-31 [962427] Clin Pharmacol Ther. 1978 Jan;23(1):73-80 [618711] Ann N Y Acad Sci. 1983;411:170-9 [6309056] Ann N Y Acad Sci. 1983;411:84-93 [6576724] Ann N Y Acad Sci. 1983;411:94-9 [6576725] Blood. 1990 Feb 1;75(3):781-6 [2297578] Bone Marrow Transplant. 1990 Jan;5 Suppl 1:25-7 [1969303] Bone Marrow Transplant. 1991 May;7(5):401-3 [2070152] Bone Marrow Transplant. 1992 Nov;10(5):435-8 [1464006] Bone Marrow Transplant. 1994 Sep;14(3):363-7 [7994256] Bone Marrow Transplant. 1999 Mar;23(6):533-7 [10217182] JAMA. 2005 Apr 6;293(13):1653-62 [15811985] Semin Hematol. 2007 Jan;44(1):51-9 [17198847] J Appl Physiol. 1949 Jan;1(7):469-89 [18104040] Nat Med. 2002 Dec;8(12):1383-9 [12426562] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1182/blood-2011-11-392654 ER - TY - JOUR T1 - Circulating Microbial Products and Acute Phase Proteins as Markers of Pathogenesis in Lymphatic Filarial Disease AN - 1328508644; 16836894 AB - Lymphatic filariasis can be associated with development of serious pathology in the form of lymphedema, hydrocele, and elephantiasis in a subset of infected patients. Dysregulated host inflammatory responses leading to systemic immune activation are thought to play a central role in filarial disease pathogenesis. We measured the plasma levels of microbial translocation markers, acute phase proteins, and inflammatory cytokines in individuals with chronic filarial pathology with (CP Ag+) or without (CP Ag-) active infection; with clinically asymptomatic infections (INF); and in those without infection (endemic normal [EN]). Comparisons between the two actively infected groups (CP Ag+ compared to INF) and those without active infection (CP Ag- compared to EN) were used preliminarily to identify markers of pathogenesis. Thereafter, we tested for group effects among all the four groups using linear models on the log transformed responses of the markers. Our data suggest that circulating levels of microbial translocation products (lipopolysaccharide and LPS-binding protein), acute phase proteins (haptoglobin and serum amyloid protein-A), and inflammatory cytokines (IL-1 beta , IL-12, and TNF- alpha ) are associated with pathogenesis of disease in lymphatic filarial infection and implicate an important role for circulating microbial products and acute phase proteins. Lymphatic filariasis afflicts over 120 million people worldwide. While the infection is mostly clinically asymptomatic, approximately 40 million people suffer from overt, morbid clinical pathology, characterized by swelling of the scrotal area and lower limbs (hydrocele and lymphedema). Host immunologic factors that influence the pathogenesis of disease in these individuals are not completely understood. Circulating microbial products such as LPS and markers associated with microbial translocation have been shown to play an important role in disease pathogenesis of certain infections like HIV. Similarly, proteins associated with the acute phase response and related cytokines also play an important role in pathogenesis. We have attempted to elucidate the role of the above mentioned factors in disease pathogenesis by comparing the plasma levels of the various markers in four groups of individuals: chronic pathology individuals with or without active filarial infection, asymptomatic, filarial infected individuals and uninfected, endemic normal individuals. We show that circulating levels of LPS, acute phase proteins and certain cytokines are significantly elevated in filarial disease with active infection but not in the other groups indicating that filarial infection induced increased production of these factors correlated with the development of filarial lymphatic pathology. JF - PLoS Pathogens AU - Anuradha, R AU - George, PJovvian AU - Pavan Kumar, N AU - Fay, Michael P AU - Kumaraswami, V AU - Nutman, Thomas B AU - Babu, Subash AD - National Institutes of Health, International Center for Excellence in Research, Chennai, India Y1 - 2012/06/07/ PY - 2012 DA - 2012 Jun 07 PB - Public Library of Science, 185 Berry Street San Francisco CA 94107 United States VL - 8 IS - 6 SN - 1553-7366, 1553-7366 KW - Biotechnology and Bioengineering Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Protein transport KW - Data processing KW - Interleukin 1 KW - Filariasis KW - Inflammation KW - Lymphedema KW - Acute phase substances KW - Interleukin 12 KW - Plasma levels KW - Limbs KW - Haptoglobin KW - Human immunodeficiency virus KW - Chronic infection KW - LPS-binding protein KW - Lipopolysaccharides KW - Cytokines KW - Tumor necrosis factor- alpha KW - Immune response KW - Translocation KW - Amyloid KW - W 30925:Genetic Engineering KW - A 01300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1328508644?accountid=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=PLoS+Pathogens&rft.atitle=Circulating+Microbial+Products+and+Acute+Phase+Proteins+as+Markers+of+Pathogenesis+in+Lymphatic+Filarial+Disease&rft.au=Anuradha%2C+R%3BGeorge%2C+PJovvian%3BPavan+Kumar%2C+N%3BFay%2C+Michael+P%3BKumaraswami%2C+V%3BNutman%2C+Thomas+B%3BBabu%2C+Subash&rft.aulast=Anuradha&rft.aufirst=R&rft.date=2012-06-07&rft.volume=8&rft.issue=6&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+Pathogens&rft.issn=15537366&rft_id=info:doi/10.1371%2Fjournal.ppat.1002749 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-04-01 N1 - Last updated - 2013-08-23 N1 - SubjectsTermNotLitGenreText - Protein transport; Data processing; Interleukin 1; Filariasis; Inflammation; Lymphedema; Interleukin 12; Acute phase substances; Plasma levels; Limbs; Haptoglobin; Chronic infection; LPS-binding protein; Cytokines; Lipopolysaccharides; Immune response; Tumor necrosis factor- alpha; Translocation; Amyloid; Human immunodeficiency virus DO - http://dx.doi.org/10.1371/journal.ppat.1002749 ER - TY - JOUR T1 - Biological responses of human mesenchymal stem cells to titanium wear debris particles. AN - 968101322; 22083964 AB - Wear debris-induced osteolysis is a major cause of orthopedic implant aseptic loosening, and various cell types, including macrophages, monocytes, osteoblasts, and osteoclasts, are involved. We recently showed that mesenchymal stem/osteoprogenitor cells (MSCs) are another target, and that endocytosis of titanium (Ti) particles causes reduced MSC proliferation and osteogenic differentiation. Here we investigated the mechanistic aspects of the endocytosis-mediated responses of MSCs to Ti particulates. Dose-dependent effects were observed on cell viability, with doses >300 Ti particles/cell resulting in drastic cell death. To maintain cell viability and analyze particle-induced effects, doses <300 particles/cell were used. Increased production of interleukin-8 (IL-8), but not IL-6, was observed in treated MSCs, while levels of TGF-β, IL-1β, and TNF-α were undetectable in treated or control cells, suggesting MSCs as a likely major producer of IL-8 in the periprosthetic zone. Disruptions in cytoskeletal and adherens junction organization were also observed in Ti particles-treated MSCs. However, neither IL-8 and IL-6 treatment nor conditioned medium from Ti particle-treated MSCs failed to affect MSC osteogenic differentiation. Among other Ti particle-induced cytokines, only GM-CSF appeared to mimic the effects of reduced cell viability and osteogenesis. Taken together, these results strongly suggest that MSCs play both responder and initiator roles in mediating the osteolytic effects of the presence of wear debris particles in periprosthetic zones. Copyright © 2011 Orthopaedic Research Society. JF - Journal of orthopaedic research : official publication of the Orthopaedic Research Society AU - Haleem-Smith, Hana AU - Argintar, Evan AU - Bush, Curtis AU - Hampton, Daniel AU - Postma, William F AU - Chen, Faye H AU - Rimington, Todd AU - Lamb, Joshua AU - Tuan, Rocky S AD - Cartilage Biology and Orthopaedics Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Department of Health and Human Service, Bethesda, Maryland 20892, USA. Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 853 EP - 863 VL - 30 IS - 6 KW - Culture Media, Conditioned KW - 0 KW - Interleukin-6 KW - Interleukin-8 KW - Particulate Matter KW - Titanium KW - D1JT611TNE KW - Index Medicus KW - Adherens Junctions -- drug effects KW - Culture Media, Conditioned -- pharmacology KW - Gene Expression -- drug effects KW - Dose-Response Relationship, Drug KW - Humans KW - Interleukin-6 -- metabolism KW - Interleukin-6 -- pharmacology KW - Interleukin-8 -- pharmacology KW - Cytoskeleton -- drug effects KW - Gene Expression Profiling KW - Apoptosis -- genetics KW - Cell Survival -- drug effects KW - Cells, Cultured KW - Apoptosis -- drug effects KW - Endocytosis -- drug effects KW - Cell Adhesion -- drug effects KW - Interleukin-8 -- metabolism KW - Cell Proliferation -- drug effects KW - Mesenchymal Stromal Cells -- drug effects KW - Titanium -- adverse effects KW - Particulate Matter -- adverse effects KW - Osteogenesis -- drug effects KW - Mesenchymal Stromal Cells -- metabolism KW - Mesenchymal Stromal Cells -- pathology KW - Osteolysis -- chemically induced KW - Osteogenesis -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/968101322?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+orthopaedic+research+%3A+official+publication+of+the+Orthopaedic+Research+Society&rft.atitle=Biological+responses+of+human+mesenchymal+stem+cells+to+titanium+wear+debris+particles.&rft.au=Haleem-Smith%2C+Hana%3BArgintar%2C+Evan%3BBush%2C+Curtis%3BHampton%2C+Daniel%3BPostma%2C+William+F%3BChen%2C+Faye+H%3BRimington%2C+Todd%3BLamb%2C+Joshua%3BTuan%2C+Rocky+S&rft.aulast=Haleem-Smith&rft.aufirst=Hana&rft.date=2012-06-01&rft.volume=30&rft.issue=6&rft.spage=853&rft.isbn=&rft.btitle=&rft.title=Journal+of+orthopaedic+research+%3A+official+publication+of+the+Orthopaedic+Research+Society&rft.issn=1554-527X&rft_id=info:doi/10.1002%2Fjor.22002 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-22 N1 - Date created - 2012-04-04 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Int J Oral Maxillofac Implants. 2011;26 Suppl:50-62; discussion 63-9 [21464999] Orthop Traumatol Surg Res. 2010 Dec;96(8):894-904 [20832379] Bone. 2010 Mar;46(3):613-27 [19857615] J Arthroplasty. 1999 Oct;14(7):840-8 [10537260] Clin Orthop Relat Res. 1999 Sep;(366):147-54 [10627728] Arch Orthop Trauma Surg. 2000;120(5-6):328-32 [10853906] Biorheology. 2001;38(2-3):161-83 [11381173] J Bone Miner Res. 2001 Nov;16(11):2082-91 [11697805] J Orthop Res. 2002 Sep;20(5):1060-9 [12382974] J Orthop Res. 2002 Nov;20(6):1175-84 [12472226] J Orthop Res. 2003 Jul;21(4):697-707 [12798071] Stem Cells. 2003;21(6):681-93 [14595128] Proc Natl Acad Sci U S A. 2004 Aug 24;101(34):12555-60 [15316116] Proc Natl Acad Sci U S A. 1985 Jun;82(11):3871-5 [3923482] Clin Orthop Relat Res. 1990 Dec;(261):171-85 [2245543] J Arthroplasty. 1992 Sep;7(3):315-23 [1402950] Clin Orthop Relat Res. 1993 Aug;(293):160-73 [8339477] J Bone Joint Surg Am. 1997 Jan;79(1):107-12 [9010191] J Bone Joint Surg Am. 1998 Oct;80(10):1447-58 [9801213] J Biomed Mater Res. 1999 Sep 5;46(3):399-407 [10397998] J Cell Biochem. 2004 Dec 15;93(6):1210-30 [15486964] J Bone Joint Surg Am. 2005 Jul;87(7):1487-97 [15995115] J Arthroplasty. 2005 Dec;20(8):1049-54 [16376262] Cytokine. 2005 Dec 21;32(6):270-9 [16377203] J Biomed Mater Res A. 2006 Apr;77(1):192-201 [16392133] J Orthop Res. 2006 Mar;24(3):461-73 [16450379] J Cell Biochem. 2006 Jun 1;98(3):538-54 [16317727] J Bone Miner Res. 2006 Jun;21(6):946-55 [16753025] Clin Orthop Relat Res. 2006 Dec;453:299-304 [16906105] J Orthop Res. 2007 Apr;25(4):450-7 [17205559] J Orthop Res. 2007 May;25(5):665-77 [17290432] Arthritis Res Ther. 2007;9 Suppl 1:S6 [17634145] J Biomed Mater Res A. 2007 Dec 15;83(4):1200-8 [17600327] Int Orthop. 2007 Dec;31(6):759-65 [17634942] Am J Physiol Cell Physiol. 2008 Mar;294(3):C675-82 [18234850] J Orthop Res. 2008 Jul;26(7):932-6 [18302244] J Am Acad Orthop Surg. 2008;16 Suppl 1:S42-8 [18612013] J Bone Joint Surg Am. 2009 Jan;91(1):128-33 [19122087] J Cell Physiol. 2009 Apr;219(1):77-83 [19089992] Biomed Mater Eng. 2008;18(6):395-403 [19197116] J Biomed Mater Res A. 2009 Apr;89(1):242-7 [18442106] J Biomed Mater Res A. 2009 May;89(2):370-8 [18431768] J Am Acad Orthop Surg. 2009 May;17(5):296-305 [19411641] J Immunol. 2009 Sep 1;183(5):3390-9 [19641137] J Cell Biochem. 2009 Oct 15;108(3):577-88 [19650110] J Orthop Res. 2010 May;28(5):571-7 [20014320] J Bone Joint Surg Am. 2010 Apr;92(4):840-5 [20360506] J Biomed Mater Res A. 2010 Aug;94(2):485-8 [20186767] Mediators Inflamm. 2010;2010:865601 [20628526] J Biomed Mater Res A. 2010 Dec 1;95(3):727-34 [20725976] Cell Transplant. 2011;20(5):693-706 [21176394] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/jor.22002 ER - TY - JOUR T1 - Challenges and opportunities in research on early-life events/exposures and cancer development later in life AN - 1842511819; 16730982 AB - It is becoming increasingly evident that early-life events and exposures have important consequences for cancer development later in life. However, epidemiological studies of early-life factors and cancer development later in life have had significant methodological challenges such as the long latency period, the distinctiveness of each cancer, and large number of subjects that must be studied, all likely to increase costs. These traditional hurdles might be mitigated by leveraging several existing large-scale prospective studies in the United States (US) and globally, as well as birth databases and birth cohorts, in order to launch both association and mechanistic studies of early-life exposures and cancer development later in life. Dedicated research funding will be needed to advance this paradigm shift in cancer research, and it seems justified by its potential to produce transformative understanding of how cancer develops over the life-course. This in turn has the potential to transform cancer prevention strategies through interventions in early-life rather than later in life, as is the current practice, where it is perhaps less effective. JF - Cancer Causes & Control AU - Mahabir, Somdat AU - Aagaard, Kjersti AU - Anderson, Lucy M AU - Herceg, Zdenko AU - Hiatt, Robert A AU - Hoover, Robert N AU - Linet, Martha S AU - Medina, Daniel AU - Potischman, Nancy AU - Tretli, Steinar AU - Trichopoulos, Dimitrios AU - Troisi, Rebecca AD - Modifiable Risk Factors Branch, Epidemiology and Genetics Research Program, Division of Cancer Control and Population Sciences (DCCPS), National Cancer Institute (NCI), 6130 Executive Blvd., Bethesda, MD, 20892, USA, mahabir@mail.nih.gov Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 983 EP - 990 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 23 IS - 6 SN - 0957-5243, 0957-5243 KW - Toxicology Abstracts KW - Databases KW - Cancer KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1842511819?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Causes+%26+Control&rft.atitle=Challenges+and+opportunities+in+research+on+early-life+events%2Fexposures+and+cancer+development+later+in+life&rft.au=Mahabir%2C+Somdat%3BAagaard%2C+Kjersti%3BAnderson%2C+Lucy+M%3BHerceg%2C+Zdenko%3BHiatt%2C+Robert+A%3BHoover%2C+Robert+N%3BLinet%2C+Martha+S%3BMedina%2C+Daniel%3BPotischman%2C+Nancy%3BTretli%2C+Steinar%3BTrichopoulos%2C+Dimitrios%3BTroisi%2C+Rebecca&rft.aulast=Mahabir&rft.aufirst=Somdat&rft.date=2012-06-01&rft.volume=23&rft.issue=6&rft.spage=983&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-9962-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-11-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Databases; Cancer DO - http://dx.doi.org/10.1007/s10552-012-9962-5 ER - TY - JOUR T1 - Caveolin binds independently to claudin-2 and occludin AN - 1780514683; PQ0002829199 AB - Treatment of epithelial and endothelial cells with proinflammatory cytokines can stimulate tight junction protein endocytosis, with associated loss of physiologic barrier function. In some instances, the endocytic scaffolding protein, caveolin-1, has been implicated in the cytokine-dependent retrieval of the tight junction proteins occludin and claudins. How caveolin-1 interacts with these proteins, however, remains undefined. Using co-immunoprecipitation assays, we found that caveolin-1 separately interacts with claudin-2 and occludin, but not with ZO-1, ZO-2, or claudin-4. Further, we found that the interactions of caveolin-1 with claudin-2 and occludin were not disrupted by cholesterol removal, suggesting that they were not dependent on co-localization to cholesterol-rich lipid rafts. Co-immunoprecipitation of caveolin-1 with chimeras between claudin-2 and -4 indicated that the C-terminal cytoplasmic domain of claudin-2 is required for association with caveolin-1; similar analysis showed that the ZO-1 binding region of occludin is not required for its interaction with caveolin-1. The finding that caveolin-1 interacts with claudin-2 and occludin, but not with claudin-4 or ZO-1, suggests a potential mechanism for selective retrieval of tight junction components. JF - Annals of the New York Academy of Sciences AU - Itallie, Christina MVan AU - Anderson, James M AD - National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland. Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 103 EP - 107 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 1257 IS - 1 SN - 0077-8923, 0077-8923 KW - Environment Abstracts KW - Lipids KW - Proteins KW - Cholesterol KW - ENA 07:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780514683?accountid=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=Caveolin+binds+independently+to+claudin-2+and+occludin&rft.au=Itallie%2C+Christina+MVan%3BAnderson%2C+James+M&rft.aulast=Itallie&rft.aufirst=Christina&rft.date=2012-06-01&rft.volume=1257&rft.issue=1&rft.spage=103&rft.isbn=&rft.btitle=&rft.title=Annals+of+the+New+York+Academy+of+Sciences&rft.issn=00778923&rft_id=info:doi/10.1111%2Fj.1749-6632.2012.06535.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-04-29 N1 - SubjectsTermNotLitGenreText - Lipids; Proteins; Cholesterol DO - http://dx.doi.org/10.1111/j.1749-6632.2012.06535.x ER - TY - JOUR T1 - Foamy Virus Vector-mediated Gene Correction of a Mouse Model of Wiskott-Aldrich Syndrome AN - 1668268907; PQ0001244571 AB - The Wiskott-Aldrich syndrome (WAS) is an X-linked disorder characterized by eczema, thrombocytopenia and immunodeficiency. Hematopoietic cell transplantation can cure the disease and gene therapy is being tested as an alternative treatment option. In this study, we assessed the use of foamy virus (FV) vectors as a gene transfer system for WAS, using a Was knockout (KO) mouse model. Preliminary experiments using FV vectors expressing the green fluorescent protein under the transcriptional control of the endogenous WAS promoter or a ubiquitously acting chromatin opening element allowed us to define transduction conditions resulting in high (>40%) and long-term in-vivo marking of blood cells after transplantation. In following experiments, Was KO mice were treated with FV vectors containing the human WAS complementary DNA (cDNA). Transplanted animals expressed the WAS protein (WASp) in T and B lymphocytes, as well as platelets and showed restoration of both T-cell receptor-mediated responses and B-cell migration. We also observed recovery of platelet adhesion and podosome formation in dendritic cells (DCs) of treated mice. These data demonstrate that FV vectors can be effective for hematopoietic stem cell (HSC)-directed gene correction of WAS. JF - Molecular Therapy AU - Uchiyama, Toru AU - Adriani, Marsilio AU - Jagadeesh, G Jayashree AU - Paine, Adam AU - Candotti, Fabio AD - Disorders of Immunity Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, USA; Department of Pediatrics, Tohoku University School of Medicine, Sendai, Japan, fabio@nhgri.nih.gov Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 1270 EP - 1279 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 20 IS - 6 SN - 1525-0016, 1525-0016 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Data processing KW - Gene therapy KW - Chromatin KW - Foamy virus KW - Lymphocytes B KW - X chromosome KW - Green fluorescent protein KW - Animal models KW - Immunodeficiency KW - Transcription KW - Fv KW - Leukocyte migration KW - Promoters KW - Wiskott-Aldrich syndrome KW - Dendritic cells KW - Thrombocytopenia KW - Lymphocytes T KW - Platelets KW - DNA KW - Blood cells KW - Hymenoptera KW - W 30905:Medical Applications KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668268907?accountid=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=Foamy+Virus+Vector-mediated+Gene+Correction+of+a+Mouse+Model+of+Wiskott-Aldrich+Syndrome&rft.au=Uchiyama%2C+Toru%3BAdriani%2C+Marsilio%3BJagadeesh%2C+G+Jayashree%3BPaine%2C+Adam%3BCandotti%2C+Fabio&rft.aulast=Uchiyama&rft.aufirst=Toru&rft.date=2012-06-01&rft.volume=20&rft.issue=6&rft.spage=1270&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2011.282 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Data processing; Chromatin; Gene therapy; Lymphocytes B; X chromosome; Immunodeficiency; Animal models; Green fluorescent protein; Transcription; Fv; Leukocyte migration; Dendritic cells; Wiskott-Aldrich syndrome; Promoters; Thrombocytopenia; DNA; Platelets; Lymphocytes T; Blood cells; Foamy virus; Hymenoptera DO - http://dx.doi.org/10.1038/mt.2011.282 ER - TY - JOUR T1 - Challenges in Vector and Trial Design Using Retroviral Vectors for Long-Term Gene Correction in Hematopoietic Stem Cell Gene Therapy AN - 1668266892; PQ0001244550 AB - Over the past two decades, incredible progress has been made using gene therapy for inherited severe immunodeficiency disorders, such as X-linked severe combined immunodeficiency disorder (SCID-X1) and adenosine deaminase deficiency-severe combined immunodeficiency disorder (ADA-SCID).[1-3] However, for reasons that remain unclear, gene transfer for SCID-X1 has also been associated with some cases of vector-induced leukemia whereas no cases have been seen in the ADA-SCID trials despite the common use of gamma -retroviral vectors. The first case was reported in a Prench gene transfer trial for SCID-X1.[4] Over the next six years, an additional three cases were reported in that trial and one in a second SCID-X1 trial that enrolled a combined total of 20 subects.[2] Unfortunately, genotoxicity would not remain confined to SCID-X1. Recent reports of insertional mutagenesis leading to myelodysplastic syndrome in a trial for chronic granulomatous disease and a case of leukemia in a trial for Wiskott-Aldrich syndrome (WAS), both of which used gamma -retroviral vectors, underscored that this type of toxicity can also apply to other disease settings.[5-7] In all these cases, insertion of the gamma -retroviral vector near known proto-oncogenes led to enhancer-mediated expression of these proto-oncogenes. proto-oncogenes. JF - Molecular Therapy AU - Corrigan-Curay, Jacqueline AU - Cohen-Haguenauer, Odile AU - O'Reilly, Marina AU - Ross, Susan R AU - Fan, Hung AU - Rosenberg, Naomi AU - Somia, Nikunj AU - King, Nancy AU - Friedmann, Theodore AU - Dunbar, Cynthia AD - Office of Biotechnology Activities, Office of the Director, National Institutes of Health, Bethesda, Maryland, USA Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 1084 EP - 1094 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 20 IS - 6 SN - 1525-0016, 1525-0016 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Gene therapy KW - Genotoxicity KW - X chromosome KW - Expression vectors KW - Myelodysplastic syndrome KW - Wiskott-Aldrich syndrome KW - Leukemia KW - Stem cells KW - insertional mutagenesis KW - Severe combined immunodeficiency KW - Chronic granulomatous disease KW - Proto-oncogenes KW - Adenosine deaminase KW - W 30905:Medical Applications KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668266892?accountid=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=Challenges+in+Vector+and+Trial+Design+Using+Retroviral+Vectors+for+Long-Term+Gene+Correction+in+Hematopoietic+Stem+Cell+Gene+Therapy&rft.au=Corrigan-Curay%2C+Jacqueline%3BCohen-Haguenauer%2C+Odile%3BO%27Reilly%2C+Marina%3BRoss%2C+Susan+R%3BFan%2C+Hung%3BRosenberg%2C+Naomi%3BSomia%2C+Nikunj%3BKing%2C+Nancy%3BFriedmann%2C+Theodore%3BDunbar%2C+Cynthia&rft.aulast=Corrigan-Curay&rft.aufirst=Jacqueline&rft.date=2012-06-01&rft.volume=20&rft.issue=6&rft.spage=1084&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2012.93 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Gene therapy; X chromosome; Genotoxicity; Expression vectors; Leukemia; Wiskott-Aldrich syndrome; Myelodysplastic syndrome; Stem cells; insertional mutagenesis; Severe combined immunodeficiency; Chronic granulomatous disease; Proto-oncogenes; Adenosine deaminase DO - http://dx.doi.org/10.1038/mt.2012.93 ER - TY - JOUR T1 - Isolating neural components of threat bias in pediatric anxiety AN - 1550985420; 201424873 AB - Background: Attention biases toward threat are often detected in individuals with anxiety disorders. Threat biases can be measured experimentally through dot-probe paradigms, in which individuals detect a probe following a stimulus pair including a threat. On these tasks, individuals with anxiety tend to detect probes that occur in a location previously occupied by a threat (i.e., congruent) faster than when opposite threats (i.e., incongruent). In pediatric anxiety disorders, dot-probe paradigms detect abnormal attention biases toward threat and abnormal ventrolateral prefrontal cortex (vlPFC) function. However, it remains unclear if this aberrant vlPFC activation occurs while subjects process threats (e.g., angry faces) or, alternatively, while they process and respond to probes. This magnetoencephalography (MEG) study was designed to answer this question. Methods: Adolescents with either generalized anxiety disorder (GAD, n=17) or no psychiatric diagnosis (n=25) performed a dot-probe task involving angry and neutral faces while MEG data were collected. Synthetic Aperture Magnetometry (SAM) beamformer technique was used to determine whether there were group differences in power ratios while subjects processed threats (i.e., angry vs. neutral faces) or when subjects responded to incongruent versus. congruent probes. Results: Group differences in vlPFC activation during the response period emerged with a 1-30Hz frequency band. No group differences in vlPFC activation were detected in response to angry-face cues. Conclusions: In the dot-probe task, anxiety-related perturbations in vlPFC activation reflect abnormal attention control when responding to behaviorally relevant probes, but not to angry faces. Given that motor responses to these probes are used to calculate threat bias, this study provides insight into the pathophysiology reflected in this commonly used marker of anxiety. In addition, this finding may inform the development of novel anxiety-disorder treatments targeting the vlPFC to enhance attention control to task-relevant demands. Adapted from the source document. JF - The Journal of Child Psychology and Psychiatry AU - Britton, Jennifer C AU - Bar-Haim, Yair AU - Carver, Frederick W AU - Holroyd, Tom AU - Norcross, Maxine A AU - Detloff, Allison AU - Leibenluft, Ellen AU - Ernst, Monique AU - Pine, Daniel S AD - Section on Development and Affective Neuroscience, National Institute of Mental Health, Bethesda, MD, USA Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 678 EP - 686 PB - Blackwell Publishing, Oxford UK VL - 53 IS - 6 SN - 0021-9630, 0021-9630 KW - Paediatrics KW - Generalized anxiety disorders KW - Anxiety disorders KW - Bias KW - Anger KW - Models KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1550985420?accountid=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=Isolating+neural+components+of+threat+bias+in+pediatric+anxiety&rft.au=Britton%2C+Jennifer+C%3BBar-Haim%2C+Yair%3BCarver%2C+Frederick+W%3BHolroyd%2C+Tom%3BNorcross%2C+Maxine+A%3BDetloff%2C+Allison%3BLeibenluft%2C+Ellen%3BErnst%2C+Monique%3BPine%2C+Daniel+S&rft.aulast=Britton&rft.aufirst=Jennifer&rft.date=2012-06-01&rft.volume=53&rft.issue=6&rft.spage=678&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Child+Psychology+and+Psychiatry&rft.issn=00219630&rft_id=info:doi/10.1111%2Fj.1469-7610.2011.02503.x LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-08-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JPPDAI N1 - SubjectsTermNotLitGenreText - Anger; Paediatrics; Generalized anxiety disorders; Models; Bias; Anxiety disorders DO - http://dx.doi.org/10.1111/j.1469-7610.2011.02503.x ER - TY - JOUR T1 - Schistosomiasis and bladder cancer: similarities and differences from urothelial cancer AN - 1520379712; 16864329 AB - Through the years, schistosoma-associated bladder cancer was believed to be a unique entity of disease, different from urothelial cancer. As carcinogenesis is a highly complex process resulting from the accumulation of many genetic and epigenetic changes leading to alterations in the cell proliferation and regulation process, confirmation of their minute differences or similarities are extremely difficult. In bladder cancer, many of these carcinogenic cascades were not fully documented in spite of the efforts undertaken. The control of schistosomiasis and the subsequent decrease in the intensity of infestation showed feature changes approaching that of urothelial tumors. However, schistosoma-associated bladder cancer still presents in more advanced stages than schistosoma-non-associated urothelial cancer. Furthermore, many data were collected proving 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 the different etiologies. JF - Expert Review of Anticancer Therapy AU - Zaghloul, Mohamed S AU - Gouda, Iman AD - Radiation Oncology and Pathology Departments, Children's Cancer Hospital and National Cancer Institute, 1 Sekket El Emmam, El Sayeda Zainab, Cairo University, Cairo, Egypt, mszagh@yahoo.com Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 753 EP - 763 PB - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom VL - 12 IS - 6 SN - 1473-7140, 1473-7140 KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality KW - bilharziasis KW - biology KW - bladder cancer KW - chemotherapy KW - cytogenetics KW - pathology KW - radical cystectomy KW - radiotherapy KW - schistosomiasis KW - Infestation KW - Bladders KW - Schistosoma KW - Carcinogenesis KW - Disease control KW - Therapy KW - Schistosomiasis KW - Tumours KW - Aetiology KW - Q1 08485:Species interactions: pests and control KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520379712?accountid=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=Expert+Review+of+Anticancer+Therapy&rft.atitle=Schistosomiasis+and+bladder+cancer%3A+similarities+and+differences+from+urothelial+cancer&rft.au=Zaghloul%2C+Mohamed+S%3BGouda%2C+Iman&rft.aulast=Zaghloul&rft.aufirst=Mohamed&rft.date=2012-06-01&rft.volume=12&rft.issue=6&rft.spage=753&rft.isbn=&rft.btitle=&rft.title=Expert+Review+of+Anticancer+Therapy&rft.issn=14737140&rft_id=info:doi/10.1586%2Fera.12.49 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Number of references - 94 N1 - Last updated - 2014-12-11 N1 - SubjectsTermNotLitGenreText - Infestation; Bladders; Carcinogenesis; Therapy; Disease control; Schistosomiasis; Tumours; Aetiology; Schistosoma DO - http://dx.doi.org/10.1586/era.12.49 ER - TY - JOUR T1 - Global environmental health and sustainable development: the role at Rio+20 AN - 1494749407; 201401322 AB - The Rio+20 United Nations Conference on Sustainable Development represents a crucial opportunity to place environmental health at the forefront of the sustainable development agenda. Billions of people living in low- and middle-income countries continue to be afflicted by preventable diseases due to modifiable environmental exposures, causing needless suffering and perpetuating a cycle of poverty. Current processes of economic development, while alleviating many social and health problems, are increasingly linked to environmental health threats, ranging from air pollution and physical inactivity to global climate change. Sustainable development practices attempt to reduce environmental impacts and should, in theory, reduce adverse environmental health consequences compared to traditional development. Yet these efforts could also result in unintended harm and impaired economic development if the new 'Green Economy' is not carefully assessed for adverse environmental and occupational health impacts. The environmental health community has an essential role to play in underscoring these relationships as international leaders gather to craft sustainable development policies. Adapted from the source document. JF - Ciencia & Saude Coletiva AU - Furie, Gregg Lawrence AU - Balbus, John AD - Robert Wood Johnson Foundation Clinical Scholars Program, Yale School of Medicine, Yale University, Connecticut, USA Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 1427 EP - 1432 PB - ABRASCO, Rio De Janeiro Brazil VL - 17 IS - 6 SN - 1413-8123, 1413-8123 KW - sustainable development KW - environmental health KW - global health KW - climate change KW - Rio+20 KW - Suffering KW - Handicapped KW - Sustainable Development KW - Health Problems KW - Economic Development KW - Health KW - United Nations KW - Threat KW - Leadership KW - article KW - 2656: environmental interactions; environmental interactions UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1494749407?accountid=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=Ciencia+%26+Saude+Coletiva&rft.atitle=Global+environmental+health+and+sustainable+development%3A+the+role+at+Rio%2B20&rft.au=Furie%2C+Gregg+Lawrence%3BBalbus%2C+John&rft.aulast=Furie&rft.aufirst=Gregg&rft.date=2012-06-01&rft.volume=17&rft.issue=6&rft.spage=1427&rft.isbn=&rft.btitle=&rft.title=Ciencia+%26+Saude+Coletiva&rft.issn=14138123&rft_id=info:doi/10.1590%2FS1413-81232012000600007 LA - English DB - Sociological Abstracts N1 - Date revised - 2014-01-01 N1 - Last updated - 2016-09-28 N1 - SubjectsTermNotLitGenreText - Sustainable Development; Health Problems; Health; Economic Development; Leadership; Suffering; United Nations; Threat; Handicapped DO - http://dx.doi.org/10.1590/S1413-81232012000600007 ER - TY - JOUR T1 - Brilliant violet fluorophores: A new class of ultrabright fluorescent compounds for immunofluorescence experiments AN - 1492655101; 18967516 AB - The Nobel Prize in Chemistry was awarded in 2000 for the discovery of conductive organic polymers, which have subsequently been adapted for applications in ultrasensitive biological detection. Here, we report the first use of this new class of fluorescent probes in a diverse range of cytometric and imaging applications. We demonstrate that these "Brilliant Violet" reporters are dramatically brighter than other UV-violet excitable dyes, and are of similar utility to phycoerythrin (PE) and allophycocyanin (APC). They are thus ideally suited for cytometric assays requiring high sensitivity, such as MHC-multimer staining or detection of intracellular antigens. Furthermore, these reporters are sensitive and spectrally distinct options for fluorescence imaging, two-photon microscopy and imaging cytometry. These ultra-bright materials provide the first new high-sensitivity fluorescence probes in over 25 years and will have a dramatic impact on the design and implementation of multicolor panels for high-sensitivity immunofluorescence assays. Published 2012 Wiley Periodicals, Inc. JF - Cytometry Part A AU - Chattopadhyay, Pratip K AU - Gaylord, Brent AU - Palmer, Adrian AU - Jiang, Nan AU - Raven, Mary A AU - Lewis, Geoff AU - Reuter, Morgan A AU - Nur-ur Rahman, AKM AU - Price, David A AU - Betts, Michael R AU - Roederer, Mario AD - Sirigen, Ringwood, Hampshire, United Kingdom., pchattop@mail.nih.gov Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 456 EP - 466 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 81A IS - 6 SN - 1552-4922, 1552-4922 KW - Biotechnology and Bioengineering Abstracts KW - Cytometry KW - imaging KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1492655101?accountid=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=Brilliant+violet+fluorophores%3A+A+new+class+of+ultrabright+fluorescent+compounds+for+immunofluorescence+experiments&rft.au=Chattopadhyay%2C+Pratip+K%3BGaylord%2C+Brent%3BPalmer%2C+Adrian%3BJiang%2C+Nan%3BRaven%2C+Mary+A%3BLewis%2C+Geoff%3BReuter%2C+Morgan+A%3BNur-ur+Rahman%2C+AKM%3BPrice%2C+David+A%3BBetts%2C+Michael+R%3BRoederer%2C+Mario&rft.aulast=Chattopadhyay&rft.aufirst=Pratip&rft.date=2012-06-01&rft.volume=81A&rft.issue=6&rft.spage=456&rft.isbn=&rft.btitle=&rft.title=Cytometry+Part+A&rft.issn=15524922&rft_id=info:doi/10.1002%2Fcyto.a.22043 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-01-01 N1 - Last updated - 2014-02-11 N1 - SubjectsTermNotLitGenreText - imaging DO - http://dx.doi.org/10.1002/cyto.a.22043 ER - TY - JOUR T1 - Particulate-Bound Mercury (Hg[p]) Size Distributions in Central Taiwan AN - 1283715486; 17487303 AB - This study focuses on particulate-bound Hg (Hg[p]) composition (ng/g) (defined as ng/g), concentrations (ng/m super(3)) and dry deposition (ng/m super(2)*min) variations for PM sub(18), PM sub(10), PM sub(2.5), and PM sub(1.0). Three characteristic sampling sites collected 1-day ambient suspended particles during November and December 2010 using MOUDI-100S4 samplers. Additionally, Hg(p) size distributions are also characterized. Composition variations of Hg(p) in PM sub(18) were in the order of 0.158 plus or minus 0.055 ng/g (Quan-xing sampling site) > 0.086 plus or minus 0.097 ng/g (Hung-kuang sampling site) > 0.083 plus or minus 0.065 ng/g (Gao-mei sampling site). Further, composition variations of Hg(p) in PM sub(10) were in the order of 0.115 plus or minus 0.038 ng/g (Quan-xing site) > 0.107 plus or minus 0.080 ng/g (Gao-mei site) > 0.103 plus or minus 0.060 ng/g (Hung-kuang site). Composition variations of Hg(p) in PM sub(2.5) were in the order of 0.885 plus or minus 0.423 ng/g (Quan-xing site) > 0.458 plus or minus 0.105 ng/g (Gao-mei site) > 0.372 plus or minus 0.157 ng/g (Hung-kuang site). Finally, composition variations of Hg(p) in PM sub(1.0) were in the order of 0.913 plus or minus 0.441 ng/g (Quan-xing site) > 0.698 plus or minus 0.293 ng/g (Hung-kuang site) > 0.508 plus or minus 0.270 ng/g (Gao-mei site). The Hg(p) size distribution peaked at 1.0 mu m at the Quan-xin site, and the lowest average Hg(p) size distribution was 18 mu m at the Hung-kung site. The main possible sources for atmospheric particulate-bound mercury Hg(p) were likely from transportation, chemical plant and fossil fuel combustion (Fang et al., 2011). In addition to the above findings, other possible nearby sources at Taichung Thermal Power Plant (TTPP) and Central Taiwan Science Park (CTSP) were: steel industry, electronic industry, plastic industry, chemical industry, basic metal manufacturing, machinery manufacturing, coal products and petroleum. Our sampling sites were in the regions of all of the above sources. JF - Environmental Forensics AU - Chen, Shui-Jen AU - Lo, Chaur-Tsuen AU - Fang, Guor-Cheng AU - Huang, Ci-Song AD - Department of Environmental Engineering and Science, National Pingtung University of Science and Technology, Nei Pu, 91207, Ping Tun, Taiwan Y1 - 2012/06/01/ PY - 2012 DA - 2012 Jun 01 SP - 98 EP - 104 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 13 IS - 2 SN - 1527-5922, 1527-5922 KW - Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE) KW - Coal KW - Combustion KW - Concentration (composition) KW - Electronics KW - Mercury KW - Particle size distribution KW - Sampling KW - Thermoelectricity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1283715486?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvironmentalengabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Forensics&rft.atitle=Particulate-Bound+Mercury+%28Hg%5Bp%5D%29+Size+Distributions+in+Central+Taiwan&rft.au=Chen%2C+Shui-Jen%3BLo%2C+Chaur-Tsuen%3BFang%2C+Guor-Cheng%3BHuang%2C+Ci-Song&rft.aulast=Chen&rft.aufirst=Shui-Jen&rft.date=2012-06-01&rft.volume=13&rft.issue=2&rft.spage=98&rft.isbn=&rft.btitle=&rft.title=Environmental+Forensics&rft.issn=15275922&rft_id=info:doi/10.1080%2F15275922.2012.676602 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-01 N1 - Last updated - 2013-03-11 DO - http://dx.doi.org/10.1080/15275922.2012.676602 ER - TY - JOUR T1 - An Insight into the Sialotranscriptome of Triatoma matogrossensis, a Kissing Bug Associated with Fogo Selvagem in South America AN - 1113220867; 17254127 AB - Triatoma matogrossensis is a Hemiptera that belongs to the oliveirai complex, a vector of Chagas' disease that feeds on vertebrate blood in all life stages. Hematophagous insects' salivary glands (SGs) produce potent pharmacologic compounds that counteract host hemostasis, including anticlotting, antiplatelet, and vasodilatory molecules. Exposure to T. matogrossensis was also found to be a risk factor associated with the endemic form of the autoimmune skin disease pemphigus foliaceus, which is described in the same regions where Chagas' disease is observed in Brazil. To obtain a further insight into the salivary biochemical and pharmacologic diversity of this kissing bug and to identify possible allergens that might be associated with this autoimmune disease, a cDNA library from its SGs was randomly sequenced. We present the analysis of a set of 2,230 (SG) cDNA sequences, 1,182 of which coded for proteins of a putative secretory nature. JF - American Journal of Tropical Medicine and Hygiene AU - Assumpcao, TCF AU - Eaton, D P AU - Pham, V M AU - Francischetti, IMB AU - Aoki, V AU - Hans-Filho, G AU - Rivitti, E A AU - Valenzuela, J G AU - Diaz, LA AU - Ribeiro, JMC AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 12735 Twinbrook Parkway, Room 2E-32D, Rockville, MD 20892, USA, jribeiro@niaid.nih.gov Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 1005 EP - 1014 VL - 86 IS - 6 SN - 0002-9637, 0002-9637 KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Entomology Abstracts; Risk Abstracts KW - Biochemistry KW - Autoimmune diseases KW - Hosts KW - Salivary gland KW - Public health KW - Disease transmission KW - Endemic species KW - Allergens KW - Risk factors KW - Glands KW - Triatoma KW - Aquatic insects KW - Vectors KW - Developmental stages KW - Pemphigus foliaceus KW - Insects KW - Hemiptera KW - Blood KW - Skin diseases KW - hemostasis KW - Brazil KW - Species diversity KW - Proteins KW - Hygiene KW - Feeds KW - Chagas' disease KW - J 02410:Animal Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - Z 05350:Medical, Veterinary, and Agricultural Entomology KW - Q5 08524:Public health, medicines, dangerous organisms KW - K 03310:Genetics & Taxonomy KW - R2 23010:General: Models, forecasting UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1113220867?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=An+Insight+into+the+Sialotranscriptome+of+Triatoma+matogrossensis%2C+a+Kissing+Bug+Associated+with+Fogo+Selvagem+in+South+America&rft.au=Assumpcao%2C+TCF%3BEaton%2C+D+P%3BPham%2C+V+M%3BFrancischetti%2C+IMB%3BAoki%2C+V%3BHans-Filho%2C+G%3BRivitti%2C+E+A%3BValenzuela%2C+J+G%3BDiaz%2C+LA%3BRibeiro%2C+JMC&rft.aulast=Assumpcao&rft.aufirst=TCF&rft.date=2012-06-01&rft.volume=86&rft.issue=6&rft.spage=1005&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.2012.11-0690 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2016-03-17 N1 - SubjectsTermNotLitGenreText - Endemic species; Glands; Species diversity; Hosts; Hygiene; Aquatic insects; Disease transmission; Public health; Blood; Skin diseases; hemostasis; Risk factors; Allergens; Autoimmune diseases; Developmental stages; Vectors; Salivary gland; Pemphigus foliaceus; Chagas' disease; Biochemistry; Proteins; Insects; Feeds; Triatoma; Hemiptera; Brazil DO - http://dx.doi.org/10.4269/ajtmh.2012.11-0690 ER - TY - JOUR T1 - Geographic Variation in the Relationship between Human Lyme Disease Incidence and Density of Infected Host-Seeking Ixodes scapularis Nymphs in the Eastern United States AN - 1113218144; 17254137 AB - Prevention and control of Lyme disease is difficult because of the complex biology of the pathogen's (Borrelia burgdorferi) vector (Ixodes scapularis) and multiple reservoir hosts with varying degrees of competence. Cost-effective implementation of tick- and host-targeted control methods requires an understanding of the relationship between pathogen prevalence in nymphs, nymph abundance, and incidence of human cases of Lyme disease. We quantified the relationship between estimated acarological risk and human incidence using county-level human case data and nymphal prevalence data from field-derived estimates in 36 eastern states. The estimated density of infected nymphs (mDIN) was significantly correlated with human incidence (r = 0.69). The relationship was strongest in high-prevalence areas, but it varied by region and state, partly because of the distribution of B. burgdorferi genotypes. More information is needed in several high-prevalence states before DIN can be used for cost-effectiveness analyses. JF - American Journal of Tropical Medicine and Hygiene AU - Pepin, K M AU - Eisen, R J AU - Mead, P S AU - Piesman, J AU - Fish, D AU - Hoen, A G AU - Barbour, A G AU - Hamer, S AU - Diuk-Wasser, MA AD - Fogarty International Center, National Institutes of Health, 31 Center Drive, MSC 2220, Bethesda, MO 20892-2220, USA, uzu2@cdc.gov Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 1062 EP - 1071 VL - 86 IS - 6 SN - 0002-9637, 0002-9637 KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; Risk Abstracts KW - Data processing KW - Borrelia burgdorferi KW - Abundance KW - Vectors KW - Ixodes scapularis KW - Pathogens KW - Genotypes KW - Cost benefit analysis KW - USA KW - Prevention KW - Economics KW - Geographical variations KW - Reservoirs KW - Lyme disease KW - J 02410:Animal Diseases KW - R2 23060:Medical and environmental health KW - K 03420:Plant Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1113218144?accountid=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=Geographic+Variation+in+the+Relationship+between+Human+Lyme+Disease+Incidence+and+Density+of+Infected+Host-Seeking+Ixodes+scapularis+Nymphs+in+the+Eastern+United+States&rft.au=Pepin%2C+K+M%3BEisen%2C+R+J%3BMead%2C+P+S%3BPiesman%2C+J%3BFish%2C+D%3BHoen%2C+A+G%3BBarbour%2C+A+G%3BHamer%2C+S%3BDiuk-Wasser%2C+MA&rft.aulast=Pepin&rft.aufirst=K&rft.date=2012-06-01&rft.volume=86&rft.issue=6&rft.spage=1062&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.2012.11-0630 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Data processing; Abundance; Vectors; Genotypes; Geographical variations; Pathogens; Lyme disease; Prevention; Economics; Reservoirs; Cost benefit analysis; Borrelia burgdorferi; Ixodes scapularis; USA DO - http://dx.doi.org/10.4269/ajtmh.2012.11-0630 ER - TY - JOUR T1 - Regression analysis for a summed missing data problem under an outcome-dependent sampling scheme AN - 1112141450; 4349342 AB - // ABSTRACT IN ENGLISH: In this paper, we consider a regression analysis for a missing data problem in which the variables of primary interest are unobserved under a general biased sampling scheme, an outcome-dependent sampling (ODS) design. We propose a semiparametric empirical likelihood method for accessing the association between a continuous outcome response and unobservable interesting factors. Simulation study results show that ODS design can produce more efficient estimators than the simple random design of the same sample size. We demonstrate the proposed approach with a data set from an environmental study for the genetic effects on human lung function in COPD smokers. // ABSTRACT IN FRENCH: Dans cet article, nous considérons une analyse de régression pour un problème de données manquantes dans lequel les variables d'intérêt primaires sont non observées sous un plan échantillonnal général biaisé, le plan d'échantillonnage dépendant de la réponse (ODS). Nous proposons une méthode de vraisemblance semi-paramétrique empirique pour étudier l'association entre la variable réponse continue et les facteurs d'intérêt non observés. Les résultats d'une étude de simulation montrent que le plan ODS peut produire des estimateurs plus efficaces que le plan d'échantillonnage aléatoire simple pour la même taille échantillonnale. Nous illustrons l'approche proposée à l'aide d'un jeu de données provenant d'une étude environnementale sur l'effet génétique pour la fonction pulmonaire chez les fumeurs ayant une bronchopneumopathie chronique obstructive. JF - Canadian journal of statistics AU - Ding, Jieli AU - Liu, Yanyan AU - Peden, David B AU - Kleeberger, Steven R AU - Zhou, Haibo AD - University of North Carolina, Chapel Hill ; National Institute of Environmental Health Sciences, USA Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 282 EP - 303 VL - 40 IS - 2 SN - 0319-5724, 0319-5724 KW - Economics KW - Lung function KW - Smoking KW - Regression analysis KW - Simulation KW - Maximum likelihood method KW - Estimation KW - Data analysis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1112141450?accountid=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=Regression+analysis+for+a+summed+missing+data+problem+under+an+outcome-dependent+sampling+scheme&rft.au=Ding%2C+Jieli%3BLiu%2C+Yanyan%3BPeden%2C+David+B%3BKleeberger%2C+Steven+R%3BZhou%2C+Haibo&rft.aulast=Ding&rft.aufirst=Jieli&rft.date=2012-06-01&rft.volume=40&rft.issue=2&rft.spage=282&rft.isbn=&rft.btitle=&rft.title=Canadian+journal+of+statistics&rft.issn=03195724&rft_id=info:doi/10.1002%2Fcjs.11131 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2013-06-12 N1 - Last updated - 2013-09-16 N1 - SubjectsTermNotLitGenreText - 10739 12228 10919; 7837 8160 8163 12230; 11755 5707 6071 1542 11325; 3279 971 3286; 11670; 4403 7854 DO - http://dx.doi.org/10.1002/cjs.11131 ER - TY - JOUR T1 - Hazard Ratio Estimation for Biomarker-Calibrated Dietary Exposures AN - 1093454808; 16887382 AB - Summary Uncertainty concerning the measurement error properties of self-reported diet has important implications for the reliability of nutritional epidemiology reports. Biomarkers based on the urinary recovery of expended nutrients can provide an objective measure of short-term nutrient consumption for certain nutrients and, when applied to a subset of a study cohort, can be used to calibrate corresponding self-report nutrient consumption assessments. A nonstandard measurement error model that makes provision for systematic error and subject-specific error, along with the usual independent random error, is needed for the self-report data. Three estimation procedures for hazard ratio (Cox model) parameters are extended for application to this more complex measurement error structure. These procedures are risk set regression calibration, conditional score, and nonparametric corrected score. An estimator for the cumulative baseline hazard function is also provided. The performance of each method is assessed in a simulation study. The methods are then applied to an example from the Women's Health Initiative Dietary Modification Trial. JF - Biometrics AU - Shaw, Pamela A AU - Prentice, Ross L AD - Biostatistics Research Branch, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892, U.S.A. Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 397 EP - 407 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 68 IS - 2 SN - 0006-341X, 0006-341X KW - Health & Safety Science Abstracts KW - Bioindicators KW - Diets KW - H 12000:Epidemiology and Public Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1093454808?accountid=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=Biometrics&rft.atitle=Hazard+Ratio+Estimation+for+Biomarker-Calibrated+Dietary+Exposures&rft.au=Shaw%2C+Pamela+A%3BPrentice%2C+Ross+L&rft.aulast=Shaw&rft.aufirst=Pamela&rft.date=2012-06-01&rft.volume=68&rft.issue=2&rft.spage=397&rft.isbn=&rft.btitle=&rft.title=Biometrics&rft.issn=0006341X&rft_id=info:doi/10.1111%2Fj.1541-0420.2011.01690.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Document feature - figure 0 N1 - Last updated - 2014-02-21 N1 - SubjectsTermNotLitGenreText - Diets DO - http://dx.doi.org/10.1111/j.1541-0420.2011.01690.x ER - TY - JOUR T1 - Precursor ion exclusion for enhanced identification of plasma biomarkers AN - 1069201109; 17140177 AB - Purpose: Our study aims to establish a plasma biomarker analysis workflow, with fewer fractionation steps, for enhanced identification of plasma biomarkers by precursor ion exclusion (PIE). Experimental design: Plasma samples were depleted for highly abundant proteins, then further fractionated by molecular weight (MW), before trypsinization for LTQ-Orbitrap mass analysis. Data-dependent acquisition (DDA) was used for baseline analysis. PIE involves the re-injection of samples with exclusion of the previously identified peptides. We compared analyses using multiple PIE iterations, compared to DDA, for plasma interrogation Results: A higher percentage of unique plasma peptides was identified with PIE, compared to DDA. The first PIE iteration reveals an increase of 75-112% more peptides than the DDA method alone. PIE can interrogate complex plasma samples with the percentage of peptides identified successively increasing with even greater than or equal to 4 iterations. The total number of peptides identified increases rapidly across the first three PIE iterations and then continues more slowly up to nine iterations. Conclusions and clinical relevance: Iterative injections with PIE resulted in many more peptide identifications in plasma samples of varying degrees of complexity, compared to re-injections using similar DDA parameters. PIE methods may therefore expand our ability to recover plasma peptides for plasma biomarker discovery. JF - Proteomics Clinical Applications AU - Wu, W W AU - Shen, R-F AU - Park, S-S AU - Martin, B AU - Maudsley, S AD - Receptor Pharmacology Unit, National Institute on Aging, National Institutes of Health, 251 Bayview Blvd., Baltimore, MD 21224, USA, maudsleyst@grc.nia.nih.gov Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 304 EP - 308 VL - 6 IS - 5-6 SN - 1862-8346, 1862-8346 KW - Biotechnology and Bioengineering Abstracts KW - Molecular weight KW - Therapeutic applications KW - biomarkers KW - proteomics KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1069201109?accountid=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+Clinical+Applications&rft.atitle=Precursor+ion+exclusion+for+enhanced+identification+of+plasma+biomarkers&rft.au=Wu%2C+W+W%3BShen%2C+R-F%3BPark%2C+S-S%3BMartin%2C+B%3BMaudsley%2C+S&rft.aulast=Wu&rft.aufirst=W&rft.date=2012-06-01&rft.volume=6&rft.issue=5-6&rft.spage=304&rft.isbn=&rft.btitle=&rft.title=Proteomics+Clinical+Applications&rft.issn=18628346&rft_id=info:doi/10.1002%2Fprca.201100107 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-09-01 N1 - Last updated - 2012-10-08 N1 - SubjectsTermNotLitGenreText - Molecular weight; Therapeutic applications; proteomics; biomarkers DO - http://dx.doi.org/10.1002/prca.201100107 ER - TY - JOUR T1 - Application of systems biology principles to protein biomarker discovery: Urinary exosomal proteome in renal transplantation AN - 1069196829; 17140173 AB - Purpose: In mass spectrometry (MS)-based studies to discover urinary protein biomarkers, an important question is how to analyze the data to find the most promising potential biomarkers to be advanced to large-scale validation studies. Here, we describe a "systems biology-based" approach to address this question. Experimental design: We analyzed large-scale liquid chromatography-tandem mass spectrometry (LC-MS/MS) data of urinary exosomes from renal allograft recipients with biopsy-proven evidence of immunological rejection or tubular injury (TI). We asked whether bioinformatic analysis of urinary exosomal proteins can identify biological-process based protein groups that correlate with biopsy findings and whether the protein groups fit with general knowledge of the pathophysiological mechanisms involved. Results: LC-MS/MS analysis of urinary exosomal proteomes identified more than 1000 proteins in each pathologic group. These protein lists were analyzed computationally to identify the Biological Process and Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathway terms that are significantly associated with each pathological group. Among the most informative terms for each group were: "sodium ion transport" for TI; "immune response" for all rejection; "epithelial cell differentiation" for cell-mediated rejection; and "acute inflammatory response" for antibody-mediated rejection. Based on these terms, candidate biomarkers were identified using a novel strategy to allow a dichotomous classification between different pathologic categories. Conclusions and clinical relevance: The terms and candidate biomarkers identified make rational connections to pathophysiological mechanisms, suggesting that the described bioinformatic approach will be useful in advancing large-scale biomarker identification studies toward a validation phase. JF - Proteomics Clinical Applications AU - Pisitkun, T AU - Gandolfo, M T AU - Das, S AU - Knepper, MA AU - Bagnasco, S M AD - Epithelial Systems Biology Laboratory, Building 10, Room 6N260, National Institutes of Health, Bethesda, MD 20892-1603, USA, knepperm@nhlbi.nih.gov Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 268 EP - 278 VL - 6 IS - 5-6 SN - 1862-8346, 1862-8346 KW - Biotechnology and Bioengineering Abstracts KW - Bioinformatics KW - Biopsy KW - Data processing KW - Differentiation KW - Epithelial cells KW - Genomes KW - Graft rejection KW - Immune response KW - Inflammation KW - Injuries KW - Kidney transplantation KW - Mass spectroscopy KW - Sodium KW - Therapeutic applications KW - biomarkers KW - exosomes KW - proteomics KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1069196829?accountid=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+Clinical+Applications&rft.atitle=Application+of+systems+biology+principles+to+protein+biomarker+discovery%3A+Urinary+exosomal+proteome+in+renal+transplantation&rft.au=Pisitkun%2C+T%3BGandolfo%2C+M+T%3BDas%2C+S%3BKnepper%2C+MA%3BBagnasco%2C+S+M&rft.aulast=Pisitkun&rft.aufirst=T&rft.date=2012-06-01&rft.volume=6&rft.issue=5-6&rft.spage=268&rft.isbn=&rft.btitle=&rft.title=Proteomics+Clinical+Applications&rft.issn=18628346&rft_id=info:doi/10.1002%2Fprca.201100108 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-09-01 N1 - Last updated - 2012-10-08 N1 - SubjectsTermNotLitGenreText - Genomes; Epithelial cells; Data processing; Injuries; Graft rejection; exosomes; Kidney transplantation; Therapeutic applications; Biopsy; biomarkers; Mass spectroscopy; Inflammation; Sodium; Differentiation; Bioinformatics; Immune response; proteomics DO - http://dx.doi.org/10.1002/prca.201100108 ER - TY - JOUR T1 - Events, politics and patterns of policy-making: impact of major incidents on health sector regulatory reforms in the UK and Japan AN - 1040990802; 4335300 AB - This article examines the major malpractice incidents in the late 1990s through early 2000s in the UK and Japan, comparing how these incidents opened up pathways for a new type of hospital regulation in each case. Applying John Kingdon's three-stream model of agenda-setting and policy change, the article argues that governance arrangements as well as the policy instruments that a government has at its disposal determine how an event could be translated into a political agenda by throwing light on the problems within the public domain. The long-term effect of such adverse events is therefore determined by how open the relevant institutional arrangements are, and is enhanced if actors constantly scrutinize the system by proactively setting the agenda. A higher level of political accountability in the UK led to British politicians taking a greater role in promoting patient-led reforms than Japanese counterparts. However, a political system with clear accountability is more conscious of its own involvement and any potential blame it might receive for policy failures. Therefore, the political class could become more engaged in continuous reforms and the delegation of tasks rather than a constant search for remedial actions. The article sheds light on the interactive aspects of the particular triggering events discussed through the decade of regulatory developments in the two health-care systems. Reprinted by permission of Blackwell Publishers JF - Social policy and administration AU - Kodate, Naonori AD - National Institutes of Health Research Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 280 EP - 301 VL - 46 IS - 3 SN - 0144-5596, 0144-5596 KW - Political Science KW - Health care KW - Political reform KW - Public sphere KW - Policy making KW - Japan KW - United Kingdom KW - Framing KW - Political systems KW - Politicians UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1040990802?accountid=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=Social+policy+and+administration&rft.atitle=Events%2C+politics+and+patterns+of+policy-making%3A+impact+of+major+incidents+on+health+sector+regulatory+reforms+in+the+UK+and+Japan&rft.au=Kodate%2C+Naonori&rft.aulast=Kodate&rft.aufirst=Naonori&rft.date=2012-06-01&rft.volume=46&rft.issue=3&rft.spage=280&rft.isbn=&rft.btitle=&rft.title=Social+policy+and+administration&rft.issn=01445596&rft_id=info:doi/10.1111%2Fj.1467-9515.2011.00814.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 - 9625 9628; Framing; 10488; 9807 9637; 9796; 9763 9653 10691; 5775 13521; 438 462 129 302; 191 300 30 DO - http://dx.doi.org/10.1111/j.1467-9515.2011.00814.x ER - TY - JOUR T1 - The potential use of toxin antibodies as a strategy for controlling acute Staphylococcus aureus infections AN - 1038604610; 16919435 AB - Introduction: The pandemic human pathogen, Staphylococcus aureus, displays high levels of antibiotic resistance and is a major cause of hospital- and community-associated infections. S. aureus disease manifestation is to a great extent due to the production of a large arsenal of virulence factors, which include a series of secreted toxins. Antibodies to S. aureus toxins are found in people who are infected or asymptomatically colonized with S. aureus. Immunotherapies consisting of neutralizing anti-toxin antibodies could provide immediate aid to patients with impaired immune systems or in advanced stages of disease. Areas covered: Important S. aureus toxins, their roles in pathogenesis, rationales for selecting S. aureus toxins for immunization efforts, and caveats associated with monoclonal antibody-based passive immunization are discussed. This review will focus on hyper-virulent community-associated methicillin-resistant S. aureus because of their recent surge and clinical importance. Expert opinion: Antibodies against genome-encoded toxins may be more broadly applicable than those directed against toxins found only in a sub-population of S. aureus isolates. Furthermore, there is substantial functional redundancy among S. aureus toxins. Thus, an optimal anti-S. aureus formulation may consist of multiple antibodies directed against a series of key S. aureus genome-encoded toxins. JF - Expert Opinion on Therapeutic Targets AU - Cheung, Gordon Yc AU - Otto, Michael AD - Laboratory of Human Bacterial Pathogenesis, NIAID, NIH, Bldg. 33, Room 1W10, 9000 Rockville Pike, Bethesda, MD 20892, USA +1 301 443 5209, motto@niaid.nih.gov Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 601 EP - 612 PB - Ashley Publications Ltd., Unitec House, 3rd Floor London, N3 1QB United Kingdom VL - 16 IS - 6 SN - 1472-8222, 1472-8222 KW - Toxicology Abstracts; Microbiology Abstracts B: Bacteriology KW - virulence factors KW - Immune system KW - Immunotherapy KW - Drug resistance KW - Pathogens KW - Infection KW - Toxins KW - Antibodies KW - pandemics KW - Reviews KW - Immunization (passive) KW - Staphylococcus aureus KW - Antibiotic resistance KW - X 24310:Pharmaceuticals KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1038604610?accountid=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+Therapeutic+Targets&rft.atitle=The+potential+use+of+toxin+antibodies+as+a+strategy+for+controlling+acute+Staphylococcus+aureus+infections&rft.au=Cheung%2C+Gordon+Yc%3BOtto%2C+Michael&rft.aulast=Cheung&rft.aufirst=Gordon&rft.date=2012-06-01&rft.volume=16&rft.issue=6&rft.spage=601&rft.isbn=&rft.btitle=&rft.title=Expert+Opinion+on+Therapeutic+Targets&rft.issn=14728222&rft_id=info:doi/http%3A%2F%2Fdx.doi.org%2F10.1517%2F14728222.2012.682573 L2 - http://www.ingentaconnect.com/content/apl/ett/2012/00000016/00000006/art00007 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-09-01 N1 - Last updated - 2013-10-21 N1 - SubjectsTermNotLitGenreText - pandemics; Antibodies; virulence factors; Drug resistance; Reviews; Immunotherapy; Immune system; Immunization (passive); Pathogens; Infection; Antibiotic resistance; Toxins; Staphylococcus aureus DO - http://dx.doi.org/10.1517/14728222.2012.682573 ER - TY - JOUR T1 - Molecular Analysis of Mitochondrial Compromise in Rodent Cardiomyocytes Exposed Long Term to Nucleoside Reverse Transcriptase Inhibitors (NRTIs) AN - 1034823212; 17048614 AB - Despite the highly effective impact of NRTI therapy in patients infected with the human immunodeficiency virus type 1 (HIV-1), long-term treatment has revealed cardiotoxicity, considered to be due to mitochondrial dysfunction. To evaluate mitochondrial damage, and design therapeutic interventions, we established cultures of rat H9c2 and mouse HL-1 cardiomyocytes and exposed them to the NRTIs zidovudine (AZT), and AZT plus didanosine (ddI). Proliferation assays showed that H9c2 cells grew well in 50 mu M AZT and 50 mu M AZT/50 mu M ddI and that HL-1 cells grew well in 10 mu M AZT and 10 mu M AZT/10 mu M ddI. Both types of cells were exposed to the drugs for 39 passages (P), and mitochondrial integrity in the form of oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) was examined by Seahorse XF24 analyzer. In NRTI-exposed H9c2 cells at most passages, OCR was reduced, in both the basal and uncoupled states, compared to unexposed controls (P < 0.05). NRTI-exposed HL-1 cells showed a different pattern of mitochondrial compromise, with inhibition of OCR, in basal and uncoupled cells, occurring largely before P14 and after P17 (P < 0.05). The ECAR response in uncoupled cells of both types was unchanged at early passages, but increased after P18 (P < 0.05). Evaluation of mitochondrial biogenesis in H9c2 cells revealed reduction before P29, no change at P29, and reduction at P39 in NRTI-exposed cells, compared to unexposed cells (P < 0.05). Western blotting of transcription factors critical for mitochondrial biogenesis, PGC-1 alpha , Nrf-1 and mtTFA, showed downregulation in NRTI-exposed H9c2 cells compared to unexposed controls. In addition, electron microscopy (EM) revealed increasing mitochondrial morphological damage in H9c2 cells over passages. For both cell types, AZT/ddI was more damaging than AZT alone. These studies demonstrate progressive mitochondrial compromise in cardiomyocytes-exposed long term, and the model will be used to evaluate potentially protective intervention strategies. JF - Cardiovascular Toxicology AU - Liu, Yongmin AU - Nguyen, Phuonggiang AU - Baris, Tara Z AU - Poirier, Miriam C AD - Carcinogen-DNA Interactions Section, Laboratory of Cancer Biology and Genetics, CCR, National Cancer Institute, Bldg 37 Rm 4032, NIH, 37 Convent Drive, MSC-4255, Bethesda, MD, 20892-4255, USA, yongminl@mail.nih.gov Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 123 EP - 134 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 12 IS - 2 SN - 1530-7905, 1530-7905 KW - Biochemistry Abstracts 2: Nucleic Acids; Toxicology Abstracts KW - Acidification KW - Cell culture KW - Cell proliferation KW - Didanosine KW - Drugs KW - Electron microscopy KW - Mitochondria KW - Oxygen consumption KW - PGC-1 protein KW - Therapeutic applications KW - Transcription factors KW - Western blotting KW - Zidovudine KW - cardiomyocytes KW - nucleoside reverse transcriptase inhibitors KW - Human immunodeficiency virus 1 KW - N 14840:Antisense, Nucleotide Analogs KW - X 24310:Pharmaceuticals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1034823212?accountid=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=Cardiovascular+Toxicology&rft.atitle=Molecular+Analysis+of+Mitochondrial+Compromise+in+Rodent+Cardiomyocytes+Exposed+Long+Term+to+Nucleoside+Reverse+Transcriptase+Inhibitors+%28NRTIs%29&rft.au=Liu%2C+Yongmin%3BNguyen%2C+Phuonggiang%3BBaris%2C+Tara+Z%3BPoirier%2C+Miriam+C&rft.aulast=Liu&rft.aufirst=Yongmin&rft.date=2012-06-01&rft.volume=12&rft.issue=2&rft.spage=123&rft.isbn=&rft.btitle=&rft.title=Cardiovascular+Toxicology&rft.issn=15307905&rft_id=info:doi/10.1007%2Fs12012-011-9148-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-08-01 N1 - Last updated - 2012-10-19 N1 - SubjectsTermNotLitGenreText - Oxygen consumption; Western blotting; Therapeutic applications; Mitochondria; Zidovudine; Cell culture; cardiomyocytes; Didanosine; Transcription factors; Acidification; PGC-1 protein; Cell proliferation; Drugs; Electron microscopy; nucleoside reverse transcriptase inhibitors; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1007/s12012-011-9148-5 ER - TY - JOUR T1 - Caffeine Intake, Smoking, and Risk of Parkinson Disease in Men and Women AN - 1028035714; 16838097 AB - The authors prospectively examined whether caffeine intake was associated with lower risk of Parkinson disease (PD) in both men and women among 304,980 participants in the National Institutes of Health-AARP Diet and Health Study and whether smoking affected this relation. Multivariate odds ratios and 95% confidence intervals were derived from logistic regression models. Higher caffeine intake as assessed in 1995-1996 was monotonically associated with lower PD risk (diagnosed in 2000-2006) in both men and women. After adjustment for age, race, and physical activity, the odds ratio comparing the highest quintile of caffeine intake with the lowest was 0.75 (95% confidence interval: 0.60, 0.94; P sub(trend) = 0.005) for men and 0.60 (95% confidence interval: 0.39, 0.91; P sub(trend) = 0.005) for women. Further adjustment for duration of smoking and analyses carried out among never smokers showed similar results. A joint analysis with smoking suggested that smoking and caffeine may act independently in relation to PD risk. Finally, the authors conducted a meta-analysis of prospective studies and confirmed that caffeine intake was inversely associated with PD risk in both men and women. These findings suggest no gender difference in the relation between caffeine and PD. JF - American Journal of Epidemiology AU - Liu, Rui AU - Guo, Xuguang AU - Park, Yikyung AU - Huang, Xuemei AU - Sinha, Rashmi AU - Freedman, Neal D AU - Hollenbeck, Albert R AU - Blair, Aaron AU - Chen, Honglei Y1 - 2012/06/01/ PY - 2012 DA - 2012 Jun 01 SP - 1200 EP - 1207 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 175 IS - 11 SN - 0002-9262, 0002-9262 KW - CSA Neurosciences Abstracts; Risk Abstracts; Health & Safety Science Abstracts KW - Diets KW - Age KW - caffeine KW - Males KW - Physical activity KW - Parkinson's disease KW - Sex differences KW - Models KW - Smoking KW - Neurodegenerative diseases KW - Movement disorders KW - Reviews KW - Risk factors KW - Gender KW - Regression analysis KW - Caffeine KW - Females KW - Races KW - N3 11028:Neuropharmacology & toxicology KW - H 12000:Epidemiology and Public Health KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028035714?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Epidemiology&rft.atitle=Caffeine+Intake%2C+Smoking%2C+and+Risk+of+Parkinson+Disease+in+Men+and+Women&rft.au=Liu%2C+Rui%3BGuo%2C+Xuguang%3BPark%2C+Yikyung%3BHuang%2C+Xuemei%3BSinha%2C+Rashmi%3BFreedman%2C+Neal+D%3BHollenbeck%2C+Albert+R%3BBlair%2C+Aaron%3BChen%2C+Honglei&rft.aulast=Liu&rft.aufirst=Rui&rft.date=2012-06-01&rft.volume=175&rft.issue=11&rft.spage=1200&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Epidemiology&rft.issn=00029262&rft_id=info:doi/10.1093%2Faje%2Fkwr451 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2013-11-04 N1 - SubjectsTermNotLitGenreText - Diets; Age; Parkinson's disease; Physical activity; Sex differences; Models; Neurodegenerative diseases; Smoking; Movement disorders; Risk factors; Reviews; Regression analysis; Caffeine; Races; caffeine; Males; Gender; Females DO - http://dx.doi.org/10.1093/aje/kwr451 ER - TY - JOUR T1 - Tumors and proliferative lesions in adult offspring after maternal exposure to methylarsonous acid during gestation in CD1 mice AN - 1028035283; 16824565 AB - Developmental exposure to inorganic arsenic is carcinogenic in humans and mice, and adult offspring of mice exposed to inorganic arsenic can develop tumors of the lung, liver, adrenal, uterus, and ovary. It has been suggested that methylarsonous acid (MMA3+), a product of the biological methylation of inorganic arsenic, could be a key carcinogenic species. Thus, pregnant CD1 mice were provided drinking water containing MMA3+ at 0 (control), 12.5, or 25 parts per million (ppm) from gestational days 8 to 18. Tumors were assessed in groups of male or female (initial n = 25) offspring up to 2 years of age. In utero treatment had no effect on survival or body weights. Female offspring exhibited increases in total epithelial uterine tumors (control 0%; 12.5 ppm 26%; 25 ppm 30%), oviduct hyperplasia (control 4%; 12.5 ppm 35%; 25 ppm 43%), adrenal cortical adenoma at 25 ppm (control 0%; 12.5 ppm 9%; 25 ppm 26%), and total epithelial ovarian tumors (control 0%; 12.5 ppm 39%; 25 ppm 26%). Male offspring showed dose-related increases in hepatocellular carcinoma (control 0%; 12.5 ppm 12%; 25 ppm 22%), adrenal adenoma (control 0%; 12.5 ppm 28%; 25 ppm 17%), and lung adenocarcinoma (control 17%; 12.5 ppm 44%). Male offspring had unusual testicular lesions, including two rete testis carcinomas, two adenomas, and three interstitial cell tumors. Overall, maternal consumption of MMA3+ during pregnancy in CD1 mice produced some similar proliferative lesions as gestationally applied inorganic arsenic in the offspring during adulthood. JF - Archives of Toxicology AU - Tokar, Erik J AU - Diwan, Bhalchandra A AU - Thomas, David J AU - Waalkes, Michael P AD - Inorganic Toxicology Group, National Toxicology Program Laboratory Branch, Division of the National Toxicology Program, The National Institute of Environmental Health Sciences, 111 Alexander Drive, P.O. Box 12233, MD E1-07, Research Triangle Park, NC, 27709, USA, waalkes@niehs.nih.gov Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 975 EP - 982 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 86 IS - 6 SN - 0340-5761, 0340-5761 KW - Toxicology Abstracts KW - Testes KW - Uterus KW - Arsenic KW - Tumors KW - Pregnancy KW - Carcinoma KW - Hyperplasia KW - Cortex KW - Oviduct KW - Lung KW - Interstitial cells KW - Gestation KW - Progeny KW - Ovaries KW - Drinking water KW - Adenocarcinoma KW - Methylation KW - Adenoma KW - Hepatocellular carcinoma KW - X 24360:Metals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028035283?accountid=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=Tumors+and+proliferative+lesions+in+adult+offspring+after+maternal+exposure+to+methylarsonous+acid+during+gestation+in+CD1+mice&rft.au=Tokar%2C+Erik+J%3BDiwan%2C+Bhalchandra+A%3BThomas%2C+David+J%3BWaalkes%2C+Michael+P&rft.aulast=Tokar&rft.aufirst=Erik&rft.date=2012-06-01&rft.volume=86&rft.issue=6&rft.spage=975&rft.isbn=&rft.btitle=&rft.title=Archives+of+Toxicology&rft.issn=03405761&rft_id=info:doi/10.1007%2Fs00204-012-0820-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2013-11-04 N1 - SubjectsTermNotLitGenreText - Testes; Arsenic; Uterus; Tumors; Carcinoma; Pregnancy; Hyperplasia; Oviduct; Cortex; Interstitial cells; Lung; Gestation; Progeny; Ovaries; Adenocarcinoma; Drinking water; Adenoma; Methylation; Hepatocellular carcinoma DO - http://dx.doi.org/10.1007/s00204-012-0820-8 ER - TY - JOUR T1 - Candidate Antibody-Based Therapeutics Against HIV-1 AN - 1028034297; 16919163 AB - Antibody-based therapeutics have been successfully used for the treatment of various diseases and as research tools. Several well characterized, broadly neutralizing monoclonal antibodies (bnmAbs) targeting HIV-1 envelope glycoproteins or related host cell surface proteins show sterilizing protection of animals, but they are not effective when used for therapy of an established infection in humans. Recently, a number of novel bnmAbs, engineered antibody domains (eAds), and multifunctional fusion proteins have been reported which exhibit exceptionally potent and broad neutralizing activity against a wide range of HIV-1 isolates from diverse genetic subtypes. eAds could be more effective in vivo than conventional full-size antibodies generated by the human immune system. Because of their small size (12~15kD), they can better access sterically restricted epitopes and penetrate densely packed tissue where HIV-1 replicates than the larger full-size antibodies. HIV-1 possesses a number of mechanisms to escape neutralization by full-size antibodies but could be less likely to develop resistance to eAds. Here, we review the in vitro and in vivo antiviral efficacies of existing HIV-1 bnmAbs, summarize the development of eAds and multispecific fusion proteins as novel types of HIV-1 inhibitors, and discuss possible strategies to generate more potent antibody-based candidate therapeutics against HIV-1, including some that could be used to eradicate the virus. JF - BioDrugs AU - Gong, Rui AU - Chen, Weizao AU - Dimitrov, Dimiter S AD - Protein Interactions Group, Frederick National Laboratory for Cancer Research, National Institutes of Health, Frederick, MD, USA Y1 - 2012/06/01/ PY - 2012 DA - 2012 Jun 01 SP - 143 EP - 162 PB - Adis International Ltd., 41 Centorian Drive Auckland 10 New Zealand VL - 26 IS - 3 SN - 1173-8804, 1173-8804 KW - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts KW - Cell surface KW - Envelopes KW - Monoclonal antibodies KW - Immune system KW - Reviews KW - Human immunodeficiency virus 1 KW - Genetic diversity KW - Fusion protein KW - Glycoproteins KW - Infection KW - Epitopes KW - V 22360:AIDS and HIV KW - W 30940:Products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028034297?accountid=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=BioDrugs&rft.atitle=Candidate+Antibody-Based+Therapeutics+Against+HIV-1&rft.au=Gong%2C+Rui%3BChen%2C+Weizao%3BDimitrov%2C+Dimiter+S&rft.aulast=Gong&rft.aufirst=Rui&rft.date=2012-06-01&rft.volume=26&rft.issue=3&rft.spage=143&rft.isbn=&rft.btitle=&rft.title=BioDrugs&rft.issn=11738804&rft_id=info:doi/ L2 - http://www.ingentaconnect.com/content/adis/bio/2012/00000026/00000003/art00002 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2015-04-02 N1 - SubjectsTermNotLitGenreText - Cell surface; Envelopes; Monoclonal antibodies; Reviews; Immune system; Genetic diversity; Glycoproteins; Fusion protein; Infection; Epitopes; Human immunodeficiency virus 1 ER - TY - JOUR T1 - Reassessment of Immune Correlates in Human Visceral Leishmaniasis as Defined by Cytokine Release in Whole Blood AN - 1028025544; 16833554 AB - Depressed cell-mediated immunity in human visceral leishmaniasis (VL) (also known as kala-azar), revealed as the inability of peripheral blood mononuclear cells (PBMCs) to respond to Leishmania antigen, remains a hallmark of and is thought to underlie the progressive nature of this disease. We recently reported the ability of a whole-blood, gamma interferon (IFN- gamma ) release assay to detect subclinical infections among healthy individuals living in an area where kala-azar is endemic (Bihar, India) and the surprising result that patients with active VL also secreted significant levels of antigen-specific IFN- gamma in this assay. We were interested in ascertaining whether these findings would be true for a larger cohort of subjects and in employing the whole-blood assay to detect additional cytokines that might better correlate with the disease status of infected individuals. We evaluated IFN- gamma , tumor necrosis factor alpha (TNF- alpha ), and interleukin-10 (IL-10) release in 35 patients with active VL, 54 patients with VL who were cured, 27 patients with other diseases, 52 healthy controls who lived in regions where VL or kala-azar is not endemic (NEHCs [for nonendemic healthy controls]), and 147 healthy controls who lived in regions where kala-azar is endemic (EHCs [for endemic healthy controls]). The cellular responses of the EHCs were correlated with their serological antibody titers against Leishmania donovani and Phlebotomus argentipes saliva. The whole-blood cells from the majority of both active (80%) and cured (85%) VL patients, as well as 24% of EHCs with presumed subclinical infections, produced significantly elevated levels of IFN- gamma . The findings do not support a severe Th1 response defect in kala-azar. Importantly, only the patients with active VL also produced IL-10, which in conjunction with IFN- gamma better reflects the immune responses that distinguish individuals with active disease from cured or subclinically infected, immune individuals. JF - Clinical and Vaccine Immunology AU - Prakash Singh, Om AU - Gidwani, Kamlesh AU - Kumar, Rajiv AU - Jones, Stephen L AU - Boelaert, Marleen AU - Sacks, David AU - Sundar, Shyam AD - Infectious Disease Research Laboratory, Department of Medicine, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India, DavidSacks,dsacks{at}nih.gov. Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 961 EP - 966 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 19 IS - 6 SN - 1556-6811, 1556-6811 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts KW - gamma -Interferon KW - India, Bihar KW - Helper cells KW - Disease control KW - Subclinical infection KW - Interleukin 10 KW - India KW - Public health KW - Leishmania donovani KW - Phlebotomus argentipes KW - Peripheral blood mononuclear cells KW - Endemic species KW - Antigens KW - Lymphocytes T KW - Cytokines KW - Disease detection KW - Visceral leishmaniasis KW - Immunity KW - Blood KW - Antibodies KW - Immunity (cell-mediated) KW - alpha -Interferon KW - Immune response KW - Saliva KW - Tumor necrosis factor- alpha KW - Vaccines KW - K 03350:Immunology KW - F 06905:Vaccines 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/1028025544?accountid=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=Clinical+and+Vaccine+Immunology&rft.atitle=Reassessment+of+Immune+Correlates+in+Human+Visceral+Leishmaniasis+as+Defined+by+Cytokine+Release+in+Whole+Blood&rft.au=Prakash+Singh%2C+Om%3BGidwani%2C+Kamlesh%3BKumar%2C+Rajiv%3BJones%2C+Stephen+L%3BBoelaert%2C+Marleen%3BSacks%2C+David%3BSundar%2C+Shyam&rft.aulast=Prakash+Singh&rft.aufirst=Om&rft.date=2012-06-01&rft.volume=19&rft.issue=6&rft.spage=961&rft.isbn=&rft.btitle=&rft.title=Clinical+and+Vaccine+Immunology&rft.issn=15566811&rft_id=info:doi/10.1128%2FCVI.00143-12 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Number of references - 28 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Blood; Antibodies; Endemic species; Antigens; Disease control; Immunity; Disease detection; Vaccines; Public health; gamma -Interferon; Visceral leishmaniasis; Helper cells; Subclinical infection; Interleukin 10; Peripheral blood mononuclear cells; Immunity (cell-mediated); alpha -Interferon; Lymphocytes T; Cytokines; Tumor necrosis factor- alpha; Saliva; Immune response; Leishmania donovani; Phlebotomus argentipes; India, Bihar; India DO - http://dx.doi.org/10.1128/CVI.00143-12 ER - TY - JOUR T1 - Impact of vancomycin MIC creep on patients with methicillin-resistant Staphylococcus aureus bacteremia AN - 1024668090; 16866591 AB - Background/Purpose: To date, vancomycin is still the standard treatment for methicillin-resistant Staphylococcus aureus (MRSA) infections, but minimum inhibitory concentration (MIC) creep is becoming a major concern. The aims of this study were to investigate trends in vancomycin use and MIC values over the last decade at our institute and to evaluate the outcomes of bacteremic patients infected with MRSA isolates with reduced vancomycin susceptibility. Methods: Vancomycin use and density were evaluated using the defined daily doses (DDD) method. Patients with MRSA bacteremia were enrolled retrospectively. Patient demographic data and clinical outcomes were analyzed. The first isolate from each patient was collected for E-testing in order to determine vancomycin MIC. MIC trends were assessed as MIC sub(50), MIC sub(90), and the geometric mean. Results: Vancomycin use has increased over the last decade. One hundred and forty patients were enrolled and their respective isolates were retrieved, including isolates from 45 patients in 2001, 46 patients in 2005, and 49 patients in 2009. The geometric mean ( plus or minus standard deviation) of the vancomycin MIC for MRSA isolates obtained in 2009 was 1.39 plus or minus 0.30 mu g/mL, which is significantly higher than the mean vancomycin MIC obtained in 2001 (1.19 plus or minus 0.34 mu g/mL, p 1.5 ng/mL or < 1.5 ng/mL. Conclusion: We identified a significant upward trend in the use of vancomycin and its MIC over the last decade. This study shows that patients infected with MRSA isolates with high MICs greater than or equal to 1.5 mu g/mL) do not have a significantly higher mortality rate compared with isolates with low MICs (<1.5 mu g/mL). JF - Journal of Microbiology, Immunology and Infection AU - Yeh, Y-C AU - Yeh, K-M AU - Lin, T-Y AU - Chiu, S-K AU - Yang, Y-S AU - Wang, Y-C AU - Lin, J-C AD - Division of Infectious Diseases and Tropical Medicine, Department of Internal Medicine, Tri-Service General Hospital, Medical Defense Medical Center, No. 325 Cheng-Kung Road, Section 2, Nei-hu 114, Taipei, Taiwan, jclin@ndmctsgh.edu.tw Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 214 EP - 220 VL - 45 IS - 3 SN - 1684-1182, 1684-1182 KW - Microbiology Abstracts B: Bacteriology KW - Bacteremia KW - Data processing KW - Demography KW - Drug resistance KW - Infection KW - Minimum inhibitory concentration KW - Mortality KW - Standard deviation KW - Vancomycin KW - Staphylococcus aureus KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1024668090?accountid=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+Microbiology%2C+Immunology+and+Infection&rft.atitle=Impact+of+vancomycin+MIC+creep+on+patients+with+methicillin-resistant+Staphylococcus+aureus+bacteremia&rft.au=Yeh%2C+Y-C%3BYeh%2C+K-M%3BLin%2C+T-Y%3BChiu%2C+S-K%3BYang%2C+Y-S%3BWang%2C+Y-C%3BLin%2C+J-C&rft.aulast=Yeh&rft.aufirst=Y-C&rft.date=2012-06-01&rft.volume=45&rft.issue=3&rft.spage=214&rft.isbn=&rft.btitle=&rft.title=Journal+of+Microbiology%2C+Immunology+and+Infection&rft.issn=16841182&rft_id=info:doi/10.1016%2Fj.jmii.2011.11.006 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2012-07-27 N1 - SubjectsTermNotLitGenreText - Demography; Mortality; Data processing; Standard deviation; Drug resistance; Bacteremia; Vancomycin; Infection; Minimum inhibitory concentration; Staphylococcus aureus DO - http://dx.doi.org/10.1016/j.jmii.2011.11.006 ER - TY - JOUR T1 - Characterization of Engineered Cartilage Constructs Using Multiexponential T sub(2) Relaxation Analysis and Support Vector Regression AN - 1024660102; 16862338 AB - Increased sensitivity in the characterization of cartilage matrix status by magnetic resonance (MR) imaging, through the identification of surrogate markers for tissue quality, would be of great use in the noninvasive evaluation of engineered cartilage. Recent advances in MR evaluation of cartilage include multiexponential and multiparametric analysis, which we now extend to engineered cartilage. We studied constructs which developed from chondrocytes seeded in collagen hydrogels. MR measurements of transverse relaxation times were performed on samples after 1, 2, 3, and 4 weeks of development. Corresponding biochemical measurements of sulfated glycosaminoglycan (sGAG) were also performed. sGAG per wet weight increased from 7.74 plus or minus 1.34 mu g/mg in week 1 to 21.06 plus or minus 4.14 mu g/mg in week 4. Using multiexponential T sub(2) analysis, we detected at least three distinct water compartments, with T sub(2) values and weight fractions of (45 ms, 3%), (200 ms, 4%), and (500 ms, 97%), respectively. These values are consistent with known properties of engineered cartilage and previous studies of native cartilage. Correlations between sGAG and MR measurements were examined using conventional univariate analysis with T sub(2) data from monoexponential fits with individual multiexponential compartment fractions and sums of these fractions, through multiple linear regression based on linear combinations of fractions, and, finally, with multivariate analysis using the support vector regression (SVR) formalism. The phenomenological relationship between T sub(2) from monoexponential fitting and sGAG exhibited a correlation coefficient of r super(2) = 0.56, comparable to the more physically motivated correlations between individual fractions or sums of fractions and sGAG; the correlation based on the sum of the two proteoglycan-associated fractions was r super(2) = 0.58. Correlations between measured sGAG and those calculated using standard linear regression were more modest, with r super(2) in the range 0.43-0.54. However, correlations using SVR exhibited r super(2) values in the range 0.68-0.93. These results indicate that the SVR-based multivariate approach was able to determine tissue sGAG with substantially higher accuracy than conventional monoexponential T sub(2) measurements or conventional regression modeling based on water fractions. This combined technique, in which the results of multiexponential analysis are examined with multivariate statistical techniques, holds the potential to greatly improve the accuracy of cartilage matrix characterization in engineered constructs using noninvasive MR data. JF - Tissue Engineering, Part C: Methods AU - Irrechukwu, ON AU - Reiter, DA AU - Lin, P-C AU - Roque, R A AU - Fishbein, K W AU - Spencer, R G AD - Magnetic Resonance Imaging and Spectroscopy Section, Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA, spencer@helix.nih.gov Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 433 EP - 443 VL - 18 IS - 6 SN - 1937-3384, 1937-3384 KW - Calcium & Calcified Tissue Abstracts; Biotechnology and Bioengineering Abstracts KW - Cartilage KW - Chondrocytes KW - Collagen KW - Computed tomography KW - Data processing KW - Glycosaminoglycans KW - Magnetic resonance imaging KW - Multivariate analysis KW - Noninvasive evaluation KW - Statistical analysis KW - Tissue engineering KW - hydrogels KW - T 2030:Cartilage and Cartilage Diseases KW - W 30920:Tissue Engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1024660102?accountid=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=Tissue+Engineering%2C+Part+C%3A+Methods&rft.atitle=Characterization+of+Engineered+Cartilage+Constructs+Using+Multiexponential+T+sub%282%29+Relaxation+Analysis+and+Support+Vector+Regression&rft.au=Irrechukwu%2C+ON%3BReiter%2C+DA%3BLin%2C+P-C%3BRoque%2C+R+A%3BFishbein%2C+K+W%3BSpencer%2C+R+G&rft.aulast=Irrechukwu&rft.aufirst=ON&rft.date=2012-06-01&rft.volume=18&rft.issue=6&rft.spage=433&rft.isbn=&rft.btitle=&rft.title=Tissue+Engineering%2C+Part+C%3A+Methods&rft.issn=19373384&rft_id=info:doi/10.1089%2Ften.tec.2011.0509 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2012-10-19 N1 - SubjectsTermNotLitGenreText - Glycosaminoglycans; Data processing; Noninvasive evaluation; hydrogels; Multivariate analysis; Cartilage; Computed tomography; Magnetic resonance imaging; Statistical analysis; Chondrocytes; Tissue engineering; Collagen DO - http://dx.doi.org/10.1089/ten.tec.2011.0509 ER - TY - JOUR T1 - Salivary Cortisol: A Tool for Biobehavioral Research in Children AN - 1023094764; 201215605 AB - The measurement of salivary cortisol has been widely used in pediatric research for more than 20 years as a biomarker of hypothalamic pituitary adrenal (HPA) axis activity during normal activity and in response to stress. The inclusion of salivary cortisol as an outcome measure will provide a useful biological marker with future research to investigate the following: stress in children undergoing painful procedures, weight loss, sleep problems, and caregiver stress. The use of salivary cortisol in pediatric biobehavioral research has revealed important information about the pattern of cortisol secretion during childhood, the response to stressors in a nonclinical environment, the response to therapeutic interventions, and the identification of dysfunctional patterns of secretion in children. Salivary cortisol is a reliable noninvasive method to assess HPA function; however, collection and measurement of specimens with infants and children require special consideration. This article will summarize pertinent issues related to salivary cortisol collection to encourage "broader employment" of this method in pediatric biobehavioral research. [Copyright Elsevier B.V.] JF - Journal of Pediatric Nursing AU - Keil, Margaret F AD - Program in Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, The National Institutes of Health keilm@mail.nih.gov Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 287 EP - 289 PB - Elsevier Ltd, The Netherlands VL - 27 IS - 3 SN - 0882-5963, 0882-5963 KW - Measurement KW - Paediatrics KW - Salivary cortisol KW - Caretaker syndrome KW - Biological markers KW - Children KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1023094764?accountid=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+Pediatric+Nursing&rft.atitle=Salivary+Cortisol%3A+A+Tool+for+Biobehavioral+Research+in+Children&rft.au=Keil%2C+Margaret+F&rft.aulast=Keil&rft.aufirst=Margaret&rft.date=2012-06-01&rft.volume=27&rft.issue=3&rft.spage=287&rft.isbn=&rft.btitle=&rft.title=Journal+of+Pediatric+Nursing&rft.issn=08825963&rft_id=info:doi/10.1016%2Fj.pedn.2012.02.003 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-07-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Salivary cortisol; Children; Paediatrics; Caretaker syndrome; Biological markers; Measurement DO - http://dx.doi.org/10.1016/j.pedn.2012.02.003 ER - TY - JOUR T1 - Methadone and metabolites in hair of methadone-assisted pregnant women and their infants. AN - 1022848882; 22495425 AB - Methadone is the recommended pharmacotherapy for opioid-dependent pregnant women. The primary aims of this study were to determine whether a dose-concentration relationship exists between cumulative maternal methadone dose, methadone and metabolite concentrations in maternal hair during pregnancy and whether maternal hair methadone and metabolite concentrations predict neonatal outcomes. Hair specimens were collected monthly from opioid-dependent mothers enrolled in methadone treatment and 4 of their infants. Hair specimens were segmented (3 cm), washed (maternal hair only), and analyzed for methadone, 2-ethylidene-1,5-dimethyl-3,3-diphenylpyrrolidine (EDDP), and 2-ethyl-5-methyl-3,3-diphenylpyrroline by liquid chromatography tandem mass spectrometry. There was large intersubject variability and no dose-concentration relationship for cumulative methadone dose and methadone, EDDP, 2-ethyl-5-methyl-3,3-diphenylpyrroline, or total concentrations in hair. For individual women, a positive trend was noted for cumulative methadone dose and methadone and EDDP concentrations in hair. There was a positive linear trend for cumulative methadone dose and EDDP/methadone ratio in maternal hair, perhaps reflecting methadone's induction of its own metabolism. Maternal methadone concentrations were higher than those in infant hair, and infant EDDP hair concentrations were higher than those in maternal hair. Maternal methadone dose, and methadone and EDDP hair concentrations were not correlated with peak infant neonatal abstinence syndrome (NAS) scores, days to peak NAS, duration of NAS, time to NAS onset, birth length, head circumference, or amount of neonatal morphine pharmacotherapy. Maternal cumulative third trimester methadone dose was positively correlated with infant birth weight. Methadone and EDDP in pregnant women's hair are markers of methadone exposure and do not predict total methadone dose, nor neonatal outcomes from in utero methadone exposure. JF - Therapeutic drug monitoring AU - Himes, Sarah K AU - Goodwin, Robert S AU - Rock, Colleen M AU - Jones, Hendrée E AU - Johnson, Rolley E AU - Wilkins, Diana G AU - Huestis, Marilyn A AD - Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD 21224, USA. Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 337 EP - 344 VL - 34 IS - 3 KW - Methadone KW - UC6VBE7V1Z KW - Index Medicus KW - Neonatal Abstinence Syndrome -- metabolism KW - Young Adult KW - Opiate Substitution Treatment -- adverse effects KW - Humans KW - Adult KW - Opiate Substitution Treatment -- methods KW - Infant, Newborn KW - Neonatal Abstinence Syndrome -- diagnosis KW - Adolescent KW - Female KW - Pregnancy KW - Opioid-Related Disorders -- metabolism KW - Prenatal Exposure Delayed Effects -- metabolism KW - Methadone -- therapeutic use KW - Hair -- metabolism KW - Hair -- chemistry KW - Prenatal Exposure Delayed Effects -- diagnosis KW - Methadone -- metabolism KW - Opioid-Related Disorders -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1022848882?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Therapeutic+drug+monitoring&rft.atitle=Methadone+and+metabolites+in+hair+of+methadone-assisted+pregnant+women+and+their+infants.&rft.au=Himes%2C+Sarah+K%3BGoodwin%2C+Robert+S%3BRock%2C+Colleen+M%3BJones%2C+Hendr%C3%A9e+E%3BJohnson%2C+Rolley+E%3BWilkins%2C+Diana+G%3BHuestis%2C+Marilyn+A&rft.aulast=Himes&rft.aufirst=Sarah&rft.date=2012-06-01&rft.volume=34&rft.issue=3&rft.spage=337&rft.isbn=&rft.btitle=&rft.title=Therapeutic+drug+monitoring&rft.issn=1536-3694&rft_id=info:doi/10.1097%2FFTD.0b013e3182512b26 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-03-11 N1 - Date created - 2012-05-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Obstet Gynecol. 1976 May 15;125(2):135-42 [1266895] Science. 1972 Feb 11;175(4022):654-6 [5009766] J Pharmacol Exp Ther. 1985 Apr;233(1):1-6 [3981450] Neurobehav Toxicol Teratol. 1986 Jul-Aug;8(4):353-5 [3762845] Am J Dis Child. 1987 Nov;141(11):1163-7 [3673965] J Anal Toxicol. 1990 Jan-Feb;14(1):1-7 [2314055] J Paediatr Child Health. 1991 Apr;27(2):96-100 [1883657] J Pediatr. 1973 Dec;83(6):1055-61 [4757521] Mt Sinai J Med. 1974 Mar-Apr;41(2):254-9 [4544621] Am J Obstet Gynecol. 1975 Mar 1;121(5):617-21 [1115163] Am J Drug Alcohol Abuse. 1974;1(3):409-19 [4619541] Forensic Sci Int. 1993 Dec;63(1-3):185-206 [8138220] J Pharm Biomed Anal. 1995 Jun;13(7):829-39 [8562606] Int J Legal Med. 1996;108(6):285-93 [8793635] J Anal Toxicol. 1996 Oct;20(6):355-61 [8889670] J Subst Abuse Treat. 1996 Jul-Aug;13(4):321-9 [9076650] Obstet Gynecol Clin North Am. 1998 Mar;25(1):139-51 [9547764] J Pharm Sci. 1998 Apr;87(4):435-40 [9548895] J Anal Toxicol. 1998 Oct;22(6):526-30 [9788529] Br J Clin Pharmacol. 1999 Jul;48(1):43-52 [10383559] Ann N Y Acad Sci. 1951 Mar;53(3):562-8 [14819882] J Invest Dermatol. 1960 Dec;35:323-7 [13764567] Biochem Pharmacol. 2005 Jan 1;69(1):187-97 [15588727] J Pharmacol Exp Ther. 2005 May;313(2):909-15 [15743923] Drug Alcohol Depend. 2005 Jul;79(1):1-10 [15943939] Clin Dermatol. 2006 Mar-Apr;24(2):80-3 [16487877] Ther Drug Monit. 2006 Jun;28(3):442-6 [16778731] J Subst Abuse Treat. 2007 Jan;32(1):19-25 [17175395] Pediatrics. 2008 Jan;121(1):106-14 [18166563] Clin Pharmacol Ther. 2008 Nov;84(5):604-12 [18701886] Br J Clin Pharmacol. 2009 Jan;67(1):29-37 [19133059] Expert Opin Drug Metab Toxicol. 2010 Jun;6(6):689-99 [20367533] Addiction. 2010 Dec;105(12):2151-9 [20854338] N Engl J Med. 2010 Dec 9;363(24):2320-31 [21142534] Clin Chem. 2011 Mar;57(3):449-58 [21245372] Forensic Sci Int. 2011 Jul 15;210(1-3):110-6 [21382678] Ther Drug Monit. 2011 Aug;33(4):443-52 [21743375] J Addict Dis. 1999;18(4):51-61 [10631963] Forensic Sci Int. 2000 Jan 10;107(1-3):225-32 [10689574] J Pharmacol Toxicol Methods. 1999 Oct;42(2):61-6 [10924887] J Anal Toxicol. 2000 Sep;24(6):448-9 [10999352] J Chromatogr B Biomed Sci Appl. 2000 Sep 15;746(2):255-64 [11076079] Forensic Sci Int. 2001 Apr 1;117(3):175-84 [11248447] J Anal Toxicol. 2003 Jan-Feb;27(1):20-3 [12587678] Ther Drug Monit. 2003 Aug;25(4):421-32 [12883224] Biochem Pharmacol. 2004 Aug 1;68(3):583-91 [15242824] Pediatrics. 1976 Nov;58(5):681-5 [980601] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1097/FTD.0b013e3182512b26 ER - TY - JOUR T1 - The importance of exposure rate on odds ratios by cigarette smoking and alcohol consumption for esophageal adenocarcinoma and squamous cell carcinoma in the Barrett's Esophagus and Esophageal Adenocarcinoma Consortium AN - 1022564175; 16790417 AB - Background: Cigarette smoking is associated with esophageal adenocarcinoma (EAC), esophagogastric junctional adenocarcinoma (EGJA) and esophageal squamous cell carcinoma (ESCC), and alcohol consumption with ESCC. However, no analyses have examined how delivery rate modifies the strength of odds ratio (OR) trends with total exposure, i.e., the impact on the OR for a fixed total exposure of high exposure rate for short duration compared with low exposure rate for long duration. Methods: The authors pooled data from 12 case-control studies from the Barrett's Esophagus and Esophageal Adenocarcinoma Consortium (BEACON), including 1242 (EAC), 1263 (EGJA) and 954 (ESCC) cases and 7053 controls, modeled joint ORs for cumulative exposure and exposure rate for cigarette smoking and alcohol consumption, and evaluated effect modification by sex, body mass index (BMI), age and self-reported acid reflux. Results: For smoking, all sites exhibited inverse delivery rate effects, whereby ORs with pack-years increased, but trends weakened with increasing cigarettes/day. None of the examined factors modified associations, except for ESCC where younger ages at diagnosis enhanced smoking effects (P<0.01). For EAC and EGJA, ORs with drink-years exhibited inverse associations in <5drinks/day consumers and no association in heavier consumers. For ESCC, ORs with drink-years increased, with trends strengthening with greater drinks/day. There was no significant effect modification, except for EAC and EGJA where acid reflux mitigated the inverse associations (P=0.02). For ESCC, younger ages at diagnosis enhanced drinking-related ORs (P<0.01). Conclusions: Patterns of ORs by pack-years and drink-years, delivery rate effects and effect modifiers revealed common as well as distinct etiologic elements for these diseases. JF - Cancer Epidemiology AU - Lubin, Jay H AU - Cook, Michael B AU - Pandeya, Nirmala AU - Vaughan, Thomas L AU - Abnet, Christian C AU - Giffen, Carol AU - Webb, Penelope M AU - Murray, Liam J AU - Casson, Alan G AU - Risch, Harvey A AU - Ye, Weimin AU - Kamangar, Farin AU - Bernstein, Leslie AU - Sharp, Linda AU - Nyren, Olof AU - Gammon, Marilie D AU - Corley, Douglas A AU - Wu, Anna H AU - Brown, Linda M AU - Chow, Wong-Ho AU - Ward, Mary H AU - Freedman, Neal D AU - Whiteman, David C AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, MD, USA, lubinj@mail.nih.gov Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 306 EP - 316 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 36 IS - 3 SN - 1877-7821, 1877-7821 KW - Risk Abstracts KW - Age KW - Alcohol KW - Body mass KW - Cancer KW - Cigarette smoking KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1022564175?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Epidemiology&rft.atitle=The+importance+of+exposure+rate+on+odds+ratios+by+cigarette+smoking+and+alcohol+consumption+for+esophageal+adenocarcinoma+and+squamous+cell+carcinoma+in+the+Barrett%27s+Esophagus+and+Esophageal+Adenocarcinoma+Consortium&rft.au=Lubin%2C+Jay+H%3BCook%2C+Michael+B%3BPandeya%2C+Nirmala%3BVaughan%2C+Thomas+L%3BAbnet%2C+Christian+C%3BGiffen%2C+Carol%3BWebb%2C+Penelope+M%3BMurray%2C+Liam+J%3BCasson%2C+Alan+G%3BRisch%2C+Harvey+A%3BYe%2C+Weimin%3BKamangar%2C+Farin%3BBernstein%2C+Leslie%3BSharp%2C+Linda%3BNyren%2C+Olof%3BGammon%2C+Marilie+D%3BCorley%2C+Douglas+A%3BWu%2C+Anna+H%3BBrown%2C+Linda+M%3BChow%2C+Wong-Ho%3BWard%2C+Mary+H%3BFreedman%2C+Neal+D%3BWhiteman%2C+David+C&rft.aulast=Lubin&rft.aufirst=Jay&rft.date=2012-06-01&rft.volume=36&rft.issue=3&rft.spage=306&rft.isbn=&rft.btitle=&rft.title=Cancer+Epidemiology&rft.issn=18777821&rft_id=info:doi/10.1016%2Fj.canep.2012.03.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Last updated - 2012-06-29 N1 - SubjectsTermNotLitGenreText - Alcohol; Age; Body mass; Cigarette smoking; Cancer DO - http://dx.doi.org/10.1016/j.canep.2012.03.001 ER - TY - JOUR T1 - Modifications in erythrocyte membrane zeta potential by Plasmodium falciparum infection AN - 1022564168; 16790391 AB - The zeta potential (ZP) is an electrochemical property of cell surfaces that is determined by the net electrical charge of molecules exposed at the surface of cell membranes. Membrane proteins contribute to the total net electrical charge of cell surfaces and can alter ZP through variation in their copy number and changes in their intermolecular interactions. Plasmodium falciparumextensively remodels its host red blood cell (RBC) membrane by placing 'knob'-like structures at the cell surface. Using an electrophoretic mobility assay, we found that the mean ZP of human RBCs was -15.7mV. In RBCs infected with P. falciparumtrophozoites ('iRBCs'), the mean ZP was significantly lower (-14.6mV, p<0.001). Removal of sialic acid from the cell surface by neuraminidase treatment significantly decreased the ZP of both RBCs (-6.06mV) and iRBCs (-4.64mV). Parasite-induced changes in ZP varied by P. falciparum clone and the presence of knobs on the iRBC surface. Variations in ZP values were accompanied by altered binding of iRBCs to human microvascular endothelial cells (MVECs). These data suggest that parasite-derived knob proteins contribute to the ZP of iRBCs, and that electrostatic and hydrophobic interactions between iRBC and MVEC membranes are involved in cytoadherence. JF - Experimental Parasitology AU - Tokumasu, Fuyuki AU - Ostera, Graciela R AU - Amaratunga, Chanaki AU - Fairhurst, Rick M AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-8132, USA, ftokumasu@niaid.nih.gov Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 245 EP - 251 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 131 IS - 2 SN - 0014-4894, 0014-4894 KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - Zeta potential KW - Plasmodium falciparum KW - Knob KW - Cytoadherence KW - Erythrocyte membrane KW - Clones KW - Cell surface KW - Microvasculature KW - Parasites KW - Data processing KW - Electrophoresis KW - Erythrocytes KW - Disease control KW - Electrostatic properties KW - Hydrophobicity KW - Membrane proteins KW - Hosts KW - Infection KW - Electrophoretic mobility KW - copy number KW - Endothelial cells KW - Cell membranes KW - Exo- alpha -sialidase KW - Sialic acids KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08524:Public health, medicines, dangerous organisms KW - K 03320:Cell Biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1022564168?accountid=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=Experimental+Parasitology&rft.atitle=Modifications+in+erythrocyte+membrane+zeta+potential+by+Plasmodium+falciparum+infection&rft.au=Tokumasu%2C+Fuyuki%3BOstera%2C+Graciela+R%3BAmaratunga%2C+Chanaki%3BFairhurst%2C+Rick+M&rft.aulast=Tokumasu&rft.aufirst=Fuyuki&rft.date=2012-06-01&rft.volume=131&rft.issue=2&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=Experimental+Parasitology&rft.issn=00144894&rft_id=info:doi/10.1016%2Fj.exppara.2012.03.005 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Last updated - 2014-12-11 N1 - SubjectsTermNotLitGenreText - Clones; Parasites; Electrophoresis; Cell membranes; Erythrocytes; Disease control; Hosts; Microvasculature; Cell surface; Data processing; Hydrophobicity; Electrostatic properties; Membrane proteins; Electrophoretic mobility; Infection; copy number; Endothelial cells; Zeta potential; Exo- alpha -sialidase; Sialic acids; Plasmodium falciparum DO - http://dx.doi.org/10.1016/j.exppara.2012.03.005 ER - TY - JOUR T1 - Systems immunology of human malaria AN - 1020850319; 16790256 AB - Plasmodium falciparum malaria remains a global public health threat. Optimism that a highly effective malaria vaccine can be developed stems in part from the observation that humans can acquire immunity to malaria through experimental and natural P. falciparum infection. Recent advances in systems immunology could accelerate efforts to unravel the mechanisms of acquired immunity to malaria. Here, we review the tools of systems immunology, their current limitations in the context of human malaria research, and the human 'models' of malaria immunity to which these tools can be applied. JF - Trends in Parasitology AU - Tran, Tuan M AU - Samal, Babru AU - Kirkness, Ewen AU - Crompton, Peter D AD - Laboratory of Immunogenetics (LIG), National Institute of Allergy and Infectious Diseases, National Institutes of Health, 12441 Parklawn Drive, Rockville, MD 20852, USA, pcrompton@niaid.nih.gov Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 248 EP - 257 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 28 IS - 6 SN - 1471-4922, 1471-4922 KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts KW - systems immunology KW - malaria KW - Plasmodium falciparum KW - Parasites KW - Human diseases KW - Immunology KW - Disease control KW - Malaria KW - Immunity KW - Infection KW - Public health KW - Reviews KW - Vaccines KW - K 03400:Human Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - F 06910:Microorganisms & Parasites KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020850319?accountid=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=Trends+in+Parasitology&rft.atitle=Systems+immunology+of+human+malaria&rft.au=Tran%2C+Tuan+M%3BSamal%2C+Babru%3BKirkness%2C+Ewen%3BCrompton%2C+Peter+D&rft.aulast=Tran&rft.aufirst=Tuan&rft.date=2012-06-01&rft.volume=28&rft.issue=6&rft.spage=248&rft.isbn=&rft.btitle=&rft.title=Trends+in+Parasitology&rft.issn=14714922&rft_id=info:doi/10.1016%2Fj.pt.2012.03.006 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Last updated - 2015-10-28 N1 - SubjectsTermNotLitGenreText - Parasites; Human diseases; Immunology; Disease control; Malaria; Vaccines; Immunity; Public health; Reviews; Infection; Plasmodium falciparum DO - http://dx.doi.org/10.1016/j.pt.2012.03.006 ER - TY - JOUR T1 - Meropenem-Clavulanic Acid Shows Activity against Mycobacterium tuberculosis In Vivo AN - 1020850265; 16780394 AB - The carbapenems imipenem and meropenem in combination with clavulanic acid reduced the bacterial burden in Mycobacterium tuberculosis-infected macrophages by 2 logs over 6 days. Despite poor stability in solution and a short half-life in rodents, treatment of chronically infected mice revealed significant reductions of bacterial burden in the lungs and spleens. Our results show that meropenem has activity in two in vivo systems, but stability and pharmacokinetics of long-term administration will offer significant challenges to clinical evaluation. JF - Antimicrobial Agents & Chemotherapy AU - England, Kathleen AU - Boshoff, Helena IM AU - Arora, Kriti AU - Weiner, Danielle AU - Dayao, Emmanuel AU - Schimel, Daniel AU - Via, Laura E AU - Barry, Clifton E, III AD - Tuberculosis Research Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, USA, CliftonE.BarryIII,cbarry{at}niaid.nih.gov. Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 3384 EP - 3387 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 56 IS - 6 SN - 0066-4804, 0066-4804 KW - Microbiology Abstracts B: Bacteriology; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Carbapenems KW - Clavulanic acid KW - Imipenem KW - Lung KW - Macrophages KW - Meropenem KW - Pharmacokinetics KW - Spleen KW - Mycobacterium tuberculosis KW - J 02410:Animal Diseases KW - A 01340:Antibiotics & Antimicrobials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020850265?accountid=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=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Meropenem-Clavulanic+Acid+Shows+Activity+against+Mycobacterium+tuberculosis+In+Vivo&rft.au=England%2C+Kathleen%3BBoshoff%2C+Helena+IM%3BArora%2C+Kriti%3BWeiner%2C+Danielle%3BDayao%2C+Emmanuel%3BSchimel%2C+Daniel%3BVia%2C+Laura+E%3BBarry%2C+Clifton+E%2C+III&rft.aulast=England&rft.aufirst=Kathleen&rft.date=2012-06-01&rft.volume=56&rft.issue=6&rft.spage=3384&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.05690-11 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Number of references - 20 N1 - Last updated - 2012-09-10 N1 - SubjectsTermNotLitGenreText - Macrophages; Lung; Clavulanic acid; Meropenem; Spleen; Carbapenems; Pharmacokinetics; Imipenem; Mycobacterium tuberculosis DO - http://dx.doi.org/10.1128/AAC.05690-11 ER - TY - JOUR T1 - Intestinal Lymphangiectasis and Lipidosis in Rats Following Subchronic Exposure to Indole-3-Carbinol via Oral Gavage AN - 1020844110; 16806059 AB - To investigate the toxicity and carcinogenic potential of indole-3-carbinol (I3C), the National Toxicology Program has conducted 13-week subchronic studies in Fisher 344 rats and B6C3F1 mice, and chronic 2-year bioassays in Sprague-Dawley rats and B6C3F1 mice. While the chronic study results are not yet available, subchronic study results and short-term special evaluations of interim sacrifices in the 2-year rat bioassay are presented. F344 rats were orally gavaged less than or equal to 300 mg I3C/kg body weight 5 days a week for 13 weeks. Rats treated with greater than or equal to 150 mg/kg demonstrated a dose-related dilation of lymphatics (lymphangiectasis) of the duodenum, jejunum, and mesenteric lymph nodes. Material within dilated lacteals stained positively for Oil Red O and Sudan Black, consistent with lipid. Electron microscopic evaluation confirmed extracellular lipid accumulation within the villar lamina propria, lacteals, and within villar macrophages. Analyses of hepatic and pulmonary CYP1A enzymes demonstrated dose-dependent I3C induction of CYP1A1 and 1A2. B6C3F1 mice orally gavaged less than or equal to 250 mg I3C/kg body weight did not demonstrate histopathological changes; however, hepatic CYP induction was similar to that in rats. The histopathologic changes of intestinal lymphangiectasis and lipidosis in this study share similarities with intestinal lymphangiectasia as observed in humans and dogs. However, the resultant clinical spectrum of protein-losing enteropathy was not present. JF - Toxicologic Pathology AU - Boyle, Michael C AU - Crabbs, Torrie A AU - Wyde, Michael E AU - Painter, JTodd AU - Hill, Georgette D AU - Malarkey, David E AU - Lieuallen, Warren G AU - Nyska, Abraham AD - National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA, anyska@bezeqint.net Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 561 EP - 576 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 40 IS - 4 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - Body weight KW - CYP1A protein KW - Cytochrome P450 KW - Duodenum KW - Enzymes KW - Indole-3-carbinol KW - Intestine KW - Jejunum KW - Lipids KW - Liver KW - Lung KW - Lymph nodes KW - Lymphangiectasis KW - Lymphatic system KW - Macrophages KW - Toxicity KW - lamina propria KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020844110?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Intestinal+Lymphangiectasis+and+Lipidosis+in+Rats+Following+Subchronic+Exposure+to+Indole-3-Carbinol+via+Oral+Gavage&rft.au=Boyle%2C+Michael+C%3BCrabbs%2C+Torrie+A%3BWyde%2C+Michael+E%3BPainter%2C+JTodd%3BHill%2C+Georgette+D%3BMalarkey%2C+David+E%3BLieuallen%2C+Warren+G%3BNyska%2C+Abraham&rft.aulast=Boyle&rft.aufirst=Michael&rft.date=2012-06-01&rft.volume=40&rft.issue=4&rft.spage=561&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623311436178 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Number of references - 77 N1 - Last updated - 2012-06-29 N1 - SubjectsTermNotLitGenreText - Macrophages; Duodenum; Lipids; Enzymes; Toxicity; Lymphangiectasis; Lymph nodes; Indole-3-carbinol; CYP1A protein; Body weight; Lung; Jejunum; Intestine; Liver; Cytochrome P450; lamina propria; Lymphatic system DO - http://dx.doi.org/10.1177/0192623311436178 ER - TY - JOUR T1 - Pesticide exposure and amyotrophic lateral sclerosis AN - 1020843282; 16792731 AB - Our objectives were to summarize literature on the association of amyotrophic lateral sclerosis (ALS) with pesticides as a group and to evaluate associations of ALS with specific pesticides. We conducted a meta-analysis of published studies of ALS and pesticides as a group and investigated the association of ALS with specific pesticides, using data from the Agricultural Health Study (AHS), a cohort including 84,739 private pesticide applicators and spouses. AHS participants provided information on pesticide use at enrollment in 1993-1997. In mortality data collected through February 2010, ALS was recorded on death certificates of 41 individuals whom we compared to the remaining cohort (controls), using unconditional logistic regression adjusted for age and gender to calculate odds ratios (ORs) and 95% confidence intervals. In the meta-analysis, ALS was associated with use of pesticides as a group (1.9, 1.1-3.1). In the AHS, ALS was not associated with pesticides as a group, but was associated with use of organochlorine insecticides (OCs) (1.6, 0.8-3.5), pyrethroids (1.4, 0.6-3.4), herbicides (1.6, 0.7-3.7), and fumigants (1.8, 0.8-3.9). ORs were elevated forever use of the specific OCs aldrin (2.1, 0.8-5.1), dieldrin (2.6, 0.9-7.3), DDT (2.1, 0.9-5.0), and toxaphene (2.0, 0.8-4.9). None of these associations was statistically significant. Similar results were observed in an analysis restricted to men. In conclusion, the meta-analysis suggests that ALS risk is associated with use of pesticides as a group, and our analysis of AHS data points to OC use in particular. The latter results are novel but based on a small number of cases and require replication in other populations. JF - Neurotoxicology AU - Kamel, Freya AU - Umbach, David M AU - Bedlack, Richard S AU - Richards, Marie AU - Watson, Mary AU - Alavanja, Michael CR AU - Blair, Aaron AU - Hoppin, Jane A AU - Schmidt, Silke AU - Sandler, Dale P AD - Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, NC, USA, kamel@niehs.nih.gov Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 457 EP - 462 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 33 IS - 3 SN - 0161-813X, 0161-813X KW - Health & Safety Science Abstracts; CSA Neurosciences Abstracts; Toxicology Abstracts KW - Aldrin KW - Amyotrophic lateral sclerosis KW - DDT KW - Data processing KW - Dieldrin KW - Fumigants KW - Herbicides KW - Insecticides KW - Mortality KW - Organochlorine compounds KW - Pesticides KW - Pyrethroids KW - Replication KW - Reviews KW - Statistical analysis KW - Toxaphene KW - H 5000:Pesticides KW - N3 11027:Neurology & neuropathology KW - X 24330:Agrochemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020843282?accountid=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=Neurotoxicology&rft.atitle=Pesticide+exposure+and+amyotrophic+lateral+sclerosis&rft.au=Kamel%2C+Freya%3BUmbach%2C+David+M%3BBedlack%2C+Richard+S%3BRichards%2C+Marie%3BWatson%2C+Mary%3BAlavanja%2C+Michael+CR%3BBlair%2C+Aaron%3BHoppin%2C+Jane+A%3BSchmidt%2C+Silke%3BSandler%2C+Dale+P&rft.aulast=Kamel&rft.aufirst=Freya&rft.date=2012-06-01&rft.volume=33&rft.issue=3&rft.spage=457&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology&rft.issn=0161813X&rft_id=info:doi/10.1016%2Fj.neuro.2012.04.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Last updated - 2012-12-14 N1 - SubjectsTermNotLitGenreText - Mortality; Data processing; Organochlorine compounds; Fumigants; Replication; Aldrin; Dieldrin; Statistical analysis; Herbicides; Amyotrophic lateral sclerosis; Insecticides; Reviews; Pesticides; DDT; Pyrethroids; Toxaphene DO - http://dx.doi.org/10.1016/j.neuro.2012.04.001 ER - TY - JOUR T1 - Fenofibrate-associated changes in renal function and relationship to clinical outcomes among individuals with type 2 diabetes: the Action to Control Cardiovascular Risk in Diabetes (ACCORD) experience AN - 1020841874; 16750014 AB - Aims/hypothesis: Fenofibrate has been noted to cause an elevation in serum creatinine in some individuals. Participants in the Action to Control Cardiovascular Risk in Diabetes Lipid Study were studied to better characterise who is at risk of an increase in creatinine level and to determine whether those with creatinine elevation have a differential risk of adverse renal or cardiovascular outcomes. Methods: A fenofibrate-associated creatinine increase (FACI) was defined as an increase in serum creatinine of at least 20% from baseline to month 4 in participants assigned to fenofibrate. Baseline patient characteristics, and baseline and 4-month drug, clinical, laboratory characteristics and study outcomes were examined by FACI status. Results: Of the sample, 48% of those randomised to receive fenofibrate had at least a 20% increase in serum creatinine within 4 months. In multivariable analysis, participants who were older, male, used an ACE inhibitor at baseline, used a thiazolidinedione (TZD) at 4 months post-randomisation, had baseline CVD, and had lower baseline serum creatinine and LDL-cholesterol levels were all more likely to meet the criteria for FACI. Participants in the FACI group were also more likely to have a decrease in their serum triacylglycerol level from baseline to 4 months. No differences in study outcomes were seen by FACI criteria. Conclusions/interpretation: Several characteristics predict a rapid rise in serum creatinine upon starting fenofibrate. Participants who met the criteria for FACI also had a greater change in triacylglycerol levels. In the setting of careful renal function surveillance and reduction of fenofibrate dose as indicated, no increase in renal disease or cardiovascular outcome was seen in those individuals demonstrating FACI. Trial registration: ClincalTrials.gov: NCT00000620 Funding: The ACCORD Trial was supported by grants (N01-HC-95178, N01-HC-95179, N01-HC-95180, N01-HC-95181, N01-HC-95182, N01-HC-95183, N01-HC-95184, IAA-Y1-HC-9035 and IAA-Y1-HC-1010) from the National Heart, Lung, and Blood Institute; by the National Institute of Diabetes and Digestive and Kidney Diseases, the National Institute on Aging, and the National Eye Institute; by the Centers for Disease Control and Prevention; by General Clinical Research Centers and by the Clinical and Translational Science Awards. Abbott Laboratories, Amylin Pharmaceutical, AstraZeneca Pharmaceuticals LP, Bayer HealthCare LLC, Closer Healthcare, GlaxoSmithKline Pharmaceuticals, King Pharmaceuticals, Merck, Novartis Pharmaceuticals, Novo Nordisk, Omron Healthcare, sanofi-aventis US and Takeda Pharmaceuticals provided study medications, equipment or supplies. JF - Diabetologia AU - Bonds, DE AU - Craven, TE AU - Buse, J AU - Crouse, J R AU - Cuddihy, R AU - Elam, M AU - Ginsberg, H N AU - Kirchner, K AU - Marcovina, S AU - Mychaleckyj, J C AU - O'Connor, P J AU - Sperl-Hillen, J-A AD - Division of Cardiovascular Sciences, National Heart, Lung and Blood Institute, National Institutes of Health, Rockledge Center 2, MSC 7936, 6701 Rockledge Drive, Suite 10018, Bethesda, MD, 20892-7936, USA, bondsde@nhlbi.nih.gov Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 1641 EP - 1650 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 55 IS - 6 SN - 0012-186X, 0012-186X KW - Risk Abstracts; Health & Safety Science Abstracts KW - Clinical trials KW - Drugs KW - Eye KW - Health care KW - Kidney KW - Lipids KW - awards KW - diabetes mellitus KW - renal function 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/1020841874?accountid=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=Diabetologia&rft.atitle=Fenofibrate-associated+changes+in+renal+function+and+relationship+to+clinical+outcomes+among+individuals+with+type+2+diabetes%3A+the+Action+to+Control+Cardiovascular+Risk+in+Diabetes+%28ACCORD%29+experience&rft.au=Bonds%2C+DE%3BCraven%2C+TE%3BBuse%2C+J%3BCrouse%2C+J+R%3BCuddihy%2C+R%3BElam%2C+M%3BGinsberg%2C+H+N%3BKirchner%2C+K%3BMarcovina%2C+S%3BMychaleckyj%2C+J+C%3BO%27Connor%2C+P+J%3BSperl-Hillen%2C+J-A&rft.aulast=Bonds&rft.aufirst=DE&rft.date=2012-06-01&rft.volume=55&rft.issue=6&rft.spage=1641&rft.isbn=&rft.btitle=&rft.title=Diabetologia&rft.issn=0012186X&rft_id=info:doi/10.1007%2Fs00125-012-2524-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - diabetes mellitus; Eye; Health care; awards; Lipids; renal function; Kidney; Clinical trials; Drugs DO - http://dx.doi.org/10.1007/s00125-012-2524-2 ER - TY - JOUR T1 - Compromising σ-1 receptors at the endoplasmic reticulum render cytotoxicity to physiologically relevant concentrations of dopamine in a nuclear factor-κB/Bcl-2-dependent mechanism: potential relevance to Parkinson's disease. AN - 1015248916; 22399814 AB - The endoplasmic reticulum (ER) chaperone σ-1 receptor (Sig-1R) is cytoprotective against ER stress-induced apoptosis. The level of Sig-1Rs in the brain was reported to be lower in early parkinsonian patients. Because dopamine (DA) toxicity is well known to be involved in the etiology of Parkinson's disease, we tested in this study whether a relationship might exist between Sig-1Rs and DA-induced cytotoxicity in a cellular model by using Chinese hamster ovary (CHO) cells. DA in physiological concentrations (e.g., lower than 10 μM) does not cause apoptosis. However, the same concentrations of DA cause apoptosis in Sig-1R knockdown CHO cells. In search of a mechanistic explanation, we found that unfolded protein response is not involved. Rather, the level of protective protein Bcl-2 is critically involved in this DA/Sig-1R knockdown-induced apoptosis. Specifically, the DA/Sig-1R knockdown causes a synergistic proteasomal conversion of nuclear factor κB (NF-κB) p105 to the active form of p50, which is known to down-regulate the transcription of Bcl-2. It is noteworthy that the DA/Sig-1R knockdown-induced apoptosis is blocked by the overexpression of Bcl-2. Our results therefore indicate that DA is involved in the activation of NF-κB and suggest that endogenous Sig-1Rs are tonically inhibiting the proteasomal conversion/activation of NF-κB caused by physiologically relevant concentrations of DA that would otherwise cause apoptosis. Thus, Sig-1Rs and associated ligands may represent new therapeutic targets for the treatment of parkinsonism. JF - The Journal of pharmacology and experimental therapeutics AU - Mori, Tomohisa AU - Hayashi, Teruo AU - Su, Tsung-Ping AD - Cellular Pathobiology Section, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD 21224, USA. Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 663 EP - 671 VL - 341 IS - 3 KW - Dopamine Agents KW - 0 KW - NF-kappa B KW - Proto-Oncogene Proteins c-bcl-2 KW - Reactive Oxygen Species KW - Receptors, sigma KW - sigma-1 receptor KW - Superoxides KW - 11062-77-4 KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Reactive Oxygen Species -- metabolism KW - Animals KW - Superoxides -- metabolism KW - CHO Cells -- metabolism KW - Blotting, Western KW - Cricetulus KW - Transfection KW - Gene Silencing KW - CHO Cells -- drug effects KW - Models, Biological KW - Parkinson Disease -- drug therapy KW - Cricetinae KW - Endoplasmic Reticulum -- metabolism KW - Dopamine -- pharmacology KW - Receptors, sigma -- genetics KW - Receptors, sigma -- metabolism KW - Proto-Oncogene Proteins c-bcl-2 -- metabolism KW - Dopamine Agents -- pharmacology KW - Apoptosis -- drug effects KW - NF-kappa B -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1015248916?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Compromising+%CF%83-1+receptors+at+the+endoplasmic+reticulum+render+cytotoxicity+to+physiologically+relevant+concentrations+of+dopamine+in+a+nuclear+factor-%CE%BAB%2FBcl-2-dependent+mechanism%3A+potential+relevance+to+Parkinson%27s+disease.&rft.au=Mori%2C+Tomohisa%3BHayashi%2C+Teruo%3BSu%2C+Tsung-Ping&rft.aulast=Mori&rft.aufirst=Tomohisa&rft.date=2012-06-01&rft.volume=341&rft.issue=3&rft.spage=663&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+pharmacology+and+experimental+therapeutics&rft.issn=1521-0103&rft_id=info:doi/10.1124%2Fjpet.111.190868 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-24 N1 - Date created - 2012-05-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Pharmacol Exp Ther. 2010 Feb;332(2):388-97 [19855099] Cent Nerv Syst Agents Med Chem. 2009 Sep;9(3):190-6 [20021353] Cell Mol Neurobiol. 2001 Jun;21(3):215-35 [11569535] Mol Cell. 2003 Mar;11(3):619-33 [12667446] J Biol Chem. 2003 May 23;278(21):19367-77 [12598533] Neuron. 2003 Sep 11;39(6):889-909 [12971891] Science. 1971 Dec 24;174(4016):1346-9 [4332627] Trends Biochem Sci. 1997 Feb;22(2):63-7 [9048485] Mol Cancer Ther. 2005 Apr;4(4):578-86 [15827331] J Cell Physiol. 2005 Aug;204(2):549-59 [15799019] Acta Neurol Scand. 2005 Aug;112(2):103-7 [16008536] Hum Mol Genet. 2005 Dec 15;14(24):3801-11 [16239241] Cell Death Differ. 2006 Mar;13(3):374-84 [16397578] J Pharmacol Exp Ther. 2007 Jan;320(1):202-10 [17050780] Biochem Biophys Res Commun. 2007 Mar 16;354(3):707-11 [17254549] Cell. 2007 Nov 2;131(3):596-610 [17981125] Proc Natl Acad Sci U S A. 2007 Nov 20;104(47):18754-9 [18000063] Curr Med Chem. 2008;15(4):404-14 [18288995] Int J Biochem Cell Biol. 2008;40(8):1425-30 [17693123] J Neurochem. 2008 Jul;106(1):333-46 [18384645] Annu Rev Biochem. 2009;78:769-96 [19489733] J Neurochem. 2009 Jun;109(6):1791-9 [19457134] J Pharmacol Exp Ther. 2010 Mar;332(3):1054-63 [19940104] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1124/jpet.111.190868 ER - TY - JOUR T1 - Neuroinflammation: a need to understand microglia as resident cells of the developing brain. AN - 1015247519; 22507950 AB - Neuroinflammation and microglia as the resident immune cells of the brain has garnered a significant amount of interest with regards to brain injury and neurotoxicology. Much of this interest and research has been focused on responses in the adult brain with little attention paid to the role of these cells during development. The available data suggests that one must view microglia and their processes during development somewhat differently. In addition, modification to microglia during development may lay a framework for subtle to significant changes in the susceptibility of the mature brain to secondary insults. A number of these point are now being raised for consideration. Published by Elsevier B.V. JF - Neurotoxicology AU - Harry, G Jean AD - National Toxicology Program Laboratory, National Institute of Environmental Health Sciences, PO Box 12233, MD C1-04, Research Triangle Park, NC 27709, USA. harry@niehs.nih.gov Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 558 EP - 559 VL - 33 IS - 3 KW - Index Medicus KW - Animals KW - Age Factors KW - Risk Factors KW - Humans KW - Risk Assessment KW - Inflammation -- physiopathology KW - Brain -- pathology KW - Brain -- drug effects KW - Microglia -- immunology KW - Neurotoxicity Syndromes -- physiopathology KW - Inflammation -- immunology KW - Brain -- immunology KW - Microglia -- pathology KW - Microglia -- drug effects KW - Neurotoxicity Syndromes -- pathology KW - Brain -- growth & development KW - Neurotoxicity Syndromes -- immunology KW - Inflammation -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1015247519?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurotoxicology&rft.atitle=Neuroinflammation%3A+a+need+to+understand+microglia+as+resident+cells+of+the+developing+brain.&rft.au=Harry%2C+G+Jean&rft.aulast=Harry&rft.aufirst=G&rft.date=2012-06-01&rft.volume=33&rft.issue=3&rft.spage=558&rft.isbn=&rft.btitle=&rft.title=Neurotoxicology&rft.issn=1872-9711&rft_id=info:doi/10.1016%2Fj.neuro.2012.03.013 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-18 N1 - Date created - 2012-05-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.neuro.2012.03.013 ER - TY - JOUR T1 - Altered Ig hypermutation pattern and frequency in complementary mouse models of DNA polymerase ζ activity. AN - 1015244824; 22547703 AB - To test the hypothesis that DNA polymerase ζ participates in Ig hypermutation, we generated two mouse models of Pol ζ function: a B cell-specific conditional knockout and a knock-in strain with a Pol ζ mutagenesis-enhancing mutation. Pol ζ-deficient B cells had a reduction in mutation frequency at Ig loci in the spleen and in Peyer's patches, whereas knock-in mice with a mutagenic Pol ζ displayed a marked increase in mutation frequency in Peyer's patches, revealing a pattern that was similar to mutations in yeast strains with a homologous mutation in the gene encoding the catalytic subunit of Pol ζ. Combined, these data are best explained by a direct role for DNA polymerase ζ in Ig hypermutation. JF - Journal of immunology (Baltimore, Md. : 1950) AU - Daly, Janssen AU - Bebenek, Katarzyna AU - Watt, Danielle L AU - Richter, Kathleen AU - Jiang, Chuancang AU - Zhao, Ming-Lang AU - Ray, Madhumita AU - McGregor, W Glenn AU - Kunkel, Thomas A AU - Diaz, Marilyn AD - Somatic Hypermutation Group, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC 27709, USA. Y1 - 2012/06/01/ PY - 2012 DA - 2012 Jun 01 SP - 5528 EP - 5537 VL - 188 IS - 11 KW - DNA polymerase zeta KW - EC 2.7.7.- KW - Rev3 protein, mouse KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - Abridged Index Medicus KW - Index Medicus KW - Models, Animal KW - Animals KW - B-Lymphocytes -- pathology KW - Gene Rearrangement, B-Lymphocyte, Heavy Chain KW - B-Lymphocytes -- immunology KW - Mice KW - Mice, Transgenic KW - Mice, Knockout KW - Enzyme Activation -- genetics KW - DNA-Directed DNA Polymerase -- physiology KW - Gene Knock-In Techniques KW - Mice, Inbred C57BL KW - B-Lymphocytes -- enzymology KW - Enzyme Activation -- immunology KW - DNA-Directed DNA Polymerase -- deficiency KW - DNA-Directed DNA Polymerase -- genetics KW - Somatic Hypermutation, Immunoglobulin -- genetics KW - Somatic Hypermutation, Immunoglobulin -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1015244824?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.atitle=Altered+Ig+hypermutation+pattern+and+frequency+in+complementary+mouse+models+of+DNA+polymerase+%CE%B6+activity.&rft.au=Daly%2C+Janssen%3BBebenek%2C+Katarzyna%3BWatt%2C+Danielle+L%3BRichter%2C+Kathleen%3BJiang%2C+Chuancang%3BZhao%2C+Ming-Lang%3BRay%2C+Madhumita%3BMcGregor%2C+W+Glenn%3BKunkel%2C+Thomas+A%3BDiaz%2C+Marilyn&rft.aulast=Daly&rft.aufirst=Janssen&rft.date=2012-06-01&rft.volume=188&rft.issue=11&rft.spage=5528&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunology+%28Baltimore%2C+Md.+%3A+1950%29&rft.issn=1550-6606&rft_id=info:doi/10.4049%2Fjimmunol.1102629 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-14 N1 - Date created - 2012-05-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell. 2000 Sep 1;102(5):553-63 [11007474] Adv Protein Chem. 2004;69:137-65 [15588842] Curr Biol. 2000 Oct 5;10(19):1213-6 [11050391] Curr Biol. 2000 Oct 5;10(19):1217-20 [11050392] Curr Biol. 2000 Oct 5;10(19):1221-4 [11050393] Philos Trans R Soc Lond B Biol Sci. 2001 Jan 29;356(1405):67-72 [11205333] Immunity. 2001 May;14(5):643-53 [11371365] Nat Immunol. 2001 Jun;2(6):530-6 [11376340] Nat Immunol. 2001 Jun;2(6):537-41 [11376341] J Immunol. 2001 Jul 1;167(1):327-35 [11418667] Nature. 2002 Jul 4;418(6893):99-103 [12097915] Genes Dev. 2002 Aug 1;16(15):1872-83 [12154119] Biochem Soc Trans. 2002 Aug;30(4):815-8 [12196205] Nature. 2002 Oct 31;419(6910):944-7 [12410315] EMBO J. 2003 Apr 1;22(7):1654-64 [12660171] Genetics. 2005 Feb;169(2):575-82 [15520252] Trends Immunol. 2005 Apr;26(4):215-20 [15797512] Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):13986-91 [16172387] EMBO J. 2005 Nov 2;24(21):3757-69 [16222339] J Immunol. 2007 Jun 1;178(11):7422-31 [17513793] DNA Repair (Amst). 2007 Dec 1;6(12):1829-38 [17715002] Nature. 2008 May 29;453(7195):667-71 [18449194] Immunology. 2009 Jan;126(1):102-13 [18624728] J Exp Med. 2009 Feb 16;206(2):477-90 [19204108] Nucleic Acids Res. 2009 Jun;37(11):3774-87 [19380376] Int Immunol. 2009 Aug;21(8):947-55 [19556307] J Exp Med. 2009 Nov 23;206(12):2603-11 [19901081] Curr Opin Immunol. 2011 Jun;23(3):383-90 [21524897] World J Gastroenterol. 2003 Jun;9(6):1165-9 [12800216] Nature. 1970 Dec 12;228(5276):1045-7 [5483159] J Exp Med. 1972 Aug 1;136(2):241-60 [4114497] EMBO J. 1986 Oct;5(10):2459-68 [2430792] Eur J Immunol. 1994 Nov;24(11):2918-21 [7957583] Nature. 1995 Jul 27;376(6538):352-5 [7543183] Nucleic Acids Res. 1997 Mar 15;25(6):1317-8 [9092650] Immunol Rev. 1998 Apr;162:13-24 [9602348] Proc Natl Acad Sci U S A. 1998 Jun 9;95(12):6876-80 [9618506] Mutat Res. 1999 Mar 10;433(2):109-16 [10102037] Int Immunol. 1999 May;11(5):825-33 [10330287] Cell. 2000 Sep 1;102(5):565-75 [11007475] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.4049/jimmunol.1102629 ER - TY - JOUR T1 - At the cancer steering wheel: defining key genomic drivers of liver cancer with next generation sequencing. AN - 1015244059; 22286003 JF - Journal of hepatology AU - Budhu, Anuradha AU - Wang, Xin Wei AD - Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 1412 EP - 1414 VL - 56 IS - 6 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1015244059?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+hepatology&rft.atitle=At+the+cancer+steering+wheel%3A+defining+key+genomic+drivers+of+liver+cancer+with+next+generation+sequencing.&rft.au=Budhu%2C+Anuradha%3BWang%2C+Xin+Wei&rft.aulast=Budhu&rft.aufirst=Anuradha&rft.date=2012-06-01&rft.volume=56&rft.issue=6&rft.spage=1412&rft.isbn=&rft.btitle=&rft.title=Journal+of+hepatology&rft.issn=1600-0641&rft_id=info:doi/10.1016%2Fj.jhep.2011.12.024 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-17 N1 - Date created - 2012-05-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Comment On: Nat Genet. 2011 Sep;43(9):828-9 [21822264] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.jhep.2011.12.024 ER - TY - JOUR T1 - Clinical evaluation of TRICOM vector therapeutic cancer vaccines. AN - 1015096756; 22595052 AB - We have developed an "off-the-shelf" vector-based vaccine platform containing transgenes for carcinoma-associated antigens and multiple costimulatory molecules (designated TRICOM). Two TRICOM platforms have been evaluated both preclinically and in clinical trials. PROSTVAC consists of rV, rF-PSA-TRICOM and is being used in prostate cancer therapy trials. PANVAC consists of rV, rF-CEA-MUC1-TRICOM; the expression of the two pan-carcinoma transgenes CEA and MUC-1 renders PANVAC vaccination applicable for therapeutic applications for a range of human carcinomas. Many new paradigms have emerged as a consequence of completed and ongoing TRICOM vaccine trials, including (1) clinical evidence of patient benefit may be delayed, because multiple vaccinations may be necessary to induce a sufficient anti-tumor immune response; (2) survival, and not strict adherence to RECIST criteria or time-to-progression, may be the most appropriate trial endpoint when TRICOM vaccines are used as monotherapy; (3) certain patient populations are more likely to benefit from vaccine therapy as compared to other therapeutics; and (4) TRICOM vaccines combined with standard-of-care therapeutics, either concomitantly or sequentially, are feasible because of the limited toxicity of vaccines. Published by Elsevier Inc. JF - Seminars in oncology AU - Madan, Ravi A AU - Bilusic, Marijo AU - Heery, Christopher AU - Schlom, Jeffrey AU - Gulley, James L AD - Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 296 EP - 304 VL - 39 IS - 3 KW - Antigens, Neoplasm KW - 0 KW - Cancer Vaccines KW - Vaccines, Synthetic KW - Index Medicus KW - Animals KW - Humans KW - Vaccines, Synthetic -- immunology KW - Transgenes KW - Clinical Trials as Topic KW - Antigens, Neoplasm -- immunology KW - Vaccines, Synthetic -- pharmacology KW - Male KW - Cancer Vaccines -- pharmacology KW - Prostatic Neoplasms -- immunology KW - Cancer Vaccines -- immunology KW - Cancer Vaccines -- genetics KW - Prostatic Neoplasms -- drug therapy KW - Immunotherapy -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1015096756?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Seminars+in+oncology&rft.atitle=Clinical+evaluation+of+TRICOM+vector+therapeutic+cancer+vaccines.&rft.au=Madan%2C+Ravi+A%3BBilusic%2C+Marijo%3BHeery%2C+Christopher%3BSchlom%2C+Jeffrey%3BGulley%2C+James+L&rft.aulast=Madan&rft.aufirst=Ravi&rft.date=2012-06-01&rft.volume=39&rft.issue=3&rft.spage=296&rft.isbn=&rft.btitle=&rft.title=Seminars+in+oncology&rft.issn=1532-8708&rft_id=info:doi/10.1053%2Fj.seminoncol.2012.02.010 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-18 N1 - Date created - 2012-05-18 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer Res. 2002 Oct 15;62(20):5770-7 [12384537] Lancet Oncol. 2012 May;13(5):501-8 [22326924] J Clin Oncol. 2003 Apr 1;21(7):1232-7 [12663709] Clin Cancer Res. 2003 May;9(5):1837-49 [12738742] Cancer Res. 2003 Nov 15;63(22):7942-9 [14633725] Cancer Res. 2004 May 15;64(10):3668-78 [15150127] J Clin Oncol. 2004 Jul 1;22(13):2532-9 [15226321] N Engl J Med. 2004 Oct 7;351(15):1502-12 [15470213] Cell Immunol. 1999 May 25;194(1):78-89 [10357883] J Clin Oncol. 2005 Feb 1;23(4):720-31 [15613691] Clin Cancer Res. 2005 Feb 15;11(4):1597-607 [15746065] J Gastrointest Surg. 2005 Mar;9(3):374-80 [15749600] Ann Surg. 2005 May;241(5):715-22, discussion 722-4 [15849507] Clin Cancer Res. 2005 Jun 15;11(12):4430-6 [15958627] Clin Cancer Res. 2005 Aug 1;11(15):5603-15 [16061879] J Immunol. 2005 Sep 15;175(6):3715-23 [16148117] Clin Cancer Res. 2006 Feb 1;12(3 Pt 1):878-87 [16467102] Clin Cancer Res. 2006 Feb 15;12(4):1260-9 [16489082] Clin Cancer Res. 2006 Mar 15;12(6):1897-905 [16551875] Eur J Cancer. 2006 May;42(8):1031-9 [16616487] J Exp Med. 2006 May 15;203(5):1259-71 [16636135] Expert Opin Biol Ther. 2007 Apr;7(4):543-54 [17373905] Cancer Immunol Immunother. 2007 Sep;56(9):1471-84 [17318654] Clin Cancer Res. 2007 Jul 1;13(13):3776-82 [17606707] J Urol. 2007 Oct;178(4 Pt 1):1515-20 [17707059] Expert Rev Anticancer Ther. 2007 Nov;7(11):1517-27 [18020921] World J Surg. 2008 Jan;32(1):93-103 [18027020] Ann Surg Oncol. 2008 Jan;15(1):134-43 [17909911] Clin Cancer Res. 2008 May 15;14(10):3060-9 [18483372] Clin Cancer Res. 2008 Jun 1;14(11):3536-44 [18519787] Clin Cancer Res. 2008 Jul 1;14(13):4241-9 [18594006] Cancer Immunol Immunother. 2009 Apr;58(4):503-15 [18690438] Cancer. 2009 Aug 15;115(16):3670-9 [19536890] Clin Cancer Res. 2009 Sep 1;15(17):5323-37 [19723653] Cancer Immunol Immunother. 2010 Mar;59(3):397-408 [19756595] J Clin Oncol. 2010 Mar 1;28(7):1099-105 [20100959] Cancer Immunol Immunother. 2010 May;59(5):663-74 [19890632] Expert Opin Biol Ther. 2010 Jan;10(1):19-28 [19857185] J Am Coll Surg. 2010 May;210(5):744-52, 752-5 [20421043] Cancer Res. 1999 Nov 15;59(22):5800-7 [10582702] N Engl J Med. 2000 Jun 29;342(26):1946-52 [10874062] Clin Cancer Res. 2000 Jun;6(6):2219-28 [10873071] Cancer Res. 2000 Sep 15;60(18):5040-4 [11016626] J Clin Oncol. 2000 Dec 1;18(23):3964-73 [11099326] Clin Cancer Res. 2001 May;7(5):1181-91 [11350882] Ann Surg. 2002 Jun;235(6):759-66 [12035031] N Engl J Med. 2010 Aug 19;363(8):711-23 [20525992] N Engl J Med. 2010 Jul 29;363(5):411-22 [20818862] Oncologist. 2010;15(9):969-75 [20798195] J Natl Cancer Inst. 2010 Sep 22;102(18):1388-97 [20826737] Lancet. 2010 Oct 2;376(9747):1147-54 [20888992] Clin Cancer Res. 2011 Feb 15;17(4):907-17 [21106727] Nat Rev Clin Oncol. 2011 Mar;8(3):151-60 [21364688] N Engl J Med. 2011 May 26;364(21):1995-2005 [21612468] Eur J Cancer. 2011 Jul;47(11):1676-81 [21565490] Expert Opin Biol Ther. 2011 Nov;11(11):1409-18 [21871012] Cancer Res. 2002 Dec 1;62(23):6944-51 [12460911] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1053/j.seminoncol.2012.02.010 ER - TY - JOUR T1 - Molecular analysis of the Noggin (NOG) gene in holoprosencephaly patients. AN - 1015094988; 22503063 AB - Holoprosencephaly (HPE) is the most common structural anomaly of the human forebrain. Various genetic and teratogenic causes have been implicated in its pathogenesis. A recent report in mice described Noggin (NOG) as a candidate gene involved in the etiogenesis of microform HPE. Here, we present for the first time genetic analysis of a large HPE cohort for sequence variations in NOG. On the basis of our study, we conclude that mutations in the coding region of NOG are rare, and play at most an uncommon role in human HPE. Published by Elsevier Inc. JF - Molecular genetics and metabolism AU - Srivastava, Kshitij AU - Hu, Ping AU - Solomon, Benjamin D AU - Ming, Jeffrey E AU - Roessler, Erich AU - Muenke, Maximilian AD - Medical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 241 EP - 243 VL - 106 IS - 2 KW - Carrier Proteins KW - 0 KW - noggin protein KW - 148294-77-3 KW - Index Medicus KW - Polymorphism, Single Nucleotide KW - Humans KW - Mutation KW - Amino Acid Substitution KW - Carrier Proteins -- genetics KW - Holoprosencephaly -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1015094988?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+genetics+and+metabolism&rft.atitle=Molecular+analysis+of+the+Noggin+%28NOG%29+gene+in+holoprosencephaly+patients.&rft.au=Srivastava%2C+Kshitij%3BHu%2C+Ping%3BSolomon%2C+Benjamin+D%3BMing%2C+Jeffrey+E%3BRoessler%2C+Erich%3BMuenke%2C+Maximilian&rft.aulast=Srivastava&rft.aufirst=Kshitij&rft.date=2012-06-01&rft.volume=106&rft.issue=2&rft.spage=241&rft.isbn=&rft.btitle=&rft.title=Molecular+genetics+and+metabolism&rft.issn=1096-7206&rft_id=info:doi/10.1016%2Fj.ymgme.2012.03.008 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-18 N1 - Date created - 2012-05-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Brain Dev. 1999 Dec;21(8):513-21 [10598051] Nat Cell Biol. 1999 Jul;1(3):158-64 [10559902] Clin Genet. 2001 Dec;60(6):447-51 [11846737] Development. 2002 Nov;129(21):4975-87 [12397106] Am J Hum Genet. 2002 Nov;71(5):1017-32 [12395298] Curr Biol. 2003 Mar 4;13(5):411-5 [12620190] Dev Biol. 2004 Mar 15;267(2):374-86 [15013800] Cell. 1992 Sep 4;70(5):829-40 [1339313] Genes Dev. 1998 May 15;12(10):1438-52 [9585504] Science. 1998 May 29;280(5368):1455-7 [9603738] Nature. 1999 Feb 25;397(6721):707-10 [10067895] Trends Genet. 1999 Aug;15(8):314-9 [10431193] Dev Biol. 2005 Oct 1;286(1):149-57 [16122729] Dev Cell. 2006 May;10(5):657-65 [16647303] Orphanet J Rare Dis. 2007;2:8 [17274816] Expert Rev Mol Med. 2007;9(26):1-17 [17888203] Hum Mutat. 2008 Jan;29(1):6-13 [18000842] J Clin Invest. 2009 Jun;119(6):1403-13 [19487816] Am J Med Genet C Semin Med Genet. 2010 Feb 15;154C(1):52-61 [20104595] Am J Med Genet C Semin Med Genet. 2010 Feb 15;154C(1):133-41 [20104608] Hum Mol Genet. 2010 Aug 1;19(15):3030-42 [20508035] Panminerva Med. 2010 Dec;52(4):345-54 [21183895] Hum Mutat. 2011 Aug;32(8):877-86 [21538686] Am J Hum Genet. 2011 Aug 12;89(2):231-40 [21802063] Hum Mol Genet. 2011 Oct 15;20(20):4005-15 [21821669] Hum Genet. 2012 Feb;131(2):301-10 [21842183] Mol Genet Metab. 2012 Apr;105(4):658-64 [22310223] Nature. 2000 Feb 10;403(6770):658-61 [10688202] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.ymgme.2012.03.008 ER - TY - JOUR T1 - Inducible Expression of Neurotrophic Factors by Mesenchymal Progenitor Cells Derived from Traumatically Injured Human Muscle AN - 1014108845; 16666745 AB - Peripheral nerve damage frequently accompanies musculoskeletal trauma and repair of these nerves could be enhanced by the targeted application of neurotrophic factors (NTFs), which are typically expressed by endogenous cells that support nerve regeneration. Injured muscle tissues express NTFs to promote reinnervation as the tissue regenerates, but the source of these factors from within the muscles is not fully understood. We have previously identified a population of mesenchymal progenitor cells (MPCs) in traumatized muscle tissue with properties that support tissue regeneration, and our hypothesis was that MPCs also secrete the NTFs that are associated with muscle tissue reinnervation. We determined that MPCs express genes associated with neurogenic function and measured the protein-level expression of specific NTFs with known functions to support nerve regeneration. We also demonstrated the effectiveness of a neurotrophic induction protocol to enhance the expression of the NTFs, which suggests that the expression of these factors may be modulated by the cellular environment. Finally, neurotrophic induction affected the expression of cell surface markers and proliferation rate of the MPCs. Our findings indicate that traumatized muscle-derived MPCs may be useful as a therapeutic cell type to enhance peripheral nerve regeneration following musculoskeletal injury. JF - Molecular Biotechnology AU - Bulken-Hoover, Jamie D AU - Jackson, Wesley M AU - Ji, Youngmi AU - Volger, Jared A AU - Tuan, Rocky S AU - Nesti, Leon J AD - Cartilage Biology and Orthopaedic Branch, Department of Health and Human Services, National Institute of Arthritis and Musculoskeletal and Skin Disease, National Institutes of Health, 50 South Drive, Room 1525, Bethesda, MD, MSC 8022, USA, rst13@pitt.edu Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 128 EP - 136 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 51 IS - 2 SN - 1073-6085, 1073-6085 KW - Biotechnology and Bioengineering Abstracts KW - Cell surface KW - Injuries KW - Mesenchyme KW - Muscles KW - Neurotrophic factors KW - Peripheral nerves KW - Regeneration KW - Reinnervation KW - Stem cells KW - Trauma KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1014108845?accountid=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+Biotechnology&rft.atitle=Inducible+Expression+of+Neurotrophic+Factors+by+Mesenchymal+Progenitor+Cells+Derived+from+Traumatically+Injured+Human+Muscle&rft.au=Bulken-Hoover%2C+Jamie+D%3BJackson%2C+Wesley+M%3BJi%2C+Youngmi%3BVolger%2C+Jared+A%3BTuan%2C+Rocky+S%3BNesti%2C+Leon+J&rft.aulast=Bulken-Hoover&rft.aufirst=Jamie&rft.date=2012-06-01&rft.volume=51&rft.issue=2&rft.spage=128&rft.isbn=&rft.btitle=&rft.title=Molecular+Biotechnology&rft.issn=10736085&rft_id=info:doi/10.1007%2Fs12033-011-9445-z LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Cell surface; Stem cells; Injuries; Neurotrophic factors; Regeneration; Muscles; Reinnervation; Mesenchyme; Peripheral nerves; Trauma DO - http://dx.doi.org/10.1007/s12033-011-9445-z ER - TY - JOUR T1 - Sigma-2 Receptor as Potential Indicator of Stem Cell Differentiation AN - 1014106076; 16667198 AB - Purpose: The sigma-2 ( sigma sub(2)) receptor is a potential biomarker of proliferative status of solid tumors. Specific synthetic probes using N-substituted-9-azabicyclo [3.3.1]nonan-3 alpha -yl carbamate analogs have been designed and implemented for experimental cancer diagnosis and therapy. Procedures: We employed the fluorescently labeled sigma sub(2) receptor probe, SW120, to evaluate sigma sub(2) receptor expression in human stem cells (SC), including: bone marrow stromal, neural progenitor, amniotic fluid, hematopoetic, and embryonic stem cells. We concurrently evaluated the intensity of SW120 and 5-ethynyl-2'-deoxyuridine (EdU) relative to passage number and multi-potency. Results: We substantiated significantly higher sigma sub(2) receptor density among proliferating SC relative to lineage-restricted cell types. Additionally, cellular internalization of the sigma sub(2) receptor in SC was consistent with receptor-mediated endocytosis and confocal microscopy indicated SW120 specific co-localization with a fluorescent marker of lysosomes in all SC imaged. Conclusion: These results suggest that sigma sub(2) receptors may serve to monitor stem cell differentiation in future experimental studies. JF - Molecular Imaging and Biology AU - Haller, Jodi L AU - Panyutin, Irina AU - Chaudhry, Aneeka AU - Zeng, Chenbo AU - Mach, Robert H AU - Frank, Joseph A AD - Frank Laboratory, Department of Radiology and Imaging Sciences, Clinical Center, National Institutes of Health, Clinical Center, Bldg. 10, Room BIN256, Bethesda, MD, 20892, USA, hallerjod@cc.nih.gov Y1 - 2012/06// PY - 2012 DA - Jun 2012 SP - 325 EP - 335 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 14 IS - 3 SN - 1536-1632, 1536-1632 KW - Biotechnology and Bioengineering Abstracts KW - Amniotic fluid KW - Bone marrow KW - Cancer KW - Confocal microscopy KW - Differentiation KW - Embryo cells KW - Endocytosis KW - Fluorescent indicators KW - Lysosomes KW - Neural stem cells KW - Probes KW - Receptor density KW - Serotonin S2 receptors KW - Solid tumors KW - Stem cells KW - biomarkers KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1014106076?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Imaging+and+Biology&rft.atitle=Sigma-2+Receptor+as+Potential+Indicator+of+Stem+Cell+Differentiation&rft.au=Haller%2C+Jodi+L%3BPanyutin%2C+Irina%3BChaudhry%2C+Aneeka%3BZeng%2C+Chenbo%3BMach%2C+Robert+H%3BFrank%2C+Joseph+A&rft.aulast=Haller&rft.aufirst=Jodi&rft.date=2012-06-01&rft.volume=14&rft.issue=3&rft.spage=325&rft.isbn=&rft.btitle=&rft.title=Molecular+Imaging+and+Biology&rft.issn=15361632&rft_id=info:doi/10.1007%2Fs11307-011-0493-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Amniotic fluid; Solid tumors; Probes; Bone marrow; biomarkers; Serotonin S2 receptors; Cancer; Differentiation; Endocytosis; Stem cells; Embryo cells; Confocal microscopy; Receptor density; Fluorescent indicators; Neural stem cells; Lysosomes DO - http://dx.doi.org/10.1007/s11307-011-0493-3 ER - TY - JOUR T1 - Evaluation of γ-retroviral vectors that mediate the inducible expression of IL-12 for clinical application. AN - 1013921530; 22576348 AB - The clinical application of interleukin-12 (IL-12) has been hindered by the toxicity associated with its systemic administration. To potentially overcome this problem, we developed a promoter designed to direct IL-12 expression within the tumor environment using an inducible composite promoter containing binding motifs for the nuclear factor of activated T cells (NFAT) linked to a minimal IL-2 promoter. In this study, the NFAT promoter was coupled to a single-chain human IL-12 gene and inserted into 2 γ-retroviral self-inactivating vectors (SERS.NFAT.hIL12 and SERS.NFAT.hIL12.PA2) and 1 γ-retroviral vector (MSGV1.NFAT.hIL.12 PA2). Peripheral blood lymphocytes (PBLs) were double transduced with an antigen-specific T-cell receptor and the 3 NFAT.hIL12 vectors. Evaluation of inducible IL-12 expression, transduction efficiency, and vector production considerations led to the choice of the MSGV1.NFAT.hIL12.PA2 vector for clinical application. MSGV1.NFAT.hIL12.PA2 PG13 retroviral vector producer cell clones were screened by transduction of tumor antigen-specific PBLs. On the basis of expression studies in PBL, clone D3 was chosen to produce clinical-grade viral vector supernatant and was demonstrated to efficiently transduce young tumor-infiltrating lymphocytes (TIL). The vector-transduced young TIL with known tumor recognition demonstrated specific inducible IL-12 production after coculture with HLA-matched tumor targets and had augmented effector function as demonstrated by increased IFN-γ secretion. These results support the clinical application of adoptive transfer of young TIL engineered with the NFAT.hIL12 vector as a new approach for cancer immunotherapy. JF - Journal of immunotherapy (Hagerstown, Md. : 1997) AU - Zhang, Ling AU - Feldman, Steven A AU - Zheng, Zhili AU - Chinnasamy, Nachimuthu AU - Xu, Hui AU - Nahvi, Azam V AU - Dudley, Mark E AU - Rosenberg, Steven A AU - Morgan, Richard A AD - Surgery Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 430 EP - 439 VL - 35 IS - 5 KW - HLA Antigens KW - 0 KW - Receptors, Antigen, T-Cell KW - Interleukin-12 KW - 187348-17-0 KW - Interferon-gamma KW - 82115-62-6 KW - Index Medicus KW - Coculture Techniques KW - Lymphocytes, Tumor-Infiltrating -- immunology KW - Humans KW - Immunotherapy KW - Transduction, Genetic KW - Gene Expression KW - Interferon-gamma -- biosynthesis KW - Receptors, Antigen, T-Cell -- immunology KW - Receptors, Antigen, T-Cell -- biosynthesis KW - Interferon-gamma -- immunology KW - Lymphocyte Activation KW - Promoter Regions, Genetic KW - Adoptive Transfer KW - Genetic Vectors KW - HLA Antigens -- immunology KW - Receptors, Antigen, T-Cell -- genetics KW - Interleukin-12 -- immunology KW - Gammaretrovirus -- genetics KW - Interleukin-12 -- biosynthesis KW - Gammaretrovirus -- immunology KW - Neoplasms -- therapy KW - Interleukin-12 -- genetics KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1013921530?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+immunotherapy+%28Hagerstown%2C+Md.+%3A+1997%29&rft.atitle=Evaluation+of+%CE%B3-retroviral+vectors+that+mediate+the+inducible+expression+of+IL-12+for+clinical+application.&rft.au=Zhang%2C+Ling%3BFeldman%2C+Steven+A%3BZheng%2C+Zhili%3BChinnasamy%2C+Nachimuthu%3BXu%2C+Hui%3BNahvi%2C+Azam+V%3BDudley%2C+Mark+E%3BRosenberg%2C+Steven+A%3BMorgan%2C+Richard+A&rft.aulast=Zhang&rft.aufirst=Ling&rft.date=2012-06-01&rft.volume=35&rft.issue=5&rft.spage=430&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunotherapy+%28Hagerstown%2C+Md.+%3A+1997%29&rft.issn=1537-4513&rft_id=info:doi/10.1097%2FCJI.0b013e31825898e8 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-05-16 N1 - Date created - 2012-05-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Blood. 2000 Jul 15;96(2):459-66 [10887106] J Gene Med. 2012 Mar;14(3):169-81 [22262359] Science. 1995 Nov 10;270(5238):908 [7481785] Hum Gene Ther. 1997 Jul 1;8(10):1189-94 [9215736] Blood. 1997 Oct 1;90(7):2541-8 [9326219] Hum Gene Ther. 2005 Apr;16(4):457-72 [15871677] Blood. 2006 Oct 15;108(8):2545-53 [16825499] Mol Ther. 2007 Jun;15(6):1167-73 [17406345] Clin Cancer Res. 2007 Aug 15;13(16):4677-85 [17699845] Semin Oncol. 2007 Dec;34(6):524-31 [18083376] J Clin Oncol. 2008 Nov 10;26(32):5233-9 [18809613] Clin Cancer Res. 2010 May 1;16(9):2646-55 [20406835] J Immunol. 2010 Jun 1;184(11):5988-98 [20427771] Cancer Res. 2010 Sep 1;70(17):6725-34 [20647327] Mol Ther. 2010 Nov;18(11):1891 [21042293] Clin Cancer Res. 2010 Dec 15;16(24):6122-31 [20668005] Hum Gene Ther. 2011 Jan;22(1):107-15 [20662590] Mol Ther. 2011 Apr;19(4):751-9 [21285960] Mol Ther. 2012 Jan;20(1):84-90 [22008914] J Immunol Methods. 1990 Apr 17;128(2):189-201 [1691237] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1097/CJI.0b013e31825898e8 ER - TY - JOUR T1 - Suppression of endogenous PPARγ increases vulnerability to methamphetamine-induced injury in mouse nigrostriatal dopaminergic pathway. AN - 1013760386; 22160138 AB - Methamphetamine is a commonly abused drug and dopaminergic neurotoxin. Repeated administration of high doses of methamphetamine induces programmed cell death, suppression of dopamine release, and reduction in locomotor activity. Previous studies have shown that pretreatment with peroxisome proliferator-activated receptor gamma (PPARγ) agonist reduced methamphetamine-induced neurodegeneration. The purpose of this study was to examine the role of endogenous PPARγ in protecting against methamphetamine toxicity. Adeno-associated virus (AAV) encoding the Cre recombinase gene was unilaterally injected into the left substantia nigra of loxP-PPARγ or control wild-type mice. Animals were treated with high doses of methamphetamine 1 month after viral injection. Behavioral tests were examined using rotarod and rotometer. In vivo voltammetry was used to examine dopamine release/clearance and at 2 months after methamphetamine injection. Administration of AAV-Cre selectively removed PPARγ in left nigra in loxP-PPARγ mice but not in the wild-type mice. The loxP-PPARγ/AAV-Cre mice that received methamphetamine showed a significant reduction in time on the rotarod and exhibited increased ipsilateral rotation using a rotometer. The peak of dopamine release induced by local application of KCl and the rate of dopamine clearance were significantly attenuated in the left striatum of loxP-PPARγ/AAV-Cre animals. Tyrosine hydroxylase immunoreactivity was reduced in the left, compared to right, nigra, and dorsal striatum in loxP-PPARγ/AAV-Cre mice receiving high doses of methamphetamine. A deficiency in PPARγ increases vulnerability to high doses of methamphetamine. Endogenous PPARγ may play an important role in reducing methamphetamine toxicity in vivo. JF - Psychopharmacology AU - Yu, Seong-Jin AU - Airavaara, Mikko AU - Shen, Hui AU - Chou, Jenny AU - Harvey, Brandon K AU - Wang, Yun AD - National Institute on Drug Abuse, IRP, Neural Protection and Regeneration Section, 251 Bayview Boulevard, 06-721A, Baltimore, MD 21224, USA. Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 479 EP - 492 VL - 221 IS - 3 KW - PPAR gamma KW - 0 KW - Methamphetamine KW - 44RAL3456C KW - Potassium Chloride KW - 660YQ98I10 KW - Tyrosine 3-Monooxygenase KW - EC 1.14.16.2 KW - Cre recombinase KW - EC 2.7.7.- KW - Integrases KW - Dopamine KW - VTD58H1Z2X KW - Index Medicus KW - Animals KW - Tyrosine 3-Monooxygenase -- metabolism KW - Dose-Response Relationship, Drug KW - Corpus Striatum -- metabolism KW - Potassium Chloride -- pharmacology KW - Dependovirus -- genetics KW - Substantia Nigra -- drug effects KW - Mice KW - Mice, Knockout KW - Substantia Nigra -- metabolism KW - Behavior, Animal -- drug effects KW - Recombination, Genetic KW - Mice, Inbred C57BL KW - Corpus Striatum -- drug effects KW - Male KW - Methamphetamine -- administration & dosage KW - Integrases -- genetics KW - Dopamine -- metabolism KW - PPAR gamma -- metabolism KW - PPAR gamma -- genetics KW - Methamphetamine -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1013760386?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psychopharmacology&rft.atitle=Suppression+of+endogenous+PPAR%CE%B3+increases+vulnerability+to+methamphetamine-induced+injury+in+mouse+nigrostriatal+dopaminergic+pathway.&rft.au=Yu%2C+Seong-Jin%3BAiravaara%2C+Mikko%3BShen%2C+Hui%3BChou%2C+Jenny%3BHarvey%2C+Brandon+K%3BWang%2C+Yun&rft.aulast=Yu&rft.aufirst=Seong-Jin&rft.date=2012-06-01&rft.volume=221&rft.issue=3&rft.spage=479&rft.isbn=&rft.btitle=&rft.title=Psychopharmacology&rft.issn=1432-2072&rft_id=info:doi/10.1007%2Fs00213-011-2595-7 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-11-26 N1 - Date created - 2012-05-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Stroke. 2001 Mar;32(3):775-82 [11239201] Nature. 1998 Jan 1;391(6662):82-6 [9422509] J Pharmacol Exp Ther. 2002 Sep;302(3):1201-11 [12183681] Proc Natl Acad Sci U S A. 2002 Sep 3;99(18):11854-9 [12192090] J Neurosci Methods. 2002 Nov 15;121(1):41-52 [12393160] J Neurosci. 2003 Jul 2;23(13):5762-70 [12843280] J Neurosci. 2003 Aug 27;23(21):7958-65 [12944527] J Neurochem. 2004 Jan;88(2):494-501 [14690537] Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15712-7 [14660788] J Neurosci Res. 2004 May 15;76(4):512-8 [15114623] Brain Res. 1970 Dec 18;24(3):485-93 [5494536] Brain Res. 1993 Oct 29;626(1-2):167-74 [8281427] J Neurosci. 1996 Nov 1;16(21):6965-74 [8824333] Brain Res. 1997 Feb 28;749(2):188-99 [9138718] J Virol. 1998 Mar;72(3):2224-32 [9499080] J Pharmacol Exp Ther. 1998 Nov;287(2):487-96 [9808671] J Neurosci. 1999 Sep 1;19(17):7653-60 [10460271] Ann N Y Acad Sci. 2004 Oct;1025:69-75 [15542702] Proc Natl Acad Sci U S A. 2005 Jan 18;102(3):868-73 [15644446] Stroke. 2005 Feb;36(2):353-9 [15618443] Eur J Neurosci. 2005 Jul;22(1):278-82 [16029218] Neurotoxicology. 2006 Jan;27(1):131-6 [16165214] Eur J Neurosci. 2006 Sep;24(6):1653-63 [17004929] J Neurosci Methods. 2006 Dec 15;158(2):219-23 [16837051] Neurochem Res. 2006 Nov;31(11):1305-16 [17053972] J Neurochem. 2007 Apr;101(1):41-56 [17394460] Hum Gene Ther. 2007 Mar;18(3):195-206 [17343566] Neuropsychopharmacology. 2007 May;32(5):1133-40 [17019405] CNS Drugs. 2008;22(1):1-14 [18072811] Neuroscience. 2008 Jan 2;151(1):92-103 [18082966] Virology. 2008 Mar 1;372(1):24-34 [18035387] Br J Pharmacol. 2008 May;154(1):226-33 [18332857] Nat Protoc. 2008;3(6):1101-8 [18546601] Neurochem Res. 2009 Apr;34(4):764-74 [18946735] Eur J Neurosci. 2009 Mar;29(5):954-63 [19245367] J Neurosci. 2009 May 13;29(19):6186-95 [19439596] Surg Endosc. 2009 Jun;23(6):1292-7 [18855061] Dev Neurobiol. 2009 Sep 1;69(10):674-88 [19551873] Brain Res. 2010 Jan 11;1307:149-57 [19853588] Neurotoxicol Teratol. 2010 May-Jun;32(3):346-55 [20096350] Neurosci Lett. 2010 Aug 9;480(1):64-8 [20573573] PLoS One. 2010;5(12):e15193 [21151937] Inflamm Bowel Dis. 2011 Feb;17(2):680-1 [20848495] Neuroscience. 2011 Oct 27;194:170-80 [21867746] Mol Cell. 1999 Oct;4(4):585-95 [10549290] Proc Natl Acad Sci U S A. 2002 Feb 19;99(4):2320-5 [11842206] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s00213-011-2595-7 ER - TY - JOUR T1 - Methyl bromide exposure and cancer risk in the Agricultural Health Study. AN - 1012746332; 22527160 AB - Methyl bromide is a genotoxic soil fumigant with high acute toxicity, but unknown human carcinogenicity. Although many countries have reduced methyl bromide use because of its ozone depleting properties, some uses remain in the United States and other countries, warranting further investigation of human health effects. We used Poisson regression to calculate rate ratios (RR) and 95 % confidence intervals (CI) for associations between methyl bromide use and all cancers combined, as well as 12 specific sites, among 53,588 Agricultural Health Study pesticide applicators with follow-up from 1993 to 2007. We also evaluated interactions with a family history for four common cancers (prostate, lung, colon, and lymphohematopoietic). We categorized methyl bromide exposure based on lifetime days applied weighted by an intensity score. A total of 7,814 applicators (14.6 %) used methyl bromide, predominantly before enrollment. Based on 15 exposed cases, stomach cancer risk increased monotonically with increasing methyl bromide use (RR = 1.42; 95 % CI, 0.51-3.95 and RR = 3.13; 95 % CI, 1.25-7.80 for low and high use compared with no use; p (trend) = 0.02). No other sites displayed a significant monotonic pattern. Although we previously observed an association with prostate cancer (follow-up through 1999), the association did not persist with longer follow-up. We observed a nonsignificant elevated risk of prostate cancer with methyl bromide use among those with a family history of prostate cancer, but the interaction with a family history did not achieve statistical significance. Our results provide little evidence of methyl bromide associations with cancer risk for most sites examined; however, we observed a significant exposure-dependent increase in stomach cancer risk. Small numbers of exposed cases and declining methyl bromide use might have influenced our findings. Further study is needed in more recently exposed populations to expand on these results. JF - Cancer causes & control : CCC AU - Barry, Kathryn Hughes AU - Koutros, Stella AU - Lubin, Jay H AU - Coble, Joseph B AU - Barone-Adesi, Francesco AU - Beane Freeman, Laura E AU - Sandler, Dale P AU - Hoppin, Jane A AU - Ma, Xiaomei AU - Zheng, Tongzhang AU - Alavanja, Michael C R AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 6120 Executive Blvd., Bethesda, MD 20892-7240, USA. barrykh@mail.nih.gov Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 807 EP - 818 VL - 23 IS - 6 KW - Herbicides KW - 0 KW - Hydrocarbons, Brominated KW - methyl bromide KW - 9V42E1Z7B6 KW - Index Medicus KW - Agriculture KW - Humans KW - North Carolina -- epidemiology KW - Poisson Distribution KW - Risk Factors KW - Herbicides -- poisoning KW - Cohort Studies KW - Surveys and Questionnaires KW - Confidence Intervals KW - Follow-Up Studies KW - Middle Aged KW - Female KW - Iowa -- epidemiology KW - Male KW - Occupational Exposure -- statistics & numerical data KW - Stomach Neoplasms -- chemically induced KW - Agricultural Workers' Diseases -- epidemiology KW - Agricultural Workers' Diseases -- chemically induced KW - Occupational Exposure -- adverse effects KW - Stomach Neoplasms -- epidemiology KW - Hydrocarbons, Brominated -- poisoning UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1012746332?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+causes+%26+control+%3A+CCC&rft.atitle=Methyl+bromide+exposure+and+cancer+risk+in+the+Agricultural+Health+Study.&rft.au=Barry%2C+Kathryn+Hughes%3BKoutros%2C+Stella%3BLubin%2C+Jay+H%3BCoble%2C+Joseph+B%3BBarone-Adesi%2C+Francesco%3BBeane+Freeman%2C+Laura+E%3BSandler%2C+Dale+P%3BHoppin%2C+Jane+A%3BMa%2C+Xiaomei%3BZheng%2C+Tongzhang%3BAlavanja%2C+Michael+C+R&rft.aulast=Barry&rft.aufirst=Kathryn&rft.date=2012-06-01&rft.volume=23&rft.issue=6&rft.spage=807&rft.isbn=&rft.btitle=&rft.title=Cancer+causes+%26+control+%3A+CCC&rft.issn=1573-7225&rft_id=info:doi/10.1007%2Fs10552-012-9949-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-11-08 N1 - Date created - 2012-05-11 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Epidemiology. 2002 Jan;13(1):94-9 [11805592] J Expo Sci Environ Epidemiol. 2012 Jul;22(4):409-16 [22569205] J Expo Anal Environ Epidemiol. 2002 Sep;12(5):313-8 [12198579] Environ Health Perspect. 2002 Dec;110(12):1175-84 [12460795] J Occup Environ Med. 2003 Mar;45(3):249-58 [12661182] Am J Epidemiol. 2003 May 1;157(9):800-14 [12727674] Br J Ind Med. 1984 Feb;41(1):15-24 [6318800] Toxicol Appl Pharmacol. 1984 Feb;72(2):262-71 [6695375] Toxicol Appl Pharmacol. 1986 Oct;86(1):131-9 [3764933] Toxicol Pathol. 1988;16(2):165-71 [3055226] Food Chem Toxicol. 1990 Feb;28(2):109-19 [2341089] Food Chem Toxicol. 1991 Jan;29(1):31-9 [1825644] Food Chem Toxicol. 1991 Aug;29(8):557-63 [1894222] Environ Health Perspect. 1996 Apr;104(4):362-9 [8732939] Mutat Res. 1998 Sep 11;417(2-3):115-28 [9733941] IARC Monogr Eval Carcinog Risks Hum. 1999;71 Pt 1:1-315 [10507919] Environ Res. 2007 Jun;104(2):282-9 [17196584] J Expo Sci Environ Epidemiol. 2010 Sep;20(6):559-69 [19888312] Am J Epidemiol. 2011 Jun 1;173(11):1280-8 [21447478] Occup Environ Med. 2011 Jul;68(7):537-41 [21257983] Int J Environ Res Public Health. 2011 Dec;8(12):4608-22 [22408592] Ann Occup Hyg. 2002 Mar;46(2):245-60 [12074034] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s10552-012-9949-2 ER - TY - JOUR T1 - DLC1 interaction with α-catenin stabilizes adherens junctions and enhances DLC1 antioncogenic activity. AN - 1012745206; 22473989 AB - The DLC1 (for deleted in liver cancer 1) tumor suppressor gene encodes a RhoGAP protein that inactivates Rho GTPases, which are implicated in regulation of the cytoskeleton and adherens junctions (AJs), a cell-cell adhesion protein complex associated with the actin cytoskeleton. Malignant transformation and tumor progression to metastasis are often associated with changes in cytoskeletal organization and cell-cell adhesion. Here we have established in human cells that the AJ-associated protein α-catenin is a new binding partner of DLC1. Their binding was mediated by the N-terminal amino acids 340 to 435 of DLC1 and the N-terminal amino acids 117 to 161 of α-catenin. These proteins colocalized in the cytosol and in the plasma membrane, where together they associated with E-cadherin and β-catenin, constitutive AJ proteins. Binding of DLC1 to α-catenin led to their accumulation at the plasma membrane and required DLC1 GAP activity. Knocking down α-catenin in DLC1-positive cells diminished DLC1 localization at the membrane. The DLC1-α-catenin complex reduced the Rho GTP level at the plasma membrane, increased E-cadherin's mobility, affected actin organization, and stabilized AJs. This process eventually contributed to a robust oncosuppressive effect of DLC1 in metastatic prostate carcinoma cells. Together, these results unravel a new mechanism through which DLC1 exerts its strong oncosuppressive function by positively influencing AJ stability. JF - Molecular and cellular biology AU - Tripathi, Veenu AU - Popescu, Nicholas C AU - Zimonjic, Drazen B AD - Laboratory of Experimental Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 2145 EP - 2159 VL - 32 IS - 11 KW - Cadherins KW - 0 KW - DLC1 protein, human KW - GTPase-Activating Proteins KW - Tumor Suppressor Proteins KW - alpha Catenin KW - rho GTP-Binding Proteins KW - EC 3.6.5.2 KW - Index Medicus KW - Cell Movement KW - Cadherins -- metabolism KW - Humans KW - Neoplasm Metastasis KW - Cell Line, Tumor KW - Protein Binding KW - Male KW - rho GTP-Binding Proteins -- metabolism KW - Cell Adhesion KW - Binding Sites KW - alpha Catenin -- metabolism KW - GTPase-Activating Proteins -- metabolism KW - Tumor Suppressor Proteins -- metabolism KW - Adherens Junctions -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1012745206?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biology&rft.atitle=DLC1+interaction+with+%CE%B1-catenin+stabilizes+adherens+junctions+and+enhances+DLC1+antioncogenic+activity.&rft.au=Tripathi%2C+Veenu%3BPopescu%2C+Nicholas+C%3BZimonjic%2C+Drazen+B&rft.aulast=Tripathi&rft.aufirst=Veenu&rft.date=2012-06-01&rft.volume=32&rft.issue=11&rft.spage=2145&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biology&rft.issn=1098-5549&rft_id=info:doi/10.1128%2FMCB.06580-11 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-11-19 N1 - Date created - 2012-05-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Pathol. 2009 Oct;175(4):1662-74 [19745064] PLoS One. 2009;4(11):e8027 [19956566] Int J Oncol. 2010 Apr;36(4):999-1005 [20198346] Nature. 2010 Apr 15;464(7291):999-1005 [20393555] Folia Histochem Cytobiol. 2010 Jan 1;48(1):37-45 [20529814] Folia Histochem Cytobiol. 2010 Jan 1;48(1):128-33 [20529828] Gastroenterology. 2010 Oct;139(4):1397-407 [20600027] Cancer Res. 2010 Nov 1;70(21):8270-5 [20861185] Nat Rev Cancer. 2010 Dec;10(12):842-57 [21102635] Cancer Res. 2011 Apr 15;71(8):2916-25 [21372205] Genes Chromosomes Cancer. 2012 Jan;51(1):66-76 [21965145] Mol Cancer Res. 2012 Jan;10(1):34-9 [22064653] J Clin Pathol. 1999 Jan;52(1):10-6 [10343606] Br J Cancer. 1999 May;80(3-4):477-82 [10408856] FEBS Lett. 2005 Feb 14;579(5):1191-6 [15710412] Cancer Res. 2005 Jul 15;65(14):6042-53 [16024604] Nat Cell Biol. 2005 Oct;7(10):954-60 [16184169] Cancer Res. 2005 Oct 1;65(19):8861-8 [16204057] Cell. 2005 Dec 2;123(5):903-15 [16325583] Clin Cancer Res. 2006 Mar 1;12(5):1412-9 [16533763] J Cell Sci. 2006 May 1;119(Pt 9):1801-11 [16608875] Cancer Res. 2006 Sep 1;66(17):8367-72 [16951145] J Cell Biol. 2007 Jan 1;176(1):43-9 [17190795] J Surg Oncol. 2007 Feb 1;95(2):148-55 [17262732] Proc Natl Acad Sci U S A. 2007 May 22;104(21):9012-7 [17517630] Exp Cell Res. 2007 Nov 1;313(18):3868-80 [17888903] J Cell Mol Med. 2007 Sep-Oct;11(5):1185-207 [17979893] Int J Biochem Cell Biol. 2008;40(5):843-7 [17521951] Mol Carcinog. 2008 May;47(5):326-37 [17932950] Cancer Gene Ther. 2008 Jun;15(6):371-81 [18369381] Int J Oncol. 2008 Jun;32(6):1285-91 [18497990] Front Biosci. 2008;13:3975-85 [18508491] Genes Dev. 2008 Jun 1;22(11):1439-44 [18519636] Nature. 2008 Jun 5;453(7196):751-6 [18480755] Genes Dev. 2008 Jul 1;22(13):1724-30 [18593873] J Biol Chem. 2008 Nov 21;283(47):32762-70 [18786931] J Cell Sci. 2009 Jan 1;122(Pt 1):92-102 [19066281] J Cell Sci. 2009 Feb 1;122(Pt 3):414-24 [19158340] Leukemia. 2009 Feb;23(2):383-90 [18923442] Cancer Metastasis Rev. 2009 Jun;28(1-2):5-14 [19153674] Cancer Metastasis Rev. 2009 Jun;28(1-2):77-83 [19221866] Cell. 2000 Jan 7;100(1):57-70 [10647931] Genome Res. 2000 Feb;10(2):244-57 [10673282] Cell. 2001 Feb 23;104(4):605-17 [11239416] J Clin Pathol. 2001 May;54(5):391-5 [11328840] Head Neck. 2001 Jul;23(7):573-8 [11400246] Clin Cancer Res. 2001 Oct;7(10):3139-43 [11595707] Breast Cancer Res. 2001;3(5):289-93 [11597316] Science. 2002 May 31;296(5573):1644-6 [12040179] Nat Cell Biol. 2002 Jun;4(6):408-15 [11992112] Histopathology. 2002 Jun;40(6):536-46 [12047765] Cancer Genet Cytogenet. 2002 May;135(1):63-90 [12072205] Nat Rev Cancer. 2002 Jun;2(6):442-54 [12189386] Nat Rev Cancer. 2002 Feb;2(2):133-42 [12635176] Oncogene. 2004 Feb 12;23(6):1308-13 [14647417] Oncogene. 2004 Feb 19;23(7):1405-11 [14661059] Science. 1987 Jan 16;235(4786):305-11 [3541204] Cancer Res. 1994 Jan 1;54(1):291-6 [8261454] Am J Pathol. 1994 Apr;144(4):667-74 [8160768] Proc Natl Acad Sci U S A. 1995 Sep 12;92(19):8813-7 [7568023] Cancer Res. 1995 Oct 15;55(20):4722-8 [7553655] Cancer Res. 1995 Nov 15;55(22):5390-5 [7585607] Mol Cell Biol. 1997 Aug;17(8):4501-8 [9234707] Cancer Res. 1997 Aug 1;57(15):3189-93 [9242448] J Cell Sci. 1997 Aug;110 ( Pt 15):1759-65 [9264463] Cancer Res. 1998 May 15;58(10):2196-9 [9605766] Am J Pathol. 1998 Aug;153(2):333-9 [9708792] Int J Cancer. 1998 Oct 23;79(5):546-50 [9761128] Oncogene. 2009 Mar 19;28(11):1401-9 [19151751] Cancer Res. 2009 Apr 1;69(7):2714-9 [19318551] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1128/MCB.06580-11 ER - TY - JOUR T1 - Loss of c-Met accelerates development of liver fibrosis in response to CCl(4) exposure through deregulation of multiple molecular pathways. AN - 1010232328; 22386877 AB - HGF/c-Met signaling plays a pivotal role in hepatocyte survival and tissue remodeling during liver regeneration. HGF treatment accelerates resolution of fibrosis in experimental animal models. Here, we utilized Met(fl/fl);Alb-Cre(+/-) conditional knockout mice and a carbon tetrachloride(CCl(4))-induced liver fibrosis model to formally address the role of c-Met signaling in hepatocytes in the context of chronic tissue injury. Histological changes during injury (4weeks) and healing phase (4weeks) were monitored by immunohistochemistry; expression levels of selected key fibrotic molecules were evaluated by western blotting, and time-dependent global transcriptomic changes were examined using a microarray platform. Loss of hepatocyte c-Met signaling altered hepatic microenvironment and aggravated hepatic fibrogenesis. Greater liver damage was associated with decreased hepatocyte proliferation, excessive stellate cell activation and rapid dystrophic calcification of necrotic areas. Global transcriptome analysis revealed a broad impact of c-Met on critical signaling pathways associated with fibrosis. Loss of hepatocyte c-Met caused a strong deregulation of chemotactic and inflammatory signaling (MCP-1, RANTES, Cxcl10) in addition to modulation of genes involved in reorganization of the cytoskeletal network (Actb, Tuba1a, Tuba8), intercellular communications and adhesion (Adam8, Icam1, Itgb2), control of cell proliferation (Ccng2, Csnk2a, Cdc6, cdk10), DNA damage and stress response (Rad9, Rad52, Ercc4, Gsta1 and 2, Jun). Our study demonstrates that deletion of c-Met receptor in hepatocytes results in pronounced changes in hepatic metabolism and microenvironment, and establishes an essential role for c-Met in maintaining the structural integrity and adaptive plasticity of the liver under adverse conditions. Published by Elsevier B.V. JF - Biochimica et biophysica acta AU - Marquardt, Jens U AU - Seo, Daekwan AU - Gómez-Quiroz, Luis E AU - Uchida, Koichi AU - Gillen, Matthew C AU - Kitade, Mitsuteru AU - Kaposi-Novak, Pal AU - Conner, Elizabeth A AU - Factor, Valentina M AU - Thorgeirsson, Snorri S AD - Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, USA. Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 942 EP - 951 VL - 1822 IS - 6 SN - 0006-3002, 0006-3002 KW - Hepatocyte Growth Factor KW - 67256-21-7 KW - Carbon Tetrachloride KW - CL2T97X0V0 KW - Proto-Oncogene Proteins c-met KW - EC 2.7.10.1 KW - Index Medicus KW - Animals KW - Liver -- pathology KW - DNA Repair KW - Hepatocyte Growth Factor -- genetics KW - Hepatocyte Growth Factor -- metabolism KW - Liver -- metabolism KW - Transcription, Genetic KW - Mice KW - Hepatocytes -- pathology KW - Liver Regeneration KW - Cell Proliferation KW - Mice, Knockout KW - Hepatic Stellate Cells -- metabolism KW - Signal Transduction -- immunology KW - Cell Communication KW - Transcriptome KW - Female KW - Cell Adhesion KW - Hepatocytes -- metabolism KW - Proto-Oncogene Proteins c-met -- deficiency KW - Proto-Oncogene Proteins c-met -- genetics KW - Liver Cirrhosis -- pathology KW - Liver Cirrhosis -- chemically induced KW - Proto-Oncogene Proteins c-met -- metabolism KW - Liver Cirrhosis -- metabolism KW - Liver Cirrhosis -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1010232328?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Loss+of+c-Met+accelerates+development+of+liver+fibrosis+in+response+to+CCl%284%29+exposure+through+deregulation+of+multiple+molecular+pathways.&rft.au=Marquardt%2C+Jens+U%3BSeo%2C+Daekwan%3BG%C3%B3mez-Quiroz%2C+Luis+E%3BUchida%2C+Koichi%3BGillen%2C+Matthew+C%3BKitade%2C+Mitsuteru%3BKaposi-Novak%2C+Pal%3BConner%2C+Elizabeth+A%3BFactor%2C+Valentina+M%3BThorgeirsson%2C+Snorri+S&rft.aulast=Marquardt&rft.aufirst=Jens&rft.date=2012-06-01&rft.volume=1822&rft.issue=6&rft.spage=942&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbadis.2012.02.012 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-27 N1 - Date created - 2012-04-27 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - GSE25583; GEO N1 - SuppNotes - Cited By: J Biol Chem. 2000 Dec 1;275(48):37984-92 [10964914] Hepatology. 2012 Apr;55(4):1215-26 [22095660] J Hepatol. 2002 Feb;36(2):169-78 [11830328] Hepatology. 2002 May;35(5):1093-103 [11981759] Nat Rev Mol Cell Biol. 2002 Dec;3(12):893-905 [12461556] Hepatology. 2003 Mar;37(3):493-503 [12601343] J Leukoc Biol. 2003 Sep;74(3):360-9 [12949239] Expert Rev Mol Med. 2003 Feb;5(5):1-23 [14987408] Proc Natl Acad Sci U S A. 2004 Mar 30;101(13):4477-82 [15070743] Semin Liver Dis. 2004 Feb;24(1):3-20 [15085483] Proc Natl Acad Sci U S A. 2004 Jul 20;101(29):10608-13 [15249655] DNA Cell Biol. 2004 Sep;23(9):592-603 [15383179] J Am Soc Nephrol. 2004 Nov;15(11):2868-81 [15504940] Methods Enzymol. 1978;52:302-10 [672633] Anal Biochem. 1981 Mar 15;112(1):70-5 [7258630] Biochem Biophys Res Commun. 1985 Dec 31;133(3):1042-50 [3910043] Biochem Biophys Res Commun. 1992 Mar 16;183(2):739-42 [1532309] J Hepatol. 1991 Nov;13(3):372-4 [1808228] Curr Opin Gastroenterol. 2009 May;25(3):223-9 [19396960] J Cell Physiol. 1995 Nov;165(2):398-405 [7593218] J Biochem. 1995 Sep;118(3):643-9 [8690730] Lancet. 1997 Mar 22;349(9055):825-32 [9121257] J Pathol. 1998 Jul;185(3):298-302 [9771484] Nat Med. 1999 Feb;5(2):226-30 [9930873] Am J Pathol. 2004 Dec;165(6):2157-66 [15579457] J Clin Invest. 2005 Feb;115(2):209-18 [15690074] Am J Pathol. 2005 Apr;166(4):1017-28 [15793283] Am J Pathol. 2006 May;168(5):1500-12 [16651617] J Clin Invest. 2006 Jun;116(6):1582-95 [16710476] Gastroenterology. 2006 Jul;131(1):272-5 [16831609] Hepatology. 2007 Jan;45(1):242-9 [17187439] Cancer Res. 2007 Oct 15;67(20):9844-51 [17942915] Arch Pathol Lab Med. 2007 Nov;131(11):1728-34 [17979495] Gastroenterology. 2008 Apr;134(4):1180-90 [18395096] Proc Am Thorac Soc. 2008 Apr 15;5(3):338-42 [18403330] Gastroenterology. 2008 May;134(6):1655-69 [18471545] J Biol Chem. 2008 May 23;283(21):14581-9 [18348981] Am J Pathol. 2008 Jul;173(1):30-41 [18502824] Expert Rev Gastroenterol Hepatol. 2008 Dec;2(6):803-16 [19090740] Biochem Pharmacol. 2000 Mar 15;59(6):681-90 [10677585] Genesis. 2000 Feb;26(2):149-50 [10686614] J Hepatol. 2000;32(1 Suppl):19-31 [10728791] Gastroenterology. 2009 Jul;137(1):297-308, 308.e1-4 [19208365] Pharmacol Rev. 2010 Mar;62(1):1-96 [20103563] Hepatology. 2010 Apr;51(4):1401-9 [20054870] Int J Clin Exp Pathol. 2010;3(7):675-80 [20830238] PLoS One. 2010;5(9). pii: e12739. doi: 10.1371/journal.pone.0012739 [20862286] J Autoimmun. 2010 Dec;35(4):424-35 [20932719] Cell Mol Life Sci. 2011 Jan;68(1):15-26 [20730552] Nat Rev Drug Discov. 2011 Jan;10(1):47-60 [21193867] Hepatology. 2011 Feb;53(2):596-603 [21274880] Mol Cell Proteomics. 2011 Mar;10(3):M110.000901 [21139050] Eur J Clin Invest. 2011 Jun;41(6):642-51 [21250982] Semin Liver Dis. 2001;21(1):3-16 [11296695] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.bbadis.2012.02.012 ER - TY - JOUR T1 - Heavy metals and couple fecundity, the LIFE Study. AN - 1001953474; 22309709 AB - The effect of heavy metals at environmentally relevant concentrations on couple fecundity has received limited study despite ubiquitous exposure. In 2005-2009, couples (n=501) desiring pregnancy and discontinuing contraception were recruited and asked to complete interviews and to provide blood specimens for the quantification of cadmium (μg L(-1)), lead (μg dL(-1)) and mercury (μg L(-1)) using inductively coupled plasma-mass spectrometry. Couples completed daily journals on lifestyle and intercourse along with menstruation and pregnancy testing for women. Couples were followed for 12 months or until pregnant. Fecundability odds ratios (FORs) and 95% confidence intervals (CIs) were estimated adjusting for age, body mass index, cotinine, and serum lipids in relation to female then male exposures. FORs <1 denote a longer time to pregnancy. In adjusted models, reduced FORs were observed for both female cadmium (0.78; 95% CI 0.63-0.97) and male lead (0.85; 95% CI 0.73-0.98) concentrations. When jointly modeling couples' exposures, only male lead concentration significantly reduced the FOR (0.82; 95% CI 0.68, 0.97), though the FOR remained <1 for female cadmium (0.80; 95% CI 0.64, 1.00). This prospective couple based cohort with longitudinal capture of time to pregnancy is suggestive of cadmium and lead's reproductive toxicity at environmentally relevant concentrations. Published by Elsevier Ltd. JF - Chemosphere AU - Buck Louis, Germaine M AU - Sundaram, Rajeshwari AU - Schisterman, Enrique F AU - Sweeney, Anne M AU - Lynch, Courtney D AU - Gore-Langton, Robert E AU - Chen, Zhen AU - Kim, Sungduk AU - Caldwell, Kathleen L AU - Barr, Dana Boyd AD - Division of Epidemiology, Statistics and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Rockville, MD 20852, United States. louisg@mail.nih.gov Y1 - 2012/06// PY - 2012 DA - June 2012 SP - 1201 EP - 1207 VL - 87 IS - 11 KW - Environmental Pollutants KW - 0 KW - Lipids KW - Metals, Heavy KW - Cadmium KW - 00BH33GNGH KW - Lead KW - 2P299V784P KW - Mercury KW - FXS1BY2PGL KW - Cotinine KW - K5161X06LL KW - Index Medicus KW - Cotinine -- analysis KW - Lipids -- blood KW - Young Adult KW - Mass Spectrometry KW - Odds Ratio KW - Mercury -- blood KW - Humans KW - Body Mass Index KW - Longitudinal Studies KW - Lead -- blood KW - Pregnancy KW - Adult KW - Cohort Studies KW - Adolescent KW - Cadmium -- blood KW - Female KW - Male KW - Environmental Pollutants -- toxicity KW - Metals, Heavy -- toxicity KW - Fertility -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1001953474?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Heavy+metals+and+couple+fecundity%2C+the+LIFE+Study.&rft.au=Buck+Louis%2C+Germaine+M%3BSundaram%2C+Rajeshwari%3BSchisterman%2C+Enrique+F%3BSweeney%2C+Anne+M%3BLynch%2C+Courtney+D%3BGore-Langton%2C+Robert+E%3BChen%2C+Zhen%3BKim%2C+Sungduk%3BCaldwell%2C+Kathleen+L%3BBarr%2C+Dana+Boyd&rft.aulast=Buck+Louis&rft.aufirst=Germaine&rft.date=2012-06-01&rft.volume=87&rft.issue=11&rft.spage=1201&rft.isbn=&rft.btitle=&rft.title=Chemosphere&rft.issn=1879-1298&rft_id=info:doi/10.1016%2Fj.chemosphere.2012.01.017 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-01 N1 - Date created - 2012-04-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Epidemiology. 2000 Mar;11(2):141-7 [11021610] Paediatr Perinat Epidemiol. 2011 Sep;25(5):413-24 [21819423] Hum Reprod. 2002 May;17(5):1399-403 [11980771] Environ Res. 2002 Mar;88(3):145-55 [12051792] Occup Environ Med. 2003 Oct;60(10):752-8 [14504363] Environ Health Perspect. 2004 Jan;112(1):79-86 [14698935] Br Med Bull. 2003;68:167-82 [14757716] Fertil Steril. 2004 Feb;81(2):384-92 [14967378] Occup Environ Med. 2004 Nov;61(11):915-23 [15477285] Arch Environ Health. 1986 Nov-Dec;41(6):387-90 [3619496] Am J Public Health. 1988 Jun;78(6):699-701 [3369604] Int J Epidemiol. 1988 Jun;17(2):378-84 [3403134] Arch Environ Contam Toxicol. 1989 Jul-Aug;18(4):495-500 [2505694] Clin Chim Acta. 1989 Oct 16;184(3):219-26 [2611996] Fertil Steril. 1996 Mar;65(3):503-9 [8774277] Paediatr Perinat Epidemiol. 1997 Jul;11(3):345-58 [9246695] Clin Chem. 1997 Dec;43(12):2281-91 [9439445] Hum Reprod. 1998 Jun;13(6):1532-9 [9688387] Occup Environ Med. 1998 Jun;55(6):364-74 [9764095] Environ Health Perspect. 1998 Nov;106(11):745-50 [9799191] Biometals. 2004 Dec;17(6):735-43 [15689116] Hum Reprod. 2006 May;21(5):1279-84 [16410331] Environ Res. 2006 Jul;101(3):380-6 [16360143] Epidemiology. 2006 Jul;17(4):440-9 [16755258] Reprod Toxicol. 2006 Jul;22(1):13-9 [16439098] Hum Reprod. 2007 Jun;22(6):1634-7 [17344224] Stat Med. 2008 Sep 10;27(20):4094-106 [18344178] Environ Health Perspect. 2008 Nov;116(11):1473-9 [19057699] Hum Reprod. 2009 Feb;24(2):451-8 [18940895] Epidemiology. 2009 Jan;20(1):56-9 [19057382] J Toxicol Environ Health B Crit Rev. 2009 Mar;12(3):206-23 [19466673] Epidemiology. 2009 Jul;20(4):488-95 [19525685] Syst Biol Reprod Med. 2010 Apr;56(2):147-67 [20377313] Environ Health Perspect. 2010 May;118(5):699-704 [20103495] Reprod Toxicol. 2011 Feb;31(2):158-63 [20933593] Hum Reprod Update. 2011 May-Jun;17(3):418-33 [21266373] Environ Health Perspect. 2011 Jul;119(7):1010-6 [21345762] Environ Health Perspect. 2011 Aug;119(8):1156-61 [21543284] Hum Reprod. 2000 Dec;15(12):2478-82 [11098014] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.chemosphere.2012.01.017 ER - TY - JOUR T1 - Dietary intake of meat, fruits, vegetables, and selective micronutrients and risk of bladder cancer in the New England region of the United States AN - 1020854979; 16759325 AB - Background: Despite many studies on diet and bladder cancer, there are areas that remain unexplored including meat mutagens, specific vegetable groups, and vitamins from diet. Methods: We conducted a population-based case-control study of bladder cancer in Maine, New Hampshire, and Vermont. A total of 1171 cases were ascertained through hospital pathology records and cancer registries from 2001 to 2004. Overall, 1418 controls were identified from the Department of Motor Vehicles (<65 years) and Center for Medicaid and Medicare Services (65-79 years) and were frequency-matched to cases by state, sex, and age (within 5 years). Diet was assessed with a self-administered Diet History Questionnaire. Unconditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI). Results: Processed meat intake was positively associated with bladder cancer (highest vs lowest quartile OR: 1.28; 95% CI: 1.00-1.65; P sub(trend)=0.035), with a stronger association for processed red meat (OR: 1.41; 95% CI: 1.08-1.84; P sub(trend)=0.024). There were no associations between intake of fruits or vegetables and bladder cancer. We did, however, observe an inverse association with vitamin B12 intake (OR: 0.77; 95% CI: 0.61-0.99; P=0.019). Conclusion: Vitamin B12 from diet may be protective against bladder cancer, whereas consuming processed meat may increase risk. JF - British Journal of Cancer AU - Wu, J W AU - Cross, A J AU - Baris, D AU - Ward, M H AU - Karagas, M R AU - Johnson, A AU - Schwenn, M AU - Cherala, S AU - Colt, J S AU - Cantor, K P AU - Rothman, N AU - Silverman, D T AU - Sinha, R AD - National Cancer Institute, National Institutes of Health, Department of Health and Human Services, 6120 Executive Blvd, Rockville, MD 20852, USA Y1 - 2012/05/22/ PY - 2012 DA - 2012 May 22 SP - 1891 EP - 1898 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 106 IS - 11 SN - 0007-0920, 0007-0920 KW - Risk Abstracts KW - Cancer KW - Diets KW - Fruits KW - Hospitals KW - Meat KW - Pathology KW - micronutrients KW - urinary bladder KW - vitamins KW - USA, New England KW - USA, New Hampshire KW - USA, Maine KW - USA, Vermont KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020854979?accountid=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=Dietary+intake+of+meat%2C+fruits%2C+vegetables%2C+and+selective+micronutrients+and+risk+of+bladder+cancer+in+the+New+England+region+of+the+United+States&rft.au=Wu%2C+J+W%3BCross%2C+A+J%3BBaris%2C+D%3BWard%2C+M+H%3BKaragas%2C+M+R%3BJohnson%2C+A%3BSchwenn%2C+M%3BCherala%2C+S%3BColt%2C+J+S%3BCantor%2C+K+P%3BRothman%2C+N%3BSilverman%2C+D+T%3BSinha%2C+R&rft.aulast=Wu&rft.aufirst=J&rft.date=2012-05-22&rft.volume=106&rft.issue=11&rft.spage=1891&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2012.187 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Meat; Diets; Fruits; urinary bladder; vitamins; Pathology; micronutrients; Cancer; Hospitals; USA, New England; USA, Maine; USA, New Hampshire; USA, Vermont DO - http://dx.doi.org/10.1038/bjc.2012.187 ER - TY - JOUR T1 - Testing an aflatoxin B1 gene signature in rat archival tissues. AN - 1015246531; 22545673 AB - Archival tissues from laboratory studies represent a unique opportunity to explore the relationship between genomic changes and agent-induced disease. In this study, we evaluated the applicability of qPCR for detecting genomic changes in formalin-fixed, paraffin-embedded (FFPE) tissues by determining if a subset of 14 genes from a 90-gene signature derived from microarray data and associated with eventual tumor development could be detected in archival liver, kidney, and lung of rats exposed to aflatoxin B1 (AFB1) for 90 days in feed at 1 ppm. These tissues originated from the same rats used in the microarray study. The 14 genes evaluated were Adam8, Cdh13, Ddit4l, Mybl2, Akr7a3, Akr7a2, Fhit, Wwox, Abcb1b, Abcc3, Cxcl1, Gsta5, Grin2c, and the C8orf46 homologue. The qPCR FFPE liver results were compared to the original liver microarray data and to qPCR results using RNA from fresh frozen liver. Archival liver paraffin blocks yielded 30 to 50 μg of degraded RNA that ranged in size from 0.1 to 4 kB. qPCR results from FFPE and fresh frozen liver samples were positively correlated (p ≤ 0.05) by regression analysis and showed good agreement in direction and proportion of change with microarray data for 11 of 14 genes. All 14 transcripts could be amplified from FFPE kidney RNA except the glutamate receptor gene Grin2c; however, only Abcb1b was significantly upregulated from control. Abundant constitutive transcripts, S18 and β-actin, could be amplified from lung FFPE samples, but the narrow RNA size range (25-500 bp length) prevented consistent detection of target transcripts. Overall, a discrete gene signature derived from prior transcript profiling and representing cell cycle progression, DNA damage response, and xenosensor and detoxication pathways was successfully applied to archival liver and kidney by qPCR and indicated that gene expression changes in response to subchronic AFB1 exposure occurred predominantly in the liver, the primary target for AFB1-induced tumors. We conclude that an evaluation of gene signatures in archival tissues can be an important toxicological tool for evaluating critical molecular events associated with chemical exposures. JF - Chemical research in toxicology AU - Merrick, B Alex AU - Auerbach, Scott S AU - Stockton, Patricia S AU - Foley, Julie F AU - Malarkey, David E AU - Sills, Robert C AU - Irwin, Richard D AU - Tice, Raymond R AD - Biomolecular Screening Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences , Research Triangle Park, NC 27709, United States. merrick@niehs.nih.gov Y1 - 2012/05/21/ PY - 2012 DA - 2012 May 21 SP - 1132 EP - 1144 VL - 25 IS - 5 KW - Carcinogens KW - 0 KW - RNA KW - 63231-63-0 KW - Aflatoxin B1 KW - 9N2N2Y55MH KW - Index Medicus KW - Rats KW - Animals KW - Rats, Inbred F344 KW - Paraffin Embedding KW - RNA -- isolation & purification KW - Kidney KW - Liver -- metabolism KW - Gene Expression Regulation KW - Lung -- metabolism KW - Tissue Fixation KW - Male KW - RNA -- genetics KW - Carcinogens -- metabolism KW - Aflatoxin B1 -- metabolism KW - Real-Time Polymerase Chain Reaction -- methods KW - Gene Expression Profiling -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1015246531?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Testing+an+aflatoxin+B1+gene+signature+in+rat+archival+tissues.&rft.au=Merrick%2C+B+Alex%3BAuerbach%2C+Scott+S%3BStockton%2C+Patricia+S%3BFoley%2C+Julie+F%3BMalarkey%2C+David+E%3BSills%2C+Robert+C%3BIrwin%2C+Richard+D%3BTice%2C+Raymond+R&rft.aulast=Merrick&rft.aufirst=B&rft.date=2012-05-21&rft.volume=25&rft.issue=5&rft.spage=1132&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=1520-5010&rft_id=info:doi/10.1021%2Ftx3000945 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-10 N1 - Date created - 2012-05-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Carcinogenesis. 2005 Mar;26(3):689-99 [15618236] BMC Genomics. 2011 Dec 23;12 Suppl 5:S6 [22369133] BMC Mol Biol. 2006;7:3 [16448564] Cancer Res. 2006 May 15;66(10):5346-53 [16707461] J Histochem Cytochem. 2006 Nov;54(11):1229-37 [16864893] FASEB J. 2006 Nov;20(13):2291-301 [17077306] Toxicol Appl Pharmacol. 2006 Dec 15;217(3):299-307 [17070881] Mutat Res. 2008 Jan 1;637(1-2):23-39 [17689568] BMC Mol Biol. 2007;8:118 [18154675] BMC Mol Biol. 2008;9:102 [19014500] Nucleic Acids Res. 1999 Nov 15;27(22):4436-43 [10536153] Exp Mol Pathol. 2012 Feb;92(1):33-43 [21963600] Lancet. 2012 Mar 3;379(9818):823-32 [22285053] Virchows Arch. 2012 Feb;460(2):131-40 [22270699] Int J Cancer. 2001 Nov15;94(4):492-9 [11745434] FEBS Lett. 2002 Jul 17;523(1-3):213-8 [12123834] Cancer Res. 1967 Dec;27(12):2370-6 [4295478] Cancer Res. 1969 Dec;29(12):2206-11 [4318833] J Biol Chem. 1996 Apr 19;271(16):9363-7 [8621601] Environ Health Perspect. 1997 Nov;105(11):1182-4 [9432466] Mutat Res. 1998 Jun 18;402(1-2):121-8 [9675258] Chem Biol Interact. 1998 Apr 24;111-112:51-67 [9679543] Carcinogenesis. 1999 Jul;20(7):1215-23 [10383892] Toxicol Sci. 2009 May;109(1):1-3 [19293422] Cancer Lett. 2008 Dec 8;272(1):160-6 [18752886] Biotechniques. 2009 Jul;47(1):587-96 [19594443] BMC Urol. 2009;9:6 [19552816] Int J Mol Med. 2009 Nov;24(5):613-22 [19787195] Genomics. 2009 Nov;94(5):341-8 [19660539] Mol Cancer. 2010;9:3 [20059769] Toxicol Appl Pharmacol. 2010 Mar 15;243(3):300-14 [20004213] BMC Genomics. 2010;11:132 [20178649] Oral Oncol. 2010 May;46(5):379-86 [20371203] J Mol Med (Berl). 2010 May;88(5):497-505 [20119708] Biotechniques. 2010 May;48(5):389-97 [20569212] Oncogene. 2010 Jul 1;29(26):3758-69 [20453887] J Mol Diagn. 2010 Jul;12(4):409-17 [20522636] Genes Chromosomes Cancer. 2010 Sep;49(9):775-90 [20607704] BMC Cancer. 2010;10:336 [20584321] Clin Cancer Res. 2010 Oct 15;16(20):5038-47 [20739434] Handb Exp Pharmacol. 2011;(201):261-83 [21103972] Methods Mol Biol. 2011;700:171-84 [21204034] Int J Clin Exp Pathol. 2011;4(2):156-61 [21326810] Int J Oncol. 2011 Apr;38(4):1075-81 [21305253] Toxicol Sci. 2011 Mar;120 Suppl 1:S28-48 [20881231] Br J Cancer. 2011 Mar 15;104(6):971-81 [21407225] Histol Histopathol. 2011 Jun;26(6):797-810 [21472693] Hepatology. 2011 Apr;53(4):1226-36 [21480327] Clin Cancer Res. 2011 Jun 15;17(12):4145-54 [21467161] Rep Carcinog. 2011;12:32-4 [21829243] Cancer Res. 2011 Aug 15;71(16):5370-3 [21828240] PLoS One. 2011;6(8):e23780 [21858221] Clin Cancer Res. 2011 Sep 1;17(17):5705-14 [21742808] J Toxicol Sci. 2011 Oct;36(5):507-14 [22008526] Toxicol Sci. 2011 Nov;124(1):54-74 [21813463] J Clin Oncol. 2011 Dec 10;29(35):4620-6 [22067406] Food Addit Contam Part A Chem Anal Control Expo Risk Assess. 2012;29(2):249-57 [21623489] J Mol Diagn. 2012 Mar-Apr;14(2):140-8 [22240448] J Biol Chem. 2005 Mar 18;280(11):9769-72 [15632201] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1021/tx3000945 ER - TY - JOUR T1 - Opportunities and Challenges for Cost-Efficient Implementation of New Point-of-Care Diagnostics for HIV and Tuberculosis AN - 1635035781; 20899936 AB - Stakeholders agree that supporting high-quality diagnostics is essential if we are to continue to make strides in the fight against human immunodeficiency virus (HIV) and tuberculosis. Despite the need to strengthen existing laboratory infrastructure, which includes expanding and developing new laboratories, there are clear diagnostic needs where conventional laboratory support is insufficient. Regarding HIV, rapid point-of-care (POC) testing for initial HIV diagnosis has been successful, but several needs remain. For tuberculosis, several new diagnostic tests have recently been endorsed by the World Health Organization, but a POC test remains elusive. Human immunodeficiency virus and tuberculosis are coendemic in many high prevalence locations, making parallel diagnosis of these conditions an important consideration. Despite its clear advantages, POC testing has important limitations, and laboratory-based testing will continue to be an important component of future diagnostic networks. Ideally, a strategic deployment plan should be used to define where and how POC technologies can be most efficiently and cost effectively integrated into diagnostic algorithms and existing test networks prior to widespread scale-up. In this fashion, the global community can best harness the tremendous capacity of novel diagnostics in fighting these 2 scourges. JF - Journal of Infectious Diseases AU - Schito, Marco AU - Peter, Trevor F AU - Cavanaugh, Sean AU - Piatek, Amy S AU - Young, Gloria J AU - Alexander, Heather AU - Coggin, William AU - Domingo, Gonzalo J AU - Ellenberger, Dennis AU - Ermantraut, Eugen AU - Jani, Ilesh V AU - Katamba, Achilles AU - Palamountain, Kara M AU - Essajee, Shaffiq AU - Dowdy, David W AD - Henry M. Jackson Foundation for the Advancement of Military Medicine, Vaccine Clinical Research Branch, Division of AIDS, NIAID, NIH, 6700-B Rockledge Dr, Rm 5255, Bethesda, MD 20892-7628, schitom@niaid.nih.gov Y1 - 2012/05/15/ PY - 2012 DA - 2012 May 15 SP - S169 EP - S180 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 205 SN - 0022-1899, 0022-1899 KW - Virology & AIDS Abstracts; Microbiology Abstracts B: Bacteriology KW - Human immunodeficiency virus KW - Mycobacterium KW - Algorithms KW - Tuberculosis KW - Fighting KW - V 22360:AIDS and HIV KW - J 02300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635035781?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Opportunities+and+Challenges+for+Cost-Efficient+Implementation+of+New+Point-of-Care+Diagnostics+for+HIV+and+Tuberculosis&rft.au=Schito%2C+Marco%3BPeter%2C+Trevor+F%3BCavanaugh%2C+Sean%3BPiatek%2C+Amy+S%3BYoung%2C+Gloria+J%3BAlexander%2C+Heather%3BCoggin%2C+William%3BDomingo%2C+Gonzalo+J%3BEllenberger%2C+Dennis%3BErmantraut%2C+Eugen%3BJani%2C+Ilesh+V%3BKatamba%2C+Achilles%3BPalamountain%2C+Kara+M%3BEssajee%2C+Shaffiq%3BDowdy%2C+David+W&rft.aulast=Schito&rft.aufirst=Marco&rft.date=2012-05-15&rft.volume=205&rft.issue=&rft.spage=S169&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjis044 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Algorithms; Tuberculosis; Fighting; Mycobacterium; Human immunodeficiency virus DO - http://dx.doi.org/10.1093/infdis/jis044 ER - TY - JOUR T1 - A prospective protocol for nasopharyngeal carcinoma in children and adolescents: the Italian Rare Tumors in Pediatric Age (TREP) project. AN - 1020511001; 21918965 AB - Nasopharyngeal carcinoma (NPC) is very rare in childhood. It differs from its adult counterpart in the prevalence of the nonkeratinizing, undifferentiated subtype and by an advanced clinical stage at onset and better chances of survival. The risk of long-term treatment-related toxicity also may be a more important issue in younger individuals. A prospective chemoradiotherapy protocol for pediatric NPC was started in Italy in 2000 within the framework of the Rare Tumors in Pediatric Age (TREP) project. Three courses of cisplatin/5-fluorouracil induction chemotherapy were followed by radiotherapy (doses up to 65 grays) with concomitant cisplatin. Forty-six patients (ages 9-17 years) were considered eligible for the study over a 10-year period. The ratio of observed to expected cases based on epidemiological data was approximately 1 for both children and adolescents. All but 1 patient had lymph node involvement, and 5 patients had distant metastases. The rate of response to primary chemotherapy was 90%. The 5-year overall and progression-free survival rates were 80.9% and 79.3%, respectively (median follow-up, 62 months). The only statistically significant prognostic variable was the presence or absence of distant metastases. A 65% incidence of late sequelae was reported. This study demonstrates the feasibility and efficacy of a prospective protocol even for such rare tumors as pediatric NPC. The use of lower radiotherapy doses than those used in adults did not affect locoregional failure rates. Long-term follow-up will be needed to obtain more information on both survival and treatment sequelae. The next objective will be to establish broader, international prospective cooperation schemes. Copyright © 2011 American Cancer Society. JF - Cancer AU - Casanova, Michela AU - Bisogno, Gianni AU - Gandola, Lorenza AU - Cecchetto, Giovanni AU - Di Cataldo, Andrea AU - Basso, Eleonora AU - Indolfi, Paolo AU - D'Angelo, Paolo AU - Favini, Francesca AU - Collini, Paola AU - Potepan, Paolo AU - Ferrari, Andrea AU - Rare Tumors in Pediatric Age Group AD - Foundation for the Research and Cure of Cancer, National Cancer Institute, Milan, Italy. ; Rare Tumors in Pediatric Age Group Y1 - 2012/05/15/ PY - 2012 DA - 2012 May 15 SP - 2718 EP - 2725 VL - 118 IS - 10 KW - DNA, Viral KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Disease-Free Survival KW - Prospective Studies KW - Neoplasm Staging KW - DNA, Viral -- analysis KW - Humans KW - Treatment Outcome KW - Child KW - Chemoradiotherapy KW - Adolescent KW - Male KW - Female KW - Herpesvirus 4, Human -- isolation & purification KW - Nasopharyngeal Neoplasms -- mortality KW - Nasopharyngeal Neoplasms -- virology KW - Nasopharyngeal Neoplasms -- therapy KW - Nasopharyngeal Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020511001?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+prospective+protocol+for+nasopharyngeal+carcinoma+in+children+and+adolescents%3A+the+Italian+Rare+Tumors+in+Pediatric+Age+%28TREP%29+project.&rft.au=Casanova%2C+Michela%3BBisogno%2C+Gianni%3BGandola%2C+Lorenza%3BCecchetto%2C+Giovanni%3BDi+Cataldo%2C+Andrea%3BBasso%2C+Eleonora%3BIndolfi%2C+Paolo%3BD%27Angelo%2C+Paolo%3BFavini%2C+Francesca%3BCollini%2C+Paola%3BPotepan%2C+Paolo%3BFerrari%2C+Andrea%3BRare+Tumors+in+Pediatric+Age+Group&rft.aulast=Casanova&rft.aufirst=Michela&rft.date=2012-05-15&rft.volume=118&rft.issue=10&rft.spage=2718&rft.isbn=&rft.btitle=&rft.title=Cancer&rft.issn=1097-0142&rft_id=info:doi/10.1002%2Fcncr.26528 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-21 N1 - Date created - 2012-05-04 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/cncr.26528 ER - TY - JOUR T1 - Crystal structures of multidrug-resistant HIV-1 protease in complex with two potent anti-malarial compounds AN - 1022563672; 16790778 AB - Two potent inhibitors (compounds 1 and 2) of malarial aspartyl protease, plasmepsin-II, were evaluated against wild type (NL4-3) and multidrug-resistant clinical isolate 769 (MDR) variants of human immunodeficiency virus type-1 (HIV-1) aspartyl protease. Enzyme inhibition assays showed that both 1 and 2 have better potency against NL4-3 than against MDR protease. Crystal structures of MDR protease in complex with 1 and 2 were solved and analyzed. Crystallographic analysis revealed that the MDR protease exhibits a typical wide-open conformation of the flaps (Gly48 to Gly52) causing an overall expansion in the active site cavity, which, in turn caused unstable binding of the inhibitors. Due to the expansion of the active site cavity, both compounds showed loss of direct contacts with the MDR protease compared to the docking models of NL4-3. Multiple water molecules showed a rich network of hydrogen bonds contributing to the stability of the ligand binding in the distorted binding pockets of the MDR protease in both crystal structures. Docking analysis of 1 and 2 showed a decrease in the binding affinity for both compounds against MDR supporting our structure-function studies. Thus, compounds 1 and 2 show promising inhibitory activity against HIV-1 protease variants and hence are good candidates for further development to enhance their potency against NL4-3 as well as MDR HIV-1 protease variants. JF - Biochemical and Biophysical Research Communications AU - Yedidi, Ravikiran S AU - Liu, Zhigang AU - Wang, Yong AU - Brunzelle, Joseph S AU - Kovari, Iulia A AU - Woster, Patrick M AU - Kovari, Ladislau C AU - Gupta, Deepak AD - Department of Biochemistry and Molecular Biology, School of Medicine, Wayne State University, 540 E. Canfield Avenue, Detroit, MI 48201, USA, yedidirs@mail.nih.gov Y1 - 2012/05/11/ PY - 2012 DA - 2012 May 11 SP - 413 EP - 417 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 421 IS - 3 SN - 0006-291X, 0006-291X KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Virology & AIDS Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - HIV-1 protease KW - Plasmepsin-II KW - Aspartyl protease KW - Multidrug-resistance KW - Mechanism-based inhibitors KW - Crystallography KW - Docking KW - Clinical isolates KW - Molecular structure KW - Drug resistance KW - Enzymes KW - Metabolites KW - Berthing KW - Models KW - aspartic endopeptidase KW - Hydrogen bonding KW - Human immunodeficiency virus 1 KW - Human immunodeficiency virus 2 KW - Crystal structure KW - Inhibitors KW - Ligands KW - Conformation KW - V 22360:AIDS and HIV KW - K 03330:Biochemistry KW - Q1 08485:Species interactions: pests and control KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1022563672?accountid=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=Biochemical+and+Biophysical+Research+Communications&rft.atitle=Crystal+structures+of+multidrug-resistant+HIV-1+protease+in+complex+with+two+potent+anti-malarial+compounds&rft.au=Yedidi%2C+Ravikiran+S%3BLiu%2C+Zhigang%3BWang%2C+Yong%3BBrunzelle%2C+Joseph+S%3BKovari%2C+Iulia+A%3BWoster%2C+Patrick+M%3BKovari%2C+Ladislau+C%3BGupta%2C+Deepak&rft.aulast=Yedidi&rft.aufirst=Ravikiran&rft.date=2012-05-11&rft.volume=421&rft.issue=3&rft.spage=413&rft.isbn=&rft.btitle=&rft.title=Biochemical+and+Biophysical+Research+Communications&rft.issn=0006291X&rft_id=info:doi/10.1016%2Fj.bbrc.2012.03.096 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Last updated - 2016-10-12 N1 - SubjectsTermNotLitGenreText - Molecular structure; Inhibitors; Metabolites; Berthing; Ligands; Clinical isolates; aspartic endopeptidase; Hydrogen bonding; Drug resistance; Crystal structure; Enzymes; Models; Conformation; Human immunodeficiency virus 1; Human immunodeficiency virus 2 DO - http://dx.doi.org/10.1016/j.bbrc.2012.03.096 ER - TY - JOUR T1 - A Three-Stage Algorithm to Make Toxicologically Relevant Activity Calls from Quantitative High Throughput Screening Data AN - 1093465994; 17168273 AB - Background: The ability of a substance to induce a toxicological response is better understood by analyzing the response profile over a broad range of concentrations than at a single concentration. In vitro quantitative high throughput screening (qHTS) assays are multiple-concentration experiments with an important role in the National Toxicology Program's (NTP) efforts to advance toxicology from a predominantly observational science at the level of disease-specific models to a more predictive science based on broad inclusion of biological observations. Objective: We developed a systematic approach to classify substances from large-scale concentration-response data into statistically supported, toxicologically relevant activity categories. Methods: The first stage of the approach finds active substances with robust concentration-response profiles within the tested concentration range. The second stage finds substances with activity at the lowest tested concentration not captured in the first stage. The third and final stage separates statistically significant (but not robustly statistically significant) profiles from responses that lack statistically compelling support (i.e., "inactives"). The performance of the proposed algorithm was evaluated with simulated qHTS data sets. Results: The proposed approach performed well for 14-point-concentration-response curves with typical levels of residual error ( sigma less than or equal to 25%) or when maximal response (|RMAX|) was > 25% of the positive control response. The approach also worked well in most cases for smaller sample sizes when |RMAX| greater than or equal to 50%, even with as few as four data points. Conclusions: The three-stage classification algorithm performed better than one-stage classification approaches based on overall F-tests, t-tests, or linear regression. JF - Environmental Health Perspectives AU - Shockley, Keith R AD - Biostatistics Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA Y1 - 2012/05/10/ PY - 2012 DA - 2012 May 10 SP - 1107 EP - 1115 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 120 IS - 8 SN - 0091-6765, 0091-6765 KW - Environment Abstracts; Health & Safety Science Abstracts KW - activity calls KW - concentration-response KW - Hill equation KW - quantitative high throughput screening KW - Tox21 KW - Classification KW - Toxicology KW - H 12000:Epidemiology and Public Health KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1093465994?accountid=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=A+Three-Stage+Algorithm+to+Make+Toxicologically+Relevant+Activity+Calls+from+Quantitative+High+Throughput+Screening+Data&rft.au=Shockley%2C+Keith+R&rft.aulast=Shockley&rft.aufirst=Keith&rft.date=2012-05-10&rft.volume=120&rft.issue=8&rft.spage=1107&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1104688 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2015-05-13 N1 - SubjectsTermNotLitGenreText - Classification; Toxicology DO - http://dx.doi.org/10.1289/ehp.1104688 ER - TY - CPAPER T1 - Visualization of IL-22 in mouse intestinal inflammation with an IL-22 tdTomato reporter mouse T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313116369; 6139092 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Shen, Wei AU - Li, Wenqing AU - Feigenbaum, Lionel AU - Hixon, Julie AU - Durum, Scott Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Interleukin 22 KW - Intestine KW - Inflammation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313116369?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Visualization+of+IL-22+in+mouse+intestinal+inflammation+with+an+IL-22+tdTomato+reporter+mouse&rft.au=Shen%2C+Wei%3BLi%2C+Wenqing%3BFeigenbaum%2C+Lionel%3BHixon%2C+Julie%3BDurum%2C+Scott&rft.aulast=Shen&rft.aufirst=Wei&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Thymic stromal lymphopoietin is produced by dendritic cells. T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313112421; 6139909 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Kashyap, Mohit AU - Rochman, Yrina AU - Spolski, Rosanne AU - Samsel, Leigh AU - Leonard, Warren Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Thymic stromal lymphopoietin KW - Dendritic cells UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313112421?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Thymic+stromal+lymphopoietin+is+produced+by+dendritic+cells.&rft.au=Kashyap%2C+Mohit%3BRochman%2C+Yrina%3BSpolski%2C+Rosanne%3BSamsel%2C+Leigh%3BLeonard%2C+Warren&rft.aulast=Kashyap&rft.aufirst=Mohit&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Genetic polymorphism in the human LILRB3/LILRA6 locus T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313112280; 6139993 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Bashirova, Arman AU - Apps, Richard AU - Vince, Nicolas AU - Yu, Xu AU - Carringotn, Mary Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Gene polymorphism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313112280?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Genetic+polymorphism+in+the+human+LILRB3%2FLILRA6+locus&rft.au=Bashirova%2C+Arman%3BApps%2C+Richard%3BVince%2C+Nicolas%3BYu%2C+Xu%3BCarringotn%2C+Mary&rft.aulast=Bashirova&rft.aufirst=Arman&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Type I Interferon Regulates the Dynamics of Innate Myeloid Sentinel Cells During Persistent Viral Infection T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313089229; 6140187 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Nayak, Debasis AU - Johnson, Kory AU - Heydari, Sara AU - Roth, Theodore AU - Zynselmeyer, Bernd AU - McGavern, Dorian Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Infection KW - Interferon KW - Viral diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313089229?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Type+I+Interferon+Regulates+the+Dynamics+of+Innate+Myeloid+Sentinel+Cells+During+Persistent+Viral+Infection&rft.au=Nayak%2C+Debasis%3BJohnson%2C+Kory%3BHeydari%2C+Sara%3BRoth%2C+Theodore%3BZynselmeyer%2C+Bernd%3BMcGavern%2C+Dorian&rft.aulast=Nayak&rft.aufirst=Debasis&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Chronic IL-33 exposure induces a hypo-responsive mast cell phenotype T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313088176; 6139822 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Jung, Mi-Yeon AU - Smrz, Daniel AU - Desai, Avanti AU - Bandara, Geethani AU - Ito, Tomonobu AU - Kang, Jeong-Han AU - Beaven, Michael AU - Metcalfe, Dean AU - Gilfillan, Alasdair Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Mast cells KW - Phenotypes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313088176?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Chronic+IL-33+exposure+induces+a+hypo-responsive+mast+cell+phenotype&rft.au=Jung%2C+Mi-Yeon%3BSmrz%2C+Daniel%3BDesai%2C+Avanti%3BBandara%2C+Geethani%3BIto%2C+Tomonobu%3BKang%2C+Jeong-Han%3BBeaven%2C+Michael%3BMetcalfe%2C+Dean%3BGilfillan%2C+Alasdair&rft.aulast=Jung&rft.aufirst=Mi-Yeon&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - IL-12 induced Fas expression in myeloid-derived cells within tumors delivers a co-stimulatory signal for adoptively transferred CD8+ T cells T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313086741; 6139275 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Kerkar, Sid AU - Restifo, Nicholas Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Tumors KW - CD95 antigen KW - CD8 antigen KW - Lymphocytes T KW - Fas antigen KW - Interleukin 12 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313086741?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=IL-12+induced+Fas+expression+in+myeloid-derived+cells+within+tumors+delivers+a+co-stimulatory+signal+for+adoptively+transferred+CD8%2B+T+cells&rft.au=Kerkar%2C+Sid%3BRestifo%2C+Nicholas&rft.aulast=Kerkar&rft.aufirst=Sid&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - A proteomic study of early signaling events regulating the Fas-FasL Death Inducing Signaling Complex T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313086337; 6139326 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Ramaswamy, Madhu AU - Do, Thao AU - Barden, Mary AU - Cruz, Anthony AU - Siegel, Richard Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Mortality KW - proteomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313086337?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=A+proteomic+study+of+early+signaling+events+regulating+the+Fas-FasL+Death+Inducing+Signaling+Complex&rft.au=Ramaswamy%2C+Madhu%3BDo%2C+Thao%3BBarden%2C+Mary%3BCruz%2C+Anthony%3BSiegel%2C+Richard&rft.aulast=Ramaswamy&rft.aufirst=Madhu&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Enhancing cancer immunotherapy by combining Notch 1 and death receptor activation T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313085975; 6139222 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Shanker, Anil AU - Malhotra, Anshu AU - Dikov, Mikhail AU - Biktasova, Asel AU - Sayers, Thomas AU - Carbone, David Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Cancer KW - Immunotherapy KW - Mortality KW - Notch protein KW - death receptors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313085975?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Enhancing+cancer+immunotherapy+by+combining+Notch+1+and+death+receptor+activation&rft.au=Shanker%2C+Anil%3BMalhotra%2C+Anshu%3BDikov%2C+Mikhail%3BBiktasova%2C+Asel%3BSayers%2C+Thomas%3BCarbone%2C+David&rft.aulast=Shanker&rft.aufirst=Anil&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Behavior-modulating function of the Duffy Antigen Receptor for Chemokines (DARC) in mice under homeostatic conditions T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313085476; 6139102 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Schneider, Erich AU - Gao, Ji-Liang AU - Holmes, Gibran AU - Fowler, Stephen AU - Peiper, Stephen AU - Murphy, Philip Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Mice KW - Receptor mechanisms KW - Chemokines KW - Duffy antigen KW - Antigens UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313085476?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Behavior-modulating+function+of+the+Duffy+Antigen+Receptor+for+Chemokines+%28DARC%29+in+mice+under+homeostatic+conditions&rft.au=Schneider%2C+Erich%3BGao%2C+Ji-Liang%3BHolmes%2C+Gibran%3BFowler%2C+Stephen%3BPeiper%2C+Stephen%3BMurphy%2C+Philip&rft.aulast=Schneider&rft.aufirst=Erich&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Increased immune activation during chronic SIV infection drives the TFH dynamics T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313083924; 6138844 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Petrovas, Constantinos AU - Yamamoto, Takuya AU - Gerner, Michael AU - Boswell, Kristin AU - Roederer, Mario AU - Seder, Robert AU - Germain, Ronald AU - Haddas, Elias AU - Koup, Richard Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Infection KW - Immune response KW - Chronic infection KW - Simian immunodeficiency virus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313083924?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Increased+immune+activation+during+chronic+SIV+infection+drives+the+TFH+dynamics&rft.au=Petrovas%2C+Constantinos%3BYamamoto%2C+Takuya%3BGerner%2C+Michael%3BBoswell%2C+Kristin%3BRoederer%2C+Mario%3BSeder%2C+Robert%3BGermain%2C+Ronald%3BHaddas%2C+Elias%3BKoup%2C+Richard&rft.aulast=Petrovas&rft.aufirst=Constantinos&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Identification of matrix metalloproteinases involved in the activation induced CD16 down-modulation by primary NK cells T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313079561; 6140473 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Peruzzi, Giovanna AU - Femnou, Laurette AU - Borrego, Francisco AU - Krzewski, Konrad AU - Coligan, John Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - CD16 antigen KW - Matrix metalloproteinase KW - Natural killer cells UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313079561?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Identification+of+matrix+metalloproteinases+involved+in+the+activation+induced+CD16+down-modulation+by+primary+NK+cells&rft.au=Peruzzi%2C+Giovanna%3BFemnou%2C+Laurette%3BBorrego%2C+Francisco%3BKrzewski%2C+Konrad%3BColigan%2C+John&rft.aulast=Peruzzi&rft.aufirst=Giovanna&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - The IgM Fc receptor, FCMR, promotes B cell development and modulates antigen-driven immune responses T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313077262; 6140076 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Choi, Seung-Chul AU - Wang, Hongsheng AU - Tian, Linjie AU - Murakami, Yousuke AU - Shin, Dong-Mi AU - Borrego, Francisco AU - Morse, Herbert AU - Coligan, John Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Lymphocytes B KW - Immunoglobulin M KW - Fc receptors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313077262?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=The+IgM+Fc+receptor%2C+FCMR%2C+promotes+B+cell+development+and+modulates+antigen-driven+immune+responses&rft.au=Choi%2C+Seung-Chul%3BWang%2C+Hongsheng%3BTian%2C+Linjie%3BMurakami%2C+Yousuke%3BShin%2C+Dong-Mi%3BBorrego%2C+Francisco%3BMorse%2C+Herbert%3BColigan%2C+John&rft.aulast=Choi&rft.aufirst=Seung-Chul&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Cell type specific role of B7 for T-dependnet antibody response in vivo T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313077121; 6140074 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Watanabe, Masashi AU - Hodes, Richard Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - B7 antigen KW - Antibody response KW - Antibodies UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313077121?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Cell+type+specific+role+of+B7+for+T-dependnet+antibody+response+in+vivo&rft.au=Watanabe%2C+Masashi%3BHodes%2C+Richard&rft.aulast=Watanabe&rft.aufirst=Masashi&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Gut commensal bacteria promote anti-tumor innate immune responses in distant tumors after immunotherapy and chemotherapy T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313076213; 6139141 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Iida, Noriho AU - Stewart, Charles AU - Goldszmid, Romina AU - Dzutsev, Amiran AU - Trinchieri, Giorgio Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Chemotherapy KW - Immunotherapy KW - Tumors KW - Immune response KW - Digestive tract KW - Commensals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313076213?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Gut+commensal+bacteria+promote+anti-tumor+innate+immune+responses+in+distant+tumors+after+immunotherapy+and+chemotherapy&rft.au=Iida%2C+Noriho%3BStewart%2C+Charles%3BGoldszmid%2C+Romina%3BDzutsev%2C+Amiran%3BTrinchieri%2C+Giorgio&rft.aulast=Iida&rft.aufirst=Noriho&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Viral Infection Triggers Rapid Differentiation of Human Blood Monocytes into Dendritic Cells T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313075883; 6139134 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Hou, Wanqiu AU - Gibbs, James AU - Lu, Xiuju AU - Brooke, Christopher AU - Roy, Devika AU - Modlin, Robert AU - Bennink, Jack AU - Yewdell, Jonathan Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Infection KW - Blood KW - Dendritic cells KW - Differentiation KW - Monocytes KW - Viral diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313075883?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Viral+Infection+Triggers+Rapid+Differentiation+of+Human+Blood+Monocytes+into+Dendritic+Cells&rft.au=Hou%2C+Wanqiu%3BGibbs%2C+James%3BLu%2C+Xiuju%3BBrooke%2C+Christopher%3BRoy%2C+Devika%3BModlin%2C+Robert%3BBennink%2C+Jack%3BYewdell%2C+Jonathan&rft.aulast=Hou&rft.aufirst=Wanqiu&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Encounter with antigen-specific CD4 T cells promotes down-regulation of MHC-II in Dendritic cells T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313073868; 6138905 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Furuta, Kazuyuki AU - Ishido, Satoshi AU - Roche, Paul Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Dendritic cells KW - Lymphocytes T KW - CD4 antigen KW - Major histocompatibility complex UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313073868?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Encounter+with+antigen-specific+CD4+T+cells+promotes+down-regulation+of+MHC-II+in+Dendritic+cells&rft.au=Furuta%2C+Kazuyuki%3BIshido%2C+Satoshi%3BRoche%2C+Paul&rft.aulast=Furuta&rft.aufirst=Kazuyuki&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Transmembrane domain sequences regulate the association of MHC- class II with lipid raft microdomains T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313073831; 6138904 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Khandelwal, Sanjay AU - Roche, Paul Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Lipid rafts KW - Transmembrane domains KW - Major histocompatibility complex UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313073831?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Transmembrane+domain+sequences+regulate+the+association+of+MHC-+class+II+with+lipid+raft+microdomains&rft.au=Khandelwal%2C+Sanjay%3BRoche%2C+Paul&rft.aulast=Khandelwal&rft.aufirst=Sanjay&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Bcl-3 is a regulator of dendritic cell functions T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313068780; 6140452 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Tassi, Ilaria AU - Claudio, Estefania AU - Wang, Hongshan AU - Siebenist, Ulrich Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Bcl-3 protein KW - Dendritic cells UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313068780?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Bcl-3+is+a+regulator+of+dendritic+cell+functions&rft.au=Tassi%2C+Ilaria%3BClaudio%2C+Estefania%3BWang%2C+Hongshan%3BSiebenist%2C+Ulrich&rft.aulast=Tassi&rft.aufirst=Ilaria&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Transcriptional factor E2A regulates the differentiation of Th17 cells T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313067717; 6140360 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Nakatsukasa, Hiroko AU - Maruyama, Takashi AU - Chen, Wanjun Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Differentiation KW - Helper cells UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313067717?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Transcriptional+factor+E2A+regulates+the+differentiation+of+Th17+cells&rft.au=Nakatsukasa%2C+Hiroko%3BMaruyama%2C+Takashi%3BChen%2C+Wanjun&rft.aulast=Nakatsukasa&rft.aufirst=Hiroko&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - IRF8 Interacts with the BCL6 Co-repressor, BCOR T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313067284; 6138939 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Yoon, Jeong AU - Feng, Jianxun AU - Morse III, Herbert Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Bcl-6 protein UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313067284?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=IRF8+Interacts+with+the+BCL6+Co-repressor%2C+BCOR&rft.au=Yoon%2C+Jeong%3BFeng%2C+Jianxun%3BMorse+III%2C+Herbert&rft.aulast=Yoon&rft.aufirst=Jeong&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - An IL15-dependent novel immune cell subset with multiple functionalities affecting the onset and severity of autoimmune disease T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313067112; 6140348 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Voynova, Elisaveta AU - Bolland, Silvia Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Autoimmune diseases KW - Interleukin 1 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313067112?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=An+IL15-dependent+novel+immune+cell+subset+with+multiple+functionalities+affecting+the+onset+and+severity+of+autoimmune+disease&rft.au=Voynova%2C+Elisaveta%3BBolland%2C+Silvia&rft.aulast=Voynova&rft.aufirst=Elisaveta&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - IFN-gamma is the primary cause of aplastic anemia not autoreactive T cells T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313064629; 6139392 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Lin, Fanching AU - Macfarlane, Michael AU - Saleh, Bahara AU - Hodge, Deborah AU - Young, Howard Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Anemia KW - g-Interferon KW - Lymphocytes T KW - Aplastic anemia UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313064629?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=IFN-gamma+is+the+primary+cause+of+aplastic+anemia+not+autoreactive+T+cells&rft.au=Lin%2C+Fanching%3BMacfarlane%2C+Michael%3BSaleh%2C+Bahara%3BHodge%2C+Deborah%3BYoung%2C+Howard&rft.aulast=Lin&rft.aufirst=Fanching&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Innate immune response contributes to virus-mediated neuronal death through activation of SARM T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313055666; 6140306 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Peterson, Karin AU - Woods, Tyson AU - Mukherjee, Piyali Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Immune response KW - Mortality KW - Immunity KW - Defense mechanisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313055666?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Innate+immune+response+contributes+to+virus-mediated+neuronal+death+through+activation+of+SARM&rft.au=Peterson%2C+Karin%3BWoods%2C+Tyson%3BMukherjee%2C+Piyali&rft.aulast=Peterson&rft.aufirst=Karin&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - The adaptor protein CIKS/Act1 is essential for imiquimod-induced psoriasis. T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313055367; 6140387 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Ha, Hye-Lin AU - Wang, Hongshan AU - Siebenlis, Ulrich Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - psoriasis KW - Psoriasis KW - adaptor proteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313055367?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=The+adaptor+protein+CIKS%2FAct1+is+essential+for+imiquimod-induced+psoriasis.&rft.au=Ha%2C+Hye-Lin%3BWang%2C+Hongshan%3BSiebenlis%2C+Ulrich&rft.aulast=Ha&rft.aufirst=Hye-Lin&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - The Glucocorticoid-Induced Tumor necrosis-factor related Receptor (GITR) is a redundant costimulatory molecule for conventional T (Tconv) cells and plays a dual role on Regulatory T cells (Treg). T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313055021; 6139692 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Ephrem, Amal AU - Epstein, Alan AU - Shevach, Ethan Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Tumors KW - Lymphocytes T KW - Immunoregulation KW - Costimulator UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313055021?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=The+Glucocorticoid-Induced+Tumor+necrosis-factor+related+Receptor+%28GITR%29+is+a+redundant+costimulatory+molecule+for+conventional+T+%28Tconv%29+cells+and+plays+a+dual+role+on+Regulatory+T+cells+%28Treg%29.&rft.au=Ephrem%2C+Amal%3BEpstein%2C+Alan%3BShevach%2C+Ethan&rft.aulast=Ephrem&rft.aufirst=Amal&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Interaction of TNF and TNFR2 stabilizes the phenotype and function of CD4+FoxP3+ regulatory T cells in the inflammatory environment T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313054992; 6139691 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Chen, Xin AU - Wu, Xueqiang AU - Howard, O M AU - Oppenheim, Joost Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Tumor necrosis factor KW - Lymphocytes T KW - Immunoregulation KW - Foxp3 protein KW - CD4 antigen KW - Inflammation KW - Phenotypes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313054992?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Interaction+of+TNF+and+TNFR2+stabilizes+the+phenotype+and+function+of+CD4%2BFoxP3%2B+regulatory+T+cells+in+the+inflammatory+environment&rft.au=Chen%2C+Xin%3BWu%2C+Xueqiang%3BHoward%2C+O+M%3BOppenheim%2C+Joost&rft.aulast=Chen&rft.aufirst=Xin&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Identification of novel subsets of CD5+ B-1a cells reveals layered populations with distinct innate-like functions T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313054783; 6140197 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Wang, Hongsheng AU - Shin, Dong-Mi AU - Abbasi, Sadia AU - Kovalchuk, Alexander AU - Jain, Shweta AU - Morse, Herbert Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313054783?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Identification+of+novel+subsets+of+CD5%2B+B-1a+cells+reveals+layered+populations+with+distinct+innate-like+functions&rft.au=Wang%2C+Hongsheng%3BShin%2C+Dong-Mi%3BAbbasi%2C+Sadia%3BKovalchuk%2C+Alexander%3BJain%2C+Shweta%3BMorse%2C+Herbert&rft.aulast=Wang&rft.aufirst=Hongsheng&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Identifying an IDO-expressing "fibrocyte" subset of myeloid suppressor cells in pediatric cancer patients. T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313054366; 6139236 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Zhang, Hua AU - Mackall, Crystal Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Cancer KW - Pediatrics KW - Suppressor cells KW - Suppressors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313054366?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Identifying+an+IDO-expressing+%22fibrocyte%22+subset+of+myeloid+suppressor+cells+in+pediatric+cancer+patients.&rft.au=Zhang%2C+Hua%3BMackall%2C+Crystal&rft.aulast=Zhang&rft.aufirst=Hua&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Interleukin-22 promotes liver progenitor cell proliferation in mice and patients with in viral hepatitis T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313053782; 6139109 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Feng, Dechun AU - Kong, Xiaoni AU - Weng, Honglei AU - Park, Ogyi AU - Wang, Hua AU - Dooley, Steve AU - Gershwin, Eric AU - Gao, Bin Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Hepatitis KW - Mice KW - Liver KW - Interleukin 22 KW - Hepatocytes KW - Stem cells UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313053782?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Interleukin-22+promotes+liver+progenitor+cell+proliferation+in+mice+and+patients+with+in+viral+hepatitis&rft.au=Feng%2C+Dechun%3BKong%2C+Xiaoni%3BWeng%2C+Honglei%3BPark%2C+Ogyi%3BWang%2C+Hua%3BDooley%2C+Steve%3BGershwin%2C+Eric%3BGao%2C+Bin&rft.aulast=Feng&rft.aufirst=Dechun&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Role of Regulatory T cells and TGF-{beta} in an Experimental Model of Psoriasis in mice T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313052892; 6140009 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Zanvit, Peter AU - Chen, Wanjun Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - psoriasis KW - Mice KW - Psoriasis KW - Animal models KW - Lymphocytes T KW - Immunoregulation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313052892?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Role+of+Regulatory+T+cells+and+TGF-%7Bbeta%7D+in+an+Experimental+Model+of+Psoriasis+in+mice&rft.au=Zanvit%2C+Peter%3BChen%2C+Wanjun&rft.aulast=Zanvit&rft.aufirst=Peter&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Interleukin-22 Ameliorates Cerulein-Induced Pancreatitis in Mice by In-hibiting the Autophagic Pathway T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313050832; 6139110 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Park, Ogyi AU - Feng, Dechun AU - Radaeva, Svetlana AU - Wang, Hua AU - Yin, Shi AU - Kong, Xiaoni AU - Zheng, Mingquan AU - Zakhari, Sam AU - Kolls, Jay AU - Gao, Bin Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Mice KW - Interleukin 22 KW - Pancreatitis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313050832?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Interleukin-22+Ameliorates+Cerulein-Induced+Pancreatitis+in+Mice+by+In-hibiting+the+Autophagic+Pathway&rft.au=Park%2C+Ogyi%3BFeng%2C+Dechun%3BRadaeva%2C+Svetlana%3BWang%2C+Hua%3BYin%2C+Shi%3BKong%2C+Xiaoni%3BZheng%2C+Mingquan%3BZakhari%2C+Sam%3BKolls%2C+Jay%3BGao%2C+Bin&rft.aulast=Park&rft.aufirst=Ogyi&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Loss of IFN-gamma 3'untranslated region AU-rich element affects B220+ B cell and plasmacytoid dendritic cell populations in novel murine lupus model T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313048180; 6139064 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Hodge, Deborah AU - Berthet, Cyril AU - Coppola, Vincenzo AU - Shirota, Hidekazu AU - Reynolds, Della AU - Klinman, Dennis AU - Young, Howard Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Lymphocytes B KW - g-Interferon KW - Dendritic cells UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313048180?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Loss+of+IFN-gamma+3%27untranslated+region+AU-rich+element+affects+B220%2B+B+cell+and+plasmacytoid+dendritic+cell+populations+in+novel+murine+lupus+model&rft.au=Hodge%2C+Deborah%3BBerthet%2C+Cyril%3BCoppola%2C+Vincenzo%3BShirota%2C+Hidekazu%3BReynolds%2C+Della%3BKlinman%2C+Dennis%3BYoung%2C+Howard&rft.aulast=Hodge&rft.aufirst=Deborah&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - The G protein-coupled receptor mFPR2 promotes anti-tumor host defense T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313048044; 6139060 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Wang, Ji AU - Liu, Ying AU - Chen, Keqiang AU - Liu, Mingyong AU - Gong, Wanghua AU - Yoshimura, Teizo AU - Ford, Jill AU - McVicar, Daniel Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - G protein-coupled receptors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313048044?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=The+G+protein-coupled+receptor+mFPR2+promotes+anti-tumor+host+defense&rft.au=Wang%2C+Ji%3BLiu%2C+Ying%3BChen%2C+Keqiang%3BLiu%2C+Mingyong%3BGong%2C+Wanghua%3BYoshimura%2C+Teizo%3BFord%2C+Jill%3BMcVicar%2C+Daniel&rft.aulast=Wang&rft.aufirst=Ji&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - In vivo analysis of antigen presentation during acute CNS viral infection T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313047362; 6138916 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Fan, Ying AU - Nayak, Debasis AU - McGavern, Dorian Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Infection KW - Central nervous system KW - Antigen presentation KW - Viral diseases KW - Antigens UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313047362?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=In+vivo+analysis+of+antigen+presentation+during+acute+CNS+viral+infection&rft.au=Fan%2C+Ying%3BNayak%2C+Debasis%3BMcGavern%2C+Dorian&rft.aulast=Fan&rft.aufirst=Ying&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Enhanced T cell activation in lymphocytes from transgenic mice expressing LAT molecules resistant to ubiquitination T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313046363; 6140373 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Rodriguez-Pena, Ana AU - Balagopalan, Lakshmi AU - Gomez-Rodriguez, Julio AU - Kortum, Robert AU - Feigenbaum, Lionel AU - Sommers, Connie AU - Samelson, Lawrence Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Mice KW - Lymphocytes KW - Lymphocytes T KW - Cell activation KW - ubiquitination KW - Transgenic mice UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313046363?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Enhanced+T+cell+activation+in+lymphocytes+from+transgenic+mice+expressing+LAT+molecules+resistant+to+ubiquitination&rft.au=Rodriguez-Pena%2C+Ana%3BBalagopalan%2C+Lakshmi%3BGomez-Rodriguez%2C+Julio%3BKortum%2C+Robert%3BFeigenbaum%2C+Lionel%3BSommers%2C+Connie%3BSamelson%2C+Lawrence&rft.aulast=Rodriguez-Pena&rft.aufirst=Ana&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Defective nuclear IKK{alpha} function in patients with ectodermal dysplasia with immune deficiency T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313037181; 6139548 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Jain, Ashish AU - Ma, Chi AU - Zhao, Yongge AU - Temmerman, Stephane Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Dysplasia UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313037181?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Defective+nuclear+IKK%7Balpha%7D+function+in+patients+with+ectodermal+dysplasia+with+immune+deficiency&rft.au=Jain%2C+Ashish%3BMa%2C+Chi%3BZhao%2C+Yongge%3BTemmerman%2C+Stephane&rft.aulast=Jain&rft.aufirst=Ashish&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Molecular mechanisms of Innate DNA recognition by the AIM2 and IFI16 inflammasomes T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313015689; 6140280 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Jin, Tengchuan AU - Perry, Andrew AU - Jiang, Jiansheng AU - Smith, Patrick AU - Curry, James AU - Unterholzner, Leonie AU - Jiang, Zhaozhao AU - Horvath, Gabor AU - Rathinam, Vijay AU - Hornung, Veit AU - Johnstone, Ricky AU - Latz, Eicke AU - Bowie, Andrew AU - Fitzgerald, Katherine AU - Xiao, T Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Molecular modelling UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313015689?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Molecular+mechanisms+of+Innate+DNA+recognition+by+the+AIM2+and+IFI16+inflammasomes&rft.au=Jin%2C+Tengchuan%3BPerry%2C+Andrew%3BJiang%2C+Jiansheng%3BSmith%2C+Patrick%3BCurry%2C+James%3BUnterholzner%2C+Leonie%3BJiang%2C+Zhaozhao%3BHorvath%2C+Gabor%3BRathinam%2C+Vijay%3BHornung%2C+Veit%3BJohnstone%2C+Ricky%3BLatz%2C+Eicke%3BBowie%2C+Andrew%3BFitzgerald%2C+Katherine%3BXiao%2C+T&rft.aulast=Jin&rft.aufirst=Tengchuan&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Progression of acute lymphoblastic leukemia (ALL) results in compartment-restricted T cell expression of PD-1 and T cell dysfunction T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313013093; 6139260 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Su, Paul AU - Burk, Chad AU - Fix, William AU - Qin, Hai-Ying AU - Fry, Terry Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Acute lymphatic leukemia KW - Lymphocytes T KW - PD-1 protein UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313013093?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Progression+of+acute+lymphoblastic+leukemia+%28ALL%29+results+in+compartment-restricted+T+cell+expression+of+PD-1+and+T+cell+dysfunction&rft.au=Su%2C+Paul%3BBurk%2C+Chad%3BFix%2C+William%3BQin%2C+Hai-Ying%3BFry%2C+Terry&rft.aulast=Su&rft.aufirst=Paul&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Functional and structural basis of T cell recognition in autoimmune gastritis: mapping of autoantigenic peptides of the alpha-chain of the H/K ATPase and X-ray structure of the I-Ad/peptide complexes T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1313008075; 6138898 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Revilleza, Maria AU - Levin, Ditza AU - Mage, Michael AU - Candon, Sophie AU - Natarajan, Kannan AU - Rui, Wang AU - Teyton, Luc AU - Robinson, Howard AU - Shevach, Ethan AU - Margulies, David Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Mapping KW - Peptide mapping KW - Ionizing radiation KW - Structure-function relationships KW - Gastritis KW - Lymphocytes T UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313008075?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Functional+and+structural+basis+of+T+cell+recognition+in+autoimmune+gastritis%3A+mapping+of+autoantigenic+peptides+of+the+alpha-chain+of+the+H%2FK+ATPase+and+X-ray+structure+of+the+I-Ad%2Fpeptide+complexes&rft.au=Revilleza%2C+Maria%3BLevin%2C+Ditza%3BMage%2C+Michael%3BCandon%2C+Sophie%3BNatarajan%2C+Kannan%3BRui%2C+Wang%3BTeyton%2C+Luc%3BRobinson%2C+Howard%3BShevach%2C+Ethan%3BMargulies%2C+David&rft.aulast=Revilleza&rft.aufirst=Maria&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Leucine rich repeats and calponin homology containing protein 4 (Lrch4) is a novel regulator of Toll-like receptor signaling T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1312990860; 6140277 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Aloor, Jim AU - Gowdy, Kymberly AU - Azzam, Kathleen AU - Madenspacher, Jennifer AU - Draper, David AU - Guardiola-Bright, John AU - Merrick, Alex AU - Dhungana, Suraj AU - Fessler, Michael Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Homology KW - Calponin KW - Toll-like receptors KW - Leucine UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312990860?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Leucine+rich+repeats+and+calponin+homology+containing+protein+4+%28Lrch4%29+is+a+novel+regulator+of+Toll-like+receptor+signaling&rft.au=Aloor%2C+Jim%3BGowdy%2C+Kymberly%3BAzzam%2C+Kathleen%3BMadenspacher%2C+Jennifer%3BDraper%2C+David%3BGuardiola-Bright%2C+John%3BMerrick%2C+Alex%3BDhungana%2C+Suraj%3BFessler%2C+Michael&rft.aulast=Aloor&rft.aufirst=Jim&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - IL27p28 inhibits induction and expression of experimental autoimmune uveitis by concurrently antagonizing autoaggressive Th1 and Th17 responses. T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1312988769; 6139582 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Chong, Wai AU - Horai, Reiko AU - Silver, Phyllis AU - Mattapallil, Mary AU - Chen, Jun AU - Caspi, Rachel Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Lymphocytes T KW - Helper cells KW - experimental autoimmune uveitis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312988769?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=IL27p28+inhibits+induction+and+expression+of+experimental+autoimmune+uveitis+by+concurrently+antagonizing+autoaggressive+Th1+and+Th17+responses.&rft.au=Chong%2C+Wai%3BHorai%2C+Reiko%3BSilver%2C+Phyllis%3BMattapallil%2C+Mary%3BChen%2C+Jun%3BCaspi%2C+Rachel&rft.aulast=Chong&rft.aufirst=Wai&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Effective prevention and treatment of CD8 T cell-mediated graft-versus-host-like disease (GvHD) using a JAK inhibitor T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1312988706; 6139791 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Okiyama, Naoko AU - Furumoto, Yasuko AU - Villarroel, Vadim AU - Gutermuth, Jan AU - Ghoreschi, Kamran AU - Gadina, Massimo AU - Katz, Stephen Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Prevention KW - Graft-versus-host reaction KW - CD8 antigen KW - Inhibitors KW - Disease control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312988706?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Effective+prevention+and+treatment+of+CD8+T+cell-mediated+graft-versus-host-like+disease+%28GvHD%29+using+a+JAK+inhibitor&rft.au=Okiyama%2C+Naoko%3BFurumoto%2C+Yasuko%3BVillarroel%2C+Vadim%3BGutermuth%2C+Jan%3BGhoreschi%2C+Kamran%3BGadina%2C+Massimo%3BKatz%2C+Stephen&rft.aulast=Okiyama&rft.aufirst=Naoko&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - The nascent truncation of Fc{epsilon}RI{beta} confers calmodulin binding which is essential for microtubule formation and degranulation in human mast cells T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1312988571; 6139818 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Cruse, Glenn AU - Beaven, Michael AU - Bradding, Peter AU - Gilfillan, Alasdair AU - Metcalfe, Dean Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Mast cells KW - Microtubules KW - Calmodulin KW - Degranulation KW - Calcium-binding protein UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312988571?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=The+nascent+truncation+of+Fc%7Bepsilon%7DRI%7Bbeta%7D+confers+calmodulin+binding+which+is+essential+for+microtubule+formation+and+degranulation+in+human+mast+cells&rft.au=Cruse%2C+Glenn%3BBeaven%2C+Michael%3BBradding%2C+Peter%3BGilfillan%2C+Alasdair%3BMetcalfe%2C+Dean&rft.aulast=Cruse&rft.aufirst=Glenn&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - T Cell Factor-1 and beta-catenin regulate the development of memory-like CD8 thymocytes T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1312988120; 6139350 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Sharma, Archna AU - Chen, Qinghua AU - Nguyen, Trang AU - Yu, Qing AU - Sen, Jyoti Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Thymocytes KW - CD8 antigen KW - Lymphocytes T KW - catenin UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312988120?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=T+Cell+Factor-1+and+beta-catenin+regulate+the+development+of+memory-like+CD8+thymocytes&rft.au=Sharma%2C+Archna%3BChen%2C+Qinghua%3BNguyen%2C+Trang%3BYu%2C+Qing%3BSen%2C+Jyoti&rft.aulast=Sharma&rft.aufirst=Archna&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - T-cell education of dendritic cell responsiveness T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1312987429; 6139123 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Abdi, Kaveh Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Education KW - Dendritic cells KW - Lymphocytes T UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312987429?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=T-cell+education+of+dendritic+cell+responsiveness&rft.au=Abdi%2C+Kaveh&rft.aulast=Abdi&rft.aufirst=Kaveh&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Migratory properties of pulmonary dendritic cells are developmentally programmed T2 - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AN - 1312985305; 6139036 JF - 99th Annual Meeting of the American Association of Immunologists (IMMUNOLOGY2012) AU - Cook, Donald AU - Burgents, Joseph AU - Nakano, Hideki Y1 - 2012/05/04/ PY - 2012 DA - 2012 May 04 KW - Lung KW - Dendritic cells KW - Cell migration UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312985305?accountid=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=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.atitle=Migratory+properties+of+pulmonary+dendritic+cells+are+developmentally+programmed&rft.au=Cook%2C+Donald%3BBurgents%2C+Joseph%3BNakano%2C+Hideki&rft.aulast=Cook&rft.aufirst=Donald&rft.date=2012-05-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=99th+Annual+Meeting+of+the+American+Association+of+Immunologists+%28IMMUNOLOGY2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.jimmunol.org/content/vol188/1_MeetingAbstracts LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Profiling Environmental Chemicals for Activity in the Antioxidant Response Element Signaling Pathway Using a High Throughput Screening Approach AN - 1677976035; 17168283 AB - Background: Oxidative stress has been implicated in the pathogenesis of a variety of diseases ranging from cancer to neurodegeneration, highlighting the need to identify chemicals that can induce this effect. The antioxidant response element (ARE) signaling pathway plays an important role in the amelioration of oxidative stress. Thus, assays that detect the up-regulation of this pathway could be useful for identifying chemicals that induce oxidative stress. Objectives: We used cell-based reporter methods and informatics tools to efficiently screen a large collection of environmental chemicals and identify compounds that induce oxidative stress. Methods: We utilized two cell-based ARE assay reporters, beta -lactamase and luciferase, to screen a U.S. National Toxicology Program 1,408-compound library (NTP 1408, which contains 1,340 unique compounds) for their ability to induce oxidative stress in HepG2 cells using quantitative high throughput screening (qHTS). Results: Roughly 3% (34 of 1,340) of the unique compounds demonstrated activity across both cell-based assays. Based on biological activity and structure-activity relationship profiles, we selected 50 compounds for retesting in the two ARE assays and in an additional follow-up assay that employed a mutated ARE linked to beta -lactamase. Using this strategy, we identified 30 compounds that demonstrated activity in the ARE-bla and ARE-luc assays and were able to determine structural features conferring compound activity across assays. Conclusions: Our results support the robustness of using two different cell-based approaches for identifying compounds that induce ARE signaling. Together, these methods are useful for prioritizing chemicals for further in-depth mechanism-based toxicity testing. JF - Environmental Health Perspectives AU - Shukla, Sunita J AU - Huang, Ruili AU - Simmons, Steven O AU - Tice, Raymond R AU - Witt, Kristine L AU - VanLeer, Danielle AU - Ramabhadran, Ram AU - Austin, Christopher P AU - Xia, Menghang AD - NIH Chemical Genomics Center, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland, USA Y1 - 2012/05/02/ PY - 2012 DA - 2012 May 02 SP - 1150 EP - 1156 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 120 IS - 8 SN - 0091-6765, 0091-6765 KW - Environmental Engineering Abstracts (EN); CSA / ASCE Civil Engineering Abstracts (CE) KW - ARE KW - Nrf2 KW - oxidative stress KW - qHTS KW - toxicity KW - Tox21 KW - Screening KW - Assaying KW - Screens KW - Antioxidants KW - Pathways KW - Diseases KW - Stresses KW - Toxicity testing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1677976035?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aenvironmentalengabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Profiling+Environmental+Chemicals+for+Activity+in+the+Antioxidant+Response+Element+Signaling+Pathway+Using+a+High+Throughput+Screening+Approach&rft.au=Shukla%2C+Sunita+J%3BHuang%2C+Ruili%3BSimmons%2C+Steven+O%3BTice%2C+Raymond+R%3BWitt%2C+Kristine+L%3BVanLeer%2C+Danielle%3BRamabhadran%2C+Ram%3BAustin%2C+Christopher+P%3BXia%2C+Menghang&rft.aulast=Shukla&rft.aufirst=Sunita&rft.date=2012-05-02&rft.volume=120&rft.issue=8&rft.spage=1150&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1104709 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-11-01 N1 - Last updated - 2015-05-04 DO - http://dx.doi.org/10.1289/ehp.1104709 ER - TY - JOUR T1 - Contribution of hepatic lineage stage-specific donor memory to the differential potential of induced mouse pluripotent stem cells. AN - 993319180; 22378611 AB - Recent studies suggested that induced pluripotent stem cells (iPSCs) retain a residual donor cell gene expression, which may impact their capacity to differentiate into cell of origin. Here, we addressed a contribution of a lineage stage-specific donor cell memory in modulating the functional properties of iPSCs. iPSCs were generated from hepatic lineage cells at an early (hepatoblast-derived, HB-iPSCs) and end stage (adult hepatocyte, AH-iPSCs) of hepatocyte differentiation as well as from mouse embryonic fibroblasts (MEFs-iPSCs) using a lentiviral vector encoding four pluripotency-inducing factors Oct4, Sox2, Klf4, and c-Myc. All resulting iPSC lines acquired iPSCs phenotype as judged by the accepted criteria including morphology, expression of pluripotency markers, silencing of transducing factors, capacity of multilineage differentiation in teratoma assay, and normal diploid karyotype. However, HB-iPSCs were more efficient in directed differentiation toward hepatocytic lineage as compared to AH-iPSCs, MEF-iPSCs, or mouse embryonic stem cells (mESCs). Extensive comparative transcriptome analyses of the early passage iPSCs, donor cells, and mESCs revealed that despite global similarities in gene expression patterns between generated iPSCs and mESCs, HB-iPSCs retained a transcriptional memory (seven upregulated and 17 downregulated genes) typical of the original cells. Continuous passaging of HB-iPSCs erased most of these differences including a superior capacity for hepatic redifferentiation. These results suggest that retention of lineage stage-specific donor memory in iPSCs may facilitate differentiation into donor cell type. The identified gene set may help to improve hepatic differentiation for therapeutic applications and contribute to the better understanding of liver development. Copyright © 2012 AlphaMed Press. JF - Stem cells (Dayton, Ohio) AU - Lee, Seung Bum AU - Seo, Daekwan AU - Choi, Dongho AU - Park, Kye-Yoon AU - Holczbauer, Agnes AU - Marquardt, Jens U AU - Conner, Elizabeth A AU - Factor, Valentina M AU - Thorgeirsson, Snorri S AD - Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892, USA. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 997 EP - 1007 VL - 30 IS - 5 KW - Transcription Factors KW - 0 KW - Index Medicus KW - Animals KW - Lentivirus KW - Humans KW - HEK293 Cells KW - Transduction, Genetic KW - Mice KW - Induced Pluripotent Stem Cells -- metabolism KW - Cell Dedifferentiation KW - Liver -- cytology KW - Liver -- metabolism KW - Induced Pluripotent Stem Cells -- cytology KW - Hepatocytes -- cytology KW - Transcription Factors -- genetics KW - Transcription Factors -- biosynthesis KW - Hepatocytes -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/993319180?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+cells+%28Dayton%2C+Ohio%29&rft.atitle=Contribution+of+hepatic+lineage+stage-specific+donor+memory+to+the+differential+potential+of+induced+mouse+pluripotent+stem+cells.&rft.au=Lee%2C+Seung+Bum%3BSeo%2C+Daekwan%3BChoi%2C+Dongho%3BPark%2C+Kye-Yoon%3BHolczbauer%2C+Agnes%3BMarquardt%2C+Jens+U%3BConner%2C+Elizabeth+A%3BFactor%2C+Valentina+M%3BThorgeirsson%2C+Snorri+S&rft.aulast=Lee&rft.aufirst=Seung&rft.date=2012-05-01&rft.volume=30&rft.issue=5&rft.spage=997&rft.isbn=&rft.btitle=&rft.title=Stem+cells+%28Dayton%2C+Ohio%29&rft.issn=1549-4918&rft_id=info:doi/10.1002%2Fstem.1074 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-30 N1 - Date created - 2012-04-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Genes Dev. 2000 Feb 15;14(4):464-74 [10691738] Nat Rev Gastroenterol Hepatol. 2010 May;7(5):288-98 [20368738] J Anat. 2001 May;198(Pt 5):555-9 [11430694] Genes Dev. 2001 Aug 1;15(15):1879-84 [11485983] Genes Dev. 2001 Aug 1;15(15):1998-2009 [11485993] Nat Rev Genet. 2002 Jul;3(7):499-512 [12094228] Exp Cell Res. 2002 Oct 1;279(2):330-43 [12243758] Mol Cell. 2003 Feb;11(2):377-89 [12620226] Dev Biol. 2003 Aug 15;260(2):426-37 [12921743] Nat Med. 2004 Jan;10(1):55-63 [14702635] Biochem Biophys Res Commun. 1996 May 6;222(1):64-70 [8630075] EMBO J. 1999 Apr 15;18(8):2127-36 [10205167] J Biol Chem. 2005 Feb 11;280(6):4929-39 [15563463] EMBO J. 2005 Sep 21;24(18):3313-24 [16138077] J Biochem. 2006 Feb;139(2):177-88 [16452305] Cell. 2006 Aug 25;126(4):663-76 [16904174] Hepatology. 2006 Dec;44(6):1478-86 [17133486] Mol Cell Biol. 2007 Apr;27(8):3056-64 [17283045] Nat Genet. 2007 Aug;39(8):963-5 [17632510] Cell. 2007 Nov 30;131(5):861-72 [18035408] Curr Protoc Mol Biol. 2001 May;Chapter 23:Unit 23.2 [18265203] Proc Natl Acad Sci U S A. 2008 May 6;105(18):6656-61 [18448678] Nature. 2008 Jul 3;454(7200):49-55 [18509334] Science. 2008 Aug 1;321(5889):699-702 [18276851] Cell. 2008 Sep 5;134(5):877-86 [18691744] Nat Biotechnol. 2010 Aug;28(8):848-55 [20644536] Nature. 2010 Sep 16;467(7313):285-90 [20644535] Cell Stem Cell. 2010 Oct 8;7(4):521-31 [20887957] Stem Cell Rev. 2010 Dec;6(4):622-32 [20821352] Genes Dev. 2010 Oct 15;24(20):2239-63 [20952534] Cell. 2010 Nov 12;143(4):508-25 [21074044] Cell. 2010 Nov 12;143(4):527-39 [21074045] Blood. 2010 Dec 16;116(25):5670-8 [20829371] Nature. 2011 Mar 3;471(7336):68-73 [21289626] Nat Cell Biol. 2011 May;13(5):541-9 [21499256] Nat Cell Biol. 2011 May;13(5):523-5 [21540851] Cell Stem Cell. 2011 Jul 8;9(1):17-23 [21726830] Gene. 2011 Nov 1;487(1):21-8 [21803131] Blood. 2003 Nov 1;102(9):3154-62 [12855584] Cell Stem Cell. 2008 Oct 9;3(4):402-15 [18940732] Cell Res. 2009 Mar;19(3):296-306 [19238173] Nat Biotechnol. 2009 Apr;27(4):353-60 [19330000] Cell Stem Cell. 2009 Jul 2;5(1):111-23 [19570518] PLoS One. 2009;4(9):e7076 [19763270] Stem Cells. 2009 Nov;27(11):2686-90 [19711451] Nat Genet. 2009 Dec;41(12):1350-3 [19881528] Hepatology. 2010 Jan;51(1):297-305 [19998274] PLoS One. 2010;5(2):e8975 [20126639] Dev Cell. 2010 Feb 16;18(2):175-89 [20159590] Proc Natl Acad Sci U S A. 2010 Mar 2;107(9):4335-40 [20160098] Differentiation. 2010 Feb;79(2):65-73 [19883970] Differentiation. 2010 Mar;79(3):171-81 [20106584] Stem Cells. 2010 Apr;28(4):704-12 [20155819] Hepatology. 2010 May;51(5):1810-9 [20432258] Nat Genet. 2000 Dec;26(4):484-9 [11101851] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/stem.1074 ER - TY - JOUR T1 - Cnot1, Cnot2, and Cnot3 maintain mouse and human ESC identity and inhibit extraembryonic differentiation. AN - 993315680; 22367759 AB - Embryonic stem cell (ESC) identity and self-renewal is maintained by extrinsic signaling pathways and intrinsic gene regulatory networks. Here, we show that three members of the Ccr4-Not complex, Cnot1, Cnot2, and Cnot3, play critical roles in maintaining mouse and human ESC identity as a protein complex and inhibit differentiation into the extraembryonic lineages. Enriched in the inner cell mass of blastocysts, these Cnot genes are highly expressed in ESC and downregulated during differentiation. In mouse ESCs, Cnot1, Cnot2, and Cnot3 are important for maintenance in both normal conditions and the 2i/LIF medium that supports the ground state pluripotency. Genetic analysis indicated that they do not act through known self-renewal pathways or core transcription factors. Instead, they repress the expression of early trophectoderm (TE) transcription factors such as Cdx2. Importantly, these Cnot genes are also necessary for the maintenance of human ESCs, and silencing them mainly lead to TE and primitive endoderm differentiation. Together, our results indicate that Cnot1, Cnot2, and Cnot3 represent a novel component of the core self-renewal and pluripotency circuitry conserved in mouse and human ESCs. Copyright © 2012 AlphaMed Press. JF - Stem cells (Dayton, Ohio) AU - Zheng, Xiaofeng AU - Dumitru, Raluca AU - Lackford, Brad L AU - Freudenberg, Johannes M AU - Singh, Ajeet P AU - Archer, Trevor K AU - Jothi, Raja AU - Hu, Guang AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, RTP, North Carolina, USA. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 910 EP - 922 VL - 30 IS - 5 KW - CNOT1 protein, human KW - 0 KW - CNOT2 protein, human KW - CNOT3 protein, human KW - CNOT3 protein, mouse KW - Repressor Proteins KW - Transcription Factors KW - Index Medicus KW - Animals KW - Humans KW - Cell Differentiation -- genetics KW - Mice KW - Cell Line KW - Mice, Knockout KW - Embryonic Stem Cells -- metabolism KW - Embryonic Stem Cells -- cytology KW - Gene Silencing -- physiology KW - Transcription Factors -- metabolism KW - Repressor Proteins -- metabolism KW - Transcription Factors -- genetics KW - Repressor Proteins -- genetics KW - Pluripotent Stem Cells -- metabolism KW - Pluripotent Stem Cells -- cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/993315680?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Stem+cells+%28Dayton%2C+Ohio%29&rft.atitle=Cnot1%2C+Cnot2%2C+and+Cnot3+maintain+mouse+and+human+ESC+identity+and+inhibit+extraembryonic+differentiation.&rft.au=Zheng%2C+Xiaofeng%3BDumitru%2C+Raluca%3BLackford%2C+Brad+L%3BFreudenberg%2C+Johannes+M%3BSingh%2C+Ajeet+P%3BArcher%2C+Trevor+K%3BJothi%2C+Raja%3BHu%2C+Guang&rft.aulast=Zheng&rft.aufirst=Xiaofeng&rft.date=2012-05-01&rft.volume=30&rft.issue=5&rft.spage=910&rft.isbn=&rft.btitle=&rft.title=Stem+cells+%28Dayton%2C+Ohio%29&rft.issn=1549-4918&rft_id=info:doi/10.1002%2Fstem.1070 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-30 N1 - Date created - 2012-04-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nat Genet. 2000 Apr;24(4):372-6 [10742100] J Mol Biol. 2001 Dec 7;314(4):683-94 [11733989] Bioinformatics. 2003 Jan 22;19(2):185-93 [12538238] Prog Nucleic Acid Res Mol Biol. 2003;73:221-50 [12882519] Gene. 2003 Aug 14;313:1-16 [12957374] Cell. 2003 Oct 31;115(3):281-92 [14636556] Methods Enzymol. 2003;365:327-41 [14696356] Nat Med. 2004 Jan;10(1):55-63 [14702635] J Biol Chem. 2004 Mar 19;279(12):10848-54 [14707134] Prog Nucleic Acid Res Mol Biol. 2004;77:289-322 [15196896] Mol Cell Biol. 2004 Jul;24(13):5808-20 [15199137] Genome Biol. 2004;5(10):R80 [15461798] Genes Dev. 1994 Mar 1;8(5):525-37 [7926748] Genes Dev. 1998 Jul 1;12(13):2048-60 [9649508] Science. 1998 Dec 11;282(5396):2072-5 [9851926] Stem Cells. 2005 Mar;23(3):299-305 [15749924] Genes Dev. 2005 May 15;19(10):1129-55 [15905405] Cell. 2005 Sep 23;122(6):947-56 [16153702] J Cell Sci. 2005 Oct 1;118(Pt 19):4495-509 [16179608] Nucleic Acids Res. 2005;33(20):e175 [16284200] Cell. 2005 Dec 2;123(5):917-29 [16325584] Nat Genet. 2006 Apr;38(4):431-40 [16518401] Stem Cells. 2006 Mar;24(3):568-74 [16282444] EMBO J. 2006 Jul 12;25(13):3089-99 [16778766] Nature. 2006 Aug 3;442(7102):533-8 [16767105] Nature. 2006 Nov 16;444(7117):364-8 [17093407] BMC Bioinformatics. 2009;10:234 [19640299] Cell Stem Cell. 2009 Oct 2;5(4):420-33 [19796622] Development. 2010 Feb;137(3):395-403 [20081188] Genome Biol. 2009;10(11):R130 [19919682] Cell Stem Cell. 2010 Apr 2;6(4):369-81 [20362541] Cell Stem Cell. 2010 Apr 2;6(4):382-95 [20362542] Cell. 2010 Apr 2;141(1):142-53 [20371351] Genes Cells. 2010 May;15(5):455-70 [20384793] Biochem Soc Trans. 2010 Aug;38(4):1027-32 [20658998] Nature. 2010 Nov 11;468(7321):316-20 [20953172] Biochem Soc Trans. 2010 Dec;38(6):1531-6 [21118121] Protein Cell. 2010 May;1(5):443-52 [21203959] Cell. 2011 Mar 18;144(6):940-54 [21414485] Genes Cells. 2011 Apr;16(4):368-79 [21299754] Cell Stem Cell. 2011 Apr 8;8(4):363-9 [21474100] Nat Methods. 2011 May;8(5):424-9 [21478862] Nat Cell Biol. 2011 May;13(5):490-6 [21540844] Nat Cell Biol. 2011 Jul;13(7):838-45 [21685889] Cell Stem Cell. 2011 Jul 8;9(1):37-49 [21726832] Nat Cell Biol. 2011 Aug;13(8):903-13 [21785422] Annu Rev Genomics Hum Genet. 2011;12:165-85 [21801025] Protein Cell. 2011 Sep;2(9):755-63 [21976065] EMBO J. 2011 Nov 16;30(22):4678-91 [21897366] Development. 2007 Feb;134(4):635-46 [17215298] Development. 2007 Aug;134(16):2895-902 [17660198] Cell. 2008 Feb 22;132(4):661-80 [18295582] J Biol Chem. 2008 Mar 14;283(11):6806-16 [18180299] Cell. 2008 Mar 21;132(6):1049-61 [18358816] Nature. 2008 May 22;453(7194):519-23 [18497825] Cell. 2008 Jun 13;133(6):1106-17 [18555785] Nat Protoc. 2008;3(7):1194-201 [18600225] Cell. 2008 Jul 11;134(1):162-74 [18614019] Genome Biol. 2008;9(8):R126 [18700969] PLoS Biol. 2008 Oct 21;6(10):e253 [18942890] DNA Res. 2009 Feb;16(1):73-80 [19112179] Genes Dev. 2009 Apr 1;23(7):837-48 [19339689] Cell Stem Cell. 2009 May 8;4(5):403-15 [19345177] Cell Stem Cell. 2009 Jun 5;4(6):487-92 [19497275] Biochem J. 2009 Sep 15;422(3):443-53 [19558367] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/stem.1070 ER - TY - JOUR T1 - The molecular interaction of a copper chelate with human P-glycoprotein. AN - 934257633; 22258826 AB - One of the major reasons for multidrug resistance (MDR) in cancer is the overexpression of P-glycoprotein (P-gp, ABCB1), a drug efflux pump. A novel copper complex, namely, copper (II) N-(2-hydroxyacetophenone) glycinate (CuNG) previously synthesized and characterized by the authors had been tested in this study. In a cell-based assay system with human MDR1 cDNA overexpressed mouse fibroblast NIH MDR1-G185 cell line, we demonstrated that this metal complex can directly interact with this transporter. As CuNG increased cellular accumulation of doxorubicin in P-gp-expressing cells, we presumed that of CuNG may be potential to reverse P-gp-mediated drug resistance probably by lowering the P-gp expression at the protein as well as mRNA level. Interestingly, our studies on UIC2 (a conformation sensitive monoclonal antibody) binding assay indicated the direct interaction of CuNG with P-gp. However, CuNG did not compete for the substrate binding as photoaffinity labeling of P-gp with a substrate analog [(125)I] iodoarylazidoprazosin ([(125)I] IAAP) showed approximately twofold increase in [(125)I] IAAP binding in presence of CuNG. In vitro study showed that CuNG significantly stimulated P-gp-specific ATPase activity in isolated membrane preparations from NIH MDR1-G185 cells. This result further confirmed the CuNG-P-gp direct interaction. This study also demonstrated that CuNG has a drug interaction site different from verapamil-, vinblastine- and progesterone-binding sites on P-gp. Taken together, this is the first report of molecular interaction of any Schiff's base metal chelate CuNG with human P-gp. This information may be useful to design more efficacious nontoxic metal-based drugs as MDR-reversing agents. JF - Molecular and cellular biochemistry AU - Ghosh, Ruma Dey AU - Chakraborty, Paramita AU - Banerjee, Kaushik AU - Adhikary, Arghya AU - Sarkar, Avijit AU - Chatterjee, Mitali AU - Das, Tanya AU - Choudhuri, Soumitra Kumar AD - Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata 700 026, India. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 309 EP - 320 VL - 364 IS - 1-2 KW - ABCB1 protein, human KW - 0 KW - Chelating Agents KW - Organometallic Compounds KW - P-Glycoprotein KW - P-Glycoproteins KW - copper (N-2-hydroxyacetophenone)glycinate KW - Copper KW - 789U1901C5 KW - Doxorubicin KW - 80168379AG KW - Adenosine Triphosphatases KW - EC 3.6.1.- KW - Glycine KW - TE7660XO1C KW - Index Medicus KW - Animals KW - Glycine -- chemistry KW - Organometallic Compounds -- pharmacology KW - Humans KW - Adenosine Triphosphatases -- metabolism KW - Mice KW - Glycine -- analogs & derivatives KW - Fibroblasts -- metabolism KW - Organometallic Compounds -- chemistry KW - Doxorubicin -- pharmacology KW - Glycine -- pharmacology KW - Cell Line KW - Chelating Agents -- pharmacology KW - Chelating Agents -- chemistry KW - P-Glycoprotein -- genetics KW - P-Glycoprotein -- metabolism KW - P-Glycoprotein -- biosynthesis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/934257633?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biochemistry&rft.atitle=The+molecular+interaction+of+a+copper+chelate+with+human+P-glycoprotein.&rft.au=Ghosh%2C+Ruma+Dey%3BChakraborty%2C+Paramita%3BBanerjee%2C+Kaushik%3BAdhikary%2C+Arghya%3BSarkar%2C+Avijit%3BChatterjee%2C+Mitali%3BDas%2C+Tanya%3BChoudhuri%2C+Soumitra+Kumar&rft.aulast=Ghosh&rft.aufirst=Ruma&rft.date=2012-05-01&rft.volume=364&rft.issue=1-2&rft.spage=309&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biochemistry&rft.issn=1573-4919&rft_id=info:doi/10.1007%2Fs11010-012-1232-z LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-20 N1 - Date created - 2012-03-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s11010-012-1232-z ER - TY - JOUR T1 - The H6D variant of NAG-1/GDF15 inhibits prostate xenograft growth in vivo. AN - 929504691; 21809352 AB - Non-steroidal anti-inflammatory drug-activated gene (NAG-1), a divergent member of the transforming growth factor-beta superfamily, has been implicated in many cellular processes, including inflammation, early bone formation, apoptosis, and tumorigenesis. Recent clinical studies suggests that a C to G single nucleotide polymorphism at position 6 (histidine to aspartic acid substitution, or H6D) of the NAG-1 protein is associated with lower human prostate cancer incidence. The objective of the current study is to investigate the activity of NAG-1 H6D variant in prostate cancer tumorigenesis in vivo. Human prostate cancer DU145 cells expressing the H6D NAG-1 or wild-type (WT) NAG-1 were injected subcutaneously into nude mice and tumor growth was monitored. Serum and tumor samples were collected for subsequent analysis. The H6D variant was more potent than the WT NAG-1 and inhibited tumor growth significantly compared to control mice. Mice with tumors expressing the WT NAG-1 have greater reduced both body weight and abdominal fat than mice with H6D variant tumors suggesting different activities of the WT NAG-1 and the H6D NAG-1. A significant reduction in adiponectin, leptin, and IGF-1 serum levels was observed in the tumor-bearing mice with a more profound reduction observed with expression of H6D variant. Cyclin D1 expression was suppressed in the tumors with a dramatic reduction observed in the tumor expressing the H6D variant. Our data suggest that the H6D variant of NAG-1 inhibits prostate tumorigenesis by suppressing IGF-1 and cyclin D1 expression but likely additional mechanisms are operative. Copyright © 2011 Wiley Periodicals, Inc. JF - The Prostate AU - Wang, Xingya AU - Chrysovergis, Kali AU - Bienstock, Rachelle J AU - Shim, Minsub AU - Eling, Thomas E AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, 111 T.W. Alexander Dr. Research Triangle Park, North Carolina 27709, USA. Y1 - 2012/05/01/ PY - 2012 DA - 2012 May 01 SP - 677 EP - 689 VL - 72 IS - 6 KW - Adiponectin KW - 0 KW - GDF15 protein, human KW - Growth Differentiation Factor 15 KW - Leptin KW - Cyclin D1 KW - 136601-57-5 KW - Insulin-Like Growth Factor I KW - 67763-96-6 KW - Index Medicus KW - Animals KW - Humans KW - Insulin-Like Growth Factor I -- metabolism KW - Cell Line, Tumor KW - Cyclin D1 -- genetics KW - Mice KW - Mice, Nude KW - Leptin -- blood KW - Neoplasm Transplantation KW - Alleles KW - Cyclin D1 -- metabolism KW - Transplantation, Heterologous KW - Adiponectin -- blood KW - Male KW - Prostatic Neoplasms -- metabolism KW - Prostatic Neoplasms -- pathology KW - Polymorphism, Single Nucleotide KW - Growth Differentiation Factor 15 -- metabolism KW - Prostate -- metabolism KW - Prostatic Neoplasms -- genetics KW - Growth Differentiation Factor 15 -- genetics KW - Prostate -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/929504691?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Prostate&rft.atitle=The+H6D+variant+of+NAG-1%2FGDF15+inhibits+prostate+xenograft+growth+in+vivo.&rft.au=Wang%2C+Xingya%3BChrysovergis%2C+Kali%3BBienstock%2C+Rachelle+J%3BShim%2C+Minsub%3BEling%2C+Thomas+E&rft.aulast=Wang&rft.aufirst=Xingya&rft.date=2012-05-01&rft.volume=72&rft.issue=6&rft.spage=677&rft.isbn=&rft.btitle=&rft.title=The+Prostate&rft.issn=1097-0045&rft_id=info:doi/10.1002%2Fpros.21471 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-09 N1 - Date created - 2012-03-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Cell Physiol. 2006 Sep;208(3):566-74 [16741990] Expert Opin Investig Drugs. 2006 Aug;15(8):917-31 [16859394] J Biochem Mol Biol. 2006 Nov 30;39(6):649-55 [17129398] Nat Rev Cancer. 2007 Apr;7(4):256-69 [17384581] Cancer Epidemiol Biomarkers Prev. 2007 Jun;16(6):1309-11 [17548705] Biochemistry. 2007 Oct 30;46(43):12238-47 [17924656] Cancer Lett. 2008 Mar 18;261(2):253-62 [18164124] Curr Protoc Bioinformatics. 2006 Oct;Chapter 5:Unit 5.6 [18428767] Ann Intern Med. 2008 Oct 7;149(7):461-71, W83-8 [18838726] Oncogene. 2008 Oct 23;27(49):6365-75 [18679417] EMBO J. 2009 Apr 8;28(7):937-47 [19229295] Carcinogenesis. 2009 May;30(5):818-23 [19269999] Cancer Epidemiol Biomarkers Prev. 2009 Oct;18(10):2569-78 [19755644] Arq Bras Endocrinol Metabol. 2009 Nov;53(8):969-75 [20126849] J Cell Physiol. 2010 Sep;224(3):626-35 [20578239] Cancer Biomark. 2010;7(1):11-5 [21045260] Aging Cell. 2010 Dec;9(6):1057-64 [20854422] Cancer Res. 2010 Nov 15;70(22):9106-17 [21062988] Cytokine. 2011 Mar;53(3):282-5 [21167737] J Cell Physiol. 2011 May;226(5):1274-82 [20945385] FASEB J. 1999 Dec;13(15):2105-24 [10593858] Proc Natl Acad Sci U S A. 2000 Jan 4;97(1):109-14 [10618379] EMBO J. 2000 May 15;19(10):2212-20 [10811612] Clin Cancer Res. 2000 May;6(5):1891-5 [10815912] Nat Struct Biol. 2000 Jun;7(6):492-6 [10881198] Annu Rev Biophys Biomol Struct. 2000;29:291-325 [10940251] J Clin Endocrinol Metab. 2000 Dec;85(12):4781-8 [11134143] Biochemistry. 2001 Jan 9;40(1):65-73 [11141057] Mol Pharmacol. 2001 Apr;59(4):901-8 [11259636] J Biol Chem. 2002 Jul 19;277(29):26662-72 [11994274] Cancer Cell. 2003 Jun;3(6):531-6 [12842082] Clin Cancer Res. 2003 Jul;9(7):2642-50 [12855642] Cancer Res. 2003 Aug 15;63(16):5034-40 [12941831] J Natl Cancer Inst. 2004 Aug 18;96(16):1248-54 [15316060] J Biol Chem. 1998 May 29;273(22):13760-7 [9593718] Cancer Res. 1999 Jan 1;59(1):227-33 [9892211] Cancer Res. 1999 May 1;59(9):2203-9 [10232609] Novartis Found Symp. 2004;262:193-9; discussion 199-204, 265-8 [15562830] Trends Mol Med. 2005 Feb;11(2):52-5 [15694866] Biochem Biophys Res Commun. 2005 Apr 15;329(3):1076-86 [15752764] Cancer Res. 2005 Mar 1;65(5):1808-13 [15753378] J Allergy Clin Immunol. 2005 May;115(5):911-9; quiz 920 [15867843] Cancer Epidemiol Biomarkers Prev. 2005 May;14(5):1270-3 [15894684] J Mol Biol. 2005 Jun 24;349(5):933-47 [15890363] J Cell Physiol. 2006 Apr;207(1):12-22 [16110483] Circ Res. 2006 Feb 17;98(3):342-50 [16397142] Cancer Res. 2006 May 15;66(10):4983-6 [16707416] Cancer Epidemiol Biomarkers Prev. 2006 Jun;15(6):1223-5 [16775185] Gastroenterology. 2006 Nov;131(5):1553-60 [17101328] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/pros.21471 ER - TY - JOUR T1 - Chemopreventive efficacy of Targretin in rodent models of urinary bladder, colon/intestine, head and neck and mammary cancers. AN - 926879607; 22307264 AB - The chemopreventive efficacy of Targretin was evaluated in various rodent cancer models. In the rat model of 4-hydroxybutyl(butyl)nitrosamine (OH-BBN)-induced urinary bladder cancer, it was found that Targretin administered in the diet (beginning one week after the last OH-BBN treatment) for 5.5 months increased the number and size of urinary bladder cancers. In the azoxymethane (AOM)-induced model of colon carcinogenesis (in which rats develop minimally invasive colonic cancers), Targretin was ineffective as a chemopreventive agent, decreasing neither tumor incidence nor multiplicity. Treatment of Min mice with Targretin for 45 days similarly failed to decrease the multiplicity of small intestinal tumors. Similarly, no preventive efficacy was noted for Targretin when the incidence of tumors in the head and neck model (squamous cell tongue tumors) induced by 4-nitroquinoline 1-oxide (4-NQO) were examined. In contrast, use of even a suboptimal dose of Targretin (40 ppm) in a sensitive breast cancer model [methylnitrosourea (MNU)-induced ER+ mammary cancers] reduced cancer multiplicity by 60%. Finally, based on the hypothesis that Targretin may decrease the expression of COX‑2, the effects of Targretin and COX inhibitors were compared in these models. There was minimal overlap of efficacy. That is, models which were relatively susceptible to NSAIDs or COX-2 inhibitors tended not to be sensitive to Targretin and vice versa. JF - Oncology reports AU - Lubet, Ronald A AU - Clapper, Margie L AU - McCormick, David L AU - Pereira, Michael A AU - Chang, W-C L AU - Steele, Vernon E AU - Fischer, Susan M AU - Juliana, M Margaret AU - Grubbs, Clinton J AD - Division of Cancer Prevention, National Cancer Institute, Bethesda, MD 20852, USA. lubetr@mail.nih.gov Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 1400 EP - 1406 VL - 27 IS - 5 KW - Anti-Inflammatory Agents, Non-Steroidal KW - 0 KW - Anticarcinogenic Agents KW - Cyclooxygenase 2 Inhibitors KW - Pyrazoles KW - Sulfonamides KW - Tetrahydronaphthalenes KW - bexarotene KW - A61RXM4375 KW - Celecoxib KW - JCX84Q7J1L KW - Index Medicus KW - Animals KW - Anti-Inflammatory Agents, Non-Steroidal -- therapeutic use KW - Head and Neck Neoplasms -- prevention & control KW - Disease Models, Animal KW - Pyrazoles -- therapeutic use KW - Mice KW - Sulfonamides -- therapeutic use KW - Mice, Knockout KW - Intestinal Neoplasms -- prevention & control KW - Rats KW - Rats, Sprague-Dawley KW - Rats, Inbred F344 KW - Urinary Bladder Neoplasms -- prevention & control KW - Cyclooxygenase 2 Inhibitors -- therapeutic use KW - Mammary Neoplasms, Animal -- prevention & control KW - Colonic Neoplasms -- prevention & control KW - Female KW - Male KW - Tetrahydronaphthalenes -- therapeutic use KW - Anticarcinogenic Agents -- therapeutic use KW - Neoplasms -- chemically induced KW - Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/926879607?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncology+reports&rft.atitle=Chemopreventive+efficacy+of+Targretin+in+rodent+models+of+urinary+bladder%2C+colon%2Fintestine%2C+head+and+neck+and+mammary+cancers.&rft.au=Lubet%2C+Ronald+A%3BClapper%2C+Margie+L%3BMcCormick%2C+David+L%3BPereira%2C+Michael+A%3BChang%2C+W-C+L%3BSteele%2C+Vernon+E%3BFischer%2C+Susan+M%3BJuliana%2C+M+Margaret%3BGrubbs%2C+Clinton+J&rft.aulast=Lubet&rft.aufirst=Ronald&rft.date=2012-05-01&rft.volume=27&rft.issue=5&rft.spage=1400&rft.isbn=&rft.btitle=&rft.title=Oncology+reports&rft.issn=1791-2431&rft_id=info:doi/10.3892%2For.2012.1673 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-23 N1 - Date created - 2012-03-07 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.3892/or.2012.1673 ER - TY - JOUR T1 - The age-specific prevalence of human papillomavirus and risk of cytologic abnormalities in rural Nigeria: implications for screen-and-treat strategies. AN - 923574078; 21630264 AB - Cervical screening for carcinogenic human papillomavirus (HPV) infection is being considered for low-income countries. Effectiveness requires targeted screening in older women in whom prevalent infections are more likely to be persistent and predictive of precancer. Some studies in West Africa have found unusually high HPV prevalences across all adult ages, which may reduce the positive predictive value (PPV) of HPV-based screening, if positivity in older women does not sufficiently predict elevated risk. We conducted a population-based study in rural Nigeria to identify HPV prevalence and associated cervical abnormalities. Using stratified random sampling, we enrolled women age 15+. Nonvirgins had a cervical exam including liquid-based cytology and PCR HPV DNA testing from residual cytology specimens. Two-thirds of invited women participated, and 14.7% had detectable carcinogenic HPV, a proportion that did not decline with age (p-trend = 0.36) and showed slight peaks in the 15-29 and 60-69 age groups. Among women of the age typically considered for screen-and-treat programs (30-49 years), 12.8% were HPV positive, and the PPV for high-grade or worse cytology was 16.4%. Comparatively, women age < 30 were more likely to be HPV positive (18.9%, p = 0.03) with a lower PPV (4.2% p = 0.05). Among women age 50+ (typically excluded from screening in resource-poor settings because inexpensive treatment is not available), HPV positivity was 14.2% with a PPV of 13.9%. In Irun and similar settings where HPV does not decline with age, HPV-based screen-and-treat programs might be feasible for mid-adult women because prevalence is sufficiently low and positivity predicts elevated risk of more easily treated precancer. Copyright © 2011 UICC. JF - International journal of cancer AU - Gage, Julia C AU - Ajenifuja, Kayode O AU - Wentzensen, Nicolas A AU - Adepiti, Akinfolarin C AU - Eklund, Claire AU - Reilly, Mary AU - Hutchinson, Martha AU - Wacholder, Sholom AU - Harford, Joe AU - Soliman, Amr S AU - Burk, Robert D AU - Schiffman, Mark AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, DHHS, Bethesda, MD, USA. gagej@mail.nih.gov Y1 - 2012/05/01/ PY - 2012 DA - 2012 May 01 SP - 2111 EP - 2117 VL - 130 IS - 9 KW - DNA, Viral KW - 0 KW - Index Medicus KW - Papillomaviridae -- pathogenicity KW - Age Factors KW - Cytodiagnosis KW - Humans KW - Aged KW - Mass Screening KW - DNA, Viral -- analysis KW - Papillomaviridae -- isolation & purification KW - Adult KW - Vaginal Smears KW - Middle Aged KW - Nigeria -- epidemiology KW - Adolescent KW - Female KW - Papillomavirus Infections -- epidemiology KW - Papillomavirus Infections -- diagnosis KW - Uterine Cervical Neoplasms -- epidemiology KW - Uterine Cervical Neoplasms -- diagnosis KW - Papillomavirus Infections -- virology KW - Uterine Cervical Neoplasms -- pathology KW - Uterine Cervical Neoplasms -- virology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/923574078?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=The+age-specific+prevalence+of+human+papillomavirus+and+risk+of+cytologic+abnormalities+in+rural+Nigeria%3A+implications+for+screen-and-treat+strategies.&rft.au=Gage%2C+Julia+C%3BAjenifuja%2C+Kayode+O%3BWentzensen%2C+Nicolas+A%3BAdepiti%2C+Akinfolarin+C%3BEklund%2C+Claire%3BReilly%2C+Mary%3BHutchinson%2C+Martha%3BWacholder%2C+Sholom%3BHarford%2C+Joe%3BSoliman%2C+Amr+S%3BBurk%2C+Robert+D%3BSchiffman%2C+Mark&rft.aulast=Gage&rft.aufirst=Julia&rft.date=2012-05-01&rft.volume=130&rft.issue=9&rft.spage=2111&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.26211 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-15 N1 - Date created - 2012-02-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Lancet. 2001 Oct 27;358(9291):1429-30 [11705494] J Infect Dis. 2005 Jun 1;191(11):1796-807 [15871111] J Natl Cancer Inst. 2003 Jan 1;95(1):46-52 [12509400] Br J Cancer. 2005 Oct 31;93(9):1068-76 [16106268] N Engl J Med. 2005 Nov 17;353(20):2158-68 [16291985] Br J Cancer. 2006 Aug 7;95(3):355-62 [16832413] Vaccine. 2006 Aug 31;24 Suppl 3:S3/71-7 [16950020] J Med Virol. 2002 Nov;68(3):417-23 [12226831] N Engl J Med. 2003 Feb 6;348(6):518-27 [12571259] Cancer Epidemiol Biomarkers Prev. 2003 Jun;12(6):477-84 [12814990] Int J Cancer. 2007 Sep 15;121(6):1306-11 [17417776] J Adolesc Health. 2008 Oct;43(4 Suppl):S5-25, S25.e1-41 [18809145] BMJ. 2008;337:a1754 [18852164] N Engl J Med. 2009 Apr 2;360(14):1385-94 [19339719] Br J Cancer. 2009 Jul 7;101(1):202-8 [19536089] J Natl Cancer Inst. 2010 Oct 20;102(20):1557-67 [20884893] Br J Cancer. 2004 Feb 9;90(3):638-45 [14760378] J Med Virol. 2004 Jul;73(3):481-5 [15170646] Acta Obstet Gynecol Scand. 1983;62(1):39-42 [6858622] Gynecol Oncol. 1985 Sep;22(1):23-31 [4018658] Obstet Gynecol. 1985 Dec;66(6):793-8 [3934610] Gynecol Oncol. 1992 Jun;45(3):240-2 [1612498] J Natl Cancer Inst. 1993 Jun 16;85(12):958-64 [8388478] Int J Cancer. 1997 Apr 10;71(2):159-65 [9139836] Cancer Causes Control. 1997 Sep;8(5):755-63 [9328198] J Pathol. 1999 Sep;189(1):12-9 [10451482] Br J Cancer. 2005 Feb 14;92(3):601-6 [15668709] Int J Cancer. 2006 Dec 1;119(11):2677-84 [16991121] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1002/ijc.26211 ER - TY - JOUR T1 - Accounting for Uncertainty in Heteroscedasticity in Nonlinear Regression. AN - 1826555568; 22345900 AB - Toxicologists and pharmacologists often describe toxicity of a chemical using parameters of a nonlinear regression model. Thus estimation of parameters of a nonlinear regression model is an important problem. The estimates of the parameters and their uncertainty estimates depend upon the underlying error variance structure in the model. Typically, a priori the researcher would know if the error variances are homoscedastic (i.e., constant across dose) or if they are heteroscedastic (i.e., the variance is a function of dose). Motivated by this concern, in this article we introduce an estimation procedure based on preliminary test which selects an appropriate estimation procedure accounting for the underlying error variance structure. Since outliers and influential observations are common in toxicological data, the proposed methodology uses M-estimators. The asymptotic properties of the preliminary test estimator are investigated; in particular its asymptotic covariance matrix is derived. The performance of the proposed estimator is compared with several standard estimators using simulation studies. The proposed methodology is also illustrated using a data set obtained from the National Toxicology Program. JF - Journal of statistical planning and inference AU - Lim, Changwon AU - Sen, Pranab K AU - Peddada, Shyamal D AD - Biostatistics Branch, NIEHS, NIH, 111 T. W. Alexander Dr, RTP, NC 27709. Y1 - 2012/05/01/ PY - 2012 DA - 2012 May 01 SP - 1047 EP - 1062 VL - 142 IS - 5 SN - 0378-3758, 0378-3758 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1826555568?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+statistical+planning+and+inference&rft.atitle=Accounting+for+Uncertainty+in+Heteroscedasticity+in+Nonlinear+Regression.&rft.au=Lim%2C+Changwon%3BSen%2C+Pranab+K%3BPeddada%2C+Shyamal+D&rft.aulast=Lim&rft.aufirst=Changwon&rft.date=2012-05-01&rft.volume=142&rft.issue=5&rft.spage=1047&rft.isbn=&rft.btitle=&rft.title=Journal+of+statistical+planning+and+inference&rft.issn=03783758&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date created - 2012-02-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Selective Embedding of Capillaries within Murine Slow Twitch Skeletal Muscle Fibers Visualized Using In Vivo Microscopy AN - 1717501408; PQ0002008802 AB - Evaluate the in vivo, 3D spatial relationship between CAP, MITO, and three fiber types within murine Tibialis anterior (TA) muscle. Two photon excitation microscopy was utilized for simultaneous imaging of MITO (NADH autofluorescence), vasculature, and interstitial space using selective dyes. ~825 x 825 x 280 mu m volumes of the TA were analyzed in vivo with flowing blood. A custom contour drawing and analysis program was used to trace fiber boundaries and determine the contact and volume ratios between CAP and muscle fibers for 98 fibers. Microscopy revealed that a significant fraction of ST fiber CAP (51.7 + or - 4.0%) had at least 50% of their circumference embedded in a groove in the sarcolemma, in vivo. Embedded CAP were tightly associated with dense MITO populations lateral to the CAP grooves and nearly absent below the groove where fibrils dominated. CAP embedding was significantly lower in IT (25.7 + or - 4.5%) and FT (14.1 + or - 2.1%). JF - Medicine & Science in Sports & Exercise AU - Glancy, Brian AU - Hsu, Li-Yueh AU - Dao, Lam AU - Bakalar, Matthew AU - French, Stephanie AU - Chess, David J AU - Taylor, Joni L AU - Daniels, Mathew P AU - Esfahani, Shervin AU - Balaban, Robert S AD - National Institutes of Health, Bethesda, MD Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 682 PB - Lippincott Williams & Wilkins, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 44 IS - 5S SN - 0195-9131, 0195-9131 KW - Physical Education Index KW - Blood KW - Programs KW - Muscles (size) KW - Scanning KW - Analysis KW - Sport science KW - Muscles (type) KW - Circulatory system KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1717501408?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medicine+%26+Science+in+Sports+%26+Exercise&rft.atitle=Selective+Embedding+of+Capillaries+within+Murine+Slow+Twitch+Skeletal+Muscle+Fibers+Visualized+Using+In+Vivo+Microscopy&rft.au=Glancy%2C+Brian%3BHsu%2C+Li-Yueh%3BDao%2C+Lam%3BBakalar%2C+Matthew%3BFrench%2C+Stephanie%3BChess%2C+David+J%3BTaylor%2C+Joni+L%3BDaniels%2C+Mathew+P%3BEsfahani%2C+Shervin%3BBalaban%2C+Robert+S&rft.aulast=Glancy&rft.aufirst=Brian&rft.date=2012-05-01&rft.volume=44&rft.issue=5S&rft.spage=682&rft.isbn=&rft.btitle=&rft.title=Medicine+%26+Science+in+Sports+%26+Exercise&rft.issn=01959131&rft_id=info:doi/ LA - English DB - Physical Education Index N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Blood; Programs; Muscles (size); Scanning; Analysis; Sport science; Muscles (type); Circulatory system ER - TY - JOUR T1 - Effects of a 10-week Aerobic Exercise Program on Cardiorespiratory Function in Patients with Interstitial Lung Disease AN - 1717500873; PQ0002008523 AB - To examine the effects of a 10-week aerobic exercise program on measures of functional capacity and cardiorespiratory function in patients with ILD. Six patients with ILD (3 males, 3 females; Age: 61 + or - 7 yrs; BMI: 30 + or - 5 kg/m2; mean + or - SD) completed treadmill cardiopulmonary exercise tests (CPET) and 6-minute walk tests (6MWT) before and after a 10-week aerobic exercise training program (AET). The AET was comprised of treadmill walking at an intensity of 70-80% of heart rate reserve determined from the initial CPET, for 30-45 minutes, 3 times per week on non-consecutive days. The AET resulted in significant increases in peak VO2 (from 17.93 + or - 6.29 to 19.93 + or - 5.31 ml/kg/min; p = 0.029), anaerobic threshold (from 10.2 + or - 2.0 to 13.4 + or - 2.4 ml/kg/min; p = 0.002), 6MWT (from 456 + or - 67 to 494 + or - 48 m; p = 0.022), and CPET duration (from 711 + or - 93 to 837 + or - 110 s; p = 0.002). JF - Medicine & Science in Sports & Exercise AU - Woolstenhulme, Joshua G AU - Keyser, Randall E AU - Drinkard, Bart E AU - Chin, Lisa AU - Kennedy, Michelle AU - Nathan, Steven D AU - Connors, Gerilynn AU - Chan, Leighton AD - National Institutes of Health, Bethesda, MD Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 601 PB - Lippincott Williams & Wilkins, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 44 IS - 5S SN - 0195-9131, 0195-9131 KW - Physical Education Index KW - Anaerobic threshold KW - Aerobics KW - Heart rate KW - Sport science KW - Patients KW - Cardiorespiratory KW - Exercise (programs) KW - Maximum oxygen consumption KW - Treadmill ergometry KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1717500873?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medicine+%26+Science+in+Sports+%26+Exercise&rft.atitle=Effects+of+a+10-week+Aerobic+Exercise+Program+on+Cardiorespiratory+Function+in+Patients+with+Interstitial+Lung+Disease&rft.au=Woolstenhulme%2C+Joshua+G%3BKeyser%2C+Randall+E%3BDrinkard%2C+Bart+E%3BChin%2C+Lisa%3BKennedy%2C+Michelle%3BNathan%2C+Steven+D%3BConnors%2C+Gerilynn%3BChan%2C+Leighton&rft.aulast=Woolstenhulme&rft.aufirst=Joshua&rft.date=2012-05-01&rft.volume=44&rft.issue=5S&rft.spage=601&rft.isbn=&rft.btitle=&rft.title=Medicine+%26+Science+in+Sports+%26+Exercise&rft.issn=01959131&rft_id=info:doi/ LA - English DB - Physical Education Index N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Anaerobic threshold; Aerobics; Heart rate; Sport science; Cardiorespiratory; Patients; Maximum oxygen consumption; Exercise (programs); Treadmill ergometry ER - TY - JOUR T1 - Severity of Exercise Intolerance and Functional Aerobic Impairment in Patients with Pulmonary Hypertension AN - 1717499705; PQ0002008521 AB - To examine cardiorespiratory capacity and exercise tolerance in patients with PH. Twenty-three patients with PH (Age: 52 + or - 11 yrs; BMI: 31 + or - 7 kg/m super(2); mean + or - SD) and nine sedentary healthy controls (CON; 48 + or - 9 yrs; 30 + or - 9 kg/m super(2)) completed symptomlimited treadmill cardiopulmonary exercise tests (CPET) and 6-minute walk tests (6MWT) as part of the NIH Exercise Therapy for Advanced Lung Disease Trial. Compared to CON, patients with PH had significantly lower peak VO sub(2) (14.0 + or - 4.7 vs. 23.9 + or - 6.5 ml/min/kg; P = 0.002), time to peak exercise (630 + or - 192 vs. 1144 + or - 393 s; P = 0.002), peak work rate (93 + or - 48 vs. 228 + or - 61 W; P <= 0.001) and VO sub(2) at anaerobic threshold (9.3 + or - 5.0 vs. 13.2 + or - 3.7 ml/kg/min; P = 0.015). 6MWT distance was also shorter (P = 0.006) in PH (409 + or - 81 m) than in CON (553 + or - 130 m). JF - Medicine & Science in Sports & Exercise AU - Chin, Lisa M K AU - Keyser, Randall E AU - Woolstenhulme, Joshua AU - Kennedy, Michelle AU - Drinkard, Bart AU - Connors, Gerilynn AU - Nathan, Steven D AU - Chan, Leighton AD - National Institutes of Health, Bethesda, MD Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 600 PB - Lippincott Williams & Wilkins, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 44 IS - 5S SN - 0195-9131, 0195-9131 KW - Physical Education Index KW - Acid base balance KW - Aerobics KW - Motor performance tests KW - Sport science KW - Patients KW - Cardiorespiratory KW - Exercise KW - Maximum oxygen consumption KW - Hypertension KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1717499705?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medicine+%26+Science+in+Sports+%26+Exercise&rft.atitle=Severity+of+Exercise+Intolerance+and+Functional+Aerobic+Impairment+in+Patients+with+Pulmonary+Hypertension&rft.au=Chin%2C+Lisa+M+K%3BKeyser%2C+Randall+E%3BWoolstenhulme%2C+Joshua%3BKennedy%2C+Michelle%3BDrinkard%2C+Bart%3BConnors%2C+Gerilynn%3BNathan%2C+Steven+D%3BChan%2C+Leighton&rft.aulast=Chin&rft.aufirst=Lisa+M&rft.date=2012-05-01&rft.volume=44&rft.issue=5S&rft.spage=600&rft.isbn=&rft.btitle=&rft.title=Medicine+%26+Science+in+Sports+%26+Exercise&rft.issn=01959131&rft_id=info:doi/ LA - English DB - Physical Education Index N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Acid base balance; Aerobics; Sport science; Motor performance tests; Cardiorespiratory; Patients; Exercise; Maximum oxygen consumption; Hypertension ER - TY - JOUR T1 - Validation of a Previous Day Recall Measuring Time Spent in Physically Active and Sedentary Behaviors AN - 1717488309; PQ0002008664 AB - Test the validity of a PDR administered by phone against a valid reference measure. Adolescents (n=91; 12-17 yrs; 53% female) and adults (n=88; 18-71 yrs; 55% female) wore an activPAL (aPAL) for 7 days to measure sedentary (sit/lie) and active time (standing/stepping) and completed up to three PDRs. Interviewers conducted PDRs eliciting open-ended reports of time spent sleeping and in specific active and sedentary behaviors at home, work/school and in the community. Bland-Altman methods and measurement error models evaluated PDR validity versus aPAL on days matched by date and observation time. Adolescents and adults reported 10.0 (SD=2.2) and 9.9 (SD=2.8) hr/d of sedentary time, and 4.2 (SD=1.8) and 5.2 (SD=2.6) hr/d of active time, respectively. Total PDR active and sedentary time was greater than aPAL wear time (difference=0.58 hr/d, p0.05) negative bias for active time in adolescents (bias=-0.27 (SD=1.37) hr/d) and adults (bias=-0.13 (SD=1.44) hr/d). JF - Medicine & Science in Sports & Exercise AU - Matthews, Charles E AU - Keadle, Sarah AU - Sampson, Joshua AU - Lyden, Kate AU - Libertine, Amanda AU - Bowles, Heather R AU - Freedson, Patty S AU - Fowke, Jay H AD - National Cancer Institute, Bethesda, MD Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 642 PB - Lippincott Williams & Wilkins, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 44 IS - 5S SN - 0195-9131, 0195-9131 KW - Physical Education Index KW - Stepping KW - Home KW - Adolescence KW - Analysis KW - Validity KW - Sport science KW - Work KW - Adults KW - Standing KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1717488309?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medicine+%26+Science+in+Sports+%26+Exercise&rft.atitle=Validation+of+a+Previous+Day+Recall+Measuring+Time+Spent+in+Physically+Active+and+Sedentary+Behaviors&rft.au=Matthews%2C+Charles+E%3BKeadle%2C+Sarah%3BSampson%2C+Joshua%3BLyden%2C+Kate%3BLibertine%2C+Amanda%3BBowles%2C+Heather+R%3BFreedson%2C+Patty+S%3BFowke%2C+Jay+H&rft.aulast=Matthews&rft.aufirst=Charles&rft.date=2012-05-01&rft.volume=44&rft.issue=5S&rft.spage=642&rft.isbn=&rft.btitle=&rft.title=Medicine+%26+Science+in+Sports+%26+Exercise&rft.issn=01959131&rft_id=info:doi/ LA - English DB - Physical Education Index N1 - Date revised - 2015-09-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Stepping; Home; Analysis; Adolescence; Validity; Work; Sport science; Adults; Standing ER - TY - JOUR T1 - Human Tumor Xenografts: The Good, the Bad, and the Ugly AN - 1668268911; PQ0001244520 AB - There has been a robust discussion for many years now on the utility, or lack thereof, of mouse tumor xenograft models in the study of human cell and gene therapies.[1-4] Of course, the reality is that the value of a model depends on what the modeler is trying to accomplish. A good use of human tumor xenograft models would be to support an experimental hypothesis, a bad use would be to present animal data that add little to the value of in vitro data, and an ugly use of tumor xenografts would be to facilitate publication of a manuscript or give a false sense of safety or efficacy. JF - Molecular Therapy AU - Morgan, Richard A AD - Surgery Branch, National Cancer Institute, Building 10, CRC Room 3-5940, 10 Center Drive, MSC1201, Bethesda, Maryland 20892, USA, rmorgan@mail.nih.gov Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 882 EP - 884 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 20 IS - 5 SN - 1525-0016, 1525-0016 KW - Biotechnology and Bioengineering Abstracts KW - Data processing KW - Animal models KW - Xenografts KW - Tumors KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668268911?accountid=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=Human+Tumor+Xenografts%3A+The+Good%2C+the+Bad%2C+and+the+Ugly&rft.au=Morgan%2C+Richard+A&rft.aulast=Morgan&rft.aufirst=Richard&rft.date=2012-05-01&rft.volume=20&rft.issue=5&rft.spage=882&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2012.73 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Data processing; Animal models; Tumors; Xenografts DO - http://dx.doi.org/10.1038/mt.2012.73 ER - TY - JOUR T1 - Relationship of Substance Abuse to Dependence in the U.S. General Population AN - 1463068796; 201326443 AB - Objective: The diagnostic categories of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, for substance abuse and dependence are commonly used in clinical work and research studies, but whether abuse and dependence represent two different syndromes has been debated. The purpose of this article is to investigate the relationship of substance abuse and dependence for cannabis, cocaine, stimulants and sedatives among lifetime users of these substances in the National Epidemiologic Survey on Alcohol and Related Conditions, a nationally representative survey conducted in 2001-2002. Method: The multiple indicators multiple causes (MIMIC) model addresses three sets of relationships: those between (1) diagnostic criteria and latent factors, (2) latent factors and covariates, and (3) criteria and covariates. This approach allows for the detection of and compensation for noninvariance of the measurement of criteria across subgroups. Results: Compared with one-factor models, two-factor models (factors roughly corresponding to abuse and dependence) fit significantly better across all substances, with abuse and dependence factors highly correlated. The MIMIC model indicated that race/ethnicity, age, income, and marital status showed some differential relationships across substance groups, although most covariates showed similar associations to dependence and abuse factors. Noninvariance of criteria measurement by demographic covariates was most pronounced for cannabis abuse and dependence criteria. Conclusions: The general relationship of abuse to dependence was consistent across substances. Results were equivocal on the value of retaining separate factors; therefore, investigating the relationships of specific genetic variants and treatment outcomes to dimensional indicators of abuse, dependence, and measures combining these criteria is warranted. Measurement of cannabis abuse and dependence criteria appears most affected by demographic characteristics. Adapted from the source document. JF - Journal of Studies on Alcohol and Drugs AU - Saha, Tulshi D AU - Harford, Thomas AU - Goldstein, Rise B AU - Kerridge, Bradley T AD - Laboratory of Epidemiology and Biometry, Room 3083, Division of Intramural Clinical and Biological Research, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, M.S. 9304, 5634 Fishers Lane, Bethesda, MD 20892-9304 sahatd@mail.nih.gov Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 368 EP - 378 PB - Center of Alcohol Studies, Rutgers, The State University of New Jersey, Piscataway VL - 73 IS - 3 SN - 1937-1888, 1937-1888 KW - Measurement KW - Compensation KW - Cannabis KW - Substance dependency KW - Drug dependency KW - Substance abuse KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1463068796?accountid=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=Relationship+of+Substance+Abuse+to+Dependence+in+the+U.S.+General+Population&rft.au=Saha%2C+Tulshi+D%3BHarford%2C+Thomas%3BGoldstein%2C+Rise+B%3BKerridge%2C+Bradley+T&rft.aulast=Saha&rft.aufirst=Tulshi&rft.date=2012-05-01&rft.volume=73&rft.issue=3&rft.spage=368&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 - Substance abuse; Cannabis; Drug dependency; Substance dependency; Measurement; Compensation ER - TY - JOUR T1 - Effects of Self-Affirmation on Implementation Intentions and the Moderating Role of Affect AN - 1449096478; 201323348 AB - Self-affirmation may offset defensiveness to threatening messages, increase intentions to engage in protective behaviors, and facilitate actual change. Relatively little is known about the conditions under which self-affirmation is most beneficial. The authors examined whether self-affirmation facilitates the forming of implementation intentions-plans to engage in specific steps that facilitate behavior change -- and whether effects differ by affective state. Undergraduate female drinkers (N = 265) were self-affirmed or not prior to reading an article linking excessive alcohol consumption to breast cancer susceptibility. They then had the opportunity to report implementation intentions, by listing specific steps they planned to take to reduce consumption. Consistent with predictions, self-affirmation promoted formation of implementation intentions, an effect found only among individuals manifesting positive (as opposed to negative) affect following receipt of the message. Self-affirmation may facilitate behavior change by encouraging development of implementation intentions, an effect that is likely enhanced among those experiencing positive affect. [Reprinted by permission of Sage Publications Inc., copyright holder.] JF - Social Psychological and Personality Science AU - Ferrer, Rebecca A AU - Shmueli, Dikla AU - Bergman, Hannah E AU - Harris, Peter R AU - Klein, William M P AD - Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Rockville, MD, USA ferrerra@mail.nih.gov Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 300 EP - 307 PB - Sage Publications, Thousand Oaks CA VL - 3 IS - 3 SN - 1948-5506, 1948-5506 KW - self-affirmation implementation intentions positive affect alcohol health behavior change KW - Behavioural changes KW - Consumption KW - Breast cancer KW - Positive affect KW - Selfaffirmation KW - Susceptibility KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1449096478?accountid=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=Social+Psychological+and+Personality+Science&rft.atitle=Effects+of+Self-Affirmation+on+Implementation+Intentions+and+the+Moderating+Role+of+Affect&rft.au=Ferrer%2C+Rebecca+A%3BShmueli%2C+Dikla%3BBergman%2C+Hannah+E%3BHarris%2C+Peter+R%3BKlein%2C+William+M+P&rft.aulast=Ferrer&rft.aufirst=Rebecca&rft.date=2012-05-01&rft.volume=3&rft.issue=3&rft.spage=300&rft.isbn=&rft.btitle=&rft.title=Social+Psychological+and+Personality+Science&rft.issn=19485506&rft_id=info:doi/10.1177%2F1948550611419265 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-11-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Selfaffirmation; Behavioural changes; Positive affect; Consumption; Susceptibility; Breast cancer DO - http://dx.doi.org/10.1177/1948550611419265 ER - TY - JOUR T1 - WISC-IV Profile in High-Functioning Autism Spectrum Disorders: Impaired Processing Speed is Associated with Increased Autism Communication Symptoms and Decreased Adaptive Communication Abilities AN - 1323339513; 201304680 AB - Changes in the Wechsler Intelligence Scales for Children-IV (WISC-IV) may affect the IQ profile characteristic of autism spectrum disorders (ASD). Moreover, the association of particular component cognitive abilities (unlike overall IQ) with symptomatology and adaptive functioning in ASD remains unclear. This archival study characterizes the WISC-IV IQ profile among 56 high-functioning (IQ > 70) children with ASD and correlates WISC-IV performance with ASD and ADHD symptomatology and adaptive functioning. The ASD WISC-IV profile included strengths on Matrix Reasoning and Similarities, weaknesses on Comprehension (which correlated negatively with social symptoms) and the subtests comprising the Processing Speed Index (Coding, Symbol Search). Processing speed task performance correlated negatively with communication symptoms and positively with communication abilities, indicating its importance to functional outcomes in ASD. Adapted from the source document. JF - Journal of Autism and Developmental Disorders AU - Oliveras-Rentas, Rafael E AU - Kenworthy, Lauren AU - Roberson, Richard B AU - Martin, Alex AU - Wallace, Gregory L AD - Center for Autism Spectrum Disorders, Children's National Medical Center, Washington, DC, USA Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 655 EP - 664 PB - Springer, Dordrecht The Netherlands VL - 42 IS - 5 SN - 0162-3257, 0162-3257 KW - High functioning KW - Symptoms KW - Communication skills KW - Adaptive behaviour KW - Intelligence quotient KW - Autistic spectrum disorders KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1323339513?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Autism+and+Developmental+Disorders&rft.atitle=WISC-IV+Profile+in+High-Functioning+Autism+Spectrum+Disorders%3A+Impaired+Processing+Speed+is+Associated+with+Increased+Autism+Communication+Symptoms+and+Decreased+Adaptive+Communication+Abilities&rft.au=Oliveras-Rentas%2C+Rafael+E%3BKenworthy%2C+Lauren%3BRoberson%2C+Richard+B%3BMartin%2C+Alex%3BWallace%2C+Gregory+L&rft.aulast=Oliveras-Rentas&rft.aufirst=Rafael&rft.date=2012-05-01&rft.volume=42&rft.issue=5&rft.spage=655&rft.isbn=&rft.btitle=&rft.title=Journal+of+Autism+and+Developmental+Disorders&rft.issn=01623257&rft_id=info:doi/10.1007%2Fs10803-011-1289-7 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2013-04-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JADDDQ N1 - SubjectsTermNotLitGenreText - Autistic spectrum disorders; Intelligence quotient; Symptoms; High functioning; Communication skills; Adaptive behaviour DO - http://dx.doi.org/10.1007/s10803-011-1289-7 ER - TY - JOUR T1 - Advancing the science of mHealth AN - 1272078470; 4386012 AB - Mobile health (mHealth) technologies have the potential to greatly impact health research, health care, and health outcomes, but the exponential growth of the technology has outpaced the science. This article outlines two initiatives designed to enhance the science of mHealth. The mHealth Evidence Workshop used an expert panel to identify optimal methodological approaches for mHealth research. The NIH mHealth Training Institutes address the silos among the many academic and technology areas in mHealth research and is an effort to build the interdisciplinary research capacity of the field. Both address the growing need for high quality mobile health research both in the United States and internationally. mHealth requires a solid, interdisciplinary scientific approach that pairs the rapid change associated with technological progress with a rigorous evaluation approach. The mHealth Evidence Workshop and the NIH mHealth Training Institutes were both designed to address and further develop this scientific approach to mHealth. Reprinted by permission of Taylor & Francis Ltd. JF - Journal of health communication AU - Nilsen, Wendy AU - Kumar, Santosh AU - Shar, Albert AU - Varoquiers, Carrie AU - Wiley, Tisha AU - Riley, William T AU - Pavel, Misha AU - Atienza, Audie A AD - National Institutes of Health ; University of Memphis ; Robert Wood Johnson Foundation ; McKesson Foundation ; National Science Foundation Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 5 EP - 10 VL - 17 IS - Supp.1 SN - 1081-0730, 1081-0730 KW - Sociology KW - Evaluation KW - Information KW - Interdisciplinary research KW - Medical research KW - Health KW - Mobile phones KW - Technological change KW - Information and communication technologies UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1272078470?accountid=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=Advancing+the+science+of+mHealth&rft.au=Nilsen%2C+Wendy%3BKumar%2C+Santosh%3BShar%2C+Albert%3BVaroquiers%2C+Carrie%3BWiley%2C+Tisha%3BRiley%2C+William+T%3BPavel%2C+Misha%3BAtienza%2C+Audie+A&rft.aulast=Nilsen&rft.aufirst=Wendy&rft.date=2012-05-01&rft.volume=17&rft.issue=Supp.1&rft.spage=5&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 - 8154 12647 12641 2572; 6518; 5772; 6515; 7886 10902; 12616 12622; 4551; 6631 10902 ER - TY - JOUR T1 - Animal Models and Medical Countermeasures Development for Radiation-Induced Lung Damage: Report from an NIAID Workshop AN - 1171879282; 16825693 AB - Since 9/11, there have been concerns that terrorists may detonate a radiological or nuclear device in an American city. Aside from several decorporation and blocking agents for use against internal radionuclide contamination, there are currently no medications within the Strategic National Stockpile that are approved to treat the immediate or delayed complications resulting from accidental exposure to radiation. Although the majority of research attention has focused on developing countermeasures that target the bone marrow and gastrointestinal tract, since they represent the most acutely radiosensitive organs, individuals who survive early radiation syndromes will likely suffer late effects in the months that follow. Of particular concern are the delayed effects seen in the lung that play a major role in late mortality seen in radiation-exposed patients and accident victims. To address these concerns, the National Institute of Allergy and Infectious Diseases convened a workshop to discuss pulmonary model development, mechanisms of radiation-induced lung injury, targets for medical countermeasures development, and end points to evaluate treatment efficacy. Other topics covered included guidance on the challenges of developing and licensing drugs and treatments specific to a radiation lung damage indication. This report reviews the data presented, as well as key points from the ensuing discussion. JF - Radiation Research AU - Williams, Jacqueline P AU - Jackson, Isabel L AU - Shah, Jui R AU - Czarniecki, Christine W AU - Maidment, Bert W AU - DiCarlo, Andrea L AD - University of Rochester Medical Center, Rochester, New York, cohena@niaid.nih.gov Y1 - 2012/05// PY - 2012 DA - May 2012 SP - e0025 EP - e0039 PB - Radiation Research Society VL - 177 IS - 5 SN - 0033-7587, 0033-7587 KW - Pollution Abstracts KW - Allergies KW - Lung KW - P 8000:RADIATION UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1171879282?accountid=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=Radiation+Research&rft.atitle=Animal+Models+and+Medical+Countermeasures+Development+for+Radiation-Induced+Lung+Damage%3A+Report+from+an+NIAID+Workshop&rft.au=Williams%2C+Jacqueline+P%3BJackson%2C+Isabel+L%3BShah%2C+Jui+R%3BCzarniecki%2C+Christine+W%3BMaidment%2C+Bert+W%3BDiCarlo%2C+Andrea+L&rft.aulast=Williams&rft.aufirst=Jacqueline&rft.date=2012-05-01&rft.volume=177&rft.issue=5&rft.spage=e0025&rft.isbn=&rft.btitle=&rft.title=Radiation+Research&rft.issn=00337587&rft_id=info:doi/10.1667%2FRROL04.1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-11-01 N1 - Number of references - 1 N1 - Last updated - 2014-02-21 N1 - SubjectsTermNotLitGenreText - Lung DO - http://dx.doi.org/10.1667/RROL04.1 ER - TY - JOUR T1 - Geographic Variability and Anti-Staphylococcal Activity of the Chrysophaentins and Their Synthetic Fragments AN - 1093462828; 17211845 AB - Drug-resistant Staphylococcus aureus is a continuing public health concern, both in the hospital and community settings. Antibacterial compounds that possess novel structural scaffolds and are effective against multiple S. aureus strains, including current drug-resistant ones, are needed. Previously, we have described the chrysophaentins, a family of bisdiarylbutene macrocycles from the chrysophyte alga Chrysophaeum taylori that inhibit the growth of S. aureus and methicillin-resistant S. aureus (MRSA). In this study we have analyzed the geographic variability of chrysophaentin production in C. taylori located at different sites on the island of St. John, U.S. Virgin Islands, and identified two new linear chrysophaentin analogs, E2 and E3. In addition, we have expanded the structure activity relationship through synthesis of fragments comprising conserved portions of the chrysophaentins, and determined the antimicrobial activity of natural chrysophaentins and their synthetic analogs against five diverse S. aureus strains. We find that the chrysophaentins show similar activity against all S. aureus strains, regardless of their drug sensitivity profiles. The synthetic chrysophaentin fragments indeed mimic the natural compounds in their spectrum of antibacterial activity, and therefore represent logical starting points for future medicinal chemistry studies of the natural products and their analogs. JF - Marine Drugs AU - Keffer, J L AU - Hammill, J T AU - Lloyd, J R AU - Plaza, A AU - Wipf, P AU - Bewley, CA AD - Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 1103 EP - 1125 VL - 10 IS - 5 SN - 1660-3397, 1660-3397 KW - Microbiology Abstracts B: Bacteriology; ASFA 1: Biological Sciences & Living Resources; Oceanic Abstracts; ASFA Marine Biotechnology Abstracts KW - Marine KW - Antimicrobial activity KW - Antibacterial activity KW - Drug resistance KW - Analogs KW - natural products KW - Antibiotics KW - Metabolites KW - Disease resistance KW - Strains KW - scaffolds KW - Public health KW - Growth KW - Islands KW - Aquatic drugs KW - Staphylococcus aureus KW - Drugs KW - Hospitals KW - Q4 27740:Products KW - O 5040:Processing, Products and Marketing KW - Q1 08625:Non-edible products KW - J 02340:Antibiotics & Antimicrobials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1093462828?accountid=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=Marine+Drugs&rft.atitle=Geographic+Variability+and+Anti-Staphylococcal+Activity+of+the+Chrysophaentins+and+Their+Synthetic+Fragments&rft.au=Keffer%2C+J+L%3BHammill%2C+J+T%3BLloyd%2C+J+R%3BPlaza%2C+A%3BWipf%2C+P%3BBewley%2C+CA&rft.aulast=Keffer&rft.aufirst=J&rft.date=2012-05-01&rft.volume=10&rft.issue=5&rft.spage=1103&rft.isbn=&rft.btitle=&rft.title=Marine+Drugs&rft.issn=16603397&rft_id=info:doi/10.3390%2Fmd10051103 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2014-05-05 N1 - SubjectsTermNotLitGenreText - Growth; Aquatic drugs; Analogs; Metabolites; Antibiotics; Disease resistance; Strains; Public health; Antimicrobial activity; Islands; Antibacterial activity; Drug resistance; natural products; Drugs; scaffolds; Hospitals; Staphylococcus aureus; Marine DO - http://dx.doi.org/10.3390/md10051103 ER - TY - JOUR T1 - Targeting malignant B cells with an immunotoxin against ROR1. AN - 1039039326; 22531447 AB - The selective cell surface expression of receptor tyrosine kinase-like orphan receptor 1 (ROR1) in chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL) has made ROR1 a novel and promising target for therapeutic monoclonal antibodies (mAbs). Four mouse mAbs generated by hybridoma technology exhibited specific binding to human ROR1. Epitope mapping studies showed that two mAbs (2A2 and 2D11) recognized N-terminal epitopes in the extracellular region of ROR1 and the other two (1A1 and 1A7) recognized C-terminal epitopes. A ROR1- immunotoxin (BT-1) consisting of truncated Pseudomonas exotoxin A (PE38) and the VH and VL fragments of 2A2-IgG was made recombinantly. Both 2A2-IgG and BT-1 showed dose-dependent and selective binding to primary CLL and MCL cells and MCL cell lines. Kinetic analyses revealed 0.12-nM (2A2-IgG) to 65-nM (BT-1) avidity/affinity to hROR1, depicting bivalent and monovalent interactions, respectively. After binding to cell surface ROR1, 2A2-IgG and BT-1 were partially internalized by primary CLL cells and MCL cell lines, and BT-1 induced profound apoptosis of ROR1-expressing MCL cell lines in vitro (EC 50 = 16 pM-16 nM), but did not affect ROR1-negative cell lines. Our data suggest that ROR1-immunotoxins such as BT-1 could serve as targeted therapeutic agents for ROR1-expressing B cell malignancies and other cancers. JF - mAbs AU - Baskar, Sivasubramanian AU - Wiestner, Adrian AU - Wilson, Wyndham H AU - Pastan, Ira AU - Rader, Christoph AD - Experimental Transplantation and Immunology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA. baskars@mail.nih.gov PY - 2012 SP - 349 EP - 361 VL - 4 IS - 3 KW - Bacterial Toxins KW - 0 KW - Biomarkers, Tumor KW - Exotoxins KW - Immunoglobulin Variable Region KW - Immunotoxins KW - Recombinant Fusion Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - ROR1 protein, human KW - EC 2.7.10.1 KW - Receptor Tyrosine Kinase-like Orphan Receptors KW - Index Medicus KW - Biomarkers, Tumor -- metabolism KW - Animals KW - Apoptosis KW - Humans KW - Immunoglobulin Variable Region -- immunology KW - Mice KW - Cell Line, Tumor KW - Recombinant Fusion Proteins -- therapeutic use KW - Receptor Tyrosine Kinase-like Orphan Receptors -- immunology KW - Virulence Factors -- therapeutic use KW - Bacterial Toxins -- therapeutic use KW - Receptor Tyrosine Kinase-like Orphan Receptors -- antagonists & inhibitors KW - Immunotoxins -- therapeutic use KW - Lymphoma, Mantle-Cell -- therapy KW - Molecular Targeted Therapy -- methods KW - Exotoxins -- therapeutic use KW - Leukemia, Lymphocytic, Chronic, B-Cell -- therapy KW - ADP Ribose Transferases -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1039039326?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=mAbs&rft.atitle=Targeting+malignant+B+cells+with+an+immunotoxin+against+ROR1.&rft.au=Baskar%2C+Sivasubramanian%3BWiestner%2C+Adrian%3BWilson%2C+Wyndham+H%3BPastan%2C+Ira%3BRader%2C+Christoph&rft.aulast=Baskar&rft.aufirst=Sivasubramanian&rft.date=2012-05-01&rft.volume=4&rft.issue=3&rft.spage=349&rft.isbn=&rft.btitle=&rft.title=mAbs&rft.issn=1942-0870&rft_id=info:doi/10.4161%2Fmabs.19870 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-02-06 N1 - Date created - 2012-09-10 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Immunol. 1988 Dec 15;141(12):4410-7 [2461993] Leukemia. 2012 Jun;26(6):1348-55 [22289919] Cancer Treat Res. 1988;37:161-73 [2908624] Proc Natl Acad Sci U S A. 1990 Nov;87(21):8291-5 [2236041] Int J Cancer. 1992 Oct 21;52(4):631-5 [1399146] Blood. 1992 Nov 1;80(9):2344-52 [1421405] J Biol Chem. 1992 Dec 25;267(36):26181-90 [1334494] Cancer Res. 1995 Sep 1;55(17):3763-71 [7641191] Nat Biotechnol. 1996 Oct;14(10):1239-45 [9631086] Science. 1998 Aug 28;281(5381):1312-6 [9721091] Blood. 1999 May 15;93(10):3309-16 [10233883] Nat Cell Biol. 2005 Jun;7(6):591-600 [15864305] J Clin Oncol. 2005 Sep 20;23(27):6719-29 [16061911] Nat Rev Cancer. 2006 Jul;6(7):559-65 [16794638] Clin Cancer Res. 2006 Jul 1;12(13):4027-35 [16818702] Curr Drug Targets. 2006 Oct;7(10):1301-11 [17073592] Blood. 2008 Jan 1;111(1):338-43 [17895404] Clin Cancer Res. 2000 Apr;6(4):1476-87 [10778980] J Exp Med. 2001 Dec 3;194(11):1625-38 [11733577] J Exp Med. 2001 Dec 3;194(11):1639-47 [11733578] Clin Cancer Res. 2002 Jul;8(7):2345-55 [12114439] Cancer Immunol Immunother. 2003 May;52(5):338-41 [12700949] Methods Mol Biol. 2004;248:503-18 [14970517] Blood. 2004 Apr 1;103(7):2718-26 [14525789] J Exp Med. 1984 Jan 1;159(1):208-20 [6319530] Cell. 1987 Jan 16;48(1):129-36 [3098436] Clin Cancer Res. 2008 Jan 15;14(2):396-404 [18223214] Proc Natl Acad Sci U S A. 2008 Feb 26;105(8):3047-52 [18287027] Int J Cancer. 2008 Sep 1;123(5):1190-5 [18546292] Cancer Res. 2008 Aug 1;68(15):6300-5 [18676854] Curr Protoc Cytom. 2001 May;Chapter 9:Unit 9.14 [18770751] Cancer Res. 2008 Sep 15;68(18):7512-9 [18794139] Clin Cancer Res. 2009 Feb 1;15(3):832-9 [19188153] J Clin Oncol. 2009 Jun 20;27(18):2983-90 [19414673] Leuk Lymphoma. 2009 Aug;50(8):1361-8 [19562616] Br J Haematol. 2010 Jan;148(1):99-109 [19821820] Cancer Immunol Immunother. 2010 May;59(5):737-46 [20091030] Blood. 2010 Apr 1;115(13):2619-29 [19965642] J Immunother. 2010 Apr;33(3):297-304 [20445350] Mol Cancer Ther. 2010 Jul;9(7):2007-15 [20587662] PLoS One. 2010;5(7):e11859 [20686606] Br J Haematol. 2010 Nov;151(4):327-35 [20813009] Blood. 2010 Nov 25;116(22):4532-41 [20702778] Clin Cancer Res. 2010 Dec 15;16(24):6132-8 [21037025] Hematol Oncol. 2011 Mar;29(1):17-21 [20597086] Proc Natl Acad Sci U S A. 2011 Apr 5;108(14):5742-7 [21436054] Cancer Res. 2011 Apr 15;71(8):3132-41 [21487037] Blood. 2011 May 19;117(20):5463-72 [21385850] PLoS One. 2011;6(6):e21018 [21698301] Clin Cancer Res. 2011 Aug 1;17(15):5101-12 [21712452] J Biol Chem. 1990 Mar 25;265(9):4923-8 [2138622] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.4161/mabs.19870 ER - TY - JOUR T1 - Medications development to treat alcohol dependence: a vision for the next decade AN - 1028034780; 16921867 AB - ABSTRACT More than 76 million people world-wide are estimated to have diagnosable alcohol use disorders (AUDs) (alcohol abuse or dependence), making these disorders a major global health problem. Pharmacotherapy offers promising means for treating AUDs, and significant progress has been made in the past 20 years. The US Food and Drug Administration approved three of the four medications for alcoholism in the last two decades. Unfortunately, these medications do not work for everyone, prompting the need for a personalized approach to optimize clinical benefit or more efficacious medications that can treat a wider range of patients, or both. To promote global health, the potential reorganization of the National Institutes of Health (NIH) must continue to support the National Institute on Alcohol Abuse and Alcoholism's (NIAAA's) vision of ensuring the development and delivery of new and more efficacious medications to treat AUDs in the coming decade. To achieve this objective, the NIAAA Medications Development Team has identified three fundamental long-range goals: (1) to make the drug development process more efficient; (2) to identify more efficacious medications, personalize treatment approaches, or both; and (3) to facilitate the implementation and adaptation of medications in real-world treatment settings. These goals will be carried out through seven key objectives. This paper describes those objectives in terms of rationale and strategy. Successful implementation of these objectives will result in the development of more efficacious and safe medications, provide a greater selection of therapy options and ultimately lessen the impact of this devastating disorder. JF - Addiction Biology AU - Litten, Raye Z AU - Egli, Mark AU - Heilig, Markus AU - Cui, Changhai AU - Fertig, Joanne B AU - Ryan, Megan L AU - Falk, Daniel E AU - Moss, Howard AU - Huebner, Robert AU - Noronha, Antonio AD - National Institute on Alcohol Abuse and Alcoholism, Bethesda, MD, USA Y1 - 2012/05/01/ PY - 2012 DA - 2012 May 01 SP - 513 EP - 527 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 17 IS - 3 SN - 1355-6215, 1355-6215 KW - Toxicology Abstracts; CSA Neurosciences Abstracts KW - Adaptations KW - Addiction KW - Alcoholism KW - Drug abuse KW - Drug dependence KW - Drug development KW - Ethanol KW - Vision KW - N3 11001:Behavioral and Cognitive Neuroscience UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028034780?accountid=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=Addiction+Biology&rft.atitle=Medications+development+to+treat+alcohol+dependence%3A+a+vision+for+the+next+decade&rft.au=Litten%2C+Raye+Z%3BEgli%2C+Mark%3BHeilig%2C+Markus%3BCui%2C+Changhai%3BFertig%2C+Joanne+B%3BRyan%2C+Megan+L%3BFalk%2C+Daniel+E%3BMoss%2C+Howard%3BHuebner%2C+Robert%3BNoronha%2C+Antonio&rft.aulast=Litten&rft.aufirst=Raye&rft.date=2012-05-01&rft.volume=17&rft.issue=3&rft.spage=513&rft.isbn=&rft.btitle=&rft.title=Addiction+Biology&rft.issn=13556215&rft_id=info:doi/http%3A%2F%2Fdx.doi.org%2F10.1111%2Fj.1369-1600.2012.00454.x L2 - http://www.ingentaconnect.com/content/bpl/adb/2012/00000017/00000003/art00003 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2012-10-08 N1 - SubjectsTermNotLitGenreText - Drug dependence; Adaptations; Vision; Alcoholism; Drug development; Addiction; Drug abuse; Ethanol DO - http://dx.doi.org/10.1111/j.1369-1600.2012.00454.x ER - TY - JOUR T1 - Small proteins link coat and cortex assembly during sporulation in Bacillus subtilis AN - 1028025285; 16682233 AB - Mature spores of the bacterium Bacillus subtilis are encased by two concentric shells: an inner shell (the 'cortex'), made of peptidoglycan; and an outer proteinaceous shell (the 'coat'), whose basement layer is anchored to the surface of the developing spore via a 26-amino-acid-long protein called SpoVM. During sporulation, initiation of cortex assembly depends on the successful initiation of coat assembly, but the mechanisms that co-ordinate the morphogenesis of both structures are largely unknown. Here, we describe a sporulation pathway involving SpoVM and a 37-amino-acid-long protein named 'CmpA' that is encoded by a previously un-annotated gene and is expressed under control of two sporulation-specific transcription factors ( sigma E and SpoIIID). CmpA localized to the surface of the developing spore and deletion of cmpA resulted in cells progressing through the sporulation programme more quickly. Overproduction of CmpA did not affect normal growth or cell division, but delayed entry into sporulation and abrogated cortex assembly. In those cells that had successfully initiated coat assembly, CmpA was removed by a post-translational mechanism, presumably in order to overcome the sporulation inhibition it imposed. We propose a model in which CmpA participates in a developmental checkpoint that ensures the proper orchestration of coat and cortex morphogenesis by repressing cortex assembly until coat assembly successfully initiates. JF - Molecular Microbiology AU - Ebmeier, Sarah E AU - Tan, Irene S AU - Clapham, Katie Rose AU - Ramamurthi, Kumaran S AD - Laboratory of Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 682 EP - 696 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 84 IS - 4 SN - 0950-382X, 0950-382X KW - Microbiology Abstracts B: Bacteriology KW - Cell division KW - Bacillus subtilis KW - Cortex KW - Post-translation KW - Transcription factors KW - Morphogenesis KW - Sporulation KW - peptidoglycans KW - Shells KW - Spores KW - J 02320:Cell Biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028025285?accountid=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=Small+proteins+link+coat+and+cortex+assembly+during+sporulation+in+Bacillus+subtilis&rft.au=Ebmeier%2C+Sarah+E%3BTan%2C+Irene+S%3BClapham%2C+Katie+Rose%3BRamamurthi%2C+Kumaran+S&rft.aulast=Ebmeier&rft.aufirst=Sarah&rft.date=2012-05-01&rft.volume=84&rft.issue=4&rft.spage=682&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/10.1111%2Fj.1365-2958.2012.08052.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Document feature - figure 8 N1 - Last updated - 2016-04-29 N1 - SubjectsTermNotLitGenreText - Cell division; Cortex; Post-translation; Transcription factors; Morphogenesis; Sporulation; peptidoglycans; Shells; Spores; Bacillus subtilis DO - http://dx.doi.org/10.1111/j.1365-2958.2012.08052.x ER - TY - JOUR T1 - Clinical research nursing: A critical resource in the national research enterprise AN - 1023093626; 201214989 AB - Translational clinical research has emerged as an important priority for the national research enterprise, with a clearly stated mandate to more quickly deliver prevention strategies, treatments and cures based on scientific innovations to the public. Within this national effort, a lack of consensus persists concerning the need for clinical nurses with expertise and specialized training in study implementation and the delivery of care to research participants. This paper reviews efforts to define and document the role of practicing nurses in implementing studies and coordinating clinical research in a variety of clinical settings, and differentiates this clinical role from the role of nurses as scientists and principal investigators. We propose an agenda for building evidence that having nurses provide and coordinate study treatments and procedures can potentially improve research efficiency, participant safety, and the quality of research data. We also provide recommendations for the development of the emerging specialty of clinical research nursing. [Copyright Elsevier B.V.] JF - Nursing Outlook AU - Hastings, Clare E AU - Fisher, Cheryl A AU - McCabe, Margaret A AD - National Institutes of Health Clinical Center, Bethesda, Maryland, USA Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 149 EP - 156 PB - Elsevier Ltd, The Netherlands VL - 60 IS - 3 SN - 0029-6554, 0029-6554 KW - Clinical research KW - Research nursing KW - Clinical trials KW - Good Clinical Practice KW - Clinical nursing KW - Professional training KW - Nurses KW - Expertise KW - Enterprises KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1023093626?accountid=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=Nursing+Outlook&rft.atitle=Clinical+research+nursing%3A+A+critical+resource+in+the+national+research+enterprise&rft.au=Hastings%2C+Clare+E%3BFisher%2C+Cheryl+A%3BMcCabe%2C+Margaret+A&rft.aulast=Hastings&rft.aufirst=Clare&rft.date=2012-05-01&rft.volume=60&rft.issue=3&rft.spage=149&rft.isbn=&rft.btitle=&rft.title=Nursing+Outlook&rft.issn=00296554&rft_id=info:doi/ LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-07-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Clinical research; Clinical nursing; Nurses; Enterprises; Expertise; Professional training ER - TY - JOUR T1 - TGI Monday? Drug-Dependent Outpatients Report Lower Stress and More Happiness at Work than Elsewhere AN - 1023090845; 201214188 AB - In the general population, experience-sampling studies show that work is the aspect of daily life most associated with momentary unhappiness and a desire to be elsewhere. We assessed whether this holds true for urban outpatients in treatment for heroin and cocaine dependence. In a 25-week natural-history study, 79 employed methadone-maintained misusers of heroin and cocaine carried electronic diaries on which mood and behavior were assessed up to five times per day. Being at work was associated with lower stress, greater happiness, and lower drug craving. Work accounted for 14% of the variance in stress, 30% of the variance in happiness, and 50% of the variance in cocaine craving. Participants with skilled jobs reported more positive and less negative mood states (and lower cocaine craving) at all times compared to participants with semi/unskilled jobs, although the latter reported greater mood improvement at work. In all participants, mood improvements occurred specifically in the presence of coworkers (not other companions). Our seemingly unusual findings might be specific to substance-disorder patients (for whom work may be a respite from drug-using companions), but might also hold for other urban dwellers of similar socioeconomic backgrounds (for whom work may be a respite from environmental stressors). Adapted from the source document. JF - The American Journal on Addictions AU - Epstein, David H AU - Preston, Kenzie L AD - NIDA Intramural Research Program, Treatment Section, Clinical Pharmacology & Therapeutics Branch, Room 01B-606, 251 Bayview Blvd., Suite 200, Baltimore, MD 21224 depstein@intra.nida.nih.gov Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 189 EP - 198 PB - Wiley Publishing, Malden, MA 02148 VL - 21 IS - 3 SN - 1055-0496, 1055-0496 KW - Companions KW - Craving KW - Moods KW - Occupational stress KW - Cocaine KW - Happiness KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1023090845?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+Journal+on+Addictions&rft.atitle=TGI+Monday%3F+Drug-Dependent+Outpatients+Report+Lower+Stress+and+More+Happiness+at+Work+than+Elsewhere&rft.au=Epstein%2C+David+H%3BPreston%2C+Kenzie+L&rft.aulast=Epstein&rft.aufirst=David&rft.date=2012-05-01&rft.volume=21&rft.issue=3&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+on+Addictions&rft.issn=10550496&rft_id=info:doi/10.1111%2Fj.1521-0391.2012.00230.x LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-07-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Moods; Craving; Occupational stress; Cocaine; Happiness; Companions DO - http://dx.doi.org/10.1111/j.1521-0391.2012.00230.x ER - TY - JOUR T1 - Longitudinal penalized functional regression for cognitive outcomes on neuronal tract measurements AN - 1021123237; 4305393 AB - We describe and analyse a longitudinal diffusion tensor imaging study relating changes in the microstructure of intracranial white matter tracts to cognitive disability in multiple-sclerosis patients. In this application the scalar outcome and the functional exposure are measured longitudinally. This data structure is new and raises challenges that cannot be addressed with current methods and software. To analyse the data, we introduce a penalized functional regression model and inferential tools designed specifically for these emerging types of data. Our proposed model extends the generalized linear mixed model by adding functional predictors; this method is computationally feasible and is applicable when the functional predictors are measured densely, sparsely or with error. On-line supplements compare two implementations, one likelihood based and the other Bayesian, and provide the software that is used in simulations; the likelihood-based implementation is included as the lpfr() function in the R package refund that is available in the Comprehensive R Archive Network. Reprinted by permission of Blackwell Publishers JF - Journal of the Royal Statistical Society AU - Goldsmith, Jeff AU - Crainiceanu, Ciprian M AU - Caffo, Brian AU - Reich, Daniel AD - Johns Hopkins University ; National Institutes of Health Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 453 EP - 469 VL - 61 IS - 3 SN - 0035-9254, 0035-9254 KW - Economics KW - Longitudinal studies KW - Computational methods KW - Computer programmes KW - Images KW - Models KW - Bayesian method KW - Neurology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1021123237?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+Royal+Statistical+Society&rft.atitle=Longitudinal+penalized+functional+regression+for+cognitive+outcomes+on+neuronal+tract+measurements&rft.au=Goldsmith%2C+Jeff%3BCrainiceanu%2C+Ciprian+M%3BCaffo%2C+Brian%3BReich%2C+Daniel&rft.aulast=Goldsmith&rft.aufirst=Jeff&rft.date=2012-05-01&rft.volume=61&rft.issue=3&rft.spage=453&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+Royal+Statistical+Society&rft.issn=00359254&rft_id=info:doi/10.1111%2Fj.1467-9876.2011.01031.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 - 6224; 7541 7537 971; 8635; 2671 10919; 1512 3865 4025; 8163; 2677 DO - http://dx.doi.org/10.1111/j.1467-9876.2011.01031.x ER - TY - JOUR T1 - Development of a Haptic Elbow Spasticity Simulator (HESS) for Improving Accuracy and Reliability of Clinical Assessment of Spasticity AN - 1020855814; 16770379 AB - This paper presents the framework for developing a robotic system to improve accuracy and reliability of clinical assessment. Clinical assessment of spasticity tends to have poor reliability because of the nature of the in-person assessment. To improve accuracy and reliability of spasticity assessment, a haptic device, named the HESS (Haptic Elbow Spasticity Simulator) has been designed and constructed to recreate the clinical "feel" of elbow spasticity based on quantitative measurements. A mathematical model representing the spastic elbow joint was proposed based on clinical assessment using the Modified Ashworth Scale (MAS) and quantitative data (position, velocity, and torque) collected on subjects with elbow spasticity. Four haptic models (HMs) were created to represent the haptic feel of MAS 1, 1 + , 2, and 3. The four HMs were assessed by experienced clinicians; three clinicians performed both in-person and haptic assessments, and had 100% agreement in MAS scores; and eight clinicians who were experienced with MAS assessed the four HMs without receiving any training prior to the test. Inter-rater reliability among the eight clinicians had substantial agreement ( Kappa = 0.626 ) . The eight clinicians also rated the level of realism ( 7.63 plus or minus 0.92 out of 10) as compared to their experience with real patients. JF - IEEE Transactions on Neural Systems and Rehabilitation Engineering AU - Park, Hyung-Soon AU - Kim, Jonghyun AU - Damiano, Diane L AD - Rehabilitation Medicine Department, National Institutes of Health, Clinical Center, Bethesda, MD, USA Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 361 EP - 370 PB - Institute of Electrical and Electronics Engineers, Inc., 3 Park Avenue, 17th Fl New York NY 10016-5997 United States VL - 20 IS - 3 SN - 1534-4320, 1534-4320 KW - Biotechnology and Bioengineering Abstracts KW - Mathematical models KW - Data processing KW - Rehabilitation KW - robotics KW - spasticity KW - Elbow KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020855814?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IEEE+Transactions+on+Neural+Systems+and+Rehabilitation+Engineering&rft.atitle=Development+of+a+Haptic+Elbow+Spasticity+Simulator+%28HESS%29+for+Improving+Accuracy+and+Reliability+of+Clinical+Assessment+of+Spasticity&rft.au=Park%2C+Hyung-Soon%3BKim%2C+Jonghyun%3BDamiano%2C+Diane+L&rft.aulast=Park&rft.aufirst=Hyung-Soon&rft.date=2012-05-01&rft.volume=20&rft.issue=3&rft.spage=361&rft.isbn=&rft.btitle=&rft.title=IEEE+Transactions+on+Neural+Systems+and+Rehabilitation+Engineering&rft.issn=15344320&rft_id=info:doi/10.1109%2FTNSRE.2012.2195330 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Data processing; Mathematical models; Rehabilitation; robotics; Elbow; spasticity DO - http://dx.doi.org/10.1109/TNSRE.2012.2195330 ER - TY - JOUR T1 - Maternal and cord steroid sex hormones, angiogenic factors, and insulin-like growth factor axis in African-American preeclamptic and uncomplicated pregnancies AN - 1020851346; 16734455 AB - Background: A history of a preeclamptic pregnancy has been associated with subsequent increased risk of cardiovascular disease in the mother and decreased risk of breast cancer in both the mother and offspring. The concentrations of steroid sex hormones, angiogenic factors, and other proteins during pregnancy are important components of the in utero environment and may mediate the association of preeclampsia with later health outcomes. This study sought to compare an extensive profile of biological markers in both maternal and umbilical cord samples in preeclamptic and uncomplicated pregnancies of a predominantly African-American population. Methods: Steroid sex hormones, angiogenic factors, and components of the insulin-like growth factor axis were measured in maternal and umbilical cord sera from 48 pregnancies complicated by preeclampsia and 43 uncomplicated pregnancies. Regression models estimated the associations of these markers with preeclampsia, after adjusting for maternal and gestational age. Results: Concentrations of androgens (testosterone p = 0.06 and androstenedione p = 0.08) and the anti-angiogenic factors soluble fms-like kinase 1 (p = 0.004) and soluble endoglin (p = 0.004) were higher in the maternal circulation of women diagnosed with preeclampsia. These findings also were noted when the analyses were restricted to only African-American participants (77% of overall study population). Furthermore, among African-Americans, cord insulin-like growth factor-1 was lower in preeclamptic pregnancies than in controls. Conclusions: The associations of maternal androgens and anti-angiogenic factors with preeclampsia are consistent with prior reports from predominantly Caucasian populations. Alterations in these analytes as well as other maternal and fetal biomarkers in preeclampsia could mediate the associations of preeclampsia with later health consequences. JF - Cancer Causes & Control AU - Faupel-Badger, Jessica M AU - Wang, Yuping AU - Staff, Anne Cathrine AU - Karumanchi, SAnanth AU - Stanczyk, Frank Z AU - Pollak, Michael AU - Hoover, Robert N AU - Troisi, Rebecca AD - Cancer Prevention Fellowship Program, Center for Cancer Training, National Cancer Institute, 6120 Executive Blvd (EPS), Suite 150E, MSC 7105, Bethesda, MD, 20892-7105, USA, badgerje@mail.nih.gov Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 779 EP - 784 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 23 IS - 5 SN - 0957-5243, 0957-5243 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Bioindicators KW - Breast cancer KW - steroids KW - Growth factors KW - Offspring KW - Hormones KW - Steroids KW - Ethnic groups KW - Cancer KW - Pregnancy KW - offspring 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/1020851346?accountid=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=Maternal+and+cord+steroid+sex+hormones%2C+angiogenic+factors%2C+and+insulin-like+growth+factor+axis+in+African-American+preeclamptic+and+uncomplicated+pregnancies&rft.au=Faupel-Badger%2C+Jessica+M%3BWang%2C+Yuping%3BStaff%2C+Anne+Cathrine%3BKarumanchi%2C+SAnanth%3BStanczyk%2C+Frank+Z%3BPollak%2C+Michael%3BHoover%2C+Robert+N%3BTroisi%2C+Rebecca&rft.aulast=Faupel-Badger&rft.aufirst=Jessica&rft.date=2012-05-01&rft.volume=23&rft.issue=5&rft.spage=779&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-9934-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Last updated - 2013-09-09 N1 - SubjectsTermNotLitGenreText - Bioindicators; Breast cancer; Offspring; Growth factors; steroids; Steroids; Hormones; Cancer; Ethnic groups; offspring; Pregnancy DO - http://dx.doi.org/10.1007/s10552-012-9934-9 ER - TY - JOUR T1 - Poultry and livestock exposure and cancer risk among farmers in the agricultural health study AN - 1020851333; 16734453 AB - Purpose: The purpose of this study is to evaluate cancer risk associated with raising animals as commodities, which is associated with a variety of exposures, such as infectious agents and endotoxins. Methods: Information was available for 49,884 male farmers in the Agricultural Health Study, who reported livestock and poultry production at enrollment (1993-1997). Cancer incidence data were obtained through annual linkage to state registries. Using Poisson regression analyses, we evaluated whether the number and type of animals raised on the farm impacted cancer risk. Results: Overall, 31,848 (63.8%) male farmers reported raising any animals. Lung cancer risk decreased with increasing number of livestock on the farm (p trend = 0.04) and with raising poultry (Relative Risk (RR) = 0.6; 95% confidence interval (CI): 0.4-0.97). Raising poultry was associated with an increased risk of colon cancer (RR = 1.4; 95% CI: 0.99-2.0) with further increased with larger flocks (p trend = 0.02). Risk of non-Hodgkin lymphoma was also elevated in those who raised poultry (RR = 1.6; 95% CI: 1.0-2.4), but there was no evidence of increased risk with larger flocks (p trend = 0.5). Raising sheep was associated with a significantly increased risk of multiple myeloma (RR = 4.9; 95% CI: 2.4-12.0). Performing veterinary services increased the risk of Hodgkin lymphoma (RR = 12.2; 95% CI: 1.6-96.3). Conclusions: We observed an inverse association between raising poultry and livestock and lung cancer risk and some evidence of increased risk of specific lymphohematopoietic malignancies with specific types of animals and performing veterinary services. Further research into associations between raising animals and cancer risk should focus on identification of etiologic agents. JF - Cancer Causes & Control AU - Beane Freeman, Laura E AU - DeRoos, Anneclaire J AU - Koutros, Stella AU - Blair, Aaron AU - Ward, Mary H AU - Alavanja, Michael AU - Hoppin, Jane A AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 6120 Executive Boulevard, MSC 7240, Bethesda, MD, 20892, USA, freemala@mail.nih.gov Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 663 EP - 670 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 23 IS - 5 SN - 0957-5243, 0957-5243 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Endotoxins KW - Poultry KW - Farms KW - multiple myeloma KW - Sheep KW - lymphoma KW - Cancer KW - Lung cancer KW - Livestock 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/1020851333?accountid=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=Poultry+and+livestock+exposure+and+cancer+risk+among+farmers+in+the+agricultural+health+study&rft.au=Beane+Freeman%2C+Laura+E%3BDeRoos%2C+Anneclaire+J%3BKoutros%2C+Stella%3BBlair%2C+Aaron%3BWard%2C+Mary+H%3BAlavanja%2C+Michael%3BHoppin%2C+Jane+A&rft.aulast=Beane+Freeman&rft.aufirst=Laura&rft.date=2012-05-01&rft.volume=23&rft.issue=5&rft.spage=663&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-9921-1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Last updated - 2016-11-23 N1 - SubjectsTermNotLitGenreText - Endotoxins; Poultry; Farms; multiple myeloma; Sheep; lymphoma; Cancer; Livestock; Lung cancer DO - http://dx.doi.org/10.1007/s10552-012-9921-1 ER - TY - JOUR T1 - Analysis of the Conformation and Function of the Plasmodium falciparum Merozoite Proteins MTRAP and PTRAMP AN - 1020839216; 16765221 AB - Thrombospondin repeat (TSR)-like domains are structures involved with cell adhesion. Plasmodium falciparum proteins containing TSR domains play crucial roles in parasite development. In particular, the preerythrocytic P. falciparum circumsporozoite protein is involved in hepatocyte invasion. The importance of these domains in two other malaria proteins, the merozoite-specific thrombospondin-related anonymous protein (MTRAP) and the thrombospondin-related apical membrane protein (PTRAMP), were assessed using near-full-length recombinant proteins composed of the extracellular domains produced in Escherichia coli. MTRAP is thought to be released from invasive organelles identified as micronemes during merozoite invasion to mediate motility and host cell invasion through an interaction with aldolase, an actin binding protein involved in the moving junction. PTRAMP function remains unknown. In this study, the conformation of recombinant MTRAP (rMTRAP) appeared to be a highly extended protein (2 nm by 33 nm, width by length, respectively), whereas rPTRAMP had a less extended structure. Using an erythrocyte binding assay, rMTRAP but not rPTRAMP bound human erythrocytes; rMTRAP binding was mediated through the TSR domain. MTRAP- and in general PTRAMP-specific antibodies failed to inhibit P. falciparum development in vitro. Altogether, MTRAP is a highly extended bifunctional protein that binds to an erythrocyte receptor and the merozoite motor. JF - Eukaryotic Cell AU - Uchime, Onyinyechukwu AU - Herrera, Raul AU - Reiter, Karine AU - Kotova, Svetlana AU - Shimp, Richard L, Jr AU - Miura, Kazutoyo AU - Jones, Dominique AU - Lebowitz, Jacob AU - Ambroggio, Xavier AU - Hurt, Darrell E AD - Laboratory of Malaria Immunology and Vaccinology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, USA, DavidL.Narum,dnarum{at}niaid.nih.gov. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 615 EP - 625 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 11 IS - 5 SN - 1535-9778, 1535-9778 KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - Parasites KW - Hepatocytes KW - Erythrocytes KW - Malaria KW - Membrane proteins KW - Development KW - Hosts KW - Public health KW - circumsporozoite protein KW - Escherichia coli KW - Actin KW - Cell migration KW - Thrombospondin KW - Plasmodium falciparum KW - Adhesion KW - Cell adhesion KW - Recombinants KW - Motility KW - Antibodies KW - Micronemes KW - Merozoites KW - Organelles KW - thrombospondin-related anonymous protein KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08524:Public health, medicines, dangerous organisms KW - K 03320:Cell Biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020839216?accountid=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=Eukaryotic+Cell&rft.atitle=Analysis+of+the+Conformation+and+Function+of+the+Plasmodium+falciparum+Merozoite+Proteins+MTRAP+and+PTRAMP&rft.au=Uchime%2C+Onyinyechukwu%3BHerrera%2C+Raul%3BReiter%2C+Karine%3BKotova%2C+Svetlana%3BShimp%2C+Richard+L%2C+Jr%3BMiura%2C+Kazutoyo%3BJones%2C+Dominique%3BLebowitz%2C+Jacob%3BAmbroggio%2C+Xavier%3BHurt%2C+Darrell+E&rft.aulast=Uchime&rft.aufirst=Onyinyechukwu&rft.date=2012-05-01&rft.volume=11&rft.issue=5&rft.spage=615&rft.isbn=&rft.btitle=&rft.title=Eukaryotic+Cell&rft.issn=15359778&rft_id=info:doi/10.1128%2FEC.00039-12 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Number of references - 43 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Recombinants; Parasites; Antibodies; Erythrocytes; Actin; Hosts; Adhesion; Public health; Hepatocytes; Thrombospondin; Malaria; Development; Membrane proteins; Cell adhesion; circumsporozoite protein; Motility; Micronemes; Merozoites; Cell migration; Organelles; thrombospondin-related anonymous protein; Escherichia coli; Plasmodium falciparum DO - http://dx.doi.org/10.1128/EC.00039-12 ER - TY - JOUR T1 - Loss of dopamine D2 receptors induces atrophy in the temporal and parietal cortices and the caudal thalamus of ethanol-consuming mice. AN - 1020189287; 22017419 AB - The need of an animal model of alcoholism becomes apparent when we consider the genetic diversity of the human populations, an example being dopamine D2 receptor (DRD2) expression levels. Research suggests that low DRD2 availability is associated with alcohol abuse, while higher DRD2 levels may be protective against alcoholism. This study aims to establish whether (i) the ethanol-consuming mouse is a suitable model of alcohol-induced brain atrophy and (ii) DRD2 protect the brain against alcohol toxicity. Adult Drd2+/+ and Drd2-/- mice drank either water or 20% ethanol solution for 6 months. At the end of the treatment period, the mice underwent magnetic resonance (MR) imaging under anesthesia. MR images were registered to a common space, and regions of interest were manually segmented. We found that chronic ethanol intake induced a decrease in the volume of the temporal and parietal cortices as well as the caudal thalamus in Drd2-/- mice. The result suggests that (i) normal DRD2 expression has a protective role against alcohol-induced brain atrophy and (ii) in the absence of Drd2 expression, prolonged ethanol intake reproduces a distinct feature of human brain pathology in alcoholism, the atrophy of the temporal and parietal cortices. Copyright © 2011 by the Research Society on Alcoholism. JF - Alcoholism, clinical and experimental research AU - Delis, Foteini AU - Benveniste, Helene AU - Xenos, Michalis AU - Grandy, David AU - Wang, Gene-Jack AU - Volkow, Nora D AU - Thanos, Panayotis K AD - Laboratory of Neuroimaging, National Institute on Alcohol Abuse and Alcoholism, NIH, Bethesda, Maryland, USA. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 815 EP - 825 VL - 36 IS - 5 KW - Central Nervous System Depressants KW - 0 KW - Receptors, Dopamine D2 KW - Ethanol KW - 3K9958V90M KW - Index Medicus KW - Magnetic Resonance Imaging KW - Atrophy -- chemically induced KW - Animals KW - Alcoholism -- pathology KW - Mice KW - Atrophy -- metabolism KW - Male KW - Organ Size -- drug effects KW - Mice, Knockout KW - Cerebral Cortex -- drug effects KW - Central Nervous System Depressants -- toxicity KW - Cerebral Cortex -- pathology KW - Thalamus -- pathology KW - Ethanol -- toxicity KW - Thalamus -- drug effects KW - Receptors, Dopamine D2 -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020189287?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=Loss+of+dopamine+D2+receptors+induces+atrophy+in+the+temporal+and+parietal+cortices+and+the+caudal+thalamus+of+ethanol-consuming+mice.&rft.au=Delis%2C+Foteini%3BBenveniste%2C+Helene%3BXenos%2C+Michalis%3BGrandy%2C+David%3BWang%2C+Gene-Jack%3BVolkow%2C+Nora+D%3BThanos%2C+Panayotis+K&rft.aulast=Delis&rft.aufirst=Foteini&rft.date=2012-05-01&rft.volume=36&rft.issue=5&rft.spage=815&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=1530-0277&rft_id=info:doi/10.1111%2Fj.1530-0277.2011.01667.x LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-10 N1 - Date created - 2012-05-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1111/j.1530-0277.2011.01667.x ER - TY - JOUR T1 - Annual Research Review: Impact of advances in genetics in understanding developmental psychopathology AN - 1018375833; 201209927 AB - It was hoped that diagnostic guidelines for, and treatment of, child psychiatric disorders in DSM-5 would be informed by the wealth of clinical genetic research related to neurodevelopmental disorders. In spite of remarkable advances in genetic technology, this has not been the case. Candidate gene, genome-wide association, and rare copy number variant (CNV) studies have been carried out for attention-deficit/hyperactivity disorder (ADHD), Autism, Tourette's Syndrome, and schizophrenia, with intriguing results, but environmental factors, incomplete penetrance, pleiotropy, and genetic heterogeneity, underlying any given phenotype have limited clinical translation. One promising approach may be the use of developmental brain imaging measures as more relevant phenotypes. This is particularly important, as subtle abnormalities in timing and expression of gene pathways underlying brain development may well link these disorders and be the ultimate target of treatments. Adapted from the source document. JF - The Journal of Child Psychology and Psychiatry AU - Addington, Anjene M AU - Rapoport, Judith L AD - Child Psychiatry Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 510 EP - 518 PB - Blackwell Publishing, Oxford UK VL - 53 IS - 5 SN - 0021-9630, 0021-9630 KW - Schizophrenia KW - Genes KW - Attention deficit hyperactivity disorder KW - Heterogeneity KW - Phenotypes KW - Technology KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1018375833?accountid=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=Annual+Research+Review%3A+Impact+of+advances+in+genetics+in+understanding+developmental+psychopathology&rft.au=Addington%2C+Anjene+M%3BRapoport%2C+Judith+L&rft.aulast=Addington&rft.aufirst=Anjene&rft.date=2012-05-01&rft.volume=53&rft.issue=5&rft.spage=510&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Child+Psychology+and+Psychiatry&rft.issn=00219630&rft_id=info:doi/10.1111%2Fj.1469-7610.2011.02478.x LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-06-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JPPDAI N1 - SubjectsTermNotLitGenreText - Phenotypes; Genes; Heterogeneity; Technology; Attention deficit hyperactivity disorder; Schizophrenia DO - http://dx.doi.org/10.1111/j.1469-7610.2011.02478.x ER - TY - JOUR T1 - Exploiting the Anti-HIV-1 Activity of Acyclovir: Suppression of Primary and Drug-Resistant HIV Isolates and Potentiation of the Activity by Ribavirin AN - 1017973902; 16723993 AB - Multiple clinical trials have demonstrated that herpes simplex virus 2 (HSV-2) suppressive therapy using acyclovir (ACV) or valacyclovir in HIV-1/HSV-2-infected persons increased the patient's survival and decreased the HIV-1 load. It has been shown that the incorporation of ACV-monophosphate into the nascent DNA chain instead of dGMP results in the termination of viral DNA elongation and directly inhibits laboratory strains of HIV-1. We evaluated here the anti-HIV activity of ACV against primary HIV-1 isolates of different clades and coreceptor specificity and against viral isolates resistant to currently used drugs, including zidovudine, lamivudine, nevirapine, a combination of nucleoside reverse transcriptase inhibitors (NRTIs), a fusion inhibitor, and two protease inhibitors. We found that, at clinically relevant concentrations, ACV inhibits the replication of these isolates in human tissues infected ex vivo. Moreover, addition of ribavirin, an antiviral capable of depleting the pool of intracellular dGTP, potentiated the ACV-mediated HIV-1 suppression. These data warrant further clinical investigations of the benefits of using inexpensive and safe ACV alone or in combination with other drugs against HIV-1, especially to complement or delay highly active antiretroviral therapy (HAART) initiation in low-resource settings. JF - Antimicrobial Agents & Chemotherapy AU - Vanpouille, Christophe AU - Lisco, Andrea AU - Introini, Andrea AU - Grivel, Jean-Charles AU - Munawwar, Arshi AU - Merbah, Melanie AU - Schinazi, Raymond F AU - Derudas, Marco AU - McGuigan, Christopher AU - Balzarini, Jan AD - Eunice Kennedy Shriver National Institute of Child Health and Human Development, Program of Physical Biology, National Institutes of Health, Bethesda, Maryland, USA, LeonidMargolis,margolis{at}helix.nih.gov. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 2604 EP - 2611 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 56 IS - 5 SN - 0066-4804, 0066-4804 KW - Virology & AIDS Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology KW - Antiviral activity KW - Antiviral agents KW - Clinical trials KW - DNA KW - Data processing KW - Drug resistance KW - Elongation KW - Lamivudine KW - Nevirapine KW - Potentiation KW - Proteinase inhibitors KW - Replication KW - Ribavirin KW - Survival KW - Zidovudine KW - acyclovir KW - highly active antiretroviral therapy KW - nucleoside reverse transcriptase inhibitors KW - valacyclovir KW - Human immunodeficiency virus 1 KW - Herpes simplex virus 2 KW - Human immunodeficiency virus KW - A 01340:Antibiotics & Antimicrobials KW - V 22360:AIDS and HIV UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1017973902?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Antimicrobial+Agents+%26+Chemotherapy&rft.atitle=Exploiting+the+Anti-HIV-1+Activity+of+Acyclovir%3A+Suppression+of+Primary+and+Drug-Resistant+HIV+Isolates+and+Potentiation+of+the+Activity+by+Ribavirin&rft.au=Vanpouille%2C+Christophe%3BLisco%2C+Andrea%3BIntroini%2C+Andrea%3BGrivel%2C+Jean-Charles%3BMunawwar%2C+Arshi%3BMerbah%2C+Melanie%3BSchinazi%2C+Raymond+F%3BDerudas%2C+Marco%3BMcGuigan%2C+Christopher%3BBalzarini%2C+Jan&rft.aulast=Vanpouille&rft.aufirst=Christophe&rft.date=2012-05-01&rft.volume=56&rft.issue=5&rft.spage=2604&rft.isbn=&rft.btitle=&rft.title=Antimicrobial+Agents+%26+Chemotherapy&rft.issn=00664804&rft_id=info:doi/10.1128%2FAAC.05986-11 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Number of references - 46 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Data processing; Replication; Potentiation; Drug resistance; Proteinase inhibitors; Ribavirin; Lamivudine; Survival; Zidovudine; acyclovir; Antiviral activity; valacyclovir; Clinical trials; Elongation; Nevirapine; Antiviral agents; highly active antiretroviral therapy; DNA; nucleoside reverse transcriptase inhibitors; Human immunodeficiency virus; Human immunodeficiency virus 1; Herpes simplex virus 2 DO - http://dx.doi.org/10.1128/AAC.05986-11 ER - TY - JOUR T1 - H-NS Regulation of IraD and IraM Antiadaptors for Control of RpoS Degradation AN - 1017972522; 16724132 AB - RpoS, the master sigma factor during stationary phase and under a variety of stress conditions, is regulated at multiple levels, including regulated degradation. Degradation is dependent upon ClpXP and the RssB adaptor protein. H-NS, a nucleoid-associated protein, affects the regulated degradation of RpoS; in the absence of H-NS, RpoS is stable. The mechanisms involved in this regulation were not known. We have found that H-NS inhibits the expression of iraD and iraM, the genes coding for two antiadaptor proteins that stabilize RpoS when overexpressed. The regulation by H-NS of iraM is independent from the previously demonstrated regulation by the PhoP/PhoQ two-component system. Moreover, differences in the behavior of several hns alleles are explained by a role for StpA, an H-NS-like protein, in the regulation of RpoS stability. This finding parallels recent observations for a role of StpA in regulation of RpoS stability in Salmonella. JF - Journal of Bacteriology AU - Battesti, A AU - Gottesman, S AD - Laboratory of Molecular Biology, National Cancer Institute, Bethesda, Maryland, USA, S.Gottesman,susang{at}helix.nih.gov. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 2470 EP - 2478 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 194 IS - 10 SN - 0021-9193, 0021-9193 KW - Microbiology Abstracts B: Bacteriology KW - stationary phase KW - adaptor proteins KW - Stress KW - Sigma factor KW - Salmonella KW - J 02320:Cell Biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1017972522?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Bacteriology&rft.atitle=H-NS+Regulation+of+IraD+and+IraM+Antiadaptors+for+Control+of+RpoS+Degradation&rft.au=Battesti%2C+A%3BGottesman%2C+S&rft.aulast=Battesti&rft.aufirst=A&rft.date=2012-05-01&rft.volume=194&rft.issue=10&rft.spage=2470&rft.isbn=&rft.btitle=&rft.title=Journal+of+Bacteriology&rft.issn=00219193&rft_id=info:doi/10.1128%2FJB.00132-12 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Number of references - 37 N1 - Last updated - 2013-07-15 N1 - SubjectsTermNotLitGenreText - stationary phase; adaptor proteins; Stress; Sigma factor; Salmonella DO - http://dx.doi.org/10.1128/JB.00132-12 ER - TY - JOUR T1 - MicroRNA Targeting of Neurotropic Flavivirus: Effective Control of Virus Escape and Reversion to Neurovirulent Phenotype AN - 1017971744; 16723760 AB - Neurotropic flaviviruses can efficiently replicate in the developing and mature central nervous systems (CNS) of mice causing lethal encephalitis. Insertion of a single copy of a target for brain-expressed microRNAs (miRNAs) in the 3' noncoding region (3'NCR) of the flavivirus genome (chimeric tick-borne encephalitis virus/dengue virus) abolished virus neurovirulence in the mature mouse CNS. However, in the developing CNS of highly permissive suckling mice, the miRNA-targeted viruses can revert to a neurovirulent phenotype by accumulating deletions or mutations within the miRNA target sequence. Virus escape from miRNA-mediated suppression in the developing CNS was markedly diminished by increasing the number of miRNA target sites and by extending the distance between these sites in the virus genome. Insertion of multiple miRNA targets into the 3'NCR altered virus neuroinvasiveness, decreased neurovirulence and neuroinflammatory responses, and prevented neurodegeneration without loss of immunogenicity. Although the onset of encephalitis was delayed, a small number of suckling mice still succumbed to lethal intracerebral infection with the miRNA-targeted viruses. Sequence analysis of brain isolates from moribund mice revealed that the viruses escaped from miRNA-mediated suppression exclusively through the deletion of miRNA targets and viral genome sequence located between the two miRNA targets separated by the greatest distance. These findings offer a general strategy to control the reversion of virus to a virulent phenotype: a simultaneous miRNA targeting of the viral genome at many different functionally important regions could prevent virus escape from miRNA-based attenuation, since a deletion of the targeted genomic sequences located between the inserted miRNA binding sites would be lethal for the virus. JF - Journal of Virology AU - Thach, Dzung C AU - Speicher, James M AU - Pletnev, Alexander G AD - Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA, AlexanderG.Pletnev,apletnev{at}niaid.nih.gov. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 5647 EP - 5659 PB - American Society for Microbiology, 1752 N Street N.W. Washington, DC 20036 United States VL - 86 IS - 10 SN - 0022-538X, 0022-538X KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; CSA Neurosciences Abstracts; Virology & AIDS Abstracts KW - Dengue virus KW - Genomes KW - Virology KW - Central nervous system KW - Invasiveness KW - Nucleotide sequence KW - Viruses KW - Reversion KW - Infection KW - Neurodegeneration KW - Phenotypes KW - Flavivirus KW - Tick-borne encephalitis KW - Gene deletion KW - genomics KW - Tick-borne encephalitis virus KW - Mutations KW - miRNA KW - Neurovirulence KW - Brain KW - Suckling behavior KW - Encephalitis KW - Inflammation KW - Viral diseases KW - Immunogenicity KW - Insertion KW - Mutation KW - V 22350:Immunology KW - Q1 08485:Species interactions: pests and control KW - Q5 08524:Public health, medicines, dangerous organisms KW - N3 11027:Neurology & neuropathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1017971744?accountid=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+Virology&rft.atitle=MicroRNA+Targeting+of+Neurotropic+Flavivirus%3A+Effective+Control+of+Virus+Escape+and+Reversion+to+Neurovirulent+Phenotype&rft.au=Thach%2C+Dzung+C%3BSpeicher%2C+James+M%3BPletnev%2C+Alexander+G&rft.aulast=Thach&rft.aufirst=Dzung&rft.date=2012-05-01&rft.volume=86&rft.issue=10&rft.spage=5647&rft.isbn=&rft.btitle=&rft.title=Journal+of+Virology&rft.issn=0022538X&rft_id=info:doi/10.1128%2FJVI.07125-11 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Number of references - 37 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Virology; Genomes; Central nervous system; Viral diseases; Mutations; Viruses; Brain; Phenotypes; Invasiveness; Nucleotide sequence; miRNA; Neurovirulence; Reversion; Suckling behavior; Infection; Neurodegeneration; Encephalitis; Inflammation; Tick-borne encephalitis; Gene deletion; Insertion; Immunogenicity; genomics; Mutation; Dengue virus; Tick-borne encephalitis virus; Flavivirus DO - http://dx.doi.org/10.1128/JVI.07125-11 ER - TY - JOUR T1 - Bovine AAV transcytosis inhibition by tannic acid results in functional expression of CFTR in vitro and altered biodistribution in vivo AN - 1017961396; 16683326 AB - Bovine adeno-associated virus (BAAV) can enter a cell either through a transcytosis or transduction pathway. We previously demonstrated that particles entering via the transcytosis pathway can be redirected to transduce the cell by blocking particle exocytosis with tannic acid (TA). To investigate whether this approach is useful in lung gene therapy applications, we tested the effect of TA on BAAV transduction in cystic fibrosis airway epithelia in vitro, and in mouse lung in vivo. Our findings suggest that BAAV transcytosis can occur in vivo and that treatment with TA reduces transcytosis and increases lung transduction. TA treatment did not impair the sorting and the activity of the BAAV expressed cystic fibrosis transmembrane regulator membrane protein. JF - Gene Therapy AU - Di Pasquale, G AU - Ostedgaard, L AU - Vermeer, D AU - Swaim, W D AU - Karp, P AU - Chiorini, J A AD - Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 576 EP - 581 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 19 IS - 5 SN - 0969-7128, 0969-7128 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Cystic fibrosis KW - Cystic fibrosis transmembrane conductance regulator KW - Exocytosis KW - Gene therapy KW - Lung KW - Membrane proteins KW - Respiratory tract KW - Tannic acid KW - Bovine adeno-associated virus KW - Adeno-associated virus KW - W 30905:Medical Applications KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1017961396?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene+Therapy&rft.atitle=Bovine+AAV+transcytosis+inhibition+by+tannic+acid+results+in+functional+expression+of+CFTR+in+vitro+and+altered+biodistribution+in+vivo&rft.au=Di+Pasquale%2C+G%3BOstedgaard%2C+L%3BVermeer%2C+D%3BSwaim%2C+W+D%3BKarp%2C+P%3BChiorini%2C+J+A&rft.aulast=Di+Pasquale&rft.aufirst=G&rft.date=2012-05-01&rft.volume=19&rft.issue=5&rft.spage=576&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2011.138 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2012-06-01 N1 - SubjectsTermNotLitGenreText - Gene therapy; Lung; Exocytosis; Cystic fibrosis transmembrane conductance regulator; Membrane proteins; Tannic acid; Cystic fibrosis; Respiratory tract; Bovine adeno-associated virus; Adeno-associated virus DO - http://dx.doi.org/10.1038/gt.2011.138 ER - TY - JOUR T1 - Circulating Antibody Free Light Chains and Risk of Posttransplant Lymphoproliferative Disorder AN - 1017959719; 16679581 AB - Posttransplant lymphoproliferative disorder (PTLD) is a major complication of solid-organ transplantation. With human immunodeficiency virus infection (an analogous immunosuppressive state), elevated kappa and lambda immunoglobulin free light chains (FLCs) in peripheral blood are associated with increased risk of lymphoma. To assess the role of B-cell dysfunction in PTLD, we measured circulating FLCs among Canadian transplant recipients, including 29 individuals with PTLD and 57 matched transplant recipients who were PTLD-free. Compared with controls, PTLD cases had higher kappa FLCs (median 1.53 vs. 1.07 times upper limit of normal) and lambda FLCs (1.03 vs. 0.68). Using samples obtained on average 3.5 months before PTLD diagnosis, cases were more likely to have polyclonal FLC elevations (i.e. elevated kappa and/or lambda with normal kappa/lambda ratio: odds ratio [OR] 4.2, 95%CI 1.1-15) or monoclonal elevations (elevated kappa and/or lambda with abnormal ratio: OR 3.0, 95%CI 0.5-18). Strong FLC-PTLD associations were also observed at diagnosis/selection. Among recipients with Epstein-Barr virus (EBV) DNA measured in blood, EBV DNAemia was associated with FLC abnormalities (ORs 6.2 and 3.2 for monoclonal and polyclonal elevations). FLC elevations are common in transplant recipients and associated with heightened PTLD risk. FLCs likely reflect B-cell dysfunction, perhaps related to EBV-driven lymphoproliferation. The authors demonstrate that elevated circulating levels of immunoglobulin free light chains are associated with an increased risk of posttransplant lymphoproliferative disorder. JF - American Journal of Transplantation AU - Engels, E A AU - Preiksaitis, J AU - Zingone, A AU - Landgren, O AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, MD Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 1268 EP - 1274 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 12 IS - 5 SN - 1600-6135, 1600-6135 KW - Immunology Abstracts; Risk Abstracts KW - DNA KW - Immunoglobulins KW - Infection KW - Light chains KW - Lymphocytes B KW - Lymphoma KW - Peripheral blood KW - complications KW - lymphoma KW - posttransplant lymphoproliferative disorders KW - Epstein-Barr virus KW - Human immunodeficiency virus KW - F 06955:Immunomodulation & Immunopharmacology KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1017959719?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Transplantation&rft.atitle=Circulating+Antibody+Free+Light+Chains+and+Risk+of+Posttransplant+Lymphoproliferative+Disorder&rft.au=Engels%2C+E+A%3BPreiksaitis%2C+J%3BZingone%2C+A%3BLandgren%2C+O&rft.aulast=Engels&rft.aufirst=E&rft.date=2012-05-01&rft.volume=12&rft.issue=5&rft.spage=1268&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Transplantation&rft.issn=16006135&rft_id=info:doi/10.1111%2Fj.1600-6143.2011.03954.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Document feature - figure 0 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Light chains; Lymphocytes B; DNA; Peripheral blood; posttransplant lymphoproliferative disorders; Infection; Lymphoma; Immunoglobulins; complications; lymphoma; Epstein-Barr virus; Human immunodeficiency virus DO - http://dx.doi.org/10.1111/j.1600-6143.2011.03954.x ER - TY - JOUR T1 - RESPONSE OF THE U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES IN PROTECTING CIVILIAN AMERICANS IN JAPAN DURING THE FUKUSHIMA NUCLEAR CRISIS AN - 1014105555; 16644562 AB - Following the earthquake and tsunami in northern Japan on 11 March 2011 and the ensuing damage to the Fukushima Daiichi Nuclear Power Plant complex, a request by the U.S. Ambassador to Japan to the U.S. Department of Health and Human Services (DHHS) Assistant Secretary for Preparedness and Response (ASPR) resulted in deployment of a five-person team of subject matter experts to the U.S. Embassy. The primary purpose of the deployment was to provide the U.S. Embassy in Tokyo with guidance on health and medical issues related to potential radiation exposure of U.S. citizens in Japan, including employees of the U.S. Department of State at consulates in Japan and American citizens living in or visiting Japan. At the request of the Government of Japan (GOJ), the deployed health team also assisted Japanese experts in their public health response to the radiation incident. Over a 3-wk period in Japan and continuing for weeks after their return to the U.S., the team provided expertise in the areas of medical and radiation oncology; health physics; assessment of radiation dose and cancer risk, particularly to U.S. citizens living in Tokyo and the surrounding areas; food and water contamination and the acceptable limits; countermeasures to exposure such as potassium iodide (KI); the use of KI and an offered donation from the United States; , evacuation and re-entry issues; and health/emergency-related communication strategies. This paper describes the various strategies used and observations made by the DHHS team during the first 2 mo after the Fukushima crisis began. JF - Health Physics AU - Simon, S L AU - Coleman, C N AU - Noska, MA AU - Bowman, T AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA, ssimon@mail.nih.gov Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 570 EP - 579 PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States VL - 102 IS - 5 SN - 0017-9078, 0017-9078 KW - Pollution Abstracts; Health & Safety Science Abstracts KW - Earthquakes KW - Nuclear power plants KW - USA KW - Communications KW - iodides KW - crises KW - Seismic activity KW - Japan, Honshu, Tokyo Prefect., Tokyo KW - evacuation KW - Cancer KW - Public health KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - P 2000:FRESHWATER POLLUTION UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1014105555?accountid=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=Health+Physics&rft.atitle=RESPONSE+OF+THE+U.S.+DEPARTMENT+OF+HEALTH+AND+HUMAN+SERVICES+IN+PROTECTING+CIVILIAN+AMERICANS+IN+JAPAN+DURING+THE+FUKUSHIMA+NUCLEAR+CRISIS&rft.au=Simon%2C+S+L%3BColeman%2C+C+N%3BNoska%2C+MA%3BBowman%2C+T&rft.aulast=Simon&rft.aufirst=S&rft.date=2012-05-01&rft.volume=102&rft.issue=5&rft.spage=570&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0b013e31824c79e5 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2013-08-12 N1 - SubjectsTermNotLitGenreText - Earthquakes; Nuclear power plants; Communications; iodides; crises; Seismic activity; evacuation; Cancer; Public health; USA; Japan, Honshu, Tokyo Prefect., Tokyo DO - http://dx.doi.org/10.1097/HP.0b013e31824c79e5 ER - TY - JOUR T1 - Dynamic Sagittal Plane Trunk Control During Anterior Cruciate Ligament Injury AN - 1014104729; 16630185 AB - Background: Recent studies have demonstrated that trunk control likely plays a role in anterior cruciate ligament (ACL) injury. Yet, the majority of ACL research remains focused on the lower limb, with limited information on the trunk position at the time of injury.Hypotheses: Athletes experiencing a noncontact ACL injury after a 1-legged landing position their center of mass (COM) more posterior from the base of support (BOS) at initial ground contact in comparison with uninjured athletes. The distance from the COM to the BOS (COM_BOS) is larger in female, as compared with male, athletes during 1-legged landing.Study Design: Case control study; Level of evidence, 3.Methods: Movie captures of 20 athletes performing a 1-legged landing maneuver resulting in a torn ACL were compared with matched (for gender, sport, and activity just before landing) movie captures of 20 athletes performing a similar maneuver that did not result in an ACL disruption (controls). The COM_BOS, trunkG angle, and limbG angle (both relative to the gravity vector) were measured in the sagittal plane at initial ground-foot contact. A 2-way ANOVA (injury status gender) was used to examine the hypotheses.Results: There was a significant difference in all 3 measures based on injury status but not on gender. The COM_BOS, normalized by femur length, and limbG angle were greater ( Delta = 0.9, P < .001 and Delta = 16 degree , P = .004, respectively), and the trunkG angle was smaller ( Delta = 12 degree , P = .016) in the participants who sustained an ACL injury as compared with controls. The average COM was calculated as 38 cm more posterior relative to the BOS in the participants who sustained an ACL injury as compared with controls.Conclusion: Landing with the COM far posterior to the BOS may be a risk factor for noncontact ACL injury and potentially can be addressed in prevention programs. JF - American Journal of Sports Medicine AU - Sheehan, Frances T AU - Sipprell, William H AU - Boden, Barry P AD - Functional and Applied Biomechanics Section in Rehabilitation Medicine, National Institutes of Health, Bethesda, Maryland, bboden@starpower.net Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 1068 EP - 1074 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 40 IS - 5 SN - 0363-5465, 0363-5465 KW - Physical Education Index KW - Athletes KW - Center of gravity KW - Films KW - Gender KW - Injuries KW - Landing KW - Ligaments KW - Preventive health KW - Trunk KW - PE 090:Sports Medicine & Exercise Sport Science UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1014104729?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Sports+Medicine&rft.atitle=Dynamic+Sagittal+Plane+Trunk+Control+During+Anterior+Cruciate+Ligament+Injury&rft.au=Sheehan%2C+Frances+T%3BSipprell%2C+William+H%3BBoden%2C+Barry+P&rft.aulast=Sheehan&rft.aufirst=Frances&rft.date=2012-05-01&rft.volume=40&rft.issue=5&rft.spage=1068&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Sports+Medicine&rft.issn=03635465&rft_id=info:doi/10.1177%2F0363546512437850 LA - English DB - Physical Education Index N1 - Date revised - 2012-05-01 N1 - Number of references - 32 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Ligaments; Trunk; Landing; Injuries; Preventive health; Gender; Center of gravity; Films; Athletes DO - http://dx.doi.org/10.1177/0363546512437850 ER - TY - JOUR T1 - Immunotoxin resistance via reversible methylation of the DPH4 promoter is a unique survival strategy. AN - 1011175407; 22509046 AB - HA22 is a recombinant immunotoxin composed of an anti-CD22 Fv fused to a portion of Pseudomonas exotoxin A. HA22 produced a high rate of complete remissions in drug-resistant hairy cell leukemia and has a lower response rate in pediatric acute lymphoblastic leukemia (ALL). To understand why patients with ALL have poorer responses, we isolated an ALL cell line that is resistant to killing by HA22. The resistance is unstable; without HA22 the cells revert to HA22 sensitivity in 4 mo. We showed that in the resistant cell line, HA22 is unable to ADP ribosylate and inactivate elongation factor-2 (EF2), owing to a low level of DPH4 mRNA and protein, which prevents diphthamide biosynthesis and renders EF2 refractory to HA22. Analysis of the promoter region of the DPH4 gene shows that the CpG island was hypomethylated in the HA22-sensitive cells, heavily methylated in the resistant cells, and reverted to low methylation in the revertant cells. Our data show that immunotoxin resistance is associated with reversible CpG island methylation and silencing of DPH4 gene transcription. Incubation of sensitive cells with the methylation inhibitor 5-azacytidine prevented the emergence of resistant cells, suggesting that this agent in combination with HA22 may be useful in the treatment of some cases of ALL. JF - Proceedings of the National Academy of Sciences of the United States of America AU - Wei, Hui AU - Xiang, Laiman AU - Wayne, Alan S AU - Chertov, Oleg AU - FitzGerald, David J AU - Bera, Tapan K AU - Pastan, Ira AD - Laboratory of Molecular Biology and Pediatric Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/05/01/ PY - 2012 DA - 2012 May 01 SP - 6898 EP - 6903 VL - 109 IS - 18 KW - Bacterial Toxins KW - 0 KW - CD22 protein, human KW - DNA, Neoplasm KW - DNAJC24 protein, human KW - Exotoxins KW - HSP40 Heat-Shock Proteins KW - Immunotoxins KW - Peptide Elongation Factor 2 KW - RNA, Messenger KW - RNA, Neoplasm KW - Sialic Acid Binding Ig-like Lectin 2 KW - immunotoxin HA22 KW - Azacitidine KW - M801H13NRU KW - Index Medicus KW - Peptide Elongation Factor 2 -- metabolism KW - Azacitidine -- pharmacology KW - Humans KW - Cell Line, Tumor KW - RNA, Neoplasm -- genetics KW - RNA, Messenger -- genetics KW - Base Sequence KW - Sialic Acid Binding Ig-like Lectin 2 -- immunology KW - RNA, Messenger -- metabolism KW - CpG Islands KW - Drug Resistance, Neoplasm -- genetics KW - Molecular Sequence Data KW - DNA, Neoplasm -- genetics KW - DNA, Neoplasm -- metabolism KW - RNA, Neoplasm -- metabolism KW - Drug Resistance, Neoplasm -- drug effects KW - Promoter Regions, Genetic KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- metabolism KW - HSP40 Heat-Shock Proteins -- genetics KW - Exotoxins -- pharmacology KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- immunology KW - DNA Methylation -- drug effects KW - Bacterial Toxins -- pharmacology KW - Immunotoxins -- pharmacology KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- drug therapy KW - Precursor Cell Lymphoblastic Leukemia-Lymphoma -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1011175407?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Immunotoxin+resistance+via+reversible+methylation+of+the+DPH4+promoter+is+a+unique+survival+strategy.&rft.au=Wei%2C+Hui%3BXiang%2C+Laiman%3BWayne%2C+Alan+S%3BChertov%2C+Oleg%3BFitzGerald%2C+David+J%3BBera%2C+Tapan+K%3BPastan%2C+Ira&rft.aulast=Wei&rft.aufirst=Hui&rft.date=2012-05-01&rft.volume=109&rft.issue=18&rft.spage=6898&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.1204523109 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-10 N1 - Date created - 2012-05-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Oncogene. 2001 Sep 13;20(41):5865-77 [11593392] Int J Oncol. 2010 May;36(5):1235-41 [20372798] J Clin Oncol. 2002 May 15;20(10):2441-52 [12011121] N Engl J Med. 2003 Nov 20;349(21):2042-54 [14627790] Genes Dev. 2004 Feb 1;18(3):320-32 [14744934] Methods Mol Biol. 2004;248:503-18 [14970517] Blood. 2004 Apr 1;103(7):2718-26 [14525789] Nature. 2004 May 27;429(6990):457-63 [15164071] Nature. 1989 Jun 1;339(6223):394-7 [2498664] Adv Exp Med Biol. 1999;457:543-50 [10500832] Cancer Cell. 2005 Apr;7(4):375-86 [15837626] Nat Clin Pract Oncol. 2005 Dec;2 Suppl 1:S4-11 [16341240] Mol Cell Biol. 2006 May;26(10):3835-41 [16648478] N Engl J Med. 2006 Oct 12;355(15):1572-82 [17035650] Blood. 2010 Jun 10;115(23):4798-809 [20215641] Mol Cell Biol. 2010 Jul;30(14):3444-52 [20457813] Br J Haematol. 2010 Aug;150(3):352-8 [20528877] Leuk Lymphoma. 2011 Jan;52(1):134-6 [20858102] Nat Med. 2011 Mar;17(3):288-9 [21383739] Biochemistry. 2010 Nov 9;49(44):9649-57 [20873788] Arthritis Rheum. 2011 May;63(5):1376-86 [21538319] FEBS J. 2011 Aug;278(15):2613-24 [21624055] J Biol Chem. 2011 Aug 5;286(31):27761-8 [21669876] Cancer Res. 2011 Oct 15;71(20):6300-9 [21998010] J Biol Chem. 2006 Oct 27;281(43):32639-48 [16950777] Leukemia. 2007 May;21(5):906-11 [17344919] Cancer Res. 2007 May 1;67(9):4482-90 [17483364] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15805-10 [17890317] Urology. 2008 Jun;71(6):1220-5 [18538698] Cancer Res. 2008 Aug 1;68(15):6300-5 [18676854] Nature. 2008 Aug 7;454(7205):766-70 [18600261] J Natl Cancer Inst. 2008 Sep 17;100(18):1271-3 [18780861] J Cell Sci. 2008 Oct 1;121(Pt 19):3140-5 [18765564] Blood. 2009 Jun 18;113(25):6296-303 [19383969] J Clin Oncol. 2009 Jun 20;27(18):2983-90 [19414673] Leukemia. 2009 Jul;23(7):1342-3 [19322208] N Engl J Med. 2000 Nov 9;343(19):1350-4 [11070098] Cancer Res. 2000 Nov 1;60(21):6039-44 [11085525] Cancer Res. 2010 Feb 1;70(3):1082-9 [20103626] Clin Cancer Res. 2010 Mar 15;16(6):1894-903 [20215554] Cell. 2010 Apr 2;141(1):69-80 [20371346] J Clin Oncol. 2002 May 15;20(10):2429-40 [12011120] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1073/pnas.1204523109 ER - TY - JOUR T1 - P2X7 receptor-NADPH oxidase axis mediates protein radical formation and Kupffer cell activation in carbon tetrachloride-mediated steatohepatitis in obese mice. AN - 1010636818; 22343416 AB - While some studies show that carbon tetrachloride-mediated metabolic oxidative stress exacerbates steatohepatitic-like lesions in obese mice, the redox mechanisms that trigger the innate immune system and accentuate the inflammatory cascade remain unclear. Here we have explored the role of the purinergic receptor P2X7-NADPH oxidase axis as a primary event in recognizing the heightened release of extracellular ATP from CCl(4)-treated hepatocytes and generating redox-mediated Kupffer cell activation in obese mice. We found that an underlying condition of obesity led to the formation of protein radicals and posttranslational nitration, primarily in Kupffer cells, at 24h post-CCl(4) administration. The free radical-mediated oxidation of cellular macromolecules, which was NADPH oxidase and P2X7 receptor-dependent, correlated well with the release of TNF-α and MCP-2 from Kupffer cells. The Kupffer cells in CCl(4)-treated mice exhibited increased expression of MHC Class II proteins and showed an activated phenotype. Increased expression of MHC Class II was inhibited by the NADPH oxidase inhibitor apocynin , P2X7 receptor antagonist A438709 hydrochloride, and genetic deletions of the NADPH oxidase p47 phox subunit or the P2X7 receptor. The P2X7 receptor acted upstream of NADPH oxidase activation by up-regulating the expression of the p47 phox subunit and p47 phox binding to the membrane subunit, gp91 phox. We conclude that the P2X7 receptor is a primary mediator of oxidative stress-induced exacerbation of inflammatory liver injury in obese mice via NADPH oxidase-dependent mechanisms. Published by Elsevier Inc. JF - Free radical biology & medicine AU - Chatterjee, Saurabh AU - Rana, Ritu AU - Corbett, Jean AU - Kadiiska, Maria B AU - Goldstein, Joyce AU - Mason, Ronald P AD - Free Radical Metabolism Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA. chatterjees2@niehs.nih.gov Y1 - 2012/05/01/ PY - 2012 DA - 2012 May 01 SP - 1666 EP - 1679 VL - 52 IS - 9 KW - Receptors, Purinergic P2X7 KW - 0 KW - Carbon Tetrachloride KW - CL2T97X0V0 KW - NADPH Oxidase KW - EC 1.6.3.1 KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Microscopy, Confocal KW - Coculture Techniques KW - Animals KW - Oxidative Stress KW - Mice, Inbred C57BL KW - Mice KW - Male KW - NADPH Oxidase -- metabolism KW - Obesity -- metabolism KW - Fatty Liver -- chemically induced KW - Fatty Liver -- metabolism KW - Receptors, Purinergic P2X7 -- metabolism KW - Kupffer Cells -- metabolism KW - Carbon Tetrachloride -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1010636818?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=P2X7+receptor-NADPH+oxidase+axis+mediates+protein+radical+formation+and+Kupffer+cell+activation+in+carbon+tetrachloride-mediated+steatohepatitis+in+obese+mice.&rft.au=Chatterjee%2C+Saurabh%3BRana%2C+Ritu%3BCorbett%2C+Jean%3BKadiiska%2C+Maria+B%3BGoldstein%2C+Joyce%3BMason%2C+Ronald+P&rft.aulast=Chatterjee&rft.aufirst=Saurabh&rft.date=2012-05-01&rft.volume=52&rft.issue=9&rft.spage=1666&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2012.02.010 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-28 N1 - Date created - 2012-05-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Chem Biol Interact. 2000 Mar 15;125(3):233-43 [10731522] J Biol Chem. 1998 Jun 12;273(24):14906-11 [9614094] J Mol Med (Berl). 1999 Jan;77(1):8-13 [9930921] Am J Pathol. 1999 Jun;154(6):1711-20 [10362796] J Biol Chem. 2005 Jul 22;280(29):27179-94 [15917250] Immunol Cell Biol. 2005 Aug;83(4):336-43 [16033528] Free Radic Biol Med. 2005 Oct 15;39(8):1050-8 [16198232] Hepatology. 2006 Feb;43(2 Suppl 1):S99-S112 [16447287] Glia. 2006 Aug 15;54(3):234-42 [16817206] World J Gastroenterol. 2006 Dec 14;12(46):7413-20 [17167827] Hepatology. 2007 Feb;45(2):391-403 [17256749] J Gastroenterol Hepatol. 2007 Jun;22 Suppl 1:S20-7 [17567459] Biochem Soc Trans. 2007 Nov;35(Pt 5):1168-70 [17956304] Nat Rev Immunol. 2008 Apr;8(4):279-89 [18340345] J Immunol. 2008 Jun 15;180(12):8410-20 [18523309] Autoimmun Rev. 2008 Jul;7(7):567-73 [18625446] Free Radic Biol Med. 2009 Feb 15;46(4):454-61 [19049863] Sci Signal. 2009;2(56):pe6 [19193605] J Hepatol. 2009 Jul;51(1):212-23 [19447517] J Immunol. 2009 Sep 15;183(6):4055-66 [19717511] Hepatology. 2010 Feb;51(2):474-81 [19902480] Gastroenterol Clin North Am. 2010 Mar;39(1):57-68 [20202579] Chem Biol Interact. 2010 Apr 29;185(2):94-100 [20227401] Hepatology. 2010 Oct;52(4):1420-30 [20690191] Science. 2010 Oct 15;330(6002):362-6 [20947763] Nat Med. 2010 Dec;16(12):1434-8 [21102458] Circ Res. 2011 Jan 21;108(2):235-48 [21252151] Free Radic Biol Med. 2011 Apr 15;50(8):988-99 [21215311] Front Biosci. 2008;13:2588-603 [17981736] J Neurochem. 2000 Sep;75(3):965-72 [10936177] Hepatology. 2001 Aug;34(2):288-97 [11481614] Free Radic Biol Med. 2001 Dec 15;31(12):1544-9 [11744328] Toxicology. 2002 Aug 1;177(1):1-9 [12126791] J Biol Chem. 2003 Apr 11;278(15):13309-17 [12551918] Crit Rev Toxicol. 2003;33(2):105-36 [12708612] Diabetes. 2004 Jan;53(1):185-94 [14693714] Hepatology. 2004 Apr;39(4):1017-27 [15057906] Carcinogenesis. 1984 Aug;5(8):993-1001 [6430587] J Free Radic Biol Med. 1985;1(1):27-38 [3915301] J Exp Med. 1989 Sep 1;170(3):985-90 [2527946] J Pharmacol Exp Ther. 1990 Dec;255(3):1371-6 [2124623] J Pharmacol Exp Ther. 1990 Dec;255(3):1377-84 [1979817] Hepatology. 1991 May;13(5):815-9 [2029987] Mol Cell Biol. 1993 Jul;13(7):4365-73 [8391636] Hepatology. 1994 Apr;19(4):948-61 [8138270] J Clin Invest. 1995 Jul;96(1):620-30 [7615836] Mol Pharmacol. 1995 Nov;48(5):825-34 [7476912] Gastroenterology. 1996 Apr;110(4):1175-81 [8613007] Proc Natl Acad Sci U S A. 1996 Nov 12;93(23):12908-13 [8917518] Annu Rev Immunol. 1997;15:323-50 [9143691] Gastroenterology. 1998 Apr;114(4):764-74 [9516397] Gastroenterology. 1998 Apr;114(4):842-5 [9547102] Hepatology. 1998 Jun;27(6):1600-6 [9620333] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.freeradbiomed.2012.02.010 ER - TY - JOUR T1 - Immune activation in the pathogenesis of treated chronic HIV disease: a workshop summary. AN - 1010230997; 21854232 AB - With the advent of highly effective antiretroviral therapy (ART), infection with human immunodeficiency virus (HIV) has become a chronic disease rather than a death sentence. Nevertheless, effectively treated individuals have a higher than normal risk for developing noninfectious comorbidities, including cardiovascular and renal disease. Although traditional risk factors of aging as well as treatment toxicity contribute to this risk, many investigators consider chronic HIV-associated inflammation a significant factor in such end-organ disease. Despite effective viral suppression, chronic inflammation persists at levels higher than in uninfected people, yet the stimuli for the inflammation and the mechanism by which inflammation persists and promotes disease pathology remain incompletely understood. This critical gap in scientific understanding complicates and hampers effective decision making about appropriate medical intervention. To better understand the mechanism(s) of chronic immune activation in treated HIV disease, three questions need answers: (1) what is the cause of persistent immune activation during treated HIV infection, (2) what are the best surrogate markers of chronic immune activation in this setting, and (3) what therapeutic intervention(s) could prevent or reverse this process? The NIH sponsored and convened a meeting to discuss the state of knowledge concerning these questions and the best course for developing effective therapeutic strategies. This report summarizes the findings of that NIH meeting. JF - AIDS research and human retroviruses AU - Plaeger, Susan F AU - Collins, Brenda S AU - Musib, Runa AU - Deeks, Steven G AU - Read, Sarah AU - Embry, Alan AD - Division of AIDS, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. splaeger@niaid.nih.gov Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 469 EP - 477 VL - 28 IS - 5 KW - Anti-HIV Agents KW - 0 KW - Index Medicus KW - AIDS/HIV KW - Viral Load KW - Animals KW - Anti-HIV Agents -- therapeutic use KW - Risk Factors KW - Humans KW - Inflammation -- immunology KW - Primates KW - Simian Acquired Immunodeficiency Syndrome -- immunology KW - Acquired Immunodeficiency Syndrome -- complications KW - Kidney Diseases -- physiopathology KW - Acquired Immunodeficiency Syndrome -- physiopathology KW - Cardiovascular Diseases -- etiology KW - Simian Acquired Immunodeficiency Syndrome -- physiopathology KW - Intestinal Mucosa -- immunology KW - Kidney Diseases -- etiology KW - Simian Acquired Immunodeficiency Syndrome -- complications KW - Cardiovascular Diseases -- physiopathology KW - Cardiovascular Diseases -- immunology KW - Lymphocyte Activation -- immunology KW - Acquired Immunodeficiency Syndrome -- immunology KW - Kidney Diseases -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1010230997?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Immune+activation+in+the+pathogenesis+of+treated+chronic+HIV+disease%3A+a+workshop+summary.&rft.au=Plaeger%2C+Susan+F%3BCollins%2C+Brenda+S%3BMusib%2C+Runa%3BDeeks%2C+Steven+G%3BRead%2C+Sarah%3BEmbry%2C+Alan&rft.aulast=Plaeger&rft.aufirst=Susan&rft.date=2012-05-01&rft.volume=28&rft.issue=5&rft.spage=469&rft.isbn=&rft.btitle=&rft.title=AIDS+research+and+human+retroviruses&rft.issn=1931-8405&rft_id=info:doi/10.1089%2FAID.2011.0213 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-17 N1 - Date created - 2012-04-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Blood. 2011 Jul 28;118(4):847-54 [21505193] Science. 2006 Jun 9;312(5779):1530-3 [16763152] Immunology. 2007 Apr;120(4):526-35 [17343615] Mol Med. 2006 Nov-Dec;12(11-12):342-4 [17380202] Nat Immunol. 2000 Oct;1(4):285-9 [11017098] Br J Pharmacol. 2001 Jul;133(5):687-94 [11429393] Rev Med Virol. 2003 Jan-Feb;13(1):39-56 [12516061] Clin Liver Dis. 2003 Feb;7(1):89-105 [12691460] J Gen Virol. 2003 Jul;84(Pt 7):1649-61 [12810858] AIDS. 2003 Sep 5;17(13):1881-8 [12960820] Blood. 2004 Mar 15;103(6):2180-6 [14604962] Cell Signal. 2004 Nov;16(11):1201-10 [15337520] Mol Immunol. 2005 Feb;42(2):161-82 [15488606] J Immunol. 1987 Jun 1;138(11):3720-4 [2953790] Clin Exp Immunol. 1988 Aug;73(2):165-7 [3263225] N Engl J Med. 1990 Jan 18;322(3):166-72 [1967191] J Acquir Immune Defic Syndr. 1993 Aug;6(8):904-12 [7686224] J Clin Immunol. 1994 May;14(3):149-61 [7929692] J Acquir Immune Defic Syndr Hum Retrovirol. 1997 Oct 1;16(2):83-92 [9358102] Nature. 1998 Sep 17;395(6699):284-8 [9751057] Clin Diagn Lab Immunol. 1999 Jan;6(1):89-95 [9874670] J Infect Dis. 1999 Apr;179(4):859-70 [10068581] Immunol Today. 1999 Oct;20(10):446-50 [10500291] J Exp Med. 2006 Jun 12;203(6):1533-41 [16735692] Infection. 2006 Jun;34(3):186-8 [16804667] Immunol Cell Biol. 2007 Feb-Mar;85(2):85-92 [17213831] Blood. 2007 Apr 15;109(8):3351-9 [17158233] J Immunol. 2007 Sep 1;179(5):3047-56 [17709519] J Exp Med. 2007 Sep 3;204(9):2171-85 [17724130] J Immunol. 2007 Dec 15;179(12):8252-63 [18056369] J Virol. 2008 Feb;82(3):1155-65 [18045946] Nat Med. 2008 Mar;14(3):266-74 [18311149] Curr HIV/AIDS Rep. 2008 Feb;5(1):13-9 [18417030] Semin Immunol. 2008 Jun;20(3):181-6 [18595731] PLoS One. 2008;3(12):e3664 [19048100] Mucosal Immunol. 2008 Jan;1(1):23-30 [19079157] Curr HIV Res. 2009 Jan;7(1):57-72 [19149555] J Virol. 2009 Feb;83(4):1617-24 [19052081] AIDS Res Hum Retroviruses. 2009 Feb;25(2):183-91 [19239357] Nat Med. 2009 Aug;15(8):955-9 [19597505] Cytokine. 2010 Jan;49(1):1-9 [19775907] Clin Cancer Res. 2010 Feb 1;16(3):784-9 [20103670] Immunology. 2010 Mar;129(3):311-21 [20409152] Front Biosci (Elite Ed). 2010;2:1299-303 [20515802] Curr Opin HIV AIDS. 2010 Nov;5(6):498-503 [20978393] Cell. 2010 Nov 24;143(5):789-801 [21111238] Curr Opin HIV AIDS. 2011 Jan;6(1):30-6 [21242891] Nat Rev Immunol. 2011 Feb;11(2):131-42 [21267014] PLoS One. 2011;6(1):e15924 [21305005] AIDS Res Hum Retroviruses. 2011 Apr;27(4):355-64 [21309730] J Clin Invest. 2011 Mar;121(3):998-1008 [21393864] Curr HIV Res. 2011 Apr;9(3):148-53 [21457131] J Thromb Haemost. 2009 Jul;7 Suppl 1:136-9 [19630786] J Immunol. 2009 Apr 1;182(7):4313-20 [19299731] J Clin Invest. 2009 Dec;119(12):3544-55 [19959873] J Clin Invest. 2009 Dec;119(12):3556-72 [19959874] J Biol. 2009;8(10):93 [19943952] Immunol Lett. 2005 Feb 15;97(1):19-29 [15626472] J Immunol. 2006 Jun 1;176(11):6690-701 [16709828] J Immunol. 2010 Nov 1;185(9):5169-79 [20889546] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1089/AID.2011.0213 ER - TY - JOUR T1 - Monoclonal antibody-based candidate therapeutics against HIV type 1. AN - 1010230993; 21827278 AB - Treatment of HIV-1 infection has been highly successful with small molecule drugs. However, resistance still develops. In addition, long-term use can lead to toxicity with unpredictable effects on health. Finally, current drugs do not lead to HIV-1 eradication. The presence of the virus leads to chronic inflammation, which can result in increased morbidity and mortality after prolonged periods of infection. Monoclonal antibodies (mAbs) have been highly successful during the past two decades for therapy of many diseases, primarily cancers and immune disorders. They are relatively safe, especially human mAbs that have evolved in humans at high concentrations to fight diseases and long-term use may not lead to toxicities. Several broadly neutralizing mAbs (bnmAbs) against HIV-1 can protect animals but are not effective when used for therapy of an established infection. We have hypothesized that HIV-1 has evolved strategies to effectively escape neutralization by full-size antibodies in natural infections but not by smaller antibody fragments. Therefore, a promising direction of research is to discover and exploit antibody fragments as potential candidate therapeutics against HIV-1. Here we review several bnmAbs and engineered antibody domains (eAds), their in vitro and in vivo antiviral efficacy, mechanisms used by HIV-1 to escape them, and strategies that could be effective to develop more powerful mAb-based HIV-1 therapeutics. JF - AIDS research and human retroviruses AU - Chen, Weizao AU - Dimitrov, Dimiter S AD - Protein Interactions Group, Center for Cancer Research Nanobiology Program, National Cancer Institute (NCI)-Frederick, National Institutes of Health (NIH) , Frederick, MD 21702, USA. chenw3@mail.nih.gov Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 425 EP - 434 VL - 28 IS - 5 KW - Anti-HIV Agents KW - 0 KW - Antibodies, Monoclonal KW - HIV Antibodies KW - Index Medicus KW - AIDS/HIV KW - Animals KW - Macaca KW - Humans KW - Neutralization Tests KW - Mice KW - HIV-1 -- immunology KW - Anti-HIV Agents -- immunology KW - HIV Antibodies -- immunology KW - Anti-HIV Agents -- pharmacology KW - HIV Antibodies -- drug effects KW - Antibodies, Monoclonal -- pharmacology KW - HIV Seropositivity -- immunology KW - HIV-1 -- drug effects KW - HIV Seropositivity -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1010230993?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Monoclonal+antibody-based+candidate+therapeutics+against+HIV+type+1.&rft.au=Chen%2C+Weizao%3BDimitrov%2C+Dimiter+S&rft.aulast=Chen&rft.aufirst=Weizao&rft.date=2012-05-01&rft.volume=28&rft.issue=5&rft.spage=425&rft.isbn=&rft.btitle=&rft.title=AIDS+research+and+human+retroviruses&rft.issn=1931-8405&rft_id=info:doi/10.1089%2FAID.2011.0226 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-17 N1 - Date created - 2012-04-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochem Biophys Res Commun. 2006 Sep 29;348(3):1107-15 [16904645] J Immunol Methods. 2006 Dec 20;317(1-2):21-30 [17078964] Cancer. 2007 Jan 15;109(2):170-9 [17154393] Clin Vaccine Immunol. 2007 Feb;14(2):157-67 [17167037] J Immunol. 2007 Apr 1;178(7):4424-35 [17372000] J Virol. 2007 Apr;81(8):4033-43 [17287272] Virology. 2007 Apr 10;360(2):294-304 [17123566] Virology. 2007 Jun 20;363(1):79-90 [17306322] J Virol. 2007 Aug;81(16):8793-808 [17567707] Nature. 2007 Sep 6;449(7158):101-4 [17805298] Proc Natl Acad Sci U S A. 2008 Mar 11;105(10):3739-44 [18322015] Vaccine. 2008 Jun 6;26(24):3078-85 [18241961] J Virol. 2008 Jul;82(14):6869-79 [18480433] J Virol. 2008 Oct;82(20):10032-41 [18667502] J Infect Dis. 2008 Nov 1;198(9):1345-52 [18771406] Proc Natl Acad Sci U S A. 2008 Nov 4;105(44):17121-6 [18957538] Protein Sci. 2008 Dec;17(12):2091-100 [18802030] J Virol. 2008 Dec;82(24):12069-81 [18842738] J Biol Chem. 2009 Feb 20;284(8):5175-85 [19097993] J Virol. 2011 Sep;85(18):9395-405 [21715496] J Virol. 2011 Nov;85(21):11401-8 [21880764] Nat Med. 2000 Feb;6(2):200-6 [10655110] Nat Med. 2000 Feb;6(2):207-10 [10655111] J Virol. 2004 Sep;78(17):9233-42 [15308718] Cancer Res. 1988 Dec 15;48(24 Pt 1):7022-32 [3191477] J Virol. 1992 Aug;66(8):4784-93 [1378510] J Immunol. 1992 Sep 1;149(5):1779-87 [1380539] J Virol. 1994 Aug;68(8):4821-8 [7518527] J Exp Med. 1994 Sep 1;180(3):885-95 [8064239] AIDS Res Hum Retroviruses. 1994 Apr;10(4):359-69 [7520721] AIDS. 1995 Jun;9(6):F1-6 [7662189] J Virol. 1996 Feb;70(2):1100-8 [8551569] AIDS Res Hum Retroviruses. 1997 May 20;13(8):647-56 [9168233] AIDS Res Hum Retroviruses. 1997 Jul 20;13(11):933-43 [9223409] J Virol. 1998 Apr;72(4):3235-40 [9525650] AIDS Res Hum Retroviruses. 1998 May 1;14(7):545-50 [9591708] Nature. 1998 Jun 18;393(6686):648-59 [9641677] J Virol. 1999 May;73(5):4009-18 [10196297] J Virol. 1999 May;73(5):4145-55 [10196311] J Antimicrob Chemother. 2004 Nov;54(5):915-20 [15456731] J Virol. 2004 Dec;78(23):13232-52 [15542675] J Biol Chem. 2005 Apr 1;280(13):12567-72 [15657041] Biochim Biophys Acta. 2009 Mar;1788(3):660-5 [19100711] J Virol. 2001 Jan;75(2):579-88 [11134270] J Virol. 2001 Jan;75(2):645-53 [11134278] J Virol. 2001 Feb;75(3):1165-71 [11152489] J Virol. 2001 Sep;75(17):8340-7 [11483779] AIDS. 2002 Jan 25;16(2):227-33 [11807307] Toxicology. 2002 Apr 2;172(3):191-203 [11893418] Proc Natl Acad Sci U S A. 2002 May 14;99(10):6913-8 [11997472] AIDS Res Hum Retroviruses. 2002 Jul 20;18(11):747-55 [12167266] AIDS. 2003 Feb 14;17(3):301-9 [12556683] J Virol. 2003 Mar;77(5):2859-65 [12584309] Nat Med. 2003 Mar;9(3):343-6 [12579198] Nature. 2003 Mar 20;422(6929):307-12 [12646921] Vaccine. 2003 Jul 28;21(24):3370-3 [12850342] J Virol. 2003 Oct;77(19):10557-65 [12970440] J Immunol Methods. 2003 Dec;283(1-2):17-25 [14659896] J Mol Biol. 2004 Jan 2;335(1):209-19 [14659751] J Infect Dis. 2004 Jan 15;189(2):286-91 [14722894] AIDS Res Hum Retroviruses. 2004 Jul;20(7):755-62 [15307922] Methods Mol Biol. 2009;525:1-27, xiii [19252861] Curr Opin HIV AIDS. 2009 Mar;4(2):112-7 [19339949] Proc Natl Acad Sci U S A. 2009 May 5;106(18):7385-90 [19372381] PLoS Pathog. 2009 May;5(5):e1000433 [19436712] J Virol. 2009 Sep;83(17):8451-62 [19515770] Antiviral Res. 2009 Sep;83(3):257-66 [19559732] Science. 2009 Oct 9;326(5950):285-9 [19729618] Virology. 2009 Nov 10;394(1):91-8 [19744690] Proc Natl Acad Sci U S A. 2009 Dec 1;106(48):20234-9 [19906992] Science. 2009 Nov 20;326(5956):1123-7 [19965434] J Virol. 2010 Jan;84(1):261-9 [19864392] MAbs. 2009 Sep-Oct;1(5):462-74 [20065653] Proc Natl Acad Sci U S A. 2010 Jan 5;107(1):181-6 [20018688] PLoS One. 2010;5(1):e8805 [20098712] Retrovirology. 2010;7:11 [20158904] MAbs. 2010 May-Jun;2(3):266-74 [20305395] Science. 2010 Aug 13;329(5993):856-61 [20616233] Antiviral Res. 2010 Oct;88(1):107-15 [20709110] Nat Med. 2005 Jun;11(6):615-22 [15880120] Curr Drug Targets Infect Disord. 2005 Jun;5(2):95-111 [15975016] Science. 2005 Jun 24;308(5730):1906-8 [15860590] Expert Opin Biol Ther. 2006 May;6(5):523-31 [16610981] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1089/AID.2011.0226 ER - TY - JOUR T1 - Analysis of chromatin dynamics during glucocorticoid receptor activation. AN - 1010230197; 22451486 AB - Steroid hormone receptors initiate a genetic program tightly regulated by the chromatin environment of the responsive regions. Using the glucocorticoid receptor (GR) as a model factor for transcriptional initiation, we classified chromatin structure through formaldehyde-assisted isolation of regulatory elements (FAIRE). We looked at dynamic changes in FAIRE signals during GR activation specifically at regions of receptor interaction. We found a distribution of GR-responsive regions with diverse responses to activation and chromatin modulation. The majority of GR binding regions demonstrate increases in FAIRE signal in response to ligand. However, the majority GR-responsive regions shared a similar FAIRE signal in the basal chromatin state, suggesting a common chromatin structure for GR recruitment. Supporting this notion, global FAIRE sequencing (seq) data indicated an enrichment of signal surrounding the GR binding site prior to activation. Brg-1 knockdown showed response element-specific effects of ATPase-dependent chromatin remodeling. FAIRE induction was universally decreased by Brg-1 depletion, but to varying degrees in a target specific manner. Taken together, these data suggest classes of nuclear receptor response regions that react to activation through different chromatin regulatory events and identify a chromatin structure that classifies the majority of response elements tested. JF - Molecular and cellular biology AU - Burd, Craig J AU - Ward, James M AU - Crusselle-Davis, Valerie J AU - Kissling, Grace E AU - Phadke, Dhiral AU - Shah, Ruchir R AU - Archer, Trevor K AD - Chromatin and Gene Expression Group, Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 1805 EP - 1817 VL - 32 IS - 10 KW - Chromatin KW - 0 KW - Ligands KW - Receptors, Glucocorticoid KW - Formaldehyde KW - 1HG84L3525 KW - Index Medicus KW - Humans KW - Chromatin Assembly and Disassembly KW - Cell Line, Tumor KW - Response Elements -- physiology KW - Protein Binding KW - Binding Sites KW - Chromatin -- metabolism KW - Chromatin -- chemistry KW - Receptors, Glucocorticoid -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1010230197?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+and+cellular+biology&rft.atitle=Analysis+of+chromatin+dynamics+during+glucocorticoid+receptor+activation.&rft.au=Burd%2C+Craig+J%3BWard%2C+James+M%3BCrusselle-Davis%2C+Valerie+J%3BKissling%2C+Grace+E%3BPhadke%2C+Dhiral%3BShah%2C+Ruchir+R%3BArcher%2C+Trevor+K&rft.aulast=Burd&rft.aufirst=Craig&rft.date=2012-05-01&rft.volume=32&rft.issue=10&rft.spage=1805&rft.isbn=&rft.btitle=&rft.title=Molecular+and+cellular+biology&rft.issn=1098-5549&rft_id=info:doi/10.1128%2FMCB.06206-11 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-07-05 N1 - Date created - 2012-04-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 2008 Dec 12;283(50):34976-82 [18922793] J Cell Biochem. 2008 Aug 1;104(5):1580-6 [18393355] Genome Biol. 2009;10(3):R25 [19261174] Genes Dev. 2009 Jul 1;23(13):1522-33 [19515975] Methods. 2009 Jul;48(3):233-9 [19303047] Mol Cell Biol. 2009 Oct;29(20):5413-25 [19687299] Genome Res. 2009 Dec;19(12):2163-71 [19801529] Cold Spring Harb Protoc. 2009 Sep;2009(9):pdb.prot5279 [20147264] Mol Cell. 2010 May 28;38(4):576-89 [20513432] Mol Cell. 2010 May 28;38(4):590-602 [20513433] Curr Opin Pharmacol. 2010 Dec;10(6):620-8 [20926342] Nat Rev Genet. 2011 Jan;12(1):7-18 [21116306] Nat Genet. 2011 Mar;43(3):264-8 [21258342] Cell. 2011 Aug 19;146(4):544-54 [21835447] Nature. 2001 Feb 15;409(6822):860-921 [11237011] Trends Endocrinol Metab. 2001 Jul;12(5):191-7 [11397643] Oncogene. 2001 May 28;20(24):3047-54 [11420720] J Biol Chem. 2001 Oct 26;276(43):39885-91 [11518712] Mol Cell. 2002 Feb;9(2):279-89 [11864602] Mol Cell Biol. 2004 Apr;24(8):3347-58 [15060156] Vitam Horm. 2004;68:93-122 [15193452] Essays Biochem. 2004;40:73-88 [15242340] Cell. 1983 May;33(1):65-76 [6088056] Cell. 1984 Aug;38(1):29-38 [6088072] EMBO J. 1991 Sep;10(9):2569-76 [1678348] Science. 1992 Mar 20;255(5051):1573-6 [1347958] Science. 1992 Dec 4;258(5088):1598-604 [1360703] EMBO J. 1993 Nov;12(11):4279-90 [8223438] Mol Cell Biol. 1994 Jan;14(1):32-41 [8264599] Cold Spring Harb Symp Quant Biol. 1993;58:63-71 [7956078] Mol Endocrinol. 1994 Sep;8(9):1154-62 [7838148] Trends Biochem Sci. 1995 Apr;20(4):143-6 [7770913] Science. 1996 Jul 26;273(5274):513-6 [8662543] Cell Mol Neurobiol. 1996 Apr;16(2):85-101 [8743962] Nature. 1998 May 7;393(6680):88-91 [9590696] Mol Endocrinol. 2005 Jun;19(6):1429-38 [15914712] J Cell Sci. 2006 Oct 1;119(Pt 19):4101-16 [16968748] J Biol Chem. 2007 Mar 16;282(11):8284-91 [17186943] Genome Res. 2007 Jun;17(6):877-85 [17179217] PLoS Genet. 2007 Aug;3(8):e136 [17708682] Mol Cell Biol. 2008 Feb;28(4):1413-26 [18086889] Nucl Recept Signal. 2008;6:e004 [18301784] Nucl Recept Signal. 2008;6:e005 [18301785] Mol Cell. 2008 Mar 14;29(5):611-24 [18342607] Genome Res. 2009 Mar;19(3):372-80 [19129543] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1128/MCB.06206-11 ER - TY - JOUR T1 - Adaptation of a genotype 3 hepatitis E virus to efficient growth in cell culture depends on an inserted human gene segment acquired by recombination. AN - 1009812519; 22398290 AB - An infectious cDNA clone of a genotype 3 strain of hepatitis E virus adapted to growth in HepG2/C3A human hepatoma cells was constructed. This virus was unusual in that the hypervariable region of the adapted virus contained a 171-nucleotide insertion that encoded 58 amino acids of human S17 ribosomal protein. Analyses of virus from six serial passages indicated that genomes with this insert, although initially rare, were selected during the first passage, suggesting it conferred a significant growth advantage. RNA transcripts from this cDNA and the viruses encoded by them were infectious for cells of both human and swine origin, the major host species for this zoonotic virus. Mutagenesis studies demonstrated that the S17 insert was a major factor in cell culture adaptation. Introduction of 54 synonymous mutations into the insert had no detectable effect, thus implicating protein, rather than RNA, as the important component. Truncation of the insert by 50% decreased the levels of successful transfection by ~3-fold. Substitution of the S17 sequence by a different ribosomal protein sequence or by GTPase-activating protein sequence resulted in a partial enhancement of transfection levels, whereas substitution with 58 amino acids of green fluorescent protein had no effect. Therefore, both the sequence length and the amino acid composition of the insert were important. The S17 sequence did not affect transfection of human hepatoma cells when inserted into the hypervariable region of a genotype 1 strain, but this chimeric genome acquired a dramatic ability to replicate in hamster cells. JF - Journal of virology AU - Shukla, P AU - Nguyen, H T AU - Faulk, K AU - Mather, K AU - Torian, U AU - Engle, R E AU - Emerson, S U AD - Molecular Hepatitis and Hepatitis Viruses Sections, Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 5697 EP - 5707 VL - 86 IS - 10 KW - Ribosomal Proteins KW - 0 KW - ribosomal protein S17 KW - Index Medicus KW - Swine KW - Genotype KW - Animals KW - Humans KW - Molecular Sequence Data KW - Cell Line, Tumor KW - Hepatitis E virus -- isolation & purification KW - Ribosomal Proteins -- metabolism KW - Ribosomal Proteins -- genetics KW - Hepatitis E -- metabolism KW - Hepatitis E virus -- growth & development KW - Hepatitis E virus -- classification KW - Recombination, Genetic KW - Hepatitis E virus -- genetics KW - Hepatitis E -- genetics KW - Hepatitis E -- virology KW - Mutagenesis, Insertional UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1009812519?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Adaptation+of+a+genotype+3+hepatitis+E+virus+to+efficient+growth+in+cell+culture+depends+on+an+inserted+human+gene+segment+acquired+by+recombination.&rft.au=Shukla%2C+P%3BNguyen%2C+H+T%3BFaulk%2C+K%3BMather%2C+K%3BTorian%2C+U%3BEngle%2C+R+E%3BEmerson%2C+S+U&rft.aulast=Shukla&rft.aufirst=P&rft.date=2012-05-01&rft.volume=86&rft.issue=10&rft.spage=5697&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=1098-5514&rft_id=info:doi/10.1128%2FJVI.00146-12 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-18 N1 - Date created - 2012-04-25 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - JQ679021; GENBANK; JQ679022; JQ679020; JQ679015; JQ679024; JQ679014; JQ679023; JQ679013; JQ679025; JQ679019; JQ679018; JQ679017; JQ679016 N1 - SuppNotes - Cited By: Emerg Infect Dis. 2009 Jan;15(1):110-4 [19116067] J Virol. 2009 Jan;83(1):384-95 [18945785] J Clin Microbiol. 2009 Jun;47(6):1906-10 [19369433] J Gen Virol. 2009 Aug;90(Pt 8):1880-91 [19339479] N Engl J Med. 2009 Sep 3;361(10):1025-7 [19726781] Vet Microbiol. 2010 Jan 27;140(3-4):256-65 [19361937] Am J Transplant. 2010 May;10(5):1321-4 [20346067] Vet Res. 2010 Nov-Dec;41(6):46 [20359452] Minerva Gastroenterol Dietol. 2010 Jun;56(2):121-8 [20485250] Virol J. 2010;7:129 [20546601] J Virol. 2010 Sep;84(18):9059-69 [20610720] J Gen Virol. 2011 Feb;92(Pt 2):269-78 [21068219] Emerg Infect Dis. 2011 Feb;17(2):173-9 [21291585] Rev Med Virol. 2011 Jan;21(1):18-31 [21294213] Proc Natl Acad Sci U S A. 2011 Feb 8;108(6):2438-43 [21262830] Gastroenterology. 2011 May;140(5):1481-9 [21354150] J Gen Virol. 2011 Sep;92(Pt 9):2088-92 [21653754] J Virol. 2011 Oct;85(19):10031-40 [21775444] Virus Res. 2011 Oct;161(1):47-58 [21345356] J Gen Virol. 2012 Mar;93(Pt 3):526-30 [22113007] Proc Natl Acad Sci U S A. 2001 Dec 18;98(26):15270-5 [11742081] Nucleic Acids Res. 2003 Jul 1;31(13):3406-15 [12824337] J Virol. 2004 May;78(9):4838-46 [15078965] Nature. 1989 Jul 13;340(6229):156-7 [2544809] Virology. 1991 Feb;180(2):602-16 [1846490] J Virol. 1994 Oct;68(10):6547-52 [8083991] J Virol. 2005 Jun;79(11):6680-9 [15890906] J Virol. 2006 Jun;80(12):5919-26 [16731930] J Gastroenterol Hepatol. 2006 Jul;21(7):1223-4 [16824086] J Gen Virol. 2007 Mar;88(Pt 3):903-11 [17325363] J Gen Virol. 2009 Feb;90(Pt 2):457-62 [19141456] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1128/JVI.00146-12 ER - TY - JOUR T1 - CLIC4 is a tumor suppressor for cutaneous squamous cell cancer. AN - 1009812279; 22387366 AB - Chloride intracellular channel (CLIC) 4 is a member of a redox-regulated, metamorphic multifunctional protein family, first characterized as intracellular chloride channels. Current knowledge indicates that CLICs participate in signaling, cytoskeleton integrity and differentiation functions of multiple tissues. In metabolically stressed skin keratinocytes, cytoplasmic CLIC4 is S-nitrosylated and translocates to the nucleus where it enhances transforming growth factor-β (TGF-β) signaling by protecting phospho-Smad 2 and 3 from dephosphorylation. CLIC4 expression is diminished in multiple human epithelial cancers, and the protein is excluded from the nucleus. We now show that CLIC4 expression is reduced in chemically induced mouse skin papillomas, mouse and human squamous carcinomas and squamous cancer cell lines, and the protein is excluded from the nucleus. The extent of reduction in CLIC4 coincides with progression of squamous tumors from benign to malignant. Inhibiting antioxidant defense in tumor cells increases S-nitrosylation and nuclear translocation of CLIC4. Adenoviral-mediated reconstitution of nuclear CLIC4 in squamous cancer cells enhances TGF-β-dependent transcriptional activity and inhibits growth. Adenoviral targeting of CLIC4 to the nucleus of tumor cells in orthografts inhibits tumor growth, whereas elevation of CLIC4 in transgenic epidermis reduces de novo chemically induced skin tumor formation. In parallel, overexpression of exogenous CLIC4 in squamous tumor orthografts suppresses tumor growth and enhances TGF-β signaling. These results indicate that CLIC4 suppresses the growth of squamous cancers, that reduced CLIC4 expression and nuclear residence detected in cancer cells is associated with the altered redox state of tumor cells and the absence of detectable nuclear CLIC4 in cancers contributes to TGF-β resistance and enhances tumor development. JF - Carcinogenesis AU - Suh, K Stephen AU - Malik, Mariam AU - Shukla, Anjali AU - Ryscavage, Andrew AU - Wright, Lisa AU - Jividen, Kasey AU - Crutchley, John M AU - Dumont, Rebecca A AU - Fernandez-Salas, Ester AU - Webster, Joshua D AU - Simpson, R Mark AU - Yuspa, Stuart H AD - Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892, USA. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 986 EP - 995 VL - 33 IS - 5 KW - CLIC protein, mouse KW - 0 KW - CLIC4 protein, human KW - Chloride Channels KW - Mitochondrial Proteins KW - Transforming Growth Factor beta KW - Tumor Suppressor Proteins KW - Index Medicus KW - Animals KW - Cell Nucleus -- metabolism KW - Cell Transformation, Neoplastic -- metabolism KW - Humans KW - Cell Line, Tumor KW - Mice KW - Papilloma -- genetics KW - Mice, Inbred BALB C KW - Fibroblasts -- metabolism KW - Oxidation-Reduction KW - Keratinocytes -- metabolism KW - Mice, Inbred SENCAR KW - Transforming Growth Factor beta -- genetics KW - Transforming Growth Factor beta -- metabolism KW - Signal Transduction KW - Papilloma -- metabolism KW - Cell Nucleus -- genetics KW - Cell Transformation, Neoplastic -- genetics KW - Male KW - Protein Transport KW - Tumor Suppressor Proteins -- biosynthesis KW - Skin Neoplasms -- genetics KW - Mitochondrial Proteins -- biosynthesis KW - Tumor Suppressor Proteins -- metabolism KW - Tumor Suppressor Proteins -- genetics KW - Mitochondrial Proteins -- genetics KW - Chloride Channels -- metabolism KW - Neoplasms, Squamous Cell -- genetics KW - Chloride Channels -- biosynthesis KW - Mitochondrial Proteins -- metabolism KW - Skin Neoplasms -- metabolism KW - Neoplasms, Squamous Cell -- metabolism KW - Chloride Channels -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1009812279?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=CLIC4+is+a+tumor+suppressor+for+cutaneous+squamous+cell+cancer.&rft.au=Suh%2C+K+Stephen%3BMalik%2C+Mariam%3BShukla%2C+Anjali%3BRyscavage%2C+Andrew%3BWright%2C+Lisa%3BJividen%2C+Kasey%3BCrutchley%2C+John+M%3BDumont%2C+Rebecca+A%3BFernandez-Salas%2C+Ester%3BWebster%2C+Joshua+D%3BSimpson%2C+R+Mark%3BYuspa%2C+Stuart+H&rft.aulast=Suh&rft.aufirst=K&rft.date=2012-05-01&rft.volume=33&rft.issue=5&rft.spage=986&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgs115 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-10 N1 - Date created - 2012-04-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochem J. 2001 Oct 1;359(Pt 1):55-64 [11563969] Curr Pharm Biotechnol. 2011 Dec;12(12):2138-49 [21619543] Am J Pathol. 2002 Aug;161(2):471-80 [12163372] Mol Membr Biol. 2003 Jan-Mar;20(1):1-11 [12745921] Cell Motil Cytoskeleton. 2003 Nov;56(3):159-72 [14569596] J Biol Chem. 2004 Feb 6;279(6):4632-41 [14610078] Nat Biotechnol. 2004 Apr;22(4):411-7 [15024388] FEBS Lett. 2004 May 21;566(1-3):136-40 [15147883] Exp Eye Res. 2004 Aug;79(2):239-47 [15325571] J Biol Chem. 1999 Jan 15;274(3):1621-7 [9880541] J Neurosci. 1999 Apr 15;19(8):2919-28 [10191309] Cancer Res. 2005 Jan 15;65(2):562-71 [15695400] World J Gastroenterol. 2005 Jun 14;11(22):3351-6 [15948238] Curr Pharm Des. 2005;11(21):2753-64 [16101453] Cell. 2005 Sep 9;122(5):707-21 [16143103] FEBS J. 2005 Oct;272(19):4996-5007 [16176272] Cell. 2005 Sep 23;122(6):947-56 [16153702] Curr Opin Struct Biol. 2005 Dec;15(6):716-23 [16263269] J Biol Chem. 1999 Dec 17;274(51):36488-97 [10593946] Biochem Biophys Res Commun. 2001 Sep 21;287(2):435-9 [11554747] J Biol Chem. 2005 Dec 23;280(51):42397-404 [16239224] J Biol Chem. 2006 Feb 3;281(5):2750-6 [16316993] Biophys J. 2006 Mar 1;90(5):1628-38 [16339885] Cell Death Differ. 2006 Jul;13(7):1138-46 [16224490] J Mol Biol. 2006 Jun 23;359(5):1316-33 [16737711] Cancer Cell. 2006 Sep;10(3):241-52 [16959615] J Immunol. 2006 Nov 15;177(10):6952-61 [17082610] Clin Cancer Res. 2007 Jan 1;13(1):121-31 [17200346] Cancer Res. 2007 Apr 1;67(7):3450-60 [17409456] J Cell Sci. 2007 Aug 1;120(Pt 15):2631-40 [17636002] Mol Carcinog. 2007 Aug;46(8):599-604 [17443730] Curr Opin Pharmacol. 2007 Aug;7(4):392-7 [17611157] Oncogene. 2007 Oct 18;26(48):6885-95 [17525749] PLoS One. 2007;2(10):e1112 [17971875] Proteins. 2008 Apr;71(1):364-78 [17985355] Toxicol Appl Pharmacol. 2008 Mar 15;227(3):400-16 [18191166] Nat Protoc. 2008;3(5):799-810 [18451788] Antioxid Redox Signal. 2008 Aug;10(8):1343-74 [18522489] J Neurosci Res. 2008 Aug 15;86(11):2488-98 [18438938] Antioxid Redox Signal. 2008 Oct;10(10):1675-86 [18522493] Mol Nutr Food Res. 2009 Jan;53(1):87-103 [18979503] Am J Pathol. 2009 Mar;174(3):1084-96 [19197003] Nat Cell Biol. 2009 Jun;11(6):777-84 [19448624] Mol Biol Cell. 2009 Nov;20(22):4664-72 [19776349] FEBS Lett. 2010 May 17;584(10):2093-101 [20085760] Methods Enzymol. 2010;474:255-75 [20609915] J Biol Chem. 2010 Jul 30;285(31):23818-28 [20504765] FEBS J. 2011 May;278(10):1662-75 [21388519] Mol Cell Biol. 2002 Jun;22(11):3610-20 [11997498] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/carcin/bgs115 ER - TY - JOUR T1 - A multicenter phase III prospective randomized trial of high-dose epirubicin in combination with cyclophosphamide (EC) versus docetaxel followed by EC in node-positive breast cancer. GOIM (Gruppo Oncologico Italia Meridionale) 9902 study. AN - 1009801719; 21965475 AB - The Gruppo Oncologico Italia Meridionale 9902 trial compared four cycles of high-dose epirubicin plus cyclophosphamide (EC) with four cycles of docetaxel (Taxotere, D) followed by four cycles of EC as adjuvant treatment of node-positive breast cancer. Patients were randomly assigned to EC (E 120 mg/m(2), C 600 mg/m(2), arm A) for four cycles or four cycles of D (100 mg/m(2)) followed by four cycles of EC (arm B), both regimens every 21 days. Hormone receptor-positive patients were given hormonal therapy for 5 years. Primary end point was 5-year disease-free survival (DFS). Secondary objectives were overall survival (OS) and safety. There were 750 patients enrolled. With a median follow-up of 64 months, 5-year DFS was 73.4% in both arms, and 5-year OS was 89.5% versus 90.7% in arm A and B [hazard ratio was 0.99 (95% confidence interval for DFS 0.75-1.31; P = 0.95)], respectively. Grade 3-4 toxicity was more common in arm B. This study did not show advantages from the addition of docetaxel to high-dose EC as adjuvant chemotherapy in node-positive breast cancer. The small sample size and low number of DFS events may have limited the ability to observe statistically significant difference between the two arms. JF - Annals of oncology : official journal of the European Society for Medical Oncology AU - Vici, P AU - Brandi, M AU - Giotta, F AU - Foggi, P AU - Schittulli, F AU - Di Lauro, L AU - Gebbia, N AU - Massidda, B AU - Filippelli, G AU - Giannarelli, D AU - Di Benedetto, A AU - Mottolese, M AU - Colucci, G AU - Lopez, M AD - Division of Medical Oncology B, Regina Elena National Cancer Institute, Rome, Italy. pvici@ifo.it Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 1121 EP - 1129 VL - 23 IS - 5 KW - Taxoids KW - 0 KW - docetaxel KW - 15H5577CQD KW - Epirubicin KW - 3Z8479ZZ5X KW - Cyclophosphamide KW - 8N3DW7272P KW - Index Medicus KW - Disease-Free Survival KW - Prospective Studies KW - Lymphatic Metastasis KW - Dose-Response Relationship, Drug KW - Humans KW - Adult KW - Lymph Nodes -- pathology KW - Algorithms KW - Middle Aged KW - Italy KW - Female KW - Survival Analysis KW - Breast Neoplasms -- drug therapy KW - Cyclophosphamide -- administration & dosage KW - Taxoids -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Epirubicin -- adverse effects KW - Antineoplastic Combined Chemotherapy Protocols -- adverse effects KW - Taxoids -- administration & dosage KW - Cyclophosphamide -- adverse effects KW - Breast Neoplasms -- mortality KW - Breast Neoplasms -- pathology KW - Carcinoma -- pathology KW - Carcinoma -- drug therapy KW - Epirubicin -- administration & dosage KW - Carcinoma -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1009801719?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Annals+of+oncology+%3A+official+journal+of+the+European+Society+for+Medical+Oncology&rft.atitle=A+multicenter+phase+III+prospective+randomized+trial+of+high-dose+epirubicin+in+combination+with+cyclophosphamide+%28EC%29+versus+docetaxel+followed+by+EC+in+node-positive+breast+cancer.+GOIM+%28Gruppo+Oncologico+Italia+Meridionale%29+9902+study.&rft.au=Vici%2C+P%3BBrandi%2C+M%3BGiotta%2C+F%3BFoggi%2C+P%3BSchittulli%2C+F%3BDi+Lauro%2C+L%3BGebbia%2C+N%3BMassidda%2C+B%3BFilippelli%2C+G%3BGiannarelli%2C+D%3BDi+Benedetto%2C+A%3BMottolese%2C+M%3BColucci%2C+G%3BLopez%2C+M&rft.aulast=Vici&rft.aufirst=P&rft.date=2012-05-01&rft.volume=23&rft.issue=5&rft.spage=1121&rft.isbn=&rft.btitle=&rft.title=Annals+of+oncology+%3A+official+journal+of+the+European+Society+for+Medical+Oncology&rft.issn=1569-8041&rft_id=info:doi/10.1093%2Fannonc%2Fmdr412 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-07 N1 - Date created - 2012-04-25 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Clin Oncol. 2001 Jul 15;19(14):3367-75 [11454884] Br J Cancer. 2002 Mar 4;86(5):692-7 [11875727] Ann Oncol. 2002 Aug;13(8):1225-35 [12181246] Ann Oncol. 2003 Mar;14(3):433-40 [12598350] J Clin Oncol. 2003 Mar 15;21(6):976-83 [12637460] J Clin Oncol. 2003 Sep 15;21(18):3462-8 [12972521] Clin Breast Cancer. 2003 Oct;4(4):286-91 [14651774] Ann Oncol. 2004 Mar;15(3):433-9 [14998845] Biometrics. 1975 Mar;31(1):103-15 [1100130] J Clin Oncol. 1985 Jun;3(6):818-26 [3859587] J Clin Oncol. 1988 Apr;6(4):679-88 [2895801] J Clin Oncol. 1988 Jun;6(6):976-82 [2897433] J Clin Oncol. 1990 Sep;8(9):1483-96 [2202791] J Clin Oncol. 1996 Apr;14(4):1146-55 [8648369] J Clin Oncol. 1998 Jan;16(1):86-92 [9440727] Lancet. 1998 Sep 19;352(9132):930-42 [9752815] J Clin Oncol. 1999 Jan;17(1):93-100 [10458222] Lancet. 2005 May 14-20;365(9472):1687-717 [15894097] Ann Oncol. 2005 Jun;16(6):915-22 [15894546] N Engl J Med. 2005 Jun 2;352(22):2302-13 [15930421] Ann Oncol. 2005 Nov;16(11):1762-71 [16148021] N Engl J Med. 2006 Feb 23;354(8):809-20 [16495393] J Clin Oncol. 2006 May 1;24(13):2019-27 [16606972] Cancer. 2006 Jun 1;106(11):2337-44 [16649217] J Clin Oncol. 2006 Dec 20;24(36):5664-71 [17116941] Ann Oncol. 2007 Jan;18(1):52-7 [17047001] J Clin Oncol. 2007 May 20;25(15):2127-32 [17513820] Cochrane Database Syst Rev. 2007;(4):CD004421 [17943815] J Clin Oncol. 2008 Jan 1;26(1):44-53 [18165639] J Natl Cancer Inst. 2008 Jan 16;100(2):121-33 [18182617] J Clin Oncol. 2008 Apr 1;26(10):1691-7 [18316792] J Clin Oncol. 2008 Jun 1;26(16):2636-43 [18509176] J Natl Cancer Inst. 2008 Jun 4;100(11):805-14 [18505968] J Clin Oncol. 2008 Sep 1;26(25):4092-9 [18678836] Breast Cancer Res Treat. 2009 Mar;114(1):103-12 [18344024] J Clin Oncol. 2009 Feb 10;27(5):720-5 [19103732] Breast Cancer Res Treat. 2009 Apr;114(3):479-84 [18463977] J Clin Oncol. 2009 Mar 10;27(8):1177-83 [19204201] Lancet. 2009 May 16;373(9676):1681-92 [19447249] J Clin Oncol. 2009 May 20;27(15):2474-81 [19332727] Cancer Invest. 2009 Jun;27(5):489-95 [19479486] Breast Cancer Res. 2009;11(2):204 [19344489] Breast Cancer Res Treat. 2010 Jan;119(1):95-104 [19636702] J Clin Oncol. 2010 Jan 1;28(1):77-82 [19901117] Oncology. 2010;78(3-4):274-81 [20530973] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/annonc/mdr412 ER - TY - JOUR T1 - Genome-wide association study identifies three common variants associated with serologic response to vitamin E supplementation in men. AN - 1009133177; 22437554 AB - Vitamin E inhibits lipid peroxidation in cell membranes, prevents oxidative damage to DNA by scavenging free radicals, and reduces carcinogen production. No study to our knowledge, however, has examined the association between genetic variants and response to long-term vitamin E supplementation. We conducted a genome-wide association study (GWAS) of common variants associated with circulating α-tocopherol concentrations following 3 y of controlled supplementation. The study population included 2112 middle-aged, male smokers in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study cohort who received a trial supplementation of α-tocopherol (50 mg/d) and had fasting serum α-tocopherol concentrations measured after 3 y. Serum concentrations were log-transformed for statistical analysis and general linear models adjusted for age, BMI, serum total cholesterol, and cancer case status. Associations with serum response to α-tocopherol supplementation achieved genome-wide significance for 2 single nucleotide polymorphisms (SNP): rs964184 on 11q23.3 (P = 2.6 × 10(-12)) and rs2108622 on 19pter-p13.11 (P = 2.2 × 10(-7)), and approached genome-wide significance for one SNP, rs7834588 on 8q12.3 (P = 6.2 × 10(-7)). Combined, these SNP explain 3.4% of the residual variance in serum α-tocopherol concentrations during controlled vitamin E supplementation. A GWAS has identified 3 genetic variants at different loci that appear associated with serum concentrations after vitamin E supplementation in men. Identifying genetic variants that influence serum nutrient biochemical status (e.g., α-tocopherol) under supplementation conditions improves our understanding of the biological determinants of these nutritional exposures and their associations with cancer etiology. JF - The Journal of nutrition AU - Major, Jacqueline M AU - Yu, Kai AU - Chung, Charles C AU - Weinstein, Stephanie J AU - Yeager, Meredith AU - Wheeler, William AU - Snyder, Kirk AU - Wright, Margaret E AU - Virtamo, Jarmo AU - Chanock, Stephen AU - Albanes, Demetrius AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD, USA. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 866 EP - 871 VL - 142 IS - 5 KW - Vitamins KW - 0 KW - beta Carotene KW - 01YAE03M7J KW - alpha-Tocopherol KW - H4N855PNZ1 KW - Index Medicus KW - beta Carotene -- administration & dosage KW - Phenotype KW - Genotype KW - Genetic Variation KW - Vitamins -- blood KW - beta Carotene -- blood KW - Genetic Predisposition to Disease -- genetics KW - Humans KW - Vitamins -- administration & dosage KW - Aged KW - Middle Aged KW - Male KW - Polymorphism, Single Nucleotide KW - alpha-Tocopherol -- blood KW - alpha-Tocopherol -- administration & dosage KW - Neoplasms -- prevention & control KW - Neoplasms -- genetics KW - Neoplasms -- metabolism KW - Genome-Wide Association Study UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1009133177?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+nutrition&rft.atitle=Genome-wide+association+study+identifies+three+common+variants+associated+with+serologic+response+to+vitamin+E+supplementation+in+men.&rft.au=Major%2C+Jacqueline+M%3BYu%2C+Kai%3BChung%2C+Charles+C%3BWeinstein%2C+Stephanie+J%3BYeager%2C+Meredith%3BWheeler%2C+William%3BSnyder%2C+Kirk%3BWright%2C+Margaret+E%3BVirtamo%2C+Jarmo%3BChanock%2C+Stephen%3BAlbanes%2C+Demetrius&rft.aulast=Major&rft.aufirst=Jacqueline&rft.date=2012-05-01&rft.volume=142&rft.issue=5&rft.spage=866&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+nutrition&rft.issn=1541-6100&rft_id=info:doi/10.3945%2Fjn.111.156349 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-12 N1 - Date created - 2012-04-23 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00342992; ClinicalTrials.gov N1 - SuppNotes - Cited By: Nat Genet. 2004 Jul;36(7):700-6 [15184900] Hum Mol Genet. 2011 Dec 1;20(23):4724-31 [21878437] Clin Chim Acta. 2000 Dec;302(1-2):213-9 [11074077] Lipids. 2001;36 Suppl:S53-63 [11837994] Diabetes Care. 2002 Dec;25(12):2172-7 [12453956] Genetics. 2003 Dec;165(4):2213-33 [14704198] Cancer Epidemiol Biomarkers Prev. 2004 Mar;13(3):378-82 [15006912] Science. 2004 Apr 23;304(5670):581-4 [15105499] J Clin Chem Clin Biochem. 1984 Mar;22(3):245-51 [6327876] Clin Chem. 1986 May;32(5):874-6 [3084131] Biochim Biophys Acta. 1990 May 9;1024(1):32-40 [2159804] Arch Biochem Biophys. 1990 Aug 15;281(1):96-105 [2166481] Cancer Res. 1993 Sep 15;53(18):4230-7 [8364919] Ann Epidemiol. 1994 Jan;4(1):1-10 [8205268] Eur J Cancer B Oral Oncol. 1996 Mar;32B(2):114-9 [8736173] Nutr Cancer. 1997;28(1):30-5 [9200147] Nutr Rev. 1998 Jan;56(1 Pt 2):S49-58 [9481124] Biofactors. 1998;7(1-2):21-30 [9523025] J Natl Cancer Inst. 2005 Mar 2;97(5):396-9 [15741576] JAMA. 2005 Mar 16;293(11):1338-47 [15769967] IUBMB Life. 2004 Oct;56(10):615-20 [15814460] Bioinformatics. 2006 Dec 15;22(24):3061-6 [17060358] Bioinformatics. 2007 Mar 15;23(6):774-6 [17234637] J Lipid Res. 2007 Nov;48(11):2506-13 [17693622] Nat Genet. 2008 Feb;40(2):161-9 [18193043] Biochem Pharmacol. 2008 Jun 15;75(12):2263-75 [18433732] Nutr Rev. 2008 Jul;66(7):406-14 [18667016] Nat Genet. 2008 Oct;40(10):1160-2 [18776911] Nat Genet. 2009 Jan;41(1):56-65 [19060906] JAMA. 2009 Jan 7;301(1):39-51 [19066370] Am J Hum Genet. 2009 Feb;84(2):123-33 [19185284] Cancer Res. 2009 Feb 15;69(4):1429-38 [19190344] Circ Cardiovasc Genet. 2010 Feb;3(1):31-8 [20160193] Pak J Pharm Sci. 2010 Apr;23(2):125-30 [20363687] Hum Mol Genet. 2010 Jul 1;19(13):2739-45 [20418485] Nature. 2010 Aug 5;466(7307):707-13 [20686565] Atherosclerosis. 2010 Oct;212(2):543-7 [20688329] Biochem Pharmacol. 2010 Dec 1;80(11):1613-31 [20696139] Nature. 2010 Oct 28;467(7319):1061-73 [20981092] Am J Clin Nutr. 2011 Mar;93(3):644-51 [21228269] Fam Pract. 2011 Jun;28(3):243-52 [21273283] Hum Mol Genet. 2011 Oct 1;20(19):3876-83 [21729881] JAMA. 2011 Oct 12;306(14):1549-56 [21990298] Cancer Causes Control. 2000 Mar;11(3):197-205 [10782653] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3945/jn.111.156349 ER - TY - JOUR T1 - Reduced-intensity allogeneic stem cell transplantation in children and young adults with ultrahigh-risk pediatric sarcomas. AN - 1009127687; 21896345 AB - Some subsets of pediatric sarcoma patients have very poor survival rates. We sought to determine the feasibility and efficacy of allogeneic hematopoietic stem cell transplantation (alloHSCT) in pediatric sarcoma populations with <25% predicted overall survival (OS). Patients with ultrahigh-risk Ewing's sarcoma family of tumors (ESFT), alveolar rhabdomyosarcoma, or desmoplastic small round cell tumors received EPOCH-fludarabine induction, a cyclophosphamide/fludarabine/melphalan preparative regimen, and HLA matched related peripheral blood stem cells. Thirty patients enrolled; 7 did not undergo alloHSCT because of progressive disease with diminishing performance status during induction. All 23 alloHSCT recipients experienced rapid full-donor engraftment, with no peritransplantation mortality. Five of 23 alloHSCT recipients (22%) remain alive (OS of 30% by Kaplan-Meier analysis at 3 years), including 3 of 7 (42%) transplanted without overt disease (median survival 14.5 versus 29.0 months from alloHSCT for patients transplanted with versus without overt disease, respectively). Among the 28 patients who progressed on the study, the median survival from date of progression was 1.9 months for the 7 who did not receive a transplant compared with 11.4 months for the 21 transplanted (P = .0003). We found prolonged survival after posttransplantation progression with several patients exhibiting indolent tumor growth. We also saw several patients with enhanced antitumor effects from posttransplantation chemotherapy (objective response to pretransplantation EPOCH-F was 24% versus 67% to posttransplantation EOCH); however, this was associated with increased toxicity. This largest reported series of alloHSCT in sarcomas demonstrates that alloHSCT is safe in this population, and that patients undergoing alloHSCT without overt disease show higher survival rates than reported using standard therapies. Enhanced chemo- and radiosensitivity of tumors and normal tissues was observed posttransplantation. Published by Elsevier Inc. JF - Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation AU - Baird, Kristin AU - Fry, Terry J AU - Steinberg, Seth M AU - Bishop, Michael R AU - Fowler, Daniel H AU - Delbrook, Cynthia P AU - Humphrey, Jennifer L AU - Rager, Alison AU - Richards, Kelly AU - Wayne, Alan S AU - Mackall, Crystal L AD - Pediatric Oncology Branch, National Cancer Institute, Center for Cancer Research, National Institutes of Health, Bethesda, Maryland 20892, USA. kbaird@mail.nih.gov Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 698 EP - 707 VL - 18 IS - 5 KW - Antineoplastic Agents KW - 0 KW - Index Medicus KW - Kaplan-Meier Estimate KW - Risk KW - Age Factors KW - Humans KW - Graft Survival -- immunology KW - Cohort Studies KW - Adult KW - Child KW - Transplantation, Homologous KW - Adolescent KW - Male KW - Female KW - Remission Induction KW - Transplantation Conditioning KW - Sarcoma -- mortality KW - Antineoplastic Agents -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- administration & dosage KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Antineoplastic Agents -- therapeutic use KW - Sarcoma -- immunology KW - Sarcoma -- therapy KW - Hematopoietic Stem Cell Transplantation -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1009127687?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biology+of+blood+and+marrow+transplantation+%3A+journal+of+the+American+Society+for+Blood+and+Marrow+Transplantation&rft.atitle=Reduced-intensity+allogeneic+stem+cell+transplantation+in+children+and+young+adults+with+ultrahigh-risk+pediatric+sarcomas.&rft.au=Baird%2C+Kristin%3BFry%2C+Terry+J%3BSteinberg%2C+Seth+M%3BBishop%2C+Michael+R%3BFowler%2C+Daniel+H%3BDelbrook%2C+Cynthia+P%3BHumphrey%2C+Jennifer+L%3BRager%2C+Alison%3BRichards%2C+Kelly%3BWayne%2C+Alan+S%3BMackall%2C+Crystal+L&rft.aulast=Baird&rft.aufirst=Kristin&rft.date=2012-05-01&rft.volume=18&rft.issue=5&rft.spage=698&rft.isbn=&rft.btitle=&rft.title=Biology+of+blood+and+marrow+transplantation+%3A+journal+of+the+American+Society+for+Blood+and+Marrow+Transplantation&rft.issn=1523-6536&rft_id=info:doi/10.1016%2Fj.bbmt.2011.08.020 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-05-03 N1 - Date created - 2012-04-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Clin Oncol. 2000 Jan;18(1):4-11 [10623687] Bone Marrow Transplant. 2004 Sep;34(6):471-6 [15273708] Ann Oncol. 2000 Nov;11(11):1451-62 [11142486] J Clin Oncol. 2001 Jun 1;19(11):2812-20 [11387352] Br J Cancer. 2001 Nov 30;85(11):1646-54 [11742482] Ann Oncol. 2002 Jan;13(1):23-30 [11863105] Bone Marrow Transplant. 2003 Jul;32(1):103-6 [12815485] Bone Marrow Transplant. 1995 May;15(5):697-705 [7670398] Br J Haematol. 2004 Sep;126(6):837-43 [15352988] Cancer Chemother Rep. 1966 Mar;50(3):163-70 [5910392] Am J Med. 1980 Aug;69(2):204-17 [6996481] Control Clin Trials. 1989 Mar;10(1):1-10 [2702835] Hematol Oncol Clin North Am. 1990 Jun;4(3):625-39 [2193015] J Clin Oncol. 1993 Aug;11(8):1482-8 [8101562] J Clin Oncol. 1993 Oct;11(10):1911-8 [8410118] Bone Marrow Transplant. 1994 Jul;14(1):37-46 [7951119] J Clin Oncol. 1998 May;16(5):1697-706 [9586881] Ann Surg Oncol. 1998 Oct-Nov;5(7):573-9 [9831103] Immunobiology. 1999 Feb;200(1):1-20 [10084692] J Clin Oncol. 2004 Dec 1;22(23):4787-94 [15570080] J Clin Oncol. 2005 Jan 1;23(1):242-4 [15625381] J Pediatr Surg. 2005 Jan;40(1):251-5 [15868593] Biol Blood Marrow Transplant. 2005 Jul;11(7):551-7 [15983555] Expert Rev Anticancer Ther. 2005 Oct;5(5):835-46 [16221053] Biol Blood Marrow Transplant. 2005 Nov;11(11):823-61 [16275588] Expert Rev Anticancer Ther. 2006 Feb;6(2):225-37 [16445375] Transplantation. 2006 Jul 15;82(1):142-4 [16861958] Nat Med. 2007 Jan;13(1):54-61 [17187072] Biol Blood Marrow Transplant. 2007 Sep;13(9):1022-30 [17697964] Oncologist. 2007 Aug;12(8):1007-18 [17766661] Nat Med. 2007 Sep;13(9):1050-9 [17704786] Haematologica. 2008 Feb;93(2):265-72 [18245651] Surg Oncol. 2008 Aug;17(2):107-12 [18191563] Nat Clin Pract Oncol. 2008 May;5(5):256-67 [18398414] J Clin Oncol. 2008 May 10;26(14):2384-9 [18467730] Pediatr Blood Cancer. 2008 Jul;51(1):142-4 [18266223] Bone Marrow Transplant. 2008 Oct;42 Suppl 2:S25-30 [18978740] J Pathol. 2009 Jun;218(2):222-31 [19274709] Pediatr Blood Cancer. 2009 Jul;53(1):120-4 [19215002] Nat Med. 2009 Oct;15(10):1170-8 [19767732] Cancer. 2010 Jan 15;116(2):443-50 [19924786] J Clin Oncol. 2010 Mar 1;28(7):1099-105 [20100959] Pediatr Clin North Am. 2010 Feb;57(1):47-66 [20307711] Eur J Cancer. 2010 Jun;46(9):1588-95 [20338746] J Clin Oncol. 2010 Jul 10;28(20):3284-91 [20547982] Clin Cancer Res. 2010 Aug 1;16(15):3819-21 [20554750] N Engl J Med. 2010 Jul 29;363(5):411-22 [20818862] Oncologist. 2010;15(9):969-75 [20798195] Clin Cancer Res. 2011 Feb 15;17(4):907-17 [21106727] Bone Marrow Transplant. 2004 Jul;34(1):37-41 [15170176] J Clin Oncol. 2000 Sep;18(17):3108-14 [10963639] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.bbmt.2011.08.020 ER - TY - JOUR T1 - Sulforaphane, a natural constituent of broccoli, prevents cell death and inflammation in nephropathy. AN - 1008829017; 21684138 AB - Cisplatin (cis-diamminedichloroplatinum II, CIS) is a potent and widely used chemotherapeutic agent to treat various malignancies, but its therapeutic use is limited because of dose-dependent nephrotoxicity. Cell death and inflammation play a key role in the development and progression of CIS-induced nephropathy. Sulforaphane (SFN), a natural constituent of cruciferous vegetables such as broccoli, Brussels sprouts, etc., has been shown to exert various protective effects in models of tissue injury and cancer. In this study, we have investigated the role of prosurvival, cell death and inflammatory signaling pathways using a rodent model of CIS-induced nephropathy, and explored the effects of SFN on these processes. Cisplatin triggered marked activation of stress signaling pathways [p53, Jun N-terminal kinase (JNK), and p38-α mitogen-activated protein kinase (MAPK)] and promoted cell death in the kidneys (increased DNA fragmentation, caspases-3/7 activity, terminal deoxynucleotidyl transferase-mediated uridine triphosphate nick-end labeling), associated with attenuation of various prosurvival signaling pathways [e.g., extracellular signal-regulated kinase (ERK) and p38-β MAPK]. Cisplatin also markedly enhanced inflammation in the kidneys [promoted NF-κB activation, increased expression of adhesion molecules ICAM and VCAM, enhanced tumor necrosis factor-α (TNF-α) levels and inflammatory cell infiltration]. These effects were significantly attenuated by pretreatment of rodents with SFN. Thus, the cisplatin-induced nephropathy is associated with activation of various cell death and proinflammatory pathways (p53, JNK, p38-α, TNF-α and NF-κB) and impairments of key prosurvival signaling mechanisms (ERK and p38-β). SFN is able to prevent the CIS-induced renal injury by modulating these pathways, providing a novel approach for preventing this devastating complication of chemotherapy. Published by Elsevier Inc. JF - The Journal of nutritional biochemistry AU - Guerrero-Beltrán, Carlos Enrique AU - Mukhopadhyay, Partha AU - Horváth, Béla AU - Rajesh, Mohanraj AU - Tapia, Edilia AU - García-Torres, Itzhel AU - Pedraza-Chaverri, José AU - Pacher, Pál AD - Section on Oxidative Stress Tissue Injury, Laboratory of Physiological Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892-9413, USA. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 494 EP - 500 VL - 23 IS - 5 KW - Antineoplastic Agents KW - 0 KW - Isothiocyanates KW - Thiocyanates KW - JNK Mitogen-Activated Protein Kinases KW - EC 2.7.11.24 KW - sulforafan KW - GA49J4310U KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Rats KW - Animals KW - Cisplatin -- toxicity KW - Rats, Wistar KW - Antineoplastic Agents -- toxicity KW - Signal Transduction KW - Male KW - JNK Mitogen-Activated Protein Kinases -- metabolism KW - Thiocyanates -- pharmacology KW - Brassica -- chemistry KW - Kidney Diseases -- pathology KW - Kidney Diseases -- metabolism KW - Inflammation -- prevention & control KW - Kidney Diseases -- prevention & control KW - Inflammation -- metabolism KW - Cell Death -- drug effects KW - Kidney Diseases -- chemically induced UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008829017?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+nutritional+biochemistry&rft.atitle=Sulforaphane%2C+a+natural+constituent+of+broccoli%2C+prevents+cell+death+and+inflammation+in+nephropathy.&rft.au=Guerrero-Beltr%C3%A1n%2C+Carlos+Enrique%3BMukhopadhyay%2C+Partha%3BHorv%C3%A1th%2C+B%C3%A9la%3BRajesh%2C+Mohanraj%3BTapia%2C+Edilia%3BGarc%C3%ADa-Torres%2C+Itzhel%3BPedraza-Chaverri%2C+Jos%C3%A9%3BPacher%2C+P%C3%A1l&rft.aulast=Guerrero-Beltr%C3%A1n&rft.aufirst=Carlos&rft.date=2012-05-01&rft.volume=23&rft.issue=5&rft.spage=494&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+nutritional+biochemistry&rft.issn=1873-4847&rft_id=info:doi/10.1016%2Fj.jnutbio.2011.02.004 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-06-24 N1 - Date created - 2012-04-20 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Food Chem Toxicol. 1999 Sep-Oct;37(9-10):973-9 [10541453] Mol Ther. 2011 Jan;19(1):188-95 [20940707] J Am Soc Nephrol. 2002 Apr;13(4):858-65 [11912244] J Pharmacol Exp Ther. 2002 Jul;302(1):8-17 [12065694] J Clin Invest. 2002 Sep;110(6):835-42 [12235115] Kidney Int. 2003 Jan;63(1):72-82 [12472770] Am J Physiol Renal Physiol. 2003 Oct;285(4):F610-8 [12865254] J Lab Clin Med. 2003 Sep;142(3):178-86 [14532906] J Pharmacol Exp Ther. 2004 Jul;310(1):263-71 [14988420] Am J Kidney Dis. 1986 Nov;8(5):368-79 [3538860] Biochem Biophys Res Commun. 1989 Mar 31;159(3):1121-7 [2930553] Am J Physiol Renal Physiol. 2005 Jul;289(1):F166-74 [15701814] J Am Soc Nephrol. 2005 Jul;16(7):1985-92 [15901768] J Mol Cell Cardiol. 2006 Apr;40(4):529-39 [16516911] Nutr Cancer. 2006;55(1):53-62 [16965241] Free Radic Res. 2006 Oct;40(10):1066-75 [17015251] Exp Biol Med (Maywood). 2007 Feb;232(2):227-34 [17259330] Biochem Pharmacol. 2007 May 1;73(9):1499-510 [17291459] Mol Cancer Ther. 2007 Apr;6(4):1338-47 [17431112] FASEB J. 2007 Jun;21(8):1788-800 [17327359] Arch Toxicol. 2007 Jul;81(7):495-504 [17216432] Br J Nutr. 2008 Mar;99(3):559-64 [17868493] Toxicology. 2008 Mar 12;245(1-2):18-23 [18243469] Kidney Int. 2008 May;73(9):994-1007 [18272962] Biochem Pharmacol. 2008 Jun 1;75(11):2214-23 [18407246] Mol Nutr Food Res. 2008 Jun;52 Suppl 1:S128-38 [18327872] Mol Nutr Food Res. 2008 Jun;52 Suppl 1:S7-17 [18327874] Nephrol Dial Transplant. 2008 Jul;23(7):2198-205 [18385389] Biochem Pharmacol. 2008 Sep 1;76(5):597-607 [18656455] Biochim Biophys Acta. 2008 Sep;1782(9):498-503 [18555028] Gastroenterology. 2008 Oct;135(4):1344-57 [18778711] Kidney Int. 2008 Dec;74(12):1538-47 [18716605] Kidney Int. 2009 Feb;75(3):304-11 [18843260] Toxicol Appl Pharmacol. 2009 Feb 15;235(1):57-67 [19071154] J Pharmacol Exp Ther. 2009 Mar;328(3):708-14 [19074681] J Agric Food Chem. 2008 Nov 26;56(22):10505-9 [18950181] Life Sci. 2009 Apr 24;84(17-18):590-7 [19302802] Am J Physiol Heart Circ Physiol. 2009 May;296(5):H1466-83 [19286953] Cancer Lett. 2009 Oct 18;284(1):15-20 [19409695] Nephrol Dial Transplant. 2009 Oct;24(10):3012-20 [19474282] J Am Soc Nephrol. 2009 Nov;20(11):2412-25 [19797168] Oncol Rep. 2009 Dec;22(6):1473-8 [19885601] Biochem Pharmacol. 2010 Jan 15;79(2):137-46 [19699182] AAPS J. 2010 Mar;12(1):87-97 [20013083] Free Radic Biol Med. 2010 Feb 1;48(3):457-67 [19969072] Cardiovasc Res. 2010 Mar 1;85(4):773-84 [19942623] Mediators Inflamm. 2009;2009:137072 [20182538] Free Radic Biol Med. 2010 Apr 15;48(8):1051-63 [20096777] Cardiovasc Toxicol. 2010 Jun;10(2):139-45 [20405237] World J Gastroenterol. 2010 Jun 28;16(24):3002-10 [20572303] Chem Res Toxicol. 2010 Aug 16;23(8):1307-9 [20707406] J Am Coll Cardiol. 2010 Dec 14;56(25):2115-25 [21144973] J Biol Chem. 2000 Oct 20;275(42):32592-7 [10938077] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jnutbio.2011.02.004 ER - TY - CONF T1 - Incorporating nonchemical stressors into cumulative risk assessments. AN - 1002794633; 22345310 AB - The role of nonchemical stressors in modulating the human health risk associated with chemical exposures is an area of increasing attention. On 9 March 2011, a workshop titled "Approaches for Incorporating Nonchemical Stressors into Cumulative Risk Assessment" took place during the 50th Anniversary Annual Society of Toxicology Meeting in Washington D.C. Objectives of the workshop included describing the current state of the science from various perspectives (i.e., regulatory, exposure, modeling, and risk assessment) and presenting expert opinions on currently available methods for incorporating nonchemical stressors into cumulative risk assessments. Herein, distinct frameworks for characterizing exposure to, joint effects of, and risk associated with chemical and nonchemical stressors are discussed. JF - Toxicological sciences : an official journal of the Society of Toxicology AU - Rider, Cynthia V AU - Dourson, Michael L AU - Hertzberg, Richard C AU - Mumtaz, Moiz M AU - Price, Paul S AU - Simmons, Jane Ellen Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 10 EP - 17 VL - 127 IS - 1 KW - Environmental Pollutants KW - 0 KW - Index Medicus KW - Socioeconomic Factors KW - Environmental Monitoring KW - District of Columbia KW - Education KW - Computer Simulation KW - Humans KW - Risk Assessment -- methods KW - Models, Biological KW - Environmental Pollutants -- toxicity KW - Stress, Psychological KW - Toxicology -- education KW - Environmental Exposure -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1002794633?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&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=Toxicological+sciences+%3A+an+official+journal+of+the+Society+of+Toxicology&rft.atitle=Incorporating+nonchemical+stressors+into+cumulative+risk+assessments.&rft.au=Rider%2C+Cynthia+V%3BDourson%2C+Michael+L%3BHertzberg%2C+Richard+C%3BMumtaz%2C+Moiz+M%3BPrice%2C+Paul+S%3BSimmons%2C+Jane+Ellen&rft.aulast=Rider&rft.aufirst=Cynthia&rft.date=2012-05-01&rft.volume=127&rft.issue=1&rft.spage=10&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%2Fkfs088 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-08 N1 - Date created - 2012-04-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Ann Occup Hyg. 2001 Apr;45 Suppl 1:S131-42 [11290359] Toxicol Sci. 2002 Mar;66(1):1-3 [11861966] Environ Res. 2003 May;92(1):1-7 [12706749] Brain Res Brain Res Rev. 1997 Feb;23(1-2):79-133 [9063588] Environ Health Perspect. 2004 Dec;112(17):1645-53 [15579407] J Expo Anal Environ Epidemiol. 2005 Nov;15(6):473-81 [15856075] Physiol Behav. 2012 Apr 12;106(1):29-39 [21888923] Environ Health Perspect. 2007 May;115(5):817-24 [17520073] Environ Toxicol Chem. 2007 Jun;26(6):1233-42 [17571690] J Expo Sci Environ Epidemiol. 2008 Sep;18(5):462-76 [18073786] Environ Health Perspect. 2010 Jun;118(6):769-75 [20194079] Risk Anal. 2010 Oct;30(10):1590-601 [20626684] Nature. 2011 Feb 17;470(7334):320-2 [21331018] Metabolism. 2006 Oct;55(10 Suppl 2):S20-3 [16979422] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/toxsci/kfs088 ER - TY - JOUR T1 - Incomplete splicing, cell division defects, and hematopoietic blockage in dhx8 mutant zebrafish. AN - 1002541166; 22411201 AB - Vertebrate hematopoiesis is a complex developmental process that is controlled by genes in diverse pathways. To identify novel genes involved in early hematopoiesis, we conducted an ENU (N-ethyl-N-nitrosourea) mutagenesis screen in zebrafish. The mummy (mmy) line was investigated because of its multiple hematopoietic defects. Homozygous mmy embryos lacked circulating blood cell types and were dead by 30 hr post-fertilization (hpf). The mmy mutants did not express myeloid markers and had significantly decreased expression of progenitor and erythroid markers in primitive hematopoiesis. Through positional cloning, we identified a truncation mutation in dhx8 in the mmy fish. dhx8 is the zebrafish ortholog of the yeast splicing factor prp22, which is a DEAH-box RNA helicase. mmy mutants had splicing defects in many genes, including several hematopoietic genes. mmy embryos also showed cell division defects as characterized by disorganized mitotic spindles and formation of multiple spindle poles in mitotic cells. These cell division defects were confirmed by DHX8 knockdown in HeLa cells. Together, our results confirm that dhx8 is involved in mRNA splicing and suggest that it is also important for cell division during mitosis. This is the first vertebrate model for dhx8, whose function is essential for primitive hematopoiesis in developing embryos. Copyright © 2012 Wiley Periodicals, Inc. JF - Developmental dynamics : an official publication of the American Association of Anatomists AU - English, Milton A AU - Lei, Lin AU - Blake, Trevor AU - Wincovitch, Stephen M AU - Sood, Raman AU - Azuma, Mizuki AU - Hickstein, Dennis AU - Liu, P Paul AD - Oncogenesis and Development Section, National Human Genome Research Institute/NIH, Bethesda, MD 20892, USA. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 879 EP - 889 VL - 241 IS - 5 KW - Zebrafish Proteins KW - 0 KW - DHX8 protein, zebrafish KW - EC 3.6.1.- KW - DEAD-box RNA Helicases KW - EC 3.6.4.13 KW - Index Medicus KW - Animals KW - Cell Differentiation -- genetics KW - Embryo, Nonmammalian -- metabolism KW - Hematopoietic System -- metabolism KW - RNA Splicing -- genetics KW - DEAD-box RNA Helicases -- metabolism KW - Zebrafish -- metabolism KW - DEAD-box RNA Helicases -- genetics KW - Zebrafish Proteins -- genetics KW - Zebrafish -- genetics KW - Zebrafish Proteins -- metabolism KW - Hematopoiesis -- genetics KW - Cell Division -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1002541166?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Developmental+dynamics+%3A+an+official+publication+of+the+American+Association+of+Anatomists&rft.atitle=Incomplete+splicing%2C+cell+division+defects%2C+and+hematopoietic+blockage+in+dhx8+mutant+zebrafish.&rft.au=English%2C+Milton+A%3BLei%2C+Lin%3BBlake%2C+Trevor%3BWincovitch%2C+Stephen+M%3BSood%2C+Raman%3BAzuma%2C+Mizuki%3BHickstein%2C+Dennis%3BLiu%2C+P+Paul&rft.aulast=English&rft.aufirst=Milton&rft.date=2012-05-01&rft.volume=241&rft.issue=5&rft.spage=879&rft.isbn=&rft.btitle=&rft.title=Developmental+dynamics+%3A+an+official+publication+of+the+American+Association+of+Anatomists&rft.issn=1097-0177&rft_id=info:doi/10.1002%2Fdvdy.23774 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-20 N1 - Date created - 2012-04-17 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: EMBO J. 2000 Dec 1;19(23):6582-91 [11101530] Mol Cell. 2008 Jun 20;30(6):743-54 [18570877] Proc Natl Acad Sci U S A. 2008 Aug 26;105(34):12337-42 [18719100] Blood. 2009 Dec 10;114(25):5162-72 [19843882] Genes Dev. 2011 Apr 1;25(7):701-16 [21460037] Blood. 2001 Aug 1;98(3):643-51 [11468162] Blood. 2001 Nov 15;98(10):3087-96 [11698295] Int J Hematol. 2001 Oct;74(3):252-7 [11721959] Genetics. 2002 Feb;160(2):407-15 [11861548] Development. 2002 Apr;129(8):2015-30 [11934867] Proc Natl Acad Sci U S A. 2002 Apr 16;99(8):5454-9 [11960002] J Biol Chem. 2002 May 3;277(18):15452-8 [11856747] Oncogene. 2002 May 13;21(21):3262-9 [12032767] Immunity. 2002 May;16(5):661-72 [12049718] Dev Biol. 2002 Jun 15;246(2):274-95 [12051816] Dev Biol. 2002 Aug 15;248(2):307-18 [12167406] Curr Biol. 2002 Dec 10;12(23):2023-8 [12477391] Exp Hematol. 2002 Dec;30(12):1381-9 [12482499] Curr Top Dev Biol. 2003;53:139-58 [12510667] Methods. 2003 Dec;31(4):265-73 [14597310] J Biol Chem. 2004 Mar 5;279(10):8617-26 [14688266] Proc Natl Acad Sci U S A. 2004 May 11;101(19):7369-74 [15123839] PLoS Biol. 2004 Aug;2(8):E237 [15314655] Genome Biol. 2004;5(10):R80 [15461798] Nature. 1991 Feb 7;349(6309):487-93 [1992352] Mol Cell Biol. 1994 Nov;14(11):7611-20 [7935475] Development. 1995 Oct;121(10):3141-50 [7588049] Dev Dyn. 1995 Jul;203(3):253-310 [8589427] Genes Dev. 1996 Apr 15;10(8):997-1007 [8608946] Cell. 1996 Sep 20;86(6):897-906 [8808625] Development. 1996 Dec;123:303-9 [9007250] Development. 1996 Dec;123:311-9 [9007251] EMBO J. 1998 Apr 1;17(7):2086-94 [9524130] Dev Biol. 1998 May 15;197(2):248-69 [9630750] Development. 1998 Nov;125(22):4575-83 [9778515] Dev Dyn. 1999 Apr;214(4):323-36 [10213388] Development. 1999 Sep;126(17):3735-45 [10433904] Nature. 2004 Dec 23;432(7020):1036-40 [15616564] Proc Natl Acad Sci U S A. 2005 Jan 11;102(2):407-12 [15630097] Biochemistry. 2005 Jul 19;44(28):9795-803 [16008364] Reprod Biol Endocrinol. 2005;3:53 [16197550] Annu Rev Genet. 2005;39:481-501 [16285869] Nat Struct Mol Biol. 2006 Jun;13(6):482-90 [16680161] Nature. 2006 Sep 21;443(7109):337-9 [16988712] Gene Expr Patterns. 2007 Jan;7(1-2):39-46 [16815100] Immunity. 2006 Dec;25(6):963-75 [17157041] Cell Cycle. 2007 Feb 1;6(3):364-70 [17297293] Blood. 2007 Jun 15;109(12):5208-14 [17327398] RNA. 2007 Sep;13(9):1437-44 [17626844] Dev Biol. 2007 Oct 1;310(1):10-22 [17719025] PLoS One. 2007;2(10):e979 [17912356] Nat Protoc. 2008;3(1):59-69 [18193022] Dev Neurobiol. 2008 Feb 15;68(3):392-408 [18161852] Cell. 2008 Feb 22;132(4):631-44 [18295580] Circ Res. 2008 May 9;102(9):1057-64 [18388326] Circ Res. 2008 May 9;102(9):1005-7 [18467639] Blood. 2000 Dec 15;96(13):4178-84 [11110689] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/dvdy.23774 ER - TY - JOUR T1 - Human papillomavirus load measured by Linear Array correlates with quantitative PCR in cervical cytology specimens. AN - 1001954189; 22337992 AB - Carcinogenic human papillomavirus (HPV) infections are necessary causes of most anogenital cancers. Viral load has been proposed as a marker for progression to cancer precursors but has been confirmed only for HPV16. Challenges in studying viral load are related to the lack of validated assays for a large number of genotypes. We compared viral load measured by Linear Array (LA) HPV genotyping with the gold standard, quantitative PCR (Q-PCR). LA genotyping and Q-PCR were performed in 143 cytology specimens from women referred to colposcopy. LA signal strength was measured by densitometry. Correlation coefficients and receiver operating characteristic (ROC) analyses were used to evaluate analytical and clinical performance. We observed a moderate to strong correlation between the two quantitative viral load measurements, ranging from an R value of 0.61 for HPV31 to an R value of 0.86 for HPV52. We also observed agreement between visual LA signal strength evaluation and Q-PCR. Both quantifications agreed on the disease stages with highest viral load, which varied by type (cervical intraepithelial neoplasia grade 2 [CIN2] for HPV52, CIN3 for HPV16 and HPV33, and cancer for HPV18 and HPV31). The area under the curve (AUC) for HPV16 Q-PCR at the CIN3 cutoff was 0.72 (P = 0.004), and the AUC for HPV18 LA at the CIN2 cutoff was 0.78 (P = 0.04). Quantification of LA signals correlates with the current gold standard for viral load, Q-PCR. Analyses of viral load need to address multiple infections and type attribution to evaluate whether viral load has clinical value beyond the established HPV16 finding. Our findings support conducting comprehensive studies of viral load and cervical cancer precursors using quantitative LA genotyping data. JF - Journal of clinical microbiology AU - Wentzensen, Nicolas AU - Gravitt, Patti E AU - Long, Rodney AU - Schiffman, Mark AU - Dunn, S Terence AU - Carreon, J Daniel AU - Allen, Richard A AU - Gunja, Munira AU - Zuna, Rosemary E AU - Sherman, Mark E AU - Gold, Michael A AU - Walker, Joan L AU - Wang, Sophia S AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland, USA. wentzenn@mail.nih.gov Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 1564 EP - 1570 VL - 50 IS - 5 KW - Index Medicus KW - Severity of Illness Index KW - Young Adult KW - ROC Curve KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - Adolescent KW - Female KW - Papillomavirus Infections -- pathology KW - Cervix Uteri -- pathology KW - Viral Load -- methods KW - Papillomaviridae -- isolation & purification KW - Papillomavirus Infections -- virology KW - Cervix Uteri -- virology KW - Molecular Diagnostic Techniques -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1001954189?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Human+papillomavirus+load+measured+by+Linear+Array+correlates+with+quantitative+PCR+in+cervical+cytology+specimens.&rft.au=Wentzensen%2C+Nicolas%3BGravitt%2C+Patti+E%3BLong%2C+Rodney%3BSchiffman%2C+Mark%3BDunn%2C+S+Terence%3BCarreon%2C+J+Daniel%3BAllen%2C+Richard+A%3BGunja%2C+Munira%3BZuna%2C+Rosemary+E%3BSherman%2C+Mark+E%3BGold%2C+Michael+A%3BWalker%2C+Joan+L%3BWang%2C+Sophia+S&rft.aulast=Wentzensen&rft.aufirst=Nicolas&rft.date=2012-05-01&rft.volume=50&rft.issue=5&rft.spage=1564&rft.isbn=&rft.btitle=&rft.title=Journal+of+clinical+microbiology&rft.issn=1098-660X&rft_id=info:doi/10.1128%2FJCM.06240-11 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-16 N1 - Date created - 2012-04-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Lancet. 2002 Jul 20;360(9328):228-9 [12133661] J Infect Dis. 2011 May 15;203(10):1425-33 [21415020] Cancer Epidemiol Biomarkers Prev. 2003 Oct;12(10):1038-44 [14578140] J Clin Virol. 2004 Oct;31(2):140-7 [15364271] Cancer Epidemiol Biomarkers Prev. 2005 Sep;14(9):2200-7 [16172232] J Clin Virol. 2006 Mar;35(3):270-7 [16214397] Cancer Res. 2006 Oct 15;66(20):10112-9 [17047075] Dis Markers. 2007;23(4):297-313 [17627064] J Clin Microbiol. 2007 Oct;45(10):3245-50 [17699644] Int J Cancer. 2007 Dec 15;121(12):2787-93 [17722112] J Clin Microbiol. 2008 Aug;46(8):2759-65 [18550741] Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):113-20 [19124488] J Virol Methods. 2009 Mar;156(1-2):152-6 [19022296] Int J Cancer. 2009 Nov 1;125(9):2151-8 [19585494] Cancer Epidemiol Biomarkers Prev. 2009 Nov;18(11):2992-9 [19861526] J Natl Cancer Inst. 2011 Mar 2;103(5):368-83 [21282563] J Clin Virol. 2011 May;51(1):44-9 [21388867] J Virol Methods. 2003 Sep;112(1-2):23-33 [12951209] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1128/JCM.06240-11 ER - TY - JOUR T1 - Genetic profiling of intrahepatic cholangiocarcinoma. AN - 1000405796; 22395571 AB - Intrahepatic cholangiocarcinoma (ICC) is a treatment-refractory disease with a dismal outcome. Limited success in the clinical management and a persistent increase in the incidence world-wide have made ICC one of the most lethal and fastest growing malignancies. However, recent advancements in genome-wide technologies combined with the application of integrative multidimensional analytical approaches have begun to provide both detailed insight into the underlying biological traits of ICC and identified new therapeutic opportunities. In comparison with other cancers, genomic studies of ICC have been limited. We and others have recently procured large cohorts of ICC patients intended for genome-wide analyses. In our study, samples from ICC patients were obtained from three cancer centers and subjected to integrated genetic and genomic analyses. We provided new insights into both pathogenesis and optimal treatment options demonstrating the presence of unique subclasses of patients, based partly on KRAS mutations and increased levels of receptor tyrosine kinase signaling. The group of patients with the worst prognosis was characterized by transcriptional enrichment of genes regulating inflammation and proteasome activities, suggesting a combination of tyrosine kinase inhibitors and anti-inflammatory drugs as a new therapeutic option for these patients. We have critically examined the progress in genome-wide studies of ICC including genetic profiling, transcriptomics, and epigenomics. Current limitations in applying these technologies to archival samples and the insufficient access to fresh-frozen material are partly the cause of the delayed implementation of the omics-based investigations of ICC compared to other hepatobiliary diseases. Thus, selected candidate single-gene studies will also be discussed. JF - Current opinion in gastroenterology AU - Andersen, Jesper B AU - Thorgeirsson, Snorri S AD - Laboratory of Experimental Carcinogenesis, NCI/CCR, NIH, Bethesda, Maryland 20892-4262, USA. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 266 EP - 272 VL - 28 IS - 3 KW - 4-amino-5-(4-methylphenyl)-7-(tert-butyl)pyrazolo(3,4-d)pyrimidine KW - 0 KW - Anti-Inflammatory Agents KW - Pyrazoles KW - Pyrimidines KW - Index Medicus KW - Pyrazoles -- administration & dosage KW - DNA Mutational Analysis KW - Humans KW - Prognosis KW - Anti-Inflammatory Agents -- administration & dosage KW - Patient Selection KW - Pyrimidines -- administration & dosage KW - Genome-Wide Association Study KW - Drug Therapy, Combination KW - Genes, ras KW - Bile Ducts, Intrahepatic KW - Risk Factors KW - Bile Duct Neoplasms KW - Mutation KW - Female KW - Male KW - Cholangiocarcinoma -- genetics KW - Gene Expression Profiling KW - Cholangiocarcinoma -- mortality KW - Liver Neoplasms -- drug therapy KW - Cholangiocarcinoma -- drug therapy KW - Liver Neoplasms -- mortality KW - Liver Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1000405796?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+gastroenterology&rft.atitle=Genetic+profiling+of+intrahepatic+cholangiocarcinoma.&rft.au=Andersen%2C+Jesper+B%3BThorgeirsson%2C+Snorri+S&rft.aulast=Andersen&rft.aufirst=Jesper&rft.date=2012-05-01&rft.volume=28&rft.issue=3&rft.spage=266&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+gastroenterology&rft.issn=1531-7056&rft_id=info:doi/10.1097%2FMOG.0b013e3283523c7e LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-25 N1 - Date created - 2012-04-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Radiat Res. 1999 Dec;152(6 Suppl):S118-24 [10564951] Gastroenterology. 2012 Apr;142(4):1021-1031.e15 [22178589] Gut. 2000 Nov;47(5):721-7 [11034592] Cancer. 2001 Feb 1;91(3):570-7 [11169940] Gut. 2001 Mar;48(3):403-8 [11171833] J Pathol. 2001 Mar;193(3):310-7 [11241409] Oncology. 2001;60(2):151-61 [11244331] J Korean Med Sci. 2004 Oct;19(5):682-7 [15483344] Cancer Genet Cytogenet. 2001 Oct 1;130(1):22-8 [11672769] Hepatogastroenterology. 2002 May-Jun;49(45):604-8 [12063950] Hepatology. 2002 Aug;36(2):439-50 [12143054] J Pathol. 2002 Aug;197(5):624-31 [12210082] Mod Pathol. 2004 Nov;17(11):1386-91 [15181454] Am J Pathol. 2002 Sep;161(3):1015-22 [12213730] Semin Liver Dis. 2002 Aug;22(3):303-13 [12360423] J Hepatol. 2002 Nov;37(5):633-9 [12399230] Gut. 2003 May;52(5):706-12 [12692057] Am J Surg. 2004 May;187(5):612-7 [15135676] J Hepatol. 2004 Aug;41(2):292-8 [15288479] Cancer. 1992 Mar 1;69(5):1115-8 [1739910] Mol Carcinog. 1993;8(4):312-8 [8280380] Gastroenterology. 1995 Nov;109(5):1612-7 [7557145] Jpn J Cancer Res. 1996 Oct;87(10):1056-62 [8957064] J Surg Res. 1999 Jun 1;84(1):88-93 [10334895] Cancer Genet Cytogenet. 2005 Feb;157(1):37-41 [15676145] Mod Pathol. 2005 Mar;18(3):412-20 [15467712] Br J Cancer. 2005 Mar 14;92(5):935-41 [15756261] Hepatology. 2005 Jun;41(6):1339-48 [15880566] Gastroenterology. 2005 Jun;128(7):2054-65 [15940637] Liver Int. 2005 Aug;25(4):704-16 [15998419] Int J Oncol. 2005 Oct;27(4):973-80 [16142313] J Cancer Res Clin Oncol. 2005 Oct;131(10):649-52 [16032426] Hepatology. 2005 Dec;42(6):1329-38 [16317687] Clin Cancer Res. 2006 Mar 15;12(6):1680-5 [16551849] Int J Oncol. 2006 May;28(5):1269-77 [16596244] Biochem Biophys Res Commun. 2006 Jul 7;345(3):1022-32 [16712791] Gastroenterology. 2006 Jun;130(7):2113-29 [16762633] J Hepatobiliary Pancreat Surg. 2006;13(4):274-9 [16858537] Hepatology. 2006 Oct;44(4):1025-38 [17006947] Cancer Res. 2006 Nov 1;66(21):10517-24 [17079474] Gastroenterology. 2007 Jan;132(1):384-96 [17241887] J Biol Chem. 2007 Mar 16;282(11):8256-64 [17220301] Arch Pathol Lab Med. 2007 Jun;131(6):923-30 [17550320] Oncogene. 2007 Sep 13;26(42):6133-40 [17404574] World J Gastroenterol. 2007 Dec 28;13(48):6465-9 [18161915] Liver Int. 2008 Jan;28(1):12-27 [18031477] Oncogene. 2008 Jan 10;27(3):378-86 [17621267] Genes Chromosomes Cancer. 2008 May;47(5):363-7 [18181165] World J Gastroenterol. 2008 Dec 14;14(46):7033-58 [19084911] J Hepatol. 2009 Feb;50(2):358-69 [19070389] Parasitol Res. 2009 Apr;104(5):1035-46 [19039603] Hepatology. 2009 May;49(5):1595-601 [19296468] Hum Pathol. 2009 Jun;40(6):834-42 [19200581] J Exp Clin Cancer Res. 2009;28:62 [19435499] Oncol Rep. 2009 Aug;22(2):227-32 [19578760] J Nippon Med Sch. 2009 Aug;76(4):188-97 [19755794] Hepatology. 2010 Mar;51(3):881-90 [20146264] Sci Transl Med. 2010 Oct 20;2(54):54ra77 [20962331] Biomed Pharmacother. 2011 Feb;65(1):22-6 [21051183] BMC Cancer. 2011;11:78 [21333016] Br J Cancer. 2011 Apr 12;104(8):1313-8 [21448164] HPB (Oxford). 2011 May;13(5):309-19 [21492330] Hum Pathol. 2000 Sep;31(9):1011-7 [11014564] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1097/MOG.0b013e3283523c7e ER - TY - JOUR T1 - Active surveillance for prostate cancer: past, present and future. AN - 1000404827; 22450149 AB - This article reviews recent developments in the use of active surveillance for localized prostate cancer. The treatment of localized prostate cancer continues to be a major challenge for urologic oncologists. Screening with prostate-specific antigen has resulted in increased numbers of low-risk prostate cancers being detected. Aggressive whole-gland therapy with surgery, or radiation therapy is associated with potentially life-altering treatment-related side effects such as urinary incontinence, bowel toxicity and erectile dysfunction. The goal of active surveillance is to avoid or delay the adverse events associated with prostate cancer therapy while still allowing for curative intervention in the future, if needed. Active surveillance is a reasonable treatment option for many men with low-risk, and some men with intermediate-risk, prostate cancer. Additional research is needed to determine the optimal active surveillance inclusion criteria, monitoring schedule, and treatment triggers. It is hoped that advances in prostate imaging, biomarkers, and focal therapy will foster greater use of active surveillance in appropriately selected men to optimize quality-of-life without compromising cancer outcomes. JF - Current opinion in oncology AU - Singer, Eric A AU - Kaushal, Aradhana AU - Turkbey, Baris AU - Couvillon, Anna AU - Pinto, Peter A AU - Parnes, Howard L AD - Urologic Oncology Branch, Center for Cancer Research, Division of Cancer Prevention, National Cancer Institute, Bethesda, Maryland, United States. Y1 - 2012/05// PY - 2012 DA - May 2012 SP - 243 EP - 250 VL - 24 IS - 3 KW - Biomarkers, Tumor KW - 0 KW - Prostate-Specific Antigen KW - EC 3.4.21.77 KW - Index Medicus KW - Prostatectomy -- adverse effects KW - Humans KW - Erectile Dysfunction -- etiology KW - Patient Selection KW - Biomarkers, Tumor -- blood KW - Early Diagnosis KW - Male KW - Prostatic Neoplasms -- immunology KW - Prostatic Neoplasms -- diagnosis KW - Watchful Waiting KW - Prostatic Neoplasms -- surgery KW - Prostate-Specific Antigen -- blood KW - Quality of Life KW - Prostatic Neoplasms -- therapy KW - Prostatic Neoplasms -- radiotherapy KW - Population Surveillance UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1000404827?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Current+opinion+in+oncology&rft.atitle=Active+surveillance+for+prostate+cancer%3A+past%2C+present+and+future.&rft.au=Singer%2C+Eric+A%3BKaushal%2C+Aradhana%3BTurkbey%2C+Baris%3BCouvillon%2C+Anna%3BPinto%2C+Peter+A%3BParnes%2C+Howard+L&rft.aulast=Singer&rft.aufirst=Eric&rft.date=2012-05-01&rft.volume=24&rft.issue=3&rft.spage=243&rft.isbn=&rft.btitle=&rft.title=Current+opinion+in+oncology&rft.issn=1531-703X&rft_id=info:doi/10.1097%2FCCO.0b013e3283527f99 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-19 N1 - Date created - 2012-04-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1097/CCO.0b013e3283527f99 ER - TY - JOUR T1 - Concentration of endogenous estrogens and estrogen metabolites in the NCI-60 human tumor cell lines AN - 1113238799; 17213621 AB - Endogenous estrogens and estrogen metabolites play an important role in the pathogenesis and development of human breast, endometrial, and ovarian cancers. Increasing evidence also supports their involvement in the development of certain lung, colon and prostate cancers. In this study we systemically surveyed endogenous estrogen and estrogen metabolite levels in each of the NCI-60 human tumor cell lines, which include human breast, central nerve system, colon, ovarian, prostate, kidney and non-small cell lung cancers, as well as melanomas and leukemia. The absolute abundances of these metabolites were measured using a liquid chromatography-tandem mass spectrometry method that has been previously utilized for biological fluids such as serum and urine. Endogenous estrogens and estrogen metabolites were found in all NCI-60 human tumor cell lines and some were substantially elevated and exceeded the levels found in well known estrogen-dependent and estrogen receptor-positive tumor cells such as MCF-7 and T-47D. While estrogens were expected to be present at high levels in cell lines representing the female reproductive system (that is, breast and ovarian), other cell lines, such as leukemia and colon, also contained very high levels of these steroid hormones. The leukemia cell line RMPI-8226 contained the highest levels of estrone (182.06 pg/106 cells) and 17 beta -estradiol (753.45 pg/106 cells). In comparison, the ovarian cancer cell line with the highest levels of these estrogens contained only 19.79 and 139.32 pg/106 cells of estrone and 17 beta -estradiol, respectively. The highest levels of estrone and 17 beta -estradiol in breast cancer cell lines were only 8.45 and 87.37 pg/106 cells in BT-549 and T-47D cells, respectively. The data provided evidence for the presence of significant amounts of endogenous estrogens and estrogen metabolites in cell lines not commonly associated with these steroid hormones. This broad discovery of endogenous estrogens and estrogen metabolites in these cell lines suggest that several human tumors may be beneficially treated using endocrine therapy aimed at estrogen biosynthesis and estrogen-related signaling pathways. JF - Genome Medicine AU - Xu, Xia AU - Veenstra, Timothy D AD - Laboratory of Proteomics and Analytical Technologies, SAIC-Frederick, Inc., National Cancer Institute at Frederick, Frederick, MD 21702, USA, xuxi@mail.nih.gov Y1 - 2012/04/30/ PY - 2012 DA - 2012 Apr 30 SP - 31 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 4 IS - 4 KW - Biotechnology and Bioengineering Abstracts; Genetics Abstracts KW - 17 beta -Estradiol KW - Breast cancer KW - Colon KW - Data processing KW - Endometrium KW - Estrogens KW - Estrone KW - Kidney KW - Mass spectroscopy KW - Melanoma KW - Metabolites KW - Non-small cell lung carcinoma KW - Ovarian cancer KW - Reproductive system KW - Signal transduction KW - Steroid hormones KW - Tumor cell lines KW - Tumors KW - Urine KW - G 07730:Development & Cell Cycle KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1113238799?accountid=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=Genome+Medicine&rft.atitle=Concentration+of+endogenous+estrogens+and+estrogen+metabolites+in+the+NCI-60+human+tumor+cell+lines&rft.au=Xu%2C+Xia%3BVeenstra%2C+Timothy+D&rft.aulast=Xu&rft.aufirst=Xia&rft.date=2012-04-30&rft.volume=4&rft.issue=4&rft.spage=31&rft.isbn=&rft.btitle=&rft.title=Genome+Medicine&rft.issn=1756-994X&rft_id=info:doi/10.1186%2Fgm330 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2012-11-20 N1 - SubjectsTermNotLitGenreText - Ovarian cancer; Estrogens; Endometrium; Data processing; Non-small cell lung carcinoma; Metabolites; Steroid hormones; Tumors; Reproductive system; Mass spectroscopy; Melanoma; Tumor cell lines; Colon; Urine; Kidney; Breast cancer; 17 beta -Estradiol; Signal transduction; Estrone DO - http://dx.doi.org/10.1186/gm330 ER - TY - JOUR T1 - Structure of the Plasmodium 6-cysteine s48/45 domain AN - 1017959200; 16643226 AB - The s48/45 domain was first noted in Plasmodium proteins more than 15 y ago. Previously believed to be unique to Plasmodium, the s48/45 domain is present in other aconoidasidans. In Plasmodium, members of the s48/45 family of proteins are localized on the surface of the parasite in different stages, mostly by glycosylphosphatydylinositol-anchoring. Members such as P52 and P36 seem to play a role in invasion of hepatocytes, and Pfs230 and Pfs48/45 are involved in fertilization in the sexual stages and have been consistently studied as targets of transmission-blocking vaccines for years. In this report, we present the molecular structure for the s48/45 domain corresponding to the C-terminal domain of the blood-stage protein Pf12 from Plasmodium falciparum, obtained by NMR. Our results indicate that this domain is a beta -sandwich formed by two sheets with a mixture of parallel and antiparallel strands. Of the six conserved cysteines, two pairs link the beta -sheets by two disulfide bonds, and the third pair forms a bond outside the core. The structure of the s48/45 domain conforms well to the previously defined surface antigen 1 (SAG1)-related-sequence (SRS) fold observed in the SAG family of surface antigens found in Toxoplasma gondii. Despite extreme sequence divergence, remarkable spatial conservation of one of the disulfide bonds is observed, supporting the hypothesis that the domains have evolved from a common ancestor. Furthermore, a homologous domain is present in ephrins, raising the possibility that the precursor of the s48/45 and SRS domains emerged from an ancient transfer to Apicomplexa from metazoan hosts. JF - Proceedings of the National Academy of Sciences, USA AU - Arredondo, Silvia A AU - Cai, Mengli AU - Takayama, Yuki AU - MacDonald, Nicholas J AU - Anderson, DEric AU - Aravind, L AU - Clore, GMarius AU - Miller, Louis H AD - Laboratory of Immunogenetics, Laboratory of Malaria Immunology and Vaccinology, and Laboratory of Malaria Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852 Y1 - 2012/04/24/ PY - 2012 DA - 2012 Apr 24 SP - 6692 EP - 6697 PB - National Academy of Sciences, 2101 Constitution Ave. Washington DC 20418 United States VL - 109 IS - 17 SN - 0027-8424, 0027-8424 KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology; Ecology Abstracts KW - Molecular structure KW - Parasites KW - sexual stages KW - Hepatocytes KW - Nucleotide sequence KW - Disulfide bonds KW - Disease control KW - ephrins KW - Hosts KW - Fertilization KW - Antigens KW - Conserved sequence KW - N.M.R. KW - Plasmodium falciparum KW - surface antigens KW - Cysteine KW - Toxoplasma gondii KW - Apicomplexa KW - Vaccines KW - Metazoa KW - K 03330:Biochemistry KW - D 04040:Ecosystem and Ecology Studies 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/1017959200?accountid=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=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Structure+of+the+Plasmodium+6-cysteine+s48%2F45+domain&rft.au=Arredondo%2C+Silvia+A%3BCai%2C+Mengli%3BTakayama%2C+Yuki%3BMacDonald%2C+Nicholas+J%3BAnderson%2C+DEric%3BAravind%2C+L%3BClore%2C+GMarius%3BMiller%2C+Louis+H&rft.aulast=Arredondo&rft.aufirst=Silvia&rft.date=2012-04-24&rft.volume=109&rft.issue=17&rft.spage=6692&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2014-12-11 N1 - SubjectsTermNotLitGenreText - Molecular structure; Parasites; Antigens; Hepatocytes; Cysteine; Nucleotide sequence; Disease control; Hosts; Vaccines; Fertilization; sexual stages; surface antigens; Disulfide bonds; Conserved sequence; ephrins; N.M.R.; Toxoplasma gondii; Apicomplexa; Plasmodium falciparum; Metazoa ER - TY - CPAPER T1 - Sirtuins, protein acetylation and selective mitophagy T2 - Experimental Biology 2012 (EB 2012) AN - 1313121095; 6161729 JF - Experimental Biology 2012 (EB 2012) AU - Sack, M Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Acetylation KW - Sirtuins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313121095?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=Sirtuins%2C+protein+acetylation+and+selective+mitophagy&rft.au=Sack%2C+M&rft.aulast=Sack&rft.aufirst=M&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - A three-part mixed-effects model to estimate usual total nutrient distributions from food and dietary supplements T2 - Experimental Biology 2012 (EB 2012) AN - 1313120908; 6160870 JF - Experimental Biology 2012 (EB 2012) AU - Dodd, K AU - Verkaik-Kloosterman, J AU - Dekkers, A AU - vantVeer, P AU - Ocke, M Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Dietary supplements KW - Nutrients KW - Food KW - Models UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313120908?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=A+three-part+mixed-effects+model+to+estimate+usual+total+nutrient+distributions+from+food+and+dietary+supplements&rft.au=Dodd%2C+K%3BVerkaik-Kloosterman%2C+J%3BDekkers%2C+A%3BvantVeer%2C+P%3BOcke%2C+M&rft.aulast=Dodd&rft.aufirst=K&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Combining self-report dietary assessment instruments to reduce the effects of measurement error T2 - Experimental Biology 2012 (EB 2012) AN - 1313120895; 6160868 JF - Experimental Biology 2012 (EB 2012) AU - Midthune, D AU - Carroll, R AU - Subar, A AU - Freedman, L AU - Thompson, F AU - Kipnis, V Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Diets UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313120895?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=Combining+self-report+dietary+assessment+instruments+to+reduce+the+effects+of+measurement+error&rft.au=Midthune%2C+D%3BCarroll%2C+R%3BSubar%2C+A%3BFreedman%2C+L%3BThompson%2C+F%3BKipnis%2C+V&rft.aulast=Midthune&rft.aufirst=D&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Methods for large scale quantitative proteomics T2 - Experimental Biology 2012 (EB 2012) AN - 1313119854; 6160446 JF - Experimental Biology 2012 (EB 2012) AU - Hoffert, J Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - proteomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313119854?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=Methods+for+large+scale+quantitative+proteomics&rft.au=Hoffert%2C+J&rft.aulast=Hoffert&rft.aufirst=J&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Antibiotics induce mistranslation of selenocysteine residue in selenoproteins T2 - Experimental Biology 2012 (EB 2012) AN - 1313102705; 6161605 JF - Experimental Biology 2012 (EB 2012) AU - Tobe, R AU - Naranjo- Suarez, S. AU - Turanov, A AU - Carlson, B AU - Tsuji, P AU - Yoo, M-H AU - Everley, R AU - Gladyshev, V Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Residues KW - Antibiotics KW - Selenocysteine KW - selenoproteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313102705?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=Antibiotics+induce+mistranslation+of+selenocysteine+residue+in+selenoproteins&rft.au=Tobe%2C+R%3BNaranjo-+Suarez%2C+S.%3BTuranov%2C+A%3BCarlson%2C+B%3BTsuji%2C+P%3BYoo%2C+M-H%3BEverley%2C+R%3BGladyshev%2C+V&rft.aulast=Tobe&rft.aufirst=R&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Mammalian selenocysteine tRNA Um34 methylase and its role in selenoprotein synthesis T2 - Experimental Biology 2012 (EB 2012) AN - 1313102660; 6161602 JF - Experimental Biology 2012 (EB 2012) AU - Chen, F AU - Hofmann, P AU - Carlson, B AU - Tobe, R AU - Schomburg, L AU - Gladyshev, V AU - Schweizer, U AU - Hatfield, D Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - tRNA Sec KW - Methylase KW - Selenocysteine KW - selenoproteins UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313102660?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=Mammalian+selenocysteine+tRNA+Um34+methylase+and+its+role+in+selenoprotein+synthesis&rft.au=Chen%2C+F%3BHofmann%2C+P%3BCarlson%2C+B%3BTobe%2C+R%3BSchomburg%2C+L%3BGladyshev%2C+V%3BSchweizer%2C+U%3BHatfield%2C+D&rft.aulast=Chen&rft.aufirst=F&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Inhibition of selenocysteine tRNA[Ser]Sec aminoacylation provides evidence that aminoacylation is required for regulatory methylation of this tRNA T2 - Experimental Biology 2012 (EB 2012) AN - 1313102641; 6161601 JF - Experimental Biology 2012 (EB 2012) AU - Carlson, B AU - Kim, J AU - Xu, X-M AU - Yoo, M AU - Zeng, Y AU - Chen, S AU - Gladyshev, V AU - Lee, B AU - Hatfield, D Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Aminoacylation KW - Selenocysteine KW - Methylation KW - tRNA UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313102641?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=Inhibition+of+selenocysteine+tRNA%5BSer%5DSec+aminoacylation+provides+evidence+that+aminoacylation+is+required+for+regulatory+methylation+of+this+tRNA&rft.au=Carlson%2C+B%3BKim%2C+J%3BXu%2C+X-M%3BYoo%2C+M%3BZeng%2C+Y%3BChen%2C+S%3BGladyshev%2C+V%3BLee%2C+B%3BHatfield%2C+D&rft.aulast=Carlson&rft.aufirst=B&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Humanized mouse lines and their application for prediction of human drug metabolism and toxicological risk assessment T2 - Experimental Biology 2012 (EB 2012) AN - 1313102391; 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6161751 JF - Experimental Biology 2012 (EB 2012) AU - Yoo, M-H AU - Carlson, B AU - Tsuji, P AU - Gladyshev, V AU - Hatfield, D Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Cancer KW - Oxidative stress KW - thioredoxin reductase UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313086765?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=Thioredoxin+reductase+1%3A+role+in+oxidative+stress+within+cancer+cells&rft.au=Yoo%2C+M-H%3BCarlson%2C+B%3BTsuji%2C+P%3BGladyshev%2C+V%3BHatfield%2C+D&rft.aulast=Yoo&rft.aufirst=M-H&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - After the Interlude: Cell-Level Systems Biology in the 21st Century T2 - Experimental Biology 2012 (EB 2012) AN - 1313077804; 6161272 JF - Experimental Biology 2012 (EB 2012) AU - Knepper, M Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Ecology KW - Botany KW - Food KW - Microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313077804?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=After+the+Interlude%3A+Cell-Level+Systems+Biology+in+the+21st+Century&rft.au=Knepper%2C+M&rft.aulast=Knepper&rft.aufirst=M&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - National Heart, Lung, and Blood Institute resources to advance molecular and cellular therapies T2 - Experimental Biology 2012 (EB 2012) AN - 1313072461; 6161281 JF - Experimental Biology 2012 (EB 2012) AU - Mockrin, S Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Lung KW - Blood KW - Heart KW - Therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313072461?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=National+Heart%2C+Lung%2C+and+Blood+Institute+resources+to+advance+molecular+and+cellular+therapies&rft.au=Mockrin%2C+S&rft.aulast=Mockrin&rft.aufirst=S&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Molecular analysis of genetic variation in prions of Saccharomyces cerevisiae T2 - Experimental Biology 2012 (EB 2012) AN - 1313069825; 6161124 JF - Experimental Biology 2012 (EB 2012) AU - Kelly, A AU - Shewmaker, F AU - Wickner, R Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Genetic diversity KW - Prion protein KW - Saccharomyces cerevisiae UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313069825?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=Molecular+analysis+of+genetic+variation+in+prions+of+Saccharomyces+cerevisiae&rft.au=Kelly%2C+A%3BShewmaker%2C+F%3BWickner%2C+R&rft.aulast=Kelly&rft.aufirst=A&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Evidence for proliferation of airway-delivered donor type II cells in lungs of recipient mice following intratracheal bleomycin T2 - Experimental Biology 2012 (EB 2012) AN - 1313068948; 6161057 JF - Experimental Biology 2012 (EB 2012) AU - Wang, P AU - Martin II, W Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Lung KW - Mice KW - Trachea KW - Cell proliferation KW - Bleomycin UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313068948?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=Evidence+for+proliferation+of+airway-delivered+donor+type+II+cells+in+lungs+of+recipient+mice+following+intratracheal+bleomycin&rft.au=Wang%2C+P%3BMartin+II%2C+W&rft.aulast=Wang&rft.aufirst=P&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Clinical methods to assess cardiac sympathetic innervation and function T2 - Experimental Biology 2012 (EB 2012) AN - 1313061847; 6160038 JF - Experimental Biology 2012 (EB 2012) AU - Goldstein, D Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Heart KW - Innervation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313061847?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=Clinical+methods+to+assess+cardiac+sympathetic+innervation+and+function&rft.au=Goldstein%2C+D&rft.aulast=Goldstein&rft.aufirst=D&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Reprogramming the cancer epigenome by metabolic transduction T2 - Experimental Biology 2012 (EB 2012) AN - 1313048849; 6161039 JF - Experimental Biology 2012 (EB 2012) AU - Byun, J AU - Gardner, K Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Cancer KW - Transduction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313048849?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=Reprogramming+the+cancer+epigenome+by+metabolic+transduction&rft.au=Byun%2C+J%3BGardner%2C+K&rft.aulast=Byun&rft.aufirst=J&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - The National Cancer Institute's automated selfadministered 24-hour dietary recall T2 - Experimental Biology 2012 (EB 2012) AN - 1313026124; 6160908 JF - Experimental Biology 2012 (EB 2012) AU - Subar, A AU - Kirkpatrick, S AU - Mittl, B AU - Zimmerman, T AU - Thompson, F AU - Bingley, C AU - Willis, G AU - McNutt, S AU - Potischman, N Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Cancer KW - Diets KW - Automation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313026124?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=The+National+Cancer+Institute%27s+automated+selfadministered+24-hour+dietary+recall&rft.au=Subar%2C+A%3BKirkpatrick%2C+S%3BMittl%2C+B%3BZimmerman%2C+T%3BThompson%2C+F%3BBingley%2C+C%3BWillis%2C+G%3BMcNutt%2C+S%3BPotischman%2C+N&rft.aulast=Subar&rft.aufirst=A&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Biomarkers of nutrition for development: an overview T2 - Experimental Biology 2012 (EB 2012) AN - 1313023374; 6160062 JF - Experimental Biology 2012 (EB 2012) AU - Raghavan, R AU - Darnton-Hill, I AU - Raiten, D Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Bioindicators KW - Nutrition KW - Reviews KW - biomarkers KW - Biomarkers UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313023374?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=Biomarkers+of+nutrition+for+development%3A+an+overview&rft.au=Raghavan%2C+R%3BDarnton-Hill%2C+I%3BRaiten%2C+D&rft.aulast=Raghavan&rft.aufirst=R&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - O-GlcNAc cycling and epigenetics T2 - Experimental Biology 2012 (EB 2012) AN - 1313015008; 6161554 JF - Experimental Biology 2012 (EB 2012) AU - Hanover, J AU - Wang, P AU - Ghosh, S AU - Keembiyehetty, C AU - Comly, M AU - Bond, M AU - Krause, M AU - Love, D Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - epigenetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313015008?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=O-GlcNAc+cycling+and+epigenetics&rft.au=Hanover%2C+J%3BWang%2C+P%3BGhosh%2C+S%3BKeembiyehetty%2C+C%3BComly%2C+M%3BBond%2C+M%3BKrause%2C+M%3BLove%2C+D&rft.aulast=Hanover&rft.aufirst=J&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - A microRNA pulldown approach uncovers regulation of p53 activity and growth factor signaling by miR- 34a T2 - Experimental Biology 2012 (EB 2012) AN - 1313003122; 6161398 JF - Experimental Biology 2012 (EB 2012) AU - Lal, A AU - Thomas, M AU - Navarro, F AU - Li, X. AU - Lieberman, J Y1 - 2012/04/21/ PY - 2012 DA - 2012 Apr 21 KW - Growth factors KW - miRNA KW - p53 protein KW - Growth UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313003122?accountid=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=Experimental+Biology+2012+%28EB+2012%29&rft.atitle=A+microRNA+pulldown+approach+uncovers+regulation+of+p53+activity+and+growth+factor+signaling+by+miR-+34a&rft.au=Lal%2C+A%3BThomas%2C+M%3BNavarro%2C+F%3BLi%2C+X.%3BLieberman%2C+J&rft.aulast=Lal&rft.aufirst=A&rft.date=2012-04-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Experimental+Biology+2012+%28EB+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://experimentalbiology.org/eb/pages/upload/file/pdfs/Final%20Print.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Prostaglandin E2 Suppresses Antifungal Immunity by Inhibiting Interferon Regulatory Factor 4 Function and Interleukin-17 Expression in T Cells AN - 1022566422; 16825155 AB - T helper 17 (Th17) cells play an important role in mucosal host defense through production of the signature cytokines IL-17 and IL-22. Prostaglandin E2 (PGE2) has been shown to enhance IL-17 production by mature Th17 cells. However, when present during Th17 cell differentiation, we found that PGE2 inhibited the transcription factor IRF4 and suppressed production of IL-17 but not IL-22. We show that IRF4 was required for IL-17 expression but inhibited IL-22 expression, highlighting the potential for discordant regulation of these two cytokines in Th17 cells. The pathogenic fungus Cryptococcus neoformans produces PGE2, and we found that it uses PGE2- and IRF4-dependent mechanisms to specifically inhibit induction of IL-17 during Th17 cell differentiation. Blockade of host PGE2 during infection led to increased IL-17 production from CD4 super(+) T cells and increased survival of mice. These findings suggest that host-or pathogen-derived PGE2 can act directly on Th17 cells during differentiation to inhibit IL-17-dependent antimicrobial responses. JF - Immunity AU - Valdez, P A AU - Vithayathil, P J AU - Janelsins, B M AU - Shaffer, AL AU - Williamson, PR AU - Datta, S K AD - Bacterial Pathogenesis Unit, Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA Y1 - 2012/04/20/ PY - 2012 DA - 2012 Apr 20 VL - 36 IS - 4 SN - 1074-7613, 1074-7613 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts KW - Antimicrobial agents KW - CD4 antigen KW - Cell survival KW - Differentiation KW - Helper cells KW - Infection KW - Interferon regulatory factor 4 KW - Interleukin 17 KW - Interleukin 22 KW - Lymphocytes T KW - Mucosa KW - Prostaglandin E2 KW - Transcription factors KW - Cryptococcus neoformans KW - A 01340:Antibiotics & Antimicrobials KW - F 06910:Microorganisms & Parasites KW - K 03320:Cell Biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1022566422?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologya&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Immunity&rft.atitle=Prostaglandin+E2+Suppresses+Antifungal+Immunity+by+Inhibiting+Interferon+Regulatory+Factor+4+Function+and+Interleukin-17+Expression+in+T+Cells&rft.au=Valdez%2C+P+A%3BVithayathil%2C+P+J%3BJanelsins%2C+B+M%3BShaffer%2C+AL%3BWilliamson%2C+PR%3BDatta%2C+S+K&rft.aulast=Valdez&rft.aufirst=P&rft.date=2012-04-20&rft.volume=36&rft.issue=4&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Immunity&rft.issn=10747613&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Last updated - 2012-09-10 N1 - SubjectsTermNotLitGenreText - Cell survival; Helper cells; Interferon regulatory factor 4; Mucosa; Prostaglandin E2; Infection; Antimicrobial agents; Differentiation; Interleukin 22; CD4 antigen; Interleukin 17; Transcription factors; Lymphocytes T; Cryptococcus neoformans ER - TY - JOUR T1 - Activation of tumor cell proliferation by thyroid hormone in a mouse model of follicular thyroid carcinoma. AN - 1008825539; 21909131 AB - Thyroid cancers are the most common malignancy of the endocrine system in humans. To understand the molecular genetic events underlying thyroid carcinogenesis, we have generated a mouse model that spontaneously develops follicular thyroid carcinoma similar to human thyroid cancer (Thrb(PV/PV) mouse). This mutant mouse harbors a dominant-negative mutated thyroid hormone receptor β (denoted PV). The PV mutation was identified in a patient with resistance to thyroid hormone (TH). Thrb(PV/PV) mice exhibit highly elevated serum thyroid-stimulating hormone levels and increased TH. We have previously shown that thyroid-stimulating hormone is required, but not sufficient to induce metastatic follicular thyroid cancer in Thrb(PV/PV) mice. However, whether the elevated TH also contributes to the thyroid carcinogenesis of Thrb(PV/PV) mice was not elucidated. To understand the role of TH in thyroid carcinogenesis, we blocked the production of TH by treating Thrb(PV/PV) mice with propylthiouracil (Thrb(PV/PV)-PTU mice) and compared the development of thyroid cancer in Thrb(PV/PV)-PTU and untreated Thrb(PV/PV) mice. We found that thyroid tumor growth was reduced by ∼42% in Thrb(PV/PV)-PTU mice as compared with Thrb(PV/PV) mice. Analysis by bromodeoxyuridine-nuclear labeling showed decreased incorporation of bromodeoxyuridine in thyroid tumor cells of Thrb(PV/PV)-PTU mice, indicative of decreased tumor cell proliferation. However, cleaved-caspase 3 staining showed no apparent changes in apoptosis of tumor cells in Thrb(PV/PV)-PTU mice. Molecular studies identified a marked attenuation of the PI3K-AKT-β-catenin signaling pathway that led to decreased protein levels of cyclin D2, thereby decreasing tumor cell proliferation in Thrb(PV/PV)-PTU mice. Furthermore, matrix metalloproteinase-2, a downstream target of β-catenin and a key regulator during tumor invasion and metastasis, was also decreased. Thus, the present study uncovers a critical role of TH in promoting the thyroid carcinogenesis of Thrb(PV/PV) mice via membrane signaling events. Importantly, these findings suggest that anti-thyroid drugs could be considered as possible therapeutic agents of thyroid cancer. JF - Oncogene AU - Lu, C AU - Zhu, X AU - Willingham, M C AU - Cheng, S-Y AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892-4264, USA. Y1 - 2012/04/19/ PY - 2012 DA - 2012 Apr 19 SP - 2007 EP - 2016 VL - 31 IS - 16 KW - Antithyroid Agents KW - 0 KW - Cyclin D2 KW - Thyroid Hormone Receptors beta KW - Thyroid Hormones KW - Propylthiouracil KW - 721M9407IY KW - Thyrotropin KW - 9002-71-5 KW - Index Medicus KW - Cell Proliferation -- drug effects KW - Adenocarcinoma, Follicular KW - Animals KW - Thyrotropin -- blood KW - Disease Models, Animal KW - Propylthiouracil -- pharmacology KW - Mice KW - Thyroid Hormone Receptors beta -- genetics KW - Antithyroid Agents -- pharmacology KW - Signal Transduction KW - Cyclin D2 -- metabolism KW - Thyroid Neoplasms -- genetics KW - Thyroid Hormones -- physiology KW - Thyroid Neoplasms -- metabolism KW - Thyroid Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008825539?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Oncogene&rft.atitle=Activation+of+tumor+cell+proliferation+by+thyroid+hormone+in+a+mouse+model+of+follicular+thyroid+carcinoma.&rft.au=Lu%2C+C%3BZhu%2C+X%3BWillingham%2C+M+C%3BCheng%2C+S-Y&rft.aulast=Lu&rft.aufirst=C&rft.date=2012-04-19&rft.volume=31&rft.issue=16&rft.spage=2007&rft.isbn=&rft.btitle=&rft.title=Oncogene&rft.issn=1476-5594&rft_id=info:doi/10.1038%2Fonc.2011.390 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-20 N1 - Date created - 2012-04-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell Cycle. 2009 Nov 1;8(21):3562-70 [19838061] Am J Physiol Endocrinol Metab. 2009 Dec;297(6):E1238-46 [19755667] Thyroid. 2009 Dec;19(12):1351-61 [19895341] Endocrinology. 2010 Jan;151(1):211-20 [19887570] Thyroid. 2010 Mar;20(3):281-6 [20187783] Endocrinology. 2010 Apr;151(4):1929-39 [20133453] Mol Cell Endocrinol. 2010 May 28;321(1):20-8 [19897009] Carcinogenesis. 2007 Dec;28(12):2451-8 [17660507] Oncogene. 2008 Jan 31;27(6):823-30 [17653082] Mol Cell Biol. 2008 Jul;28(14):4598-608 [18474620] Oncogene. 2008 Sep 18;27(41):5477-85 [18794882] Eur J Endocrinol. 2009 Jan;160(1):71-9 [18952764] Cancer Res. 2009 Mar 1;69(5):1867-76 [19223551] Thyroid. 2009 Apr;19(4):333-40 [19355823] Am J Physiol Cell Physiol. 2009 May;296(5):C980-91 [19158403] Mol Cell Endocrinol. 2009 Sep 24;308(1-2):63-9 [19549593] Endocr Rev. 2010 Apr;31(2):139-70 [20051527] Cell. 2010 Apr 2;141(1):52-67 [20371345] Thyroid. 2010 Jul;20(7):697-706 [20578891] Clin Oncol (R Coll Radiol). 2010 Aug;22(6):395-404 [20627675] Cancer Res. 2010 Oct 15;70(20):8149-58 [20736363] Endocrinology. 2010 Nov;151(11):5528-36 [20844001] Oncogene. 2010 Oct 21;29(42):5678-86 [20676139] Curr Opin Oncol. 2011 Jan;23(1):13-21 [21045687] Steroids. 2011 Aug;76(9):885-91 [21473875] Proc Natl Acad Sci U S A. 2000 Nov 21;97(24):13209-14 [11069286] Thyroid. 2002 Nov;12(11):963-9 [12490073] J Clin Endocrinol Metab. 2003 May;88(5):2341-7 [12727994] Cell Cycle. 2003 Jul-Aug;2(4):339-45 [12851486] Cancer Res. 2003 Sep 1;63(17):5274-80 [14500358] Cell Cycle. 2004 Feb;3(2):145-8 [14712077] Circ Res. 2004 Jun 11;94(11):1500-6 [15117822] J Clin Endocrinol Metab. 1991 Nov;73(5):990-4 [1682340] J Clin Invest. 1991 Dec;88(6):2123-30 [1661299] Mol Cell Biol. 2005 Jan;25(1):124-35 [15601836] Mol Endocrinol. 2005 Jan;19(1):102-12 [15388791] Endocr Pathol. 2004 Winter;15(4):319-27 [15681856] Endocrinology. 2005 Jul;146(7):2864-71 [15802494] Thyroid. 2005 Jun;15(6):551-61 [16029121] Proc Natl Acad Sci U S A. 2006 Feb 7;103(6):1780-5 [16446424] JAMA. 2006 May 10;295(18):2164-7 [16684987] J Clin Invest. 2006 Nov;116(11):2972-84 [17039256] Int Angiol. 2006 Dec;25(4):407-13 [17164749] J Mol Endocrinol. 2007 Feb;38(1-2):221-33 [17293442] Clin Cancer Res. 2007 Feb 15;13(4):1161-70 [17317825] Steroids. 2007 Feb;72(2):180-7 [17174366] J Biol Chem. 2007 Apr 13;282(15):11221-9 [17287208] Carcinogenesis. 2007 May;28(5):932-9 [17127711] Arch Otolaryngol Head Neck Surg. 2007 May;133(5):503-10 [17515507] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1038/onc.2011.390 ER - TY - CPAPER T1 - Structure-Guided Development of AIDS Therapeutics: Successes, Challenges, and Opportunities T2 - The 25th International Conference on Antiviral Research AN - 1313084833; 6128984 JF - The 25th International Conference on Antiviral Research AU - Mitsuya, Hiroaki Y1 - 2012/04/16/ PY - 2012 DA - 2012 Apr 16 KW - Acquired immune deficiency syndrome KW - Drug development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313084833?accountid=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=The+25th+International+Conference+on+Antiviral+Research&rft.atitle=Structure-Guided+Development+of+AIDS+Therapeutics%3A+Successes%2C+Challenges%2C+and+Opportunities&rft.au=Mitsuya%2C+Hiroaki&rft.aulast=Mitsuya&rft.aufirst=Hiroaki&rft.date=2012-04-16&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=The+25th+International+Conference+on+Antiviral+Research&rft.issn=&rft_id=info:doi/ L2 - http://www.isar-icar.com/resource/resmgr/docs/final_program_2012.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Mapping of the UGT1A locus identifies an uncommon coding variant that affects mRNA expression and protects from bladder cancer. AN - 959144571; 22228101 AB - A recent genome-wide association study of bladder cancer identified the UGT1A gene cluster on chromosome 2q37.1 as a novel susceptibility locus. The UGT1A cluster encodes a family of UDP-glucuronosyltransferases (UGTs), which facilitate cellular detoxification and removal of aromatic amines. Bioactivated forms of aromatic amines found in tobacco smoke and industrial chemicals are the main risk factors for bladder cancer. The association within the UGT1A locus was detected by a single nucleotide polymorphism (SNP) rs11892031. Now, we performed detailed resequencing, imputation and genotyping in this region. We clarified the original genetic association detected by rs11892031 and identified an uncommon SNP rs17863783 that explained and strengthened the association in this region (allele frequency 0.014 in 4035 cases and 0.025 in 5284 controls, OR = 0.55, 95%CI = 0.44-0.69, P = 3.3 × 10(-7)). Rs17863783 is a synonymous coding variant Val209Val within the functional UGT1A6.1 splicing form, strongly expressed in the liver, kidney and bladder. We found the protective T allele of rs17863783 to be associated with increased mRNA expression of UGT1A6.1 in in-vitro exontrap assays and in human liver tissue samples. We suggest that rs17863783 may protect from bladder cancer by increasing the removal of carcinogens from bladder epithelium by the UGT1A6.1 protein. Our study shows an example of genetic and functional role of an uncommon protective genetic variant in a complex human disease, such as bladder cancer. JF - Human molecular genetics AU - Tang, Wei AU - Fu, Yi-Ping AU - Figueroa, Jonine D AU - Malats, Núria AU - Garcia-Closas, Montserrat AU - Chatterjee, Nilanjan AU - Kogevinas, Manolis AU - Baris, Dalsu AU - Thun, Michael AU - Hall, Jennifer L AU - De Vivo, Immaculata AU - Albanes, Demetrius AU - Porter-Gill, Patricia AU - Purdue, Mark P AU - Burdett, Laurie AU - Liu, Luyang AU - Hutchinson, Amy AU - Myers, Timothy AU - Tardón, Adonina AU - Serra, Consol AU - Carrato, Alfredo AU - Garcia-Closas, Reina AU - Lloreta, Josep AU - Johnson, Alison AU - Schwenn, Molly AU - Karagas, Margaret R AU - Schned, Alan AU - Black, Amanda AU - Jacobs, Eric J AU - Diver, W Ryan AU - Gapstur, Susan M AU - Virtamo, Jarmo AU - Hunter, David J AU - Fraumeni, Joseph F AU - Chanock, Stephen J AU - Silverman, Debra T AU - Rothman, Nathaniel AU - Prokunina-Olsson, Ludmila AD - Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD 20892, USA. Y1 - 2012/04/15/ PY - 2012 DA - 2012 Apr 15 SP - 1918 EP - 1930 VL - 21 IS - 8 KW - Carcinogens KW - 0 KW - Protein Isoforms KW - RNA, Messenger KW - irinotecan KW - 0H43101T0J KW - UDP-glucuronosyltransferase, UGT1A6 KW - EC 2.4.1.- KW - Glucuronosyltransferase KW - EC 2.4.1.17 KW - Camptothecin KW - XT3Z54Z28A KW - Index Medicus KW - Urinary Bladder -- metabolism KW - Humans KW - Liver -- metabolism KW - RNA, Messenger -- genetics KW - Chromosome Mapping KW - Camptothecin -- administration & dosage KW - Genome-Wide Association Study KW - Phenotype KW - Carcinogens -- metabolism KW - RNA, Messenger -- metabolism KW - Risk Factors KW - Camptothecin -- analogs & derivatives KW - Case-Control Studies KW - Genetic Predisposition to Disease KW - Protein Isoforms -- genetics KW - Polymorphism, Single Nucleotide KW - Glucuronosyltransferase -- genetics KW - Urinary Bladder Neoplasms -- prevention & control KW - Urinary Bladder Neoplasms -- genetics KW - Glucuronosyltransferase -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/959144571?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Human+molecular+genetics&rft.atitle=Mapping+of+the+UGT1A+locus+identifies+an+uncommon+coding+variant+that+affects+mRNA+expression+and+protects+from+bladder+cancer.&rft.au=Tang%2C+Wei%3BFu%2C+Yi-Ping%3BFigueroa%2C+Jonine+D%3BMalats%2C+N%C3%BAria%3BGarcia-Closas%2C+Montserrat%3BChatterjee%2C+Nilanjan%3BKogevinas%2C+Manolis%3BBaris%2C+Dalsu%3BThun%2C+Michael%3BHall%2C+Jennifer+L%3BDe+Vivo%2C+Immaculata%3BAlbanes%2C+Demetrius%3BPorter-Gill%2C+Patricia%3BPurdue%2C+Mark+P%3BBurdett%2C+Laurie%3BLiu%2C+Luyang%3BHutchinson%2C+Amy%3BMyers%2C+Timothy%3BTard%C3%B3n%2C+Adonina%3BSerra%2C+Consol%3BCarrato%2C+Alfredo%3BGarcia-Closas%2C+Reina%3BLloreta%2C+Josep%3BJohnson%2C+Alison%3BSchwenn%2C+Molly%3BKaragas%2C+Margaret+R%3BSchned%2C+Alan%3BBlack%2C+Amanda%3BJacobs%2C+Eric+J%3BDiver%2C+W+Ryan%3BGapstur%2C+Susan+M%3BVirtamo%2C+Jarmo%3BHunter%2C+David+J%3BFraumeni%2C+Joseph+F%3BChanock%2C+Stephen+J%3BSilverman%2C+Debra+T%3BRothman%2C+Nathaniel%3BProkunina-Olsson%2C+Ludmila&rft.aulast=Tang&rft.aufirst=Wei&rft.date=2012-04-15&rft.volume=21&rft.issue=8&rft.spage=1918&rft.isbn=&rft.btitle=&rft.title=Human+molecular+genetics&rft.issn=1460-2083&rft_id=info:doi/10.1093%2Fhmg%2Fddr619 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-18 N1 - Date created - 2012-03-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Hum Genet. 2011 Jul;130(1):59-78 [21678065] Annu Rev Pharmacol Toxicol. 2000;40:581-616 [10836148] World J Urol. 2001 Apr;19(2):151-3 [11374319] Am J Hum Genet. 2001 Jul;69(1):124-37 [11404818] Pharmacogenetics. 2001 Jun;11(4):357-68 [11434514] Trends Genet. 2001 Sep;17(9):502-10 [11525833] Mol Pharmacol. 2002 Sep;62(3):446-50 [12181419] Mutat Res. 2002 Sep 30;506-507:65-77 [12351146] Pharmacogenetics. 2002 Dec;12(9):725-33 [12464801] Nucleic Acids Res. 2003 Jul 1;31(13):3568-71 [12824367] Nat Rev Cancer. 2003 Oct;3(10):733-44 [14570033] Pharmacoeconomics. 2003;21(18):1315-30 [14750899] Toxicol Appl Pharmacol. 1979 Sep 30;50(3):479-84 [516060] Chem Biol Interact. 1980 Sep;31(3):265-78 [7408035] Cancer Res. 1982 Feb;42(2):642-8 [6275985] Crit Rev Biochem Mol Biol. 1991;26(2):129-50 [1914494] Semin Urol. 1993 Aug;11(3):113-26 [8210833] J Am Diet Assoc. 1995 Jul;95(7):791-7 [7797810] Science. 1996 Oct 25;274(5287):536-9 [8928008] Nat Genet. 1999 Jan;21(1 Suppl):56-60 [9915503] Br J Ind Med. 1954 Jul;11(3):213-6 [13182161] J Urol. 1959 Feb;81(2):339-43 [13631832] Bioinformatics. 2005 Jan 15;21(2):263-5 [15297300] Nat Rev Genet. 2005 Feb;6(2):109-18 [15716907] Lancet. 2005 Aug 20-26;366(9486):649-59 [16112301] Mol Cell Proteomics. 2005 Dec;4(12):1920-32 [16127175] Pharmacogenomics J. 2006 Jan-Feb;6(1):63-75 [16314888] Oncogene. 2006 Mar 13;25(11):1659-72 [16550166] Nat Genet. 2006 Jun;38(6):659-62 [16715099] Urol Oncol. 2006 Jul-Aug;24(4):338-43 [16818188] Drug Metab Rev. 2006;38(3):393-409 [16877259] BMC Cancer. 2006;6:239 [17026750] Mol Cancer Ther. 2007 Mar;6(3):820-32 [17339364] Pharmacogenet Genomics. 2007 Jul;17(7):497-504 [17558305] Int J Epidemiol. 2007 Apr;36(2):445-8 [17470492] Cancer Epidemiol Biomarkers Prev. 2007 Aug;16(8):1595-600 [17684133] Am J Hum Genet. 2007 Sep;81(3):559-75 [17701901] Am J Epidemiol. 2007 Oct 1;166(7):741-51 [17675654] Am J Hum Genet. 2008 Jan;82(1):100-12 [18179889] Curr Atheroscler Rep. 2008 Jun;10(3):194-200 [18489846] JAMA. 2008 May 28;299(20):2423-36 [18505952] Nat Genet. 2008 Jun;40(6):695-701 [18509313] Am J Hum Genet. 2008 Jul;83(1):112-9 [18589396] Drug Metab Dispos. 2008 Aug;36(8):1461-4 [18480185] Scand J Urol Nephrol Suppl. 2008 Sep;(218):110-5 [18815925] Proc Natl Acad Sci U S A. 2009 Jun 9;106(23):9362-7 [19474294] Curr Opin Genet Dev. 2009 Jun;19(3):212-9 [19481926] PLoS Genet. 2009 Jun;5(6):e1000529 [19543373] Hum Mol Genet. 2009 Jul 15;18(14):2700-10 [19414484] Hum Mol Genet. 2009 Jul 15;18(14):2711-8 [19419973] Nature. 2009 Oct 8;461(7265):747-53 [19812666] PLoS Biol. 2010 Jan;8(1):e1000294 [20126254] Methods Mol Biol. 2010;641:1-12 [20407938] Am J Hum Genet. 2010 May 14;86(5):730-42 [20434130] Hum Genomics. 2010 Apr;4(4):238-49 [20511137] Nature. 2010 Aug 5;466(7307):714-9 [20686566] Nature. 2010 Sep 2;467(7311):52-8 [20811451] CA Cancer J Clin. 2010 Sep-Oct;60(5):277-300 [20610543] Am J Epidemiol. 2010 Oct 15;172(8):869-89 [20876667] Nat Genet. 2010 Nov;42(11):978-84 [20972438] Nature. 2010 Oct 28;467(7319):1061-73 [20981092] PLoS Biol. 2011;9(1):e1001008 [21267066] Am J Hum Genet. 2011 Apr 8;88(4):458-68 [21457907] Carcinogenesis. 2011 Jun;32(6):843-7 [21402590] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/hmg/ddr619 ER - TY - JOUR T1 - Formation of reactive sulfite-derived free radicals by the activation of human neutrophils: an ESR study. AN - 948911246; 22326772 AB - The objective of this study was to determine the effect of (bi)sulfite (hydrated sulfur dioxide) on human neutrophils and the ability of these immune cells to produce reactive free radicals due to (bi)sulfite oxidation. Myeloperoxidase (MPO) is an abundant heme protein in neutrophils that catalyzes the formation of cytotoxic oxidants implicated in asthma and inflammatory disorders. In this study sulfite ((•)SO(3)(-)) and sulfate (SO(4)(•-)) anion radicals are characterized with the ESR spin-trapping technique using 5,5-dimethyl-1-pyrroline N-oxide (DMPO) in the reaction of (bi)sulfite oxidation by human MPO and human neutrophils via sulfite radical chain reaction chemistry. After treatment with (bi)sulfite, phorbol 12-myristate 13-acetate-stimulated neutrophils produced DMPO-sulfite anion radical, -superoxide, and -hydroxyl radical adducts. The last adduct probably resulted, in part, from the conversion of DMPO-sulfate to DMPO-hydroxyl radical adduct via a nucleophilic substitution reaction of the radical adduct. This anion radical (SO(4)(•-)) is highly reactive and, presumably, can oxidize target proteins to protein radicals, thereby initiating protein oxidation. Therefore, we propose that the potential toxicity of (bi)sulfite during pulmonary inflammation or lung-associated diseases such as asthma may be related to free radical formation. Published by Elsevier Inc. JF - Free radical biology & medicine AU - Ranguelova, Kalina AU - Rice, Annette B AU - Khajo, Abdelahad AU - Triquigneaux, Mathilde AU - Garantziotis, Stavros AU - Magliozzo, Richard S AU - Mason, Ronald P AD - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Y1 - 2012/04/15/ PY - 2012 DA - 2012 Apr 15 SP - 1264 EP - 1271 VL - 52 IS - 8 KW - Free Radicals KW - 0 KW - Spin Labels KW - Sulfites KW - Peroxidase KW - EC 1.11.1.7 KW - Index Medicus KW - Oxidation-Reduction KW - Cells, Cultured KW - Humans KW - Peroxidase -- metabolism KW - Peroxidase -- antagonists & inhibitors KW - Neutrophils -- metabolism KW - Neutrophil Activation KW - Electron Spin Resonance Spectroscopy -- methods KW - Sulfites -- metabolism KW - Neutrophils -- enzymology KW - Free Radicals -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/948911246?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Formation+of+reactive+sulfite-derived+free+radicals+by+the+activation+of+human+neutrophils%3A+an+ESR+study.&rft.au=Ranguelova%2C+Kalina%3BRice%2C+Annette+B%3BKhajo%2C+Abdelahad%3BTriquigneaux%2C+Mathilde%3BGarantziotis%2C+Stavros%3BMagliozzo%2C+Richard+S%3BMason%2C+Ronald+P&rft.aulast=Ranguelova&rft.aufirst=Kalina&rft.date=2012-04-15&rft.volume=52&rft.issue=8&rft.spage=1264&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2012.01.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-16 N1 - Date created - 2012-03-26 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Eur J Biochem. 2000 Oct;267(19):5858-64 [10998045] J Biol Chem. 2010 Jul 30;285(31):24195-205 [20501663] Chem Biol. 2002 May;9(5):555-65 [12031662] Scand J Clin Lab Invest Suppl. 1968;97:77-89 [4179068] J Biol Chem. 1971 Jan 25;246(2):359-66 [5542006] Am J Pathol. 1974 Apr;75(1):45-60 [4133056] Environ Health Perspect. 1974 Aug;8:97-121 [4470921] Biochemistry. 1976 Jul 13;15(14):3059-63 [8081] Biochem Biophys Res Commun. 1977 Aug 22;77(4):1486-91 [197963] Biochim Biophys Acta. 1979 Dec 6;548(3):608-15 [228717] Proc Natl Acad Sci U S A. 1980 Jun;77(6):3715-9 [6997882] Food Cosmet Toxicol. 1981 Oct;19(5):667-82 [6171492] J Biol Chem. 1982 May 10;257(9):5050-5 [6279657] J Clin Invest. 1982 Sep;70(3):598-607 [6286728] Mol Pharmacol. 1982 Nov;22(3):732-7 [6296662] J Allergy Clin Immunol. 1984 Oct;74(4 Pt 1):469-72 [6491092] J Leukoc Biol. 1985 Apr;37(4):431-47 [3855949] J Biol Chem. 1985 Apr 10;260(7):4003-6 [2984193] Adv Food Res. 1986;30:1-76 [3526827] Proc Natl Acad Sci U S A. 1986 Oct;83(20):7593-7 [3020550] CRC Crit Rev Toxicol. 1987;17(3):185-214 [3556020] Biochem Pharmacol. 1988 Aug 1;37(15):2907-13 [2840082] Arch Biochem Biophys. 1988 Dec;267(2):681-9 [2850769] Ann Allergy. 1989 May;62(5):402-5 [2719349] Am J Respir Cell Mol Biol. 1990 Nov;3(5):507-11 [2223105] Methods Enzymol. 1990;186:127-33 [2172700] Free Radic Biol Med. 1990;9(3):235-43 [2272532] Biochem Pharmacol. 1991 May 15;41(10):1485-92 [1850278] Arch Biochem Biophys. 1991 Aug 15;289(1):145-52 [1654843] Chest. 1991 Nov;100(5):1319-22 [1657539] Free Radic Biol Med. 1993 Jun;14(6):661-8 [8392022] Biochemistry. 1994 Feb 15;33(6):1447-54 [8312264] J Toxicol Environ Health. 1994 Mar;41(3):285-97 [8126751] Pharmacol Toxicol. 1994 Feb;74(2):136-40 [8190702] J Magn Reson B. 1994 Jun;104(2):105-10 [8049862] Lancet. 1994 Oct 1;344(8927):930-3 [7934352] J Biolumin Chemilumin. 1994 May-Jun;9(3):171-5 [7942122] Clin Chem. 1995 Jun;41(6 Pt 1):897-903 [7768009] J Am Coll Nutr. 1995 Jun;14(3):229-32 [8586770] Mech Ageing Dev. 1996 Jul 5;88(1-2):95-109 [8803926] Biochem J. 1997 Jan 15;321 ( Pt 2):503-8 [9020887] FEBS Lett. 1997 Feb 17;403(2):127-30 [9042951] Arch Biochem Biophys. 1997 Mar 1;339(1):200-9 [9056250] Clin Exp Immunol. 1997 Apr;108(1):167-74 [9097926] Biochemistry. 1998 Dec 22;37(51):17923-30 [9922160] J Biol Chem. 1999 Apr 2;274(14):9494-502 [10092633] Free Radic Biol Med. 1999 Aug;27(3-4):411-21 [10468216] J Biol Chem. 1961 Jun;236:1836-40 [13701912] Can J Physiol Pharmacol. 2005 Jan;83(1):69-75 [15759052] Biochem J. 2005 May 1;387(Pt 3):841-7 [15595925] J Leukoc Biol. 2005 May;77(5):598-625 [15689384] Free Radic Biol Med. 2007 Oct 1;43(7):995-1022 [17761297] Am J Physiol Lung Cell Mol Physiol. 2007 Nov;293(5):L1293-9 [17720872] Chem Biol Interact. 2008 Aug 11;174(3):147-54 [18579106] Free Radic Biol Med. 2009 Jul 15;47(2):128-34 [19362142] Clin Exp Allergy. 2009 Nov;39(11):1643-51 [19775253] Environ Health Perspect. 2010 Jul;118(7):970-5 [20348042] Free Radic Biol Med. 2010 Aug 1;49(3):317-22 [20406682] Eur J Pharmacol. 2001 Apr 6;417(1-2):37-43 [11301057] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.freeradbiomed.2012.01.016 ER - TY - JOUR T1 - β-Caryophyllene ameliorates cisplatin-induced nephrotoxicity in a cannabinoid 2 receptor-dependent manner. AN - 948905437; 22326488 AB - (E)-β-caryophyllene (BCP) is a natural sesquiterpene found in many essential oils of spice (best known for contributing to the spiciness of black pepper) and food plants with recognized anti-inflammatory properties. Recently it was shown that BCP is a natural agonist of endogenous cannabinoid 2 (CB(2)) receptors, which are expressed in immune cells and mediate anti-inflammatory effects. In this study we aimed to test the effects of BCP in a clinically relevant murine model of nephropathy (induced by the widely used antineoplastic drug cisplatin) in which the tubular injury is largely dependent on inflammation and oxidative/nitrative stress. β-caryophyllene dose-dependently ameliorated cisplatin-induced kidney dysfunction, morphological damage, and renal inflammatory response (chemokines MCP-1 and MIP-2, cytokines TNF-α and IL-1β, adhesion molecule ICAM-1, and neutrophil and macrophage infiltration). It also markedly mitigated oxidative/nitrative stress (NOX-2 and NOX-4 expression, 4-HNE and 3-NT content) and cell death. The protective effects of BCP against biochemical and histological markers of nephropathy were absent in CB(2) knockout mice. Thus, BCP may be an excellent therapeutic agent to prevent cisplatin-induced nephrotoxicity through a CB(2) receptor-dependent pathway. Given the excellent safety profile of BCP in humans it has tremendous therapeutic potential in a multitude of diseases associated with inflammation and oxidative stress. Published by Elsevier Inc. JF - Free radical biology & medicine AU - Horváth, Béla AU - Mukhopadhyay, Partha AU - Kechrid, Malek AU - Patel, Vivek AU - Tanchian, Galin AU - Wink, David A AU - Gertsch, Jürg AU - Pacher, Pál AD - Laboratory of Physiologic Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/04/15/ PY - 2012 DA - 2012 Apr 15 SP - 1325 EP - 1333 VL - 52 IS - 8 KW - Antineoplastic Agents KW - 0 KW - DNA Primers KW - Nitrates KW - Receptor, Cannabinoid, CB2 KW - Sesquiterpenes KW - caryophyllene KW - BHW853AU9H KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Animals KW - Base Sequence KW - Oxidative Stress KW - Nitrates -- metabolism KW - Mice, Inbred C57BL KW - Mice KW - Male KW - Kidney -- metabolism KW - Cisplatin -- toxicity KW - Kidney -- drug effects KW - Antineoplastic Agents -- toxicity KW - Receptor, Cannabinoid, CB2 -- physiology KW - Sesquiterpenes -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/948905437?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=%CE%B2-Caryophyllene+ameliorates+cisplatin-induced+nephrotoxicity+in+a+cannabinoid+2+receptor-dependent+manner.&rft.au=Horv%C3%A1th%2C+B%C3%A9la%3BMukhopadhyay%2C+Partha%3BKechrid%2C+Malek%3BPatel%2C+Vivek%3BTanchian%2C+Galin%3BWink%2C+David+A%3BGertsch%2C+J%C3%BCrg%3BPacher%2C+P%C3%A1l&rft.aulast=Horv%C3%A1th&rft.aufirst=B%C3%A9la&rft.date=2012-04-15&rft.volume=52&rft.issue=8&rft.spage=1325&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2012.01.014 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-16 N1 - Date created - 2012-03-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: FASEB J. 2009 Jul;23(7):2120-30 [19246487] J Leukoc Biol. 2007 Dec;82(6):1382-9 [17652447] J Pharm Pharmacol. 2007 Dec;59(12):1643-7 [18053325] Toxicol Lett. 2008 Jan 4;176(1):48-57 [18063323] Br J Pharmacol. 2008 Jan;153(2):263-70 [17906675] Br J Pharmacol. 2008 Jan;153(2):252-62 [18026124] Kidney Int. 2008 May;73(9):994-1007 [18272962] Int J Cancer. 2008 Sep 1;123(5):1025-33 [18546271] Proc Natl Acad Sci U S A. 2008 Jul 1;105(26):9099-104 [18574142] Arch Biochem Biophys. 2008 Sep 15;477(2):183-95 [18602883] Inflamm Bowel Dis. 2009 Nov;15(11):1678-85 [19408320] Biochemistry. 2010 Feb 9;49(5):835-42 [20050630] Free Radic Biol Med. 2010 Feb 1;48(3):457-67 [19969072] Farmaco. 2001 May-Jul;56(5-7):387-9 [11482764] J Am Soc Nephrol. 2001 Dec;12(12):2683-90 [11729237] Pharmacol Rev. 2002 Jun;54(2):161-202 [12037135] J Clin Invest. 2002 Sep;110(6):835-42 [12235115] Free Radic Biol Med. 2002 Dec 1;33(11):1451-64 [12446202] Am J Respir Crit Care Med. 2002 Dec 15;166(12 Pt 2):S4-8 [12471082] Nat Rev Drug Discov. 2004 Sep;3(9):771-84 [15340387] Cancer Res. 1979 Feb;39(2 Pt 1):365-9 [570092] J Pharm Sci. 1981 Jun;70(6):710-1 [7252830] Xenobiotica. 1986 Aug;16(8):753-67 [3765656] Arch Biochem Biophys. 1991 Aug 1;288(2):481-7 [1654835] Arch Biochem Biophys. 1992 Nov 1;298(2):446-51 [1329657] Free Radic Biol Med. 1996;21(6):855-69 [8902531] Planta Med. 1996 Oct;62(5):427-30 [8923808] Am J Physiol. 1996 Nov;271(5 Pt 1):C1424-37 [8944624] Planta Med. 1996 Oct;62(5):469-70 [9005452] Nature. 1998 Jan 22;391(6665):393-7 [9450756] Nature. 2005 Apr 7;434(7034):782-6 [15815632] CMAJ. 2005 Jun 21;172(13):1672 [15967965] J Agric Food Chem. 2006 Jan 11;54(1):174-81 [16390196] Am J Physiol Renal Physiol. 2006 Sep;291(3):F578-87 [16622172] Pharmacol Rev. 2006 Sep;58(3):389-462 [16968947] FASEB J. 2006 Dec;20(14):2633-5 [17065222] Physiol Rev. 2007 Jan;87(1):315-424 [17237348] Life Sci. 2007 Feb 13;80(10):932-9 [17188718] J Biol Chem. 2007 Mar 2;282(9):6854-62 [17202146] FASEB J. 2007 Jun;21(8):1788-800 [17327359] J Cereb Blood Flow Metab. 2007 Jul;27(7):1387-96 [17245417] Cardiovasc Res. 2010 Mar 1;85(4):773-84 [19942623] Pharmacol Ther. 2010 Apr;126(1):21-38 [20117132] Br J Pharmacol. 2010 Jun;160(3):523-9 [20590562] Br J Pharmacol. 2010 Jun;160(3):657-68 [20590569] Hepatology. 2010 Sep;52(3):1046-59 [20597071] Fundam Clin Pharmacol. 2010 Dec;24(6):749-58 [20015227] J Am Coll Cardiol. 2010 Dec 14;56(25):2115-25 [21144973] Free Radic Biol Med. 2011 Jan 1;50(1):179-95 [21070851] Am J Pathol. 2011 Mar;178(3):1153-66 [21356367] Prog Lipid Res. 2011 Apr;50(2):193-211 [21295074] Mol Med Rep. 2011 Jan-Feb;4(1):151-5 [21461578] Curr Med Chem. 2011;18(11):1575-83 [21428888] Free Radic Biol Med. 2011 May 15;50(10):1368-81 [21362471] Diabetologia. 2011 Jun;54(6):1567-78 [21373835] J Immunol. 2011 Jun 1;186(11):6465-73 [21502376] Diabetes. 2011 Sep;60(9):2386-96 [21810593] Hepatology. 2011 Oct;54(4):1217-26 [21735467] Free Radic Biol Med. 2011 Nov 1;51(9):1774-88 [21884784] Free Radic Biol Med. 2012 Jan 15;52(2):497-506 [22120494] Br J Pharmacol. 2012 Apr;165(8):2462-78 [21449982] Eur Heart J. 2012 Apr;33(7):846-56 [22112961] J Nutr Biochem. 2012 May;23(5):494-500 [21684138] Nat Rev Drug Discov. 2007 Aug;6(8):662-80 [17667957] Am J Physiol Heart Circ Physiol. 2007 Oct;293(4):H2210-8 [17660390] J Pharmacol Exp Ther. 2009 Mar;328(3):708-14 [19074681] J Mol Cell Cardiol. 2009 May;46(5):612-20 [19162037] Microvasc Res. 2009 Jun;78(1):86-94 [19332079] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.freeradbiomed.2012.01.014 ER - TY - JOUR T1 - Switch from cytology-based to human papillomavirus test-based cervical screening: implications for colposcopy. AN - 923575002; 21607948 AB - Human papillomavirus (HPV) testing is more sensitive than cytology; some cervical cancer prevention programs will switch from cytology to carcinogenic HPV test-based screening. The objective of our study is to evaluate the clinical implications of a switch to HPV test-based screening on performance and workload of colposcopy. Women in the population-based, 7-year Guanacaste cohort study were screened at enrollment using cytology. We also took another specimen for HPV DNA testing and collected magnified cervical photographic images (cervigrams). A final case diagnosis (≥cervical intraepithelial neoplasia [CIN] grade 3, CIN2, 27 Mya, suggesting an ancient, conserved relationship between these parasite and host proteins that may serve to attenuate potentially damaging inflammatory responses. JF - Proceedings of the National Academy of Sciences, USA AU - Waisberg, Michael AU - Cerqueira, Gustavo C AU - Yager, Stephanie B AU - Francischetti, Ivo MB AU - Lu, Jinghua AU - Gera, Nidhi AU - Srinivasan, Prakash AU - Miura, Kazutoyo AU - Rada, Balazs AU - Lukszo, Jan AU - Barbian, Kent D AU - Leto, Thomas L AU - Porcella, Stephen F AU - Narum, David L AU - El-Sayed, Najib AU - Miller, Louis H AU - Pierce, Susan K AD - Laboratory of Immunogenetics, Laboratory of Host Defenses, Laboratory of Malaria and Vector Research, Research Technologies Branch, and Laboratory of Malaria Immunology and Vaccinology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852 Y1 - 2012/04/03/ PY - 2012 DA - 2012 Apr 03 SP - 5429 EP - 5434 PB - National Academy of Sciences, 2101 Constitution Ave. Washington DC 20418 United States VL - 109 IS - 14 SN - 0027-8424, 0027-8424 KW - ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology; ASFA 1: Biological Sciences & Living Resources KW - Parasites KW - Human diseases KW - Allelles KW - Immune system KW - Erythrocytes KW - Leukocytes (neutrophilic) KW - Merozoite surface protein 1 KW - Malaria KW - Plasmodium falciparum KW - Hosts KW - Chemotaxis KW - Inflammation KW - Cell activation KW - Public health KW - Proteins KW - Monocytes KW - Host-parasite interactions KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08524:Public health, medicines, dangerous organisms KW - K 03310:Genetics & Taxonomy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1014100146?accountid=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=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Plasmodium+falciparum+merozoite+surface+protein+1+blocks+the+proinflammatory+protein+S100P&rft.au=Waisberg%2C+Michael%3BCerqueira%2C+Gustavo+C%3BYager%2C+Stephanie+B%3BFrancischetti%2C+Ivo+MB%3BLu%2C+Jinghua%3BGera%2C+Nidhi%3BSrinivasan%2C+Prakash%3BMiura%2C+Kazutoyo%3BRada%2C+Balazs%3BLukszo%2C+Jan%3BBarbian%2C+Kent+D%3BLeto%2C+Thomas+L%3BPorcella%2C+Stephen+F%3BNarum%2C+David+L%3BEl-Sayed%2C+Najib%3BMiller%2C+Louis+H%3BPierce%2C+Susan+K&rft.aulast=Waisberg&rft.aufirst=Michael&rft.date=2012-04-03&rft.volume=109&rft.issue=14&rft.spage=5429&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2015-10-28 N1 - SubjectsTermNotLitGenreText - Parasites; Human diseases; Allelles; Erythrocytes; Proteins; Malaria; Hosts; Chemotaxis; Public health; Immune system; Leukocytes (neutrophilic); Merozoite surface protein 1; Monocytes; Host-parasite interactions; Cell activation; Inflammation; Plasmodium falciparum ER - TY - JOUR T1 - Parkinson's disease: don't mess with calcium. AN - 963831626; 22446181 AB - The hallmark of the movement disorder Parkinson's disease (PD) is progressive degeneration of dopaminergic neurons. Mitochondrial dysfunction, impaired ubiquitin-mediated proteolysis of α-synuclein, and ER stress are each implicated in the complex and poorly understood sequence of events leading to dopaminergic neuron demise. In this issue of the JCI, Selvaraj et al. report that in a mouse neurotoxin-based model of PD, reduced Ca2+ influx through transient receptor potential C1 (TRPC1) channels in the plasma membrane of dopaminergic neurons triggers a cell death-inducing ER stress response. These new findings suggest that TRPC1 channels normally function in Ca2+-mediated signaling pathways that couple adaptive/neurotrophic responses to metabolic and oxidative stress and suggest that disruption of these pathways may contribute to PD. JF - The Journal of clinical investigation AU - Mattson, Mark P AD - Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA. mattsonm@grc.nia.nih.gov Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 1195 EP - 1198 VL - 122 IS - 4 KW - TRPC Cation Channels KW - 0 KW - transient receptor potential cation channel, subfamily C, member 1 KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine KW - 9P21XSP91P KW - TOR Serine-Threonine Kinases KW - EC 2.7.1.1 KW - mTOR protein, mouse KW - Akt1 protein, mouse KW - EC 2.7.11.1 KW - Proto-Oncogene Proteins c-akt KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Humans KW - Male KW - Dopaminergic Neurons -- drug effects KW - Unfolded Protein Response -- drug effects KW - Calcium Signaling -- physiology KW - TOR Serine-Threonine Kinases -- physiology KW - 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine -- pharmacology KW - TRPC Cation Channels -- biosynthesis KW - Proto-Oncogene Proteins c-akt -- antagonists & inhibitors KW - Parkinsonian Disorders -- metabolism KW - Endoplasmic Reticulum Stress -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/963831626?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+clinical+investigation&rft.atitle=Parkinson%27s+disease%3A+don%27t+mess+with+calcium.&rft.au=Mattson%2C+Mark+P&rft.aulast=Mattson&rft.aufirst=Mark&rft.date=2012-04-01&rft.volume=122&rft.issue=4&rft.spage=1195&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+clinical+investigation&rft.issn=1558-8238&rft_id=info:doi/10.1172%2FJCI62835 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-06 N1 - Date created - 2012-04-02 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Neurology. 2004 May 25;62(10):1835-8 [15159488] Science. 1983 Feb 25;219(4587):979-80 [6823561] Ann Neurol. 1998 Sep;44(3 Suppl 1):S110-4 [9749581] Proc Natl Acad Sci U S A. 2004 Dec 28;101(52):18171-6 [15604149] Eur J Pharmacol. 2008 Oct 24;595(1-3):7-12 [18703048] Neuron. 2008 Dec 10;60(5):748-66 [19081372] J Neurosci. 2010 Jan 20;30(3):1166-75 [20089925] PLoS One. 2011;6(1):e16706 [21304957] Cell Death Differ. 2011 May;18(5):769-82 [21113145] Biofactors. 2011 May-Jun;37(3):228-40 [21674642] Nat Rev Neurosci. 2011 Aug;12(8):437-52 [21772323] Annu Rev Genomics Hum Genet. 2011;12:301-25 [21639795] J Neurosci. 2011 Oct 12;31(41):14754-62 [21994391] Neuroscience. 2011 Dec 15;198:221-31 [21884755] Hum Mol Genet. 2012 Mar 1;21(5):963-77 [22045699] Nat Rev Neurosci. 2012 Mar;13(3):209-16 [22251954] J Clin Invest. 2012 Apr;122(4):1354-67 [22446186] Comment On: J Clin Invest. 2012 Apr;122(4):1354-67 [22446186] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1172/JCI62835 ER - TY - JOUR T1 - Relationship between liver function and brain shrinkage in patients with alcohol dependence. AN - 963492097; 21995416 AB - Oxidative stress has been proposed as one of the mechanisms of alcohol-induced brain shrinkage and alcohol-induced hepatotoxicity. The aim of this study was to assess the correlations between liver function and brain volume (BV) measurements in patients with alcohol dependence. We recruited 124 patients with alcohol dependence and 111 healthy control subjects from National Institute of Health, National Institute on Alcohol Abuse and Alcoholism inpatient alcohol treatment program. Gamma-glutamyl transferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT), as well as hematocrit (Hct) and albumin were assayed shortly after admission. Magnetic resonance imaging examination was conducted in both groups (after 3-week abstinence in the patient group). We used stepwise linear regression analyses to determine the variables most strongly correlated with brain shrinkage. Patients with alcohol dependence had lower BV, and greater brain shrinkage as measured by gray matter ratio (GMR), white matter ratio (WMR), brain ratio (BR), and higher cerebrospinal fluid ratio ratio (CSFR) compared with their healthy counterparts. Age and sex were significantly correlated with some BV measurements in both patient and control groups. Body mass index (BMI) was significantly correlated with CSFR, BR, GMR, and WMR; Hct with CSFR and BR; serum GGT level with BV, CSFR, BR, GMR, and WMF in the patient group. No biological variables were correlated with BV indices in the control group. In gender-stratified analysis, age was significantly correlated with brain shrinkage in male patients but not in female patients. Serum GGT level in male and female patients, Hct in male patients, and AST levels in female patients were significantly correlated with brain shrinkage. Our results showed that the higher levels of liver function indices, especially GGT, correlated with BV shrinkage as measured using CSFR, BR, GMR, and WMR in patients with alcohol dependence but not in controls. Serum GGT level outweighed aging effect on brain shrinkage in female patients. No claim to original US government works.Copyright © 2011 by the Research Society on Alcoholism. JF - Alcoholism, clinical and experimental research AU - Chen, Chun-Hsin AU - Walker, Jonathan AU - Momenan, Reza AU - Rawlings, Robert AU - Heilig, Markus AU - Hommer, Daniel W AD - Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 625 EP - 632 VL - 36 IS - 4 KW - Index Medicus KW - Magnetic Resonance Imaging KW - Educational Status KW - Age of Onset KW - Sex Characteristics KW - Humans KW - Linear Models KW - Aged KW - Body Mass Index KW - Liver Function Tests KW - Smoking -- epidemiology KW - Socioeconomic Factors KW - Aging -- physiology KW - Middle Aged KW - Image Processing, Computer-Assisted KW - Male KW - Diagnostic and Statistical Manual of Mental Disorders KW - Female KW - Liver -- physiopathology KW - Alcoholism -- pathology KW - Brain -- pathology KW - Alcoholism -- cerebrospinal fluid KW - Alcoholism -- physiopathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/963492097?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Alcoholism%2C+clinical+and+experimental+research&rft.atitle=Relationship+between+liver+function+and+brain+shrinkage+in+patients+with+alcohol+dependence.&rft.au=Chen%2C+Chun-Hsin%3BWalker%2C+Jonathan%3BMomenan%2C+Reza%3BRawlings%2C+Robert%3BHeilig%2C+Markus%3BHommer%2C+Daniel+W&rft.aulast=Chen&rft.aufirst=Chun-Hsin&rft.date=2012-04-01&rft.volume=36&rft.issue=4&rft.spage=625&rft.isbn=&rft.btitle=&rft.title=Alcoholism%2C+clinical+and+experimental+research&rft.issn=1530-0277&rft_id=info:doi/10.1111%2Fj.1530-0277.2011.01662.x LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-18 N1 - Date created - 2012-03-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Alcohol Clin Exp Res. 1995 Oct;19(5):1177-91 [8561288] Hepatology. 1996 May;23(5):1025-9 [8621128] J Histochem Cytochem. 1996 Oct;44(10):1101-8 [8813074] Biochem Mol Biol Int. 1996 Dec;40(6):1123-33 [8988324] Free Radic Biol Med. 1997;22(5):853-60 [9119254] Am J Cardiol. 1997 Aug 15;80(4):481-5 [9285662] Free Radic Biol Med. 1998 Nov 1;25(7):786-92 [9823544] Hepatology. 1999 Jan;29(1):14-20 [9862843] Curr Pharm Des. 2005;11(8):973-84 [15777248] Alcohol Clin Exp Res. 2005 May;29(5):896-901 [15897736] Am J Gastroenterol. 2005 Jun;100(6):1303-10 [15929761] J Pharmacol Exp Ther. 2005 Aug;314(2):780-8 [15878999] Alcohol Clin Exp Res. 2006 Nov;30(11):1938-49 [17067360] Cell Mol Neurobiol. 2006 Jul-Aug;26(4-6):385-405 [16633891] Glia. 2007 Apr 1;55(5):453-62 [17203472] AJNR Am J Neuroradiol. 2007 Aug;28(7):1328-31 [17698536] J Gastroenterol Hepatol. 2008 Mar;23 Suppl 1:S98-103 [18336675] Alcohol. 2008 Sep;42(6):513-8 [18579335] Alcohol Alcohol. 2009 Mar-Apr;44(2):115-27 [18940959] J Formos Med Assoc. 2009 Jul;108(7):560-9 [19586830] Neuropsychopharmacology. 2010 Apr;35(5):1120-8 [20043000] Free Radic Biol Med. 2000 Nov 1;29(9):825-33 [11063908] Alcohol Clin Exp Res. 2011 Feb;35(2):338-44 [21070251] N Engl J Med. 2000 Apr 27;342(17):1266-71 [10781624] Radiology. 2000 Sep;216(3):672-82 [10966694] J Clin Invest. 2000 Oct;106(7):867-72 [11018074] Am J Psychiatry. 2001 Feb;158(2):188-97 [11156800] Am J Psychiatry. 2001 Feb;158(2):198-204 [11156801] J Biol Chem. 2001 Feb 9;276(6):3798-804 [11080500] Crit Rev Clin Lab Sci. 2001 Aug;38(4):263-355 [11563810] Alcohol Clin Exp Res. 2002 Apr;26(4):558-64 [11981133] J Nutr. 2003 Mar;133 Suppl 3:933S-940S [12612179] Am J Pathol. 2003 Sep;163(3):1137-46 [12937155] Addiction. 2003 Dec;98 Suppl 2:31-43 [14984240] Alcohol Alcohol. 2004 Mar-Apr;39(2):113-8 [14998827] Am J Psychiatry. 2004 Jul;161(7):1190-6 [15229050] Free Radic Biol Med. 2004 Oct 1;37(7):1018-23 [15336318] J Lab Clin Med. 1981 Sep;98(3):417-24 [7264437] J Hepatol. 1986;2(1):33-42 [3950362] Alcohol. 1986 Jul-Aug;3(4):223-6 [2875722] Scand J Gastroenterol. 1987 Dec;22(10):1251-6 [3433014] Alcohol Clin Exp Res. 1988 Feb;12(1):81-7 [3279864] Alcohol Clin Exp Res. 1991 Jun;15(3):418-27 [1877728] Stat Med. 1991 Nov;10(11):1711-8 [1792465] Ups J Med Sci. 1992;97(2):183-94 [1361697] Alcohol Clin Exp Res. 1992 Dec;16(6):1078-89 [1471762] Arch Biochem Biophys. 1993 Jan;300(1):401-8 [8380969] Alcohol. 1993 Nov-Dec;10(6):459-64 [8123200] Am J Respir Cell Mol Biol. 1994 Nov;11(5):586-92 [7946387] JAMA. 1995 Jul 12;274(2):149-54 [7596003] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1111/j.1530-0277.2011.01662.x ER - TY - JOUR T1 - Hepatocyte growth factor/c-met signaling is required for stem-cell-mediated liver regeneration in mice. AN - 963489051; 22095660 AB - Hepatocyte growth factor (HGF)/c-Met supports a pleiotrophic signal transduction pathway that controls stem cell homeostasis. Here, we directly addressed the role of c-Met in stem-cell-mediated liver regeneration by utilizing mice harboring c-met floxed alleles and Alb-Cre or Mx1-Cre transgenes. To activate oval cells, the hepatic stem cell (HSC) progeny, we used a model of liver injury induced by diet containing the porphyrinogenic agent, 3,5-diethocarbonyl-1,4-dihydrocollidine (DDC). Deletion of c-met in oval cells was confirmed in both models by polymerase chain reaction analysis of fluorescence-activated cell-sorted epithelial cell adhesion molecule (EpCam)-positive cells. Loss of c-Met receptor decreased the sphere-forming capacity of oval cells in vitro as well as reduced oval cell pool, impaired migration, and decreased hepatocytic differentiation in vivo, as demonstrated by double immunofluorescence using oval- (A6 and EpCam) and hepatocyte-specific (i.e. hepatocyte nuclear factor 4-alpha) antibodies. Furthermore, lack of c-Met had a profound effect on tissue remodeling and overall composition of HSC niche, which was associated with greatly reduced matrix metalloproteinase (MMP)9 activity and decreased expression of stromal-cell-derived factor 1. Using a combination of double immunofluorescence of cell-type-specific markers with MMP9 and gelatin zymography on the isolated cell populations, we identified macrophages as a major source of MMP9 in DDC-treated livers. The Mx1-Cre-driven c-met deletion caused the greatest phenotypic impact on HSCs response, as compared to the selective inactivation in the epithelial cell lineages achieved in c-Met(fl/fl); Alb-Cre(+/-) mice. However, in both models, genetic loss of c-met triggered a similar cascade of events, leading to the failure of HSC mobilization and death of the mice. These results establish a direct contribution of c-Met in the regulation of HSC response and support a unique role for HGF/c-Met as an essential growth-factor-signaling pathway for regeneration of diseased liver. Copyright © 2011 American Association for the Study of Liver Diseases. JF - Hepatology (Baltimore, Md.) AU - Ishikawa, Tsuyoshi AU - Factor, Valentina M AU - Marquardt, Jens U AU - Raggi, Chiara AU - Seo, Daekwan AU - Kitade, Mitsuteru AU - Conner, Elizabeth A AU - Thorgeirsson, Snorri S AD - Laboratory of Experimental Carcinogenesis, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-4262, USA. Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 1215 EP - 1226 VL - 55 IS - 4 KW - 3,5-diethoxycarbonyl-1,4-dihydrocollidine KW - 0 KW - Chemokine CXCL12 KW - Pyridines KW - Hepatocyte Growth Factor KW - 67256-21-7 KW - Proto-Oncogene Proteins c-met KW - EC 2.7.10.1 KW - Matrix Metalloproteinase 9 KW - EC 3.4.24.35 KW - Index Medicus KW - Animals KW - Chemical and Drug Induced Liver Injury -- pathology KW - Disease Models, Animal KW - Mice KW - Mice, Transgenic KW - Chemical and Drug Induced Liver Injury -- therapy KW - Chemokine CXCL12 -- metabolism KW - Matrix Metalloproteinase 9 -- metabolism KW - Mice, Mutant Strains KW - Cell Differentiation -- physiology KW - Cell Movement -- physiology KW - Stem Cell Transplantation KW - Pyridines -- adverse effects KW - Chemical and Drug Induced Liver Injury -- metabolism KW - Male KW - Proto-Oncogene Proteins c-met -- deficiency KW - Signal Transduction -- physiology KW - Proto-Oncogene Proteins c-met -- genetics KW - Hepatocyte Growth Factor -- physiology KW - Stem Cells -- cytology KW - Hepatocyte Growth Factor -- deficiency KW - Hepatocyte Growth Factor -- genetics KW - Proto-Oncogene Proteins c-met -- physiology KW - Stem Cells -- physiology KW - Liver Regeneration -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/963489051?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Hepatocyte+growth+factor%2Fc-met+signaling+is+required+for+stem-cell-mediated+liver+regeneration+in+mice.&rft.au=Ishikawa%2C+Tsuyoshi%3BFactor%2C+Valentina+M%3BMarquardt%2C+Jens+U%3BRaggi%2C+Chiara%3BSeo%2C+Daekwan%3BKitade%2C+Mitsuteru%3BConner%2C+Elizabeth+A%3BThorgeirsson%2C+Snorri+S&rft.aulast=Ishikawa&rft.aufirst=Tsuyoshi&rft.date=2012-04-01&rft.volume=55&rft.issue=4&rft.spage=1215&rft.isbn=&rft.btitle=&rft.title=Hepatology+%28Baltimore%2C+Md.%29&rft.issn=1527-3350&rft_id=info:doi/10.1002%2Fhep.24796 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-22 N1 - Date created - 2012-03-30 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Lab Invest. 2010 Aug;90(8):1199-208 [20440274] J Hepatol. 2010 Sep;53(3):500-7 [20561705] PLoS One. 2010;5(9). pii: e12739. doi: 10.1371/journal.pone.0012739 [20862286] Clin Liver Dis. 2010 Nov;14(4):705-18 [21055691] Nat Rev Mol Cell Biol. 2010 Dec;11(12):834-48 [21102609] J Gastroenterol Hepatol. 2011 Jan;26 Suppl 1:203-12 [21199532] Int J Biochem Cell Biol. 2011 Feb;43(2):222-9 [19914396] J Biochem. 2011 Mar;149(3):231-9 [21217146] Gut. 2011 Apr;60(4):525-33 [21106552] Future Med Chem. 2009 Sep;1(6):1095-1111 [20161478] Cell Stem Cell. 2011 May 6;8(5):486-98 [21549325] Hepatology. 1999 Dec;30(6):1425-33 [10573521] Am J Pathol. 2001 Apr;158(4):1313-23 [11290549] Nature. 2003 Apr 24;422(6934):897-901 [12665832] Proc Natl Acad Sci U S A. 2003 Jun 10;100(12):7075-80 [12756303] Nat Genet. 2003 Jul;34(3):292-6 [12808453] J Clin Invest. 2003 Jul;112(2):160-9 [12865405] Semin Liver Dis. 2003 Nov;23(4):303-12 [14722808] Proc Natl Acad Sci U S A. 2004 Mar 30;101(13):4477-82 [15070743] Hepatology. 2004 May;39(5):1353-61 [15122764] Proc Natl Acad Sci U S A. 2004 Jul 20;101(29):10608-13 [15249655] Carcinogenesis. 1987 Nov;8(11):1737-40 [3664968] Differentiation. 1990 Oct;45(1):29-37 [2292360] Am J Pathol. 1993 Jun;142(6):1823-30 [8506951] Cell Growth Differ. 1993 Jul;4(7):555-61 [7691152] Proc Soc Exp Biol Med. 1993 Dec;204(3):253-60 [7694304] Am J Pathol. 1994 Aug;145(2):409-22 [8053498] Nature. 1995 Feb 23;373(6516):699-702 [7854452] Nature. 1995 Feb 23;373(6516):702-5 [7854453] Science. 1995 Sep 8;269(5229):1427-9 [7660125] Science. 1997 Apr 4;276(5309):60-6 [9082986] Lab Invest. 1999 Feb;79(2):103-9 [10068199] FASEB J. 2005 Feb;19(2):234-6 [15550552] Cell Res. 2005 Jan;15(1):49-51 [15686627] J Clin Invest. 2005 Sep;115(9):2330-40 [16110324] Hepatology. 2007 Jan;45(1):213-22 [17187438] J Immunol. 2007 Apr 15;178(8):5288-95 [17404313] Hepatology. 2007 Dec;46(6):1993-2002 [17924446] Hepatology. 2008 Jan;47(1):288-95 [17929301] Cancer Metastasis Rev. 2008 Mar;27(1):85-94 [18175071] Gastroenterology. 2008 Mar;134(3):781-92 [18325391] Matrix Biol. 2008 Oct;27(8):674-81 [18678246] Hepatology. 2009 May;49(5):1625-35 [19296469] Development. 2009 Jun;136(11):1951-60 [19429791] Gastroenterology. 2009 Jul;137(1):297-308, 308.e1-4 [19208365] Gastroenterology. 2009 Aug;137(2):466-81 [19470389] Mech Dev. 2009 Aug-Sep;126(8-9):665-76 [19527784] Hepatology. 2009 Nov;50(5):1617-24 [19725107] Gut. 2010 May;59(5):645-54 [20427399] Proc Jpn Acad Ser B Phys Biol Sci. 2010;86(6):588-610 [20551596] Hepatology. 2010 Jul;52(1):291-302 [20578156] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/hep.24796 ER - TY - JOUR T1 - Sterculic acid antagonizes 7-ketocholesterol-mediated inflammation and inhibits choroidal neovascularization. AN - 929124028; 22342272 AB - Sterculic acid is a cyclopropene fatty acid with numerous biological activities. In this study we demonstrate that sterculic acid is a potent inhibitor of endoplasmic reticulum (ER) stress and related inflammation caused by 7-ketocholesterol (7KCh). 7KCh is a highly toxic oxysterol suspected in the pathogenesis of various age-related diseases such as atherosclerosis, Alzheimer's disease and age-related macular degeneration. Sterculic acid demonstrated to be 5-10 times more effective than other anti-inflammatory fatty acids at inhibiting 7KCh-mediated inflammatory responses in cultured cells. In vivo, sterculic acid was effective at inhibiting the formation of choroidal neovascularization (CNV) in the laser-injury rat model. Our data suggests that sterculic acid may be useful in treating CNV in certain forms of age-related macular degeneration. Published by Elsevier B.V. JF - Biochimica et biophysica acta AU - Huang, Jiahn-Dar AU - Amaral, Juan AU - Lee, Jung Wha AU - Larrayoz, Ignacio M AU - Rodriguez, Ignacio R AD - Mechanism of Retinal Diseases Section, Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 637 EP - 646 VL - 1821 IS - 4 SN - 0006-3002, 0006-3002 KW - Cyclopropanes KW - 0 KW - Cytokines KW - DDIT3 protein, human KW - Enzyme Inhibitors KW - Fatty Acids KW - Fatty Acids, Monounsaturated KW - Heat-Shock Proteins KW - Inflammation Mediators KW - Ketocholesterols KW - Vascular Endothelial Growth Factor A KW - molecular chaperone GRP78 KW - Transcription Factor CHOP KW - 147336-12-7 KW - sterculic acid KW - MXV06G5ROK KW - 7-ketocholesterol KW - O7676FE78M KW - Index Medicus KW - Gene Expression -- drug effects KW - Animals KW - Cytokines -- genetics KW - Humans KW - Endoplasmic Reticulum Stress -- genetics KW - Retinal Pigment Epithelium -- drug effects KW - Rats, Inbred BN KW - Lasers -- adverse effects KW - Fatty Acids -- pharmacology KW - Rats KW - Retinal Pigment Epithelium -- cytology KW - Transcription Factor CHOP -- genetics KW - Retinal Pigment Epithelium -- metabolism KW - Male KW - Heat-Shock Proteins -- metabolism KW - Immunoblotting KW - Transcription Factor CHOP -- metabolism KW - Dose-Response Relationship, Drug KW - Cytokines -- metabolism KW - Reverse Transcriptase Polymerase Chain Reaction KW - Inflammation Mediators -- metabolism KW - Cells, Cultured KW - Enzyme Inhibitors -- pharmacology KW - Drug Antagonism KW - Vascular Endothelial Growth Factor A -- genetics KW - Heat-Shock Proteins -- genetics KW - Vascular Endothelial Growth Factor A -- metabolism KW - Endoplasmic Reticulum Stress -- drug effects KW - Fatty Acids, Monounsaturated -- pharmacology KW - Ketocholesterols -- pharmacology KW - Inflammation -- prevention & control KW - Choroidal Neovascularization -- etiology KW - Choroidal Neovascularization -- prevention & control KW - Inflammation -- genetics KW - Cyclopropanes -- pharmacology KW - Inflammation -- metabolism KW - Choroidal Neovascularization -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/929124028?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimica+et+biophysica+acta&rft.atitle=Sterculic+acid+antagonizes+7-ketocholesterol-mediated+inflammation+and+inhibits+choroidal+neovascularization.&rft.au=Huang%2C+Jiahn-Dar%3BAmaral%2C+Juan%3BLee%2C+Jung+Wha%3BLarrayoz%2C+Ignacio+M%3BRodriguez%2C+Ignacio+R&rft.aulast=Huang&rft.aufirst=Jiahn-Dar&rft.date=2012-04-01&rft.volume=1821&rft.issue=4&rft.spage=637&rft.isbn=&rft.btitle=&rft.title=Biochimica+et+biophysica+acta&rft.issn=00063002&rft_id=info:doi/10.1016%2Fj.bbalip.2012.01.013 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-02-04 N1 - Date created - 2012-03-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Prog Retin Eye Res. 2009 Nov;28(6):393-422 [19698799] J Clin Immunol. 2009 Jul;29(4):397-405 [19408108] Cardiovasc Ther. 2010 Aug;28(4):202-15 [20633023] J Lipid Res. 2010 Oct;51(10):2847-62 [20567027] Invest Ophthalmol Vis Sci. 2010 Oct;51(10):4942-55 [20554621] Circ Res. 2010 Oct 1;107(7):839-50 [20884885] Prog Retin Eye Res. 2010 Nov;29(6):500-19 [20488255] Mol Med. 2010 Nov-Dec;16(11-12):535-42 [20683548] Ophthalmology. 2010 Dec;117(12):2395-401 [20630597] Curr Drug Targets. 2011 Feb;12(2):173-81 [20887245] Am J Clin Nutr. 2011 Feb;93(2):446-54 [21147858] Nat Cell Biol. 2011 Mar;13(3):184-90 [21364565] Cell. 2011 Apr 29;145(3):341-55 [21529710] Free Radic Res. 2001 Jul;35(1):31-41 [11697115] Proc Natl Acad Sci U S A. 2002 May 14;99(10):7172-7 [11997456] Cell Death Differ. 2003 Jan;10(1):45-65 [12655295] Brain Pathol. 2003 Jul;13(3):250-62 [12946016] Invest Ophthalmol Vis Sci. 2004 Aug;45(8):2830-7 [15277510] Arch Ophthalmol. 1989 Feb;107(2):264-9 [2464985] Arterioscler Thromb. 1994 Jul;14(7):1177-85 [8018675] Lipids. 1996 May;31(5):453-87 [8727640] J Lipid Res. 1997 Sep;38(9):1730-45 [9323583] Can J Biochem Physiol. 1959 Aug;37(8):911-7 [13671378] J Biol Chem. 2005 Feb 25;280(8):7377-87 [15591071] Am J Clin Nutr. 2006 Jun;83(6 Suppl):1505S-1519S [16841861] Am J Cardiol. 2006 Aug 21;98(4A):3i-18i [16919512] Invest Ophthalmol Vis Sci. 2006 Dec;47(12):5163-70 [17122098] Metabolism. 2007 Mar;56(3):357-62 [17292724] Invest Ophthalmol Vis Sci. 2007 Sep;48(9):4328-34 [17724224] Arch Ophthalmol. 2008 Jun;126(6):826-33 [18541848] J Atheroscler Thromb. 2008 Jun;15(3):130-7 [18603819] Arch Ophthalmol. 2008 Sep;126(9):1274-9 [18779490] Invest Ophthalmol Vis Sci. 2009 Feb;50(2):523-32 [18936140] Curr Med Chem. 2009;16(6):685-705 [19199932] Circ Res. 2009 Feb 13;104(3):328-36 [19106412] J Nutr Biochem. 2009 May;20(5):321-36 [19345313] Mol Aspects Med. 2009 Jun;30(3):153-70 [19248805] Mol Aspects Med. 2009 Jun;30(3):180-9 [19248806] Z Naturforsch C. 2009 Mar-Apr;64(3-4):307-10 [19526729] Invest Ophthalmol Vis Sci. 2010 Jun;51(6):2813-26 [20484600] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.bbalip.2012.01.013 ER - TY - JOUR T1 - New paradigms in translational science research in cancer biomarkers. AN - 929120092; 22424436 AB - Despite significant investments in basic science by the US National Institutes of Health, there is a concern that the return on this investment has been limited in terms of clinical utility. In the field of biomarkers, translational research is used to bridge the gap between the results of basic research that identify biomolecules involved in or the consequence of carcinogenesis and their incorporation into medical application. The cultural separation between different scientific disciplines often makes it difficult to establish the multidisciplinary and multi-skilled teams that are necessary for successful translational research. The field of biomarker research requires extensive interactions between academic researchers and industrial developers, and clinicians are needed to help shape the research direction that can be addressed only by a multidisciplinary, multi-institutional approach. In this article, we provide our perspective on the relatively slow pace of cancer biomarker translation, especially those for early detection and screening. Published by Mosby, Inc. JF - Translational research : the journal of laboratory and clinical medicine AU - Wagner, Paul D AU - Srivastava, Sudhir AD - Cancer Biomarkers Research Group, Division of Cancer Prevention, National Cancer Institute, 6130 Executive Boulevard, Rockville, MD 20852, USA. Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 343 EP - 353 VL - 159 IS - 4 KW - Biomarkers KW - 0 KW - Biomarkers, Tumor KW - Abridged Index Medicus KW - Index Medicus KW - Humans KW - Biomarkers, Tumor -- metabolism KW - Neoplasms -- diagnosis KW - Biomarkers -- metabolism KW - Translational Medical Research -- trends KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/929120092?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Translational+research+%3A+the+journal+of+laboratory+and+clinical+medicine&rft.atitle=New+paradigms+in+translational+science+research+in%C2%A0cancer+biomarkers.&rft.au=Wagner%2C+Paul+D%3BSrivastava%2C+Sudhir&rft.aulast=Wagner&rft.aufirst=Paul&rft.date=2012-04-01&rft.volume=159&rft.issue=4&rft.spage=343&rft.isbn=&rft.btitle=&rft.title=Translational+research+%3A+the+journal+of+laboratory+and+clinical+medicine&rft.issn=1878-1810&rft_id=info:doi/10.1016%2Fj.trsl.2012.01.015 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-08 N1 - Date created - 2012-03-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Clin Pharmacol Ther. 2001 Mar;69(3):89-95 [11240971] J Proteome Res. 2011 Aug 5;10(8):3429-38 [21574648] J Natl Cancer Inst. 2005 Aug 17;97(16):1180-4 [16106022] Clin Trials. 2006;3(1):43-56 [16539089] Cancer Epidemiol Biomarkers Prev. 2007 Oct;16(10):1918-20 [17932336] J Clin Epidemiol. 2007 Dec;60(12):1205-19 [17998073] Clin Cancer Res. 2008 Sep 15;14(18):5672-7 [18794074] J Natl Cancer Inst. 2008 Oct 15;100(20):1432-8 [18840817] Gastroenterology. 2009 Jul;137(1):110-8 [19362088] J Natl Cancer Inst. 2009 Aug 19;101(16):1116-9 [19574417] J Clin Oncol. 2010 Feb 1;28(4):698-704 [20038718] Semin Oncol. 2010 Jun;37(3):224-42 [20709207] J Natl Cancer Inst. 2010 Oct 6;102(19):1462-7 [20705936] Cancer Epidemiol Biomarkers Prev. 2010 Dec;19(12):2995-9 [20962299] Cancer Prev Res (Phila). 2011 Mar;4(3):375-83 [21372037] Obstet Gynecol. 2011 Aug;118(2 Pt 1):280-8 [21775843] J Natl Cancer Inst. 2001 Jul 18;93(14):1054-61 [11459866] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.trsl.2012.01.015 ER - TY - JOUR T1 - Primary outcome indices in illicit drug dependence treatment research: systematic approach to selection and measurement of drug use end-points in clinical trials AN - 928988980; 4279053 AB - Aims Clinical trials test the safety and efficacy of behavioral and pharmacological interventions in drug-dependent individuals. However, there is no consensus about the most appropriate outcome(s) to consider in determining treatment efficacy or on the most appropriate methods for assessing selected outcome(s). We summarize the discussion and recommendations of treatment and research experts, convened by the US National Institute on Drug Abuse, to select appropriate primary outcomes for drug dependence treatment clinical trials, and in particular the feasibility of selecting a common outcome to be included in all or most trials. Methods A brief history of outcomes employed in prior drug dependence treatment research, incorporating perspectives from tobacco and alcohol research, is included. The relative merits and limitations of focusing on drug-taking behavior, as measured by self-report and qualitative or quantitative biological markers, are evaluated. Results Drug-taking behavior, measured ideally by a combination of self-report and biological indicators, is seen as the most appropriate proximal primary outcome in drug dependence treatment clinical trials. Conclusions We conclude that the most appropriate outcome will vary as a function of salient variables inherent in the clinical trial, such as the type of intervention, its target, treatment goals (e.g. abstinence or reduction of use) and the perspective being taken (e.g. researcher, clinical program, patient, society). It is recommended that a decision process, based on such trial variables, be developed to guide the selection of primary and secondary outcomes as well as the methods to assess them. Reprinted by permission of Blackwell Publishing JF - Addiction AU - Wells, Elizabeth A AU - Donovan, Dennis M AU - Bigelow, George E AU - Brigham, Gregory S AU - Carroll, Kathleen M AU - Cohen, Allan J AU - Gardin, John G AU - Hamilton, John A AU - Huestis, Marilyn A AU - Hughes, John R AU - Lindblad, Robert AU - Marlatt, G Alan AU - Preston, Kenzie L AU - Selzer, Jeffrey A AU - Somoza, Eugene C AU - Wakim, Paul G AD - University of Washington, Seattle ; Johns Hopkins University ; Yale University ; Bay Area Addiction Research and Treatment ; ADAPT, Roseburg ; Regional Network of Programs, Shelton ; National Institute on Drug Abuse, Baltimore ; University of Vermont ; EMMES Corporation, Rockville ; Committee for Physician Health, Albany ; University of Cincinnati ; National Institute on Drug Abuse, Bethesda Y1 - 2012/04// PY - 2012 DA - Apr 2012 SP - 694 EP - 708 VL - 107 IS - 4 SN - 0965-2140, 0965-2140 KW - Sociology KW - Alcohol KW - Pharmacology KW - Drug use KW - Drug users KW - Alcoholism KW - Tobacco KW - Drug addicts KW - Addiction KW - Drug abuse KW - Drug addiction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/928988980?accountid=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=Primary+outcome+indices+in+illicit+drug+dependence+treatment+research%3A+systematic+approach+to+selection+and+measurement+of+drug+use+end-points+in+clinical+trials&rft.au=Wells%2C+Elizabeth+A%3BDonovan%2C+Dennis+M%3BBigelow%2C+George+E%3BBrigham%2C+Gregory+S%3BCarroll%2C+Kathleen+M%3BCohen%2C+Allan+J%3BGardin%2C+John+G%3BHamilton%2C+John+A%3BHuestis%2C+Marilyn+A%3BHughes%2C+John+R%3BLindblad%2C+Robert%3BMarlatt%2C+G+Alan%3BPreston%2C+Kenzie+L%3BSelzer%2C+Jeffrey+A%3BSomoza%2C+Eugene+C%3BWakim%2C+Paul+G&rft.aulast=Wells&rft.aufirst=Elizabeth&rft.date=2012-04-01&rft.volume=107&rft.issue=4&rft.spage=694&rft.isbn=&rft.btitle=&rft.title=Addiction&rft.issn=09652140&rft_id=info:doi/10.1111%2Fj.1360-0443.2011.03473.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 - 3744 561 6220; 3745 562; 12766 3055 798 10286; 909; 913 561 6220; 561 6220; 3742 1121 11776 3753 3755; 3753 3755; 3754 3755; 9476 7894 DO - http://dx.doi.org/10.1111/j.1360-0443.2011.03473.x ER - TY - JOUR T1 - Phosphorylation of serine 212 confers novel activity to human estrogen receptor α. AN - 928375796; 22266331 AB - Estrogen receptor α (ERα) can be phosphorylated at various residues, one of which is serine 212 in the DNA binding domain. The majority of human nuclear receptors conserves, as a motif, this serine residue within their DNA binding domain. Among these nuclear receptors, phosphorylation of the corresponding threonine 38 in the nuclear receptor CAR is essential for determining its activity [9]. Here, we have investigated the role of phosphorylated serine 212 in the regulation of ERα activity by comparing it with serine 236, another potential phosphorylation site within the DNA binding domain, and demonstrated that phosphorylation of serine 212 confers upon ERα a distinct activity regulating gene expression in Huh-7 cells. In Western blot analysis, wild type ERα and mutants ERα S212A, ERα S212D, ERα S236A and ERα S236D were equally expressed in the nucleus, thus indicating that phosphorylation does not determine nuclear localization of ERα. ERα S212D, but not ERα S236D, retained its capability of activating an ERE-reporter gene in luciferase assays. Similar results were also obtained for human ERβ; the ERβ S176D mutant retained its trans-activation activity, but the ERβ S200D mutant did not. cDNA microarray and Ingenuity Pathway Analysis, employed on Huh-7 cells ectopically expressing either ERα S212A or ERα S212D, revealed that phosphorylation of serine 212 enabled ERα to regulate a unique set of genes and cellular functions. Published by Elsevier Inc. JF - Steroids AU - Shindo, Sawako AU - Sakuma, Tsutomu AU - Negishi, Masahiko AU - Squires, James AD - Pharmacogenetics Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 448 EP - 453 VL - 77 IS - 5 KW - Estrogen Receptor alpha KW - 0 KW - estrogen receptor alpha, human KW - Serine KW - 452VLY9402 KW - Index Medicus KW - Blotting, Western KW - Phosphorylation KW - Oligonucleotide Array Sequence Analysis KW - Humans KW - Molecular Sequence Data KW - Cell Line, Tumor KW - Amino Acid Sequence KW - Binding Sites -- genetics KW - Reverse Transcriptase Polymerase Chain Reaction KW - Mutation KW - Transcriptional Activation KW - Gene Expression Regulation, Neoplastic KW - Gene Expression Profiling KW - Estrogen Receptor alpha -- genetics KW - Estrogen Receptor alpha -- metabolism KW - Serine -- metabolism KW - Serine -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/928375796?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Steroids&rft.atitle=Phosphorylation+of+serine+212+confers+novel+activity+to+human+estrogen+receptor+%CE%B1.&rft.au=Shindo%2C+Sawako%3BSakuma%2C+Tsutomu%3BNegishi%2C+Masahiko%3BSquires%2C+James&rft.aulast=Shindo&rft.aufirst=Sawako&rft.date=2012-04-01&rft.volume=77&rft.issue=5&rft.spage=448&rft.isbn=&rft.btitle=&rft.title=Steroids&rft.issn=1878-5867&rft_id=info:doi/10.1016%2Fj.steroids.2012.01.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-14 N1 - Date created - 2012-03-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Steroids. 2003 Jan;68(1):1-9 [12475718] Mol Cell Biol. 1998 Oct;18(10):5652-8 [9742082] Mol Cell Biol. 1999 Feb;19(2):1002-15 [9891036] Steroids. 2007 Mar;72(3):231-46 [17284330] Endocr Relat Cancer. 2008 Sep;15(3):755-63 [18550720] Mol Cell Proteomics. 2009 Mar;8(3):467-80 [18984578] Mol Cancer Res. 2009 Jun;7(6):977-86 [19470599] Mol Endocrinol. 2009 Oct;23(10):1544-55 [19574448] J Biol Chem. 2009 Dec 11;284(50):34785-92 [19858220] Traffic. 2010 Apr;11(4):533-47 [20028487] Endocr Relat Cancer. 2011 Feb;18(1):R1-14 [21149515] Blood. 2011 Oct 20;118(16):4401-10 [21865343] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.steroids.2012.01.001 ER - TY - JOUR T1 - Oxidative damage in muscular dystrophy correlates with the severity of the pathology: role of glutathione metabolism. AN - 927833077; 22219131 AB - Muscular dystrophies (MDs) such as Duchenne muscular dystrophy (DMD), sarcoglycanopathy (Sgpy) and dysferlinopathy (Dysfy) are recessive genetic neuromuscular diseases that display muscle degeneration. Although these MDs have comparable endpoints of muscle pathology, the onset, severity and the course of these diseases are diverse. Different mechanisms downstream of genetic mutations might underlie the disparity in these pathologies. We surmised that oxidative damage and altered antioxidant function might contribute to these differences. The oxidant and antioxidant markers in the muscle biopsies from patients with DMD (n = 15), Sgpy (n = 15) and Dysfy (n = 15) were compared to controls (n = 10). Protein oxidation and lipid peroxidation was evident in all MDs and correlated with the severity of pathology, with DMD, the most severe dystrophic condition showing maximum damage, followed by Sgpy and Dysfy. Oxidative damage in DMD and Sgpy was attributed to the depletion of glutathione (GSH) and lowered antioxidant activities while loss of GSH peroxidase and GSH-S-transferase activities was observed in Dysfy. Lower GSH level in DMD was due to lowered activity of gamma-glutamyl cysteine ligase, the rate limiting enzyme in GSH synthesis. Similar analysis in cardiotoxin (CTX) mouse model of MD showed that the dystrophic muscle pathology correlated with GSH depletion and lipid peroxidation. Depletion of GSH prior to CTX exposure in C2C12 myoblasts exacerbated oxidative damage and myotoxicity. We deduce that the pro and anti-oxidant mechanisms could be correlated to the severity of MD and might influence the dystrophic pathology to a different extent in various MDs. On a therapeutic note, this could help in evolving novel therapies that offer myoprotection in MD. JF - Neurochemical research AU - Renjini, R AU - Gayathri, N AU - Nalini, A AU - Srinivas Bharath, M M AD - Department of Neurochemistry, National Institute of Mental Health and Neurosciences-NIMHANS, Hosur Road, Bangalore 560029, Karnataka, India. Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 885 EP - 898 VL - 37 IS - 4 KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Oxidation-Reduction KW - Young Adult KW - Animals KW - Humans KW - Adult KW - Mice KW - Child KW - Adolescent KW - Male KW - Female KW - Cell Line KW - Child, Preschool KW - Severity of Illness Index KW - Muscular Dystrophies -- metabolism KW - Oxidative Stress -- physiology KW - Muscular Dystrophies -- pathology KW - Glutathione -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/927833077?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurochemical+research&rft.atitle=Oxidative+damage+in+muscular+dystrophy+correlates+with+the+severity+of+the+pathology%3A+role+of+glutathione+metabolism.&rft.au=Renjini%2C+R%3BGayathri%2C+N%3BNalini%2C+A%3BSrinivas+Bharath%2C+M+M&rft.aulast=Renjini&rft.aufirst=R&rft.date=2012-04-01&rft.volume=37&rft.issue=4&rft.spage=885&rft.isbn=&rft.btitle=&rft.title=Neurochemical+research&rft.issn=1573-6903&rft_id=info:doi/10.1007%2Fs11064-011-0683-z LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-11-26 N1 - Date created - 2012-03-12 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s11064-011-0683-z ER - TY - JOUR T1 - A novel approach for the rapid mutagenesis and directed evolution of the structural genes of west nile virus. AN - 927832723; 22258236 AB - Molecular clone technology has proven to be a powerful tool for investigating the life cycle of flaviviruses, their interactions with the host, and vaccine development. Despite the demonstrated utility of existing molecular clone strategies, the feasibility of employing these existing approaches in large-scale mutagenesis studies is limited by the technical challenges of manipulating relatively large molecular clone plasmids that can be quite unstable when propagated in bacteria. We have developed a novel strategy that provides an extremely rapid approach for the introduction of mutations into the structural genes of West Nile virus (WNV). The backbone of this technology is a truncated form of the genome into which DNA fragments harboring the structural genes are ligated and transfected directly into mammalian cells, bypassing entirely the requirement for cloning in bacteria. The transfection of cells with this system results in the rapid release of WNV that achieves a high titer (∼10(7) infectious units/ml in 48 h). The suitability of this approach for large-scale mutagenesis efforts was established in two ways. First, we constructed and characterized a library of variants encoding single defined amino acid substitutions at the 92 residues of the "pr" portion of the precursor-to-membrane (prM) protein. Analysis of a subset of these variants identified a mutation that conferred resistance to neutralization by an envelope protein-specific antibody. Second, we employed this approach to accelerate the identification of mutations that allow escape from neutralizing antibodies. Populations of WNV encoding random changes in the E protein were produced in the presence of a potent monoclonal antibody, E16. Viruses resistant to neutralization were identified in a single passage. Together, we have developed a simple and rapid approach to produce infectious WNV that accelerates the process of manipulating the genome to study the structure and function of the structural genes of this important human pathogen. JF - Journal of virology AU - Lin, Tsai-Yu AU - Dowd, Kimberly A AU - Manhart, Carolyn J AU - Nelson, Steevenson AU - Whitehead, Stephen S AU - Pierson, Theodore C AD - Viral Pathogenesis Section, Laboratory of Viral Diseases, National Institutes of Health, Bethesda, Maryland, USA. Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 3501 EP - 3512 VL - 86 IS - 7 KW - Viral Envelope Proteins KW - 0 KW - Index Medicus KW - Animals KW - Humans KW - Molecular Sequence Data KW - Cell Line KW - Mutagenesis KW - Mutagenesis, Site-Directed -- methods KW - Directed Molecular Evolution -- methods KW - West Nile Fever -- virology KW - West Nile virus -- genetics KW - Viral Envelope Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/927832723?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+novel+approach+for+the+rapid+mutagenesis+and+directed+evolution+of+the+structural+genes+of+west+nile+virus.&rft.au=Lin%2C+Tsai-Yu%3BDowd%2C+Kimberly+A%3BManhart%2C+Carolyn+J%3BNelson%2C+Steevenson%3BWhitehead%2C+Stephen+S%3BPierson%2C+Theodore+C&rft.aulast=Lin&rft.aufirst=Tsai-Yu&rft.date=2012-04-01&rft.volume=86&rft.issue=7&rft.spage=3501&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=1098-5514&rft_id=info:doi/10.1128%2FJVI.06435-11 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-11 N1 - Date created - 2012-03-12 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - JQ582805; GENBANK; JQ582804 N1 - SuppNotes - Cited By: J Virol. 2001 Jul;75(14):6719-28 [11413342] Cell. 2002 Mar 8;108(5):717-25 [11893341] Vaccine. 2002 Mar 15;20(13-14):1823-30 [11906771] Adv Virus Res. 2003;59:141-75 [14696329] Nature. 1979 May 17;279(5710):246-8 [86955] Proc Natl Acad Sci U S A. 1985 May;82(10):3355-9 [2987922] J Virol. 1989 May;63(5):1852-60 [2522997] Gene. 1989 Apr 15;77(1):51-9 [2744487] New Biol. 1989 Dec;1(3):285-96 [2487295] J Gen Virol. 1991 Jun;72 ( Pt 6):1323-9 [1710648] Virology. 1992 Dec;191(2):921-31 [1280384] Virology. 1994 Jan;198(1):109-17 [8259646] J Virol. 1997 Nov;71(11):8475-81 [9343204] J Virol. 1998 Jul;72(7):5967-77 [9621059] Lancet. 1998 Sep 5;352(9130):767-71 [9737281] Emerg Infect Dis. 1999 Sep-Oct;5(5):643-50 [10511520] Nat Med. 2004 Dec;10(12 Suppl):S98-109 [15577938] Nat Rev Microbiol. 2005 Jan;3(1):13-22 [15608696] Virus Res. 2005 Feb;107(2):141-9 [15649560] Virology. 2005 Mar 30;334(1):28-40 [15749120] Virology. 2005 Apr 25;335(1):99-105 [15823609] Nat Med. 2005 May;11(5):522-30 [15852016] J Virol. 2005 Jul;79(13):8339-47 [15956579] Virol J. 2005;2:53 [15985182] Vector Borne Zoonotic Dis. 2005 Fall;5(3):252-7 [16187894] Nature. 2005 Sep 29;437(7059):764-9 [16193056] J Clin Neurosci. 2005 Sep;12(7):822-4 [16169227] J Virol. 2006 Feb;80(3):1290-301 [16415006] Virology. 2006 Mar 1;346(1):53-65 [16325883] Proc Natl Acad Sci U S A. 2006 Aug 15;103(33):12400-4 [16895988] J Virol. 2006 Oct;80(19):9557-68 [16973559] J Virol. 2006 Dec;80(23):11467-74 [16987985] J Virol. 2006 Dec;80(24):12149-59 [17035317] J Gen Virol. 2007 Apr;88(Pt 4):1169-74 [17374760] J Virol. 2007 Jun;81(11):6141-5 [17376919] Clin Infect Dis. 2007 Jun 15;44(12):1617-24 [17516407] Virology. 2007 Sep 30;366(2):349-60 [17719070] J Virol. 2007 Oct;81(20):11526-31 [17670824] J Virol. 2007 Nov;81(21):11737-48 [17715227] J Virol. 2007 Nov;81(21):11828-39 [17715236] Cell Host Microbe. 2007 Apr 19;1(2):135-45 [18005691] Nat Struct Mol Biol. 2008 Mar;15(3):312-7 [18264114] Science. 2008 Mar 28;319(5871):1830-4 [18369147] Science. 2008 Mar 28;319(5871):1834-7 [18369148] PLoS Pathog. 2008 May;4(5):e1000060 [18464894] Nat Struct Mol Biol. 2008 Jul;15(7):690-8 [18596815] J Virol. 2008 Aug;82(16):7846-62 [18524814] J Virol. 2008 Sep;82(17):8828-37 [18562544] Cell Host Microbe. 2008 Sep 11;4(3):229-38 [18779049] Virology. 2008 Nov 10;381(1):67-74 [18801552] Virology. 2009 Feb 5;384(1):16-20 [19101005] Virus Res. 2009 Feb;139(2):230-9 [18703097] J Infect Dis. 2009 Jul 15;200(2):202-5 [19527169] Cell Host Microbe. 2009 Oct 22;6(4):381-91 [19837377] EMBO J. 2009 Oct 21;28(20):3269-76 [19713934] J Virol. 2009 Dec;83(23):12631-5 [19776132] PLoS Pathog. 2010 Jan;6(1):e1000718 [20062797] Vector Borne Zoonotic Dis. 2010 Apr;10(3):267-74 [19619041] Science. 2010 May 7;328(5979):745-8 [20448183] Clin Lab Med. 2010 Mar;30(1):47-65 [20513541] Virology. 2010 Jul 20;403(1):85-91 [20447672] J Virol. 2010 Aug;84(16):8353-8 [20519400] PLoS Pathog. 2010;6(7):e1001005 [20661479] Cell Host Microbe. 2010 Sep 16;8(3):271-83 [20833378] Proc Natl Acad Sci U S A. 2010 Nov 2;107(44):18950-5 [20956322] Virology. 2011 Feb 5;410(1):30-7 [21084104] J Biol Chem. 2011 Jan 21;286(3):2067-77 [21078673] Virology. 2011 Mar 15;411(2):306-15 [21255816] PLoS Pathog. 2011 Jun;7(6):e1002111 [21738473] J Virol. 2002 Jun;76(12):5847-56 [12021317] J Virol. 2002 Dec;76(24):13097-100 [12438639] J Gen Virol. 2003 Jan;84(Pt 1):183-91 [12533715] EMBO J. 2003 Jun 2;22(11):2604-13 [12773377] Adv Virus Res. 1999;53:183-207 [10582099] J Virol. 2000 Apr;74(7):3253-63 [10708442] Clin Infect Dis. 2000 Mar;30(3):413-8 [10722421] Virology. 2001 Mar 15;281(2):294-304 [11277701] J Gen Virol. 2001 May;82(Pt 5):1013-25 [11297676] J Virol. 2001 May;75(10):4633-40 [11312333] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1128/JVI.06435-11 ER - TY - JOUR T1 - Spontaneous transformation of murine epithelial cells requires the early acquisition of specific chromosomal aneuploidies and genomic imbalances. AN - 921143690; 22161874 AB - Human carcinomas are defined by recurrent chromosomal aneuploidies, which result in a tissue-specific distribution of genomic imbalances. In order to develop models for these genome mutations and to determine their role in tumorigenesis, we generated 45 spontaneously transformed murine cell lines from normal epithelial cells derived from bladder, cervix, colon, kidney, lung, and mammary gland. Phenotypic changes, chromosomal aberrations, centrosome number, and telomerase activity were assayed in control uncultured cells and in three subsequent stages of transformation. Supernumerary centrosomes, binucleate cells, and tetraploidy were observed as early as 48 hr after explantation. In addition, telomerase activity increased throughout progression. Live-cell imaging revealed that failure of cytokinesis, not cell fusion, promoted genome duplication. Spectral karyotyping demonstrated that aneuploidy preceded immortalization, consisting predominantly of whole chromosome losses (4, 9, 12, 13, 16, and Y) and gains (1, 10, 15, and 19). After transformation, focal amplifications of the oncogenes Myc and Mdm2 were frequently detected. Fifty percent of the transformed lines resulted in tumors on injection into immunocompromised mice. The phenotypic and genomic alterations observed in spontaneously transformed murine epithelial cells recapitulated the aberration pattern observed during human carcinogenesis. The dominant aberration of these cell lines was the presence of specific chromosomal aneuploidies. We propose that our newly derived cancer models will be useful tools to dissect the sequential steps of genome mutations during malignant transformation, and also to identify cancer-specific genes, signaling pathways, and the role of chromosomal instability in this process. Copyright © 2011 Wiley Periodicals, Inc. JF - Genes, chromosomes & cancer AU - Padilla-Nash, Hesed M AU - Hathcock, Karen AU - McNeil, Nicole E AU - Mack, David AU - Hoeppner, Daniel AU - Ravin, Rea AU - Knutsen, Turid AU - Yonescu, Raluca AU - Wangsa, Danny AU - Dorritie, Kathleen AU - Barenboim, Linda AU - Hu, Yue AU - Ried, Thomas AD - Genetics Branch, National Cancer Institute, Bethesda, MD 20892, USA. nashh@mail.nih.gov Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 353 EP - 374 VL - 51 IS - 4 KW - Mdm2 protein, mouse KW - EC 2.3.2.27 KW - Proto-Oncogene Proteins c-mdm2 KW - Index Medicus KW - Phenotype KW - Animals KW - Proto-Oncogene Proteins c-mdm2 -- genetics KW - Genes, myc KW - Humans KW - Mice, Inbred C57BL KW - Mice, Nude KW - Mice KW - Cell Line, Transformed KW - Male KW - Female KW - Epithelial Cells -- metabolism KW - Aneuploidy KW - Epithelial Cells -- pathology KW - Chromosomal Instability -- genetics KW - Cell Transformation, Neoplastic -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/921143690?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Genes%2C+chromosomes+%26+cancer&rft.atitle=Spontaneous+transformation+of+murine+epithelial+cells+requires+the+early+acquisition+of+specific+chromosomal+aneuploidies+and+genomic+imbalances.&rft.au=Padilla-Nash%2C+Hesed+M%3BHathcock%2C+Karen%3BMcNeil%2C+Nicole+E%3BMack%2C+David%3BHoeppner%2C+Daniel%3BRavin%2C+Rea%3BKnutsen%2C+Turid%3BYonescu%2C+Raluca%3BWangsa%2C+Danny%3BDorritie%2C+Kathleen%3BBarenboim%2C+Linda%3BHu%2C+Yue%3BRied%2C+Thomas&rft.aulast=Padilla-Nash&rft.aufirst=Hesed&rft.date=2012-04-01&rft.volume=51&rft.issue=4&rft.spage=353&rft.isbn=&rft.btitle=&rft.title=Genes%2C+chromosomes+%26+cancer&rft.issn=1098-2264&rft_id=info:doi/10.1002%2Fgcc.21921 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-11 N1 - Date created - 2012-02-09 N1 - Date revised - 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Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/gcc.21921 ER - TY - JOUR T1 - Inhibition of androgen-responsive LNCaP prostate cancer cell tumor xenograft growth by dietary phenethyl isothiocyanate correlates with decreased angiogenesis and inhibition of cell attachment. AN - 919648565; 22266918 AB - Phenethyl isothiocyanate (PEITC) is a candidate anticancer compound found in certain cruciferous vegetables. In our tumor cell xenograft model, dietary administration of PEITC (100-150 mg/kg body weight/d) inhibited androgen-responsive LNCaP human prostate cancer cell tumor growth. We found that dietary treatment with PEITC significantly inhibited tumor platelet/endothelial cell adhesion molecule (PECAM-1/CD31) expression, a marker of angiogenesis. By contrast, we did not find the inhibitory effects of PEITC on tumor growth to be associated with alteration of specific markers for apoptosis, cell proliferation or androgen receptor-mediated pathways. Consistent with in vivo results, PEITC exerted little effects on cell proliferation, cell cycle and androgen-dependent pathways. Interestingly, PEITC significantly attenuated LNCaP cell plating efficiency that correlated with inhibition of integrin family proteins integrin β1, α2 and α6 mRNA expression. Thus, PEITC may be a dietary factor that inhibits androgen-responsive prostate tumor growth indirectly by selectively targeting factors involved in the tumor microenvironment. JF - International journal of oncology AU - Hudson, Tamaro S AU - Perkins, Susan N AU - Hursting, Stephen D AU - Young, Heather A AU - Kim, Young S AU - Wang, Tien-Chung AU - Wang, Thomas T Y AD - Laboratory of Cellular Regulation and Carcinogenesis, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 1113 EP - 1121 VL - 40 IS - 4 KW - Angiogenesis Inhibitors KW - 0 KW - Anticarcinogenic Agents KW - Isothiocyanates KW - phenethyl isothiocyanate KW - 6U7TFK75KV KW - Index Medicus KW - Cell Growth Processes -- drug effects KW - Animals KW - Humans KW - Xenograft Model Antitumor Assays KW - Mice, Nude KW - Mice KW - Mice, Inbred BALB C KW - Immunohistochemistry KW - Male KW - Anticarcinogenic Agents -- administration & dosage KW - Angiogenesis Inhibitors -- administration & dosage KW - Prostatic Neoplasms -- pathology KW - Cell-Matrix Junctions -- genetics KW - Isothiocyanates -- administration & dosage KW - Prostatic Neoplasms -- genetics KW - Cell-Matrix Junctions -- metabolism KW - Prostatic Neoplasms -- drug therapy KW - Cell-Matrix Junctions -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/919648565?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+oncology&rft.atitle=Inhibition+of+androgen-responsive+LNCaP+prostate+cancer+cell+tumor+xenograft+growth+by+dietary+phenethyl+isothiocyanate+correlates+with+decreased+angiogenesis+and+inhibition+of+cell+attachment.&rft.au=Hudson%2C+Tamaro+S%3BPerkins%2C+Susan+N%3BHursting%2C+Stephen+D%3BYoung%2C+Heather+A%3BKim%2C+Young+S%3BWang%2C+Tien-Chung%3BWang%2C+Thomas+T+Y&rft.aulast=Hudson&rft.aufirst=Tamaro&rft.date=2012-04-01&rft.volume=40&rft.issue=4&rft.spage=1113&rft.isbn=&rft.btitle=&rft.title=International+journal+of+oncology&rft.issn=1791-2423&rft_id=info:doi/10.3892%2Fijo.2012.1335 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-31 N1 - Date created - 2012-02-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochem Pharmacol. 2001 Jan 15;61(2):165-77 [11163331] J Cell Physiol. 2010 Aug;224(2):283-8 [20432448] J Nutr. 2001 Nov;131(11 Suppl):3027S-33S [11694642] Am J Physiol Cell Physiol. 2002 May;282(5):C1181-90 [11940533] Cancer Res. 2002 Jul 1;62(13):3615-9 [12097262] J Biol Chem. 2002 Oct 18;277(42):39334-42 [12171915] Mol Cell Endocrinol. 2002 Nov 29;197(1-2):239-50 [12431818] Curr Cancer Drug Targets. 2003 Jun;3(3):205-17 [12769689] Cancer Sci. 2004 Jan;95(1):65-71 [14720329] Mol Cancer Ther. 2004 May;3(5):567-75 [15141014] Prev Med. 1980 Sep;9(5):630-49 [6159622] Cancer Res. 1981 Aug;41(8):2991-4 [6788365] Carcinogenesis. 1987 Dec;8(12):1971-3 [3677323] Cancer Lett. 1990 Mar;49(3):225-30 [2317784] Cancer Res. 1991 Apr 15;51(8):2063-8 [2009525] Am J Pathol. 1993 Aug;143(2):401-9 [7688183] Lancet. 1993 Sep 18;342(8873):752 [8103867] Cancer Lett. 1993 Aug 16;72(1-2):103-10 [8402566] Cancer. 1994 Feb 15;73(4):1270-5 [8313330] Proc Natl Acad Sci U S A. 1994 Apr 12;91(8):3147-50 [8159717] J Natl Cancer Inst. 1995 Mar 1;87(5):354-60 [7531773] Prostate. 1995 Feb;26(2):87-93 [7855002] J Cell Biochem Suppl. 1995;22:195-209 [8538199] Br J Urol. 1996 Apr;77(4):481-93 [8777605] Cancer Res. 1998 Feb 1;58(3):402-8 [9458080] J Urol. 1999 Jan;161(1):152-5 [10037388] J Nutr. 1999 Sep;129(9):1628-35 [10460196] Oncogene. 2005 Jun 30;24(28):4486-95 [15856023] Methods Mol Med. 2005;112:277-89 [16010024] Oncogene. 2005 Sep 15;24(41):6256-68 [15940258] Carcinogenesis. 2005 Nov;26(11):1896-904 [15958518] Carcinogenesis. 2006 Mar;27(3):475-82 [16299382] Cancer Res. 2006 Aug 15;66(16):8091-9 [16912186] Mol Carcinog. 2006 Dec;45(12):943-56 [16865672] Cancer Res. 2007 Mar 1;67(5):2239-46 [17332354] Neoplasia. 2008 Aug;10(8):797-803 [18670640] Carcinogenesis. 2008 Oct;29(10):2001-10 [18586690] Cancer Biother Radiopharm. 2001 Feb;16(1):55-62 [11279798] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.3892/ijo.2012.1335 ER - TY - JOUR T1 - Simple and efficient purification of Escherichia coli DNA polymerase V: Cofactor requirements for optimal activity and processivity in vitro AN - 1735916666; PQ0002257265 AB - Most damage induced mutagenesis in Escherichia coli is dependent upon the protein complex, which comprises DNA polymerase V (pol V). Biochemical characterization of pol V has been hindered by the fact that the enzyme is notoriously difficult to purify, largely because overproduced UmuC is insoluble. Here, we report a simple and efficient protocol for the rapid purification of milligram quantities of pol V from just 4L of bacterial culture. Rather than over producing the UmuC protein, it was expressed at low basal levels, while was expressed in trans from a high copy-number plasmid with an inducible promoter. We have also developed strategies to purify the beta -clamp and gamma -clamp loader free from contaminating polymerases. Using these highly purified proteins, we determined the cofactor requirements for optimal activity of pol V in vitro and found that pol V shows robust activity on an SSB-coated circular DNA template in the presence of the beta / gamma -complex and a RecA nucleoprotein filament (RecA*) formed in trans. This strong activity was attributed to the unexpectedly high processivity of pol V Mut (), which was efficiently recruited to a primer terminus by SSB. JF - DNA Repair AU - Karata, Kiyonobu AU - Vaisman, Alexandra AU - Goodman, Myron F AU - Woodgate, Roger AD - Laboratory of Genomic Integrity, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-3371, USA Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 431 EP - 440 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 11 IS - 4 SN - 1568-7864, 1568-7864 KW - Microbiology Abstracts B: Bacteriology; Genetics Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - UmuC KW - UmuD' KW - SOS mutagenesis KW - Y-family DNA polymerase KW - Mutagenesis KW - Translesion DNA synthesis KW - Circular DNA KW - Nucleoproteins KW - Enzymes KW - Plasmids KW - DNA repair KW - Promoters KW - Cofactors KW - DNA-directed DNA polymerase KW - Escherichia coli KW - Primers KW - Filaments KW - RecA protein KW - G 07880:Human Genetics KW - N 14820:DNA Metabolism & Structure KW - J 02300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1735916666?accountid=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=DNA+Repair&rft.atitle=Simple+and+efficient+purification+of+Escherichia+coli+DNA+polymerase+V%3A+Cofactor+requirements+for+optimal+activity+and+processivity+in+vitro&rft.au=Karata%2C+Kiyonobu%3BVaisman%2C+Alexandra%3BGoodman%2C+Myron+F%3BWoodgate%2C+Roger&rft.aulast=Karata&rft.aufirst=Kiyonobu&rft.date=2012-04-01&rft.volume=11&rft.issue=4&rft.spage=431&rft.isbn=&rft.btitle=&rft.title=DNA+Repair&rft.issn=15687864&rft_id=info:doi/10.1016%2Fj.dnarep.2012.01.012 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-11-01 N1 - Last updated - 2016-02-29 N1 - SubjectsTermNotLitGenreText - Promoters; Circular DNA; Cofactors; DNA-directed DNA polymerase; Nucleoproteins; Enzymes; Primers; DNA repair; Plasmids; Filaments; RecA protein; Mutagenesis; Escherichia coli DO - http://dx.doi.org/10.1016/j.dnarep.2012.01.012 ER - TY - JOUR T1 - Dietary lignan and proanthocyanidin consumption and colorectal adenoma recurrence in the Polyp Prevention Trial AN - 1562665830; 20634535 AB - Lignans and proanthocyanidins are plant polyphenols that have shown protective properties against colorectal neoplasms in some human studies. Using logistic regression, we estimated odds ratios (ORs) and 95% confidence intervals (CIs) to prospectively evaluate the association between lignan and proanthocyanidin intake, estimated from databases linked to a food frequency questionnaire, and adenoma recurrence in 1,859 participants of the Polyp Prevention Trial. Overall, individual or total lignans or proanthocyanidins were not associated with colorectal adenoma recurrence. However, in sex-specific analyses, total lignan intake was positively associated with any adenoma recurrence in women (highest vs. lowest lignan intake quartile OR = 2.07, 95% CI: 1.22-3.52, p trend = 0.004) but not in men (p interaction = 0.04). To conclude, dietary lignan and proanthocyanidin consumption were not generally related to colorectal adenoma recurrence; however, high lignan intake may increase the risk of adenoma recurrence in women. JF - International Journal of Cancer AU - Bobe, Gerd AU - Murphy, Gwen AU - Albert, Paul S AU - Sansbury, Leah B AU - Lanza, Elaine AU - Schatzkin, Arthur AU - Cross, Amanda J AD - Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute (NCI), National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Frederick, MD. Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 1649 EP - 1659 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 130 IS - 7 SN - 0020-7136, 0020-7136 KW - Risk Abstracts KW - Diets KW - Health risks KW - Prevention KW - Polyps KW - Cancer KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1562665830?accountid=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=Dietary+lignan+and+proanthocyanidin+consumption+and+colorectal+adenoma+recurrence+in+the+Polyp+Prevention+Trial&rft.au=Bobe%2C+Gerd%3BMurphy%2C+Gwen%3BAlbert%2C+Paul+S%3BSansbury%2C+Leah+B%3BLanza%2C+Elaine%3BSchatzkin%2C+Arthur%3BCross%2C+Amanda+J&rft.aulast=Bobe&rft.aufirst=Gerd&rft.date=2012-04-01&rft.volume=130&rft.issue=7&rft.spage=1649&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.26184 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Diets; Health risks; Prevention; Polyps; Cancer DO - http://dx.doi.org/10.1002/ijc.26184 ER - TY - JOUR T1 - Antibodies reactive to Plasmodium falciparum serine repeat antigen in children with Burkitt lymphoma from Ghana AN - 1560118989; 20634558 AB - The role of protective immunity to Plasmodium falciparum (Pf) malaria in Burkitt lymphoma (BL) is unknown. We investigated the association between BL and antibodies reactive to SE36 antigen, a recombinant protein based on P. falciparum serine repeat antigen 5 gene, targeted by protective malaria immune responses. Cases were children (0-14 years) enrolled at the Korle-Bu Teaching Hospital, Accra, Ghana, during 1965-1994 with BL confirmed by histology or cytology (92% of cases). Controls were apparently healthy children enrolled contemporaneous to the cases from the nearest neighbor house to the case house and were age,- sex-frequency-matched to the cases. Anti-SE36 IgG antibodies were measured using enzyme-linked absorbent immunoassays (ELISAs). SE36 titers were estimated by extrapolating ELISA optical density readings to a standard fitting curve. Anti-SE36 titers were log-transformed for analysis. Odds ratios (ORs) and two-sided 95% confidence intervals (95% CIs) were estimated using unconditional logistic regression. The mean log endpoint dilution titers were 0.63 logs lower in cases than in controls (8.26 [SD 1.68] vs. 8.89 [SD 1.75], Student's t-test, p = 0.019). Lower titers were observed in cases than controls aged 0-4 years (p = 0.05) and in those aged 5-14 years (p = 0.06). Low and medium tertiles of anti-SE36 IgG antibodies were associated with increased OR for BL ([OR 1.67, 95% CI 1.21-2.31] and [OR 1.33, 95% CI 0.96-1.86], respectively, p sub(trend) = 0.002) in analyses adjusting for age, sex, calendar period and test plate. Our findings suggest that compared to similarly aged children enrolled from the same community, children with BL in Ghana have lower antibodies to SE36 antigen. JF - International Journal of Cancer AU - Guech-Ongey, Mercy AU - Yagi, Masanori AU - Palacpac, Nirianne Marie Q AU - Emmanuel, Benjamin AU - Talisuna, Ambrose O AU - Bhatia, Kishor AU - Stefan, DCristina AU - Biggar, Robert J AU - Nkrumah, Francis AU - Neequaye, Janet AU - Tougan, Takahiro AU - Horii, Toshihiro AU - Mbulaiteye, Sam M AD - Division of Cancer Epidemiology and Genetics, DCEG, NCI, Bethesda, MD. Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 1908 EP - 1914 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 130 IS - 8 SN - 0020-7136, 0020-7136 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Immunology Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - Parasites KW - Age KW - Human diseases KW - Malaria KW - Public health KW - Burkitt's lymphoma KW - Antigens KW - Optical density KW - ELISA KW - Cytology KW - Serine KW - Sex KW - Ghana KW - Houses KW - Enzyme-linked immunosorbent assay KW - Plasmodium falciparum KW - Immunity KW - Children KW - Antibodies KW - Immunoglobulin G KW - Language KW - Immune response KW - serine repeat antigen KW - Immunoassays KW - Hospitals KW - K 03400:Human Diseases KW - F 06915:Cancer Immunology KW - Q1 08423:Behaviour KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1560118989?accountid=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=International+Journal+of+Cancer&rft.atitle=Antibodies+reactive+to+Plasmodium+falciparum+serine+repeat+antigen+in+children+with+Burkitt+lymphoma+from+Ghana&rft.au=Guech-Ongey%2C+Mercy%3BYagi%2C+Masanori%3BPalacpac%2C+Nirianne+Marie+Q%3BEmmanuel%2C+Benjamin%3BTalisuna%2C+Ambrose+O%3BBhatia%2C+Kishor%3BStefan%2C+DCristina%3BBiggar%2C+Robert+J%3BNkrumah%2C+Francis%3BNeequaye%2C+Janet%3BTougan%2C+Takahiro%3BHorii%2C+Toshihiro%3BMbulaiteye%2C+Sam+M&rft.aulast=Guech-Ongey&rft.aufirst=Mercy&rft.date=2012-04-01&rft.volume=130&rft.issue=8&rft.spage=1908&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=00207136&rft_id=info:doi/10.1002%2Fijc.26203 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Last updated - 2016-04-29 N1 - SubjectsTermNotLitGenreText - Parasites; Human diseases; Antibodies; Antigens; Cytology; ELISA; Malaria; Serine; Public health; Age; Enzyme-linked immunosorbent assay; Houses; Immunity; Children; Burkitt's lymphoma; Optical density; Immunoglobulin G; Language; Immune response; serine repeat antigen; Immunoassays; Hospitals; Sex; Plasmodium falciparum; Ghana DO - http://dx.doi.org/10.1002/ijc.26203 ER - TY - JOUR T1 - Symmetric Epistasis Estimation (SEE) and its application to dissecting interaction map of Plasmodium falciparum AN - 1560116960; 20516657 AB - It is being increasingly recognized that many important phenotypic traits, including various diseases, are governed by a combination of weak genetic effects and their interactions. While the detection of epistatic interactions that involve a non-additive effect of two loci on a quantitative trait is particularly challenging, this interaction type is fundamental for the understanding of genome organization and gene regulation. However, current methods that detect epistatic interactions typically rely on the existence of a strong primary effect, considerably limiting the sensitivity of the search. To fill this gap, we developed a new method, SEE (Symmetric Epistasis Estimation), allowing the genome-wide detection of epistatic interactions without the need for a strong primary effect. We applied our approach to progeny crosses of the human malaria parasite P. falciparumand S. cerevisiae. We found an abundance of epistatic interactions in the parasite and a much smaller number of such interactions in yeast. The genome of P. falciparumalso harboured several epistatic interaction hotspots that putatively play a role in drug resistance mechanisms. The abundance of observed epistatic interactions might suggest a mechanism of compensation for the extremely limited repertoire of transcription factors. Interestingly, epistatic interaction hotspots were associated with elevated levels of linkage disequilibrium, an observation that suggests selection pressure acting on P. falciparum, potentially reflecting host-pathogen interactions or drug-induced selection. JF - Molecular BioSystems AU - Huang, Yang AU - Siwo, Geoffrey AU - Wuchty, Stefan AU - Ferdig, Michael T AU - Przytycka, Teresa M AD - National Center for Biotechnology Information; NLM; NIH; 8600 Rockville Pike; Building 38A; Bethesda; MD 20894; USA; 301-480-4637; 301-402-1723; , przytyck@mail.nih.gov Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 1544 EP - 1552 PB - Royal Society of Chemistry VL - 8 IS - 5 SN - 1742-206X, 1742-206X KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - Genomes KW - Yeasts KW - Parasites KW - Human diseases KW - Hot spots KW - Drug resistance KW - Abundance KW - Transcription KW - Malaria KW - Plasmodium falciparum KW - Phenotypes KW - Public health KW - Linkage disequilibrium KW - Epistasis KW - Transcription factors KW - Gene regulation KW - Host-pathogen interactions KW - Genetic crosses KW - K 03300:Methods 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/1560116960?accountid=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=Molecular+BioSystems&rft.atitle=Symmetric+Epistasis+Estimation+%28SEE%29+and+its+application+to+dissecting+interaction+map+of+Plasmodium+falciparum&rft.au=Huang%2C+Yang%3BSiwo%2C+Geoffrey%3BWuchty%2C+Stefan%3BFerdig%2C+Michael+T%3BPrzytycka%2C+Teresa+M&rft.aulast=Huang&rft.aufirst=Yang&rft.date=2012-04-01&rft.volume=8&rft.issue=5&rft.spage=1544&rft.isbn=&rft.btitle=&rft.title=Molecular+BioSystems&rft.issn=1742206X&rft_id=info:doi/10.1039%2Fc2mb05333k LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-09-01 N1 - Number of references - 32 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Yeasts; Genomes; Parasites; Human diseases; Hot spots; Transcription; Malaria; Phenotypes; Public health; Linkage disequilibrium; Drug resistance; Host-pathogen interactions; Gene regulation; Transcription factors; Epistasis; Abundance; Genetic crosses; Plasmodium falciparum DO - http://dx.doi.org/10.1039/c2mb05333k ER - TY - JOUR T1 - Mass spectrometry-based targeted quantitative proteomics: Achieving sensitive and reproducible detection of proteins AN - 1529957692; 19893184 AB - Traditional shotgun proteomics used to detect a mixture of hundreds to thousands of proteins through mass spectrometric analysis, has been the standard approach in research to profile protein content in a biological sample which could lead to the discovery of new (and all) protein candidates with diagnostic, prognostic, and therapeutic values. In practice, this approach requires significant resources and time, and does not necessarily represent the goal of the researcher who would rather study a subset of such discovered proteins (including their variations or posttranslational modifications) under different biological conditions. In this context, targeted proteomics is playing an increasingly important role in the accurate measurement of protein targets in biological samples in the hope of elucidating the molecular mechanism of cellular function via the understanding of intricate protein networks and pathways. One such (targeted) approach, selected reaction monitoring (or multiple reaction monitoring) mass spectrometry (MRM-MS), offers the capability of measuring multiple proteins with higher sensitivity and throughput than shotgun proteomics. Developing and validating MRM-MS-based assays, however, is an extensive and iterative process, requiring a coordinated and collaborative effort by the scientific community through the sharing of publicly accessible data and datasets, bioinformatic tools, standard operating procedures, and well characterized reagents. JF - Proteomics AU - Boja, Emily S AU - Rodriguez, Henry AD - Office of Cancer Clinical Proteomics Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2012/04// PY - 2012 DA - Apr 2012 SP - 1093 EP - 1110 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 12 IS - 8 SN - 1615-9853, 1615-9853 KW - Biotechnology and Bioengineering Abstracts KW - Molecular modelling KW - Data processing KW - proteomics KW - Bioinformatics KW - Mass spectroscopy KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1529957692?accountid=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=Mass+spectrometry-based+targeted+quantitative+proteomics%3A+Achieving+sensitive+and+reproducible+detection+of+proteins&rft.au=Boja%2C+Emily+S%3BRodriguez%2C+Henry&rft.aulast=Boja&rft.aufirst=Emily&rft.date=2012-04-01&rft.volume=12&rft.issue=8&rft.spage=1093&rft.isbn=&rft.btitle=&rft.title=Proteomics&rft.issn=16159853&rft_id=info:doi/10.1002%2Fpmic.201100387 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-05-01 N1 - Last updated - 2014-06-12 N1 - SubjectsTermNotLitGenreText - Molecular modelling; Data processing; Bioinformatics; proteomics; Mass spectroscopy DO - http://dx.doi.org/10.1002/pmic.201100387 ER - TY - JOUR T1 - Fast and accurate modeling of protein-protein interactions by combining template-interface-based docking with flexible refinement AN - 1434018368; 18498773 AB - The similarity between folding and binding led us to posit the concept that the number of protein-protein interface motifs in nature is limited, and interacting protein pairs can use similar interface architectures repeatedly, even if their global folds completely vary. Thus, known protein-protein interface architectures can be used to model the complexes between two target proteins on the proteome scale, even if their global structures differ. This powerful concept is combined with a flexible refinement and global energy assessment tool. The accuracy of the method is highly dependent on the structural diversity of the interface architectures in the template dataset. Here, we validate this knowledge-based combinatorial method on the Docking Benchmark and show that it efficiently finds high-quality models for benchmark complexes and their binding regions even in the absence of template interfaces having sequence similarity to the targets. Compared to "classical" docking, it is computationally faster; as the number of target proteins increases, the difference becomes more dramatic. Further, it is able to distinguish binders from nonbinders. These features allow performing large-scale network modeling. The results on an independent target set (proteins in the p53 molecular interaction map) show that current method can be used to predict whether a given protein pair interacts. Overall, while constrained by the diversity of the template set, this approach efficiently produces high-quality models of protein-protein complexes. We expect that with the growing number of known interface architectures, this type of knowledge-based methods will be increasingly used by the broad proteomics community. Proteins 2012; [copy 2011 Wiley Periodicals, Inc. JF - Proteins: Structure, Function and Bioinformatics AU - Tuncbag, Nurcan AU - Keskin, Ozlem AU - Nussinov, Ruth AU - Gursoy, Attila AD - Basic Science Program, SAIC-Frederick, Inc, Center for Cancer Research Nanobiology Program, NCI-Frederick, Frederick, Maryland 21702., okeskin@ku.edu.tr Y1 - 2012/04// PY - 2012 DA - Apr 2012 SP - 1239 EP - 1249 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030 United States VL - 80 IS - 4 SN - 0887-3585, 0887-3585 KW - Biotechnology and Bioengineering Abstracts KW - Protein structure KW - Energy KW - proteomics KW - Bioinformatics KW - Protein interaction KW - Models KW - p53 protein KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434018368?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.atitle=Fast+and+accurate+modeling+of+protein-protein+interactions+by+combining+template-interface-based+docking+with+flexible+refinement&rft.au=Tuncbag%2C+Nurcan%3BKeskin%2C+Ozlem%3BNussinov%2C+Ruth%3BGursoy%2C+Attila&rft.aulast=Tuncbag&rft.aufirst=Nurcan&rft.date=2012-04-01&rft.volume=80&rft.issue=4&rft.spage=1239&rft.isbn=&rft.btitle=&rft.title=Proteins%3A+Structure%2C+Function+and+Bioinformatics&rft.issn=08873585&rft_id=info:doi/10.1002%2Fprot.24022 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Last updated - 2013-09-20 N1 - SubjectsTermNotLitGenreText - Protein structure; Energy; Bioinformatics; proteomics; Protein interaction; p53 protein; Models DO - http://dx.doi.org/10.1002/prot.24022 ER - TY - JOUR T1 - Dietary Nitrate and Nitrite Intake and Non-Hodgkin Lymphoma Survival AN - 1257774424; 17452193 AB - Nitrate and nitrite are precursors in the formation of N-nitroso compounds. We recently found a 40% increased risk of NHL with higher dietary nitrite intake and significant increases in risk for follicular and T-cell lymphoma. It is possible that these compounds also affect NHL prognosis by enhancing cancer progression in addition to development by further impairing immune system function. To test the hypothesis that nitrate and nitrite intake affects NHL survival, we evaluated the association in study participants that have been followed post-disease diagnosis in a population-based case-control study among women in Connecticut. We did not observe a significant increasing trend of mortality for NHL overall or by subtype for nitrate or nitrite intake for deaths from NHL or death from any cause, although a borderline significant protective trend was observed for follicular lymphoma with increasing nitrate intake. We did not identify a difference in overall survival for nitrate (P = 0.39) or for nitrite (P = 0.66) or for NHL specific survival for nitrate (P = 0.96) or nitrite (P = 0.17). Thus, our null findings do not confer support for the possibility that dietary nitrate and nitrite intake impacts NHL survival by promoting immune unresponsiveness. JF - Nutrition and Cancer AU - Aschebrook-Kilfoy, Briseis AU - Ward, Mary H AU - Zheng, Tongzhang AU - Holford, Theodore R AU - Boyle, Peter AU - Leaderer, Brian AU - Zhang, Yawei AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, Maryland, USA, brisa@uchicago.edu Y1 - 2012/04/01/ PY - 2012 DA - 2012 Apr 01 SP - 488 EP - 492 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 64 IS - 3 SN - 0163-5581, 0163-5581 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Cancer KW - Diets KW - Immune system KW - Lymphoma KW - Mortality KW - Nitrates KW - Nitrites KW - Non-Hodgkin's lymphoma KW - Survival KW - lymphoma KW - USA, Connecticut 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/1257774424?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nutrition+and+Cancer&rft.atitle=Dietary+Nitrate+and+Nitrite+Intake+and+Non-Hodgkin+Lymphoma+Survival&rft.au=Aschebrook-Kilfoy%2C+Briseis%3BWard%2C+Mary+H%3BZheng%2C+Tongzhang%3BHolford%2C+Theodore+R%3BBoyle%2C+Peter%3BLeaderer%2C+Brian%3BZhang%2C+Yawei&rft.aulast=Aschebrook-Kilfoy&rft.aufirst=Briseis&rft.date=2012-04-01&rft.volume=64&rft.issue=3&rft.spage=488&rft.isbn=&rft.btitle=&rft.title=Nutrition+and+Cancer&rft.issn=01635581&rft_id=info:doi/10.1080%2F01635581.2012.658136 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-12-01 N1 - Last updated - 2013-05-06 N1 - SubjectsTermNotLitGenreText - Diets; Non-Hodgkin's lymphoma; Mortality; Nitrates; Nitrites; Immune system; Survival; Lymphoma; lymphoma; Cancer; USA, Connecticut DO - http://dx.doi.org/10.1080/01635581.2012.658136 ER - TY - JOUR T1 - Promoting Good Clinical Laboratory Practices and Laboratory Accreditation to Support Clinical Trials in Sub-Saharan Africa AN - 1093471373; 17172201 AB - Laboratory capacity in the developing world frequently lacks quality management systems (QMS) such as good clinical laboratory practices, proper safety precautions, and adequate facilities; impacting the ability to conduct biomedical research where it is needed most. As the regulatory climate changes globally, higher quality laboratory support is needed to protect study volunteers and to accurately assess biological parameters. The University of Bamako and its partners have undertaken a comprehensive QMS plan to improve quality and productivity using the Clinical and Laboratory Standards Institute standards and guidelines. The clinical laboratory passed the College of American Pathologists inspection in April 2010, and received full accreditation in June 2010. Our efforts to implement high-quality standards have been valuable for evaluating safety and immunogenicity of malaria vaccine candidates in Mali. Other disease-specific research groups in resource-limited settings may benefit by incorporating similar training initiatives, QMS methods, and continual improvement practices to ensure best practices. JF - American Journal of Tropical Medicine and Hygiene AU - Guindo, MA AU - Shott, J P AU - Saye, R AU - Diakite, M L AU - Sanogo, S AU - Dembele, M B AU - Keita, S AU - Nagel, M C AU - Ellis, R D AU - Aebig, JA AU - Diallo, DA AU - Doumbo, OK AD - 33 N Drive, MSC 3207, Bethesda, MD 20892, USA, Shottj@mail.nih.gov Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 573 EP - 579 VL - 86 IS - 4 SN - 0002-9637, 0002-9637 KW - Microbiology Abstracts C: Algology, Mycology & Protozoology; Microbiology Abstracts B: Bacteriology; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Sustainability Science Abstracts; Health & Safety Science Abstracts KW - Human diseases KW - Mali KW - Training KW - Best practices KW - Guidelines KW - Disease control KW - Malaria KW - Clinical trials KW - Education establishments KW - Public health KW - Training centres KW - Immunogenicity KW - Vaccines KW - Inspection KW - Hygiene KW - accreditation KW - M3 1010:Issues in Sustainable Development KW - K 03400:Human Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - J 02350:Immunology KW - Q5 08524:Public health, medicines, dangerous organisms KW - H 4000:Food and Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1093471373?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.atitle=Promoting+Good+Clinical+Laboratory+Practices+and+Laboratory+Accreditation+to+Support+Clinical+Trials+in+Sub-Saharan+Africa&rft.au=Guindo%2C+MA%3BShott%2C+J+P%3BSaye%2C+R%3BDiakite%2C+M+L%3BSanogo%2C+S%3BDembele%2C+M+B%3BKeita%2C+S%3BNagel%2C+M+C%3BEllis%2C+R+D%3BAebig%2C+JA%3BDiallo%2C+DA%3BDoumbo%2C+OK&rft.aulast=Guindo&rft.aufirst=MA&rft.date=2012-04-01&rft.volume=86&rft.issue=4&rft.spage=573&rft.isbn=&rft.btitle=&rft.title=American+Journal+of+Tropical+Medicine+and+Hygiene&rft.issn=00029637&rft_id=info:doi/10.4269%2Fajtmh.2012.11-0691 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Human diseases; Training centres; Disease control; Malaria; Vaccines; Hygiene; Education establishments; Public health; Immunogenicity; Clinical trials; Training; Best practices; Guidelines; Inspection; accreditation; Mali DO - http://dx.doi.org/10.4269/ajtmh.2012.11-0691 ER - TY - JOUR T1 - Flexicate molecules as a potential new class of antibiotics AN - 1038596166; 17011993 AB - Evaluation of: Howson SE, Bolhuis A, Brabec V et al. Optically pure, water-stable metallo-helical 'flexicate'' assemblies with antibiotic activity. Nat. Chem. 4(1), 31-36 (2011). Helicates are alpha -helical, nonpeptide complexes that bind to DNA and exhibit antimicrobial activity. In the past, enthusiasm for the use of helicates in biological applications was limited, at least in part, by the presence of a racemic mixture of enantiomers or the formation of complexes that are insoluble in aqueous solutions. Recently, Howson et al. overcame the barriers associated with helicate synthesis by generating helicate-like complexes that are soluble and stable in water, optically pure and synthetically flexible. The mechanism synthesizes nonpeptide mimetic alpha -helical 'flexicates'' that bind to DNA and show broad-spectrum antimicrobial activity against representative Gram-positive and Gram-negative bacterial pathogens. Although the application of flexicates as an antimicrobial therapy remains to be determined, this study provides important insight into flexicate activity and the prospective use of flexicates as microbicidal agents. JF - Future Microbiology AU - Rasmussen, Devon L AU - Kobayashi, Scott D AU - DeLeo, Frank R AD - Laboratory of Bacterial Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy & Infectious Diseases, National Institutes of Health, 903 South 4th Street, Hamilton, MT 59840, USA, fdeleo@niaid.nih.gov Y1 - 2012/04// PY - 2012 DA - Apr 2012 SP - 445 EP - 448 PB - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom VL - 7 IS - 4 SN - 1746-0913, 1746-0913 KW - Biotechnology and Bioengineering Abstracts; Microbiology Abstracts B: Bacteriology KW - Antibiotics KW - Antimicrobial activity KW - W 30915:Pharmaceuticals & Vaccines KW - J 02450:Ecology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1038596166?accountid=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=Future+Microbiology&rft.atitle=Flexicate+molecules+as+a+potential+new+class+of+antibiotics&rft.au=Rasmussen%2C+Devon+L%3BKobayashi%2C+Scott+D%3BDeLeo%2C+Frank+R&rft.aulast=Rasmussen&rft.aufirst=Devon&rft.date=2012-04-01&rft.volume=7&rft.issue=4&rft.spage=445&rft.isbn=&rft.btitle=&rft.title=Future+Microbiology&rft.issn=17460913&rft_id=info:doi/10.2217%2Ffmb.12.26 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-09-01 N1 - Number of references - 1 N1 - Last updated - 2014-02-11 N1 - SubjectsTermNotLitGenreText - Antimicrobial activity DO - http://dx.doi.org/10.2217/fmb.12.26 ER - TY - JOUR T1 - Sleep disordered breathing in community psychiatric patients AN - 1038109400; 201221960 AB - Background and Objectives: Sleep disturbance is prominent in many neuropsychiatric disorders and may precipitate or exacerbate a range of psychiatric conditions. Few studies have investigated sleep disordered breathing and in particular obstructive sleep apnoea in community psychiatric patients and the commonly used screening instruments have not been evaluated in patients with psychiatric disorders. The objective is to evaluate the prevalence of sleep disordered breathing in a community cohort with chronic mental illness on long term psychotropic medication, and to assess the effectiveness of commonly used screening instruments to detect abnormal sleep. Methods: 52 patients completed sleep questionnaires and 50 undertook overnight oximetry. Results: 52% (n = 26) had sleep-disordered breathing; 20% (n = 10) had moderate/severe sleep apnoea. The Epworth Sleepiness Score and the Pittsburgh Sleep Quality Inventory did not predict sleep disordered breathing. Conclusions: Patients with psychiatric disorders in the community have a high rate of undiagnosed sleep disordered breathing, which is not reliably detected by established sleep disorder screening questionnaires. Adapted from the source document. JF - The European Journal of Psychiatry AU - Anderson, Kirstie N AU - Waton, Tony AU - Armstrong, Daniel AU - Watkinson, Helen M AU - Mackin, Paul AD - Department of Neurology, Royal Victoria Infirmary Queen Victoria Road, Newcastle upon Tyne NEI 4LP Phone: +0191 282 3833, Fax: +0191 282 3435 kirstie.anderson@nuth.nhs.uk Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 86 EP - 95 PB - Faculty of Medicine, Universy of Zaragoza, Spain VL - 26 IS - 2 SN - 0213-6163, 0213-6163 KW - Sleep disorders, Polysomnography, Obstructive sleep apnoea KW - Screening KW - Mentally ill people KW - Breathing KW - Sleep disorders KW - Sleep KW - Psychiatric disorders KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1038109400?accountid=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+European+Journal+of+Psychiatry&rft.atitle=Sleep+disordered+breathing+in+community+psychiatric+patients&rft.au=Anderson%2C+Kirstie+N%3BWaton%2C+Tony%3BArmstrong%2C+Daniel%3BWatkinson%2C+Helen+M%3BMackin%2C+Paul&rft.aulast=Anderson&rft.aufirst=Kirstie&rft.date=2012-04-01&rft.volume=26&rft.issue=2&rft.spage=86&rft.isbn=&rft.btitle=&rft.title=The+European+Journal+of+Psychiatry&rft.issn=02136163&rft_id=info:doi/ LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-09-01 N1 - Last updated - 2016-09-27 N1 - CODEN - EJOPEO N1 - SubjectsTermNotLitGenreText - Sleep; Breathing; Mentally ill people; Screening; Psychiatric disorders; Sleep disorders ER - TY - JOUR T1 - A Brief Primer on Self-Esteem AN - 1023096159; 201217784 AB - Since the construct of self-esteem was first introduced over 100 years ago, a wealth of knowledge has been accumulated. Several conclusions about the nature of self-esteem can be reached that provide a foundation for future practice and research. In general, research shows that high self-esteem is associated with the behaviors, goals, and coping processes that facilitate success in school, work, and relationships, while low self-esteem is a risk-factor for mental health problems, antisocial behavior, and substance abuse. This article provides a brief primer on self-esteem and reviews the literature on self-esteem intervention programs. Adapted from the source document. JF - Prevention Researcher AU - Robins, Richard W AU - Trzesniewski, Kali H AU - Donnellan, M Brent AD - Psychology, University of California, Davis, and a member of the core faculty for the NIMH Training Program in Affective Science rwrobins@ucdavis.edu Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 3 EP - 7 PB - Integrated Research Services, Eugene OR VL - 19 IS - 2 SN - 1086-4385, 1086-4385 KW - Goals KW - Risk factors KW - Psychiatric disorders KW - Wealth KW - Selfesteem KW - Substance abuse KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1023096159?accountid=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=Prevention+Researcher&rft.atitle=A+Brief+Primer+on+Self-Esteem&rft.au=Robins%2C+Richard+W%3BTrzesniewski%2C+Kali+H%3BDonnellan%2C+M+Brent&rft.aulast=Robins&rft.aufirst=Richard&rft.date=2012-04-01&rft.volume=19&rft.issue=2&rft.spage=3&rft.isbn=&rft.btitle=&rft.title=Prevention+Researcher&rft.issn=10864385&rft_id=info:doi/ LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-07-01 N1 - Last updated - 2016-09-27 N1 - CODEN - PRREFE N1 - SubjectsTermNotLitGenreText - Selfesteem; Substance abuse; Psychiatric disorders; Wealth; Goals; Risk factors ER - TY - JOUR T1 - Talking About End-of-Life Preferences With Advanced Cancer Patients: Factors Influencing Feasibility AN - 1023091655; 201212992 AB - Context. The End-of-Life Preferences Interview (ELPI) was developed with the purpose of supporting physicians in communicating with advanced cancer patients. Objectives. This study aimed to evaluate ELPI feasibility and compare home care/hospice (HC-H) vs. outpatient (OU) care settings. Methods. Twenty-eight physicians were trained in the use of the ELPI and were asked to apply the new instrument in their daily clinical practice for two months. ELPI feasibility was evaluated through three indices: the percentage of eligible patients, the percentage of patients to whom the ELPI was proposed, and the percentage of completed interviews. Results. The 23 physicians participating in the data collection screened 633 patients, and 156 of them (25%, 95% confidence interval 21%-28%) were judged to be eligible. Eligibility in HC-H was lower than that in the OU setting (18% vs. 46%; P < 0.0001), whereas the differences were reduced when looking at patients to whom the ELPI was proposed (12% vs. 20%; P = 0.017) and who completed the ELPI (8% vs. 18%; P < 0.001). The percentage of eligible patients refusing the interview was very low in the entire sample (1.9%). Conclusion. Results indicate that discussing end-of-life preferences in an earlier disease phase, such as in the OU setting, could be preferable but that its accomplishment in this setting may be more difficult, mainly as a result of organizational reasons. This observation could indicate that the system is not yet ready to offer patients such an opportunity and although communication on these sensitive issues cannot be reduced to a procedure, the ELPI can become a useful tool to help physicians in accomplishing this difficult task. [Copyright U.S. Cancer Pain Relief Committee. Published by Elsevier Inc.] JF - Journal of Pain and Symptom Management AU - Borreani, Claudia AU - Brunelli, Cinzia AU - Bianchi, Elisabetta AU - Piva, Laura AU - Moro, Cecilia AU - Miccinesi, Guido AD - Clinical Psychology Unit, IRCCS Foundation, National Cancer Institute, Via Venezian 1, 20133 Milan, Italy claudia.borreani@istitutotumori.mi.it Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 739 EP - 746 PB - Elsevier, New York NY VL - 43 IS - 4 SN - 0885-3924, 0885-3924 KW - End of life, preferences, advanced cancer, communication, decision making KW - Feasibility KW - Doctors KW - Preferences KW - End of life decisions KW - Confidence intervals KW - Terminally ill people KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1023091655?accountid=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+Pain+and+Symptom+Management&rft.atitle=Talking+About+End-of-Life+Preferences+With+Advanced+Cancer+Patients%3A+Factors+Influencing+Feasibility&rft.au=Borreani%2C+Claudia%3BBrunelli%2C+Cinzia%3BBianchi%2C+Elisabetta%3BPiva%2C+Laura%3BMoro%2C+Cecilia%3BMiccinesi%2C+Guido&rft.aulast=Borreani&rft.aufirst=Claudia&rft.date=2012-04-01&rft.volume=43&rft.issue=4&rft.spage=739&rft.isbn=&rft.btitle=&rft.title=Journal+of+Pain+and+Symptom+Management&rft.issn=08853924&rft_id=info:doi/10.1016%2Fj.jpainsymman.2011.05.011 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-07-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JSPME2 N1 - SubjectsTermNotLitGenreText - Doctors; Feasibility; End of life decisions; Preferences; Terminally ill people; Confidence intervals DO - http://dx.doi.org/10.1016/j.jpainsymman.2011.05.011 ER - TY - JOUR T1 - A small RNA that regulates motility and biofilm formation in response to changes in nutrient availability in Escherichia coli AN - 1020856963; 16510265 AB - In bacteria, many small regulatory RNAs (sRNAs) are induced in response to specific environmental signals or stresses and act by base-pairing with mRNA targets to affect protein translation or mRNA stability. In Escherichia coli, the gene for the sRNA IS061/IsrA, here renamed McaS, was predicted to reside in an intergenic region between abgR, encoding a transcription regulator and ydaL, encoding a small MutS-related protein. We show that McaS is a similar to 95nt transcript whose expression increases over growth, peaking in early-to-mid stationary phase, or when glucose is limiting. McaS uses three discrete single-stranded regions to regulate mRNA targets involved in various aspects of biofilm formation. McaS represses csgD, the transcription regulator of curli biogenesis and activates flhD, the master transcription regulator of flagella synthesis leading to increased motility, a process not previously reported to be regulated by sRNAs. McaS also regulates pgaA, a porin required for the export of the polysaccharide poly beta -1,6-N-acetyl-d-glucosamine. Consequently, high levels of McaS result in increased biofilm formation while a strain lacking mcaS shows reduced biofilm formation. Based on our observations, we propose that, in response to limited nutrient availability, increasing levels of McaS modulate steps in the progression to a sessile lifestyle. JF - Molecular Microbiology AU - Thomason, Maureen K AU - Fontaine, Fanette AU - De Lay, Nicholas AU - Storz, Gisela AD - Cell Biology and Metabolism Program, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD, USA. Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 17 EP - 35 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 84 IS - 1 SN - 0950-382X, 0950-382X KW - Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology KW - Translation KW - mRNA stability KW - Porins KW - Nutrient availability KW - Glucose KW - Transcription KW - Stress KW - Polysaccharides KW - stationary phase KW - Motility KW - Escherichia coli KW - Biofilms KW - Flagella KW - J 02320:Cell Biology KW - N 14830:RNA UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020856963?accountid=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+small+RNA+that+regulates+motility+and+biofilm+formation+in+response+to+changes+in+nutrient+availability+in+Escherichia+coli&rft.au=Thomason%2C+Maureen+K%3BFontaine%2C+Fanette%3BDe+Lay%2C+Nicholas%3BStorz%2C+Gisela&rft.aulast=Thomason&rft.aufirst=Maureen&rft.date=2012-04-01&rft.volume=84&rft.issue=1&rft.spage=17&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/10.1111%2Fj.1365-2958.2012.07965.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Document feature - figure 7 N1 - Last updated - 2016-04-29 N1 - SubjectsTermNotLitGenreText - stationary phase; Translation; mRNA stability; Motility; Porins; Nutrient availability; Glucose; Stress; Transcription; Biofilms; Polysaccharides; Flagella; Escherichia coli DO - http://dx.doi.org/10.1111/j.1365-2958.2012.07965.x ER - TY - JOUR T1 - Passing years, changing fears? Conceptualizing and measuring risk perceptions for chronic disease in younger and middle-aged women AN - 1018377177; 201210777 AB - As is true for many behavioral theory constructs, no consensus exists on how best to measure perceived risk; therefore, it is unclear whether different measures of disease risk perception are conceptually equivalent and whether such measures are equally appropriate for people with different objective disease risk. To investigate these issues, we used four commonly utilized risk perception items (measuring beliefs about personal risk, others' risk, disease prevalence, and mortality) to assess susceptibility to cardiovascular disease, breast cancer, and lung cancer among 454 younger (ages 18-25) and 169 middle-aged (40-64) women. We examined age- and ethnicity-related differences in participants' responses to the items. We also used structural equation modeling to test whether these items reflect a multidimensional, disease-specific latent construct of risk perception; and to test whether consistency exists in participants' disease-specific risk perceptions. Despite differences in responses to individual items, hypothesized models of perceived risk fit both age groups, suggesting that risk perception can be conceptualized in younger and middle-aged women as a multidimensional construct that is specific to disease yet reflective of global risk-related beliefs. Adapted from the source document. JF - Journal of Behavioral Medicine AU - Hamilton, Jada G AU - Lobel, Marci AD - Department of Psychology, Stony Brook University, Stony Brook, NY, USA hamiltonjg@mail.nih.gov Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 124 EP - 138 PB - Springer Science+Business Media, Inc., Dordrecht, The Netherlands VL - 35 IS - 2 SN - 0160-7715, 0160-7715 KW - Middle aged women KW - Mortality KW - Young women KW - Women KW - Risk perception KW - Morbidity KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1018377177?accountid=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+Behavioral+Medicine&rft.atitle=Passing+years%2C+changing+fears%3F+Conceptualizing+and+measuring+risk+perceptions+for+chronic+disease+in+younger+and+middle-aged+women&rft.au=Hamilton%2C+Jada+G%3BLobel%2C+Marci&rft.aulast=Hamilton&rft.aufirst=Jada&rft.date=2012-04-01&rft.volume=35&rft.issue=2&rft.spage=124&rft.isbn=&rft.btitle=&rft.title=Journal+of+Behavioral+Medicine&rft.issn=01607715&rft_id=info:doi/10.1007%2Fs10865-011-9342-8 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-06-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JBMEDD N1 - SubjectsTermNotLitGenreText - Risk perception; Middle aged women; Young women; Morbidity; Women; Mortality DO - http://dx.doi.org/10.1007/s10865-011-9342-8 ER - TY - JOUR T1 - MicroRNA-1 is a candidate tumor suppressor and prognostic marker in human prostate cancer. AN - 1018367720; 22210864 AB - We previously reported that miR-1 is among the most consistently down-regulated miRs in primary human prostate tumors. In this follow-up study, we further corroborated this finding in an independent data set and made the novel observation that miR-1 expression is further reduced in distant metastasis and is a candidate predictor of disease recurrence. Moreover, we performed in vitro experiments to explore the tumor suppressor function of miR-1. Cell-based assays showed that miR-1 is epigenetically silenced in human prostate cancer. Overexpression of miR-1 in these cells led to growth inhibition and down-regulation of genes in pathways regulating cell cycle progression, mitosis, DNA replication/repair and actin dynamics. This observation was further corroborated with protein expression analysis and 3'-UTR-based reporter assays, indicating that genes in these pathways are either direct or indirect targets of miR-1. A gene set enrichment analysis revealed that the miR-1-mediated tumor suppressor effects are globally similar to those of histone deacetylase inhibitors. Lastly, we obtained preliminary evidence that miR-1 alters the cellular organization of F-actin and inhibits tumor cell invasion and filipodia formation. In conclusion, our findings indicate that miR-1 acts as a tumor suppressor in prostate cancer by influencing multiple cancer-related processes and by inhibiting cell proliferation and motility. JF - Nucleic acids research AU - Hudson, Robert S AU - Yi, Ming AU - Esposito, Dominic AU - Watkins, Stephanie K AU - Hurwitz, Arthur A AU - Yfantis, Harris G AU - Lee, Dong H AU - Borin, James F AU - Naslund, Michael J AU - Alexander, Richard B AU - Dorsey, Tiffany H AU - Stephens, Robert M AU - Croce, Carlo M AU - Ambs, Stefan AD - Laboratory of Human Carcinogenesis, Center for Cancer Research (CCR), National Cancer Institute (NCI), National Institutes of Health, Bethesda, MD, USA. Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 3689 EP - 3703 VL - 40 IS - 8 KW - Biomarkers, Tumor KW - 0 KW - Histone Deacetylase Inhibitors KW - MIRN1 microRNA, human KW - MicroRNAs KW - Index Medicus KW - Cell Movement KW - Histone Deacetylase Inhibitors -- pharmacology KW - Genes, Tumor Suppressor KW - Humans KW - Prognosis KW - Cell Line, Tumor KW - Cell Proliferation KW - Epigenesis, Genetic KW - DNA Repair -- genetics KW - Mitosis KW - Neoplasm Recurrence, Local -- diagnosis KW - Neoplasm Metastasis KW - Xenograft Model Antitumor Assays KW - Cell Cycle -- genetics KW - Male KW - Prostatic Neoplasms -- metabolism KW - Biomarkers, Tumor -- metabolism KW - Prostatic Neoplasms -- pathology KW - Biomarkers, Tumor -- genetics KW - MicroRNAs -- metabolism KW - MicroRNAs -- genetics KW - Prostatic Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1018367720?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=MicroRNA-1+is+a+candidate+tumor+suppressor+and+prognostic+marker+in+human+prostate+cancer.&rft.au=Hudson%2C+Robert+S%3BYi%2C+Ming%3BEsposito%2C+Dominic%3BWatkins%2C+Stephanie+K%3BHurwitz%2C+Arthur+A%3BYfantis%2C+Harris+G%3BLee%2C+Dong+H%3BBorin%2C+James+F%3BNaslund%2C+Michael+J%3BAlexander%2C+Richard+B%3BDorsey%2C+Tiffany+H%3BStephens%2C+Robert+M%3BCroce%2C+Carlo+M%3BAmbs%2C+Stefan&rft.aulast=Hudson&rft.aufirst=Robert&rft.date=2012-04-01&rft.volume=40&rft.issue=8&rft.spage=3689&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=1362-4962&rft_id=info:doi/10.1093%2Fnar%2Fgkr1222 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-09 N1 - Date created - 2012-04-24 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - GSE31620; 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16592474 AB - Epigenetic regulation of gene expression is important in maintaining self-renewal of embryonic stem (ES) and trophoblast stem (TS) cells. Histone deacetylases (HDACs) negatively control histone acetylation by removing covalent acetylation marks from histone tails. Because histone acetylation is a known mark for active transcription, HDACs presumably associate with inactive genes. Here, we used genome-wide chromatin immunoprecipitation to investigate targets of HDAC1 in ES and TS cells. Through evaluation of genes associated with acetylated histone H3 marks, and global expression analysis of Hdac1 knockout ES and trichostatin A-treated ES and TS cells, we found that HDAC1 occupies mainly active genes, including important regulators of ES and TS cells self-renewal. We also observed occupancy of methyl-CpG binding domain protein 3 (MBD3), a subunit of the nucleosome remodeling and histone deacetylation (NuRD) complex, at a subset of HDAC1-occupied sequences in ES cells, including the pluripotency regulators Oct4, Nanog and Kfl4. By mapping HDAC1 targets on a global scale, our results describe further insight into epigenetic mechanisms of ES and TS cells self-renewal. JF - Nucleic Acids Research AU - Kidder, Benjamin L AU - Palmer, Stephen AD - super(1)EMD Serono Research Institute, Billerica, MA 01821 and super(2)Systems Biology Center, National Heart, Lung and Blood Institute, NIH, Bethesda, MD 20892, USA, Benjamin.kidder@nih.gov Y1 - 2012/04// PY - 2012 DA - Apr 2012 SP - 2925 EP - 2939 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 40 IS - 7 SN - 0305-1048, 0305-1048 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Acetylation KW - Chromatin KW - Deacetylation KW - Embryo cells KW - Embryos KW - Gene expression KW - Gene mapping KW - Histone H3 KW - Histone deacetylase KW - Immunoprecipitation KW - MBD3 protein KW - NuRD protein KW - Nucleosomes KW - Oct-4 protein KW - Stem cells KW - Transcription KW - Trophoblasts KW - epigenetics KW - G 07720:Immunogenetics KW - N 14820:DNA Metabolism & Structure KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1017963039?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=HDAC1+regulates+pluripotency+and+lineage+specific+transcriptional+networks+in+embryonic+and+trophoblast+stem+cells&rft.au=Kidder%2C+Benjamin+L%3BPalmer%2C+Stephen&rft.aulast=Kidder&rft.aufirst=Benjamin&rft.date=2012-04-01&rft.volume=40&rft.issue=7&rft.spage=2925&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/10.1093%2Fnar%2Fgkr1151 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2013-01-25 N1 - SubjectsTermNotLitGenreText - Histone deacetylase; Chromatin; Immunoprecipitation; Trophoblasts; Transcription; NuRD protein; Deacetylation; Gene expression; Acetylation; Nucleosomes; Stem cells; Embryo cells; epigenetics; MBD3 protein; Embryos; Histone H3; Oct-4 protein; Gene mapping DO - http://dx.doi.org/10.1093/nar/gkr1151 ER - TY - JOUR T1 - Bronchial and Bronchiolar Fibrosis in Rats Exposed to 2,3-Pentanedione Vapors: Implications for Bronchiolitis Obliterans in Humans AN - 1017961512; 16590151 AB - 2,3-Pentanedione (PD) is a component of artificial butter flavorings. The use of PD is increasing since diacetyl, a major butter flavorant, was associated with bronchiolitis obliterans (BO) in workers and has been removed from many products. Because the toxicity of inhaled PD is unknown, these studies were conducted to characterize the toxicity of inhaled PD across a range of concentrations in rodents. Male and female Wistar-Han rats and B6C3F1 mice were exposed to 0, 50, 100, or 200 ppm PD 6 h/d, 5 d/wk for up to 2 wk. Bronchoalveolar lavage fluid (BALF) was collected after 1, 3, 5, and 10 exposures, and histopathology was evaluated after 12 exposures. MCP-1, MCP-3, CRP, FGF-9, fibrinogen, and OSM were increased 2- to 9-fold in BALF of rats exposed for 5 and 10 days to 200 ppm. In mice, only fibrinogen was increased after 5 exposures to 200 ppm. The epithelium lining the respiratory tract was the site of toxicity in all mice and rats exposed to 200 ppm. Significantly, PD also caused both intraluminal and intramural fibrotic airway lesions in rats. The histopathological and biological changes observed in rats raise concerns that PD inhalation may cause BO in exposed humans. JF - Toxicologic Pathology AU - Morgan, Daniel L AU - Jokinen, Micheal P AU - Price, Herman C AU - Gwinn, William M AU - Palmer, Scott M AU - Flake, Gordon P AD - National Institute of Environmental Health Sciences, National Toxicology Program, Research Triangle Park, North Carolina, USA, morgan3@niehs.nih.gov Y1 - 2012/04// PY - 2012 DA - Apr 2012 SP - 448 EP - 465 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 40 IS - 3 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - Alveoli KW - Bronchus KW - Butter KW - Diacetyl KW - Epithelium KW - Fibrinogen KW - Fibroblast growth factor receptor 9 KW - Fibrosis KW - Flavorants KW - Flavorings KW - Inhalation KW - Monocyte chemoattractant protein 1 KW - Respiratory tract KW - Toxicity KW - Vapors KW - Workers KW - bronchiolitis obliterans KW - X 24320:Food Additives & Contaminants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1017961512?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Bronchial+and+Bronchiolar+Fibrosis+in+Rats+Exposed+to+2%2C3-Pentanedione+Vapors%3A+Implications+for+Bronchiolitis+Obliterans+in+Humans&rft.au=Morgan%2C+Daniel+L%3BJokinen%2C+Micheal+P%3BPrice%2C+Herman+C%3BGwinn%2C+William+M%3BPalmer%2C+Scott+M%3BFlake%2C+Gordon+P&rft.aulast=Morgan&rft.aufirst=Daniel&rft.date=2012-04-01&rft.volume=40&rft.issue=3&rft.spage=448&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623311431946 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Number of references - 42 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Inhalation; Flavorants; Monocyte chemoattractant protein 1; Fibrosis; Fibrinogen; Flavorings; Toxicity; Diacetyl; Alveoli; Workers; Vapors; Bronchus; Butter; Epithelium; bronchiolitis obliterans; Fibroblast growth factor receptor 9; Respiratory tract DO - http://dx.doi.org/10.1177/0192623311431946 ER - TY - JOUR T1 - Differentiation of Rodent Immune and Hematopoietic System Reactive Lesions from Neoplasias AN - 1017961483; 16590149 AB - The immune and hematopoietic systems play an important role in the normal homeostasis of blood and blood cells and for immune responses to endogenous and exogenous processes and insults. In order to interpret histopathologic changes in the immune and hematopoietic systems, it is important to understand the normal anatomy and histology of the thymus, spleen, lymph nodes, bone marrow, and other tissues. The thymus, spleen, and lymph nodes can be categorized by anatomical compartments, each of which contributes to specific immune functions. Lesions may be diagnosed by interpretive or descriptive (semiquantitative) methods. The interpretation of these tissues by lesion in anatomical compartments should allow for better understanding of these reactions and more definitive pathologic findings. Proliferative lesions may be difficult to differentiate from lymphomas and leukemias. The use of immunohistochemistry, compartmental pathology, and methods for the evaluation of clonality will make interpretation easier. JF - Toxicologic Pathology AU - Ward, Jerrold M AU - Rehg, Jerold E AU - Morse, Herbert C AD - Global VetPathology and Laboratory of Immunopathology, NIAID, NIH, Bethesda, Maryland, USA, globalvetpathology@gmail.com Y1 - 2012/04// PY - 2012 DA - Apr 2012 SP - 425 EP - 434 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 40 IS - 3 SN - 0192-6233, 0192-6233 KW - Immunology Abstracts; Toxicology Abstracts KW - Blood cells KW - Bone marrow KW - Differentiation KW - Hemopoiesis KW - Homeostasis KW - Immune response KW - Immunohistochemistry KW - Leukemia KW - Lymph nodes KW - Lymphoma KW - Neoplasia KW - Spleen KW - Thymus KW - F 06955:Immunomodulation & Immunopharmacology KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1017961483?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Differentiation+of+Rodent+Immune+and+Hematopoietic+System+Reactive+Lesions+from+Neoplasias&rft.au=Ward%2C+Jerrold+M%3BRehg%2C+Jerold+E%3BMorse%2C+Herbert+C&rft.aulast=Ward&rft.aufirst=Jerrold&rft.date=2012-04-01&rft.volume=40&rft.issue=3&rft.spage=425&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623311431467 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Number of references - 62 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Thymus; Bone marrow; Spleen; Homeostasis; Lymph nodes; Neoplasia; Leukemia; Differentiation; Hemopoiesis; Immune response; Blood cells; Immunohistochemistry; Lymphoma DO - http://dx.doi.org/10.1177/0192623311431467 ER - TY - JOUR T1 - Identification of Two Novel Coccidian Species Shed by California Sea Lions (Zalophus californianus) AN - 1017961249; 16624580 AB - Routine fecal examination revealed novel coccidian oocysts in asymptomatic California sea lions (Zalophus californianus) in a rehabilitation facility. Coccidian oocysts were observed in fecal samples collected from 15 of 410 California sea lions admitted to The Marine Mammal Center between April 2007 and October 2009. Phylogenetic analysis using the full ITS-1 region, partial small subunit 18S rDNA sequence, and the Apicomplexa rpoB region identified 2 distinct sequence clades, referred to as Coccidia A and Coccidia B, and placed them in the Sarcocystidae, grouped with the tissue-cyst-forming coccidia. Both sequence clades resolved as individual taxa at ITS-1 and rpoB and were most closely related to Neospora caninum. Coccidia A was identified in 11 and Coccidia B in 4 of 12 sea lion oocyst samples successfully sequenced (3 of those sea lions were co-infected with both parasites). Shedding of Coccidia A oocysts was not associated with age class, sex, or stranding location, but yearlings represented the majority of shedders (8/15). This is the first study to use molecular phylogenetics to identify and describe coccidian parasites shed by a marine mammal. JF - Journal of Parasitology AU - Carlson-Bremer, Daphne AU - Johnson, Christine K AU - Miller, Robin H AU - Gulland, Frances MD AU - Conrad, Patricia A AU - Wasmuth, James D AU - Colegrove, Kathleen M AU - Grigg, Michael E Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 347 EP - 354 PB - American Society of Parasitologists VL - 98 IS - 2 SN - 0022-3395, 0022-3395 KW - Oceanic Abstracts; ASFA 1: Biological Sciences & Living Resources; Ecology Abstracts KW - Phylogeny KW - Marine KW - Parasites KW - Juveniles KW - Age KW - Sarcocystidae KW - Oocysts KW - Rehabilitation KW - Nucleotide sequence KW - Zalophus californianus KW - Stranding KW - Neospora caninum KW - INE, USA, California KW - Marine mammals KW - DNA KW - Apicomplexa KW - Coccidia KW - RpoB protein KW - Phylogenetics KW - Sex KW - New species KW - O 1070:Ecology/Community Studies KW - D 04040:Ecosystem and Ecology Studies KW - Q1 08484:Species interactions: parasites and diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1017961249?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aecology&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Parasitology&rft.atitle=Identification+of+Two+Novel+Coccidian+Species+Shed+by+California+Sea+Lions+%28Zalophus+californianus%29&rft.au=Carlson-Bremer%2C+Daphne%3BJohnson%2C+Christine+K%3BMiller%2C+Robin+H%3BGulland%2C+Frances+MD%3BConrad%2C+Patricia+A%3BWasmuth%2C+James+D%3BColegrove%2C+Kathleen+M%3BGrigg%2C+Michael+E&rft.aulast=Carlson-Bremer&rft.aufirst=Daphne&rft.date=2012-04-01&rft.volume=98&rft.issue=2&rft.spage=347&rft.isbn=&rft.btitle=&rft.title=Journal+of+Parasitology&rft.issn=00223395&rft_id=info:doi/10.1645%2FGE-2752.1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Number of references - 36 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Juveniles; Parasites; Nucleotide sequence; Marine mammals; DNA; Stranding; Phylogenetics; New species; Phylogeny; Age; Rehabilitation; Oocysts; RpoB protein; Sex; Sarcocystidae; Neospora caninum; Coccidia; Apicomplexa; Zalophus californianus; INE, USA, California; Marine DO - http://dx.doi.org/10.1645/GE-2752.1 ER - TY - JOUR T1 - Five-factor personality traits and age trajectories of self-rated health: the role of question framing AN - 1015466619; 4294299 AB - We examined the influence of personality traits on mean levels and age trends in 4 single-item measures of self-rated health: general rating, comparison to age peers, comparison to past health, and expectations for future health. Community-dwelling participants (N = 1,683) completed 7,474 self-rated health assessments over a period of up to 19 years. In hierarchical linear modeling analyses, age-associated declines differed across the 4 health items. Across age groups, high Neuroticism and low Conscientiousness, low Extraversion, and low Openness were associated with worse health ratings, with notable differences across the 4 health items. Furthermore, high Neuroticism predicted steeper declines in health ratings involving temporal comparisons. We consider theoretical implications regarding the mechanisms behind associations among personality traits and self-rated health. Reprinted by permission of Blackwell Publishers JF - Journal of personality AU - Ferrucci, Luigi AU - Costa, Paul T AU - Löckenhoff, Corinna E AU - Terracciano, Antonio AD - Cornell University ; National Institute on Aging Y1 - 2012/04// PY - 2012 DA - Apr 2012 SP - 375 EP - 401 VL - 80 IS - 2 SN - 0022-3506, 0022-3506 KW - Sociology KW - Comparative analysis KW - Self-evaluation KW - Consciousness KW - Age KW - Neuroses KW - Personality traits KW - Personality KW - Health KW - Framing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1015466619?accountid=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+personality&rft.atitle=Five-factor+personality+traits+and+age+trajectories+of+self-rated+health%3A+the+role+of+question+framing&rft.au=Ferrucci%2C+Luigi%3BCosta%2C+Paul+T%3BL%C3%B6ckenhoff%2C+Corinna+E%3BTerracciano%2C+Antonio&rft.aulast=Ferrucci&rft.aufirst=Luigi&rft.date=2012-04-01&rft.volume=80&rft.issue=2&rft.spage=375&rft.isbn=&rft.btitle=&rft.title=Journal+of+personality&rft.issn=00223506&rft_id=info:doi/10.1111%2Fj.1467-6494.2011.00724.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 - 9416 2153; 9429 9416 2153; 646; 11474 4551; 5772; Framing; 2630 971; 8638 7951 6220 7954; 2724 DO - http://dx.doi.org/10.1111/j.1467-6494.2011.00724.x ER - TY - JOUR T1 - Neutrophilic Inflammatory Response and Oxidative Stress in Premenopausal Women Chronically Exposed to Indoor Air Pollution from Biomass Burning AN - 1011214049; 16524813 AB - The possibility of inflammation and neutrophil activation in response to indoor air pollution (IAP) from biomass fuel use has been investigated. For this, 142 premenopausal, never-smoking women (median age, 34 years) who cook exclusively with biomass (wood, dung, crop wastes) and 126 age-matched control women who cook with cleaner fuel liquefied petroleum gas (LPG) were enrolled. The neutrophil count in blood and sputum was significantly higher (p<0.05) in biomass users than the control group. Flow cytometric analysis revealed marked increase in the surface expression of CD35 (complement receptor-1), CD16 (F sub(C) gamma receptor III), and beta sub(2) Mac-1 integrin (CD11b/CD18) on circulating neutrophils of biomass users. Besides, enzyme-linked immunosorbent assay showed that they had 72%, 67%, and 54% higher plasma levels of the proinflammatory cytokines tumor necrosis factor-alpha, interleukin-6, and interleukin-12, respectively, and doubled neutrophil chemoattractant interleukin-8. Immunocytochemical study revealed significantly higher percentage of airway neutrophils expressing inducible nitric oxide synthase, while the serum level of nitric oxide was doubled in women who cooked with biomass. Spectrophotometric analysis documented higher myeloperoxidase activity in circulating neutrophils of biomass users, suggesting neutrophil activation. Flow cytometry showed excess generation of reactive oxygen species (ROS) by leukocytes of biomass-using women, whereas their erythrocytes contained a depleted level of antioxidant enzyme superoxide dismutase (SOD). Indoor air of biomass-using households had two to four times more particulate matter with diameters of <10 mu m (PM sub(10)) and <2.5 mu m (PM sub(2.5)) as measured by real-time laser photometer. After controlling potential confounders, rise in proinflammatory mediators among biomass users were positively associated with PM sub(10) and PM sub(2.5) in indoor air, suggesting a close relationship between IAP and neutrophil activation. Besides, the levels of neutrophil activation and inflammation markers were positively associated with generation of ROS and negatively with SOD, indicating a role of oxidative stress in mediating neutrophilic inflammatory response following chronic inhalation of biomass smoke. JF - Inflammation AU - Banerjee, Anirban AU - Mondal, Nandan Kumar AU - Das, Debangshu AU - Ray, Manas Ranjan AD - Department of Experimental Hematology, Chittaranjan National Cancer Institute, 37, S. P. Mukherjee Road, Kolkata, 700 026, India, nandan_gm@yahoo.com Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 671 EP - 683 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 35 IS - 2 SN - 0360-3997, 0360-3997 KW - Immunology Abstracts; Health & Safety Science Abstracts; Pollution Abstracts KW - Indoor air pollution KW - Peroxidase KW - Fuels KW - Particulate matter KW - Erythrocytes KW - Cell activation KW - Flow cytometry KW - IAP protein KW - Interleukin 12 KW - Reactive oxygen species KW - Superoxide dismutase KW - Oxidative stress KW - Integrins KW - Petroleum KW - Respiratory tract KW - Particle size KW - Enzyme-linked immunosorbent assay KW - Leukocytes (neutrophilic) KW - Wood KW - Enzymes KW - Biomass KW - oxidative stress KW - Fc receptors KW - Inflammation KW - Serum levels KW - Smoke KW - Air pollution KW - Blood KW - Mac1 protein KW - Chemotactic factors KW - Dung KW - Nitric oxide KW - Burning KW - Sputum KW - Indoor environments KW - P 0000:AIR POLLUTION KW - H 0500:General KW - F 06935:Development, Aging & Organ Systems UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1011214049?accountid=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=Inflammation&rft.atitle=Neutrophilic+Inflammatory+Response+and+Oxidative+Stress+in+Premenopausal+Women+Chronically+Exposed+to+Indoor+Air+Pollution+from+Biomass+Burning&rft.au=Banerjee%2C+Anirban%3BMondal%2C+Nandan+Kumar%3BDas%2C+Debangshu%3BRay%2C+Manas+Ranjan&rft.aulast=Banerjee&rft.aufirst=Anirban&rft.date=2012-04-01&rft.volume=35&rft.issue=2&rft.spage=671&rft.isbn=&rft.btitle=&rft.title=Inflammation&rft.issn=03603997&rft_id=info:doi/10.1007%2Fs10753-011-9360-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Fuels; Peroxidase; Erythrocytes; Particulate matter; Cell activation; IAP protein; Flow cytometry; Interleukin 12; Reactive oxygen species; Integrins; Oxidative stress; Superoxide dismutase; Petroleum; Respiratory tract; Enzyme-linked immunosorbent assay; Leukocytes (neutrophilic); Enzymes; Biomass; Inflammation; Fc receptors; Air pollution; Smoke; Serum levels; Blood; Mac1 protein; Chemotactic factors; Dung; Nitric oxide; Sputum; Burning; Particle size; Indoor air pollution; Wood; Indoor environments; oxidative stress DO - http://dx.doi.org/10.1007/s10753-011-9360-2 ER - TY - JOUR T1 - Pulmonary non-tuberculous mycobacterial infection in congenital contractual arachnodactyly AN - 1011213748; 16564198 AB - Congenital contractural arachnodactyly (CCA) is caused by mutations within the fibrillin-2 gene (FBN2), which is crucial for microfibril structure. Affected individuals may have contractures, chest wall deformities, scoliosis, abnormal ear folding and elongated limbs. We describe a novel FBN2 mutation in a woman with CCA who also had pulmonary non-tuberculous mycobacteria (NTM) infection. The population with pulmonary NTM infections shares phenotypic features with CCA, such as elongated body habitus, scoliosis and pectus deformities. While it is unlikely that FBN2 defects account for susceptibility to NTM infection in the majority of cases, the overlap between these two diseases suggests some shared pathophysiology. JF - International Journal of Tuberculosis and Lung Disease AU - Paulson, M L AU - Olivier, K N AU - Holland, S M AD - Laboratory of Clinical Infectious Diseases, SAIC-Frederick, Inc. National Cancer Institute-Frederick, Frederick, Maryland, NIH 9000 Rockville Pike, CRC B3-4141, MSC 1684, Bethesda, MD 20892 - 1684, USA, paulsonm@niaid.nih.gov Y1 - 2012/04// PY - 2012 DA - Apr 2012 SP - 561 EP - 563 PB - International Union Against Tuberculosis and Lung Disease VL - 16 IS - 4 SN - 1027-3719, 1027-3719 KW - Microbiology Abstracts B: Bacteriology KW - Scoliosis KW - Limbs KW - Mycobacterium KW - Microfibrils KW - Lung diseases KW - Tuberculosis KW - Ear KW - Infection KW - Chest KW - Mutation KW - Arachnodactyly KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1011213748?accountid=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=International+Journal+of+Tuberculosis+and+Lung+Disease&rft.atitle=Pulmonary+non-tuberculous+mycobacterial+infection+in+congenital+contractual+arachnodactyly&rft.au=Paulson%2C+M+L%3BOlivier%2C+K+N%3BHolland%2C+S+M&rft.aulast=Paulson&rft.aufirst=M&rft.date=2012-04-01&rft.volume=16&rft.issue=4&rft.spage=561&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Tuberculosis+and+Lung+Disease&rft.issn=10273719&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2013-09-20 N1 - SubjectsTermNotLitGenreText - Scoliosis; Limbs; Lung diseases; Microfibrils; Ear; Tuberculosis; Chest; Infection; Mutation; Arachnodactyly; Mycobacterium ER - TY - JOUR T1 - Iron deficiency in blood donors: the REDS-II Donor Iron Status Evaluation (RISE) study AN - 1011210005; 16550260 AB - BACKGROUND: Blood donors are at risk of iron deficiency. We evaluated the effects of blood donation intensity on iron and hemoglobin (Hb) in a prospective study. STUDY DESIGN AND METHODS: Four cohorts of frequent and first-time or reactivated (FT/RA) blood donors (no donation in 2 years), female and male, totaling 2425, were characterized and followed as they donated blood frequently. At enrollment and the final visit, ferritin, soluble transferrin receptor (sTfR), and Hb were determined. Models to predict iron deficiency and Hb deferral were developed. Iron depletion was defined at two levels: iron deficiency erythropoiesis (IDE) [log(sTfR/ferritin) greater than or equal to 2.07] and absent iron stores (AIS; ferritin<12ng/mL). RESULTS: Among returning female FT and RA donors, 20 and 51% had AIS and IDE at their final visit, respectively; corresponding proportions for males were 8 and 20%. Among female frequent donors who returned, 27 and 62% had AIS and IDE, respectively, while corresponding proportions for males were 18 and 47%. Predictors of IDE and/or AIS included a higher frequency of blood donation in the past 2 years, a shorter interdonation interval, and being female and young; conversely, taking iron supplements reduced the risk of iron depletion. Predictors of Hb deferral included female sex, black race, and a shorter interdonation interval. CONCLUSIONS: There is a high prevalence of iron depletion in frequent blood donors. Increasing the interdonation interval would reduce the prevalence of iron depletion and Hb deferral. Alternatively, replacement with iron supplements may allow frequent donation without the adverse outcome of iron depletion. JF - Transfusion AU - Cable, Ritchard G AU - Glynn, Simone A AU - Kiss, Joseph E AU - Mast, Alan E AU - Steele, Whitney R AU - Murphy, Edward L AU - Wright, David J AU - Sacher, Ronald A AU - Gottschall, Jerry L AU - Tobler, Leslie H AU - Simon, Toby L AD - From the New England Region, American Red Cross Blood Services, Farmington, Connecticut; Transfusion Medicine and Cellular Therapies, National Heart, Lung, and Blood Institute, Bethesda, Maryland; the Institute for Transfusion Medicine, Pittsburgh, Pennsylvania; BloodCenter of Wisconsin and the Department of Cell Biology, Neurobiology and Anatomy, Medical College of Wisconsin, Milwaukee, Wisconsin; Westat, Rockville, Maryland; the University of California, San Francisco and Blood Systems Research Institute, San Francisco, California; Hoxworth Blood Center, University of Cincinnati Academic Health Center, Cincinnati, Ohio; and CSL Plasma, Boca Raton, Florida. Y1 - 2012/04// PY - 2012 DA - Apr 2012 SP - 702 EP - 711 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 52 IS - 4 SN - 0041-1132, 0041-1132 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Iron KW - blood donors KW - H 13000:Medical Safety KW - R2 23010:General: Models, forecasting UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1011210005?accountid=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=Iron+deficiency+in+blood+donors%3A+the+REDS-II+Donor+Iron+Status+Evaluation+%28RISE%29+study&rft.au=Cable%2C+Ritchard+G%3BGlynn%2C+Simone+A%3BKiss%2C+Joseph+E%3BMast%2C+Alan+E%3BSteele%2C+Whitney+R%3BMurphy%2C+Edward+L%3BWright%2C+David+J%3BSacher%2C+Ronald+A%3BGottschall%2C+Jerry+L%3BTobler%2C+Leslie+H%3BSimon%2C+Toby+L&rft.aulast=Cable&rft.aufirst=Ritchard&rft.date=2012-04-01&rft.volume=52&rft.issue=4&rft.spage=702&rft.isbn=&rft.btitle=&rft.title=Transfusion&rft.issn=00411132&rft_id=info:doi/10.1111%2Fj.1537-2995.2011.03401.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Document feature - figure 3 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - blood donors; Iron DO - http://dx.doi.org/10.1111/j.1537-2995.2011.03401.x ER - TY - JOUR T1 - Δ8-Tetrahydrocannabivarin prevents hepatic ischaemia/reperfusion injury by decreasing oxidative stress and inflammatory responses through cannabinoid CB2 receptors. AN - 1010488231; 21470208 AB - Activation of cannabinoid CB(2) receptors protects against various forms of ischaemia-reperfusion (I/R) injury. Δ(8) -Tetrahydrocannabivarin (Δ(8) -THCV) is a synthetic analogue of the plant cannabinoid Δ(9) -tetrahydrocannabivarin, which exhibits anti-inflammatory effects in rodents involving activation of CB(2) receptors. Here, we assessed effects of Δ(8) -THCV and its metabolite 11-OH-Δ(8) -THCV on CB(2) receptors and against hepatic I/R injury. Effects in vitro were measured with human CB(2) receptors expressed in CHO cells. Hepatic I/R injury was assessed in mice with 1h ischaemia and 2, 6 or 24h reperfusion in vivo. Displacement of [(3) H]CP55940 by Δ(8) -THCV or 11-OH-Δ(8) -THCV from specific binding sites in CHO cell membranes transfected with human CB(2) receptors (hCB(2) ) yielded K(i) values of 68.4 and 59.95 nM respectively. Δ(8) -THCV or 11-OH-Δ(8) -THCV inhibited forskolin-stimulated cAMP production by hCB(2) CHO cells (EC(50) = 12.95 and 14.3 nM respectively). Δ(8) -THCV, given before induction of I/R, attenuated hepatic injury (measured by serum alanine aminotransferase and aspartate aminotransferase levels), decreased tissue protein carbonyl adducts, 4-hydroxy-2-nonenal, the chemokines CCL3 and CXCL2,TNF-α, intercellular adhesion molecule 1 (CD54) mRNA levels, tissue neutrophil infiltration, caspase 3/7 activity and DNA fragmentation. Protective effects of Δ(8) -THCV against liver damage were still present when the compound was given at the beginning of reperfusion. Pretreatment with a CB(2) receptor antagonist attenuated the protective effects of Δ(8) -THCV, while a CB(1) antagonist tended to enhance it. Δ(8) -THCV activated CB(2) receptors in vitro, and decreased tissue injury and inflammation in vivo, associated with I/R partly via CB(2) receptor activation. This article is part of a themed section on Cannabinoids in Biology and Medicine. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2012.165.issue-8. To view Part I of Cannabinoids in Biology and Medicine visit http://dx.doi.org/10.1111/bph.2011.163.issue-7. Published 2011. This article is a U.S. Government work and is in the public domain in the USA. JF - British journal of pharmacology AU - Bátkai, Sándor AU - Mukhopadhyay, Partha AU - Horváth, Bėla AU - Rajesh, Mohanraj AU - Gao, Rachel Y AU - Mahadevan, Anu AU - Amere, Mukkanti AU - Battista, Natalia AU - Lichtman, Aron H AU - Gauson, Lisa A AU - Maccarrone, Mauro AU - Pertwee, Roger G AU - Pacher, Pál AD - Laboratory of Physiologic Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA. Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 2450 EP - 2461 VL - 165 IS - 8 KW - Aldehydes KW - 0 KW - Cytokines KW - Protective Agents KW - RNA, Messenger KW - Receptor, Cannabinoid, CB2 KW - delta8-tetrahydrocannabivarin KW - Dronabinol KW - 7J8897W37S KW - Aspartate Aminotransferases KW - EC 2.6.1.1 KW - Alanine Transaminase KW - EC 2.6.1.2 KW - 4-hydroxy-2-nonenal KW - K1CVM13F96 KW - Index Medicus KW - Animals KW - Liver -- pathology KW - Cytokines -- genetics KW - Cricetulus KW - Humans KW - Liver -- metabolism KW - Inflammation -- drug therapy KW - Mice KW - Aspartate Aminotransferases -- blood KW - Alanine Transaminase -- blood KW - RNA, Messenger -- metabolism KW - Liver -- drug effects KW - Apoptosis -- drug effects KW - Oxidative Stress -- drug effects KW - Mice, Inbred C57BL KW - Aldehydes -- metabolism KW - CHO Cells KW - Inflammation -- metabolism KW - DNA Fragmentation KW - Male KW - Inflammation -- pathology KW - Cricetinae KW - Reperfusion Injury -- metabolism KW - Receptor, Cannabinoid, CB2 -- metabolism KW - Protective Agents -- metabolism KW - Dronabinol -- analogs & derivatives KW - Dronabinol -- therapeutic use KW - Dronabinol -- metabolism KW - Reperfusion Injury -- drug therapy KW - Protective Agents -- therapeutic use KW - Receptor, Cannabinoid, CB2 -- agonists KW - Reperfusion Injury -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1010488231?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+pharmacology&rft.atitle=%CE%948-Tetrahydrocannabivarin+prevents+hepatic+ischaemia%2Freperfusion+injury+by+decreasing+oxidative+stress+and+inflammatory+responses+through+cannabinoid+CB2+receptors.&rft.au=B%C3%A1tkai%2C+S%C3%A1ndor%3BMukhopadhyay%2C+Partha%3BHorv%C3%A1th%2C+B%C4%97la%3BRajesh%2C+Mohanraj%3BGao%2C+Rachel+Y%3BMahadevan%2C+Anu%3BAmere%2C+Mukkanti%3BBattista%2C+Natalia%3BLichtman%2C+Aron+H%3BGauson%2C+Lisa+A%3BMaccarrone%2C+Mauro%3BPertwee%2C+Roger+G%3BPacher%2C+P%C3%A1l&rft.aulast=B%C3%A1tkai&rft.aufirst=S%C3%A1ndor&rft.date=2012-04-01&rft.volume=165&rft.issue=8&rft.spage=2450&rft.isbn=&rft.btitle=&rft.title=British+journal+of+pharmacology&rft.issn=1476-5381&rft_id=info:doi/10.1111%2Fj.1476-5381.2011.01410.x LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-27 N1 - Date created - 2012-03-26 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: J Invest Surg. 2003 May-Jun;16(3):127-40 [12775429] Coron Artery Dis. 2003 Apr;14(2):115-22 [12655275] Biochem Pharmacol. 1973 Dec 1;22(23):3099-108 [4202581] J Clin Invest. 1987 Jun;79(6):1564-70 [3294898] Br J Pharmacol. 1999 Feb;126(3):665-72 [10188977] Br J Pharmacol. 2005 Dec;146(7):917-26 [16205722] Pharmacol Rev. 2006 Mar;58(1):87-114 [16507884] Am J Physiol Gastrointest Liver Physiol. 2006 Jun;290(6):G1083-8 [16687579] Physiol Rev. 2007 Jan;87(1):315-424 [17237348] Br J Pharmacol. 2007 Mar;150(5):586-94 [17245367] FASEB J. 2007 Jun;21(8):1788-800 [17327359] J Cereb Blood Flow Metab. 2007 Jul;27(7):1387-96 [17245417] J Leukoc Biol. 2007 Dec;82(6):1382-9 [17652447] Br J Pharmacol. 2008 Jan;153(2):199-215 [17828291] Br J Pharmacol. 2008 Jan;153(2):252-62 [18026124] Nat Neurosci. 2008 Feb;11(2):152-9 [18204441] Br J Pharmacol. 2008 May;154(1):204-15 [18311186] Nat Protoc. 2008;3(6):1101-8 [18546601] Gastroenterology. 2008 Oct;135(4):1344-57 [18778711] J Pharmacol Exp Ther. 2009 Mar;328(3):708-14 [19074681] J Mol Cell Cardiol. 2009 May;46(5):612-20 [19162037] Br J Pharmacol. 2009 Apr;156(7):1154-66 [19378378] Am J Physiol Heart Circ Physiol. 2009 May;296(5):H1466-83 [19286953] J Neuroimmune Pharmacol. 2009 Jun;4(2):249-59 [19255856] Microvasc Res. 2009 Jun;78(1):86-94 [19332079] FASEB J. 2009 Jul;23(7):2120-30 [19246487] Gut. 2009 Aug;58(8):1135-43 [19282305] J Cell Mol Med. 2009 Aug;13(8B):2330-41 [19175688] Cardiovasc Res. 2010 Mar 1;85(4):773-84 [19942623] FASEB J. 2010 Mar;24(3):788-98 [19884325] Br J Pharmacol. 2010 Jun;160(3):677-87 [20590571] Epilepsia. 2010 Aug;51(8):1522-32 [20196794] J Am Coll Cardiol. 2010 Dec 14;56(25):2115-25 [21144973] Free Radic Biol Med. 2011 Jan 1;50(1):179-95 [21070851] Prog Lipid Res. 2011 Apr;50(2):193-211 [21295074] Br J Pharmacol. 2011 Nov;164 Suppl 1:S1-324 [22040146] Br J Pharmacol. 2003 Feb;138(4):532-43 [12598407] Nature. 1970 Oct 10;228(5267):134-6 [5466704] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1111/j.1476-5381.2011.01410.x ER - TY - JOUR T1 - Acute depletion of Tet1-dependent 5-hydroxymethylcytosine levels impairs LIF/Stat3 signaling and results in loss of embryonic stem cell identity. AN - 1009530223; 22210859 AB - The TET family of FE(II) and 2-oxoglutarate-dependent enzymes (Tet1/2/3) promote DNA demethylation by converting 5-methylcytosine to 5-hydroxymethylcytosine (5hmC), which they further oxidize into 5-formylcytosine and 5-carboxylcytosine. Tet1 is robustly expressed in mouse embryonic stem cells (mESCs) and has been implicated in mESC maintenance. Here we demonstrate that, unlike genetic deletion, RNAi-mediated depletion of Tet1 in mESCs led to a significant reduction in 5hmC and loss of mESC identity. The differentiation phenotype due to Tet1 depletion positively correlated with the extent of 5hmC loss. Meta-analyses of genomic data sets suggested interaction between Tet1 and leukemia inhibitory factor (LIF) signaling. LIF signaling is known to promote self-renewal and pluripotency in mESCs partly by opposing MAPK/ERK-mediated differentiation. Withdrawal of LIF leads to differentiation of mESCs. We discovered that Tet1 depletion impaired LIF-dependent Stat3-mediated gene activation by affecting Stat3's ability to bind to its target sites on chromatin. Nanog overexpression or inhibition of MAPK/ERK signaling, both known to maintain mESCs in the absence of LIF, rescued Tet1 depletion, further supporting the dependence of LIF/Stat3 signaling on Tet1. These data support the conclusion that analysis of mESCs in the hours/days immediately following efficient Tet1 depletion reveals Tet1's normal physiological role in maintaining the pluripotent state that may be subject to homeostatic compensation in genetic models. JF - Nucleic acids research AU - Freudenberg, Johannes M AU - Ghosh, Swati AU - Lackford, Brad L AU - Yellaboina, Sailu AU - Zheng, Xiaofeng AU - Li, Ruifang AU - Cuddapah, Suresh AU - Wade, Paul A AU - Hu, Guang AU - Jothi, Raja AD - Systems Biology Section, Biostatistics Branch, National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health (NIH), 111 TW Alexander Drive, Research Triangle Park, NC 27709, USA. Y1 - 2012/04// PY - 2012 DA - April 2012 SP - 3364 EP - 3377 VL - 40 IS - 8 KW - DNA-Binding Proteins KW - 0 KW - Homeodomain Proteins KW - Leukemia Inhibitory Factor KW - Lif protein, mouse KW - Nanog Homeobox Protein KW - Nanog protein, mouse KW - Proto-Oncogene Proteins KW - STAT3 Transcription Factor KW - Stat3 protein, mouse KW - TET1 protein, mouse KW - 5-hydroxymethylcytosine KW - 1123-95-1 KW - Cytosine KW - 8J337D1HZY KW - DNA (Cytosine-5-)-Methyltransferase KW - EC 2.1.1.37 KW - DNA methyltransferase 3B KW - Index Medicus KW - Gene Expression Profiling KW - Animals KW - MAP Kinase Signaling System KW - Cells, Cultured KW - Homeodomain Proteins -- metabolism KW - Mice KW - Gene Expression Regulation KW - RNA Interference KW - DNA (Cytosine-5-)-Methyltransferase -- metabolism KW - Signal Transduction KW - Embryonic Stem Cells -- enzymology KW - Leukemia Inhibitory Factor -- metabolism KW - Proto-Oncogene Proteins -- antagonists & inhibitors KW - Embryonic Stem Cells -- metabolism KW - Embryonic Stem Cells -- cytology KW - DNA-Binding Proteins -- genetics KW - DNA-Binding Proteins -- physiology KW - DNA-Binding Proteins -- antagonists & inhibitors KW - STAT3 Transcription Factor -- metabolism KW - Proto-Oncogene Proteins -- genetics KW - Cytosine -- analogs & derivatives KW - Proto-Oncogene Proteins -- physiology KW - Cytosine -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1009530223?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+acids+research&rft.atitle=Acute+depletion+of+Tet1-dependent+5-hydroxymethylcytosine+levels+impairs+LIF%2FStat3+signaling+and+results+in+loss+of+embryonic+stem+cell+identity.&rft.au=Freudenberg%2C+Johannes+M%3BGhosh%2C+Swati%3BLackford%2C+Brad+L%3BYellaboina%2C+Sailu%3BZheng%2C+Xiaofeng%3BLi%2C+Ruifang%3BCuddapah%2C+Suresh%3BWade%2C+Paul+A%3BHu%2C+Guang%3BJothi%2C+Raja&rft.aulast=Freudenberg&rft.aufirst=Johannes&rft.date=2012-04-01&rft.volume=40&rft.issue=8&rft.spage=3364&rft.isbn=&rft.btitle=&rft.title=Nucleic+acids+research&rft.issn=1362-4962&rft_id=info:doi/10.1093%2Fnar%2Fgkr1253 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-09 N1 - Date created - 2012-04-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cell Stem Cell. 2009 May 8;4(5):403-15 [19345177] Science. 2009 May 15;324(5929):930-5 [19372391] Science. 2009 May 15;324(5929):929-30 [19372393] Cell Cycle. 2009 Jun 1;8(11):1698-710 [19411852] N Engl J Med. 2009 May 28;360(22):2289-301 [19474426] Genome Biol. 2009;10(3):R25 [19261174] Cell Stem Cell. 2009 Jun 5;4(6):487-92 [19497275] Nature. 2009 Jul 2;460(7251):118-22 [19571885] BMC Bioinformatics. 2009;10:234 [19640299] Nat Rev Mol Cell Biol. 2009 Oct;10(10):672-81 [19738627] Cell Stem Cell. 2009 Oct 2;5(4):420-33 [19796622] Nature. 2011 Sep 29;477(7366):606-10 [21892189] Science. 2011 Oct 14;334(6053):194 [21940858] Cell. 1999 Oct 29;99(3):247-57 [10555141] Genome Res. 2002 Jun;12(6):996-1006 [12045153] Bioinformatics. 2003 Jan 22;19(2):185-93 [12538238] Cell. 2003 May 30;113(5):643-55 [12787505] Genome Biol. 2004;5(10):R80 [15461798] Nucleic Acids Res. 1978 Sep;5(9):3231-6 [704354] Cell. 1992 Jun 12;69(6):915-26 [1606615] Genes Dev. 1998 Jul 1;12(13):2048-60 [9649508] Nucleic Acids Res. 2005;33(20):e175 [16284200] Nat Genet. 2006 Apr;38(4):431-40 [16518401] Nature. 2006 Aug 3;442(7102):533-8 [16767105] Cell Stem Cell. 2009 Dec 4;5(6):597-609 [19951688] Genes Dev. 2010 Feb 1;24(3):265-76 [20123906] Nat Rev Mol Cell Biol. 2010 Sep;11(9):607-20 [20683471] Nature. 2010 Aug 26;466(7310):1129-33 [20639862] Annu Rev Cell Dev Biol. 2010;26:503-32 [20624054] Nat Biotechnol. 2010 Oct;28(10):1097-105 [20852635] Nature. 2010 Dec 9;468(7325):839-43 [21057493] Nat Biotechnol. 2011 Jan;29(1):68-72 [21151123] Cell Stem Cell. 2011 Feb 4;8(2):200-13 [21295276] Proc Natl Acad Sci U S A. 2011 Mar 1;108(9):3642-7 [21321204] Cell. 2011 Mar 18;144(6):940-54 [21414485] Genes Dev. 2011 Apr 1;25(7):679-84 [21460036] Cell. 2011 Apr 29;145(3):423-34 [21496894] Nat Cell Biol. 2011 May;13(5):490-6 [21540844] Nature. 2011 May 19;473(7347):389-93 [21451524] Nature. 2011 May 19;473(7347):398-402 [21460836] Nature. 2011 May 19;473(7347):343-8 [21490601] Nature. 2011 May 19;473(7347):293-4 [21593859] Mol Cell. 2011 May 20;42(4):451-64 [21514197] Cell. 2011 Jun 10;145(6):835-50 [21663790] Nat Cell Biol. 2011 Jul;13(7):762-70 [21685894] Cell. 2011 Jul 8;146(1):67-79 [21722948] Cancer Cell. 2011 Jul 12;20(1):11-24 [21723200] Nat Cell Biol. 2011 Aug;13(8):903-13 [21785422] Cell Stem Cell. 2011 Aug 5;9(2):166-75 [21816367] Cell Cycle. 2011 Aug 1;10(15):2428-36 [21750410] Proc Natl Acad Sci U S A. 2011 Aug 30;108(35):14566-71 [21873190] Blood. 2011 Sep 1;118(9):2551-5 [21734233] Cell Stem Cell. 2011 Sep 2;9(3):193-204 [21885017] Science. 2011 Sep 2;333(6047):1300-3 [21778364] Science. 2011 Sep 2;333(6047):1303-7 [21817016] Annu Rev Genomics Hum Genet. 2011;12:165-85 [21801025] Cell. 2011 Sep 16;146(6):866-72 [21925312] Genes Dev. 2006 Nov 15;20(22):3089-103 [17085482] PLoS Comput Biol. 2006 Nov 24;2(11):e158 [17121458] Mol Cell Biol. 2007 May;27(10):3769-79 [17339329] Cell. 2008 Feb 22;132(4):567-82 [18295576] Nat Cell Biol. 2008 Mar;10(3):353-60 [18264089] Nature. 2008 May 22;453(7194):519-23 [18497825] Cell. 2008 Jun 13;133(6):1106-17 [18555785] Cell. 2008 Jun 27;133(7):1145-8 [18585349] Cell. 2008 Jul 11;134(1):162-74 [18614019] Nature. 2008 Aug 7;454(7205):766-70 [18600261] Cell. 2008 Aug 8;134(3):521-33 [18692474] Nucleic Acids Res. 2008 Sep;36(16):5221-31 [18684996] PLoS Genet. 2008 Oct;4(10):e1000242 [18974828] Cell Stem Cell. 2008 Nov 6;3(5):543-54 [18804426] Mol Cell. 2008 Nov 21;32(4):491-502 [19026780] Genome Res. 2009 Jan;19(1):24-32 [19056695] Proc Natl Acad Sci U S A. 2009 Mar 31;106(13):5187-91 [19279218] Proc Natl Acad Sci U S A. 2009 Mar 31;106(13):5181-6 [19279220] Genes Dev. 2009 Apr 1;23(7):837-48 [19339689] BMC Genomics. 2009;10:73 [19203379] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/nar/gkr1253 ER - TY - JOUR T1 - PET imaging of angiogenesis after myocardial infarction/reperfusion using a one-step labeled integrin-targeted tracer super(18)F-AlF-NOTA-PRGD2 AN - 1008846941; 16516065 AB - Purpose: The alpha sub(v) beta sub(3) integrin represents a potential target for noninvasive imaging of angiogenesis. The purpose of this study was to evaluate a novel one-step labeled integrin alpha sub(v) beta sub(3)-ta rgeting positron emission tomography (PET) probe, super(18)F-AlF-NOTA-PRGD2, for angiogenesis imaging in a myocardial infarction/reperfusion (MI/R) animal model. Methods: Male Sprague-Dawley rats underwent 45-min transient left coronary artery occlusion followed by reperfusion. The myocardial infarction was confirmed by ECG, super(18)F-fluorodeoxyglucose (FDG) imaging, and cardiac ultrasound. In vivo PET imaging was used to determine myocardial uptake of super(18)F-AlF-NOTA-PRGD2 at different time points following reperfusion. The control peptide RAD was labeled with a similar procedure and used to confirm the specificity. Ex vivo autoradiographic analysis and CD31/CD61 double immunofluorescence staining were performed to validate the PET results. Results: Myocardial origin of the super(18)F-AlF-NOTA-PRGD2 accumulation was confirmed by super(18)F-FDG and autoradiography. PET imaging demonstrated increased focal accumulation of super(18)F-AlF-NOTA-PRGD2 in the infarcted area which started at day 3 (0.28 plus or minus 0.03%ID/g, p<0.05) and peaked between 1 and 3 weeks (0.59 plus or minus 0.16 and 0.55 plus or minus 0.13%ID/g, respectively). The focal accumulation decreased but still kept at a higher level than the sham group after 4 months of reperfusion (0.31 plus or minus 0.01%ID/g, p<0.05). Pretreatment with unlabeled arginine-glycine-aspartic acid (RGD) peptide significantly decreased tracer uptake, indicating integrin specificity of this tracer. At 1 week after MI/R, uptake of the control tracer super(18)F-AlF-NOTA-RAD that does not bind to integrin, in the infarcted area, was only 0.21 plus or minus 0.01%ID/g. Autoradiographic imaging showed the same trend of uptake in the myocardial infarction area. The time course of focal tracer uptake was consistent with the pattern of vascular density and integrin beta sub(3) expression as measured by CD31 and CD61 immunostaining analysis. Conclusion: PET imaging using one-step labeled super(18)F-AlF-NOTA-PRGD2 allows noninvasive visualization of ischemia/reperfusion-induced myocardial angiogenesis longitudinally. The favorable in vivo kinetics and easy production method of this integrin-targeted PET tracer facilitates its future clinical translation for lesion evaluation and therapy response monitoring in patients with occlusive cardiovascular diseases. JF - European Journal of Nuclear Medicine and Molecular Imaging AU - Gao, Haokao AU - Lang, Lixin AU - Guo, Ning AU - Cao, Feng AU - Quan, Qimeng AU - Hu, Shuo AU - Kiesewetter, Dale O AU - Niu, Gang AU - Chen, Xiaoyuan AD - Department of Cardiology, Xijing Hospital, The Fourth Military Medical University, Xi'an, China, 710032, niug@mail.nih.gov Y1 - 2012/04// PY - 2012 DA - Apr 2012 SP - 683 EP - 692 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 39 IS - 4 SN - 1619-7070, 1619-7070 KW - Biotechnology and Bioengineering Abstracts KW - Angiogenesis KW - Animal models KW - Autoradiography KW - Cardiovascular diseases KW - EKG KW - Heart KW - Immunofluorescence KW - Integrins KW - Ischemia KW - Kinetics KW - Myocardial infarction KW - Nuclear medicine KW - Occlusion KW - Positron emission tomography KW - Probes KW - Reperfusion KW - Tracers KW - Translation KW - coronary artery KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008846941?accountid=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=PET+imaging+of+angiogenesis+after+myocardial+infarction%2Freperfusion+using+a+one-step+labeled+integrin-targeted+tracer+super%2818%29F-AlF-NOTA-PRGD2&rft.au=Gao%2C+Haokao%3BLang%2C+Lixin%3BGuo%2C+Ning%3BCao%2C+Feng%3BQuan%2C+Qimeng%3BHu%2C+Shuo%3BKiesewetter%2C+Dale+O%3BNiu%2C+Gang%3BChen%2C+Xiaoyuan&rft.aulast=Gao&rft.aufirst=Haokao&rft.date=2012-04-01&rft.volume=39&rft.issue=4&rft.spage=683&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.issn=16197070&rft_id=info:doi/10.1007%2Fs00259-011-2052-1 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-05-18 N1 - SubjectsTermNotLitGenreText - Heart; Translation; Probes; Animal models; Angiogenesis; Immunofluorescence; Ischemia; Autoradiography; Myocardial infarction; EKG; coronary artery; Reperfusion; Tracers; Integrins; Occlusion; Kinetics; Positron emission tomography; Nuclear medicine; Cardiovascular diseases DO - http://dx.doi.org/10.1007/s00259-011-2052-1 ER - TY - JOUR T1 - Gene therapy in a murine model of methylmalonic acidemia using rAAV9-mediated gene delivery AN - 1008842493; 16533679 AB - Methylmalonic acidemia (MMA), an inherited metabolic disorder caused by deficient activity of methylmalonyl-CoA mutase, carries a poor prognosis for long-term survival. While administration of a recombinant adeno-associated virus serotype 8 vector (rAAV8) can rescue Mut super(-/-) mice from neonatal lethality and provide sustained phenotypic correction, translation of gene therapy to human subjects will likely require multiple rounds of systemic administration and, ideally, the use of a vector that transduces the kidney. To examine the effectiveness of alternative rAAVs in the treatment of MMA, a serotype 9 rAAV expressing the Mut cDNA was constructed and delivered to newborn Mut super(-/-) mice (n=11). rAAV9 gene therapy directed hepatic transgene expression within 24 h and effectively rescued the Mut super(-/-) mice from lethality, conferred long-term survival, markedly improved metabolism and resulted in striking preservation of renal function and histology. Systemic readministration of the vector at a dose similar to that used in human clinical trials (2.5 10 super(9) GC of rAAV9 per gram) to older, treated Mut super(-/-) mice (n=5) lowered circulating metabolites, increased in vivo propionate oxidative capacity and produced transgene expression in the kidney and liver. Our data support the use of an rAAV9 vector in the acute and chronic treatment of MMA, and highlight the renal tropism afforded by this novel serotype. JF - Gene Therapy AU - Senac, J S AU - Chandler, R J AU - Sysol, J R AU - Li, L AU - Venditti, C P AD - Organic Acid Research Section, Genetics and Molecular Biology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA Y1 - 2012/04// PY - 2012 DA - Apr 2012 SP - 385 EP - 391 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 19 IS - 4 SN - 0969-7128, 0969-7128 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Clinical trials KW - Expression vectors KW - Gene therapy KW - Gene transfer KW - Guanylate cyclase KW - Lethality KW - Liver KW - Metabolic disorders KW - Metabolites KW - Neonates KW - Preservation KW - Prognosis KW - Propionic acid KW - Renal function KW - Serotypes KW - Survival KW - Transgenes KW - Translation KW - Tropism KW - Adeno-associated virus KW - W 30905:Medical Applications KW - G 07870:Mammals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008842493?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Gene+Therapy&rft.atitle=Gene+therapy+in+a+murine+model+of+methylmalonic+acidemia+using+rAAV9-mediated+gene+delivery&rft.au=Senac%2C+J+S%3BChandler%2C+R+J%3BSysol%2C+J+R%3BLi%2C+L%3BVenditti%2C+C+P&rft.aulast=Senac&rft.aufirst=J&rft.date=2012-04-01&rft.volume=19&rft.issue=4&rft.spage=385&rft.isbn=&rft.btitle=&rft.title=Gene+Therapy&rft.issn=09697128&rft_id=info:doi/10.1038%2Fgt.2011.108 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Translation; Serotypes; Gene therapy; Metabolic disorders; Transgenes; Tropism; Prognosis; Propionic acid; Survival; Metabolites; Clinical trials; Expression vectors; Guanylate cyclase; Lethality; Renal function; Gene transfer; Liver; Preservation; Neonates; Adeno-associated virus DO - http://dx.doi.org/10.1038/gt.2011.108 ER - TY - JOUR T1 - Minimally invasive input function for 2- super(18)F-fluoro-A-85380 brain PET studies AN - 1008831275; 16516052 AB - Purpose: Quantitative neuroreceptor positron emission tomography (PET) studies often require arterial cannulation to measure input function. While population-based input function (PBIF) would be a less invasive alternative, it has only rarely been used in conjunction with neuroreceptor PET tracers. The aims of this study were (1) to validate the use of PBIF for 2- super(18)F-fluoro-A-85380, a tracer for nicotinic receptors; (2) to compare the accuracy of measures obtained via PBIF to those obtained via blood-scaled image-derived input function (IDIF) from carotid arteries; and (3) to explore the possibility of using venous instead of arterial samples for both PBIF and IDIF. Methods: Ten healthy volunteers underwent a dynamic 2- super(18)F-fluoro-A-85380 brain PET scan with arterial and, in seven subjects, concurrent venous serial blood sampling. PBIF was obtained by averaging the normalized metabolite-corrected arterial input function and subsequently scaling each curve with individual blood samples. IDIF was obtained from the carotid arteries using a blood-scaling method. Estimated Logan distribution volume (V sub(T)) values were compared to the reference values obtained from arterial cannulation. Results: For all subjects, PBIF curves scaled with arterial samples were similar in shape and magnitude to the reference arterial input function. The Logan V sub(T) ratio was 1.00 plus or minus 0.05; all subjects had an estimation error <10%. IDIF gave slightly less accurate results (V sub(T) ratio 1.03 plus or minus 0.07; eight of ten subjects had an error <10%). PBIF scaled with venous samples yielded inaccurate results (V sub(T) ratio 1.13 plus or minus 0.13; only three of seven subjects had an error <10%). Due to arteriovenous differences at early time points, IDIF could not be calculated using venous samples. Conclusion: PBIF scaled with arterial samples accurately estimates Logan V sub(T) for 2- super(18)F-fluoro-A-85380. Results obtained with PBIF were slightly better than those obtained with IDIF. Due to arteriovenous concentration differences, venous samples cannot be substituted for arterial samples. JF - European Journal of Nuclear Medicine and Molecular Imaging AU - Zanotti-Fregonara, Paolo AU - Maroy, Renaud AU - Peyronneau, Marie-Anne AU - Trebossen, Regine AU - Bottlaender, Michel AD - Molecular Imaging Branch, National Institute of Mental Health, NIH, 10 Center Drive, MSC-1026, Bethesda, MD, 20892-2035, USA, zanottifregonp@mail.nih.gov Y1 - 2012/04// PY - 2012 DA - Apr 2012 SP - 651 EP - 659 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 39 IS - 4 SN - 1619-7070, 1619-7070 KW - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts KW - Acetylcholine receptors (nicotinic) KW - Brain KW - Cannulation KW - Carotid artery KW - Neuroimaging KW - Nuclear medicine KW - Positron emission tomography KW - Sampling KW - Scaling KW - Tracers KW - W 30910:Imaging KW - N3 11145:Methodology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008831275?accountid=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=Minimally+invasive+input+function+for+2-+super%2818%29F-fluoro-A-85380+brain+PET+studies&rft.au=Zanotti-Fregonara%2C+Paolo%3BMaroy%2C+Renaud%3BPeyronneau%2C+Marie-Anne%3BTrebossen%2C+Regine%3BBottlaender%2C+Michel&rft.aulast=Zanotti-Fregonara&rft.aufirst=Paolo&rft.date=2012-04-01&rft.volume=39&rft.issue=4&rft.spage=651&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.issn=16197070&rft_id=info:doi/10.1007%2Fs00259-011-2004-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2013-04-05 N1 - SubjectsTermNotLitGenreText - Tracers; Neuroimaging; Brain; Carotid artery; Positron emission tomography; Nuclear medicine; Sampling; Cannulation; Scaling; Acetylcholine receptors (nicotinic) DO - http://dx.doi.org/10.1007/s00259-011-2004-9 ER - TY - CPAPER T1 - Using embryonic melanoblast transcriptome analysis to identify novel mechanisms promoting metastatic melanoma T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313121833; 6163660 JF - 2012 American Association for Cancer Research Annual Meeting AU - Mishra, Pravin AU - Guo, Theresa AU - Zaidi, Raza AU - Davis, Sean AU - Arnheiter, Heinz AU - Walker, Robert AU - Meltzer, Paul AU - Merlino, Glenn Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Melanoma KW - Gene expression KW - Embryos KW - Metastases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313121833?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Using+embryonic+melanoblast+transcriptome+analysis+to+identify+novel+mechanisms+promoting+metastatic+melanoma&rft.au=Mishra%2C+Pravin%3BGuo%2C+Theresa%3BZaidi%2C+Raza%3BDavis%2C+Sean%3BArnheiter%2C+Heinz%3BWalker%2C+Robert%3BMeltzer%2C+Paul%3BMerlino%2C+Glenn&rft.aulast=Mishra&rft.aufirst=Pravin&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Therapeutic targeting of B cell receptor signaling in activated B cell-like (ABC) diffuse large B cell lymphoma with the BTK inhibitor Ibrutinib (PCI-32765) T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313121777; 6163441 JF - 2012 American Association for Cancer Research Annual Meeting AU - Staudt, Louis Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - lymphoma KW - Lymphocytes B KW - Bruton's tyrosine kinase KW - B-cell lymphoma KW - Inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313121777?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Therapeutic+targeting+of+B+cell+receptor+signaling+in+activated+B+cell-like+%28ABC%29+diffuse+large+B+cell+lymphoma+with+the+BTK+inhibitor+Ibrutinib+%28PCI-32765%29&rft.au=Staudt%2C+Louis&rft.aulast=Staudt&rft.aufirst=Louis&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Therapeutic strategies in lymphoma inspired by functional and structural genomics T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313121724; 6163471 JF - 2012 American Association for Cancer Research Annual Meeting AU - Staudt, Louis Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - lymphoma KW - Lymphoma KW - Structure-function relationships KW - genomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313121724?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Therapeutic+strategies+in+lymphoma+inspired+by+functional+and+structural+genomics&rft.au=Staudt%2C+Louis&rft.aulast=Staudt&rft.aufirst=Louis&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Maintenance of genome stability T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313102973; 6163849 JF - 2012 American Association for Cancer Research Annual Meeting AU - Nussenzweig, Andre Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Genomes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313102973?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Maintenance+of+genome+stability&rft.au=Nussenzweig%2C+Andre&rft.aulast=Nussenzweig&rft.aufirst=Andre&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Resources for users from genome data analysis centers T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313102834; 6163571 JF - 2012 American Association for Cancer Research Annual Meeting AU - Eley, Greg Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Genomes KW - Data processing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313102834?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Resources+for+users+from+genome+data+analysis+centers&rft.au=Eley%2C+Greg&rft.aulast=Eley&rft.aufirst=Greg&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Applying for access to controlled databases T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313102817; 6163570 JF - 2012 American Association for Cancer Research Annual Meeting AU - Ozenberger, Brad Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Databases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313102817?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Applying+for+access+to+controlled+databases&rft.au=Ozenberger%2C+Brad&rft.aulast=Ozenberger&rft.aufirst=Brad&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - TCGA - Strategy, Goals and Data Availability T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313102799; 6163569 JF - 2012 American Association for Cancer Research Annual Meeting AU - Shaw, Kenna Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Data processing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313102799?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=TCGA+-+Strategy%2C+Goals+and+Data+Availability&rft.au=Shaw%2C+Kenna&rft.aulast=Shaw&rft.aufirst=Kenna&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Overview of the PI3K/Akt/mTOR pathway T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313100074; 6163383 JF - 2012 American Association for Cancer Research Annual Meeting AU - Dennis, Phillip Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - 1-Phosphatidylinositol 3-kinase KW - Reviews KW - AKT protein KW - TOR protein UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313100074?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Overview+of+the+PI3K%2FAkt%2FmTOR+pathway&rft.au=Dennis%2C+Phillip&rft.aulast=Dennis&rft.aufirst=Phillip&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Risk of diffuse large B-cell lymphoma in solid organ transplant recipients T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313099676; 6163584 JF - 2012 American Association for Cancer Research Annual Meeting AU - Gibson, Todd AU - Engels, Eric AU - Clarke, Christina AU - Pfeiffer, Ruth AU - Lynch, Charles AU - Chang, Ellen AU - Hall, Erin AU - Weisenburger, Dennis AU - Morton, Lindsay Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - lymphoma KW - Organs KW - B-cell lymphoma KW - Transplants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313099676?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Risk+of+diffuse+large+B-cell+lymphoma+in+solid+organ+transplant+recipients&rft.au=Gibson%2C+Todd%3BEngels%2C+Eric%3BClarke%2C+Christina%3BPfeiffer%2C+Ruth%3BLynch%2C+Charles%3BChang%2C+Ellen%3BHall%2C+Erin%3BWeisenburger%2C+Dennis%3BMorton%2C+Lindsay&rft.aulast=Gibson&rft.aufirst=Todd&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Introduction to DNase-seq and its applications T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313094941; 6163184 JF - 2012 American Association for Cancer Research Annual Meeting AU - Hager, Gordon Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Cancer KW - Genetics KW - Bioinformatics KW - Oncology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313094941?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Introduction+to+DNase-seq+and+its+applications&rft.au=Hager%2C+Gordon&rft.aulast=Hager&rft.aufirst=Gordon&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Strategies for effective grantsmanship for team science T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313092974; 6163730 JF - 2012 American Association for Cancer Research Annual Meeting AU - Croyle, Robert Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Cancer KW - Genetics KW - Bioinformatics KW - Oncology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313092974?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Strategies+for+effective+grantsmanship+for+team+science&rft.au=Croyle%2C+Robert&rft.aulast=Croyle&rft.aufirst=Robert&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Developing and using team science to address health disparities T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313092913; 6163728 JF - 2012 American Association for Cancer Research Annual Meeting AU - Fagan, Pebbles Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Cancer KW - Genetics KW - Bioinformatics KW - Oncology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313092913?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Developing+and+using+team+science+to+address+health+disparities&rft.au=Fagan%2C+Pebbles&rft.aulast=Fagan&rft.aufirst=Pebbles&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - The molecular epidemiology of myeloma T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313084853; 6163761 JF - 2012 American Association for Cancer Research Annual Meeting AU - Landgren, Ola Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Myeloma KW - Epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313084853?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=The+molecular+epidemiology+of+myeloma&rft.au=Landgren%2C+Ola&rft.aulast=Landgren&rft.aufirst=Ola&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Development of clinical trials incorporating genomic signatures: Lessons learned T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313083674; 6163322 JF - 2012 American Association for Cancer Research Annual Meeting AU - McShane, Lisa Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Clinical trials KW - genomics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313083674?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Development+of+clinical+trials+incorporating+genomic+signatures%3A+Lessons+learned&rft.au=McShane%2C+Lisa&rft.aulast=McShane&rft.aufirst=Lisa&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Epstein-Barr virus (EBV) and cancer: Opportunities for etiologic research and prevention T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313081185; 6163812 JF - 2012 American Association for Cancer Research Annual Meeting AU - Hildesheim, Allan Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Cancer KW - Prevention KW - Epstein-Barr virus UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313081185?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Epstein-Barr+virus+%28EBV%29+and+cancer%3A+Opportunities+for+etiologic+research+and+prevention&rft.au=Hildesheim%2C+Allan&rft.aulast=Hildesheim&rft.aufirst=Allan&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Target-molecular specific near infrared cancer photoimmunotherapy: Detection, treatment, and monitoring of tumors with a theranostic fluorescent probe T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313065946; 6163624 JF - 2012 American Association for Cancer Research Annual Meeting AU - Kobayashi, Hisataka AU - Mitsunaga, Makoto AU - Nakajima, Takahito AU - Sano, Kohei AU - Choyke, Peter Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Cancer KW - Tumors KW - Fluorescent indicators UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313065946?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Target-molecular+specific+near+infrared+cancer+photoimmunotherapy%3A+Detection%2C+treatment%2C+and+monitoring+of+tumors+with+a+theranostic+fluorescent+probe&rft.au=Kobayashi%2C+Hisataka%3BMitsunaga%2C+Makoto%3BNakajima%2C+Takahito%3BSano%2C+Kohei%3BChoyke%2C+Peter&rft.aulast=Kobayashi&rft.aufirst=Hisataka&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Transfer of T cells with artificial T cell receptors to target cancers T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313064809; 6163249 JF - 2012 American Association for Cancer Research Annual Meeting AU - Dudley, Mark Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Cancer KW - T-cell receptor KW - Lymphocytes T UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313064809?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Transfer+of+T+cells+with+artificial+T+cell+receptors+to+target+cancers&rft.au=Dudley%2C+Mark&rft.aulast=Dudley&rft.aufirst=Mark&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Inherited variation at chromosome 12p13.33 including RAD52 influences squamous cell lung carcinoma risk T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313049557; 6163886 JF - 2012 American Association for Cancer Research Annual Meeting AU - Shi, Jianxin AU - Chatterjee, Nilanjan AU - Rotunno, Melissa AU - Wang, Yufei AU - Pesatori, Angela AU - Consonni, Dario AU - Li, Peng AU - Broderick, Peter AU - Henrion, Marc AU - Eisen, Timothy AU - Wang, Zhaoming AU - Chen, Wei AU - Dong, Qiong AU - Albanes, Demetrius AU - Thun, Michael AU - Spitz, Margaret AU - Bertazzi, Pier AU - Caporaso, Neil AU - Chanock, Stephen AU - Amos, Christopher AU - Houlston, Richard AU - Landi, Maria Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Lung KW - Chromosomes KW - Rad52 protein KW - Chromosome 12 KW - Lung carcinoma KW - Squamous cells KW - Tumors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313049557?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Inherited+variation+at+chromosome+12p13.33+including+RAD52+influences+squamous+cell+lung+carcinoma+risk&rft.au=Shi%2C+Jianxin%3BChatterjee%2C+Nilanjan%3BRotunno%2C+Melissa%3BWang%2C+Yufei%3BPesatori%2C+Angela%3BConsonni%2C+Dario%3BLi%2C+Peng%3BBroderick%2C+Peter%3BHenrion%2C+Marc%3BEisen%2C+Timothy%3BWang%2C+Zhaoming%3BChen%2C+Wei%3BDong%2C+Qiong%3BAlbanes%2C+Demetrius%3BThun%2C+Michael%3BSpitz%2C+Margaret%3BBertazzi%2C+Pier%3BCaporaso%2C+Neil%3BChanock%2C+Stephen%3BAmos%2C+Christopher%3BHoulston%2C+Richard%3BLandi%2C+Maria&rft.aulast=Shi&rft.aufirst=Jianxin&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Chromatin remodeling proteins in transcription and development T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313048599; 6163911 JF - 2012 American Association for Cancer Research Annual Meeting AU - Archer, Trevor AU - Trotter, Kevin AU - Singh, Ajeet Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Chromatin remodeling KW - Transcription UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313048599?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Chromatin+remodeling+proteins+in+transcription+and+development&rft.au=Archer%2C+Trevor%3BTrotter%2C+Kevin%3BSingh%2C+Ajeet&rft.aulast=Archer&rft.aufirst=Trevor&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Innovative Molecular Analysis Technologies (IMAT) T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313045967; 6163752 JF - 2012 American Association for Cancer Research Annual Meeting AU - Dickherber, Anthony Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Innovations KW - Technology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313045967?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Innovative+Molecular+Analysis+Technologies+%28IMAT%29&rft.au=Dickherber%2C+Anthony&rft.aulast=Dickherber&rft.aufirst=Anthony&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Thyroid doses in exposed populations: How Fukushima can be compared to Chernobyl and other nuclear reactor accidents T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313033868; 6163508 JF - 2012 American Association for Cancer Research Annual Meeting AU - Drozdovitch, Vladimir Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Ukraine, Chernobyl KW - Accidents KW - Nuclear reactors KW - Thyroid UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313033868?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Thyroid+doses+in+exposed+populations%3A+How+Fukushima+can+be+compared+to+Chernobyl+and+other+nuclear+reactor+accidents&rft.au=Drozdovitch%2C+Vladimir&rft.aulast=Drozdovitch&rft.aufirst=Vladimir&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - NCI best practices for biospecimen resources T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313033811; 6163751 JF - 2012 American Association for Cancer Research Annual Meeting AU - Vaught, Jimmie Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Best practices UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313033811?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=NCI+best+practices+for+biospecimen+resources&rft.au=Vaught%2C+Jimmie&rft.aulast=Vaught&rft.aufirst=Jimmie&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Discussion of research opportunities and the NCI perspective T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313033472; 6163744 JF - 2012 American Association for Cancer Research Annual Meeting AU - Croyle, Robert Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Cancer KW - Genetics KW - Bioinformatics KW - Oncology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313033472?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Discussion+of+research+opportunities+and+the+NCI+perspective&rft.au=Croyle%2C+Robert&rft.aulast=Croyle&rft.aufirst=Robert&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Molecular mechanisms that modulate oncogenic Ras/Raf signaling T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313027691; 6163779 JF - 2012 American Association for Cancer Research Annual Meeting AU - Morrison, Deborah Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Raf protein KW - Ras protein KW - Molecular modelling KW - RAS UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313027691?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Molecular+mechanisms+that+modulate+oncogenic+Ras%2FRaf+signaling&rft.au=Morrison%2C+Deborah&rft.aulast=Morrison&rft.aufirst=Deborah&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Assessment of the dynamics of tumor hypoxia: Distinguishing chronic and cycling hypoxic regions and the response to therapy T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313025808; 6163286 JF - 2012 American Association for Cancer Research Annual Meeting AU - Cherukuri, Murali Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Hypoxia KW - Tumors KW - Therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313025808?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Assessment+of+the+dynamics+of+tumor+hypoxia%3A+Distinguishing+chronic+and+cycling+hypoxic+regions+and+the+response+to+therapy&rft.au=Cherukuri%2C+Murali&rft.aulast=Cherukuri&rft.aufirst=Murali&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Leveraging epidemiology studies in cancer outcomes research T2 - 2012 American Association for Cancer Research Annual Meeting AN - 1313015136; 6163799 JF - 2012 American Association for Cancer Research Annual Meeting AU - Elena, Joanne Y1 - 2012/03/31/ PY - 2012 DA - 2012 Mar 31 KW - Cancer KW - Epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313015136?accountid=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+American+Association+for+Cancer+Research+Annual+Meeting&rft.atitle=Leveraging+epidemiology+studies+in+cancer+outcomes+research&rft.au=Elena%2C+Joanne&rft.aulast=Elena&rft.aufirst=Joanne&rft.date=2012-03-31&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+American+Association+for+Cancer+Research+Annual+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/start.aspx?mkey={2D8C569E-B72C-4E7D-AB3B-070BEC7EB280} LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - A structural basis for reversible photoswitching of absorbance spectra in red fluorescent protein rsTagRFP. AN - 926507689; 22310052 AB - rsTagRFP is the first monomeric red fluorescent protein (FP) with reversibly photoswitchable absorbance spectra. The switching is realized by irradiation of rsTagRFP with blue (440 nm) and yellow (567 nm) light, turning the protein fluorescence ON and OFF, respectively. It is perhaps the most useful probe in this color class that has yet been reported. Because of the photoswitchable absorbance, rsTagRFP can be used as an acceptor in photochromic Förster resonance energy transfer. Yellow FPs, YPet and mVenus, are demonstrated to be excellent photochromic Förster resonance energy transfer donors for the rsTagRFP acceptor in its fusion constructs. Analysis of X-ray structures has shown that photoswitching of rsTagRFP is accompanied by cis-trans isomerization and protonation/deprotonation of the chromophore, with the deprotonated cis- and protonated trans-isomers corresponding to its ON and OFF states, respectively. Unlike in other photoswitchable FPs, both conformers of rsTagRFP chromophore are essentially coplanar. Two other peculiarities of the rsTagRFP chromophore are an essentially hydrophobic environment of its p-hydroxyphenyl site and the absence of direct hydrogen bonding between this moiety and the protein scaffold. The influence of the immediate environment on rsTagRFP chromophore was probed by site-directed mutagenesis. Residues Glu145 and His197 were found to participate in protonation/deprotonation of the chromophore accompanying the photoswitching of rsTagRFP fluorescence, whereas residues Met160 and Leu174 were shown to spatially restrict chromophore isomerization, favoring its radiative decay. Copyright © 2012 Elsevier Ltd. All rights reserved. JF - Journal of molecular biology AU - Pletnev, Sergei AU - Subach, Fedor V AU - Dauter, Zbigniew AU - Wlodawer, Alexander AU - Verkhusha, Vladislav V AD - Synchrotron Radiation Research Section, Macromolecular Crystallography Laboratory, National Cancer Institute, Argonne, IL 60439, USA. pletnevs@mail.nih.gov Y1 - 2012/03/30/ PY - 2012 DA - 2012 Mar 30 SP - 144 EP - 151 VL - 417 IS - 3 KW - Luminescent Proteins KW - 0 KW - Protons KW - Recombinant Fusion Proteins KW - red fluorescent protein KW - Green Fluorescent Proteins KW - 147336-22-9 KW - Methionine KW - AE28F7PNPL KW - Leucine KW - GMW67QNF9C KW - Index Medicus KW - Hydrophobic and Hydrophilic Interactions KW - Green Fluorescent Proteins -- chemistry KW - Models, Molecular KW - Fluorescence Resonance Energy Transfer KW - Leucine -- chemistry KW - Recombinant Fusion Proteins -- chemistry KW - Recombinant Fusion Proteins -- genetics KW - Isomerism KW - Photochemical Processes KW - Crystallography, X-Ray KW - Hydrogen Bonding KW - Methionine -- chemistry KW - Protein Conformation KW - Luminescent Proteins -- chemistry KW - Luminescent Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/926507689?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+molecular+biology&rft.atitle=A+structural+basis+for+reversible+photoswitching+of+absorbance+spectra+in+red+fluorescent+protein+rsTagRFP.&rft.au=Pletnev%2C+Sergei%3BSubach%2C+Fedor+V%3BDauter%2C+Zbigniew%3BWlodawer%2C+Alexander%3BVerkhusha%2C+Vladislav+V&rft.aulast=Pletnev&rft.aufirst=Sergei&rft.date=2012-03-30&rft.volume=417&rft.issue=3&rft.spage=144&rft.isbn=&rft.btitle=&rft.title=Journal+of+molecular+biology&rft.issn=1089-8638&rft_id=info:doi/10.1016%2Fj.jmb.2012.01.044 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-18 N1 - Date created - 2012-03-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 2000 Aug 25;275(34):25879-82 [10852900] Proc Natl Acad Sci U S A. 2000 Oct 24;97(22):11996-2001 [11050231] Nat Biotechnol. 2002 Jan;20(1):87-90 [11753368] Nat Biotechnol. 2003 Feb;21(2):191-4 [12524551] Science. 2004 Nov 19;306(5700):1370-3 [15550670] Nat Biotechnol. 2005 Mar;23(3):355-60 [15696158] Biochemistry. 2005 Apr 19;44(15):5774-87 [15823036] Proc Natl Acad Sci U S A. 2005 Sep 13;102(37):13070-4 [16135569] Proc Natl Acad Sci U S A. 2005 Dec 6;102(49):17565-9 [16314572] Physiology (Bethesda). 2006 Jun;21:162-70 [16714474] Angew Chem Int Ed Engl. 2007;46(4):530-6 [17094157] Biochem J. 2007 Feb 15;402(1):35-42 [17117927] Proc Natl Acad Sci U S A. 2007 Apr 17;104(16):6672-7 [17420458] Biophys J. 2007 Jun 15;92(12):L97-9 [17384059] Nat Methods. 2007 Jul;4(7):555-7 [17572680] Proc Natl Acad Sci U S A. 2007 Aug 7;104(32):13005-9 [17646653] J Am Chem Soc. 2007 Nov 14;129(45):13970-7 [17956094] J Am Chem Soc. 2007 Dec 26;129(51):16132-41 [18047340] PLoS Comput Biol. 2008 Mar;4(3):e1000034 [18369426] Proc Natl Acad Sci U S A. 2008 Jul 8;105(27):9227-32 [18574155] Biophys J. 2008 Sep 15;95(6):2989-97 [18658221] Nat Biotechnol. 2008 Sep;26(9):1035-40 [18724362] Proc Natl Acad Sci U S A. 2008 Nov 25;105(47):18343-8 [19017808] Nat Methods. 2009 Feb;6(2):153-9 [19169259] Curr Opin Chem Biol. 2010 Feb;14(1):23-9 [19914857] Chem Biol. 2010 Apr 23;17(4):333-41 [20416505] J Biol Chem. 2010 May 7;285(19):14603-9 [20236929] Chem Biol. 2010 Jul 30;17(7):745-55 [20659687] Biochem J. 2011 Feb 1;433(3):411-22 [21235524] Curr Opin Cell Biol. 2011 Jun;23(3):310-7 [21242078] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.jmb.2012.01.044 ER - TY - CPAPER T1 - The NIH Undiagnosed Diseases Program: Success rate in identifying candidate genes using exome sequencing T2 - 2012 ACMG Annual Clinical Genetics Meeting AN - 1313024667; 6108025 JF - 2012 ACMG Annual Clinical Genetics Meeting AU - Markello, Thomas AU - Adams, David AU - Tifft, Cynthia AU - Sincan, Murat AU - Cherukuri, Praveen AU - Toro, Camilo AU - Fischer, Roxanne AU - Fuentes-Fajaro, Karin AU - Gahl, William AU - Boerkoel, Cornelius Y1 - 2012/03/27/ PY - 2012 DA - 2012 Mar 27 KW - Genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313024667?accountid=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+ACMG+Annual+Clinical+Genetics+Meeting&rft.atitle=The+NIH+Undiagnosed+Diseases+Program%3A+Success+rate+in+identifying+candidate+genes+using+exome+sequencing&rft.au=Markello%2C+Thomas%3BAdams%2C+David%3BTifft%2C+Cynthia%3BSincan%2C+Murat%3BCherukuri%2C+Praveen%3BToro%2C+Camilo%3BFischer%2C+Roxanne%3BFuentes-Fajaro%2C+Karin%3BGahl%2C+William%3BBoerkoel%2C+Cornelius&rft.aulast=Markello&rft.aufirst=Thomas&rft.date=2012-03-27&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+ACMG+Annual+Clinical+Genetics+Meeting&rft.issn=&rft_id=info:doi/ L2 - http://submissions.miracd.com/acmg2012/Itinerary/SearchResultsProgram.asp LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Common genetic variants in the PSCA gene influence gene expression and bladder cancer risk AN - 1028018446; 16524253 AB - Genome-wide association studies have identified a SNP, rs2294008, on 8q24.3 within the prostate stem cell antigen (PSCA) gene, as a risk factor for bladder cancer. To fine-map this region, we imputed 642 SNPs within 100 Kb of rs2294008 in addition to 33 markers genotyped in one of the reported genome-wide association study in 8,652 subjects. A multivariable logistic regression model adjusted for rs2294008 revealed a unique signal, rs2978974 (r2 = 0.02, D' = 0.19 with rs2294008). In the combined analysis of 5,393 cases and 7,324 controls, we detected a per-allele odds ratio (OR) = 1.11 [95% confidence interval (CI) = 1.06-1.17, P = 5.8 x 10 super(-5)] for rs2294008 and OR = 1.07 (95% CI = 1.02-1.13, P = 9.7 x 10 super(-3)) for rs2978974. The effect was stronger in carriers of both risk variants (OR = 1.24, 95% CI = 1.08-1.41, P = 1.8 x 10 super(-3)) and there was a significant multiplicative interaction (P = 0.035) between these two SNPs, which requires replication in future studies. The T risk allele of rs2294008 was associated with increased PSCA mRNA expression in two sets of bladder tumor samples (n = 36, P = 0.0007 and n = 34, P = 0.0054) and in normal bladder samples (n = 35, P = 0.0155), but rs2978974 was not associated with PSCA expression. SNP rs2978974 is located 10 Kb upstream of rs2294008, within an alternative untranslated first exon of PSCA. The non-risk allele G of rs2978974 showed strong interaction with nuclear proteins from five cell lines tested, implying a regulatory function. In conclusion, a joint effect of two PSCA SNPs, rs2294008 and rs2978974, suggests that both variants may be important for bladder cancer susceptibility, possibly through different mechanisms that influence the control of mRNA expression and interaction with regulatory factors. JF - Proceedings of the National Academy of Sciences, USA AU - Fu, Yi-Ping AU - Kohaar, Indu AU - Rothman, Nathaniel AU - Earl, Julie AU - Figueroa, Jonine D AU - Ye, Yuanqing AU - Malats, Nuria AU - Tang, Wei AU - Liu, Luyang AU - Garcia-Closas, Montserrat AU - Muchmore, Brian AU - Chatterjee, Nilanjan AU - Tarway, McAnthony AU - Kogevinas, Manolis AU - Porter-Gill, Patricia AU - Baris, Dalsu AU - Mumy, Adam AU - Albanes, Demetrius AU - Purdue, Mark P AU - Hutchinson, Amy AU - Carrato, Alfredo AU - Tardon, Adonina AU - Serra, Consol AU - Garcia-Closas, Reina AU - Lloreta, Josep AU - Johnson, Alison AU - Schwenn, Molly AU - Karagas, Margaret R AU - Schned, Alan AU - Diver, WRyan AU - Gapstur, Susan M AU - Thun, Michael J AU - Virtamo, Jarmo AU - Chanock, Stephen J AU - Fraumeni, Joseph F AU - Silverman, Debra T AU - Wu, Xifeng AU - Real, Francisco X AU - Prokunina-Olsson, Ludmila AD - Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, and Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892 Y1 - 2012/03/27/ PY - 2012 DA - 2012 Mar 27 SP - 4974 EP - 4979 PB - National Academy of Sciences, 2101 Constitution Ave. Washington DC 20418 United States VL - 109 IS - 13 SN - 0027-8424, 0027-8424 KW - Risk Abstracts; Health & Safety Science Abstracts; Genetics Abstracts KW - Cancer KW - Exons KW - Gene expression KW - Prostate KW - Proteins KW - Regression analysis KW - Replication KW - Risk factors KW - Single-nucleotide polymorphism KW - Stem cells KW - Tumors KW - Upstream KW - Urinary bladder KW - G 07720:Immunogenetics KW - H 8000:Radiation Safety/Electrical Safety KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028018446?accountid=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=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Common+genetic+variants+in+the+PSCA+gene+influence+gene+expression+and+bladder+cancer+risk&rft.au=Fu%2C+Yi-Ping%3BKohaar%2C+Indu%3BRothman%2C+Nathaniel%3BEarl%2C+Julie%3BFigueroa%2C+Jonine+D%3BYe%2C+Yuanqing%3BMalats%2C+Nuria%3BTang%2C+Wei%3BLiu%2C+Luyang%3BGarcia-Closas%2C+Montserrat%3BMuchmore%2C+Brian%3BChatterjee%2C+Nilanjan%3BTarway%2C+McAnthony%3BKogevinas%2C+Manolis%3BPorter-Gill%2C+Patricia%3BBaris%2C+Dalsu%3BMumy%2C+Adam%3BAlbanes%2C+Demetrius%3BPurdue%2C+Mark+P%3BHutchinson%2C+Amy%3BCarrato%2C+Alfredo%3BTardon%2C+Adonina%3BSerra%2C+Consol%3BGarcia-Closas%2C+Reina%3BLloreta%2C+Josep%3BJohnson%2C+Alison%3BSchwenn%2C+Molly%3BKaragas%2C+Margaret+R%3BSchned%2C+Alan%3BDiver%2C+WRyan%3BGapstur%2C+Susan+M%3BThun%2C+Michael+J%3BVirtamo%2C+Jarmo%3BChanock%2C+Stephen+J%3BFraumeni%2C+Joseph+F%3BSilverman%2C+Debra+T%3BWu%2C+Xifeng%3BReal%2C+Francisco+X%3BProkunina-Olsson%2C+Ludmila&rft.aulast=Fu&rft.aufirst=Yi-Ping&rft.date=2012-03-27&rft.volume=109&rft.issue=13&rft.spage=4974&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Last updated - 2012-11-20 N1 - SubjectsTermNotLitGenreText - Gene expression; Stem cells; Exons; Replication; Single-nucleotide polymorphism; Urinary bladder; Risk factors; Regression analysis; Tumors; Prostate; Cancer; Upstream; Proteins ER - TY - JOUR T1 - Childhood infections, orchitis and testicular germ cell tumours: a report from the STEED study and a meta-analysis of existing data AN - 1014109299; 16504220 AB - Background: Similarities between the age-specific incidence pattern of testicular germ cell tumours (TGCTs) and the age-specific incidence pattern of cancers of viral origin prompted us to evaluate the relationship between common infections occurring during childhood or young adult life and TGCT using existing data from the US Servicemen's Testicular Tumor Environmental and Endocrine Determinants (STEED) case-control study. Methods: TGCT cases diagnosed between 2002 and 2005 (n=767) were matched on age, race and serum draw date to at least one control (n=929). Results: None of the infections evaluated were associated with TGCT risk. Further, a meta-analysis of mumps and mumps orchitis or orchitis infection did not support an association with TGCT (mumps pooled odds ratio (OR): 1.03, 95% confidence interval (CI): 0.89-1.20; mumps orchitis or orchitis pooled OR: 1.80, 95% CI: 0.74-4.42). Conclusion: Based on our evaluation of childhood and early life infections and meta-analyses of mumps and mumps orchitis and/or orchitis, TGCT does not appear to be associated with common childhood infections. JF - British Journal of Cancer AU - Trabert, B AU - Graubard, B I AU - Erickson, R L AU - McGlynn, K A AD - Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, 6120 Executive Boulevard, Suite 550, Rockville, MD 20852-7234, USA Y1 - 2012/03/27/ PY - 2012 DA - 2012 Mar 27 SP - 1331 EP - 1334 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 106 IS - 7 SN - 0007-0920, 0007-0920 KW - Risk Abstracts KW - Age KW - infection KW - tumors KW - Children KW - young adults KW - Cancer KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1014109299?accountid=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=Childhood+infections%2C+orchitis+and+testicular+germ+cell+tumours%3A+a+report+from+the+STEED+study+and+a+meta-analysis+of+existing+data&rft.au=Trabert%2C+B%3BGraubard%2C+B+I%3BErickson%2C+R+L%3BMcGlynn%2C+K+A&rft.aulast=Trabert&rft.aufirst=B&rft.date=2012-03-27&rft.volume=106&rft.issue=7&rft.spage=1331&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2012.45 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2013-06-28 N1 - SubjectsTermNotLitGenreText - Age; infection; tumors; young adults; Children; Cancer DO - http://dx.doi.org/10.1038/bjc.2012.45 ER - TY - JOUR T1 - A recurrent fusion gene in high-grade endometrial stromal sarcoma: a new tool for diagnosis and therapy? AN - 1113230539; 17213626 AB - High-grade endometrial stromal sarcomas (ESSs) are an aggressive group of endometrial stromal tumors. A recent study described a recurrent chromosomal translocation (t(10; 17)) occurring in ESS, which joins the gene 14-3-3 epsilon with either FAM22A or FAM22B. Expression of the resulting fusion gene leads to malignant transformation, and silencing of its expression reverses the malignant phenotype. Because the fusion can be readily detected in diagnostic samples using fluorescent in situ hybridization, this chromosomal aberration could be used to differentiate high-grade ESS from the low-grade, less aggressive form. Discovery of the new oncoprotein could also provide entry points for targeted therapies. JF - Genome Medicine AU - Ried, Thomas AU - Gaiser, Timo AD - Genetics Branch, National Cancer Institute, National Institutes of Health, 50 South Drive, Bethesda, MD 20892, USA, riedt@mail.nih.gov Y1 - 2012/03/19/ PY - 2012 DA - 2012 Mar 19 SP - 20 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 4 IS - 3 KW - Biotechnology and Bioengineering Abstracts; Genetics Abstracts KW - Chromosome aberrations KW - Chromosome translocations KW - Endometrium KW - Fluorescence in situ hybridization KW - Fusion protein KW - Sarcoma KW - Transformation KW - Tumors KW - W 30925:Genetic Engineering KW - G 07880:Human Genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1113230539?accountid=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=Genome+Medicine&rft.atitle=A+recurrent+fusion+gene+in+high-grade+endometrial+stromal+sarcoma%3A+a+new+tool+for+diagnosis+and+therapy%3F&rft.au=Ried%2C+Thomas%3BGaiser%2C+Timo&rft.aulast=Ried&rft.aufirst=Thomas&rft.date=2012-03-19&rft.volume=4&rft.issue=3&rft.spage=20&rft.isbn=&rft.btitle=&rft.title=Genome+Medicine&rft.issn=1756-994X&rft_id=info:doi/10.1186%2Fgm319 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2012-11-20 N1 - SubjectsTermNotLitGenreText - Transformation; Endometrium; Chromosome translocations; Sarcoma; Tumors; Fusion protein; Chromosome aberrations; Fluorescence in situ hybridization DO - http://dx.doi.org/10.1186/gm319 ER - TY - JOUR T1 - Class B Scavenger Receptor Types I and II and CD36 Targeting Improves Sepsis Survival and Acute Outcomes in Mice AN - 968168714; 16427029 AB - Class B scavenger receptors (SR-Bs), such as SR-BI/II or CD36, bind lipoproteins but also mediate bacterial recognition and phagocytosis. In evaluating whether blocking receptors can prevent intracellular bacterial proliferation, phagocyte cytotoxicity, and proinflammatory signaling in bacterial infection/sepsis, we found that SR-BI/II- or CD36-deficient phagocytes are characterized by a reduced intracellular bacterial survival and a lower cytokine response and were protected from bacterial cytotoxicity in the presence of antibiotics. Mice deficient in either SR-BI/II or CD36 are protected from antibiotic-treated cecal ligation and puncture (CLP)-induced sepsis, with greatly increased peritoneal granulocytic phagocyte survival (8-fold), a drastic diminution in peritoneal bacteria counts, and a 50-70% reduction in systemic inflammation (serum levels of IL-6, TNF- alpha , and IL-10) and organ damage relative to CLP in wild-type mice. The survival rate of CD36-deficient mice after CLP was 58% compared with 17% in control mice. When compensated for mineralocorticoid and glucocorticoid deficiency, SR-BI/II-deficient mice had nearly a 50% survival rate versus 5% in mineralo-/glucocorticoid-treated controls. Targeting SR-B receptors with L-37pA, a peptide that functions as an antagonist of SR-BI/II and CD36 receptors, also increased peritoneal granulocyte counts, as well as reduced peritoneal bacteria and bacterium-induced cytokine secretion. In the CLP mouse sepsis model, L-37pA improved survival from 6 to 27%, reduced multiple organ damage, and improved kidney function. These results demonstrate that the reduction of both SR-BI/II- and CD36-dependent bacterial invasion and inflammatory response in the presence of antibiotic treatment results in granulocyte survival and local bacterial containment, as well as reduces systemic inflammation and organ damage and improves animal survival during severe infections. JF - Journal of Immunology AU - Leelahavanichkul, Asada AU - Bocharov, Alexander V AU - Kurlander, Roger AU - Baranova, Irina N AU - Vishnyakova, Tatyana G AU - Souza, Ana CP AU - Hu, Xuzhen AU - Doi, Kent AU - Vaisman, Boris AU - Amar, Marcelo AU - Sviridov, Denis AU - Chen, Zhigang AU - Remaley, Alan T AU - Csako, Gyorgy AU - Patterson, Amy P AU - Yuen, Peter ST AU - Star, Robert A AU - Eggerman, Thomas L AD - Renal Diagnostics and Therapeutics Unit, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 Y1 - 2012/03/15/ PY - 2012 DA - 2012 Mar 15 SP - 2749 EP - 2758 PB - American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 United States VL - 188 IS - 6 SN - 0022-1767, 0022-1767 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Interleukin 6 KW - Animal models KW - Survival KW - Antibiotics KW - Infection KW - Interleukin 10 KW - Renal function KW - Phagocytes KW - Cytokines KW - Cecum KW - Phagocytosis KW - scavenger receptors KW - Intracellular signalling KW - CD36 antigen KW - Peritoneum KW - Glucocorticoids KW - Inflammation KW - Serum levels KW - Leukocytes (granulocytic) KW - Corticoids KW - Cytotoxicity KW - Sepsis KW - Lipoproteins KW - Tumor necrosis factor- alpha KW - J 02350:Immunology KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/968168714?accountid=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=Class+B+Scavenger+Receptor+Types+I+and+II+and+CD36+Targeting+Improves+Sepsis+Survival+and+Acute+Outcomes+in+Mice&rft.au=Leelahavanichkul%2C+Asada%3BBocharov%2C+Alexander+V%3BKurlander%2C+Roger%3BBaranova%2C+Irina+N%3BVishnyakova%2C+Tatyana+G%3BSouza%2C+Ana+CP%3BHu%2C+Xuzhen%3BDoi%2C+Kent%3BVaisman%2C+Boris%3BAmar%2C+Marcelo%3BSviridov%2C+Denis%3BChen%2C+Zhigang%3BRemaley%2C+Alan+T%3BCsako%2C+Gyorgy%3BPatterson%2C+Amy+P%3BYuen%2C+Peter+ST%3BStar%2C+Robert+A%3BEggerman%2C+Thomas+L&rft.aulast=Leelahavanichkul&rft.aufirst=Asada&rft.date=2012-03-15&rft.volume=188&rft.issue=6&rft.spage=2749&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunology&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2013-09-09 N1 - SubjectsTermNotLitGenreText - Interleukin 6; Intracellular signalling; CD36 antigen; Peritoneum; Animal models; Survival; Antibiotics; Infection; Glucocorticoids; Interleukin 10; Inflammation; Serum levels; Corticoids; Leukocytes (granulocytic); Sepsis; Cytotoxicity; Renal function; Phagocytes; Lipoproteins; Cecum; Cytokines; Tumor necrosis factor- alpha; Phagocytosis; scavenger receptors ER - TY - JOUR T1 - Stabilization of ribozyme-like cis-noncoding rRNAs induces apoptotic and nonapoptotic death in lung cells. AN - 928905604; 22419110 AB - Bidirectional non-protein-coding RNAs are ubiquitously transcribed from the genome. Convergent sense and antisense transcripts may regulate each other. Here, we examined the convergent cis-noncoding rRNAs (nc-rRNAs) in A5 and E9 lung cancer models. Sense nc-rRNAs extending from rDNA intergenic region to internal transcribed spacer of around 10 kb in length were identified. nc-rRNAs in sense direction exhibited in vitro characteristics of ribozymes, namely, degradation upon incubation with MgCl(2) and stabilization by complementary oligonucleotides. Detection of endogenous cleavage-ligation products carrying internal deletion of hundreds to thousands nucleotides by massively parallel sequencing confirmed the catalytic properties. Transfection of oligonucleotides pairing with antisense nc-rRNAs stabilized both target and complementary transcripts, perturbed rRNA biogenesis, and induced massive cell death via apoptotic and/or nonapoptotic mechanisms depending on cell type and treatment. Oligonucleotides targeting cellular sense transcripts are less responsive. Spontaneously detached cells, though rare, also showed accumulation of nc-rRNAs and perturbation of rRNA biogenesis. Direct participation of nc-rRNAs in apoptotic and nonapoptotic death was demonstrated by transfection of synthetic nc-rRNAs encompassing the rDNA promoter. In sum, convergent cis-nc-rRNAs follow a feed-forward mechanism to regulate each other and rRNA biogenesis. This opens an opportunity to disrupt rRNA biogenesis, commonly upregulated in cancers, via inhibition of ribozyme-like activities in nc-rRNAs. JF - Cell death & disease AU - Gee, M AU - Gu, Y AU - Fields, J R AU - Shiao, Y-H AD - Laboratory of Comparative Carcinogenesis, National Cancer Institute at Frederick, Frederick, MD 21702, USA. Y1 - 2012/03/15/ PY - 2012 DA - 2012 Mar 15 SP - 1 VL - 3 KW - DNA, Ribosomal KW - 0 KW - Oligonucleotides, Antisense KW - RNA, Catalytic KW - RNA, Ribosomal KW - RNA, Untranslated KW - Magnesium Chloride KW - 02F3473H9O KW - Index Medicus KW - Animals KW - Magnesium Chloride -- metabolism KW - Oligonucleotides, Antisense -- genetics KW - DNA, Ribosomal -- metabolism KW - Transcription, Genetic KW - Cell Line, Tumor KW - Mice KW - Promoter Regions, Genetic KW - Base Sequence KW - Transfection KW - Lung Neoplasms KW - Molecular Sequence Data KW - Cell Death -- genetics KW - Oligonucleotides, Antisense -- metabolism KW - Adenocarcinoma KW - Cell Cycle -- genetics KW - DNA, Ribosomal -- genetics KW - Signal Transduction KW - High-Throughput Nucleotide Sequencing KW - Epithelial Cells -- metabolism KW - RNA, Ribosomal -- metabolism KW - RNA, Catalytic -- metabolism KW - RNA, Untranslated -- metabolism KW - RNA, Catalytic -- genetics KW - Apoptosis KW - Epithelial Cells -- pathology KW - RNA, Ribosomal -- genetics KW - Lung -- pathology KW - Lung -- metabolism KW - RNA, Untranslated -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/928905604?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+death+%26+disease&rft.atitle=Stabilization+of+ribozyme-like+cis-noncoding+rRNAs+induces+apoptotic+and+nonapoptotic+death+in+lung+cells.&rft.au=Gee%2C+M%3BGu%2C+Y%3BFields%2C+J+R%3BShiao%2C+Y-H&rft.aulast=Gee&rft.aufirst=M&rft.date=2012-03-15&rft.volume=3&rft.issue=&rft.spage=e281&rft.isbn=&rft.btitle=&rft.title=Cell+death+%26+disease&rft.issn=2041-4889&rft_id=info:doi/10.1038%2Fcddis.2012.19 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-24 N1 - Date created - 2012-03-15 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nat Genet. 2004 Jan;36(1):40-5 [14702039] Nat Biotechnol. 2003 Apr;21(4):379-86 [12640466] Nucleic Acids Res. 2004;32(16):4812-20 [15356298] Mol Pharmacol. 1985 Feb;27(2):308-13 [2578606] Nucleic Acids Res. 1985 Jul 11;13(13):4905-19 [4022778] Cell. 1986 Dec 26;47(6):891-900 [3779844] EMBO J. 1987 Nov;6(11):3487-92 [3428263] Cancer Res. 1994 Feb 1;54(3):632-6 [8306322] Prog Nucleic Acid Res Mol Biol. 1994;49:197-239 [7863007] Eur J Hum Genet. 2005 Aug;13(8):894-7 [15970949] Science. 2005 Sep 2;309(5740):1564-6 [16141073] Am J Respir Cell Mol Biol. 2005 Nov;33(5):490-9 [16055672] Curr Opin Chem Biol. 2005 Dec;9(6):665-73 [16233986] RNA. 2006 May;12(5):797-806 [16556935] Hum Mol Genet. 2006 Apr 15;15 Spec No 1:R17-29 [16651366] Mol Cell. 2006 May 5;22(3):351-61 [16678107] Nature. 2007 Feb 8;445(7128):666-70 [17237763] Hepatology. 2008 Feb;47(2):686-97 [18161049] Nat Med. 2008 Jul;14(7):723-30 [18587408] IUBMB Life. 2008 Oct;60(10):669-83 [18636557] Trends Genet. 2008 Dec;24(12):622-9 [18980784] J Neurosci. 2008 Nov 26;28(48):12759-64 [19036968] Nat Rev Mol Cell Biol. 2009 Sep;10(9):637-43 [19638999] Mol Cell. 2009 Aug 28;35(4):414-25 [19716787] PLoS One. 2009;4(10):e7505 [19838300] J Biol Chem. 2010 Apr 16;285(16):12416-25 [20159984] Mol Cell Biol. 2010 Jul;30(13):3142-50 [20421411] Cold Spring Harb Symp Quant Biol. 2010;75:357-64 [21502405] Cell Death Dis. 2011;2:e239 [22158478] Nature. 2002 Dec 5;420(6915):563-73 [12466851] Nat Rev Cancer. 2003 Mar;3(3):179-92 [12612653] Nature. 2004 Jun 3;429(6991):571-4 [15175754] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1038/cddis.2012.19 ER - TY - JOUR T1 - Body fat distribution, weight change during adulthood, and thyroid cancer risk in the NIH-AARP Diet and Health Study. AN - 917161157; 21544808 AB - Body mass index (BMI) has been positively associated with thyroid cancer risk in several studies, but the underlying mechanisms remain unclear. We examined the associations for waist and hip circumference and weight change during adulthood with thyroid cancer risk among 125,347 men and 72,363 women in the NIH-AARP Diet and Health Study who completed a second mailed questionnaire in 1996-1997. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated separately by sex and adjusted for race/ethnicity, education and smoking status. During follow-up (median = 10.1 years), 106 men and 105 women were diagnosed with a first primary thyroid cancer, as identified through linkage to state cancer registries. Having a large waist circumference (above the clinical cutpoint for normal: > 102 cm in men and > 88 cm in women) was associated with increased risk in both men (HR = 1.79, 95% CI: 1.21-2.63) and women (HR = 1.54, 95% CI: 1.05-2.26). Having both a large waist and BMI in the obese range (≥ 30 kg/m2) approximately doubled the risk of thyroid cancer (HR in men = 2.13, 95% CI: 1.18-3.85; HR in women = 1.91, 95% CI: 1.31-3.25) compared to having a normal waist circumference/normal BMI (18.5-24.9 kg/m2). We also observed positive association for weight gain between ages 18-35 in men (gained ≥ 10.0 kg vs. lost/gained < 5 kg, HR = 1.49, 95% CI: 0.93-2.39, p-trend = 0.03), but the association was less pronounced in women. No clear association for weight gain in later life was observed. These results support a potential role for hormonal and metabolic parameters common to central adiposity in thyroid carcinogenesis. Copyright © 2011 UICC. JF - International journal of cancer AU - Kitahara, Cari M AU - Platz, Elizabeth A AU - Park, Yikyung AU - Hollenbeck, Albert R AU - Schatzkin, Arthur AU - Berrington de González, Amy AD - Division of Cancer Epidemiology and Genetics, NCI, National Institutes of Health, Rockville, MD 20852, USA. kitaharac@mail.nih.gov. Y1 - 2012/03/15/ PY - 2012 DA - 2012 Mar 15 SP - 1411 EP - 1419 VL - 130 IS - 6 KW - Index Medicus KW - Humans KW - Aged KW - Body Mass Index KW - Risk Assessment -- methods KW - Prospective Studies KW - Waist-Hip Ratio KW - Risk Factors KW - National Institutes of Health (U.S.) KW - Surveys and Questionnaires KW - Follow-Up Studies KW - Middle Aged KW - United States -- epidemiology KW - Female KW - Male KW - Hip KW - Proportional Hazards Models KW - Thyroid Neoplasms -- epidemiology KW - Body Fat Distribution -- statistics & numerical data KW - Waist Circumference KW - Weight Gain UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/917161157?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Body+fat+distribution%2C+weight+change+during+adulthood%2C+and+thyroid+cancer+risk+in+the+NIH-AARP+Diet+and+Health+Study.&rft.au=Kitahara%2C+Cari+M%3BPlatz%2C+Elizabeth+A%3BPark%2C+Yikyung%3BHollenbeck%2C+Albert+R%3BSchatzkin%2C+Arthur%3BBerrington+de+Gonz%C3%A1lez%2C+Amy&rft.aulast=Kitahara&rft.aufirst=Cari&rft.date=2012-03-15&rft.volume=130&rft.issue=6&rft.spage=1411&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.26161 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-01 N1 - Date created - 2012-01-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Endocrinology. 1999 Dec;140(12):5705-11 [10579335] Am J Clin Nutr. 2002 Apr;75(4):683-8 [11916754] J Clin Endocrinol Metab. 2001 Mar;86(3):1072-7 [11238488] Obes Rev. 2001 Aug;2(3):141-7 [12120099] Horm Metab Res. 2002 Nov-Dec;34(11-12):731-6 [12660891] Epidemiology. 1990 Nov;1(6):466-73 [2090285] Cancer Causes Control. 1993 Sep;4(5):431-40 [8218875] World Health Organ Tech Rep Ser. 1995;854:1-452 [8594834] Cancer Epidemiol Biomarkers Prev. 1997 Nov;6(11):863-73 [9367058] Environ Health Perspect. 1998 Aug;106(8):427-36 [9681969] N Engl J Med. 1999 Aug 5;341(6):427-34 [10432328] J Clin Oncol. 2005 Jul 20;23(21):4742-54 [16034050] Br J Cancer. 2005 Oct 31;93(9):1062-7 [16234822] Diabetologia. 2006 May;49(5):945-52 [16557372] Cancer Causes Control. 2006 Sep;17(7):901-9 [16841257] Br J Cancer. 2006 Aug 7;95(3):366-70 [16832414] Gastroenterology. 2007 May;132(6):2087-102 [17498505] Am J Epidemiol. 2007 Nov 15;166(10):1140-9 [17855390] Lancet. 2008 Feb 16;371(9612):569-78 [18280327] Am J Epidemiol. 2008 Mar 1;167(5):586-97 [18270373] J Clin Endocrinol Metab. 2008 Mar;93(3):809-14 [18160464] Arch Intern Med. 2008 Mar 24;168(6):568-9 [18362247] Am J Epidemiol. 2008 Jun 15;167(12):1465-75 [18417494] Am J Epidemiol. 2008 Aug 1;168(3):268-77 [18544571] Cancer Causes Control. 2008 Dec;19(10):1233-42 [18618280] Cancer Epidemiol Biomarkers Prev. 2009 Mar;18(3):784-91 [19240234] Gend Med. 2009;6 Suppl 1:60-75 [19318219] Cancer Causes Control. 2009 Jul;20(5):581-90 [19043789] Am J Epidemiol. 2009 Jul 1;170(1):53-64 [19403842] Br J Cancer. 2009 Oct 6;101(7):1202-6 [19690552] Am J Epidemiol. 2010 Jan 15;171(2):242-52 [19951937] Int J Cancer. 2010 Jun 15;126(12):2947-56 [19795465] Int J Cancer. 2010 Jun 15;126(12):2984-90 [19950225] Thyroid. 2010 Nov;20(11):1285-93 [20932181] Cancer Epidemiol Biomarkers Prev. 2011 Mar;20(3):464-72 [21266520] JAMA. 2001 May 16;285(19):2486-97 [11368702] Diabetes Care. 2001 May;24(5):925-32 [11347756] Int J Cancer. 2001 Sep 1;93(5):745-50 [11477590] Am J Epidemiol. 2001 Dec 15;154(12):1119-25 [11744517] Cancer Causes Control. 2000 Feb;11(2):137-44 [10710197] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/ijc.26161 ER - TY - JOUR T1 - Circulating micro-RNA expression profiles in early stage nonsmall cell lung cancer. AN - 917161143; 21544802 AB - Circulating micro-RNA (miR) profiles have been proposed as promising diagnostic and prognostic biomarkers for cancer, including lung cancer. We have developed methods to accurately and reproducibly measure micro-RNA levels in serum and plasma. Here, we study paired serum and plasma samples from 220 patients with early stage nonsmall cell lung cancer (NSCLC) and 220 matched controls. We use qRT-PCR to measure the circulating levels of 30 different miRs that have previously been reported to be differently expressed in lung cancer tissue. Duplicate RNA extractions were performed for 10% of all samples, and micro-RNA measurements were highly correlated among those duplicates. This demonstrates high reproducibility of our assay. The expressions of miR-146b, miR-221, let-7a, miR-155, miR-17-5p, miR-27a and miR-106a were significantly reduced in the serum of NSCLC cases, while miR-29c was significantly increased. No significant differences were observed in plasma of patients compared with controls. Overall, expression levels in serum did not correlate well with levels in plasma. In secondary analyses, reduced plasma expression of let-7b was modestly associated with worse cancer-specific mortality in all patients, and reduced serum expression of miR-223 was modestly associated with cancer-specific mortality in stage IA/B patients. MiR profiles also showed considerable differences comparing African American and European Americans. In summary, we found significant differences in miR expression when comparing cases and controls and find evidence that expression of let-7b is associated with prognosis in NSCLC. Copyright © 2011 UICC. JF - International journal of cancer AU - Heegaard, Niels H H AU - Schetter, Aaron J AU - Welsh, Judith A AU - Yoneda, Mitsuhiro AU - Bowman, Elise D 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 - 2012/03/15/ PY - 2012 DA - 2012 Mar 15 SP - 1378 EP - 1386 VL - 130 IS - 6 KW - MicroRNAs KW - 0 KW - Index Medicus KW - Gene Expression Regulation, Neoplastic KW - Aged, 80 and over KW - Risk Factors KW - Humans KW - Neoplasm Staging -- methods KW - Adult KW - Real-Time Polymerase Chain Reaction -- methods KW - Aged KW - Middle Aged KW - Male KW - Gene Expression Profiling -- methods KW - Female KW - Carcinoma, Non-Small-Cell Lung -- metabolism KW - Carcinoma, Non-Small-Cell Lung -- blood KW - MicroRNAs -- metabolism KW - MicroRNAs -- genetics KW - Lung Neoplasms -- blood KW - Carcinoma, Non-Small-Cell Lung -- genetics KW - MicroRNAs -- blood KW - Lung Neoplasms -- genetics KW - Lung Neoplasms -- pathology KW - Lung Neoplasms -- metabolism KW - Carcinoma, Non-Small-Cell Lung -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/917161143?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Circulating+micro-RNA+expression+profiles+in+early+stage+nonsmall+cell+lung+cancer.&rft.au=Heegaard%2C+Niels+H+H%3BSchetter%2C+Aaron+J%3BWelsh%2C+Judith+A%3BYoneda%2C+Mitsuhiro%3BBowman%2C+Elise+D%3BHarris%2C+Curtis+C&rft.aulast=Heegaard&rft.aufirst=Niels+H&rft.date=2012-03-15&rft.volume=130&rft.issue=6&rft.spage=1378&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.26153 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-01 N1 - Date created - 2012-01-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nat Struct Mol Biol. 2009 Sep;16(9):961-6 [19668211] Cancer Res. 2009 Jul 15;69(14):5776-83 [19584273] Lancet Oncol. 2009 Oct;10(10):1001-10 [19796752] Exp Lung Res. 2009 Oct;35(8):646-64 [19895320] Cancer Epidemiol Biomarkers Prev. 2009 Dec;18(12):3375-83 [19959685] Cancer Cell. 2009 Dec 8;16(6):498-509 [19962668] Cancer Res. 2010 Jan 1;70(1):36-45 [20028859] Carcinogenesis. 2010 Jan;31(1):37-49 [19955394] Clin Cancer Res. 2010 Jan 15;16(2):430-41 [20068076] Cancer Res. 2010 Feb 15;70(4):1668-78 [20124479] Blood. 2010 Mar 4;115(9):1768-78 [20029046] Methods. 2010 Apr;50(4):298-301 [20146939] Technol Cancer Res Treat. 2010 Apr;9(2):123-38 [20218735] J Cancer Res Clin Oncol. 2010 Jul;136(7):1023-8 [20033209] Transpl Int. 2000;13(2):146-50 [10836652] Carcinogenesis. 2003 Feb;24(2):269-74 [12584177] Cancer Res. 2004 Jun 1;64(11):3753-6 [15172979] Nucleic Acids Res. 1991 Nov 11;19(21):6051 [1719488] Biotechniques. 1997 Jul;23(1):24, 26, 28 [9232220] Cell. 2005 Mar 11;120(5):635-47 [15766527] Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2257-61 [16461460] Cancer Cell. 2006 Mar;9(3):189-98 [16530703] Nat Cell Biol. 2007 Jun;9(6):654-9 [17486113] Proc Natl Acad Sci U S A. 2007 Oct 2;104(40):15805-10 [17890317] Cancer Cell. 2008 Jan;13(1):48-57 [18167339] Nat Rev Cancer. 2008 May;8(5):329-40 [18404148] Br J Haematol. 2008 May;141(5):672-5 [18318758] Oncogene. 2008 Jun 19;27(27):3845-55 [18246122] Gastroenterology. 2008 Jul;135(1):257-69 [18555017] Proc Natl Acad Sci U S A. 2008 Jul 29;105(30):10513-8 [18663219] PLoS One. 2008;3(9):e3148 [18773077] Cell Res. 2008 Oct;18(10):997-1006 [18766170] Nat Cell Biol. 2008 Dec;10(12):1470-6 [19011622] Clin Lung Cancer. 2009 Jan;10(1):42-6 [19289371] Curr Cancer Drug Targets. 2009 Jun;9(4):572-94 [19519323] Transfusion. 2009 Jul;49(7):1443-50 [19389023] Methods Mol Biol. 2009;578:277-92 [19768601] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/ijc.26153 ER - TY - JOUR T1 - 3'-UTR and Functional Secretor Haplotypes in Mannose-Binding Lectin 2 Are Associated with Increased Colon Cancer Risk in African Americans AN - 1014108782; 16473715 AB - Because chronic intestinal inflammation is a risk factor for colorectal cancer, we hypothesized that genetic variants of inflammatory mediators, such as mannose-binding lectin 2 (MBL2), are associated with colon cancer susceptibility. Here, we report the association of 24 MBL2 single-nucleotide polymorphisms (SNP) and corresponding haplotypes with colon cancer risk in a case-control study. Four SNPs in the 3'-untranslated region (UTR) of the gene (rs10082466, rs2120132, rs2099902, and rs10450310) were associated with an increased risk of colon cancer in African Americans. ORs for homozygous variants versus wild-type ranged from 3.17 [95% confidence interval (CI), 1.57-6.40] to 4.51 (95% CI, 1.94-10.50), whereas the 3'-UTR region haplotype consisting of these four variants had an OR of 2.10 (95% CI, 1.42-3.12). The C allele of rs10082466 exhibited a binding affinity of miR-27a and this allele was associated with both lower MBL plasma levels and activity. We found that 5' secretor haplotypes known to correlate with moderate and low MBL serum levels exhibited associations with increased risk of colon cancer in African Americans, specifically as driven by two haplotypes, LYPA and LYQC, relative to the referent HYPA haplotype (LYPA: OR, 2.60; 95% CI, 1.33-5.08 and LYQC: OR, 2.28; 95% CI, 1.20-4.30). Similar associations were not observed in Caucasians. Together, our results support the hypothesis that genetic variations in MBL2 increase colon cancer susceptibility in African Americans. Cancer Res; 72(6); 1467-77. [copy]2012 AACR. JF - Cancer Research AU - Zanetti, Krista A AU - Haznadar, Majda AU - Welsh, Judith A AU - Robles, Ana I AU - Ryan, Brid M AU - McClary, Andrew C AU - Bowman, Elise D AU - Goodman, Julie E AU - Bernig, Toralf AU - Chanock, Stephen J AU - Harris, Curtis C AD - Authors' Affiliations: Laboratory of Human Carcinogenesis, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland Y1 - 2012/03/15/ PY - 2012 DA - 2012 Mar 15 SP - 1467 EP - 1477 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 72 IS - 6 SN - 0008-5472, 0008-5472 KW - Risk Abstracts; Health & Safety Science Abstracts; Immunology Abstracts KW - 3' Untranslated regions KW - Colorectal cancer KW - Genetic diversity KW - Colon cancer KW - Cancer KW - Inflammation KW - Serum levels KW - Mannose-binding lectin KW - Plasma levels KW - Haplotypes KW - Single-nucleotide polymorphism KW - Risk factors KW - Intestine KW - Colorectal carcinoma KW - Ethnic groups KW - H 11000:Diseases/Injuries/Trauma KW - F 06915:Cancer Immunology KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1014108782?accountid=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+Research&rft.atitle=3%27-UTR+and+Functional+Secretor+Haplotypes+in+Mannose-Binding+Lectin+2+Are+Associated+with+Increased+Colon+Cancer+Risk+in+African+Americans&rft.au=Zanetti%2C+Krista+A%3BHaznadar%2C+Majda%3BWelsh%2C+Judith+A%3BRobles%2C+Ana+I%3BRyan%2C+Brid+M%3BMcClary%2C+Andrew+C%3BBowman%2C+Elise+D%3BGoodman%2C+Julie+E%3BBernig%2C+Toralf%3BChanock%2C+Stephen+J%3BHarris%2C+Curtis+C&rft.aulast=Zanetti&rft.aufirst=Krista&rft.date=2012-03-15&rft.volume=72&rft.issue=6&rft.spage=1467&rft.isbn=&rft.btitle=&rft.title=Cancer+Research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2013-09-09 N1 - SubjectsTermNotLitGenreText - Serum levels; Mannose-binding lectin; Plasma levels; 3' Untranslated regions; Haplotypes; Single-nucleotide polymorphism; Risk factors; Intestine; Colorectal cancer; Colon cancer; Inflammation; Genetic diversity; Colorectal carcinoma; Ethnic groups; Cancer ER - TY - CPAPER T1 - New Partnerships to Accelerate Translation T2 - 2012 Annual Meeting of the American Society for Clinical Pharmacology and Therapeutics (ASCPT 2012) AN - 1313092980; 6126134 JF - 2012 Annual Meeting of the American Society for Clinical Pharmacology and Therapeutics (ASCPT 2012) AU - Collins, Francis Y1 - 2012/03/12/ PY - 2012 DA - 2012 Mar 12 KW - Translation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313092980?accountid=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+Clinical+Pharmacology+and+Therapeutics+%28ASCPT+2012%29&rft.atitle=New+Partnerships+to+Accelerate+Translation&rft.au=Collins%2C+Francis&rft.aulast=Collins&rft.aufirst=Francis&rft.date=2012-03-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Annual+Meeting+of+the+American+Society+for+Clinical+Pharmacology+and+Therapeutics+%28ASCPT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascpt.org/Portals/8/docs/Meetings/2012%20Annual%20Meeting/ASCPT%20Final%20Program_website.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Codevelopment of Investigational Drugs to Treat Cancer: Overview, Background, and Scientific Rationale T2 - 2012 Annual Meeting of the American Society for Clinical Pharmacology and Therapeutics (ASCPT 2012) AN - 1313021435; 6126172 JF - 2012 Annual Meeting of the American Society for Clinical Pharmacology and Therapeutics (ASCPT 2012) AU - Chen, Helen Y1 - 2012/03/12/ PY - 2012 DA - 2012 Mar 12 KW - Cancer KW - Drugs KW - Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313021435?accountid=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+Clinical+Pharmacology+and+Therapeutics+%28ASCPT+2012%29&rft.atitle=Codevelopment+of+Investigational+Drugs+to+Treat+Cancer%3A+Overview%2C+Background%2C+and+Scientific+Rationale&rft.au=Chen%2C+Helen&rft.aulast=Chen&rft.aufirst=Helen&rft.date=2012-03-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Annual+Meeting+of+the+American+Society+for+Clinical+Pharmacology+and+Therapeutics+%28ASCPT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.ascpt.org/Portals/8/docs/Meetings/2012%20Annual%20Meeting/ASCPT%20Final%20Program_website.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Generation of a Convalescent Model of Virulent Francisella tularensis Infection for Assessment of Host Requirements for Survival of Tularemia AN - 1011210553; 16495215 AB - Francisella tularensis is a facultative intracellular bacterium and the causative agent of tularemia. Development of novel vaccines and therapeutics for tularemia has been hampered by the lack of understanding of which immune components are required to survive infection. Defining these requirements for protection against virulent F. tularensis, such as strain SchuS4, has been difficult since experimentally infected animals typically die within 5 days after exposure to as few as 10 bacteria. Such a short mean time to death typically precludes development, and therefore assessment, of immune responses directed against virulent F. tularensis. To enable identification of the components of the immune system that are required for survival of virulent F. tularensis, we developed a convalescent model of tularemia in C57Bl/6 mice using low dose antibiotic therapy in which the host immune response is ultimately responsible for clearance of the bacterium. Using this model we demonstrate alpha beta TCR+ cells, gamma delta TCR+ cells, and B cells are necessary to survive primary SchuS4 infection. Analysis of mice deficient in specific soluble mediators shows that IL-12p40 and IL-12p35 are essential for survival of SchuS4 infection. We also show that IFN- gamma is required for survival of SchuS4 infection since mice lacking IFN- gamma R succumb to disease during the course of antibiotic therapy. Finally, we found that both CD4+ and CD8+ cells are the primary producers of IFN- gamma and that gamma delta TCR+ cells and NK cells make a minimal contribution toward production of this cytokine throughout infection. Together these data provide a novel model that identifies key cells and cytokines required for survival or exacerbation of infection with virulent F. tularensis and provides evidence that this model will be a useful tool for better understanding the dynamics of tularemia infection. JF - PLoS ONE AU - Crane, Deborah D AU - Scott, Dana P AU - Bosio, Catharine M AD - Immunity to Pulmonary Pathogens, Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, NIAID, National Institutes of Health, Hamilton, Montana, United States of America Y1 - 2012/03/12/ PY - 2012 DA - 2012 Mar 12 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 7 IS - 3 KW - Microbiology Abstracts B: Bacteriology KW - Animal models KW - Antibiotics KW - CD4 antigen KW - CD8 antigen KW - Cell survival KW - Cytokines KW - Data processing KW - Immune response KW - Infection KW - Interleukin 12 KW - Lymphocytes B KW - Natural killer cells KW - Survival KW - Tularemia KW - Vaccines KW - gamma -Interferon KW - Francisella tularensis KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1011210553?accountid=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=PLoS+ONE&rft.atitle=Generation+of+a+Convalescent+Model+of+Virulent+Francisella+tularensis+Infection+for+Assessment+of+Host+Requirements+for+Survival+of+Tularemia&rft.au=Crane%2C+Deborah+D%3BScott%2C+Dana+P%3BBosio%2C+Catharine+M&rft.aulast=Crane&rft.aufirst=Deborah&rft.date=2012-03-12&rft.volume=7&rft.issue=3&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+ONE&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0033349 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2012-05-18 N1 - SubjectsTermNotLitGenreText - Cell survival; gamma -Interferon; Data processing; Lymphocytes B; Natural killer cells; Animal models; Survival; Antibiotics; CD8 antigen; Infection; Interleukin 12; Tularemia; CD4 antigen; Cytokines; Immune response; Vaccines; Francisella tularensis DO - http://dx.doi.org/10.1371/journal.pone.0033349 ER - TY - CPAPER T1 - Early-Life Exposures to Endocrineactive Chemicals Promotes Breast Cancer Risk Later in Life T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313106896; 6137098 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Birnbaum, L Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - Chemicals KW - Breast cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313106896?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=Early-Life+Exposures+to+Endocrineactive+Chemicals+Promotes+Breast+Cancer+Risk+Later+in+Life&rft.au=Birnbaum%2C+L&rft.aulast=Birnbaum&rft.aufirst=L&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Mode of Action of Methylated Trivalent Arsenic with a Focus on the Potential Action as a Carcinogen T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313097726; 6137469 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Waalkes, M AU - Kojima, C AU - Orihuela, R AU - Tokar, E Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - Carcinogens KW - Arsenic UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313097726?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=Mode+of+Action+of+Methylated+Trivalent+Arsenic+with+a+Focus+on+the+Potential+Action+as+a+Carcinogen&rft.au=Waalkes%2C+M%3BKojima%2C+C%3BOrihuela%2C+R%3BTokar%2C+E&rft.aulast=Waalkes&rft.aufirst=M&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Redundancy and Cross-Talk in Pathways and Functions in Dna Damage Responses to the Highly Toxic Dna Double-Strand Break. T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313087371; 6137007 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Paules, R AU - Palii, S AU - Cui, Y AU - Hesse, J AU - Innes, C AU - Sleckman, B Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - DNA damage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313087371?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=Redundancy+and+Cross-Talk+in+Pathways+and+Functions+in+Dna+Damage+Responses+to+the+Highly+Toxic+Dna+Double-Strand+Break.&rft.au=Paules%2C+R%3BPalii%2C+S%3BCui%2C+Y%3BHesse%2C+J%3BInnes%2C+C%3BSleckman%2C+B&rft.aulast=Paules&rft.aufirst=R&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Overview of the Niehs-Sponsored Nanogo Program T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313080118; 6137195 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Nadadur, S Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313080118?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=Overview+of+the+Niehs-Sponsored+Nanogo+Program&rft.au=Nadadur%2C+S&rft.aulast=Nadadur&rft.aufirst=S&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Free Radicals and Oxidized Macromolecules: Roles in Biomarker Toxicology T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313079912; 6137388 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Kadiiska, M Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - Bioindicators KW - Toxicology KW - Macromolecules KW - Free radicals KW - biomarkers KW - Biomarkers UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313079912?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=Free+Radicals+and+Oxidized+Macromolecules%3A+Roles+in+Biomarker+Toxicology&rft.au=Kadiiska%2C+M&rft.aulast=Kadiiska&rft.aufirst=M&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - The Effects of Antiandrogens on Epididymal Development in the Rat T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313079599; 6137034 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Foster, P Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - antiandrogens UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313079599?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=The+Effects+of+Antiandrogens+on+Epididymal+Development+in+the+Rat&rft.au=Foster%2C+P&rft.aulast=Foster&rft.aufirst=P&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Novel Topics in Environmental Polycyclic Aromatic Hydrocarbon Metabolism Leading to Carcinogenesis T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313078913; 6137290 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Carlin, D AU - Moorthy, B Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - Metabolism KW - Carcinogenesis KW - Polycyclic aromatic hydrocarbons KW - Pollution effects KW - Aromatic hydrocarbons UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313078913?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=Novel+Topics+in+Environmental+Polycyclic+Aromatic+Hydrocarbon+Metabolism+Leading+to+Carcinogenesis&rft.au=Carlin%2C+D%3BMoorthy%2C+B&rft.aulast=Carlin&rft.aufirst=D&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Urine Micrornas as Kidney Injury Biomarkers: The Case for Exosomes T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313069823; 6137257 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Yuen, P Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - Bioindicators KW - Kidneys KW - Injuries KW - Urine KW - exosomes KW - miRNA KW - biomarkers KW - Biomarkers UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313069823?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=Urine+Micrornas+as+Kidney+Injury+Biomarkers%3A+The+Case+for+Exosomes&rft.au=Yuen%2C+P&rft.aulast=Yuen&rft.aufirst=P&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Sufficient Similarity of Whole Representative Mixtures or a Relative Potency Factor Approach: Polycyclic Aromatic Hydrocarbons as a Case Study T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313065868; 6137199 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Rider, C Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - Case studies KW - Polycyclic aromatic hydrocarbons KW - Aromatic hydrocarbons UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313065868?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=Sufficient+Similarity+of+Whole+Representative+Mixtures+or+a+Relative+Potency+Factor+Approach%3A+Polycyclic+Aromatic+Hydrocarbons+as+a+Case+Study&rft.au=Rider%2C+C&rft.aulast=Rider&rft.aufirst=C&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Evaluating Tools and Models Used for Quantitative Extrapolation of in Vitro to in Vivo Data for Neurotoxicants T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313060550; 6137332 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Chan, M AU - DeVito, M AU - Shafer, T AU - Tornero-Velez, R AU - Hughes, M Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - Neurotoxicity KW - Data processing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313060550?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=Evaluating+Tools+and+Models+Used+for+Quantitative+Extrapolation+of+in+Vitro+to+in+Vivo+Data+for+Neurotoxicants&rft.au=Chan%2C+M%3BDeVito%2C+M%3BShafer%2C+T%3BTornero-Velez%2C+R%3BHughes%2C+M&rft.aulast=Chan&rft.aufirst=M&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Refining Your Science Communication Skills T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313060530; 6137547 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Mercado- Feliciano, M AU - Pastoor, T AU - Gray, G AU - Walker, N AU - Beck, N Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - Communication UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313060530?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=Refining+Your+Science+Communication+Skills&rft.au=Mercado-+Feliciano%2C+M%3BPastoor%2C+T%3BGray%2C+G%3BWalker%2C+N%3BBeck%2C+N&rft.aulast=Mercado-+Feliciano&rft.aufirst=M&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Bronchial Fibrosis in Rats Exposed to 2,3-Butanedione and 2,3-Pentanedione Vapors T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313059661; 6137162 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Morgan, D AU - Jokinen, M AU - Johnson, C AU - Gwinn, W AU - Price, H AU - Flake, G Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - Vapors KW - Rats KW - Fibrosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313059661?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=Bronchial+Fibrosis+in+Rats+Exposed+to+2%2C3-Butanedione+and+2%2C3-Pentanedione+Vapors&rft.au=Morgan%2C+D%3BJokinen%2C+M%3BJohnson%2C+C%3BGwinn%2C+W%3BPrice%2C+H%3BFlake%2C+G&rft.aulast=Morgan&rft.aufirst=D&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Cell Signaling in Response to Parp Inhibition and Alkylating Agent Exposure T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313058038; 6137004 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Wilson, S AU - Horton, J AU - Stefanick, D AU - Heacock, M AU - Kedar, P AU - Carrozza, M Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - Poly(ADP-ribose) polymerase KW - Alkylating agents UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313058038?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=Cell+Signaling+in+Response+to+Parp+Inhibition+and+Alkylating+Agent+Exposure&rft.au=Wilson%2C+S%3BHorton%2C+J%3BStefanick%2C+D%3BHeacock%2C+M%3BKedar%2C+P%3BCarrozza%2C+M&rft.aulast=Wilson&rft.aufirst=S&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Dna Damage Responses and Repair T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313057963; 6137002 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Paules, R AU - Samson, L Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - DNA damage UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313057963?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=Dna+Damage+Responses+and+Repair&rft.au=Paules%2C+R%3BSamson%2C+L&rft.aulast=Paules&rft.aufirst=R&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Ahr-Mediated Gene Expression across Multiple Developing Mouse Tissues T2 - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AN - 1313012754; 6137414 JF - 51st Annual Meeting of the Society of Toxicology (SOT 2012) AU - Chang, X AU - Foley, J AU - Gohlke, J AU - Portier, C AU - Devito, M Y1 - 2012/03/11/ PY - 2012 DA - 2012 Mar 11 KW - Gene expression UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313012754?accountid=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=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.atitle=Ahr-Mediated+Gene+Expression+across+Multiple+Developing+Mouse+Tissues&rft.au=Chang%2C+X%3BFoley%2C+J%3BGohlke%2C+J%3BPortier%2C+C%3BDevito%2C+M&rft.aulast=Chang&rft.aufirst=X&rft.date=2012-03-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=51st+Annual+Meeting+of+the+Society+of+Toxicology+%28SOT+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.toxicology.org/AI/PUB/Program12.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Renal, hepatic, pulmonary and adrenal tumors induced by prenatal inorganic arsenic followed by dimethylarsinic acid in adulthood in CD1 mice. AN - 920370083; 22230260 AB - Inorganic arsenic, an early life carcinogen in humans and mice, can initiate lesions promotable by other agents in later life. The biomethylation product of arsenic, dimethylarsinic acid (DMA), is a multi-site tumor promoter. Thus, pregnant CD1 mice were given drinking water (0 ppm or 85 ppm arsenic) from gestation day 8 to 18 and after weaning male offspring received DMA (0 ppm or 200 ppm; drinking water) for up to 2 years. No renal tumors occurred in controls or DMA alone treated mice while gestational arsenic exposure plus later DMA induced a significant renal tumor incidence of 17% (primarily renal cell carcinoma). Arsenic plus DMA or arsenic alone also increased renal hyperplasia over control but DMA alone did not. Arsenic alone, DMA alone and arsenic plus DMA all induced urinary bladder hyperplasia (33-35%) versus control (2%). Compared to control (6%), arsenic alone tripled hepatocellular carcinoma (20%), and arsenic plus DMA doubled this rate again (43%), but DMA alone had no effect. DMA alone, arsenic alone, and arsenic plus DMA increased lung adenocarcinomas and adrenal adenomas versus control. Overall, DMA in adulthood promoted tumors/lesions initiated by prenatal arsenic in the kidney and liver, but acted independently in the urinary bladder, lung and adrenal. Published by Elsevier Ireland Ltd. JF - Toxicology letters AU - Tokar, Erik J AU - Diwan, Bhalchandra A AU - Waalkes, Michael P AD - Inorganic Toxicology Group, National Toxicology Program Laboratory Branch, Division of the National Toxicology Program, the National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. Y1 - 2012/03/07/ PY - 2012 DA - 2012 Mar 07 SP - 179 EP - 185 VL - 209 IS - 2 KW - Cacodylic Acid KW - AJ2HL7EU8K KW - Arsenic KW - N712M78A8G KW - Index Medicus KW - Animals KW - Random Allocation KW - Mice KW - Histocytochemistry KW - Male KW - Female KW - Survival Analysis KW - Pregnancy KW - Arsenic -- toxicity KW - Kidney Neoplasms -- chemically induced KW - Liver Neoplasms -- chemically induced KW - Adrenal Gland Neoplasms -- chemically induced KW - Lung Neoplasms -- chemically induced KW - Cacodylic Acid -- toxicity KW - Prenatal Exposure Delayed Effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920370083?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicology+letters&rft.atitle=Renal%2C+hepatic%2C+pulmonary+and+adrenal+tumors+induced+by+prenatal+inorganic+arsenic+followed+by+dimethylarsinic+acid+in+adulthood+in+CD1+mice.&rft.au=Tokar%2C+Erik+J%3BDiwan%2C+Bhalchandra+A%3BWaalkes%2C+Michael+P&rft.aulast=Tokar&rft.aufirst=Erik&rft.date=2012-03-07&rft.volume=209&rft.issue=2&rft.spage=179&rft.isbn=&rft.btitle=&rft.title=Toxicology+letters&rft.issn=1879-3169&rft_id=info:doi/10.1016%2Fj.toxlet.2011.12.016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-04 N1 - Date created - 2012-02-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Int J Toxicol. 2010 May-Jun;29(3):291-6 [20448261] Environ Health Prev Med. 2011 May;16(3):164-70 [21431798] Epidemiology. 2010 Jan;21(1):103-8 [20010213] Cancer Res. 2008 Oct 15;68(20):8278-85 [18922899] Cancer Epidemiol Biomarkers Prev. 2008 Aug;17(8):1982-7 [18708388] J Biol Chem. 2008 Jul 11;283(28):19342-50 [18487201] Environ Health Perspect. 2008 Feb;116(2):158-64 [18288312] Toxicol Appl Pharmacol. 2007 Aug 1;222(3):271-80 [17306315] Cancer Sci. 2007 Jun;98(6):803-14 [17441966] J Intern Med. 2007 May;261(5):412-7 [17444880] Toxicol Appl Pharmacol. 2006 Sep 15;215(3):295-305 [16712894] Environ Health Perspect. 2006 Aug;114(8):1293-6 [16882542] Toxicology. 2006 Jun 1;223(1-2):82-100 [16677751] Semin Fetal Neonatal Med. 2006 Apr;11(2):73-8 [16368278] Cancer Res. 2006 Feb 1;66(3):1337-45 [16452187] Carcinogenesis. 1999 Sep;20(9):1873-6 [10469637] Cancer Lett. 1998 Mar 13;125(1-2):83-8 [9566700] Carcinogenesis. 1996 Nov;17(11):2435-9 [8968060] Cancer Res. 1995 Mar 15;55(6):1271-6 [7882321] Proc West Pharmacol Soc. 1983;26:413-5 [6688469] Carcinogenesis. 2004 Jan;25(1):133-41 [14514661] Toxicol Appl Pharmacol. 2003 Dec 15;193(3):309-34 [14678742] Toxicol Appl Pharmacol. 2003 Jan 1;186(1):7-17 [12583988] Carcinogenesis. 2002 Aug;23(8):1387-97 [12151359] Crit Rev Toxicol. 2010 Nov;40(10):912-27 [20812815] Toxicol Sci. 2011 Mar;120 Suppl 1:S192-203 [21071725] J Natl Cancer Inst. 2009 Dec 16;101(24):1670-81 [19933942] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.toxlet.2011.12.016 ER - TY - JOUR T1 - Hierarchical Scale-Based Multiobject Recognition of 3-D Anatomical Structures AN - 968164670; 16429395 AB - Segmentation of anatomical structures from medical images is a challenging problem, which depends on the accurate recognition (localization) of anatomical structures prior to delineation. This study generalizes anatomy segmentation problem via attacking two major challenges: 1) automatically locating anatomical structures without doing search or optimization, and 2) automatically delineating the anatomical structures based on the located model assembly. For 1), we propose intensity weighted ball-scale object extraction concept to build a hierarchical transfer function from image space to object (shape) space such that anatomical structures in 3-D medical images can be recognized without the need to perform search or optimization. For 2), we integrate the graph-cut (GC) segmentation algorithm with prior shape model. This integrated segmentation framework is evaluated on clinical 3-D images consisting of a set of 20 abdominal CT scans. In addition, we use a set of 11 foot MR images to test the generalizability of our method to the different imaging modalities as well as robustness and accuracy of the proposed methodology. Since MR image intensities do not possess a tissue specific numeric meaning, we also explore the effects of intensity nonstandardness on anatomical object recognition. Experimental results indicate that: 1) effective recognition can make the delineation more accurate; 2) incorporating a large number of anatomical structures via a model assembly in the shape model improves the recognition and delineation accuracy dramatically; 3) ball-scale yields useful information about the relationship between the objects and the image; 4) intensity variation among scenes in an ensemble degrades object recognition performance. JF - IEEE Transactions on Medical Imaging AU - Bagci, Ulas AU - Chen, Xinjian AU - Udupa, Jayaram K AD - Center for Infectious Disease Imaging, Department of Radiology and Imaging Sciences, National Institutes of Health, Bethesda, US Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 777 EP - 789 PB - Institute of Electrical and Electronics Engineers, Inc., 345 E. 47th St. NY NY 10017-2394 United States VL - 31 IS - 3 SN - 0278-0062, 0278-0062 KW - Biotechnology and Bioengineering Abstracts KW - Pattern recognition KW - Guanylate cyclase KW - Computed tomography KW - Segmentation KW - Foot KW - Algorithms KW - Image processing KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/968164670?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=IEEE+Transactions+on+Medical+Imaging&rft.atitle=Hierarchical+Scale-Based+Multiobject+Recognition+of+3-D+Anatomical+Structures&rft.au=Bagci%2C+Ulas%3BChen%2C+Xinjian%3BUdupa%2C+Jayaram+K&rft.aulast=Bagci&rft.aufirst=Ulas&rft.date=2012-03-01&rft.volume=31&rft.issue=3&rft.spage=777&rft.isbn=&rft.btitle=&rft.title=IEEE+Transactions+on+Medical+Imaging&rft.issn=02780062&rft_id=info:doi/10.1109%2FTMI.2011.2180920 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Guanylate cyclase; Pattern recognition; Computed tomography; Algorithms; Foot; Segmentation; Image processing DO - http://dx.doi.org/10.1109/TMI.2011.2180920 ER - TY - JOUR T1 - Racial variation in umbilical cord blood sex steroid hormones and the insulin-like growth factor axis in African-American and white female neonates AN - 954651107; 16417601 AB - Purpose: To evaluate whether there is racial variation in venous umbilical cord blood concentrations of sex steroid hormones and the insulin-like growth factor (IGF) axis between female African-American and white neonates. Methods: Maternal and birth characteristics and venous umbilical cord blood samples were collected from 77 African-American and 41 white full-term uncomplicated births at two urban hospitals in 2004 and 2005. Cord blood was measured for testosterone, dehydroespiandrosterone-sulfate, estradiol, and sex steroid hormone-binding globulin (SHBG) by immunoassay. IGF-1, IGF-2, and IGF-binding protein-3 (IGFBP-3) were measured by ELISA. Crude and multivariable-adjusted geometric mean concentrations were computed for the hormones. Results: African-American neonates weighed less at birth (3,228 g vs. 3,424 g, p < 0.004) than whites. Birth weight was positively correlated with IGF-1, IGFBP-3, and the molar ratio of IGF-1 to IGFBP-3, but inversely correlated with the molar ratio of IGF-2 to IGFBP-3. Adjusted models showed higher testosterone (1.82 ng/ml vs. 1.47 ng/ml, p = 0.006) and the molar ratio of testosterone to SHBG (0.42 vs. 0.30, p = 0.03) in African-American compared to white female neonates. IGF-1, IGF-2, and IGFBP-3 were lower in African-American compared to white female neonates, but only the difference for IGF-2 remained significant (496.5 ng/ml vs. 539.2 ng/ml, p = 0.04). Conclusion: We provide evidence of racial variation in cord blood testosterone and testosterone to SHBG in African-American compared to white female neonates, and higher IGF-2 in white compared to African-American female neonates. Findings suggest plausible explanations for a prenatal influence on subsequent breast cancer risk and mortality. Further work is needed to confirm these observations. JF - Cancer Causes & Control AU - Agurs-Collins, Tanya AU - Rohrmann, Sabine AU - Sutcliffe, Catherine AU - Bienstock, Jessica L AU - Monsegue, Deborah AU - Akereyeni, Folasade AU - Bradwin, Gary AU - Rifai, Nader AU - Pollak, Michael N AU - Platz, Elizabeth A AD - Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD, USA, collinsta@mail.nih.gov Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 445 EP - 454 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 23 IS - 3 SN - 0957-5243, 0957-5243 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Mortality KW - Birth weight KW - Prenatal experience KW - Breast cancer KW - Neonates KW - Steroid hormones KW - Growth factors KW - Hormones KW - Ethnic groups KW - Cancer KW - Hospitals 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/954651107?accountid=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=Racial+variation+in+umbilical+cord+blood+sex+steroid+hormones+and+the+insulin-like+growth+factor+axis+in+African-American+and+white+female+neonates&rft.au=Agurs-Collins%2C+Tanya%3BRohrmann%2C+Sabine%3BSutcliffe%2C+Catherine%3BBienstock%2C+Jessica+L%3BMonsegue%2C+Deborah%3BAkereyeni%2C+Folasade%3BBradwin%2C+Gary%3BRifai%2C+Nader%3BPollak%2C+Michael+N%3BPlatz%2C+Elizabeth+A&rft.aulast=Agurs-Collins&rft.aufirst=Tanya&rft.date=2012-03-01&rft.volume=23&rft.issue=3&rft.spage=445&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-011-9893-6 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-03-01 N1 - Last updated - 2013-09-09 N1 - SubjectsTermNotLitGenreText - Birth weight; Mortality; Prenatal experience; Breast cancer; Growth factors; Steroid hormones; Neonates; Hormones; Cancer; Ethnic groups; Hospitals DO - http://dx.doi.org/10.1007/s10552-011-9893-6 ER - TY - JOUR T1 - Molecular basis of Staphylococcus epidermidis infections AN - 954650631; 16398595 AB - Staphylococcus epidermidis is the most important member of the coagulase-negative staphylococci and one of the most abundant colonizers of human skin. While for a long time regarded as innocuous, it has been identified as the most frequent cause of device-related infections occurring in the hospital setting and is therefore now recognized as an important opportunistic pathogen. S. epidermidis produces a series of molecules that provide protection from host defenses. Specifically, many proteins and exopolymers, such as the exopolysaccharide PIA, contribute to biofilm formation and inhibit phagocytosis and the activity of human antimicrobial peptides. Furthermore, recent research has identified a family of pro-inflammatory peptides in S. epidermidis, the phenol-soluble modulins (PSMs), which have multiple functions in immune evasion and biofilm development, and may be cytolytic. However, in accordance with the relatively benign relationship that S. epidermidis has with its host, production of aggressive members of the PSM family is kept at a low level. Interestingly, in contrast to S. aureus with its large arsenal of toxins developed for causing infection in the human host, most if not all "virulence factors" of S. epidermidis appear to have original functions in the commensal lifestyle of this bacterium. JF - Seminars in Immunopathology AU - Otto, Michael AD - Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, NIAID, NIH, 9000 Rockville Pike, Bethesda, MD, 20892, USA, motto@niaid.nih.gov Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 201 EP - 214 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 34 IS - 2 SN - 1863-2297, 1863-2297 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Antimicrobial peptides KW - Benign KW - Biofilms KW - Commensals KW - Hospitals KW - Infection KW - Inflammation KW - Opportunist infection KW - Pathogens KW - Phagocytosis KW - Skin KW - Toxins KW - exopolysaccharides KW - virulence factors KW - Staphylococcus aureus KW - Staphylococcus epidermidis KW - F 06960:Molecular Immunology KW - J 02350:Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/954650631?accountid=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=Seminars+in+Immunopathology&rft.atitle=Molecular+basis+of+Staphylococcus+epidermidis+infections&rft.au=Otto%2C+Michael&rft.aulast=Otto&rft.aufirst=Michael&rft.date=2012-03-01&rft.volume=34&rft.issue=2&rft.spage=201&rft.isbn=&rft.btitle=&rft.title=Seminars+in+Immunopathology&rft.issn=18632297&rft_id=info:doi/10.1007%2Fs00281-011-0296-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-03-01 N1 - Last updated - 2012-05-18 N1 - SubjectsTermNotLitGenreText - Skin; virulence factors; Commensals; Pathogens; Infection; exopolysaccharides; Toxins; Inflammation; Opportunist infection; Biofilms; Phagocytosis; Antimicrobial peptides; Hospitals; Benign; Staphylococcus aureus; Staphylococcus epidermidis DO - http://dx.doi.org/10.1007/s00281-011-0296-2 ER - TY - JOUR T1 - Neutrophils in innate host defense against Staphylococcus aureus infections AN - 954650628; 16398594 AB - Staphylococcus aureus has been an important human pathogen throughout history and is currently a leading cause of bacterial infections worldwide. S. aureus has the unique ability to cause a continuum of diseases, ranging from minor skin infections to fatal necrotizing pneumonia. Moreover, the emergence of highly virulent, drug-resistant strains such as methicillin-resistant S. aureus in both healthcare and community settings is a major therapeutic concern. Neutrophils are the most prominent cellular component of the innate immune system and provide an essential primary defense against bacterial pathogens such as S. aureus. Neutrophils are rapidly recruited to sites of infection where they bind and ingest invading S. aureus, and this process triggers potent oxidative and non-oxidative antimicrobial killing mechanisms that serve to limit pathogen survival and dissemination. S. aureus has evolved numerous mechanisms to evade host defense strategies employed by neutrophils, including the ability to modulate normal neutrophil turnover, a process critical to the resolution of acute inflammation. Here we provide an overview of the role of neutrophils in host defense against bacterial pathogens and discuss strategies employed by S. aureus to circumvent neutrophil function. JF - Seminars in Immunopathology AU - Rigby, Kevin M AU - DeLeo, Frank R AD - Laboratory of Human Pathogenesis, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 South 4th Street, Hamilton, MT, 59840, USA, fdeleo@niaid.nih.gov Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 237 EP - 259 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 34 IS - 2 SN - 1863-2297, 1863-2297 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Antimicrobial agents KW - Cell survival KW - Drug resistance KW - Immune system KW - Infection KW - Inflammation KW - Leukocytes (neutrophilic) KW - Pathogens KW - Pneumonia KW - Reviews KW - Staphylococcus aureus KW - J 02350:Immunology KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/954650628?accountid=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=Seminars+in+Immunopathology&rft.atitle=Neutrophils+in+innate+host+defense+against+Staphylococcus+aureus+infections&rft.au=Rigby%2C+Kevin+M%3BDeLeo%2C+Frank+R&rft.aulast=Rigby&rft.aufirst=Kevin&rft.date=2012-03-01&rft.volume=34&rft.issue=2&rft.spage=237&rft.isbn=&rft.btitle=&rft.title=Seminars+in+Immunopathology&rft.issn=18632297&rft_id=info:doi/10.1007%2Fs00281-011-0295-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-03-01 N1 - Last updated - 2012-05-18 N1 - SubjectsTermNotLitGenreText - Cell survival; Reviews; Immune system; Drug resistance; Leukocytes (neutrophilic); Pathogens; Infection; Pneumonia; Antimicrobial agents; Inflammation; Staphylococcus aureus DO - http://dx.doi.org/10.1007/s00281-011-0295-3 ER - TY - JOUR T1 - Unopposed estrogen and estrogen plus progestin menopausal hormone therapy and lung cancer risk in the NIH-AARP Diet and Health Study Cohort AN - 954641788; 16417606 AB - Purpose: Previous studies have reported that lung cancer risk may be decreased, increased, or unaffected by prior use of menopausal hormone therapy (MHT). Methods: To assess this issue further, we examined relationships among 118,008 women, ages 50-71 years who were recruited during 1995-1996 for the NIH-AARP Diet and Health Study and in whom 2,097 incident lung carcinomas were identified during follow-up through 2006. Multivariable Cox proportional hazards models estimated relative risks (RR) and 95% confidence intervals (CIs) associated with various measures of self-reported MHT use. Results: We found no evidence that either estrogen therapy (ET)-only or estrogen plus progestin therapy (EPT) use was substantially related to subsequent lung cancer risk (respective RRs and 95% CIs for ever use = 0.97, 0.86-1.09 and 1.03, 0.90-1.17). There were no significant variations according to currency or duration of use of either formulation, nor was there evidence that risks varied within subgroups defined by cigarette smoking or body size. The absence of effect was seen for nearly all lung cancer subtypes, with the exception of an increased risk of undifferentiated/large cell cancers associated with long-term ET-only use (p sub(trend) = 0.02), a relationship not observed among EPT users. Conclusions: Our results failed to support any substantial alterations in lung cancer risk associated with use of either unopposed estrogen or estrogen plus progestin MHT, even when detailed exposure measures and other risk predictors were considered. JF - Cancer Causes & Control AU - Brinton, Louise A AU - Schwartz, Lauren AU - Spitz, Margaret R AU - Park, Yikyung AU - Hollenbeck, Albert R AU - Gierach, Gretchen L AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 6120 Executive Blvd., Room 5018, Suite 550, Rockville, MD, 20852, USA, brinton@nih.gov Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 487 EP - 496 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 23 IS - 3 SN - 0957-5243, 0957-5243 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Age KW - Body size KW - Cancer KW - Cigarettes KW - Diets KW - Estrogens KW - Hormones KW - Lung cancer KW - body size KW - estrogens 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/954641788?accountid=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=Unopposed+estrogen+and+estrogen+plus+progestin+menopausal+hormone+therapy+and+lung+cancer+risk+in+the+NIH-AARP+Diet+and+Health+Study+Cohort&rft.au=Brinton%2C+Louise+A%3BSchwartz%2C+Lauren%3BSpitz%2C+Margaret+R%3BPark%2C+Yikyung%3BHollenbeck%2C+Albert+R%3BGierach%2C+Gretchen+L&rft.aulast=Brinton&rft.aufirst=Louise&rft.date=2012-03-01&rft.volume=23&rft.issue=3&rft.spage=487&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-9904-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-03-01 N1 - Last updated - 2012-08-10 N1 - SubjectsTermNotLitGenreText - Diets; Estrogens; Age; Cigarettes; Body size; body size; Hormones; Cancer; estrogens; Lung cancer DO - http://dx.doi.org/10.1007/s10552-012-9904-2 ER - TY - JOUR T1 - Physical activity, diabetes, and thyroid cancer risk: a pooled analysis of five prospective studies AN - 954641777; 16417604 AB - Purpose: Although many studies have linked obesity with increased risk of thyroid cancer, few have investigated the role of obesity-related lifestyle characteristics and medical conditions in the etiology of this disease. We examined the associations of self-reported physical activity and diabetes history with thyroid cancer risk in a large pooled analysis of prospective cohort studies. Methods: Data from five prospective studies in the U.S. (n = 362,342 men, 312,149 women) were coded using standardized exposure, covariate, and outcome definitions. Hazard ratios (HR) and 95% confidence intervals (CI) for thyroid cancer were estimated using age as the time metric and adjusting for sex, education, race, marital status, cigarette smoking, body mass index, alcohol intake, and cohort. Effect modification by other risk factors (e.g., age, sex, and body mass index) and differences by cancer subtype (e.g., papillary, follicular) were also examined. Results: Over follow-up (median = 10.5 years), 308 men and 510 women were diagnosed with a first primary thyroid cancer. Overall, subjects reporting the greatest amount of physical activity had an increased risk of the disease (HR = 1.18, 95% CI:1.00-1.39); however, this association was restricted to participants who were overweight/obese ( greater than or equal to 25 kg/m super(2); HR = 1.34, 95% CI:1.09-1.64) as opposed to normal-weight (<25 kg/m super(2); HR = 0.92, 95% CI:0.69-1.22; P-interaction = 0.03). We found no overall association between self-reported history of diabetes and thyroid cancer risk (HR = 1.08, 95% CI:0.83-1.40). Conclusion: Neither physical inactivity nor diabetes history was associated with increased risk of thyroid cancer. While it may have been a chance finding, the possible increased risk associated with greater physical activity warrants further investigation. JF - Cancer Causes & Control AU - Kitahara, Cari M AU - Platz, Elizabeth A AU - Beane Freeman, Laura E AU - Black, Amanda AU - Hsing, Ann W AU - Linet, Martha S AU - Park, Yikyung 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 - 2012/03// PY - 2012 DA - Mar 2012 SP - 463 EP - 471 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 23 IS - 3 SN - 0957-5243, 0957-5243 KW - Physical Education Index; Risk Abstracts; Health & Safety Science Abstracts KW - Historical account KW - Alcohol KW - Obesity KW - Age KW - Cigarettes KW - Men KW - Body mass KW - Women KW - Thyroid KW - Exercise KW - Cancer KW - Diabetes KW - USA KW - diabetes mellitus KW - body mass KW - Analysis KW - Diseases KW - physical activity KW - H 11000:Diseases/Injuries/Trauma KW - R2 23060:Medical and environmental health KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/954641777?accountid=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=Physical+activity%2C+diabetes%2C+and+thyroid+cancer+risk%3A+a+pooled+analysis+of+five+prospective+studies&rft.au=Kitahara%2C+Cari+M%3BPlatz%2C+Elizabeth+A%3BBeane+Freeman%2C+Laura+E%3BBlack%2C+Amanda%3BHsing%2C+Ann+W%3BLinet%2C+Martha+S%3BPark%2C+Yikyung%3BSchairer%2C+Catherine%3BBerrington+de+Gonzalez%2C+Amy&rft.aulast=Kitahara&rft.aufirst=Cari&rft.date=2012-03-01&rft.volume=23&rft.issue=3&rft.spage=463&rft.isbn=&rft.btitle=&rft.title=Cancer+Causes+%26+Control&rft.issn=09575243&rft_id=info:doi/10.1007%2Fs10552-012-9896-y LA - English DB - Physical Education Index; ProQuest Environmental Science Collection N1 - Date revised - 2012-03-01 N1 - Last updated - 2013-11-15 N1 - SubjectsTermNotLitGenreText - Obesity; Men; Body mass; Analysis; Women; Diseases; Exercise; Cancer; Diabetes; Alcohol; Historical account; Age; diabetes mellitus; Cigarettes; body mass; Thyroid; physical activity; USA DO - http://dx.doi.org/10.1007/s10552-012-9896-y ER - TY - JOUR T1 - Psychiatric comorbidity and the persistence of drug use disorders in the United States AN - 928988928; 4279041 AB - Aims DSM-IV drug use disorders, a major public health problem, are highly comorbid with other psychiatric disorders, but little is known about the role of this comorbidity when studied prospectively in the general population. Our aims were to determine the role of comorbid psychopathology in the 3-year persistence of drug use disorders. Design and setting Secondary data analysis using waves 1 (2001–02) and 2 (2005–05) of the National Epidemiologic Survey on Alcohol and Related Conditions. Participants Respondents with current DSM-IV drug use disorder at wave 1 who participated in wave 2 (n = 613). Measurements Alcohol Use Disorders and Associated Disabilities Interview Schedule IV (AUDADIS-IV) obtained DSM-IV Axis I and II diagnoses. Persistent drug use disorder was defined as meeting full criteria for any drug use disorder between waves 1 and 2. Findings Drug use disorders persisted in 30.9% of respondents. No Axis I disorders predicted persistence. Antisocial [odds ratio (OR) = 2.75; 95% confidence interval (CI): 1.27–5.99], borderline (OR = 1.91; 95% CI: 1.06–3.45) and schizotypal (OR = 2.77; 95% CI: 1.42–5.39) personality disorders were significant predictors of persistent drug use disorders, controlling for demographics, psychiatric comorbidity, family history, treatment and number of drug use disorders. Deceitfulness and lack of remorse were the strongest antisocial criteria predictors of drug use disorder persistence, identity disturbance and self-damaging impulsivity were the strongest borderline criteria predictors, and ideas of reference and social anxiety were the strongest schizotypal criteria predictors. Conclusions Antisocial, borderline and schizotypal personality disorders are specific predictors of drug use disorder persistence over a 3-year period. Reprinted by permission of Blackwell Publishing JF - Addiction AU - Hasin, Deborah S AU - Fenton, Miriam C AU - Keyes, Katherine AU - Geier, Timothy AU - Greenstein, Eliana AU - Skodol, Andrew AU - Krueger, Bob AU - Grant, Bridget F AD - Columbia University ; New York State Psychiatric Institute ; University of Wisconsin, Madison ; University of Minnesota ; University of Arizona ; National Institute on Alcohol Abuse and Alcoholism, Rockville Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 599 EP - 609 VL - 107 IS - 3 SN - 0965-2140, 0965-2140 KW - Sociology KW - Alcohol KW - Drug use KW - Family history KW - Interviews KW - U.S.A. KW - Psychiatry KW - Deceit KW - Personality disorders UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/928988928?accountid=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=Psychiatric+comorbidity+and+the+persistence+of+drug+use+disorders+in+the+United+States&rft.au=Hasin%2C+Deborah+S%3BFenton%2C+Miriam+C%3BKeyes%2C+Katherine%3BGeier%2C+Timothy%3BGreenstein%2C+Eliana%3BSkodol%2C+Andrew%3BKrueger%2C+Bob%3BGrant%2C+Bridget+F&rft.aulast=Hasin&rft.aufirst=Deborah&rft.date=2012-03-01&rft.volume=107&rft.issue=3&rft.spage=599&rft.isbn=&rft.btitle=&rft.title=Addiction&rft.issn=09652140&rft_id=info:doi/10.1111%2Fj.1360-0443.2011.03638.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 - 909; 10391; 6832 10919; 4767 5889; 3753 3755; 9423 10412 7951 6220 7954; 3315; 433 293 14 DO - http://dx.doi.org/10.1111/j.1360-0443.2011.03638.x ER - TY - JOUR T1 - super(18)F-radiolabeled analogs of exendin-4 for PET imaging of GLP-1 in insulinoma AN - 926905216; 16335077 AB - Purpose: Glucagon-like peptide type 1 (GLP-1) is an incretin peptide that augments glucose-stimulated insulin release following oral consumption of nutrients. Its message is transmitted via a G protein-coupled receptor called GLP-1R, which is colocalized with pancreatic beta -cells. The GLP-1 system is responsible for enhancing insulin release, inhibiting glucagon production, inhibiting hepatic gluconeogenesis, inhibiting gastric mobility, and suppression of appetite. The abundance of GLP-1R in pancreatic beta -cells in insulinoma, a cancer of the pancreas, and the activity of GLP-1 in the cardiovascular system have made GLP-1R a target for molecular imaging. Methods: We prepared super(18)F radioligands for GLP-1R by the reaction of [ super(18)F]FBEM, a maleimide prosthetic group, with [Cys super(0)] and [Cys super(40)] analogs of exendin-4. The binding affinity, cellular uptake and internalization, in vitro stability, and uptake and specificity of uptake of the resulting compounds were determined in an INS-1 xenograft model in nude mice. Results: The [ super(18)F]FBEM-[Cys super(x)]-exendin-4 analogs were obtained in good yield (34.3 plus or minus 3.4%, n=11), based on the starting compound [ super(18)F]FBEM), and had a specific activity of 45.51 plus or minus 16.28 GBq/ mu mol (1.23 plus or minus 0.44 Ci/ mu mol, n=7) at the end of synthesis. The C-terminal isomer, [ super(18)F]FBEM-[Cys super(40)]-exendin-4, had higher affinity for INS-1 tumor cells (IC sub(50) 1.11 plus or minus 0.057 nM) and higher tumor uptake (25.25 plus or minus 3.39 %ID/g at 1 h) than the N-terminal isomer, [ super(18)F]FBEM-[Cys super(0)]-exendin-4 (IC sub(50) 2.99 plus or minus 0.06 nM, uptake 7.20 plus or minus 1.26 %ID/g at 1 h). Uptake of both isomers into INS-1 tumor, pancreas, stomach, and lung could be blocked by preinjection of nonradiolabeled [Cys super(x)]-exendin-4 (p<0.05). Conclusion: [ super(18)F]FBEM-[Cys super(40)]-exendin-4 and [ super(18)F]FBEM-[Cys super(0)]-exendin-4 have high affinity for GLP-1R and display similar in vitro cell internalization. The higher uptake into INS-1 xenograft tumors exhibited by [ super(18)F]FBEM-[Cys super(40)]-exendin-4 suggests that this compound would be the better tracer for imaging GLP-1R. JF - European Journal of Nuclear Medicine and Molecular Imaging AU - Kiesewetter, Dale O AU - Gao, Haokao AU - Ma, Ying AU - Niu, Gang AU - Quan, Qimeng AU - Guo, Ning AU - Chen, Xiaoyuan AD - Laboratory of Molecular Imaging and Nanomedicine (LOMIN), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institutes of Health (NIH), 31 Center Drive, Suite 1 C14, Bethesda, MD, 20892, USA, shawn.chen@nih.gov Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 463 EP - 473 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 39 IS - 3 SN - 1619-7070, 1619-7070 KW - Biotechnology and Bioengineering Abstracts KW - Beta cells KW - Cancer KW - Cardiovascular system KW - G protein-coupled receptors KW - Glucagon KW - Insulin KW - Insulinoma KW - Isomers KW - Lung KW - Mobility KW - Nuclear medicine KW - Nutrients KW - Pancreas KW - Pancreatic cancer KW - Radioisotopes KW - Tumor cells KW - Tumors KW - Xenografts KW - imaging KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/926905216?accountid=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=super%2818%29F-radiolabeled+analogs+of+exendin-4+for+PET+imaging+of+GLP-1+in+insulinoma&rft.au=Kiesewetter%2C+Dale+O%3BGao%2C+Haokao%3BMa%2C+Ying%3BNiu%2C+Gang%3BQuan%2C+Qimeng%3BGuo%2C+Ning%3BChen%2C+Xiaoyuan&rft.aulast=Kiesewetter&rft.aufirst=Dale&rft.date=2012-03-01&rft.volume=39&rft.issue=3&rft.spage=463&rft.isbn=&rft.btitle=&rft.title=European+Journal+of+Nuclear+Medicine+and+Molecular+Imaging&rft.issn=16197070&rft_id=info:doi/10.1007%2Fs00259-011-1980-0 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-03-01 N1 - Last updated - 2012-05-18 N1 - SubjectsTermNotLitGenreText - Cardiovascular system; Mobility; Pancreas; Glucagon; Insulinoma; Pancreatic cancer; Beta cells; Nutrients; Tumors; imaging; Tumor cells; Cancer; Insulin; Isomers; G protein-coupled receptors; Lung; Radioisotopes; Nuclear medicine; Xenografts DO - http://dx.doi.org/10.1007/s00259-011-1980-0 ER - TY - JOUR T1 - Growth rate regulation in Escherichia coli AN - 926904380; 16384322 AB - Growth rate regulation in bacteria has been an important issue in bacterial physiology for the past 50 years. This review, using Escherichia coli as a paradigm, summarizes the mechanisms for the regulation of rRNA synthesis in the context of systems biology, particularly, in the context of genome-wide competition for limited RNA polymerase (RNAP) in the cell under different growth conditions including nutrient starvation. The specific location of the seven rrn operons in the chromosome and the unique properties of the rrn promoters contribute to growth rate regulation. The length of the rrn transcripts, coupled with gene dosage effects, influence the distribution of RNAP on the chromosome in response to growth rate. Regulation of rRNA synthesis depends on multiple factors that affect the structure of the nucleoid and the allocation of RNAP for global gene expression. The magic spot ppGpp, which acts with DksA synergistically, is a key effector in both the growth rate regulation and the stringent response induced by nutrient starvation, mainly because the ppGpp level changes in response to environmental cues. It regulates rRNA synthesis via a cascade of events including both transcription initiation and elongation, and can be explained by an RNAP redistribution (allocation) model. Using E. coli as a paradigm, this review summarizes the research on the growth regulation in the past 50 years, with a focus on the regulation of rRNA in the context of genome-wide competition for limited RNA polymerase in the cell under different growth conditions. JF - FEMS Microbiology Reviews AU - Jin, Ding Jun AU - Cagliero, Cedric AU - Zhou, Yan Ning AD - Transcription Control Section, Gene Regulation and Chromosome Biology Laboratory, National Cancer Institute-Frederick, National Institutes of Health, Frederick, MD, USA Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 269 EP - 287 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 36 IS - 2 SN - 0168-6445, 0168-6445 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology KW - Chromosomes KW - DNA-directed RNA polymerase KW - Elongation KW - Gene dosage KW - Gene expression KW - Growth conditions KW - Growth rate KW - Nucleoids KW - Nutrients KW - Operons KW - Promoters KW - Starvation KW - Stringent response KW - Transcription initiation KW - rRNA KW - Escherichia coli KW - A 01450:Environmental Pollution & Waste Treatment KW - J 02320:Cell Biology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/926904380?accountid=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=FEMS+Microbiology+Reviews&rft.atitle=Growth+rate+regulation+in+Escherichia+coli&rft.au=Jin%2C+Ding+Jun%3BCagliero%2C+Cedric%3BZhou%2C+Yan+Ning&rft.aulast=Jin&rft.aufirst=Ding&rft.date=2012-03-01&rft.volume=36&rft.issue=2&rft.spage=269&rft.isbn=&rft.btitle=&rft.title=FEMS+Microbiology+Reviews&rft.issn=01686445&rft_id=info:doi/10.1111%2Fj.1574-6976.2011.00279.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-03-01 N1 - Document feature - figure 4 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Stringent response; Growth rate; Starvation; Growth conditions; Nutrients; Transcription initiation; Gene expression; rRNA; Elongation; Promoters; Chromosomes; DNA-directed RNA polymerase; Gene dosage; Nucleoids; Operons; Escherichia coli DO - http://dx.doi.org/10.1111/j.1574-6976.2011.00279.x ER - TY - JOUR T1 - Elevated temperature impairs onset of symbiosis and reduces survivorship in larvae of the Hawaiian coral, Fungia scutaria AN - 926903589; 16381765 AB - Many corals obtain their obligate intracellular dinoflagellate symbionts from the environment as larvae or juveniles. The process of symbiont acquisition remains largely unexplored, especially under stress. This study addressed both the ability of Fungia scutaria (Lamarck 1801) larvae to establish symbiosis with Symbiodinium sp. C1f while exposed to elevated temperature and the survivorship of aposymbiotic and newly symbiotic larvae under these conditions. Larvae were exposed to 27, 29, or 31 degree C for 1 h prior to infection, throughout a 3-h infection period, and up to 72 h following infection. Exposure to elevated temperatures impaired the ability of coral larvae to establish symbiosis and reduced larval survivorship. At 31 degree C, the presence of symbionts further reduced larval survivorship. As sea surface temperatures rise, coral larvae exposed to elevated temperatures during symbiosis onset will likely be negatively impacted, which in turn could affect the establishment of future generations of corals. JF - Marine Biology AU - Schnitzler, CE AU - Hollingsworth, L L AU - Krupp, DA AU - Weis, V M AD - Department of Zoology, Oregon State University, Corvallis, OR, 97331, USA, christine.schnitzler@nih.gov Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 633 EP - 642 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 159 IS - 3 SN - 0025-3162, 0025-3162 KW - Ecology Abstracts; Oceanic Abstracts; ASFA 1: Biological Sciences & Living Resources KW - Temperature effects KW - Marine KW - Symbiodinium KW - Symbionts KW - Symbiosis KW - Larvae KW - Survival KW - Stress KW - Phytoplankton KW - Infection KW - Fungia scutaria KW - Dinoflagellates KW - Coral KW - Survivorship KW - Corals KW - D 04040:Ecosystem and Ecology Studies KW - Q1 08422:Environmental effects KW - O 4060:Pollution - Environment UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/926903589?accountid=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=Marine+Biology&rft.atitle=Elevated+temperature+impairs+onset+of+symbiosis+and+reduces+survivorship+in+larvae+of+the+Hawaiian+coral%2C+Fungia+scutaria&rft.au=Schnitzler%2C+CE%3BHollingsworth%2C+L+L%3BKrupp%2C+DA%3BWeis%2C+V+M&rft.aulast=Schnitzler&rft.aufirst=CE&rft.date=2012-03-01&rft.volume=159&rft.issue=3&rft.spage=633&rft.isbn=&rft.btitle=&rft.title=Marine+Biology&rft.issn=00253162&rft_id=info:doi/10.1007%2Fs00227-011-1842-0 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-03-01 N1 - Last updated - 2016-03-30 N1 - SubjectsTermNotLitGenreText - Symbiosis; Symbionts; Larvae; Coral; Phytoplankton; Survivorship; Temperature effects; Dinoflagellates; Stress; Survival; Corals; Infection; Fungia scutaria; Symbiodinium; Marine DO - http://dx.doi.org/10.1007/s00227-011-1842-0 ER - TY - JOUR T1 - Common genetic variation in the indoleamine-2,3-dioxygenase genes and antidepressant treatment outcome in major depressive disorder. AN - 926155053; 22282879 AB - The essential amino acid tryptophan is the precursor to serotonin, but it can also be metabolized into kynurenine through indoleamine-2,3-dioxygenase (IDO). Increased immune activation has long been associated with symptoms of depression and has been shown to upregulate the expression of IDO. The presence of additional IDO directs more tryptophan down the kynurenine pathway, leaving less available for synthesis of serotonin and its metabolites. Kynurenine can be metabolized through a series of enzymes to quinolinic acid, a potent N-methyl-D-aspartate receptor agonist with demonstrated neurotoxic effects. We tested the hypothesis that IDO plays a role in outcome of treatment with the selective serotonin reuptake inhibitor, citalopram. Patients consisted of 1953 participants enrolled in the Sequenced Treatment Alternatives to Relieve Depression study (STAR*D). Genotypes corresponding to 94 single nucleotide polymorphisms (SNPs) in the genes IDO1 and IDO2, which encode IDO and IDO2, were extracted from a larger genome-wide set and analyzed using single marker tests to look for association with previously defined response, remission and QIDS-C score change phenotypes, with adequate correction for racial stratification and multiple testing. One SNP, rs2929115, showed evidence of association with citalopram response (OR = 0.64, p = 0.0005) after experiment-wide correction for multiple testing. Another closely associated marker, rs2929116 (OR = 0.64, p = 0.0006) had an experiment-wide significant result. Both implicated SNPs are located between 26 kb and 28 kb downstream of IDO2. We conclude that common genetic variation in IDO1 and IDO2 may play a role in antidepressant treatment outcome. These results are modest in a genome-wide context and need to be replicated in an independent sample. JF - Journal of psychopharmacology (Oxford, England) AU - Cutler, Jessica A AU - Rush, A John AU - McMahon, Francis J AU - Laje, Gonzalo AD - Genetic Basis of Mood and Anxiety Disorders Unit, National Institute of Mental Health, Bethesda, MD 20892-3719, USA. Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 360 EP - 367 VL - 26 IS - 3 KW - 3' Untranslated Regions KW - 0 KW - Antidepressive Agents KW - Indoleamine-Pyrrole 2,3,-Dioxygenase KW - Isoenzymes KW - Serotonin Uptake Inhibitors KW - Citalopram KW - 0DHU5B8D6V KW - Index Medicus KW - United States KW - Young Adult KW - Psychiatric Status Rating Scales KW - Humans KW - Adult KW - Genetic Association Studies KW - Drug Resistance KW - Aged KW - Middle Aged KW - Adolescent KW - Isoenzymes -- genetics KW - Isoenzymes -- metabolism KW - Diagnostic and Statistical Manual of Mental Disorders KW - Remission Induction KW - Citalopram -- therapeutic use KW - Polymorphism, Single Nucleotide KW - Depressive Disorder, Major -- drug therapy KW - Depressive Disorder, Major -- metabolism KW - Serotonin Uptake Inhibitors -- therapeutic use KW - Depressive Disorder, Major -- psychology KW - Antidepressive Agents -- therapeutic use KW - Indoleamine-Pyrrole 2,3,-Dioxygenase -- metabolism KW - Depressive Disorder, Major -- genetics KW - Indoleamine-Pyrrole 2,3,-Dioxygenase -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/926155053?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+psychopharmacology+%28Oxford%2C+England%29&rft.atitle=Common+genetic+variation+in+the+indoleamine-2%2C3-dioxygenase+genes+and+antidepressant+treatment+outcome+in+major+depressive+disorder.&rft.au=Cutler%2C+Jessica+A%3BRush%2C+A+John%3BMcMahon%2C+Francis+J%3BLaje%2C+Gonzalo&rft.aulast=Cutler&rft.aufirst=Jessica&rft.date=2012-03-01&rft.volume=26&rft.issue=3&rft.spage=360&rft.isbn=&rft.btitle=&rft.title=Journal+of+psychopharmacology+%28Oxford%2C+England%29&rft.issn=1461-7285&rft_id=info:doi/10.1177%2F0269881111434622 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-03 N1 - Date created - 2012-03-01 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1177/0269881111434622 ER - TY - JOUR T1 - Prolonged remission after long-term treatment with steroidogenesis inhibitors in Cushing's syndrome caused by ectopic ACTH secretion. AN - 925717026; 22190002 AB - Spontaneous remission is rare in ectopic ACTH syndrome (EAS). We describe four patients with presumed EAS in whom long-term treatment with steroidogenesis inhibitors was followed by prolonged remission of hypercortisolemia. Biochemical testing was consistent with EAS, but imaging failed to identify a tumor. Patients were treated with ketoconazole alone or with mitotane and/or metyrapone to control hypercortisolemia. Dexamethasone was added when a block and replace strategy was used. Treatment with steroidogenesis inhibitors for 3-10 years in these patients was followed by a prolonged period of remission (15-60 months). During remission, the first patient had an elevated ACTH, low cortisol and 24-h urinary free cortisol (UFC), and adrenal atrophy on computerized tomography scan during remission, suggesting a direct toxic effect on the adrenal glands. Cases 2 and 3 had normal to low ACTH levels and low-normal UFC, consistent with an effect at the level of the ectopic tumor. They did not have a history of cyclicity and case 3 has been in remission for ~5 years, making cyclic Cushing's syndrome less likely. Case 4, with a history of cyclic hypercortisolism, had normal to slightly elevated ACTH levels and low-normal UFC during remission. The most likely etiology of remission is cyclic production of ACTH by the ectopic tumor. Spontaneous and sustained remission of hypercortisolemia is possible in EAS after long-term treatment with steroidogenesis inhibitors; a drug holiday may be warranted during chronic therapy to evaluate this. The pathophysiology remains unclear but may involve several different mechanisms. JF - European journal of endocrinology AU - Sharma, S T AU - Nieman, L K AD - Program in Reproductive and Adult Endocrinology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Building 10, CRC, 1 East, Rm 3140, Bethesda, Maryland 20892-1109, USA. sharmast@mail.nih.gov Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 531 EP - 536 VL - 166 IS - 3 KW - Hormone Antagonists KW - 0 KW - Steroids KW - Index Medicus KW - Humans KW - Adult KW - Treatment Outcome KW - Middle Aged KW - Time Factors KW - Male KW - Female KW - Remission Induction KW - Steroids -- biosynthesis KW - ACTH Syndrome, Ectopic -- blood KW - Hormone Antagonists -- therapeutic use KW - Cushing Syndrome -- blood KW - Cushing Syndrome -- drug therapy KW - Steroids -- antagonists & inhibitors KW - ACTH Syndrome, Ectopic -- drug therapy KW - Hormone Antagonists -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/925717026?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+endocrinology&rft.atitle=Prolonged+remission+after+long-term+treatment+with+steroidogenesis+inhibitors+in+Cushing%27s+syndrome+caused+by+ectopic+ACTH+secretion.&rft.au=Sharma%2C+S+T%3BNieman%2C+L+K&rft.aulast=Sharma&rft.aufirst=S&rft.date=2012-03-01&rft.volume=166&rft.issue=3&rft.spage=531&rft.isbn=&rft.btitle=&rft.title=European+journal+of+endocrinology&rft.issn=1479-683X&rft_id=info:doi/10.1530%2FEJE-11-0949 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-04-20 N1 - Date created - 2012-02-29 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Eur J Endocrinol. 1996 Oct;135(4):440-3 [8921826] Arch Intern Med. 1993 Jan 25;153(2):251-5 [8422213] Horm Res. 2007;67(5):257-62 [17220632] Eur J Endocrinol. 2007 Sep;157(3):245-54 [17766705] Eur J Endocrinol. 2009 Jun;160(6):1011-8 [19289537] Expert Opin Emerg Drugs. 2009 Dec;14(4):661-71 [19939210] J Clin Endocrinol Metab. 2010 Mar;95(3):1207-19 [20089611] J Clin Endocrinol Metab. 2011 Sep;96(9):2796-804 [21752886] Pituitary. 2002;5(2):77-82 [12675504] J Endocrinol. 2003 Jun;177(3):365-72 [12773116] Endocr Pract. 2003 Mar-Apr;9(2):147-51 [12917078] Pituitary. 2003;6(3):119-26 [14971736] Am J Med. 1966 Oct;41(4):581-92 [5923599] N Engl J Med. 1975 Oct 30;293(18):893-6 [1177986] Lancet. 1977 May 28;1(8022):1148-9 [68240] Clin Endocrinol (Oxf). 1981 May;14(5):485-92 [6273022] J Clin Invest. 1985 Nov;76(5):1892-8 [2997296] J Clin Pathol. 1986 Sep;39(9):955-60 [3020095] Arch Intern Med. 1991 Jan;151(1):185-9 [1985595] Acta Endocrinol (Copenh). 1991 Sep;125(3):331-4 [1659100] Pituitary. 2004;7(1):45-9 [15638298] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1530/EJE-11-0949 ER - TY - JOUR T1 - A gynecologic oncology group phase II trial of two p53 peptide vaccine approaches: subcutaneous injection and intravenous pulsed dendritic cells in high recurrence risk ovarian cancer patients. AN - 923576327; 21927947 AB - Peptide antigens have been administered by different approaches as cancer vaccine therapy, including direct injection or pulsed onto dendritic cells; however, the optimal delivery method is still debatable. In this study, we describe the immune response elicited by two vaccine approaches using the wild-type (wt) p53 vaccine. Twenty-one HLA-A2.1 patients with stage III, IV, or recurrent ovarian cancer overexpressing the p53 protein with no evidence of disease were treated in two cohorts. Arm A received SC wt p53:264-272 peptide admixed with Montanide and GM-CSF. Arm B received wt p53:264-272 peptide-pulsed dendritic cells IV. Interleukin-2 (IL-2) was administered to both cohorts in alternative cycles. Nine of 13 patients (69%) in arm A and 5 of 6 patients (83%) in arm B developed an immunologic response as determined by ELISPOT and tetramer assays. The vaccine caused no serious systemic side effects. IL-2 administration resulted in grade 3 and 4 toxicities in both arms and directly induced the expansion of T regulatory cells. The median overall survival was 40.8 and 29.6 months for arm A and B, respectively; the median progression-free survival was 4.2 and. 8.7 months, respectively. We found that using either vaccination approach generates comparable specific immune responses against the p53 peptide with minimal toxicity. Accordingly, our findings suggest that the use of less demanding SC approach may be as effective. Furthermore, the use of low-dose SC IL-2 as an adjuvant might have interfered with the immune response. Therefore, it may not be needed in future trials. JF - Cancer immunology, immunotherapy : CII AU - Rahma, Osama E AU - Ashtar, Ed AU - Czystowska, Malgorzata AU - Szajnik, Marta E AU - Wieckowski, Eva AU - Bernstein, Sarah AU - Herrin, Vincent E AU - Shams, Mortada A AU - Steinberg, Seth M AU - Merino, Maria AU - Gooding, William AU - Visus, Carmen AU - Deleo, Albert B AU - Wolf, Judith K AU - Bell, Jeffrey G AU - Berzofsky, Jay A AU - Whiteside, Theresa L AU - Khleif, Samir N AD - Vaccine Branch, CCR, NCI, 41 Medlars Dr., Building 41 Room B900, Bethesda, MD 20892, USA. Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 373 EP - 384 VL - 61 IS - 3 KW - Cancer Vaccines KW - 0 KW - HLA-A2 Antigen KW - Interleukin-2 KW - Tumor Suppressor Protein p53 KW - Vaccines, Subunit KW - Granulocyte-Macrophage Colony-Stimulating Factor KW - 83869-56-1 KW - Index Medicus KW - Cancer Vaccines -- administration & dosage KW - Interleukin-2 -- administration & dosage KW - Interleukin-2 -- adverse effects KW - Cancer Vaccines -- adverse effects KW - Humans KW - Aged KW - Granulocyte-Macrophage Colony-Stimulating Factor -- administration & dosage KW - Cancer Vaccines -- immunology KW - HLA-A2 Antigen -- immunology KW - Adult KW - Treatment Outcome KW - Injections, Subcutaneous KW - Fatigue -- etiology KW - T-Lymphocytes -- drug effects KW - T-Lymphocytes -- immunology KW - Granulocyte-Macrophage Colony-Stimulating Factor -- immunology KW - Vaccination -- methods KW - Injections, Intravenous KW - Combined Modality Therapy KW - Lymphopenia -- etiology KW - Kaplan-Meier Estimate KW - T-Lymphocytes -- metabolism KW - Risk Factors KW - Cohort Studies KW - Interleukin-2 -- immunology KW - Middle Aged KW - Vaccination -- adverse effects KW - Neoplasm Recurrence, Local KW - Female KW - Dendritic Cells -- immunology KW - Ovarian Neoplasms -- pathology KW - Vaccines, Subunit -- administration & dosage KW - Vaccines, Subunit -- immunology KW - Dendritic Cells -- transplantation KW - Tumor Suppressor Protein p53 -- immunology KW - Ovarian Neoplasms -- therapy KW - Vaccines, Subunit -- adverse effects KW - Ovarian Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/923576327?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+immunology%2C+immunotherapy+%3A+CII&rft.atitle=A+gynecologic+oncology+group+phase+II+trial+of+two+p53+peptide+vaccine+approaches%3A+subcutaneous+injection+and+intravenous+pulsed+dendritic+cells+in+high+recurrence+risk+ovarian+cancer+patients.&rft.au=Rahma%2C+Osama+E%3BAshtar%2C+Ed%3BCzystowska%2C+Malgorzata%3BSzajnik%2C+Marta+E%3BWieckowski%2C+Eva%3BBernstein%2C+Sarah%3BHerrin%2C+Vincent+E%3BShams%2C+Mortada+A%3BSteinberg%2C+Seth+M%3BMerino%2C+Maria%3BGooding%2C+William%3BVisus%2C+Carmen%3BDeleo%2C+Albert+B%3BWolf%2C+Judith+K%3BBell%2C+Jeffrey+G%3BBerzofsky%2C+Jay+A%3BWhiteside%2C+Theresa+L%3BKhleif%2C+Samir+N&rft.aulast=Rahma&rft.aufirst=Osama&rft.date=2012-03-01&rft.volume=61&rft.issue=3&rft.spage=373&rft.isbn=&rft.btitle=&rft.title=Cancer+immunology%2C+immunotherapy+%3A+CII&rft.issn=1432-0851&rft_id=info:doi/10.1007%2Fs00262-011-1100-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-11 N1 - Date created - 2012-02-23 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Cell Mol Med. 2008 Apr;12(2):690-700 [18419605] Clin Cancer Res. 2007 Nov 1;13(21):6301-11 [17975141] Cancer Immunol Immunother. 2008 Sep;57(9):1413-20 [18297281] Expert Rev Vaccines. 2008 Sep;7(7):1031-40 [18767952] Br J Dermatol. 2008 Sep;159(3):606-14 [18616776] Int J Oncol. 2009 Sep;35(3):569-81 [19639177] Int J Oncol. 2001 Mar;18(3):475-8 [11179474] J Clin Oncol. 2001 Mar 15;19(6):1848-54 [11251017] J Exp Med. 2001 Jan 15;193(2):233-8 [11208863] J Exp Med. 2001 Jan 15;193(2):F5-9 [11208869] Immunity. 2001 Apr;14(4):357-68 [11336681] Int J Cancer. 2001 Jul 15;93(2):243-51 [11410873] J Clin Invest. 2002 Feb;109(3):409-17 [11828001] Cancer. 2003 Jan 1;97(1):186-200 [12491520] Curr Opin Immunol. 2003 Apr;15(2):138-47 [12633662] Cancer Res. 2003 May 1;63(9):2127-33 [12727829] J Immunother. 2003 Jul-Aug;26(4):349-56 [12843797] Blood. 2003 Oct 1;102(7):2338-44 [12714511] J Clin Oncol. 2003 Oct 15;21(20):3826-35 [14551301] J Clin Oncol. 2003 Nov 1;21(21):4016-26 [14581425] Br J Cancer. 2004 Feb 23;90(4):773-80 [14970852] Cancer Immunol Immunother. 2004 Jul;53(7):633-41 [14985857] Proc Natl Acad Sci U S A. 1993 Apr 15;90(8):3539-43 [8097319] Int Immunol. 1993 Aug;5(8):849-57 [8398980] Cell Immunol. 1996 May 25;170(1):101-10 [8665590] Cell Immunol. 1996 May 25;170(1):111-9 [8665591] Nat Med. 1998 Mar;4(3):321-7 [9500606] Clin Cancer Res. 1997 Mar;3(3):483-90 [9815709] J Immunother. 1999 Mar;22(2):155-65 [10093040] J Clin Oncol. 2004 Nov 15;22(22):4474-85 [15542798] Nat Med. 2004 Dec;10(12):1359-65 [15568033] J Immunol. 2005 Mar 15;174(6):3798-807 [15749921] Nat Biotechnol. 2005 Nov;23(11):1407-13 [16258544] Clin Exp Immunol. 2005 Dec;142(3):555-68 [16297169] J Clin Invest. 2005 Dec;115(12):3623-33 [16308572] Eur J Med Res. 2006 Jan 31;11(1):7-12 [16504954] Ann Oncol. 2006 Apr;17(4):563-70 [16418308] Int J Cancer. 2006 Jun 15;118(12):3022-9 [16425257] Ann Oncol. 2006 Jun;17(6):974-80 [16600979] Am J Clin Oncol. 2006 Aug;29(4):352-60 [16891861] J Clin Invest. 2007 May;117(5):1195-203 [17476349] Cancer Immunol Immunother. 2007 Sep;56(9):1485-99 [17285289] Vaccine. 2007 Aug 1;25(31):5882-91 [17602804] Clin Immunol. 2007 Oct;125(1):43-51 [17631051] Clin Cancer Res. 2008 Jun 15;14(12):3706-15 [18559587] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s00262-011-1100-9 ER - TY - JOUR T1 - Thiazolidinedione treatment decreases oxidative stress in spontaneously hypertensive heart failure rats through attenuation of inducible nitric oxide synthase-mediated lipid radical formation. AN - 923189886; 22315311 AB - The current study was designed to test the hypothesis that inducible nitric oxide synthase (iNOS)-mediated lipid free radical overproduction exists in an insulin-resistant rat model and that reducing the accumulation of toxic metabolites is associated with improved insulin signaling and metabolic response. Lipid radical formation was detected by electron paramagnetic resonance spectroscopy with in vivo spin trapping in an obese rat model, with or without thiazolidinedione treatment. Lipid radical formation was accompanied by accumulation of toxic end products in the liver, such as 4-hydroxynonenal and nitrotyrosine, and was inhibited by the administration of the selective iNOS inhibitor 1400 W. The model showed impaired phosphorylation of the insulin signaling pathway. Ten-day rosiglitazone injection not only improved the response to an oral glucose tolerance test and corrected insulin signaling but also decreased iNOS levels. Similar to the results with specific iNOS inhibition, thiazolidinedione dramatically decreased lipid radical formation. We demonstrate a novel mechanism where a thiazolidinedione treatment can reduce oxidative stress in this model through reducing iNOS-derived lipid radical formation. Our results suggest that hepatic iNOS expression may underlie the accumulation of lipid end products and that reducing the accumulation of toxic lipid metabolites contributes to a better redox status in insulin-sensitive tissues. JF - Diabetes AU - Kadiiska, Maria B AU - Bonini, Marcelo G AU - Ruggiero, Christine AU - Cleland, Ellen AU - Wicks, Shawna AU - Stadler, Krisztian AD - Laboratory of Pharmacology and Chemistry, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA. Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 586 EP - 596 VL - 61 IS - 3 KW - Aldehydes KW - 0 KW - Free Radicals KW - Nitrites KW - Thiazolidinediones KW - 3-nitrotyrosine KW - 3604-79-3 KW - Tyrosine KW - 42HK56048U KW - Nitric Oxide Synthase Type II KW - EC 1.14.13.39 KW - 4-hydroxy-2-nonenal KW - K1CVM13F96 KW - Abridged Index Medicus KW - Index Medicus KW - Animals KW - Rats, Inbred WKY KW - Rats, Inbred SHR KW - Nitrites -- metabolism KW - Glucose Intolerance KW - Liver -- metabolism KW - Body Composition KW - Free Radicals -- metabolism KW - Rats KW - Aldehydes -- metabolism KW - Tyrosine -- metabolism KW - Tyrosine -- analogs & derivatives KW - Insulin Resistance KW - Muscle, Skeletal -- metabolism KW - Male KW - Hypertension -- complications KW - Nitric Oxide Synthase Type II -- antagonists & inhibitors KW - Thiazolidinediones -- pharmacology KW - Oxidative Stress -- drug effects KW - Nitric Oxide Synthase Type II -- physiology KW - Heart Failure -- metabolism KW - Lipid Peroxidation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/923189886?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Diabetes&rft.atitle=Thiazolidinedione+treatment+decreases+oxidative+stress+in+spontaneously+hypertensive+heart+failure+rats+through+attenuation+of+inducible+nitric+oxide+synthase-mediated+lipid+radical+formation.&rft.au=Kadiiska%2C+Maria+B%3BBonini%2C+Marcelo+G%3BRuggiero%2C+Christine%3BCleland%2C+Ellen%3BWicks%2C+Shawna%3BStadler%2C+Krisztian&rft.aulast=Kadiiska&rft.aufirst=Maria&rft.date=2012-03-01&rft.volume=61&rft.issue=3&rft.spage=586&rft.isbn=&rft.btitle=&rft.title=Diabetes&rft.issn=1939-327X&rft_id=info:doi/10.2337%2Fdb11-1091 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-04-10 N1 - Date created - 2012-02-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Hypertension. 2004 Oct;44(4):484-9 [15302844] Free Radic Biol Med. 1991;11(1):81-128 [1937131] Arch Biochem Biophys. 1993 Jun;303(2):185-94 [8390216] Mol Aspects Med. 1993;14(3):217-28 [8264336] Biochem Biophys Res Commun. 1995 Feb 6;207(1):80-8 [7531975] J Biol Chem. 1997 Feb 21;272(8):4959-63 [9030556] Biochem J. 1997 Jul 15;325 ( Pt 2):487-93 [9230132] J Clin Invest. 1997 Jul 15;100(2):290-5 [9218505] Diabetes. 1997 Nov;46(11):1691-700 [9356014] Proc Natl Acad Sci U S A. 1998 Mar 3;95(5):2498-502 [9482914] Diabetologia. 1999 May;42(5):539-44 [10333045] Am J Cardiol. 1999 Jul 8;84(1A):11J-14J [10418852] Am J Cardiol. 1999 Jul 8;84(1A):33J-36J [10418857] Free Radic Biol Med. 2005 Jan 1;38(1):125-35 [15589381] Diabetes. 2005 Apr;54(4):959-67 [15793233] Diabetes. 2005 May;54(5):1340-8 [15855318] Methods Enzymol. 2008;441:217-36 [18554537] J Biol Chem. 2008 Aug 8;283(32):21837-41 [18445586] Free Radic Biol Med. 2008 Sep 15;45(6):866-74 [18620046] Biochim Biophys Acta. 2009 May;1792(5):409-16 [18852044] Diabetes. 2010 Apr;59(4):861-71 [20103705] Chem Res Toxicol. 2010 Apr 19;23(4):821-35 [20170094] Proc Natl Acad Sci U S A. 2000 Feb 15;97(4):1784-9 [10677535] J Biol Chem. 2000 Mar 24;275(12):9047-54 [10722755] Trends Endocrinol Metab. 2000 Aug;11(6):212-7 [10878750] J Biol Chem. 2001 Jun 15;276(24):20831-8 [11259420] Diabetologia. 2001 Jul;44(7):834-8 [11508267] Nat Med. 2001 Oct;7(10):1138-43 [11590438] J Biol Chem. 2002 Jan 11;277(2):1531-7 [11606564] Am J Physiol Endocrinol Metab. 2002 Feb;282(2):E386-94 [11788371] Diabetes. 2002 Apr;51(4):1076-82 [11916928] Diabetes Care. 2002 Jul;25(7):1177-84 [12087016] Am J Physiol Endocrinol Metab. 2002 Sep;283(3):E413-22 [12169433] FASEB J. 2002 Sep;16(11):1335-47 [12205025] FASEB J. 2002 Nov;16(13):1713-20 [12409313] Circulation. 2002 Nov 19;106(21):2680-6 [12438293] Diabetes. 2003 Jan;52(1):1-8 [12502486] Mol Aspects Med. 2003 Aug-Oct;24(4-5):219-30 [12893000] Int J Obes Relat Metab Disord. 2003 Dec;27 Suppl 3:S46-8 [14704744] Eur J Pharmacol. 2004 Jan 1;483(1):79-93 [14709329] Nat Med. 2004 Mar;10(3):268-74 [14770177] J Endocrinol. 2004 Jun;181(3):419-27 [15171690] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.2337/db11-1091 ER - TY - JOUR T1 - Clozapine protects dopaminergic neurons from inflammation-induced damage by inhibiting microglial overactivation. AN - 922763097; 21870076 AB - Increasing evidence suggests a possible involvement of neuroinflammation in some psychiatric disorders, and also pharmacological reports indicate that anti-inflammatory effects are associated with therapeutic actions of psychoactive drugs, such as anti-depressants and antipsychotics. The purpose of this study was to explore whether clozapine, a widely used antipsychotic drugs, displays anti-inflammatory and neuroprotective effects. Using primary cortical and mesencephalic neuron-glia cultures, we found that clozapine was protective against inflammation-related neurodegeneration induced by lipopolysaccharide (LPS). Pretreatment of cortical or mesencephalic neuron-glia cultures with clozapine (0.1 or 1 μM) for 24 h attenuated LPS-induced neurotoxicity. Clozapine also protected neurons against 1-methyl-4-phenylpyridinium(+) (MPP(+))-induced neurotoxicity, but only in cultures containing microglia, indicating an indispensable role of microglia in clozapine-afforded neuroprotection. Further observation revealed attenuated LPS-induced microglial activation in primary neuron-glia cultures and in HAPI microglial cell line with clozapine pretreatment. Clozapine ameliorated the production of microglia-derived superoxide and intracellular reactive oxygen species (ROS), as well as the production of nitric oxide and TNF-α following LPS. In addition, the protective effect of clozapine was not observed in neuron-glia cultures from mice lacking functional NADPH oxidase (PHOX), a key enzyme for superoxide production in immune cells. Further mechanistic studies demonstrated that clozapine pretreatment inhibited LPS-induced translocation of cytosolic subunit p47(phox) to the membrane in microglia, which was most likely through inhibiting the phosphoinositide 3-kinase (PI3K) pathway. Taken together, this study demonstrates that clozapine exerts neuroprotective effect via the attenuation of microglia activation through inhibition of PHOX-generated ROS production and suggests potential use of antipsychotic drugs for neuroprotection. JF - Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology AU - Hu, Xiaoming AU - Zhou, Hui AU - Zhang, Dan AU - Yang, Sufen AU - Qian, Li AU - Wu, Hung-Ming AU - Chen, Po-See AU - Wilson, Belinda AU - Gao, Hui-Ming AU - Lu, Ru-band AU - Hong, Jau-Shyong AD - Neuropharmacology Section, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA. Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 187 EP - 201 VL - 7 IS - 1 KW - Anti-Inflammatory Agents KW - 0 KW - Antipsychotic Agents KW - Lipopolysaccharides KW - Neuroprotective Agents KW - Clozapine KW - J60AR2IKIC KW - Index Medicus KW - Microscopy, Confocal KW - Animals KW - Coculture Techniques KW - Antipsychotic Agents -- pharmacology KW - Nerve Degeneration -- chemically induced KW - Mice KW - Nerve Degeneration -- prevention & control KW - Neuroprotective Agents -- pharmacology KW - Rats KW - Blotting, Western KW - Cell Survival -- drug effects KW - Mice, Inbred C57BL KW - Lipopolysaccharides -- toxicity KW - Flow Cytometry KW - Inflammation -- prevention & control KW - Dopaminergic Neurons -- drug effects KW - Inflammation -- chemically induced KW - Clozapine -- pharmacology KW - Dopaminergic Neurons -- immunology KW - Dopaminergic Neurons -- pathology KW - Microglia -- drug effects KW - Microglia -- metabolism KW - Anti-Inflammatory Agents -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/922763097?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+neuroimmune+pharmacology+%3A+the+official+journal+of+the+Society+on+NeuroImmune+Pharmacology&rft.atitle=Clozapine+protects+dopaminergic+neurons+from+inflammation-induced+damage+by+inhibiting+microglial+overactivation.&rft.au=Hu%2C+Xiaoming%3BZhou%2C+Hui%3BZhang%2C+Dan%3BYang%2C+Sufen%3BQian%2C+Li%3BWu%2C+Hung-Ming%3BChen%2C+Po-See%3BWilson%2C+Belinda%3BGao%2C+Hui-Ming%3BLu%2C+Ru-band%3BHong%2C+Jau-Shyong&rft.aulast=Hu&rft.aufirst=Xiaoming&rft.date=2012-03-01&rft.volume=7&rft.issue=1&rft.spage=187&rft.isbn=&rft.btitle=&rft.title=Journal+of+neuroimmune+pharmacology+%3A+the+official+journal+of+the+Society+on+NeuroImmune+Pharmacology&rft.issn=1557-1904&rft_id=info:doi/10.1007%2Fs11481-011-9309-0 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-12 N1 - Date created - 2012-02-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Cell Biol. 1996 Dec;135(5):1249-60 [8947549] Acta Psychiatr Scand. 1996 Sep;94(3):198-204 [8891088] Biol Psychiatry. 1998 May 1;43(9):674-9 [9583001] Exp Gerontol. 1998 Aug;33(5):371-8 [9762518] Am J Psychiatry. 1999 Feb;156(2):286-93 [9989565] Blood. 1999 Mar 1;93(5):1464-76 [10029572] Curr Opin Neurol. 2005 Jun;18(3):315-21 [15891419] J Neuropsychiatry Clin Neurosci. 2005 Spring;17(2):227-31 [15939978] Folia Neuropathol. 2005;43(2):81-9 [16012909] J Mol Neurosci. 2005;27(1):43-64 [16055946] J Psychiatry Neurosci. 2006 Jan;31(1):32-7 [16496033] Int Immunopharmacol. 2006 Jun;6(6):903-7 [16644475] J Psychopharmacol. 2006 Sep;20(5):636-42 [16478754] Cell Signal. 2006 Nov;18(11):1876-86 [16542821] FASEB J. 2006 Dec;20(14):2496-511 [17142799] Nat Rev Neurosci. 2007 Jan;8(1):57-69 [17180163] Brain Res. 2007 Mar 23;1138:196-202 [17275793] J Exp Med. 2007 Mar 19;204(3):571-82 [17339406] Ann N Y Acad Sci. 2007 Jan;1096:70-7 [17405917] Schizophr Res. 2000 Apr 7;42(2):157-64 [10742653] J Neuropathol Exp Neurol. 2000 Feb;59(2):137-50 [10749103] Med Hypotheses. 2000 Feb;54(2):198-202 [10790752] Proc Natl Acad Sci U S A. 2001 Feb 13;98(4):1982-7 [11172062] Mol Psychiatry. 2001 Jan;6(1):66-73 [11244487] Neuropsychopharmacology. 2001 May;24(5):531-44 [11282253] Nat Cell Biol. 2001 Jul;3(7):679-82 [11433301] J Cell Biol. 2001 Oct 1;155(1):19-25 [11581283] Am J Psychiatry. 2002 Jan;159(1):59-65 [11772691] Am J Psychiatry. 2002 Feb;159(2):244-50 [11823266] J Neurochem. 2002 Jun;81(6):1285-97 [12068076] J Neurosci Res. 2002 Jul 15;69(2):278-83 [12111809] Glia. 2002 Nov;40(2):184-94 [12379906] J Neurochem. 2002 Nov;83(4):973-83 [12421370] Ann N Y Acad Sci. 2002 Nov;973:505-7 [12485919] J Pharmacol Exp Ther. 2003 Jan;304(1):1-7 [12490568] Psychiatry Res. 2003 Jan 25;117(1):85-8 [12581823] Neuropsychobiology. 2003;47(2):73-7 [12707488] Eur J Neurosci. 2003 Apr;17(8):1563-70 [12752374] FASEB J. 2003 Oct;17(13):1954-6 [12897068] FEBS Lett. 2004 Feb 27;560(1-3):115-9 [14988008] Arch Gen Psychiatry. 1990 Nov;47(11):1029-34 [2241505] Arch Gen Psychiatry. 1992 Mar;49(3):195-205 [1567274] Trends Neurosci. 1996 Aug;19(8):312-8 [8843599] Prostaglandins Leukot Essent Fatty Acids. 1996 Aug;55(1-2):33-43 [8888121] J Bone Joint Surg Am. 2007 May;89(5):1019-27 [17473139] Glia. 2007 Oct;55(13):1362-73 [17654704] Neuropsychopharmacology. 2007 Oct;32(10):2057-66 [17327887] Biochem Soc Trans. 2007 Nov;35(Pt 5):1127-32 [17956294] Environ Health Perspect. 2008 May;116(5):593-8 [18470306] J Neuroinflammation. 2008;5:21 [18507839] Trends Immunol. 2008 Aug;29(8):357-65 [18599350] Biol Psychiatry. 2008 Nov 1;64(9):820-2 [18534557] Blood. 2008 Nov 1;112(9):3867-77 [18711001] Blood. 2008 Dec 15;112(13):5202-11 [18755982] J Nucl Med. 2009 Nov;50(11):1801-7 [19837763] Biol Psychiatry. 2010 Mar 15;67(6):503-4 [20185031] Eur J Pharmacol. 2010 May 25;634(1-3):84-8 [20184876] J Neural Transm (Vienna). 2010 Aug;117(8):971-9 [20571837] J Neuroinflammation. 2011;8(1):3 [21232086] Psychiatry Res. 1997 Jul 4;74(3):141-50 [9255859] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s11481-011-9309-0 ER - TY - JOUR T1 - Shining a light on xeroderma pigmentosum. AN - 921723625; 22217736 AB - Xeroderma pigmentosum (XP) is a rare, autosomal recessive disorder of DNA repair characterized by sun sensitivity and UV radiation-induced skin and mucous membrane cancers. Initially described in 1874 by Moriz Kaposi in Vienna, nearly 100 years later, James Cleaver in San Francisco reported defective DNA repair in XP cells. This eventually provided the basis for a mechanistic link between sun exposure, DNA damage, somatic mutations, and skin cancer. XP cells were found to have defects in seven of the proteins of the nucleotide excision repair pathway and in DNA polymerase η. XP cells are hypersensitive to killing by UV radiation, and XP cancers have characteristic "UV signature" mutations. Clinical studies at the National Institutes of Health found a nearly 10,000-fold increase in skin cancer in XP patients under the age of 20 years, demonstrating the substantial importance of DNA repair in cancer prevention in the general population. Approximately 25% of XP patients have progressive neurological degeneration with progressive loss of neurons, probably from DNA damage induced by oxidative metabolism, which kills nondividing cells in the nervous system. Interestingly, patients with another disorder, trichothiodystrophy, have defects in some of the same genes as XP, but they have primary developmental abnormalities without an increase in skin cancer. JF - The Journal of investigative dermatology AU - DiGiovanna, John J AU - Kraemer, Kenneth H AD - DNA Repair Section, Dermatology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland 20892-4258, USA. Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 785 EP - 796 VL - 132 IS - 3 Pt 2 KW - Index Medicus KW - Sunlight -- adverse effects KW - Humans KW - Xeroderma Pigmentosum -- pathology KW - Skin Neoplasms -- genetics KW - Skin Neoplasms -- physiopathology KW - DNA Repair -- physiology KW - Xeroderma Pigmentosum -- physiopathology KW - Xeroderma Pigmentosum -- genetics KW - Skin Neoplasms -- pathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/921723625?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+investigative+dermatology&rft.atitle=Shining+a+light+on+xeroderma+pigmentosum.&rft.au=DiGiovanna%2C+John+J%3BKraemer%2C+Kenneth+H&rft.aulast=DiGiovanna&rft.aufirst=John&rft.date=2012-03-01&rft.volume=132&rft.issue=3+Pt+2&rft.spage=785&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+investigative+dermatology&rft.issn=1523-1747&rft_id=info:doi/10.1038%2Fjid.2011.426 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-04-10 N1 - Date created - 2012-02-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 2002 Sep 1;62(17):4899-902 [12208738] DNA Repair (Amst). 2002 Feb 28;1(2):143-57 [12509261] Cancer Res. 2004 May 15;64(10):3559-65 [15150112] Nat Genet. 2004 Jul;36(7):677-8 [15226750] Proc Natl Acad Sci U S A. 2004 Oct 26;101(43):15410-5 [15486090] Nature. 1968 May 18;218(5142):652-6 [5655953] JAMA. 1969 Mar 17;207(11):2073-9 [5818379] Proc Natl Acad Sci U S A. 1969 Nov;64(3):1035-41 [5264135] Science. 1970 Jun 19;168(3938):1477-8 [5445941] Photochem Photobiol. 1970 Jun;11(6):547-50 [5456279] J Lab Clin Med. 1971 May;77(5):759-67 [5557662] J Invest Dermatol. 1972 Mar;58(3):124-8 [5013606] Nat New Biol. 1972 Jul 19;238(81):80-3 [4505415] Ann Intern Med. 1974 Feb;80(2):221-48 [4811796] Proc Natl Acad Sci U S A. 1975 Jan;72(1):59-63 [164028] Mutat Res. 1975 Dec;33(2-3):327-40 [1243579] Mutat Res. 1977 Apr;43(1):117-38 [865487] Mutat Res. 1979 Jan;59(1):143-6 [431549] Cancer Res. 1998 Oct 1;58(19):4402-9 [9766670] Mol Med Today. 1999 Feb;5(2):86-94 [10200950] Nature. 1999 Jun 17;399(6737):700-4 [10385124] Science. 1999 Jul 9;285(5425):263-5 [10398605] Proc Natl Acad Sci U S A. 1962 Jul 15;48:1250-7 [13910967] Mutat Res. 2005 Apr 1;571(1-2):43-56 [15748637] Carcinogenesis. 2005 Jun;26(6):1085-90 [15731165] DNA Repair (Amst). 2005 Sep 28;4(10):1068-74 [16054878] Cancer Res. 2005 Nov 15;65(22):10298-306 [16288018] Mutat Res. 2006 Oct 10;601(1-2):171-8 [16905156] Proc Natl Acad Sci U S A. 2007 Jan 23;104(4):1389-94 [17229834] Neuroscience. 2007 Apr 14;145(4):1388-96 [17276014] Cancer Epidemiol Biomarkers Prev. 2008 Mar;17(3):507-17 [18349268] J Med Genet. 2008 Sep;45(9):564-71 [18628313] J Am Acad Dermatol. 2008 Nov;59(5):881-6 [19119101] Pediatr Radiol. 2009 Feb;39 Suppl 1:S27-31 [19083227] DNA Repair (Amst). 2009 Feb 1;8(2):153-61 [18996499] Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6279-84 [19329485] Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6209-14 [19329487] Cancer Res. 2009 Sep 1;69(17):6857-64 [19706757] Nat Genet. 2009 Oct;41(10):1127-32 [19718025] Nature. 2010 Jan 14;463(7278):191-6 [20016485] Hum Mutat. 2010 Feb;31(2):113-26 [19894250] Clin Genet. 2010 Apr;77(4):365-73 [20002457] Nat Rev Cancer. 2011 Feb;11(2):96-110 [21258395] J Invest Dermatol. 2011 Mar;131(3):785-8 [21107348] J Med Genet. 2011 Mar;48(3):168-76 [21097776] Nat Genet. 2011 May;43(5):442-6 [21499247] Surv Ophthalmol. 2011 Jul-Aug;56(4):348-61 [21684361] Prenat Diagn. 2011 Nov;31(11):1046-53 [21800331] J Am Acad Dermatol. 2005 Feb;52(2):224-32 [15692466] Mutat Res. 1979 Aug;62(1):183-90 [492197] Radiat Res. 1981 Oct;88(1):194-208 [7302127] Proc Natl Acad Sci U S A. 1985 Oct;82(19):6622-6 [2995975] Proc Natl Acad Sci U S A. 1986 Nov;83(21):8273-7 [3464953] Arch Dermatol. 1987 Feb;123(2):241-50 [3545087] Environ Health Perspect. 1987 Dec;76:33-9 [3129287] N Engl J Med. 1988 Jun 23;318(25):1633-7 [3287161] JAMA. 1989 Oct 20;262(15):2097-100 [2795783] Mol Cell Biol. 1990 Jun;10(6):2570-81 [2111438] Cell. 1990 Aug 24;62(4):777-91 [2167179] Nature. 1990 Nov 1;348(6296):73-6 [2234061] Genomics. 1990 Dec;8(4):623-33 [2276736] Brain. 1991 Jun;114 ( Pt 3):1335-61 [2065254] Proc Natl Acad Sci U S A. 1992 Jan 1;89(1):261-5 [1729695] Nature. 1992 Dec 10;360(6404):610 [1461286] Genes Chromosomes Cancer. 1992 Nov;5(4):335-42 [1283322] Cancer Res. 1994 Jul 15;54(14):3837-44 [8033104] Arch Dermatol. 1994 Aug;130(8):1018-21 [8053698] Nature. 1995 Sep 14;377(6545):162-5 [7675084] Nature. 1995 Sep 14;377(6545):169-73 [7675086] Genomics. 1995 Sep 1;29(1):62-9 [8530102] Br J Dermatol. 1996 Jun;134(6):1147-50 [8763445] Cell. 1996 Sep 6;86(5):811-22 [8797827] J Cutan Med Surg. 1998 Jan;2(3):153-8 [9479081] Cancer Res. 2000 Mar 15;60(6):1580-4 [10749126] Carcinogenesis. 2000 Oct;21(10):1821-5 [11023539] Lancet. 2001 Mar 24;357(9260):926-9 [11289350] Cancer Res. 2001 Apr 15;61(8):3321-5 [11309287] Nat Immunol. 2001 Jun;2(6):537-41 [11376341] Mutat Res. 2001 Jun 2;477(1-2):31-40 [11376684] Nat Med. 2001 Aug;7(8):961-6 [11479630] Proc Natl Acad Sci U S A. 2001 Nov 6;98(23):13379-84 [11687625] J Invest Dermatol. 2002 Jun;118(6):972-82 [12060391] Nucleic Acids Res. 2002 Aug 15;30(16):3624-31 [12177305] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1038/jid.2011.426 ER - TY - JOUR T1 - Perfluorinated compounds and subfecundity in pregnant women. AN - 921143530; 22081060 AB - Perfluorinated compounds are ubiquitous pollutants; epidemiologic data suggest they may be associated with adverse health outcomes, including subfecundity. We examined subfecundity in relation to 2 perfluorinated compounds-perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA). This case-control analysis included 910 women enrolled in the Norwegian Mother and Child Cohort Study in 2003 and 2004. Around gestational week 17, women reported their time to pregnancy and provided blood samples. Cases consisted of 416 women with a time to pregnancy greater than 12 months, considered subfecund. Plasma concentrations of perfluorinated compounds were analyzed using liquid chromatography-mass spectrometry. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated for each pollutant quartile using logistic regression. Estimates were further stratified by parity. The median plasma concentration of PFOS was 13.0 ng/mL (interquartile range [IQR] = 10.3-16.6 ng/mL) and of PFOA was 2.2 ng/mL (IQR = 1.7-3.0 ng/mL). The relative odds of subfecundity among parous women was 2.1 (95% CI = 1.2-3.8) for the highest PFOS quartile and 2.1 (1.0-4.0) for the highest PFOA quartile. Among nulliparous women, the respective relative odds were 0.7 (0.4-1.3) and 0.5 (0.2-1.2). Previous studies suggest that the body burden of perfluorinated compounds decreases during pregnancy and lactation through transfer to the fetus and to breast milk. Afterward, the body burden may increase again. Among parous women, increased body burden may be due to a long interpregnancy interval rather than the cause of a long time to pregnancy. Therefore, data from nulliparous women may be more informative regarding toxic effects of perfluorinated compounds. Our results among nulliparous women did not support an association with subfecundity. JF - Epidemiology (Cambridge, Mass.) AU - Whitworth, Kristina W AU - Haug, Line S AU - Baird, Donna D AU - Becher, Georg AU - Hoppin, Jane A AU - Skjaerven, Rolv AU - Thomsen, Cathrine AU - Eggesbo, Merete AU - Travlos, Gregory AU - Wilson, Ralph AU - Longnecker, Matthew P AD - Department of Health and Human Services, National Institute for Environmental Health Sciences, National Institutes of Health, Durham, NC 27709, USA. whitworthkw@niehs.nih.gov Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 257 EP - 263 VL - 23 IS - 2 KW - Alkanesulfonic Acids KW - 0 KW - Caprylates KW - Fluorocarbons KW - perfluorooctanoic acid KW - 947VD76D3L KW - perfluorooctane sulfonic acid KW - 9H2MAI21CL KW - Index Medicus KW - Parity KW - Odds Ratio KW - Norway -- epidemiology KW - Pregnancy -- drug effects KW - Logistic Models KW - Humans KW - Body Burden KW - Adult KW - Gas Chromatography-Mass Spectrometry KW - Case-Control Studies KW - Female KW - Caprylates -- blood KW - Caprylates -- adverse effects KW - Fluorocarbons -- blood KW - Fluorocarbons -- adverse effects KW - Alkanesulfonic Acids -- blood KW - Alkanesulfonic Acids -- adverse effects KW - Fertility -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/921143530?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Epidemiology+%28Cambridge%2C+Mass.%29&rft.atitle=Perfluorinated+compounds+and+subfecundity+in+pregnant+women.&rft.au=Whitworth%2C+Kristina+W%3BHaug%2C+Line+S%3BBaird%2C+Donna+D%3BBecher%2C+Georg%3BHoppin%2C+Jane+A%3BSkjaerven%2C+Rolv%3BThomsen%2C+Cathrine%3BEggesbo%2C+Merete%3BTravlos%2C+Gregory%3BWilson%2C+Ralph%3BLongnecker%2C+Matthew+P&rft.aulast=Whitworth&rft.aufirst=Kristina&rft.date=2012-03-01&rft.volume=23&rft.issue=2&rft.spage=257&rft.isbn=&rft.btitle=&rft.title=Epidemiology+%28Cambridge%2C+Mass.%29&rft.issn=1531-5487&rft_id=info:doi/10.1097%2FEDE.0b013e31823b5031 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-25 N1 - Date created - 2012-02-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Int J Toxicol. 2001 Mar-Apr;20(2):101-9 [11354466] Environ Sci Technol. 2010 Dec 15;44(24):9550-6 [21090747] Environ Sci Technol. 2002 Apr 1;36(7):146A-152A [11999053] Crit Rev Toxicol. 2004 Jul-Aug;34(4):351-84 [15328768] J Epidemiol Community Health. 1995 Jun;49(3):314-9 [7629471] Toxicol Sci. 2006 Apr;90(2):510-8 [16415327] Int J Epidemiol. 2006 Oct;35(5):1146-50 [16926217] Tohoku J Exp Med. 2007 May;212(1):63-70 [17464105] Environ Health Perspect. 2007 Sep;115(9):1298-305 [17805419] Toxicol Sci. 2007 Oct;99(2):366-94 [17519394] Environ Health Perspect. 2007 Nov;115(11):1596-602 [18007991] Environ Health Perspect. 2007 Nov;115(11):1670-6 [18008002] Environ Health Perspect. 2007 Nov;115(11):1677-82 [18008003] Environ Sci Technol. 2008 Jul 1;42(13):4989-95 [18678038] J Chromatogr A. 2009 Jan 16;1216(3):385-93 [19026423] Int J Hyg Environ Health. 2009 May;212(3):239-70 [18565792] Hum Reprod. 2009 May;24(5):1200-5 [19176540] Environ Sci Technol. 2009 Mar 15;43(6):2131-6 [19368225] Reprod Toxicol. 2009 Jun;27(3-4):319-30 [19162172] Reprod Toxicol. 2009 Jun;27(3-4):212-30 [19429401] Environ Sci Technol. 2009 Apr 1;43(7):2641-7 [19452929] Epidemiology. 2010 Jan;21(1):160-1; author reply 161 [20010224] Environ Int. 2010 Aug;36(6):584-92 [20494442] Rev Environ Contam Toxicol. 2010;208:161-77 [20811864] Environ Sci Technol. 2010 Sep 15;44(18):7123-9 [20722423] Anal Bioanal Chem. 2010 Nov;398(6):2413-27 [20680618] Environ Int. 2011 Jan;37(1):178-83 [20880590] Comment In: Epidemiology. 2012 Mar;23(2):264-6 [22317809] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1097/EDE.0b013e31823b5031 ER - TY - JOUR T1 - RAD53 is limiting in double-strand break repair and in protection against toxicity associated with ribonucleotide reductase inhibition. AN - 920366373; 22277748 AB - The yeast Chk2/Chk1 homolog Rad53 is a central component of the DNA damage checkpoint system. While it controls genotoxic stress responses such as cell cycle arrest, replication fork stabilization and increase in dNTP pools, little is known about the consequences of reduced Rad53 levels on the various cellular endpoints or about its roles in dealing with chronic vs. acute genotoxic challenges. Using a tetraploid gene dosage model in which only one copy of the yeast RAD53 is functional (simplex), we found that the simplex strain was not sensitive to acute UV radiation or chronic MMS exposure. However, the simplex strain was sensitized to chronic exposure of the ribonucleotide reductase inhibitor hydroxyurea (HU). Surprisingly, reduced RAD53 gene dosage did not affect sensitivity to HU acute exposure, indicating that immediate checkpoint responses and recovery from HU-induced stress were not compromised. Interestingly, cells of most of the colonies that arise after chronic HU exposure acquired heritable resistance to HU. We also found that short HU exposure before and after treatment of G₂ cells with ionizing radiation (IR) reduced the capability of RAD53 simplex cells to repair DSBs, in agreement with sensitivity of RAD53 simplex strain to high doses of IR. We propose that a modest reduction in Rad53 activity can impact the activation of the ribonucleotide reductase catalytic subunit Rnr1 following stress, reducing the ability to generate nucleotide pools sufficient for DNA repair and replication. At the same time, reduced Rad53 activity may lead to genome instability and to the acquisition of drug resistance before and/or during the chronic exposure to HU. These results have implications for developing drug enhancers as well as for understanding mechanisms of drug resistance in cells compromised for DNA damage checkpoint. Published by Elsevier B.V. JF - DNA repair AU - Covo, Shay AU - Westmoreland, James W AU - Reddy, Amit K AU - Gordenin, Dmitry A AU - Resnick, Michael A AD - Chromosome Stability Group, Laboratory of Molecular Genetics, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, NC 27709, USA. Y1 - 2012/03/01/ PY - 2012 DA - 2012 Mar 01 SP - 317 EP - 323 VL - 11 IS - 3 KW - Cell Cycle Proteins KW - 0 KW - Mutagens KW - Saccharomyces cerevisiae Proteins KW - Ribonucleotide Reductases KW - EC 1.17.4.- KW - Rnr1 protein, S cerevisiae KW - Checkpoint Kinase 2 KW - EC 2.7.1.11 KW - Protein-Serine-Threonine Kinases KW - EC 2.7.11.1 KW - RAD53 protein, S cerevisiae KW - EC 2.7.12.1 KW - Hydroxyurea KW - X6Q56QN5QC KW - Index Medicus KW - Genomic Instability -- radiation effects KW - Drug Resistance -- drug effects KW - Drug Resistance -- radiation effects KW - Stress, Physiological -- drug effects KW - Mutagens -- toxicity KW - Microbial Viability -- drug effects KW - Genomic Instability -- drug effects KW - Stress, Physiological -- radiation effects KW - Radiation, Ionizing KW - Microbial Viability -- radiation effects KW - Saccharomyces cerevisiae Proteins -- metabolism KW - DNA Breaks, Double-Stranded -- drug effects KW - Protein-Serine-Threonine Kinases -- metabolism KW - Cytoprotection -- radiation effects KW - Saccharomyces cerevisiae Proteins -- antagonists & inhibitors KW - Ribonucleotide Reductases -- antagonists & inhibitors KW - DNA Breaks, Double-Stranded -- radiation effects KW - Cytoprotection -- drug effects KW - Saccharomyces cerevisiae -- enzymology KW - DNA Repair -- drug effects KW - Hydroxyurea -- toxicity KW - Cell Cycle Proteins -- metabolism KW - DNA Repair -- radiation effects KW - Ribonucleotide Reductases -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920366373?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=DNA+repair&rft.atitle=RAD53+is+limiting+in+double-strand+break+repair+and+in+protection+against+toxicity+associated+with+ribonucleotide+reductase+inhibition.&rft.au=Covo%2C+Shay%3BWestmoreland%2C+James+W%3BReddy%2C+Amit+K%3BGordenin%2C+Dmitry+A%3BResnick%2C+Michael+A&rft.aulast=Covo&rft.aufirst=Shay&rft.date=2012-03-01&rft.volume=11&rft.issue=3&rft.spage=317&rft.isbn=&rft.btitle=&rft.title=DNA+repair&rft.issn=1568-7856&rft_id=info:doi/10.1016%2Fj.dnarep.2011.12.008 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-10 N1 - Date created - 2012-02-07 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Genes Dev. 2010 Dec 1;24(23):2705-16 [21123655] PLoS Genet. 2010 Jul;6(7):e1001006 [20617204] Pediatr Dent. 2011 Jan-Feb;33(1):67-74 [21406151] Curr Opin Hematol. 2011 May;18(3):158-65 [21372708] Lancet Oncol. 2011 Jul;12(7):693-702 [21163702] Br J Cancer. 2011 Jul 26;105(3):372-81 [21730979] Science. 1999 Nov 5;286(5442):1166-71 [10550056] Mol Cell Biol. 2000 Dec;20(23):9076-83 [11074005] EMBO J. 2001 Jul 2;20(13):3544-53 [11432841] Proc Natl Acad Sci U S A. 2002 Mar 19;99(6):3746-51 [11904430] Science. 2002 Jul 26;297(5581):599-602 [12142537] Cell. 2003 Feb 7;112(3):391-401 [12581528] Nature. 2003 Oct 16;425(6959):737-41 [14562106] J Biol Chem. 2004 Jan 2;279(1):223-30 [14573610] Cell. 2004 Sep 17;118(6):699-713 [15369670] Mol Gen Genet. 1976 Jan 16;143(2):119-29 [765749] Mutat Res. 1990 Aug;231(2):177-86 [2200955] Mutat Res. 1996 Jul 5;354(1):69-75 [8692208] Cell. 1997 Sep 19;90(6):1097-106 [9323137] Cell. 1998 Sep 4;94(5):595-605 [9741624] Genes Dev. 1998 Sep 15;12(18):2956-70 [9744871] Nature. 1998 Oct 8;395(6702):615-8 [9783589] Yeast. 1999 Oct;15(14):1541-53 [10514571] Mol Cancer Ther. 2005 Aug;4(8):1268-76 [16093443] Nat Cell Biol. 2006 Feb;8(2):148-55 [16429127] Exp Cell Res. 2006 Aug 15;312(14):2654-9 [16859682] Nature. 2006 Oct 5;443(7111):541-7 [17024086] Cell. 2006 Nov 3;127(3):509-22 [17081974] Nucleic Acids Res. 2006;34(20):5852-62 [17062626] Proc Natl Acad Sci U S A. 2007 Jan 23;104(4):1183-8 [17227840] DNA Repair (Amst). 2007 Jul 1;6(7):900-13 [17379579] Proc Natl Acad Sci U S A. 2007 Jun 19;104(25):10364-9 [17563356] Oncogene. 2007 Dec 10;26(56):7816-24 [18066095] Mol Cell. 2007 Dec 14;28(5):739-45 [18082599] Proc Natl Acad Sci U S A. 2008 Aug 19;105(33):11845-50 [18701715] Mol Cell. 2008 Oct 10;32(1):70-80 [18851834] EMBO J. 2009 Apr 22;28(8):1131-41 [19322196] DNA Repair (Amst). 2009 Jun 4;8(6):720-31 [19269260] PLoS Genet. 2009 Sep;5(9):e1000656 [19763170] DNA Repair (Amst). 2009 Nov 2;8(11):1258-63 [19713159] Genetics. 2009 Dec;183(4):1249-60 [19805819] Cell Cycle. 2010 Jan 1;9(1):25-6 [20016261] PLoS Biol. 2010 Jan;8(1):e1000286 [20126259] Nucleic Acids Res. 2010 Mar;38(4):1195-203 [19965764] Nucleic Acids Res. 2010 Jul;38(12):3975-83 [20215435] Nat Med. 2010 Jul;16(7):774-80 [20601951] J Clin Oncol. 2011 Feb 10;29(5):573-82 [21220604] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.dnarep.2011.12.008 ER - TY - JOUR T1 - Polymorphisms in complement system genes and risk of non-Hodgkin lymphoma. AN - 919956461; 22170086 AB - The complement system plays an important role in inflammatory and immune responses, and recent evidence has suggested that it may also play a role in lymphomagenesis. We evaluated the association between genetic variation in complement system genes and risk of non-Hodgkin lymphoma (NHL) in a population-based case-control study conducted among women in Connecticut. Tag SNPs in 30 complement genes were genotyped in 432 Caucasian incident cases and 494 frequency-matched controls. A gene-based analysis that adjusted for the number of tag SNPs genotyped in each gene showed a significant association with NHL overall (P = 0.04) as well as with diffuse large B-cell lymphoma (DLBCL) (P = 0.01) for the C1RL gene. A SNP-based analysis showed that a C>T base substitution for C1RL rs3813729 (odds ratio (OR)(CT) = 0.60, 95% confidence interval (CI) = 0.42-0.87, P(trend) = 0.0062) was associated with a decreased risk of overall NHL, as well as for DLBCL (OR(CT) = 0.39, 95% CI = 0.20-0.73; P(trend) = 0.0034). Additionally, SNPs (C2 rs497309, A>C and C3 rs344550, G>C) in two complement genes were positively associated with marginal zone lymphoma (MZL) and C1QG was associated with CLL/SLL, but these results were based on a limited number of cases. Our results suggest a potential role of the complement system in susceptibility to NHL; however, our results should be viewed as exploratory and further replication is needed to clarify these preliminary findings. Copyright © 2011 Wiley Periodicals, Inc. JF - Environmental and molecular mutagenesis AU - Bassig, Bryan A AU - Zheng, Tongzhang AU - Zhang, Yawei AU - Berndt, Sonja I AU - Holford, Theodore R AU - Hosgood, H Dean AU - Hu, Wei AU - Leaderer, Brian AU - Yeager, Meredith AU - Menashe, Idan AU - Boyle, Peter AU - Xu, Jun AU - Zou, Kaiyong AU - Zhu, Yong AU - Chanock, Stephen AU - Rothman, Nathaniel AU - Lan, Qing AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, Maryland 20892-7240, USA. bryan.bassig@yale.edu Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 145 EP - 151 VL - 53 IS - 2 KW - Complement System Proteins KW - 9007-36-7 KW - Serine Endopeptidases KW - EC 3.4.21.- KW - C1RL protein, human KW - Ec 3.4.21.- KW - Index Medicus KW - Young Adult KW - Risk KW - Serine Endopeptidases -- genetics KW - Aged, 80 and over KW - Humans KW - Adult KW - Case-Control Studies KW - Aged KW - Middle Aged KW - Genetic Predisposition to Disease KW - Female KW - Lymphoma, Non-Hodgkin -- genetics KW - Complement System Proteins -- genetics KW - Polymorphism, Single Nucleotide KW - Complement System Proteins -- immunology KW - Lymphoma, Non-Hodgkin -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/919956461?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+and+molecular+mutagenesis&rft.atitle=Polymorphisms+in+complement+system+genes+and+risk+of+non-Hodgkin+lymphoma.&rft.au=Bassig%2C+Bryan+A%3BZheng%2C+Tongzhang%3BZhang%2C+Yawei%3BBerndt%2C+Sonja+I%3BHolford%2C+Theodore+R%3BHosgood%2C+H+Dean%3BHu%2C+Wei%3BLeaderer%2C+Brian%3BYeager%2C+Meredith%3BMenashe%2C+Idan%3BBoyle%2C+Peter%3BXu%2C+Jun%3BZou%2C+Kaiyong%3BZhu%2C+Yong%3BChanock%2C+Stephen%3BRothman%2C+Nathaniel%3BLan%2C+Qing&rft.aulast=Bassig&rft.aufirst=Bryan&rft.date=2012-03-01&rft.volume=53&rft.issue=2&rft.spage=145&rft.isbn=&rft.btitle=&rft.title=Environmental+and+molecular+mutagenesis&rft.issn=1098-2280&rft_id=info:doi/10.1002%2Fem.21675 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-03-27 N1 - Date created - 2012-02-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Immunology. 2003 Feb;108(2):144-51 [12562322] Mol Cancer Res. 2010 Nov;8(11):1453-65 [20870736] Am J Clin Pathol. 2004 Jun;121 Suppl:S97-104 [15298155] Proc Natl Acad Sci U S A. 2004 Oct 5;101(40):14390-5 [15385675] Mol Biol Evol. 1995 Sep;12(5):921-7 [7476138] Pathol Oncol Res. 1998;4(4):271-6 [9887357] Hum Genet. 2004 Sep;115(4):295-301 [15278436] Medicine (Baltimore). 2005 Jan;84(1):23-34 [15643297] Biochem J. 2005 Apr 1;387(Pt 1):165-73 [15527420] J Rheumatol. 2005 Oct;32(10):1884-7 [16206341] Lancet Oncol. 2006 Jan;7(1):27-38 [16389181] J Natl Cancer Inst. 2006 Jan 4;98(1):51-60 [16391371] Blood. 2006 May 15;107(10):4101-8 [16449530] Br J Haematol. 2006 Jul;134(2):180-3 [16740140] Genet Epidemiol. 2006 Sep;30(6):495-507 [16755536] Cancer Epidemiol Biomarkers Prev. 2007 Mar;16(3):401-4 [17337646] Carcinogenesis. 2007 Mar;28(3):704-12 [17056605] Cancer Res. 2007 May 15;67(10):5042-54 [17510437] Am J Pathol. 2007 Sep;171(3):715-27 [17640961] Autoimmunity. 2007 Dec;40(8):560-6 [18075790] Rheumatology (Oxford). 2008 Feb;47(2):158-64 [18174230] Trans R Soc Trop Med Hyg. 2008 Aug;102(8):735-42 [18486167] Nat Genet. 2008 Oct;40(10):1204-10 [18758461] Nat Immunol. 2008 Nov;9(11):1225-35 [18820683] Exp Dermatol. 2009 Jan;18(1):30-4 [18631248] Br J Haematol. 2009 Jun;145(5):614-23 [19344414] Trends Immunol. 2009 Jun;30(6):286-92 [19428302] Nat Genet. 2009 Aug;41(8):873-5 [19620980] Cancer Res. 2009 Aug 15;69(16):6367-70 [19654288] Nat Genet. 2010 Feb;42(2):132-6 [20062064] J Autoimmun. 2010 May;34(3):J276-86 [20005073] Nat Genet. 2010 Aug;42(8):661-4 [20639881] Cancer Causes Control. 2003 Sep;14(7):687-94 [14575367] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/em.21675 ER - TY - JOUR T1 - Heme iron from meat and risk of adenocarcinoma of the esophagus and stomach. AN - 916851426; 22044848 AB - Iron can cause oxidative stress and DNA damage, and heme iron can catalyze endogenous formation of N-nitroso compounds, which are potent carcinogens. Dietary iron promotes esophageal cancer incidence in animal studies and has been identified as a growth factor for Helicobacter pylori, an established risk factor for stomach cancer. We conducted a population-based case-control study of adenocarcinoma of the esophagus (n=124) and stomach (n=154) and 449 controls in Nebraska. Heme iron and total iron intake were estimated from a food frequency questionnaire and databases of heme and total iron. We used logistic regression to calculate odds ratios (ORs) and 95% confidence intervals (CIs) adjusted for known risk factors. Esophageal cancer was positively associated with higher intakes of heme iron (ORQ4 vs. Q1=3.04, 95% CI: 1.20-7.72; P trend=0.009) and total iron from meat sources (ORQ4 vs. Q1=2.67, 95% CI: 0.99-7.16; P trend=0.050). Risk of stomach cancer was elevated among those with higher intakes of heme iron (ORQ4 vs.Q1=1.99, 95% CI: 1.00-3.95; P trend=0.17) and total iron from meat (OR=2.26, 95% CI: 1.14-4.46; P trend=0.11). Iron intake from all dietary sources was not significantly associated with risk of either cancer. Our results suggest that high intakes of heme and iron from meat may be important dietary risk factors for esophageal and stomach cancer and may partly explain associations with red meat. JF - European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) AU - Ward, Mary H AU - Cross, Amanda J AU - Abnet, Christian C AU - Sinha, Rashmi AU - Markin, Rodney S AU - Weisenburger, Dennis D AD - Department of Health and Human Services, Occupational and Environmental Epidemiology Branch , National Cancer Institute, National Institutes of Health, Bethesda, MD 20892-7240, USA. wardm@mail.nih.gov Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 134 EP - 138 VL - 21 IS - 2 KW - Iron, Dietary KW - 0 KW - Heme KW - 42VZT0U6YR KW - Index Medicus KW - Young Adult KW - Eating -- physiology KW - Feeding Behavior -- physiology KW - Humans KW - Aged KW - Nutrition Surveys KW - Heme -- adverse effects KW - Aged, 80 and over KW - Risk Factors KW - Adult KW - Case-Control Studies KW - Middle Aged KW - Heme -- analysis KW - Female KW - Male KW - Adenocarcinoma -- epidemiology KW - Meat -- adverse effects KW - Iron, Dietary -- analysis KW - Adenocarcinoma -- etiology KW - Iron, Dietary -- adverse effects KW - Meat -- analysis KW - Stomach Neoplasms -- epidemiology KW - Stomach Neoplasms -- etiology KW - Esophageal Neoplasms -- etiology KW - Iron, Dietary -- administration & dosage KW - Esophageal Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/916851426?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+cancer+prevention+%3A+the+official+journal+of+the+European+Cancer+Prevention+Organisation+%28ECP%29&rft.atitle=Heme+iron+from+meat+and+risk+of+adenocarcinoma+of+the+esophagus+and+stomach.&rft.au=Ward%2C+Mary+H%3BCross%2C+Amanda+J%3BAbnet%2C+Christian+C%3BSinha%2C+Rashmi%3BMarkin%2C+Rodney+S%3BWeisenburger%2C+Dennis+D&rft.aulast=Ward&rft.aufirst=Mary&rft.date=2012-03-01&rft.volume=21&rft.issue=2&rft.spage=134&rft.isbn=&rft.btitle=&rft.title=European+journal+of+cancer+prevention+%3A+the+official+journal+of+the+European+Cancer+Prevention+Organisation+%28ECP%29&rft.issn=1473-5709&rft_id=info:doi/10.1097%2FCEJ.0b013e32834c9b6c LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-07 N1 - Date created - 2012-01-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Carcinogenesis. 2001 Aug;22(8):1119-29 [11470739] Nutr Cancer. 2002;42(1):33-40 [12235648] Cancer Res. 2003 May 15;63(10):2358-60 [12750250] Am J Epidemiol. 1985 Jul;122(1):13-26 [4014190] Epidemiology. 1990 Sep;1(5):349-56 [2078610] Epidemiology. 1990 Jan;1(1):58-64 [2081241] Cancer Epidemiol Biomarkers Prev. 1993 Jul-Aug;2(4):305-12 [8348053] Int J Cancer. 1995 Jan 17;60(2):160-2 [7829208] Alcohol. 1995 Mar-Apr;12(2):97-104 [7772272] Cancer Lett. 1995 Jun 29;93(1):17-48 [7600541] Int J Cancer. 1996 Mar 28;66(1):130-4 [8608956] Int J Cancer. 1997 Mar 28;71(1):14-9 [9096659] J Gastroenterol Hepatol. 1999 Mar;14(3):202-14 [10197487] Mol Nutr Food Res. 2005 Jul;49(7):648-55 [15986387] Int J Cancer. 2005 Nov 20;117(4):643-7 [15929082] Cancer Res. 1999 Nov 15;59(22):5704-9 [10582688] Am J Gastroenterol. 2011 Mar;106(3):432-42 [20978481] Cancer Causes Control. 2010 Dec;21(12):2269-79 [20936528] Int J Occup Environ Health. 2008 Jul-Sep;14(3):193-7 [18686719] Carcinogenesis. 2007 Mar;28(3):685-90 [17052997] World J Gastroenterol. 2006 Jul 21;12(27):4296-303 [16865769] Carcinogenesis. 2006 Jul;27(7):1497-501 [16571648] J Natl Cancer Inst. 2006 Mar 1;98(5):345-54 [16507831] Eur J Gastroenterol Hepatol. 2000 Dec;12(12):1263-5 [11192313] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1097/CEJ.0b013e32834c9b6c ER - TY - JOUR T1 - Activated microglia proliferate at neurites of mutant huntingtin-expressing neurons. AN - 916522179; 21482444 AB - In Huntington's disease (HD), mutated huntingtin (mhtt) causes striatal neurodegeneration which is paralleled by elevated microglia cell numbers. In vitro corticostriatal slice and primary neuronal culture models, in which neuronal expression of mhtt fragments drives HD-like neurotoxicity, were employed to examine wild type microglia during both the initiation and progression of neuronal pathology. As neuronal pathology progressed, microglia initially localized in the vicinity of neurons expressing mhtt fragments increased in number, demonstrated morphological evidence of activation, and expressed the proliferation marker, Ki67. These microglia were positioned along irregular neurites, but did not localize with mhtt inclusions nor exacerbate mhtt fragment-induced neurotoxicity. Prior to neuronal pathology, microglia upregulated ionized calcium binding adaptor molecule 1 (Iba1), signaling a functional shift. With neurodegeneration, interleukin-6 and complement component 1q were increased. The results suggest a stimulatory, proliferative signal for microglia present at the onset of mhtt fragment-induced neurodegeneration. Thus, microglia effect a localized inflammatory response to neuronal mhtt expression that may serve to direct microglial removal of dysfunctional neurites or aberrant synapses, as is required for reparative actions in vivo. Published by Elsevier Inc. JF - Neurobiology of aging AU - Kraft, Andrew D AU - Kaltenbach, Linda S AU - Lo, Donald C AU - Harry, G Jean AD - Neurotoxicology Group, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, USA. Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 621.e17 EP - 33 VL - 33 IS - 3 KW - Htt protein, mouse KW - 0 KW - Huntingtin Protein KW - Huntingtin protein, rat KW - Nerve Tissue Proteins KW - Nuclear Proteins KW - Index Medicus KW - Animals KW - Mice KW - Nerve Degeneration -- genetics KW - Mice, Transgenic KW - Rats KW - Synapses -- genetics KW - Animals, Newborn KW - Rats, Sprague-Dawley KW - Cells, Cultured KW - Nerve Degeneration -- metabolism KW - Nerve Degeneration -- pathology KW - Synapses -- pathology KW - Cell Death -- genetics KW - Organ Culture Techniques KW - Nuclear Proteins -- genetics KW - Neurons -- metabolism KW - Nerve Tissue Proteins -- biosynthesis KW - Cell Proliferation KW - Nerve Tissue Proteins -- genetics KW - Neurons -- pathology KW - Huntington Disease -- metabolism KW - Nuclear Proteins -- biosynthesis KW - Mutation -- genetics KW - Neurites -- pathology KW - Huntington Disease -- pathology KW - Neurites -- metabolism KW - Microglia -- pathology KW - Huntington Disease -- genetics KW - Microglia -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/916522179?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurobiology+of+aging&rft.atitle=Activated+microglia+proliferate+at+neurites+of+mutant+huntingtin-expressing+neurons.&rft.au=Kraft%2C+Andrew+D%3BKaltenbach%2C+Linda+S%3BLo%2C+Donald+C%3BHarry%2C+G+Jean&rft.aulast=Kraft&rft.aufirst=Andrew&rft.date=2012-03-01&rft.volume=33&rft.issue=3&rft.spage=621.e17&rft.isbn=&rft.btitle=&rft.title=Neurobiology+of+aging&rft.issn=1558-1497&rft_id=info:doi/10.1016%2Fj.neurobiolaging.2011.02.015 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-28 N1 - Date created - 2012-01-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Neuron. 1994 Dec;13(6):1263-8 [7993619] Nature. 1995 Apr 13;374(6523):647-50 [7715705] Nat Genet. 1995 May;10(1):104-10 [7647777] Proc Natl Acad Sci U S A. 1995 Sep 12;92(19):8710-4 [7568002] J Cereb Blood Flow Metab. 1999 Nov;19(11):1256-62 [10566972] Ann Neurol. 1999 Dec;46(6):842-9 [10589536] J Neuropathol Exp Neurol. 2001 Feb;60(2):161-72 [11273004] Science. 2001 Mar 23;291(5512):2423-8 [11264541] J Exp Med. 2001 Sep 17;194(6):781-95 [11560994] J Neuroimmunol. 2001 Oct 1;119(2):269-77 [11585630] J Neurosci. 2001 Nov 1;21(21):8473-81 [11606636] J Immunol. 2001 Nov 1;167(9):5004-10 [11673508] Methods. 2001 Dec;25(4):402-8 [11846609] Cell Death Differ. 2002 Aug;9(8):801-6 [12107823] Nat Neurosci. 2002 Aug;5(8):731-6 [12089530] Neuron. 2002 Aug 29;35(5):819-22 [12372277] Glia. 2002 Nov;40(2):156-63 [12379903] Hum Mol Genet. 2002 Nov 1;11(23):2905-17 [12393802] FASEB J. 2003 Jun;17(9):1110-1 [12692086] Glia. 2003 Sep;43(3):274-80 [12898706] Trends Mol Med. 2003 Oct;9(10):414-20 [14557053] Proc Natl Acad Sci U S A. 2003 Oct 14;100(21):12171-6 [14527999] Mol Immunol. 2004 Jan;40(10):709-16 [14644096] J Neurosci. 2004 Feb 4;24(5):1101-12 [14762128] FASEB J. 2004 Feb;18(2):412-4 [14688201] Mol Cell Biol. 2004 Sep;24(18):8195-209 [15340079] J Neurosci. 2004 Sep 29;24(39):8500-9 [15456824] EMBO Rep. 2004 Oct;5(10):958-63 [15459747] Nature. 2004 Oct 14;431(7010):805-10 [15483602] J Neurosci. 1995 Nov;15(11):6999-7011 [7472456] Acta Neuropathol. 1996;91(4):385-95 [8928615] Cell Tissue Res. 1997 Feb;287(3):447-58 [9023076] Science. 1997 Sep 26;277(5334):1990-3 [9302293] Glia. 1998 Feb;22(2):180-8 [9537838] Hum Mol Genet. 1998 May;7(5):783-90 [9536081] Cell. 1998 Oct 2;95(1):55-66 [9778247] Brain Res. 1998 Dec 7;813(2):241-53 [9838143] Ann Neurol. 1999 Jan;45(1):25-32 [9894873] J Neuropathol Exp Neurol. 1999 Feb;58(2):165-73 [10029099] J Neurosci. 1999 Apr 1;19(7):2522-34 [10087066] J Neurosci. 1999 May 15;19(10):3791-800 [10234011] Nature. 1999 May 20;399(6733):263-7 [10353249] Hum Mol Genet. 1999 Jul;8(7):1227-36 [10369868] Exp Neurol. 1999 Oct;159(2):362-76 [10506508] J Neurocytol. 2004 Sep;33(5):517-33 [15906159] J Neurosci Res. 2005 Aug 1;81(3):302-13 [15954124] Cell Mol Life Sci. 2005 Sep;62(17):1901-12 [15968465] Nat Rev Neurosci. 2005 Dec;6(12):919-30 [16288298] J Cell Biol. 2005 Dec 19;171(6):1001-12 [16365166] Neurology. 2006 Jun 13;66(11):1638-43 [16769933] Neuroscience. 2009 Feb 6;158(3):1030-8 [18644426] Brain. 2009 Feb;132(Pt 2):288-95 [18567623] J Neurosci. 2009 Apr 1;29(13):3974-80 [19339593] FASEB J. 2009 Jun;23(6):1893-906 [19171786] Neurotoxicology. 2009 Sep;30(5):785-93 [19596372] Prog Neurobiol. 2009 Nov;89(3):277-87 [19686799] J Neurochem. 2010 Feb;112(3):733-43 [19919576] Trends Immunol. 2010 Apr;31(4):154-63 [20153254] Hum Mol Genet. 2010 May 1;19(9):1756-65 [20147317] Nat Rev Neurol. 2010 Apr;6(4):193-201 [20234358] J Biomol Screen. 2010 Aug;15(7):806-19 [20581077] Brain Res Brain Res Rev. 1995 Mar;20(3):269-87 [7550361] Z Zellforsch Mikrosk Anat. 1968;85(2):145-57 [5706753] J Cell Biol. 1980 Jun;85(3):890-902 [6248568] Science. 1985 Feb 15;227(4688):770-3 [3155875] N Engl J Med. 1986 Nov 13;315(20):1267-76 [2877396] Neurosci Lett. 1988 Mar 10;85(3):317-21 [3362421] Glia. 2007 Mar;55(4):360-8 [17136771] Brain Res Bull. 2007 Apr 30;72(2-3):148-51 [17352938] Prog Neurobiol. 2007 Apr;81(5-6):253-71 [17169479] Glia. 2007 Jun;55(8):873-84 [17405148] Glia. 2007 Aug 1;55(10):1074-84 [17551926] J Proteome Res. 2007 Jul;6(7):2833-40 [17552550] Nat Neurosci. 2007 Nov;10(11):1387-94 [17965659] Cell. 2007 Dec 14;131(6):1164-78 [18083105] J Biol Chem. 2008 Mar 21;283(12):7390-400 [18079112] J Exp Med. 2008 Aug 4;205(8):1869-77 [18625748] Hum Mol Genet. 2008 Sep 1;17(17):2738-51 [18558632] J Neurosci. 2008 Sep 24;28(39):9723-31 [18815258] N Engl J Med. 1990 May 3;322(18):1293-8 [1691447] Cell. 1993 Mar 26;72(6):971-83 [8458085] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.neurobiolaging.2011.02.015 ER - TY - JOUR T1 - How Do Body Diagrams Affect the Accuracy and Consistency of Childrenʼs Reports of Bodily Touch Across Repeated Interviews? AN - 1665157033 AB - We examined the amount, accuracy, and consistency of information reported by 58 5- to 7-year-old children about a staged event that included physical contact/touching. Both 1 and 7months following the event, children were asked both open and yes/no questions about touch [i] when provided with human body diagrams (HBDs), [ii] following instruction and practice using the HBDs, or [iii] without HBDs. Children interviewed with HBDs reported more information at 7months, but a high proportion of inaccurate touches. Children seldom repeated touch-related information across the two interviews and did not incorporate errors made in the 1-month interview into their open-ended accounts 6months later. Asking children to talk about innocuous touch may lead them to report unreliable information, especially when HBDs are used as aids and repeated interviews are conducted across delays that resemble those typical of forensic contexts. Copyright © 2011 John Wiley & Sons, Ltd. JF - Applied Cognitive Psychology AU - Brown, Deirdre AU - Pipe, Margaret-Ellen AU - Lewis, Charlie AU - Lamb, Michael E AU - Orbach, Yael AD - University of Victoria, Wellington, New Zealand. ; Brooklyn College, New York, USA. ; University of Lancaster, Lancaster, UK. ; University of Cambridge, Cambridge, UK. ; National Institute of Child Health and Human Development, Bethesda, USA. ; University of Victoria, Wellington, New Zealand. Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 174 EP - 181 CY - Bognor Regis PB - Wiley Subscription Services, Inc. VL - 26 IS - 2 SN - 0888-4080 KW - Psychology KW - Accuracy KW - Children KW - Diagrams KW - Touch UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1665157033?accountid=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=Applied+Cognitive+Psychology&rft.atitle=How+Do+Body+Diagrams+Affect+the+Accuracy+and+Consistency+of+Children%CA%BCs+Reports+of+Bodily+Touch+Across+Repeated+Interviews%3F&rft.au=Brown%2C+Deirdre%3BPipe%2C+Margaret-Ellen%3BLewis%2C+Charlie%3BLamb%2C+Michael+E%3BOrbach%2C+Yael&rft.aulast=Brown&rft.aufirst=Deirdre&rft.date=2012-03-01&rft.volume=26&rft.issue=2&rft.spage=174&rft.isbn=&rft.btitle=&rft.title=Applied+Cognitive+Psychology&rft.issn=08884080&rft_id=info:doi/10.1002%2Facp.1828 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2015-01-09 N1 - Last updated - 2016-08-16 DO - http://dx.doi.org/10.1002/acp.1828 ER - TY - JOUR T1 - A randomized controlled trial of rituximab following failure of antiviral therapy for hepatitis C virus-associated cryoglobulinemic vasculitis AN - 1534820750; 19767661 AB - Objective To perform a randomized controlled trial of rituximab in patients with hepatitis C virus (HCV)-associated mixed cryoglobulinemic vasculitis. Methods We conducted a single-center, open-label, randomized controlled trial of rituximab (375 mg/ m super(2)/week for 4 weeks) compared to the best available therapy (maintenance or increase in immunosuppressive therapy) for HCV-associated cryoglobulinemic vasculitis in patients in whom antiviral therapy had failed to induce remission. The primary end point was disease remission at 6 months from study entry. Results A total of 24 patients were enrolled (12 in each treatment group). Baseline disease activity and organ involvement were similar in the two groups. Ten patients in the rituximab group (83%) were in remission at study month 6, as compared with 1 patient in the control group (8%), a result that met the criterion for stopping the study (P < 0.001). The median duration of remission for rituximab-treated patients who reached the primary end point was 7 months. No adverse effects of rituximab on HCV plasma viremia or on hepatic transaminase levels were observed. Conclusion Rituximab was a well-tolerated and effective treatment in patients with HCV-associated cryoglobulinemic vasculitis in whom antiviral therapy failed to induce remission. JF - Arthritis & Rheumatism AU - Sneller, Michael C AU - Hu, Zonghui AU - Langford, Carol A AD - National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland. Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 835 EP - 842 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 64 IS - 3 SN - 0004-3591, 0004-3591 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - Vasculitis KW - Hepatitis C virus KW - rituximab KW - Liver KW - Remission KW - Hepatitis C KW - Viremia KW - Clinical trials KW - Immunosuppressive agents KW - Side effects KW - transaminase KW - A 01340:Antibiotics & Antimicrobials KW - V 22400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1534820750?accountid=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=Arthritis+%26+Rheumatism&rft.atitle=A+randomized+controlled+trial+of+rituximab+following+failure+of+antiviral+therapy+for+hepatitis+C+virus-associated+cryoglobulinemic+vasculitis&rft.au=Sneller%2C+Michael+C%3BHu%2C+Zonghui%3BLangford%2C+Carol+A&rft.aulast=Sneller&rft.aufirst=Michael&rft.date=2012-03-01&rft.volume=64&rft.issue=3&rft.spage=835&rft.isbn=&rft.btitle=&rft.title=Arthritis+%26+Rheumatism&rft.issn=00043591&rft_id=info:doi/10.1002%2Fart.34322 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-06-01 N1 - Last updated - 2015-11-25 N1 - SubjectsTermNotLitGenreText - Vasculitis; rituximab; Liver; Remission; Viremia; Hepatitis C; Immunosuppressive agents; Clinical trials; transaminase; Side effects; Hepatitis C virus DO - http://dx.doi.org/10.1002/art.34322 ER - TY - JOUR T1 - Selective killing of Kaposi's sarcoma-associated herpesvirus lytically infected cells with a recombinant immunotoxin targeting the viral gpK8.1A envelope glycoprotein. AN - 1515642298; 22377676 AB - Kaposi sarcoma-associated herpesvirus (KSHV, human herpesvirus 8) is etiologically associated with three neoplastic syndromes: Kaposi sarcoma and the uncommon HIV-associated B-cell lymphoproliferative disorders primary effusion lymphoma and multicentric Castleman disease. The incidence of the latter B-cell pathology has been increasing in spite of antiretroviral therapy; its association with lytic virus replication has prompted interest in therapeutic strategies aimed at this phase of the virus life cycle. We designed and expressed a recombinant immunotoxin (2014-PE38) targeting the gpK8.1A viral glycoprotein expressed on the surface of the virion and infected cells. We show that this immunotoxin selectively kills KSHV-infected cells in dose-dependent fashion, resulting in major reductions of infectious virus release. The immunotoxin and ganciclovir, an inhibitor of viral DNA replication, showed marked reciprocal potentiation of antiviral activities. These results suggest that the immunotoxin, alone or in combination, may represent a new approach to treat diseases associated with KSHV lytic replication. JF - mAbs AU - Chatterjee, Deboeeta AU - Chandran, Bala AU - Berger, Edward A AD - Laboratory of Viral Diseases; National Institute of Allergy and Infectious Diseases; National Institutes of Health; Bethesda, MD USA. ; Departiment of Microbiology and Immunology; Rosalind Franklin University of Medicine and Science; Chicago, IL USA. PY - 2012 SP - 233 EP - 242 VL - 4 IS - 2 KW - Antibodies, Viral KW - 0 KW - Antiviral Agents KW - DNA, Viral KW - Glycoproteins KW - Immunotoxins KW - K8.1 protein, Human herpesvirus 8 KW - Recombinant Proteins KW - Viral Proteins KW - Index Medicus KW - ganciclovir KW - reciprocal drug potentiation KW - Pseudomonas exotoxin A KW - KSHV surface glycoprotein KW - targeted cytotoxic proteins KW - human herpesvirus-8 KW - KSHV lytic infection KW - multicentric Castleman disease KW - Virus Replication KW - Animals KW - Base Sequence KW - Recombinant Proteins -- pharmacology KW - DNA Replication -- immunology KW - Humans KW - DNA, Viral -- immunology KW - Cercopithecus aethiops KW - Recombinant Proteins -- immunology KW - Molecular Sequence Data KW - Vero Cells KW - Recombinant Proteins -- genetics KW - DNA Replication -- drug effects KW - Viral Proteins -- immunology KW - Viral Proteins -- genetics KW - Glycoproteins -- antagonists & inhibitors KW - Antibodies, Viral -- pharmacology KW - Herpesviridae Infections -- pathology KW - Herpesvirus 8, Human -- physiology KW - Glycoproteins -- genetics KW - Herpesviridae Infections -- immunology KW - Antibodies, Viral -- immunology KW - Glycoproteins -- immunology KW - Antibodies, Viral -- genetics KW - Immunotoxins -- immunology KW - Antiviral Agents -- pharmacology KW - Immunotoxins -- genetics KW - Herpesviridae Infections -- drug therapy KW - Antiviral Agents -- immunology KW - Immunotoxins -- pharmacology KW - Viral Proteins -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1515642298?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=mAbs&rft.atitle=Selective+killing+of+Kaposi%27s+sarcoma-associated+herpesvirus+lytically+infected+cells+with+a+recombinant+immunotoxin+targeting+the+viral+gpK8.1A+envelope+glycoprotein.&rft.au=Chatterjee%2C+Deboeeta%3BChandran%2C+Bala%3BBerger%2C+Edward+A&rft.aulast=Chatterjee&rft.aufirst=Deboeeta&rft.date=2012-03-01&rft.volume=4&rft.issue=2&rft.spage=233&rft.isbn=&rft.btitle=&rft.title=mAbs&rft.issn=1942-0870&rft_id=info:doi/10.4161%2Fmabs.4.2.19262 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2015-02-12 N1 - Date created - 2014-04-11 N1 - Date revised - 2017-01-13 N1 - Genetic sequence - JQ434470; 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author reply 349 [20146033] J Infect Dis. 2010 Jun 15;201(12):1919-22 [20443737] PLoS Pathog. 2010;6(6):e1000803 [20548940] Curr Opin Chem Biol. 2010 Aug;14(4):529-37 [20643572] J Clin Oncol. 2010 Aug 10;28(23):3701-8 [20625121] Proc Natl Acad Sci U S A. 2010 Sep 21;107(38):16637-42 [20817853] Blood. 2010 Nov 25;116(22):4415-21 [20688959] Curr Opin HIV AIDS. 2011 Jan;6(1):80-5 [21242898] Immunotherapy. 2011 Mar;3(3):349-70 [21395378] Proc Natl Acad Sci U S A. 2011 Apr 5;108(14):5742-7 [21436054] Oncologist. 2011;16(4):497-511 [21441298] Expert Opin Drug Deliv. 2011 May;8(5):605-21 [21453191] Cancer Lett. 2011 Jun 28;305(2):163-74 [21493001] Antiviral Res. 2011 Jun;90(3):143-50 [21440007] Drug Discov Today. 2011 Jun;16(11-12):495-503 [21511052] J Clin Oncol. 2011 Jun 20;29(18):2481-6 [21555697] Curr Opin Infect Dis. 2011 Aug;24(4):295-301 [21666458] Blood. 2011 Jun 30;117(26):6977-86 [21487108] Blood. 2011 Jul 14;118(2):271-5 [21511959] J Med Virol. 2011 Oct;83(10):1696-703 [21837785] J Immunother. 2011 Nov-Dec;34(9):611-28 [21989410] Clin Cancer Res. 2011 Oct 15;17(20):6389-97 [22003066] Clin Cancer Res. 2011 Oct 15;17(20):6398-405 [22003067] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.4161/mabs.4.2.19262 ER - TY - JOUR T1 - Incentive effect on inhibitory control in adolescents with early-life stress: An antisaccade study AN - 1512194543; 201406440 AB - Early-life stress (ES) such as adoption, change of caregiver, or experience of emotional neglect may influence the way in which affected individuals respond to emotional stimuli of positive or negative valence. These modified responses may stem from a direct alteration of how emotional stimuli are coded, and/or the cognitive function implicated in emotion modulation, such as self-regulation or inhibition. These ES effects have been probed on tasks either targeting reward and inhibitory function. Findings revealed deficits in both reward processing and inhibitory control in ES youths. However, no work has yet examined whether incentives can improve automatic response or inhibitory control in ES youths. To determine whether incentives would only improve self-regulated voluntary actions or generalize to automated motoric responses, participants were tested on a mixed eye movement task that included reflex-like prosaccades and voluntary controlled antisaccade eye movements. Seventeen adopted children (10 females, mean age 11.3 years) with a documented history of neglect and 29 typical healthy youths (16 females, mean age 11.9 years) performed the mixed prosaccade/antisaccade task during monetary incentive conditions or during no-incentive conditions. Across both saccade types, ES adolescents responded more slowly than controls. As expected, control participants committed fewer errors on antisaccades during the monetary incentive condition relative to the no-incentive condition. By contrast, ES youths failed to show this incentive-related improvement on inhibitory control. No significant incentive effects were found with prepotent prosaccades trials in either group. Finally, co-morbid psychopathology did not modulate the findings. These data suggest that youths with experience of early stress exhibit deficient modulation of inhibitory control by reward processes, in tandem with a reward-independent deficit in preparation for both automatic and controlled responses. These data may be relevant to interventions in ES youths. [Copyright Elsevier Ltd.] JF - Child Abuse & Neglect AU - Mueller, Sven C AU - Hardin, Michael G AU - Korelitz, Katherine AU - Daniele, Teresa AU - Bemis, Jessica AU - Dozier, Mary AU - Peloso, Elizabeth AU - Maheu, Francoise S AU - Pine, Daniel S AU - Ernst, Monique AD - Section of Developmental and Affective Neuroscience National Institute of Mental Health, National Institute of Health, Bethesda, MD, USA Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 217 EP - 225 PB - Elsevier Science, Amsterdam The Netherlands VL - 36 IS - 3 SN - 0145-2134, 0145-2134 KW - Reward Antisaccade Cognitive control Early adversity Stress KW - Inhibitory processes KW - Eye movements KW - Caretaker syndrome KW - Incentives KW - Rewards KW - Adolescents KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1512194543?accountid=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+Abuse+%26+Neglect&rft.atitle=Incentive+effect+on+inhibitory+control+in+adolescents+with+early-life+stress%3A+An+antisaccade+study&rft.au=Mueller%2C+Sven+C%3BHardin%2C+Michael+G%3BKorelitz%2C+Katherine%3BDaniele%2C+Teresa%3BBemis%2C+Jessica%3BDozier%2C+Mary%3BPeloso%2C+Elizabeth%3BMaheu%2C+Francoise+S%3BPine%2C+Daniel+S%3BErnst%2C+Monique&rft.aulast=Mueller&rft.aufirst=Sven&rft.date=2012-03-01&rft.volume=36&rft.issue=3&rft.spage=217&rft.isbn=&rft.btitle=&rft.title=Child+Abuse+%26+Neglect&rft.issn=01452134&rft_id=info:doi/10.1016%2Fj.chiabu.2011.10.010 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2014-04-01 N1 - Last updated - 2016-09-27 N1 - CODEN - CABND3 N1 - SubjectsTermNotLitGenreText - Incentives; Inhibitory processes; Rewards; Eye movements; Caretaker syndrome; Adolescents DO - http://dx.doi.org/10.1016/j.chiabu.2011.10.010 ER - TY - JOUR T1 - The World Library of Toxicology, Chemical Safety, and Environmental Health (WLT) AN - 1434030174; 18507346 AB - The World Library of Toxicology, Chemical Safety, and Environmental Health, commonly referred to as the World Library of Toxicology (WLT), is a multilingual online portal of links to key global resources, representing a host of individual countries and multilateral organizations. The Site is designed as a network of, and gateway to, toxicological information and activities from around the world. It is built on a Wiki platform by a roster of Country Correspondents, with the aim of efficiently exchanging information and stimulating collaboration among colleagues, and building capacity, with the ultimate objective of serving as a tool to help improve global public health. The WLT was publicly launched on September 7, 2009, at the Seventh Congress of Toxicology in Developing Countries (CTDC-VII) in Sun City, South Africa. JF - Human & Experimental Toxicology AU - Wexler, Philip AU - Gilbert, Steven G AU - Thorp, Nick AU - Faustman, Elaine AU - Breskin, Donna D AD - US National Library of Medicine, Bethesda, MD, USA, wexlerp@mail.nih.gov Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 207 EP - 214 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 31 IS - 3 SN - 0960-3271, 0960-3271 KW - Pollution Abstracts; Environment Abstracts; Toxicology Abstracts; Health & Safety Science Abstracts KW - Congress KW - Environmental health KW - Public health KW - Sun KW - South Africa KW - Developing countries KW - Toxicology KW - Internet KW - Urban areas KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - X 24490:Other KW - P 6000:TOXICOLOGY AND HEALTH KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1434030174?accountid=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=Human+%26+Experimental+Toxicology&rft.atitle=The+World+Library+of+Toxicology%2C+Chemical+Safety%2C+and+Environmental+Health+%28WLT%29&rft.au=Wexler%2C+Philip%3BGilbert%2C+Steven+G%3BThorp%2C+Nick%3BFaustman%2C+Elaine%3BBreskin%2C+Donna+D&rft.aulast=Wexler&rft.aufirst=Philip&rft.date=2012-03-01&rft.volume=31&rft.issue=3&rft.spage=207&rft.isbn=&rft.btitle=&rft.title=Human+%26+Experimental+Toxicology&rft.issn=09603271&rft_id=info:doi/10.1177%2F0960327110389500 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-09-01 N1 - Number of references - 2 N1 - Last updated - 2014-05-02 N1 - SubjectsTermNotLitGenreText - Sun; Developing countries; Internet; Public health; Congress; Environmental health; Toxicology; Urban areas; South Africa DO - http://dx.doi.org/10.1177/0960327110389500 ER - TY - JOUR T1 - Self-assembling nanocomplexes by combining ferumoxytol, heparin and protamine for cell tracking by magnetic resonance imaging AN - 1419362554; 16823978 AB - We report on a new straightforward magnetic cell-labeling approach that combines three US Food and Drug Administration (FDA)-approved drugs-ferumoxytol, heparin and protamine-in serum-free medium to form self-assembling nanocomplexes that effectively label cells for in vivo magnetic resonance imaging (MRI). We observed that the ferumoxytol-heparin-protamine (HPF) nanocomplexes were stable in serum-free cell culture medium. HPF nanocomplexes show a threefold increase in T2 relaxivity compared to ferumoxytol. Electron microscopy showed internalized HPF in endosomes, which we confirmed by Prussian blue staining of labeled cells. There was no long-term effect or toxicity on cellular physiology or function of HPF-labeled hematopoietic stem cells, bone marrow stromal cells, neural stem cells or T cells when compared to controls. In vivo MRI detected 1,000 HPF-labeled cells implanted in rat brains. This HPF labeling method should facilitate the monitoring by MRI of infused or implanted cells in clinical trials. JF - Nature Medicine AU - Thu, Mya S AU - Bryant, L Henry AU - Coppola, Tiziana AU - Jordan, E Kay AU - Budde, Matthew D AU - Lewis, Bobbi K AU - Chaudhry, Aneeka AU - Ren, Jiaqiang AU - Varma, Nadimpalli Ravi S AU - Arbab, Ali S AU - Frank, Joseph A AD - Frank Laboratory and Laboratory of Diagnostic Radiology Research, Department of Radiology and Imaging Sciences, US National Institutes of Health (NIH), Bethesda, Maryland, USA. Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 463 EP - 467 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 18 IS - 3 SN - 1078-8956, 1078-8956 KW - Toxicology Abstracts KW - stromal cells KW - Magnetic resonance imaging KW - Bone marrow KW - Brain KW - Cell culture KW - Toxicity KW - Clinical trials KW - Long-term effects KW - Stem cells KW - serum-free medium KW - endosomes KW - protamine KW - Lymphocytes T KW - Neural stem cells KW - Heparin KW - Electron microscopy KW - X 24390:Radioactive Materials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1419362554?accountid=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+Medicine&rft.atitle=Self-assembling+nanocomplexes+by+combining+ferumoxytol%2C+heparin+and+protamine+for+cell+tracking+by+magnetic+resonance+imaging&rft.au=Thu%2C+Mya+S%3BBryant%2C+L+Henry%3BCoppola%2C+Tiziana%3BJordan%2C+E+Kay%3BBudde%2C+Matthew+D%3BLewis%2C+Bobbi+K%3BChaudhry%2C+Aneeka%3BRen%2C+Jiaqiang%3BVarma%2C+Nadimpalli+Ravi+S%3BArbab%2C+Ali+S%3BFrank%2C+Joseph+A&rft.aulast=Thu&rft.aufirst=Mya&rft.date=2012-03-01&rft.volume=18&rft.issue=3&rft.spage=463&rft.isbn=&rft.btitle=&rft.title=Nature+Medicine&rft.issn=10788956&rft_id=info:doi/10.1038%2Fnm.2666 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-08-01 N1 - Last updated - 2013-10-04 N1 - SubjectsTermNotLitGenreText - stromal cells; Magnetic resonance imaging; Brain; Bone marrow; Cell culture; Toxicity; Clinical trials; Long-term effects; endosomes; serum-free medium; Stem cells; protamine; Lymphocytes T; Heparin; Neural stem cells; Electron microscopy DO - http://dx.doi.org/10.1038/nm.2666 ER - TY - JOUR T1 - "You're too young for this": Adolescent and Young Adults' Perspectives on Cancer Survivorship AN - 1364704462; 201304163 AB - Adolescent and young adult cancer survivors face unique challenges not systematically addressed by cancer clinicians. Four focus groups and two individual interviews were conducted with 19 survivors to profile experiences and identify key concerns for future interventions. The resultant themes reflect cancer care continuum challenges (such as delays in diagnosis, problems with adherence), psychosocial concerns (such as infertility and reproductive concerns, changing social relationships, financial burden), and the paradox of being diagnosed with cancer as a young adult. Future intervention development for adolescent and young adult survivors should involve patient voices at each stage of the research process. Adapted from the source document. JF - Journal of Psychosocial Oncology AU - Kent, Erin E AU - Parry, Carla AU - Montoya, Michael J AU - Sender, Leonard S AU - Morris, Rebecca A AU - Anton-Culver, Hoda AD - Cancer Prevention Fellowship Program and Office of Cancer Survivorship, National Cancer Institute, National Institutes of Health erin.kent@nih.gov Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 260 EP - 279 PB - Taylor & Francis, Philadelphia PA VL - 30 IS - 2 SN - 0734-7332, 0734-7332 KW - Adult Development KW - Intervention KW - Patients KW - Young Adults KW - Adolescent Development KW - Adolescents KW - Cancer KW - article KW - 6121: therapeutic interventions UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1364704462?accountid=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=Journal+of+Psychosocial+Oncology&rft.atitle=%22You%27re+too+young+for+this%22%3A+Adolescent+and+Young+Adults%27+Perspectives+on+Cancer+Survivorship&rft.au=Kent%2C+Erin+E%3BParry%2C+Carla%3BMontoya%2C+Michael+J%3BSender%2C+Leonard+S%3BMorris%2C+Rebecca+A%3BAnton-Culver%2C+Hoda&rft.aulast=Kent&rft.aufirst=Erin&rft.date=2012-03-01&rft.volume=30&rft.issue=2&rft.spage=260&rft.isbn=&rft.btitle=&rft.title=Journal+of+Psychosocial+Oncology&rft.issn=07347332&rft_id=info:doi/10.1080%2F07347332.2011.644396 LA - English DB - Social Services Abstracts N1 - Date revised - 2013-06-01 N1 - Last updated - 2016-09-28 N1 - CODEN - JPONED N1 - SubjectsTermNotLitGenreText - Cancer; Young Adults; Adolescents; Intervention; Patients; Adolescent Development; Adult Development DO - http://dx.doi.org/10.1080/07347332.2011.644396 ER - TY - JOUR T1 - Discussions of cancer clinical trials with the National Cancer Institute's Cancer Information Service AN - 1272075723; 4385947 AB - Clinical trials are essential for the development of new and effective treatments for cancer; however, participation rates are low. One reason for this is lack of knowledge about clinical trials. This study assessed how often clinical trials are discussed on calls to National Cancer Institute's Cancer Information Service (CIS). The authors quantitatively analyzed 283,094 calls to the CIS (1-800-4-CANCER) over 3 years (2006-2008). They calculated descriptive statistics and multivariate regressions to determine whether specific caller characteristics are associated with the presence of a clinical trials discussion. In addition, 2 focus groups were conducted with CIS information specialists ( n = 12) to provide insight into the findings. The authors found that approximately 9.3% of CIS calls discussed clinical trials, with higher percentages for patients (12.5%) and family members (15.4%). Calls with Hispanics, Blacks, and Spanish speakers were less likely to include a conversation. For all cancers, patients who are in treatment or experiencing a recurrence were statistically significantly more likely to discuss clinical trials. CIS information specialists reported callers' limited knowledge of clinical trials. The CIS has the unique ability to make a substantial effect in educating patients about clinical trials as an option in cancer treatment and care. Reprinted by permission of Taylor & Francis Ltd. JF - Journal of health communication AU - Byrne, Margaret M AU - Kornfeld, Julie AU - Vanderpool, Robin AU - Belanger, Marc AD - University of Miami ; University of Kentucky ; National Cancer Institute Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 319 EP - 337 VL - 17 IS - 3 SN - 1081-0730, 1081-0730 KW - Sociology KW - Clinical trials KW - Information services KW - Health education KW - Medical research KW - Focus groups KW - Medical treatment KW - Patients KW - U.S.A. KW - Knowledge KW - Ethnic groups KW - Cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1272075723?accountid=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=Discussions+of+cancer+clinical+trials+with+the+National+Cancer+Institute%27s+Cancer+Information+Service&rft.au=Byrne%2C+Margaret+M%3BKornfeld%2C+Julie%3BVanderpool%2C+Robin%3BBelanger%2C+Marc&rft.aulast=Byrne&rft.aufirst=Margaret&rft.date=2012-03-01&rft.volume=17&rft.issue=3&rft.spage=319&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 - 1939 3617 6220; 6532 6515; 5077 10519 3279 971 3286 10919; 9271 7890 5792 10484; 7886 10902; 4424; 7073; 7890 5792 10484; 5779 4049; 433 293 14 ER - TY - JOUR T1 - Impact of Circulating Vitamin D Binding Protein Levels on the Association between 25-Hydroxyvitamin D and Pancreatic Cancer Risk: A Nested Case-Control Study AN - 1093449079; 16426614 AB - High concentrations of circulating 25-hydroxyvitamin D [25(OH)D] have been associated with elevated pancreatic cancer risk. As this is contrary to an expected inverse association between vitamin D status and cancer, we examined whether vitamin D binding protein (DBP), the primary carrier of vitamin D compounds in circulation, plays a role in this relationship. Prediagnostic serum DBP and 25(OH)D were studied in relation to risk of pancreatic cancer in a nested case-control study of 234 cases and 234 controls in the Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study of Finnish men. ORs and 95% CIs were estimated using logistic regression, and statistical tests were two-sided. We found that DBP and 25(OH)D were correlated (r = 0.27, P < 0.0001), and DBP was inversely associated with pancreatic cancer risk (OR = 0.66, 95% CI = 0.39-1.12, for the highest vs. lowest quartile; Ptrend = 0.02). Importantly, this association seemed to have a threshold between quartiles 2 to 4 and quartile 1, and was primarily evident among men with concurrent high 25(OH)D concentrations (OR = 0.33, 95% CI = 0.16-0.70 for highest vs. lowest quartile; Ptrend = 0.002), with no association in men with lower serum 25(OH)D (OR = 1.28, 95% CI = 0.62-2.61 for highest vs. lowest quartile, Ptrend 0.63, Pinteraction = 0.01). Men with higher 25(OH)D concentrations and serum DBP below the median showed greatly elevated risk of pancreatic cancer (OR = 5.01, 95% CI 2.33-10.78, for highest vs. lowest quartile; Ptrend < 0.0001), while risk was weakly inversely associated with serum 25(OH)D when DBP concentrations were higher (Pinteraction = 0.001). Taken together, our findings indicate that higher DBP concentrations may sequester more 25(OH)D and reduce free 25(OH)D bioavailability. Simultaneous examination of DBP and 25(OH)D may be important in determining the association of vitamin D with cancer risk. Cancer Res; 72(5); 1190-8. [copy]2012 AACR. JF - Cancer Research AU - Weinstein, Stephanie J AU - Stolzenberg-Solomon, Rachael Z AU - Kopp, William AU - Rager, Helen AU - Virtamo, Jarmo AU - Albanes, Demetrius AD - Authors' Affiliations: Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda Y1 - 2012/03/01/ PY - 2012 DA - 2012 Mar 01 SP - 1190 EP - 1198 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 72 IS - 5 SN - 0008-5472, 0008-5472 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Bioavailability KW - Cancer KW - Pancreatic cancer KW - Prevention KW - Proteins KW - Vitamins 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/1093449079?accountid=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+Research&rft.atitle=Impact+of+Circulating+Vitamin+D+Binding+Protein+Levels+on+the+Association+between+25-Hydroxyvitamin+D+and+Pancreatic+Cancer+Risk%3A+A+Nested+Case-Control+Study&rft.au=Weinstein%2C+Stephanie+J%3BStolzenberg-Solomon%2C+Rachael+Z%3BKopp%2C+William%3BRager%2C+Helen%3BVirtamo%2C+Jarmo%3BAlbanes%2C+Demetrius&rft.aulast=Weinstein&rft.aufirst=Stephanie&rft.date=2012-03-01&rft.volume=72&rft.issue=5&rft.spage=1190&rft.isbn=&rft.btitle=&rft.title=Cancer+Research&rft.issn=00085472&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2012-10-19 N1 - SubjectsTermNotLitGenreText - Bioavailability; Prevention; Vitamins; Pancreatic cancer; Proteins; Cancer ER - TY - JOUR T1 - Structure of the cytoplasmic domain of Yersinia pestis YscD, an essential component of the type III secretion system AN - 1038302393; 16885267 AB - The Yersinia pestis YscD protein is an essential component of the type III secretion system. YscD consists of an N-terminal cytoplasmic domain (residues 1-121), a transmembrane linker (122-142) and a large periplasmic domain (143-419). Both the cytoplasmic and the periplasmic domains are required for the assembly of the type III secretion system. Here, the structure of the YscD cytoplasmic domain solved by SAD phasing is presented. Although the three-dimensional structure is similar to those of forkhead-associated (FHA) domains, comparison with the structures of canonical FHA domains revealed that the cytoplasmic domain of YscD lacks the conserved residues that are required for binding phosphothreonine and is therefore unlikely to function as a true FHA domain. JF - Acta Crystallographica Section D AU - Lountos, George T AU - Tropea, Joseph E AU - Waugh, David S AD - Basic Science Program, SAIC-Frederick Inc., National Cancer Institute at Frederick, Frederick, MD 21702-1201, USA Y1 - 2012/03/01/ PY - 2012 DA - 2012 Mar 01 SP - 201 EP - 209 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 68 IS - 3 SN - 0907-4449, 0907-4449 KW - Microbiology Abstracts B: Bacteriology KW - Secretion KW - Yersinia pestis KW - J 02330:Biochemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1038302393?accountid=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+D&rft.atitle=Structure+of+the+cytoplasmic+domain+of+Yersinia+pestis+YscD%2C+an+essential+component+of+the+type+III+secretion+system&rft.au=Lountos%2C+George+T%3BTropea%2C+Joseph+E%3BWaugh%2C+David+S&rft.aulast=Lountos&rft.aufirst=George&rft.date=2012-03-01&rft.volume=68&rft.issue=3&rft.spage=201&rft.isbn=&rft.btitle=&rft.title=Acta+Crystallographica+Section+D&rft.issn=09074449&rft_id=info:doi/10.1107%2FS0907444911054308 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-09-01 N1 - Document feature - figure 0 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Secretion; Yersinia pestis DO - http://dx.doi.org/10.1107/S0907444911054308 ER - TY - JOUR T1 - Transcriptional regulation of the c-Myc promoter by NFAT1 involves negative and positive NFAT-responsive elements. AN - 1034658107; 22333584 AB - A number of physiological processes in both normal and cancer cells are regulated by the proto-oncogene c-Myc. Among them, processes such as cell cycle regulation, apoptosis, angiogenesis and metastasis are also controlled by the nuclear factor of activated T cells (NFAT) family of transcription factors. It is already known that NFAT upregulates c-Myc expression by binding to an element located in the minimal c-Myc promoter. However, the importance of other NFAT sites in the context of the full promoter has not been evaluated. In this work, we demonstrate that the regulation of c-Myc by NFAT1 is more complex than previously conceived. In addition to the proximal site, NFAT1 directly binds to distal sites in the c-Myc promoter with different affinities. Promoter deletions and site-directed mutagenesis of NFAT binding sites in HEK293T cells suggest that in NFAT1-mediated transactivation, some NFAT elements are negative and dominant and others are positive and recessive. Furthermore, we demonstrate that cooperation with partner proteins, such as p300, enhances NFAT1-mediated transactivation of the c-Myc promoter. At last, the newly identified sites are also responsive to NFAT2 in HEK293T cells. However, in NIH3T3 cells, the regulation mediated by NFAT proteins is not dependent on the known NFAT sites, including the site previously described. Thus, our data suggest that the contribution of NFAT to the regulation of c-Myc expression may depend on a balance between the binding to positive and negative NFAT-responsive elements and cooperation with transcriptional cofactors, which may differ according to the context and/or cell type. JF - Cell cycle (Georgetown, Tex.) AU - Mognol, Giuliana P AU - de Araujo-Souza, Patricia S AU - Robbs, Bruno K AU - Teixeira, Leonardo K AU - Viola, Joao P B AD - Program of Cellular Biology, Brazilian National Cancer Institute (INCA), Rio de Janeiro, Brazil. Y1 - 2012/03/01/ PY - 2012 DA - 2012 Mar 01 SP - 1014 EP - 1028 VL - 11 IS - 5 KW - NFATC Transcription Factors KW - 0 KW - Proto-Oncogene Proteins c-myc KW - p300-CBP Transcription Factors KW - EC 2.3.1.48 KW - Calcineurin KW - EC 3.1.3.16 KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Animals KW - Calcineurin -- metabolism KW - HEK293 Cells KW - Humans KW - CD4-Positive T-Lymphocytes -- immunology KW - Transcription, Genetic KW - Mice KW - NIH 3T3 Cells KW - Binding Sites KW - Calcium -- metabolism KW - Mutagenesis, Site-Directed KW - Promoter Regions, Genetic KW - CD4-Positive T-Lymphocytes -- metabolism KW - p300-CBP Transcription Factors -- metabolism KW - Mice, Inbred C57BL KW - Protein Structure, Tertiary KW - Signal Transduction KW - NFATC Transcription Factors -- chemistry KW - Proto-Oncogene Proteins c-myc -- genetics KW - Proto-Oncogene Proteins c-myc -- metabolism KW - NFATC Transcription Factors -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1034658107?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+cycle+%28Georgetown%2C+Tex.%29&rft.atitle=Transcriptional+regulation+of+the+c-Myc+promoter+by+NFAT1+involves+negative+and+positive+NFAT-responsive+elements.&rft.au=Mognol%2C+Giuliana+P%3Bde+Araujo-Souza%2C+Patricia+S%3BRobbs%2C+Bruno+K%3BTeixeira%2C+Leonardo+K%3BViola%2C+Joao+P+B&rft.aulast=Mognol&rft.aufirst=Giuliana&rft.date=2012-03-01&rft.volume=11&rft.issue=5&rft.spage=1014&rft.isbn=&rft.btitle=&rft.title=Cell+cycle+%28Georgetown%2C+Tex.%29&rft.issn=1551-4005&rft_id=info:doi/10.4161%2Fcc.11.5.19518 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-04 N1 - Date created - 2012-08-21 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.4161/cc.11.5.19518 ER - TY - JOUR T1 - Retained platinum uptake and indifference to p53 status make novel transplatinum agents active in platinum-resistant cells compared to cisplatin and oxaliplatin. AN - 1034658106; 22333583 AB - Despite the clinical success of platinum-containing drugs in the treatment of solid tumors, acquired resistance remains a major obstacle. We previously identified a group of novel transplanaramine or transplatinum compounds based on distinct activity profiles in the NCI-60 panel. In the present study, parental KB-3.1 cells with wild-type p53 and its cisplatin- and oxaliplatin-resistant sublines harboring mutant p53 proteins were used to contrast several transplatinum compounds with cisplatin and oxaliplatin. The transplatinum compounds retained cytotoxic activity in the resistant cell lines. While intracellular accumulation and DNA platination of cisplatin and oxaliplatin was decreased in the resistant cells, the transplatinum compounds both accumulated intracellularly and platinated DNA at comparable levels in all cell lines. Cytoflow analysis confirmed that cisplatin and oxaliplatin alter the cell cycle distribution and result in apoptosis; however, at comparably toxic concentrations, the transplatinum compounds did not alter the cell cycle distribution. Analysis of the cytoplasmic fraction treated with acetone showed that cisplatin and oxaliplatin readily bound to macromolecules in the pellet, whereas a larger percentage of the transplatinum compounds remained in the supernatant. We concluded that, distinct from platinum compounds currently in use, transplatinum compounds accumulate intracellularly in resistant cells at levels comparable to those in drug-sensitive cells, do not affect the cell cycle and thus retain cytotoxicity independent of p53 status and likely have cytoplasmic targets that are important in their activity. JF - Cell cycle (Georgetown, Tex.) AU - Murphy, Robert F AU - Komlodi-Pasztor, Edina AU - Robey, Robert AU - Balis, Frank M AU - Farrell, Nicholas P AU - Fojo, Tito AD - Pediatric Oncology Branch, National Cancer Institute, National Institutes of Health (NIH), Bethesda, MD, USA. murphyb@mail.nih.gov Y1 - 2012/03/01/ PY - 2012 DA - 2012 Mar 01 SP - 963 EP - 973 VL - 11 IS - 5 KW - Antineoplastic Agents KW - 0 KW - Organoplatinum Compounds KW - Tumor Suppressor Protein p53 KW - oxaliplatin KW - 04ZR38536J KW - DNA KW - 9007-49-2 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Humans KW - DNA -- metabolism KW - Apoptosis -- drug effects KW - Cell Cycle Checkpoints -- drug effects KW - DNA -- chemistry KW - Cell Line, Tumor KW - Drug Resistance, Neoplasm -- drug effects KW - Cisplatin -- chemistry KW - Organoplatinum Compounds -- chemistry KW - Cisplatin -- toxicity KW - Antineoplastic Agents -- toxicity KW - Organoplatinum Compounds -- toxicity KW - Antineoplastic Agents -- chemistry KW - Tumor Suppressor Protein p53 -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1034658106?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cell+cycle+%28Georgetown%2C+Tex.%29&rft.atitle=Retained+platinum+uptake+and+indifference+to+p53+status+make+novel+transplatinum+agents+active+in+platinum-resistant+cells+compared+to+cisplatin+and+oxaliplatin.&rft.au=Murphy%2C+Robert+F%3BKomlodi-Pasztor%2C+Edina%3BRobey%2C+Robert%3BBalis%2C+Frank+M%3BFarrell%2C+Nicholas+P%3BFojo%2C+Tito&rft.aulast=Murphy&rft.aufirst=Robert&rft.date=2012-03-01&rft.volume=11&rft.issue=5&rft.spage=963&rft.isbn=&rft.btitle=&rft.title=Cell+cycle+%28Georgetown%2C+Tex.%29&rft.issn=1551-4005&rft_id=info:doi/10.4161%2Fcc.11.5.19447 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-01-04 N1 - Date created - 2012-08-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Inorg Chem. 2006 Jul 24;45(15):5733-5 [16841974] Cancer Lett. 2006 Mar 8;234(1):34-9 [16297532] Cancer Chemother Pharmacol. 2006 Dec;58(6):759-64 [16847673] Cell Cycle. 2006 Oct;5(19):2253-9 [16969106] Biochem Pharmacol. 2007 Jun 1;73(11):1749-57 [17418817] Biochem J. 2008 Feb 1;409(3):731-40 [17944601] Clin Cancer Res. 2008 Mar 1;14(5):1291-5 [18316546] Drug Resist Updat. 2008 Feb-Apr;11(1-2):1-16 [18394950] Expert Rev Anticancer Ther. 2008 May;8(5):683-8 [18471041] N Engl J Med. 2008 Sep 11;359(11):1116-27 [18784101] Gynecol Oncol. 2009 Jan;112(1):275-81 [18977023] J Clin Oncol. 2009 Apr 20;27(12):2046-51 [19289620] Oncogene. 2009 Sep 3;28(35):3111-20 [19581934] Breast Cancer Res Treat. 2009 Nov;118(2):361-7 [19459042] J Clin Oncol. 2009 Nov 10;27(32):5431-8 [19805692] Drug Metab Dispos. 2003 Jul;31(7):916-23 [12814969] Oncogene. 2003 Oct 20;22(47):7265-79 [14576837] Clin Cancer Res. 2004 Jul 15;10(14):4661-9 [15269138] Eur J Cancer. 2004 Aug;40(12):1872-7 [15288289] Chem Biol Interact. 1975 Sep;11(3):145-61 [1157188] Toxicology. 1980;17(2):169-76 [7209999] Biochemistry. 1985 Jan 29;24(3):707-13 [4039603] Pharmacol Ther. 1987;34(2):155-66 [3317449] J Med Chem. 1989 Oct;32(10):2240-1 [2795596] Anticancer Res. 1989 Sep-Oct;9(5):1301-12 [2686531] J Natl Cancer Inst. 1990 Jul 4;82(13):1107-12 [2359136] Jpn J Cancer Res. 1990 May;81(5):527-35 [2116401] Cancer Res. 1992 Sep 15;52(18):5065-72 [1516063] Cancer Res. 1992 Nov 15;52(22):6188-93 [1423261] Br J Cancer. 1992 Dec;66(6):1109-15 [1457352] Curr Opin Oncol. 1992 Dec;4(6):1073-9 [1457521] J Biol Chem. 1993 Sep 25;268(27):20116-25 [8376370] Anticancer Drugs. 1994 Feb;5(1):64-8 [8186432] Eur J Med Chem. 2010 Jan;45(1):134-41 [19853978] Clin Cancer Res. 2011 Feb 15;17(4):783-91 [21097693] Biochem Pharmacol. 1996 Dec 24;52(12):1855-65 [8951344] J Inorg Biochem. 1999 Oct;77(1-2):47-50 [10626353] Cancer Res. 2000 Mar 1;60(5):1312-6 [10728692] Clin Cancer Res. 2001 Oct;7(10):2984-97 [11595686] Cancer Res. 1997 Oct 1;57(19):4285-300 [9331090] Clin Cancer Res. 1999 Mar;5(3):655-63 [10100719] Semin Cancer Biol. 1998;8(5):345-57 [10101800] Cell Growth Differ. 1999 Jul;10(7):473-8 [10437915] Crit Rev Oncol Hematol. 2005 Jan;53(1):25-34 [15607933] Mol Cancer Ther. 2004 Dec;3(12):1543-9 [15634647] J Med Chem. 2005 Sep 8;48(18):5651-4 [16134932] Virchows Arch. 2005 Sep;447(3):626-33 [15968547] J Med Chem. 2006 Jan 12;49(1):224-31 [16392807] Cancer Res. 2006 Sep 1;66(17):8847-57 [16951202] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.4161/cc.11.5.19447 ER - TY - JOUR T1 - The development of communicative and narrative skills among preschoolers: lessons from forensic interviews about child abuse AN - 1033286148; 4321669 AB - This study examined age differences in 299 preschoolers' responses to investigative interviewers' questions exploring the suspected occurrence of child abuse. Analyses focused on the children's tendencies to respond (a) at all, (b) appropriately to the issue raised by the investigator, and (c) informatively, providing previously undisclosed information. Linear developmental trends characterized all types of responding. When the types of prompts were considered, three- to four-year-olds responded slightly more informatively to specific (directive) recall prompts than to open-ended prompts whereas children aged five and older were more responsive to open-ended recall prompts. The findings suggest that even three-year-olds can provide information about experienced events when recall processes are activated, although the ability to provide narrative responses to open-ended recall prompts only becomes reliable later in development. Reprinted by permission of the University of Chicago Press. © All rights reserved JF - Child development AU - Hershkowitz, Irit AU - Lamb, Michael E AU - Orbach, Yael AU - Katz, Carmit AU - Horowitz, Dvora AD - University of Haifa ; University of Cambridge ; National Institute of Child Health and Human Development, Maryland ; Child Investigation Unit, Israel Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 611 EP - 622 VL - 83 IS - 2 SN - 0009-3920, 0009-3920 KW - Sociology KW - Preschoolers KW - Perception KW - Child abuse KW - Communication KW - Age difference KW - Narratives KW - Interviews KW - Developmental psychology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1033286148?accountid=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=The+development+of+communicative+and+narrative+skills+among+preschoolers%3A+lessons+from+forensic+interviews+about+child+abuse&rft.au=Hershkowitz%2C+Irit%3BLamb%2C+Michael+E%3BOrbach%2C+Yael%3BKatz%2C+Carmit%3BHorowitz%2C+Dvora&rft.aulast=Hershkowitz&rft.aufirst=Irit&rft.date=2012-03-01&rft.volume=83&rft.issue=2&rft.spage=611&rft.isbn=&rft.btitle=&rft.title=Child+development&rft.issn=00093920&rft_id=info:doi/10.1111%2Fj.1467-8624.2011.01704.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 - 648 646; 3518 10404; 2189 2212; 6832 10919; 9382; 2572; 8470 DO - http://dx.doi.org/10.1111/j.1467-8624.2011.01704.x ER - TY - JOUR T1 - An intergenerational women's empowerment intervention to mitigate domestic violence: results of a pilot study in Bengaluru, India AN - 1033283702; 4321557 AB - A growing body of literature has documented the global prevalence of domestic violence against women of reproductive age, as well as the association between violence and an array of adverse reproductive, psychosocial, and child health outcomes. However, there is a dearth of research on domestic violence prevention interventions in the peer-reviewed literature to guide program planning and policy-making efforts. In this article, the authors describe the development and assessment of the feasibility, acceptability, and potential effectiveness of an intergenerational women's empowerment-based intervention to mitigate domestic violence and related adverse health outcomes in low-income urban communities in Southern India. Reprinted by permission of Sage Publications Ltd JF - Violence against women AU - Krishnan, Suneeta AU - Subbiah, Kalyani AU - Khanum, Sajida AU - Chandra, Prabha S AU - Padian, Nancy S AD - RTI International ; St. John's National Academy of Health Sciences ; National Institute of Mental Health and Neurosciences, India ; University of California, Berkeley Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 346 EP - 370 VL - 18 IS - 3 SN - 1077-8012, 1077-8012 KW - Sociology KW - Bengaluru KW - Prevention KW - Fertility KW - Women KW - Karnataka KW - Domestic violence KW - Urban communities KW - Social policy KW - Low income KW - India UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1033283702?accountid=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=Violence+against+women&rft.atitle=An+intergenerational+women%27s+empowerment+intervention+to+mitigate+domestic+violence%3A+results+of+a+pilot+study+in+Bengaluru%2C+India&rft.au=Krishnan%2C+Suneeta%3BSubbiah%2C+Kalyani%3BKhanum%2C+Sajida%3BChandra%2C+Prabha+S%3BPadian%2C+Nancy+S&rft.aulast=Krishnan&rft.aufirst=Suneeta&rft.date=2012-03-01&rft.volume=18&rft.issue=3&rft.spage=346&rft.isbn=&rft.btitle=&rft.title=Violence+against+women&rft.issn=10778012&rft_id=info:doi/10.1177%2F1077801212442628 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2013-06-12 N1 - Last updated - 2013-09-16 N1 - SubjectsTermNotLitGenreText - 3708 13325; 4869 3409 6306; 11888 10472; 10072; 7553 6271; 13162 2603; 13598 5421 6091; 197 175 387 30; 175 387 30 DO - http://dx.doi.org/10.1177/1077801212442628 ER - TY - JOUR T1 - Stability of language in childhood: A multiage, multidomain, multimeasure, and multisource study AN - 1023036912; 201208294 AB - The stability of language across childhood is traditionally assessed by exploring longitudinal relations between individual language measures. However, language encompasses many domains and varies with different sources (child speech, parental report, experimenter assessment). This study evaluated individual variation in multiple age-appropriate measures of child language derived from multiple sources and stability between their latent variables in 192 young children across more than 2 years. Structural equation modeling demonstrated the loading of multiple measures of child language from different sources on single latent variables of language at ages 20 months and 48 months. A large stability coefficient (r = .84) obtained between the 2 language latent variables. This stability obtained even when accounting for family socioeconomic status, maternal verbal intelligence, education, speech, tendency to respond in a socially desirable fashion, and child social competence. Stability was also equivalent for children in diverse childcare situations and for girls and boys. Across age, from the beginning of language acquisition to just before school entry, aggregating multiple age-appropriate methods and measures at each age and multiple reporters, children show a strong stability of individual differences in general language development. [Copyright American Psychological Association] JF - Developmental Psychology AU - Bornstein, Marc H AU - Putnick, Diane L Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 477 EP - 491 VL - 48 IS - 2 SN - 0012-1649, 0012-1649 KW - Child Language (11800) KW - Language Acquisition (41600) KW - Children (11850) KW - article KW - 4015: psycholinguistics; child language acquisition UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1023036912?accountid=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=Developmental+Psychology&rft.atitle=Stability+of+language+in+childhood%3A+A+multiage%2C+multidomain%2C+multimeasure%2C+and+multisource+study&rft.au=Bornstein%2C+Marc+H%3BPutnick%2C+Diane+L&rft.aulast=Bornstein&rft.aufirst=Marc&rft.date=2012-03-01&rft.volume=48&rft.issue=2&rft.spage=477&rft.isbn=&rft.btitle=&rft.title=Developmental+Psychology&rft.issn=00121649&rft_id=info:doi/ LA - English DB - Linguistics and Language Behavior Abstracts (LLBA) N1 - Date revised - 2012-07-01 N1 - Last updated - 2016-09-27 N1 - CODEN - DEVPA9 N1 - SubjectsTermNotLitGenreText - Children (11850); Child Language (11800); Language Acquisition (41600) ER - TY - JOUR T1 - Cognitive functioning self-assessment scale (CFSS): Preliminary psychometric data AN - 1018376910; 201209981 AB - The cognitive functioning is included in the concept of quality of life. Many times well-being remains incomplete because of cognitive difficulties, that people are not always able to properly recognize and explain. Nonetheless, only few instruments, specifically thought for non-clinical neurologic populations, are available to measure them. The present study is an attempt at providing a self-report instrument -- cognitive functioning self-assessment scale (CFSS) -- to measure the individual cognitive functioning in general population. The CFSS is itemized into18 questions to which participants answer on a five-point scale. Two hundred and eighty-two patients in a General Practitioner study have filled-in the CFSS together with a clinical and socio-demographic data form. Explorative factor analysis, using principal component analysis, suggests the consideration ofthe CFSS as one-dimensional; internal reliability = 0.856. Non-parametric testshave shown that women report a worse cognitive functioning than men, while no differences emerged in relation to age, manual prevalence, presence of an illness or being in pharmacological treatment. Although further verifications are necessary, the CFSS seems to be a promising self-report cognitive functioning measure. Adapted from the source document. JF - Psychology, Health & Medicine AU - Annunziata, M A AU - Muzzatti, B AU - Giovannini, L AU - Lucchini, G AD - Unit of Oncological Psychology, IRCCS Centro di Riferimento Oncologico, National Cancer Institute, Italy Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 207 EP - 212 PB - Routledge/Taylor & Francis, Abingdon UK VL - 17 IS - 2 SN - 1354-8506, 1354-8506 KW - cognitive functioning general population psychometrics self-assessment quality of life KW - Cognitive functioning KW - Treatment methods KW - Selfreport KW - Selfassessment KW - Quality of life KW - Prevalence KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1018376910?accountid=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%2C+Health+%26+Medicine&rft.atitle=Cognitive+functioning+self-assessment+scale+%28CFSS%29%3A+Preliminary+psychometric+data&rft.au=Annunziata%2C+M+A%3BMuzzatti%2C+B%3BGiovannini%2C+L%3BLucchini%2C+G&rft.aulast=Annunziata&rft.aufirst=M&rft.date=2012-03-01&rft.volume=17&rft.issue=2&rft.spage=207&rft.isbn=&rft.btitle=&rft.title=Psychology%2C+Health+%26+Medicine&rft.issn=13548506&rft_id=info:doi/10.1080%2F13548506.2011.596552 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-06-01 N1 - Last updated - 2016-09-27 N1 - CODEN - PHMEFL N1 - SubjectsTermNotLitGenreText - Cognitive functioning; Selfreport; Selfassessment; Prevalence; Quality of life; Treatment methods DO - http://dx.doi.org/10.1080/13548506.2011.596552 ER - TY - JOUR T1 - The effect of intravenous alcohol on the neural correlates of risky decision making in healthy social drinkers AN - 1017962418; 16685788 AB - ABSTRACT Alcohol is thought to contribute to an increase in risk-taking behavior, but the neural correlates underlying this effect are not well understood. In this study, participants were given intravenous alcohol or placebo while undergoing functional magnetic resonance imaging (fMRI) and playing a risk-taking game. The game allowed us to examine the neural response to choosing a safe or risky option, anticipating outcome and receiving feedback. We found that alcohol increased risk-taking behavior, particularly among participants who experienced more stimulating effects of alcohol. fMRI scans demonstrated that alcohol increased activation in the striatum to risky compared with safe choices and dampened the neural response to notification of both winning and losing throughout the caudate, thalamus and insula. This study suggests that alcohol may increase risk-taking behavior by both activating brain regions involved in reward when a decision is made, and dampening the response to negative and positive feedback. JF - Addiction Biology AU - Gilman, Jodi M AU - Smith, Ashley R AU - Ramchandani, Vijay A AU - Momenan, Reza AU - Hommer, Daniel W AD - Section of Brain Electrophysiology and Imaging, Laboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA Y1 - 2012/03/01/ PY - 2012 DA - 2012 Mar 01 SP - 465 EP - 478 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 17 IS - 2 SN - 1355-6215, 1355-6215 KW - Health & Safety Science Abstracts; Risk Abstracts; CSA Neurosciences Abstracts KW - Addiction KW - Alcohol KW - Brain KW - Brain mapping KW - Computed tomography KW - Decision making KW - Feedback KW - Functional magnetic resonance imaging KW - Intravenous administration KW - Neostriatum KW - Reinforcement KW - Risk taking KW - Thalamus KW - alcohols KW - risk taking KW - N3 11001:Behavioral and Cognitive Neuroscience 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/1017962418?accountid=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=Addiction+Biology&rft.atitle=The+effect+of+intravenous+alcohol+on+the+neural+correlates+of+risky+decision+making+in+healthy+social+drinkers&rft.au=Gilman%2C+Jodi+M%3BSmith%2C+Ashley+R%3BRamchandani%2C+Vijay+A%3BMomenan%2C+Reza%3BHommer%2C+Daniel+W&rft.aulast=Gilman&rft.aufirst=Jodi&rft.date=2012-03-01&rft.volume=17&rft.issue=2&rft.spage=465&rft.isbn=&rft.btitle=&rft.title=Addiction+Biology&rft.issn=13556215&rft_id=info:doi/http%3A%2F%2Fdx.doi.org%2F10.1111%2Fj.1369-1600.2011.00383.x L2 - http://www.ingentaconnect.com/content/bpl/adb/2012/00000017/00000002/art00022 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2012-10-08 N1 - SubjectsTermNotLitGenreText - Decision making; Brain mapping; Intravenous administration; Functional magnetic resonance imaging; Neostriatum; Computed tomography; Reinforcement; alcohols; Feedback; Addiction; Thalamus; Alcohol; Brain; Risk taking; risk taking DO - http://dx.doi.org/10.1111/j.1369-1600.2011.00383.x ER - TY - JOUR T1 - Microbial activity and functional diversity in Psamment soils in a forested coastal dune-swale system AN - 1015460669; 2012-047466 AB - The aim of the study was to examine soil microbial activity and functional diversity in different parts of coastal landscapes influenced by recurring saltwater intrusion in the Ravenna area (Italy). For this reason, seven profiles were selected in the San Vitale Pinewood, in low-lying interdune spot and next to dune crests and swales. Soils were classified as Typic Psammaquent, Typic Ustipsamment, Aquic Ustipsamment and Sodic Psammaquent. Chemical, physical and biochemical properties of soil horizons, such as microbial biomass metabolic quotient and enzyme activity, were determined to examine the effects of soil salinity and sodicity levels on microbial activity and functional diversity. The various soils and horizons could be split into distinct groups based on Differential Function Analysis of their properties. Cellulase, xylosidase and arylsulfatase showed a peak of their activity in surface horizons of sodic soils. alpha -glucosidase activity also was high in deeper horizons of those soils. Moreover, functional diversity, evaluated through calculation of Shannon's diversity index, was higher in the surface and deeper horizons of saline soils than non-saline soils. Conversely, soil with shallow water-table showed similar enzyme activity to soil located in the highest spots of the dune system. However, the highest values of specific activity (per unit of organic carbon) recorded in the deep horizons of the Typic Ustipsamment soil suggested more efficient hydrolytic activity of organic substrates due to oxygenation of soil. In conclusion, hydromorphic conditions in these soils influence the efficiency of organic substrate hydrolysis while soil salinity and sodicity increase both biochemical activity and functional diversity of microbial communities. JF - Geoderma AU - Marinari, S AU - Carbone, S AU - Vittori Antisari, L AU - Grego, S AU - Vianello, G Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 249 EP - 257 PB - Elsevier, Amsterdam VL - 173-174 SN - 0016-7061, 0016-7061 KW - eolian features KW - San Vitale Italy KW - dunes KW - salt-water intrusion KW - Psamments KW - characterization KW - Europe KW - salinity KW - enzymes KW - Italy KW - Southern Europe KW - ground water KW - Hydromorphic soils KW - Entisols KW - Emilia-Romagna Italy KW - coastal dunes KW - Ravenna Italy KW - coastal aquifers KW - soils KW - forests KW - shore features KW - soil profiles KW - physicochemical properties KW - alkali metals KW - sodium KW - aquifers KW - organic compounds KW - biogenic processes KW - metals KW - proteins KW - microorganisms KW - 25:Soils UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1015460669?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ageorefmodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Geoderma&rft.atitle=Microbial+activity+and+functional+diversity+in+Psamment+soils+in+a+forested+coastal+dune-swale+system&rft.au=Marinari%2C+S%3BCarbone%2C+S%3BVittori+Antisari%2C+L%3BGrego%2C+S%3BVianello%2C+G&rft.aulast=Marinari&rft.aufirst=S&rft.date=2012-03-01&rft.volume=173-174&rft.issue=&rft.spage=249&rft.isbn=&rft.btitle=&rft.title=Geoderma&rft.issn=00167061&rft_id=info:doi/10.1016%2Fj.geoderma.2011.12.023 L2 - http://www.sciencedirect.com/science/journal/00167061 LA - English DB - GeoRef N1 - Copyright - GeoRef, Copyright 2012, American Geosciences Institute. Reference includes data from CAPCAS, Elsevier Scientific Publishers, Amsterdam, Netherlands N1 - Date revised - 2012-01-01 N1 - Number of references - 60 N1 - Document feature - illus. incl. 7 tables, sketch map N1 - Last updated - 2012-06-07 N1 - CODEN - GEDMAB N1 - SubjectsTermNotLitGenreText - alkali metals; aquifers; biogenic processes; characterization; coastal aquifers; coastal dunes; dunes; Emilia-Romagna Italy; Entisols; enzymes; eolian features; Europe; forests; ground water; Hydromorphic soils; Italy; metals; microorganisms; organic compounds; physicochemical properties; proteins; Psamments; Ravenna Italy; salinity; salt-water intrusion; San Vitale Italy; shore features; sodium; soil profiles; soils; Southern Europe DO - http://dx.doi.org/10.1016/j.geoderma.2011.12.023 ER - TY - JOUR T1 - Short Communication: Fracture Risk by HIV Infection Status in Perinatally HIV-Exposed Children AN - 1011215018; 16590264 AB - The objective of this study was to examine the incidence of fractures in HIV-infected children and comparable HIV-exposed, uninfected (HEU) children in a multicenter, prospective cohort study (PACTG 219/219C) in the United States. The main outcome was first fracture during the risk period. Nine fractures occurred in 7 of 1326 HIV-infected and 2 of 649 HEU children, corresponding to incidence rates of 1.2 per 1000 person-years and 1.1 per 1000 person-years, respectively. The incidence rate ratio was 1.1 (95% CI 0.2, 5.5). There was no evidence of a substantially increased risk of fracture in HIV-infected compared to HEU children. JF - AIDS Research and Human Retroviruses AU - Siberry, G K AU - Li, H AU - Jacobson, D AD - Pediatric, Adolescent, and Maternal AIDS (PAMA) Branch, Center for Research for Mothers and Children, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, 6100 Executive Boulevard, Room 4B11H, Bethesda, Maryland 20892-7510, USA, siberryg@mail.nih.gov Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 247 EP - 250 VL - 28 IS - 3 SN - 0889-2229, 0889-2229 KW - Risk Abstracts; Health & Safety Science Abstracts; Virology & AIDS Abstracts KW - Risk assessment KW - USA KW - Acquired immune deficiency syndrome KW - Retrovirus KW - Communications KW - Human immunodeficiency virus KW - Fractures KW - Children KW - Infection KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - V 22360:AIDS and HIV KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1011215018?accountid=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=AIDS+Research+and+Human+Retroviruses&rft.atitle=Short+Communication%3A+Fracture+Risk+by+HIV+Infection+Status+in+Perinatally+HIV-Exposed+Children&rft.au=Siberry%2C+G+K%3BLi%2C+H%3BJacobson%2C+D&rft.aulast=Siberry&rft.aufirst=G&rft.date=2012-03-01&rft.volume=28&rft.issue=3&rft.spage=247&rft.isbn=&rft.btitle=&rft.title=AIDS+Research+and+Human+Retroviruses&rft.issn=08892229&rft_id=info:doi/10.1089%2Faid.2011.0064 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2013-09-09 N1 - SubjectsTermNotLitGenreText - Risk assessment; Fractures; Infection; Children; Acquired immune deficiency syndrome; Communications; Human immunodeficiency virus; Retrovirus; USA DO - http://dx.doi.org/10.1089/aid.2011.0064 ER - TY - JOUR T1 - An empirical approach to evaluating the validity of alternative low-risk drinking guidelines AN - 1010708059; 201208150 AB - Introduction and Aims. This paper proposes an approach for evaluating the validity of alternative low-risk drinking guidelines. Design and Methods. Twenty-seven alternative guidelines were evaluated in terms of their ability to predict nine measures of concurrent and prospective alcohol-related harm, using longitudinal data from a nationally representative sample of US adults (n = 26 438 to 12 339 depending upon outcome). Parameters compared included sensitivity, specificity, adjusted odds ratios and measures of model fit. Results. Performance varied by harm. The guidelines that best predicted concurrent alcohol-related harm comprised daily-only limits of 4/3 drinks for men/women, but gender-invariant limits of 4/4 drinks also performed well. Adding weekly limits did little to improve the prediction of concurrent harm. The guidelines that best predicted prospective harm comprised daily limits of 4/4 drinks combined with weekly limits of 14 drinks for men and 7 drinks for women, with weekly limits of 14/14 drinks running second. When concurrent and incident harms were aggregated, daily-only limits of 4/3 drinks performed nearly on a par with the combination of 14/14 drinks per week and 4/3 drinks per day. Discussion and Conclusions. This paper supported gender-specific daily limits and suggested that optimal guidelines might take daily limits from analyses of concurrent harms and weekly limits from analyses of prospective harms. This paper illustrates a mechanism for validating the ability of low-risk drinking guidelines to accurately predict a range of alcohol-related harms, whereby countries could use their own data on consumption and its association with harm to evaluate their low-risk drinking guidelines. Adapted from the source document. JF - Drug and Alcohol Review AU - DAWSON, Deborah A AU - SMITH, Sharon M AU - PICKERING, Roger P AU - GRANT, Bridget F AD - Laboratory of Epidemiology and Biometry, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health ddawson@mail.nih.gov Y1 - 2012/03// PY - 2012 DA - March 2012 SP - 141 EP - 150 PB - Wiley-Blackwell, UK VL - 31 IS - 2 SN - 0959-5236, 0959-5236 KW - drinking guideline KW - alcohol-related harm KW - validity KW - prediction KW - Sensitivity KW - Parameters KW - Drinks KW - Grants KW - Consumption KW - Alcohol related KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1010708059?accountid=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=Drug+and+Alcohol+Review&rft.atitle=An+empirical+approach+to+evaluating+the+validity+of+alternative+low-risk+drinking+guidelines&rft.au=DAWSON%2C+Deborah+A%3BSMITH%2C+Sharon+M%3BPICKERING%2C+Roger+P%3BGRANT%2C+Bridget+F&rft.aulast=DAWSON&rft.aufirst=Deborah&rft.date=2012-03-01&rft.volume=31&rft.issue=2&rft.spage=141&rft.isbn=&rft.btitle=&rft.title=Drug+and+Alcohol+Review&rft.issn=09595236&rft_id=info:doi/10.1111%2Fj.1465-3362.2011.00335.x LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-05-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Drinks; Alcohol related; Parameters; Consumption; Sensitivity; Grants DO - http://dx.doi.org/10.1111/j.1465-3362.2011.00335.x ER - TY - JOUR T1 - Retinopathy in old persons with and without diabetes mellitus: the Age, Gene/Environment Susceptibility-Reykjavik Study (AGES-R) AN - 1008830020; 16382806 AB - Aims/hypothesis: We aimed to describe the prevalence of retinopathy in an aged cohort of Icelanders with and without diabetes mellitus. Methods: The study population consisted of 4,994 persons aged greater than or equal to 67 years, who participated in the Age, Gene/Environment Susceptibility-Reykjavik Study (AGES-R). Type 2 diabetes mellitus was defined as HbA sub(1c) greater than or equal to 6.5% (>48 mmol/mol). Retinopathy was assessed by grading fundus photographs using the modified Airlie House adaptation of the Early Treatment Diabetic Retinopathy Study protocol. Associations between retinopathy and risk factors were estimated using odds ratios obtained from multivariate analyses. Results: The overall prevalence of retinopathy in AGES-R was 12.4%. Diabetes mellitus was present in 516 persons (10.3%), for 512 of whom gradable fundus photos were available, including 138 persons (27.0%, 95% CI 23.2, 31.0) with any retinopathy. Five persons (1.0%, 95% CI 0.3, 2.3) had proliferative retinopathy. Clinically significant macular oedema was present in five persons (1.0%, 95% CI 0.3, 2.3). Independent risk factors for retinopathy in diabetic patients in a multivariate model included HbA sub(1c), insulin use and use of oral hypoglycaemic agents, the last two being indicators of longer disease duration. In 4478 participants without diabetes mellitus, gradable fundus photos were available for 4,453 participants, with retinopathy present in 476 (10.7%, 95% CI 9.8, 11.6) and clinically significant macular oedema in three persons. Independent risk factors included increasing age and microalbuminuria. Conclusions/interpretation: Over three-quarters (78%) of retinopathy cases were found in persons without diabetes and a strong association between microalbuminuria and non-diabetic retinopathy was found. These results may have implications for patient management of the aged. JF - Diabetologia AU - Gunnlaugsdottir, E AU - Halldorsdottir, S AU - Klein, R AU - Eiriksdottir, G AU - Klein, B E AU - Benediktsson, R AU - Harris, T B AU - Launer, L J AU - Aspelund, T AU - Gudnason, V AU - Cotch, M F AU - Jonasson, F AD - University Eye Department, Landspitalinn, 101, Reykjavik, Iceland, mfc@nei.nih.gov Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 671 EP - 680 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 55 IS - 3 SN - 0012-186X, 0012-186X KW - Risk Abstracts; Environment Abstracts KW - Age KW - Housing KW - Residential areas KW - Risk factors KW - adaptability KW - diabetes mellitus KW - insulin KW - R2 23060:Medical and environmental health KW - ENA 07:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008830020?accountid=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=Diabetologia&rft.atitle=Retinopathy+in+old+persons+with+and+without+diabetes+mellitus%3A+the+Age%2C+Gene%2FEnvironment+Susceptibility-Reykjavik+Study+%28AGES-R%29&rft.au=Gunnlaugsdottir%2C+E%3BHalldorsdottir%2C+S%3BKlein%2C+R%3BEiriksdottir%2C+G%3BKlein%2C+B+E%3BBenediktsson%2C+R%3BHarris%2C+T+B%3BLauner%2C+L+J%3BAspelund%2C+T%3BGudnason%2C+V%3BCotch%2C+M+F%3BJonasson%2C+F&rft.aulast=Gunnlaugsdottir&rft.aufirst=E&rft.date=2012-03-01&rft.volume=55&rft.issue=3&rft.spage=671&rft.isbn=&rft.btitle=&rft.title=Diabetologia&rft.issn=0012186X&rft_id=info:doi/10.1007%2Fs00125-011-2395-y LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-05-18 N1 - SubjectsTermNotLitGenreText - Age; diabetes mellitus; Housing; insulin; Risk factors; Residential areas; adaptability DO - http://dx.doi.org/10.1007/s00125-011-2395-y ER - TY - JOUR T1 - Effect of diet composition on energy expenditure during weight loss: the POUNDS LOST Study AN - 1008826668; 16450257 AB - Background: Weight loss reduces energy expenditure, but the contribution of different macronutrients to this change is unclear.Hypothesis:We tested the hypothesis that macronutrient composition of the diet might affect the partitioning of energy expenditure during weight loss.Design:A substudy of 99 participants from the Preventing Overweight Using Novel Dietary Strategies (POUNDS LOST) trial had total energy expenditure (TEE) measured by doubly labeled water, and resting energy expenditure (REE) measured by indirect calorimetry at baseline and repeated at 6 months in 89 participants. Participants were randomly assigned to one of four diets with either 15 or 25% protein and 20 or 40% fat. Results: TEE and REE were positively correlated with each other and with fat-free mass and body fat, at baseline and 6 months. The average weight loss of 8.1+/-0.65 kg (least-square mean+/-s.e.) reduced TEE by 120+/-56 kcal per day and REE by 136+/-18 kcal per day. A greater weight loss at 6 months was associated with a greater decrease in TEE and REE. Participants eating the high-fat diet (HF) lost significantly more fat-free mass (1.52+/-0.55 kg) than the low-fat (LF) diet group (P<0.05). Participants eating the LF diet had significantly higher measures of physical activity than the HF group. Conclusion: A greater weight loss was associated with a larger decrease in both TEE and REE. The LF diet was associated with significant changes in fat-free body mass and energy expenditure from physical activity compared with the HF diet. JF - International Journal of Obesity AU - Bray, G A AU - Smith, S R AU - DeJonge, L AU - de Souza, R AU - Rood, J AU - Champagne, C M AU - Laranjo, N AU - Carey, V AU - Obarzanek, E AU - Loria, C M AU - Anton, S D AU - Ryan, D H AU - Greenway, F L AU - Williamson, D AU - Sacks, F M AD - 1] Pennington Biomedical Research Center, Baton Rouge, LA, USA [2] Harvard School of Public Health and Harvard Medical School-Brigham and Women's Hospital, Boston, MA, USA [3] The National Heart, Lung, and Blood Institute, Bethesda, MD, USA Y1 - 2012/03// PY - 2012 DA - Mar 2012 SP - 448 EP - 455 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 36 IS - 3 SN - 0307-0565, 0307-0565 KW - Physical Education Index; Environment Abstracts KW - Body mass KW - Calorimetry KW - Diet (effects) KW - Diets KW - Eating disorders KW - Energy cost KW - Exercise KW - Measurement KW - Obesity KW - Proteins KW - Weight control KW - body mass KW - obesity KW - physical activity KW - ENA 08:International KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008826668?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Obesity&rft.atitle=Effect+of+diet+composition+on+energy+expenditure+during+weight+loss%3A+the+POUNDS+LOST+Study&rft.au=Bray%2C+G+A%3BSmith%2C+S+R%3BDeJonge%2C+L%3Bde+Souza%2C+R%3BRood%2C+J%3BChampagne%2C+C+M%3BLaranjo%2C+N%3BCarey%2C+V%3BObarzanek%2C+E%3BLoria%2C+C+M%3BAnton%2C+S+D%3BRyan%2C+D+H%3BGreenway%2C+F+L%3BWilliamson%2C+D%3BSacks%2C+F+M&rft.aulast=Bray&rft.aufirst=G&rft.date=2012-03-01&rft.volume=36&rft.issue=3&rft.spage=448&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Obesity&rft.issn=03070565&rft_id=info:doi/10.1038%2Fijo.2011.173 LA - English DB - Physical Education Index; ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-08-24 N1 - SubjectsTermNotLitGenreText - Energy cost; Obesity; Measurement; Diet (effects); Weight control; Eating disorders; Body mass; Exercise; Diets; body mass; obesity; Proteins; Calorimetry; physical activity DO - http://dx.doi.org/10.1038/ijo.2011.173 ER - TY - JOUR T1 - Productive Replication of Ebola Virus Is Regulated by the c-Abl1 Tyrosine Kinase AN - 1285091791; 17492135 AB - Ebola virus causes a fulminant infection in humans resulting in diffuse bleeding, vascular instability, hypotensive shock, and often death. Because of its high mortality and ease of transmission from human to human, Ebola virus remains a biological thre at for which effective preventive and therapeutic interventions are needed. An understanding of the mechanisms of Ebola virus pathogenesis is critical for developing antiviral therapeutics. Here, we report that productive replication of Ebola virus is modulated by the c-Abl1 tyrosine kinase. Release of Ebola virus-like particles (VLPs) in a cell culture cotransfection system was inhibited by c-Abl1-specific small interfering RMA (siRNA) or by Abl-specific kinase inhibitors and required tyrosine phosphorylation of the Ebola matrix protein VP40. Expression of c-Abl1 stimulated an increase in phosphorylation of tyrosine 13 (Y super(13)) of VP40, and mutation of Y super(13) to alanine decreased the release of Ebola VLPs. Productive replication of the highly pathogenic Ebola virus Zaire strain was inhibited by c-Abl1-specific siRNAs or by the Abl-family inhibitor nilotinib by up to four orders of magnitude. These data indicate that c-Abl1 regulates budding or release of filoviruses through a mechanism involving phosphorylation of VP40. This step of the virus life cycle therefore may represent a target for antiviral therapy. JF - Science Translational Medicine AU - Garcia, M AU - Cooper, A AU - Shi, W AU - Bornmann, W AU - Carrion, R AU - Kalman, D AU - Nabel, G J Y1 - 2012/02/29/ PY - 2012 DA - 2012 Feb 29 VL - 4 IS - 123 SN - 1946-6234, 1946-6234 KW - Biotechnology and Bioengineering Abstracts; Virology & AIDS Abstracts KW - Translation KW - Mortality KW - Data processing KW - Virus-like particles KW - Alanine KW - Replication KW - Life cycle KW - Therapeutic applications KW - Ebola virus KW - Cell culture KW - VP40 protein KW - Infection KW - matrix protein KW - Shock KW - siRNA KW - Phosphorylation KW - Ebola virus zaire KW - Filovirus KW - Protein-tyrosine kinase KW - Bleeding KW - Mutation KW - Budding KW - V 22320:Replication KW - W 30945:Fermentation & Cell Culture UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285091791?accountid=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=Science+Translational+Medicine&rft.atitle=Productive+Replication+of+Ebola+Virus+Is+Regulated+by+the+c-Abl1+Tyrosine+Kinase&rft.au=Garcia%2C+M%3BCooper%2C+A%3BShi%2C+W%3BBornmann%2C+W%3BCarrion%2C+R%3BKalman%2C+D%3BNabel%2C+G+J&rft.aulast=Garcia&rft.aufirst=M&rft.date=2012-02-29&rft.volume=4&rft.issue=123&rft.spage=123ra24&rft.isbn=&rft.btitle=&rft.title=Science+Translational+Medicine&rft.issn=19466234&rft_id=info:doi/10.1126%2Fscitranslmed.3003500 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-01 N1 - Last updated - 2013-08-12 N1 - SubjectsTermNotLitGenreText - Mortality; Translation; Virus-like particles; Data processing; Alanine; Replication; Therapeutic applications; Life cycle; Cell culture; VP40 protein; Infection; matrix protein; Phosphorylation; siRNA; Shock; Protein-tyrosine kinase; Bleeding; Mutation; Budding; Ebola virus zaire; Filovirus; Ebola virus DO - http://dx.doi.org/10.1126/scitranslmed.3003500 ER - TY - JOUR T1 - Exposure to animals and increased risk of marginal zone B-cell lymphomas of the ocular adnexae AN - 1008837931; 16429898 AB - Background: Ocular adnexal marginal zone B-cell lymphoma (OAMZL) has been associated with Chlamydophila psittaci, an infection that may be transmitted by carrier animals. However, it is still unclear whether exposure to animals affects the risk of OAMZL in comparison with other lymphoma histotypes. We therefore investigated the role of professional and/or domestic exposures to animals in the occurrence of OAMZL, as compared with other types of lymphoma. Methods: A hospital-based case-control study was carried out on 43 consecutive OAMZL patients (cases) and 87 consecutive patients with nodal non-Hodgkin's lymphomas (NHLs; controls). Multiple logistic regression (MLR) odds ratios (ORs), and 95% confidence intervals (CIs) were used to estimate the association between exposures to animals and OAMZL risk. Results: A higher proportion of cases reported a lifetime exposure to household animals (79.1% vs 64.4% among controls), with a non-statistical significant MLR-OR of 2.18 (95% CI: 0.85-5.62). The OAMZL cases more frequently reported a history of occupation in breeding and/or slaughtering than controls (34.9% vs 6.9%), with an overall increased risk of 7.69 (95%CI: 2.65-22.34). Conclusion: These results indicate that, compared with nodal NHLs, the risk of OAMZL is markedly increased by contact with animals, particularly by occupational exposures. JF - British Journal of Cancer AU - Dolcetti, R AU - Serraino, D AU - Dognini, G AU - Govi, S AU - Crocchiolo, R AU - Ghia, P AU - Pasini, E AU - Ponzoni, M AU - Talamini, R AU - De Paoli, P AU - Doglioni, C AU - Ferreri, A J M AD - Centro di Riferimento Oncologico - IRCCS, National Cancer Institute, 33081, Aviano, Italy Y1 - 2012/02/28/ PY - 2012 DA - 2012 Feb 28 SP - 966 EP - 969 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 106 IS - 5 SN - 0007-0920, 0007-0920 KW - Immunology Abstracts; Risk Abstracts; Health & Safety Science Abstracts KW - non-Hodgkin's lymphoma KW - Historical account KW - Animals KW - double prime B-cell lymphoma KW - Infection KW - Non-Hodgkin's lymphoma KW - households KW - breeding KW - Breeding KW - infection KW - Slaughter KW - Occupational exposure KW - Cancer KW - Chlamydophila psittaci KW - lymphoma KW - F 06915:Cancer Immunology 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/1008837931?accountid=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=Exposure+to+animals+and+increased+risk+of+marginal+zone+B-cell+lymphomas+of+the+ocular+adnexae&rft.au=Dolcetti%2C+R%3BSerraino%2C+D%3BDognini%2C+G%3BGovi%2C+S%3BCrocchiolo%2C+R%3BGhia%2C+P%3BPasini%2C+E%3BPonzoni%2C+M%3BTalamini%2C+R%3BDe+Paoli%2C+P%3BDoglioni%2C+C%3BFerreri%2C+A+J+M&rft.aulast=Dolcetti&rft.aufirst=R&rft.date=2012-02-28&rft.volume=106&rft.issue=5&rft.spage=966&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2012.2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-04-23 N1 - SubjectsTermNotLitGenreText - Non-Hodgkin's lymphoma; double prime B-cell lymphoma; Breeding; Slaughter; Infection; Occupational exposure; non-Hodgkin's lymphoma; Animals; Historical account; households; breeding; infection; lymphoma; Cancer; Chlamydophila psittaci DO - http://dx.doi.org/10.1038/bjc.2012.2 ER - TY - CPAPER T1 - NIH Funding Opportunity on Spatial Uncertainty T2 - 2012 Annual Meeting of the Association of American Geographers (AAG 2012) AN - 1412154640; 6220649 JF - 2012 Annual Meeting of the Association of American Geographers (AAG 2012) AU - Zhu, Li Y1 - 2012/02/24/ PY - 2012 DA - 2012 Feb 24 KW - Financing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1412154640?accountid=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+Association+of+American+Geographers+%28AAG+2012%29&rft.atitle=NIH+Funding+Opportunity+on+Spatial+Uncertainty&rft.au=Zhu%2C+Li&rft.aulast=Zhu&rft.aufirst=Li&rft.date=2012-02-24&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Annual+Meeting+of+the+Association+of+American+Geographers+%28AAG+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://meridian.aag.org/callforpapers/program/index.cfm?mtgID=57 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-06-30 N1 - Last updated - 2013-07-25 ER - TY - CPAPER T1 - The beads task, information sampling and impulsivity T2 - 2012 Workshop on Computational and Systems Neuroscience (Cosyne 2012) AN - 1326136559; 6205073 JF - 2012 Workshop on Computational and Systems Neuroscience (Cosyne 2012) AU - Averbeck, Bruno AU - Furl, Nicholas AU - Djamshidian, Atbin AU - Lees, Andrew Y1 - 2012/02/23/ PY - 2012 DA - 2012 Feb 23 KW - Sampling KW - impulsive behavior UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1326136559?accountid=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+Workshop+on+Computational+and+Systems+Neuroscience+%28Cosyne+2012%29&rft.atitle=The+beads+task%2C+information+sampling+and+impulsivity&rft.au=Averbeck%2C+Bruno%3BFurl%2C+Nicholas%3BDjamshidian%2C+Atbin%3BLees%2C+Andrew&rft.aulast=Averbeck&rft.aufirst=Bruno&rft.date=2012-02-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Workshop+on+Computational+and+Systems+Neuroscience+%28Cosyne+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.cosyne.org/c/index.php?title=Cosyne_12 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-03-31 N1 - Last updated - 2013-04-12 ER - TY - CPAPER T1 - Critical exponents derived for neuronal avalanches in alert non-human primate T2 - 2012 Workshop on Computational and Systems Neuroscience (Cosyne 2012) AN - 1326135720; 6205110 JF - 2012 Workshop on Computational and Systems Neuroscience (Cosyne 2012) AU - Yu, Shan AU - Yang, Hongdian AU - Plenz, Dietmar Y1 - 2012/02/23/ PY - 2012 DA - 2012 Feb 23 KW - Avalanches KW - Primates UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1326135720?accountid=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+Workshop+on+Computational+and+Systems+Neuroscience+%28Cosyne+2012%29&rft.atitle=Critical+exponents+derived+for+neuronal+avalanches+in+alert+non-human+primate&rft.au=Yu%2C+Shan%3BYang%2C+Hongdian%3BPlenz%2C+Dietmar&rft.aulast=Yu&rft.aufirst=Shan&rft.date=2012-02-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Workshop+on+Computational+and+Systems+Neuroscience+%28Cosyne+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.cosyne.org/c/index.php?title=Cosyne_12 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-03-31 N1 - Last updated - 2013-04-12 ER - TY - CPAPER T1 - What does information seeking tell us about reinforcement learning? T2 - 2012 Workshop on Computational and Systems Neuroscience (Cosyne 2012) AN - 1326135537; 6205331 JF - 2012 Workshop on Computational and Systems Neuroscience (Cosyne 2012) AU - Bromberg-Martin, Ethan AU - Hikosaka, Okihide Y1 - 2012/02/23/ PY - 2012 DA - 2012 Feb 23 KW - Learning KW - Reinforcement UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1326135537?accountid=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+Workshop+on+Computational+and+Systems+Neuroscience+%28Cosyne+2012%29&rft.atitle=What+does+information+seeking+tell+us+about+reinforcement+learning%3F&rft.au=Bromberg-Martin%2C+Ethan%3BHikosaka%2C+Okihide&rft.aulast=Bromberg-Martin&rft.aufirst=Ethan&rft.date=2012-02-23&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Workshop+on+Computational+and+Systems+Neuroscience+%28Cosyne+2012%29&rft.issn=&rft_id=info:doi/ L2 - http://www.cosyne.org/c/index.php?title=Cosyne_12 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-03-31 N1 - Last updated - 2013-04-12 ER - TY - JOUR T1 - Estrogen metabolism and risk of breast cancer in postmenopausal women. AN - 923191202; 22232133 AB - Estrogens are recognized causal factors in breast cancer. Interindividual variation in estrogen metabolism may also influence the risk of breast cancer and could provide clues to mechanisms of breast carcinogenesis. Long-standing hypotheses about how estrogen metabolism might influence breast cancer have not been adequately evaluated in epidemiological studies because of the lack of accurate, reproducible, and high-throughput assays for estrogen metabolites. We conducted a prospective case-control study nested within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO). Participants included 277 women who developed invasive breast cancer (case subjects) and 423 matched control subjects; at PLCO baseline, all subjects were aged 55-74 years, postmenopausal and not using hormone therapy, and provided a blood sample. Liquid chromatography-tandem mass spectrometry was used to measure serum concentrations of 15 estrogens and estrogen metabolites, in unconjugated and conjugated forms, including the parent estrogens, estrone and estradiol, and estrogen metabolites in pathways defined by irreversible hydroxylation at the C-2, C-4, or C-16 positions of the steroid ring. We calculated hazard ratios (HRs) approximating risk in highest vs lowest deciles of individual estrogens and estrogen metabolites, estrogens and estrogen metabolites grouped by metabolic pathways, and metabolic pathway ratios using multivariable Cox proportional hazards models. All statistical tests were two-sided. Nearly all estrogens, estrogen metabolites, and metabolic pathway groups were associated with an increased risk of breast cancer; the serum concentration of unconjugated estradiol was strongly associated with the risk of breast cancer (HR = 2.07, 95% confidence interval [CI] = 1.19 to 3.62). No estrogen, estrogen metabolite, or metabolic pathway group remained statistically significantly associated with the risk of breast cancer after adjusting for unconjugated estradiol. The ratio of the 2-hydroxylation pathway to parent estrogens (HR = 0.66, 95% CI = 0.51 to 0.87) and the ratio of 4-hydroxylation pathway catechols to 4-hydroxylation pathway methylated catechols (HR = 1.34, 95% CI = 1.04 to 1.72) were statistically significantly associated with the risk of breast cancer and remained so after adjustment for unconjugated estradiol. More extensive 2-hydroxylation of parent estrogens is associated with lower risk, and less extensive methylation of potentially genotoxic 4-hydroxylation pathway catechols is associated with higher risk of postmenopausal breast cancer. JF - Journal of the National Cancer Institute AU - Fuhrman, Barbara J AU - Schairer, Catherine AU - Gail, Mitchell H AU - Boyd-Morin, Jennifer AU - Xu, Xia AU - Sue, Laura Y AU - Buys, Saundra S AU - Isaacs, Claudine AU - Keefer, Larry K AU - Veenstra, Timothy D AU - Berg, Christine D AU - Hoover, Robert N AU - Ziegler, Regina G AD - Hormonal and Reproductive Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD 20892, USA. fuhrmanb@mail.nih.gov Y1 - 2012/02/22/ PY - 2012 DA - 2012 Feb 22 SP - 326 EP - 339 VL - 104 IS - 4 KW - Biomarkers, Tumor KW - 0 KW - Estrogens KW - Estrogens, Catechol KW - Hydroxyestrones KW - Receptors, Estrogen KW - Estrone KW - 2DI9HA706A KW - Estradiol KW - 4TI98Z838E KW - Index Medicus KW - Randomized Controlled Trials as Topic KW - Odds Ratio KW - Humans KW - Aged KW - Predictive Value of Tests KW - Tandem Mass Spectrometry KW - Receptors, Estrogen -- metabolism KW - Estrone -- metabolism KW - Risk Assessment KW - Multivariate Analysis KW - Estradiol -- metabolism KW - Hydroxylation KW - Prospective Studies KW - Postmenopause KW - Risk Factors KW - Estrogens, Catechol -- metabolism KW - Confounding Factors (Epidemiology) KW - Hydroxyestrones -- metabolism KW - Case-Control Studies KW - Chromatography, Liquid KW - Middle Aged KW - Methylation KW - Female KW - Proportional Hazards Models KW - Biomarkers, Tumor -- metabolism KW - Estrogens -- metabolism KW - Neoplasms, Hormone-Dependent -- metabolism KW - Breast Neoplasms -- etiology KW - Breast Neoplasms -- metabolism KW - Neoplasms, Hormone-Dependent -- etiology KW - Estrogens -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/923191202?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Estrogen+metabolism+and+risk+of+breast+cancer+in+postmenopausal+women.&rft.au=Fuhrman%2C+Barbara+J%3BSchairer%2C+Catherine%3BGail%2C+Mitchell+H%3BBoyd-Morin%2C+Jennifer%3BXu%2C+Xia%3BSue%2C+Laura+Y%3BBuys%2C+Saundra+S%3BIsaacs%2C+Claudine%3BKeefer%2C+Larry+K%3BVeenstra%2C+Timothy+D%3BBerg%2C+Christine+D%3BHoover%2C+Robert+N%3BZiegler%2C+Regina+G&rft.aulast=Fuhrman&rft.aufirst=Barbara&rft.date=2012-02-22&rft.volume=104&rft.issue=4&rft.spage=326&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+National+Cancer+Institute&rft.issn=1460-2105&rft_id=info:doi/10.1093%2Fjnci%2Fdjr531 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-04-12 N1 - Date created - 2012-02-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: JAMA. 2010 Oct 20;304(15):1684-92 [20959578] Hum Mol Genet. 2010 Oct 1;19(19):3873-84 [20634197] J Natl Cancer Inst Monogr. 2000;(27):113-24 [10963623] Epidemiology. 2000 Nov;11(6):635-40 [11055622] Oncogene. 2001 Nov 29;20(55):7945-53 [11753677] J Natl Cancer Inst. 2002 Apr 17;94(8):606-16 [11959894] Curr Drug Metab. 2002 Jun;3(3):321-49 [12083324] Steroids. 2003 Jan;68(1):65-72 [12475724] Epidemiology. 2003 Nov;14(6):740-4 [14569192] J Steroid Biochem. 1980 Feb;13(2):231-44 [6991820] J Steroid Biochem. 1983 Jul;19(1B):627-33 [6310246] J Steroid Biochem. 1986 Jan;24(1):353-6 [3009986] Proc Natl Acad Sci U S A. 1986 Jul;83(14):5301-5 [3460092] Ann N Y Acad Sci. 1986;464:138-51 [3014947] N Engl J Med. 1986 Nov 20;315(21):1305-9 [3773953] Chem Res Toxicol. 1996 Jul-Aug;9(5):851-9 [8828920] Eur J Cancer Prev. 1997 Feb;6(1):3-10 [9161806] Environ Health Perspect. 1997 Apr;105 Suppl 3:607-14 [9168003] Cancer Epidemiol Biomarkers Prev. 1997 Jul;6(7):505-9 [9232337] Proc Natl Acad Sci U S A. 1997 Sep 30;94(20):10937-42 [9380738] Ann Acad Med Singapore. 1998 Mar;27(2):294-9 [9663330] Br J Cancer. 1998 Nov;78(9):1250-5 [9820189] J Natl Cancer Inst. 1999 Jun 16;91(12):1067-72 [10379970] Cancer Epidemiol Biomarkers Prev. 2005 Sep;14(9):2137-42 [16172222] Mutat Res. 2005 Dec 30;592(1-2):147-54 [16054167] Epidemiology. 2006 Jan;17(1):80-8 [16357599] Int J Cancer. 2006 Mar 1;118(5):1292-301 [16161054] N Engl J Med. 2006 Jan 19;354(3):270-82 [16421368] Chem Res Toxicol. 2006 Mar;19(3):475-9 [16544955] Endocrinology. 2006 Sep;147(9):4132-50 [16728493] Cancer Epidemiol Biomarkers Prev. 2006 Sep;15(9):1578-81 [16985015] Cancer Epidemiol Biomarkers Prev. 2006 Sep;15(9):1620-9 [16985022] J Steroid Biochem Mol Biol. 2006 Nov;101(4-5):204-15 [16982187] Ann N Y Acad Sci. 2006 Nov;1089:286-301 [17261777] Anal Chem. 2007 Oct 15;79(20):7813-21 [17848096] Free Radic Biol Med. 2007 Dec 1;43(11):1534-40 [17964424] Cancer Epidemiol Biomarkers Prev. 2008 Aug;17(8):2029-35 [18708395] Chem Res Toxicol. 2008 Aug;21(8):1622-30 [18582124] BMC Cancer. 2009;9:84 [19292893] Cancer Epidemiol Biomarkers Prev. 2009 Aug;18(8):2273-9 [19661086] Cancer Epidemiol Biomarkers Prev. 2010 Jan;19(1):292-300 [20056650] J Steroid Biochem Mol Biol. 2010 Aug;121(3-5):491-5 [20470886] Cancer Epidemiol Biomarkers Prev. 2000 Jan;9(1):81-7 [10667467] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/jnci/djr531 ER - TY - JOUR T1 - Charged linker sequence modulates eukaryotic heat shock protein 90 (Hsp90) chaperone activity AN - 1520375831; 16407454 AB - Hsp90 is an essential and highly conserved modular molecular chaperone whose N and middle domains are separated by a disordered region termed the charged linker. Although its importance has been previously disregarded, because a minimal linker length is sufficient for Hsp90 activity, the evolutionary persistence of extensive charged linkers of divergent sequence in Hsp90 proteins of most eukaryotes remains unexplained. To examine this question further, we introduced human and plasmodium native and length-matched artificial linkers into yeast Hsp90. After evaluating ATPase activity and biophysical characteristics in vitro, and chaperone function in vivo, we conclude that linker sequence affects Hsp90 function, cochaperone interaction, and conformation. We propose that the charged linker, in addition to providing the flexibility necessary for Hsp90 domain rearrangements-likely its original purpose-has evolved in eukaryotes to serve as a rheostat for the Hsp90 chaperone machine. JF - Proceedings of the National Academy of Sciences, USA AU - Tsutsumi, Shinji AU - Mollapour, Mehdi AU - Prodromou, Chrisostomos AU - Lee, Chung-Tien AU - Panaretou, Barry AU - Yoshida, Soichiro AU - Mayer, Matthias P AU - Neckers, Leonard M AD - Urologic Oncology Branch, National Cancer Institute, Bethesda, MD 20892 Y1 - 2012/02/21/ PY - 2012 DA - 2012 Feb 21 SP - 2937 EP - 2942 PB - National Academy of Sciences, 2101 Constitution Ave. Washington DC 20418 United States VL - 109 IS - 8 SN - 0027-8424, 0027-8424 KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality KW - Yeasts KW - Plasmodium KW - Nucleotide sequence KW - Proteins KW - Heat shock KW - Q1 08206:Physiology, biochemistry, biophysics KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1520375831?accountid=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=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=Charged+linker+sequence+modulates+eukaryotic+heat+shock+protein+90+%28Hsp90%29+chaperone+activity&rft.au=Tsutsumi%2C+Shinji%3BMollapour%2C+Mehdi%3BProdromou%2C+Chrisostomos%3BLee%2C+Chung-Tien%3BPanaretou%2C+Barry%3BYoshida%2C+Soichiro%3BMayer%2C+Matthias+P%3BNeckers%2C+Leonard+M&rft.aulast=Tsutsumi&rft.aufirst=Shinji&rft.date=2012-02-21&rft.volume=109&rft.issue=8&rft.spage=2937&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-04-01 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Yeasts; Nucleotide sequence; Heat shock; Proteins; Plasmodium ER - TY - CPAPER T1 - Novel GPCR-Regulated Oncogenic and Pro-Metastatic Signaling Circuitries T2 - 2012 Keystone Symposia Meeting on G Protein-Coupled Receptors: Molecular Mechanisms and Novel Functional Insights AN - 1326136899; 6207513 JF - 2012 Keystone Symposia Meeting on G Protein-Coupled Receptors: Molecular Mechanisms and Novel Functional Insights AU - Gutkind, J Y1 - 2012/02/17/ PY - 2012 DA - 2012 Feb 17 KW - Bioremediation KW - Public health KW - G protein-coupled receptors KW - Molecular modelling UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1326136899?accountid=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+Keystone+Symposia+Meeting+on+G+Protein-Coupled+Receptors%3A+Molecular+Mechanisms+and+Novel+Functional+Insights&rft.atitle=Novel+GPCR-Regulated+Oncogenic+and+Pro-Metastatic+Signaling+Circuitries&rft.au=Gutkind%2C+J&rft.aulast=Gutkind&rft.aufirst=J&rft.date=2012-02-17&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Keystone+Symposia+Meeting+on+G+Protein-Coupled+Receptors%3A+Molecular+Mechanisms+and+Novel+Functional+Insights&rft.issn=&rft_id=info:doi/ L2 - http://www.keystonesymposia.org/index.cfm?e=Web.Meeting.Program&MeetingID=1130 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-03-31 N1 - Last updated - 2013-04-12 ER - TY - JOUR T1 - Epithelial Nitration by a Peroxidase/NOX5 System Mediates Mosquito Antiplasmodial Immunity AN - 1008848121; 16377306 AB - Plasmodium ookinetes traverse midgut epithelial cells before they encounter the complement system in the mosquito hemolymph. We identified a heme peroxidase (HPX2) and NADPH oxidase 5 (NOX5) as critical mediators of midgut epithelial nitration and antiplasmodial immunity that enhance nitric oxide toxicity in Anopheles gambiae. We show that the two immune mechanisms that target ookinetes-epithelial nitration and thioester-containing protein 1 (TEP1)-mediated lysis-work sequentially, and we propose that epithelial nitration works as an opsonization-like system that promotes activation of the mosquito complement cascade. JF - Science (Washington) AU - de Almeida Oliveira, Giselle AU - Lieberman, Joshua AU - Barillas-Mury, Carolina AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health (NIH), Rockville, MD 20892, USA Y1 - 2012/02/17/ PY - 2012 DA - 2012 Feb 17 SP - 856 EP - 859 PB - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States VL - 335 IS - 6070 SN - 0036-8075, 0036-8075 KW - Entomology Abstracts; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources KW - Epithelial cells KW - Hemolymph KW - Heme KW - Zygotes KW - Peroxidase KW - Immunity KW - Toxicity KW - Anopheles gambiae KW - Plasmodium KW - Complement activation KW - Nitration KW - NAD(P)H oxidase KW - Nitric oxide KW - Antiprotozoal agents KW - Midgut KW - Aquatic insects KW - Q1 08306:Physiology, biochemistry, biophysics KW - K 03350:Immunology KW - F 06945:Insect Immunity KW - Z 05350:Medical, Veterinary, and Agricultural Entomology KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008848121?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Science+%28Washington%29&rft.atitle=Epithelial+Nitration+by+a+Peroxidase%2FNOX5+System+Mediates+Mosquito+Antiplasmodial+Immunity&rft.au=de+Almeida+Oliveira%2C+Giselle%3BLieberman%2C+Joshua%3BBarillas-Mury%2C+Carolina&rft.aulast=de+Almeida+Oliveira&rft.aufirst=Giselle&rft.date=2012-02-17&rft.volume=335&rft.issue=6070&rft.spage=856&rft.isbn=&rft.btitle=&rft.title=Science+%28Washington%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2014-05-29 N1 - SubjectsTermNotLitGenreText - Toxicity; Immunity; Aquatic insects; Hemolymph; Epithelial cells; Heme; Zygotes; Peroxidase; Complement activation; Nitration; Nitric oxide; NAD(P)H oxidase; Midgut; Antiprotozoal agents; Plasmodium; Anopheles gambiae ER - TY - JOUR T1 - Modeled nitrate levels in well water supplies and prevalence of abnormal thyroid conditions among the Old Order Amish in Pennsylvania AN - 1008834763; 16494919 AB - Nitrate is a widespread contaminant of drinking water supplies, especially in agricultural areas. Nitrate intake from drinking water and dietary sources can interfere with the uptake of iodide by the thyroid, thus potentially impacting thyroid function. We assessed the relation of estimated nitrate levels in well water supplies with thyroid health in a cohort of 2,543 Old Order Amish residing in Lancaster, Chester, and Lebanon counties in Pennsylvania for whom thyroid stimulating hormone (TSH) levels were measured during 1995-2008. Nitrate measurement data (1976-2006) for 3,613 wells in the study area were obtained from the U.S. Geological Survey and we used these data to estimate concentrations at study participants' residences using a standard linear mixed effects model that included hydrogeological covariates and kriging of the wells' residuals. Nitrate levels estimated by the model ranged from 0.35 mg/L to 16.4 mg/L N-NO3-, with a median value of 6.5 mg/L, which was used as the cutpoint to define high and low nitrate exposure. In a validation analysis of the model, we calculated that the sensitivity of the model was 67% and the specificity was 93%. TSH levels were used to define the following outcomes: clinical hyperthyroidism (n = 10), clinical hypothyroidism (n = 56), subclinical hyperthyroidism (n = 25), and subclinical hypothyroidism (n = 228). In women, high nitrate exposure was significantly associated with subclinical hypothyroidism (OR = 1.60; 95% CI: 1.11-2.32). Nitrate was not associated with subclinical thyroid disease in men or with clinical thyroid disease in men or women. Although these data do not provide strong support for an association between nitrate in drinking water and thyroid health, our results do suggest that further exploration of this hypothesis is warranted using studies that incorporate individual measures of both dietary and drinking water nitrate intake. JF - Environmental Health (London) AU - Aschebrook-Kilfoy, Briseis AU - Heltshe, Sonya L AU - Nuckols, John R AU - Sabra, Mona M AU - Shuldiner, Alan R AU - Mitchell, Braxton D AU - Airola, Matt AU - Holford, Theodore R AU - Zhang, Yawei AU - Ward, Mary H AD - Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Rockville, MD, USA, brisa@uchicago.edu Y1 - 2012/02/17/ PY - 2012 DA - 2012 Feb 17 SP - 6 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 11 KW - Health & Safety Science Abstracts; Pollution Abstracts KW - Diets KW - Nitrates KW - iodides KW - USA, Pennsylvania KW - geological surveys KW - Lebanon KW - Thyroid KW - Water wells KW - Drinking water KW - Water supplies KW - Hormones KW - H 3000:Environment and Ecology KW - P 2000:FRESHWATER POLLUTION UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008834763?accountid=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+%28London%29&rft.atitle=Modeled+nitrate+levels+in+well+water+supplies+and+prevalence+of+abnormal+thyroid+conditions+among+the+Old+Order+Amish+in+Pennsylvania&rft.au=Aschebrook-Kilfoy%2C+Briseis%3BHeltshe%2C+Sonya+L%3BNuckols%2C+John+R%3BSabra%2C+Mona+M%3BShuldiner%2C+Alan+R%3BMitchell%2C+Braxton+D%3BAirola%2C+Matt%3BHolford%2C+Theodore+R%3BZhang%2C+Yawei%3BWard%2C+Mary+H&rft.aulast=Aschebrook-Kilfoy&rft.aufirst=Briseis&rft.date=2012-02-17&rft.volume=11&rft.issue=&rft.spage=6&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+%28London%29&rft.issn=1476-069X&rft_id=info:doi/10.1186%2F1476-069X-11-6 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2013-06-28 N1 - SubjectsTermNotLitGenreText - Diets; Nitrates; iodides; geological surveys; Thyroid; Water wells; Drinking water; Hormones; Water supplies; USA, Pennsylvania; Lebanon DO - http://dx.doi.org/10.1186/1476-069X-11-6 ER - TY - JOUR T1 - TE-dependent spatial and spectral specificity of functional connectivity AN - 920799543; 16257709 AB - Previous studies suggest that spontaneous fluctuations in the resting-state fMRI (RS-fMRI) signal may reflect fluctuations in transverse relaxation time (T[sub]2[super]*) rather than spin density (S[sub]0). However, such S[sub]0 and T[sub]2[super]* features have not been well characterized. In this study, spatial and spectral characteristics of functional connectivity on sensorimotor, default-mode, dorsal attention, and primary visual systems were examined using a multiple gradient-echo sequence at 3 T. In the spatial domain, we found broad, local correlations at short echo times (TE less than or equal to 14 ms) due to dominant S[sub]0 contribution, whereas long-range connections mediated by T[sub]2[super]* became explicit at TEs longer than 22 ms. In the frequency domain, compared with the flat spectrum of S[sub]0, spectral power of the T[sub]2[super]*-weighted signal elevated significantly with increasing TE, particularly in the frequency ranges of 0.008-0.023 Hz and 0.037-0.043 Hz. Using the S[sub]0 spectrum as a reference, we propose two indices to measure spectral signal change (SSC) and spectral contrast-to-noise ratio (SCNR), respectively, for quantifying the RS-fMRI signal. These indices demonstrated te dependency of connectivity-related fluctuation strength, resembling functional contrasts in activation-based fMRI. These findings further confirm that large-scale functional circuit connectivity based on BOLD contrast may be constrained within specific frequency ranges in every brain network, and the spectral features of S[sub]0 and T[sub]2[super]* could be valuable for interpreting and quantifying RS-fMRI data. JF - NeuroImage AU - Wu, Changwei W AU - Gu, Hong AU - Zou, Qihong AU - Lu, Hanbing AU - Stein, Elliot A AU - Yang, Yihong AD - Neuroimaging Research Branch, National Institute on Drug Abuse, National Institutes of Health, Baltimore, MD, USA, YihongYang@intra.nida.nih.gov Y1 - 2012/02/15/ PY - 2012 DA - 2012 Feb 15 SP - 3075 EP - 3084 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 59 IS - 4 SN - 1053-8119, 1053-8119 KW - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts KW - fMRI KW - Spontaneous fluctuations KW - Functional connectivity KW - Echo time KW - Frequency KW - sensorimotor system KW - Brain mapping KW - Visual pathways KW - Neuroimaging KW - Data processing KW - Neural networks KW - Functional magnetic resonance imaging KW - Visual system KW - Circuits KW - Attention KW - W 30910:Imaging KW - N3 11006:Neuroanatomy, histology & cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920799543?accountid=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=NeuroImage&rft.atitle=TE-dependent+spatial+and+spectral+specificity+of+functional+connectivity&rft.au=Wu%2C+Changwei+W%3BGu%2C+Hong%3BZou%2C+Qihong%3BLu%2C+Hanbing%3BStein%2C+Elliot+A%3BYang%2C+Yihong&rft.aulast=Wu&rft.aufirst=Changwei&rft.date=2012-02-15&rft.volume=59&rft.issue=4&rft.spage=3075&rft.isbn=&rft.btitle=&rft.title=NeuroImage&rft.issn=10538119&rft_id=info:doi/10.1016%2Fj.neuroimage.2011.11.030 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-02-01 N1 - Last updated - 2015-04-09 N1 - SubjectsTermNotLitGenreText - Visual pathways; Brain mapping; sensorimotor system; Neuroimaging; Data processing; Neural networks; Functional magnetic resonance imaging; Visual system; Circuits; Attention DO - http://dx.doi.org/10.1016/j.neuroimage.2011.11.030 ER - TY - JOUR T1 - Serotonin-1A receptors in major depression quantified using PET: Controversies, confounds, and recommendations AN - 920799534; 16257708 AB - The serotonin-1A (5-HT[sub]1A) receptor is of particular interest in human positron emission tomography (PET) studies of major depressive disorder (MDD). Of the eight studies investigating this issue in the brains of patients with MDD, four reported decreased 5-HT[sub]1A receptor density, two reported no change, and two reported increased 5-HT[sub]1A receptor density. While clinical heterogeneity may have contributed to these differing results, methodological factors by themselves could also explain the discrepancies. This review highlights several of these factors, including the use of the cerebellum as a reference region and the imprecision of measuring the concentration of parent radioligand in arterial plasma, the method otherwise considered to be the 'gold standard'. Other potential confounds also exist that could restrict or unexpectedly affect the interpretation of results. For example, the radioligand may be a substrate for an efflux transporter - like P-gp - at the blood-brain barrier; furthermore, the binding of the radioligand to the receptor in various stages of cellular trafficking is unknown. Efflux transport and cellular trafficking may also be differentially expressed in patients compared to healthy subjects. We believe that, taken together, the existing disparate findings do not reliably answer the question of whether 5-HT[sub]1A receptors are altered in MDD or in subgroups of patients with MDD. In addition, useful meta-analysis is precluded because only one of the imaging centers acquired all the data necessary to address these methodological concerns. We recommend that in the future, individual centers acquire more thorough data capable of addressing methodological concerns, and that multiple centers collaborate to meaningfully pool their data for meta-analysis. JF - NeuroImage AU - Shrestha, Saurav AU - Hirvonen, Jussi AU - Hines, Christina S AU - Henter, Ioline D AU - Svenningsson, Per AU - Pike, Victor W AU - Innis, Robert B AD - Molecular Imaging Branch, National Institute of Mental Health, National Institutes of Health, 10 Center Drive, MSC 1026, Bldg 10, Room B1D43, Bethesda, MD 20892, USA, saurav.shrestha@nih.gov Y1 - 2012/02/15/ PY - 2012 DA - 2012 Feb 15 SP - 3243 EP - 3251 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 59 IS - 4 SN - 1053-8119, 1053-8119 KW - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts KW - Blood-brain barrier KW - Data processing KW - W 30910:Imaging KW - N3:11001 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920799534?accountid=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=NeuroImage&rft.atitle=Serotonin-1A+receptors+in+major+depression+quantified+using+PET%3A+Controversies%2C+confounds%2C+and+recommendations&rft.au=Shrestha%2C+Saurav%3BHirvonen%2C+Jussi%3BHines%2C+Christina+S%3BHenter%2C+Ioline+D%3BSvenningsson%2C+Per%3BPike%2C+Victor+W%3BInnis%2C+Robert+B&rft.aulast=Shrestha&rft.aufirst=Saurav&rft.date=2012-02-15&rft.volume=59&rft.issue=4&rft.spage=3243&rft.isbn=&rft.btitle=&rft.title=NeuroImage&rft.issn=10538119&rft_id=info:doi/10.1016%2Fj.neuroimage.2011.11.029 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-02-01 N1 - Last updated - 2014-02-21 N1 - SubjectsTermNotLitGenreText - Data processing DO - http://dx.doi.org/10.1016/j.neuroimage.2011.11.029 ER - TY - JOUR T1 - Automatic identification and normalization of dosage forms in drug monographs AN - 1008836466; 16494886 AB - Each day, millions of health consumers seek drug-related information on the Web. Despite some efforts in linking related resources, drug information is largely scattered in a wide variety of websites of different quality and credibility. As a step toward providing users with integrated access to multiple trustworthy drug resources, we aim to develop a method capable of identifying drug's dosage form information in addition to drug name recognition. We developed rules and patterns for identifying dosage forms from different sections of full-text drug monographs, and subsequently normalized them to standardized RxNorm dosage forms. Our method represents a significant improvement compared with a baseline lookup approach, achieving overall macro-averaged Precision of 80%, Recall of 98%, and F-Measure of 85%. We successfully developed an automatic approach for drug dosage form identification, which is critical for building links between different drug-related resources. JF - BMC Medical Informatics and Decision Making AU - Li, Jiao AU - Lu, Zhiyong AD - National Library of Medicine, Bethesda, MD 20894, USA, lij10@ncbi.nlm.nih.gov Y1 - 2012/02/15/ PY - 2012 DA - 2012 Feb 15 SP - 9 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 12 KW - Biotechnology and Bioengineering Abstracts KW - Decision making KW - Informatics KW - Consumers KW - Drugs KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008836466?accountid=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+Medical+Informatics+and+Decision+Making&rft.atitle=Automatic+identification+and+normalization+of+dosage+forms+in+drug+monographs&rft.au=Li%2C+Jiao%3BLu%2C+Zhiyong&rft.aulast=Li&rft.aufirst=Jiao&rft.date=2012-02-15&rft.volume=12&rft.issue=&rft.spage=9&rft.isbn=&rft.btitle=&rft.title=BMC+Medical+Informatics+and+Decision+Making&rft.issn=1472-6947&rft_id=info:doi/10.1186%2F1472-6947-12-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-04-23 N1 - SubjectsTermNotLitGenreText - Decision making; Informatics; Consumers; Drugs DO - http://dx.doi.org/10.1186/1472-6947-12-9 ER - TY - JOUR T1 - Probing the donor and acceptor substrate specificity of the γ-glutamyl transpeptidase. AN - 921564716; 22257032 AB - γ-Glutamyl transpeptidase (GGT) is a two-substrate enzyme that plays a central role in glutathione metabolism and is a potential target for drug design. GGT catalyzes the cleavage of γ-glutamyl donor substrates and the transfer of the γ-glutamyl moiety to an amine of an acceptor substrate or water. Although structures of bacterial GGT have revealed details of the protein-ligand interactions at the donor site, the acceptor substrate site is relatively undefined. The recent identification of a species-specific acceptor site inhibitor, OU749, suggests that these inhibitors may be less toxic than glutamine analogues. Here we investigated the donor and acceptor substrate preferences of Bacillus anthracis GGT (CapD) and applied computational approaches in combination with kinetics to probe the structural basis of the enzyme's substrate and inhibitor binding specificities and compare them with human GGT. Site-directed mutagenesis studies showed that the R432A and R520S variants exhibited 6- and 95-fold decreases in hydrolase activity, respectively, and that their activity was not stimulated by the addition of the l-Cys acceptor substrate, suggesting an additional role in acceptor binding and/or catalysis of transpeptidation. Rat GGT (and presumably HuGGT) has strict stereospecificity for L-amino acid acceptor substrates, while CapD can utilize both L- and D-acceptor substrates comparably. Modeling and kinetic analysis suggest that R520 and R432 allow two alternate acceptor substrate binding modes for L- and D-acceptors. R432 is conserved in Francisella tularensis, Yersinia pestis, Burkholderia mallei, Helicobacter pylori and Escherichia coli, but not in human GGT. Docking and MD simulations point toward key residues that contribute to inhibitor and acceptor substrate binding, providing a guide to designing novel and specific GGT inhibitors. JF - Biochemistry AU - Hu, Xin AU - Legler, Patricia M AU - Khavrutskii, Ilja AU - Scorpio, Angelo AU - Compton, Jaimee R AU - Robertson, Kelly L AU - Friedlander, Arthur M AU - Wallqvist, Anders AD - Biotechnology HPC Software Applications Institute, Telemedicine and Advanced Technology Research Center, US Army Medical Research and Materiel Command, Fort Detrick, Maryland 21702, United States. xin.hu@nih.gov Y1 - 2012/02/14/ PY - 2012 DA - 2012 Feb 14 SP - 1199 EP - 1212 VL - 51 IS - 6 KW - Bacterial Proteins KW - 0 KW - Ligands KW - N-(5-(4-methoxybenzyl)-1,3,4-thiadiazol-2-yl)benzenesulfonamide KW - Sulfonamides KW - Thiadiazoles KW - gamma-Glutamyltransferase KW - EC 2.3.2.2 KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Swine KW - Animals KW - Bacterial Capsules -- genetics KW - Thiadiazoles -- metabolism KW - Glutathione -- metabolism KW - Humans KW - Computational Biology -- methods KW - Catalytic Domain KW - Mice KW - Thiadiazoles -- pharmacology KW - Protein Binding KW - Sulfonamides -- metabolism KW - Rats KW - Sulfonamides -- pharmacology KW - Bacterial Capsules -- chemistry KW - Substrate Specificity KW - Bacterial Capsules -- metabolism KW - Sequence Homology, Amino Acid KW - Bacillus anthracis -- enzymology KW - gamma-Glutamyltransferase -- chemistry KW - Bacterial Proteins -- genetics KW - Bacterial Proteins -- antagonists & inhibitors KW - Bacterial Proteins -- chemistry KW - gamma-Glutamyltransferase -- genetics KW - gamma-Glutamyltransferase -- antagonists & inhibitors UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/921564716?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochemistry&rft.atitle=Probing+the+donor+and+acceptor+substrate+specificity+of+the+%CE%B3-glutamyl+transpeptidase.&rft.au=Hu%2C+Xin%3BLegler%2C+Patricia+M%3BKhavrutskii%2C+Ilja%3BScorpio%2C+Angelo%3BCompton%2C+Jaimee+R%3BRobertson%2C+Kelly+L%3BFriedlander%2C+Arthur+M%3BWallqvist%2C+Anders&rft.aulast=Hu&rft.aufirst=Xin&rft.date=2012-02-14&rft.volume=51&rft.issue=6&rft.spage=1199&rft.isbn=&rft.btitle=&rft.title=Biochemistry&rft.issn=1520-4995&rft_id=info:doi/10.1021%2Fbi200987b LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-04 N1 - Date created - 2012-02-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1021/bi200987b ER - TY - CPAPER T1 - Is the ghost in your genes a sugar? O-GlcNAc and epigenetics T2 - 2012 Gordon Research Conference on Aging, Biology Of AN - 1313024630; 6148026 JF - 2012 Gordon Research Conference on Aging, Biology Of AU - Hanover, John Y1 - 2012/02/12/ PY - 2012 DA - 2012 Feb 12 KW - Sugar KW - epigenetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313024630?accountid=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+Gordon+Research+Conference+on+Aging%2C+Biology+Of&rft.atitle=Is+the+ghost+in+your+genes+a+sugar%3F+O-GlcNAc+and+epigenetics&rft.au=Hanover%2C+John&rft.aulast=Hanover&rft.aufirst=John&rft.date=2012-02-12&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Gordon+Research+Conference+on+Aging%2C+Biology+Of&rft.issn=&rft_id=info:doi/ L2 - http://www.grc.org/programs.aspx?year=2012&program=aging LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Endocytic collagen degradation: A novel mechanism involved in the protection against liver fibrosis T2 - 2012 Gordon Research Conference on Plasminogen Activation And Extracellular Proteolysis AN - 1313095873; 6146999 JF - 2012 Gordon Research Conference on Plasminogen Activation And Extracellular Proteolysis AU - Madsen, Daniel Y1 - 2012/02/11/ PY - 2012 DA - 2012 Feb 11 KW - Degradation KW - Liver KW - Fibrosis KW - Collagen UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313095873?accountid=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+Gordon+Research+Conference+on+Plasminogen+Activation+And+Extracellular+Proteolysis&rft.atitle=Endocytic+collagen+degradation%3A+A+novel+mechanism+involved+in+the+protection+against+liver+fibrosis&rft.au=Madsen%2C+Daniel&rft.aulast=Madsen&rft.aufirst=Daniel&rft.date=2012-02-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Gordon+Research+Conference+on+Plasminogen+Activation+And+Extracellular+Proteolysis&rft.issn=&rft_id=info:doi/ L2 - http://www.grc.org/programs.aspx?year=2012&program=grs_plsmno LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - SRT2104, a molecule designed to activate SIRT1, extends lifespan and healthspan of C57BL6/J mice T2 - 2012 Gordon-Kenan Research Seminar Aging, Biology Of AN - 1312994637; 6154694 JF - 2012 Gordon-Kenan Research Seminar Aging, Biology Of AU - Mitchell, Sarah Y1 - 2012/02/11/ PY - 2012 DA - 2012 Feb 11 KW - Mice KW - Life span KW - SIRT1 protein UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312994637?accountid=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+Gordon-Kenan+Research+Seminar+Aging%2C+Biology+Of&rft.atitle=SRT2104%2C+a+molecule+designed+to+activate+SIRT1%2C+extends+lifespan+and+healthspan+of+C57BL6%2FJ+mice&rft.au=Mitchell%2C+Sarah&rft.aulast=Mitchell&rft.aufirst=Sarah&rft.date=2012-02-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Gordon-Kenan+Research+Seminar+Aging%2C+Biology+Of&rft.issn=&rft_id=info:doi/ L2 - http://www.grc.org/programs.aspx?year=2012&program=grs_aging LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Unraveling the Global microRNAome Responses to Ionizing Radiation in Human Embryonic Stem Cells AN - 1008848013; 16344288 AB - MicroRNAs (miRNA) comprise a group of short ribonucleic acid molecules implicated in regulation of key biological processes and functions at the post-transcriptional level. Ionizing radiation (IR) causes DNA damage and generally triggers cellular stress response. However, the role of miRNAs in IR-induced response in human embryonic stem cells (hESC) has not been defined yet. Here, by using system biology approaches, we show for the first time, that miRNAome undergoes global alterations in hESC (H1 and H9 lines) after IR. Interrogation of expression levels of 1,090 miRNA species in irradiated hESC showed statistically significant changes in 54 genes following 1 Gy of X-ray exposures; global miRNAome alterations were found to be highly temporally and cell line - dependent in hESC. Time-course studies showed that the 16 hr miRNAome radiation response of hESC is much more robust compared to 2 hr-response signature (only eight genes), and may be involved in regulating the cell cycle. Quantitative real-time PCR performed on some miRNA species confirms the robustness of our miRNA microarray platform. Positive regulation of differentiation-, cell cycle-, ion transport- and endomembrane system-related processes were predicted to be negatively affected by miRNAome changes in irradiated hESC. Our findings reveal a fundamental role of miRNAome in modulating the radiation response, and identify novel molecular targets of radiation in hESC. JF - PLoS ONE AU - Sokolov, Mykyta V AU - Panyutin, Irina V AU - Neumann, Ronald D AD - Nuclear Medicine Division, Department of Radiology and Imaging Sciences, Clinical Center, National Institutes of Health, Bethesda, Maryland, United States of America Y1 - 2012/02/08/ PY - 2012 DA - 2012 Feb 08 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 7 IS - 2 KW - Biotechnology and Bioengineering Abstracts; Genetics Abstracts; Environment Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Cell cycle KW - DNA KW - DNA damage KW - Embryo cells KW - Ionizing radiation KW - Polymerase chain reaction KW - Post-transcription KW - Statistical analysis KW - Stem cells KW - Stress KW - miRNA KW - stem cells KW - ENA 14:Radiological Contamination KW - N 14820:DNA Metabolism & Structure KW - G 07730:Development & Cell Cycle KW - W 30945:Fermentation & Cell Culture UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008848013?accountid=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=PLoS+ONE&rft.atitle=Unraveling+the+Global+microRNAome+Responses+to+Ionizing+Radiation+in+Human+Embryonic+Stem+Cells&rft.au=Sokolov%2C+Mykyta+V%3BPanyutin%2C+Irina+V%3BNeumann%2C+Ronald+D&rft.aulast=Sokolov&rft.aufirst=Mykyta&rft.date=2012-02-08&rft.volume=7&rft.issue=2&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+ONE&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0031028 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2013-04-05 N1 - SubjectsTermNotLitGenreText - DNA damage; Stem cells; Embryo cells; Ionizing radiation; Cell cycle; miRNA; Statistical analysis; Polymerase chain reaction; Stress; Post-transcription; stem cells; DNA DO - http://dx.doi.org/10.1371/journal.pone.0031028 ER - TY - JOUR T1 - Endosulfan upregulates AP-1 binding and ARE-mediated transcription via ERK1/2 and p38 activation in HepG2 cells. AN - 914666051; 22146149 AB - Endosulfan is an organochlorine insecticide and has been implicated in neurotoxicity, hepatotoxicity, immunosuppression and teratogenicity. However, the molecular mechanism of endosulfan toxicity is not yet clear. Recent studies demonstrated that oxidative stress induced by endosulfan is involved in its toxicity and accumulating evidence suggests that endosulfan can modulate the activities of stress-responsive signal transduction pathways including extracellular signal regulated kinases (ERK) 1/2. However, none of the previous studies investigated the ability of endosulfan to modulate activating protein-1 (AP-1) binding and antioxidant response element (ARE)-mediated transcription as an underlying mechanism of endosulfan toxicity. In this report, we show that treatment of HepG2 cells with endosulfan significantly increased oxidative stress-responsive transcription via AP-1 activation. In addition, endosulfan-induced transcription was enhanced in cells depleted of glutathione by buthionine sulfoximine (BSO) treatment. Exposure to endosulfan resulted in a significant increase in the activities of MAPKs, ERK1/2 and p38. Endosulfan-induced increases in enzymatic activities of these MAPKs were consistent with MAPK phosphorylation. Endosulfan exposure also caused an increase in c-Jun phosphorylation. These results suggest a model for endosulfan toxicity in which endosulfan increases ERK1/2 and p38 activities and these activated MAPKs then increase c-Jun phosphorylation. Phosphorylated c-Jun, in turn, increases AP-1 activity, which results in activation of ARE-mediated transcription. Copyright © 2011 Elsevier Ireland Ltd. All rights reserved. JF - Toxicology AU - Song, Min Ok AU - Lee, Chang-Ho AU - Yang, Hyun Ok AU - Freedman, Jonathan H AD - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. songmo@kist.re.kr Y1 - 2012/02/06/ PY - 2012 DA - 2012 Feb 06 SP - 23 EP - 32 VL - 292 IS - 1 KW - Transcription Factor AP-1 KW - 0 KW - MAPK1 protein, human KW - EC 2.7.11.24 KW - Mitogen-Activated Protein Kinase 1 KW - Mitogen-Activated Protein Kinase 3 KW - p38 Mitogen-Activated Protein Kinases KW - Endosulfan KW - OKA6A6ZD4K KW - Index Medicus KW - Transcription, Genetic -- drug effects KW - Hep G2 Cells KW - Humans KW - Enzyme Activation -- drug effects KW - Transcriptional Activation -- physiology KW - Transcriptional Activation -- drug effects KW - Enzyme Activation -- physiology KW - Transcription, Genetic -- physiology KW - Up-Regulation -- physiology KW - Mitogen-Activated Protein Kinase 3 -- metabolism KW - Transcription Factor AP-1 -- metabolism KW - Mitogen-Activated Protein Kinase 1 -- metabolism KW - Up-Regulation -- drug effects KW - p38 Mitogen-Activated Protein Kinases -- physiology KW - Endosulfan -- toxicity KW - p38 Mitogen-Activated Protein Kinases -- metabolism KW - Mitogen-Activated Protein Kinase 1 -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/914666051?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Endosulfan+upregulates+AP-1+binding+and+ARE-mediated+transcription+via+ERK1%2F2+and+p38+activation+in+HepG2+cells.&rft.au=Song%2C+Min+Ok%3BLee%2C+Chang-Ho%3BYang%2C+Hyun+Ok%3BFreedman%2C+Jonathan+H&rft.aulast=Song&rft.aufirst=Min&rft.date=2012-02-06&rft.volume=292&rft.issue=1&rft.spage=23&rft.isbn=&rft.btitle=&rft.title=Toxicology&rft.issn=1879-3185&rft_id=info:doi/10.1016%2Fj.tox.2011.11.013 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-02-27 N1 - Date created - 2012-01-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Toxicol In Vitro. 2005 Mar;19(2):261-73 [15649640] Toxicol Sci. 2005 Aug;86(2):444-52 [15888667] J Steroid Biochem Mol Biol. 2006 Feb;98(2-3):122-32 [16413991] Cancer Res. 2009 Feb 15;69(4):1284-92 [19190345] Environ Pollut. 2011 Jun;159(6):1737-43 [21429639] Chemosphere. 2011 May;83(10):1398-405 [21470655] Mol Cell Biol. 1999 Apr;19(4):2435-44 [10082509] Toxicol Appl Pharmacol. 2000 Mar 1;163(2):188-94 [10698677] Biochem Pharmacol. 2000 Jun 1;59(11):1433-9 [10751553] Toxicology. 2000 May 5;146(2-3):171-6 [10814849] Mol Cell Biochem. 2000 Feb;205(1-2):53-66 [10821422] J Biol Chem. 2000 Jun 2;275(22):16709-16 [10828062] Toxicol Sci. 2001 Sep;63(1):65-73 [11509745] J Vet Med Sci. 2001 Nov;63(11):1183-90 [11767051] Toxicol Appl Pharmacol. 2002 Mar 15;179(3):172-84 [11906247] Biochemistry (Mosc). 2002 Mar;67(3):281-92 [11970728] Nat Cell Biol. 2002 May;4(5):E131-6 [11988758] Bull Environ Contam Toxicol. 2002 May;68(5):725-31 [12068940] Mol Cell Biochem. 2003 May;247(1-2):1-7 [12841624] Mol Cell Biochem. 2003 May;247(1-2):127-38 [12841640] Biofactors. 2003;17(1-4):287-96 [12897450] J Biochem Mol Toxicol. 2003;17(4):207-13 [12898644] Carcinogenesis. 2004 Feb;25(2):249-61 [14604893] Toxicol Lett. 2004 Jul 15;151(2):357-65 [15183460] Rev Environ Contam Toxicol. 2004;183:99-113 [15369323] J Environ Sci Health C. 1978;13(1):49-62 [26707] Toxicology. 1979 Jun-Jul;13(2):115-30 [390767] Med Biol. 1982 Oct;60(5):237-54 [6759800] Arch Toxicol. 1986 Dec;59(4):279-84 [3827596] J Toxicol Environ Health. 1989;28(4):473-81 [2531805] Indian J Exp Biol. 1989 Aug;27(8):725-8 [2633982] J Biol Chem. 1991 Mar 5;266(7):4556-61 [1900296] J Biol Chem. 1991 Jun 25;266(18):11632-9 [1646813] Nature. 1991 Oct 17;353(6345):670-4 [1922387] Nature. 1991 Dec 12;354(6353):494-6 [1749429] Pharmacol Ther. 1991;51(2):155-94 [1784629] Mol Cell Biol. 1992 Aug;12(8):3507-13 [1630458] Biochem Biophys Res Commun. 1993 Jan 15;190(1):15-9 [8380689] Oncogene. 1994 Feb;9(2):565-71 [8290267] Pharmacogenetics. 1994 Feb;4(1):1-10 [8004128] Bull Environ Contam Toxicol. 1995 Feb;54(2):258-65 [7537992] Biol Trace Elem Res. 1995 Jan-Mar;47(1-3):321-6 [7779565] J Biol Chem. 1995 Jun 23;270(25):14843-6 [7797459] J Biol Chem. 1995 Jul 14;270(28):16483-6 [7622446] Food Chem Toxicol. 1995 Nov;33(11):941-50 [7590542] Vet Hum Toxicol. 1995 Dec;37(6):547-9 [8588293] Curr Opin Cell Biol. 1995 Dec;7(6):798-805 [8608010] Mol Reprod Dev. 1995 Dec;42(4):459-67 [8607977] FASEB J. 1996 May;10(7):709-20 [8635688] EMBO J. 1996 Aug 1;15(15):3943-50 [8670899] Curr Opin Immunol. 1996 Jun;8(3):402-11 [8793994] Curr Opin Cell Biol. 1997 Apr;9(2):240-6 [9069263] Genes Dev. 1997 Jul 1;11(13):1748-58 [9224723] J Androl. 1997 Nov-Dec;18(6):571-5 [9432128] EMBO J. 1998 Aug 3;17(15):4404-13 [9687508] Annu Rev Pharmacol Toxicol. 1999;39:67-101 [10331077] Pharmacol Toxicol. 1999 May;84(5):201-10 [10361976] J Biol Chem. 1999 Sep 24;274(39):27545-52 [10488090] Singapore Med J. 2006 Dec;47(12):1030-2 [17139397] J Appl Toxicol. 2007 Mar-Apr;27(2):143-51 [17186572] Clin Toxicol (Phila). 2007 Jun-Aug;45(5):530-2 [17503261] J Cell Physiol. 2007 Oct;213(1):177-86 [17503468] J Cell Biochem. 2007 Dec 15;102(6):1442-57 [17471497] FASEB J. 2008 Apr;22(4):954-65 [18039929] Toxicol In Vitro. 2008 Sep;22(6):1595-604 [18640261] Hum Exp Toxicol. 1999 Sep;18(9):583-9 [10523873] Environ Health Perspect. 2004 Nov;112(15):1481-7 [15531431] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.tox.2011.11.013 ER - TY - CPAPER T1 - Robust automated detection, segmentation and classification of hepatic tumors from CT data T2 - 2012 Conference on Biomedical Applications in Molecular, Structural, and Functional Imaging AN - 1313120363; 6159811 JF - 2012 Conference on Biomedical Applications in Molecular, Structural, and Functional Imaging AU - Linguraru, Marius AU - Richbourg, William AU - Pamulapati, Vivek AU - Wang, Shijun AU - Summers, Ronald Y1 - 2012/02/04/ PY - 2012 DA - 2012 Feb 04 KW - Classification KW - Tumors KW - Data processing KW - Segmentation KW - Liver KW - Automation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313120363?accountid=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+Conference+on+Biomedical+Applications+in+Molecular%2C+Structural%2C+and+Functional+Imaging&rft.atitle=Robust+automated+detection%2C+segmentation+and+classification+of+hepatic+tumors+from+CT+data&rft.au=Linguraru%2C+Marius%3BRichbourg%2C+William%3BPamulapati%2C+Vivek%3BWang%2C+Shijun%3BSummers%2C+Ronald&rft.aulast=Linguraru&rft.aufirst=Marius&rft.date=2012-02-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Conference+on+Biomedical+Applications+in+Molecular%2C+Structural%2C+and+Functional+Imaging&rft.issn=&rft_id=info:doi/ L2 - http://spie.org/documents/conferencesexhibitions/MI12-Final-lr.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - GPU-based iterative relative fuzzy connectedness image segmentation T2 - 2012 Conference on Image-Guided Procedures, Robotic Interventions, and Modeling AN - 1313091200; 6159741 JF - 2012 Conference on Image-Guided Procedures, Robotic Interventions, and Modeling AU - Zhuge, Ying AU - Udupa, Jayaram AU - Miller, Robert Y1 - 2012/02/04/ PY - 2012 DA - 2012 Feb 04 KW - Segmentation KW - Image processing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313091200?accountid=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+Conference+on+Image-Guided+Procedures%2C+Robotic+Interventions%2C+and+Modeling&rft.atitle=GPU-based+iterative+relative+fuzzy+connectedness+image+segmentation&rft.au=Zhuge%2C+Ying%3BUdupa%2C+Jayaram%3BMiller%2C+Robert&rft.aulast=Zhuge&rft.aufirst=Ying&rft.date=2012-02-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Conference+on+Image-Guided+Procedures%2C+Robotic+Interventions%2C+and+Modeling&rft.issn=&rft_id=info:doi/ L2 - http://spie.org/documents/conferencesexhibitions/MI12-Final-lr.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Quantitative evaluation of phase processing approaches in susceptibility weighted imaging T2 - 2012 Conference on Biomedical Applications in Molecular, Structural, and Functional Imaging AN - 1313090405; 6159820 JF - 2012 Conference on Biomedical Applications in Molecular, Structural, and Functional Imaging AU - Li, Ningzhi AU - Wang, Wen-tung AU - Sati, Pascal AU - Pham, Dzung AU - Butman, John Y1 - 2012/02/04/ PY - 2012 DA - 2012 Feb 04 KW - Imaging techniques UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313090405?accountid=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+Conference+on+Biomedical+Applications+in+Molecular%2C+Structural%2C+and+Functional+Imaging&rft.atitle=Quantitative+evaluation+of+phase+processing+approaches+in+susceptibility+weighted+imaging&rft.au=Li%2C+Ningzhi%3BWang%2C+Wen-tung%3BSati%2C+Pascal%3BPham%2C+Dzung%3BButman%2C+John&rft.aulast=Li&rft.aufirst=Ningzhi&rft.date=2012-02-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Conference+on+Biomedical+Applications+in+Molecular%2C+Structural%2C+and+Functional+Imaging&rft.issn=&rft_id=info:doi/ L2 - http://spie.org/documents/conferencesexhibitions/MI12-Final-lr.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Computer-assisted diagnostic tool to quantify the pulmonary veins in sickle cell associated pulmonary hypertension T2 - 2012 Conference on Biomedical Applications in Molecular, Structural, and Functional Imaging AN - 1313060092; 6159866 JF - 2012 Conference on Biomedical Applications in Molecular, Structural, and Functional Imaging AU - Jajamovich, Guido AU - Pamulapati, Vivek AU - Alam, Shoaib AU - Mehari, Alem AU - Kato, Gregory AU - Wood, Bradford AU - Linguraru, Marius Y1 - 2012/02/04/ PY - 2012 DA - 2012 Feb 04 KW - Hypertension KW - Lung KW - Veins KW - Circulatory system KW - Heart UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313060092?accountid=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+Conference+on+Biomedical+Applications+in+Molecular%2C+Structural%2C+and+Functional+Imaging&rft.atitle=Computer-assisted+diagnostic+tool+to+quantify+the+pulmonary+veins+in+sickle+cell+associated+pulmonary+hypertension&rft.au=Jajamovich%2C+Guido%3BPamulapati%2C+Vivek%3BAlam%2C+Shoaib%3BMehari%2C+Alem%3BKato%2C+Gregory%3BWood%2C+Bradford%3BLinguraru%2C+Marius&rft.aulast=Jajamovich&rft.aufirst=Guido&rft.date=2012-02-04&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Conference+on+Biomedical+Applications+in+Molecular%2C+Structural%2C+and+Functional+Imaging&rft.issn=&rft_id=info:doi/ L2 - http://spie.org/documents/conferencesexhibitions/MI12-Final-lr.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Mutagenesis of human immunodeficiency virus reverse transcriptase p51 subunit defines residues contributing to vinylogous urea inhibition of ribonuclease H activity. AN - 920232574; 22105069 AB - The vinylogous urea, NSC727447, was proposed to allosterically inhibit ribonuclease H (RNase H) activity of human immunodeficiency virus type 1 reverse transcriptase (HIV-1 RT) by interacting with the thumb subdomain of its non-catalytic p51 subunit. Proximity of the p51 thumb to the p66 RNase H domain implied that inhibitor binding altered active site geometry, whereas protein footprinting suggested a contribution from α-helix I residues Cys-280 and Lys-281. To more thoroughly characterize the vinylogous urea binding site, horizontal alanine scanning mutagenesis between p51 residues Lys-275 and Thr-286 (comprising α-helix I and portions of the neighboring αH/αI and αI/αJ connecting loops) was combined with a limited vertical scan of Cys-280. A contribution from Cys-280 was strengthened by our observation that all substitutions at this position rendered selectively mutated, reconstituted p66/p51 heterodimers ∼45-fold less sensitive to inhibition. An ∼19-fold reduced IC(50) for p51 mutant T286A coupled with a 2-8-fold increased IC(50) when intervening residues were substituted supports our original proposal of p51 α-helix I as the vinylogous urea binding site. In contrast to these allosteric inhibitors, mutant enzymes retained equivalent sensitivity to the natural product α-hydroxytropolone inhibitor manicol, which x-ray crystallography has demonstrated functions by chelating divalent metal at the p66 RNase H active site. Finally, reduced DNA strand-transfer activity together with increased vinylogous urea sensitivity of p66/p51 heterodimers containing short p51 C-terminal deletions suggests an additional role for the p51 C terminus in nucleic acid binding that is compromised by inhibitor binding. JF - The Journal of biological chemistry AU - Chung, Suhman AU - Miller, Jennifer T AU - Johnson, Barry C AU - Hughes, Stephen H AU - Le Grice, Stuart F J AD - HIV Drug Resistance Program, National Cancer Institute-Frederick, National Institutes of Health, Frederick, Maryland 21702, USA. Y1 - 2012/02/03/ PY - 2012 DA - 2012 Feb 03 SP - 4066 EP - 4075 VL - 287 IS - 6 KW - Enzyme Inhibitors KW - 0 KW - NSC 727447 KW - Thiophenes KW - Ribonuclease H, Human Immunodeficiency Virus KW - EC 3.1.26.4 KW - Index Medicus KW - Protein Structure, Secondary KW - Humans KW - Crystallography, X-Ray KW - Protein Structure, Tertiary KW - Mutation, Missense KW - Cell Line KW - Amino Acid Substitution KW - Mutagenesis KW - HIV-1 -- genetics KW - Thiophenes -- chemistry KW - Ribonuclease H, Human Immunodeficiency Virus -- antagonists & inhibitors KW - Ribonuclease H, Human Immunodeficiency Virus -- genetics KW - Enzyme Inhibitors -- chemistry KW - HIV-1 -- enzymology KW - Ribonuclease H, Human Immunodeficiency Virus -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920232574?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mutagenesis+of+human+immunodeficiency+virus+reverse+transcriptase+p51+subunit+defines+residues+contributing+to+vinylogous+urea+inhibition+of+ribonuclease+H+activity.&rft.au=Chung%2C+Suhman%3BMiller%2C+Jennifer+T%3BJohnson%2C+Barry+C%3BHughes%2C+Stephen+H%3BLe+Grice%2C+Stuart+F+J&rft.aulast=Chung&rft.aufirst=Suhman&rft.date=2012-02-03&rft.volume=287&rft.issue=6&rft.spage=4066&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M111.314781 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-03-25 N1 - Date created - 2012-02-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biochemistry. 2000 Feb 15;39(6):1427-33 [10684624] J Med Chem. 2011 Jul 14;54(13):4462-73 [21568335] EMBO J. 2001 Mar 15;20(6):1449-61 [11250910] Biochemistry. 2002 Apr 16;41(15):4856-65 [11939780] J Biol Chem. 2003 Jan 31;278(5):2777-80 [12480948] J Mol Biol. 2003 Mar 14;327(1):19-30 [12614605] Nucleic Acids Res. 2003 Dec 1;31(23):6852-9 [14627818] J Med Chem. 2004 May 6;47(10):2550-60 [15115397] Eur J Biochem. 1990 Jan 26;187(2):307-14 [1688798] EMBO J. 1991 Dec;10(12):3905-11 [1718745] Proc Natl Acad Sci U S A. 1992 Nov 15;89(22):10763-7 [1279694] Science. 1992 Nov 13;258(5085):1112-8 [1279806] Proc Natl Acad Sci U S A. 1993 Jul 1;90(13):6320-4 [7687065] J Biol Chem. 1994 Jan 14;269(2):1388-93 [7507107] Proc Natl Acad Sci U S A. 1994 Jul 19;91(15):7242-6 [7518928] Nucleic Acids Res. 1994 Nov 11;22(22):4625-33 [7527138] Eur J Biochem. 1996 Nov 15;242(1):98-103 [8954159] J Mol Biol. 1996 Dec 20;264(5):1085-100 [9000632] Biochemistry. 1997 May 13;36(19):5758-68 [9153416] Proc Natl Acad Sci U S A. 1997 Jun 24;94(13):6700-5 [9192628] J Mol Biol. 1998 Nov 27;284(2):313-23 [9813120] Science. 1998 Nov 27;282(5394):1669-75 [9831551] Prog Biophys Mol Biol. 2005 Jun;88(2):209-31 [15572156] Biochemistry. 2005 Feb 8;44(5):1595-606 [15683243] Nucleic Acids Res. 2005;33(4):1249-56 [15741178] J Med Chem. 2005 Mar 24;48(6):1901-9 [15771434] Curr Pharm Des. 2006;12(15):1879-94 [16724954] Curr Pharm Des. 2006;12(15):1909-22 [16724956] J Med Chem. 2006 Aug 10;49(16):4834-41 [16884295] J Virol. 2006 Dec;80(24):12283-92 [17020946] ACS Chem Biol. 2006 Dec 20;1(11):702-12 [17184135] Virology. 2007 May 25;362(1):131-8 [17258261] Proc Natl Acad Sci U S A. 2008 Feb 5;105(5):1466-71 [18230722] Nature. 2008 May 8;453(7192):184-9 [18464735] ACS Chem Biol. 2008 Oct 17;3(10):635-44 [18831589] J Mol Biol. 2009 May 8;388(3):462-74 [19289131] J Med Chem. 2009 Oct 8;52(19):5781-4 [19791799] J Med Chem. 2009 Oct 22;52(20):6467-73 [19775161] Structure. 2009 Dec 9;17(12):1625-35 [20004166] J Virol. 2010 Aug;84(15):7625-33 [20484498] Antimicrob Agents Chemother. 2010 Sep;54(9):3913-21 [20547794] Antimicrob Agents Chemother. 2011 Jun;55(6):2905-15 [21464257] J Biol Chem. 2000 May 26;275(21):16015-22 [10748161] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1074/jbc.M111.314781 ER - TY - JOUR T1 - Hydrogen sulfide is an endogenous potentiator of T cell activation. AN - 920230848; 22167178 AB - H(2)S is an endogenous signaling molecule that may act via protein sulfhydrylation to regulate various physiological functions. H(2)S is also a byproduct of dietary sulfate metabolism by gut bacteria. Inflammatory bowel diseases such as ulcerative colitis are associated with an increase in the colonization of the intestine by sulfate reducing bacteria along with an increase in H(2)S production. Consistent with its increased production, H(2)S is implicated as a mediator of ulcerative colitis both in its genesis or maintenance. As T cells are well established mediators of inflammatory bowel disease, we investigated the effect of H(2)S exposure on T cell activation. Using primary mouse T lymphocytes (CD3+), OT-II CD4+ T cells, and the human Jurkat T cell line, we show that physiological levels of H(2)S potentiate TCR-induced activation. Nanomolar levels of H(2)S (50-500 nM) enhance T cell activation assessed by CD69 expression, interleukin-2 expression, and CD25 levels. Exposure of T cells to H(2)S dose-dependently enhances TCR-stimulated proliferation with a maximum at 300 nM (30% increase, p < 0.01). Furthermore, activation increases the capacity of T cells to make H(2)S via increased expression of cystathionine γ-lyase and cystathionine β-synthase. Disrupting this response by silencing these H(2)S producing enzymes impairs T cell activation, and proliferation and can be rescued by the addition of 300 nM H(2)S. Thus, H(2)S represents a novel autocrine immunomodulatory molecule in T cells. JF - The Journal of biological chemistry AU - Miller, Thomas W AU - Wang, Evelyn A AU - Gould, Serge AU - Stein, Erica V AU - Kaur, Sukhbir AU - Lim, Langston AU - Amarnath, Shoba AU - Fowler, Daniel H AU - Roberts, David D AD - Laboratory of Pathology, Center for Cancer Research, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA. Y1 - 2012/02/03/ PY - 2012 DA - 2012 Feb 03 SP - 4211 EP - 4221 VL - 287 IS - 6 KW - Air Pollutants KW - 0 KW - Antigens, CD KW - Antigens, Differentiation, T-Lymphocyte KW - CD69 antigen KW - IL2 protein, human KW - IL2RA protein, human KW - Il2ra protein, mouse KW - Interleukin-2 KW - Interleukin-2 Receptor alpha Subunit KW - Lectins, C-Type KW - Cystathionine beta-Synthase KW - EC 4.2.1.22 KW - Cystathionine gamma-Lyase KW - EC 4.4.1.1 KW - Hydrogen Sulfide KW - YY9FVM7NSN KW - Index Medicus KW - Cell Proliferation -- drug effects KW - Cystathionine gamma-Lyase -- genetics KW - Animals KW - Interleukin-2 Receptor alpha Subunit -- genetics KW - Lectins, C-Type -- immunology KW - Humans KW - Gene Expression Regulation -- immunology KW - Jurkat Cells KW - Cystathionine beta-Synthase -- immunology KW - Antigens, CD -- genetics KW - Mice KW - Interleukin-2 -- genetics KW - Mice, Transgenic KW - Gene Expression Regulation -- genetics KW - Antigens, Differentiation, T-Lymphocyte -- genetics KW - Cystathionine beta-Synthase -- genetics KW - Cystathionine gamma-Lyase -- immunology KW - Lectins, C-Type -- genetics KW - Interleukin-2 Receptor alpha Subunit -- immunology KW - Interleukin-2 -- immunology KW - Gene Expression Regulation -- drug effects KW - Antigens, Differentiation, T-Lymphocyte -- immunology KW - Antigens, CD -- immunology KW - Lymphocyte Activation -- drug effects KW - Air Pollutants -- pharmacology KW - Lymphocyte Activation -- genetics KW - Lymphocyte Activation -- immunology KW - Hydrogen Sulfide -- pharmacology KW - CD4-Positive T-Lymphocytes -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920230848?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Hydrogen+sulfide+is+an+endogenous+potentiator+of+T+cell+activation.&rft.au=Miller%2C+Thomas+W%3BWang%2C+Evelyn+A%3BGould%2C+Serge%3BStein%2C+Erica+V%3BKaur%2C+Sukhbir%3BLim%2C+Langston%3BAmarnath%2C+Shoba%3BFowler%2C+Daniel+H%3BRoberts%2C+David+D&rft.aulast=Miller&rft.aufirst=Thomas&rft.date=2012-02-03&rft.volume=287&rft.issue=6&rft.spage=4211&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+biological+chemistry&rft.issn=1083-351X&rft_id=info:doi/10.1074%2Fjbc.M111.307819 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-03-25 N1 - Date created - 2012-02-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Antioxid Redox Signal. 2010 May 15;12(10):1167-78 [19769462] Antioxid Redox Signal. 2010 May 15;12(10):1219-34 [19803742] Respir Physiol Neurobiol. 2010 Jul 31;172(3):169-78 [20576528] Clin Exp Pharmacol Physiol. 2010 Jul;37(7):764-71 [20148917] Arterioscler Thromb Vasc Biol. 2010 Oct;30(10):1998-2004 [20634473] Antioxid Redox Signal. 2011 Jul 1;15(1):39-47 [20673163] Inflamm Bowel Dis. 2011 Jul;17(7):1620-5 [21674719] PLoS One. 2011;6(6):e21077 [21701688] J Immunol. 2001 Feb 15;166(4):2427-36 [11160302] Immunity. 2001 Mar;14(3):315-29 [11290340] Comp Biochem Physiol B Biochem Mol Biol. 2001 May;129(1):129-37 [11337256] Biochemistry. 2002 Oct 1;41(39):11552-65 [12269799] J Biol Chem. 2003 Oct 17;278(42):41034-46 [12896977] Nat Rev Immunol. 2004 Feb;4(2):110-22 [15040584] Trends Immunol. 2004 May;25(5):257-65 [15099566] Cell Immunol. 1980 Mar 15;50(2):416-31 [6965617] Eur J Biochem. 1982 Mar;123(1):159-64 [7067695] Int Arch Allergy Appl Immunol. 1982;68(1):84-9 [6281197] J Cell Physiol. 1983 Aug;116(2):127-34 [6134740] Science. 1986 Jul 11;233(4760):203-6 [3523754] J Exp Med. 1986 Dec 1;164(6):1988-2005 [2946796] Cell Immunol. 1990 Aug;129(1):32-46 [2364441] Annu Rev Pharmacol Toxicol. 1992;32:109-34 [1605565] J Immunol. 1993 Aug 15;151(4):1881-93 [7688389] J Immunol. 1994 Jun 15;152(12):5633-42 [8207197] J Exp Med. 1995 Feb 1;181(2):577-84 [7836913] J Neurosci. 1996 Feb 1;16(3):1066-71 [8558235] Cancer. 1996 Apr 15;77(8 Suppl):1701-6 [8608565] Gut. 1996 Jul;39(1):1-4 [8881797] Dig Dis Sci. 1997 Aug;42(8):1571-9 [9286219] Biochem Biophys Res Commun. 1997 Aug 28;237(3):527-31 [9299397] Am J Gastroenterol. 1998 Jan;93(1):83-7 [9448181] J Cell Biol. 1998 Feb 23;140(4):861-71 [9472038] J Immunother. 1999 Jul;22(4):336-45 [10404435] J Clin Invest. 1999 Oct;104(8):1107-14 [10525049] Lab Invest. 2005 Jan;85(1):154-9 [15543203] Science. 2005 Apr 22;308(5721):518 [15845845] Br J Pharmacol. 2005 May;145(2):141-4 [15753944] Br J Pharmacol. 2005 Oct;146(4):498-505 [16100527] J Biomol Screen. 2005 Dec;10(8):795-805 [16234347] Shock. 2006 Aug;26(2):154-61 [16878023] FASEB J. 2006 Oct;20(12):2118-20 [16912151] Free Radic Biol Med. 2007 Mar 1;42(5):706-19 [17291994] Shock. 2007 Apr;27(4):370-2 [17414418] Am J Physiol Lung Cell Mol Physiol. 2007 Apr;292(4):L960-71 [17209138] Indian J Biochem Biophys. 2007 Jun;44(3):179-82 [17650588] Proc Natl Acad Sci U S A. 2007 Sep 25;104(39):15560-5 [17878306] J Cell Physiol. 2007 Dec;213(3):826-33 [17516567] Dig Dis Sci. 2008 Jan;53(1):277-83 [17551834] Circulation. 2008 May 6;117(18):2351-60 [18443240] Life Sci. 2008 Jun 6;82(23-24):1196-202 [18482739] Eur J Pharmacol. 2008 Aug 20;590(1-3):127-35 [18585702] Am J Physiol Heart Circ Physiol. 2008 Aug;295(2):H801-6 [18567706] Am J Physiol Heart Circ Physiol. 2008 Sep;295(3):H1330-H1340 [18660450] Lab Invest. 2008 Oct;88(10):1038-48 [18679378] Science. 2008 Oct 24;322(5901):587-90 [18948540] Am J Physiol Regul Integr Comp Physiol. 2008 Nov;295(5):R1479-85 [18799635] PLoS One. 2008;3(12):e3861 [19060950] Nat Med. 2009 Feb;15(2):200-5 [19136963] Shock. 2009 Mar;31(3):267-74 [18636044] Toxicology. 2009 Oct 1;264(1-2):96-103 [19647029] Nat Chem Biol. 2009 Oct;5(10):721-3 [19718041] Sci Signal. 2009;2(96):ra72 [19903941] Proc Natl Acad Sci U S A. 2009 Dec 22;106(51):21972-7 [19955410] Neurochem Int. 2010 Jan;56(1):3-10 [19703504] Cell Mol Life Sci. 2010 Apr;67(7):1119-32 [20063035] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1074/jbc.M111.307819 ER - TY - CPAPER T1 - Association between variants on 8q24 and prostate cancer: A review and meta-analysis T2 - 2012 Genitourinary Cancers Symposium AN - 1313072383; 6150048 JF - 2012 Genitourinary Cancers Symposium AU - Troutman, Sarah Y1 - 2012/02/02/ PY - 2012 DA - 2012 Feb 02 KW - Reviews KW - Prostate cancer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313072383?accountid=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+Genitourinary+Cancers+Symposium&rft.atitle=Association+between+variants+on+8q24+and+prostate+cancer%3A+A+review+and+meta-analysis&rft.au=Troutman%2C+Sarah&rft.aulast=Troutman&rft.aufirst=Sarah&rft.date=2012-02-02&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Genitourinary+Cancers+Symposium&rft.issn=&rft_id=info:doi/ L2 - http://www.gucasymposium.org/2012/2012GenitourinaryCancersSymposium/MeetingProgram.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Assessment of Compound Hepatotoxicity Using Human Plateable Cryopreserved Hepatoeytesin a 1536-Well-Plate Format AN - 968185566; 16507593 AB - Hepatotoxicity is a major concern for both drug development and toxicological evaluation of environmental chemicals. The assessment of compound-induced hepatotoxicity has traditionally relied on in vivo testing; however, it is being replaced by human in vitro models due to an emphasis on the reduction of animal testing and species-specific differences. Since most cell lines and hybridomas lack the full complement of enzymes at physiological levels found in the liver, primary hepatoeytes are the gold standard to study liver toxicities in vitro due to the retention of most of their in vivo activities. Here, we optimized a cell viability assay using plateable cryopreserved human hepatoeytes in a 1536-well-plate format. The assay was validated by deriving inhibitory concentration at 50% values for 12 known compounds, including tamoxifen, staurosporine, and phenylmercurie acetate, with regard to hepatotoxicity and general cytotoxicity using multiple hepatocyte donors. The assay performed well, and the cytotoxicity of these compounds was confirmed in comparison to HepG2 cells. This is the first study to report the reliability of using plateable cryopreserved human hepatoeytes for cytotoxicity studies in a 1536-well-plate format. These results suggest that plateable cryopreserved human hepatoeytes can be scaled up for screening a large compound library and may be amenable to other hepatocytic assays such as metabolic or drug safety studies. JF - Assay and Drug Development Technologies AU - Moeller, T A AU - Shukla, S J AU - Xia, M AD - NIH Chemical Genomies Center, National Institutes of Health, 9800 Medical Center Drive, MSC 3370, Bethesda, MD 20892-3370, USA, mxia@mail.nih.gov Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 78 EP - 87 VL - 10 IS - 1 SN - 1540-658X, 1540-658X KW - Toxicology Abstracts; Biotechnology and Bioengineering Abstracts KW - Hepatocytes KW - Enzymes KW - Drug development KW - Toxicity KW - Tamoxifen KW - Acetic acid KW - Cryopreservation KW - hepatotoxicity KW - Hybridoma KW - Cytotoxicity KW - Staurosporine KW - Liver KW - Drugs KW - X 24310:Pharmaceuticals KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/968185566?accountid=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=Assay+and+Drug+Development+Technologies&rft.atitle=Assessment+of+Compound+Hepatotoxicity+Using+Human+Plateable+Cryopreserved+Hepatoeytesin+a+1536-Well-Plate+Format&rft.au=Moeller%2C+T+A%3BShukla%2C+S+J%3BXia%2C+M&rft.aulast=Moeller&rft.aufirst=T&rft.date=2012-02-01&rft.volume=10&rft.issue=1&rft.spage=78&rft.isbn=&rft.btitle=&rft.title=Assay+and+Drug+Development+Technologies&rft.issn=1540658X&rft_id=info:doi/10.1089%2Fadt.2010.0365 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2016-06-22 N1 - SubjectsTermNotLitGenreText - Hepatocytes; Enzymes; Drug development; Toxicity; Cryopreservation; Acetic acid; Tamoxifen; hepatotoxicity; Hybridoma; Cytotoxicity; Staurosporine; Liver; Drugs DO - http://dx.doi.org/10.1089/adt.2010.0365 ER - TY - JOUR T1 - Abscopal Regression of Antigen Disparate Tumors by Antigen Cascade After Systemic Tumor Vaccination in Combination with Local Tumor Radiation AN - 968184479; 16506871 AB - Radiation is a primary modality in cancer treatment. Radiation can also reduce tumor growth outside the treatment field, often referred to as the abscopal effect. The mechanisms and therapeutic potential of the abscopal effect have not been fully elucidated. We evaluated the role of vaccination directed against a tumor-associated antigen (TAA) in the induction and amplification of radiation induced abscopal effects. Active-specific immunotherapy with a TAA-specific vaccine regimen was used to induce and potentiate T-cell responses against carcinoembryonic antigen (CEA) in combination with local irradiation of subcutaneous tumors. We examined the potential synergy of a poxvirus-based CEA vaccine regimen in CEA-transgenic (Tg) mice in combination with either external beam radiation or brachytherapy of local tumors. The induction of CD8 super(+) T cells specific for multiple TAAs not encoded by the vaccine was observed after the combination therapy. In two tumor models, the antigen cascade responses induced by vaccine and local irradiation mediated the regression of antigen negative metastases at distal subcutaneous or pulmonary sites. Clinically, local control of the primary tumor is necessary and can sometimes prevent metastases; however, irradiation generally fails to control preexisting metastases. These studies suggest that by coupling tumor irradiation with immunotherapy, the abscopal effect can transcend from anecdotal observation to a defined mechanism that can be exploited for the treatment of systemic disease. JF - Cancer Biotherapy and Radiopharmaceuticals AU - Hodge, J W AU - Sharp, HJ AU - Gameiro AD - Laboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 10 Center Drive, Room 8B13, Bethesda, MD, 20892, USA, jh241d@nih.gov Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 12 EP - 22 VL - 27 IS - 1 SN - 1084-9785, 1084-9785 KW - Environment Abstracts; Immunology Abstracts; Biotechnology and Bioengineering Abstracts KW - Animal models KW - Antigen (tumor-associated) KW - Brachytherapy KW - CD8 antigen KW - Cancer KW - Carcinoembryonic antigen KW - Immunotherapy KW - Irradiation KW - Lung KW - Lymphocytes T KW - Metastases KW - Mice KW - Pharmaceuticals KW - Radiation KW - Radioisotopes KW - Regression analysis KW - Tumors KW - Vaccination KW - Vaccines KW - exploitation KW - tumors KW - vaccines KW - F 06915:Cancer Immunology KW - W 30915:Pharmaceuticals & Vaccines KW - ENA 07:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/968184479?accountid=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+Biotherapy+and+Radiopharmaceuticals&rft.atitle=Abscopal+Regression+of+Antigen+Disparate+Tumors+by+Antigen+Cascade+After+Systemic+Tumor+Vaccination+in+Combination+with+Local+Tumor+Radiation&rft.au=Hodge%2C+J+W%3BSharp%2C+HJ%3BGameiro&rft.aulast=Hodge&rft.aufirst=J&rft.date=2012-02-01&rft.volume=27&rft.issue=1&rft.spage=12&rft.isbn=&rft.btitle=&rft.title=Cancer+Biotherapy+and+Radiopharmaceuticals&rft.issn=10849785&rft_id=info:doi/10.1089%2Fcbr.2012.1202 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-05-18 N1 - SubjectsTermNotLitGenreText - Immunotherapy; Carcinoembryonic antigen; Animal models; Tumors; CD8 antigen; Vaccination; Cancer; Metastases; Brachytherapy; Radiation; Lung; Antigen (tumor-associated); Radioisotopes; Lymphocytes T; Regression analysis; Pharmaceuticals; Vaccines; vaccines; Irradiation; exploitation; Mice; tumors DO - http://dx.doi.org/10.1089/cbr.2012.1202 ER - TY - JOUR T1 - Recent Advances in Therapeutic Cancer Vaccines AN - 968184443; 16506869 AB - The Food and Drug Administration (FDA) approval of sipuleucel-T super(1) as the first therapeutic cancer vaccine represents a major stride for this field. Sipuleucel-T consists of autologous peripheral blood mononuclear cells, including antigen-presenting cells that have been activated ex vivo with a recombinant fusion protein. In addition to this vaccine, numerous other vaccine platforms are currently demonstrating evidence of patient benefit in multicenter, randomized Phase II and Phase III studies in a range of human cancers. JF - Cancer Biotherapy and Radiopharmaceuticals AU - Schlom, J AD - Laboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 10 Center Drive, Room 8B09, Bethesda, MD 20892, USA, js141c@nih.gov Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 2 EP - 5 VL - 27 IS - 1 SN - 1084-9785, 1084-9785 KW - Biotechnology and Bioengineering Abstracts KW - Cancer vaccines KW - Peripheral blood mononuclear cells KW - Radioisotopes KW - Pharmaceuticals KW - Antigen-presenting cells KW - Fusion protein KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/968184443?accountid=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+Biotherapy+and+Radiopharmaceuticals&rft.atitle=Recent+Advances+in+Therapeutic+Cancer+Vaccines&rft.au=Schlom%2C+J&rft.aulast=Schlom&rft.aufirst=J&rft.date=2012-02-01&rft.volume=27&rft.issue=1&rft.spage=2&rft.isbn=&rft.btitle=&rft.title=Cancer+Biotherapy+and+Radiopharmaceuticals&rft.issn=10849785&rft_id=info:doi/10.1089%2Fcbr.2012.1200 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-04-23 N1 - SubjectsTermNotLitGenreText - Cancer vaccines; Peripheral blood mononuclear cells; Radioisotopes; Pharmaceuticals; Fusion protein; Antigen-presenting cells DO - http://dx.doi.org/10.1089/cbr.2012.1200 ER - TY - JOUR T1 - Defining the Molecular Signature of Chemotherapy-Mediated Lung Tumor Phenotype Modulation and Increased Susceptibility to T-Cell Killing AN - 968183645; 16506872 AB - Chemotherapy with platinum doublets, including cisplatin plus vinorelbine, is standard of care for non-small-cell lung cancer. Sublethal exposure to certain chemotherapeutic agents has been demonstrated to alter the phenotype or biology of human tumor cells, rendering them more susceptible to cytotoxic T lymphocyte (CTL)-mediated lysis. The effects of cisplatin/vinorelbine on tumor sensitivity to T-cell cytotoxicity and its molecular mechanisms, however, have not been fully elucidated. We examined the effect of this chemotherapy on growth, cell-surface phenotype, and CTL-mediated lysis of five distinct human lung carcinoma cell lines in vitro and examined the molecular mechanisms associated with enhanced CTL sensitivity. These studies demonstrate that sublethal exposure of human lung tumor cells to the platinum doublet modulates tumor cell phenotype and increases sensitivity to major histocompatibility complex-restricted perforin/granzyme-mediated CTL killing. These studies also demonstrate that exposure to chemotherapy markedly decreased the protein secretion ratio of transforming growth factor- beta /interleukin (IL)-8. We examined the gene expression profile of two lung tumor cell lines to identify a shared gene signature in response to sublethal cisplatin/vinorelbine and found coordinate expression of only 16 transcripts, including those for cytokine/chemokine expression and apoptosis such as tumor necrosis factor- alpha , IL8, CXCL5, and B cell lymphoma-2-like genes (BCL-2). Overall, these results suggest that sublethal exposure to cisplatin/vinorelbine increases sensitivity to perforin/granzyme-mediated CTL killing by modulation of (a) tumor phenotype, (b) cytokine/chemokine milieu, and (c) the proapoptotic/antiapoptotic gene ratio. The data presented here propose a complex mechanism that is distinct from and complementary to that of immunogenic cell death. This molecular signature may be useful in predicting responses to immunotherapy as well as provide the rationale for the potential clinical benefit of the combined use of vaccine with cisplatin/vinorelbine regimens. JF - Cancer Biotherapy and Radiopharmaceuticals AU - Gameiro AU - Caballero, JA AU - Hodge, J W AD - Laboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 10 Center Drive, Room 8B13, Bethesda, MD, 20892, USA, jh241d@nih.gov Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 23 EP - 35 VL - 27 IS - 1 SN - 1084-9785, 1084-9785 KW - Immunology Abstracts; Biotechnology and Bioengineering Abstracts KW - Molecular modelling KW - Chemokines KW - Apoptosis KW - Chemotherapy KW - Immunotherapy KW - Interleukins KW - Interleukin 8 KW - vinorelbine KW - Gene expression KW - Tumor cell lines KW - Cisplatin KW - Combined vaccines KW - Lymphocytes T KW - Platinum KW - Bcl-2 protein KW - Lung cancer KW - Perforin KW - Data processing KW - Lymphocytes B KW - Lung carcinoma KW - Cytotoxicity KW - Immunogenicity KW - Histocompatibility KW - Transforming growth factor- beta KW - Radioisotopes KW - Pharmaceuticals KW - Tumor necrosis factor- alpha KW - W 30910:Imaging KW - F 06915:Cancer Immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/968183645?accountid=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+Biotherapy+and+Radiopharmaceuticals&rft.atitle=Defining+the+Molecular+Signature+of+Chemotherapy-Mediated+Lung+Tumor+Phenotype+Modulation+and+Increased+Susceptibility+to+T-Cell+Killing&rft.au=Gameiro%3BCaballero%2C+JA%3BHodge%2C+J+W&rft.aulast=Gameiro&rft.aufirst=&rft.date=2012-02-01&rft.volume=27&rft.issue=1&rft.spage=23&rft.isbn=&rft.btitle=&rft.title=Cancer+Biotherapy+and+Radiopharmaceuticals&rft.issn=10849785&rft_id=info:doi/10.1089%2Fcbr.2012.1203 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-04-23 N1 - SubjectsTermNotLitGenreText - Molecular modelling; Chemokines; Apoptosis; Immunotherapy; Chemotherapy; Interleukins; vinorelbine; Interleukin 8; Gene expression; Tumor cell lines; Cisplatin; Combined vaccines; Platinum; Lymphocytes T; Bcl-2 protein; Lung cancer; Perforin; Data processing; Lung carcinoma; Lymphocytes B; Cytotoxicity; Immunogenicity; Histocompatibility; Transforming growth factor- beta; Radioisotopes; Pharmaceuticals; Tumor necrosis factor- alpha DO - http://dx.doi.org/10.1089/cbr.2012.1203 ER - TY - JOUR T1 - Positron Emission Tomography Imaging of Tumors Expressing the Human Chemokine Receptor CXCR4 in Mice with the Use of super(64)Cu-AMD3100 AN - 926891839; 16370947 AB - Purpose: Expression of CXCR4 in cancers has been correlated with poor prognosis and increased metastasis. Quantifying CXCR4 expression non-invasively might aid in prognostication and monitoring therapy. We evaluated a radiolabeled antagonist of CXCR4, super(64)Cu-AMD3100, as a positron-emitting imaging agent. Procedures: CXCR4-transfected or non-transfected cell lines were injected into mice to form xenografts. Accumulation of super(64)Cu-AMD3100 in tumors was analyzed by small-animal PET and biodistribution assays. Results: super(64)Cu-AMD3100 accumulated in CXCR4-expressing, but not CXCR4-negative, tumors. For CXCR4-expressing tumors, tumor-to-blood and tumor-to-muscle ratios were 23-41 and 50-59, respectively, depending on tumor type. Excess of unlabeled Cu-AMD3100 or AMD3100 significantly reduced super(64)Cu-AMD3100 accumulation in CXCR4-expressing tumors. Human-absorbed dose calculations predicted a dose limit of 444 MBq. Conclusions: CXCR4 can be imaged in tumors using super(64)Cu-AMD3100. Dosimetry studies suggest that imaging in humans is feasible. We conclude that super(64)Cu-AMD3100 should be investigated as a potential agent for imaging and quantifying CXCR4 in tumors. JF - Molecular Imaging and Biology AU - Weiss, Ido D AU - Jacobson, Orit AU - Kiesewetter, Dale O AU - Jacobus, John P AU - Szajek, Lawrence P AU - Chen, Xiaoyuan AU - Farber, Joshua M AD - Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, 10 Center Drive, Room 11N111, Bethesda, MD, 20892, USA, jfarber@niaid.nih.gov Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 106 EP - 114 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 14 IS - 1 SN - 1536-1632, 1536-1632 KW - Immunology Abstracts; Biotechnology and Bioengineering Abstracts KW - CXCR4 protein KW - Cancer KW - Chemokine receptors KW - Dosimetry KW - Metastases KW - Positron emission tomography KW - Prognosis KW - Tumors KW - Xenografts KW - W 30910:Imaging KW - F 06920:Transplantation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/926891839?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Imaging+and+Biology&rft.atitle=Positron+Emission+Tomography+Imaging+of+Tumors+Expressing+the+Human+Chemokine+Receptor+CXCR4+in+Mice+with+the+Use+of+super%2864%29Cu-AMD3100&rft.au=Weiss%2C+Ido+D%3BJacobson%2C+Orit%3BKiesewetter%2C+Dale+O%3BJacobus%2C+John+P%3BSzajek%2C+Lawrence+P%3BChen%2C+Xiaoyuan%3BFarber%2C+Joshua+M&rft.aulast=Weiss&rft.aufirst=Ido&rft.date=2012-02-01&rft.volume=14&rft.issue=1&rft.spage=106&rft.isbn=&rft.btitle=&rft.title=Molecular+Imaging+and+Biology&rft.issn=15361632&rft_id=info:doi/10.1007%2Fs11307-010-0466-y LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-03-01 N1 - Last updated - 2012-05-18 N1 - SubjectsTermNotLitGenreText - Metastases; CXCR4 protein; Dosimetry; Prognosis; Positron emission tomography; Chemokine receptors; Xenografts; Tumors; Cancer DO - http://dx.doi.org/10.1007/s11307-010-0466-y ER - TY - JOUR T1 - Molecular Imaging and Contrast Agent Database (MICAD): Evolution and Progress AN - 926884374; 16370958 AB - The purpose of writing this review is to showcase the Molecular Imaging and Contrast Agent Database (MICAD; www.micad.nlm.nih.gov) to students, researchers, and clinical investigators interested in the different aspects of molecular imaging. This database provides freely accessible, current, online scientific information regarding molecular imaging (MI) probes and contrast agents (CA) used for positron emission tomography, single-photon emission computed tomography, magnetic resonance imaging, X-ray/computed tomography, optical imaging and ultrasound imaging. Detailed information on >1,000 agents in MICAD is provided in a chapter format and can be accessed through PubMed. Lists containing >4,250 unique MI probes and CAs published in peer-reviewed journals and agents approved by the United States Food and Drug Administration as well as a comma separated values file summarizing all chapters in the database can be downloaded from the MICAD homepage. Users can search for agents in MICAD on the basis of imaging modality, source of signal/contrast, agent or target category, pre-clinical or clinical studies, and text words. Chapters in MICAD describe the chemical characteristics (structures linked to PubChem), the in vitro and in vivo activities, and other relevant information regarding an imaging agent. All references in the chapters have links to PubMed. A Supplemental Information Section in each chapter is available to share unpublished information regarding an agent. A Guest Author Program is available to facilitate rapid expansion of the database. Members of the imaging community registered with MICAD periodically receive an e-mail announcement (eAnnouncement) that lists new chapters uploaded to the database. Users of MICAD are encouraged to provide feedback, comments, or suggestions for further improvement of the database by writing to the editors at micadlm.nih.gov. JF - Molecular Imaging and Biology AU - Chopra, Arvind AU - Shan, Liang AU - Eckelman, W C AU - Leung, Kam AU - Latterner, Martin AU - Bryant, Stephen H AU - Menkens, Anne AD - National Center of Biotechnology Information, National Library of Medicine, 8600 Rockville Pike, Bethesda, MD, 20894, USA, chopraa@mail.nih.gov Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 4 EP - 13 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 14 IS - 1 SN - 1536-1632, 1536-1632 KW - Biotechnology and Bioengineering Abstracts KW - Computed tomography KW - Computer programs KW - Contrast media KW - Databases KW - Evolution KW - Feedback KW - Internet KW - Ionizing radiation KW - Magnetic resonance imaging KW - Positron emission tomography KW - Probes KW - Ultrasound KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/926884374?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Molecular+Imaging+and+Biology&rft.atitle=Molecular+Imaging+and+Contrast+Agent+Database+%28MICAD%29%3A+Evolution+and+Progress&rft.au=Chopra%2C+Arvind%3BShan%2C+Liang%3BEckelman%2C+W+C%3BLeung%2C+Kam%3BLatterner%2C+Martin%3BBryant%2C+Stephen+H%3BMenkens%2C+Anne&rft.aulast=Chopra&rft.aufirst=Arvind&rft.date=2012-02-01&rft.volume=14&rft.issue=1&rft.spage=4&rft.isbn=&rft.btitle=&rft.title=Molecular+Imaging+and+Biology&rft.issn=15361632&rft_id=info:doi/10.1007%2Fs11307-011-0521-3 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-03-01 N1 - Last updated - 2012-05-18 N1 - SubjectsTermNotLitGenreText - Computer programs; Databases; Ionizing radiation; Magnetic resonance imaging; Computed tomography; Positron emission tomography; Probes; Contrast media; Feedback; Ultrasound; Internet; Evolution DO - http://dx.doi.org/10.1007/s11307-011-0521-3 ER - TY - JOUR T1 - Metabolism of sugars by genetically diverse species of oral Leptotrichia AN - 920804226; 16239863 AB - Leptotrichia buccalis ATCC 14201 is a gram-negative, anaerobic rod-shaped bacterium resident in oral biofilm at the tooth surface. The sequenced genome of this organism reveals three contiguous genes at loci: Lebu_1525, Lebu_1526 and Lebu_1527. The translation products of these genes exhibit significant homology with phospho- alpha -glucosidase (Pagl), a regulatory protein (GntR) and a phosphoenol pyruvate-dependent sugar transport protein (EIICB), respectively. In non-oral bacterial species, these genes comprise the sim operon that facilitates sucrose isomer metabolism. Growth studies showed that L. buccalis fermented a wide variety of carbohydrates, including four of the five isomers of sucrose. Growth on the isomeric disaccharides elicited expression of a 50-kDa polypeptide comparable in size to that encoded by Lebu_1525. The latter gene was cloned, and the expressed protein was purified to homogeneity from Escherichia coli TOP10 cells. In the presence of two cofactors, NAD+ and Mn2+ ions, the enzyme readily hydrolyzed p-nitrophenyl- alpha -glucopyranoside 6-phosphate (pNP alpha G6P), a chromogenic analogue of the phosphorylated isomers of sucrose. By comparative sequence alignment, immunoreactivity and signature motifs, the enzyme can be assigned to the phospho- alpha -glucosidase (Pagl) clade of Family 4 of the glycosyl hydrolase super family. We suggest that the products of Lebu_1527 and Lebu_1525, catalyze the phosphorylative translocation and hydrolysis of sucrose isomers in L. buccalis, respectively. Four genetically diverse, but 16S rDNA-related, species of Leptotrichia have recently been described: L. goodfellowii, L. hofstadii, L. shahii and L. wadei. The phenotypic traits of these new species, with respect to carbohydrate utilization, have also been determined. JF - Molecular Oral Microbiology AU - Thompson, J AU - Pikis, A AD - Microbial Biochemistry and Genetics Unit, Oral Infection and Immunity Branch, NIDCR, National Institutes of Health, Bethesda, MD, USA Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 34 EP - 44 PB - Wiley-Blackwell, Rosenoerns Alle 1 Copenhagen V 1502 Denmark VL - 27 IS - 1 SN - 2041-1006, 2041-1006 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology KW - Teeth KW - Genomes KW - Translation KW - Leptotrichia KW - Nucleotide sequence KW - Isomers KW - regulatory proteins KW - Sucrose KW - Immunoreactivity KW - Escherichia coli KW - Glycosyl hydrolase KW - Carbohydrates KW - Biofilms KW - Translocation KW - Ions KW - Sugar KW - Protein transport KW - Enzymes KW - Hydrolysis KW - Disaccharides KW - Cofactors KW - Homology KW - Operons KW - Metabolism KW - New species KW - J 02310:Genetics & Taxonomy KW - A 01310:Products of Microorganisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920804226?accountid=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+Oral+Microbiology&rft.atitle=Metabolism+of+sugars+by+genetically+diverse+species+of+oral+Leptotrichia&rft.au=Thompson%2C+J%3BPikis%2C+A&rft.aulast=Thompson&rft.aufirst=J&rft.date=2012-02-01&rft.volume=27&rft.issue=1&rft.spage=34&rft.isbn=&rft.btitle=&rft.title=Molecular+Oral+Microbiology&rft.issn=20411006&rft_id=info:doi/10.1111%2Fj.2041-1014.2011.00627.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-02-01 N1 - Document feature - figure 3 N1 - Last updated - 2016-09-01 N1 - SubjectsTermNotLitGenreText - Genomes; Teeth; Protein transport; Translation; Sugar; Ions; Nucleotide sequence; Enzymes; Hydrolysis; Isomers; Disaccharides; Cofactors; Homology; regulatory proteins; Sucrose; Immunoreactivity; Glycosyl hydrolase; Biofilms; Carbohydrates; Operons; Translocation; Metabolism; New species; Leptotrichia; Escherichia coli DO - http://dx.doi.org/10.1111/j.2041-1014.2011.00627.x ER - TY - JOUR T1 - Class B Scavenger Receptor Types I and II and CD36 Mediate Bacterial Recognition and Proinflammatory Signaling Induced by Escherichia coli, Lipopolysaccharide, and Cytosolic Chaperonin 60 AN - 920795101; 16278888 AB - Class B scavenger receptors (SR-B) are lipoprotein receptors that also mediate pathogen recognition, phagocytosis, and clearance as well as pathogen-induced signaling. In this study we report that three members of the SR-B family, namely, CLA-1, CLA-2, and CD36, mediate recognition of bacteria not only through interaction with cell wall LPS but also with cytosolic chaperonin 60. HeLa cells stably transfected with any of these SR-Bs demonstrated markedly (3- to 5-fold) increased binding and endocytosis of Escherichia coli, LPS, and chaperonin 60 (GroEL) as revealed by both FACS analysis and confocal microscopy imaging. Increased pathogen (E. coli, LPS, and GroEL) binding to SR-Bs was also associated with the dose-dependent stimulation of cytokine secretion in the order of CD36 > CLA-2 > CLA-1 in HEK293 cells. Pathogen-induced IL-6-secretion was reduced in macrophages from CD36- and SR-BI/II-null mice by 40-50 and 30-40%, respectively. Intravenous GroEL administration increased plasma IL-6 and CXCL1 levels in mice. The cytokine responses were 40-60% lower in CD36-/- relative to wild-type mice, whereas increased cytokine responses were found in SR-BI/II-/- mice. While investigating the discrepancy of in vitro versus in vivo data in SR-BI/II deficiency, SR-BI/II-/- mice were found to respond to GroEL administration without increases in either plasma corticosterone or aldosterone as normally seen in wild-type mice. SR-BI/II-/- mice with mineralocorticoid replacement demonstrated an similar to 40-50% reduction in CXCL1 and IL-6 responses. These results demonstrate that, by recognizing and mediating inflammatory signaling of both bacterial cell wall LPS and cytosolic GroEL, all three SR-B family members play important roles in innate immunity and host defense. JF - Journal of Immunology AU - Baranova, Irina N AU - Vishnyakova, Tatyana G AU - Bocharov, Alexander V AU - Leelahavanichkul, Asada AU - Kurlander, Roger AU - Chen, Zhigang AU - Souza, Ana CP AU - Yuen, Peter ST AU - Star, Robert A AU - Csako, Gyorgy AU - Patterson, Amy P AU - Eggerman, Thomas L AD - Department of Laboratory Medicine, Clinical Center, National Institute of Diabetes and Digestive Kidney Diseases, National Institutes of Health, Bethesda, MD 20892 Y1 - 2012/02/01/ PY - 2012 DA - 2012 Feb 01 SP - 1371 EP - 1380 PB - American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 United States VL - 188 IS - 3 SN - 0022-1767, 0022-1767 KW - Microbiology Abstracts B: Bacteriology; Immunology Abstracts KW - Interleukin 6 KW - Macrophages KW - Intravenous administration KW - CD36 antigen KW - Data processing KW - Chaperonins KW - Pathogens KW - lipoprotein receptors KW - Immunity KW - Inflammation KW - Flow cytometry KW - Endocytosis KW - Corticoids KW - Corticosterone KW - Confocal microscopy KW - Computed tomography KW - Escherichia coli KW - Lipopolysaccharides KW - Aldosterone KW - Phagocytosis KW - scavenger receptors KW - Cell walls KW - J 02350:Immunology KW - F 06910:Microorganisms & Parasites UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920795101?accountid=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=Class+B+Scavenger+Receptor+Types+I+and+II+and+CD36+Mediate+Bacterial+Recognition+and+Proinflammatory+Signaling+Induced+by+Escherichia+coli%2C+Lipopolysaccharide%2C+and+Cytosolic+Chaperonin+60&rft.au=Baranova%2C+Irina+N%3BVishnyakova%2C+Tatyana+G%3BBocharov%2C+Alexander+V%3BLeelahavanichkul%2C+Asada%3BKurlander%2C+Roger%3BChen%2C+Zhigang%3BSouza%2C+Ana+CP%3BYuen%2C+Peter+ST%3BStar%2C+Robert+A%3BCsako%2C+Gyorgy%3BPatterson%2C+Amy+P%3BEggerman%2C+Thomas+L&rft.aulast=Baranova&rft.aufirst=Irina&rft.date=2012-02-01&rft.volume=188&rft.issue=3&rft.spage=1371&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunology&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-02-01 N1 - Last updated - 2013-09-09 N1 - SubjectsTermNotLitGenreText - Macrophages; Interleukin 6; Intravenous administration; Data processing; CD36 antigen; Chaperonins; Immunity; lipoprotein receptors; Pathogens; Inflammation; Flow cytometry; Corticosterone; Corticoids; Endocytosis; Computed tomography; Confocal microscopy; Lipopolysaccharides; Aldosterone; Phagocytosis; scavenger receptors; Cell walls; Escherichia coli ER - TY - JOUR T1 - Genetic variation in nucleotide excision repair pathway genes, pesticide exposure and prostate cancer risk. AN - 920232196; 22102698 AB - Previous research demonstrates increased prostate cancer risk for pesticide applicators and pesticide manufacturing workers. Although underlying mechanisms are unknown, human biomonitoring studies indicate increased genetic damage (e.g. chromosomal aberrations) with pesticide exposure. Given that the nucleotide excision repair (NER) pathway repairs a broad range of DNA damage, we evaluated interactions between pesticide exposure and 324 single-nucleotide polymorphisms (SNPs) tagging 27 NER genes among 776 prostate cancer cases and 1444 male controls in a nested case-control study of white Agricultural Health Study pesticide applicators. We determined interaction P values using likelihood ratio tests from logistic regression models and three-level pesticide variables (none/low/high) based on lifetime days of use weighted to an intensity score. We adjusted for multiple comparisons using the false discovery rate (FDR) method. Of the 17 interactions that met FDR <0.2, 3 displayed a monotonic increase in prostate cancer risk with increasing exposure in one genotype group and no significant association in the other group. Men carrying the variant A allele at ERCC1 rs2298881 exhibited increased prostate cancer risk with high versus no fonofos use [odds ratio (OR) 2.98; 95% confidence interval (CI) 1.65-5.39; P(interact) = 3.6 × 10(-4); FDR-adjusted P = 0.11]. Men carrying the homozygous wild-type TT genotype at two correlated CDK7 SNPs, rs11744596 and rs2932778 (r(2) = 1.0), exhibited increased risk with high versus no carbofuran use (OR 2.01; 95% CI 1.31-3.10 for rs11744596; P(interact) = 7.2 × 10(-4); FDR-adjusted P = 0.09). In contrast, we did not observe associations among men with other genotypes at these loci. While requiring replication, our findings suggest a role for NER genetic variation in pesticide-associated prostate cancer risk. JF - Carcinogenesis AU - Barry, Kathryn Hughes AU - Koutros, Stella AU - Andreotti, Gabriella AU - Sandler, Dale P AU - Burdette, Laurie A AU - Yeager, Meredith AU - Beane Freeman, Laura E AU - Lubin, Jay H AU - Ma, Xiaomei AU - Zheng, Tongzhang AU - Alavanja, Michael C R AU - Berndt, Sonja I AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, MD 20892-7240, USA. barrykh@mail.nih.gov Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 331 EP - 337 VL - 33 IS - 2 KW - Pesticides KW - 0 KW - Index Medicus KW - Polymorphism, Single Nucleotide KW - Odds Ratio KW - Homozygote KW - Humans KW - Aged KW - Genotype KW - Alleles KW - Aged, 80 and over KW - Logistic Models KW - Risk Factors KW - Adult KW - Cohort Studies KW - Case-Control Studies KW - Middle Aged KW - Follow-Up Studies KW - Genetic Predisposition to Disease KW - Male KW - DNA Repair KW - Pesticides -- poisoning KW - Prostatic Neoplasms -- chemically induced KW - Prostatic Neoplasms -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920232196?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+variation+in+nucleotide+excision+repair+pathway+genes%2C+pesticide+exposure+and+prostate+cancer+risk.&rft.au=Barry%2C+Kathryn+Hughes%3BKoutros%2C+Stella%3BAndreotti%2C+Gabriella%3BSandler%2C+Dale+P%3BBurdette%2C+Laurie+A%3BYeager%2C+Meredith%3BBeane+Freeman%2C+Laura+E%3BLubin%2C+Jay+H%3BMa%2C+Xiaomei%3BZheng%2C+Tongzhang%3BAlavanja%2C+Michael+C+R%3BBerndt%2C+Sonja+I&rft.aulast=Barry&rft.aufirst=Kathryn&rft.date=2012-02-01&rft.volume=33&rft.issue=2&rft.spage=331&rft.isbn=&rft.btitle=&rft.title=Carcinogenesis&rft.issn=1460-2180&rft_id=info:doi/10.1093%2Fcarcin%2Fbgr258 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-12 N1 - Date created - 2012-02-06 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Exp Cell Res. 1988 Mar;175(1):184-91 [3345800] Mutat Res. 1986 Nov;168(3):301-25 [3796654] Am J Ind Med. 1997 Feb;31(2):233-42 [9028440] Mutagenesis. 1998 Mar;13(2):157-66 [9568589] Mutat Res. 1998 Aug 7;416(1-2):101-13 [9725996] Cancer Res. 1998 Sep 15;58(18):4117-21 [9751622] J Biol Chem. 1999 Jun 25;274(26):18173-80 [10373416] Bioinformatics. 2005 Jan 15;21(2):263-5 [15297300] Int Arch Occup Environ Health. 2004 Nov;77(8):559-70 [15688248] Cancer Lett. 2005 Apr 8;220(2):125-35 [15766587] Mutat Res. 2005 Sep 4;577(1-2):275-83 [15922366] Hum Exp Toxicol. 2005 Sep;24(9):439-45 [16235732] Cancer Causes Control. 2006 May;17(4):353-73 [16596288] Environ Health Perspect. 2006 Dec;114(12):1838-42 [17185272] Am J Hum Genet. 2007 Sep;81(3):559-75 [17701901] Can Fam Physician. 2007 Oct;53(10):1712-20 [17934035] Food Chem Toxicol. 2007 Dec;45(12):2488-98 [17673351] Nat Genet. 2008 Mar;40(3):310-5 [18264096] Nat Genet. 2008 Mar;40(3):316-21 [18264097] Mutat Res. 2008 Jul 31;654(2):168-75 [18603015] Methods Mol Biol. 2009;471:361-85 [19109789] Environ Mol Mutagen. 2009 Jan;50(1):37-45 [19031420] J Agromedicine. 2009;14(2):206-14 [19437279] Environ Sci Technol. 2009 Aug 15;43(16):6370-7 [19746739] Environ Health Perspect. 2010 Aug;118(8):1117-25 [20444670] J Expo Sci Environ Epidemiol. 2010 Sep;20(6):559-69 [19888312] J Occup Environ Med. 2010 Nov;52(11):1098-105 [21063187] Cancer Res. 2010 Nov 15;70(22):9224-33 [20978189] Environ Health Perspect. 2011 Dec;119(12):1726-32 [21810555] Ecotoxicology. 2003 Feb-Aug;12(1-4):345-63 [12739880] Mutat Res. 2000 Feb 16;465(1-2):123-9 [10708977] Science. 2001 Feb 16;291(5507):1284-9 [11181991] Toxicology. 2001 Dec 14;169(2):153-61 [11718956] Epidemiology. 2002 Jan;13(1):94-9 [11805592] Cancer Epidemiol Biomarkers Prev. 2002 May;11(5):493-6 [12010865] Ann Occup Hyg. 2002 Mar;46(2):245-60 [12074034] J Expo Anal Environ Epidemiol. 2002 Sep;12(5):313-8 [12198579] Mutagenesis. 2003 Mar;18(2):201-5 [12621077] Am J Epidemiol. 2003 May 1;157(9):800-14 [12727674] Mutat Res. 2003 Jun;543(3):251-72 [12787816] Am J Hum Genet. 2004 Jan;74(1):106-20 [14681826] Cancer Res. 2004 Feb 1;64(3):1197-201 [14871857] Mutat Res. 1982 Mar;101(1):19-29 [7043246] Mutat Res. 1983 Mar;116(3-4):185-216 [6339892] Environ Health Perspect. 1996 Apr;104(4):362-9 [8732939] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/carcin/bgr258 ER - TY - JOUR T1 - Plasminogen activator inhibitor 1 RNAi suppresses gastric cancer metastasis in vivo. AN - 919956250; 22098548 AB - Cancer metastasis remains the primary cause of pain, suffering, and death in cancer patients, and even the most current therapeutic strategies have not been highly successful in preventing or inhibiting metastasis. In most patients with scirrhous gastric cancer (one of the most aggressive of diffuse-type gastric cancer), recurrence occurs even after potentially curative resection, most frequently in the form of peritoneal metastasis. Given that the occurrence of diffuse-type gastric cancers has been increasing, the development of new strategies to combat metastasis of this disease is critically important. Plasminogen activator inhibitor-1 (PAI-1) is a critical factor in cancer progression; thus, PAI-1 RNAi may be an effective therapy against cancer metastasis. In the present study, we used an RNAi technique to reduce PAI-1 expression in an in vivo model system for gastric cancer metastasis. Ex vivo plasmid transfection and adenovirus infection were tested as mechanisms to incorporate specific PAI-1 RNAi vectors into human gastric carcinoma cells. Both approaches significantly decreased peritoneal tumor growth and the formation of bloody ascites in the mouse model, suggesting that this approach may provide a new, effective strategy for inhibiting cancer metastasis. © 2012 Japanese Cancer Association. JF - Cancer science AU - Nishioka, Nobuaki AU - Matsuoka, Tasuku AU - Yashiro, Masakazu AU - Hirakawa, Kosei AU - Olden, Kenneth AU - Roberts, John D AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA. Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 228 EP - 232 VL - 103 IS - 2 KW - Plasminogen Activator Inhibitor 1 KW - 0 KW - RNA, Small Interfering KW - Index Medicus KW - Animals KW - Neoplasm Metastasis -- genetics KW - Neoplasm Recurrence, Local -- drug therapy KW - Transfection KW - Plasmids -- genetics KW - Neoplasm Metastasis -- drug therapy KW - Humans KW - Mice, Nude KW - Mice KW - Cell Line, Tumor KW - Neoplasm Recurrence, Local -- genetics KW - Adenoviridae -- genetics KW - Stomach Neoplasms -- pathology KW - Plasminogen Activator Inhibitor 1 -- genetics KW - Plasminogen Activator Inhibitor 1 -- biosynthesis KW - Stomach Neoplasms -- genetics KW - RNA, Small Interfering -- administration & dosage KW - Plasminogen Activator Inhibitor 1 -- metabolism KW - RNA, Small Interfering -- pharmacology KW - RNA Interference UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/919956250?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+science&rft.atitle=Plasminogen+activator+inhibitor+1+RNAi+suppresses+gastric+cancer+metastasis+in+vivo.&rft.au=Nishioka%2C+Nobuaki%3BMatsuoka%2C+Tasuku%3BYashiro%2C+Masakazu%3BHirakawa%2C+Kosei%3BOlden%2C+Kenneth%3BRoberts%2C+John+D&rft.aulast=Nishioka&rft.aufirst=Nobuaki&rft.date=2012-02-01&rft.volume=103&rft.issue=2&rft.spage=228&rft.isbn=&rft.btitle=&rft.title=Cancer+science&rft.issn=1349-7006&rft_id=info:doi/10.1111%2Fj.1349-7006.2011.02155.x LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-03-25 N1 - Date created - 2012-02-02 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1111/j.1349-7006.2011.02155.x ER - TY - JOUR T1 - Nitroxide derivatives of non-steroidal anti-inflammatory drugs exert anti-inflammatory and superoxide dismutase scavenging properties in A459 cells. AN - 918579427; 21658022 AB - Inflammation and reactive oxygen species are associated with the promotion of various cancers. The use of non-steroidal anti-inflammatory drugs (NSAIDs) in cancer prevention treatments has been promising in numerous cancers. We report the evaluation of NSAIDs chemically modified by the addition of a redox-active nitroxide group. TEMPO-aspirin (TEMPO-ASA) and TEMPO-indomethacin (TEMPO-IND) were synthesized and evaluated in the lung cancer cell line A549. We evaluated physico-chemical properties of TEMPO-ASA and TEMPO-IND by electron paramagnetic resonance and cyclic voltammetry. Superoxide dismutase-like properties was assayed by measuring cytochrome c reduction and anti-inflammatory effects were assayed by measuring production of prostaglandin E(2) (PGE(2) ) and leukotriene B(4) (LTB(4) ). MTT proliferation assay and clonogenic assay were evaluated in the A549 lung carcinoma cell line. Maximum tolerated doses (MTD) and acute ulcerogenic index were also evaluated in in vivo. MTD were: TEMPO (140 mg·kg(-1) ), ASA (100 mg·kg(-1) ), indomethacin (5 mg·kg(-1) ), TEMPO-ASA (100 mg·kg(-1) ) and TEMPO-IND (40 mg·kg(-1) ). While TEMPO-ASA was as well tolerated as ASA, TEMPO-IND showed an eightfold improvement over indomethacin. TEMPO-IND showed markedly less gastric toxicity than the parent NSAID. Both TEMPO-ASA and TEMPO-IND inhibited production of PGE(2) and LTB(4) in A549 cells with maximum effects at 100 µg·mL(-1) or 10 µg·mL(-1) respectively. The nitroxide-NSAIDs retained superoxide scavenging capacity of the parent nitroxide and anti-inflammatory effects, inhibiting cyclooxygenase and 5-lipoxygenase enzymes. These redox-modified NSAIDs might be potential drug candidates, as they exhibit the pharmacological properties of the parent NSAID with antioxidant activity decreasing NSAID-associated toxicity. Published 2011. This article is a U.S. Government work and is in the public domain in the USA. JF - British journal of pharmacology AU - Flores-Santana, Wilmarie AU - Moody, Terry AU - Chen, Weibin AU - Gorczynski, Michael J AU - Shoman, Mai E AU - Velázquez, Carlos AU - Thetford, Angela AU - Mitchell, James B AU - Cherukuri, Murali K AU - King, S Bruce AU - Wink, David A AD - Radiation Biology Branch National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 1058 EP - 1067 VL - 165 IS - 4b KW - Anti-Inflammatory Agents, Non-Steroidal KW - 0 KW - Antioxidants KW - Cyclic N-Oxides KW - Leukotriene B4 KW - 1HGW4DR56D KW - Carrageenan KW - 9000-07-1 KW - Superoxide Dismutase KW - EC 1.15.1.1 KW - Dinoprostone KW - K7Q1JQR04M KW - Aspirin KW - R16CO5Y76E KW - TEMPO KW - VQN7359ICQ KW - Indomethacin KW - XXE1CET956 KW - Index Medicus KW - Cell Proliferation -- drug effects KW - Animals KW - Leukotriene B4 -- metabolism KW - Humans KW - Superoxide Dismutase -- metabolism KW - Disease Models, Animal KW - Mice, Nude KW - Mice KW - Cell Line, Tumor KW - Edema -- drug therapy KW - Stomach Ulcer -- chemically induced KW - Rats KW - Edema -- chemically induced KW - Stomach Ulcer -- drug therapy KW - Cell Survival -- drug effects KW - Dinoprostone -- metabolism KW - Female KW - Antioxidants -- toxicity KW - Aspirin -- toxicity KW - Anti-Inflammatory Agents, Non-Steroidal -- toxicity KW - Indomethacin -- pharmacology KW - Indomethacin -- chemistry KW - Anti-Inflammatory Agents, Non-Steroidal -- chemistry KW - Antioxidants -- pharmacology KW - Aspirin -- chemistry KW - Cyclic N-Oxides -- pharmacology KW - Cyclic N-Oxides -- toxicity KW - Antioxidants -- chemistry KW - Cyclic N-Oxides -- chemistry KW - Indomethacin -- toxicity KW - Aspirin -- pharmacology KW - Anti-Inflammatory Agents, Non-Steroidal -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/918579427?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+pharmacology&rft.atitle=Nitroxide+derivatives+of+non-steroidal+anti-inflammatory+drugs+exert+anti-inflammatory+and+superoxide+dismutase+scavenging+properties+in+A459+cells.&rft.au=Flores-Santana%2C+Wilmarie%3BMoody%2C+Terry%3BChen%2C+Weibin%3BGorczynski%2C+Michael+J%3BShoman%2C+Mai+E%3BVel%C3%A1zquez%2C+Carlos%3BThetford%2C+Angela%3BMitchell%2C+James+B%3BCherukuri%2C+Murali+K%3BKing%2C+S+Bruce%3BWink%2C+David+A&rft.aulast=Flores-Santana&rft.aufirst=Wilmarie&rft.date=2012-02-01&rft.volume=165&rft.issue=4b&rft.spage=1058&rft.isbn=&rft.btitle=&rft.title=British+journal+of+pharmacology&rft.issn=1476-5381&rft_id=info:doi/10.1111%2Fj.1476-5381.2011.01527.x LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-15 N1 - Date created - 2012-01-27 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5537-41 [1319064] Cancer Res. 1992 Apr 1;52(7):1750-3 [1551104] J Biol Chem. 1996 Oct 18;271(42):26026-31 [8824242] Free Radic Biol Med. 1996;21(4):463-70 [8886796] Annu Rev Pharmacol Toxicol. 1998;38:97-120 [9597150] Trends Pharmacol Sci. 1999 Aug;20(8):319-23 [10431210] Proc Soc Exp Biol Med. 1962 Dec;111:544-7 [14001233] Clin Cancer Res. 2005 May 1;11(9):3342-8 [15867233] J Med Chem. 2005 Jun 16;48(12):4061-7 [15943479] Free Radic Biol Med. 2005 Sep 1;39(5):567-83 [16085176] Clin Cancer Res. 2005 Oct 15;11(20):7564-8 [16243832] Am J Physiol Regul Integr Comp Physiol. 2006 Jan;290(1):R37-43 [16179488] Nat Rev Cancer. 2006 Feb;6(2):130-40 [16491072] Free Radic Biol Med. 2007 Mar 1;42(5):706-19 [17291994] Drugs. 2007;67(6):821-45 [17428102] Free Radic Biol Med. 2007 Jun 1;42(11):1632-50 [17462532] Bioorg Med Chem. 2007 Jul 15;15(14):4767-74 [17509888] Curr Pharm Des. 2007;13(22):2215-27 [17691994] Cancer Res. 2008 Mar 1;68(5):1601-8 [18316625] Circulation. 2008 May 20;117(20):2626-36 [18474817] J Physiol Pharmacol. 2008 Aug;59 Suppl 2:117-33 [18812633] Radiat Res. 2009 Dec;172(6):706-17 [19929417] Inflammation. 2010 Aug;33(4):224-34 [20084447] Free Radic Biol Med. 2010 Aug 15;49(4):667-73 [20561604] Cancer Chemother Pharmacol. 2010 Jan;65(2):267-76 [19506872] Biochim Biophys Acta. 2001 Feb 16;1525(1-2):70-6 [11342255] Prostaglandins Other Lipid Mediat. 2002 Feb;67(2):107-20 [11936617] Ann Rheum Dis. 2003 Jun;62(6):501-9 [12759283] Dig Liver Dis. 2003 May;35 Suppl 2:S27-34 [12846441] J Natl Cancer Inst. 2003 Oct 1;95(19):1440-52 [14519750] Antioxid Redox Signal. 2004 Jun;6(3):587-95 [15130285] J Immunol. 2004 Aug 1;173(3):2011-22 [15265936] Nat New Biol. 1971 Jun 23;231(25):232-5 [5284360] Biochim Biophys Acta. 1980 Jun 26;623(2):457-60 [6249381] Biochim Biophys Acta. 1986 Aug 29;888(1):82-90 [3741890] Free Radic Res Commun. 1990;9(3-6):241-9 [2167262] Free Radic Res Commun. 1991;12-13 Pt 1:187-94 [1649088] Am J Med. 1991 Sep 30;91(3C):14S-22S [1928205] Environ Mol Mutagen. 1992;19(1):21-6 [1310080] Gut. 1994 Sep;35(9):1181-8 [7959222] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1111/j.1476-5381.2011.01527.x ER - TY - JOUR T1 - Phase I study of the synthetic triterpenoid, 2-cyano-3, 12-dioxoolean-1, 9-dien-28-oic acid (CDDO), in advanced solid tumors. AN - 918033004; 21805353 AB - The triterpenoid 2-cyano-3,12-dioxoolean-1,9-dien-28-oic Acid (CDDO, previously RTA 401) is a multifunctional molecule that controls cellular growth and differentiation. While CDDO is capable of activating the transcription factor peroxisome proliferator activator receptor-γ (PPARγ), its apoptotic effects in malignant cells have been shown to occur independently of PPARγ. A phase I dose-escalation study was conducted to determine the toxicity, the maximum tolerated dose, and the pharmacokinetics and pharmacodynamics of CDDO, administered as a 5-day continuous infusion every 28 days in patients with advanced cancers. An accelerated titration design was followed, with one patient per cohort entered, and doses ranging from 0.6 to 38.4 mg/m(2)/h. Pharmacokinetics of CDDO was assessed and cleaved poly (ADP-ribose) polymerase (c-PARP), as a marker of apoptosis, was measured in peripheral blood mononuclear cells to assess drug effect. Seven patients, one patient per dose level up to dose level 7 (38.4 mg/m(2)/h), were enrolled and received a total of 11 courses of treatment. Cmax increased proportionally with dose. Preclinically determined efficacious blood level (1 μM) of drug was attained at the highest dose level. One patient, at dose level 6, experienced grade 2 mucositis, nausea, vomiting, and anorexia. Four patients developed thromboembolic events subsequently considered as dose-limiting toxicity. No antitumor activity was noted. A causal relationship of observed thromboembolic events to CDDO was considered possible but could not be established. JF - Cancer chemotherapy and pharmacology AU - Speranza, Giovanna AU - Gutierrez, Martin E AU - Kummar, Shivaani AU - Strong, John M AU - Parker, Robert J AU - Collins, Jerry AU - Yu, Yunkai AU - Cao, Liang AU - Murgo, Anthony J AU - Doroshow, James H AU - Chen, Alice AD - Division of Cancer Treatment and Diagnosis, National Cancer Institute, Bethesda, MD, USA. Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 431 EP - 438 VL - 69 IS - 2 KW - 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid KW - 0 KW - Oleanolic Acid KW - 6SMK8R7TGJ KW - Poly(ADP-ribose) Polymerases KW - EC 2.4.2.30 KW - Index Medicus KW - Immunoblotting KW - Drug Administration Schedule KW - Infusions, Intravenous KW - Dose-Response Relationship, Drug KW - Humans KW - Vomiting -- chemically induced KW - Jurkat Cells KW - Mucositis -- chemically induced KW - Metabolic Clearance Rate KW - Thromboembolism -- chemically induced KW - Poly(ADP-ribose) Polymerases -- metabolism KW - Nausea -- chemically induced KW - Cell Survival -- drug effects KW - Half-Life KW - Apoptosis -- drug effects KW - Treatment Outcome KW - Middle Aged KW - Anorexia -- chemically induced KW - Female KW - Male KW - Neoplasms -- drug therapy KW - Neoplasms -- pathology KW - Oleanolic Acid -- pharmacokinetics KW - Oleanolic Acid -- analogs & derivatives KW - Oleanolic Acid -- therapeutic use KW - Oleanolic Acid -- adverse effects KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/918033004?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+chemotherapy+and+pharmacology&rft.atitle=Phase+I+study+of+the+synthetic+triterpenoid%2C+2-cyano-3%2C+12-dioxoolean-1%2C+9-dien-28-oic+acid+%28CDDO%29%2C+in+advanced+solid+tumors.&rft.au=Speranza%2C+Giovanna%3BGutierrez%2C+Martin+E%3BKummar%2C+Shivaani%3BStrong%2C+John+M%3BParker%2C+Robert+J%3BCollins%2C+Jerry%3BYu%2C+Yunkai%3BCao%2C+Liang%3BMurgo%2C+Anthony+J%3BDoroshow%2C+James+H%3BChen%2C+Alice&rft.aulast=Speranza&rft.aufirst=Giovanna&rft.date=2012-02-01&rft.volume=69&rft.issue=2&rft.spage=431&rft.isbn=&rft.btitle=&rft.title=Cancer+chemotherapy+and+pharmacology&rft.issn=1432-0843&rft_id=info:doi/10.1007%2Fs00280-011-1712-y LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-03-20 N1 - Date created - 2012-01-25 N1 - Date revised - 2017-01-14 N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00280-011-1712-y ER - TY - JOUR T1 - A primer on using pooled shRNA libraries for functional genomic screens. AN - 917858236; 22271906 AB - The discovery of RNA interference (RNAi) has revolutionized genetic analysis in mammalian cells. Loss-of-function RNAi screens enable rapid, functional annotation of the genome. Of the various RNAi approaches, pooled shRNA libraries have received considerable attention because of their versatility. A number of genome-wide shRNA libraries have been constructed against the human and mouse genomes, and these libraries can be readily applied to a variety of screens to interrogate the function of human and mouse genes in an unbiased fashion. We provide an introduction to the technical aspects of using pooled shRNA libraries for genetic screens. JF - Acta biochimica et biophysica Sinica AU - Hu, Guang AU - Luo, Ji AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA. hug4@niehs.nih.gov Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 103 EP - 112 VL - 44 IS - 2 KW - RNA, Small Interfering KW - 0 KW - Index Medicus KW - Validation Studies as Topic KW - Animals KW - Genome, Human KW - Humans KW - Genetic Vectors KW - Oligonucleotide Array Sequence Analysis -- methods KW - Mice KW - RNA Interference KW - Genomics -- methods KW - Genomics -- statistics & numerical data KW - RNA, Small Interfering -- genetics KW - Genomics -- standards KW - Genomic Library UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/917858236?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Acta+biochimica+et+biophysica+Sinica&rft.atitle=A+primer+on+using+pooled+shRNA+libraries+for+functional+genomic+screens.&rft.au=Hu%2C+Guang%3BLuo%2C+Ji&rft.aulast=Hu&rft.aufirst=Guang&rft.date=2012-02-01&rft.volume=44&rft.issue=2&rft.spage=103&rft.isbn=&rft.btitle=&rft.title=Acta+biochimica+et+biophysica+Sinica&rft.issn=1745-7270&rft_id=info:doi/10.1093%2Fabbs%2Fgmr116 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-18 N1 - Date created - 2012-01-24 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nat Methods. 2006 Sep;3(9):707-14 [16929316] Nat Methods. 2006 Sep;3(9):715-9 [16929317] Proc Natl Acad Sci U S A. 2006 Sep 12;103(37):13759-64 [16945906] Nature. 2006 Nov 9;444(7116):230-4 [17086199] Blood. 2007 Jul 15;110(2):640-50 [17420285] Cancer Cell. 2007 Oct;12(4):395-402 [17936563] Science. 2008 Feb 1;319(5863):620-4 [18239126] Nature. 2008 Jul 10;454(7201):226-31 [18568025] Cell. 2008 Nov 28;135(5):852-64 [19012953] Curr Gene Ther. 2008 Dec;8(6):483-8 [19075631] Proc Natl Acad Sci U S A. 2008 Dec 23;105(51):20380-5 [19091943] Nat Rev Genet. 2009 Feb;10(2):94-108 [19148191] Cell Cycle. 2009 Feb 1;8(3):498-504 [19177017] Proc Natl Acad Sci U S A. 2009 Feb 17;106(7):2289-94 [19171886] Cell. 2009 May 29;137(5):821-34 [19490892] Cell. 2009 May 29;137(5):835-48 [19490893] J Biol Chem. 2009 Jul 17;284(29):19463-73 [19460752] Nat Methods. 2009 Aug;6(8):569-75 [19644458] Nat Cell Biol. 2009 Nov;11(11):1297-304 [19801974] Nature. 2009 Nov 5;462(7269):108-12 [19847166] Mol Cell. 2010 Jul 9;39(1):36-47 [20603073] Proc Natl Acad Sci U S A. 2010 Aug 10;107(32):14280-5 [20660729] Nat Cell Biol. 2010 Sep;12(9):886-93 [20711181] J Clin Invest. 2010 Nov;120(11):3940-52 [20972333] Mol Cell. 2010 Nov 24;40(4):645-57 [21055985] Genes Dev. 2010 Dec 1;24(23):2654-65 [21062900] Proc Natl Acad Sci U S A. 2011 Mar 1;108(9):3665-70 [21307310] Mol Cell. 2011 Mar 18;41(6):733-46 [21353615] Nature. 2011 Mar 24;471(7339):523-6 [21430781] Proc Natl Acad Sci U S A. 2011 Jul 26;108(30):12372-7 [21746896] Nature. 2011 Aug 18;476(7360):346-50 [21760589] Nature. 2011 Oct 27;478(7370):524-8 [21814200] Nature. 2004 Mar 25;428(6981):427-31 [15042091] Nature. 2004 Mar 25;428(6981):431-7 [15042092] Methods Enzymol. 2005;392:381-405 [15644194] Cell. 2005 Jun 17;121(6):837-48 [15960972] Proc Natl Acad Sci U S A. 2005 Sep 13;102(37):13212-7 [16141338] Nat Genet. 2005 Nov;37(11):1281-8 [16200065] Mol Cell. 2005 Dec 9;20(5):673-85 [16337592] Gene Ther. 2006 Mar;13(6):503-8 [16195700] Nat Chem Biol. 2006 Apr;2(4):202-6 [16474381] Cell. 2006 Mar 24;124(6):1283-98 [16564017] Nature. 2006 May 4;441(7089):106-10 [16572121] Nature. 2006 Jun 1;441(7093):646-50 [16511445] Nat Methods. 2006 Sep;3(9):701-6 [16929315] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/abbs/gmr116 ER - TY - JOUR T1 - Iron N-(2-hydroxy acetophenone) glycinate (FeNG), a non-toxic glutathione depletor circumvents doxorubicin resistance in Ehrlich ascites carcinoma cells in vivo. AN - 917854113; 21915630 AB - Multidrug resistance-associated protein 1 (MRP1) reduces intracellular anticancer drug accumulation either by co transporting them with glutathione (GSH) or extruding drug-GSH conjugates outside of the cell. Thus, MRP1 confers multidrug resistance (MDR) and worsen successful chemotherapeutic treatment against cancer. Although the exact mechanism of MRP1 involved in MDR remains unknown, the elevated level of intracellular GSH is considered as a key factor responsible for MDR in cancer. Hence the quest for non-toxic molecules that are able to deplete intracellular GSH has profound importance to subdue MDR. The present preclinical study depicts the resistance reversal potentiality of an iron complex; viz. Ferrous N-(2-hydroxy acetophenone) glycinate (FeNG) developed by us in doxorubicin resistant Ehrlich ascites carcinoma (EAC/Dox) cells. FeNG potentiate cytotoxic effect of doxorubicin on EAC/Dox cells ex vivo and also increases the survivability EAC/Dox bearing Swiss albino mice in vivo as well. Moreover, in vivo administration of FeNG significantly depletes intracellular GSH with ensuant increase in doxorubicin concentration in EAC/Dox cells without alternation of MRP1 expression. In addition, intra-peritoneal (i.p.) application of FeNG in normal or EAC/Dox bearing mice does not cause any systemic toxicity in preliminary trials in mouse Ehrlich ascites carcinoma model. Therefore, the present report provides evidence that FeNG may be a promising new resistance modifying agent against drug resistant cancers. JF - Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine AU - Ganguly, Avishek AU - Chakraborty, Paramita AU - Banerjee, Kaushik AU - Chatterjee, Shilpak AU - Basu, Soumya AU - Sarkar, Avijit AU - Chatterjee, Mitali AU - Choudhuri, Soumitra Kumar AD - Department of In Vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Calcutta, 700 026, India. Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 149 EP - 163 VL - 25 IS - 1 KW - Acetophenones KW - 0 KW - Antineoplastic Agents KW - Multidrug Resistance-Associated Proteins KW - Doxorubicin KW - 80168379AG KW - Iron KW - E1UOL152H7 KW - Glutathione KW - GAN16C9B8O KW - acetophenone KW - RK493WHV10 KW - multidrug resistance-associated protein 1 KW - Y49M64GZ4Q KW - Index Medicus KW - Molecular Structure KW - Animals KW - Humans KW - Mice KW - Tissue Distribution KW - Female KW - Drug Resistance, Multiple KW - Acetophenones -- metabolism KW - Glutathione -- metabolism KW - Multidrug Resistance-Associated Proteins -- metabolism KW - Carcinoma, Ehrlich Tumor -- drug therapy KW - Acetophenones -- chemistry KW - Drug Resistance, Neoplasm KW - Doxorubicin -- therapeutic use KW - Antineoplastic Agents -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/917854113?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Religion+and+Health&rft.atitle=Unbelievable%3F%21+Theistic%2FEpistemological+Viewpoint+Affects+Religion-Health+Relationship&rft.au=Speed%2C+David&rft.aulast=Speed&rft.aufirst=David&rft.date=2017-02-01&rft.volume=56&rft.issue=1&rft.spage=238&rft.isbn=&rft.btitle=&rft.title=Journal+of+Religion+and+Health&rft.issn=00224197&rft_id=info:doi/10.1007%2Fs10943-016-0271-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-21 N1 - Date created - 2012-01-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s10534-011-9493-7 ER - TY - JOUR T1 - Increased oxidative damage and decreased antioxidant function in aging human substantia nigra compared to striatum: implications for Parkinson's disease. AN - 917853736; 21971758 AB - Parkinson's disease (PD) is characterized by selective degeneration and loss of dopaminergic neurons in the substantia nigra (SN) of the ventral mid brain leading to dopamine depletion in the striatum. Oxidative stress and mitochondrial damage have been implicated in the death of SN neurons during the evolution of PD. In our previous study on human PD brains, we observed that compared to SN, striatum was significantly protected against oxidative damage and mitochondrial dysfunction. To understand whether brain aging contributes to the vulnerability of midbrain to neurodegeneration in PD compared to striatum, we assessed the status of oxidant and antioxidant markers, glutathione metabolic enzymes, glial fibrillary acidic protein (GFAP) expression and mitochondrial complex I(CI) activity in SN (n = 23) and caudate nucleus (n = 24) during physiological aging in human brains. We observed a significant increase in protein oxidation (P < 0.001), loss of CI activity (P = 0.04) and increased astrocytic proliferation indicated by GFAP expression (P < 0.001) in SN compared to CD with increasing age. These changes were attributed to significant decrease in antioxidant function represented by superoxide dismutase (SOD) (P = 0.03), glutathione (GSH) peroxidase (GPx) (P = 0.02) and GSH reductase (GR) (P = 0.03) and a decreasing trend in total GSH and catalase with increasing age. However, these parameters were relatively unaltered in CD. We propose that SN undergoes extensive oxidative damage, loss of antioxidant and mitochondrial function and increased GFAP expression during physiological aging which might make it more vulnerable to neurotoxic insults thus contributing to selective degeneration during evolution of PD. JF - Neurochemical research AU - Venkateshappa, C AU - Harish, G AU - Mythri, Rajeswara Babu AU - Mahadevan, Anita AU - Bharath, M M Srinivas AU - Shankar, S K AD - Department of Neurochemistry, National Institute of Mental Health and Neurosciences (NIMHANS), No. 2900, Hosur Road, Bangalore, Karnataka, 560029, India. Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 358 EP - 369 VL - 37 IS - 2 KW - Antioxidants KW - 0 KW - Glial Fibrillary Acidic Protein KW - Index Medicus KW - Young Adult KW - Humans KW - Adult KW - Glial Fibrillary Acidic Protein -- metabolism KW - Aged KW - Middle Aged KW - Child KW - Male KW - Female KW - Child, Preschool KW - Substantia Nigra -- metabolism KW - Antioxidants -- metabolism KW - Parkinson Disease -- metabolism KW - Oxidative Stress UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/917853736?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurochemical+research&rft.atitle=Increased+oxidative+damage+and+decreased+antioxidant+function+in+aging+human+substantia+nigra+compared+to+striatum%3A+implications+for+Parkinson%27s+disease.&rft.au=Venkateshappa%2C+C%3BHarish%2C+G%3BMythri%2C+Rajeswara+Babu%3BMahadevan%2C+Anita%3BBharath%2C+M+M+Srinivas%3BShankar%2C+S+K&rft.aulast=Venkateshappa&rft.aufirst=C&rft.date=2012-02-01&rft.volume=37&rft.issue=2&rft.spage=358&rft.isbn=&rft.btitle=&rft.title=Neurochemical+research&rft.issn=1573-6903&rft_id=info:doi/10.1007%2Fs11064-011-0619-7 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-13 N1 - Date created - 2012-01-24 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s11064-011-0619-7 ER - TY - JOUR T1 - Phase I study of heat-deployed liposomal doxorubicin during radiofrequency ablation for hepatic malignancies. AN - 917577497; 22178041 AB - A phase I dose escalation study was performed with systemically delivered lyso-thermosensitive liposomal doxorubicin (LTLD). The primary objectives were to determine the safe maximum tolerated dose (MTD), pharmacokinetic properties, and dose-limiting toxicity (DLT) of LTLD during this combination therapy. Subjects eligible for percutaneous or surgical radiofrequency (RF) ablation with primary (n = 9) or metastatic (n = 15) tumors of the liver, with four or fewer lesions as large as 7 cm in diameter, were included. RF ablation was initiated 15 minutes after starting a 30-minute intravenous LTLD infusion. Dose levels between 20 mg/m(2) and 60 mg/m(2) were evaluated. Magnetic resonance imaging, positron emission tomography, and computed tomography were performed at predetermined intervals before and after treatment until evidence of recurrence was seen, administration of additional antitumor treatment was performed, or a total of 3 years had elapsed. DLT criteria were met at 60 mg/m(2), and the MTD was defined as 50 mg/m(2). RF ablation was performed during the peak of the plasma concentration-time curve in an effort to yield maximal drug deposition. LTLD produced reversible, dose-dependent neutropenia and leukopenia. LTLD can be safely administered systemically at the MTD (50 mg/m(2)) in combination with RF ablation, with limited and manageable toxicity. Further evaluation of this agent combined with RF ablation is warranted to determine its role in the management of liver tumors. Copyright © 2012 SIR. Published by Elsevier Inc. All rights reserved. JF - Journal of vascular and interventional radiology : JVIR AU - Wood, Bradford J AU - Poon, Ronnie T AU - Locklin, Julia K AU - Dreher, Matthew R AU - Ng, K K AU - Eugeni, Michelle AU - Seidel, Geoffrey AU - Dromi, Sergio AU - Neeman, Ziv AU - Kolf, Michael AU - Black, Christopher D V AU - Prabhakar, Raj AU - Libutti, Steven K AD - Center for Interventional Oncology, Radiology and Imaging Sciences, Clinical Center, National Institutes of Health, 9000 Rockville Pk., Building 10, Room 1C364, MSC 1182, Bethesda, MD 20892, USA. locklinj@cc.nih.gov Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 248 EP - 55.e7 VL - 23 IS - 2 KW - Antibiotics, Antineoplastic KW - 0 KW - Doxorubicin KW - 80168379AG KW - Index Medicus KW - Antibiotics, Antineoplastic -- administration & dosage KW - Combined Modality Therapy KW - Aged, 80 and over KW - Humans KW - Adult KW - Treatment Outcome KW - Aged KW - Middle Aged KW - Radiography KW - Male KW - Female KW - Liver Neoplasms -- therapy KW - Catheter Ablation -- methods KW - Liver Neoplasms -- diagnostic imaging KW - Doxorubicin -- administration & dosage KW - Hyperthermia, Induced -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/917577497?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+vascular+and+interventional+radiology+%3A+JVIR&rft.atitle=Phase+I+study+of+heat-deployed+liposomal+doxorubicin+during+radiofrequency+ablation+for+hepatic+malignancies.&rft.au=Wood%2C+Bradford+J%3BPoon%2C+Ronnie+T%3BLocklin%2C+Julia+K%3BDreher%2C+Matthew+R%3BNg%2C+K+K%3BEugeni%2C+Michelle%3BSeidel%2C+Geoffrey%3BDromi%2C+Sergio%3BNeeman%2C+Ziv%3BKolf%2C+Michael%3BBlack%2C+Christopher+D+V%3BPrabhakar%2C+Raj%3BLibutti%2C+Steven+K&rft.aulast=Wood&rft.aufirst=Bradford&rft.date=2012-02-01&rft.volume=23&rft.issue=2&rft.spage=248&rft.isbn=&rft.btitle=&rft.title=Journal+of+vascular+and+interventional+radiology+%3A+JVIR&rft.issn=1535-7732&rft_id=info:doi/10.1016%2Fj.jvir.2011.10.018 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-24 N1 - Date created - 2012-01-23 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Cancer. 2000 Jun 1;88(11):2452-63 [10861420] Ann Surg Oncol. 2000 Mar;7(2):106-13 [10761788] Radiology. 2001 Oct;221(1):159-66 [11568334] Adv Drug Deliv Rev. 2001 Dec 31;53(3):285-305 [11744173] J Gastrointest Surg. 2001 Sep-Oct;5(5):477-89 [11985998] AJR Am J Roentgenol. 2002 Jul;179(1):93-101 [12076912] Radiology. 2003 Feb;226(2):441-51 [12563138] Radiology. 2003 Aug;228(2):335-45 [12893895] Cancer J Sci Am. 1995 May-Jun;1(1):73-81 [9166457] J Natl Cancer Inst. 2007 Jan 3;99(1):53-63 [17202113] Clin Cancer Res. 2007 May 1;13(9):2722-7 [17473205] Radiology. 2007 Aug;244(2):599-607 [17641378] Ann Surg. 2007 Oct;246(4):559-65; discussion 565-7 [17893492] Conf Proc IEEE Eng Med Biol Soc. 2006;1:4354-7 [17947080] Int J Hyperthermia. 2010;26(5):499-513 [20377363] Cancer Res. 2003 Oct 1;63(19):6327-33 [14559820] J Am Coll Surg. 2003 Nov;197(5):759-64 [14585410] Cancer Surv. 1993;17:219-52 [8137342] AJR Am J Roentgenol. 1996 Sep;167(3):759-68 [8751696] Surgery. 1997 Dec;122(6):1147-54; discussion 1154-5 [9426432] J Chemother. 2004 Nov;16 Suppl 5:34-6 [15675474] Int J Hyperthermia. 2004 Nov;20(7):781-802 [15675672] J Clin Oncol. 2005 Mar 1;23(7):1358-64 [15684312] Radiology. 2005 May;235(2):469-77 [15858089] Surg Endosc. 2005 May;19(5):710-4 [15759186] Ann Surg. 2005 Aug;242(2):158-71 [16041205] J Vasc Interv Radiol. 2005 Oct;16(10):1365-71 [16221908] Surg Endosc. 2005 Dec;19(12):1613-7 [16247574] Ann Surg Oncol. 2006 May;13(5):651-8 [16538411] Arch Surg. 2006 May;141(5):460-6; discussion 466-7 [16702517] Cancer Res. 2000 Mar 1;60(5):1197-201 [10728674] Cancer Res. 2000 Dec 15;60(24):6950-7 [11156395] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.jvir.2011.10.018 ER - TY - JOUR T1 - Emotional relationships in mothers and infants: culture-common and community-specific characteristics of dyads from rural and metropolitan settings in Argentina, Italy, and the United States AN - 917308197; 4261594 AB - This study uses country and regional contrasts to examine culture-common and community-specific variation in mother-infant emotional relationships. Altogether, 220 Argentine, Italian, and U.S. American mothers and their daughters and sons, living in rural and metropolitan settings, were observed at home at infant age 5 months. Both variable- and person-centered perspectives of dyadic emotional relationships were analyzed. Supporting the notion that adequate emotional relationships are a critical and culture-common characteristic of human infant development, across all samples most dyads scored in the adaptive range in terms of emotional relationships. Giving evidence of community-specific characteristics, Italian mothers were more sensitive, and Italian infants more responsive, than Argentine and U.S. mothers and infants; in addition, rural mothers were more intrusive than metropolitan mothers and rural dyads more likely than expected to be classified as midrange in emotional relationships and less likely to be classified as high in emotional relationships. Adaptive emotional relationships appear to be a culture-common characteristic of mother-infant dyads near the beginning of life, but this relational construct is moderated by a community-specific (country and regional) context. JF - Journal of cross-cultural psychology AU - Bornstein, Marc H AU - Putnick, Diane L AU - Suwalsky, Joan T.D. AU - Venuti, Paola AU - Falco, Simona de AU - Galperín, Celia Zingman de AU - Gini, Motti AU - Tichovolsky, Marianne Heslington AD - National Institutes of Health, Bethesda ; Università degli Studi di Trento ; Universidad de Belgrano ; University of Haifa ; University of Massachusetts, Amherst Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 171 EP - 197 VL - 43 IS - 2 SN - 0022-0221, 0022-0221 KW - Sociology KW - Argentina KW - Mothers KW - Parent-child relations KW - Social development KW - U.S.A. KW - Child development KW - Italy KW - Metropolitan areas KW - Rural areas KW - Infants UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/917308197?accountid=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+cross-cultural+psychology&rft.atitle=Emotional+relationships+in+mothers+and+infants%3A+culture-common+and+community-specific+characteristics+of+dyads+from+rural+and+metropolitan+settings+in+Argentina%2C+Italy%2C+and+the+United+States&rft.au=Bornstein%2C+Marc+H%3BPutnick%2C+Diane+L%3BSuwalsky%2C+Joan+T.D.%3BVenuti%2C+Paola%3BFalco%2C+Simona+de%3BGalper%C3%ADn%2C+Celia+Zingman+de%3BGini%2C+Motti%3BTichovolsky%2C+Marianne+Heslington&rft.aulast=Bornstein&rft.aufirst=Marc&rft.date=2012-02-01&rft.volume=43&rft.issue=2&rft.spage=171&rft.isbn=&rft.btitle=&rft.title=Journal+of+cross-cultural+psychology&rft.issn=00220221&rft_id=info:doi/10.1177%2F0022022110388563 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2013-06-12 N1 - Last updated - 2013-09-16 N1 - SubjectsTermNotLitGenreText - 11813 3483; 8317 9184; 6495 2212; 11156 1247; 7999; 9178 4777 6093 6823; 2197 2212 6075 3483; 24 386 14; 188 396 129; 433 293 14 DO - http://dx.doi.org/10.1177/0022022110388563 ER - TY - JOUR T1 - Use of baculovirus BacMam vectors for expression of ABC drug transporters in mammalian cells. AN - 917154817; 22041108 AB - ATP-binding cassette (ABC) drug transporters ABCB1 [P-glycoprotein (Pgp)] and ABCG2 are expressed in many tissues including those of the intestines, the liver, the kidney and the brain and are known to influence the pharmacokinetics and toxicity of therapeutic drugs. In vitro studies involving their functional characteristics provide important information that allows improvements in drug delivery or drug design. In this study, we report use of the BacMam (baculovirus-based expression in mammalian cells) expression system to express and characterize the function of Pgp and ABCG2 in mammalian cell lines. BacMam-Pgp and BacMam-ABCG2 baculovirus-transduced cell lines showed similar cell surface expression (as detected by monoclonal antibodies with an external epitope) and transport function of these transporters compared to drug-resistant cell lines that overexpress the two transporters. Transient expression of Pgp was maintained in HeLa cells for up to 72 h after transduction (48 h after removal of the BacMam virus). These BacMam-baculovirus-transduced mammalian cells expressing Pgp or ABCG2 were used for assessing the functional activity of these transporters. Crude membranes isolated from these cells were further used to study the activity of these transporters by biochemical techniques such as photo-cross-linking with transport substrate and adenosine triphosphatase assays. In addition, we show that the BacMam expression system can be exploited to coexpress both Pgp and ABCG2 in mammalian cells to determine their contribution to the transport of a common anticancer drug substrate. Collectively, these data demonstrate that the BacMam-baculovirus-based expression system can be used to simultaneously study the transport function and biochemical properties of ABC transporters. JF - Drug metabolism and disposition: the biological fate of chemicals AU - Shukla, Suneet AU - Schwartz, Candice AU - Kapoor, Khyati AU - Kouanda, Abdul AU - Ambudkar, Suresh V AD - Laboratory of Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 304 EP - 312 VL - 40 IS - 2 KW - ABCB1 protein, human KW - 0 KW - ABCG2 protein, human KW - ATP Binding Cassette Transporter, Sub-Family G, Member 2 KW - Antineoplastic Agents KW - Neoplasm Proteins KW - P-Glycoprotein KW - P-Glycoproteins KW - Radiation-Sensitizing Agents KW - Recombinant Proteins KW - Chlorophyll KW - 1406-65-1 KW - Doxorubicin KW - 80168379AG KW - Mitoxantrone KW - BZ114NVM5P KW - pheophorbide a KW - IA2WNI2HO2 KW - Index Medicus KW - Animals KW - Mammals KW - Mitoxantrone -- metabolism KW - Chlorophyll -- metabolism KW - Humans KW - Antineoplastic Agents -- metabolism KW - Biological Transport KW - Cell Line, Tumor KW - Drug Resistance, Neoplasm KW - Radiation-Sensitizing Agents -- metabolism KW - Doxorubicin -- metabolism KW - Recombinant Proteins -- metabolism KW - Cell Membrane -- metabolism KW - Chlorophyll -- analogs & derivatives KW - Neoplasms -- drug therapy KW - ATP-Binding Cassette Transporters -- metabolism KW - Baculoviridae -- metabolism KW - P-Glycoprotein -- therapeutic use KW - Transduction, Genetic -- methods KW - P-Glycoprotein -- genetics KW - P-Glycoprotein -- metabolism KW - Genetic Vectors KW - Neoplasm Proteins -- genetics KW - Neoplasm Proteins -- therapeutic use KW - ATP-Binding Cassette Transporters -- genetics KW - Drug Evaluation, Preclinical -- methods KW - ATP-Binding Cassette Transporters -- therapeutic use KW - Neoplasm Proteins -- metabolism KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/917154817?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+Religion+and+Health&rft.atitle=Factor+Structure+of+the+Brief+Multidimensional+Measure+of+Religiousness%2FSpirituality+in+US+and+Indian+Samples+with+Traumatic+Brain+Injury&rft.au=Johnstone%2C+Brick%3BBhushan%2C+Braj%3BHanks%2C+Robin%3BYoon%2C+Dong+Pil%3BCohen%2C+Daniel&rft.aulast=Johnstone&rft.aufirst=Brick&rft.date=2016-04-01&rft.volume=55&rft.issue=2&rft.spage=572&rft.isbn=&rft.btitle=&rft.title=Journal+of+Religion+and+Health&rft.issn=00224197&rft_id=info:doi/10.1007%2Fs10943-015-0170-y LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-18 N1 - Date created - 2012-01-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 2004 Feb 15;64(4):1242-6 [14973080] Biochemistry. 2002 Nov 26;41(47):13989-4000 [12437356] J Biol Chem. 1986 Jun 15;261(17):7762-70 [3711108] Proc Natl Acad Sci U S A. 1986 Oct;83(20):7785-9 [2429319] Proc Natl Acad Sci U S A. 1987 Nov;84(21):7735-8 [2444983] Anticancer Drugs. 1996 Jul;7(5):568-78 [8862725] Hum Gene Ther. 1997 Nov 20;8(17):2011-8 [9414250] Methods Enzymol. 1998;292:504-14 [9711578] Proc Natl Acad Sci U S A. 1999 Jan 5;96(1):127-32 [9874783] J Biol Chem. 2005 Feb 11;280(6):4219-27 [15557326] Nat Biotechnol. 2005 May;23(5):567-75 [15877075] Curr Drug Deliv. 2004 Jan;1(1):27-42 [16305368] Protein Expr Purif. 2006 Jun;47(2):591-8 [16481201] Biochemistry. 2006 Jul 25;45(29):8940-51 [16846237] Eur J Pharm Sci. 2006 Nov;29(3-4):269-77 [16822659] Drug Discov Today. 2007 May;12(9-10):396-403 [17467576] J Pharmacol Exp Ther. 2007 Jun;321(3):1085-94 [17347325] Curr Drug Deliv. 2007 Oct;4(4):324-33 [17979652] Curr Protoc Immunol. 2001 May;Appendix 3:Appendix 3B [18432654] Drug Discov Today. 2008 May;13(9-10):379-93 [18468555] Expert Opin Drug Metab Toxicol. 2008 Jun;4(6):721-32 [18611113] Mol Pharmacol. 2008 Oct;74(4):964-71 [18612080] BMC Neurol. 2009;9 Suppl 1:S1 [19534730] Comb Chem High Throughput Screen. 2010 Feb;13(2):112-34 [20053160] Mol Pharm. 2011 Apr 4;8(2):571-82 [21309545] PLoS One. 2011;6(4):e18438 [21483698] Nat Rev Drug Discov. 2011 May;10(5):328-9 [21532551] J Membr Biol. 2000 Feb 1;173(3):203-14 [10667916] Clin Cancer Res. 2001 Jan;7(1):145-52 [11205902] J Biol Chem. 2001 Mar 23;276(12):8657-64 [11121420] Cancer Res. 2001 Apr 15;61(8):3458-64 [11309308] Annu Rev Biochem. 2002;71:537-92 [12045106] Nature. 1985 Aug 29-Sep 4;316(6031):820-3 [2412130] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1124/dmd.111.042721 ER - TY - JOUR T1 - A phase II study of O6-benzylguanine and temozolomide in pediatric patients with recurrent or progressive high-grade gliomas and brainstem gliomas: a Pediatric Brain Tumor Consortium study. AN - 916851585; 21968943 AB - To estimate the sustained (≥8 weeks) objective response rate in pediatric patients with recurrent or progressive high-grade gliomas (HGG, Stratum A) or brainstem gliomas (BSG, Stratum B) treated with the combination of O6-benzylguanine (O6BG) and temozolomide(®) (TMZ). Patients received O6BG 120 mg/m(2)/d IV followed by TMZ 75 mg/m(2)/d orally daily for 5 consecutive days of each 28-day course. The target objective response rate to consider the combination active was 17%. A two-stage design was employed. Forty-three patients were enrolled; 41 were evaluable for response, including 25 patients with HGG and 16 patients with BSG. The combination of O6BG and TMZ was tolerable, and the primary toxicities were myelosuppression and gastrointestinal symptoms. One sustained (≥8 weeks) partial response was observed in the HGG cohort; no sustained objective responses were observed in the BSG cohort. Long-term (≥6 courses) stable disease (SD) was observed in 4 patients in Stratum A and 1 patient in Stratum B. Of the 5 patients with objective response or long-term SD, 3 underwent central review with 2 reclassified as low-grade gliomas. The combination of O6BG and TMZ did not achieve the target response rate for activity in pediatric patients with recurrent or progressive HGG and BSG. JF - Journal of neuro-oncology AU - Warren, Katherine E AU - Gururangan, Sri AU - Geyer, J Russell AU - McLendon, Roger E AU - Poussaint, Tina Young AU - Wallace, Dana AU - Balis, Frank M AU - Berg, Stacey L AU - Packer, Roger J AU - Goldman, Stewart AU - Minturn, Jane E AU - Pollack, Ian F AU - Boyett, James M AU - Kun, Larry E AD - Pediatric Oncology Branch, National Cancer Institute, Bethesda, MD 20892, USA. warrenk@mail.nih.gov Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 643 EP - 649 VL - 106 IS - 3 KW - Antineoplastic Agents KW - 0 KW - Ki-67 Antigen KW - Tumor Suppressor Proteins KW - O(6)-benzylguanine KW - 01KC87F8FE KW - Guanine KW - 5Z93L87A1R KW - Dacarbazine KW - 7GR28W0FJI KW - DNA Modification Methylases KW - EC 2.1.1.- KW - MGMT protein, human KW - EC 2.1.1.63 KW - DNA Repair Enzymes KW - EC 6.5.1.- KW - temozolomide KW - YF1K15M17Y KW - Index Medicus KW - DNA Repair Enzymes -- metabolism KW - Young Adult KW - DNA Modification Methylases -- metabolism KW - Humans KW - Retrospective Studies KW - Ki-67 Antigen -- metabolism KW - Child KW - Child, Preschool KW - Kaplan-Meier Estimate KW - Tumor Suppressor Proteins -- metabolism KW - Drug Therapy, Combination -- methods KW - Adolescent KW - Female KW - Male KW - Proportional Hazards Models KW - Brain Stem Neoplasms -- drug therapy KW - Dacarbazine -- therapeutic use KW - Glioma -- drug therapy KW - Dacarbazine -- analogs & derivatives KW - Brain Stem Neoplasms -- mortality KW - Glioma -- mortality KW - Guanine -- analogs & derivatives KW - Antineoplastic Agents -- therapeutic use KW - Guanine -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/916851585?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+neuro-oncology&rft.atitle=A+phase+II+study+of+O6-benzylguanine+and+temozolomide+in+pediatric+patients+with+recurrent+or+progressive+high-grade+gliomas+and+brainstem+gliomas%3A+a+Pediatric+Brain+Tumor+Consortium+study.&rft.au=Warren%2C+Katherine+E%3BGururangan%2C+Sri%3BGeyer%2C+J+Russell%3BMcLendon%2C+Roger+E%3BPoussaint%2C+Tina+Young%3BWallace%2C+Dana%3BBalis%2C+Frank+M%3BBerg%2C+Stacey+L%3BPacker%2C+Roger+J%3BGoldman%2C+Stewart%3BMinturn%2C+Jane+E%3BPollack%2C+Ian+F%3BBoyett%2C+James+M%3BKun%2C+Larry+E&rft.aulast=Warren&rft.aufirst=Katherine&rft.date=2012-02-01&rft.volume=106&rft.issue=3&rft.spage=643&rft.isbn=&rft.btitle=&rft.title=Journal+of+neuro-oncology&rft.issn=1573-7373&rft_id=info:doi/10.1007%2Fs11060-011-0709-z LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-21 N1 - Date created - 2012-01-18 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer. 2005 Jan 1;103(1):133-9 [15565574] Anticancer Drugs. 1999 Feb;10(2):179-85 [10211548] J Clin Oncol. 2005 Oct 20;23(30):7646-53 [16234526] Clin Cancer Res. 2005 Nov 15;11(22):8145-57 [16299247] J Clin Oncol. 2006 Oct 10;24(29):4746-53 [16954518] Mol Cancer Ther. 2006 Oct;5(10):2531-9 [17041097] Oncogene. 2007 Jan 11;26(2):186-97 [16819506] Pediatr Blood Cancer. 2007 Apr;48(4):403-7 [16609952] Neurol Med Chir (Tokyo). 2007 Aug;47(8):341-9; discussion 350 [17721049] J Clin Oncol. 2007 Sep 10;25(26):4127-36 [17827463] Cancer. 2007 Oct 1;110(7):1542-50 [17705175] Clin Cancer Res. 2007 Nov 15;13(22 Pt 1):6712-8 [18006772] J Clin Oncol. 2008 Sep 1;26(25):4189-99 [18757334] J Clin Oncol. 2009 Mar 10;27(8):1262-7 [19204199] Neuro Oncol. 2011 Mar;13(3):317-23 [21339192] Neuro Oncol. 2011 Apr;13(4):410-6 [21345842] J Clin Oncol. 1999 Sep;17(9):2762-71 [10561351] Clin Cancer Res. 2001 Feb;7(2):421-8 [11234899] Ann Oncol. 2001 Feb;12(2):259-66 [11300335] J Clin Oncol. 2002 Mar 1;20(5):1375-82 [11870182] J Clin Oncol. 2002 May 1;20(9):2277-83 [11980998] J Clin Oncol. 2002 May 1;20(9):2388-99 [11981013] Oncology. 2002;63(1):38-41 [12187069] Mol Cancer Ther. 2002 Sep;1(11):943-8 [12481416] J Clin Oncol. 2002 Dec 15;20(24):4684-91 [12488414] J Neurooncol. 2003 Feb;61(3):203-7 [12675312] Cancer Chemother Pharmacol. 2003 Dec;52(6):435-41 [13680158] J Neurooncol. 2004 Mar-Apr;67(1-2):77-81 [15072451] Cancer Res. 1987 Nov 15;47(22):5846-52 [3664486] Br J Cancer. 1992 Feb;65(2):287-91 [1739631] Biochemistry. 1994 Aug 9;33(31):9045-51 [8049205] Bioessays. 1994 Nov;16(11):833-9 [7840761] Cancer Res. 1995 Jul 1;55(13):2853-7 [7796412] Cancer Res. 1995 Oct 15;55(20):4606-10 [7553637] Br J Cancer. 1996 May;73(9):1049-52 [8624262] J Clin Oncol. 1998 Nov;16(11):3570-5 [9817277] J Clin Oncol. 1998 Dec;16(12):3851-7 [9850030] Clin Cancer Res. 2005 Apr 1;11(7):2747-55 [15814657] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s11060-011-0709-z ER - TY - JOUR T1 - Detection, monitoring, and management of trastuzumab-induced left ventricular dysfunction: an actual challenge. AN - 916851482; 22219501 AB - The antibody trastuzumab, targeted to inhibit the signalling of ErbB2, a tyrosine kinase receptor overexpressed in 20-30% of breast cancers, improves the prognosis in women affected by this tumour, but produces cardiotoxicity, since ErbB2 is also involved in myocardial homeostasis. In this review, we discuss the pathophysiology of trastuzumab cardiomyopathy and the complex interplay between ErbB2 inhibition and anthracyclines, and we focus on the actual challenges of detecting, monitoring, and managing trastuzumab cardiotoxicity: the research of new, sensitive markers of early trastuzumab toxicity, before the ejection fraction is reduced, is an active field of research. JF - European journal of heart failure AU - Tocchetti, Carlo G AU - Ragone, Gianluca AU - Coppola, Carmela AU - Rea, Domenica AU - Piscopo, Giovanna AU - Scala, Stefania AU - De Lorenzo, Claudia AU - Iaffaioli, Rosario V AU - Arra, Claudio AU - Maurea, Nicola AD - Division of Cardiology, National Cancer Institute, Sen. Pascale Foundation, Naples, Italy. cgtocchetti@iol.it Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 130 EP - 137 VL - 14 IS - 2 KW - Anthracyclines KW - 0 KW - Antibodies, Monoclonal, Humanized KW - Antineoplastic Agents KW - Biomarkers KW - ERBB2 protein, human KW - EC 2.7.10.1 KW - Receptor, ErbB-2 KW - Trastuzumab KW - P188ANX8CK KW - Index Medicus KW - Myocytes, Cardiac -- drug effects KW - Humans KW - Biomarkers -- analysis KW - Algorithms KW - Monitoring, Physiologic KW - Anthracyclines -- adverse effects KW - Antibodies, Monoclonal, Humanized -- adverse effects KW - Ventricular Dysfunction, Left -- diagnosis KW - Receptor, ErbB-2 -- antagonists & inhibitors KW - Cardiomyopathies -- diagnosis KW - Cardiomyopathies -- physiopathology KW - Cardiomyopathies -- chemically induced KW - Ventricular Dysfunction, Left -- physiopathology KW - Cardiomyopathies -- therapy KW - Ventricular Dysfunction, Left -- chemically induced KW - Ventricular Dysfunction, Left -- therapy KW - Antineoplastic Agents -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/916851482?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+heart+failure&rft.atitle=Detection%2C+monitoring%2C+and+management+of+trastuzumab-induced+left+ventricular+dysfunction%3A+an+actual+challenge.&rft.au=Tocchetti%2C+Carlo+G%3BRagone%2C+Gianluca%3BCoppola%2C+Carmela%3BRea%2C+Domenica%3BPiscopo%2C+Giovanna%3BScala%2C+Stefania%3BDe+Lorenzo%2C+Claudia%3BIaffaioli%2C+Rosario+V%3BArra%2C+Claudio%3BMaurea%2C+Nicola&rft.aulast=Tocchetti&rft.aufirst=Carlo&rft.date=2012-02-01&rft.volume=14&rft.issue=2&rft.spage=130&rft.isbn=&rft.btitle=&rft.title=European+journal+of+heart+failure&rft.issn=1879-0844&rft_id=info:doi/10.1093%2Feurjhf%2Fhfr165 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-23 N1 - Date created - 2012-01-18 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/eurjhf/hfr165 ER - TY - JOUR T1 - Pazopanib for the treatment of breast cancer. AN - 916150413; 22233389 AB - Several clinical trials have shown clinical benefit of angiogenesis inhibitors in the treatment of solid tumors. Pazopanib is a multitargeted tyrosine kinase inhibitor that is currently approved for the treatment of patients with advanced renal cell carcinoma (RCC). In this article, the clinical development of pazopanib as it relates to breast cancer is reviewed including its evaluation in clinical trials and side effect profile. Preclinical data show the anti-tumor activity of pazopanib in animal models. Several trials of pazopanib monotherapy and combination therapy in breast cancer have been completed or are underway. The development of biomarkers predictive of response and toxicity to angiogenesis inhibitors remains a challenging endeavor and is necessary to help guide treatment decision. JF - Expert opinion on investigational drugs AU - Amiri-Kordestani, Laleh AU - Tan, Antoinette R AU - Swain, Sandra M AD - National Cancer Institute, 10 Center Drive, 12N226, Bethesda, MD, USA. Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 217 EP - 225 VL - 21 IS - 2 KW - Angiogenesis Inhibitors KW - 0 KW - Biomarkers, Tumor KW - Protein Kinase Inhibitors KW - Pyrimidines KW - Sulfonamides KW - pazopanib KW - 7RN5DR86CK KW - Protein-Tyrosine Kinases KW - EC 2.7.10.1 KW - Index Medicus KW - Protein-Tyrosine Kinases -- antagonists & inhibitors KW - Humans KW - Female KW - Breast Neoplasms -- genetics KW - Breast Neoplasms -- drug therapy KW - Angiogenesis Inhibitors -- therapeutic use KW - Pyrimidines -- therapeutic use KW - Protein Kinase Inhibitors -- therapeutic use KW - Sulfonamides -- therapeutic use UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/916150413?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Expert+opinion+on+investigational+drugs&rft.atitle=Pazopanib+for+the+treatment+of+breast+cancer.&rft.au=Amiri-Kordestani%2C+Laleh%3BTan%2C+Antoinette+R%3BSwain%2C+Sandra+M&rft.aulast=Amiri-Kordestani&rft.aufirst=Laleh&rft.date=2012-02-01&rft.volume=21&rft.issue=2&rft.spage=217&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+investigational+drugs&rft.issn=1744-7658&rft_id=info:doi/10.1517%2F13543784.2012.652304 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-01 N1 - Date created - 2012-01-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1517/13543784.2012.652304 ER - TY - JOUR T1 - Weekly paclitaxel in heavily pretreated ovarian cancer patients: does this treatment still provide further advantages? AN - 916148290; 21735184 AB - To evaluate the disease control rate (DCR) in heavily pretreated and relapsed ovarian cancer patients re-challenged with a weekly paclitaxel schedule and to establish whether a correlation between dose intensity, progression-free interval (PFI) and overall survival (OS) exists. Retrospective data were collected from 30 heavily pretreated metastatic ovarian cancer patients who received 80 mg/m(2)/week paclitaxel regimen. The treatment was well tolerated and showed a DCR in 70% of the patients, with only one case of grade 3 hematological toxicity. One patient (3%) showed a complete response, 15 patients (50%) a partial response and five patients (17%) a stabilization of their disease. The regimen was mostly used as a fourth-line chemotherapy (range 2-7). The median dose intensity in responding patients was 57.5 mg/m(2)/week and in those with progressive disease 49.7 mg/m(2)/week. (p = 0.20). PFI and OS were increased in the responder patient groups with a log-rank test of 25.64 (p < 0.001) and 15.10 (p = 0.0001), respectively. Weekly administration of paclitaxel was active and well tolerated as a salvage therapy for heavily pretreated ovarian cancer patients. JF - Archives of gynecology and obstetrics AU - Miolo, Gianmaria AU - Bidoli, Ettore AU - Lombardi, Davide AU - Santeufemia, Davide Adriano AU - Capobianco, Giampiero AU - Dessole, Francesco AU - Scalone, Simona AU - Spazzapan, Simon AU - Sorio, Roberto AU - Tabaro, Gianna AU - Veronesi, Andrea AD - Department of Oncology, Division of Medical Oncology C, Centro di Riferimento Oncologico, National Cancer Institute, Aviano, Italy. Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 499 EP - 503 VL - 285 IS - 2 KW - Antineoplastic Agents, Phytogenic KW - 0 KW - Paclitaxel KW - P88XT4IS4D KW - Index Medicus KW - Disease-Free Survival KW - Humans KW - Anemia -- chemically induced KW - Retrospective Studies KW - Aged KW - Neutropenia -- chemically induced KW - Kaplan-Meier Estimate KW - Aged, 80 and over KW - Adult KW - Treatment Outcome KW - Neoplasm Metastasis KW - Middle Aged KW - Female KW - Paclitaxel -- administration & dosage KW - Paclitaxel -- adverse effects KW - Neoplasm Recurrence, Local -- drug therapy KW - Antineoplastic Agents, Phytogenic -- adverse effects KW - Ovarian Neoplasms -- pathology KW - Antineoplastic Agents, Phytogenic -- therapeutic use KW - Salvage Therapy KW - Paclitaxel -- therapeutic use KW - Antineoplastic Agents, Phytogenic -- administration & dosage KW - Ovarian Neoplasms -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/916148290?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+gynecology+and+obstetrics&rft.atitle=Weekly+paclitaxel+in+heavily+pretreated+ovarian+cancer+patients%3A+does+this+treatment+still+provide+further+advantages%3F&rft.au=Miolo%2C+Gianmaria%3BBidoli%2C+Ettore%3BLombardi%2C+Davide%3BSanteufemia%2C+Davide+Adriano%3BCapobianco%2C+Giampiero%3BDessole%2C+Francesco%3BScalone%2C+Simona%3BSpazzapan%2C+Simon%3BSorio%2C+Roberto%3BTabaro%2C+Gianna%3BVeronesi%2C+Andrea&rft.aulast=Miolo&rft.aufirst=Gianmaria&rft.date=2012-02-01&rft.volume=285&rft.issue=2&rft.spage=499&rft.isbn=&rft.btitle=&rft.title=Archives+of+gynecology+and+obstetrics&rft.issn=1432-0711&rft_id=info:doi/10.1007%2Fs00404-011-1976-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-07 N1 - Date created - 2012-01-13 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s00404-011-1976-9 ER - TY - JOUR T1 - Longitudinal analysis of carcinogenic human papillomavirus infection and associated cytologic abnormalities in the Guanacaste natural history study: looking ahead to cotesting. AN - 916147665; 22147792 AB - Few studies have addressed the timing of cervical cytologic abnormalities and human papillomavirus (HPV) positivity during the course of an infection. It remains largely unknown how infections detected by HPV and cytology wax and wane relative to each other. The aim of this analysis was to assess the longitudinal relationship of abnormal cytology and HPV positivity in a 7-year prospective study of 2500 women in Guanacaste, Costa Rica. At each semiannual or annual visit, cervical specimens were screened using liquid-based cytology and tested for >40 HPV types with use of MY09/MY11 L1 degenerate primer polymerase chain reaction-based methods. On the basis of previous work, we separated prevalent and newly detected infections in younger and older women. Among newly detected HPV- and/or cytology-positive events, HPV and cytology appeared together ∼60% of the time; when discordant, HPV tended to appear before cytology in younger and older women. Combining newly and prevalently detected events, HPV and cytology disappeared at the same time >70% of the time. When discordant, HPV tended to disappear after cytology in younger and older women. Detection of HPV DNA and associated cytological abnormalities tend to come and leave together; however, when discordant, detection of HPV DNA tends to precede and/or last longer than associated cytologic abnormalities. JF - The Journal of infectious diseases AU - Markt, Sarah Coseo AU - Rodriguez, Ana C AU - Burk, Robert D AU - Hildesheim, Allan AU - Herrero, Rolando AU - Wacholder, Sholom AU - Hutchinson, Martha AU - Schiffman, Mark AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland, USA. scoseo@hsph.harvard.edu Y1 - 2012/02/01/ PY - 2012 DA - 2012 Feb 01 SP - 498 EP - 505 VL - 205 IS - 3 KW - DNA, Viral KW - 0 KW - Abridged Index Medicus KW - Index Medicus KW - Young Adult KW - Cytological Techniques KW - Costa Rica KW - Humans KW - Aged KW - Longitudinal Studies KW - Polymerase Chain Reaction KW - Prospective Studies KW - Aged, 80 and over KW - Adult KW - DNA, Viral -- isolation & purification KW - Middle Aged KW - Adolescent KW - DNA, Viral -- genetics KW - Female KW - Viral Load KW - Papillomavirus Infections -- pathology KW - Cervix Uteri -- pathology KW - Papillomaviridae -- isolation & purification KW - Papillomavirus Infections -- virology KW - Papillomaviridae -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/916147665?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+Journal+of+infectious+diseases&rft.atitle=Longitudinal+analysis+of+carcinogenic+human+papillomavirus+infection+and+associated+cytologic+abnormalities+in+the+Guanacaste+natural+history+study%3A+looking+ahead+to+cotesting.&rft.au=Markt%2C+Sarah+Coseo%3BRodriguez%2C+Ana+C%3BBurk%2C+Robert+D%3BHildesheim%2C+Allan%3BHerrero%2C+Rolando%3BWacholder%2C+Sholom%3BHutchinson%2C+Martha%3BSchiffman%2C+Mark&rft.aulast=Markt&rft.aufirst=Sarah&rft.date=2012-02-01&rft.volume=205&rft.issue=3&rft.spage=498&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+infectious+diseases&rft.issn=1537-6613&rft_id=info:doi/10.1093%2Finfdis%2Fjir746 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-03-06 N1 - Date created - 2012-01-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Natl Cancer Inst. 2010 Mar 3;102(5):315-24 [20157096] Lancet Oncol. 2009 Jul;10(7):672-82 [19540162] JAMA. 2000 Jan 5;283(1):87-93 [10632285] JAMA. 2001 Jun 20;285(23):2995-3002 [11410098] J Pathol. 2001 Oct;195(3):300-6 [11673826] Lancet. 2001 Nov 24;358(9295):1782-3 [11734239] J Med Virol. 2002 Nov;68(3):417-23 [12226831] J Infect Dis. 2002 Oct 15;186(8):1169-72 [12355370] Rev Panam Salud Publica. 2004 Feb;15(2):75-89 [15030652] JAMA. 1989 Aug 18;262(7):931-4 [2754794] J Natl Cancer Inst. 1995 Jun 7;87(11):796-802 [7791229] J Natl Cancer Inst. 1995 Sep 20;87(18):1365-71 [7658497] J Clin Microbiol. 1997 Jun;35(6):1304-10 [9163434] Rev Panam Salud Publica. 1997 May;1(5):362-75 [9180057] Cancer. 1999 Apr 25;87(2):48-55 [10227593] Eur J Obstet Gynecol Reprod Biol. 2005 Apr 1;119(2):219-27 [15808384] Cancer Res. 2006 Oct 15;66(20):10112-9 [17047075] N Engl J Med. 2007 Oct 18;357(16):1589-97 [17942872] Int J Cancer. 2007 Dec 15;121(12):2787-93 [17722112] Lancet. 2007 Nov 24;370(9601):1764-72 [17919718] Obstet Gynecol Clin North Am. 2008 Dec;35(4):537-48; vii [19061815] Lancet Oncol. 2009 Apr;10(4):321-2 [19350698] Obstet Gynecol. 2010 Jul;116(1):76-84 [20567171] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/infdis/jir746 ER - TY - JOUR T1 - The nuclear receptor constitutive active/androstane receptor arrests DNA-damaged human hepatocellular carcinoma Huh7 cells at the G2/M phase. AN - 913721162; 21557330 AB - Here, we have demonstrated that xenobiotic activation of the nuclear receptor (CAR, NR1I3) can result in arresting DNA-damaged human hepatocellular carcinoma Huh7 cells at the G2/M phase. Huh7 cells over-expressing CAR were either treated with dimethyl sulfoxide, the CAR activator TCPOBOP (1,4-bis[2-(3,5-dichloropyridyloxy)]benzene; androstenol, 16,(5α)-androsten-3α-OL), or repressor androstenol; these treatments were then followed by adriamycin treatment to damage DNA. FACS analysis revealed that CAR-activation by TCPOBOP increased the rate of arrested Huh7 cells at the G2/M phase (4N DNA content) after DNA damage by adriamycin. This increase correlated with the increase of cell viability in TCPOBOP-treated Huh7 cells, as determined by MTT assays. Real-time polymerase chain reaction analysis determined that, as regulated by CAR, the growth arrest and DNA damage-inducible γ (GADD45γ) and Cyclin G2 genes increased and decreased, respectively, as TCPOBOP increased the number of Huh7 cells arrested at the G2/M phase. Thus, the results suggest that CAR regulates cell cycle, increasing G2/M arrest, and delaying the death of DNA-damaged cells. Copyright © 2011 Wiley Periodicals, Inc. JF - Molecular carcinogenesis AU - Kamino, Hiroki AU - Negishi, Masahiko AD - Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA. Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 206 EP - 212 VL - 51 IS - 2 KW - DNA Primers KW - 0 KW - Receptors, Cytoplasmic and Nuclear KW - constitutive androstane receptor KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Base Sequence KW - Humans KW - Flow Cytometry KW - Cell Line, Tumor KW - Receptors, Cytoplasmic and Nuclear -- physiology KW - Liver Neoplasms -- pathology KW - Liver Neoplasms -- metabolism KW - Carcinoma, Hepatocellular -- metabolism KW - DNA Damage KW - Carcinoma, Hepatocellular -- pathology KW - G2 Phase KW - Cell Division UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/913721162?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+carcinogenesis&rft.atitle=The+nuclear+receptor+constitutive+active%2Fandrostane+receptor+arrests+DNA-damaged+human+hepatocellular+carcinoma+Huh7+cells+at+the+G2%2FM+phase.&rft.au=Kamino%2C+Hiroki%3BNegishi%2C+Masahiko&rft.aulast=Kamino&rft.aufirst=Hiroki&rft.date=2012-02-01&rft.volume=51&rft.issue=2&rft.spage=206&rft.isbn=&rft.btitle=&rft.title=Molecular+carcinogenesis&rft.issn=1098-2744&rft_id=info:doi/10.1002%2Fmc.20783 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-02-13 N1 - Date created - 2012-01-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biol Chem. 2000 Jun 2;275(22):16602-8 [10747892] PLoS One. 2010;5(4):e10121 [20404936] Mol Cell Biol. 2004 Sep;24(18):7931-40 [15340055] Cancer Res. 2004 Oct 15;64(20):7197-200 [15492232] J Biol Chem. 1996 Mar 15;271(11):6050-61 [8626390] J Biol Chem. 1997 May 9;272(19):12650-61 [9139721] Mol Cell Biol. 1998 Oct;18(10):5652-8 [9742082] J Biol Chem. 1999 Mar 5;274(10):6043-6 [10037683] Oncogene. 1999 May 6;18(18):2892-900 [10362260] Cancer Res. 2004 Dec 15;64(24):8980-6 [15604262] Drug Metab Rev. 2006;38(1-2):75-87 [16684649] Toxicol Sci. 2007 Mar;96(1):72-82 [17172636] J Clin Pharmacol. 2007 May;47(5):566-78 [17442683] Curr Drug Metab. 2008 Sep;9(7):614-21 [18781913] Mol Biol Rep. 2009 Nov;36(8):2075-85 [19048389] J Cell Physiol. 2002 Sep;192(3):327-38 [12124778] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/mc.20783 ER - TY - JOUR T1 - AAV5-mediated sFLT01 gene therapy arrests retinal lesions in Ccl2(-/-)/Cx3cr1(-/-) mice. AN - 908741589; 21397984 AB - To test the effects of adeno-associated virus encoding sFLT01 (AAV5.sFLT01) on the retinal lesions in Ccl2(-/-)/Cx3cr1(-/-) mice, a model for age-related macular degeneration (AMD), AAV5.sFLT01 was injected into the subretinal space of the right eyes and the left eyes served as controls. Histology found no retinal toxicity due to the treatment after 3 months. The treated eyes showed lesion arrest compared with lesion progression in the left eyes by fundus monitoring monthly and histological evaluation 3 months after treatment. Retinal ultrastructure showed fewer lipofuscin and better preserved photoreceptors after the treatment. A2E, a major component of lipofuscin, was lower in the treated eyes than in the control eyes. Molecular analysis showed that AAV5.sFLT01 lowered retinal extracellular signal-regulated kinase (ERK) phosphorylation and inducible nitric oxide synthetase expression, which suggested the involvement of reactive nitrogen species in the retinal lesions of Ccl2(-/-)/Cx3cr1(-/-). We concluded that local delivery of AAV5.sFLT01 can stabilize retinal lesions in Ccl2(-/-)/Cx3cr1(-/-) mice. The findings provide further support for the potential beneficial effects of sFLT01 gene therapy for age-related macular degeneration. Published by Elsevier Inc. JF - Neurobiology of aging AU - Tuo, Jingsheng AU - Pang, Ji-Jing AU - Cao, Xiaoguang AU - Shen, Defen AU - Zhang, Jun AU - Scaria, Abraham AU - Wadsworth, Samuel C AU - Pechan, Peter AU - Boye, Sanford L AU - Hauswirth, William W AU - Chan, Chi-Chao AD - Immunopathology Section, Laboratory of Immunology, National Eye Institute, NIH, Bethesda, MD 20892-1857, USA. Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 433.e1 EP - 10 VL - 33 IS - 2 KW - Ccl2 protein, mouse KW - 0 KW - Chemokine CCL2 KW - Cx3cr1 protein, mouse KW - Receptors, Chemokine KW - Flt1 protein, mouse KW - EC 2.7.10.1 KW - Vascular Endothelial Growth Factor Receptor-1 KW - Index Medicus KW - Chemokine CCL2 -- genetics KW - Animals KW - Genetic Vectors KW - Receptors, Chemokine -- metabolism KW - Mice, Inbred C57BL KW - Receptors, Chemokine -- genetics KW - Mice KW - Chemokine CCL2 -- metabolism KW - Mice, Knockout KW - Vascular Endothelial Growth Factor Receptor-1 -- genetics KW - Transfection -- methods KW - Vascular Endothelial Growth Factor Receptor-1 -- therapeutic use KW - Macular Degeneration -- therapy KW - Macular Degeneration -- metabolism KW - Adenoviridae -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/908741589?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neurobiology+of+aging&rft.atitle=AAV5-mediated+sFLT01+gene+therapy+arrests+retinal+lesions+in+Ccl2%28-%2F-%29%2FCx3cr1%28-%2F-%29+mice.&rft.au=Tuo%2C+Jingsheng%3BPang%2C+Ji-Jing%3BCao%2C+Xiaoguang%3BShen%2C+Defen%3BZhang%2C+Jun%3BScaria%2C+Abraham%3BWadsworth%2C+Samuel+C%3BPechan%2C+Peter%3BBoye%2C+Sanford+L%3BHauswirth%2C+William+W%3BChan%2C+Chi-Chao&rft.aulast=Tuo&rft.aufirst=Jingsheng&rft.date=2012-02-01&rft.volume=33&rft.issue=2&rft.spage=433.e1&rft.isbn=&rft.btitle=&rft.title=Neurobiology+of+aging&rft.issn=1558-1497&rft_id=info:doi/10.1016%2Fj.neurobiolaging.2011.01.009 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-04-19 N1 - Date created - 2011-12-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Ann Med. 2006;38(7):450-71 [17101537] Int J Mol Med. 2007 Jan;19(1):75-9 [17143550] Aust Fam Physician. 2007 May;36(5):359-61 [17492074] J Biol Chem. 2000 Apr 7;275(14):10661-72 [10744763] Bioorg Med Chem Lett. 2001 Jun 18;11(12):1533-40 [11412975] Hum Gene Ther. 2001 Jul 1;12(10):1299-310 [11440623] Nat Med. 2004 Oct;10(10):1095-103 [15378055] Oncogene. 1990 Apr;5(4):519-24 [2158038] Proc Natl Acad Sci U S A. 1997 Jun 24;94(13):6916-21 [9192666] J Biol Chem. 1997 Dec 19;272(51):32521-7 [9405464] FEBS Lett. 1998 Jun 16;429(3):249-53 [9662426] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14609-13 [9843937] Mol Vis. 2005 Feb 28;11:152-62 [15765048] Proc Natl Acad Sci U S A. 2005 Mar 15;102(11):4164-9 [15749821] Folia Neuropathol. 2005;43(1):31-9 [15827888] Exp Eye Res. 2005 May;80(5):595-606 [15862166] Hum Gene Ther. 2005 May;16(5):541-50 [15916479] Mol Ther. 2005 Oct;12(4):659-68 [16023893] Mol Ther. 2006 Mar;13(3):565-72 [16223604] Adv Biochem Eng Biotechnol. 2005;99:119-45 [16568890] Invest Ophthalmol Vis Sci. 2007 Jun;48(6):2769-74 [17525211] Invest Ophthalmol Vis Sci. 2007 Aug;48(8):3827-36 [17652758] J Clin Invest. 2007 Oct;117(10):2920-8 [17909628] Exp Eye Res. 2008 Apr;86(4):675-83 [18308304] Ophthalmic Res. 2008;40(3-4):124-8 [18421225] J Biol Chem. 2008 May 2;283(18):11947-53 [18326047] Gene Ther. 2008 Jun;15(11):849-57 [18418417] Gene Ther. 2009 Jan;16(1):10-6 [18633446] Stroke. 2009 Apr;40(4):1467-73 [19228841] Cancer Lett. 2009 Jul 18;280(1):86-92 [19307054] Int Immunopharmacol. 2009 Jul;9(7-8):810-6 [19293003] J Cell Physiol. 2009 Aug;220(2):469-75 [19418485] Am J Pathol. 2009 Aug;175(2):799-807 [19608872] Neurotox Res. 2009 Oct;16(3):318-28 [19551455] Invest Ophthalmol Vis Sci. 2009 Sep;50(9):4279-87 [19357358] J Immunol. 2009 Oct 15;183(8):5113-20 [19786548] PLoS One. 2009;4(11):e7945 [19936204] J Immunol. 2010 Jan 15;184(2):545-9 [20008289] Hum Gene Ther. 2010 May;21(5):631-7 [20053138] Exp Eye Res. 2010 Jul;91(1):15-25 [20361964] Mol Ther. 2011 Feb;19(2):234-42 [21139570] J Immunol. 2004 Apr 1;172(7):4618-23 [15034080] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.neurobiolaging.2011.01.009 ER - TY - JOUR T1 - RADIATION DOSE TO THE FETUS FROM [ super(18)F]-FDG ADMINISTRATION DURING THE SECOND TRIMESTER OF PREGNANCY AN - 1691284434; 16372962 AB - The authors estimated the fetal radiation dose from [ super(18)F]-FDG in a rare case of a woman who underwent a PET/CT scan during the second trimester of pregnancy. The patient, a 27-y-old female with a paraganglioma, received 181.3 MBq [ super(18)F]-FDG. From the concentrations of radioactivity measured on the images, the time-integrated activity coefficients of the fetus and the placenta were derived. The time-integrated activity coefficients of the mother's organs were taken from the standard values of ICRP publication 106. The final fetal dose was calculated using the 6-mo pregnant model of the OLINDA/EXM software. The fetus showed an overall low and homogeneous [ super(18)F]-FDG uptake, with an average concentration of 2.41 kBq cm super(-3). The uptake in the placenta was generally higher (average concentration = 3.69 kBq cm super(-3)). The estimated time-integrated activity coefficients were 0.0130 and 0.0058 Bq h Bq super(-1) for the fetus and the placenta, respectively. The final average dose to the fetus was 1.97 x 10 super(-2) mGy MBq super(-1) (3.6 mGy in this patient who received 181.3 MBq). Therefore, the dose to the fetus from [ super(18)F]-FDG administration during the second trimester of pregnancy is low. When medically indicated, pregnancy should not be a categorical basis for withholding [ super(18)F]-FDG PET scans. JF - Health Physics AU - Zanotti-Fregonara, P AU - Koroscil, T M AU - Mantil, J AU - Satter, M AD - Molecular Imaging Branch, National Institute of Mental Health, Building 10, Room B1D43, 31 Center Drive, MSC-1026, Bethesda, MD 20892-2035, USA, zanottifregonp@mail.nih.gov Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 217 EP - 219 PB - Williams & Wilkins, 351 W. Camden St. Baltimore MD 21201 United States VL - 102 IS - 2 SN - 0017-9078, 0017-9078 KW - Environment Abstracts KW - Computer programs KW - Radioactivity KW - Organs KW - Pregnancy KW - ENA 07:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1691284434?accountid=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=Health+Physics&rft.atitle=RADIATION+DOSE+TO+THE+FETUS+FROM+%5B+super%2818%29F%5D-FDG+ADMINISTRATION+DURING+THE+SECOND+TRIMESTER+OF+PREGNANCY&rft.au=Zanotti-Fregonara%2C+P%3BKoroscil%2C+T+M%3BMantil%2C+J%3BSatter%2C+M&rft.aulast=Zanotti-Fregonara&rft.aufirst=P&rft.date=2012-02-01&rft.volume=102&rft.issue=2&rft.spage=217&rft.isbn=&rft.btitle=&rft.title=Health+Physics&rft.issn=00179078&rft_id=info:doi/10.1097%2FHP.0b013e318226ebb4 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2015-06-26 N1 - SubjectsTermNotLitGenreText - Computer programs; Radioactivity; Organs; Pregnancy DO - http://dx.doi.org/10.1097/HP.0b013e318226ebb4 ER - TY - JOUR T1 - Cardiorespiratory Fitness as a Predictor of Dementia Mortality in Men and Women AN - 1647023326; 21210966 AB - There is evidence that physical activity may reduce the risk of developing Alzheimer disease and dementia. However, few reports have examined the physical activity-dementia association with objective measures of physical activity. Cardiorespiratory fitness (hereafter called fitness) is an objective reproducible measure of recent physical activity habits. Purpose: We sought to determine whether fitness is associated with lower risk for dementia mortality in women and men. Methods: We followed 14,811 women and 45,078 men, age 20-88 yr at baseline, for an average of 17 yr. All participants completed a preventive health examination at the Cooper Clinic in Dallas, TX, during 1970-2001. Fitness was measured with a maximal treadmill exercise test, with results expressed in maximal METs. The National Death Index identified deaths through 2003. Cox proportional hazards models were used to examine the association between baseline fitness and dementia mortality, adjusting for age, sex, examination year, body mass index, smoking, alcohol use, abnormal ECGs, and health status. Results: There were 164 deaths with dementia fisted as the cause during 1,012,125 person-years of exposure. Each 1-MET increase in fitness was associated with a 14% lower adjusted risk of dementia mortality (95% confidence interval (CI) = 696-22%). With fitness expressed in tertiles, adjusted hazard ratios (HRs) for those in the middle- and high-fitness groups suggest their risk of dementia mortality was less than half that of those in the lowest fitness group (HR = 0.44, CI = 0.26-0.74 and HR = 0.49, CI = 0.26-0.90, respectively). Conclusions: Greater fitness was associated with lower risk of mortality from dementia in a large cohort of men and women. JF - Medicine & Science in Sports & Exercise AU - Liu, Rui AU - Sui, Xuemei AU - Laditka, James N AU - Church, Timothy S AU - Colabianchi, Natalie AU - Hussey, Jim AU - Blair, Steven N AD - Epidemiology Branch, National Institute of Environmental Health Sciences, in T.W. Alexander Dr. PO Box 12233, Mail drop A3-05, Research Triangle Park, NC 27709, liur2@niehs.nih.gov Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 253 EP - 259 PB - Lippincott Williams & Wilkins, 530 Walnut Street Philadelphia PA 19106-3621 United States VL - 44 IS - 2 SN - 0195-9131, 0195-9131 KW - Physical Education Index KW - PHYSICAL FITNESS KW - COGNITIVE FUNCTION KW - ALZHEIMER DISEASE KW - VASCULAR DEMENTIA KW - METS KW - Fitness KW - Death KW - Men KW - Alzheimer's disease KW - Women KW - Sport science KW - Exercise KW - Cardiorespiratory endurance KW - Professional sports KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1647023326?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medicine+%26+Science+in+Sports+%26+Exercise&rft.atitle=Cardiorespiratory+Fitness+as+a+Predictor+of+Dementia+Mortality+in+Men+and+Women&rft.au=Liu%2C+Rui%3BSui%2C+Xuemei%3BLaditka%2C+James+N%3BChurch%2C+Timothy+S%3BColabianchi%2C+Natalie%3BHussey%2C+Jim%3BBlair%2C+Steven+N&rft.aulast=Liu&rft.aufirst=Rui&rft.date=2012-02-01&rft.volume=44&rft.issue=2&rft.spage=253&rft.isbn=&rft.btitle=&rft.title=Medicine+%26+Science+in+Sports+%26+Exercise&rft.issn=01959131&rft_id=info:doi/10.1249%2FMSS.0b013e31822cf717 LA - English DB - Physical Education Index N1 - Date revised - 2015-01-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Fitness; Death; Men; Women; Alzheimer's disease; Sport science; Exercise; Professional sports; Cardiorespiratory endurance DO - http://dx.doi.org/10.1249/MSS.0b013e31822cf717 ER - TY - JOUR T1 - Impact of the 2009 Influenza Pandemic on Pneumococcal Pneumonia Hospitalizations in the United States AN - 1635019655; 20933603 AB - Background. Infection with influenza virus increases the risk for developing pneumococcal disease. The A/H1N1 influenza pandemic in autumn 2009 provided a unique opportunity to evaluate this relationship. Methods. Using weekly age-, state-, and cause-specific hospitalizations from the US State Inpatient Databases of the Healthcare Cost and Utilization Project 2003-2009, we quantified the increase in pneumococcal pneumonia hospitalization rates above a seasonal baseline during the pandemic period. Results. We found a significant increase in pneumococcal hospitalizations from late August to mid-December 2009, which corresponded to the timing of highest pandemic influenza activity. Individuals aged 5-19 years, who have a low baseline level of pneumococcal disease, experienced the largest relative increase in pneumococcal hospitalizations (ratio, 1.6 [95% confidence interval {CI}, 1.4-1.7]), whereas the largest absolute increase was observed among individuals aged 40-64 years. In contrast, there was no excess disease in the elderly. Geographical variation in the timing of excess pneumococcal hospitalizations matched geographical patterns for the fall pandemic influenza wave. Conclusions. The 2009 influenza pandemic had a significant impact on the rate of pneumococcal pneumonia hospitalizations, with the magnitude of this effect varying between age groups and states, mirroring observed variations in influenza activity. JF - Journal of Infectious Diseases AU - Weinberger, Daniel AU - Simonsen, Lone AU - Jordan, Richard AU - Steiner, Claudia AU - Miller, Mark AU - Viboud, Cecile AD - Division of International Epidemiology and Population Studies, Fogarty International Center, National Institutes of Health, Bethesda, Maryland; Division of International Epidemiology and Population Studies, National Institutes of Health, Bldg 16, 16 Center Dr, Bethesda, MD 20892, weinbergerdm@mail.nih.gov Y1 - 2012/02/01/ PY - 2012 DA - 2012 Feb 01 SP - 458 EP - 465 PB - Oxford University Press, Oxford Journals, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 205 IS - 3 SN - 0022-1899, 0022-1899 KW - Virology & AIDS Abstracts; Microbiology Abstracts B: Bacteriology; Health & Safety Science Abstracts KW - Age KW - Elderly KW - Infection KW - Influenza KW - Databases KW - USA KW - Streptococcus pneumoniae KW - pandemics KW - Influenza virus KW - Sulfur dioxide KW - Health care KW - Infectious diseases KW - Geriatrics KW - Age groups KW - Waves KW - Geographical variations KW - Seasonal variations KW - Pneumonia KW - H 13000:Medical Safety KW - J 02400:Human Diseases KW - V 22400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635019655?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Infectious+Diseases&rft.atitle=Impact+of+the+2009+Influenza+Pandemic+on+Pneumococcal+Pneumonia+Hospitalizations+in+the+United+States&rft.au=Weinberger%2C+Daniel%3BSimonsen%2C+Lone%3BJordan%2C+Richard%3BSteiner%2C+Claudia%3BMiller%2C+Mark%3BViboud%2C+Cecile&rft.aulast=Weinberger&rft.aufirst=Daniel&rft.date=2012-02-01&rft.volume=205&rft.issue=3&rft.spage=458&rft.isbn=&rft.btitle=&rft.title=Journal+of+Infectious+Diseases&rft.issn=00221899&rft_id=info:doi/10.1093%2Finfdis%2Fjir749 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Influenza; Databases; Age; pandemics; Geriatrics; Waves; Geographical variations; Infection; Pneumonia; Sulfur dioxide; Infectious diseases; Health care; Elderly; Age groups; Seasonal variations; Streptococcus pneumoniae; Influenza virus; USA DO - http://dx.doi.org/10.1093/infdis/jir749 ER - TY - JOUR T1 - Predictors of participation in physical activity for community-dwelling elderly Italians AN - 1458533353; 16034640 AB - This paper analyses variables associated with community-dwelling older people's engagement in physical activity (PA). Data were examined using the results from the European ZINCAGE study on 306 community-dwelling Italians aged 65 years and over. The lifestyle questionnaire was used to evaluate the data. Levels of regular/non-regular PA were based on greater than or equal to 1 h of weekly exercise. Logistic regression analysis was used to analyze the predictors of PA. Participants reported the time they had spent per week engaging in PA over the last year. Overall, 56.2% of them engaged in regular physical exercise. PA levels decreased in subjects with probable cognitive decline, depression and high perceived stress levels (p < 0.001). Lower age, a lower body mass index (BMI), better health status, absence of depression, being married, were all associated with regular PA. The importance of monitoring PA in the elderly emerged, in particular in those having some certain social-demographic characteristics. JF - Archives of Gerontology and Geriatrics AU - Giuli, Cinzia AU - Papa, Roberta AU - Mocchegiani, Eugenio AU - Marcellini, Fiorella AD - Unit of Geriatrics, INRCA (Italian National Institute on Aging), Contrada Mossa, I-63023 Fermo, Italy, f.marcellini@inrca.it Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 50 EP - 54 PB - Elsevier B.V., Elsevier House, Brookvale Plaza East Park Shannon, Co. Clare Ireland VL - 54 IS - 1 SN - 0167-4943, 0167-4943 KW - Physical Education Index KW - Depression KW - Analysis KW - Body mass KW - Gerontology KW - Geriatrics KW - Stress KW - Health KW - Exercise KW - Lifestyle KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1458533353?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Archives+of+Gerontology+and+Geriatrics&rft.atitle=Predictors+of+participation+in+physical+activity+for+community-dwelling+elderly+Italians&rft.au=Giuli%2C+Cinzia%3BPapa%2C+Roberta%3BMocchegiani%2C+Eugenio%3BMarcellini%2C+Fiorella&rft.aulast=Giuli&rft.aufirst=Cinzia&rft.date=2012-02-01&rft.volume=54&rft.issue=1&rft.spage=50&rft.isbn=&rft.btitle=&rft.title=Archives+of+Gerontology+and+Geriatrics&rft.issn=01674943&rft_id=info:doi/10.1016%2Fj.archger.2011.02.017 LA - English DB - Physical Education Index N1 - Date revised - 2013-11-01 N1 - Last updated - 2013-11-15 N1 - SubjectsTermNotLitGenreText - Depression; Body mass; Analysis; Geriatrics; Gerontology; Stress; Health; Exercise; Lifestyle DO - http://dx.doi.org/10.1016/j.archger.2011.02.017 ER - TY - JOUR T1 - Antiangiogenic and antitumor activity of LP-261, a novel oral tubulin binding agent, alone and in combination with bevacizumab AN - 1399903256; 17318497 AB - LP-261 is a novel tubulin targeting anticancer agent that binds at the colchicine site on tubulin, inducing G2/M arrest. Screening in the NCI60 cancer cell lines resulted in a mean GI50 of approximately 100 nM. Here, we report the results of testing in multiple mouse xenograft models and angiogenesis assays, along with bioavailability studies. To determine the antiangiogenic activity of LP-261, both in vitro and ex vivo experiments were performed. Human Umbilical Vein Endothelial cells (HUVECs) were incubated with LP-261 at 50 nM to 10 mu M. LP-261 was also tested in a rat aortic ring assay, from 20 nM to 10 mu M. Multiple mouse xenograft studies were performed to assess in vivo antitumor activity. LP-261 was tested as a single agent in colon adenocarcinoma (SW620) and prostate cancer (LNCaP and PC3) xenografts, evaluating several different dosing schedules. LP-261 was also used in combination with bevacizumab in the SW620 xenograft model. LP-261 also exhibited high oral bioavailability and apparent lack of efflux by intestinal transporters such as ABCB1. LP-261 is a very potent inhibitor of angiogenesis, preventing microvessel outgrowth in the rat aortic ring assay and HUVEC cell proliferation at nanomolar concentrations. Complete inhibition of tumor growth was achieved in the PC3 xenograft model and shown to be schedule dependent. Excellent inhibition of tumor growth in the SW620 model was observed, comparable with paclitaxel. Combining oral, low dose LP-261 with bevacizumab led to significantly improved tumor inhibition. Oral LP-261 is very effective at inhibiting tumor growth in multiple mouse xenograft models and is well tolerated. JF - Investigational New Drugs AU - Gardner, Erin R AU - Kelly, Martha AU - Springman, Eric AU - Lee, Kyoung-jin AU - Li, Haiqing AU - Moore, William AU - Figg, William D AD - Clinical Pharmacology Program, SAIC-Frederick, NCI-Frederick, Frederick, MD, 21702, USA, wdfigg@helix.nih.gov Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 90 EP - 97 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 30 IS - 1 SN - 0167-6997, 0167-6997 KW - Biotechnology and Bioengineering Abstracts KW - Aorta KW - Angiogenesis KW - Animal models KW - Bevacizumab KW - Tumors KW - umbilical vein KW - Antitumor agents KW - Endothelial cells KW - Tumor cell lines KW - Prostate cancer KW - Colon KW - Paclitaxel KW - Intestine KW - Colchicine KW - Xenografts KW - Cell proliferation KW - Tubulin KW - Adenocarcinoma KW - Antitumor activity KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1399903256?accountid=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=Investigational+New+Drugs&rft.atitle=Antiangiogenic+and+antitumor+activity+of+LP-261%2C+a+novel+oral+tubulin+binding+agent%2C+alone+and+in+combination+with+bevacizumab&rft.au=Gardner%2C+Erin+R%3BKelly%2C+Martha%3BSpringman%2C+Eric%3BLee%2C+Kyoung-jin%3BLi%2C+Haiqing%3BMoore%2C+William%3BFigg%2C+William+D&rft.aulast=Gardner&rft.aufirst=Erin&rft.date=2012-02-01&rft.volume=30&rft.issue=1&rft.spage=90&rft.isbn=&rft.btitle=&rft.title=Investigational+New+Drugs&rft.issn=01676997&rft_id=info:doi/10.1007%2Fs10637-010-9520-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-07-01 N1 - Last updated - 2013-07-15 N1 - SubjectsTermNotLitGenreText - Aorta; Animal models; Angiogenesis; Tumors; Bevacizumab; umbilical vein; Antitumor agents; Endothelial cells; Tumor cell lines; Prostate cancer; Colon; Paclitaxel; Intestine; Colchicine; Xenografts; Adenocarcinoma; Tubulin; Cell proliferation; Antitumor activity DO - http://dx.doi.org/10.1007/s10637-010-9520-5 ER - TY - CPAPER T1 - The Effect of Minocycline on the HARM MRI Marker of Blood-CSF Barrier Opening After Transient MCAO in SHR Rats T2 - 2012 International Stroke Conference AN - 1313113688; 6186881 JF - 2012 International Stroke Conference AU - Warach, Steven AU - Henning, Erica AU - Leoni, Renata AU - Arai, Allison AU - Latour, Lawrence AU - Silva, Afonso Y1 - 2012/02/01/ PY - 2012 DA - 2012 Feb 01 KW - Rats KW - Barriers KW - Magnetic resonance imaging KW - Minocycline UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313113688?accountid=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+International+Stroke+Conference&rft.atitle=The+Effect+of+Minocycline+on+the+HARM+MRI+Marker+of+Blood-CSF+Barrier+Opening+After+Transient+MCAO+in+SHR+Rats&rft.au=Warach%2C+Steven%3BHenning%2C+Erica%3BLeoni%2C+Renata%3BArai%2C+Allison%3BLatour%2C+Lawrence%3BSilva%2C+Afonso&rft.aulast=Warach&rft.aufirst=Steven&rft.date=2012-02-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+International+Stroke+Conference&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/Plan/browse.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Disappearance Of The Acute Diffusion Weighted Imaging Lesion After Treatment With tPA T2 - 2012 International Stroke Conference AN - 1313104429; 6186747 JF - 2012 International Stroke Conference AU - Freeman, Jason AU - Luby, Maire AU - Warach, Steven Y1 - 2012/02/01/ PY - 2012 DA - 2012 Feb 01 KW - Lesions KW - Diffusion KW - Imaging techniques KW - TPA UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313104429?accountid=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+International+Stroke+Conference&rft.atitle=Disappearance+Of+The+Acute+Diffusion+Weighted+Imaging+Lesion+After+Treatment+With+tPA&rft.au=Freeman%2C+Jason%3BLuby%2C+Maire%3BWarach%2C+Steven&rft.aulast=Freeman&rft.aufirst=Jason&rft.date=2012-02-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+International+Stroke+Conference&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/Plan/browse.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Approximate Volume Using "XYZ/2" Is Equivalent to Planimetric Volume Mismatch Evaluation T2 - 2012 International Stroke Conference AN - 1313087148; 6186126 JF - 2012 International Stroke Conference AU - Luby, Marie AU - Hong, Jennifer AU - Merino, Jose AU - Lynch, John AU - Hsia, Amie AU - Magadan, Alejandro AU - Song, Shlee AU - Latour, Lawrence AU - Warach, Steven Y1 - 2012/02/01/ PY - 2012 DA - 2012 Feb 01 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313087148?accountid=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+International+Stroke+Conference&rft.atitle=Approximate+Volume+Using+%22XYZ%2F2%22+Is+Equivalent+to+Planimetric+Volume+Mismatch+Evaluation&rft.au=Luby%2C+Marie%3BHong%2C+Jennifer%3BMerino%2C+Jose%3BLynch%2C+John%3BHsia%2C+Amie%3BMagadan%2C+Alejandro%3BSong%2C+Shlee%3BLatour%2C+Lawrence%3BWarach%2C+Steven&rft.aulast=Luby&rft.aufirst=Marie&rft.date=2012-02-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+International+Stroke+Conference&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/Browse.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Pretreatment MRI Markers May Predict Hemorrhagic Transformation in Patients Treated with IV tPA T2 - 2012 International Stroke Conference AN - 1313074922; 6186142 JF - 2012 International Stroke Conference AU - Luby, Marie AU - Boparai, Sundeep AU - Warach, Steven Y1 - 2012/02/01/ PY - 2012 DA - 2012 Feb 01 KW - TPA KW - Magnetic resonance imaging KW - Hemorrhage KW - Transformation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313074922?accountid=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+International+Stroke+Conference&rft.atitle=Pretreatment+MRI+Markers+May+Predict+Hemorrhagic+Transformation+in+Patients+Treated+with+IV+tPA&rft.au=Luby%2C+Marie%3BBoparai%2C+Sundeep%3BWarach%2C+Steven&rft.aulast=Luby&rft.aufirst=Marie&rft.date=2012-02-01&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+International+Stroke+Conference&rft.issn=&rft_id=info:doi/ L2 - http://www.abstractsonline.com/plan/Browse.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Time of concentration: a paradox in modern hydrology AN - 1034825728; 17032723 AB - The time of concentration is a primary parameter for a variety of modern hydrological models adopted in professional and scientific communities. Nevertheless, a universally accepted working definition of this parameter is currently lacking and several definitions can be found in the technical literature along with related estimation procedures. This study brings to light the inherent variability of these definitions through the empirical analysis of four small basins. These case studies demonstrate that available approaches for the estimation of the time of concentration may yield numerical predictions that differ from each other by up to 500%. JF - Hydrological Sciences Journal/Journal des Sciences Hydrologiques AU - Grimaldi, S AU - Petroselli, A AU - Tauro, F AU - Porfiri, M AD - Dipartimento per l'Innovazione nei sistemi Biologici, Agroalimentari e Forestali (DIBAF Department), University of Tuscia, Via San Camillo De Lellis, Viterbo, Italy,Honors Center of Italian Universities (H2CU), Sapienza University of Rome, Roma, Italy,Department of Mechanical and Aerospace Engineering, Polytechnic Institute of New York University, Six MetroTech Center, Brooklyn, NY, USA Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 217 EP - 228 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 57 IS - 2 SN - 0262-6667, 0262-6667 KW - Water Resources Abstracts; ASFA 2: Ocean Technology Policy & Non-Living Resources; Aqualine Abstracts; Meteorological & Geoastrophysical Abstracts; Environment Abstracts KW - Prediction KW - Variability KW - Hydrologic analysis KW - Case Studies KW - Concentration Time KW - Basins KW - Yield KW - Hydrologic Models KW - Case studies KW - Hydrology KW - Experts KW - SW 5010:Network design KW - AQ 00006:Sewage KW - M2 556:General (556) KW - Q2 09162:Methods and instruments KW - ENA 07:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1034825728?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hydrological+Sciences+Journal%2FJournal+des+Sciences+Hydrologiques&rft.atitle=Time+of+concentration%3A+a+paradox+in+modern+hydrology&rft.au=Grimaldi%2C+S%3BPetroselli%2C+A%3BTauro%2C+F%3BPorfiri%2C+M&rft.aulast=Grimaldi&rft.aufirst=S&rft.date=2012-02-01&rft.volume=57&rft.issue=2&rft.spage=217&rft.isbn=&rft.btitle=&rft.title=Hydrological+Sciences+Journal%2FJournal+des+Sciences+Hydrologiques&rft.issn=02626667&rft_id=info:doi/10.1080%2F02626667.2011.644244 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-08-01 N1 - Last updated - 2014-05-05 N1 - SubjectsTermNotLitGenreText - Hydrology; Experts; Hydrologic analysis; Prediction; Case studies; Basins; Yield; Variability; Hydrologic Models; Case Studies; Concentration Time DO - http://dx.doi.org/10.1080/02626667.2011.644244 ER - TY - JOUR T1 - A contextual approach to understanding breast cancer survivorship among Latinas AN - 1023095605; 201216261 AB - Objectives The purpose of this review is to describe the empirical literature on the health-related quality of life (HRQOL) in Latina breast cancer survivors by exploring the social determinants of health. In framing the key domains of survivors' quality of life within a ecological-contextual model that evaluates individual and societal contributions to health outcomes, we provide a comprehensive landscape of the diverse factors constituting Latina survivors' lived experiences and their resultant quality of life outcomes. Methods We retrieved 244 studies via search engines and reference lists, of which 37 studies met the inclusion criteria. Results Findings document the importance of the social determinants of HRQOL, with studies documenting ecological and contextual factors accounting for significant variance in HRQOL outcomes. Our review identifies a dearth of research examining community-, institutional-, and policy-level factors, such as health care access, legal and immigration factors, physical and built environments, and health care affordability and policies affecting Latina breast cancer survivors' HRQOL. Conclusions Overall research on Latina breast cancer survivorship is sparse, with even greater underrepresentation within longitudinal and intervention studies. Results highlight a need for clear documentation of the comprehensive care needs of underserved cancer survivors and interventions considering integrated systems of care to address the medical and ecological factors known to impact the HRQOL of breast cancer survivors. [Copyright John Wiley and Sons, Ltd.] JF - Psycho-Oncology AU - Lopez-Class, Maria AU - Gomez-Duarte, Jessika AU - Graves, Kristi AU - Ashing-Giwa, Kimlin AD - Eunice Kennedy Shriver National, Institute of Child Health and Human Development 6100 Executive Blvd., Room 5C01, Bethesda, MD 20892, USA Phone: 301-443-4480, Fax: 301-480-1222 Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 115 EP - 124 PB - John Wiley, Chichester UK VL - 21 IS - 2 SN - 1057-9249, 1057-9249 KW - quality of life, Latinas, contextual-ecological perspective, breast cancer survivors KW - Latin American people KW - Health care KW - Breast cancer KW - Health status KW - Survivors KW - Quality of life KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1023095605?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aassia&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Psycho-Oncology&rft.atitle=A+contextual+approach+to+understanding+breast+cancer+survivorship+among+Latinas&rft.au=Lopez-Class%2C+Maria%3BGomez-Duarte%2C+Jessika%3BGraves%2C+Kristi%3BAshing-Giwa%2C+Kimlin&rft.aulast=Lopez-Class&rft.aufirst=Maria&rft.date=2012-02-01&rft.volume=21&rft.issue=2&rft.spage=115&rft.isbn=&rft.btitle=&rft.title=Psycho-Oncology&rft.issn=10579249&rft_id=info:doi/10.1002%2Fpon.1998 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-07-01 N1 - Last updated - 2016-09-27 N1 - CODEN - POJCEE N1 - SubjectsTermNotLitGenreText - Quality of life; Health status; Breast cancer; Survivors; Latin American people; Health care DO - http://dx.doi.org/10.1002/pon.1998 ER - TY - JOUR T1 - Empirically derived subtypes of lifetime anxiety disorders: Developmental and clinical correlates in U.S. Adolescents. AN - 1023090559; 201213196 AB - Objective: The current study examined the sex- and age-specific structure and comorbidity of lifetime anxiety disorders among U.S. adolescents. Method: The sample consisted of 2,539 adolescents (1,505 females and 1,034 males) from the National Comorbidity Survey-Adolescent Supplement who met criteria for Diagnostic and Statistical Manual of Mental Disorders (4th ed., text rev. [DSM-IV-TR]) lifetime anxiety disorders (American Psychiatric Association, 2000). Adolescents ranged in age from 13 to 18 years (M = 15.2 years, SE = 0.08 years) and were 39% non-White. Multiple-group latent class analysis was conducted by adolescent sex and age to identify subgroups of adolescents with similar anxiety disorder profiles. Developmental and clinical correlates of empirically derived classes were also examined to assess the nomological validity of identified subgroups. Results: A 7-class solution provided the best fit to the data, with classes defined primarily by one rather than multiple anxiety disorders. Results also indicated that classes displayed similar diagnostic profiles across age, but varied by sex. Classes characterized by multiple anxiety disorders were consistently associated with a greater degree of persistence, clinical severity, impairment, and comorbidity with other DSM-IV-TR psychiatric disorders. Conclusions: The presentation of lifetime anxiety disorders among adolescents and the observation of unique correlates of specific classes provide initial evidence for the utility of individual DSM-IV-TR anxiety disorder categories. Although findings of the present study should be considered preliminary, results emphasize the potential value of early intervention and gender-specific conceptualization and treatment of anxiety disorders. [Copyright American Psychological Association] JF - Journal of Consulting and Clinical Psychology AU - Burstein, Marcy AU - Georgiades, Katholiki AU - Lamers, Femke AU - Swanson, Sonja A AU - Cui, Lihong AU - He, Jian-Ping AU - Avenevoli, Shelli AU - Merikangas, Kathleen R AD - Genetic Epidemiology Research Branch, National Institute of Mental Health marcy.burstein@nih.gov Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 102 EP - 115 PB - American Psychological Association, Washington DC VL - 80 IS - 1 SN - 0022-006X, 0022-006X KW - Adolescent Development KW - Anxiety Disorders KW - Comorbidity KW - Subtypes (Disorders) KW - Anxiety KW - Onset (Disorders) KW - Surveys KW - Anxiety disorders KW - Latent class analysis KW - Psychiatric disorders KW - Age differences KW - Adolescents KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1023090559?accountid=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+Consulting+and+Clinical+Psychology&rft.atitle=Empirically+derived+subtypes+of+lifetime+anxiety+disorders%3A+Developmental+and+clinical+correlates+in+U.S.+Adolescents.&rft.au=Burstein%2C+Marcy%3BGeorgiades%2C+Katholiki%3BLamers%2C+Femke%3BSwanson%2C+Sonja+A%3BCui%2C+Lihong%3BHe%2C+Jian-Ping%3BAvenevoli%2C+Shelli%3BMerikangas%2C+Kathleen+R&rft.aulast=Burstein&rft.aufirst=Marcy&rft.date=2012-02-01&rft.volume=80&rft.issue=1&rft.spage=102&rft.isbn=&rft.btitle=&rft.title=Journal+of+Consulting+and+Clinical+Psychology&rft.issn=0022006X&rft_id=info:doi/10.1037%2Fa0026069 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-07-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JCLPBC N1 - SubjectsTermNotLitGenreText - Anxiety disorders; Adolescents; Comorbidity; Psychiatric disorders; Age differences; Latent class analysis DO - http://dx.doi.org/10.1037/a0026069 ER - TY - JOUR T1 - A Path Analysis of a Randomized Promotora de Salud Cardiovascular Disease-Prevention Trial Among At-Risk Hispanic Adults AN - 1022560873; 16309366 AB - This study assessed effectiveness of an educational community intervention taught by promotoras de salud in reducing cardiovascular disease (CVD) risk among Hispanics using a structural equation modeling (SEM) approach. Model development was guided by a social ecological framework proposing CVD risk reduction through improvement of protective health behaviors, health beliefs, contextual and social factors. Participants were 328 Hispanic adults with at least one CVD risk factor. SEM analyses assessed direct and indirect effects of intervention participation on CVD risk (Framingham score) and latent variables nutrition intake and health beliefs. The model fit was adequate (root mean square error of approximation = .056 [90% confidence interval = .040, .072], comparative fit index = .967, normed fit index = .938, nonnormed fit index = .947). Intervention participation was associated with improved nutritional consumption, but not lower CVD risk. Stronger health beliefs predicted healthier nutritional habits. This project provided evidence for the adequacy of a conceptual framework that can be used to elicit new pathways toward CVD risk reduction among at-risk Hispanic populations. JF - Health Education & Behavior AU - de Heer, Hendrik Dirk AU - Balcazar, Hector G AU - Castro, Felipe AU - Schulz, Leslie AD - National Human Genome Research Institute, Bethesda, MD, USA Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 77 EP - 86 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 39 IS - 1 SN - 1090-1981, 1090-1981 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Cardiovascular diseases KW - Education KW - Ethnic groups KW - Intervention KW - Nutrition KW - Risk factors KW - Risk reduction KW - R2 23050:Environment KW - H 0500:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1022560873?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Health+Education+%26+Behavior&rft.atitle=A+Path+Analysis+of+a+Randomized+Promotora+de+Salud+Cardiovascular+Disease-Prevention+Trial+Among+At-Risk+Hispanic+Adults&rft.au=de+Heer%2C+Hendrik+Dirk%3BBalcazar%2C+Hector+G%3BCastro%2C+Felipe%3BSchulz%2C+Leslie&rft.aulast=de+Heer&rft.aufirst=Hendrik&rft.date=2012-02-01&rft.volume=39&rft.issue=1&rft.spage=77&rft.isbn=&rft.btitle=&rft.title=Health+Education+%26+Behavior&rft.issn=10901981&rft_id=info:doi/10.1177%2F1090198111408720 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Number of references - 40 N1 - Last updated - 2012-06-29 N1 - SubjectsTermNotLitGenreText - Education; Risk factors; Intervention; Cardiovascular diseases; Risk reduction; Nutrition; Ethnic groups DO - http://dx.doi.org/10.1177/1090198111408720 ER - TY - JOUR T1 - Methicillin-resistant Staphylococcus aureus infection is associated with increased mortality AN - 1020842435; 16598182 AB - Evaluation of: Hanberger H, Walther S, Leone M et al. Increased mortality associated with meticillin-resistant Staphylococcus aureus (MRSA) infection in the intensive care unit: results from the EPIC II study. Int. J. Antimicrob. Agents 38(4), 331-335 (2011). Methicillin resistance is a widespread and major source of treatment complication in Staphylococcus aureus infections. Whether infections with methicillin-resistant S. aureus are associated with a worse clinical outcome, such as higher mortality, has remained controversial. Analyzing data from a large, global multicenter study, Hanberger et al. demonstrate that methicillin-resistant S. aureus infections are associated with approximately 50% higher mortality in the intensive care unit and significantly more frequent among critically ill patients than infections with methicillin-susceptible S. aureus. These findings call for the implementation or continuation of active methicillin-resistant S. aureus surveillance measures. JF - Future Microbiology AU - Otto, Michael AD - Pathogen Molecular Genetics Section, Laboratory of Human Bacterial Pathogenesis, National Institute of Allergy & Infectious Diseases, NIH, Bethesda, MD, USA., motto@niaid.nih.gov Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 189 EP - 191 PB - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom VL - 7 IS - 2 SN - 1746-0913, 1746-0913 KW - Microbiology Abstracts B: Bacteriology KW - Data processing KW - Drug resistance KW - Infection KW - Intensive care units KW - Methicillin KW - Mortality KW - Staphylococcus aureus KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020842435?accountid=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=Future+Microbiology&rft.atitle=Methicillin-resistant+Staphylococcus+aureus+infection+is+associated+with+increased+mortality&rft.au=Otto%2C+Michael&rft.aulast=Otto&rft.aufirst=Michael&rft.date=2012-02-01&rft.volume=7&rft.issue=2&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=Future+Microbiology&rft.issn=17460913&rft_id=info:doi/10.2217%2Ffmb.11.156 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Number of references - 14 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Mortality; Methicillin; Data processing; Intensive care units; Drug resistance; Infection; Staphylococcus aureus DO - http://dx.doi.org/10.2217/fmb.11.156 ER - TY - JOUR T1 - Dendrimer-induced leukocyte procoagulant activity depends on particle size and surface charge AN - 1017979809; 16751408 AB - Aims: Thrombogenicity associated with the induction of leukocyte procoagulant activity (PCA) is a common complication in sepsis and cancer. Since nanoparticles are increasingly used for drug delivery, their interaction with coagulation systems is an important part of the safety assessment. The purpose of this study was to investigate the effects of nanoparticle physicochemical properties on leukocyte PCA, and to get insight into the mechanism of PCA induction. Materials & Methods: A total of 12 formulations of polyamidoamine (PAMAM) dendrimers, varying in size and surface charge, were studied in vitro using recalcification time assay. Results: Irrespective of their size, anionic and neutral dendrimers did not induce leukocyte PCA in vitro. Cationic particles induced PCA in a size- and charge-dependent manner. The mechanism of PCA induction was similar to that of doxorubicin. Cationic dendrimers were also found to exacerbate endotoxin-induced PCA. Conclusion: PAMAM dendrimer-induced leukocyte PCA depends on particle size, charge and density of surface groups. JF - Nanomedicine AU - Dobrovolskaia, Marina A AU - Patri, Anil K AU - Potter, Timothy M AU - Rodriguez, Jamie C AU - Hall, Jennifer B AU - McNeil, Scott E AD - Nanotechnology Characterization Lab SAIC-Frederick Inc., NCI-Frederick 1050 Boyles St., Bldg. 469 Frederick MD, 21702, USA., marina@mail.nih.gov Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 245 EP - 256 PB - Future Science Group (FSG), Unitec House, 2 Albert Place London N3 1QB United Kingdom VL - 7 IS - 2 SN - 1743-5889, 1743-5889 KW - Immunology Abstracts; Biotechnology and Bioengineering Abstracts KW - Cancer KW - Coagulation KW - Doxorubicin KW - Drug delivery KW - Leukocytes KW - Particle size KW - Physicochemical properties KW - Sepsis KW - Surface charge KW - nanoparticles KW - nanotechnology KW - polyamidoamines KW - F 06915:Cancer Immunology KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1017979809?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nanomedicine&rft.atitle=Dendrimer-induced+leukocyte+procoagulant+activity+depends+on+particle+size+and+surface+charge&rft.au=Dobrovolskaia%2C+Marina+A%3BPatri%2C+Anil+K%3BPotter%2C+Timothy+M%3BRodriguez%2C+Jamie+C%3BHall%2C+Jennifer+B%3BMcNeil%2C+Scott+E&rft.aulast=Dobrovolskaia&rft.aufirst=Marina&rft.date=2012-02-01&rft.volume=7&rft.issue=2&rft.spage=245&rft.isbn=&rft.btitle=&rft.title=Nanomedicine&rft.issn=17435889&rft_id=info:doi/10.2217%2Fnnm.11.105 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Number of references - 55 N1 - Last updated - 2012-06-29 N1 - SubjectsTermNotLitGenreText - Particle size; Drug delivery; Sepsis; Coagulation; Physicochemical properties; polyamidoamines; Leukocytes; Surface charge; nanoparticles; Doxorubicin; Cancer; nanotechnology DO - http://dx.doi.org/10.2217/nnm.11.105 ER - TY - JOUR T1 - Enhanced Histopathology of the Immune System: A Review and Update AN - 1017964019; 16590123 AB - Enhanced histopathology (EH) of the immune system is a tool that the pathologist can use to assist in the detection of lymphoid organ lesions when evaluating a suspected immunomodulatory test article within a subchronic study or as a component of a more comprehensive, tiered approach to immunotoxicity testing. There are three primary points to consider when performing EH: (1) each lymphoid organ has separate compartments that support specific immune functions; (2) these compartments should be evaluated individually; and (3) semiquantitative descriptive rather than interpretive terminology should be used to characterize any changes. Enhanced histopathology is a screening tool that should be used in conjunction with study data including clinical signs, gross changes, body weight, spleen and thymus weights, other organ or tissue changes, and clinical pathology. Points to consider include appropriate tissue collection, sectioning, and staining; lesion grading; and diligent comparison with concurrent controls. The value of EH of lymphoid organs is to aid in the identification of target cell type, changes in cell production and cell death, changes in cellular trafficking and recirculation, and determination of mechanism of action. JF - Toxicologic Pathology AU - Elmore, Susan A AD - National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA, elmore@niehs.nih.gov Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 148 EP - 156 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 40 IS - 2 SN - 0192-6233, 0192-6233 KW - Immunology Abstracts; Toxicology Abstracts KW - Body weight KW - Cell death KW - Data processing KW - Immune response KW - Immunomodulation KW - Immunotoxicity KW - Reviews KW - Sectioning KW - Spleen KW - Thymus KW - F 06955:Immunomodulation & Immunopharmacology KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1017964019?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Enhanced+Histopathology+of+the+Immune+System%3A+A+Review+and+Update&rft.au=Elmore%2C+Susan+A&rft.aulast=Elmore&rft.aufirst=Susan&rft.date=2012-02-01&rft.volume=40&rft.issue=2&rft.spage=148&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623311427571 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Number of references - 28 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Immunotoxicity; Cell death; Data processing; Body weight; Reviews; Sectioning; Thymus; Spleen; Immune response; Immunomodulation DO - http://dx.doi.org/10.1177/0192623311427571 ER - TY - JOUR T1 - Proceedings of the 2011 National Toxicology Program Satellite Symposium AN - 1017961286; 16590129 AB - The 2011 annual National Toxicology Program (NTP) Satellite Symposium, entitled "Pathology Potpourri," was held in Denver, Colorado in advance of the Society of Toxicologic Pathology's 30th Annual Meeting. The goal of the NTP Symposium is to present current diagnostic pathology or nomenclature issues to the Toxicologic Pathology community. This article presents summaries of the speakers' presentations, including diagnostic or nomenclature issues that were presented, along with select images that were used for audience voting or discussion. Some lesions and topics covered during the symposium include: proliferative lesions from various fish species including ameloblastoma, gas gland hyperplasia, nodular regenerative hepatocellular hyperplasia, and malignant granulosa cell tumor; spontaneous cystic hyperplasia in the stomach of CD1 mice and histiocytic aggregates in the duodenal villous tips of treated mice; an olfactory neuroblastoma in a cynomolgus monkey; various rodent skin lesions, including follicular parakeratotic hyperkeratosis, adnexal degeneration, and epithelial intracytoplasmic accumulations; oligodendroglioma and microgliomas in rats; a diagnostically challenging microcytic, hypochromic, responsive anemia in rats; a review of microcytes and microcytosis; nasal lesions associated with green tea extract and Ginkgo biloba in rats; corneal dystrophy in Dutch belted rabbits; valvulopathy in rats; and lymphoproliferative disease in a cynomolgus monkey. JF - Toxicologic Pathology AU - Boorman, Gary AU - Crabbs, Torrie A AU - Kolenda-Roberts, Holly AU - Latimer, Ken AU - Miller, Andrew D AU - Muravnick, Kathleen B AU - Nyska, Abraham AU - Ochoa, Ricardo AU - Pardo, Ingrid D AU - Ramot, Yuval AU - Rao, Deepa B AU - Schuh, JoAnn AU - Suttie, Andrew AU - Travlos, Greg S AU - Ward, Jerrold M AU - Wolf, Jeffrey C AU - Elmore, Susan A AD - Covance Laboratories, Inc., Chantilly, Virginia, USA, elmore@niehs.nih.gov7 Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 321 EP - 344 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 40 IS - 2 SN - 0192-6233, 0192-6233 KW - ASFA 3: Aquatic Pollution & Environmental Quality; Oceanic Abstracts KW - NTP Satellite Symposium KW - ameloblastoma KW - gas gland hyperplasia KW - stomach cystic hyperplasia KW - sodium dichromate dihydrate KW - olfactory neuroblastoma KW - cynomolgus monkey KW - adnexal degeneration KW - parakeratotic hyperkeratosis KW - oligodendroglioma KW - microglioma KW - microcytic hypochromic anemia KW - microcytosis KW - spherocytosis KW - poikilocytosis KW - green tea KW - Ginkgo biloba KW - corneal dystrophy KW - Dutch belted rabbit valvulitis KW - valvulopathy KW - post-transplant lymphoproliferative disease. KW - Pathology KW - Conferences KW - Animal physiology KW - Toxicity KW - Satellite sensing KW - USA, Colorado KW - Anaemia KW - USA, Colorado, Denver KW - Glands KW - Cynomolgus KW - Toxicology KW - Olfaction KW - O 4020:Pollution - Organisms/Ecology/Toxicology KW - Q5 08504:Effects on organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1017961286?accountid=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=Toxicologic+Pathology&rft.atitle=Proceedings+of+the+2011+National+Toxicology+Program+Satellite+Symposium&rft.au=Boorman%2C+Gary%3BCrabbs%2C+Torrie+A%3BKolenda-Roberts%2C+Holly%3BLatimer%2C+Ken%3BMiller%2C+Andrew+D%3BMuravnick%2C+Kathleen+B%3BNyska%2C+Abraham%3BOchoa%2C+Ricardo%3BPardo%2C+Ingrid+D%3BRamot%2C+Yuval%3BRao%2C+Deepa+B%3BSchuh%2C+JoAnn%3BSuttie%2C+Andrew%3BTravlos%2C+Greg+S%3BWard%2C+Jerrold+M%3BWolf%2C+Jeffrey+C%3BElmore%2C+Susan+A&rft.aulast=Boorman&rft.aufirst=Gary&rft.date=2012-02-01&rft.volume=40&rft.issue=2&rft.spage=321&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623311427713 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Number of references - 53 N1 - Last updated - 2016-09-29 N1 - SubjectsTermNotLitGenreText - Satellite sensing; Anaemia; Conferences; Pathology; Glands; Animal physiology; Toxicity; Olfaction; Toxicology; Ginkgo biloba; Cynomolgus; USA, Colorado; USA, Colorado, Denver DO - http://dx.doi.org/10.1177/0192623311427713 ER - TY - JOUR T1 - Analysis of the Sensory Profile in Children with Smith-Magenis Syndrome AN - 1010708160; 201208520 AB - This study systematically assessed sensory processing in 34 children, aged 3-14 years, with Smith-Magenis syndrome (SMS) using the Sensory Profile Caregiver Questionnaire. Scores for the SMS cohort were significantly different from scores of the national sample of children with and without disabilities in all Sensory Profile categories and quadrants (p < .001). No main effects of age or gender were found, but an interaction effect of age by gender was found in Modulation of Sensory Input Affecting Emotional Responses, in which older females presented with the lowest scores. A significant decline over time was found in the Seeking pattern, reflecting increased vulnerability (p < .05). Nonsignificant trends suggest more vulnerabilities for older versus younger children, especially older females. The neurobehavioral phenotype in children with SMS is expanded by this description of sensory processing. How children with SMS experience and respond to everyday sensations informs multidisciplinary team decisions. Adapted from the source document. JF - Physical and Occupational Therapy in Pediatrics AU - Hildenbrand, Hanna L AU - Smith, Ann C M AD - Department of Rehabilitation Medicine, National Institutes of Health, Bethesda, Maryland hhildenbrand@cc.nih.gov Y1 - 2012/02// PY - 2012 DA - February 2012 SP - 48 EP - 65 PB - Informa Healthcare, New York NY VL - 32 IS - 1 SN - 0194-2638, 0194-2638 KW - sensory processing, sensory profile caregiver questionnaire, sensory modulation, Smith-Magenis syndrome KW - Sensory processes KW - Gender KW - Vulnerability KW - Children KW - Age differences KW - Smith-Magenis syndrome KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1010708160?accountid=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=Physical+and+Occupational+Therapy+in+Pediatrics&rft.atitle=Analysis+of+the+Sensory+Profile+in+Children+with+Smith-Magenis+Syndrome&rft.au=Hildenbrand%2C+Hanna+L%3BSmith%2C+Ann+C+M&rft.aulast=Hildenbrand&rft.aufirst=Hanna&rft.date=2012-02-01&rft.volume=32&rft.issue=1&rft.spage=48&rft.isbn=&rft.btitle=&rft.title=Physical+and+Occupational+Therapy+in+Pediatrics&rft.issn=01942638&rft_id=info:doi/10.3109%2F01942638.2011.572152 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-05-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Children; Vulnerability; Sensory processes; Smith-Magenis syndrome; Gender; Age differences DO - http://dx.doi.org/10.3109/01942638.2011.572152 ER - TY - JOUR T1 - Twenty-five year results of the national cancer institute randomized breast conservation trial AN - 1008848156; 16398755 AB - Breast conservation therapy (BCT) consisting of lumpectomy and postoperative radiation has become an accepted alternative to mastectomy (MRM) for the treatment of early stage breast cancer. We currently report the 25 year outcomes of a single institution, prospective, randomized clinical trial at the National Cancer Institute. 237 women with pathologically confirmed invasive breast tumors 5 cm or less were accrued between 1979 and 1987 and randomized to receive either BCT or MRM. Overall survival was the primary endpoint. Patients with node positive disease were included and treated with doxorubicin and cyclophosphamide. Both arms received axillary dissection. BCT patients had radiation to the whole breast followed by a boost. At a median follow-up of 25.7 years, overall survival was 43.8% for the MRM group and 37.9% for BCT (P = 0.38). Although the cumulative incidence of a disease-free survival event was higher in BCT patients (29.0% MRM vs. 56.4% BCT, P = 0.0017), the additional treatment failures were primarily isolated ipsilateral breast tumor recurrences (IBTR's) requiring salvage mastectomy. 22.3% of BCT patients experienced an IBTR. Distant disease and second cancers were similar in both arms. After 25 years, long term survival between BCT and MRM continues to be similar in patients treated for early stage breast cancer. Patients receiving BCT may be at risk for additional treatment-related morbidity, which may occur as a late event. Further studies are required to delineate patients at higher risk for these events, and prolonged follow up should be encouraged after treatment for all women. JF - Breast Cancer Research and Treatment AU - Simone, Nicole L AU - Dan, Tu AU - Shih, Joanna AU - Smith, Sharon L AU - Sciuto, Linda AU - Lita, Elena AU - Lippman, Marc E AU - Glatstein, Eli AU - Swain, Sandra M AU - Danforth, David N AU - Camphausen, Kevin AD - Radiation Oncology Branch, National Cancer Institute/NIH, Building 10-CRC, Room B2-3500, 10 Center Drive, Bethesda, MD, 20892, USA, simonen@mail.nih.gov Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 197 EP - 203 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 132 IS - 1 SN - 0167-6806, 0167-6806 KW - Environment Abstracts KW - Breast cancer KW - Cancer KW - Conservation KW - Morbidity KW - clinical trials KW - survival KW - tumors KW - ENA 21:Wildlife UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008848156?accountid=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=Breast+Cancer+Research+and+Treatment&rft.atitle=Twenty-five+year+results+of+the+national+cancer+institute+randomized+breast+conservation+trial&rft.au=Simone%2C+Nicole+L%3BDan%2C+Tu%3BShih%2C+Joanna%3BSmith%2C+Sharon+L%3BSciuto%2C+Linda%3BLita%2C+Elena%3BLippman%2C+Marc+E%3BGlatstein%2C+Eli%3BSwain%2C+Sandra+M%3BDanforth%2C+David+N%3BCamphausen%2C+Kevin&rft.aulast=Simone&rft.aufirst=Nicole&rft.date=2012-02-01&rft.volume=132&rft.issue=1&rft.spage=197&rft.isbn=&rft.btitle=&rft.title=Breast+Cancer+Research+and+Treatment&rft.issn=01676806&rft_id=info:doi/10.1007%2Fs10549-011-1867-6 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-05-18 N1 - SubjectsTermNotLitGenreText - Conservation; Breast cancer; tumors; clinical trials; survival; Morbidity; Cancer DO - http://dx.doi.org/10.1007/s10549-011-1867-6 ER - TY - JOUR T1 - Variation in the risk of radiation-related contralateral breast cancer by histology and estrogen receptor expression in SEER AN - 1008830757; 16378717 AB - Radiation exposure, particularly at a young age, is an established cause of breast cancer. It is not known whether radiation-related breast cancer risk varies by molecular subtype. We characterized the relative risk (RR) of contralateral breast cancer (CBC) related to radiotherapy by histology and estrogen receptor (ER) status of the CBC in five-year survivors in the Surveillance, Epidemiology, and End Results database using Poisson regression models adjusted for attained age and calendar year, age at and year of treatment, ER status of the first breast cancer, and disease stage. 205,316 female breast cancer survivors were followed for an average of 10 years from 1973 until 2007, during which time 6924 women developed a subsequent primary invasive breast cancer in the contralateral breast. The overall RR (and 95% confidence interval (CI)) of radiotherapy-related CBC was 1.11 (1.05-1.16). There was no heterogeneity in risk according to histology of the CBC (P > 0.50) for all ages or young age at exposure, but case numbers were small for subtypes other than ductal and lobular carcinomas. Information on ER status was available from 1990 onwards for 3546 CBC cases, of which 2597 (73%) were ER+ and 949 (27%) were ER-. The RRs were 1.10 (1.02-1.19) for ER+ CBC and 1.19 (1.04-1.35) for ER- CBC (P sub(difference) = 0.33). Among women treated age <35 years, radiation-related risk of CBC was non-significantly elevated for ER- (RR = 1.38, 95% CI: 0.96-1.97) but not for ER+ tumors (RR = 0.80, 95% CI: 0.47-1.35) (P sub(difference) = 0.09). We did not find clear evidence that radiation-related risk varies by histology or ER status, but our findings, which were the first to examine this question, were suggestive of possible differences by ER status that may merit further investigation. JF - Breast Cancer Research and Treatment AU - Neta, Gila AU - Anderson, William F AU - Gilbert, Ethel AU - Berrington, Amy AD - Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 6120 Executive Blvd, Bethesda, MD, 20852, USA, netagil@mail.nih.gov Y1 - 2012/02// PY - 2012 DA - Feb 2012 SP - 1021 EP - 1027 PB - Springer Science+Business Media, Van Godewijckstraat 30 Dordrecht 3311 GX Netherlands VL - 131 IS - 3 SN - 0167-6806, 0167-6806 KW - Risk Abstracts; Environment Abstracts KW - Health risks KW - Age KW - Estrogens KW - Histology KW - Breast cancer KW - Radiotherapy KW - tumors KW - Tumors KW - radiotherapy KW - Cancer KW - estrogens KW - R2 23060:Medical and environmental health KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008830757?accountid=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=Breast+Cancer+Research+and+Treatment&rft.atitle=Variation+in+the+risk+of+radiation-related+contralateral+breast+cancer+by+histology+and+estrogen+receptor+expression+in+SEER&rft.au=Neta%2C+Gila%3BAnderson%2C+William+F%3BGilbert%2C+Ethel%3BBerrington%2C+Amy&rft.aulast=Neta&rft.aufirst=Gila&rft.date=2012-02-01&rft.volume=131&rft.issue=3&rft.spage=1021&rft.isbn=&rft.btitle=&rft.title=Breast+Cancer+Research+and+Treatment&rft.issn=01676806&rft_id=info:doi/10.1007%2Fs10549-011-1820-8 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2013-11-15 N1 - SubjectsTermNotLitGenreText - Health risks; Estrogens; Age; Histology; Radiotherapy; Breast cancer; tumors; Tumors; radiotherapy; Cancer; estrogens DO - http://dx.doi.org/10.1007/s10549-011-1820-8 ER - TY - JOUR T1 - High efficiency human memory B cell assay and its application to studying Plasmodium falciparum-specific memory B cells in natural infections AN - 920797662; 16208680 AB - Memory B cells (MBCs) are a key component of long term humoral immunity to many human infectious diseases. Despite their importance, we know little about the generation or maintenance of antigen-(Ag)-specific MBCs in humans in response to infection. A frequently employed method for quantifying Ag-specific MBCs in human peripheral blood (Crotty et al., 2004) relies on the ability of MBCs but not naive B cells to differentiate into antibody secreting cells (ASCs) in response to polyclonal activators and Toll-like receptor agonists in vitro and the measurement of Ag-specific ASCs by ELISPOT assays. Here we report on studies to optimize the efficiency of this ELISPOT-based assay and to apply this assay to the detection of Plasmodium falciparum (Pf)-specific MBCs in adults living in a malaria endemic area where immunity to Pf is acquired through natural infection. We show that the addition of IL-10 to in vitro cultures of human peripheral blood mononuclear cells increased the efficiency of the assay from 10% to over 90% without increasing the ASC burst size and without any substantial increase in background from naive B cells or plasma cells (PCs). Using this assay we were able to quantify the frequency of Pf-specific MBCs in peripheral blood of adults living in a malaria endemic area. Thus, this highly efficient assay appears to be well suited to field studies of the generation and maintenance of MBCs where the volumes of blood obtainable are often limiting. JF - Journal of Immunological Methods AU - Weiss, Greta E AU - Ndungu, Francis M AU - McKittrick, Noah AU - Li, Shanping AU - Kimani, Domtila AU - Crompton, Peter D AU - Marsh, Kevin AU - Pierce, Susan K AD - Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852, USA, weiss@burnet.edu.au Y1 - 2012/01/31/ PY - 2012 DA - 2012 Jan 31 SP - 68 EP - 74 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 375 IS - 1-2 SN - 0022-1759, 0022-1759 KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts KW - Memory B cells KW - B cell ELISPOT KW - Plasmodium falciparum KW - Malaria KW - Parasites KW - Human diseases KW - Burst size KW - Immunological memory KW - Cell culture KW - Infection KW - Interleukin 10 KW - Public health KW - Immunity (humoral) KW - Peripheral blood mononuclear cells KW - Endemic species KW - Serological studies KW - Infectious diseases KW - Enzyme-linked immunosorbent assay KW - Lymphocytes B KW - Memory cells KW - Immunity KW - Polyclonal activators KW - Blood KW - Antibodies KW - Plasma cells KW - Toll-like receptors KW - K 03400:Human Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - F 06900:Methods KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920797662?accountid=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+Immunological+Methods&rft.atitle=High+efficiency+human+memory+B+cell+assay+and+its+application+to+studying+Plasmodium+falciparum-specific+memory+B+cells+in+natural+infections&rft.au=Weiss%2C+Greta+E%3BNdungu%2C+Francis+M%3BMcKittrick%2C+Noah%3BLi%2C+Shanping%3BKimani%2C+Domtila%3BCrompton%2C+Peter+D%3BMarsh%2C+Kevin%3BPierce%2C+Susan+K&rft.aulast=Weiss&rft.aufirst=Greta&rft.date=2012-01-31&rft.volume=375&rft.issue=1-2&rft.spage=68&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunological+Methods&rft.issn=00221759&rft_id=info:doi/10.1016%2Fj.jim.2011.09.006 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-02-01 N1 - Last updated - 2015-10-28 N1 - SubjectsTermNotLitGenreText - Parasites; Blood; Antibodies; Serological studies; Endemic species; Human diseases; Malaria; Immunity; Public health; Enzyme-linked immunosorbent assay; Burst size; Lymphocytes B; Immunological memory; Memory cells; Cell culture; Infection; Interleukin 10; Polyclonal activators; Immunity (humoral); Peripheral blood mononuclear cells; Infectious diseases; Plasma cells; Toll-like receptors; Plasmodium falciparum DO - http://dx.doi.org/10.1016/j.jim.2011.09.006 ER - TY - JOUR T1 - Meat consumption and the risk of incident distal colon and rectal adenoma. AN - 919649675; 22166801 AB - Most studies of meat and colorectal adenoma have investigated prevalent events from a single screening, thus limiting our understanding of the role of meat and meat-related exposures in early colorectal carcinogenesis. Among participants in the screening arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial who underwent baseline and follow-up sigmoidoscopy (n=17,072), we identified 1008 individuals with incident distal colorectal adenoma. We calculated odds ratios (ORs) and 95% confidence intervals (95% CIs) for associations between meat and meat-related components and incident distal colorectal adenoma using multivariate logistic regression. We observed suggestive positive associations for red meat, processed meat, haeme iron, and nitrate/nitrite with distal colorectal adenoma. Grilled meat (OR=1.56, 95% CI=1.04-2.36), well or very well-done meat (OR=1.59, 95% CI=1.05-2.43), 2-amino-1-methyl-6-phenyl-imidazo[4,5-b]pyridine (PhIP) (OR=1.75, 95% CI=1.17-2.64), benzo[a]pyrene (OR=1.53, 95% CI=1.06-2.20), and total mutagenic activity (OR=1.57, 95% CI=1.03-2.40) were positively associated with rectal adenoma. Total iron (diet and supplements) (OR=0.69, 95% CI=0.56-0.86) and iron from supplements (OR=0.65, 95% CI=0.44-0.97) were inversely associated with any distal colorectal adenoma. Our findings indicate that several meat-related components may be most relevant to early neoplasia in the rectum. In contrast, total iron and iron from supplements were inversely associated with any distal colorectal adenoma. JF - British journal of cancer AU - Ferrucci, L M AU - Sinha, R AU - Huang, W-Y AU - Berndt, S I AU - Katki, H A AU - Schoen, R E AU - Hayes, R B AU - Cross, A J AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA. Y1 - 2012/01/31/ PY - 2012 DA - 2012 Jan 31 SP - 608 EP - 616 VL - 106 IS - 3 KW - Index Medicus KW - Sigmoidoscopy KW - Colon -- pathology KW - Risk Factors KW - Humans KW - Incidence KW - Aged KW - Middle Aged KW - United States -- epidemiology KW - Male KW - Female KW - Meat KW - Adenoma -- epidemiology KW - Colorectal Neoplasms -- etiology KW - Adenoma -- etiology KW - Colorectal Neoplasms -- epidemiology KW - Colorectal Neoplasms -- prevention & control UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/919649675?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=British+journal+of+cancer&rft.atitle=Meat+consumption+and+the+risk+of+incident+distal+colon+and+rectal+adenoma.&rft.au=Ferrucci%2C+L+M%3BSinha%2C+R%3BHuang%2C+W-Y%3BBerndt%2C+S+I%3BKatki%2C+H+A%3BSchoen%2C+R+E%3BHayes%2C+R+B%3BCross%2C+A+J&rft.aulast=Ferrucci&rft.aufirst=L&rft.date=2012-01-31&rft.volume=106&rft.issue=3&rft.spage=608&rft.isbn=&rft.btitle=&rft.title=British+journal+of+cancer&rft.issn=1532-1827&rft_id=info:doi/10.1038%2Fbjc.2011.549 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-03-27 N1 - Date created - 2012-02-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Nutr Cancer. 2011;63(4):583-92 [21598178] Carcinogenesis. 2011 Feb;32(2):203-9 [21081473] Cancer Prev Res (Phila). 2011 Oct;4(10):1686-97 [21803984] Cancer Res. 1999 Nov 15;59(22):5704-9 [10582688] Cancer Epidemiol Biomarkers Prev. 2000 Jun;9(6):625-30 [10868699] Carcinogenesis. 2000 Oct;21(10):1909-15 [11023550] Control Clin Trials. 2000 Dec;21(6 Suppl):273S-309S [11189684] Cancer Epidemiol Biomarkers Prev. 2001 May;10(5):559-62 [11352869] Nutr Rev. 2001 May;59(5):140-8 [11396694] Jpn J Cancer Res. 2002 May;93(5):478-83 [12036442] Mutat Res. 2002 Aug 26;519(1-2):151-61 [12160900] Mutat Res. 2002 Sep 30;506-507:175-85 [12351157] Mutat Res. 2002 Sep 30;506-507:205-14 [12351160] Am J Epidemiol. 2003 Mar 1;157(5):434-45 [12615608] Cancer Res. 2003 May 15;63(10):2358-60 [12750250] J Natl Cancer Inst. 2004 Mar 3;96(5):403-7 [14996862] J Nutr. 2004 Apr;134(4):776-84 [15051825] Eur J Cancer Prev. 2004 Jun;13(3):159-64 [15167213] Carcinogenesis. 2004 Jul;25(7):1211-8 [14988221] J Nutr. 2004 Oct;134(10):2711-6 [15465771] Mutat Res. 1975 Dec;31(6):347-64 [768755] Int J Cancer. 1981;27(4):471-4 [7275353] Mutat Res. 1991 Mar-Apr;259(3-4):399-410 [2017219] Carcinogenesis. 1991 Aug;12(8):1503-6 [1860171] Int J Cancer. 1991 Oct 21;49(4):520-5 [1917152] J Natl Cancer Inst. 1992 Jan 15;84(2):91-8 [1310511] Int J Cancer. 1994 Feb 1;56(3):379-82 [8314326] Cancer Res. 1995 Oct 15;55(20):4516-9 [7553619] Am J Epidemiol. 1995 Oct 1;142(7):692-8 [7572938] Cancer Epidemiol Biomarkers Prev. 1996 Jul;5(7):503-7 [8827353] Am J Epidemiol. 1996 Dec 1;144(11):1005-14 [8942430] Cancer Epidemiol Biomarkers Prev. 1997 Dec;6(12):1029-32 [9419398] Carcinogenesis. 1998 Jan;19(1):117-24 [9472702] Food Chem Toxicol. 1998 Apr;36(4):279-87 [9651044] Food Chem Toxicol. 1998 Apr;36(4):289-97 [9651045] Cancer Epidemiol Biomarkers Prev. 1999 Jan;8(1):15-24 [9950235] Lancet. 1999 Feb 27;353(9154):703-7 [10073512] Int J Cancer. 1999 Mar 15;80(6):852-6 [10074917] Cancer Res. 1999 Sep 1;59(17):4320-4 [10485479] Cancer Lett. 1999 Sep 1;143(2):189-94 [10503902] J Natl Cancer Inst. 2005 Feb 2;97(3):232-3; author reply 233-4 [15687367] Carcinogenesis. 2005 Mar;26(3):637-42 [15579480] J Natl Cancer Inst. 2005 Jun 15;97(12):917-26 [15956653] Mol Nutr Food Res. 2005 Jul;49(7):648-55 [15986387] Cancer Epidemiol Biomarkers Prev. 2005 Aug;14(8):2030-4 [16103456] Cancer Res. 2005 Sep 1;65(17):8034-41 [16140978] Am J Gastroenterol. 2005 Dec;100(12):2789-95 [16393237] Int J Cancer. 2006 Jun 15;118(12):3147-52 [16425287] Cancer Epidemiol Biomarkers Prev. 2006 Apr;15(4):717-25 [16614114] Cancer Epidemiol Biomarkers Prev. 2006 Jun;15(6):1120-5 [16775169] Am J Epidemiol. 2006 Dec 1;164(11):1085-93 [16990408] Med Hypotheses. 2007;68(3):562-4 [17045417] Int J Cancer. 2007 Jul 1;121(1):136-42 [17354224] Carcinogenesis. 2007 Jun;28(6):1210-6 [17277235] Br J Cancer. 2007 Jul 2;97(1):118-22 [17551493] Carcinogenesis. 2007 Sep;28(9):2019-27 [17690112] Am J Clin Nutr. 2009 May;89(5):1418-24 [19261727] Am J Gastroenterol. 2009 May;104(5):1231-40 [19367270] Cancer Res. 2010 Mar 15;70(6):2406-14 [20215514] Cancer Prev Res (Phila). 2011 Sep;4(9):1465-75 [21685236] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1038/bjc.2011.549 ER - TY - JOUR T1 - Dietary fat intake and risk of ovarian cancer in the NIH-AARP Diet and Health Study AN - 1008831905; 16429843 AB - Background: Fat intake has been postulated to increase risk of ovarian cancer, but previous studies have reported inconsistent results. Methods: The NIH-AARP Diet and Health Study, a large prospective cohort, assessed diet using a food frequency questionnaire at baseline in 1995-1996. During an average of 9 years of follow-up, 695 ovarian cancer cases were ascertained through the state cancer registry database. The relative risks (RRs) and 95% confidence interval (CI) were estimated using a Cox proportional hazard model. Results: Women in the highest vs the lowest quintile of total fat intake had a 28% increased risk of ovarian cancer (RR sub(Q5 vs Q1)=1.28, 95% CI: 1.01-1.63). Fat intake from animal sources (RR sub(Q5 vs Q1)=1.30; 95% CI: 1.02-1.66), but not from plant sources, was positively associated with ovarian cancer risk. Saturated and monounsaturated fat intakes were not related to risk of ovarian cancer, but polyunsaturated fat intake showed a weak positive association. The association between total fat intake and ovarian cancer was stronger in women who were nulliparous or never used oral contraceptives. Conclusion: Fat intake, especially from animal sources, was related to an increased risk of ovarian cancer. The association may be modified by parity and oral contraceptive use, which warrants further investigation. JF - British Journal of Cancer AU - Blank, M M AU - Wentzensen, N AU - Murphy, M A AU - Hollenbeck, A AU - Park, Y AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 6120 Executive Boulevard, Rockville, MD 20852, USA Y1 - 2012/01/31/ PY - 2012 DA - 2012 Jan 31 SP - 596 EP - 602 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 106 IS - 3 SN - 0007-0920, 0007-0920 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Cancer KW - Diets KW - Ovarian carcinoma KW - Parity KW - contraceptives KW - ovarian carcinoma KW - parity 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/1008831905?accountid=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=Dietary+fat+intake+and+risk+of+ovarian+cancer+in+the+NIH-AARP+Diet+and+Health+Study&rft.au=Blank%2C+M+M%3BWentzensen%2C+N%3BMurphy%2C+M+A%3BHollenbeck%2C+A%3BPark%2C+Y&rft.aulast=Blank&rft.aufirst=M&rft.date=2012-01-31&rft.volume=106&rft.issue=3&rft.spage=596&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2011.572 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-08-10 N1 - SubjectsTermNotLitGenreText - Parity; Diets; parity; ovarian carcinoma; Ovarian carcinoma; Cancer; contraceptives DO - http://dx.doi.org/10.1038/bjc.2011.572 ER - TY - JOUR T1 - Blood leukocyte Alu and LINE-1 methylation and gastric cancer risk in the Shanghai Women's Health Study AN - 1008831795; 16429838 AB - Background: Recent data suggest a link between blood leukocyte DNA methylation, and cancer risk. However, reports on DNA methylation from a prospective study are unavailable for gastric cancer. Methods: We explored the association between methylation in pre-diagnostic blood leukocyte DNA and gastric cancer risk in a case-control study nested in the prospective Shanghai Women's Health Study cohort. Incident gastric cancer cases (n=192) and matched controls (n=384) were included in the study. Methylation of Alu and long interspersed nucleotide elements (LINE)-1 were evaluated using bisulphite pyrosequencing. Odds ratios (ORs) and 95% confidence intervals (CI) were calculated from logistic regression adjusting for potential confounders. Results: Alu methylation was inversely associated with gastric cancer risk, mainly among cases diagnosed one or more years after blood collection. After excluding cases diagnosed during the first year of follow-up, the ORs for the third, second, and first quartiles of Alu methylation compared with the highest quartile were 2.43 (1.43-4.13), 1.47(0.85-2.57), and 2.22 (1.28-3.84), respectively. This association appeared to be modified by dietary intake, particularly isoflavone. In contrast, LINE-1 methylation levels were not associated with gastric cancer risk. Conclusion: Evidence from this prospective study is consistent with the hypothesis that DNA hypomethylation in blood leukocytes may be related to cancer risk, including risk of gastric cancer. JF - British Journal of Cancer AU - Gao, Y AU - Baccarelli, A AU - Shu, X O AU - Ji, B-T AU - Yu, K AU - Tarantini, L AU - Yang, G AU - Li, H-L AU - Hou, L AU - Rothman, N AU - Zheng, W AU - Gao, Y-T AU - Chow, W-H AD - Genetic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, 6120 Executive Boulevard, Building. EPS/Room 7110, NIH/NCI, Bethesda, MD 20892-7236, USA Y1 - 2012/01/31/ PY - 2012 DA - 2012 Jan 31 SP - 585 EP - 591 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 106 IS - 3 SN - 0007-0920, 0007-0920 KW - Biochemistry Abstracts 2: Nucleic Acids; Immunology Abstracts; Health & Safety Science Abstracts; Risk Abstracts KW - Diets KW - Data processing KW - Leukocytes KW - Ingestion KW - Dietary intake KW - Cancer KW - Isoflavones KW - Blood KW - DNA KW - DNA methylation KW - Long interspersed nucleotide elements KW - China, People's Rep., Shanghai KW - Females KW - Gastric cancer KW - H 11000:Diseases/Injuries/Trauma KW - N 14820:DNA Metabolism & Structure KW - F 06915:Cancer Immunology KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008831795?accountid=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=Blood+leukocyte+Alu+and+LINE-1+methylation+and+gastric+cancer+risk+in+the+Shanghai+Women%27s+Health+Study&rft.au=Gao%2C+Y%3BBaccarelli%2C+A%3BShu%2C+X+O%3BJi%2C+B-T%3BYu%2C+K%3BTarantini%2C+L%3BYang%2C+G%3BLi%2C+H-L%3BHou%2C+L%3BRothman%2C+N%3BZheng%2C+W%3BGao%2C+Y-T%3BChow%2C+W-H&rft.aulast=Gao&rft.aufirst=Y&rft.date=2012-01-31&rft.volume=106&rft.issue=3&rft.spage=585&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2011.562 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-05-07 N1 - SubjectsTermNotLitGenreText - Blood; Data processing; Leukocytes; DNA methylation; Long interspersed nucleotide elements; Gastric cancer; Dietary intake; Isoflavones; Diets; DNA; Females; Ingestion; Cancer; China, People's Rep., Shanghai DO - http://dx.doi.org/10.1038/bjc.2011.562 ER - TY - CPAPER T1 - Bcl-3 Is A Regulator of Dendritic Cell Functions T2 - 10th Cytokines and Inflammation Conference AN - 1313110041; 6154682 JF - 10th Cytokines and Inflammation Conference AU - Tassi, Ilaria Y1 - 2012/01/30/ PY - 2012 DA - 2012 Jan 30 KW - Bcl-3 protein KW - Dendritic cells UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313110041?accountid=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=10th+Cytokines+and+Inflammation+Conference&rft.atitle=Bcl-3+Is+A+Regulator+of+Dendritic+Cell+Functions&rft.au=Tassi%2C+Ilaria&rft.aulast=Tassi&rft.aufirst=Ilaria&rft.date=2012-01-30&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=10th+Cytokines+and+Inflammation+Conference&rft.issn=&rft_id=info:doi/ L2 - http://www.gtcbio.com/index.php?option=com_conference&file=program&cn=10th%20Cytokines%20and%20Inflammation%20Conference&cid=51 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Oncogenic IL-7R Gain-of-function Mutations in Childhood T-ALL T2 - 10th Cytokines and Inflammation Conference AN - 1313003989; 6154689 JF - 10th Cytokines and Inflammation Conference AU - Durum, Scott Y1 - 2012/01/30/ PY - 2012 DA - 2012 Jan 30 KW - Mutation KW - Children KW - Acute lymphatic leukemia KW - Lymphocytes T UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313003989?accountid=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=10th+Cytokines+and+Inflammation+Conference&rft.atitle=Oncogenic+IL-7R+Gain-of-function+Mutations+in+Childhood+T-ALL&rft.au=Durum%2C+Scott&rft.aulast=Durum&rft.aufirst=Scott&rft.date=2012-01-30&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=10th+Cytokines+and+Inflammation+Conference&rft.issn=&rft_id=info:doi/ L2 - http://www.gtcbio.com/index.php?option=com_conference&file=program&cn=10th%20Cytokines%20and%20Inflammation%20Conference&cid=51 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Pineal Cell Biology: Past, Present and Future T2 - 2012 Gordon Research Conference on Pineal Cell Biology AN - 1313075885; 6128959 JF - 2012 Gordon Research Conference on Pineal Cell Biology AU - Klein, David Y1 - 2012/01/29/ PY - 2012 DA - 2012 Jan 29 KW - Pineal gland KW - Cytology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313075885?accountid=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+Gordon+Research+Conference+on+Pineal+Cell+Biology&rft.atitle=Pineal+Cell+Biology%3A+Past%2C+Present+and+Future&rft.au=Klein%2C+David&rft.aulast=Klein&rft.aufirst=David&rft.date=2012-01-29&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Gordon+Research+Conference+on+Pineal+Cell+Biology&rft.issn=&rft_id=info:doi/ L2 - http://www.grc.org/programs.aspx?year=2012&program=pineal LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Association Between BRCA1 and BRCA2 Mutations and Survival in Women With Invasive Epithelial Ovarian Cancer AN - 1837301219; 16297586 AB - Context Approximately 10% of women with invasive epithelial ovarian cancer (EOC) carry deleterious germline mutations in BRCA1 or BRCA2. A recent article suggested that BRCA2 -related EOC was associated with an improved prognosis, but the effect of BRCA1 remains unclear. OBJECTIVE: To characterize the survival of BRCA carriers with EOC compared with noncarriers and to determine whether BRCA1 and BRCA2 carriers show similar survival patterns. Design, Setting, and Participants A pooled analysis of 26 observational studies on the survival of women with ovarian cancer, which included data from 1213 EOC cases with pathogenic germline mutations in BRCA1 (n = 909) or BRCA2 (n = 304) and from 2666 noncarriers recruited and followed up at variable times between 1987 and 2010 (the median year of diagnosis was 1998). MAIN OUTCOME MEASURE: Five-year overall mortality. RESULTS: The 5-year overall survival was 36% (95% CI, 34%-38%) for noncarriers, 44% (95% CI, 40%-48%) for BRCA1 carriers, and 52% (95% CI, 46%-58%) for BRCA2 carriers. After adjusting for study and year of diagnosis, BRCA1 and BRCA2 mutation carriers showed a more favorable survival than noncarriers (for BRCA1: hazard ratio [HR], 0.78; 95% CI, 0.68-0.89; P < .001; and for BRCA2: HR, 0.61; 95% CI, 0.50-0.76; P < .001). These survival differences remained after additional adjustment for stage, grade, histology, and age at diagnosis (for BRCA1: HR, 0.73; 95% CI, 0.64-0.84; P < .001; and for BRCA2: HR, 0.49; 95% CI, 0.39-0.61; P < .001). The BRCA1 HR estimate was significantly different from the HR estimated in the adjusted model (P for heterogeneity = .003). CONCLUSION: Among patients with invasive EOC, having a germline mutation in BRCA1 or BRCA2 was associated with improved 5-year overall survival. BRCA2 carriers had the best prognosis. JF - JAMA: Journal of the American Medical Association AU - Bolton, Kelly L AU - Chenevix- Trench, Georgia AU - Goh, Cindy AU - Sadetzki, Siegal AU - Ramus, Susan J AU - Karlan, Beth Y AU - Lambrechts, Diether AU - Despierre, Evelyn AU - Barrowdale, Daniel AU - McGuffog, Lesley AU - Healey, Sue AU - Easton, Douglas F AU - Sinilnikova, Olga AU - Benitez, Javier AU - Garcia, Maria J AU - Neuhausen, Susan AU - Gail, Mitchell H AU - Hartge, Patricia AU - Peock, Susan AU - Frost, Debra AU - Evans, DGareth AU - Eeles, Rosalind AU - Godwin, Andrew K AU - Daly, Mary B AU - Kwong, Ava AU - Ma, Edmond SK AU - Lazaro, Conxi AU - Blanco, Ignacio AU - Montagna, Marco AU - D'Andrea, Emma AU - Nicoletto, Maria Ornella AU - Johnatty, Sharon E AU - Kjaer, Susanne Krueger AU - Jensen, Allan AU - Hoegdall, Estrid AU - Goode, Ellen L AU - Fridley, Brooke L AU - Loud, Jennifer T AU - Greene, Mark H AU - Mai, Phuong L AU - Chetrit, Angela AU - Lubin, Flora AU - Hirsh-Yechezkel, Galit AU - Glendon, Gord AU - Andrulis, Irene L AU - Toland, Amanda E AU - Senter, Leigha AU - Gore, Martin E AU - Gourley, Charlie AU - Michie, Caroline O AU - Song, Honglin AU - Tyrer, Jonathan AU - Whittemore, Alice S AU - McGuire, Valerie AU - Sieh, Weiva AU - Kristoffersson, Ulf AU - Olsson, Haakan AU - Borg, Aake AU - Levine, Douglas A AU - Steele, Linda AU - Beattie, Mary S AU - Chan, Salina AU - Nussbaum, Robert L AU - Moysich, Kirsten B AU - Gross, Jenny AU - Cass, Ilana AU - Walsh, Christine AU - Li, Andrew J AU - Leuchter, Ronald AU - Gordon, Ora AU - Garcia-Closas, Montserrat AU - Gayther, Simon A AU - Chanock, Stephen J AU - Antoniou, Antonis C AU - Pharoah, Paul DP AD - Author Affiliations: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland (Drs Bolton, Gail, Chanock, and Hartge) Y1 - 2012/01/25/ PY - 2012 DA - 2012 Jan 25 SP - 382 EP - 389 PB - American Medical Association, 515 N. State St. Chicago IL 60610 United States VL - 307 IS - 4 SN - 0098-7484, 0098-7484 KW - Toxicology Abstracts KW - Ovarian cancer KW - Mortality KW - Invasiveness KW - Age KW - Data processing KW - Prognosis KW - Survival KW - BRCA2 protein KW - Models KW - BRCA1 protein KW - Breast cancer KW - Mutation KW - X 24300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1837301219?accountid=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=JAMA%3A+Journal+of+the+American+Medical+Association&rft.atitle=Association+Between+BRCA1+and+BRCA2+Mutations+and+Survival+in+Women+With+Invasive+Epithelial+Ovarian+Cancer&rft.au=Bolton%2C+Kelly+L%3BChenevix-+Trench%2C+Georgia%3BGoh%2C+Cindy%3BSadetzki%2C+Siegal%3BRamus%2C+Susan+J%3BKarlan%2C+Beth+Y%3BLambrechts%2C+Diether%3BDespierre%2C+Evelyn%3BBarrowdale%2C+Daniel%3BMcGuffog%2C+Lesley%3BHealey%2C+Sue%3BEaston%2C+Douglas+F%3BSinilnikova%2C+Olga%3BBenitez%2C+Javier%3BGarcia%2C+Maria+J%3BNeuhausen%2C+Susan%3BGail%2C+Mitchell+H%3BHartge%2C+Patricia%3BPeock%2C+Susan%3BFrost%2C+Debra%3BEvans%2C+DGareth%3BEeles%2C+Rosalind%3BGodwin%2C+Andrew+K%3BDaly%2C+Mary+B%3BKwong%2C+Ava%3BMa%2C+Edmond+SK%3BLazaro%2C+Conxi%3BBlanco%2C+Ignacio%3BMontagna%2C+Marco%3BD%27Andrea%2C+Emma%3BNicoletto%2C+Maria+Ornella%3BJohnatty%2C+Sharon+E%3BKjaer%2C+Susanne+Krueger%3BJensen%2C+Allan%3BHoegdall%2C+Estrid%3BGoode%2C+Ellen+L%3BFridley%2C+Brooke+L%3BLoud%2C+Jennifer+T%3BGreene%2C+Mark+H%3BMai%2C+Phuong+L%3BChetrit%2C+Angela%3BLubin%2C+Flora%3BHirsh-Yechezkel%2C+Galit%3BGlendon%2C+Gord%3BAndrulis%2C+Irene+L%3BToland%2C+Amanda+E%3BSenter%2C+Leigha%3BGore%2C+Martin+E%3BGourley%2C+Charlie%3BMichie%2C+Caroline+O%3BSong%2C+Honglin%3BTyrer%2C+Jonathan%3BWhittemore%2C+Alice+S%3BMcGuire%2C+Valerie%3BSieh%2C+Weiva%3BKristoffersson%2C+Ulf%3BOlsson%2C+Haakan%3BBorg%2C+Aake%3BLevine%2C+Douglas+A%3BSteele%2C+Linda%3BBeattie%2C+Mary+S%3BChan%2C+Salina%3BNussbaum%2C+Robert+L%3BMoysich%2C+Kirsten+B%3BGross%2C+Jenny%3BCass%2C+Ilana%3BWalsh%2C+Christine%3BLi%2C+Andrew+J%3BLeuchter%2C+Ronald%3BGordon%2C+Ora%3BGarcia-Closas%2C+Montserrat%3BGayther%2C+Simon+A%3BChanock%2C+Stephen+J%3BAntoniou%2C+Antonis+C%3BPharoah%2C+Paul+DP&rft.aulast=Bolton&rft.aufirst=Kelly&rft.date=2012-01-25&rft.volume=307&rft.issue=4&rft.spage=382&rft.isbn=&rft.btitle=&rft.title=JAMA%3A+Journal+of+the+American+Medical+Association&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-11-01 N1 - Last updated - 2016-12-22 N1 - SubjectsTermNotLitGenreText - Mortality; Ovarian cancer; Age; Invasiveness; Data processing; Prognosis; Breast cancer; Survival; BRCA1 protein; BRCA2 protein; Mutation; Models ER - TY - JOUR T1 - How Staphylococcus aureus biofilms develop their characteristic structure AN - 968174549; 16297741 AB - Biofilms cause significant problems in the environment and during the treatment of infections. However, the molecular mechanisms underlying biofilm formation are poorly understood. There is a particular lack of knowledge about biofilm maturation processes, such as biofilm structuring and detachment, which are deemed crucial for the maintenance of biofilm viability and the dissemination of cells from a biofilm. Here, we identify the phenol-soluble modulin (PSM) surfactant peptides as key biofilm structuring factors in the premier biofilm-forming pathogen Staphylococcus aureus. We provide evidence that all known PSM classes participate in structuring and detachment processes. Specifically, absence of PSMs in isogenic S. aureus psm deletion mutants led to strongly impaired formation of biofilm channels, abolishment of the characteristic waves of biofilm detachment and regrowth, and loss of control of biofilm expansion. In contrast, induced expression of psm loci in preformed biofilms promoted those processes. Furthermore, PSMs facilitated dissemination from an infected catheter in a mouse model of biofilm-associated infection. Moreover, formation of the biofilm structure was linked to strongly variable, quorum sensing-controlled PSM expression in biofilm microenvironments, whereas overall PSM production remained constant to ascertain biofilm homeostasis. Our study describes a mechanism of biofilm structuring in molecular detail, and the general principle (i.e., quorum-sensing controlled expression of surfactants) seems to be conserved in several bacteria, despite the divergence of the respective biofilm-structuring surfactants. These findings provide a deeper understanding of biofilm development processes, which represents an important basis for strategies to interfere with biofilm formation in the environment and human disease. JF - Proceedings of the National Academy of Sciences, USA AU - Periasamy, Saravanan AU - Joo, Hwang-Soo AU - Duong, Anthony C AU - Bach, Thanh-Huy L AU - Tan, Vee Y AU - Chatterjee, Som S AU - Cheung, Gordon YC AU - Otto, Michael AD - National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 Y1 - 2012/01/24/ PY - 2012 DA - 2012 Jan 24 SP - 1281 EP - 1286 PB - National Academy of Sciences, 2101 Constitution Ave. Washington DC 20418 United States VL - 109 IS - 4 SN - 0027-8424, 0027-8424 KW - Microbiology Abstracts B: Bacteriology KW - Animal models KW - Biofilms KW - Catheters KW - Deletion mutant KW - Homeostasis KW - Infection KW - Microenvironments KW - Molecular modelling KW - Pathogens KW - Surfactants KW - Waves KW - quorum sensing KW - Staphylococcus aureus KW - J 02410:Animal Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/968174549?accountid=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=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.atitle=How+Staphylococcus+aureus+biofilms+develop+their+characteristic+structure&rft.au=Periasamy%2C+Saravanan%3BJoo%2C+Hwang-Soo%3BDuong%2C+Anthony+C%3BBach%2C+Thanh-Huy+L%3BTan%2C+Vee+Y%3BChatterjee%2C+Som+S%3BCheung%2C+Gordon+YC%3BOtto%2C+Michael&rft.aulast=Periasamy&rft.aufirst=Saravanan&rft.date=2012-01-24&rft.volume=109&rft.issue=4&rft.spage=1281&rft.isbn=&rft.btitle=&rft.title=Proceedings+of+the+National+Academy+of+Sciences%2C+USA&rft.issn=00278424&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Molecular modelling; Deletion mutant; quorum sensing; Catheters; Animal models; Microenvironments; Waves; Homeostasis; Pathogens; Biofilms; Infection; Surfactants; Staphylococcus aureus ER - TY - CPAPER T1 - Adaptations for the acquisition and transmission of the tick-borne relapsing fever spirochete Borrelia hermsii T2 - 2012 Gordon Research Conference on the Biology of Spirochetes AN - 1312982467; 6106889 JF - 2012 Gordon Research Conference on the Biology of Spirochetes AU - Schwan, Tom Y1 - 2012/01/22/ PY - 2012 DA - 2012 Jan 22 KW - Adaptability KW - Adaptations KW - Spirochetes KW - tick-borne diseases KW - Borrelia hermsii UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312982467?accountid=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+Gordon+Research+Conference+on+the+Biology+of+Spirochetes&rft.atitle=Adaptations+for+the+acquisition+and+transmission+of+the+tick-borne+relapsing+fever+spirochete+Borrelia+hermsii&rft.au=Schwan%2C+Tom&rft.aulast=Schwan&rft.aufirst=Tom&rft.date=2012-01-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Gordon+Research+Conference+on+the+Biology+of+Spirochetes&rft.issn=&rft_id=info:doi/ L2 - http://www.grc.org/programs.aspx?year=2012&program=spirochete LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Inactivation of the locus for antigenic variation in the Relapsing Fever Spirochete Borrelia hermsii T2 - 2012 Gordon Research Conference on the Biology of Spirochetes AN - 1312982287; 6106886 JF - 2012 Gordon Research Conference on the Biology of Spirochetes AU - Stewart, Sandra Y1 - 2012/01/22/ PY - 2012 DA - 2012 Jan 22 KW - Inactivation KW - Relapsing fever KW - Spirochetes KW - Borrelia hermsii UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312982287?accountid=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+Gordon+Research+Conference+on+the+Biology+of+Spirochetes&rft.atitle=Inactivation+of+the+locus+for+antigenic+variation+in+the+Relapsing+Fever+Spirochete+Borrelia+hermsii&rft.au=Stewart%2C+Sandra&rft.aulast=Stewart&rft.aufirst=Sandra&rft.date=2012-01-22&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Gordon+Research+Conference+on+the+Biology+of+Spirochetes&rft.issn=&rft_id=info:doi/ L2 - http://www.grc.org/programs.aspx?year=2012&program=spirochete LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Theranostic imaging guided target-specific photo-activatable immunotherapy (PIT) T2 - 2012 Conference on Reporters, Markers, Dyes, Nanoparticles, and Molecular Probes for Biomedical Applications AN - 1313084425; 6107618 JF - 2012 Conference on Reporters, Markers, Dyes, Nanoparticles, and Molecular Probes for Biomedical Applications AU - Kobayashi, Hisataka Y1 - 2012/01/21/ PY - 2012 DA - 2012 Jan 21 KW - Immunotherapy KW - Imaging techniques UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313084425?accountid=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+Conference+on+Reporters%2C+Markers%2C+Dyes%2C+Nanoparticles%2C+and+Molecular+Probes+for+Biomedical+Applications&rft.atitle=Theranostic+imaging+guided+target-specific+photo-activatable+immunotherapy+%28PIT%29&rft.au=Kobayashi%2C+Hisataka&rft.aulast=Kobayashi&rft.aufirst=Hisataka&rft.date=2012-01-21&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Conference+on+Reporters%2C+Markers%2C+Dyes%2C+Nanoparticles%2C+and+Molecular+Probes+for+Biomedical+Applications&rft.issn=&rft_id=info:doi/ L2 - http://spie.org/Documents/ConferencesExhibitions/PW12-Final-lr.pdf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - A Vision for the Development of Molecularly Targeted Therapies for Colon Cancer in 2012 T2 - 2012 Gastrointestinal Cancers Symposium AN - 1313038377; 6117897 JF - 2012 Gastrointestinal Cancers Symposium AU - Doroshow, James Y1 - 2012/01/19/ PY - 2012 DA - 2012 Jan 19 KW - Colon cancer KW - Vision KW - Therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313038377?accountid=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+Gastrointestinal+Cancers+Symposium&rft.atitle=A+Vision+for+the+Development+of+Molecularly+Targeted+Therapies+for+Colon+Cancer+in+2012&rft.au=Doroshow%2C+James&rft.aulast=Doroshow&rft.aufirst=James&rft.date=2012-01-19&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Gastrointestinal+Cancers+Symposium&rft.issn=&rft_id=info:doi/ L2 - http://gicasym.org/2012GastrointestinalCancersSymposium/MeetingProgram.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - In vivo quantification of T sub(2) super(a) anisotropy in white matter fibers in marmoset monkeys AN - 915491277; 16147639 AB - T sub(2) super(a)-weighted MRI at high field is a promising approach for studying noninvasively the tissue structure and composition of the brain. However, the biophysical origin of T sub(2) super(a) contrast, especially in white matter, remains poorly understood. Recent work has shown that R sub(2) super(a) (= 1/T sub(2) super(a)) may depend on the tissue's orientation relative to the static magnetic field (B sub(0) and suggested that this dependence could be attributed to local anisotropy in the magnetic properties of brain tissue. In the present work, we analyzed high-resolution, multi-gradient-echo images of in vivo marmoset brains at 7 T, and compared them with ex vivo diffusion tensor images, to show that R) sub(2) super(a relaxation in white matter is highly sensitive to the fiber orientation relative to the main field. We directly demonstrate this orientation dependence by performing in vivo multi-gradient-echo experiments in two orthogonal brain positions, uncovering a nearly 50% change in the R) sub(2) super(a relaxation rate constant of the optic radiations. We attribute this substantial R) sub(2) super(a anisotropy to local subvoxel susceptibility effects arising from the highly ordered and anisotropic structure of the myelin sheath.) JF - NeuroImage AU - Sati, Pascal AU - Silva, Afonso C AU - Van Gelderen, Peter AU - Gaitan, Maria I AU - Wohler, Jillian E AU - Jacobson, Steven AU - Duyn, Jeff H AU - Reich, Daniel S AD - Translational Neuroradiology Unit, Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA, satip@ninds.nih.gov Y1 - 2012/01/16/ PY - 2012 DA - 2012 Jan 16 SP - 979 EP - 985 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 59 IS - 2 SN - 1053-8119, 1053-8119 KW - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts KW - Anisotropy KW - Callithrix KW - Brain KW - W 30910:Imaging KW - N3:11029 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/915491277?accountid=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=NeuroImage&rft.atitle=In+vivo+quantification+of+T+sub%282%29+super%28a%29+anisotropy+in+white+matter+fibers+in+marmoset+monkeys&rft.au=Sati%2C+Pascal%3BSilva%2C+Afonso+C%3BVan+Gelderen%2C+Peter%3BGaitan%2C+Maria+I%3BWohler%2C+Jillian+E%3BJacobson%2C+Steven%3BDuyn%2C+Jeff+H%3BReich%2C+Daniel+S&rft.aulast=Sati&rft.aufirst=Pascal&rft.date=2012-01-16&rft.volume=59&rft.issue=2&rft.spage=979&rft.isbn=&rft.btitle=&rft.title=NeuroImage&rft.issn=10538119&rft_id=info:doi/10.1016%2Fj.neuroimage.2011.08.064 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-01-01 N1 - Last updated - 2014-02-21 N1 - SubjectsTermNotLitGenreText - Brain; Callithrix DO - http://dx.doi.org/10.1016/j.neuroimage.2011.08.064 ER - TY - JOUR T1 - Direct imaging of macrovascular and microvascular contributions to BOLD fMRI in layers IV-V of the rat whisker-barrel cortex AN - 915488939; 16147580 AB - The spatiotemporal characteristics of the hemodynamic response to increased neural activity were investigated at the level of individual intracortical vessels using BOLD-fMRI in a well-established rodent model of somatosensory stimulation at 11.7 T. Functional maps of the rat barrel cortex were obtained at 150 x 150 x 500 mu m spatial resolution every 200 ms. The high spatial resolution allowed separation of active voxels into those containing intracortical macro vessels, mainly vein/venules (referred to as macrovasculature), and those enriched with arteries/capillaries and small venules (referred to as microvasculature) since the macro vessel can be readily mapped due to the fast T2* decay of blood at 11.7 T. The earliest BOLD response was observed within layers IV-V by 0.8 s following stimulation and encompassed mainly the voxels containing the microvasculature and some confined macrovasculature voxels. By 1.2 s, the BOLD signal propagated to the macrovasculature voxels where the peak BOLD signal was 2-3 times higher than that of the microvasculature voxels. The BOLD response propagated in individual venules/veins far from neuronal sources at later times. This was also observed in layers IV-V of the barrel cortex after specific stimulation of separated whisker rows. These results directly visualized that the earliest hemodynamic changes to increased neural activity occur mainly in the microvasculature and spread toward the macrovasculature. However, at peak response, the BOLD signal is dominated by penetrating venules even at layers IV-V of the cortex. JF - NeuroImage AU - Yu, Xin AU - Glen, Daniel AU - Wang, Shumin AU - Dodd, Stephen AU - Hirano, Yoshiyuki AU - Saad, Ziad AU - Reynolds, Richard AU - Silva, Afonso C AU - Koretsky, Alan P AD - National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA, koretskya@ninds.nih.gov Y1 - 2012/01/16/ PY - 2012 DA - 2012 Jan 16 SP - 1451 EP - 1460 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 59 IS - 2 SN - 1053-8119, 1053-8119 KW - CSA Neurosciences Abstracts; Biotechnology and Bioengineering Abstracts KW - Arteries KW - Microvasculature KW - W 30910:Imaging KW - N3:11029 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/915488939?accountid=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=NeuroImage&rft.atitle=Direct+imaging+of+macrovascular+and+microvascular+contributions+to+BOLD+fMRI+in+layers+IV-V+of+the+rat+whisker-barrel+cortex&rft.au=Yu%2C+Xin%3BGlen%2C+Daniel%3BWang%2C+Shumin%3BDodd%2C+Stephen%3BHirano%2C+Yoshiyuki%3BSaad%2C+Ziad%3BReynolds%2C+Richard%3BSilva%2C+Afonso+C%3BKoretsky%2C+Alan+P&rft.aulast=Yu&rft.aufirst=Xin&rft.date=2012-01-16&rft.volume=59&rft.issue=2&rft.spage=1451&rft.isbn=&rft.btitle=&rft.title=NeuroImage&rft.issn=10538119&rft_id=info:doi/10.1016%2Fj.neuroimage.2011.08.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-01-01 N1 - Last updated - 2014-02-21 N1 - SubjectsTermNotLitGenreText - Microvasculature DO - http://dx.doi.org/10.1016/j.neuroimage.2011.08.001 ER - TY - JOUR T1 - IL-10 Limits Parasite Burden and Protects against Fatal Myocarditis in a Mouse Model of Trypanosoma cruzi Infection AN - 920797842; 16199746 AB - Chagas' disease is a zoonosis prevalent in Latin America that is caused by the protozoan Trypanosoma cruzi. The immunopathogenesis of cardiomyopathy, the main clinical problem in Chagas' disease, has been extensively studied but is still poorly understood. In this study, we systematically compared clinical, microbiologic, pathologic, immunologic, and molecular parameters in two mouse models with opposite susceptibility to acute myocarditis caused by the myotropic Colombiana strain of T. cruzi: C3H/HeSnJ (100% mortality, uncontrolled parasitism) and C57BL/6J (<10% mortality, controlled parasitism). T. cruzi induced differential polarization of immunoregulatory cytokine mRNA expression in the hearts of C57BL/6J versus C3H/HeSnJ mice; however, most differences were small. The difference in IL-10 expression was exceptional (C57BL/6J 8.7-fold greater than C3H/HeSnJ). Consistent with this, hearts from infected C57BL/6J mice, but not C3H/HeSnJ mice, had a high frequency of total IL-10-producing CD8+ T cells and both CD4+ and CD8+ subsets of IFN- gamma +IL-10+ double-producing T cells. Furthermore, T. cruzi infection of IL-10-/- C57BL/6J mice phenocopied fatal infection in wild-type C3H/HeSnJ mice with complete loss of parasite control. Adoptive transfer experiments indicated that T cells were a source of protective IL-10. Thus, in this system, IL-10 production by T cells promotes T. cruzi control and protection from fatal acute myocarditis. JF - Journal of Immunology AU - Roffe, Ester AU - Rothfuchs, Antonio Gigliotti AU - Santiago, Helton C AU - Marino, Ana Paula MP AU - Ribeiro-Gomes, Flavia L AU - Eckhaus, Michael AU - Antonelli, Lis RV AU - Murphy, Philip M AD - Molecular Signaling Section, Laboratory of Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 Y1 - 2012/01/15/ PY - 2012 DA - 2012 Jan 15 SP - 649 EP - 660 PB - American Association of Immunologists, 9650 Rockville Pike Bethesda MD 20814-3998 United States VL - 188 IS - 2 SN - 0022-1767, 0022-1767 KW - ASFA 3: Aquatic Pollution & Environmental Quality; ASFA 1: Biological Sciences & Living Resources; Microbiology Abstracts C: Algology, Mycology & Protozoology; Immunology Abstracts KW - gamma -Interferon KW - Immunoregulation KW - Molecular modelling KW - Parasites KW - Animal models KW - Infection KW - Parasitism KW - Interleukin 10 KW - Public health KW - Gene expression KW - Cardiomyopathy KW - CD4 antigen KW - Lymphocytes T KW - Myocarditis KW - Heart diseases KW - Heart KW - Trypanosoma cruzi KW - Mortality KW - Immunology KW - Latin America KW - Immunopathogenesis KW - CD8 antigen KW - Polarization KW - Parasite control KW - Adoptive transfer KW - Mortality causes KW - Chagas' disease KW - K 03410:Animal Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - F 06910:Microorganisms & Parasites KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920797842?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Immunology&rft.atitle=IL-10+Limits+Parasite+Burden+and+Protects+against+Fatal+Myocarditis+in+a+Mouse+Model+of+Trypanosoma+cruzi+Infection&rft.au=Roffe%2C+Ester%3BRothfuchs%2C+Antonio+Gigliotti%3BSantiago%2C+Helton+C%3BMarino%2C+Ana+Paula+MP%3BRibeiro-Gomes%2C+Flavia+L%3BEckhaus%2C+Michael%3BAntonelli%2C+Lis+RV%3BMurphy%2C+Philip+M&rft.aulast=Roffe&rft.aufirst=Ester&rft.date=2012-01-15&rft.volume=188&rft.issue=2&rft.spage=649&rft.isbn=&rft.btitle=&rft.title=Journal+of+Immunology&rft.issn=00221767&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-02-01 N1 - Last updated - 2016-10-26 N1 - SubjectsTermNotLitGenreText - Heart; Parasite control; Parasites; Immunology; Polarization; Parasitism; Mortality causes; Public health; Molecular modelling; Immunoregulation; Mortality; gamma -Interferon; Animal models; Immunopathogenesis; CD8 antigen; Infection; Interleukin 10; Gene expression; Cardiomyopathy; CD4 antigen; Adoptive transfer; Lymphocytes T; Myocarditis; Heart diseases; Chagas' disease; Trypanosoma cruzi; Latin America ER - TY - JOUR T1 - Mitochondrial-targeted antioxidants represent a promising approach for prevention of cisplatin-induced nephropathy. AN - 914672848; 22120494 AB - Cisplatin is a widely used antineoplastic agent; however, its major limitation is the development of dose-dependent nephrotoxicity whose precise mechanisms are poorly understood. Here we show not only that mitochondrial dysfunction is a feature of cisplatin nephrotoxicity, but also that targeted delivery of superoxide dismutase mimetics to mitochondria largely prevents the renal effects of cisplatin. Cisplatin induced renal oxidative stress, deterioration of mitochondrial structure and function, an intense inflammatory response, histopathological injury, and renal dysfunction. A single systemic dose of mitochondrially targeted antioxidants, MitoQ or Mito-CP, dose-dependently prevented cisplatin-induced renal dysfunction. Mito-CP also prevented mitochondrial injury and dysfunction, renal inflammation, and tubular injury and apoptosis. Despite being broadly renoprotective against cisplatin, Mito-CP did not diminish cisplatin's antineoplastic effect in a human bladder cancer cell line. Our results highlight the central role of mitochondrially generated oxidants in the pathogenesis of cisplatin nephrotoxicity. Because similar compounds seem to be safe in humans, mitochondrially targeted antioxidants may represent a novel therapeutic approach against cisplatin nephrotoxicity. Copyright © 2011 Elsevier Inc. All rights reserved. JF - Free radical biology & medicine AU - Mukhopadhyay, Partha AU - Horváth, Béla AU - Zsengellér, Zsuzsanna AU - Zielonka, Jacek AU - Tanchian, Galin AU - Holovac, Eileen AU - Kechrid, Malek AU - Patel, Vivek AU - Stillman, Isaac E AU - Parikh, Samir M AU - Joseph, Joy AU - Kalyanaraman, Balaraman AU - Pacher, Pál AD - Laboratory of Physiologic Studies, National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/01/15/ PY - 2012 DA - 2012 Jan 15 SP - 497 EP - 506 VL - 52 IS - 2 KW - 10-(6'-ubiquinonyl)decyltriphenylphosphonium bromide KW - 0 KW - Antineoplastic Agents KW - Antioxidants KW - Cyclic N-Oxides KW - Organophosphorus Compounds KW - mito-carboxy proxyl KW - Ubiquinone KW - 1339-63-5 KW - NADH Dehydrogenase KW - EC 1.6.99.3 KW - Electron Transport Complex IV KW - EC 1.9.3.1 KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Animals KW - NADH Dehydrogenase -- metabolism KW - Kidney Tubules -- pathology KW - Humans KW - Mitochondria -- pathology KW - Inflammation -- chemically induced KW - Cytoprotection KW - Mice KW - Cell Line, Tumor KW - Kidney Tubules -- enzymology KW - Inflammation -- prevention & control KW - Cell Survival -- drug effects KW - Kidney Tubules -- drug effects KW - Mitochondria -- drug effects KW - Apoptosis -- drug effects KW - Oxidative Stress -- drug effects KW - Mice, Inbred C57BL KW - Electron Transport Complex IV -- metabolism KW - Male KW - Cyclic N-Oxides -- therapeutic use KW - Organophosphorus Compounds -- therapeutic use KW - Ubiquinone -- therapeutic use KW - Acute Kidney Injury -- prevention & control KW - Ubiquinone -- analogs & derivatives KW - Organophosphorus Compounds -- pharmacokinetics KW - Antineoplastic Agents -- adverse effects KW - Antioxidants -- pharmacology KW - Acute Kidney Injury -- chemically induced KW - Antioxidants -- therapeutic use KW - Cyclic N-Oxides -- pharmacology KW - Organophosphorus Compounds -- pharmacology KW - Cisplatin -- adverse effects KW - Ubiquinone -- pharmacology KW - Cyclic N-Oxides -- pharmacokinetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/914672848?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Mitochondrial-targeted+antioxidants+represent+a+promising+approach+for+prevention+of+cisplatin-induced+nephropathy.&rft.au=Mukhopadhyay%2C+Partha%3BHorv%C3%A1th%2C+B%C3%A9la%3BZsengell%C3%A9r%2C+Zsuzsanna%3BZielonka%2C+Jacek%3BTanchian%2C+Galin%3BHolovac%2C+Eileen%3BKechrid%2C+Malek%3BPatel%2C+Vivek%3BStillman%2C+Isaac+E%3BParikh%2C+Samir+M%3BJoseph%2C+Joy%3BKalyanaraman%2C+Balaraman%3BPacher%2C+P%C3%A1l&rft.aulast=Mukhopadhyay&rft.aufirst=Partha&rft.date=2012-01-15&rft.volume=52&rft.issue=2&rft.spage=497&rft.isbn=&rft.btitle=&rft.title=Free+radical+biology+%26+medicine&rft.issn=1873-4596&rft_id=info:doi/10.1016%2Fj.freeradbiomed.2011.11.001 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-01 N1 - Date created - 2012-01-06 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Proc Natl Acad Sci U S A. 2000 Mar 14;97(6):2826-31 [10717001] J Am Soc Nephrol. 2001 Dec;12(12):2683-90 [11729237] Kidney Int. 2001 Dec;60(6):2118-28 [11737586] J Clin Invest. 2002 Sep;110(6):743-5 [12235103] J Clin Invest. 2002 Sep;110(6):835-42 [12235115] Kidney Int. 2003 Jan;63(1):72-82 [12472770] J Clin Oncol. 2003 Mar 1;21(5):927-31 [12610195] Am J Physiol Renal Physiol. 2003 Oct;285(4):F610-8 [12865254] J Lab Clin Med. 2003 Sep;142(3):178-86 [14532906] Nephrol Dial Transplant. 2004 Feb;19(2):329-36 [14736955] Eur J Cancer. 2004 Jul;40(11):1713-23 [15251161] Am J Physiol Renal Physiol. 2004 Nov;287(5):F990-8 [15280156] Am J Kidney Dis. 1986 Nov;8(5):368-79 [3538860] Arch Biochem Biophys. 1992 Nov 1;298(2):446-51 [1329657] J Pharmacol Exp Ther. 1997 Feb;280(2):638-49 [9023274] J Clin Invest. 1998 Feb 15;101(4):777-82 [9466972] Nat Rev Drug Discov. 2005 Apr;4(4):307-20 [15789122] Am J Physiol Renal Physiol. 2005 Aug;289(2):F469-80 [15814532] Free Radic Biol Med. 2005 Sep 1;39(5):567-83 [16085176] Am J Physiol Renal Physiol. 2006 Jan;290(1):F35-42 [16106037] Physiol Rev. 2007 Jan;87(1):315-424 [17237348] Nat Protoc. 2006;1(5):2315-9 [17406473] Kidney Int. 2007 Jul;72(1):37-44 [17396112] Nat Rev Drug Discov. 2007 Aug;6(8):662-80 [17667957] Kidney Int. 2008 May;73(9):994-1007 [18272962] J Neurosci. 2008 Apr 16;28(16):4115-22 [18417691] J Am Soc Nephrol. 2008 May;19(5):923-32 [18256356] J Clin Invest. 2009 May;119(5):1275-85 [19349686] Kidney Int. 2009 Nov;76(10):1049-62 [19710628] Free Radic Biol Med. 2010 Feb 1;48(3):457-67 [19969072] Proc Natl Acad Sci U S A. 2010 May 11;107(19):8788-93 [20421486] J Biol Chem. 2010 Nov 5;285(45):34447-59 [20805228] Free Radic Biol Med. 2011 Jan 1;50(1):179-95 [21070851] Discov Med. 2011 Feb;11(57):106-14 [21356165] J Am Soc Nephrol. 2011 Jun;22(6):1041-52 [21546574] J Clin Invest. 2011 Jul;121(7):2709-22 [21633170] Free Radic Biol Med. 2011 Nov 1;51(9):1774-88 [21884784] Antioxid Redox Signal. 2011 Dec 15;15(12):3021-38 [21395490] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1016/j.freeradbiomed.2011.11.001 ER - TY - JOUR T1 - DNA methylation-mediated silencing of nonsteroidal anti-inflammatory drug-activated gene (NAG-1/GDF15) in glioma cell lines. AN - 911944789; 21437897 AB - Nonsteroidal anti-inflammatory drug-activated gene, NAG-1, a transforming growth factor-β member, is involved in tumor progression and development. The association between NAG-1 expression and development and progression of glioma has not been well defined. Glioblastoma cell lines have lower basal expression of NAG-1 than other gliomas and normal astrocytes. Most primary human gliomas have very low levels of NAG-1 expression. NAG-1 basal expression appeared to inversely correlate with tumor grade in glioma. Aberrant promoter hypermethylation is a common mechanism for silencing of tumor suppressor genes in cancer cells. In glioblastoma cell lines, NAG-1 expression was increased by the demethylating agent, 5-aza-2'-deoxycytidine. To investigate whether the NAG-1 gene was silenced by hypermethylation in glioblastoma, we examined DNA methylation status using genomic bisulfite sequencing. The NAG-1 promoter was densely methylated in several glioblastoma cell lines as well as in primary oligodendroglioma tumor samples, which have low basal expression of NAG-1. DNA methylation at two specific sites (-53 and +55 CpG sites) in the NAG-1 promoter was strongly associated with low NAG-1 expression. The methylation of the NAG-1 promoter at the -53 site blocks Egr-1 binding and thereby suppresses Nag-1 induction. Treatment of cells with low basal NAG-1 expression with NAG-1 inducer also did not increase NAG-1. Incubation with a demethylation chemical increased Nag-1 basal expression and subsequent incubation with a NAG-1 inducer increased NAG-1 expression. We concluded from these data that methylation of specific promoter sequences causes transcriptional silencing of the NAG-1 locus in glioma and may ultimately contribute to tumor progression. Copyright © 2011 UICC. JF - International journal of cancer AU - Kadowaki, Mitsutoshi AU - Yoshioka, Hiroki AU - Kamitani, Hideki AU - Watanabe, Takashi AU - Wade, Paul A AU - Eling, Thomas E AD - Laboratory of Molecular Carcinogenesis, NIEHS, National Institutes of Health, Research Triangle Park, NC 27709, USA. Y1 - 2012/01/15/ PY - 2012 DA - 2012 Jan 15 SP - 267 EP - 277 VL - 130 IS - 2 KW - Anti-Inflammatory Agents, Non-Steroidal KW - 0 KW - EGR1 protein, human KW - Early Growth Response Protein 1 KW - GDF15 protein, human KW - Growth Differentiation Factor 15 KW - Hydroxamic Acids KW - Sulindac KW - 184SNS8VUH KW - trichostatin A KW - 3X2S926L3Z KW - sulindac sulfide KW - 6UVA8S2DEY KW - decitabine KW - 776B62CQ27 KW - Azacitidine KW - M801H13NRU KW - Index Medicus KW - Azacitidine -- pharmacology KW - Gene Silencing KW - Azacitidine -- analogs & derivatives KW - Humans KW - Early Growth Response Protein 1 -- genetics KW - Cell Line, Tumor KW - Cell Growth Processes -- genetics KW - Gene Expression Regulation, Neoplastic KW - Promoter Regions, Genetic KW - Apoptosis -- genetics KW - Transfection KW - Early Growth Response Protein 1 -- metabolism KW - Sulindac -- pharmacology KW - Sulindac -- analogs & derivatives KW - Hydroxamic Acids -- pharmacology KW - Anti-Inflammatory Agents, Non-Steroidal -- pharmacology KW - Glioblastoma -- genetics KW - Brain Neoplasms -- pathology KW - DNA Methylation KW - Brain Neoplasms -- genetics KW - Glioblastoma -- pathology KW - Glioblastoma -- metabolism KW - Brain Neoplasms -- metabolism KW - Growth Differentiation Factor 15 -- biosynthesis KW - Growth Differentiation Factor 15 -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/911944789?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=DNA+methylation-mediated+silencing+of+nonsteroidal+anti-inflammatory+drug-activated+gene+%28NAG-1%2FGDF15%29+in+glioma+cell+lines.&rft.au=Kadowaki%2C+Mitsutoshi%3BYoshioka%2C+Hiroki%3BKamitani%2C+Hideki%3BWatanabe%2C+Takashi%3BWade%2C+Paul+A%3BEling%2C+Thomas+E&rft.aulast=Kadowaki&rft.aufirst=Mitsutoshi&rft.date=2012-01-15&rft.volume=130&rft.issue=2&rft.spage=267&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.26082 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-03-16 N1 - Date created - 2011-12-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Cancer Res. 2004 Oct 1;64(19):6892-9 [15466178] Am J Pathol. 2004 Oct;165(4):1151-61 [15466382] Brain Pathol. 1996 Jul;6(3):217-23; discussion 23-4 [8864278] J Neurooncol. 1998 Jan;36(2):123-40 [9525812] Clin Cancer Res. 1997 Apr;3(4):523-30 [9815715] J Leukoc Biol. 1999 Jan;65(1):2-5 [9886240] J Biol Chem. 2004 Nov 26;279(48):49617-23 [15377673] Acta Neuropathol. 2005 Jan;109(1):93-108 [15685439] Cancer Res. 2006 Jan 1;66(1):159-67 [16397228] Prog Lipid Res. 2006 Jan;45(1):1-16 [16337272] J Pharmacol Exp Ther. 2006 Aug;318(2):899-906 [16714403] Cancer Res. 2006 Aug 1;66(15):7490-501 [16885346] Gastroenterology. 2006 Nov;131(5):1553-60 [17101328] Cancer J. 2008 May-Jun;14(3):170-7 [18536556] Cancer Lett. 2008 Oct 18;270(1):30-9 [18550273] Int J Oncol. 2008 Oct;33(4):759-65 [18813789] Cancer Res. 2008 Oct 1;68(19):8094-103 [18829568] Nature. 2008 Oct 23;455(7216):1061-8 [18772890] J Biol Chem. 2008 Nov 28;283(48):33129-37 [18801729] Curr Stem Cell Res Ther. 2009 Jan;4(1):44-9 [19149629] Cancer Res. 2010 Mar 15;70(6):2141-5 [20179191] Cancer Cell. 2010 May 18;17(5):510-22 [20399149] Endocr Relat Cancer. 2000 Jun;7(2):115-29 [10903528] J Neurosci. 2000 Dec 1;20(23):8597-603 [11102463] Lab Invest. 2001 Jan;81(1):77-82 [11204276] Mol Pharmacol. 2001 Apr;59(4):901-8 [11259636] Cancer Res. 2001 Sep 1;61(17):6335-9 [11522621] J Comp Neurol. 2001 Oct 8;439(1):32-45 [11579380] Carcinogenesis. 2002 Mar;23(3):425-34 [11895857] J Nutr. 2002 Apr;132(4):773-8 [11925476] Nat Rev Genet. 2002 Jun;3(6):415-28 [12042769] Proc Natl Acad Sci U S A. 2003 Mar 18;100(6):3410-5 [12624183] Cancer Res. 2003 Aug 15;63(16):5034-40 [12941831] J Biol Chem. 2004 Feb 20;279(8):6883-92 [14662774] Cancer Metastasis Rev. 2004 Jan-Jun;23(1-2):29-39 [15000147] Clin Cancer Res. 2004 Apr 1;10(7):2386-92 [15073115] Pediatr Blood Cancer. 2004 Aug;43(2):181 [15236290] Nat Rev Neurosci. 2004 Oct;5(10):782-92 [15378038] Virchows Arch. 1995;427(2):113-8 [7582239] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/ijc.26082 ER - TY - JOUR T1 - Contribution of TMC6 and TMC8 (EVER1 and EVER2) variants to cervical cancer susceptibility. AN - 911935953; 21387292 AB - Cervical cancer (CxCa) is caused by persistent human papillomavirus (HPV) infection; genetic predisposition is also suspected to play a role. Our study is a targeted candidate gene follow-up based on: (i) strong clinical evidence demonstrating that mutations in the TMC6 and TMC8 (EVER1 and EVER2) genes associate with the HPV-associated disease epidermodysplasia verruciformis (EV) and (ii) recent epidemiological data suggesting a genetic susceptibility conferred by polymorphisms in such genes for skin and CxCa. Clarifying the association of the TMC6/8 genes with risk of CxCa will help in understanding why some HPV-infected women develop persistent infection, cervical lesions and eventually cancer while others do not. Twenty-two single nucleotide polymorphisms (SNPs) harboring the TMC6/8 genes were genotyped in 2,989 cases with cervical intraepithelial neoplasia grade III or invasive CxCa and 2,281 controls from the Swedish population. Association was evaluated in logistic regression models. Two SNPs displayed association with cervical disease: rs2290907 [odds ratio (OR)(GGvsAA) = 0.6, 95% confidence interval (95% CI): 0.3-0.9, p = 0.02)] and rs16970849 (OR(AGvsGG) = 0.8, 95% CI: 0.66-0.98, p = 0.03). The present data support the involvement of the TMC6/8 region in CxCa susceptibility but further analyses are needed to replicate our findings, fully characterize the region and understand the function of the genetic variants involved. Published 2011 UICC. JF - International journal of cancer AU - Castro, Felipe A AU - Ivansson, Emma L AU - Schmitt, Markus AU - Juko-Pecirep, Ivana AU - Kjellberg, Lennart AU - Hildesheim, Allan AU - Gyllensten, Ulf B AU - Pawlita, Michael AD - Division of Genome Modifications and Carcinogenesis, German Cancer Research Center (DKFZ), Heidelberg, Germany. felipe.castro@nih.gov Y1 - 2012/01/15/ PY - 2012 DA - 2012 Jan 15 SP - 349 EP - 355 VL - 130 IS - 2 KW - Membrane Proteins KW - 0 KW - TMC6 protein, human KW - TMC8 protein, human KW - Index Medicus KW - Genotype KW - Polymorphism, Single Nucleotide KW - Humans KW - Cohort Studies KW - Sweden -- epidemiology KW - Genetic Predisposition to Disease KW - Female KW - Cervical Intraepithelial Neoplasia -- genetics KW - Uterine Cervical Neoplasms -- epidemiology KW - Uterine Cervical Neoplasms -- genetics KW - Membrane Proteins -- genetics KW - Cervical Intraepithelial Neoplasia -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/911935953?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Contribution+of+TMC6+and+TMC8+%28EVER1+and+EVER2%29+variants+to+cervical+cancer+susceptibility.&rft.au=Castro%2C+Felipe+A%3BIvansson%2C+Emma+L%3BSchmitt%2C+Markus%3BJuko-Pecirep%2C+Ivana%3BKjellberg%2C+Lennart%3BHildesheim%2C+Allan%3BGyllensten%2C+Ulf+B%3BPawlita%2C+Michael&rft.aulast=Castro&rft.aufirst=Felipe&rft.date=2012-01-15&rft.volume=130&rft.issue=2&rft.spage=349&rft.isbn=&rft.btitle=&rft.title=International+journal+of+cancer&rft.issn=1097-0215&rft_id=info:doi/10.1002%2Fijc.26016 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-03-16 N1 - Date created - 2011-12-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Hum Mol Genet. 2004 Sep 1;13(17):1951-8 [15238505] Nat Genet. 2002 Dec;32(4):579-81 [12426567] J Invest Dermatol. 1999 Mar;112(3):259-63 [10084299] Nature. 1999 Jul 1;400(6739):29-30 [10403244] J Pathol. 1999 Sep;189(1):12-9 [10451482] Bioinformatics. 2005 Jan 15;21(2):263-5 [15297300] Nat Genet. 2005 Nov;37(11):1217-23 [16244653] Nat Cell Biol. 2005 Dec;7(12):1267-74 [16284622] Curr Biol. 2005 Dec 6;15(23):2149-55 [16289642] BMC Bioinformatics. 2006;7:209 [16620382] Am J Hum Genet. 2007 Sep;81(3):559-75 [17701901] Int J Cancer. 2007 Dec 1;121(11):2451-7 [17688234] Cell. 2007 Nov 16;131(4):643-5 [18022355] BMC Bioinformatics. 2007;8:448 [18005446] J Exp Med. 2008 Jan 21;205(1):35-42 [18158319] Biochem Biophys Res Commun. 2008 Apr 11;368(3):476-82 [18249188] Int J Cancer. 2008 May 15;122(10):2377-9 [18224692] Curr Top Microbiol Immunol. 2008;321:59-83 [18727487] Genes Immun. 2008 Oct;9(7):613-23 [18650831] Microbiol Mol Biol Rev. 2009 Jun;73(2):348-70 [19487731] Int J Cancer. 2009 Oct 15;125(8):1851-8 [19585495] PLoS One. 2010;5(1):e8667 [20084279] Gynecol Oncol. 2010 Mar;116(3):544-8 [19959217] J Invest Dermatol. 2000 Jun;114(6):1148-53 [10844558] Science. 2002 Jun 21;296(5576):2225-9 [12029063] IARC Sci Publ. 1980;(32):5-338 [7216345] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1002/ijc.26016 ER - TY - CPAPER T1 - Eukaryotic genome annotation pipeline T2 - International Plant & Animal Genome XX (PAG XX) AN - 1313091979; 6130949 JF - International Plant & Animal Genome XX (PAG XX) AU - Thibaud-Nissen, Francoise Y1 - 2012/01/14/ PY - 2012 DA - 2012 Jan 14 KW - Pipelines KW - Genomes KW - Bibliographic information UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313091979?accountid=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=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.atitle=Eukaryotic+genome+annotation+pipeline&rft.au=Thibaud-Nissen%2C+Francoise&rft.aulast=Thibaud-Nissen&rft.aufirst=Francoise&rft.date=2012-01-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.issn=&rft_id=info:doi/ L2 - https://pag.confex.com/pag/xx/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 - Primary Data Submission Portal T2 - International Plant & Animal Genome XX (PAG XX) AN - 1313091803; 6130947 JF - International Plant & Animal Genome XX (PAG XX) AU - Pruitt, Kim AU - Mizrachi, Ilene Y1 - 2012/01/14/ PY - 2012 DA - 2012 Jan 14 KW - Data processing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313091803?accountid=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=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.atitle=Primary+Data+Submission+Portal&rft.au=Pruitt%2C+Kim%3BMizrachi%2C+Ilene&rft.aulast=Pruitt&rft.aufirst=Kim&rft.date=2012-01-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.issn=&rft_id=info:doi/ L2 - https://pag.confex.com/pag/xx/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 - Annual Report of Genome Sequencing Projects T2 - International Plant & Animal Genome XX (PAG XX) AN - 1313076702; 6130951 JF - International Plant & Animal Genome XX (PAG XX) AU - Pruitt, Kim AU - Tatusova, Tatiana AU - Clark, Karen Y1 - 2012/01/14/ PY - 2012 DA - 2012 Jan 14 KW - Genomes KW - Annual reports UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313076702?accountid=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=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.atitle=Annual+Report+of+Genome+Sequencing+Projects&rft.au=Pruitt%2C+Kim%3BTatusova%2C+Tatiana%3BClark%2C+Karen&rft.aulast=Pruitt&rft.aufirst=Kim&rft.date=2012-01-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.issn=&rft_id=info:doi/ L2 - https://pag.confex.com/pag/xx/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 - Connecting the Lab to the Genome: CloneDB T2 - International Plant & Animal Genome XX (PAG XX) AN - 1313076659; 6130950 JF - International Plant & Animal Genome XX (PAG XX) AU - Church, Deanna Y1 - 2012/01/14/ PY - 2012 DA - 2012 Jan 14 KW - Genomes UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313076659?accountid=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=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.atitle=Connecting+the+Lab+to+the+Genome%3A+CloneDB&rft.au=Church%2C+Deanna&rft.aulast=Church&rft.aufirst=Deanna&rft.date=2012-01-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.issn=&rft_id=info:doi/ L2 - https://pag.confex.com/pag/xx/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 - Genome Workbench: a Desktop Application for Viewing and Analyzing Sequence Data T2 - International Plant & Animal Genome XX (PAG XX) AN - 1313075529; 6130161 JF - International Plant & Animal Genome XX (PAG XX) AU - Church, Deanna AU - Kuznetsov, Anatoliy AU - Cohen, Robert AU - Falk, Robert AU - Katargin, Roman AU - Voronov, Yuri AU - Wu, Liangshou AU - Ostell, James AU - DiCuccio, Michael Y1 - 2012/01/14/ PY - 2012 DA - 2012 Jan 14 KW - Genomes KW - Data processing KW - Nucleotide sequence UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313075529?accountid=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=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.atitle=Genome+Workbench%3A+a+Desktop+Application+for+Viewing+and+Analyzing+Sequence+Data&rft.au=Church%2C+Deanna%3BKuznetsov%2C+Anatoliy%3BCohen%2C+Robert%3BFalk%2C+Robert%3BKatargin%2C+Roman%3BVoronov%2C+Yuri%3BWu%2C+Liangshou%3BOstell%2C+James%3BDiCuccio%2C+Michael&rft.aulast=Church&rft.aufirst=Deanna&rft.date=2012-01-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.issn=&rft_id=info:doi/ L2 - https://pag.confex.com/pag/xx/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 - dbSNP and dbVar: NCBI Databases of Simple and Structural Variations T2 - International Plant & Animal Genome XX (PAG XX) AN - 1313074999; 6130046 JF - International Plant & Animal Genome XX (PAG XX) AU - Phan, Lon AU - Ward, Ming AU - Zhang, Hua AU - Rudnev, Dmitry AU - Kholodov, Mike AU - Shao, David AU - Shekhtman, Eugene AU - Maiti, Rama AU - Lopez, John AU - Hefferon, Tim AU - Garner, John AU - Church, Deanna AU - Sirotkin, Karl AU - Maglott, Donna AU - Feolo, Mike AU - Sherry, Steve Y1 - 2012/01/14/ PY - 2012 DA - 2012 Jan 14 KW - Databases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313074999?accountid=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=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.atitle=dbSNP+and+dbVar%3A+NCBI+Databases+of+Simple+and+Structural+Variations&rft.au=Phan%2C+Lon%3BWard%2C+Ming%3BZhang%2C+Hua%3BRudnev%2C+Dmitry%3BKholodov%2C+Mike%3BShao%2C+David%3BShekhtman%2C+Eugene%3BMaiti%2C+Rama%3BLopez%2C+John%3BHefferon%2C+Tim%3BGarner%2C+John%3BChurch%2C+Deanna%3BSirotkin%2C+Karl%3BMaglott%2C+Donna%3BFeolo%2C+Mike%3BSherry%2C+Steve&rft.aulast=Phan&rft.aufirst=Lon&rft.date=2012-01-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.issn=&rft_id=info:doi/ L2 - https://pag.confex.com/pag/xx/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 - NCBI SRA Toolkit Technology for Next Generation Sequence Data T2 - International Plant & Animal Genome XX (PAG XX) AN - 1313074911; 6130043 JF - International Plant & Animal Genome XX (PAG XX) AU - Sherry, Steve AU - Xiao, Chunlin AU - Yaschenko, Eugene AU - Durbrow, Kenneth AU - Kimelman, Michael AU - Rodarmer, Kurt AU - Shumway, Martin AU - Ostell, James Y1 - 2012/01/14/ PY - 2012 DA - 2012 Jan 14 KW - Technology KW - Data processing UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313074911?accountid=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=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.atitle=NCBI+SRA+Toolkit+Technology+for+Next+Generation+Sequence+Data&rft.au=Sherry%2C+Steve%3BXiao%2C+Chunlin%3BYaschenko%2C+Eugene%3BDurbrow%2C+Kenneth%3BKimelman%2C+Michael%3BRodarmer%2C+Kurt%3BShumway%2C+Martin%3BOstell%2C+James&rft.aulast=Sherry&rft.aufirst=Steve&rft.date=2012-01-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.issn=&rft_id=info:doi/ L2 - https://pag.confex.com/pag/xx/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 - Managing Multiple Assemblies: Comparative Genomics Tools for Annotation and Visualization T2 - International Plant & Animal Genome XX (PAG XX) AN - 1313065346; 6130056 JF - International Plant & Animal Genome XX (PAG XX) AU - Church, Deanna Y1 - 2012/01/14/ PY - 2012 DA - 2012 Jan 14 KW - genomics KW - Bibliographic information UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313065346?accountid=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=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.atitle=Managing+Multiple+Assemblies%3A+Comparative+Genomics+Tools+for+Annotation+and+Visualization&rft.au=Church%2C+Deanna&rft.aulast=Church&rft.aufirst=Deanna&rft.date=2012-01-14&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=International+Plant+%26+Animal+Genome+XX+%28PAG+XX%29&rft.issn=&rft_id=info:doi/ L2 - https://pag.confex.com/pag/xx/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 - Bubblegrams Reveal the Inner Body of Bacteriophage {phi}KZ AN - 954652964; 16243358 AB - Dense packing of macromolecules in cellular compartments and higher-order assemblies makes it difficult to pick out even quite large components in electron micrographs, despite nominally high resolution. Immunogold labeling and histochemical procedures offer ways to map certain components but are limited in their applicability. Here, we present a differential mapping procedure, based on the physical principle of protein's greater sensitivity to radiation damage compared with that of nucleic acid. JF - Science (Washington) AU - Wu, Weimin AU - Thomas, Julie A AU - Cheng, Naiqian AU - Black, Lindsay W AU - Steven, Alasdair C AD - Laboratory of Structural Biology, National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), National Institutes of Health, Bethesda, MD 20892, USA Y1 - 2012/01/13/ PY - 2012 DA - 2012 Jan 13 SP - 182 PB - American Association for the Advancement of Science, 1200 New York Avenue, NW Washington DC 20005 United States VL - 335 IS - 6065 SN - 0036-8075, 0036-8075 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Virology & AIDS Abstracts KW - Macromolecules KW - Bacteria KW - nucleic acids KW - A:01490 KW - V:22320 UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/954652964?accountid=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+%28Washington%29&rft.atitle=Bubblegrams+Reveal+the+Inner+Body+of+Bacteriophage+%7Bphi%7DKZ&rft.au=Wu%2C+Weimin%3BThomas%2C+Julie+A%3BCheng%2C+Naiqian%3BBlack%2C+Lindsay+W%3BSteven%2C+Alasdair+C&rft.aulast=Wu&rft.aufirst=Weimin&rft.date=2012-01-13&rft.volume=335&rft.issue=6065&rft.spage=182&rft.isbn=&rft.btitle=&rft.title=Science+%28Washington%29&rft.issn=00368075&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-03-01 N1 - Last updated - 2014-02-21 N1 - SubjectsTermNotLitGenreText - nucleic acids; Bacteria ER - TY - JOUR T1 - Endogenous interleukin-4 regulates glutathione synthesis following acetaminophen-induced liver injury in mice. AN - 916520711; 22107450 AB - In a recent study, we reported that interleukin (IL)-4 had a protective role against acetaminophen (APAP)-induced liver injury (AILI), although the mechanism of protection was unclear. Here, we carried out more detailed investigations and have shown that one way IL-4 may control the severity of AILI is by regulating glutathione (GSH) synthesis. In the present studies, the protective role of IL-4 in AILI was established definitively by showing that C57BL/6J mice made deficient in IL-4 genetically (IL-4(-/-)) or by depletion with an antibody, were more susceptible to AILI than mice not depleted of IL-4. The increased susceptibility of IL-4(-/-) mice was not due to elevated levels of hepatic APAP-protein adducts but was associated with a prolonged reduction in hepatic GSH that was attributed to decreased gene expression of γ-glutamylcysteine ligase (γ-GCL). Moreover, administration of recombinant IL-4 to IL-4(-/-) mice postacetaminophen treatment diminished the severity of liver injury and increased γ-GCL and GSH levels. We also report that the prolonged reduction of GSH in APAP-treated IL-4(-/-) mice appeared to contribute toward increased liver injury by causing a sustained activation of c-Jun-N-terminal kinase (JNK) since levels of phosphorylated JNK remained significantly higher in the IL-4(-/-) mice up to 24 h after APAP treatment. Overall, these results show for the first time that IL-4 has a role in regulating the synthesis of GSH in the liver under conditions of cellular stress. This mechanism appears to be responsible at least in part for the protective role of IL-4 against AILI in mice and may have a similar role not only in AILI in humans but also in pathologies of the liver caused by other drugs and etiologies. JF - Chemical research in toxicology AU - Ryan, Pauline M AU - Bourdi, Mohammed AU - Korrapati, Midhun C AU - Proctor, William R AU - Vasquez, Ronald A AU - Yee, Steven B AU - Quinn, Timothy D AU - Chakraborty, Mala AU - Pohl, Lance R AD - Molecular and Cellular Toxicology Section, Laboratory of Molecular Immunology, Immunology Center, National Heart, Lung and Blood Institute, National Institutes of Health , 9000 Rockville Pike, Building 10, Room 8N110, Bethesda, Maryland 20892, United States. Y1 - 2012/01/13/ PY - 2012 DA - 2012 Jan 13 SP - 83 EP - 93 VL - 25 IS - 1 KW - Analgesics, Non-Narcotic KW - 0 KW - NF-E2-Related Factor 2 KW - Nfe2l2 protein, mouse KW - Interleukin-4 KW - 207137-56-2 KW - Acetaminophen KW - 362O9ITL9D KW - Cytochrome P-450 CYP2E1 KW - EC 1.14.13.- KW - JNK Mitogen-Activated Protein Kinases KW - EC 2.7.11.24 KW - Glutamate-Cysteine Ligase KW - EC 6.3.2.2 KW - Glutathione KW - GAN16C9B8O KW - Index Medicus KW - Animals KW - Liver -- pathology KW - Liver -- drug effects KW - Mice, Inbred C57BL KW - Liver -- metabolism KW - Mice KW - Cytochrome P-450 CYP2E1 -- metabolism KW - Glutamate-Cysteine Ligase -- metabolism KW - Male KW - NF-E2-Related Factor 2 -- metabolism KW - Mice, Knockout KW - JNK Mitogen-Activated Protein Kinases -- metabolism KW - Interleukin-4 -- genetics KW - Interleukin-4 -- metabolism KW - Chemical and Drug Induced Liver Injury -- pathology KW - Interleukin-4 -- deficiency KW - Glutathione -- metabolism KW - Analgesics, Non-Narcotic -- toxicity KW - Chemical and Drug Induced Liver Injury -- metabolism KW - Acetaminophen -- toxicity UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/916520711?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chemical+research+in+toxicology&rft.atitle=Endogenous+interleukin-4+regulates+glutathione+synthesis+following+acetaminophen-induced+liver+injury+in+mice.&rft.au=Ryan%2C+Pauline+M%3BBourdi%2C+Mohammed%3BKorrapati%2C+Midhun+C%3BProctor%2C+William+R%3BVasquez%2C+Ronald+A%3BYee%2C+Steven+B%3BQuinn%2C+Timothy+D%3BChakraborty%2C+Mala%3BPohl%2C+Lance+R&rft.aulast=Ryan&rft.aufirst=Pauline&rft.date=2012-01-13&rft.volume=25&rft.issue=1&rft.spage=83&rft.isbn=&rft.btitle=&rft.title=Chemical+research+in+toxicology&rft.issn=1520-5010&rft_id=info:doi/10.1021%2Ftx2003992 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-01 N1 - Date created - 2012-01-16 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Semin Liver Dis. 2008 May;28(2):175-87 [18452117] Chem Res Toxicol. 2007 Oct;20(10):1528-35 [17854155] Hepatology. 2008 Sep;48(3):889-97 [18712839] Gastroenterology. 2008 Oct;135(4):1311-21 [18700144] J Exp Med. 2008 Oct 27;205(11):2595-608 [18852293] J Clin Invest. 2009 Feb;119(2):305-14 [19164858] Science. 2009 Mar 27;323(5922):1722-5 [19264983] Eur J Immunol. 2009 Jun;39(6):1652-63 [19499520] Handb Exp Pharmacol. 2010;(196):195-231 [20020264] Handb Exp Pharmacol. 2010;(196):369-405 [20020268] J Biol Chem. 2010 Mar 12;285(11):8244-55 [20061376] Toxicol Appl Pharmacol. 2010 Jul;246(1-2):8-17 [20423716] Biochem Biophys Res Commun. 2010 Jul 2;397(3):453-8 [20510877] Free Radic Biol Med. 2011 Jan 1;50(1):14-26 [20970495] J Hepatol. 2005 Jun;42(6):850-9 [15885356] J Biol Chem. 1989 Jun 15;264(17):9814-9 [2524496] J Pharmacol Exp Ther. 1990 Dec;255(3):935-41 [2262912] Adv Exp Med Biol. 1991;283:579-88 [2069026] J Immunol. 1992 Aug 15;149(4):1258-64 [1500716] Clin Pharmacol Ther. 2000 Mar;67(3):275-82 [10741631] Biochem Pharmacol. 2000 Jun 1;59(11):1433-9 [10751553] Hepatology. 2000 Aug;32(2):321-33 [10915739] Inflamm Res. 2000 Jun;49(6):275-9 [10939617] Cell Biol Toxicol. 2000;16(4):221-33 [11101004] Proc Nutr Soc. 2000 Nov;59(4):595-600 [11115795] Toxicol Sci. 2001 Jan;59(1):169-77 [11134556] Cytokine. 2001 Jan 21;13(2):75-84 [11145846] J Immunol. 2001 Feb 1;166(3):1903-11 [11160238] Blood. 2001 Mar 15;97(6):1742-9 [11238116] J Immunol. 2001 Apr 15;166(8):5225-35 [11290807] Genes Immun. 2001 Aug;2(5):287-9 [11528525] Respir Res. 2001;2(2):66-70 [11686867] Hepatology. 2002 Feb;35(2):289-98 [11826401] Chem Biol Interact. 2002 Nov 10;142(1-2):7-23 [12399152] Biomed Pharmacother. 2003 May-Jun;57(3-4):145-55 [12818476] Nat Rev Immunol. 2003 Jul;3(7):534-43 [12876556] J Immunol. 2003 Sep 15;171(6):3233-44 [12960353] Hepatology. 2004 May;39(5):1267-76 [15122755] Hepatology. 2004 May;39(5):1430-40 [15122773] Anal Biochem. 1969 Mar;27(3):502-22 [4388022] J Biol Chem. 1975 Feb 25;250(4):1422-6 [1112810] Biochem Pharmacol. 1976 Aug 1;25(15):1777-81 [942482] Res Commun Chem Pathol Pharmacol. 1981 Sep;33(3):463-73 [7330451] Biochem Pharmacol. 1987 Apr 15;36(8):1193-6 [3593409] J Biol Chem. 1989 Apr 25;264(12):6984-9 [2523386] Mol Cell Biol. 1992 Oct;12(10):4694-705 [1328860] Mol Pharmacol. 1993 Oct;44(4):707-15 [8232220] Free Radic Biol Med. 1995 Sep;19(3):303-10 [7557544] Res Commun Mol Pathol Pharmacol. 1996 Jun;92(3):259-73 [8827825] Drug Metab Dispos. 1996 Nov;24(11):1192-6 [8937852] J Pharmacol Exp Ther. 1997 Jan;280(1):501-5 [8996234] Adv Enzymol Relat Areas Mol Biol. 1999;73:209-67, xii [10218110] Antioxid Redox Signal. 2006 Sep-Oct;8(9-10):1865-79 [16987039] Microbiol Mol Biol Rev. 2006 Dec;70(4):1061-95 [17158707] Chem Res Toxicol. 2007 Feb;20(2):208-16 [17305405] Toxicol Appl Pharmacol. 2007 Apr 1;220(1):92-107 [17275868] Chem Res Toxicol. 2007 May;20(5):734-44 [17439248] J Biol Chem. 2007 Jun 1;282(22):16502-10 [17403689] Mol Carcinog. 2007 Aug;46(8):591-8 [17538955] J Biol Chem. 2007 Aug 17;282(33):23996-4003 [17573345] J Biol Chem. 2008 May 16;283(20):13565-77 [18337250] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1021/tx2003992 ER - TY - JOUR T1 - Evaluation of molecular modeling of agonist binding in light of the crystallographic structure of an agonist-bound A₂A adenosine receptor. AN - 916147700; 22104008 AB - Molecular modeling of agonist binding to the human A(2A) adenosine receptor (AR) was assessed and extended in light of crystallographic structures. Heterocyclic adenine nitrogens of cocrystallized agonist overlaid corresponding positions of the heterocyclic base of a bound triazolotriazine antagonist, and ribose moiety was coordinated in a hydrophilic region, as previously predicted based on modeling using the inactive receptor. Automatic agonist docking of 20 known potent nucleoside agonists to agonist-bound A(2A)AR crystallographic structures predicted new stabilizing protein interactions to provide a structural basis for previous empirical structure activity relationships consistent with previous mutagenesis results. We predicted binding of novel C2 terminal amino acid conjugates of A(2A)AR agonist CGS21680 and used these models to interpret effects on binding affinity of newly synthesized agonists. d-Amino acid conjugates were generally more potent than l-stereoisomers and free terminal carboxylates more potent than corresponding methyl esters. Amino acid moieties were coordinated close to extracellular loops 2 and 3. Thus, molecular modeling is useful in probing ligand recognition and rational design of GPCR-targeting compounds with specific pharmacological profiles. JF - Journal of medicinal chemistry AU - Deflorian, Francesca AU - Kumar, T Santhosh AU - Phan, Khai AU - Gao, Zhan-Guo AU - Xu, Fei AU - Wu, Huixian AU - Katritch, Vsevolod AU - Stevens, Raymond C AU - Jacobson, Kenneth A AD - Molecular Recognition Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Building 8A, Room B1A-19, Bethesda, Maryland 20892-0810, United States. Y1 - 2012/01/12/ PY - 2012 DA - 2012 Jan 12 SP - 538 EP - 552 VL - 55 IS - 1 KW - Adenosine A2 Receptor Agonists KW - 0 KW - Amino Acids KW - Ligands KW - Nucleosides KW - Phenethylamines KW - Receptor, Adenosine A2A KW - 2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine KW - 120225-54-9 KW - Adenosine KW - K72T3FS567 KW - Index Medicus KW - Animals KW - Stereoisomerism KW - Thermodynamics KW - Cricetulus KW - HEK293 Cells KW - Humans KW - Radioligand Assay KW - Structure-Activity Relationship KW - Binding Sites KW - Amino Acids -- chemistry KW - CHO Cells KW - Crystallography, X-Ray KW - Cricetinae KW - Protein Conformation KW - Models, Molecular KW - Adenosine -- analogs & derivatives KW - Adenosine -- chemistry KW - Phenethylamines -- chemical synthesis KW - Adenosine -- chemical synthesis KW - Adenosine A2 Receptor Agonists -- chemical synthesis KW - Nucleosides -- chemistry KW - Receptor, Adenosine A2A -- metabolism KW - Adenosine A2 Receptor Agonists -- chemistry KW - Adenosine -- pharmacology KW - Receptor, Adenosine A2A -- chemistry KW - Phenethylamines -- chemistry KW - Phenethylamines -- pharmacology KW - Adenosine A2 Receptor Agonists -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/916147700?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+medicinal+chemistry&rft.atitle=Evaluation+of+molecular+modeling+of+agonist+binding+in+light+of+the+crystallographic+structure+of+an+agonist-bound+A%E2%82%82A+adenosine+receptor.&rft.au=Deflorian%2C+Francesca%3BKumar%2C+T+Santhosh%3BPhan%2C+Khai%3BGao%2C+Zhan-Guo%3BXu%2C+Fei%3BWu%2C+Huixian%3BKatritch%2C+Vsevolod%3BStevens%2C+Raymond+C%3BJacobson%2C+Kenneth+A&rft.aulast=Deflorian&rft.aufirst=Francesca&rft.date=2012-01-12&rft.volume=55&rft.issue=1&rft.spage=538&rft.isbn=&rft.btitle=&rft.title=Journal+of+medicinal+chemistry&rft.issn=1520-4804&rft_id=info:doi/10.1021%2Fjm201461q LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-03-26 N1 - Date created - 2012-01-12 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Trends Pharmacol Sci. 2009 May;30(5):249-59 [19375807] Biochem Pharmacol. 2009 Apr 1;77(7):1117-24 [19041853] J Mol Recognit. 2009 Jul-Aug;22(4):307-18 [19353579] Bioorg Med Chem Lett. 2009 Aug 1;19(15):4471-5 [19501510] Handb Exp Pharmacol. 2009;(193):59-98 [19639279] J Med Chem. 2009 Dec 10;52(23):7669-77 [19580286] Bioorg Med Chem Lett. 2010 Feb 1;20(3):1219-24 [20031406] J Biol Chem. 2010 Apr 23;285(17):13032-44 [20147292] Science. 2010 Nov 19;330(6007):1066-71 [20929726] Nature. 2011 Jan 13;469(7329):175-80 [21228869] Nature. 2011 Jan 13;469(7329):241-4 [21228877] Nature. 2011 Mar 31;471(7340):656-60 [21389983] Nature. 2011 Mar 31;471(7340):651-5 [21389988] Science. 2011 Apr 15;332(6027):322-7 [21393508] Nature. 2011 Jun 23;474(7352):521-5 [21593763] Nature. 2011 Jul 7;475(7354):65-70 [21697825] Curr Opin Struct Biol. 2011 Aug;21(4):559-66 [21775127] Nature. 2011 Sep 29;477(7366):549-55 [21772288] Trends Pharmacol Sci. 2011 Nov;32(11):637-43 [21903279] Methods Mol Biol. 2000;126:363-74 [10685423] J Med Chem. 2000 Mar 23;43(6):1165-72 [10737749] J Med Chem. 2001 Feb 15;44(4):531-9 [11170643] Adv Drug Deliv Rev. 2001 Mar 1;46(1-3):3-26 [11259830] Nucleosides Nucleotides Nucleic Acids. 2001 Apr-Jul;20(4-7):343-60 [11563047] J Biol Chem. 2002 May 24;277(21):19056-63 [11891221] Mol Pharmacol. 2003 Jun;63(6):1256-72 [12761335] Circulation. 2004 Feb 3;109(4):457-64 [14734517] Bioorg Med Chem. 2004 May 1;12(9):2021-34 [15080906] Proteins. 2004 Nov 1;57(2):225-42 [15340911] Biochem Pharmacol. 2004 Nov 15;68(10):1985-93 [15476669] Biochem Pharmacol. 1973 Dec 1;22(23):3099-108 [4202581] J Mol Recognit. 1989 Dec;2(4):170-8 [2561548] Anal Biochem. 1990 Sep;189(2):231-4 [2177960] J Med Chem. 1991 Mar;34(3):1043-9 [2002448] Pharmacology. 1993;46(2):91-100 [8441759] J Biol Chem. 1994 Oct 7;269(40):24692-8 [7929142] J Biol Chem. 1995 Jun 9;270(23):13987-97 [7775460] Naunyn Schmiedebergs Arch Pharmacol. 1998 Jan;357(1):1-9 [9459566] Proteins. 1997;Suppl 1:215-20 [9485515] J Pharmacol Exp Ther. 1998 Aug;286(2):611-8 [9694911] Nat Rev Drug Discov. 2006 Mar;5(3):247-64 [16518376] Med Chem. 2005 Jul;1(4):405-21 [16789897] Eur J Pharmacol. 2007 Jun 14;564(1-3):219-25 [17382926] Trends Pharmacol Sci. 2008 Feb;29(2):79-83 [18194818] Nat Rev Drug Discov. 2008 Apr;7(4):339-57 [18382464] Nature. 2008 Jul 10;454(7201):183-7 [18563085] Nature. 2008 Jul 24;454(7203):486-91 [18594507] Nature. 2008 Sep 25;455(7212):497-502 [18818650] Science. 2008 Nov 21;322(5905):1211-7 [18832607] J Med Chem. 2009 May 28;52(10):3284-92 [19402631] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1021/jm201461q ER - TY - CPAPER T1 - Apoptosis - a probable mechanism of cell death in amyotrophic lateral sclerosis? :An in-vitro study T2 - 19th Biennial Meeting of the International Society for Developmental Neuroscience AN - 1313107190; 6120531 JF - 19th Biennial Meeting of the International Society for Developmental Neuroscience AU - Ghosh, S AU - Chandrasekhar Sagar, B AU - Alladi, P AU - Raju, T Y1 - 2012/01/11/ PY - 2012 DA - 2012 Jan 11 KW - Mortality KW - Amyotrophic lateral sclerosis KW - Apoptosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313107190?accountid=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+Biennial+Meeting+of+the+International+Society+for+Developmental+Neuroscience&rft.atitle=Apoptosis+-+a+probable+mechanism+of+cell+death+in+amyotrophic+lateral+sclerosis%3F+%3AAn+in-vitro+study&rft.au=Ghosh%2C+S%3BChandrasekhar+Sagar%2C+B%3BAlladi%2C+P%3BRaju%2C+T&rft.aulast=Ghosh&rft.aufirst=S&rft.date=2012-01-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=19th+Biennial+Meeting+of+the+International+Society+for+Developmental+Neuroscience&rft.issn=&rft_id=info:doi/ L2 - http://www.isdn-conference.elsevier.com/conference-programme.html LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Assessment of adult neurogenesis in the ventral subicular lesioned rats, an animal model with neurodegeneration and cognitive impairment T2 - 19th Biennial Meeting of the International Society for Developmental Neuroscience AN - 1313053512; 6120455 JF - 19th Biennial Meeting of the International Society for Developmental Neuroscience AU - Prem, N AU - Kutty, B Y1 - 2012/01/11/ PY - 2012 DA - 2012 Jan 11 KW - Animal models KW - Cognitive ability KW - Rats KW - Neurogenesis KW - Neurodegeneration UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313053512?accountid=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+Biennial+Meeting+of+the+International+Society+for+Developmental+Neuroscience&rft.atitle=Assessment+of+adult+neurogenesis+in+the+ventral+subicular+lesioned+rats%2C+an+animal+model+with+neurodegeneration+and+cognitive+impairment&rft.au=Prem%2C+N%3BKutty%2C+B&rft.aulast=Prem&rft.aufirst=N&rft.date=2012-01-11&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=19th+Biennial+Meeting+of+the+International+Society+for+Developmental+Neuroscience&rft.issn=&rft_id=info:doi/ L2 - http://www.isdn-conference.elsevier.com/conference-programme.html 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 Coenzyme F420 in the biochemistry and drug-susceptibility of Mycobacterium tuberculosis T2 - Annual Symposium of the Biochemical Society AN - 1312963831; 6129063 JF - Annual Symposium of the Biochemical Society AU - Barry, Clifton Y1 - 2012/01/10/ PY - 2012 DA - 2012 Jan 10 KW - Tuberculosis KW - Biochemistry KW - Coenzymes KW - Mycobacterium tuberculosis UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1312963831?accountid=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=Annual+Symposium+of+the+Biochemical+Society&rft.atitle=The+role+of+Coenzyme+F420+in+the+biochemistry+and+drug-susceptibility+of+Mycobacterium+tuberculosis&rft.au=Barry%2C+Clifton&rft.aulast=Barry&rft.aufirst=Clifton&rft.date=2012-01-10&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Annual+Symposium+of+the+Biochemical+Society&rft.issn=&rft_id=info:doi/ L2 - http://www.biochemistry.org/Conferences/AllConferences/tabid/379/View/Programme/Page/1/MeetingNo/SA127/Default.aspx LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Measurement of average transition-path time for protein folding in single molecule FRET experiments T2 - 2012 Gordon Research Conference on Protein Folding Dynamics Research Seminar AN - 1313077517; 6100632 JF - 2012 Gordon Research Conference on Protein Folding Dynamics Research Seminar AU - Chung, Hoi Y1 - 2012/01/07/ PY - 2012 DA - 2012 Jan 07 KW - Protein folding KW - fluorescence resonance energy transfer UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313077517?accountid=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+Gordon+Research+Conference+on+Protein+Folding+Dynamics+Research+Seminar&rft.atitle=Measurement+of+average+transition-path+time+for+protein+folding+in+single+molecule+FRET+experiments&rft.au=Chung%2C+Hoi&rft.aulast=Chung&rft.aufirst=Hoi&rft.date=2012-01-07&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Gordon+Research+Conference+on+Protein+Folding+Dynamics+Research+Seminar&rft.issn=&rft_id=info:doi/ L2 - http://www.grc.org/programs.aspx?year=2012&program=grs_protf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - CPAPER T1 - Effects of membrane lipids on the conformation and aggregation of the repeat domain of a functional amyloid, Pmel17 T2 - 2012 Gordon Research Conference on Protein Folding Dynamics Research Seminar AN - 1313045916; 6100637 JF - 2012 Gordon Research Conference on Protein Folding Dynamics Research Seminar AU - Jiang, Zhiping Y1 - 2012/01/07/ PY - 2012 DA - 2012 Jan 07 KW - Lipids KW - Membranes KW - Amyloid KW - Conformation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1313045916?accountid=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+Gordon+Research+Conference+on+Protein+Folding+Dynamics+Research+Seminar&rft.atitle=Effects+of+membrane+lipids+on+the+conformation+and+aggregation+of+the+repeat+domain+of+a+functional+amyloid%2C+Pmel17&rft.au=Jiang%2C+Zhiping&rft.aulast=Jiang&rft.aufirst=Zhiping&rft.date=2012-01-07&rft.volume=&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=2012+Gordon+Research+Conference+on+Protein+Folding+Dynamics+Research+Seminar&rft.issn=&rft_id=info:doi/ L2 - http://www.grc.org/programs.aspx?year=2012&program=grs_protf LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-26 N1 - Last updated - 2013-02-28 ER - TY - JOUR T1 - Molecular Basis for the Activation of a Catalytic Asparagine Residue in a Self-Cleaving Bacterial Autotransporter AN - 918069411; 16187680 AB - Autotransporters are secreted proteins produced by pathogenic Gram-negative bacteria. They consist of a membrane-embedded beta -domain and an extracellular passenger domain that is sometimes cleaved and released from the cell surface. We solved the structures of three noncleavable mutants of the autotransporter EspP to examine how it promotes asparagine cyclization to cleave its passenger. We found that cyclization is facilitated by multiple factors. The active-site asparagine is sterically constrained to conformations favorable for cyclization, while electrostatic interactions correctly orient the carboxamide group for nucleophilic attack. During molecular dynamics simulations, water molecules were observed to enter the active site and to form hydrogen bonds favorable for increasing the nucleophilicity of the active-site asparagine. When the activated asparagine attacks its main-chain carbonyl carbon, the resulting oxyanion is stabilized by a protonated glutamate. Upon cleavage, this proton could be transferred to the leaving amine group, helping overcome a significant energy barrier. Together, these findings provide insight into factors important for asparagine cyclization, a mechanism broadly used for protein cleavage. JF - Journal of Molecular Biology AU - Barnard, Travis J AU - Gumbart, James AU - Peterson, Janine H AU - Noinaj, Nicholas AU - Easley, Nicole C AU - Dautin, Nathalie AU - Kuszak, Adam J AU - Tajkhorshid, Emad AU - Bernstein, Harris D AU - Buchanan, Susan K AD - Laboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, US National Institutes of Health, Bethesda, MD 20892, USA, skbuchan@helix.nih.gov Y1 - 2012/01/06/ PY - 2012 DA - 2012 Jan 06 SP - 128 EP - 142 PB - Elsevier B.V., P.O. Box 211 Amsterdam 1000 AE Netherlands VL - 415 IS - 1 SN - 0022-2836, 0022-2836 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology KW - EspP KW - autocleavage KW - outer membrane protein KW - crystal structure KW - asparagine cyclization KW - Bacteria KW - Cell surface KW - Protons KW - Electrostatic properties KW - Asparagine KW - amines KW - Carbon KW - Hydrogen bonding KW - Gram-negative bacteria KW - Energy KW - Glutamic acid KW - carbonyls KW - A 01490:Miscellaneous KW - J 02450:Ecology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/918069411?accountid=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+Molecular+Biology&rft.atitle=Molecular+Basis+for+the+Activation+of+a+Catalytic+Asparagine+Residue+in+a+Self-Cleaving+Bacterial+Autotransporter&rft.au=Barnard%2C+Travis+J%3BGumbart%2C+James%3BPeterson%2C+Janine+H%3BNoinaj%2C+Nicholas%3BEasley%2C+Nicole+C%3BDautin%2C+Nathalie%3BKuszak%2C+Adam+J%3BTajkhorshid%2C+Emad%3BBernstein%2C+Harris+D%3BBuchanan%2C+Susan+K&rft.aulast=Barnard&rft.aufirst=Travis&rft.date=2012-01-06&rft.volume=415&rft.issue=1&rft.spage=128&rft.isbn=&rft.btitle=&rft.title=Journal+of+Molecular+Biology&rft.issn=00222836&rft_id=info:doi/10.1016%2Fj.jmb.2011.10.049 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-01-01 N1 - Last updated - 2015-10-28 N1 - SubjectsTermNotLitGenreText - Cell surface; amines; Carbon; Protons; Hydrogen bonding; Energy; Gram-negative bacteria; Electrostatic properties; Glutamic acid; carbonyls; Asparagine; Bacteria DO - http://dx.doi.org/10.1016/j.jmb.2011.10.049 ER - TY - JOUR T1 - Testing in Mice the Hypothesis That Melanin Is Protective in Malaria Infections AN - 926887988; 16287556 AB - Malaria has had the largest impact of any infectious disease on shaping the human genome, exerting enormous selective pressure on genes that improve survival in severe malaria infections. Modern humans originated in Africa and lost skin melanization as they migrated to temperate regions of the globe. Although it is well documented that loss of melanization improved cutaneous Vitamin D synthesis, melanin plays an evolutionary ancient role in insect immunity to malaria and in some instances melanin has been implicated to play an immunoregulatory role in vertebrates. Thus, we tested the hypothesis that melanization may be protective in malaria infections using mouse models. Congenic C57BL/6 mice that differed only in the gene encoding tyrosinase, a key enzyme in the synthesis of melanin, showed no difference in the clinical course of infection by Plasmodium yoelii 17XL, that causes severe anemia, Plasmodium berghei ANKA, that causes severe cerebral malaria or Plasmodium chabaudi AS that causes uncomplicated chronic disease. Moreover, neither genetic deficiencies in vitamin D synthesis nor vitamin D supplementation had an effect on survival in cerebral malaria. Taken together, these results indicate that neither melanin nor vitamin D production improve survival in severe malaria. JF - PLoS ONE AU - Waisberg, Michael AU - Vickers, Brandi K AU - Yager, Stephanie B AU - Lin, Christina K AU - Pierce, Susan K AD - Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America Y1 - 2012/01/05/ PY - 2012 DA - 2012 Jan 05 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 7 IS - 1 KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - Genomes KW - Immunoregulation KW - Melanin KW - Human diseases KW - Animal models KW - Survival KW - Malaria KW - Melanization KW - Supplementation KW - Public health KW - Infectious diseases KW - Plasmodium chabaudi KW - Plasmodium yoelii KW - Insect immunity KW - Aquatic insects KW - Skin KW - Anemia KW - Enzymes KW - Monophenol monooxygenase KW - Plasmodium berghei KW - Nutrient deficiency KW - Vitamin D KW - Anaemia KW - Chronic infection KW - Africa KW - Evolution KW - K 03410:Animal Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/926887988?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PLoS+ONE&rft.atitle=Testing+in+Mice+the+Hypothesis+That+Melanin+Is+Protective+in+Malaria+Infections&rft.au=Waisberg%2C+Michael%3BVickers%2C+Brandi+K%3BYager%2C+Stephanie+B%3BLin%2C+Christina+K%3BPierce%2C+Susan+K&rft.aulast=Waisberg&rft.aufirst=Michael&rft.date=2012-01-05&rft.volume=7&rft.issue=1&rft.spage=&rft.isbn=&rft.btitle=&rft.title=PLoS+ONE&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0029493 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-03-01 N1 - Last updated - 2015-10-28 N1 - SubjectsTermNotLitGenreText - Genomes; Human diseases; Anaemia; Vitamin D; Infectious diseases; Malaria; Aquatic insects; Evolution; Public health; Immunoregulation; Melanin; Skin; Animal models; Anemia; Survival; Enzymes; Melanization; Monophenol monooxygenase; Supplementation; Nutrient deficiency; Chronic infection; Insect immunity; Plasmodium chabaudi; Plasmodium yoelii; Plasmodium berghei; Africa DO - http://dx.doi.org/10.1371/journal.pone.0029493 ER - TY - JOUR T1 - Efficient extraction of vaccines formulated in aluminum hydroxide gel by including surfactants in the extraction buffer AN - 918055727; 16186399 AB - Efficient antigen extraction from vaccines formulated on aluminum hydroxide gels is a critical step for the evaluation of the quality of vaccines following formulation. It has been shown in our laboratory that the efficiency of antigen extraction from vaccines formulated on Alhydrogel decreased significantly with increased storage time. To increase antigen extraction efficiency, the present study determined the effect of surfactants on antigen recovery from vaccine formulations. The Plasmodium falciparum apical membrane antigen 1 (AMA1) formulated on Alhydrogel and stored at 2-8 degree C for 3 years was used as a model in this study. The AMA1 on Alhydrogel was extracted in the presence or absence of 30 mM sodium dodecyl sulfate (SDS) or 20 mM cetylpyridinium chloride in the extraction buffer (0.60 M citrate, 0.55 M phosphate, pH 8.5) using our standard antigen extraction protocols. Extracted AMA1 antigen was analyzed by 4-20% Tris-glycine SDS-PAGE followed by silver staining or western blotting. The results showed that inclusion of SDS or cetylpyridinium chloride in extraction buffer increased the antigen recovery dramatically and can be used for efficient characterization of Alhydrogel vaccines. JF - Vaccine AU - Zhu, Daming AU - Huang, Shuhui AU - McClellan, Holly AU - Dai, Weili AU - Syed, Najam R AU - Gebregeorgis, Elizabeth AU - Mullen, Gregory ED AU - Long, Carole AU - Martin, Laura B AU - Narum, David AU - Duffy, Patrick AU - Miller, Louis H AU - Saul, Allan AD - Laboratory of Malaria Immunology and Vaccinology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA, dzhu@niaid.nih.gov Y1 - 2012/01/05/ PY - 2012 DA - 2012 Jan 05 SP - 189 EP - 194 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 30 IS - 2 SN - 0264-410X, 0264-410X KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Immunology Abstracts KW - Alhydrogel KW - AMA1 KW - Extraction KW - SDS KW - Cetylpyridinium chloride KW - Apical membrane antigen 1 KW - Western blotting KW - Parasites KW - Storage life KW - Disease control KW - Aluminum hydroxide KW - Plasmodium falciparum KW - Citrates KW - Models KW - Gels KW - Antigens KW - Phosphate KW - Aluminium KW - Sodium lauryl sulfate KW - Vaccines KW - Hydroxides KW - pH effects KW - Surfactants KW - Citric acid KW - F 06905:Vaccines 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/918055727?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aasfaaquaticpollution&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Vaccine&rft.atitle=Efficient+extraction+of+vaccines+formulated+in+aluminum+hydroxide+gel+by+including+surfactants+in+the+extraction+buffer&rft.au=Zhu%2C+Daming%3BHuang%2C+Shuhui%3BMcClellan%2C+Holly%3BDai%2C+Weili%3BSyed%2C+Najam+R%3BGebregeorgis%2C+Elizabeth%3BMullen%2C+Gregory+ED%3BLong%2C+Carole%3BMartin%2C+Laura+B%3BNarum%2C+David%3BDuffy%2C+Patrick%3BMiller%2C+Louis+H%3BSaul%2C+Allan&rft.aulast=Zhu&rft.aufirst=Daming&rft.date=2012-01-05&rft.volume=30&rft.issue=2&rft.spage=189&rft.isbn=&rft.btitle=&rft.title=Vaccine&rft.issn=0264410X&rft_id=info:doi/10.1016%2Fj.vaccine.2011.11.025 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-01-01 N1 - Last updated - 2014-12-11 N1 - SubjectsTermNotLitGenreText - Parasites; Antigens; Storage life; Aluminium; Disease control; Vaccines; Citrates; Hydroxides; Surfactants; Gels; Apical membrane antigen 1; Western blotting; Phosphate; Sodium lauryl sulfate; Aluminum hydroxide; pH effects; Models; Citric acid; Cetylpyridinium chloride; Plasmodium falciparum DO - http://dx.doi.org/10.1016/j.vaccine.2011.11.025 ER - TY - JOUR T1 - Management of Needlestick Injuries: A House Officer Who Has a Needlestick AN - 920807576; 16199586 AB - Since its identification in 1985, human immunodeficiency virus (HIV) has challenged several aspects of health care delivery. Because HIV is a blood-borne infectious disease, from the early days of the epidemic, concern was raised about risks of occupational exposures and infections among health care workers. Despite the development of highly active antiretroviral therapy, which has effectively modulated HIV into a chronic disease in many settings, risks of occupational infection with 3 blood-borne pathogens remain in the health care workplace. Using the case of a house officer who has a needlestick during a resuscitation attempt, prevention of needlesticks including universal precautions and postexposure management of occupational HIV, hepatitis B, and hepatitis C exposures is discussed. JF - JAMA: Journal of the American Medical Association AU - Henderson, David K AD - Author Affiliation: Dr Henderson is Deputy Director for Clinical Care of the National Institutes of Health Clinical Center Y1 - 2012/01/04/ PY - 2012 DA - 2012 Jan 04 SP - 75 EP - 84 PB - American Medical Association, 515 N. State St. Chicago IL 60610 United States VL - 307 IS - 1 SN - 0098-7484, 0098-7484 KW - Risk Abstracts; Health & Safety Science Abstracts KW - Hepatitis KW - Housing KW - Health care KW - Human immunodeficiency virus KW - Residential areas KW - infection KW - Pathogens KW - Occupational exposure KW - Medical personnel KW - H 1000:Occupational Safety and Health KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920807576?accountid=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=JAMA%3A+Journal+of+the+American+Medical+Association&rft.atitle=Management+of+Needlestick+Injuries%3A+A+House+Officer+Who+Has+a+Needlestick&rft.au=Henderson%2C+David+K&rft.aulast=Henderson&rft.aufirst=David&rft.date=2012-01-04&rft.volume=307&rft.issue=1&rft.spage=75&rft.isbn=&rft.btitle=&rft.title=JAMA%3A+Journal+of+the+American+Medical+Association&rft.issn=00987484&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-02-01 N1 - Last updated - 2013-09-09 N1 - SubjectsTermNotLitGenreText - Hepatitis; Health care; Housing; Human immunodeficiency virus; infection; Residential areas; Pathogens; Medical personnel; Occupational exposure ER - TY - JOUR T1 - Pre- and Postnatal Polychlorinated Biphenyl Concentrations and Longitudinal Measures of Thymus Volume in Infants AN - 1017976399; 16725627 AB - Background: Previously, we reported an association between higher maternal polychlorinated biphenyl (PCB) concentrations and smaller thymus volume in newborns in a birth cohort residing in eastern Slovakia. Objective: In the present report we address whether thymus volume at later ages is influenced by prenatal and early postnatal PCB exposure. Methods: At the time of delivery, 1,134 mother-infant pairs were enrolled. Maternal and 6- and 16-month infant blood samples were collected and analyzed for 15 PCB congeners. Thymus volume was measured in infants shortly after birth and at ages 6 and 16 months using ultrasonography. Results: Higher maternal PCB concentration was associated with reduced thymus volume at birth [a 0.21 SD reduction in thymus volume for an increase in total maternal PCB concentration from the 10th to the 90th percentile; 95% confidence interval (CI): -0.37, -0.05], whereas maternal PCB concentration was not predictive of 6- and 16-month thymus volume. Six-month infant PCB concentration was associated with a 0.40 SD decrease in 6-month thymus volume (95% CI: -0.76, -0.04). There was also some suggestion that thymus volume at 16 months was positively associated with concurrent infant PCB concentration. Conclusions: The potential adverse effects of in utero PCB exposure on thymic development may extend beyond the neonatal period. Results from this highly exposed cohort provide suggestive evidence that postnatal PCB concentrations may be influential, but a smaller set of 6-month PCB measurements limited statistical power at that time point. Implications regarding impaired immunologic maturation or long-term clinical implications remain to be determined. JF - Environmental Health Perspectives AU - Jusko, Todd A AU - Sonneborn, Dean AU - Palkovicova, Lubica AU - Kocan, Anton AU - Drobna, Beata AU - Trnovec, Tomas AU - Hertz-Picciotto, Irva AD - Epidemiology Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, North Carolina, USA Y1 - 2012/01/03/ PY - 2012 DA - 2012 Jan 03 SP - 595 EP - 600 PB - US Government Printing Office, Superintendent of Documents, P.O. Box 371954 Pittsburgh PA 15250-7954 United States VL - 120 IS - 4 SN - 0091-6765, 0091-6765 KW - Toxicology Abstracts; Environment Abstracts KW - atrophy KW - cohort KW - epidemiology KW - immune KW - Roma KW - T cell KW - Age KW - Slovakia KW - Statistics KW - Prenatal experience KW - Thymus KW - Intrauterine exposure KW - Ultrasonography KW - prenatal experience KW - Bioaccumulation KW - polychlorinated biphenyls KW - Congeners KW - Neonates KW - PCB compounds KW - PCB KW - Side effects KW - Infants KW - X 24350:Industrial Chemicals KW - ENA 02:Toxicology & Environmental Safety UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1017976399?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Environmental+Health+Perspectives&rft.atitle=Pre-+and+Postnatal+Polychlorinated+Biphenyl+Concentrations+and+Longitudinal+Measures+of+Thymus+Volume+in+Infants&rft.au=Jusko%2C+Todd+A%3BSonneborn%2C+Dean%3BPalkovicova%2C+Lubica%3BKocan%2C+Anton%3BDrobna%2C+Beata%3BTrnovec%2C+Tomas%3BHertz-Picciotto%2C+Irva&rft.aulast=Jusko&rft.aufirst=Todd&rft.date=2012-01-03&rft.volume=120&rft.issue=4&rft.spage=595&rft.isbn=&rft.btitle=&rft.title=Environmental+Health+Perspectives&rft.issn=00916765&rft_id=info:doi/10.1289%2Fehp.1104229 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2015-05-13 N1 - SubjectsTermNotLitGenreText - Age; Prenatal experience; Statistics; polychlorinated biphenyls; Thymus; Congeners; Intrauterine exposure; Neonates; Ultrasonography; Side effects; PCB; Infants; prenatal experience; Bioaccumulation; PCB compounds; Slovakia DO - http://dx.doi.org/10.1289/ehp.1104229 ER - TY - JOUR T1 - Correlates of anti-EBV EBNA1 IgA positivity among unaffected relatives from nasopharyngeal carcinoma multiplex families AN - 1008826043; 16429782 AB - Background: To determine whether non-viral nasopharyngeal carcinoma (NPC) risk factors might be associated with (and mediated through) Epstein-Barr virus (EBV) serological responses linked to NPC risk, we evaluated predictors of risk of anti-EBNA1 IgA seropositivity and other markers among unaffected relatives from a large NPC family study in Taiwan. Methods: Multivariate logistic regression conditioned on family was used to examine the associations between sociodemographic, dietary, lifestyle, and occupational variables and risk of anti-EBV EBNA1 IgA positivity, anti-VCA IgA, and anti-DNase positivity. Results: Among 2393 unaffected relatives from 319 multiplex families, 1180 (49.3%) were anti-EBV EBNA1 IgA seropositive. None of the associations with anti-EBNA1 IgA were statistically significant, except for being 31-50 years of age (vs <30, adjusted ORs 0.51-0.57). For one or more EBV serological markers, there were suggestive associations for older age, GuangDong firm salted fish, betel use, current alcohol use, and male gender. Conclusion: Overall, we found little evidence to suggest that non-viral NPC risk factors significantly alter EBV serological patterns, suggesting that non-viral NPC risk factors act through pathways independent of EBV serological responses. JF - British Journal of Cancer AU - Chang, C M AU - Yu, K J AU - Hsu, W L AU - Major, J M AU - Chen, J Y AU - Lou, P J AU - Liu, M Y AU - Diehl, S R AU - Goldstein, A M AU - Chen, C J AU - Hildesheim, A AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, 6120 Executive Blvd., EPS 7073, Rockville, MD, USA Y1 - 2012/01/03/ PY - 2012 DA - 2012 Jan 03 SP - 206 EP - 209 PB - Nature Publishing Group, The Macmillan Building London N1 9XW United Kingdom VL - 106 IS - 1 SN - 0007-0920, 0007-0920 KW - Virology & AIDS Abstracts; Immunology Abstracts; Risk Abstracts KW - Diets KW - Alcohol KW - Taiwan KW - Age KW - Statistical analysis KW - Cancer KW - Family studies KW - Epstein-Barr virus KW - Immunoglobulin A KW - Nasopharyngeal carcinoma KW - Risk factors KW - Gender KW - alcohols KW - Geriatrics KW - Fish KW - F 06915:Cancer Immunology KW - R2 23060:Medical and environmental health KW - V 22370:Oncology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008826043?accountid=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=Correlates+of+anti-EBV+EBNA1+IgA+positivity+among+unaffected+relatives+from+nasopharyngeal+carcinoma+multiplex+families&rft.au=Chang%2C+C+M%3BYu%2C+K+J%3BHsu%2C+W+L%3BMajor%2C+J+M%3BChen%2C+J+Y%3BLou%2C+P+J%3BLiu%2C+M+Y%3BDiehl%2C+S+R%3BGoldstein%2C+A+M%3BChen%2C+C+J%3BHildesheim%2C+A&rft.aulast=Chang&rft.aufirst=C&rft.date=2012-01-03&rft.volume=106&rft.issue=1&rft.spage=206&rft.isbn=&rft.btitle=&rft.title=British+Journal+of+Cancer&rft.issn=00070920&rft_id=info:doi/10.1038%2Fbjc.2011.502 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2013-06-28 N1 - SubjectsTermNotLitGenreText - Immunoglobulin A; Nasopharyngeal carcinoma; Risk factors; Geriatrics; alcohols; Statistical analysis; Family studies; Diets; Alcohol; Age; Gender; Fish; Cancer; Epstein-Barr virus; Taiwan DO - http://dx.doi.org/10.1038/bjc.2011.502 ER - TY - JOUR T1 - Plasma clusterin concentration is associated with longitudinal brain atrophy in mild cognitive impairment AN - 902354961; 15913264 AB - Recent genetic and proteomic studies demonstrate that clusterin/apolipoprotein-J is associated with risk, pathology, and progression of Alzheimer's disease (AD). Our main aim was to examine associations between plasma clusterin concentration and longitudinal changes in brain volume in normal aging and mild cognitive impairment (MCI). A secondary objective was to examine associations between peripheral concentration of clusterin and its concentration in the brain within regions that undergo neuropathological changes in AD. Non-demented individuals (N = 139; mean baseline age 70.5 years) received annual volumetric MRI (912 MRI scans in total) over a mean six-year interval. Sixteen participants (92 MRI scans in total) were diagnosed during the course of the study with amnestic MCI. Clusterin concentration was assayed by ELISA in plasma samples collected within a year of the baseline MRI. Mixed effects regression models investigated whether plasma clusterin concentration was associated with rates of brain atrophy for control and MCI groups and whether these associations differed between groups. In a separate autopsy sample of individuals with AD (N = 17) and healthy controls (N = 4), we examined the association between antemortem clusterin concentration in plasma and postmortem levels in the superior temporal gyrus, hippocampus and cerebellum. The associations of plasma clusterin concentration with rates of change in brain volume were significantly different between MCI and control groups in several volumes including whole brain, ventricular CSF, temporal gray matter as well as parahippocampal, superior temporal and cingulate gyri. Within the MCI but not control group, higher baseline concentration of plasma clusterin was associated with slower rates of brain atrophy in these regions. In the combined autopsy sample of AD and control cases, representing a range of severity in AD pathology, we observed a significant association between clusterin concentration in the plasma and that in the superior temporal gyrus. Our findings suggest that clusterin, a plasma protein with roles in amyloid clearance, complement inhibition and apoptosis, is associated with rate of brain atrophy in MCI. Furthermore, peripheral concentration of clusterin also appears to reflect its concentration within brain regions vulnerable to AD pathology. These findings in combination suggest an influence of this multi-functional protein on early stages of progression in AD pathology. JF - NeuroImage AU - Thambisetty, Madhav AU - An, Yang AU - Kinsey, Anna AU - Koka, Deepthi AU - Saleem, Muzamil AU - GIe85% of urines were positive for modafinil, N = 36), and the lower three quartiles of modafinil 200 and 400 mg groups (N = 106). Conclusions: Although these data suggest that modafinil, plus group behavioral therapy, was not effective for decreasing methamphetamine use, the study is probably inconclusive because of inadequate compliance with taking medication. [Copyright Elsevier Ireland Ltd.] JF - Drug and Alcohol Dependence AU - Anderson, Ann L AU - Li, Shou-Hua AU - Biswas, Kousick AU - McSherry, Frances AU - Holmes, Tyson AU - Iturriaga, Erin AU - Kahn, Roberta AU - Chiang, Nora AU - Beresford, Thomas AU - Campbell, Jan AU - Haning, William AU - Mawhinney, Joseph AU - McCann, Michael AU - Rawson, Richard AU - Stock, Christopher AU - Weis, Dennis AU - Yu, Elmer AU - Elkashef, Ahmed M AD - Division of Pharmacotherapies and Medical Consequences of Drug Abuse, National Institute on Drug Abuse, National Institutes of Health, Bethesda, MD, United States Y1 - 2012///0, PY - 2012 DA - 0, 2012 SP - 135 EP - 141 PB - Elsevier Ireland, Amsterdam The Netherlands VL - 120 IS - 1-3 SN - 0376-8716, 0376-8716 KW - Methamphetamine Substance-related disorders Drug therapy Modafinil Medication adherence Attention Deficit Hyperactivity Disorders KW - Methamphetamine KW - Urine KW - Compliance KW - Clinics KW - Modafinil KW - Outpatient treatment KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/925739852?accountid=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=Drug+and+Alcohol+Dependence&rft.atitle=Modafinil+for+the+treatment+of+methamphetamine+dependence&rft.au=Anderson%2C+Ann+L%3BLi%2C+Shou-Hua%3BBiswas%2C+Kousick%3BMcSherry%2C+Frances%3BHolmes%2C+Tyson%3BIturriaga%2C+Erin%3BKahn%2C+Roberta%3BChiang%2C+Nora%3BBeresford%2C+Thomas%3BCampbell%2C+Jan%3BHaning%2C+William%3BMawhinney%2C+Joseph%3BMcCann%2C+Michael%3BRawson%2C+Richard%3BStock%2C+Christopher%3BWeis%2C+Dennis%3BYu%2C+Elmer%3BElkashef%2C+Ahmed+M&rft.aulast=Anderson&rft.aufirst=Ann&rft.date=2012-01-01&rft.volume=120&rft.issue=1-3&rft.spage=135&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 - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-05-01 N1 - Last updated - 2016-09-27 N1 - CODEN - DADEDV N1 - SubjectsTermNotLitGenreText - Modafinil; Methamphetamine; Urine; Compliance; Clinics; Outpatient treatment DO - http://dx.doi.org/10.1016/j.drugalcdep.2011.07.007 ER - TY - JOUR T1 - Sex and hedgehog: roles of genes in the hedgehog signaling pathway in mammalian sexual differentiation. AN - 922757380; 22105695 AB - The chromosome status of the mammalian embryo initiates a multistage process of sexual development in which the bipotential reproductive system establishes itself as either male or female. These events are governed by intricate cell-cell and interorgan communication that is regulated by multiple signaling pathways. The hedgehog signaling pathway was originally identified for its key role in the development of Drosophila, but is now recognized as a critical developmental regulator in many species, including humans. In addition to its developmental roles, the hedgehog signaling pathway also modulates adult organ function, and misregulation of this pathway often leads to diseases, such as cancer. The hedgehog signaling pathway acts through its morphogenetic ligands that signal from ligand-producing cells to target cells over a specified distance. The target cells then respond in a graded manner based on the concentration of the ligands that they are exposed to. Through this unique mechanism of action, the hedgehog signaling pathway elicits cell fate determination, epithelial-mesenchymal interactions, and cellular homeostasis. Here, we review current findings on the roles of hedgehog signaling in the sexually dimorphic development of the reproductive organs with an emphasis on mammals and comparative evidence in other species. JF - Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology AU - Franco, Heather L AU - Yao, Humphrey H-C AD - Reproductive Developmental Biology Group, Laboratory of Reproductive and Developmental Toxicity, National Institute of Environmental Health Sciences, 111 TW Alexander Drive, Research Triangle Park, NC 27709, USA. Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 247 EP - 258 VL - 20 IS - 1 KW - Hedgehog Proteins KW - 0 KW - Index Medicus KW - Leydig Cells -- cytology KW - Animals KW - Mammals KW - Germ Cells -- growth & development KW - Embryo, Mammalian -- metabolism KW - Germ Cells -- cytology KW - Germ Cells -- metabolism KW - Leydig Cells -- metabolism KW - Genes KW - Sex Chromosomes -- genetics KW - Embryo, Mammalian -- cytology KW - Fetal Development KW - Reproduction KW - Sex Chromosomes -- metabolism KW - Male KW - Female KW - Gene Expression Regulation, Developmental KW - Hedgehog Proteins -- metabolism KW - Hedgehog Proteins -- genetics KW - Sex Differentiation KW - Signal Transduction KW - Sex UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/922757380?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Chromosome+research+%3A+an+international+journal+on+the+molecular%2C+supramolecular+and+evolutionary+aspects+of+chromosome+biology&rft.atitle=Sex+and+hedgehog%3A+roles+of+genes+in+the+hedgehog+signaling+pathway+in+mammalian+sexual+differentiation.&rft.au=Franco%2C+Heather+L%3BYao%2C+Humphrey+H-C&rft.aulast=Franco&rft.aufirst=Heather&rft.date=2012-01-01&rft.volume=20&rft.issue=1&rft.spage=247&rft.isbn=&rft.btitle=&rft.title=Chromosome+research+%3A+an+international+journal+on+the+molecular%2C+supramolecular+and+evolutionary+aspects+of+chromosome+biology&rft.issn=1573-6849&rft_id=info:doi/10.1007%2Fs10577-011-9254-z LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-07 N1 - Date created - 2012-02-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: PLoS Genet. 2007 Jun;3(6):e102 [17590085] Biochem Biophys Res Commun. 2007 Nov 23;363(3):757-61 [17904097] J Neurosci. 2008 Jul 16;28(29):7350-8 [18632939] Rev Endocr Metab Disord. 2008 Sep;9(3):227-36 [18633712] Genes Dev. 2008 Sep 15;22(18):2454-72 [18794343] PLoS One. 2008;3(9):e3285 [18818749] Biol Reprod. 2009 Feb;80(2):258-63 [18843087] Dev Biol. 2009 Feb 1;326(1):112-20 [19041858] Dev Biol. 2009 May 1;329(1):96-103 [19268447] Dev Biol. 2009 Apr 15;328(2):355-62 [19389345] Dev Biol. 2009 Apr 15;328(2):342-54 [19389352] Mol Endocrinol. 2009 May;23(5):711-23 [19196835] Reproduction. 2009 Aug;138(2):329-39 [19433502] Microsc Res Tech. 2009 Nov;72(11):809-15 [19484749] Development. 2009 Dec;136(23):3949-57 [19906862] J Androl. 2010 Jan-Feb;31(1):11-5 [19875489] Biol Reprod. 2010 Apr;82(4):783-90 [20056671] Biol Reprod. 2010 May;82(5):991-9 [20130264] Mol Endocrinol. 2010 May;24(5):930-40 [20219888] Development. 2010 Jul;137(13):2079-94 [20530542] Zoolog Sci. 2010 Oct;27(10):804-10 [20887178] Cell. 2010 Dec 10;143(6):978-90 [21145463] Proc Natl Acad Sci U S A. 2011 Jan 4;108(1):167-72 [21173261] Reproduction. 2011 Feb;141(2):217-25 [21062903] Nat Commun. 2010;1:23 [20975695] Biol Reprod. 2011 May;84(5):894-9 [21209421] Dev Cell. 2011 May 17;20(5):677-88 [21571224] Nat Rev Genet. 2011 Jun;12(6):393-406 [21502959] Endocr Rev. 2011 Jun;32(3):404-21 [21257780] Biol Reprod. 2000 Dec;63(6):1825-38 [11090455] Development. 2001 Jul;128(14):2649-60 [11526072] Cell. 2001 Sep 21;106(6):759-69 [11572781] Biol Reprod. 2001 Nov;65(5):1392-402 [11673255] Development. 2001 Nov;128(21):4241-50 [11684660] Biol Reprod. 2001 Dec;65(6):1663-71 [11717126] Dev Biol. 2002 May 15;245(2):280-90 [11977981] Genes Dev. 2002 Jun 1;16(11):1433-40 [12050120] Dev Biol. 2002 Jun 15;246(2):356-65 [12051821] Dev Biol. 2002 Jul 1;247(1):26-46 [12074550] Development. 2002 Sep;129(17):4111-24 [12163413] Mol Endocrinol. 2002 Oct;16(10):2338-48 [12351698] Development. 2003 Jan;130(2):295-305 [12466197] Biol Reprod. 2003 Jul;69(1):8-14 [12672657] Am J Med Genet A. 2003 Nov 15;123A(1):5-28 [14556242] Nat Rev Genet. 2003 Dec;4(12):969-80 [14631357] J Androl. 2004 Jul-Aug;25(4):514-22 [15223840] J Clin Endocrinol Metab. 2004 Sep;89(9):4480-3 [15356051] Nature. 1980 Oct 30;287(5785):795-801 [6776413] Ann N Y Acad Sci. 1984;438:435-46 [6598327] Development. 1990 Jul;109(3):635-46 [2401216] Nature. 1991 May 9;351(6322):117-21 [2030730] Dev Biol. 1995 Nov;172(1):126-38 [7589793] Development. 1996 Apr;122(4):1125-35 [8620839] Curr Biol. 1996 Mar 1;6(3):298-304 [8805249] Endocrinology. 2005 Aug;146(8):3558-66 [15878962] Mol Endocrinol. 2005 Sep;19(9):2299-308 [15890675] Reproduction. 2005 Oct;130(4):509-16 [16183868] Dev Dyn. 2005 Oct;234(2):422-31 [16145667] Endocrinology. 2011 Jul;152(7):2894-903 [21586556] Dev Cell. 2011 Aug 16;21(2):315-27 [21820362] Eur J Med Genet. 2011 Nov-Dec;54(6):e529-34 [21816240] Genesis. 2011 Oct;49(10):753-75 [21735540] Genesis. 2012 Jan;50(1):28-40 [21809434] Development. 2000 May;127(10):2165-76 [10769240] Development. 2000 Jun;127(11):2471-9 [10804187] Genes Dev. 2000 Aug 1;14(15):1933-44 [10921907] Am J Hum Genet. 2000 Nov;67(5):1302-5 [11017805] Mol Hum Reprod. 2005 Nov;11(11):833-6 [16390857] J Androl. 2006 Mar-Apr;27(2):225-32 [16278368] Nat Genet. 2006 Oct;38(10):1204-9 [16951680] Dev Dyn. 2006 Nov;235(11):3063-70 [16958114] Endocrinology. 2007 Aug;148(8):3704-10 [17495005] Biol Reprod. 2007 Aug;77(2):226-36 [17392501] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s10577-011-9254-z ER - TY - JOUR T1 - Circulating Vitamin D and Risk of Prostate Cancer-Response AN - 920798085; 16199319 JF - Cancer Epidemiology, Biomarkers & Prevention AU - Albanes, Demetrius AU - Weinstein, Stephanie J AU - Mondul, Alison M AU - Virtamo, Jarmo AD - Authors' Affiliations: Nutritional Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, Maryland Y1 - 2012 PY - 2012 DA - 2012 SP - 247 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 1 SN - 1055-9965, 1055-9965 KW - Risk Abstracts KW - Bioindicators KW - vitamins KW - prevention KW - Cancer KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920798085?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Epidemiology%2C+Biomarkers+%26+Prevention&rft.atitle=Circulating+Vitamin+D+and+Risk+of+Prostate+Cancer-Response&rft.au=Albanes%2C+Demetrius%3BWeinstein%2C+Stephanie+J%3BMondul%2C+Alison+M%3BVirtamo%2C+Jarmo&rft.aulast=Albanes&rft.aufirst=Demetrius&rft.date=2012-01-01&rft.volume=21&rft.issue=1&rft.spage=247&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 - 2012-02-01 N1 - Last updated - 2012-03-29 N1 - SubjectsTermNotLitGenreText - Bioindicators; vitamins; prevention; Cancer ER - TY - JOUR T1 - Chemotherapy and Thyroid Cancer Risk: A Report from the Childhood Cancer Survivor Study AN - 920798055; 16199309 AB - BACKGROUND: Although ionizing radiation is an established environmental risk factor for thyroid cancer, the effect of chemotherapy drugs on thyroid cancer risk remains unclear. We evaluated the chemotherapy-related risk of thyroid cancer in childhood cancer survivors and the possible joint effects of chemotherapy and radiotherapy. METHODS: The study included 12,547 five-year survivors of childhood cancer diagnosed during 1970 through 1986. Chemotherapy and radiotherapy information was obtained from medical records, and radiation dose was estimated to the thyroid gland. Cumulative incidence and relative risks were calculated with life-table methods and Poisson regression. Chemotherapy-related risks were evaluated separately by categories of radiation dose. RESULTS: Histologically confirmed thyroid cancer occurred in 119 patients. Thirty years after the first childhood cancer treatment, the cumulative incidence of thyroid cancer was 1.3% (95% CI, 1.0-1.6) for females and 0.6% (0.4-0.8) for males. Among patients with thyroid radiation doses of 20 Gy or less, treatment with alkylating agents was associated with a significant 2.4-fold increased risk of thyroid cancer (95% CI, 1.3-4.5; P = 0.002). Chemotherapy risks decreased as radiation dose increased, with a significant decrease for patients treated with alkylating agents (Ptrend = 0.03). No chemotherapy-related risk was evident for thyroid radiation doses more than 20 Gy. CONCLUSIONS: Treatments with alkylating agents increased thyroid cancer risk, but only in the radiation dose range less than 20 Gy, in which cell sparing likely predominates over cell killing. IMPACT: Our study adds to the evidence for chemotherapy agent-specific increased risks of thyroid cancer, which to date, were mainly thought to be related to prior radiotherapy. Cancer Epidemiol Biomarkers Prev; 21(1); 92-101. [copy ]2011 AACR. JF - Cancer Epidemiology, Biomarkers & Prevention AU - Veiga, Lene HS AU - Bhatti, Parveen AU - Ronckers, Cecile M AU - Sigurdson, Alice J AU - Stovall, Marilyn AU - Smith, Susan A AU - Weathers, Rita AU - Leisenring, Wendy AU - Mertens, Ann C AU - Hammond, Sue AU - Neglia, Joseph P AU - Meadows, Anna T AU - Donaldson, Sarah S AU - Sklar, Charles A AU - Friedman, Debra L AU - Robison, Leslie L AU - Inskip, Peter D AD - Authors' Affiliations: Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, DHHS, Bethesda, Maryland Y1 - 2012 PY - 2012 DA - 2012 SP - 92 EP - 101 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 1 SN - 1055-9965, 1055-9965 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Bioindicators KW - Cancer KW - Chemotherapy KW - Children KW - Ionizing radiation KW - Prevention KW - Risk factors KW - Thyroid KW - chemotherapy KW - prevention KW - radiotherapy 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/920798055?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Epidemiology%2C+Biomarkers+%26+Prevention&rft.atitle=Chemotherapy+and+Thyroid+Cancer+Risk%3A+A+Report+from+the+Childhood+Cancer+Survivor+Study&rft.au=Veiga%2C+Lene+HS%3BBhatti%2C+Parveen%3BRonckers%2C+Cecile+M%3BSigurdson%2C+Alice+J%3BStovall%2C+Marilyn%3BSmith%2C+Susan+A%3BWeathers%2C+Rita%3BLeisenring%2C+Wendy%3BMertens%2C+Ann+C%3BHammond%2C+Sue%3BNeglia%2C+Joseph+P%3BMeadows%2C+Anna+T%3BDonaldson%2C+Sarah+S%3BSklar%2C+Charles+A%3BFriedman%2C+Debra+L%3BRobison%2C+Leslie+L%3BInskip%2C+Peter+D&rft.aulast=Veiga&rft.aufirst=Lene&rft.date=2012-01-01&rft.volume=21&rft.issue=1&rft.spage=92&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 - 2012-02-01 N1 - Last updated - 2012-08-10 N1 - SubjectsTermNotLitGenreText - Bioindicators; Prevention; Chemotherapy; Risk factors; Ionizing radiation; prevention; Thyroid; Children; radiotherapy; chemotherapy; Cancer ER - TY - JOUR T1 - PET and MRI of Metastatic Peritoneal and Pulmonary Colorectal Cancer in Mice with Human Epidermal Growth Factor Receptor 1-Targeted 89Zr-Labeled Panitumumab AN - 920797437; 16198716 AB - Human epidermal growth factor receptor 1 (HER1) plays an important role in the pathogenesis of colorectal cancer. Panitumumab is an anti-HER1 monoclonal antibody approved for use in colorectal cancer. However, few data exist regarding HER1 status in the corresponding distant metastases, and little corresponding information is available regarding the localization of panitumumab at primary and metastatic lesions. The utility of PET and MRI using 89Zr-panitumumab to assess the status of HER1 in distant metastases with different metastasis models is presented in this study. METHODS: In vivo biodistribution and PET studies were performed in HER1-expressing LS-174T and HER1-negative A375 tumor xenografts. Additionally, studies were performed in different models of intraperitoneal and pulmonary metastases. MRI studies were performed for metastatic models to characterize the targeting potential of 89Zr-panitumumab at different lesion sites. RESULTS: HER1-mediated targeting was achieved in all HER1-expressing models. The LS-174T tumor area under the curve (AUC) was 3.7-fold greater than the AUC for A375. The LS-174T tumor AUC of 204.13 plus or minus 9.67 was significantly greater (P < 0.001) than the LS-174T tumor AUC of 36.45 plus or minus 1.39 obtained from mice coinjected with 0.1 mg of panitumumab for blocking the target. Differences were observed in 2 intraperitoneal models; tumor uptake in mice with a 3-d tumor burden was more than 2-fold greater than the mice with a 7-d tumor burden. PET and MRI studies revealed HER1-mediated tumor targeting in all metastatic models. However, significant differences were observed between different LS-174T tumor models. Peak tumor uptake of approximately 40 percentage injected dose per gram (%ID/g) was observed at 3-4 d after injection for the subcutaneous tumor model, in contrast to approximately 75 %ID/g at 2 d after injection for the thoracic tumors and approximately 95 %ID/g at 1-2 d after injection for the intraperitoneal tumors. CONCLUSION: The potential utility of 89Zr-panitumumab in assessing HER1 status in distant metastases and understanding the variations in antibody uptake at different lesion sites is demonstrated in this study. 89Zr-panitumumab can play a vital role in patient stratification and immunotherapy and therefore warrants further investigation for clinical translation. JF - Journal of Nuclear Medicine AU - Nayak, Tapan K AU - Garmestani, Kayhan AU - Milenic, Diane E AU - Brechbiel, Martin W AD - Radioimmune and Inorganic Chemistry Section, Radiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland Y1 - 2012 PY - 2012 DA - 2012 SP - 113 EP - 120 PB - Society of Nuclear Medicine VL - 53 IS - 1 SN - 0161-5505, 0161-5505 KW - Biotechnology and Bioengineering Abstracts KW - Translation KW - Data processing KW - Monoclonal antibodies KW - Immunotherapy KW - Peritoneum KW - Magnetic resonance imaging KW - Colorectal cancer KW - Animal models KW - Epidermal growth factor receptors KW - Tumors KW - Models KW - Metastases KW - Antibodies KW - Lung KW - Thorax KW - Nuclear medicine KW - Xenografts KW - Lung cancer KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920797437?accountid=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+Nuclear+Medicine&rft.atitle=PET+and+MRI+of+Metastatic+Peritoneal+and+Pulmonary+Colorectal+Cancer+in+Mice+with+Human+Epidermal+Growth+Factor+Receptor+1-Targeted+89Zr-Labeled+Panitumumab&rft.au=Nayak%2C+Tapan+K%3BGarmestani%2C+Kayhan%3BMilenic%2C+Diane+E%3BBrechbiel%2C+Martin+W&rft.aulast=Nayak&rft.aufirst=Tapan&rft.date=2012-01-01&rft.volume=53&rft.issue=1&rft.spage=113&rft.isbn=&rft.btitle=&rft.title=Journal+of+Nuclear+Medicine&rft.issn=01615505&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-02-01 N1 - Last updated - 2012-03-29 N1 - SubjectsTermNotLitGenreText - Translation; Data processing; Monoclonal antibodies; Immunotherapy; Magnetic resonance imaging; Peritoneum; Animal models; Colorectal cancer; Epidermal growth factor receptors; Tumors; Models; Metastases; Antibodies; Lung; Thorax; Nuclear medicine; Xenografts; Lung cancer ER - TY - JOUR T1 - Long-term Cancer Risk among People Diagnosed with AIDS during Childhood AN - 920796864; 16199333 AB - BACKGROUND: Highly active antiretroviral therapy (HAART) results in partial immune restoration for people with AIDS, but its impact on cancer risk among children is unknown. METHODS: Data from the U.S. HIV/AIDS Cancer Match Study were used to evaluate cancer risk for people diagnosed with AIDS as children (diagnosed with AIDS at ages 0-14 years, during 1980-2007, followed for up to 10 years; N = 5,850). We calculated standardized incidence ratios (SIR) to compare cancer risk to the general population. Poisson regression evaluated changes in cancer incidence between the pre-HAART (1980-1995) and HAART eras (1996-2007). RESULTS: There were 106 cancers observed with significantly elevated risks for the two major AIDS-defining cancers: Kaposi sarcoma [KS; N = 20, SIR = 1,694; 95% confidence interval (CI), 986-2,712 and SIR = 1,146; 95% CI, 236-3,349] during the pre-HAART and HAART eras, respectively, and non-Hodgkin lymphoma (NHL; N = 64, SIR = 338; 95% CI, 242-458 and SIR = 116; 95% CI, 74-175). Incidence of both cancers declined 87% and 60%, respectively, in the HAART era (P < 0.05). Of non-AIDS-defining cancers, leiomyosarcoma risk (N = 9) was elevated during both time periods (SIR = 863; 95% CI, 235-2,211 and SIR = 533; 95% CI, 173-1,243). CONCLUSION: People diagnosed with AIDS during childhood remain at elevated risk for KS, NHL, and leiomyosarcoma in the HAART era. Incidence of KS and NHL declined relative to widespread HAART use, but there was no change in the incidence of other cancers. IMPACT: People diagnosed with AIDS during childhood remain at elevated risk for certain cancers. Continued monitoring is warranted as this immunosuppressed population ages into adulthood where cancer risks generally increase. Cancer Epidemiol Biomarkers Prev; 21(1); 148-54. [copy ]2011 AACR. JF - Cancer Epidemiology, Biomarkers & Prevention AU - Simard, Edgar P AU - Shiels, Meredith S AU - Bhatia, Kishor AU - Engels, Eric A AD - Authors' Affiliations: Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Rockville, Maryland Y1 - 2012 PY - 2012 DA - 2012 SP - 148 EP - 154 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 1 SN - 1055-9965, 1055-9965 KW - Virology & AIDS Abstracts; Risk Abstracts; Health & Safety Science Abstracts KW - Bioindicators KW - Acquired immune deficiency syndrome KW - Age KW - Data processing KW - Children KW - biomarkers KW - Cancer KW - USA KW - Prevention KW - Human immunodeficiency virus KW - highly active antiretroviral therapy KW - antiretroviral agents KW - prevention KW - Sarcoma KW - Standards KW - Lymphoma KW - V 22360:AIDS and HIV 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/920796864?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Epidemiology%2C+Biomarkers+%26+Prevention&rft.atitle=Long-term+Cancer+Risk+among+People+Diagnosed+with+AIDS+during+Childhood&rft.au=Simard%2C+Edgar+P%3BShiels%2C+Meredith+S%3BBhatia%2C+Kishor%3BEngels%2C+Eric+A&rft.aulast=Simard&rft.aufirst=Edgar&rft.date=2012-01-01&rft.volume=21&rft.issue=1&rft.spage=148&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 - 2012-02-01 N1 - Last updated - 2014-05-29 N1 - SubjectsTermNotLitGenreText - Age; Acquired immune deficiency syndrome; Data processing; highly active antiretroviral therapy; Sarcoma; Children; biomarkers; Lymphoma; Bioindicators; Prevention; Human immunodeficiency virus; antiretroviral agents; prevention; Standards; Cancer; USA ER - TY - JOUR T1 - Sex Hormones, Hormonal Interventions, and Gastric Cancer Risk: A Meta-analysis AN - 920796859; 16199327 AB - Estrogens may influence gastric cancer risk, but published studies are inconclusive. We therefore carried out a meta-analysis addressing the associations of gastric cancer in women with menstrual and reproductive factors and with use of estrogen- and antiestrogen-related therapies. Searches of PubMed up to June, 2011 and review of citations yielded a total of 28 independent studies, including at least one exposure of interest. Random effects pooled estimates of relative risk (RR) and corresponding 95% CIs were calculated for eight exposures reported in at least five studies, including: age at menarche, age at menopause, years of fertility, parity, age at first birth, oral contraceptive use, hormone replacement therapy (HRT), and tamoxifen treatment. Longer years of fertility (RR = 0.74, 95% CI: 0.63-0.86) and HRT (RR = 0.77; 95% CI: 0.64-0.92) were each associated with decreased gastric cancer risk. Conversely, tamoxifen treatment was associated with increased risk (RR = 1.82; 95% CI: 1.39-2.38). The other five exposures were not significantly associated. Our analysis supports the hypothesis that longer exposure to estrogen effects of either ovarian or exogenous origin may decrease risk of gastric cancer. Additional studies are warranted to extend this finding and to identify the underlying mechanisms. Cancer Epidemiol Biomarkers Prev; 21(1); 20-38. [copy ]2011 AACR. JF - Cancer Epidemiology, Biomarkers & Prevention AU - Camargo, MConstanza AU - Goto, Yasuyuki AU - Zabaleta, Jovanny AU - Morgan, Douglas R AU - Correa, Pelayo AU - Rabkin, Charles S AD - Authors' Affiliations: Division of Cancer Epidemiology and Genetics, National Cancer Institute, Rockville, Maryland Y1 - 2012 PY - 2012 DA - 2012 SP - 20 EP - 38 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 1 SN - 1055-9965, 1055-9965 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Age KW - Bioindicators KW - Cancer KW - Estrogens KW - Fertility KW - Hormones KW - Intervention KW - Reviews KW - estrogens KW - hormone replacement therapy KW - parity 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/920796859?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Ariskabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+Epidemiology%2C+Biomarkers+%26+Prevention&rft.atitle=Sex+Hormones%2C+Hormonal+Interventions%2C+and+Gastric+Cancer+Risk%3A+A+Meta-analysis&rft.au=Camargo%2C+MConstanza%3BGoto%2C+Yasuyuki%3BZabaleta%2C+Jovanny%3BMorgan%2C+Douglas+R%3BCorrea%2C+Pelayo%3BRabkin%2C+Charles+S&rft.aulast=Camargo&rft.aufirst=MConstanza&rft.date=2012-01-01&rft.volume=21&rft.issue=1&rft.spage=20&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 - 2012-02-01 N1 - Last updated - 2012-08-10 N1 - SubjectsTermNotLitGenreText - Bioindicators; Estrogens; parity; Fertility; Age; Reviews; Intervention; Hormones; hormone replacement therapy; Cancer; estrogens ER - TY - JOUR T1 - Database resources of the National Center for Biotechnology Information AN - 920795055; 16173630 AB - In addition to maintaining the GenBank registered nucleic acid sequence database, the National Center for Biotechnology Information (NCBI) provides analysis and retrieval resources for the data in GenBank and other biological data made available through the NCBI Website. NCBI resources include Entrez, the Entrez Programming Utilities, MyNCBI, PubMed, PubMed Central (PMC), Gene, the NCBI Taxonomy Browser, BLAST, BLAST Link (BLink), Primer-BLAST, COBALT, Splign, RefSeq, UniGene, HomoloGene, ProtEST, dbMHC, dbSNP, dbVar, Epigenomics, Genome and related tools, the Map Viewer, Model Maker, Evidence Viewer, Trace Archive, Sequence Read Archive, BioProject, BioSample, Retroviral Genotyping Tools, HIV-1/Human Protein Interaction Database, Gene Expression Omnibus (GEO), Probe, Online Mendelian Inheritance in Animals (OMIA), the Molecular Modeling Database (MMDB), the Conserved Domain Database (CDD), the Conserved Domain Architecture Retrieval Tool (CDART), Biosystems, Protein Clusters and the PubChem suite of small molecule databases. Augmenting many of the Web applications are custom implementations of the BLAST program optimized to search specialized data sets. All of these resources can be accessed through the NCBI home page at www.ncbi.nlm.nih.gov. JF - Nucleic Acids Research AU - Sayers, Eric W AU - Barrett, Tanya AU - Benson, Dennis A AU - Bolton, Evan AU - Bryant, Stephen H AU - Canese, Kathi AU - Chetvernin, Vyacheslav AU - Church, Deanna M AU - DiCuccio, Michael AU - Federhen, Scott AU - Feolo, Michael AU - Fingerman, Ian M AU - Geer, Lewis Y AU - Helmberg, Wolfgang AU - Kapustin, Yuri AU - Krasnov, Sergey AU - Landsman, David AU - Lipman, David J AU - Lu, Zhiyong AU - Madden, Thomas L AU - Madej, Tom AU - Maglott, Donna R AU - Marchler-Bauer, Aron AU - Miller, Vadim AU - Karsch-Mizrachi, Ilene AU - Ostell, James AU - Panchenko, Anna AU - Phan, Lon AU - Pruitt, Kim D AU - Schuler, Gregory D AU - Sequeira, Edwin AU - Sherry, Stephen T AU - Shumway, Martin AU - Sirotkin, Karl AU - Slotta, Douglas AU - Souvorov, Alexandre AU - Starchenko, Grigory AU - Tatusova, Tatiana A AU - Wagner, Lukas AU - Wang, Yanli AU - Wilbur, WJohn AU - Yaschenko, Eugene AU - Ye, Jian AD - super(1)National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Building 38A, 8600 Rockville Pike, Bethesda, MD 20894, USA and super(2)University Clinic of Blood Group Serology and Transfusion Medicine, Medical University of Graz, Auenbruggerplatz 3, A-8036 Graz, Austria, sayers@ncbi.nlm.nih.gov Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - D13 EP - D25 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 40 IS - D1 SN - 0305-1048, 0305-1048 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Cobalt KW - Computer programs KW - Conserved sequence KW - DNA probes KW - Data processing KW - Databases KW - Gene expression KW - Genomes KW - Genotyping KW - Heredity KW - Internet KW - Molecular modelling KW - Nucleotide sequence KW - Protein interaction KW - Taxonomy KW - nucleic acids KW - Human immunodeficiency virus 1 KW - G 07740:Evolution KW - N 14815:Nucleotide Sequence KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920795055?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Nucleic+Acids+Research&rft.atitle=Database+resources+of+the+National+Center+for+Biotechnology+Information&rft.au=Sayers%2C+Eric+W%3BBarrett%2C+Tanya%3BBenson%2C+Dennis+A%3BBolton%2C+Evan%3BBryant%2C+Stephen+H%3BCanese%2C+Kathi%3BChetvernin%2C+Vyacheslav%3BChurch%2C+Deanna+M%3BDiCuccio%2C+Michael%3BFederhen%2C+Scott%3BFeolo%2C+Michael%3BFingerman%2C+Ian+M%3BGeer%2C+Lewis+Y%3BHelmberg%2C+Wolfgang%3BKapustin%2C+Yuri%3BKrasnov%2C+Sergey%3BLandsman%2C+David%3BLipman%2C+David+J%3BLu%2C+Zhiyong%3BMadden%2C+Thomas+L%3BMadej%2C+Tom%3BMaglott%2C+Donna+R%3BMarchler-Bauer%2C+Aron%3BMiller%2C+Vadim%3BKarsch-Mizrachi%2C+Ilene%3BOstell%2C+James%3BPanchenko%2C+Anna%3BPhan%2C+Lon%3BPruitt%2C+Kim+D%3BSchuler%2C+Gregory+D%3BSequeira%2C+Edwin%3BSherry%2C+Stephen+T%3BShumway%2C+Martin%3BSirotkin%2C+Karl%3BSlotta%2C+Douglas%3BSouvorov%2C+Alexandre%3BStarchenko%2C+Grigory%3BTatusova%2C+Tatiana+A%3BWagner%2C+Lukas%3BWang%2C+Yanli%3BWilbur%2C+WJohn%3BYaschenko%2C+Eugene%3BYe%2C+Jian&rft.aulast=Sayers&rft.aufirst=Eric&rft.date=2012-01-01&rft.volume=40&rft.issue=D1&rft.spage=D13&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/10.1093%2Fnar%2Fgkr1184 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-02-01 N1 - Last updated - 2013-04-05 N1 - SubjectsTermNotLitGenreText - Genomes; Molecular modelling; Data processing; Heredity; DNA probes; Genotyping; Nucleotide sequence; Gene expression; Databases; Computer programs; nucleic acids; Cobalt; Conserved sequence; Taxonomy; Internet; Protein interaction; Human immunodeficiency virus 1 DO - http://dx.doi.org/10.1093/nar/gkr1184 ER - TY - JOUR T1 - IBIS (Inferred Biomolecular Interaction Server) reports, predicts and integrates multiple types of conserved interactions for proteins AN - 920794890; 16173792 AB - We have recently developed the Inferred Biomolecular Interaction Server (IBIS) and database, which reports, predicts and integrates different types of interaction partners and locations of binding sites in proteins based on the analysis of homologous structural complexes. Here, we highlight several new IBIS features and options. The server's webpage is now redesigned to allow users easier access to data for different interaction types. An entry page is added to give a quick summary of available results and to now accept protein sequence accessions. To elucidate the formation of protein complexes, not just binary interactions, IBIS currently presents an expandable interaction network. Previously, IBIS provided annotations for four different types of binding partners: proteins, small molecules, nucleic acids and peptides; in the current version a new protein-ion interaction type has been added. Several options provide easy downloads of IBIS data for all Protein Data Bank (PDB) protein chains and the results for each query. In this study, we show that about one-third of all RefSeq sequences can be annotated with IBIS interaction partners and binding sites. The IBIS server is available at http://www.ncbi.nlm.nih.gov/Structure/ibis/ibis.cgi and updated biweekly. JF - Nucleic Acids Research AU - Shoemaker, Benjamin A AU - Zhang, Dachuan AU - Tyagi, Manoj AU - Thangudu, Ratna R AU - Fong, Jessica H AU - Marchler-Bauer, Aron AU - Bryant, Stephen H AU - Madej, Thomas AU - Panchenko, Anna R AD - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, 8600 Rockville Pike, Building 38A, Bethesda, MD 20894, USA, panch@ncbi.nlm.nih.gov Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - D834 EP - D840 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 40 IS - D1 SN - 0305-1048, 0305-1048 KW - Genetics Abstracts; Environment Abstracts; Biochemistry Abstracts 2: Nucleic Acids KW - Data banks KW - Databases KW - Data processing KW - nucleic acids KW - Proteins KW - Nucleic acids KW - Amino acid sequence KW - G 07880:Human Genetics KW - N 14810:Methods KW - ENA 07:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920794890?accountid=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=Nucleic+Acids+Research&rft.atitle=IBIS+%28Inferred+Biomolecular+Interaction+Server%29+reports%2C+predicts+and+integrates+multiple+types+of+conserved+interactions+for+proteins&rft.au=Shoemaker%2C+Benjamin+A%3BZhang%2C+Dachuan%3BTyagi%2C+Manoj%3BThangudu%2C+Ratna+R%3BFong%2C+Jessica+H%3BMarchler-Bauer%2C+Aron%3BBryant%2C+Stephen+H%3BMadej%2C+Thomas%3BPanchenko%2C+Anna+R&rft.aulast=Shoemaker&rft.aufirst=Benjamin&rft.date=2012-01-01&rft.volume=40&rft.issue=D1&rft.spage=D834&rft.isbn=&rft.btitle=&rft.title=Nucleic+Acids+Research&rft.issn=03051048&rft_id=info:doi/10.1093%2Fnar%2Fgkr997 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-02-01 N1 - Last updated - 2012-05-07 N1 - SubjectsTermNotLitGenreText - Data banks; Databases; nucleic acids; Data processing; Amino acid sequence; Proteins; Nucleic acids DO - http://dx.doi.org/10.1093/nar/gkr997 ER - TY - JOUR T1 - Characterization of Polybrominated Diphenyl Ether Toxicity in Wistar Han Rats and Use of Liver Microarray Data for Predicting Disease Susceptibilities AN - 920794224; 16262300 AB - The toxicity of polybrominated diphenyl ethers (PBDEs), flame-retardant components, was characterized in offspring from Wistar Han dams exposed by gavage to a PBDE mixture (DE71) starting at gestation day 6 and continuing to weaning on postnatal day (PND) 21. Offspring from the dams underwent PBDE direct dosing by gavage at the same dose as their dams from PND 12 to PND 21, and then after weaning for another thirteen weeks. Liver samples were collected at PND 22 and week 13 for liver gene expression analysis (Affymetrix Rat Genome 230 2.0 Array). Treatment with PBDE induced 1,066 liver gene transcript changes in females and 1,200 transcriptional changes in males at PND 22 (false discovery rate < 0.01), but only 263 liver transcriptional changes at thirteen weeks in male rats (false discovery rate < 0.05). No significant differences in dose response were found between male and female pups. Transcript changes at PND 22 coded for proteins in xenobiotic, sterol, and lipid metabolism, and cell cycle regulation, and overlapped rodent liver transcript patterns after a high-fat diet or phenobarbital exposure. These findings, along with the observed PBDE-induced liver hypertrophy and vacuolization, suggest that long-term PBDE exposure has the potential to modify cell functions that contribute to metabolic disease and/or cancer susceptibilities. JF - Toxicologic Pathology AU - Dunnick, J K AU - Brix, A AU - Cunny, H AU - Vallant, M AU - Shockley, K R AD - National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA  , dunnickj@niehs.nih.gov Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - 93 EP - 106 PB - Sage Publications Ltd., 6 Bonhill St. London EC2A 4PU United Kingdom VL - 40 IS - 1 SN - 0192-6233, 0192-6233 KW - Toxicology Abstracts KW - Genomes KW - Phenobarbital KW - Data processing KW - Metabolic disorders KW - Cell cycle KW - Weaning KW - Transcription KW - Fire retardant chemicals KW - Toxicity KW - DNA microarrays KW - Cancer KW - Lipid metabolism KW - Gene expression KW - polybrominated diphenyl ethers KW - High fat diet KW - Sterols KW - Gestation KW - Liver KW - Progeny KW - X 24350:Industrial Chemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920794224?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxicologyabstracts&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Toxicologic+Pathology&rft.atitle=Characterization+of+Polybrominated+Diphenyl+Ether+Toxicity+in+Wistar+Han+Rats+and+Use+of+Liver+Microarray+Data+for+Predicting+Disease+Susceptibilities&rft.au=Dunnick%2C+J+K%3BBrix%2C+A%3BCunny%2C+H%3BVallant%2C+M%3BShockley%2C+K+R&rft.aulast=Dunnick&rft.aufirst=J&rft.date=2012-01-01&rft.volume=40&rft.issue=1&rft.spage=93&rft.isbn=&rft.btitle=&rft.title=Toxicologic+Pathology&rft.issn=01926233&rft_id=info:doi/10.1177%2F0192623311429973 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-02-01 N1 - Last updated - 2012-03-29 N1 - SubjectsTermNotLitGenreText - Genomes; Phenobarbital; Data processing; Metabolic disorders; Cell cycle; Transcription; Weaning; Toxicity; Fire retardant chemicals; DNA microarrays; Cancer; Lipid metabolism; Gene expression; polybrominated diphenyl ethers; High fat diet; Sterols; Gestation; Liver; Progeny DO - http://dx.doi.org/10.1177/0192623311429973 ER - TY - JOUR T1 - Inhibition of NADPH oxidase promotes alternative and anti-inflammatory microglial activation during neuroinflammation AN - 920791524; 16160730 AB - Like macrophages, microglia are functionally polarized into different phenotypic activation states, referred as classical and alternative. The balance of the two phenotypes may be critical to ensure proper brain homeostasis, and may be altered in brain pathological states, such as Alzheimer's disease. We investigated the role of NADPH oxidase in microglial activation state using p47phox and gp91phox-deficient mice as well as apocynin, a NADPH oxidase inhibitor during neuroinflammation induced by an intracerebroventricular injection of LPS or A beta 1-42. We showed that NADPH oxidase plays a critical role in the modulation of microglial phenotype and subsequent inflammatory response. We demonstrated that inhibition of NADPH oxidase or gene deletion of its functional p47phox subunit switched microglial activation from a classical to an alternative state in response to an inflammatory challenge. Moreover, we showed a shift in redox state towards an oxidized milieu and that subpopulations of microglia retain their detrimental phenotype in Alzheimer's disease brains. Microglia can change their activation phenotype depending on NADPH oxidase-dependent redox state of microenvironment. Inhibition of NADPH oxidase represents a promising neuroprotective approach to reduce oxidative stress and modulate microglial phenotype towards an alternative state. Inhibition of NADPH oxidase or gene deletion of p47phox subunit switched microglial activation from a classical to an alternative state in response to an inflammatory challenge. These findings suggest that NADPH oxidase acts as a guide and regulates the age-related increase in detrimental microglial activation and the accompanying increase in oxidative stress in AD.Original Abstract: J. Neurochem. (2012) 120, 292-301. JF - Journal of Neurochemistry AU - Choi, Sang-Ho AU - Aid, Saba AU - Kim, Hyung-Wook AU - Jackson, Sharon H AU - Bosetti, Francesca AD - Molecular Neuroscience Unit, National Institutes of Health, Bethesda, Maryland, USA Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - 292 EP - 301 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 120 IS - 2 SN - 0022-3042, 0022-3042 KW - Biotechnology and Bioengineering Abstracts; CSA Neurosciences Abstracts KW - Macrophages KW - Redox properties KW - Age KW - Alzheimer's disease KW - Brain KW - Neuroprotection KW - Homeostasis KW - Microglia KW - Inflammation KW - Cell activation KW - Neurodegenerative diseases KW - Gene deletion KW - Oxidative stress KW - Lipopolysaccharides KW - Microenvironments KW - NAD(P)H oxidase KW - beta -Amyloid KW - N3 11008:Neurochemistry KW - W 30965:Miscellaneous, Reviews UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920791524?accountid=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+Neurochemistry&rft.atitle=Inhibition+of+NADPH+oxidase+promotes+alternative+and+anti-inflammatory+microglial+activation+during+neuroinflammation&rft.au=Choi%2C+Sang-Ho%3BAid%2C+Saba%3BKim%2C+Hyung-Wook%3BJackson%2C+Sharon+H%3BBosetti%2C+Francesca&rft.aulast=Choi&rft.aufirst=Sang-Ho&rft.date=2012-01-01&rft.volume=120&rft.issue=2&rft.spage=292&rft.isbn=&rft.btitle=&rft.title=Journal+of+Neurochemistry&rft.issn=00223042&rft_id=info:doi/10.1111%2Fj.1471-4159.2011.07572.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-02-01 N1 - Document feature - figure 8 N1 - Last updated - 2013-08-12 N1 - SubjectsTermNotLitGenreText - Macrophages; Age; Redox properties; Alzheimer's disease; Brain; Neuroprotection; Homeostasis; Microglia; Cell activation; Inflammation; Neurodegenerative diseases; Gene deletion; Oxidative stress; Microenvironments; Lipopolysaccharides; NAD(P)H oxidase; beta -Amyloid DO - http://dx.doi.org/10.1111/j.1471-4159.2011.07572.x ER - TY - JOUR T1 - Comment on: Identification of antimicrobial activity among FDA-approved drugs for combating Mycobacterium abscessus and Mycobacterium chelonae AN - 920791124; 16180655 JF - Journal of Antimicrobial Chemotherapy AU - Mukherjee, Tathagata AU - Boshoff, Helena AU - Barry, Clifton E AD - Tuberculosis Research Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA, cbarry@niaid.nih.gov Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - 252 EP - 253 PB - Oxford University Press, Great Clarendon Street Oxford OX2 6DP United Kingdom VL - 67 IS - 1 SN - 0305-7453, 0305-7453 KW - Microbiology Abstracts A: Industrial & Applied Microbiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920791124?accountid=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+Antimicrobial+Chemotherapy&rft.atitle=Comment+on%3A+Identification+of+antimicrobial+activity+among+FDA-approved+drugs+for+combating+Mycobacterium+abscessus+and+Mycobacterium+chelonae&rft.au=Mukherjee%2C+Tathagata%3BBoshoff%2C+Helena%3BBarry%2C+Clifton+E&rft.aulast=Mukherjee&rft.aufirst=Tathagata&rft.date=2012-01-01&rft.volume=67&rft.issue=1&rft.spage=252&rft.isbn=&rft.btitle=&rft.title=Journal+of+Antimicrobial+Chemotherapy&rft.issn=03057453&rft_id=info:doi/10.1093%2Fjac%2Fdkr418 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-02-01 N1 - Last updated - 2012-03-29 DO - http://dx.doi.org/10.1093/jac/dkr418 ER - TY - JOUR T1 - Imaging proteins inside cells with fluorescent tags AN - 920790048; 16163667 AB - Watching biological molecules provides clues to their function and regulation. Some of the most powerful methods of labeling proteins for imaging use genetically encoded fluorescent fusion tags. There are four standard genetic methods of covalently tagging a protein with a fluorescent probe for cellular imaging. These use (i) autofluorescent proteins, (ii) self-labeling enzymes, (iii) enzymes that catalyze the attachment of a probe to a target sequence, and (iv) biarsenical dyes that target tetracysteine motifs. Each of these techniques has advantages and disadvantages. In this review, we cover new developments in these methods and discuss practical considerations for their use in imaging proteins inside living cells. JF - Trends in Biotechnology AU - Crivat, Georgeta AU - Taraska, Justin W AD - University of Maryland, College Park, Department of Entomology and Program in Cell and Molecular Biology, College Park, MD 20742, USA, justin.taraska@nih.gov PY - 2012 SP - 8 EP - 16 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 30 IS - 1 SN - 0167-7799, 0167-7799 KW - Microbiology Abstracts B: Bacteriology; Biotechnology and Bioengineering Abstracts KW - Dyes KW - Reviews KW - Computed tomography KW - Probes KW - Enzymes KW - Fluorescent indicators KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/920790048?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Amicrobiologyb&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Trends+in+Biotechnology&rft.atitle=Imaging+proteins+inside+cells+with+fluorescent+tags&rft.au=Crivat%2C+Georgeta%3BTaraska%2C+Justin+W&rft.aulast=Crivat&rft.aufirst=Georgeta&rft.date=2012-01-01&rft.volume=30&rft.issue=1&rft.spage=8&rft.isbn=&rft.btitle=&rft.title=Trends+in+Biotechnology&rft.issn=01677799&rft_id=info:doi/10.1016%2Fj.tibtech.2011.08.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-02-01 N1 - Last updated - 2016-01-06 N1 - SubjectsTermNotLitGenreText - Dyes; Reviews; Computed tomography; Probes; Fluorescent indicators; Enzymes DO - http://dx.doi.org/10.1016/j.tibtech.2011.08.002 ER - TY - JOUR T1 - Comparison of the cobas Human Papillomavirus (HPV) test with the hybrid capture 2 and linear array HPV DNA tests. AN - 919950580; 22075592 AB - The cobas human papillomavirus (HPV) test (cobas) was recently approved by the U.S. Food and Drug Administration (FDA) and identifies HPV16 and HPV18 separately as well as detecting a pool of 11 HR-HPV genotypes (HPV31, -33, -35, -39, -45, -51, -52, -56, -58, -59, -68) and also HPV66. We compared cobas, Linear Array (LA), and Hybrid Capture 2 (HC2) assays for detection of carcinogenic HPV DNA, and cobas and LA for detection of HPV16 and HPV18 DNA, among the first 1,852 women enrolled in the HPV Persistence and Progression Cohort (PaP Cohort) study. Specimens were tested by all 3 assays 1 year after an HC2-positive result. In 1,824 specimens with cobas results, cobas had an 85.9% agreement with HC2 and 91.0% agreement with LA for carcinogenic HPV detection. When results between cobas and HC2 disagreed, cobas tended to call more women HPV positive (P < 0.01). Categorizing cobas and LA results hierarchically according to cancer risk (HPV16, HPV18, other carcinogenic HPV genotypes, or carcinogen negative), there was a 90% agreement for all categories of HPV (n = 1,824). We found good agreement between the two U.S. FDA-approved HPV tests, with discrepancies between the two assays due to specific characteristics of the individual assays. Additional studies are needed to compare HC2 and cobas for detecting and predicting CIN3 to understand the clinical implications of the discrepant test results between the two tests. JF - Journal of clinical microbiology AU - Gage, Julia C AU - Sadorra, Mark AU - Lamere, Brandon J AU - Kail, Randi AU - Aldrich, Carrie AU - Kinney, Walter AU - Fetterman, Barbara AU - Lorey, Thomas AU - Schiffman, Mark AU - Castle, Philip E AU - PaP Cohort Study Group AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, DHHS, Bethesda, Maryland, USA. gagej@mail.nih.gov ; PaP Cohort Study Group Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 61 EP - 65 VL - 50 IS - 1 KW - DNA, Viral KW - 0 KW - Index Medicus KW - United States KW - Aged, 80 and over KW - Humans KW - Adult KW - Aged KW - Middle Aged KW - DNA, Viral -- isolation & purification KW - DNA, Viral -- genetics KW - Female KW - Papillomavirus Infections -- diagnosis KW - Papillomaviridae -- classification KW - Papillomaviridae -- isolation & purification KW - Papillomavirus Infections -- virology KW - Papillomaviridae -- genetics KW - Virology -- methods KW - Molecular Diagnostic Techniques -- methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/919950580?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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 completed - 2012-04-11 N1 - Date created - 2011-12-28 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Virol Methods. 2007 Dec;146(1-2):80-5 [17673302] J Low Genit Tract Dis. 2007 Oct;11(4):223-39 [17917567] Cancer Epidemiol Biomarkers Prev. 2008 May;17(5):1248-54 [18483347] J Clin Microbiol. 2008 Aug;46(8):2595-604 [18579716] Br J Cancer. 2008 Aug 19;99(4):563-8 [18682715] Cancer Epidemiol Biomarkers Prev. 2008 Nov;17(11):3033-42 [18957520] J Clin Microbiol. 2009 Oct;47(10):3344-7 [19675214] Am J Clin Pathol. 2011 Mar;135(3):468-75 [21350104] Lancet Oncol. 2011 Jul;12(7):663-72 [21684207] Lancet Oncol. 2011 Sep;12(9):880-90 [21865084] Am J Obstet Gynecol. 2003 Jul;189(1):295-304 [12861176] Virology. 2005 Jun 20;337(1):76-84 [15914222] J Natl Cancer Inst. 2005 Jul 20;97(14):1072-9 [16030305] Cancer Res. 2006 Oct 15;66(20):10112-9 [17047075] Br J Cancer. 2008 May 20;98(10):1704-9 [18392052] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1128/JCM.05989-11 ER - TY - JOUR T1 - Bisubstrate analogue inhibitors of 6-hydroxymethyl-7,8-dihydropterin pyrophosphokinase: New design with improved properties AN - 918061739; 16186951 AB - 6-Hydroxymethyl-7,8-dihydropterin pyrophosphokinase (HPPK), a key enzyme in the folate biosynthetic pathway, catalyzes the pyrophosphoryl transfer from ATP to 6-hydroxymethyl-7,8-dihydropterin. The enzyme is essential for microorganisms, is absent from humans, and is not the target for any existing antibiotics. Therefore, HPPK is an attractive target for developing novel antimicrobial agents. Previously, we characterized the reaction trajectory of HPPK-catalyzed pyrophosphoryl transfer and synthesized a series of bisubstrate analog inhibitors of the enzyme by linking 6-hydroxymethylpterin to adenosine through 2, 3, or 4 phosphate groups. Here, we report a new generation of bisubstrate analog inhibitors. To improve protein binding and linker properties of such inhibitors, we have replaced the pterin moiety with 7,7-dimethyl-7,8-dihydropterin and the phosphate bridge with a piperidine linked thioether. We have synthesized the new inhibitors, measured their Kd and IC50 values, determined their crystal structures in complex with HPPK, and established their structure-activity relationship. 6-Carboxylic acid ethyl ester-7,7-dimethyl-7,8-dihydropterin, a novel intermediate that we developed recently for easy derivatization at position 6 of 7,7-dimethyl-7,8-dihydropterin, offers a much high yield for the synthesis of bisubstrate analogs than that of previously established procedure. JF - Bioorganic and Medicinal Chemistry AU - Shi, Genbin AU - Shaw, Gary AU - Liang, Yu-He AU - Subburaman, Priadarsini AU - Li, Yue AU - Wu, Yan AU - Yan, Honggao AU - Ji, Xinhua AD - Macromolecular Crystallography Laboratory, National Cancer Institute, Frederick, MD 21702, USA, jix@mail.nih.gov Y1 - 2012/01/01/ PY - 2012 DA - 2012 Jan 01 SP - 47 EP - 57 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 20 IS - 1 SN - 0968-0896, 0968-0896 KW - Biotechnology and Bioengineering Abstracts KW - Enzymes KW - ATP KW - Antibiotics KW - thioethers KW - Antimicrobial agents KW - Phosphate KW - Piperidine KW - Crystal structure KW - Microorganisms KW - Folic acid KW - Adenosine KW - Structure-activity relationships KW - W 30915:Pharmaceuticals & Vaccines UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/918061739?accountid=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=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 - 2012-01-01 N1 - Last updated - 2012-03-29 N1 - SubjectsTermNotLitGenreText - Piperidine; Phosphate; Microorganisms; Crystal structure; ATP; Enzymes; Antibiotics; Folic acid; Structure-activity relationships; Adenosine; thioethers; Antimicrobial agents DO - http://dx.doi.org/10.1016/j.bmc.2011.11.032 ER - TY - JOUR T1 - Computer-assisted detection of infectious lung diseases: A review AN - 915489016; 16148114 AB - Respiratory tract infections are a leading cause of death and disability worldwide. Although radiology serves as a primary diagnostic method for assessing respiratory tract infections, visual analysis of chest radiographs and computed tomography (CT) scans is restricted by low specificity for causal infectious organisms and a limited capacity to assess severity and predict patient outcomes. These limitations suggest that computer-assisted detection (CAD) could make a valuable contribution to the management of respiratory tract infections by assisting in the early recognition of pulmonary parenchymal lesions, providing quantitative measures of disease severity and assessing the response to therapy. In this paper, we review the most common radiographic and CT features of respiratory tract infections, discuss the challenges of defining and measuring these disorders with CAD, and propose some strategies to address these challenges. JF - Computerized Medical Imaging and Graphics AU - Bagci, Ulas AU - Bray, Mike AU - Caban, Jesus AU - Yao, Jianhua AU - Mollura, Daniel J AD - Center for Infectious Disease Imaging, Department of Radiology and Imaging Sciences, National Institutes of Health (NIH), Bethesda, MD 20892, USA, ulasbagci@gmail.com Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - 72 EP - 84 PB - Elsevier B.V., 660 White Plains Rd., Floor 2 Tarrytown NY 10591-5153 United States VL - 36 IS - 1 SN - 0895-6111, 0895-6111 KW - Biotechnology and Bioengineering Abstracts KW - Infectious diseases KW - Computer assisted detection KW - Texture analysis KW - Lung CT KW - Feature extraction KW - Tomography KW - Respiratory tract diseases KW - Reviews KW - Computed tomography KW - Lung diseases KW - Radiography KW - Infection KW - Radiology KW - Chest KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/915489016?accountid=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=Computerized+Medical+Imaging+and+Graphics&rft.atitle=Computer-assisted+detection+of+infectious+lung+diseases%3A+A+review&rft.au=Bagci%2C+Ulas%3BBray%2C+Mike%3BCaban%2C+Jesus%3BYao%2C+Jianhua%3BMollura%2C+Daniel+J&rft.aulast=Bagci&rft.aufirst=Ulas&rft.date=2012-01-01&rft.volume=36&rft.issue=1&rft.spage=72&rft.isbn=&rft.btitle=&rft.title=Computerized+Medical+Imaging+and+Graphics&rft.issn=08956111&rft_id=info:doi/10.1016%2Fj.compmedimag.2011.06.002 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-01-01 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Respiratory tract diseases; Reviews; Computed tomography; Lung diseases; Radiography; Chest; Radiology; Infection DO - http://dx.doi.org/10.1016/j.compmedimag.2011.06.002 ER - TY - JOUR T1 - Engineering endomorphin drugs: state of the art. AN - 914668657; 22214283 AB - Although endomorphins-1 (EM-1; H-Tyr-Pro-Phe-Trp-NH(2)) and -2 (EM-2; H-Tyr-Pro-Phe-Phe-NH(2)) are primarily considered agonists for the μ-opioid receptor (MOR), systematic alterations to specific residues provided antagonists and ligands with mixed μ/δ-opioid properties, suitable for application to health-related topics. While the application of endomorphins as antinociceptive agents and numerous biological endpoints were experimentally delineated in laboratory animals and in vitro, clinical use is currently absent. However, structural alterations provide enhanced stability; formation of MOR antagonists or mixed and dual μ/δ-acting ligands could find considerable therapeutic potential. This review attempts to succinctly provide insight on the development and bioactivity of endomorphin analogues during the past decade. Rational design approaches will focus on the engineering of endomorphin agonists, antagonists and mixed ligands for their application as a multi-target ligand. Aside from alleviating pain, EM analogues open new horizons in the treatment of medical syndromes involving neural reward mechanisms and extraneural regulation effects on homeostasis. Highly selective MOR antagonists may be promising to reduce inflammation, attenuate addiction to drugs and excess consumption of high-caloric food, ameliorate alcoholism, affect the immune system and combat opioid bowel dysfunction. JF - Expert opinion on therapeutic patents AU - Lazarus, Lawrence H AU - Okada, Yoshio AD - National Institute of Environmental Health Sciences, Laboratory of Toxicology and Pharmacology, 111 South TW Alexander Drive, Research Triangle Park, NC 27709, USA. lazarus@niehs.nih.gov Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 1 EP - 14 VL - 22 IS - 1 KW - Ligands KW - 0 KW - Oligopeptides KW - Receptors, Opioid, mu KW - endomorphin 1 KW - endomorphin 2 KW - 3PH5M0466G KW - Index Medicus KW - Substance-Related Disorders -- physiopathology KW - Animals KW - Inflammation -- physiopathology KW - Humans KW - Substance-Related Disorders -- drug therapy KW - Inflammation -- drug therapy KW - Patents as Topic KW - Receptors, Opioid, mu -- agonists KW - Receptors, Opioid, mu -- antagonists & inhibitors KW - Oligopeptides -- pharmacology KW - Drug Design UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/914668657?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Expert+opinion+on+therapeutic+patents&rft.atitle=Engineering+endomorphin+drugs%3A+state+of+the+art.&rft.au=Lazarus%2C+Lawrence+H%3BOkada%2C+Yoshio&rft.aulast=Lazarus&rft.aufirst=Lawrence&rft.date=2012-01-01&rft.volume=22&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Expert+opinion+on+therapeutic+patents&rft.issn=1744-7674&rft_id=info:doi/10.1517%2F13543776.2012.646261 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-04-25 N1 - Date created - 2012-01-05 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Med Chem. 2004 Jul 1;47(14):3591-9 [15214786] Proc Soc Exp Biol Med. 1966 Dec;123(3):755-8 [4381176] Br J Pharmacol Chemother. 1968 Jun;33(2):266-76 [5664147] J Biol Chem. 1989 Jan 5;264(1):354-62 [2562839] Proc Natl Acad Sci U S A. 1989 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[15850502] Bioorg Med Chem Lett. 2005 May 16;15(10):2467-9 [15863298] Life Sci. 2005 Jul 22;77(10):1155-65 [15878600] J Neurosci. 2005 Aug 24;25(34):7754-62 [16120776] FEBS J. 2005 Oct;272(19):5079-97 [16176278] Nat Neurosci. 2005 Nov;8(11):1445-9 [16251986] Biochem Biophys Res Commun. 2005 Dec 16;338(2):1012-7 [16263089] Biochem Pharmacol. 2005 Dec 19;71(1-2):188-95 [16288997] Eur J Pharmacol. 2005 Dec 5;526(1-3):101-12 [16253234] Br J Pharmacol. 2006 Jan;147 Suppl 1:S153-62 [16402099] Geriatrics. 2006 Jan;61(1):31-3 [16405362] Hum Mol Genet. 2006 Mar 15;15(6):807-19 [16476706] Differentiation. 2006 Apr;74(4):174-85 [16683988] Pharmazie. 2006 May;61(5):450-2 [16724544] Bioorg Med Chem Lett. 2006 Jul 15;16(14):3688-92 [16682191] J Med Chem. 2006 Sep 7;49(18):5610-7 [16942034] J Pharmacol Exp Ther. 2006 Oct;319(1):308-16 [16803861] Peptides. 2006 Nov;27(11):2770-7 [16901587] Bioorg Med Chem. 2007 Feb 1;15(3):1237-51 [17142049] Mol Cell Proteomics. 2007 Jan;6(1):29-42 [17028301] Bioorg 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[11704620] J Pharmacol Exp Ther. 2002 Jan;300(1):265-72 [11752125] J Neuroimmunol. 2002 May;126(1-2):5-15 [12020952] J Med Chem. 2002 Jun 6;45(12):2571-8 [12036366] Neuroscience. 2002;112(2):345-53 [12044452] Ann N Y Acad Sci. 2002 Jun;966:456-63 [12114304] J Am Chem Soc. 2002 Nov 13;124(45):13352-3 [12418865] Bioorg Med Chem. 2003 Mar 6;11(5):675-8 [12537996] J Med Chem. 2003 Feb 27;46(5):677-80 [12593647] Bioorg Med Chem. 2003 May 1;11(9):1983-94 [12670649] Endocrinology. 2003 May;144(5):1753-60 [12697680] Eur J Pharmacol. 2003 Apr 25;467(1-3):219-22 [12706478] Biopolymers. 2003;71(2):86-102 [12767112] J Mol Neurosci. 2004;22(1-2):125-37 [14742917] Peptides. 2004 Jan;25(1):91-4 [15003360] CNS Spectr. 2004 Jul;9(7):516-22 [15208511] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1517/13543776.2012.646261 ER - TY - JOUR T1 - Infusion-based manganese-enhanced MRI: a new imaging technique to visualize the mouse brain. AN - 913717516; 21597966 AB - Manganese-enhanced magnetic resonance imaging is a technique that employs the divalent ion of the paramagnetic metal manganese (Mn(2+)) as an effective contrast agent to visualize, in vivo, the mammalian brain. As total achievable contrast is directly proportional to the net amount of Mn(2+) accumulated in the brain, there is a great interest in optimizing administration protocols to increase the effective delivery of Mn(2+) to the brain while avoiding the toxic effects of Mn(2+) overexposure. In this study, we investigated outcomes following continuous slow systemic infusion of manganese chloride (MnCl(2)) into the mouse via mini-osmotic pump administration. The effects of increasing fractionated rates of Mn(2+) infusion on signal enhancement in regions of the brain were analyzed in a three-treatment study. We acquired whole-brain 3-D T1-weighted images and performed region of interest quantitative analysis to compare mean normalized signal in Mn(2+) treatments spanning 3, 7, or 14 days of infusion (rates of 1, 0.5, and 0.25 μL/h, respectively). Evidence of Mn(2+) transport at the conclusion of each infusion treatment was observed throughout the brains of normally behaving mice. Regions of particular Mn(2+) accumulation include the olfactory bulbs, cortex, infralimbic cortex, habenula, thalamus, hippocampal formation, amygdala, hypothalamus, inferior colliculus, and cerebellum. Signals measured at the completion of each infusion treatment indicate comparable means for all examined fractionated rates of Mn(2+) infusion. In this current study, we achieved a significantly higher dose of Mn(2+) (180 mg/kg) than that employed in previous studies without any observable toxic effects on animal physiology or behavior. JF - Brain structure & function AU - Mok, Stephanie I AU - Munasinghe, Jeeva P AU - Young, W Scott AD - Section on Neural Gene Expression, National Institute of Mental Health, National Institutes of Health, DHHS, 9000 Rockville Pike, Building 49, Room 5A51, Bethesda, MD 20892-4483, USA. Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 107 EP - 114 VL - 217 IS - 1 KW - Chlorides KW - 0 KW - Manganese Compounds KW - Receptors, Oxytocin KW - manganese chloride KW - QQE170PANO KW - Index Medicus KW - Animals KW - Infusion Pumps, Implantable KW - Mice, Inbred C57BL KW - Receptors, Oxytocin -- genetics KW - Mice KW - Statistics, Nonparametric KW - Male KW - Mice, Knockout KW - Magnetic Resonance Imaging -- methods KW - Chlorides -- administration & dosage KW - Manganese Compounds -- pharmacokinetics KW - Brain -- anatomy & histology KW - Manganese Compounds -- administration & dosage KW - Chlorides -- pharmacokinetics KW - Brain -- physiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/913717516?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Brain+structure+%26+function&rft.atitle=Infusion-based+manganese-enhanced+MRI%3A+a+new+imaging+technique+to+visualize+the+mouse+brain.&rft.au=Mok%2C+Stephanie+I%3BMunasinghe%2C+Jeeva+P%3BYoung%2C+W+Scott&rft.aulast=Mok&rft.aufirst=Stephanie&rft.date=2012-01-01&rft.volume=217&rft.issue=1&rft.spage=107&rft.isbn=&rft.btitle=&rft.title=Brain+structure+%26+function&rft.issn=1863-2661&rft_id=info:doi/10.1007%2Fs00429-011-0324-y LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-04-23 N1 - Date created - 2012-01-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Brain Res Bull. 2001 May 15;55(2):225-8 [11470319] NMR Biomed. 2010 Oct;23(8):913-21 [20878969] J Neurosci. 2002 Dec 15;22(24):10958-65 [12486191] Magn Reson Med. 2003 Jul;50(1):33-9 [12815676] Neuroimage. 2004 Jul;22(3):1046-59 [15219577] Neurosci Biobehav Rev. 1991 Fall;15(3):333-40 [1956602] Brain Res. 1995 Oct 9;695(1):53-8 [8574647] J Neuropsychiatry Clin Neurosci. 1997 Summer;9(3):315-30 [9276837] Magn Reson Med. 1997 Sep;38(3):378-88 [9339438] NMR Biomed. 2004 Dec;17(8):544-53 [15617053] Nat Neurosci. 2005 Jul;8(7):961-8 [15924136] NMR Biomed. 2006 Dec;19(8):1028-34 [16845705] NMR Biomed. 2008 Jun;21(5):473-8 [17944008] Prog Brain Res. 2008;170:73-7 [18655873] BMC Neurosci. 2008;9:111 [19014547] Prog Neurobiol. 2009 Jun;88(2):127-51 [19482229] Neuroimage. 2010 Feb 1;49(3):2544-55 [19896539] Annu Rev Biomed Eng. 1999;1:611-48 [11701502] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s00429-011-0324-y ER - TY - JOUR T1 - Endpoints, patient selection, and biomarkers in the design of clinical trials for cancer vaccines. AN - 913439341; 22120693 AB - Therapeutic cancer vaccines are an emerging and potentially effective treatment modality. Cancer vaccines are usually very well tolerated, with minimal toxicity compared with chemotherapy. Unlike conventional cytotoxic therapies, immunotherapy does not result in immediate tumor shrinkage but may alter growth rate and thus prolong survival. Multiple randomized controlled trials of various immunotherapeutic agents have shown a delayed separation in Kaplan-Meier survival curves, with no evidence of clinical benefit within the first 6-12 months of vaccine treatment. Overall survival benefit is seen in patients with lower disease burden who are not expected to die within those initial 6-12 months. The concept of improved overall survival without marked initial tumor reduction represents a significant shift from the current paradigms established by standard cytotoxic therapies. Future clinical studies of therapeutic vaccines should enroll patients with either lower tumor burden, more indolent disease or both, and must seek to identify early markers of clinical benefit that may correlate with survival. Until then, improved overall survival is the only clear, discriminatory endpoint for therapeutic vaccines as monotherapies. JF - Cancer immunology, immunotherapy : CII AU - Bilusic, Marijo AU - Gulley, James L AD - Laboratory of Tumor Immunology and Biology and Medical Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 109 EP - 117 VL - 61 IS - 1 KW - Biomarkers, Tumor KW - 0 KW - Cancer Vaccines KW - Index Medicus KW - Endpoint Determination KW - Humans KW - Treatment Outcome KW - Patient Selection KW - Biomarkers, Tumor -- blood KW - Neoplasms -- blood KW - Cancer Vaccines -- therapeutic use KW - Clinical Trials, Phase III as Topic -- methods KW - Neoplasms -- therapy KW - Randomized Controlled Trials as Topic -- methods KW - Neoplasms -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/913439341?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Cancer+immunology%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 completed - 2012-05-08 N1 - Date created - 2012-01-02 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Oncologist. 2008 Oct;13(10):1046-54 [18838440] Blood. 2008 Aug 1;112(3):610-8 [18519811] Oncologist. 2010;15(9):969-75 [20798195] J Natl Cancer Inst. 2010 Sep 22;102(18):1388-97 [20826737] Cancer Immunol Immunother. 2011 Feb;60(2):197-206 [20976449] Clin Cancer Res. 2011 Feb 15;17(4):907-17 [21106727] Cancer Immunol Immunother. 2011 Mar;60(3):433-42 [21221967] Clin Cancer Res. 2011 Jun 15;17(12):3884-91 [21680544] Clin Cancer Res. 2011 Aug 15;17(16):5233-8 [21700764] Lancet Oncol. 2010 Feb;11(2):155-64 [20004617] J Clin Oncol. 2010 Mar 1;28(7):1099-105 [20100959] Expert Opin Biol Ther. 2010 Jan;10(1):19-28 [19857185] Semin Immunol. 2010 Jun;22(3):113-24 [20403709] Nat Rev Immunol. 2010 Aug;10(8):580-93 [20651745] N Engl J Med. 2010 Aug 19;363(8):711-23 [20525992] N Engl J Med. 2010 Jul 29;363(5):411-22 [20818862] Adv Immunol. 2000;74:181-273 [10605607] Clin Cancer Res. 2000 Jun;6(6):2175-82 [10873066] Int J Cancer. 2000 Sep 1;87(5):680-7 [10925362] J Clin Oncol. 2000 Dec 1;18(23):3894-903 [11099318] CA Cancer J Clin. 1999 Mar-Apr;49(2):101-16, 65 [11198885] Clin Cancer Res. 2001 May;7(5):1181-91 [11350882] Immunol Rev. 2001 Aug;182:18-32 [11722621] J Immunol Methods. 2002 Jan 1;259(1-2):95-110 [11730845] BJU Int. 2002 Jan;89(1):19-26 [11849155] Science. 2002 Apr 12;296(5566):301-5 [11951032] J Clin Oncol. 2002 Jun 1;20(11):2624-32 [12039923] Curr Opin Immunol. 2003 Apr;15(2):131-7 [12633661] J Clin Oncol. 2003 Apr 1;21(7):1232-7 [12663709] Eur J Immunol. 2004 Feb;34(2):336-44 [14768038] Clin Cancer Res. 2004 May 15;10(10):3273-81 [15161680] Prostate. 2004 Aug 1;60(3):197-204 [15176049] Cancer Res. 2004 Jun 15;64(12):4328-37 [15205348] Proc Natl Acad Sci U S A. 1968 Aug;60(4):1231-8 [4299942] Semin Hematol. 1985 Jan;22(1):27-40 [3155876] Cancer Surv. 1992;13:173-204 [1423323] Adv Immunol. 1997;64:1-38 [9100978] Blood. 1997 May 1;89(9):3129-35 [9129015] Clin Cancer Res. 2005 Mar 15;11(6):2416-26 [15788693] Clin Cancer Res. 2005 May 1;11(9):3353-62 [15867235] Clin Prostate Cancer. 2005 Jun;4(1):55-60 [15992463] J Clin Oncol. 2006 Jul 1;24(19):3089-94 [16809734] Expert Rev Anticancer Ther. 2006 Sep;6(9):1163-7 [17020451] Cancer Res. 2007 Feb 15;67(4):1842-52 [17293384] Curr Cancer Drug Targets. 2007 Feb;7(1):31-40 [17305476] Clin Cancer Res. 2007 Mar 15;13(6):1810-5 [17363537] J Natl Cancer Inst. 2007 Mar 21;99(6):428-32 [17374832] Immunity. 2007 Apr;26(4):397-406 [17459809] Clin Cancer Res. 2007 Jul 1;13(13):3776-82 [17606707] Vaccine. 2007 Sep 27;25 Suppl 2:B89-96 [17573164] Vaccine. 2007 Sep 27;25 Suppl 2:B97-B109 [17916465] J Clin Oncol. 2007 Oct 10;25(29):4562-8 [17876010] J Transl Med. 2007;5:42 [17822557] Clin Cancer Res. 2007 Nov 1;13(21):6247-51 [17975134] Expert Opin Biol Ther. 2007 Dec;7(12):1893-902 [18034654] Cancer Immunol Immunother. 2008 Mar;57(3):303-15 [17721781] J Clin Invest. 2008 Jun;118(6):1991-2001 [18523649] Clin Cancer Res. 2008 Jul 15;14(14):4526-31 [18628467] Clin Cancer Res. 2009 Dec 1;15(23):7412-20 [19934295] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1007/s00262-011-1141-0 ER - TY - JOUR T1 - Proline metabolism and cancer. AN - 913031447; 22201839 AB - Proline plays a special role in cancer metabolism. Proline oxidase (POX), a.k.a. proline dehydrogenase (PRODH), is among a few genes induced rapidly and robustly by P53, the tumor suppressor. Ectopic expression of POX under control of tet-off promoter initiated mitochondrial apoptosis. The mechanism activated by POX is mediated by its production of ROS. In immunodeficient mice, POX overexpression markedly retarded growth of xenograft tumors. In human tumors of the digestive tract and kidney, POX was markedly decreased, suggesting that the suppressive effect of POX was downregulated. This was not due to POX gene mutations or hypermethylation. Instead, a microRNA, miR-23b*, expressed at high levels in tumors, was a potent inhibitor of POX expression. Furthermore, antagomirs of miR-23b* reversed the downregulated expression of POX and its tumor-suppressive effect, thereby providing a therapeutic strategy. POX not only responds to genotoxic stress, but also to inflammatory and metabolic stress. Depending on microenvironmental and temporal factors, POX can mediate oppositely-directed responses-programmed cell death, on the one hand, and survival, on the other. JF - Frontiers in bioscience (Landmark edition) AU - Phang, James M AU - Liu, Wei AD - Metabolism and Cancer Susceptibility Section, Laboratory of Comparative Carcinogenesis, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD 21702, USA. phangj@mail.nih.gov Y1 - 2012/01/01/ PY - 2012 DA - 2012 Jan 01 SP - 1835 EP - 1845 VL - 17 KW - Proline KW - 9DLQ4CIU6V KW - Proline Oxidase KW - EC 1.5.3.- KW - Index Medicus KW - Animals KW - Down-Regulation KW - Genes, Tumor Suppressor KW - Humans KW - Proline Oxidase -- metabolism KW - Xenograft Model Antitumor Assays KW - Proline Oxidase -- genetics KW - Proline -- metabolism KW - Neoplasms -- genetics KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/913031447?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Frontiers+in+bioscience+%28Landmark+edition%29&rft.atitle=Proline+metabolism+and+cancer.&rft.au=Phang%2C+James+M%3BLiu%2C+Wei&rft.aulast=Phang&rft.aufirst=James&rft.date=2012-01-01&rft.volume=17&rft.issue=&rft.spage=1835&rft.isbn=&rft.btitle=&rft.title=Frontiers+in+bioscience+%28Landmark+edition%29&rft.issn=1093-4715&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-04-03 N1 - Date created - 2011-12-28 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 ER - TY - JOUR T1 - Serotonergic action on dorsal striatal function. AN - 912639426; 22166410 AB - Serotonin (5-HT) is a monoamine neurotransmitter released throughout the brain. The serotonergic system is implicated in a host of neuropsychiatric disorders including, but not limited to, Parkinson's disease and L-DOPA-induced dyskinesia. These are pathological and drug-induced states that center on dysfunction of the striatum, a basal ganglia structure necessary for voluntary movement control and action learning. 5-HT is released by dorsal raphe nucleus neurons into the dorsal striatum where it acts upon diverse 5-HT receptors that are expressed on various pre- and postsynaptic components. Here, we review the literature on serotonergic effects on dorsal striatal function and discuss possible roles for the striatal serotonergic system in physiological and parkinsonian states. Copyright © 2011 Elsevier Ltd. All rights reserved. JF - Parkinsonism & related disorders AU - Mathur, Brian N AU - Lovinger, David M AD - Laboratory for Integrative Neuroscience, National Institute on Alcohol Abuse and Alcoholism, US National Institutes of Health, Rockville, MD 20852-9411, USA. Y1 - 2012/01// PY - 2012 DA - January 2012 SP - S129 EP - S131 VL - 18 Suppl 1 KW - Antiparkinson Agents KW - 0 KW - Receptors, Serotonin KW - Serotonin KW - 333DO1RDJY KW - Index Medicus KW - Receptors, Serotonin -- physiology KW - Dyskinesia, Drug-Induced -- metabolism KW - Animals KW - Humans KW - Parkinson Disease -- metabolism KW - Antiparkinson Agents -- pharmacology KW - Receptors, Serotonin -- metabolism KW - Antiparkinson Agents -- metabolism KW - Corpus Striatum -- secretion KW - Corpus Striatum -- physiology KW - Serotonin -- secretion KW - Serotonin -- physiology KW - Corpus Striatum -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/912639426?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Parkinsonism+%26+related+disorders&rft.atitle=Serotonergic+action+on+dorsal+striatal+function.&rft.au=Mathur%2C+Brian+N%3BLovinger%2C+David+M&rft.aulast=Mathur&rft.aufirst=Brian&rft.date=2012-01-01&rft.volume=18+Suppl+1&rft.issue=&rft.spage=S129&rft.isbn=&rft.btitle=&rft.title=Parkinsonism+%26+related+disorders&rft.issn=1873-5126&rft_id=info:doi/10.1016%2FS1353-8020%2811%2970040-2 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-27 N1 - Date created - 2011-12-14 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/S1353-8020(11)70040-2 ER - TY - JOUR T1 - Overabundance of putative cancer stem cells in human skin keratinocyte cells malignantly transformed by arsenic. AN - 912638662; 22011395 AB - Arsenic is a human skin carcinogen. Cancer is probably a disease driven by stem cells (SCs), and SCs are likely a key target during arsenic oncogenesis. In utero arsenic exposure predisposes mice to skin cancers that overproduce cancer SCs (CSCs) and have distorted CSC signaling and population dynamics. Therefore, we hypothesized CSC accumulation may occur during arsenic-induced malignant transformation in vitro of human skin keratinocytes. Thus, the HaCaT cell line, malignantly transformed by arsenite (100 nM, 30 weeks; termed As-TM cells) in prior work, was further studied for the quantity and nature of SCs after this transformation. SCs were isolated from passage-matched control and As-TM cells by a magnetic bead system that enriches for CD34-positive cells. There were 2.5 times more SCs isolated from As-TM cells than control. Holoclone production from As-TM putative CSCs was 2.5-fold higher by 1 week and 3.5-fold higher by 2 weeks than control SCs. Potential malignant phenotype was assessed in isolated SC/CSCs. Transcript level of SC/CSC markers were elevated in both isolated As-TM CSCs and control SCs compared with parental cells, but compared with control SCs, As-TM putative CSCs had elevated CD34, K5, K14, K15, and K19 transcripts and dramatically stronger staining for p63, Rac1, K5, Notch1, and K19. As-TM putative CSCs also showed markedly elevated MMP-9 secretion and colony formation, indicators of cancer phenotype, even compared with total population of As-TM cells. Thus, malignant phenotype is particularly pronounced in CSCs after arsenic-induced transformation of human skin cells and occurs concurrently with a potential overproduction of these cells. JF - Toxicological sciences : an official journal of the Society of Toxicology AU - Sun, Yang AU - Tokar, Erik J AU - Waalkes, Michael P AD - National Toxicology Program Laboratory, Inorganic Toxicology Group, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA. Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 20 EP - 29 VL - 125 IS - 1 KW - Antigens, CD34 KW - 0 KW - Biomarkers KW - Matrix Metalloproteinase 9 KW - EC 3.4.24.35 KW - Arsenic KW - N712M78A8G KW - Index Medicus KW - Real-Time Polymerase Chain Reaction KW - Microscopy, Fluorescence KW - Matrix Metalloproteinase 9 -- metabolism KW - Humans KW - Biomarkers -- metabolism KW - Fluorescent Antibody Technique KW - Antigens, CD34 -- metabolism KW - Cell Line KW - Arsenic -- toxicity KW - Neoplastic Stem Cells -- pathology KW - Keratinocytes -- drug effects KW - Cell Transformation, Neoplastic -- metabolism KW - Cell Transformation, Neoplastic -- chemically induced KW - Skin Neoplasms -- pathology KW - Keratinocytes -- pathology KW - Keratinocytes -- metabolism KW - Skin Neoplasms -- metabolism KW - Neoplastic Stem Cells -- metabolism KW - Neoplastic Stem Cells -- drug effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/912638662?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Overabundance+of+putative+cancer+stem+cells+in+human+skin+keratinocyte+cells+malignantly+transformed+by+arsenic.&rft.au=Sun%2C+Yang%3BTokar%2C+Erik+J%3BWaalkes%2C+Michael+P&rft.aulast=Sun&rft.aufirst=Yang&rft.date=2012-01-01&rft.volume=125&rft.issue=1&rft.spage=20&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%2Fkfr282 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-06-06 N1 - Date created - 2011-12-22 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Environ Health Perspect. 2009 Dec;117(12):1847-52 [20049202] Cancer Biol Ther. 2009 Nov;8(21):1986-93 [19783903] J Natl Cancer Inst. 2010 May 5;102(9):638-49 [20339138] PLoS One. 2010;5(10):e13578 [21042537] Toxicol Sci. 2011 Jan;119(1):73-83 [20937726] Cell Biol Toxicol. 2011 Feb;27(1):69-81 [20680429] Cell. 2000 Feb 18;100(4):387-90 [10693755] Proc Natl Acad Sci U S A. 2001 Mar 13;98(6):3156-61 [11248048] Toxicol Appl Pharmacol. 2001 Oct 1;176(1):64-71 [11578149] J Dermatol. 2001 Nov;28(11):628-31 [11770720] Environ Health Perspect. 2002 Oct;110 Suppl 5:749-52 [12426125] J Invest Dermatol. 2003 Apr;120(4):501-11 [12648211] Genes Dev. 2003 May 15;17(10):1253-70 [12756227] J Invest Dermatol. 2003 Nov;121(5):963-8 [14708593] Nat Rev Cancer. 2003 Dec;3(12):895-902 [14737120] Crit Rev Oncol Hematol. 2004 Jul;51(1):1-28 [15207251] Proc Natl Acad Sci U S A. 1987 Apr;84(8):2302-6 [2436229] J Cell Biol. 1988 Mar;106(3):761-71 [2450098] Proc Soc Exp Biol Med. 1993 Jan;202(1):9-15 [8093814] Proc Natl Acad Sci U S A. 1994 May 10;91(10):4293-7 [8183903] J Am Acad Dermatol. 1996 Aug;35(2 Pt 1):223-42 [8708026] Mutat Res. 1997 Jun;386(3):209-18 [9219559] J Cell Sci. 1998 Nov;111 ( Pt 21):3179-88 [9763512] Cell. 1998 Oct 2;95(1):29-39 [9778245] Am J Pathol. 1998 Dec;153(6):1775-85 [9846968] Eur J Dermatol. 1999 Jul-Aug;9(5):363-5 [10417438] Toxicol Appl Pharmacol. 2005 Aug 22;207(1):69-77 [16054901] Science. 2005 Aug 5;309(5736):933-5 [16081735] Proc Natl Acad Sci U S A. 2005 Oct 11;102(41):14677-82 [16203973] Cancer Lett. 2006 Jan 18;231(2):326-38 [15893875] Cancer Res. 2006 Feb 15;66(4):1883-90; discussion 1895-6 [16488983] Oncogene. 2006 Jun 22;25(26):3680-8 [16682958] Stem Cells. 2006 Nov;24(11):2319-45 [16794264] Stem Cell Rev. 2005;1(3):225-31 [17142859] Semin Cancer Biol. 2007 Jun;17(3):219-24 [16781871] Cancer Res. 2007 May 1;67(9):4173-81 [17483328] Toxicol Appl Pharmacol. 2007 May 15;221(1):119-28 [17400267] Mol Carcinog. 2007 Aug;46(8):579-84 [17583566] J Cell Biol. 2008 Jan 28;180(2):273-84 [18209104] Cancer Res. 2008 Mar 15;68(6):1820-5 [18339862] Nature. 2008 Apr 3;452(7187):650-3 [18385740] Free Radic Biol Med. 2008 Sep 1;45(5):651-8 [18572023] Cancer Res. 2008 Oct 15;68(20):8278-85 [18922899] Lancet Oncol. 2009 May;10(5):453-4 [19418618] Toxicology. 2009 Aug 3;262(2):162-70 [19524636] Exp Dermatol. 2009 Oct;18(10):849-56 [19469895] Environ Health Perspect. 2010 Jan;118(1):108-15 [20056578] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/toxsci/kfr282 ER - TY - JOUR T1 - Large prospective investigation of meat intake, related mutagens, and risk of renal cell carcinoma. AN - 912637867; 22170360 AB - The evidence for meat intake and renal cell carcinoma (RCC) risk is inconsistent. Mutagens related to meat cooking and processing, and variation by RCC subtype may be important to consider. In a large US cohort, we prospectively investigated intake of meat and meat-related compounds in relation to risk of RCC, as well as clear cell and papillary RCC histologic subtypes. Study participants (492,186) completed a detailed dietary assessment linked to a database of heme iron, heterocyclic amines (HCA), polycyclic aromatic hydrocarbons (PAHs), nitrate, and nitrite concentrations in cooked and processed meats. Over 9 (mean) y of follow-up, we identified 1814 cases of RCC (498 clear cell and 115 papillary adenocarcinomas). HRs and 95% CIs were estimated within quintiles by using multivariable Cox proportional hazards regression. Red meat intake [62.7 g (quintile 5) compared with 9.8 g (quintile 1) per 1000 kcal (median)] was associated with a tendency toward an increased risk of RCC [HR: 1.19; 95% CI: 1.01, 1.40; P-trend = 0.06] and a 2-fold increased risk of papillary RCC [P-trend = 0.002]. Intakes of benzo(a)pyrene (BaP), a marker of PAHs, and 2-amino-1-methyl-6-phenyl-imidazo[4,5-b]pyridine (PhIP), an HCA, were associated with a significant 20-30% elevated risk of RCC and a 2-fold increased risk of papillary RCC. No associations were observed for the clear cell subtype. Red meat intake may increase the risk of RCC through mechanisms related to the cooking compounds BaP and PhIP. Our findings for RCC appeared to be driven by strong associations with the rarer papillary histologic variant. This study is registered at clinicaltrials.gov as NCT00340015. JF - The American journal of clinical nutrition AU - Daniel, Carrie R AU - Cross, Amanda J AU - Graubard, Barry I AU - Park, Yikyung AU - Ward, Mary H AU - Rothman, Nathaniel AU - Hollenbeck, Albert R AU - Chow, Wong-Ho AU - Sinha, Rashmi AD - Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Department of Health and Human Services, Rockville, MD, USA. carrie.daniel@nih.hhs.gov Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 155 EP - 162 VL - 95 IS - 1 KW - Imidazoles KW - 0 KW - Mutagens KW - Polycyclic Compounds KW - Benzo(a)pyrene KW - 3417WMA06D KW - 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine KW - 909C6UN66T KW - Abridged Index Medicus KW - Index Medicus KW - Prospective Studies KW - Risk Factors KW - Humans KW - Incidence KW - Middle Aged KW - Benzo(a)pyrene -- adverse effects KW - Male KW - Imidazoles -- adverse effects KW - Female KW - Carcinoma, Renal Cell -- etiology KW - Meat -- adverse effects KW - Mutagens -- adverse effects KW - Cooking KW - Diet KW - Polycyclic Compounds -- adverse effects KW - Carcinoma, Renal Cell -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/912637867?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=The+American+journal+of+clinical+nutrition&rft.atitle=Large+prospective+investigation+of+meat+intake%2C+related+mutagens%2C+and+risk+of+renal+cell+carcinoma.&rft.au=Daniel%2C+Carrie+R%3BCross%2C+Amanda+J%3BGraubard%2C+Barry+I%3BPark%2C+Yikyung%3BWard%2C+Mary+H%3BRothman%2C+Nathaniel%3BHollenbeck%2C+Albert+R%3BChow%2C+Wong-Ho%3BSinha%2C+Rashmi&rft.aulast=Daniel&rft.aufirst=Carrie&rft.date=2012-01-01&rft.volume=95&rft.issue=1&rft.spage=155&rft.isbn=&rft.btitle=&rft.title=The+American+journal+of+clinical+nutrition&rft.issn=1938-3207&rft_id=info:doi/10.3945%2Fajcn.111.019364 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-02-16 N1 - Date created - 2011-12-22 N1 - Date revised - 2017-01-14 N1 - Genetic sequence - NCT00340015; ClinicalTrials.gov N1 - SuppNotes - Cited By: Cancer Epidemiol Biomarkers Prev. 2004 Feb;13(2):293-8 [14973110] Br J Cancer. 2011 Sep 27;105(7):1096-104 [21897389] Int J Cancer. 1996 Jan 3;65(1):67-73 [8543399] Princess Takamatsu Symp. 1995;23:85-92 [8844799] Cancer Epidemiol Biomarkers Prev. 1997 Apr;6(4):215-23 [9107425] Lancet. 1999 Feb 27;353(9154):703-7 [10073512] Mol Nutr Food Res. 2005 Jul;49(7):648-55 [15986387] Cancer Causes Control. 2007 Mar;18(2):125-33 [17242980] Urology. 2007 Mar;69(3):452-6 [17382143] Cancer Causes Control. 2007 Dec;18(10):1141-51 [17717631] Public Health Nutr. 2008 Feb;11(2):183-95 [17610761] Hum Pathol. 2009 Jan;40(1):10-29 [19027455] J Natl Cancer Inst. 2008 Dec 3;100(23):1695-706 [19033572] J Am Diet Assoc. 2009 Apr;109(4):656-67 [19328261] Cancer Detect Prev. 2009;32(5-6):340-51 [19303221] Am J Epidemiol. 1986 Jul;124(1):17-27 [3521261] Am J Epidemiol. 2000 Aug 1;152(3):279-86 [10933275] Int J Epidemiol. 2000 Dec;29(6):1060-4 [11101548] J Soc Biol. 2000;194(1):29-38 [11107547] Carcinogenesis. 2001 Jan;22(1):199-202 [11159760] Food Chem Toxicol. 2001 May;39(5):423-36 [11313108] Epidemiology. 2001 May;12(3):327-38 [11338313] Am J Epidemiol. 2001 Dec 15;154(12):1089-99 [11744511] Am J Epidemiol. 2001 Dec 15;154(12):1119-25 [11744517] Carcinogenesis. 2002 May;23(5):809-15 [12016154] Mutat Res. 2002 Sep 30;506-507:197-204 [12351159] Redox Rep. 2002;7(4):189-97 [12396663] J Nutr. 2002 Nov;132(11 Suppl):3526S-3529S [12421882] IARC Sci Publ. 2002;156:181-6 [12484160] Cancer Res. 2003 May 15;63(10):2358-60 [12750250] Mutat Res. 2003 Dec 10;533(1-2):153-71 [14643418] Environ Mol Mutagen. 2004;43(1):53-74 [14743346] Nat Rev Urol. 2010 May;7(5):245-57 [20448658] Nat Rev Urol. 2010 May;7(5):277-85 [20448661] J Appl Toxicol. 2010 Jul;30(5):402-10 [20186696] Am J Pathol. 2011 Feb;178(2):853-60 [21281817] Comment In: J Urol. 2012 Jun;187(6):2022-3 [22579170] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.3945/ajcn.111.019364 ER - TY - JOUR T1 - Fluoxetine protects neurons against microglial activation-mediated neurotoxicity. AN - 912637708; 22166439 AB - Neuroinflammation is closely associated with the pathogenesis of Parkinson's disease (PD) and other neurological disorders. Increasing evidence suggests that inhibition of microglia-mediated neuroinflammation might represent a promising therapeutic potential for PD and related disorders. Fluoxetine, a selective serotonin reuptake inhibitor, is commonly used for the treatment of major depression due to its tolerability and safety profiles. Recent studies have shown that fluoxetine affords robust neuroprotection in a series of neurological disease models. However, the mechanism underlying fluoxetine-mediated neuroprotection remains unclear. Here, by using rat primary midbrain neuronglia cultures, we report that both R and S enantiomers of fluoxetine attenuated chronic neurodegeneration induced by a common inflammogen lipopolysaccharide (LPS) and a neurotoxin 1-methyl-4-phenylpyridinium (MPP(+)). Reconstituted cell culture studies further revealed that microglia were required for fluoxetine-mediated neuroprotection. Fluoxetine significantly inhibited LPS-induced activation of microglia and subsequent release of multiple pro-inflammatory and cytotoxic factors including tumor necrosis factor-α, interleukin-1β, nitric oxide, and reactive oxygen species. Furthermore, inhibition of microglial NF-κB signaling pathway participated in fluoxetine-mediated neuroprotection. Collectively, fluoxetine exerted neuroprotection against microglia-mediated neurotoxicity. Thus, fluoxetine might hold a potential to retard inflammation-mediated chronic neurodegenerative process of PD. Copyright © 2011 Elsevier Ltd. All rights reserved. JF - Parkinsonism & related disorders AU - Zhang, Feng AU - Zhou, Hui AU - Wilson, Belinda C AU - Shi, Jing-Shan AU - Hong, Jau-Shyong AU - Gao, Hui-Ming AD - Neuropharmacology Section, Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 27709, USA. Y1 - 2012/01// PY - 2012 DA - January 2012 SP - S213 EP - S217 VL - 18 Suppl 1 KW - NF-kappa B KW - 0 KW - Neuroprotective Agents KW - Reactive Oxygen Species KW - Fluoxetine KW - 01K63SUP8D KW - Index Medicus KW - Rats KW - Reactive Oxygen Species -- metabolism KW - Animals KW - Rats, Inbred F344 KW - Cells, Cultured KW - Neurotoxicity Syndromes -- prevention & control KW - Neurotoxicity Syndromes -- metabolism KW - Female KW - Pregnancy KW - NF-kappa B -- metabolism KW - NF-kappa B -- antagonists & inhibitors KW - Fluoxetine -- pharmacology KW - Neurons -- metabolism KW - Neurons -- drug effects KW - Parkinson Disease -- metabolism KW - Fluoxetine -- therapeutic use KW - Parkinson Disease -- prevention & control KW - Neuroprotective Agents -- therapeutic use KW - Microglia -- pathology KW - Microglia -- drug effects KW - Neuroprotective Agents -- pharmacology KW - Neurons -- pathology KW - Microglia -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/912637708?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Parkinsonism+%26+related+disorders&rft.atitle=Fluoxetine+protects+neurons+against+microglial+activation-mediated+neurotoxicity.&rft.au=Zhang%2C+Feng%3BZhou%2C+Hui%3BWilson%2C+Belinda+C%3BShi%2C+Jing-Shan%3BHong%2C+Jau-Shyong%3BGao%2C+Hui-Ming&rft.aulast=Zhang&rft.aufirst=Feng&rft.date=2012-01-01&rft.volume=18+Suppl+1&rft.issue=&rft.spage=S213&rft.isbn=&rft.btitle=&rft.title=Parkinsonism+%26+related+disorders&rft.issn=1873-5126&rft_id=info:doi/10.1016%2FS1353-8020%2811%2970066-9 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-27 N1 - Date created - 2011-12-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Neurobiol Dis. 2006 Oct;24(1):101-13 [16887358] FASEB J. 2006 Dec;20(14):2496-511 [17142799] Proc Natl Acad Sci U S A. 1997 Jul 8;94(14):7531-6 [9207126] Neurology. 1988 Aug;38(8):1285-91 [3399080] Genes Dev. 2004 Sep 15;18(18):2195-224 [15371334] Trends Pharmacol Sci. 2003 Aug;24(8):395-401 [12915048] J Neurosci. 2002 May 1;22(9):3673-82 [11978843] J Pharmacol Exp Ther. 2000 May;293(2):607-17 [10773035] J Immunol Methods. 2000 Apr 21;238(1-2):59-68 [10758236] Neuroimage. 2010 Jan 15;49(2):1259-70 [19682588] Brain Res. 2009 Jul 24;1281:108-16 [19427844] J Neurosci Res. 2009 Mar;87(4):1037-45 [18855941] Glia. 2009 Jan 1;57(1):13-23 [18661552] Trends Immunol. 2008 Aug;29(8):357-65 [18599350] Proc Natl Acad Sci U S A. 2007 Nov 20;104(47):18754-9 [18000063] Curr Neurovasc Res. 2007 Feb;4(1):19-29 [17311541] Nat Rev Drug Discov. 2005 Sep;4(9):764-74 [16121130] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/S1353-8020(11)70066-9 ER - TY - JOUR T1 - A recombinant immunotoxin engineered for increased stability by adding a disulfide bond has decreased immunogenicity. AN - 912427634; 22101015 AB - Recombinant immunotoxins (RITs) are anti-cancer agents that combine the Fv of an antibody against cancer cells with a protein toxin from bacteria or plants. Since RITs contain a non-human protein, immunogenicity can be an obstacle in their development. In this study, we have explored the hypothesis that increasing stability can reduce the immunogenicity of a RIT using HA22-LR, which is composed of an anti-CD22 Fv fused to domain III of Pseudomonas exotoxin A. We introduced a disulfide bond into domain III by identifying and mutating two structurally adjacent residues to cysteines at sites suggested by computer modeling. This RIT, HA22-LR-DB, displays a remarkable increase in thermal stability and an enhanced resistance to trypsin degradation. In addition, HA22-LR-DB retains cytotoxic and anti-tumor activity, while exhibiting significantly lower immunogenicity in mice. This study demonstrates that it is possible to design mutations in a protein molecule that will increase the stability of the protein and thereby reduce its immunogenicity. JF - Protein engineering, design & selection : PEDS AU - Liu, Wenhai AU - Onda, Masanori AU - Kim, Changhoon AU - Xiang, Laiman AU - Weldon, John E AU - Lee, Byungkook AU - Pastan, Ira AD - Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, 37 Convent Drive, Bethesda, MD 20892-4264, USA. Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 1 EP - 6 VL - 25 IS - 1 KW - Bacterial Toxins KW - 0 KW - Disulfides KW - Exotoxins KW - Immunotoxins KW - Recombinant Proteins KW - Virulence Factors KW - ADP Ribose Transferases KW - EC 2.4.2.- KW - toxA protein, Pseudomonas aeruginosa KW - EC 2.4.2.31 KW - Index Medicus KW - Animals KW - Electrophoresis, Polyacrylamide Gel KW - Humans KW - ADP Ribose Transferases -- pharmacology KW - Mice, Inbred BALB C KW - ADP Ribose Transferases -- genetics KW - Bacterial Toxins -- genetics KW - Cell Survival -- drug effects KW - Xenograft Model Antitumor Assays KW - Lymphoma -- drug therapy KW - Lymphoma -- immunology KW - Time Factors KW - Exotoxins -- genetics KW - Exotoxins -- pharmacology KW - ADP Ribose Transferases -- immunology KW - Dose-Response Relationship, Drug KW - Protein Stability KW - Virulence Factors -- genetics KW - Cell Line, Tumor KW - Bacterial Toxins -- pharmacology KW - Mice KW - Cell Survival -- immunology KW - Bacterial Toxins -- immunology KW - Exotoxins -- immunology KW - Virulence Factors -- immunology KW - Virulence Factors -- pharmacology KW - Hot Temperature KW - Mice, SCID KW - Lymphoma -- pathology KW - Mutation KW - Female KW - Disulfides -- chemistry KW - Recombinant Proteins -- pharmacology KW - Immunotoxins -- immunology KW - Recombinant Proteins -- immunology KW - Protein Engineering -- methods KW - Immunotoxins -- genetics KW - Recombinant Proteins -- chemistry KW - Disulfides -- immunology KW - Immunotoxins -- pharmacology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/912427634?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+engineering%2C+design+%26+selection+%3A+PEDS&rft.atitle=A+recombinant+immunotoxin+engineered+for+increased+stability+by+adding+a+disulfide+bond+has+decreased+immunogenicity.&rft.au=Liu%2C+Wenhai%3BOnda%2C+Masanori%3BKim%2C+Changhoon%3BXiang%2C+Laiman%3BWeldon%2C+John+E%3BLee%2C+Byungkook%3BPastan%2C+Ira&rft.aulast=Liu&rft.aufirst=Wenhai&rft.date=2012-01-01&rft.volume=25&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Protein+engineering%2C+design+%26+selection+%3A+PEDS&rft.issn=1741-0134&rft_id=info:doi/10.1093%2Fprotein%2Fgzr053 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-05-11 N1 - Date created - 2011-12-21 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Biologicals. 2010 Jan;38(1):144-9 [19783458] Annu Rev Med. 2007;58:221-37 [17059365] Clin Cancer Res. 2000 Apr;6(4):1476-87 [10778980] Biochemistry. 2000 Apr 18;39(15):4207-16 [10757967] J Immunother. 2010 Apr;33(3):297-304 [20445350] J Clin Oncol. 2010 Apr 10;28(11):1870-7 [20212249] Clin Cancer Res. 2010 Mar 15;16(6):1894-903 [20215554] J Immunol Methods. 1985 Mar 18;77(2):305-19 [3981007] Anal Biochem. 1979 Feb;93(1):98-102 [434474] Mol Cell Proteomics. 2004 Jun;3(6):608-14 [15034119] Methods Mol Biol. 2004;248:503-18 [14970517] Nat Struct Biol. 2002 Aug;9(8):621-7 [12080331] N Engl J Med. 2001 Jul 26;345(4):241-7 [11474661] J Exp Med. 2006 Sep 4;203(9):2049-55 [16908625] J Clin Oncol. 2000 Apr;18(8):1622-36 [10764422] Blood. 2009 Apr 16;113(16):3792-800 [18988862] Biophys Chem. 2009 Apr;141(1):21-8 [19155118] Proc Natl Acad Sci U S A. 2008 Aug 12;105(32):11311-6 [18678888] Clin Cancer Res. 2007 Sep 1;13(17):5144-9 [17785569] Cell. 1987 Jan 16;48(1):129-36 [3098436] J Biol Chem. 1988 Aug 25;263(24):11820-5 [2457027] Trends Biochem Sci. 1990 Jan;15(1):14-7 [2107612] Proc Natl Acad Sci U S A. 1996 Jul 9;93(14):6902-6 [8692916] Int J Cancer. 1999 Mar 31;81(1):148-55 [10077166] Leukemia. 1999 Apr;13(4):629-33 [10214872] J Biol Chem. 2004 Nov 12;279(46):47939-51 [15347644] J Clin Oncol. 2005 Sep 20;23(27):6719-29 [16061911] Anal Biochem. 2006 Jun 15;353(2):266-71 [16647035] Nat Rev Cancer. 2006 Jul;6(7):559-65 [16794638] Adv Drug Deliv Rev. 2006 Aug 7;58(5-6):640-56 [16904789] J Immunol. 2006 Dec 15;177(12):8822-34 [17142785] Nat Chem Biol. 2009 Nov;5(11):797-807 [19841629] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/protein/gzr053 ER - TY - JOUR T1 - Assaying chromatin structure and remodeling by restriction enzyme accessibility. AN - 912273624; 22183589 AB - The packaging of eukaryotic DNA into nucleosomes, the fundamental unit of chromatin, creates a barrier to nuclear processes, such as transcription, DNA replication, recombination, and repair. This obstructive nature of chromatin can be overcome by the enzymatic activity of chromatin remodeling complexes, which create a more favorable environment for the association of essential factors and regulators to sequences within target genes. Here, we describe a detailed approach for analyzing chromatin architecture and remodeling by restriction endonuclease hypersensitivity assay. This procedure uses restriction endonucleases to characterize changes in chromatin that accompany nucleosome remodeling. The specific experimental example described in this article is the BRG1 complex-dependent chromatin remodeling of the steroid hormone-responsive mouse mammary tumor virus promoter. Through the use of these methodologies one is able to quantify changes at specific nucleosomes in response to regulatory signals. JF - Methods in molecular biology (Clifton, N.J.) AU - Trotter, Kevin W AU - Archer, Trevor K AD - Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA. Y1 - 2012 PY - 2012 DA - 2012 SP - 89 EP - 102 VL - 833 KW - Chromatin KW - 0 KW - DNA Primers KW - DNA, Neoplasm KW - Nuclear Proteins KW - Oligonucleotides KW - Transcription Factors KW - DNA-Directed DNA Polymerase KW - EC 2.7.7.7 KW - DNA Restriction Enzymes KW - EC 3.1.21.- KW - SMARCA4 protein, human KW - EC 3.6.1.- KW - DNA Helicases KW - EC 3.6.4.- KW - Index Medicus KW - Animals KW - DNA Helicases -- metabolism KW - Transcription Factors -- metabolism KW - Humans KW - Cell Line, Tumor KW - Mice KW - DNA, Neoplasm -- isolation & purification KW - Oligonucleotides -- metabolism KW - Base Sequence KW - Nuclear Proteins -- metabolism KW - Staining and Labeling KW - DNA Primers -- metabolism KW - DNA, Neoplasm -- metabolism KW - DNA-Directed DNA Polymerase -- metabolism KW - Biological Assay -- methods KW - DNA Restriction Enzymes -- metabolism KW - Chromatin Assembly and Disassembly KW - Chromatin -- chemistry UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/912273624?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.atitle=Assaying+chromatin+structure+and+remodeling+by+restriction+enzyme+accessibility.&rft.au=Trotter%2C+Kevin+W%3BArcher%2C+Trevor+K&rft.aulast=Trotter&rft.aufirst=Kevin&rft.date=2012-01-01&rft.volume=833&rft.issue=&rft.spage=89&rft.isbn=&rft.btitle=&rft.title=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.issn=1940-6029&rft_id=info:doi/10.1007%2F978-1-61779-477-3_6 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-04-16 N1 - Date created - 2011-12-20 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Oncogene. 2001 May 28;20(24):3039-46 [11420719] Nat Rev Genet. 2010 Jun;11(6):426-37 [20421872] Nature. 2003 Jan 23;421(6921):448-53 [12540921] Chromosoma. 2003 May;111(8):495-504 [12743713] J Cell Biochem. 2004 Apr 15;91(6):1087-98 [15048866] Mol Cell Biol. 2004 Apr;24(8):3347-58 [15060156] J Cell Sci. 2004 Aug 1;117(Pt 17):3707-11 [15286171] EMBO J. 1986 Oct;5(10):2681-7 [3023055] Mol Cell Biol. 1991 Feb;11(2):688-98 [1846670] Science. 1992 Mar 20;255(5051):1573-6 [1347958] EMBO J. 1993 Aug;12(8):3249-59 [8344262] Cell. 1994 Apr 8;77(1):13-6 [8156588] Mol Cell Biol. 1995 Jul;15(7):3714-21 [7791778] EMBO J. 1996 May 15;15(10):2496-507 [8665857] Cell. 1999 Aug 6;98(3):285-94 [10458604] Nucleic Acids Res. 2006;34(4):e34 [16510851] Mol Cell Endocrinol. 2007 Feb;265-266:162-7 [17240047] Nucl Recept Signal. 2008;6:e004 [18301784] J Biol Chem. 2008 Mar 14;283(11):6752-63 [18174157] Mol Biol Cell. 2001 Nov;12(11):3365-74 [11694573] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/978-1-61779-477-3_6 ER - TY - JOUR T1 - Identification and mapping of linear antigenic determinants of human amyloid ß(1-42) peptide. AN - 912271003; 22181818 AB - Accumulation of cytotoxic oligomers of amyloid ß (Aß) is one of the major pathological hallmarks of Alzheimer's disease (AD). Several immunological approaches that prevent the conversion of Aß into its toxic form or that accelerate its clearance are being actively pursued worldwide. As part of these attempts, we have carried out sequential epitope analysis of Aß where antibodies raised against native Aß and its homologue Aß-KEK were screened for binding to five overlapping hexadecapeptides encompassing the full length of Aß sequence with 10 amino acid overlap. By this approach, we could identify a neutralizing epitope spanning the region 13-28 in Aß. These results demonstrate the presence of an additional stretch of Aß that can serve as mini-vaccine for AD. JF - Journal of immunoassay & immunochemistry AU - Subramanian, Sarada AU - D'Souza, Regina AU - Divya Shree, A N AD - Department of Neurochemistry, National Institute of Mental Health & Neurosciences, Bangalore, India. sarada@nimhans.kar.nic.in Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 26 EP - 34 VL - 33 IS - 1 KW - Amyloid beta-Peptides KW - 0 KW - Antibodies KW - Epitopes KW - Peptide Fragments KW - amyloid beta-protein (1-42) KW - Index Medicus KW - Antigen-Antibody Reactions KW - Humans KW - Molecular Sequence Data KW - Enzyme-Linked Immunosorbent Assay KW - Amino Acid Sequence KW - Antibodies -- immunology KW - Amyloid beta-Peptides -- chemical synthesis KW - Peptide Fragments -- chemistry KW - Amyloid beta-Peptides -- chemistry KW - Epitopes -- immunology KW - Peptide Fragments -- immunology KW - Epitope Mapping KW - Peptide Fragments -- chemical synthesis KW - Amyloid beta-Peptides -- immunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/912271003?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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+immunoassay+%26+immunochemistry&rft.atitle=Identification+and+mapping+of+linear+antigenic+determinants+of+human+amyloid+%C3%9F%281-42%29+peptide.&rft.au=Subramanian%2C+Sarada%3BD%27Souza%2C+Regina%3BDivya+Shree%2C+A+N&rft.aulast=Subramanian&rft.aufirst=Sarada&rft.date=2012-01-01&rft.volume=33&rft.issue=1&rft.spage=26&rft.isbn=&rft.btitle=&rft.title=Journal+of+immunoassay+%26+immunochemistry&rft.issn=1532-4230&rft_id=info:doi/10.1080%2F15321819.2011.591477 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-07-03 N1 - Date created - 2011-12-20 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1080/15321819.2011.591477 ER - TY - JOUR T1 - Targeting the mitochondrial pathway to induce apoptosis/necrosis through ROS by a newly developed Schiff's base to overcome MDR in cancer. AN - 911951214; 22037022 AB - Multidrug resistance (MDR) in cancer, a major obstacle to successful application of cancer chemotherapy, is often characterized by over-expression of multidrug resistance-related proteins such as MRP1, P-gp or elevated glutathione (GSH) level. Efflux of drugs by functional P-gp, MRP1 and elevated GSH level can confer resistance to apoptosis induced by a range of different stimuli. Therefore, it is necessary to develop new cell death inducers with relatively lower toxicity toward non-malignant cells that can overcome MDR by induction of apoptotic or non-apoptotic cell death pathways. Herein we report the synthesis and spectroscopic characterization of a GSH depleting, redox active Schiff's base, viz., potassium-N-(2-hydroxy-3-methoxy-benzaldehyde)-alaninate (PHMBA). Cytotoxic potential of PHMBA has been studied in doxorubicin-resistant and -sensitive T lymphoblastic leukemia cells and Ehrlich ascites carcinoma (EAC) cells. PHMBA kills both the cell types irrespective of their drug-resistance phenotype following apoptotic/necrotic pathways. Moreover, PHMBA-induced cell death is associated with oxidative stress mediated mitochondrial pathway as the H(2)O(2) inhibitor PEG-Catalase abrogated PHMBA-induced apoptosis/necrosis. PHMBA induces anti-tumor activity in both doxorubicin-sensitive and -resistant EAC-tumor-bearing Swiss albino mice. The non-toxicity of PHMBA was also confirmed through cytotoxicity studies on normal cell lines like PBMC, NIH3T3 and Chang Liver. To summarise, our data provide compelling rationale for future clinical use of this redox active Schiff's base in treatment of cancer patients irrespective of their drug-resistance status. Copyright © 2011 Elsevier Masson SAS. All rights reserved. JF - Biochimie AU - Basu, Soumya AU - Ganguly, Avishek AU - Chakraborty, Paramita AU - Sen, Rupashree AU - Banerjee, Kaushik AU - Chatterjee, Mitali AU - Efferth, Thomas AU - Choudhuri, Soumitra Kumar AD - Department of In vitro Carcinogenesis and Cellular Chemotherapy, Chittaranjan National Cancer Institute, 37, S.P. Mukherjee Road, Kolkata 700 026, India. Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 166 EP - 183 VL - 94 IS - 1 KW - Reactive Oxygen Species KW - 0 KW - Schiff Bases KW - Calpain KW - EC 3.4.22.- KW - Caspase 3 KW - Glutathione KW - GAN16C9B8O KW - Calcium KW - SY7Q814VUP KW - Index Medicus KW - Calcium -- metabolism KW - Spectroscopy, Fourier Transform Infrared KW - Animals KW - Necrosis KW - Glutathione -- metabolism KW - Spectrophotometry, Ultraviolet KW - Mice KW - Flow Cytometry KW - Cell Line, Tumor KW - Calpain -- metabolism KW - Magnetic Resonance Spectroscopy KW - Caspase 3 -- metabolism KW - Reactive Oxygen Species -- metabolism KW - Neoplasms -- pathology KW - Neoplasms -- enzymology KW - Mitochondria -- enzymology KW - Mitochondria -- drug effects KW - Apoptosis -- drug effects KW - Mitochondria -- metabolism KW - Drug Resistance, Neoplasm KW - Schiff Bases -- pharmacology KW - Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/911951214?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biochimie&rft.atitle=Targeting+the+mitochondrial+pathway+to+induce+apoptosis%2Fnecrosis+through+ROS+by+a+newly+developed+Schiff%27s+base+to+overcome+MDR+in+cancer.&rft.au=Basu%2C+Soumya%3BGanguly%2C+Avishek%3BChakraborty%2C+Paramita%3BSen%2C+Rupashree%3BBanerjee%2C+Kaushik%3BChatterjee%2C+Mitali%3BEfferth%2C+Thomas%3BChoudhuri%2C+Soumitra+Kumar&rft.aulast=Basu&rft.aufirst=Soumya&rft.date=2012-01-01&rft.volume=94&rft.issue=1&rft.spage=166&rft.isbn=&rft.btitle=&rft.title=Biochimie&rft.issn=1638-6183&rft_id=info:doi/10.1016%2Fj.biochi.2011.10.004 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-04-16 N1 - Date created - 2011-12-16 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1016/j.biochi.2011.10.004 ER - TY - JOUR T1 - A survival analysis approach to modeling human fecundity. AN - 911943994; 21697247 AB - Understanding conception probabilities is important not only for helping couples to achieve pregnancy but also in identifying acute or chronic reproductive toxicants that affect the highly timed and interrelated processes underlying hormonal profiles, ovulation, libido, and conception during menstrual cycles. Currently, 2 statistical approaches are available for estimating conception probabilities depending upon the research question and extent of data collection during the menstrual cycle: a survival approach when interested in modeling time-to-pregnancy (TTP) in relation to women or couples' purported exposure(s), or a hierarchical Bayesian approach when one is interested in modeling day-specific conception probabilities during the estimated fertile window. We propose a biologically valid discrete survival model that unifies the above 2 approaches while relaxing some assumptions that may not be consistent with human reproduction or behavior. This approach combines both the survival and the hierarchical models allowing investigators to obtain the distribution of TTP and day-specific probabilities during the fertile window in a single model. Our model allows for the consideration of covariate effects at both the cycle and the daily level while accounting for daily variation in conception. We conduct extensive simulations and utilize the New York State Angler Prospective Pregnancy Cohort Study to illustrate our approach. We also provide the code to implement the model in R software in the supplemental section of the supplementary material available at Biostatistics online. JF - Biostatistics (Oxford, England) AU - Sundaram, Rajeshwari AU - McLain, Alexander C AU - Buck Louis, Germaine M AD - Division of Epidemiology, Statistics and Prevention Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, 6100 Executive Boulevard, Rockville, MD 20852, USA. sundaramr2@mail.nih.gov Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 4 EP - 17 VL - 13 IS - 1 KW - Index Medicus KW - New York KW - Fertilization KW - Humans KW - Cohort Studies KW - Bayes Theorem KW - Time Factors KW - Male KW - Female KW - Survival Analysis KW - Pregnancy KW - Biostatistics KW - Fertility KW - Models, Biological UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/911943994?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&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 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-04-17 N1 - Date created - 2011-12-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Am J Epidemiol. 1986 Sep;124(3):470-80 [3740046] Biometrics. 1986 Sep;42(3):547-60 [3567288] J Am Stat Assoc. 1996 Dec;91(436):1,413-22 [12155400] Environ Health Perspect. 2004 Jan;112(1):79-86 [14698935] Fertil Steril. 2004 Aug;82(2):358-66 [15302284] Clin Reprod Fertil. 1985 Jun;3(2):145-9 [4052921] Fertil Steril. 1986 May;45(5):732-4 [3699176] Stat Med. 1994 Mar 15-Apr 15;13(5-7):671-81 [8023042] Biometrics. 1994 Jun;50(2):358-67 [8068836] Epidemiology. 1994 Jul;5(4):476-7 [7802800] Biometrics. 1996 Sep;52(3):945-54 [8805762] Biometrics. 1997 Mar;53(1):318-29 [9147597] Biometrics. 2005 Mar;61(1):126-33 [15737085] Am J Epidemiol. 2005 Sep 15;162(6):523-32 [16093292] Paediatr Perinat Epidemiol. 2006 Nov;20 Suppl 1:3-12 [17061968] Hum Reprod. 2009 Feb;24(2):451-8 [18940895] Epidemiology. 2009 Jan;20(1):56-9 [19057382] Biometrics. 1999 Dec;55(4):1005-13 [11315041] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/biostatistics/kxr015 ER - TY - JOUR T1 - Latent class models for joint analysis of disease prevalence and high-dimensional semicontinuous biomarker data. AN - 911943290; 21908867 AB - High-dimensional biomarker data are often collected in epidemiological studies when assessing the association between biomarkers and human disease is of interest. We develop a latent class modeling approach for joint analysis of high-dimensional semicontinuous biomarker data and a binary disease outcome. To model the relationship between complex biomarker expression patterns and disease risk, we use latent risk classes to link the 2 modeling components. We characterize complex biomarker-specific differences through biomarker-specific random effects, so that different biomarkers can have different baseline (low-risk) values as well as different between-class differences. The proposed approach also accommodates data features that are common in environmental toxicology and other biomarker exposure data, including a large number of biomarkers, numerous zero values, and complex mean-variance relationship in the biomarkers levels. A Monte Carlo EM (MCEM) algorithm is proposed for parameter estimation. Both the MCEM algorithm and model selection procedures are shown to work well in simulations and applications. In applying the proposed approach to an epidemiological study that examined the relationship between environmental polychlorinated biphenyl (PCB) exposure and the risk of endometriosis, we identified a highly significant overall effect of PCB concentrations on the risk of endometriosis. JF - Biostatistics (Oxford, England) AU - Zhang, Bo AU - Chen, Zhen AU - Albert, Paul S AD - Biostatistics and Bioinformatics Branch, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892, USA. bo.zhang@nih.gov Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 74 EP - 88 VL - 13 IS - 1 KW - Biomarkers KW - 0 KW - Polychlorinated Biphenyls KW - DFC2HB4I0K KW - Index Medicus KW - Endometriosis -- epidemiology KW - Young Adult KW - Endometriosis -- blood KW - Polychlorinated Biphenyls -- toxicity KW - Humans KW - Algorithms KW - Endometriosis -- etiology KW - Monte Carlo Method KW - Likelihood Functions KW - Polychlorinated Biphenyls -- blood KW - Adult KW - Environmental Exposure KW - Adolescent KW - Biomarkers -- blood KW - Female KW - Biostatistics KW - Models, Statistical KW - Cross-Sectional Studies -- statistics & numerical data UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/911943290?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Biostatistics+%28Oxford%2C+England%29&rft.atitle=Latent+class+models+for+joint+analysis+of+disease+prevalence+and+high-dimensional+semicontinuous+biomarker+data.&rft.au=Zhang%2C+Bo%3BChen%2C+Zhen%3BAlbert%2C+Paul+S&rft.aulast=Zhang&rft.aufirst=Bo&rft.date=2012-01-01&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 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-04-17 N1 - Date created - 2011-12-14 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Epidemiology. 2010 Jul;21 Suppl 4:S71-6 [20526202] Hum Reprod. 2005 Jan;20(1):279-85 [15513976] Biometrics. 1982 Dec;38(4):963-74 [7168798] Epidemiology. 2010 Jul;21 Suppl 4:S77-84 [21422968] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/biostatistics/kxr024 ER - TY - JOUR T1 - Fatal pancreatitis in simian immunodeficiency virus SIV(mac251)-infected macaques treated with 2',3'-dideoxyinosine and stavudine following cytotoxic-T-lymphocyte-associated antigen 4 and indoleamine 2,3-dioxygenase blockade. AN - 911934057; 22013040 AB - Human immunodeficiency virus (HIV) infection is associated with immune activation, CD4⁺-T-cell loss, and a progressive decline of immune functions. Antiretroviral therapy (ART) only partially reverses HIV-associated immune dysfunction, suggesting that approaches that target immune activation and improve virus-specific immune responses may be needed. We performed a preclinical study in rhesus macaques infected with the pathogenic simian immunodeficiency virus SIV(mac251) and treated with ART. We tested whether vaccination administered together with cytotoxic-T-lymphocyte-associated antigen 4 (CTLA-4) blockade and treatment with the indoleamine 2,3-dioxygenase (IDO) inhibitor 1-methyl-D-tryptophan (D-1mT), decreased immune activation and improved vaccine efficacy. The treatment did not augment vaccine immunogenicity; rather, it dramatically increased ART-related toxicity, causing all treated animals to succumb to acute pancreatitis and hyperglycemic coma. The onset of fulminant diabetes was associated with severe lymphocyte infiltration of the pancreas and complete loss of the islets of Langerhans. Thus, caution should be used when considering approaches aimed at targeting immune activation during ART. JF - Journal of virology AU - Vaccari, Monica AU - Boasso, Adriano AU - Fenizia, Claudio AU - Fuchs, Dietmar AU - Hryniewicz, Anna AU - Morgan, Tia AU - Weiss, Deborah AU - Doster, Melvin N AU - Heraud, Jean Michel AU - Shearer, Gene M AU - Franchini, Genoveffa AD - Animal Models & Retroviral Vaccines Section, NCI, NIH, Bethesda, Maryland, USA. Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 108 EP - 113 VL - 86 IS - 1 KW - AIDS Vaccines KW - 0 KW - Anti-HIV Agents KW - CTLA-4 Antigen KW - Indoleamine-Pyrrole 2,3,-Dioxygenase KW - Tryptophan KW - 8DUH1N11BX KW - Stavudine KW - BO9LE4QFZF KW - Didanosine KW - K3GDH6OH08 KW - Index Medicus KW - AIDS Vaccines -- administration & dosage KW - Drug Therapy, Combination -- adverse effects KW - Animals KW - Tryptophan -- analogs & derivatives KW - HIV-1 -- immunology KW - Tryptophan -- adverse effects KW - AIDS Vaccines -- immunology KW - Humans KW - Disease Models, Animal KW - Tryptophan -- therapeutic use KW - HIV-1 -- physiology KW - CTLA-4 Antigen -- antagonists & inhibitors KW - Indoleamine-Pyrrole 2,3,-Dioxygenase -- antagonists & inhibitors KW - Macaca mulatta KW - Drug Evaluation, Preclinical KW - HIV-1 -- drug effects KW - Simian Immunodeficiency Virus -- physiology KW - Simian Immunodeficiency Virus -- immunology KW - HIV Infections -- virology KW - Pancreatitis -- immunology KW - Anti-HIV Agents -- adverse effects KW - Pancreatitis -- etiology KW - Didanosine -- adverse effects KW - Didanosine -- therapeutic use KW - Anti-HIV Agents -- therapeutic use KW - Stavudine -- therapeutic use KW - HIV Infections -- complications KW - Pancreatitis -- mortality KW - Simian Immunodeficiency Virus -- drug effects KW - HIV Infections -- immunology KW - HIV Infections -- drug therapy KW - Stavudine -- adverse effects UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/911934057?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info: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=Fatal+pancreatitis+in+simian+immunodeficiency+virus+SIV%28mac251%29-infected+macaques+treated+with+2%27%2C3%27-dideoxyinosine+and+stavudine+following+cytotoxic-T-lymphocyte-associated+antigen+4+and+indoleamine+2%2C3-dioxygenase+blockade.&rft.au=Vaccari%2C+Monica%3BBoasso%2C+Adriano%3BFenizia%2C+Claudio%3BFuchs%2C+Dietmar%3BHryniewicz%2C+Anna%3BMorgan%2C+Tia%3BWeiss%2C+Deborah%3BDoster%2C+Melvin+N%3BHeraud%2C+Jean+Michel%3BShearer%2C+Gene+M%3BFranchini%2C+Genoveffa&rft.aulast=Vaccari&rft.aufirst=Monica&rft.date=2012-01-01&rft.volume=86&rft.issue=1&rft.spage=108&rft.isbn=&rft.btitle=&rft.title=Journal+of+virology&rft.issn=1098-5514&rft_id=info:doi/10.1128%2FJVI.05609-11 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-02-14 N1 - Date created - 2011-12-14 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Nat Immunol. 2003 Dec;4(12):1206-12 [14578884] Curr Med Chem. 2011;18(15):2247-56 [21517754] Annu Rev Immunol. 2004;22:531-62 [15032588] J Immunol. 2004 Aug 1;173(3):2184-9 [15265956] J Exp Med. 2004 Aug 2;200(3):331-43 [15280419] Am J Transplant. 2004 Oct;4(10):1614-27 [15367216] Nat Rev Immunol. 2004 Oct;4(10):762-74 [15459668] Science. 1987 Jan 16;235(4786):356 [3099388] Am J Gastroenterol. 1992 Jun;87(6):708-13 [1590305] Gut. 1995 Oct;37(4):565-7 [7489946] Immunol Invest. 1997 Jan-Feb;26(1-2):15-28 [9037609] Clin Chem. 1997 Dec;43(12):2424-6 [9439467] Science. 1998 Aug 21;281(5380):1191-3 [9712583] J Antimicrob Chemother. 1999 Jul;44(1):137-8 [10459826] Blood. 2004 Nov 15;104(10):3249-56 [15271794] J Clin Oncol. 2005 Feb 1;23(4):741-50 [15613700] J Clin Pharmacol. 2005 Aug;45(8):935-40 [16027404] Ann Surg Oncol. 2006 Sep;13(9):1252-8 [16952047] AIDS Rev. 2006 Jul-Sep;8(3):141-7 [17078484] Blood. 2006 Dec 1;108(12):3834-42 [16896154] Cancer Res. 2007 Jan 15;67(2):792-801 [17234791] Blood. 2007 Apr 15;109(8):3351-9 [17158233] J Clin Invest. 2007 May;117(5):1147-54 [17476344] Cancer Res. 2007 Aug 1;67(15):7082-7 [17671174] J Virol. 2007 Nov;81(21):11593-603 [17715231] J Immunother. 2007 Nov-Dec;30(8):825-30 [18049334] J Immunol. 2008 Apr 15;180(8):5439-47 [18390726] Mucosal Immunol. 2008 Nov;1(6):497-507 [19079217] J Intern Med. 2009 Jan;265(1):78-96 [19093962] Diabetes Metab Res Rev. 2009 Mar;25(3):208-18 [19214972] J Immunol. 2009 Apr 1;182(7):4313-20 [19299731] PLoS One. 2010;5(3):e9852 [20352042] J Exp Med. 2003 Dec 15;198(12):1951-7 [14662908] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1128/JVI.05609-11 ER - TY - JOUR T1 - Sex steroid hormone levels in breast adipose tissue and serum in postmenopausal women. AN - 911931520; 21870130 AB - Elevated levels of circulating estrogens and androgens are linked to higher breast cancer risk among postmenopausal women; however, little is known about hormone levels within the breast. Hormone concentrations within the breast may not be reflected in the blood and are likely important contributors to breast carcinogenesis. We used a previously validated method to measure levels of estrone, estradiol, androstenedione, and testosterone in adipose tissue removed as part of breast excisions performed for cancer in 100 postmenopausal women (69 ER/PR +/+ and 31 ER/PR -/-) participating in a breast cancer case-control study. We also measured the same steroid hormones, as well as estrone sulfate, and sex hormone-binding globulin (SHBG) in serum from these patients and 100 controls matched on ages at blood collection and on menopause. Overall, concentrations of serum hormones did not vary significantly between controls and cases. However, women with ER-/PR- breast cancers had lower circulating levels of all measured sex steroid hormones and higher SHBG levels than women with ER+/PR+ breast cancers and controls. Similarly, hormone concentrations in breast adipose tissue were higher among women with ER+/PR+ compared to ER-/PR- breast cancer, although differences were only significant for testosterone. These data demonstrate that high sex steroid concentrations in both serum and adipose tissues are more strongly related to ER+/PR+ than ER-/PR- breast cancers. Measurement of sex hormones in serum and in the microenvironment may help in understanding the hormonal etiology of breast cancer, suggest methods for prevention, and have value in gauging treatment response and prognosis. JF - Breast cancer research and treatment AU - Falk, Roni T AU - Gentzschein, Elisabet AU - Stanczyk, Frank Z AU - Garcia-Closas, Montserrat AU - Figueroa, Jonine D AU - Ioffe, Olga B AU - Lissowska, Jolanta AU - Brinton, Louise A AU - Sherman, Mark E AD - Hormonal and Reproductive Epidemiology Branch, National Cancer Institute, Bethesda, MD, USA. falkr@mail.nih.gov Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 287 EP - 294 VL - 131 IS - 1 KW - Gonadal Steroid Hormones KW - 0 KW - Receptors, Estrogen KW - Receptors, Progesterone KW - Sex Hormone-Binding Globulin KW - Estrone KW - 2DI9HA706A KW - Testosterone KW - 3XMK78S47O KW - Androstenedione KW - 409J2J96VR KW - Estradiol KW - 4TI98Z838E KW - Index Medicus KW - Humans KW - Sex Hormone-Binding Globulin -- analysis KW - Aged KW - Body Mass Index KW - Receptors, Estrogen -- metabolism KW - Androstenedione -- blood KW - Estradiol -- blood KW - Receptors, Progesterone -- metabolism KW - Postmenopause KW - Testosterone -- blood KW - Adult KW - Middle Aged KW - Estrone -- blood KW - Female KW - Adipose Tissue -- physiology KW - Gonadal Steroid Hormones -- blood KW - Breast Neoplasms -- blood UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/911931520?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Breast+cancer+research+and+treatment&rft.atitle=Sex+steroid+hormone+levels+in+breast+adipose+tissue+and+serum+in+postmenopausal+women.&rft.au=Falk%2C+Roni+T%3BGentzschein%2C+Elisabet%3BStanczyk%2C+Frank+Z%3BGarcia-Closas%2C+Montserrat%3BFigueroa%2C+Jonine+D%3BIoffe%2C+Olga+B%3BLissowska%2C+Jolanta%3BBrinton%2C+Louise+A%3BSherman%2C+Mark+E&rft.aulast=Falk&rft.aufirst=Roni&rft.date=2012-01-01&rft.volume=131&rft.issue=1&rft.spage=287&rft.isbn=&rft.btitle=&rft.title=Breast+cancer+research+and+treatment&rft.issn=1573-7217&rft_id=info:doi/10.1007%2Fs10549-011-1734-5 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-08-21 N1 - Date created - 2011-12-13 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Steroid Biochem Mol Biol. 2009 Mar;114(1-2):68-71 [19444935] J Steroid Biochem Mol Biol. 2009 Oct;117(1-3):31-41 [19591931] Cancer Epidemiol Biomarkers Prev. 2009 Nov;18(11):2942-8 [19843675] Cancer Epidemiol Biomarkers Prev. 2010 Feb;19(2):492-502 [20086116] Clin Cancer Res. 2010 Mar 15;16(6):1790-801 [20215536] J Steroid Biochem Mol Biol. 2010 Aug;121(3-5):491-5 [20470886] Cancer Prev Res (Phila). 2011 Mar;4(3):329-46 [21372033] J Natl Cancer Inst. 2011 May 4;103(9):744-52 [21483019] N Engl J Med. 2011 Jun 23;364(25):2381-91 [21639806] Cancer Prev Res (Phila). 2011 Jul;4(7):1021-9 [21622727] J Steroid Biochem Mol Biol. 2000 Jan-Feb;72(1-2):23-7 [10731634] J Natl Cancer Inst. 2002 Apr 17;94(8):606-16 [11959894] Endocr Rev. 2003 Apr;24(2):152-82 [12700178] J Steroid Biochem Mol Biol. 2003 Sep;86(3-5):245-53 [14623518] Cancer Res. 1985 Jun;45(6):2907-12 [3157451] Cancer Epidemiol Biomarkers Prev. 2004 Oct;13(10):1558-68 [15466970] Maturitas. 2004 Sep 24;49(1):25-33 [15351093] Eur J Cancer Clin Oncol. 1986 Apr;22(4):515-25 [3015631] Br Med J (Clin Res Ed). 1988 Mar 12;296(6624):741-3 [3126957] Steroids. 1987 Oct-Dec;50(4-6):537-48 [3504615] Int J Cancer. 1991 Oct 21;49(4):562-5 [1917157] Breast Cancer Res Treat. 1995;33(2):171-7 [7749143] Cancer Epidemiol Biomarkers Prev. 1995 Dec;4(8):857-60 [8634657] Int J Cancer. 1997 Mar 17;70(6):639-43 [9096642] Steroids. 1998 May-Jun;63(5-6):319-21 [9618794] J Steroid Biochem Mol Biol. 1999 Apr-Jun;69(1-6):293-7 [10419005] J Natl Cancer Inst. 2004 Dec 15;96(24):1856-65 [15601642] J Steroid Biochem Mol Biol. 2005 Feb;93(2-5):221-36 [15860265] Cancer Epidemiol Biomarkers Prev. 2005 May;14(5):1047-51 [15894651] N Engl J Med. 2006 Jan 19;354(3):270-82 [16421368] Breast Cancer. 2006;13(2):129-36 [16755106] Br J Cancer. 2006 Jul 3;95(1):123-9 [16755295] Cancer Epidemiol Biomarkers Prev. 2007 Mar;16(3):439-43 [17372238] Int J Cancer. 2007 Sep 1;121(5):1079-85 [17487843] Cancer Epidemiol Biomarkers Prev. 2008 Aug;17(8):1891-5 [18708377] Breast Cancer. 2008;15(4):270-7 [18622573] Cancer Epidemiol Biomarkers Prev. 2009 Jan;18(1):169-76 [19124495] Ann N Y Acad Sci. 2009 Feb;1155:121-31 [19250199] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/s10549-011-1734-5 ER - TY - JOUR T1 - Epithelial ovarian cancer and exposure to dietary nitrate and nitrite in the NIH-AARP Diet and Health Study. AN - 908009276; 21934624 AB - Ovarian cancer is a leading cause of cancer death among women in the United States and it has the highest mortality rate of all gynecologic cancers. Internationally, there is a five-fold variation in incidence and mortality of ovarian cancer, which suggests a role for environmental factors, including diet. Nitrate and nitrite are found in various food items and they are precursors of N-nitroso compounds, which are known carcinogens in animal models. We evaluated dietary nitrate and nitrite intake and epithelial ovarian cancer in the National Institutes of Health (NIH)-AARP Diet and Health Study, including 151 316 women aged 50-71 years at the time of the baseline questionnaire in 1995-1996. The nitrate and nitrite intake was assessed using a 124-item validated food frequency questionnaire. Through 31 December 2006, 709 incident epithelial ovarian cancer cases with complete dietary information were identified. Using Cox proportional hazards regression to estimate hazard ratios and 95% confidence intervals (CIs), women in the highest intake quintile of dietary nitrate had a 31% increased risk (95% CI: 1.01-1.68) of epithelial ovarian cancer, compared with those in the lowest intake quintile. Although there was no association for total dietary nitrite, those in the highest intake category of animal sources of nitrite had a 34% increased risk (95% CI: 1.05-1.69) of ovarian cancer. There were no clear differences in risk by histologic subtype of ovarian cancer. Our findings suggest that a role of dietary nitrate and nitrite in ovarian cancer risk should be followed in other large cohort studies. JF - European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) AU - Aschebrook-Kilfoy, Briseis AU - Ward, Mary H AU - Gierach, Gretchen L AU - Schatzkin, Arthur AU - Hollenbeck, Albert R AU - Sinha, Rashmi AU - Cross, Amanda J AD - Occupational and Environmental Epidemiology Branch, DCEG, NCI, NIH, Rockville, Maryland 20852, USA. kilfoyb@mail.nih.gov Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 65 EP - 72 VL - 21 IS - 1 KW - Nitrates KW - 0 KW - Nitrites KW - Index Medicus KW - Prospective Studies KW - Risk Factors KW - Humans KW - National Institutes of Health (U.S.) KW - Adult KW - Diet Surveys KW - Incidence KW - Aged KW - Middle Aged KW - United States -- epidemiology KW - Female KW - Adenocarcinoma, Mucinous -- epidemiology KW - Endometrial Neoplasms -- chemically induced KW - Nitrites -- adverse effects KW - Adenocarcinoma, Clear Cell -- chemically induced KW - Endometrial Neoplasms -- epidemiology KW - Adenocarcinoma, Clear Cell -- epidemiology KW - Ovarian Neoplasms -- chemically induced KW - Nitrates -- adverse effects KW - Diet KW - Adenocarcinoma, Mucinous -- chemically induced KW - Ovarian Neoplasms -- epidemiology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/908009276?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=European+journal+of+cancer+prevention+%3A+the+official+journal+of+the+European+Cancer+Prevention+Organisation+%28ECP%29&rft.atitle=Epithelial+ovarian+cancer+and+exposure+to+dietary+nitrate+and+nitrite+in+the+NIH-AARP+Diet+and+Health+Study.&rft.au=Aschebrook-Kilfoy%2C+Briseis%3BWard%2C+Mary+H%3BGierach%2C+Gretchen+L%3BSchatzkin%2C+Arthur%3BHollenbeck%2C+Albert+R%3BSinha%2C+Rashmi%3BCross%2C+Amanda+J&rft.aulast=Aschebrook-Kilfoy&rft.aufirst=Briseis&rft.date=2012-01-01&rft.volume=21&rft.issue=1&rft.spage=65&rft.isbn=&rft.btitle=&rft.title=European+journal+of+cancer+prevention+%3A+the+official+journal+of+the+European+Cancer+Prevention+Organisation+%28ECP%29&rft.issn=1473-5709&rft_id=info:doi/10.1097%2FCEJ.0b013e328347622f LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-03-20 N1 - Date created - 2011-12-01 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Br J Cancer. 2002 Mar 4;86(5):712-7 [11875731] Am J Epidemiol. 2001 Dec 15;154(12):1119-25 [11744517] Cancer Res. 1975 Nov;35(11 Pt. 2):3240-5 [1192400] Int J Cancer. 1981;27(4):471-4 [7275353] J Natl Cancer Inst. 1983 Oct;71(4):681-6 [6578362] Int J Epidemiol. 1984 Sep;13(3):324-31 [6490303] Zentralbl Bakteriol Mikrobiol Hyg B. 1985 Feb;180(2-3):311-8 [3993260] J Natl Cancer Inst. 1987 Oct;79(4):663-9 [3116309] Cancer Surv. 1987;6(4):719-38 [3330686] Am J Epidemiol. 1988 Oct;128(4):771-7 [3421242] Jpn J Cancer Res. 1988 Sep;79(9):997-1004 [3142839] J Natl Cancer Inst. 1994 Sep 7;86(17):1336-9 [8064892] Semin Surg Oncol. 1994 Jul-Aug;10(4):242-8 [8091065] Eur J Pharmacol. 1994 Nov 1;292(1):1-38 [7867685] Cancer Lett. 1995 Jun 29;93(1):17-48 [7600541] IARC Sci Publ. 1996;(139):189-201 [8923031] Eur J Cancer Prev. 1996 Sep;5 Suppl 1:131-6 [8972308] Epidemiology. 2006 Jul;17(4):375-82 [16699473] Lancet Oncol. 2006 Aug;7(8):628-9 [16900606] Environ Sci Technol. 2006 Dec 15;40(24):7834-40 [17256535] Cancer Epidemiol Biomarkers Prev. 2007 Apr;16(4):852-5 [17416784] Public Health Nutr. 2008 Feb;11(2):183-95 [17610761] Am J Epidemiol. 2009 Sep 1;170(5):598-606 [19605513] Am J Epidemiol. 2000 Aug 1;152(3):279-86 [10933275] Br J Nutr. 1999 May;81(5):349-58 [10615207] CA Cancer J Clin. 2010 Sep-Oct;60(5):277-300 [20610543] Epidemiology. 2001 May;12(3):327-38 [11338313] Int J Cancer. 2001 Sep15;93(6):911-5 [11519057] Int J Cancer. 2004 Jun 10;110(2):271-7 [15069693] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1097/CEJ.0b013e328347622f ER - TY - JOUR T1 - Why proteins in mammalian cells? AN - 897813285; 21987243 AB - Producing recombinant mammalian proteins in native or near-native conformation is fundamental to many aspects of biology. Unfortunately, it is also a task whose outcome is extremely unpredictable. A protein that has been shaped over millions of generations of evolution for expression at a level appropriate to a specific cell type or in a particular developmental stage, may be toxic to a new host cell, or become insoluble (among many possible obstacles) when overexpressed in vitro. The object of this volume, "Protein Expression in Mammalian Cells," is to offer guidance for those who wish (or who have been forced by circumstance) to overexpress a mammalian protein in mammalian cells. JF - Methods in molecular biology (Clifton, N.J.) AU - Hartley, James L AD - Protein Expression Laboratory, SAIC-Frederick, Inc., National Cancer Institute, Frederick, MD, USA. hartleyjames@mail.nih.gov Y1 - 2012 PY - 2012 DA - 2012 SP - 1 EP - 12 VL - 801 KW - Recombinant Proteins KW - 0 KW - DNA KW - 9007-49-2 KW - Index Medicus KW - Animals KW - Solubility KW - Transfection KW - DNA -- metabolism KW - DNA -- genetics KW - Protein Folding KW - Gene Expression KW - Viruses -- genetics KW - Genetic Vectors -- genetics KW - Cell Line KW - Recombinant Proteins -- biosynthesis KW - Mammals KW - Genetic Engineering -- methods KW - Recombinant Proteins -- chemistry KW - Recombinant Proteins -- genetics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/897813285?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.atitle=Why+proteins+in+mammalian+cells%3F&rft.au=Hartley%2C+James+L&rft.aulast=Hartley&rft.aufirst=James&rft.date=2012-01-01&rft.volume=801&rft.issue=&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Methods+in+molecular+biology+%28Clifton%2C+N.J.%29&rft.issn=1940-6029&rft_id=info:doi/10.1007%2F978-1-61779-352-3_1 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-02-02 N1 - Date created - 2011-10-11 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1007/978-1-61779-352-3_1 ER - TY - JOUR T1 - Tumor necrosis factor-alpha (TNF- alpha ) is a therapeutic target for impaired cutaneous wound healing AN - 1780502840; 16306189 AB - Impaired wound healing states lead to substantial morbidity and cost with treatment resulting in an expenditure of billions of dollars per annum in the US alone. Both chronic wounds and impaired acute wounds are characterized by excessive inflammation, enhanced proteolysis, and reduced matrix deposition. These confounding factors are exacerbated in the elderly, in part, as we report here, related to increased local and systemic tumor necrosis factor-alpha (TNF- alpha ) levels. Moreover, we have used a secretory leukocyte protease inhibitor (SLPI) null mouse model of severely impaired wound healing and excessive inflammation, comparable to age-related delayed human healing, to demonstrate that topical application of anti-TNF- alpha neutralizing antibodies blunts leukocyte recruitment and NF Kappa B activation, alters the balance between M1 and M2 macrophages, and accelerates wound healing. Following antagonism of TNF- alpha , matrix synthesis is enhanced, associated with suppression of both inflammatory parameters and NF Kappa B binding activity. Our data suggest that inhibiting TNF- alpha is a critical event in reversing the severely impaired healing response associated with the absence of SLPI, and may be applicable to prophylaxis and/or treatment of impaired wound healing states in humans. JF - Wound Repair and Regeneration AU - Ashcroft, Gillian S AU - Jeong, Moon-Jin AU - Ashworth, Jason J AU - Hardman, Matthew AU - Jin, Wenwen AU - Moutsopoulos, Niki AU - Wild, Teresa AU - McCartney-Francis, Nancy AU - Sim, Davis AU - McGrady, George AU - Song, Xiao-yu AU - Wahl, Sharon M AD - Oral Infection and Immunity Branch National Institute of Dental & Craniofacial Research. National Institutes of Health Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 38 EP - 49 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 20 IS - 1 SN - 1067-1927, 1067-1927 KW - Biotechnology and Bioengineering Abstracts KW - Macrophages KW - Proteolysis KW - Age KW - Data processing KW - Leukocytes KW - Proteinase inhibitors KW - Animal models KW - Wound healing KW - Antagonism KW - Morbidity KW - Cell activation KW - Inflammation KW - Topical application KW - Leukocyte migration KW - Antibodies KW - Prophylaxis KW - Geriatrics KW - Tumor necrosis factor- alpha KW - W 30940:Products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1780502840?accountid=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=Wound+Repair+and+Regeneration&rft.atitle=Tumor+necrosis+factor-alpha+%28TNF-+alpha+%29+is+a+therapeutic+target+for+impaired+cutaneous+wound+healing&rft.au=Ashcroft%2C+Gillian+S%3BJeong%2C+Moon-Jin%3BAshworth%2C+Jason+J%3BHardman%2C+Matthew%3BJin%2C+Wenwen%3BMoutsopoulos%2C+Niki%3BWild%2C+Teresa%3BMcCartney-Francis%2C+Nancy%3BSim%2C+Davis%3BMcGrady%2C+George%3BSong%2C+Xiao-yu%3BWahl%2C+Sharon+M&rft.aulast=Ashcroft&rft.aufirst=Gillian&rft.date=2012-01-01&rft.volume=20&rft.issue=1&rft.spage=38&rft.isbn=&rft.btitle=&rft.title=Wound+Repair+and+Regeneration&rft.issn=10671927&rft_id=info:doi/10.1111%2Fj.1524-475X.2011.00748.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-04-01 N1 - Last updated - 2016-05-13 N1 - SubjectsTermNotLitGenreText - Proteolysis; Macrophages; Age; Data processing; Proteinase inhibitors; Leukocytes; Animal models; Wound healing; Antagonism; Morbidity; Topical application; Inflammation; Cell activation; Leukocyte migration; Antibodies; Geriatrics; Prophylaxis; Tumor necrosis factor- alpha DO - http://dx.doi.org/10.1111/j.1524-475X.2011.00748.x ER - TY - JOUR T1 - Archaeal origin of tubulin AN - 1776660936; 16884952 AB - Tubulins are a family of GTPases that are key components of the cytoskeleton in all eukaryotes and are distantly related to the FtsZ GTPase that is involved in cell division in most bacteria and many archaea. Among prokaryotes, bona fide tubulins have been identified only in bacteria of the genus Prosthecobacter. These bacterial tubulin genes appear to have been horizontally transferred from eukaryotes. Here we describe tubulins encoded in the genomes of thaumarchaeota of the genus Nitrosoarchaeum that we denote artubulins Phylogenetic analysis results are compatible with the origin of eukaryotic tubulins from artubulins. These findings expand the emerging picture of the origin of key components of eukaryotic functional systems from ancestral forms that are scattered among the extant archaea. Reviewers: This article was reviewed by Gaspar Jekely and J. Peter Gogarten. JF - Biology Direct AU - Yutin, Natalya AU - Koonin, Eugene V AD - National Center for Biotechnology Information, National Library of Medicine. National Institutes of Health, Bethesda, MD 20894, USA Y1 - 2012///0, PY - 2012 DA - 0, 2012 SP - 10 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 7 IS - 1 SN - 1745-6150, 1745-6150 KW - Microbiology Abstracts B: Bacteriology KW - Genomes KW - Cytoskeleton KW - Phylogeny KW - Cell division KW - Archaea KW - Prosthecobacter KW - Reviews KW - Prokaryotes KW - Tubulin KW - Guanosinetriphosphatase KW - J 02310:Genetics & Taxonomy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1776660936?accountid=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=Biology+Direct&rft.atitle=Archaeal+origin+of+tubulin&rft.au=Yutin%2C+Natalya%3BKoonin%2C+Eugene+V&rft.aulast=Yutin&rft.aufirst=Natalya&rft.date=2012-01-01&rft.volume=7&rft.issue=1&rft.spage=10&rft.isbn=&rft.btitle=&rft.title=Biology+Direct&rft.issn=17456150&rft_id=info:doi/10.1186%2F1745-6150-7-10 L2 - http://www.biology-direct.com/content/7/1/10 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-03-01 N1 - Number of references - 48 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Phylogeny; Cytoskeleton; Genomes; Cell division; Reviews; Prokaryotes; Tubulin; Guanosinetriphosphatase; Archaea; Prosthecobacter DO - http://dx.doi.org/10.1186/1745-6150-7-10 ER - TY - JOUR T1 - Improving understanding of clinical trial procedures among low literacy populations: an intervention within a microbicide trial in Malawi AN - 1758242972; 17436164 AB - Background: The intervention reported in this paper was a follow up to an empirical study conducted in Malawi with the aim of assessing trial participants' understanding of randomisation, double-blinding and placebo use. In the empirical study, the majority of respondents (61.1%; n=124) obtained low scores (lower than 75%) on understanding of all three concepts under study. Based on these findings, an intervention based on a narrative which included all three concepts and their personal implications was designed. The narrative used daily examples from the field of Agriculture because Malawi has an agro-based economy. Methods: The intervention was tested using a sample of 36 women who had been identified as low scorers during the empirical study. The 36 low scorers were randomly assigned to control (n=18) and intervention arms (n=18). The control arm went through a session in which they were provided with standard informed consent information for the microbicide trial. The intervention arm went through a session in which they were provided with a narrative in ChiChewa, the local language, with the assistance of a power point presentation which included pictures as well as discussions on justification and personal implications of the concepts under study. Results: The findings on the efficacy of the intervention suggest that the 3 scientific concepts and their personal implications can be understood by low literacy populations using simple language and everyday local examples. The findings also suggest that the intervention positively impacted on understanding of trial procedures under study, as 13 of the 18 women in the intervention arm, obtained high scores (above 75%) during the post intervention assessment and none of the 18 in the control arm obtained a high score. Using Fischer's exact test, it was confirmed that the effect of the intervention on understanding of the three procedures was statistically significant (p=0.0001). Conclusions: Potential trial participants can be assisted to understand key clinical trial procedures, their justification and personal implications by using innovative tailored local narratives. JF - BMC Medical Ethics AU - Ndebele, Paul M AU - Wassenaar, Douglas AU - Munalula, Esther AU - Masiye, Francis AD - HJF-DAIDS, NIAID, NIH, 6700A Rockledge Drive Room 42A193, Second Floor, Bethesda, MD, 20817, USA PY - 2012 SP - 29 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 13 IS - 1 SN - 1472-6939, 1472-6939 KW - Microbiology Abstracts A: Industrial & Applied Microbiology KW - Assessment KW - Comprehension KW - Double-blinding KW - Informed consent KW - Intervention KW - Randomisation KW - Placebo KW - Malawi KW - Understanding KW - Agriculture KW - Ethics KW - Statistical analysis KW - Language KW - Clinical trials KW - microbicides KW - A 01340:Antibiotics & Antimicrobials UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1758242972?accountid=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=BMC+Medical+Ethics&rft.atitle=Improving+understanding+of+clinical+trial+procedures+among+low+literacy+populations%3A+an+intervention+within+a+microbicide+trial+in+Malawi&rft.au=Ndebele%2C+Paul+M%3BWassenaar%2C+Douglas%3BMunalula%2C+Esther%3BMasiye%2C+Francis&rft.aulast=Ndebele&rft.aufirst=Paul&rft.date=2012-01-01&rft.volume=13&rft.issue=1&rft.spage=29&rft.isbn=&rft.btitle=&rft.title=BMC+Medical+Ethics&rft.issn=14726939&rft_id=info:doi/10.1186%2F1472-6939-13-29 L2 - http://www.biomedcentral.com/1472-6939/13/29 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Number of references - 42 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Agriculture; Ethics; Statistical analysis; Language; Clinical trials; microbicides DO - http://dx.doi.org/10.1186/1472-6939-13-29 ER - TY - JOUR T1 - Updated clusters of orthologous genes for Archaea: a complex ancestor of the Archaea and the byways of horizontal gene transfer AN - 1758240426; 17529916 AB - Background: Collections of Clusters of Orthologous Genes (COGs) provide indispensable tools for comparative genomic analysis, evolutionary reconstruction and functional annotation of new genomes. Initially, COGs were made for all complete genomes of cellular life forms that were available at the time. However, with the accumulation of thousands of complete genomes, construction of a comprehensive COG set has become extremely computationally demanding and prone to error propagation, necessitating the switch to taxon-specific COG collections. Previously, we reported the collection of COGs for 41 genomes of Archaea (arCOGs). Here we present a major update of the arCOGs and describe evolutionary reconstructions to reveal general trends in the evolution of Archaea. Results: The updated version of the arCOG database incorporates 91% of the pangenome of 120 archaea (251,032 protein-coding genes altogether) into 10,335 arCOGs. Using this new set of arCOGs, we performed maximum likelihood reconstruction of the genome content of archaeal ancestral forms and gene gain and loss events in archaeal evolution. This reconstruction shows that the last Common Ancestor of the extant Archaea was an organism of greater complexity than most of the extant archaea, probably with over 2,500 protein-coding genes. The subsequent evolution of almost all archaeal lineages was apparently dominated by gene loss resulting in genome streamlining. Overall, in the evolution of Archaea as well as a representative set of bacteria that was similarly analyzed for comparison, gene losses are estimated to outnumber gene gains at least 4 to 1. Analysis of specific patterns of gene gain in Archaea shows that, although some groups, in particular Halobacteria, acquire substantially more genes than others, on the whole, gene exchange between major groups of Archaea appears to be largely random, with no major 'highways' of horizontal gene transfer. Conclusions: The updated collection of arCOGs is expected to become a key resource for comparative genomics, evolutionary reconstruction and functional annotation of new archaeal genomes. Given that, in spite of the major increase in the number of genomes, the conserved core of archaeal genes appears to be stabilizing, the major evolutionary trends revealed here have a chance to stand the test of time. Reviewers: This article was reviewed by (for complete reviews see the Reviewers' Reports section): Dr. PLG, Prof. PF, Dr. PL (nominated by Prof. JPG). JF - Biology Direct AU - Wolf, Yuri I AU - Makarova, Kira S AU - Yutin, Natalya AU - Koonin, Eugene V AD - National Center for Biotechnology Information, NLM, National Institutes of Health, Bethesda, MD 20894, USA Y1 - 2012///0, PY - 2012 DA - 0, 2012 SP - 46 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 7 IS - 1 SN - 1745-6150, 1745-6150 KW - Microbiology Abstracts B: Bacteriology; Genetics Abstracts KW - Archaea KW - Orthologs KW - Horizontal gene transfer KW - Genomes KW - Databases KW - Reviews KW - Genomic analysis KW - Evolutionary genetics KW - genomics KW - Evolution KW - G 07770:Bacteria KW - J 02450:Ecology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1758240426?accountid=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=Biology+Direct&rft.atitle=Updated+clusters+of+orthologous+genes+for+Archaea%3A+a+complex+ancestor+of+the+Archaea+and+the+byways+of+horizontal+gene+transfer&rft.au=Wolf%2C+Yuri+I%3BMakarova%2C+Kira+S%3BYutin%2C+Natalya%3BKoonin%2C+Eugene+V&rft.aulast=Wolf&rft.aufirst=Yuri&rft.date=2012-01-01&rft.volume=7&rft.issue=1&rft.spage=46&rft.isbn=&rft.btitle=&rft.title=Biology+Direct&rft.issn=17456150&rft_id=info:doi/10.1186%2F1745-6150-7-46 L2 - http://www.biology-direct.com/content/7/1/46 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Number of references - 75 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Genomes; Databases; Reviews; Genomic analysis; genomics; Evolutionary genetics; Evolution; Archaea DO - http://dx.doi.org/10.1186/1745-6150-7-46 ER - TY - JOUR T1 - Fecal microbial determinants of fecal and systemic estrogens and estrogen metabolites: a cross-sectional study AN - 1758239894; 17648412 AB - Background: High systemic estrogen levels contribute to breast cancer risk for postmenopausal women, whereas low levels contribute to osteoporosis risk. Except for obesity, determinants of non-ovarian systemic estrogen levels are undefined. We sought to identify members and functions of the intestinal microbial community associated with estrogen levels via enterohepatic recirculation. Methods: Fifty-one epidemiologists at the National Institutes of Health, including 25 men, 7 postmenopausal women, and 19 premenopausal women, provided urine and aliquots of feces, using methods proven to yield accurate and reproducible results. Estradiol, estrone, 13 estrogen metabolites (EM), and their sum (total estrogens) were quantified in urine and feces by liquid chromatography/tandem mass spectrometry. In feces, [beta]-glucuronidase and [beta]-glucosidase activities were determined by realtime kinetics, and microbiome diversity and taxonomy were estimated by pyrosequencing 16S rRNA amplicons. Pearson correlations were computed for each log sub(e) estrogen level, log sub(e) enzymatic activity level, and microbiome alpha diversity estimate. For the 55 taxa with mean relative abundance of at least 0.1%, ordinal levels were created [zero, low (below median of detected sequences), high] and compared to log sub(e) estrogens, [beta]-glucuronidase and [beta]-glucosidase enzymatic activity levels by linear regression. Significance was based on two-sided tests with [alpha]=0.05. Results: In men and postmenopausal women, levels of total urinary estrogens (as well as most individual EM) were very strongly and directly associated with all measures of fecal microbiome richness and alpha diversity (R> or =0.50, P or =0.6). Conclusions: Intestinal microbial richness and functions, including but not limited to [beta]-glucuronidase, influence levels of non-ovarian estrogens via enterohepatic circulation. Thus, the gut microbial community likely affects the risk for estrogen-related conditions in older adults. Understanding how Clostridia taxa relate to systemic estrogens may identify targets for interventions. Trial registration: Not applicable. JF - Journal of Translational Medicine AU - Flores, Roberto AU - Shi, Jianxin AU - Fuhrman, Barbara AU - Xu, Xia AU - Veenstra, Timothy D AU - Gail, Mitchell H AU - Gajer, Pawel AU - Ravel, Jacques AU - Goedert, James J AD - Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Boulevard, Room 7068, Rockville, MD 20852, USA PY - 2012 SP - 253 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 10 IS - 1 SN - 1479-5876, 1479-5876 KW - Microbiology Abstracts A: Industrial & Applied Microbiology KW - Microbiome KW - Feces KW - Enterohepatic circulation KW - [beta]-glucuronidase KW - [beta]-glucosidase KW - Postmenopausal estrogens KW - Fecal estrogens KW - Estrogen metabolites KW - Translation KW - Obesity KW - Estrogens KW - Abundance KW - Osteoporosis KW - Metabolites KW - Mass spectroscopy KW - Digestive tract KW - Liquid chromatography KW - Post-menopause KW - Urine KW - Kinetics KW - Intestine KW - Breast cancer KW - Taxonomy KW - Enzymatic activity KW - rRNA 16S KW - Estrone KW - A 01300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1758239894?accountid=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+Translational+Medicine&rft.atitle=Fecal+microbial+determinants+of+fecal+and+systemic+estrogens+and+estrogen+metabolites%3A+a+cross-sectional+study&rft.au=Flores%2C+Roberto%3BShi%2C+Jianxin%3BFuhrman%2C+Barbara%3BXu%2C+Xia%3BVeenstra%2C+Timothy+D%3BGail%2C+Mitchell+H%3BGajer%2C+Pawel%3BRavel%2C+Jacques%3BGoedert%2C+James+J&rft.aulast=Flores&rft.aufirst=Roberto&rft.date=2012-01-01&rft.volume=10&rft.issue=1&rft.spage=253&rft.isbn=&rft.btitle=&rft.title=Journal+of+Translational+Medicine&rft.issn=14795876&rft_id=info:doi/10.1186%2F1479-5876-10-253 L2 - http://www.translational-medicine.com/content/10/1/253 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2016-01-01 N1 - Number of references - 38 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Obesity; Translation; Estrogens; Abundance; Osteoporosis; Metabolites; Mass spectroscopy; Digestive tract; Urine; Post-menopause; Liquid chromatography; Kinetics; Intestine; Breast cancer; Taxonomy; Enzymatic activity; Feces; rRNA 16S; Estrone DO - http://dx.doi.org/10.1186/1479-5876-10-253 ER - TY - JOUR T1 - Merged satellite information and ground measurements of the precipitation for hydrological modeling AN - 1717501271; PQ0001980084 AB - The availability of detailed well distributed in space information on precipitation is of essential importance for the hydrological modeling. Conventional measurements of precipitation are in a limited number of points represented by synoptic, climatic and precipitation stations. This information is not sufficient for correct spatial distribution of precipitation. The distribution of the ground stations are quite irregular and thus distances between stations could be quite big, sometimes more then 30 km. On the other hand, precipitation has high variability in space. The results of the spatial distribution depend on the density of the ground measurements. Precipitation estimated from satellite information includes spatial information that could be used to ameliorate precipitation field based only on ground stations. This paper presents the results of an application that merges satellite information with conventional ground measurements of the precipitation for hydrological modeling purpose. Hydrological simulation will be performed with 3 types of precipitation fields. Simulation using satellite information for precipitation, simulation with real measured precipitation and with merged information for precipitation. Geographic Information System (GIS) and ArcInfo techniques will be applied for spatial distribution and spatial analysis of the precipitation data. Relevant analyses and conclusions will be provided. JF - EUMETSAT Meteorological Satellite Conference AU - Dimitrov, Dobri AU - Balabanova, Snezhanka AU - Koshinchanov, Georgy AD - NIMH - BAS Bulgaria, dimitrov.dobri@gmail.com Y1 - 2012///0, PY - 2012 DA - 0, 2012 PB - EUMETSAT, Am Kavalleriesand 31 Darmstadt D-64295 Germany SN - 1011-3932, 1011-3932 KW - Meteorological & Geoastrophysical Abstracts; ASFA 2: Ocean Technology Policy & Non-Living Resources; Aqualine Abstracts; Water Resources Abstracts KW - Remote Sensing KW - Variability KW - Precipitation data KW - Spatial distribution KW - Ecological distribution KW - Remote sensing KW - Spatial Distribution KW - Scientific satellites KW - Hydrologic Models KW - Geographic Information Systems (GIS) KW - Hydrologic Data KW - Geographical Information Systems KW - Satellite conferences KW - Modelling KW - Satellite Technology KW - Hydrologic analysis KW - Density KW - Precipitation KW - Meteorological satellites KW - Satellite sensing KW - Numerical simulations KW - Meteorological conferences KW - Precipitation variability KW - Q2 09243:Structure, mechanics and thermodynamics KW - AQ 00001:Water Resources and Supplies KW - SW 5010:Network design KW - M2 556:General (556) UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1717501271?accountid=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=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 revised - 2015-09-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Satellite sensing; Ecological distribution; Remote sensing; Scientific satellites; Modelling; Precipitation data; Hydrologic analysis; Numerical simulations; Spatial distribution; Meteorological conferences; Geographic Information Systems (GIS); Precipitation variability; Precipitation; Meteorological satellites; Satellite conferences; Remote Sensing; Satellite Technology; Variability; Hydrologic Models; Density; Spatial Distribution; Hydrologic Data; Geographical Information Systems ER - TY - JOUR T1 - Live and Let Die: A New Suicide Gene Therapy Moves to the Clinic AN - 1668269507; PQ0001270024 AB - The concept of suicide gene therapy dates from the beginning of the field of gene therapy and was one of the first clinical applications. Initially described as an anticancer therapy, it quickly found a specific application in the practice of hematopoietic stem cell transplantation. A recent publication by Di Stasi et al. presents the first clinical data on a relatively new suicide gene system that targets caspase 9-mediated apoptosis in an inducible fashion.[1] Specifically, five children undergoing haplo-identical stem cell transplantation for leukemia received donor T lymphocytes that had been genetically engineered with the inducible caspase 9 (iCasp9) gene. Four of the five patients developed graft-vs.-host disease (GVHD) caused by the donor lymphocytes that was quickly reversed by induction of the iCasp9 suicide gene. JF - Molecular Therapy AU - Morgan, Richard A AD - Surgery Branch, National Cancer Institute, Building 10, CRC Room 3-5940, 10 Center Drive, MSC 1201, Bethesda, Maryland 20892, USA, rmorgan@mail.nih.gov Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - 11 EP - 13 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 20 IS - 1 SN - 1525-0016, 1525-0016 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Caspase-9 KW - Donors KW - Apoptosis KW - Data processing KW - Gene therapy KW - stem cell transplantation KW - Therapeutic applications KW - Graft-versus-host reaction KW - Children KW - Leukemia KW - Genetic engineering KW - Lymphocytes T 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/1668269507?accountid=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=Live+and+Let+Die%3A+A+New+Suicide+Gene+Therapy+Moves+to+the+Clinic&rft.au=Morgan%2C+Richard+A&rft.aulast=Morgan&rft.aufirst=Richard&rft.date=2012-01-01&rft.volume=20&rft.issue=1&rft.spage=11&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2011.273 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Caspase-9; Donors; Data processing; Apoptosis; Gene therapy; stem cell transplantation; Therapeutic applications; Graft-versus-host reaction; Children; Leukemia; Genetic engineering; Lymphocytes T; suicide genes DO - http://dx.doi.org/10.1038/mt.2011.273 ER - TY - JOUR T1 - Evaluation of Residual Promoter Activity in gamma -Retroviral Self-inactivating (SIN) Vectors AN - 1668249647; PQ0001270033 AB - Therapeutic gene delivery mediated by retroviral vectors has the advantage of stable integration into the host genome. A major safety concern for gene delivery achieved by murine leukemia virus (MLV)-based retroviral vectors is the activation of adjacent cellular genes including oncogenes following integration into the host genome. Self-inactivating (SIN) vectors lacking viral enhancers/promoters in their 3' long terminal repeat (LTR) have been proposed as a means of overcoming this safety concern. However the MLV-based SIN vectors currently used by laboratories to assess insertional mutagenesis, integration site selection, and the potency of transgene expression are not uniform in the composition of their 3' LTRs. We constructed a series of SIN vectors representative of the currently employed vectors, but lacking an internal promoter. Green fluorescent protein (GFP) was used as a reporter gene. Target cells exposed to these vectors were evaluated for number of integrants and GFP expression at the messenger RNA (mRNA) level and protein level. We found that viral promoter activity in the 3' LTR is not attenuated in many currently employed SIN vectors. These results suggest that the influence of strong residual promoter activity should be taken into consideration when interpreting experimental results obtained using SIN vectors in gene therapy research. JF - Molecular Therapy AU - Xu, Wenqin AU - Russ, Jill L AU - Eiden, Maribeth V AD - Section on Directed Gene Transfer, Laboratory of Cellular and Molecular Regulation, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA, eidenm@mail.nih.gov Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - 84 EP - 90 PB - Elsevier B.V., The Boulevard Kidlington Oxford OX5 1GB United Kingdom VL - 20 IS - 1 SN - 1525-0016, 1525-0016 KW - Virology & AIDS Abstracts; Biotechnology and Bioengineering Abstracts KW - Genomes KW - Gene therapy KW - Long terminal repeat KW - Transgenes KW - Green fluorescent protein KW - Murine leukemia virus KW - mRNA KW - Gene expression KW - Site selection KW - Expression vectors KW - Enhancers KW - Integration KW - Promoters KW - Oncogenes KW - Gene transfer KW - Reporter gene KW - insertional mutagenesis KW - W 30905:Medical Applications KW - V 22370:Oncology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1668249647?accountid=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=Evaluation+of+Residual+Promoter+Activity+in+gamma+-Retroviral+Self-inactivating+%28SIN%29+Vectors&rft.au=Xu%2C+Wenqin%3BRuss%2C+Jill+L%3BEiden%2C+Maribeth+V&rft.aulast=Xu&rft.aufirst=Wenqin&rft.date=2012-01-01&rft.volume=20&rft.issue=1&rft.spage=84&rft.isbn=&rft.btitle=&rft.title=Molecular+Therapy&rft.issn=15250016&rft_id=info:doi/10.1038%2Fmt.2011.204 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2015-03-01 N1 - Last updated - 2015-11-16 N1 - SubjectsTermNotLitGenreText - Genomes; Gene therapy; Long terminal repeat; Transgenes; Green fluorescent protein; mRNA; Expression vectors; Site selection; Gene expression; Promoters; Integration; Enhancers; Oncogenes; Reporter gene; Gene transfer; insertional mutagenesis; Murine leukemia virus DO - http://dx.doi.org/10.1038/mt.2011.204 ER - TY - JOUR T1 - A minimum version of log-rank test for testing the existence of cancer cure using relative survival data AN - 1635034252; 21009614 AB - Cancer survival is one of the most important measures to evaluate the effectiveness of treatment and early diagnosis. The ultimate goal of cancer research and patient care is the cure of cancer. As cancer treatments progress, cure becomes a reality for many cancers if patients are diagnosed early and get effective treatment. If a cure does exist for a certain type of cancer, it is useful to estimate the time of cure. For cancers that impose excess risk of mortality, it is informative to understand the difference in survival between cancer patients and the general cancer-free population. In population-based cancer survival studies, relative survival is the standard measure of excess mortality due to cancer. Cure is achieved when the survival of cancer patients is equivalent to that of the general population. This definition of cure is usually called the statistical cure, which is an important measure of burden due to cancer. In this paper, a minimum version of the log-rank test is proposed to test the equivalence of cancer patients' survival using the relative survival data. Performance of the proposed test is evaluated by simulation. Relative survival data from population-based cancer registries in SEER Program are used to examine patients' survival after diagnosis for various major cancer sites. JF - Biometrical Journal AU - Yu, Binbing AD - Laboratory of Epidemiology, Demography and Biometry, National Institute on Aging, Bethesda, MD 20892, USA. Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - 45 EP - 60 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 54 IS - 1 SN - 0323-3847, 0323-3847 KW - Biotechnology and Bioengineering Abstracts KW - Mortality KW - Data processing KW - Statistics KW - Survival KW - Biometrics KW - Cancer KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1635034252?accountid=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=Biometrical+Journal&rft.atitle=A+minimum+version+of+log-rank+test+for+testing+the+existence+of+cancer+cure+using+relative+survival+data&rft.au=Yu%2C+Binbing&rft.aulast=Yu&rft.aufirst=Binbing&rft.date=2012-01-01&rft.volume=54&rft.issue=1&rft.spage=45&rft.isbn=&rft.btitle=&rft.title=Biometrical+Journal&rft.issn=03233847&rft_id=info:doi/10.1002%2Fbimj.201100069 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-12-01 N1 - Last updated - 2014-12-11 N1 - SubjectsTermNotLitGenreText - Mortality; Statistics; Data processing; Survival; Biometrics; Cancer DO - http://dx.doi.org/10.1002/bimj.201100069 ER - TY - JOUR T1 - Locally Learning Biomedical Data Using Diffusion Frames AN - 1627948965; 20907814 AB - Diffusion geometry techniques are useful to classify patterns and visualize high-dimensional datasets. Building upon ideas from diffusion geometry, we outline our mathematical foundations for learning a function on high-dimension biomedical data in a local fashion from training data. Our approach is based on a localized summation kernel, and we verify the computational performance by means of exact approximation rates. After these theoretical results, we apply our scheme to learn early disease stages in standard and new biomedical datasets. JF - Journal of Computational Biology AU - Ehler, M AU - Filbir, F AU - Mhaskar, H N AD - Section on Medical Biophysics, NICHD, National Institutes of Health, Bethesda, Maryland; Helmholtz Zentrum Munchen, Institute of Biomathematics and Biometry, Ingolstadter Landstrasse 1, D-85764 Neuherberg, Germany PY - 2012 SP - 1251 EP - 1264 PB - Mary Ann Liebert, Inc., 2 Madison Ave Larchmont NY 10538 United States VL - 19 IS - 11 SN - 1557-8666, 1557-8666 KW - Biotechnology and Bioengineering Abstracts KW - graphs and networks KW - machine learning KW - Learning KW - Data processing KW - Kernels KW - Diffusion KW - Computer applications KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1627948965?accountid=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+Computational+Biology&rft.atitle=Locally+Learning+Biomedical+Data+Using+Diffusion+Frames&rft.au=Ehler%2C+M%3BFilbir%2C+F%3BMhaskar%2C+H+N&rft.aulast=Ehler&rft.aufirst=M&rft.date=2012-01-01&rft.volume=19&rft.issue=11&rft.spage=1251&rft.isbn=&rft.btitle=&rft.title=Journal+of+Computational+Biology&rft.issn=15578666&rft_id=info:doi/10.1089%2Fcmb.2012.0187 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-11-01 N1 - Last updated - 2015-12-09 N1 - SubjectsTermNotLitGenreText - Learning; Data processing; Kernels; Diffusion; Computer applications DO - http://dx.doi.org/10.1089/cmb.2012.0187 ER - TY - JOUR T1 - RadRAT: a radiation risk assessment tool for lifetime cancer risk projection AN - 1611615578; 20675721 AB - Risk projection methods allow for timely assessment of the potential magnitude of radiation-related cancer risks following low-dose radiation exposures. The estimation of such risks directly through observational studies would generally require infeasibly large studies and long-term follow-up to achieve reasonable statistical power. We developed an online radiation risk assessment tool (RadRAT) which can be used to estimate the lifetime risk of radiation-related cancer with uncertainty intervals following a user-specified exposure history (https://irep.nci.nih.gov/radrat). The uncertainty intervals constitute a key component of the program because of the various assumptions that are involved in such calculations. The risk models used in RadRAT are broadly based on those developed by the BEIR VII committee for estimating lifetime risk following low-dose radiation exposure of the US population for eleven site-specific cancers. We developed new risk models for seven additional cancer sites, oral, oesophagus, gallbladder, pancreas, rectum, kidney and brain/central nervous system (CNS) cancers, using data from Japanese atomic bomb survivors. The lifetime risk estimates are slightly higher for RadRAT than for BEIR VII across all exposure ages mostly because the weighting of the excess relative risk and excess absolute risk models was conducted on an arithmetic rather than a logarithmic scale. The calculator can be used to estimate lifetime cancer risk from both uniform and non-uniform doses that are acute or chronic. It is most appropriate for low-LET radiation doses <1 Gy, and for individuals with life-expectancy and cancer rates similar to the general population in the US. JF - Journal of Radiological Protection AU - de Gonzalez, Amy Berrington AU - Apostoaei, A Iulian AU - Veiga, Lene H S AU - Rajaraman, Preetha AU - Thomas, Brian A AU - Hoffman, F Owen AU - Gilbert, Ethel AU - Land, Charles AD - Radiation Epidemiology Branch, Division of Cancer Epidemiology and Genetics, NCI, Bethesda, MD, USA, berringtona@mail.nih.gov Y1 - 2012///0, PY - 2012 DA - 0, 2012 SP - 205 EP - 222 PB - IOP Publishing, The Public Ledger Building, Suite 929 Philadelphia PA 19106 United States VL - 32 SN - 0952-4746, 0952-4746 KW - Risk Abstracts KW - Risk assessment KW - Central nervous system KW - Historical account KW - Age KW - Atomic bombs KW - Brain KW - Cancer KW - Health risks KW - Radiation KW - Committees KW - Kidney KW - Japan KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1611615578?accountid=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+Radiological+Protection&rft.atitle=RadRAT%3A+a+radiation+risk+assessment+tool+for+lifetime+cancer+risk+projection&rft.au=de+Gonzalez%2C+Amy+Berrington%3BApostoaei%2C+A+Iulian%3BVeiga%2C+Lene+H+S%3BRajaraman%2C+Preetha%3BThomas%2C+Brian+A%3BHoffman%2C+F+Owen%3BGilbert%2C+Ethel%3BLand%2C+Charles&rft.aulast=de+Gonzalez&rft.aufirst=Amy&rft.date=2012-01-01&rft.volume=32&rft.issue=&rft.spage=205&rft.isbn=&rft.btitle=&rft.title=Journal+of+Radiological+Protection&rft.issn=09524746&rft_id=info:doi/10.1088%2F0952-4746%2F32%2F3%2F205 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-10-01 N1 - Last updated - 2016-04-29 N1 - SubjectsTermNotLitGenreText - Risk assessment; Historical account; Central nervous system; Health risks; Age; Radiation; Committees; Atomic bombs; Kidney; Brain; Cancer; Japan DO - http://dx.doi.org/10.1088/0952-4746/32/3/205 ER - TY - JOUR T1 - Polymorphic toxin systems: Comprehensive characterization of trafficking modes, processing, mechanisms of action, immunity and ecology using comparative genomics AN - 1496892186; 17391613 AB - Abstract: Background: Proteinaceous toxins are observed across all levels of inter-organismal and intra-genomic conflicts. These include recently discovered prokaryotic polymorphic toxin systems implicated in intra-specific conflicts. They are characterized by a remarkable diversity of C-terminal toxin domains generated by recombination with standalone toxin-coding cassettes. Prior analysis revealed a striking diversity of nuclease and deaminase domains among the toxin modules. We systematically investigated polymorphic toxin systems using comparative genomics, sequence and structure analysis. Results: Polymorphic toxin systems are distributed across all major bacterial lineages and are delivered by at least eight distinct secretory systems. In addition to type-II, these include type-V, VI, VII (ESX), and the poorly characterized "Photorhabdus virulence cassettes (PVC)", PrsW-dependent and MuF phage-capsid-like systems. We present evidence that trafficking of these toxins is often accompanied by autoproteolytic processing catalyzed by HINT, ZU5, PrsW, caspase-like, papain-like, and a novel metallopeptidase associated with the PVC system. We identified over 150 distinct toxin domains in these systems. These span an extraordinary catalytic spectrum to include 23 distinct clades of peptidases, numerous previously unrecognized versions of nucleases and deaminases, ADP-ribosyltransferases, ADP ribosyl cyclases, RelA/SpoT-like nucleotidyltransferases, glycosyltranferases and other enzymes predicted to modify lipids and carbohydrates, and a pore-forming toxin domain. Several of these toxin domains are shared with host-directed effectors of pathogenic bacteria. Over 90 families of immunity proteins might neutralize anywhere between a single to at least 27 distinct types of toxin domains. In some organisms multiple tandem immunity genes or immunity protein domains are organized into polyimmunity loci or polyimmunity proteins. Gene-neighborhood-analysis of polymorphic toxin systems predicts the presence of novel trafficking-related components, and also the organizational logic that allows toxin diversification through recombination. Domain architecture and protein-length analysis revealed that these toxins might be deployed as secreted factors, through directed injection, or via inter-cellular contact facilitated by filamentous structures formed by RHS/YD, filamentous hemagglutinin and other repeats. Phyletic pattern and life-style analysis indicate that polymorphic toxins and polyimmunity loci participate in cooperative behavior and facultative 'cheating' in several ecosystems such as the human oral cavity and soil. Multiple domains from these systems have also been repeatedly transferred to eukaryotes and their viruses, such as the nucleo-cytoplasmic large DNA viruses. Conclusions: Along with a comprehensive inventory of toxins and immunity proteins, we present several testable predictions regarding active sites and catalytic mechanisms of toxins, their processing and trafficking and their role in intra-specific and inter-specific interactions between bacteria. These systems provide insights regarding the emergence of key systems at different points in eukaryotic evolution, such as ADP ribosylation, interaction of myosin VI with cargo proteins, mediation of apoptosis, hyphal heteroincompatibility, hedgehog signaling, arthropod toxins, cell-cell interaction molecules like teneurins and different signaling messengers. Reviewers: This article was reviewed by AM, FE and IZ. JF - Biology Direct AU - Zhang, Dapeng AU - de Souza, Robson F 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, MD, 20894, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 18 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 7 IS - 1 SN - 1745-6150, 1745-6150 KW - Toxicology Abstracts KW - Apoptosis KW - Arthropoda KW - Toxins KW - X 24360:Metals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1496892186?accountid=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=Biology+Direct&rft.atitle=Polymorphic+toxin+systems%3A+Comprehensive+characterization+of+trafficking+modes%2C+processing%2C+mechanisms+of+action%2C+immunity+and+ecology+using+comparative+genomics&rft.au=Zhang%2C+Dapeng%3Bde+Souza%2C+Robson+F%3BAnantharaman%2C+Vivek%3BIyer%2C+Lakshminarayan+M%3BAravind%2C+L&rft.aulast=Zhang&rft.aufirst=Dapeng&rft.date=2012-01-01&rft.volume=7&rft.issue=1&rft.spage=18&rft.isbn=&rft.btitle=&rft.title=Biology+Direct&rft.issn=17456150&rft_id=info:doi/10.1186%2F1745-6150-7-18 L2 - http://www.biology-direct.com/content/7/1/18 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2014-02-01 N1 - Number of references - 1 N1 - Last updated - 2014-02-11 N1 - SubjectsTermNotLitGenreText - Toxins; Arthropoda DO - http://dx.doi.org/10.1186/1745-6150-7-18 ER - TY - JOUR T1 - Potential impact of propofol immediately after motor vehicle accident on later symptoms of posttraumatic stress disorder at 6-month follow up: a retrospective cohort study AN - 1367483663; 17407653 AB - Introduction: Critically injured patients are at risk of developing posttraumatic stress disorder (PTSD). Propofol was recently reported to enhance fear memory consolidation retrospectively. Thus, we investigated here whether administration of propofol within 72 h of a motor vehicle accident (MVA) affects the subsequent development of PTSD symptoms. Methods: We examined data obtained from a prospective cohort study of MVA-related injured patients, admitted to the intensive care unit of a general hospital. We investigated the effect of propofol administration within 72 h of MVA on outcome. Primary outcome was diagnosis of full or partial PTSD as determined by the Clinician-Administered PTSD Scale (CAPS) at 6 months. Secondary outcomes were diagnosis of full or partial PTSD at 1 month and CAPS score indicating PTSD at 1 and 6 months. Multivariate analysis was conducted adjusting for being female, age, injury severity score (ISS), and administration of ketamine or midazolam within 72 h of MVA. Results: Among 300 patients recruited (mean ISS, 8.0; median Glasgow Coma Scale (GCS) score, 15.0; age, 18 to 69 years), propofol administration showed a higher risk for full or partial PTSD as determined by CAPS at 6 months (odds ratio = 6.13, 95% confidence interval (CI): 1.57 to 23.85, P = 0.009) and at 1 month (odds ratio = 1.31, 95% CI: 0.41 to 4.23, P = 0.647) in the multivariate logistic regression. Multivariate regression analysis showed a trend toward adverse effects of propofol on PTSD symptom development at 6 months after MVA ([beta] = 4.08, 95% CI: -0.49 to 8.64, P = 0.080), but not at 1 month after MVA ([beta] = -0.42, 95% CI: -6.34 to 5.51, P = 0.890). Conclusions: These findings suggest that using propofol in the acute phase after MVA might be associated with the development of PTSD symptoms 6 months later. However, since the design of this study was retrospective, these findings should be interpreted cautiously and further study is warranted. JF - Critical Care AU - Usuki, Masato AU - Matsuoka, Yutaka AU - Nishi, Daisuke AU - Yonemoto, Naohiro AU - Matsumura, Kenta AU - Otomo, Yasuhiro AU - Kim, Yoshiharu AU - Kanba, Shigenobu AD - National Institute of Mental Health, National Center of Neurology and Psychiatry, Tokyo 187-8553, Japan Y1 - 2012 PY - 2012 DA - 2012 SP - 1 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 16 IS - 5 SN - 1364-8535, 1364-8535 KW - Health & Safety Science Abstracts KW - Accidents KW - Age KW - Posttraumatic stress disorder KW - Injuries KW - Intensive care units KW - Psychology KW - Motor vehicles KW - British Isles, Scotland, Glasgow KW - Side effects KW - H 2000:Transportation UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1367483663?accountid=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=Critical+Care&rft.atitle=Potential+impact+of+propofol+immediately+after+motor+vehicle+accident+on+later+symptoms+of+posttraumatic+stress+disorder+at+6-month+follow+up%3A+a+retrospective+cohort+study&rft.au=Usuki%2C+Masato%3BMatsuoka%2C+Yutaka%3BNishi%2C+Daisuke%3BYonemoto%2C+Naohiro%3BMatsumura%2C+Kenta%3BOtomo%2C+Yasuhiro%3BKim%2C+Yoshiharu%3BKanba%2C+Shigenobu&rft.aulast=Usuki&rft.aufirst=Masato&rft.date=2012-01-01&rft.volume=16&rft.issue=5&rft.spage=R196&rft.isbn=&rft.btitle=&rft.title=Critical+Care&rft.issn=13648535&rft_id=info:doi/10.1186%2Fcc11681 L2 - http://ccforum.com/content/16/5/R196 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-06-01 N1 - Number of references - 40 N1 - Last updated - 2013-07-15 N1 - SubjectsTermNotLitGenreText - Age; Accidents; Posttraumatic stress disorder; Intensive care units; Injuries; Psychology; Motor vehicles; Side effects; British Isles, Scotland, Glasgow DO - http://dx.doi.org/10.1186/cc11681 ER - TY - JOUR T1 - Multi-walled carbon nanotubes induce COX-2 and iNOS expression via MAP Kinase-dependent and -independent mechanisms in mouse RAW264.7 macrophages AN - 1328514529; 17391597 AB - Background: Carbon nanotubes (CNTs) are engineered graphene cylinders with numerous applications in engineering, electronics and medicine. However, CNTs cause inflammation and fibrosis in the rodent lung, suggesting a potential human health risk. We hypothesized that multi-walled CNTs (MWCNTs) induce two key inflammatory enzymes in macrophages, cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), through activation of extracellular signal-regulated kinases (ERK1,2). Methods: RAW264.7 macrophages were exposed to MWCNTs or carbon black nanoparticles (CBNPs) over a range of doses and time course. Uptake and subcellular localization of MWCNTs was visualized by transmission electron microscopy (TEM). Protein levels of COX-2, iNOS, and ERK1,2 (total ERK and phosphorylated ERK) were measured by Western blot analysis. Prostaglandin-E sub(2) (PGE sub(2)) and nitric oxide (NO) levels in cell supernatants were measured by ELISA and Greiss assay, respectively. Results: MWCNTs, but not CBNPs, induced COX-2 and iNOS in a time- and dose-dependent manner. COX-2 and iNOS induction by MWCNTs correlated with increased PGE sub(2) and NO production, respectively. MWCNTs caused ERK1,2 activation and inhibition of ERK1,2 (U0126) blocked MWCNT induction of COX-2 and PGE sub(2) production, but did not reduce the induction of iNOS. Inhibition of iNOS (L-NAME) did not affect ERK1,2 activation, nor did L-NAME significantly decrease COX-2 induction by MWCNT. Nickel nanoparticles (NiNPs), which are present in MWCNTs as a residual catalyst, also induced COX-2 via ERK-1,2. However, a comparison of COX-2 induction by MWCNTs containing 4.5 and 1.8% Ni did not show a significant difference in ability to induce COX-2, indicating that characteristics of MWCNTs in addition to Ni content contribute to COX-2 induction. Conclusion: This study identifies COX-2 and subsequent PGE sub(2) production, along with iNOS induction and NO production, as inflammatory mediators involved in the macrophage response to MWCNTs. Furthermore, our work demonstrates that COX-2 induction by MWCNTs in RAW264.7 macrophages is ERK1,2-dependent, while iNOS induction by MWCNTs is ERK1,2-independent. Our data also suggest contributory physicochemical factors other than residual Ni catalyst play a role in COX-2 induction to MWCNT. JF - Particle and Fibre Toxicology AU - Lee, Jong Kwon AU - Sayers, Brian C AU - Chun, Kyung-Soo AU - Lao, Huei-Chen AU - Shipley-Phillips, Jeanette K AU - Bonner, James C AU - Langenbach, Robert AD - Laboratory of Toxicology and Pharmacology, National Institute of Environmental Health Sciences, Research Triangle Park, Durham, NC, 27709, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 14 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 9 IS - 1 SN - 1743-8977, 1743-8977 KW - Toxicology Abstracts KW - Carbon nanotubes KW - Nanoparticles KW - Lung inflammation KW - Macrophages KW - Prostaglandins KW - Nitric oxide KW - Cyclooxygenase-2 KW - Western blotting KW - Enzyme-linked immunosorbent assay KW - Data processing KW - NG-Nitroarginine methyl ester KW - Transmission electron microscopy KW - Nickel KW - Prostaglandin E2 KW - Inflammation KW - Cell activation KW - Nitric-oxide synthase KW - Extracellular signal-regulated kinase KW - Carbon KW - Lung KW - nanotubes KW - Catalysts KW - nanoparticles KW - X 24360:Metals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1328514529?accountid=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=Particle+and+Fibre+Toxicology&rft.atitle=Multi-walled+carbon+nanotubes+induce+COX-2+and+iNOS+expression+via+MAP+Kinase-dependent+and+-independent+mechanisms+in+mouse+RAW264.7+macrophages&rft.au=Lee%2C+Jong+Kwon%3BSayers%2C+Brian+C%3BChun%2C+Kyung-Soo%3BLao%2C+Huei-Chen%3BShipley-Phillips%2C+Jeanette+K%3BBonner%2C+James+C%3BLangenbach%2C+Robert&rft.aulast=Lee&rft.aufirst=Jong&rft.date=2012-01-01&rft.volume=9&rft.issue=1&rft.spage=14&rft.isbn=&rft.btitle=&rft.title=Particle+and+Fibre+Toxicology&rft.issn=17438977&rft_id=info:doi/10.1186%2F1743-8977-9-14 L2 - http://www.particleandfibretoxicology.com/content/9/1/14 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-04-01 N1 - Number of references - 50 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Cyclooxygenase-2; Macrophages; Western blotting; Enzyme-linked immunosorbent assay; Data processing; NG-Nitroarginine methyl ester; Transmission electron microscopy; Nickel; Prostaglandin E2; Cell activation; Inflammation; Nitric-oxide synthase; Extracellular signal-regulated kinase; Carbon; Lung; nanotubes; Nitric oxide; Catalysts; nanoparticles DO - http://dx.doi.org/10.1186/1743-8977-9-14 ER - TY - JOUR T1 - Dose-dependent changes in neuroinflammatory and arachidonic acid cascade markers with synaptic marker loss in rat lipopolysaccharide infusion model of neuroinflammation AN - 1328512957; 17390807 AB - Background: Neuroinflammation, caused by six days of intracerebroventricular infusion of bacterial lipopolysaccharide (LPS), stimulates rat brain arachidonic acid (AA) metabolism. The molecular changes associated with increased AA metabolism are not clear. We examined effects of a six-day infusion of a low-dose (0.5 ng/h) and a high-dose (250 ng/h) of LPS on neuroinflammatory, AA cascade, and pre- and post-synaptic markers in rat brain. We used artificial cerebrospinal fluid-infused brains as controls. Results: Infusion of low- or high-dose LPS increased brain protein levels of TNF[alpha], and iNOS, without significantly changing GFAP. High-dose LPS infusion upregulated brain protein and mRNA levels of AA cascade markers (cytosolic cPLA sub(2)-IVA, secretory sPLA sub(2)-V, cyclooxygenase-2 and 5-lipoxygenase), and of transcription factor NF-[kappa]B p50 DNA binding activity. Both LPS doses increased cPLA sub(2) and p38 mitogen-activated protein kinase levels, while reducing protein levels of the pre-synaptic marker, synaptophysin. Post-synaptic markers drebrin and PSD95 protein levels were decreased with high- but not low-dose LPS. Conclusions: Chronic LPS infusion has differential effects, depending on dose, on inflammatory, AA and synaptic markers in rat brain. Neuroinflammation associated with upregulated brain AA metabolism can lead to synaptic dysfunction. JF - BMC Neuroscience AU - Kellom, Matthew AU - Basselin, Mireille AU - Keleshian, Vasken L AU - Chen, Mei AU - Rapoport, Stanley I AU - Rao, Jagadeesh S AD - Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, 9000 Rockville Pike, Bldg. 9, 1S-126, Bethesda, MD, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 50 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 13 IS - 1 SN - 1471-2202, 1471-2202 KW - Biotechnology and Bioengineering Abstracts; CSA Neurosciences Abstracts KW - Cyclooxygenase-2 KW - MAP kinase KW - Arachidonate 5-lipoxygenase KW - Postsynaptic density proteins KW - Animal models KW - Brain KW - Glial fibrillary acidic protein KW - Arachidonic acid KW - Inflammation KW - NF- Kappa B protein KW - Nitric-oxide synthase KW - Synaptophysin KW - Nervous system KW - Transcription factors KW - DNA KW - Lipopolysaccharides KW - Metabolism KW - W 30940:Products KW - N3 11024:Neuroimmunology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1328512957?accountid=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 L2 - http://www.biomedcentral.com/1471-2202/13/50 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-04-01 N1 - Number of references - 69 N1 - Last updated - 2013-08-23 N1 - SubjectsTermNotLitGenreText - Cyclooxygenase-2; MAP kinase; Arachidonate 5-lipoxygenase; Postsynaptic density proteins; Glial fibrillary acidic protein; Brain; Animal models; Arachidonic acid; NF- Kappa B protein; Inflammation; Nitric-oxide synthase; Nervous system; Synaptophysin; Transcription factors; DNA; Lipopolysaccharides; Metabolism DO - http://dx.doi.org/10.1186/1471-2202-13-50 ER - TY - JOUR T1 - Evaluation of common genetic variants in 82 candidate genes as risk factors for neural tube defects AN - 1328512463; 17380568 AB - Background: Neural tube defects (NTDs) are common birth defects (~1 in 1000 pregnancies in the US and Europe) that have complex origins, including environmental and genetic factors. A low level of maternal folate is one well-established risk factor, with maternal periconceptional folic acid supplementation reducing the occurrence of NTD pregnancies by 50-70%. Gene variants in the folate metabolic pathway (e.g., MTHFR rs1801133 (677 C > T) and MTHFD1 rs2236225 (R653Q)) have been found to increase NTD risk. We hypothesized that variants in additional folate/B12 pathway genes contribute to NTD risk. Methods: A tagSNP approach was used to screen common variation in 82 candidate genes selected from the folate/B12 pathway and NTD mouse models. We initially genotyped polymorphisms in 320 Irish triads (NTD cases and their parents), including 301 cases and 341 Irish controls to perform case-control and family based association tests. Significantly associated polymorphisms were genotyped in a secondary set of 250 families that included 229 cases and 658 controls. The combined results for 1441 SNPs were used in a joint analysis to test for case and maternal effects. Results: Nearly 70 SNPs in 30 genes were found to be associated with NTDs at the p < 0.01 level. The ten strongest association signals (p-value range: 0.0003-0.0023) were found in nine genes (MFTC, CDKN2A, ADA, PEMT, CUBN, GART, DNMT3A, MTHFD1 and T (Brachyury)) and included the known NTD risk factor MTHFD1 R653Q (rs2236225). The single strongest signal was observed in a new candidate, MFTC rs17803441 (OR = 1.61 [1.23-2.08], p = 0.0003 for the minor allele). Though nominally significant, these associations did not remain significant after correction for multiple hypothesis testing. Conclusions: To our knowledge, with respect to sample size and scope of evaluation of candidate polymorphisms, this is the largest NTD genetic association study reported to date. The scale of the study and the stringency of correction are likely to have contributed to real associations failing to survive correction. We have produced a ranked list of variants with the strongest association signals. Variants in the highest rank of associations are likely to include true associations and should be high priority candidates for further study of NTD risk. JF - BMC Medical Genetics AU - Pangilinan, Faith AU - Molloy, Anne M AU - Mills, James L AU - Troendle, James F AU - Parle-McDermott, Anne AU - Signore, Caroline AU - O'Leary, Valerie B AU - Chines, Peter AU - Seay, Jessica M AU - Geiler-Samerotte, Kerry AU - Mitchell, Adam AU - VanderMeer, Julia E AU - Krebs, Kristine M AU - Sanchez, Angelica AU - Cornman-Homonoff, Joshua AU - Stone, Nicole AU - Conley, Mary AU - Kirke, Peadar N AU - Shane, Barry AU - Scott, John M AU - Brody, Lawrence C AD - Molecular Pathogenesis Section, Genome Technology Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 62 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 13 IS - 1 SN - 1471-2350, 1471-2350 KW - Genetics Abstracts; CSA Neurosciences Abstracts; Risk Abstracts KW - Genetic factors KW - Maternal effects KW - Gene polymorphism KW - Animal models KW - Europe KW - Methylenetetrahydrofolate reductase KW - Supplementation KW - Neural tube defects KW - Pregnancy KW - Single-nucleotide polymorphism KW - Risk factors KW - Metabolic pathways KW - Priorities KW - Congenital defects KW - Folic acid KW - N3 11003:Developmental neuroscience KW - R2 23060:Medical and environmental health KW - G 07870:Mammals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1328512463?accountid=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=BMC+Medical+Genetics&rft.atitle=Evaluation+of+common+genetic+variants+in+82+candidate+genes+as+risk+factors+for+neural+tube+defects&rft.au=Pangilinan%2C+Faith%3BMolloy%2C+Anne+M%3BMills%2C+James+L%3BTroendle%2C+James+F%3BParle-McDermott%2C+Anne%3BSignore%2C+Caroline%3BO%27Leary%2C+Valerie+B%3BChines%2C+Peter%3BSeay%2C+Jessica+M%3BGeiler-Samerotte%2C+Kerry%3BMitchell%2C+Adam%3BVanderMeer%2C+Julia+E%3BKrebs%2C+Kristine+M%3BSanchez%2C+Angelica%3BCornman-Homonoff%2C+Joshua%3BStone%2C+Nicole%3BConley%2C+Mary%3BKirke%2C+Peadar+N%3BShane%2C+Barry%3BScott%2C+John+M%3BBrody%2C+Lawrence+C&rft.aulast=Pangilinan&rft.aufirst=Faith&rft.date=2012-01-01&rft.volume=13&rft.issue=1&rft.spage=62&rft.isbn=&rft.btitle=&rft.title=BMC+Medical+Genetics&rft.issn=14712350&rft_id=info:doi/10.1186%2F1471-2350-13-62 L2 - http://www.biomedcentral.com/1471-2350/13/62 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-04-01 N1 - Number of references - 59 N1 - Last updated - 2013-08-23 N1 - SubjectsTermNotLitGenreText - Genetic factors; Maternal effects; Gene polymorphism; Animal models; Methylenetetrahydrofolate reductase; Neural tube defects; Supplementation; Pregnancy; Single-nucleotide polymorphism; Risk factors; Metabolic pathways; Congenital defects; Folic acid; Priorities; Europe DO - http://dx.doi.org/10.1186/1471-2350-13-62 ER - TY - JOUR T1 - Primer-BLAST: A tool to design target-specific primers for polymerase chain reaction AN - 1328508493; 17380063 AB - Background: Choosing appropriate primers is probably the single most important factor affecting the polymerase chain reaction (PCR). Specific amplification of the intended target requires that primers do not have matches to other targets in certain orientations and within certain distances that allow undesired amplification. The process of designing specific primers typically involves two stages. First, the primers flanking regions of interest are generated either manually or using software tools; then they are searched against an appropriate nucleotide sequence database using tools such as BLAST to examine the potential targets. However, the latter is not an easy process as one needs to examine many details between primers and targets, such as the number and the positions of matched bases, the primer orientations and distance between forward and reverse primers. The complexity of such analysis usually makes this a time-consuming and very difficult task for users, especially when the primers have a large number of hits. Furthermore, although the BLAST program has been widely used for primer target detection, it is in fact not an ideal tool for this purpose as BLAST is a local alignment algorithm and does not necessarily return complete match information over the entire primer range. Results: We present a new software tool called Primer-BLAST to alleviate the difficulty in designing target-specific primers. This tool combines BLAST with a global alignment algorithm to ensure a full primer-target alignment and is sensitive enough to detect targets that have a significant number of mismatches to primers. Primer-BLAST allows users to design new target-specific primers in one step as well as to check the specificity of pre-existing primers. Primer-BLAST also supports placing primers based on exon/intron locations and excluding single nucleotide polymorphism (SNP) sites in primers. Conclusions: We describe a robust and fully implemented general purpose primer design tool that designs target-specific PCR primers. Primer-BLAST offers flexible options to adjust the specificity threshold and other primer properties. This tool is publicly available at http://www.ncbi.nlm.nih.gov/tools/primer-blast . JF - BMC Bioinformatics AU - Ye, Jian AU - Coulouris, George AU - Zaretskaya, Irena AU - Cutcutache, Ioana AU - Rozen, Steve AU - Madden, Thomas L AD - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Building 45, 8600 Rockville Pike, Bethesda, MD, 20894, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 134 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 13 IS - 1 SN - 1471-2105, 1471-2105 KW - Biotechnology and Bioengineering Abstracts KW - Algorithms KW - Bioinformatics KW - Computer programs KW - Databases KW - Exons KW - Introns KW - Nucleotide sequence KW - Polymerase chain reaction KW - Primers KW - Single-nucleotide polymorphism KW - software KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1328508493?accountid=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+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 - http://www.biomedcentral.com/1471-2105/13/134 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-04-01 N1 - Number of references - 14 N1 - Last updated - 2013-04-19 N1 - SubjectsTermNotLitGenreText - Databases; Computer programs; software; Exons; Single-nucleotide polymorphism; Nucleotide sequence; Introns; Algorithms; Polymerase chain reaction; Primers; Bioinformatics DO - http://dx.doi.org/10.1186/1471-2105-13-134 ER - TY - JOUR T1 - Autophagy and lysosomal dysfunction as emerging mechanisms of nanomaterial toxicity AN - 1328508186; 17381267 AB - Abstract: The study of the potential risks associated with the manufacture, use, and disposal of nanoscale materials, and their mechanisms of toxicity, is important for the continued advancement of nanotechnology. Currently, the most widely accepted paradigms of nanomaterial toxicity are oxidative stress and inflammation, but the underlying mechanisms are poorly defined. This review will highlight the significance of autophagy and lysosomal dysfunction as emerging mechanisms of nanomaterial toxicity. Most endocytic routes of nanomaterial cell uptake converge upon the lysosome, making the lysosomal compartment the most common intracellular site of nanoparticle sequestration and degradation. In addition to the endo-lysosomal pathway, recent evidence suggests that some nanomaterials can also induce autophagy. Among the many physiological functions, the lysosome, by way of the autophagy (macroautophagy) pathway, degrades intracellular pathogens, and damaged organelles and proteins. Thus, autophagy induction by nanoparticles may be an attempt to degrade what is perceived by the cell as foreign or aberrant. While the autophagy and endo-lysosomal pathways have the potential to influence the disposition of nanomaterials, there is also a growing body of literature suggesting that biopersistent nanomaterials can, in turn, negatively impact these pathways. Indeed, there is ample evidence that biopersistent nanomaterials can cause autophagy and lysosomal dysfunctions resulting in toxicological consequences. JF - Particle and Fibre Toxicology AU - Stern, Stephan T AU - Adiseshaiah, Pavan P AU - Crist, Rachael M AD - Nanotechnology Characterization Laboratory, Advanced Technology Program, SAIC-Frederick, Inc., NCI-Frederick, Frederick, MD, 21702, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 20 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 9 IS - 1 SN - 1743-8977, 1743-8977 KW - Toxicology Abstracts KW - Lysosome KW - Endocytosis KW - Autophagy KW - Nanomaterials KW - Oxidative stress KW - Disposition KW - Toxicity KW - Pathogens KW - Phagocytosis KW - Organelles KW - nanoparticles KW - Lysosomes KW - Inflammation KW - nanotechnology KW - X 24500:Reviews, Legislation, Book & Conference Notices UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1328508186?accountid=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=Particle+and+Fibre+Toxicology&rft.atitle=Autophagy+and+lysosomal+dysfunction+as+emerging+mechanisms+of+nanomaterial+toxicity&rft.au=Stern%2C+Stephan+T%3BAdiseshaiah%2C+Pavan+P%3BCrist%2C+Rachael+M&rft.aulast=Stern&rft.aufirst=Stephan&rft.date=2012-01-01&rft.volume=9&rft.issue=1&rft.spage=20&rft.isbn=&rft.btitle=&rft.title=Particle+and+Fibre+Toxicology&rft.issn=17438977&rft_id=info:doi/10.1186%2F1743-8977-9-20 L2 - http://www.particleandfibretoxicology.com/content/9/1/20 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-04-01 N1 - Number of references - 140 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Oxidative stress; Disposition; Pathogens; Toxicity; Organelles; Phagocytosis; nanoparticles; Lysosomes; nanotechnology; Inflammation DO - http://dx.doi.org/10.1186/1743-8977-9-20 ER - TY - JOUR T1 - Can sedentary behavior be made more active? A randomized pilot study of TV commercial stepping versus walking AN - 1328508179; 17391476 AB - Background: There is a growing problem of physical inactivity in America, and approximately a quarter of the population report being completely sedentary during their leisure time. In the U.S., TV viewing is the most common leisure-time activity. Stepping in place during TV commercials (TV Commercial Stepping) could increase physical activity. The purpose of this study was to examine the feasibility of incorporating physical activity (PA) into a traditionally sedentary activity, by comparing TV Commercial Stepping during 90 min/d of TV programming to traditional exercise (Walking). Methods: A randomized controlled pilot study of the impact of 6 months of TV Commercial Stepping versus Walking 30 min/day in adults was conducted. 58 sedentary, overweight (body mass index 33.5 plus or minus 4.8 kg/m super(2)) adults (age 52.0 plus or minus 8.6 y) were randomly assigned to one of two 6-mo behavioral PA programs: 1) TV Commercial Stepping; or 2) Walking 30 min/day. To help facilitate behavior changes participants received 6 monthly phone calls, attended monthly meetings for the first 3 months, and received monthly newsletters for the last 3 months. Using intent-to-treat analysis, changes in daily steps, TV viewing, diet, body weight, waist and hip circumference, and percent fat were compared at baseline, 3, and 6 mo. Data were collected in 2010-2011, and analyzed in 2011. Results: Of the 58 subjects, 47 (81%) were retained for follow-up at the completion of the 6-mo program. From baseline to 6-mo, both groups significantly increased their daily steps [4611 plus or minus 1553 steps/d vs. 7605 plus or minus 2471 steps/d (TV Commercial Stepping); 4909 plus or minus 1335 steps/d vs. 7865 plus or minus 1939 steps/d (Walking); P < 0.05] with no significant difference between groups. TV viewing and dietary intake decreased significantly in both groups. Body weight did not change, but both groups had significant decreases in percent body fat (3-mo to 6-mo), and waist and hip circumference (baseline to 6-mo) over time. Conclusions: Participants in both the TV Commercial Stepping and Walking groups had favorable changes in daily steps, TV viewing, diet, and anthropometrics. PA can be performed while viewing TV commercials and this may be a feasible alternative to traditional approaches for increasing daily steps in overweight and obese adults. Trial Registration: This study is registered at ClinicalTrials.gov, NCT01342471 JF - International Journal of Behavioral Nutrition and Physical Activity AU - Steeves, Jeremy A AU - Bassett, David R AU - Fitzhugh, Eugene C AU - Raynor, Hollie A AU - Thompson, Dixie L AD - Cancer Prevention Fellowship Program, National Cancer Institute, 6120 Executive Boulevard, Bethesda, MD, 20892, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 95 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 9 IS - 1 SN - 1479-5868, 1479-5868 KW - Physical Education Index KW - Obesity KW - Stepping KW - Programs KW - Television KW - Diet (weight control) KW - Walking KW - Adults KW - Exercise KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1328508179?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Behavioral+Nutrition+and+Physical+Activity&rft.atitle=Can+sedentary+behavior+be+made+more+active%3F+A+randomized+pilot+study+of+TV+commercial+stepping+versus+walking&rft.au=Steeves%2C+Jeremy+A%3BBassett%2C+David+R%3BFitzhugh%2C+Eugene+C%3BRaynor%2C+Hollie+A%3BThompson%2C+Dixie+L&rft.aulast=Steeves&rft.aufirst=Jeremy&rft.date=2012-01-01&rft.volume=9&rft.issue=1&rft.spage=95&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Behavioral+Nutrition+and+Physical+Activity&rft.issn=14795868&rft_id=info:doi/10.1186%2F1479-5868-9-95 L2 - http://www.ijbnpa.org/content/9/1/95 LA - English DB - Physical Education Index N1 - Date revised - 2013-04-01 N1 - Number of references - 38 N1 - Last updated - 2013-05-17 N1 - SubjectsTermNotLitGenreText - Obesity; Programs; Stepping; Television; Diet (weight control); Walking; Exercise; Adults DO - http://dx.doi.org/10.1186/1479-5868-9-95 ER - TY - JOUR T1 - Predicting tissue specific cis-regulatory modules in the human genome using pairs of co-occurring motifs AN - 1328507628; 17380092 AB - Background: Researchers seeking to unlock the genetic basis of human physiology and diseases have been studying gene transcription regulation. The temporal and spatial patterns of gene expression are controlled by mainly non-coding elements known as cis-regulatory modules (CRMs) and epigenetic factors. CRMs modulating related genes share the regulatory signature which consists of transcription factor (TF) binding sites (TFBSs). Identifying such CRMs is a challenging problem due to the prohibitive number of sequence sets that need to be analyzed. Results: We formulated the challenge as a supervised classification problem even though experimentally validated CRMs were not required. Our efforts resulted in a software system named CrmMiner. The system mines for CRMs in the vicinity of related genes. CrmMiner requires two sets of sequences: a mixed set and a control set. Sequences in the vicinity of the related genes comprise the mixed set, whereas the control set includes random genomic sequences. CrmMiner assumes that a large percentage of the mixed set is made of background sequences that do not include CRMs. The system identifies pairs of closely located motifs representing vertebrate TFBSs that are enriched in the training mixed set consisting of 50% of the gene loci. In addition, CrmMiner selects a group of the enriched pairs to represent the tissue-specific regulatory signature. The mixed and the control sets are searched for candidate sequences that include any of the selected pairs. Next, an optimal Bayesian classifier is used to distinguish candidates found in the mixed set from their control counterparts. Our study proposes 62 tissue-specific regulatory signatures and putative CRMs for different human tissues and cell types. These signatures consist of assortments of ubiquitously expressed TFs and tissue-specific TFs. Under controlled settings, CrmMiner identified known CRMs in noisy sets up to 1:25 signal-to-noise ratio. CrmMiner was 21-75% more precise than a related CRM predictor. The sensitivity of the system to locate known human heart enhancers reached up to 83%. CrmMiner precision reached 82% while mining for CRMs specific to the human CD4 super(+ )T cells. On several data sets, the system achieved 99% specificity. Conclusion: These results suggest that CrmMiner predictions are accurate and likely to be tissue-specific CRMs. We expect that the predicted tissue-specific CRMs and the regulatory signatures broaden our knowledge of gene transcription regulation. JF - BMC Bioinformatics AU - Girgis, Hani Z AU - Ovcharenko, Ivan AD - Computational Biology Branch, National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health 9600 Rockville Pike, Bethesda, MD 20896, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 25 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 13 IS - 1 SN - 1471-2105, 1471-2105 KW - Genetics Abstracts; Biotechnology and Bioengineering Abstracts KW - Genomes KW - Heart KW - Data processing KW - Bayesian analysis KW - Transcription KW - Gene expression KW - Computer programs KW - Enhancers KW - CD4 antigen KW - software KW - epigenetics KW - Transcription factors KW - Gene regulation KW - Lymphocytes T KW - genomics KW - Bioinformatics KW - G 07880:Human Genetics KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1328507628?accountid=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+Bioinformatics&rft.atitle=Predicting+tissue+specific+cis-regulatory+modules+in+the+human+genome+using+pairs+of+co-occurring+motifs&rft.au=Girgis%2C+Hani+Z%3BOvcharenko%2C+Ivan&rft.aulast=Girgis&rft.aufirst=Hani&rft.date=2012-01-01&rft.volume=13&rft.issue=1&rft.spage=25&rft.isbn=&rft.btitle=&rft.title=BMC+Bioinformatics&rft.issn=14712105&rft_id=info:doi/10.1186%2F1471-2105-13-25 L2 - http://www.biomedcentral.com/1471-2105/13/25 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-04-01 N1 - Number of references - 54 N1 - Last updated - 2013-08-23 N1 - SubjectsTermNotLitGenreText - Heart; Genomes; Data processing; Bayesian analysis; Transcription; Gene expression; Enhancers; Computer programs; software; CD4 antigen; epigenetics; Gene regulation; Transcription factors; Lymphocytes T; Bioinformatics; genomics DO - http://dx.doi.org/10.1186/1471-2105-13-25 ER - TY - JOUR T1 - Factors affecting the performance, energy consumption, and carbon footprint for ultra low temperature freezers: case study at the National Institutes of Health AN - 1318696194; 17760702 AB - The National Institutes of Health (NIH) recognises an opportunity to significantly reduce the energy consumption and its carbon footprint from plug load equipment can be realised by managing -86 degree C ultra low temperature (ULT) freezers. Energy meters were installed on ULT freezers operating in actual laboratory conditions to determine how their energy consumption is influenced by various factors. Ambient temperature, freezer condition, age, capacity, and set point temperature were the factors that were examined. Based on the study, ultra low temperature freezers operated efficiently when they are: well maintained, operating in ambient temperatures less than 25 degree C, less than ten years old, are operating at a set point higher than -80 degree C, and have an internal capacity greater than 23 ft super(3). The results of the case study are presented and discussed. Freezer performance was assessed to determine how ambient temperature and the freezer condition influenced the freezer's ability to reach set point temperature. The results of the study indicate a freezer that is not maintained and operating in ambient temperatures above 32 degree C produce cabinet temperatures 12.5 degree C warmer than the desired set point temperature. JF - World Review of Science, Technology and Sustainable Development AU - Gumapas, Leo Angelo M AU - Simons, Glenn AD - US Public Health Service Commissioned Corps, Office of Research Facilities, Division of Environmental Protection, National Institutes of Health, Room 2W64, 9000 Rockville Pike Building 13, Bethesda, MD 20892, USA. Y1 - 2012 PY - 2012 DA - 2012 SP - 129 EP - 141 PB - Inderscience Publishers Ltd., PO Box 735 Olney Bucks MK46 5WB United Kingdom VL - 10 IS - 1-2-3 SN - 1741-2242, 1741-2242 KW - Health & Safety Science Abstracts; Environment Abstracts; Sustainability Science Abstracts KW - ENERGY AND ENVIRONMENT KW - MANAGEMENT AND BUSINESS KW - Environment and Sustainable Development KW - Operational Management and Marketing KW - Policy and Organisational Management KW - Age KW - Low temperature KW - Case studies KW - Reviews KW - Temperature KW - Sustainable development KW - Energy consumption KW - ENA 03:Energy KW - M3 1010:Issues in Sustainable Development KW - H 0500:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1318696194?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Assamodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=World+Review+of+Science%2C+Technology+and+Sustainable+Development&rft.atitle=Factors+affecting+the+performance%2C+energy+consumption%2C+and+carbon+footprint+for+ultra+low+temperature+freezers%3A+case+study+at+the+National+Institutes+of+Health&rft.au=Gumapas%2C+Leo+Angelo+M%3BSimons%2C+Glenn&rft.aulast=Gumapas&rft.aufirst=Leo+Angelo&rft.date=2012-01-01&rft.volume=10&rft.issue=1-2-3&rft.spage=129&rft.isbn=&rft.btitle=&rft.title=World+Review+of+Science%2C+Technology+and+Sustainable+Development&rft.issn=17412242&rft_id=info:doi/10.1504%2FWRSTSD.2013.050786 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-03-01 N1 - Last updated - 2015-03-19 N1 - SubjectsTermNotLitGenreText - Age; Case studies; Low temperature; Reviews; Temperature; Sustainable development; Energy consumption DO - http://dx.doi.org/10.1504/WRSTSD.2013.050786 ER - TY - JOUR T1 - Household food access and child malnutrition: results from the eight-country MAL-ED study AN - 1318692976; 17758372 AB - Background: Stunting results from decreased food intake, poor diet quality, and a high burden of early childhood infections, and contributes to significant morbidity and mortality worldwide. Although food insecurity is an important determinant of child nutrition, including stunting, development of universal measures has been challenging due to cumbersome nutritional questionnaires and concerns about lack of comparability across populations. We investigate the relationship between household food access, one component of food security, and indicators of nutritional status in early childhood across eight country sites. Methods: We administered a socioeconomic survey to 800 households in research sites in eight countries, including a recently validated nine-item food access insecurity questionnaire, and obtained anthropometric measurements from children aged 24 to 60 months. We used multivariable regression models to assess the relationship between household food access insecurity and anthropometry in children, and we assessed the invariance of that relationship across country sites. Results: Average age of study children was 41 months. Mean food access insecurity score (range: 0-27) was 5.8, and varied from 2.4 in Nepal to 8.3 in Pakistan. Across sites, the prevalence of stunting (42%) was much higher than the prevalence of wasting (6%). In pooled regression analyses, a 10-point increase in food access insecurity score was associated with a 0.20 SD decrease in height-for-age Z score (95% CI 0.05 to 0.34 SD; p = 0.008). A likelihood ratio test for heterogeneity revealed that this relationship was consistent across countries (p = 0.17). Conclusions: Our study provides evidence of the validity of using a simple household food access insecurity score to investigate the etiology of childhood growth faltering across diverse geographic settings. Such a measure could be used to direct interventions by identifying children at risk of illness and death related to malnutrition. JF - Population Health Metrics AU - Psaki, Stephanie AU - Bhutta, Zulfiqar A AU - Ahmed, Tahmeed AU - Ahmed, Shamsir AU - Bessong, Pascal AU - Islam, Munirul AU - John, Sushil AU - Kosek, Margaret AU - Lima, Aldo AU - Nesamvuni, Cebisa AU - Shrestha, Prakash AU - Svensen, Erling AU - McGrath, Monica AU - Richard, Stephanie AU - Seidman, Jessica AU - Caulfield, Laura AU - Miller, Mark AU - Checkley, William AD - Fogarty International Center, National Institutes of Health, Bethesda, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 24 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 10 IS - 1 SN - 1478-7954, 1478-7954 KW - Sustainability Science Abstracts KW - Children KW - Diets KW - Households KW - Infection KW - Intervention KW - Malnutrition KW - Morbidity KW - Mortality KW - Nutrition KW - Pakistan KW - Nepal KW - M3 1010:Issues in Sustainable Development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1318692976?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Assamodule&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Population+Health+Metrics&rft.atitle=Household+food+access+and+child+malnutrition%3A+results+from+the+eight-country+MAL-ED+study&rft.au=Psaki%2C+Stephanie%3BBhutta%2C+Zulfiqar+A%3BAhmed%2C+Tahmeed%3BAhmed%2C+Shamsir%3BBessong%2C+Pascal%3BIslam%2C+Munirul%3BJohn%2C+Sushil%3BKosek%2C+Margaret%3BLima%2C+Aldo%3BNesamvuni%2C+Cebisa%3BShrestha%2C+Prakash%3BSvensen%2C+Erling%3BMcGrath%2C+Monica%3BRichard%2C+Stephanie%3BSeidman%2C+Jessica%3BCaulfield%2C+Laura%3BMiller%2C+Mark%3BCheckley%2C+William&rft.aulast=Psaki&rft.aufirst=Stephanie&rft.date=2012-01-01&rft.volume=10&rft.issue=1&rft.spage=24&rft.isbn=&rft.btitle=&rft.title=Population+Health+Metrics&rft.issn=14787954&rft_id=info:doi/10.1186%2F1478-7954-10-24 L2 - http://www.pophealthmetrics.com/content/10/1/24 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-03-01 N1 - Number of references - 29 N1 - Last updated - 2013-04-05 N1 - SubjectsTermNotLitGenreText - Diets; Mortality; Malnutrition; Households; Intervention; Infection; Children; Nutrition; Morbidity; Pakistan; Nepal DO - http://dx.doi.org/10.1186/1478-7954-10-24 ER - TY - JOUR T1 - Domain enhanced lookup time accelerated BLAST AN - 1318691620; 17720934 AB - Background: BLAST is a commonly-used software package for comparing a query sequence to a database of known sequences; in this study, we focus on protein sequences. Position-specific-iterated BLAST (PSI-BLAST) iteratively searches a protein sequence database, using the matches in round i to construct a position-specific score matrix (PSSM) for searching the database in round i + 1. Biegert and Soding developed Context-sensitive BLAST (CS-BLAST), which combines information from searching the sequence database with information derived from a library of short protein profiles to achieve better homology detection than PSI-BLAST, which builds its PSSMs from scratch. Results: We describe a new method, called domain enhanced lookup time accelerated BLAST (DELTA-BLAST), which searches a database of pre-constructed PSSMs before searching a protein-sequence database, to yield better homology detection. For its PSSMs, DELTA-BLAST employs a subset of NCBI's Conserved Domain Database (CDD). On a test set derived from ASTRAL, with one round of searching, DELTA-BLAST achieves a ROC sub(5000) of 0.270 vs. 0.116 for CS-BLAST. The performance advantage diminishes in iterated searches, but DELTA-BLAST continues to achieve better ROC scores than CS-BLAST. Conclusions: DELTA-BLAST is a useful program for the detection of remote protein homologs. It is available under the "Protein BLAST" link at http://blast.ncbi.nlm.nih.gov . Reviewers: This article was reviewed by Arcady Mushegian, Nick V. Grishin, and Frank Eisenhaber. JF - Biology Direct AU - Boratyn, Grzegorz M AU - Schaeffer, Alejandro A AU - Agarwala, Richa AU - Altschul, Stephen F AU - Lipman, David J AU - Madden, Thomas L AD - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Building 38A, 8600 Rockville Pike, Bethesda, MD, 20894, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 12 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 7 IS - 1 SN - 1745-6150, 1745-6150 KW - Ecology Abstracts KW - Databases KW - Computer programs KW - software KW - Homology KW - Reviews KW - Amino acid sequence KW - D 04040:Ecosystem and Ecology Studies UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1318691620?accountid=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=Biology+Direct&rft.atitle=Domain+enhanced+lookup+time+accelerated+BLAST&rft.au=Boratyn%2C+Grzegorz+M%3BSchaeffer%2C+Alejandro+A%3BAgarwala%2C+Richa%3BAltschul%2C+Stephen+F%3BLipman%2C+David+J%3BMadden%2C+Thomas+L&rft.aulast=Boratyn&rft.aufirst=Grzegorz&rft.date=2012-01-01&rft.volume=7&rft.issue=1&rft.spage=12&rft.isbn=&rft.btitle=&rft.title=Biology+Direct&rft.issn=17456150&rft_id=info:doi/10.1186%2F1745-6150-7-12 L2 - http://www.biology-direct.com/content/7/1/12 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-03-01 N1 - Number of references - 43 N1 - Last updated - 2013-07-26 N1 - SubjectsTermNotLitGenreText - Computer programs; Databases; software; Homology; Reviews; Amino acid sequence DO - http://dx.doi.org/10.1186/1745-6150-7-12 ER - TY - JOUR T1 - Genomic organization, evolution, and expression of photoprotein and opsin genes in Mnemiopsis leidyi: a new view of ctenophore photocytes AN - 1315617865; 17699908 AB - Background: Calcium-activated photoproteins are luciferase variants found in photocyte cells of bioluminescent jellyfish (Phylum Cnidaria) and comb jellies (Phylum Ctenophora). The complete genomic sequence from the ctenophore Mnemiopsis leidyi, a representative of the earliest branch of animals that emit light, provided an opportunity to examine the genome of an organism that uses this class of luciferase for bioluminescence and to look for genes involved in light reception. To determine when photoprotein genes first arose, we examined the genomic sequence from other early-branching taxa. We combined our genomic survey with gene trees, developmental expression patterns, and functional protein assays of photoproteins and opsins to provide a comprehensive view of light production and light reception in Mnemiopsis. Results: The Mnemiopsis genome has 10 full-length photoprotein genes situated within two genomic clusters with high sequence conservation that are maintained due to strong purifying selection and concerted evolution. Photoprotein-like genes were also identified in the genomes of the non-luminescent sponge Amphimedon queenslandica and the non-luminescent cnidarian Nematostella vectensis, and phylogenomic analysis demonstrated that photoprotein genes arose at the base of all animals. Photoprotein gene expression in Mnemiopsis embryos begins during gastrulation in migrating precursors to photocytes and persists throughout development in the canals where photocytes reside. We identified three putative opsin genes in the Mnemiopsis genome and show that they do not group with well-known bilaterian opsin subfamilies. Interestingly, photoprotein transcripts are co-expressed with two of the putative opsins in developing photocytes. Opsin expression is also seen in the apical sensory organ. We present evidence that one opsin functions as a photopigment in vitro, absorbing light at wavelengths that overlap with peak photoprotein light emission, raising the hypothesis that light production and light reception may be functionally connected in ctenophore photocytes. We also present genomic evidence of a complete ciliary phototransduction cascade in Mnemiopsis. Conclusions: This study elucidates the genomic organization, evolutionary history, and developmental expression of photoprotein and opsin genes in the ctenophore Mnemiopsis leidyi, introduces a novel dual role for ctenophore photocytes in both bioluminescence and phototransduction, and raises the possibility that light production and light reception are linked in this early-branching non-bilaterian animal. JF - BMC Biology AU - Schnitzler, Christine E AU - Pang, Kevin AU - Powers, Meghan L AU - Reitzel, Adam M AU - Ryan, Joseph F AU - Simmons, David AU - Tada, Takashi AU - Park, Morgan AU - Gupta, Jyoti AU - Brooks, Shelise Y AU - Blakesley, Robert W AU - Yokoyama, Shozo AU - Haddock, Steven HD AU - Martindale, Mark Q AU - Baxevanis, Andreas D AD - Genome Technology Branch, Division of Intramural Research, National Human Genome Research Institute, National Institutes of Health, 50 South Drive, Bethesda, MD 20892, USA Y1 - 2012///0, PY - 2012 DA - 0, 2012 SP - 107 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 10 IS - 1 SN - 1741-7007, 1741-7007 KW - Genetics Abstracts; CSA Neurosciences Abstracts; Oceanic Abstracts; Ecology Abstracts; ASFA 1: Biological Sciences & Living Resources KW - Bioluminescence KW - ctenophore KW - Mnemiopsis leidyi KW - opsin KW - photocyte KW - photoprotein KW - photoreception KW - phototransduction KW - Genomes KW - Mnemiopsis KW - Gastrulation KW - photopigments KW - Nucleotide sequence KW - Development KW - Sense organs KW - Gene expression KW - opsins KW - Branches KW - Wave absorbers KW - Conserved sequence KW - Embryos KW - photocytes KW - Evolutionary genetics KW - genomics KW - Wavelength KW - Marine KW - Phototransduction KW - Embryonic development KW - Developmental stages KW - Light effects KW - Amphimedon KW - Canals KW - Ctenophora KW - Cnidaria KW - Nematostella vectensis KW - Evolution KW - Bilateria KW - Q1 08246:Physiology, biochemistry, biophysics KW - O 1085:Biotechnology KW - N3 11003:Developmental neuroscience KW - D 04040:Ecosystem and Ecology Studies KW - G 07730:Development & Cell Cycle UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1315617865?accountid=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=BMC+Biology&rft.atitle=Genomic+organization%2C+evolution%2C+and+expression+of+photoprotein+and+opsin+genes+in+Mnemiopsis+leidyi%3A+a+new+view+of+ctenophore+photocytes&rft.au=Schnitzler%2C+Christine+E%3BPang%2C+Kevin%3BPowers%2C+Meghan+L%3BReitzel%2C+Adam+M%3BRyan%2C+Joseph+F%3BSimmons%2C+David%3BTada%2C+Takashi%3BPark%2C+Morgan%3BGupta%2C+Jyoti%3BBrooks%2C+Shelise+Y%3BBlakesley%2C+Robert+W%3BYokoyama%2C+Shozo%3BHaddock%2C+Steven+HD%3BMartindale%2C+Mark+Q%3BBaxevanis%2C+Andreas+D&rft.aulast=Schnitzler&rft.aufirst=Christine&rft.date=2012-01-01&rft.volume=10&rft.issue=1&rft.spage=107&rft.isbn=&rft.btitle=&rft.title=BMC+Biology&rft.issn=17417007&rft_id=info:doi/10.1186%2F1741-7007-10-107 L2 - http://www.biomedcentral.com/1741-7007/10/107 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-03-01 N1 - Number of references - 106 N1 - Last updated - 2016-02-18 N1 - SubjectsTermNotLitGenreText - Gene expression; Genomes; Bioluminescence; Wave absorbers; Nucleotide sequence; Embryonic development; Evolution; Gastrulation; Phototransduction; photopigments; Developmental stages; Development; Sense organs; Light effects; Canals; opsins; Branches; Conserved sequence; photocytes; Embryos; Wavelength; genomics; Evolutionary genetics; Amphimedon; Mnemiopsis; Ctenophora; Mnemiopsis leidyi; Cnidaria; Nematostella vectensis; Bilateria; Marine DO - http://dx.doi.org/10.1186/1741-7007-10-107 ER - TY - JOUR T1 - Characterization of the Bat proteins in the oxidative stress response of Leptospira biflexa AN - 1291612358; 17648145 AB - Background: Leptospires lack many of the homologs for oxidative defense present in other bacteria, but do encode homologs of the Bacteriodes aerotolerance (Bat) proteins, which have been proposed to fulfill this function. Bat homologs have been identified in all families of the phylum Spirochaetes, yet a specific function for these proteins has not been experimentally demonstrated. Results: We investigated the contribution of the Bat proteins in the model organism Leptospira biflexa for their potential contributions to growth rate, morphology and protection against oxidative challenges. A genetically engineered mutant strain in which all bat ORFs were deleted did not exhibit altered growth rate or morphology, relative to the wild-type strain. Nor could we demonstrate a protective role for the Bat proteins in coping with various oxidative stresses. Further, pre-exposing L. biflexa to sublethal levels of reactive oxygen species did not appear to induce a general oxidative stress response, in contrast to what has been shown in other bacterial species. Differential proteomic analysis of the wild-type and mutant strains detected changes in the abundance of a single protein only - HtpG, which is encoded by the gene immediately downstream of the bat loci. Conclusion: The data presented here do not support a protective role for the Leptospira Bat proteins in directly coping with oxidative stress as previously proposed. L. biflexa is relatively sensitive to reactive oxygen species such as superoxide and H sub(2)O sub(2), suggesting that this spirochete lacks a strong, protective defense against oxidative damage despite being a strict aerobe. JF - BMC Microbiology AU - Stewart, Philip E AU - Carroll, James A AU - Dorward, David W AU - Stone, Hunter H AU - Sarkar, Amit AU - Picardeau, Mathieu AU - Rosa, Patricia A AD - Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 South 4th St, Hamilton, Montana, 59840, US Y1 - 2012 PY - 2012 DA - 2012 SP - 290 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 12 IS - 1 SN - 1471-2180, 1471-2180 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology KW - Aerotolerance KW - Bat protein KW - Data processing KW - Genetic engineering KW - Growth rate KW - Hydrogen peroxide KW - Models KW - Oxidative stress KW - Reactive oxygen species KW - Spirochetes KW - Superoxide KW - proteomics KW - Leptospira KW - Leptospira biflexa KW - Bacteriodes KW - J 02320:Cell Biology KW - A 01300:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1291612358?accountid=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=BMC+Microbiology&rft.atitle=Characterization+of+the+Bat+proteins+in+the+oxidative+stress+response+of+Leptospira+biflexa&rft.au=Stewart%2C+Philip+E%3BCarroll%2C+James+A%3BDorward%2C+David+W%3BStone%2C+Hunter+H%3BSarkar%2C+Amit%3BPicardeau%2C+Mathieu%3BRosa%2C+Patricia+A&rft.aulast=Stewart&rft.aufirst=Philip&rft.date=2012-01-01&rft.volume=12&rft.issue=1&rft.spage=290&rft.isbn=&rft.btitle=&rft.title=BMC+Microbiology&rft.issn=14712180&rft_id=info:doi/10.1186%2F1471-2180-12-290 L2 - http://www.biomedcentral.com/1471-2180/12/290 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-01 N1 - Number of references - 49 N1 - Last updated - 2013-03-22 N1 - SubjectsTermNotLitGenreText - Growth rate; Spirochetes; Data processing; Reactive oxygen species; Hydrogen peroxide; Oxidative stress; Superoxide; Genetic engineering; Bat protein; Aerotolerance; proteomics; Models; Bacteriodes; Leptospira; Leptospira biflexa DO - http://dx.doi.org/10.1186/1471-2180-12-290 ER - TY - JOUR T1 - Down-weighting overlapping genes improves gene set analysis AN - 1285096899; 17611239 AB - Background: The identification of gene sets that are significantly impacted in a given condition based on microarray data is a crucial step in current life science research. Most gene set analysis methods treat genes equally, regardless how specific they are to a given gene set. Results: In this work we propose a new gene set analysis method that computes a gene set score as the mean of absolute values of weighted moderated gene t-scores. The gene weights are designed to emphasize the genes appearing in few gene sets, versus genes that appear in many gene sets. We demonstrate the usefulness of the method when analyzing gene sets that correspond to the KEGG pathways, and hence we called our method Pathway Analysis with Down-weighting of Overlapping Genes (PADOG). Unlike most gene set analysis methods which are validated through the analysis of 2-3 data sets followed by a human interpretation of the results, the validation employed here uses 24 different data sets and a completely objective assessment scheme that makes minimal assumptions and eliminates the need for possibly biased human assessments of the analysis results. Conclusions: PADOG significantly improves gene set ranking and boosts sensitivity of analysis using information already available in the gene expression profiles and the collection of gene sets to be analyzed. The advantages of PADOG over other existing approaches are shown to be stable to changes in the database of gene sets to be analyzed. PADOG was implemented as an R package available at: http://bioinformaticsprb.med.wayne.edu/PADOG/ or http://www.bioconductor.org . JF - BMC Bioinformatics AU - Tarca, Adi Laurentiu AU - Draghici, Sorin AU - Bhatti, Gaurav AU - Romero, Roberto AD - Perinatology Research Branch, NICHD/NIH/DHHS, , Bethesda, Maryland, and Detroit, MI, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 136 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 13 IS - 1 SN - 1471-2105, 1471-2105 KW - Biotechnology and Bioengineering Abstracts KW - Bioinformatics KW - Data processing KW - Databases KW - Gene expression KW - W 30960:Bioinformatics & Computer Applications UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285096899?accountid=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+Bioinformatics&rft.atitle=Down-weighting+overlapping+genes+improves+gene+set+analysis&rft.au=Tarca%2C+Adi+Laurentiu%3BDraghici%2C+Sorin%3BBhatti%2C+Gaurav%3BRomero%2C+Roberto&rft.aulast=Tarca&rft.aufirst=Adi&rft.date=2012-01-01&rft.volume=13&rft.issue=1&rft.spage=136&rft.isbn=&rft.btitle=&rft.title=BMC+Bioinformatics&rft.issn=14712105&rft_id=info:doi/10.1186%2F1471-2105-13-136 L2 - http://www.biomedcentral.com/1471-2105/13/136 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-01 N1 - Number of references - 47 N1 - Last updated - 2013-03-11 N1 - SubjectsTermNotLitGenreText - Gene expression; Databases; Data processing; Bioinformatics DO - http://dx.doi.org/10.1186/1471-2105-13-136 ER - TY - JOUR T1 - Evidence for validity of five secondary data sources for enumerating retail food outlets in seven American Indian Communities in North Carolina AN - 1285094858; 17611515 AB - Background: Most studies on the local food environment have used secondary sources to describe the food environment, such as government food registries or commercial listings (e.g., Reference USA). Most of the studies exploring evidence for validity of secondary retail food data have used on-site verification and have not conducted analysis by data source (e.g., sensitivity of Reference USA) or by food outlet type (e.g., sensitivity of Reference USA for convenience stores). Few studies have explored the food environment in American Indian communities. To advance the science on measuring the food environment, we conducted direct, on-site observations of a wide range of food outlets in multiple American Indian communities, without a list guiding the field observations, and then compared our findings to several types of secondary data. Methods: Food outlets located within seven State Designated Tribal Statistical Areas in North Carolina (NC) were gathered from online Yellow Pages, Reference USA, Dun & Bradstreet, local health departments, and the NC Department of Agriculture and Consumer Services. All TIGER/Line 2009 roads (>1,500 miles) were driven in six of the more rural tribal areas and, for the largest tribe, all roads in two of its cities were driven. Sensitivity, positive predictive value, concordance, and kappa statistics were calculated to compare secondary data sources to primary data. Results: 699 food outlets were identified during primary data collection. Match rate for primary data and secondary data differed by type of food outlet observed, with the highest match rates found for grocery stores (97%), general merchandise stores (96%), and restaurants (91%). Reference USA exhibited almost perfect sensitivity (0.89). Local health department data had substantial sensitivity (0.66) and was almost perfect when focusing only on restaurants (0.91). Positive predictive value was substantial for Reference USA (0.67) and moderate for local health department data (0.49). Evidence for validity was comparatively lower for Dun & Bradstreet, online Yellow Pages, and the NC Department of Agriculture. Conclusions: Secondary data sources both over- and under-represented the food environment; they were particularly problematic for identifying convenience stores and specialty markets. More attention is needed to improve the validity of existing data sources, especially for rural local food environments. JF - International Journal of Behavioral Nutrition and Physical Activity AU - Fleischhacker, Sheila E AU - Rodriguez, Daniel A AU - Evenson, Kelly R AU - Henley, Amanda AU - Gizlice, Ziya AU - Soto, Dolly AU - Ramachandran, Gowri AD - Senior Public Health & Science Policy Advisor, NIH Division of Nutrition Research Coordination, National Institutes of Health, US Department of Health and Human Services, Two Democracy Plaza, Room 635, 6707 Democracy Boulevard, MSC 5461, Bethesda, MD, 20892-5461, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 137 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 9 IS - 1 SN - 1479-5868, 1479-5868 KW - Physical Education Index KW - Analysis KW - Diet KW - Exercise KW - Health KW - Indians KW - Observation KW - Restaurants KW - Statistics KW - Validity KW - PE 030:Exercise, Health & Physical Fitness UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285094858?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aphysicaleducation&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=International+Journal+of+Behavioral+Nutrition+and+Physical+Activity&rft.atitle=Evidence+for+validity+of+five+secondary+data+sources+for+enumerating+retail+food+outlets+in+seven+American+Indian+Communities+in+North+Carolina&rft.au=Fleischhacker%2C+Sheila+E%3BRodriguez%2C+Daniel+A%3BEvenson%2C+Kelly+R%3BHenley%2C+Amanda%3BGizlice%2C+Ziya%3BSoto%2C+Dolly%3BRamachandran%2C+Gowri&rft.aulast=Fleischhacker&rft.aufirst=Sheila&rft.date=2012-01-01&rft.volume=9&rft.issue=1&rft.spage=137&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Behavioral+Nutrition+and+Physical+Activity&rft.issn=14795868&rft_id=info:doi/10.1186%2F1479-5868-9-137 L2 - http://www.ijbnpa.org/content/9/1/137 LA - English DB - Physical Education Index N1 - Date revised - 2013-02-01 N1 - Number of references - 47 N1 - Last updated - 2013-03-11 N1 - SubjectsTermNotLitGenreText - Indians; Statistics; Restaurants; Analysis; Validity; Observation; Health; Exercise; Diet DO - http://dx.doi.org/10.1186/1479-5868-9-137 ER - TY - JOUR T1 - Yersinia pestis insecticidal-like toxin complex (Tc) family proteins: characterization of expression, subcellular localization, and potential role in infection of the flea vector AN - 1285093423; 17592639 AB - Background: Toxin complex (Tc) family proteins were first identified as insecticidal toxins in Photorhabdus luminescens and have since been found in a wide range of bacteria. The genome of Yersinia pestis, the causative agent of bubonic plague, contains a locus that encodes the Tc protein homologues YitA, YitB, YitC, and YipA and YipB. Previous microarray data indicate that the Tc genes are highly upregulated by Y. pestis while in the flea vector; however, their role in the infection of fleas and pathogenesis in the mammalian host is unclear. Results: We show that the Tc proteins YitA and YipA are highly produced by Y. pestis while in the flea but not during growth in brain heart infusion (BHI) broth at the same temperature. Over-production of the LysR-type regulator YitR from an exogenous plasmid increased YitA and YipA synthesis in broth culture. The increase in production of YitA and YipA correlated with the yitR copy number and was temperature-dependent. Although highly synthesized in fleas, deletion of the Tc proteins did not alter survival of Y. pestis in the flea or prevent blockage of the proventriculus. Furthermore, YipA was found to undergo post-translational processing and YipA and YitA are localized to the outer membrane of Y. pestis. YitA was also detected by immunofluorescence microscopy on the surface of Y. pestis. Both YitA and YipA are produced maximally at low temperature but persist for several hours after transfer to 37 degree C. Conclusions: Y. pestis Tc proteins are highly expressed in the flea but are not essential for Y. pestis to stably infect or produce a transmissible infection in the flea. However, YitA and YipA localize to the outer membrane and YitA is exposed on the surface, indicating that at least YitA is present on the surface when Y. pestis is transmitted into the mammalian host from the flea. JF - BMC Microbiology AU - Spinner, Justin L AU - Jarrett, Clayton O AU - LaRock, Doris L AU - Miller, Samuel I AU - Collins, Carleen M AU - Hinnebusch, B Joseph AD - Laboratory of Zoonotic Pathogens, Rocky Mountain Laboratories, NIAID, NIH, Hamilton, MT, 59840, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 296 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 12 IS - 1 SN - 1471-2180, 1471-2180 KW - Microbiology Abstracts A: Industrial & Applied Microbiology; Toxicology Abstracts; Microbiology Abstracts B: Bacteriology KW - Temperature effects KW - Genomes KW - Heart KW - Data processing KW - Outer membranes KW - Brain KW - Yersinia pestis KW - Survival KW - Immunofluorescence KW - Plasmids KW - Infection KW - Toxins KW - copy number KW - Expression vectors KW - Post-translation KW - Photorhabdus luminescens KW - Microscopy KW - Plague KW - J 02410:Animal Diseases KW - A 01380:Plant Protection, Fungicides & Seed Treatments KW - X 24330:Agrochemicals UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285093423?accountid=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=BMC+Microbiology&rft.atitle=Yersinia+pestis+insecticidal-like+toxin+complex+%28Tc%29+family+proteins%3A+characterization+of+expression%2C+subcellular+localization%2C+and+potential+role+in+infection+of+the+flea+vector&rft.au=Spinner%2C+Justin+L%3BJarrett%2C+Clayton+O%3BLaRock%2C+Doris+L%3BMiller%2C+Samuel+I%3BCollins%2C+Carleen+M%3BHinnebusch%2C+B+Joseph&rft.aulast=Spinner&rft.aufirst=Justin&rft.date=2012-01-01&rft.volume=12&rft.issue=1&rft.spage=296&rft.isbn=&rft.btitle=&rft.title=BMC+Microbiology&rft.issn=14712180&rft_id=info:doi/10.1186%2F1471-2180-12-296 L2 - http://www.biomedcentral.com/1471-2180/12/296 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-01 N1 - Number of references - 38 N1 - Last updated - 2013-10-21 N1 - SubjectsTermNotLitGenreText - Heart; Genomes; Temperature effects; Data processing; Outer membranes; Brain; Survival; Immunofluorescence; Infection; Plasmids; Toxins; copy number; Expression vectors; Post-translation; Microscopy; Plague; Photorhabdus luminescens; Yersinia pestis DO - http://dx.doi.org/10.1186/1471-2180-12-296 ER - TY - JOUR T1 - EPIPOI: A user-friendly analytical tool for the extraction and visualization of temporal parameters from epidemiological time series AN - 1285091332; 17528999 AB - Background: There is an increasing need for processing and understanding relevant information generated by the systematic collection of public health data over time. However, the analysis of those time series usually requires advanced modeling techniques, which are not necessarily mastered by staff, technicians and researchers working on public health and epidemiology. Here a user-friendly tool, EPIPOI, is presented that facilitates the exploration and extraction of parameters describing trends, seasonality and anomalies that characterize epidemiological processes. It also enables the inspection of those parameters across geographic regions. Although the visual exploration and extraction of relevant parameters from time series data is crucial in epidemiological research, until now it had been largely restricted to specialists. Methods: EPIPOI is freely available software developed in Matlab (The Mathworks Inc) that runs both on PC and Mac computers. Its friendly interface guides users intuitively through useful comparative analyses including the comparison of spatial patterns in temporal parameters. Results: EPIPOI is able to handle complex analyses in an accessible way. A prototype has already been used to assist researchers in a variety of contexts from didactic use in public health workshops to the main analytical tool in published research. Conclusions: EPIPOI can assist public health officials and students to explore time series data using a broad range of sophisticated analytical and visualization tools. It also provides an analytical environment where even advanced users can benefit by enabling a higher degree of control over model assumptions, such as those associated with detecting disease outbreaks and pandemics. JF - BMC Public Health AU - Alonso, Wladimir J AU - McCormick, Benjamin JJ AD - Fogarty International Center, National Institutes of Health, Bethesda, 20892, MD, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 982 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 12 IS - 1 SN - 1471-2458, 1471-2458 KW - Health & Safety Science Abstracts KW - Computer programs KW - Spatial distribution KW - Technicians KW - Outbreaks KW - Time series analysis KW - Inspection KW - Seasonal variations KW - Ethnic groups KW - Public health KW - H 12000:Epidemiology and Public Health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285091332?accountid=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=BMC+Public+Health&rft.atitle=EPIPOI%3A+A+user-friendly+analytical+tool+for+the+extraction+and+visualization+of+temporal+parameters+from+epidemiological+time+series&rft.au=Alonso%2C+Wladimir+J%3BMcCormick%2C+Benjamin+JJ&rft.aulast=Alonso&rft.aufirst=Wladimir&rft.date=2012-01-01&rft.volume=12&rft.issue=1&rft.spage=982&rft.isbn=&rft.btitle=&rft.title=BMC+Public+Health&rft.issn=14712458&rft_id=info:doi/10.1186%2F1471-2458-12-982 L2 - http://www.biomedcentral.com/1471-2458/12/982 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-01 N1 - Number of references - 31 N1 - Last updated - 2013-11-04 N1 - SubjectsTermNotLitGenreText - Computer programs; Spatial distribution; Technicians; Outbreaks; Inspection; Time series analysis; Seasonal variations; Ethnic groups; Public health DO - http://dx.doi.org/10.1186/1471-2458-12-982 ER - TY - JOUR T1 - Staphylococcus epidermidis pan-genome sequence analysis reveals diversity of skin commensal and hospital infection-associated isolates AN - 1285087855; 17593321 AB - Background: While Staphylococcus epidermidis is commonly isolated from healthy human skin, it is also the most frequent cause of nosocomial infections on indwelling medical devices. Despite its importance, few genome sequences existed and the most frequent hospital-associated lineage, ST2, had not been fully sequenced. Results: We cultivated 71 commensal S. epidermidis isolates from 15 skin sites and compared them with 28 nosocomial isolates from venous catheters and blood cultures. We produced 21 commensal and 9 nosocomial draft genomes, and annotated and compared their gene content, phylogenetic relatedness and biochemical functions. The commensal strains had an open pan-genome with 80% core genes and 20% variable genes. The variable genome was characterized by an overabundance of transposable elements, transcription factors and transporters. Biochemical diversity, as assayed by antibiotic resistance and in vitro biofilm formation, demonstrated the varied phenotypic consequences of this genomic diversity. The nosocomial isolates exhibited both large-scale rearrangements and single-nucleotide variation. We showed that S. epidermidis genomes separate into two phylogenetic groups, one consisting only of commensals. The formate dehydrogenase gene, present only in commensals, is a discriminatory marker between the two groups. Conclusions: Commensal skin S. epidermidis have an open pan-genome and show considerable diversity between isolates, even when derived from a single individual or body site. For ST2, the most common nosocomial lineage, we detect variation between three independent isolates sequenced. Finally, phylogenetic analyses revealed a previously unrecognized group of S. epidermidis strains characterized by reduced virulence and formate dehydrogenase, which we propose as a clinical molecular marker. JF - Genome Biology AU - Conlan, Sean AU - Mijares, Lilia A AU - Becker, Jesse AU - Blakesley, Robert W AU - Bouffard, Gerard G AU - Brooks, Shelise AU - Coleman, Holly AU - Gupta, Jyoti AU - Gurson, Natalie AU - Park, Morgan AU - Schmidt, Brian AU - Thomas, Pamela J AU - Otto, Michael AU - Kong, Heidi H AU - Murray, Patrick R AU - Segre, Julia A AD - National Human Genome Research Institute, NIH, Bethesda, MD 20892, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 1 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 13 IS - 7 SN - 1465-6906, 1465-6906 KW - Biochemistry Abstracts 2: Nucleic Acids; Microbiology Abstracts B: Bacteriology; Genetics Abstracts KW - Blood culture KW - Phylogeny KW - Genomes KW - Skin KW - Commensals KW - Formate dehydrogenase KW - Transposons KW - Virulence KW - Transcription factors KW - Nosocomial infection KW - Catheters KW - Biofilms KW - genomics KW - Staphylococcus epidermidis KW - Antibiotic resistance KW - Hospitals KW - J 02310:Genetics & Taxonomy KW - N 14835:Protein-Nucleic Acids Association KW - G 07770:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1285087855?accountid=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=Genome+Biology&rft.atitle=Staphylococcus+epidermidis+pan-genome+sequence+analysis+reveals+diversity+of+skin+commensal+and+hospital+infection-associated+isolates&rft.au=Conlan%2C+Sean%3BMijares%2C+Lilia+A%3BBecker%2C+Jesse%3BBlakesley%2C+Robert+W%3BBouffard%2C+Gerard+G%3BBrooks%2C+Shelise%3BColeman%2C+Holly%3BGupta%2C+Jyoti%3BGurson%2C+Natalie%3BPark%2C+Morgan%3BSchmidt%2C+Brian%3BThomas%2C+Pamela+J%3BOtto%2C+Michael%3BKong%2C+Heidi+H%3BMurray%2C+Patrick+R%3BSegre%2C+Julia+A&rft.aulast=Conlan&rft.aufirst=Sean&rft.date=2012-01-01&rft.volume=13&rft.issue=7&rft.spage=R64&rft.isbn=&rft.btitle=&rft.title=Genome+Biology&rft.issn=14656906&rft_id=info:doi/10.1186%2Fgb-2012-13-7-r64 L2 - http://genomebiology.com/content/13/7/R64 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-02-01 N1 - Number of references - 49 N1 - Last updated - 2013-11-15 N1 - SubjectsTermNotLitGenreText - Genomes; Phylogeny; Blood culture; Skin; Commensals; Formate dehydrogenase; Virulence; Transposons; Transcription factors; Nosocomial infection; Catheters; genomics; Biofilms; Antibiotic resistance; Hospitals; Staphylococcus epidermidis DO - http://dx.doi.org/10.1186/gb-2012-13-7-r64 ER - TY - JOUR T1 - Introduction to the Special Issue AN - 1283642574; 201300912 AB - Introduces a special journal issue on "Addiction-Related Issues Among Active Duty Military, Veterans and Their Families.". JF - Journal of Social Work Practice in the Addictions AU - Glass, Joseph E AU - Perron, Brian E AU - Straussner, Shulamith Lala AD - PhD Candidate and National Institute on Alcohol Abuse and Alcoholism Predoctoral Fellow, George Warren Brown School of Social Work, Washington University in St. Louis, St. Louis, Missouri, USA Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 1 EP - 5 PB - Taylor & Francis, Philadelphia PA VL - 12 IS - 1 SN - 1533-256X, 1533-256X KW - Veterans KW - Family KW - Armed Forces KW - article KW - 6129: addiction UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1283642574?accountid=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=Journal+of+Social+Work+Practice+in+the+Addictions&rft.atitle=Introduction+to+the+Special+Issue&rft.au=Glass%2C+Joseph+E%3BPerron%2C+Brian+E%3BStraussner%2C+Shulamith+Lala&rft.aulast=Glass&rft.aufirst=Joseph&rft.date=2012-01-01&rft.volume=12&rft.issue=1&rft.spage=1&rft.isbn=&rft.btitle=&rft.title=Journal+of+Social+Work+Practice+in+the+Addictions&rft.issn=1533256X&rft_id=info:doi/10.1080%2F1533256X.2012.649242 LA - English DB - Social Services Abstracts N1 - Date revised - 2013-02-01 N1 - Last updated - 2016-09-28 N1 - SubjectsTermNotLitGenreText - Family; Armed Forces; Veterans DO - http://dx.doi.org/10.1080/1533256X.2012.649242 ER - TY - JOUR T1 - Achaete-scute complex homolog-1 promotes DNA repair in the lung carcinogenesis through matrix metalloproteinase-7 and O(6)-methylguanine-DNA methyltransferase. AN - 1273343183; 23300791 AB - Lung cancer is the leading cause of cancer-related deaths in the world. Achaete-scute complex homolog-1 (Ascl1) is a member of the basic helix-loop-helix (bHLH) transcription factor family that has multiple functions in the normal and neoplastic lung such as the regulation of neuroendocrine differentiation, prevention of apoptosis and promotion of tumor-initiating cells. We now show that Ascl1 directly regulates matrix metalloproteinase-7 (MMP-7) and O(6)-methylguanine-DNA methyltransferase (MGMT). Loss- and gain-of-function experiments in human bronchial epithelial and lung carcinoma cell lines revealed that Ascl1, MMP-7 and MGMT are able to protect cells from the tobacco-specific nitrosamine NNK-induced DNA damage and the alkylating agent cisplatin-induced apoptosis. We also examined the role of Ascl1 in NNK-induced lung tumorigenesis in vivo. Using transgenic mice which constitutively expressed human Ascl1 in airway lining cells, we found that there was a delay in lung tumorigenesis. We conclude that Ascl1 potentially enhances DNA repair through activation of MMP-7 and MGMT which may impact lung carcinogenesis and chemoresistance. The study has uncovered a novel and unexpected function of Ascl1 which will contribute to better understanding of lung carcinogenesis and the broad implications of transcription factors in tobacco-related carcinogenesis. JF - PloS one AU - Wang, Xiao-Yang AU - Jensen-Taubman, Sandra M AU - Keefe, Kathleen M AU - Yang, Danlei AU - Linnoila, R Ilona AD - Cell and Cancer Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America. xiaoyangwang@gmail.com Y1 - 2012 PY - 2012 DA - 2012 SP - 1 VL - 7 IS - 12 KW - ASCL1 protein, human KW - 0 KW - Antineoplastic Agents, Alkylating KW - Basic Helix-Loop-Helix Transcription Factors KW - Nitrosamines KW - RNA, Small Interfering KW - Tumor Suppressor Proteins KW - 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone KW - 7S395EDO61 KW - DNA Modification Methylases KW - EC 2.1.1.- KW - MGMT protein, human KW - EC 2.1.1.63 KW - MMP7 protein, human KW - EC 3.4.24.23 KW - Matrix Metalloproteinase 7 KW - DNA Repair Enzymes KW - EC 6.5.1.- KW - Cisplatin KW - Q20Q21Q62J KW - Index Medicus KW - Animals KW - Antineoplastic Agents, Alkylating -- pharmacology KW - DNA Damage KW - Humans KW - Cell Transformation, Neoplastic -- metabolism KW - RNA, Small Interfering -- genetics KW - Mice KW - Cell Line, Tumor KW - Mice, Transgenic KW - Protein Binding KW - Gene Expression Regulation, Neoplastic KW - Promoter Regions, Genetic KW - Gene Knockdown Techniques KW - Adenoma -- metabolism KW - Adenoma -- chemically induced KW - Apoptosis -- drug effects KW - Cell Transformation, Neoplastic -- chemically induced KW - Cisplatin -- pharmacology KW - Enzyme Induction KW - Up-Regulation KW - DNA Repair Enzymes -- metabolism KW - DNA Modification Methylases -- metabolism KW - DNA Repair KW - Matrix Metalloproteinase 7 -- genetics KW - Basic Helix-Loop-Helix Transcription Factors -- physiology KW - Tumor Suppressor Proteins -- genetics KW - DNA Modification Methylases -- genetics KW - DNA Repair Enzymes -- genetics KW - Small Cell Lung Carcinoma -- metabolism KW - Tumor Suppressor Proteins -- metabolism KW - Matrix Metalloproteinase 7 -- metabolism KW - Lung Neoplasms -- chemically induced KW - Lung Neoplasms -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273343183?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Achaete-scute+complex+homolog-1+promotes+DNA+repair+in+the+lung+carcinogenesis+through+matrix+metalloproteinase-7+and+O%286%29-methylguanine-DNA+methyltransferase.&rft.au=Wang%2C+Xiao-Yang%3BJensen-Taubman%2C+Sandra+M%3BKeefe%2C+Kathleen+M%3BYang%2C+Danlei%3BLinnoila%2C+R+Ilona&rft.aulast=Wang&rft.aufirst=Xiao-Yang&rft.date=2012-01-01&rft.volume=7&rft.issue=12&rft.spage=e52832&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0052832 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-06-27 N1 - Date created - 2013-01-09 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Mutat Res. 2000 Apr;462(2-3):83-100 [10767620] Mol Cell Biol. 2008 Jun;28(11):3589-99 [18362162] Cancer Res. 2000 Aug 1;60(15):4005-9 [10945598] Cancer Res. 2001 Jan 15;61(2):577-81 [11212252] J Mol Biol. 2001 Oct 26;313(3):539-57 [11676538] J Biol Chem. 2001 Nov 9;276(45):42462-7 [11571274] Cancer Res. 2003 Aug 15;63(16):4842-8 [12941804] Cancer Lett. 2004 Feb 20;204(2):159-69 [15013215] Am J Clin Pathol. 1988 Dec;90(6):641-52 [2848408] J Natl Cancer Inst. 1990 Jul 4;82(13):1107-12 [2359136] Cancer Res. 1992 Jun 1;52(11):3164-73 [1591728] Environ Health Perspect. 1995 Nov;103 Suppl 8:131-42 [8741773] Nature. 1997 Apr 24;386(6627):852-5 [9126746] Cancer Res. 1997 Jun 15;57(12):2415-8 [9192819] J Biol Chem. 1998 Mar 6;273(10):5858-68 [9488723] Oncogene. 1999 Jan 14;18(2):525-32 [9927209] Cancer Res. 1999 Feb 15;59(4):793-7 [10029064] Carcinogenesis. 1999 Feb;20(2):279-84 [10069465] J Natl Cancer Inst. 1999 Apr 21;91(8):675-90 [10218505] Lab Invest. 2006 May;86(5):425-44 [16568108] Int J Oncol. 2006 Oct;29(4):745-52 [16964372] Lab Invest. 2007 Jun;87(6):527-39 [17507989] Lung Cancer. 2007 Dec;58(3):384-91 [17728005] Cancer Lett. 2008 Feb 18;260(1-2):48-55 [18037231] Br Med Bull. 2008;85:17-33 [18245773] Cancer. 2008 Jul 1;113(1):5-21 [18473355] Cancer Res. 2009 Feb 1;69(3):845-54 [19176379] Am J Pathol. 2009 Aug;175(2):592-604 [19608871] Toxicol Sci. 2010 Sep;117(1):238-48 [20554700] Int J Cancer. 2010 Dec 15;127(12):2893-917 [21351269] CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 [21296855] Genes Dev. 2011 May 1;25(9):930-45 [21536733] Lung Cancer. 2012 Jan;75(1):58-65 [21684625] CA Cancer J Clin. 2012 Jan-Feb;62(1):10-29 [22237781] Mol Biol Cell. 2012 Aug;23(15):2856-66 [22696682] J Natl Cancer Inst. 2000 Jun 7;92(11):874-97 [10841823] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1371/journal.pone.0052832 ER - TY - JOUR T1 - Restricted cell surface expression of receptor tyrosine kinase ROR1 in pediatric B-lineage acute lymphoblastic leukemia suggests targetability with therapeutic monoclonal antibodies. AN - 1273173236; 23285131 AB - Despite high cure rates for pediatric B-lineage acute lymphoblastic leukemia (B-ALL), short-term and long-term toxicities and chemoresistance are shortcomings of standard chemotherapy. Immunotherapy and chemoimmunotherapy based on monoclonal antibodies (mAbs) that target cell surface antigens with restricted expression in pediatric B-ALL may offer the potential to reduce toxicities and prevent or overcome chemoresistance. The receptor tyrosine kinase ROR1 has emerged as a candidate for mAb targeting in select B-cell malignancies. Using flow cytometry, Western blotting, immunohistochemistry, and confocal immunofluorescence microscopy, we analyzed the cell surface expression of ROR1 across major pediatric ALL subtypes represented by 14 cell lines and 56 primary blasts at diagnosis or relapse as well as in normal adult and pediatric tissues. Cell surface ROR1 expression was found in 45% of pediatric ALL patients, all of which were B-ALL, and was not limited to any particular genotype. All cell lines and primary blasts with E2A-PBX1 translocation and a portion of patients with other high risk genotypes, such as MLL rearrangement, expressed cell surface ROR1. Importantly, cell surface ROR1 expression was found in many of the pediatric B-ALL patients with multiply relapsed and refractory disease and normal karyotype or low risk cytogenetics, such as hyperdiploidy. Notably, cell surface ROR1 was virtually absent in normal adult and pediatric tissues. Collectively, this study suggests that ROR1 merits preclinical and clinical investigations as a novel target for mAb-based therapies in pediatric B-ALL. We propose cell surface expression of ROR1 detected by flow cytometry as primary inclusion criterion for pediatric B-ALL patients in future clinical trials of ROR1-targeted therapies. JF - PloS one AU - Dave, Hema AU - Anver, Miriam R AU - Butcher, Donna O AU - Brown, Patrick AU - Khan, Javed AU - Wayne, Alan S AU - Baskar, Sivasubramanian AU - Rader, Christoph AD - Experimental Transplantation and Immunology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012 PY - 2012 DA - 2012 SP - 1 VL - 7 IS - 12 KW - Antibodies, Monoclonal KW - 0 KW - Antineoplastic Agents KW - RNA, Messenger KW - ROR1 protein, human KW - EC 2.7.10.1 KW - Receptor Tyrosine Kinase-like Orphan Receptors KW - Index Medicus KW - Young Adult KW - Antibodies, Monoclonal -- metabolism KW - Humans KW - Molecular Targeted Therapy KW - Gene Expression KW - Cell Line, Tumor KW - Child KW - RNA, Messenger -- genetics KW - Antibodies, Monoclonal -- therapeutic use KW - Child, Preschool KW - Infant KW - Gene Expression Profiling KW - RNA, Messenger -- metabolism KW - Adult KW - Adolescent KW - Antineoplastic Agents -- therapeutic use KW - Immunophenotyping KW - Male KW - Female KW - Precursor B-Cell Lymphoblastic Leukemia-Lymphoma -- genetics KW - Precursor B-Cell Lymphoblastic Leukemia-Lymphoma -- metabolism KW - Receptor Tyrosine Kinase-like Orphan Receptors -- metabolism KW - Receptor Tyrosine Kinase-like Orphan Receptors -- genetics KW - Receptor Tyrosine Kinase-like Orphan Receptors -- antagonists & inhibitors KW - Precursor B-Cell Lymphoblastic Leukemia-Lymphoma -- drug therapy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273173236?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Restricted+cell+surface+expression+of+receptor+tyrosine+kinase+ROR1+in+pediatric+B-lineage+acute+lymphoblastic+leukemia+suggests+targetability+with+therapeutic+monoclonal+antibodies.&rft.au=Dave%2C+Hema%3BAnver%2C+Miriam+R%3BButcher%2C+Donna+O%3BBrown%2C+Patrick%3BKhan%2C+Javed%3BWayne%2C+Alan+S%3BBaskar%2C+Sivasubramanian%3BRader%2C+Christoph&rft.aulast=Dave&rft.aufirst=Hema&rft.date=2012-01-01&rft.volume=7&rft.issue=12&rft.spage=e52655&rft.isbn=&rft.btitle=&rft.title=PloS+one&rft.issn=1932-6203&rft_id=info:doi/10.1371%2Fjournal.pone.0052655 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-06-27 N1 - Date created - 2013-01-03 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: Dev Genes Evol. 2001 Apr;211(4):161-71 [11455430] PLoS One. 2011;6(6):e21018 [21698301] J Exp Med. 2001 Dec 3;194(11):1639-47 [11733578] Blood. 2003 Oct 15;102(8):2951-9 [12730115] Hematology Am Soc Hematol Educ Program. 2003;:102-31 [14633779] Singapore Med J. 2003 Oct;44(10):517-20 [15024455] N Engl J Med. 2004 Apr 8;350(15):1535-48 [15071128] Blood. 1990 Jul 1;76(1):117-22 [2364165] J Biol Chem. 1992 Dec 25;267(36):26181-90 [1334494] Leukemia. 1994 Apr;8(4):659-63 [8152261] Leuk Res. 2011 Oct;35(10):1390-4 [21813176] Drug Discov Today. 2011 Dec;16(23-24):1037-43 [21945861] Mol Endocrinol. 2012 Jan;26(1):110-27 [22074948] Leukemia. 2012 Feb;26(2):255-64 [21869836] PLoS One. 2012;7(3):e31127 [22403610] Cancer Cell. 2012 Mar 20;21(3):348-61 [22439932] MAbs. 2012 May-Jun;4(3):349-61 [22531447] Br J Haematol. 2012 Oct;159(1):3-17 [22881237] Genes Cells. 1999 Jan;4(1):41-56 [10231392] Nat Cell Biol. 2005 Jun;7(6):591-600 [15864305] Leukemia. 2007 Nov;21(11):2240-5 [17657218] Clin Cancer Res. 2008 Jan 15;14(2):396-404 [18223214] Proc Natl Acad Sci U S A. 2008 Feb 26;105(8):3047-52 [18287027] Int J Cancer. 2008 Sep 1;123(5):1190-5 [18546292] Leuk Lymphoma. 2008 Jul;49(7):1360-7 [18604725] J Clin Oncol. 2008 Aug 1;26(22):3756-62 [18669463] Proc Natl Acad Sci U S A. 2009 May 26;106(21):8695-700 [19433805] Clin Cancer Res. 2010 Mar 15;16(6):1894-903 [20215554] Blood. 2010 Apr 1;115(13):2619-29 [19965642] Blood. 2010 Nov 25;116(22):4532-41 [20702778] Leukemia. 2011 Jan;25(1):181-4 [20944674] Hematol Oncol. 2011 Mar;29(1):17-21 [20597086] Cancer Res. 2011 Apr 15;71(8):3132-41 [21487037] J Clin Oncol. 2011 Jun 20;29(18):2493-8 [21576633] J Exp Med. 2001 Dec 3;194(11):1625-38 [11733577] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1371/journal.pone.0052655 ER - TY - JOUR T1 - Development and validation of an immunoassay for quantification of topoisomerase I in solid tumor tissues. AN - 1273163629; 23284638 AB - Topoisomerase I (Top1) is a proven target for cancer therapeutics. Recent data from the Fluorouracil, Oxaliplatin, CPT-11: Use and Sequencing (FOCUS) trial demonstrated that nuclear staining of Top1 correlates with chemotherapeutic efficacy. Such a correlation may help identify patients likely to respond to Top1 inhibitors and illuminate their mechanism of action. Cellular response to Top1 inhibitors is complex, but Top1 target engagement is a necessary first step in this process. This paper reports the development and validation of a quantitative immunoassay for Top1 in tumors. We have developed and validated a two-site enzyme chemiluminescent immunoassay for quantifying Top1 levels in tumor biopsies. Analytical validation of the assay established the inter-day coefficient of variation at 9.3%±3.4% and a 96.5%±7.3% assay accuracy. Preclinical fit-for-purpose modeling of topotecan time- and dose-effects was performed using topotecan-responsive and -nonresponsive xenografts in athymic nude mice. Higher baseline levels of Top1 were observed in topotecan-responsive than -nonresponsive tumors. Top1 levels reached a maximal decrease 4 to 7 hours following treatment of engrafted mice with topotecan and the indenoisoquinoline NSC 724998. Our analysis of Top1 levels in control and treated tumors supports the previously proposed mechanism of action for Top1 inhibitor efficacy, wherein higher baseline Top1 levels lead to formation of more covalent-complex-dependent double-strand break damage and, ultimately, cell death. In contrast, xenografts with lower baseline Top1 levels accumulate fewer double-stand breaks, and may be more resistant to Top1 inhibitors. Our results support further investigation into the use of Top1 levels in tumors as a potential predictive biomarker. The Top1 immunoassay described in this paper has been incorporated into a Phase I clinical trial at the National Cancer Institute to assess pharmacodynamic response in tumor biopsies and determine whether baseline Top1 levels are predictive of response to indenoisoquinoline Top1 inhibitors. JF - PloS one AU - Pfister, Thomas D AU - Hollingshead, Melinda AU - Kinders, Robert J AU - Zhang, Yiping AU - Evrard, Yvonne A AU - Ji, Jiuping AU - Khin, Sonny A AU - Borgel, Suzanne AU - Stotler, Howard AU - Carter, John AU - Divelbiss, Raymond AU - Kummar, Shivaani AU - Pommier, Yves AU - Parchment, Ralph E AU - Tomaszewski, Joseph E AU - Doroshow, James H AD - Laboratory of Human Toxicology and Pharmacology, Applied/Developmental Research Support Directorate, SAIC-Frederick, Inc., Frederick National Laboratory for Cancer Research, Frederick, Maryland, United States of America. pfistert@mail.nih.gov Y1 - 2012 PY - 2012 DA - 2012 SP - 1 VL - 7 IS - 12 KW - Isoquinolines KW - 0 KW - Topoisomerase I Inhibitors KW - Topotecan KW - 7M7YKX2N15 KW - Poly(ADP-ribose) Polymerases KW - EC 2.4.2.30 KW - DNA Topoisomerases, Type I KW - EC 5.99.1.2 KW - isoquinoline KW - JGX76Y85M6 KW - Index Medicus KW - Topoisomerase I Inhibitors -- pharmacology KW - Animals KW - Dose-Response Relationship, Drug KW - Clinical Trials as Topic KW - Biopsy KW - Cell Line, Tumor KW - Mice KW - Poly(ADP-ribose) Polymerases -- metabolism KW - Leukocytes, Mononuclear -- enzymology KW - Isoquinolines -- chemistry KW - Isoquinolines -- pharmacology KW - Topotecan -- pharmacology KW - Xenograft Model Antitumor Assays KW - Leukocytes, Mononuclear -- drug effects KW - Time Factors KW - Female KW - Drug Resistance, Neoplasm -- drug effects KW - Neoplasms -- drug therapy KW - Neoplasms -- pathology KW - Neoplasms -- enzymology KW - Immunoassay -- methods KW - DNA Topoisomerases, Type I -- blood KW - DNA Topoisomerases, Type I -- metabolism UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1273163629?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=PloS+one&rft.atitle=Development+and+validation+of+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 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-06-17 N1 - Date created - 2013-01-03 N1 - Date revised - 2017-01-14 N1 - SuppNotes - Cited By: Mol Pharmacol. 1999 Apr;55(4):677-83 [10101025] J Clin Oncol. 1998 Oct;16(10):3345-52 [9779711] Clin Cancer Res. 2005 Jun 15;11(12):4338-40 [15958615] Nat Rev Cancer. 2006 Oct;6(10):789-802 [16990856] Lancet. 2007 Jul 14;370(9582):135-42 [17630036] Anticancer Res. 2007 Jul-Aug;27(4B):2541-5 [17695551] Cancer Res. 2007 Sep 15;67(18):8752-61 [17875716] Cancer Res. 2007 Nov 1;67(21):10397-405 [17974983] Ann N Y Acad Sci. 2000;922:306-8 [11193908] Cancer Res. 2001 Jan 15;61(2):504-8 [11212241] Cancer Res. 2001 Aug 1;61(15):5926-32 [11479235] Mol Cell Biol. 2003 Apr;23(7):2341-50 [12640119] Am J Clin Pathol. 2002 Jun;117 Suppl:S26-35 [14569800] Biochem Pharmacol. 2008 Mar 15;75(6):1262-71 [18061144] J Clin Oncol. 2008 Jun 1;26(16):2690-8 [18509181] Proc Natl Acad Sci U S A. 2008 Jul 1;105(26):9053-8 [18574145] J Biol Chem. 2008 Jul 25;283(30):21074-83 [18515798] Mol Cancer Ther. 2008 Oct;7(10):3212-22 [18852125] Clin Cancer Res. 2008 Nov 1;14(21):6877-85 [18980982] Nat Rev Cancer. 2008 Dec;8(12):957-67 [19005492] Eur J Cancer. 2009 Jul;45(11):1999-2006 [19457654] Chem Rev. 2009 Jul;109(7):2894-902 [19476377] Mol Cancer Ther. 2009 Jul;8(7):1878-84 [19584232] J Biol Chem. 2009 Oct 9;284(41):28084-92 [19666469] Clin Cancer Res. 2010 Feb 1;16(3):1073-84 [20103672] Clin Cancer Res. 2010 Nov 15;16(22):5447-57 [20924131] Mol Cancer Ther. 2009 May;8(5):1008-14 [19383846] Mol Cancer Ther. 2011 Aug;10(8):1490-9 [21636699] Cancer Res. 2011 Sep 1;71(17):5626-34 [21795476] Cancer Res. 2003 Nov 1;63(21):7428-35 [14612542] Cancer Res. 2003 Dec 1;63(23):8400-7 [14679002] J Med Chem. 2004 Mar 25;47(7):1609-12 [15027851] Anticancer Res. 2004 May-Jun;24(3a):1745-51 [15274350] Cancer Res. 1988 Apr 1;48(7):1722-6 [2832051] Cancer Res. 1989 Sep 15;49(18):5016-22 [2548707] Science. 1989 Nov 24;246(4933):1046-8 [2555920] J Clin Oncol. 1992 Apr;10(4):647-56 [1312588] J Med Chem. 1994 Jan 7;37(1):40-6 [8289200] Cancer Res. 1995 May 15;55(10):2116-21 [7743511] Mol Pharmacol. 1995 May;47(5):907-14 [7538195] Clin Cancer Res. 1998 Mar;4(3):545-57 [9533521] J Natl Cancer Inst. 1998 Apr 1;90(7):505-11 [9539245] Br J Cancer. 1999 Mar;79(9-10):1534-41 [10188903] N1 - Last updated - 2017-01-19 DO - http://dx.doi.org/10.1371/journal.pone.0050494 ER - TY - JOUR T1 - SspA up-regulates gene expression of the LEE pathogenicity island by decreasing H-NS levels in enterohemorrhagic Escherichia coli AN - 1272742793; 17573969 AB - Background: Enterohemorrhagic Escherichia coli (EHEC) colonizes the intestinal epithelium and causes attaching and effacing (A/E) lesions. Expression of virulence genes, particularly those from the locus of the enterocyte effacement (LEE) pathogenicity island is required for the formation of a type three secretion system, which induces A/E lesion formation. Like other horizontally acquired genetic elements, expression of the LEE is negatively regulated by H-NS. In the non-pathogenic Escherichia coli K-12 strain the stringent starvation protein A (SspA) inhibits accumulation of H-NS, and thereby allows de-repression of the H-NS regulon during the stationary phase of growth. However, the effect of SspA on the expression of H-NS-controlled virulence genes in EHEC is unknown. Results: Here we assess the effect of SspA on virulence gene expression in EHEC. We show that transcription of virulence genes including those of the LEE is decreased in an sspA mutant, rendering the mutant strain defective in forming A/E lesions. A surface exposed pocket of SspA is functionally important for the regulation of the LEE and for the A/E phenotype. Increased expression of ler alleviates LEE expression in an sspA mutant, suggesting that the level of Ler in the mutant is insufficient to counteract H-NS-mediated repression. We demonstrate that the H-NS level is two-fold higher in an sspA mutant compared to wild type, and that the defects of the sspA mutant are suppressed by an hns null mutation, indicating that hns is epistatic to sspA in regulating H-NS repressed virulence genes. Conclusions: SspA positively regulates the expression of EHEC virulence factors by restricting the intracellular level of H-NS. Since SspA is conserved in many bacterial pathogens containing horizontally acquired pathogenicity islands controlled by H-NS, our study suggests a common mechanism whereby SspA potentially regulates the expression of virulence genes in these pathogens. JF - BMC Microbiology AU - Hansen, Anne-Marie AU - Jin, Ding Jun AD - Transcription Control Section, Gene Regulation and Chromosome Biology Laboratory, Frederick National Laboratory for Cancer Research, National Cancer Institute, National Institutes of Health, Frederick, MD 21702, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 231 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 12 IS - 1 SN - 1471-2180, 1471-2180 KW - Genetics Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Microbiology Abstracts B: Bacteriology KW - Starvation KW - virulence factors KW - Secretion KW - Intracellular levels KW - Transcription KW - Pathogens KW - stationary phase KW - Gene expression KW - pathogenicity islands KW - Epistasis KW - Escherichia coli KW - Intestine KW - Epithelium KW - Mutation KW - Enterocytes KW - A 01490:Miscellaneous KW - J 02320:Cell Biology KW - G 07770:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1272742793?accountid=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=BMC+Microbiology&rft.atitle=SspA+up-regulates+gene+expression+of+the+LEE+pathogenicity+island+by+decreasing+H-NS+levels+in+enterohemorrhagic+Escherichia+coli&rft.au=Hansen%2C+Anne-Marie%3BJin%2C+Ding+Jun&rft.aulast=Hansen&rft.aufirst=Anne-Marie&rft.date=2012-01-01&rft.volume=12&rft.issue=1&rft.spage=231&rft.isbn=&rft.btitle=&rft.title=BMC+Microbiology&rft.issn=14712180&rft_id=info:doi/10.1186%2F1471-2180-12-231 L2 - http://www.biomedcentral.com/1471-2180/12/231 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-01-01 N1 - Number of references - 62 N1 - Last updated - 2013-10-21 N1 - SubjectsTermNotLitGenreText - Starvation; virulence factors; Secretion; Intracellular levels; Transcription; Pathogens; pathogenicity islands; Gene expression; stationary phase; Epistasis; Intestine; Epithelium; Mutation; Enterocytes; Escherichia coli DO - http://dx.doi.org/10.1186/1471-2180-12-231 ER - TY - JOUR T1 - Foetal haemoglobin and the dynamics of paediatric malaria AN - 1272741325; 17574246 AB - Background: Although 80% of malaria occurs in children under five years of age, infants under six months of age are known to have low rates of infection and disease. It is not clear why this youngest age group is protected; possible factors include maternal antibodies, unique nutrition (breast milk), and the presence of foetal haemoglobin (HbF). This work aims to gain insight into possible mechanisms of protection, and suggest pathways for focused empirical work, by modelling a range of possible effects of foetal haemoglobin and other red blood cell (RBC) developmental changes on parasite dynamics in infants. Methods: A set of ordinary differential equations was created to investigate the leading hypotheses about the possible protective mechanisms of HbF-containing red blood cells, in particular whether HbF suppresses parasite population growth because parasite multiplication in individual RBCs is lower, slower or absent. The model also incorporated the intrinsic changes in blood volume and haematocrit that occur with age, and the possibility of parasite affinities for HbF-containing RBCs or reticulocytes. Results: The model identified several sets of conditions in which the infant remained protected, or displayed a much slower growth of parasitaemia in the first few months of life, without any intervening immune response. The most protective of the hypothesized mechanisms would be the inhibition of schizont division in foetal RBCs so that fewer merozoites are produced. The model showed that a parasite preference for HbF-containing RBCs increases protective effects for the host, while a preference for reticulocytes has little effect. Conclusions: The results from this simple model of haematological changes in infants and their effects on Plasmodium falciparum infection dynamics emphasize the likely importance of HbF and RBC number as an explanatory factor in paediatric malaria, and suggest a framework for organizing related empirical research. JF - Malaria Journal AU - Billig, Erica MW AU - McQueen, Philip G AU - McKenzie, F Ellis AD - National Institutes of Health, Fogarty International Center, Building 16, Room 303, Bethesda, MD, 20892, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 396 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 11 IS - 1 SN - 1475-2875, 1475-2875 KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - Malaria KW - Plasmodium falciparum KW - Foetal haemoglobin KW - Parasites KW - Age KW - Human diseases KW - Population growth KW - Erythrocytes KW - Breast milk KW - Infection KW - Nutrition KW - Public health KW - Hemoglobin KW - Mathematical models KW - Pediatrics KW - Environmental impact KW - Developmental stages KW - Schizonts KW - Children KW - Endoparasites KW - Differential equations KW - Antibodies KW - Merozoites KW - Immune response KW - Reticulocytes KW - Haemoglobins KW - Infants KW - K 03400:Human Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1272741325?accountid=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=Malaria+Journal&rft.atitle=Foetal+haemoglobin+and+the+dynamics+of+paediatric+malaria&rft.au=Billig%2C+Erica+MW%3BMcQueen%2C+Philip+G%3BMcKenzie%2C+F+Ellis&rft.aulast=Billig&rft.aufirst=Erica&rft.date=2012-01-01&rft.volume=11&rft.issue=1&rft.spage=396&rft.isbn=&rft.btitle=&rft.title=Malaria+Journal&rft.issn=14752875&rft_id=info:doi/10.1186%2F1475-2875-11-396 L2 - http://www.malariajournal.com/content/11/1/396 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-01-01 N1 - Number of references - 47 N1 - Last updated - 2015-10-28 N1 - SubjectsTermNotLitGenreText - Parasites; Human diseases; Erythrocytes; Environmental impact; Malaria; Endoparasites; Haemoglobins; Differential equations; Public health; Age; Mathematical models; Pediatrics; Population growth; Breast milk; Schizonts; Developmental stages; Children; Infection; Nutrition; Hemoglobin; Antibodies; Merozoites; Immune response; Reticulocytes; Infants; Plasmodium falciparum DO - http://dx.doi.org/10.1186/1475-2875-11-396 ER - TY - JOUR T1 - Effects of multiple conformers per compound upon 3-D similarity search and bioassay data analysis AN - 1272737969; 17574570 AB - Background: To improve the utility of PubChem, a public repository containing biological activities of small molecules, the PubChem3D project adds computationally-derived three-dimensional (3-D) descriptions to the small-molecule records contained in the PubChem Compound database and provides various search and analysis tools that exploit 3-D molecular similarity. Therefore, the efficient use of PubChem3D resources requires an understanding of the statistical and biological meaning of computed 3-D molecular similarity scores between molecules. Results: The present study investigated effects of employing multiple conformers per compound upon the 3-D similarity scores between ten thousand randomly selected biologically-tested compounds (10-K set) and between non-inactive compounds in a given biological assay (156-K set). When the "best-conformer-pair" approach, in which a 3-D similarity score between two compounds is represented by the greatest similarity score among all possible conformer pairs arising from a compound pair, was employed with ten diverse conformers per compound, the average 3-D similarity scores for the 10-K set increased by 0.11, 0.09, 0.15, 0.16, 0.07, and 0.18 for ST super( ST-opt ), CT super( ST-opt ), ComboT super( ST-opt ), ST super( CT-opt ), CT super( CT-opt ), and ComboT super( CT-opt ), respectively, relative to the corresponding averages computed using a single conformer per compound. Interestingly, the best-conformer-pair approach also increased the average 3-D similarity scores for the non-inactive-non-inactive (NN) pairs for a given assay, by comparable amounts to those for the random compound pairs, although some assays showed a pronounced increase in the per-assay NN-pair 3-D similarity scores, compared to the average increase for the random compound pairs. Conclusion: These results suggest that the use of ten diverse conformers per compound in PubChem bioassay data analysis using 3-D molecular similarity is not expected to increase the separation of non-inactive from random and inactive spaces "on average", although some assays show a noticeable separation between the non-inactive and random spaces when multiple conformers are used for each compound. The present study is a critical next step to understand effects of conformational diversity of the molecules upon the 3-D molecular similarity and its application to biological activity data analysis in PubChem. The results of this study may be helpful to build search and analysis tools that exploit 3-D molecular similarity between compounds archived in PubChem and other molecular libraries in a more efficient way. JF - Journal of Cheminformatics AU - Kim, Sunghwan AU - Bolton, Evan E AU - Bryant, Stephen H AD - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Department of Health and Human Services, 8600 Rockville Pike, Bethesda, 20894, MD, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 28 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 4 IS - 1 SN - 1758-2946, 1758-2946 KW - Biotechnology and Bioengineering Abstracts KW - Data processing KW - Databases KW - Informatics KW - Statistics KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1272737969?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Abiotechresearch&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+Cheminformatics&rft.atitle=Effects+of+multiple+conformers+per+compound+upon+3-D+similarity+search+and+bioassay+data+analysis&rft.au=Kim%2C+Sunghwan%3BBolton%2C+Evan+E%3BBryant%2C+Stephen+H&rft.aulast=Kim&rft.aufirst=Sunghwan&rft.date=2012-01-01&rft.volume=4&rft.issue=1&rft.spage=28&rft.isbn=&rft.btitle=&rft.title=Journal+of+Cheminformatics&rft.issn=17582946&rft_id=info:doi/10.1186%2F1758-2946-4-28 L2 - http://www.jcheminf.com/content/4/1/28 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2013-01-01 N1 - Number of references - 55 N1 - Last updated - 2013-02-08 N1 - SubjectsTermNotLitGenreText - Databases; Statistics; Data processing; Informatics DO - http://dx.doi.org/10.1186/1758-2946-4-28 ER - TY - JOUR T1 - Open-Ended and Open-Door Treatment Groups for Young People with Mental Illness AN - 1266148106; 201300048 AB - The concept of open-ended groups is expanded to include an open-door model (OEOD) wherein members with severe mental illnesses, including schizophrenia disorders and bipolar, can join, leave, and reenter groups as their life circumstances dictate their availability and willingness for treatment. This model is grounded on the work of Schopler and Galinsky's (1984/2006) and Galinsky and Schopler's (1989) theses on the value and processes of open-ended groups and includes perspectives on mutual aid and group development. Groupwork with the OEOD format is illustrated with examples taken from a group of 79 participants diagnosed with first-episode schizophrenia/schizoaffective disorders, 40 of whom had cooccurring substance abuse. Of the 79 participants in the OEOD group program, 70 (89%) remained in treatment for the maximum of 3 years. The overall value of group treatment for this population is reviewed along with the small number of available publications on open-ended and open-door type groups. Adapted from the source document. JF - Social Work with Groups AU - Miller, Rachel AU - Mason, Susan E AD - National Institute of Mental Health, Bethesda, Maryland, USA Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 50 EP - 67 PB - Taylor & Francis, Philadelphia PA VL - 35 IS - 1 SN - 0160-9513, 0160-9513 KW - groupwork schizophrenia open-ended open-door mental illness KW - Values KW - Schizophrenia KW - Foreign Aid KW - Substance Abuse KW - Affective Illness KW - Mental Illness KW - Youth KW - article KW - 6120: social work practice UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1266148106?accountid=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=Social+Work+with+Groups&rft.atitle=Open-Ended+and+Open-Door+Treatment+Groups+for+Young+People+with+Mental+Illness&rft.au=Miller%2C+Rachel%3BMason%2C+Susan+E&rft.aulast=Miller&rft.aufirst=Rachel&rft.date=2012-01-01&rft.volume=35&rft.issue=1&rft.spage=50&rft.isbn=&rft.btitle=&rft.title=Social+Work+with+Groups&rft.issn=01609513&rft_id=info:doi/10.1080%2F01609513.2011.587099 LA - English DB - Social Services Abstracts N1 - Date revised - 2013-01-01 N1 - Last updated - 2016-09-28 N1 - CODEN - SWGRDU N1 - SubjectsTermNotLitGenreText - Schizophrenia; Values; Affective Illness; Foreign Aid; Youth; Substance Abuse; Mental Illness DO - http://dx.doi.org/10.1080/01609513.2011.587099 ER - TY - JOUR T1 - Biospecimens and Biorepositories: From Afterthought to Science AN - 1257855705; 16321572 AB - Biospecimens are recognized as critical components of biomedical research, from basic studies to clinical trials and epidemiologic investigations. Biorepositories have existed in various forms for more than 150 years, from early small collections in pathology laboratories to modern automated facilities managing millions of samples. As collaborative science has developed, it has been recognized that biospecimens must be of consistent quality. Recent years have seen a proliferation of best practices and the recognition of the field of "biospecimen science." The future of this field will depend on the development of more evidence-based practices in both the research and clinical settings. As the field matures, educating a new generation of biospecimen/biobanking scientists will be an important need. Cancer Epidemiol Biomarkers Prev; 21(2); 253-5. [copy]2012 AACR. JF - Cancer Epidemiology, Biomarkers & Prevention AU - Vaught, Jimmie B AU - Henderson, Marianne K AU - Compton, Carolyn C AD - Authors' Affiliations: Office of Biorepositories and Biospecimen Research, and Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland Y1 - 2012 PY - 2012 DA - 2012 SP - 253 EP - 255 PB - American Association for Cancer Research, 615 Chestnut St., 17th Floor Philadelphia PA 19106-4404 United States VL - 21 IS - 2 SN - 1055-9965, 1055-9965 KW - Health & Safety Science Abstracts KW - Best practices KW - Bioindicators KW - Cancer KW - Clinical trials KW - Pathology KW - Prevention KW - H 4000:Food and Drugs UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1257855705?accountid=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=Cancer+Epidemiology%2C+Biomarkers+%26+Prevention&rft.atitle=Biospecimens+and+Biorepositories%3A+From+Afterthought+to+Science&rft.au=Vaught%2C+Jimmie+B%3BHenderson%2C+Marianne+K%3BCompton%2C+Carolyn+C&rft.aulast=Vaught&rft.aufirst=Jimmie&rft.date=2012-01-01&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 - 2012-12-01 N1 - Last updated - 2013-01-11 N1 - SubjectsTermNotLitGenreText - Bioindicators; Prevention; Pathology; Best practices; Clinical trials; Cancer ER - TY - JOUR T1 - B cell analysis of ethnic groups in Mali with differential susceptibility to malaria AN - 1257750765; 17436185 AB - Background: Several studies indicate that people of the Fulani ethnic group are less susceptible to malaria compared to those of other ethnic groups living sympatrically in Africa, including the Dogon ethnic group. Although the mechanisms of this protection remain unclear, the Fulani are known to have higher levels of Plasmodium falciparum-specific antibodies of all Ig classes as compared to the Dogon. However, the proportions of B cell subsets in the Fulani and Dogon that may account for differences in the levels of Ig have not been characterized. Methods: In this cross-sectional study, venous blood was collected from asymptomatic Fulani (n = 25) and Dogon (n = 25) adults in Mali during the malaria season, and from P. falciparum-naive adults in the U.S. (n = 8). At the time of the blood collection, P. falciparum infection was detected by blood-smear in 16% of the Fulani and 36% of the Dogon volunteers. Thawed lymphocytes were analysed by flow cytometry to quantify B cell subsets, including immature and naive B cells; plasma cells; and classical, activated, and atypical memory B cells (MBCs). Results: The overall distribution of B cell subsets was similar between Fulani and Dogon adults, although the percentage of activated MBCs was higher in the Fulani group (Fulani: 11.07% [95% CI: 9.317 - 12.82]; Dogon: 8.31% [95% CI: 6.378 - 10.23]; P = 0.016). The percentage of atypical MBCs was similar between Fulani and Dogon adults (Fulani: 28.3% [95% CI: 22.73 - 34.88]; Dogon: 29.3% [95% CI: 25.06 - 33.55], but higher than U.S. adults (U.S.: 3.0% [95% CI: -0.21 - 6.164]; P < 0.001). Plasmodium falciparum infection was associated with a higher percentage of plasma cells among Fulani (Fulani infected: 3.3% [95% CI: 1.788 - 4.744]; Fulani uninfected: 1.71% [95% CI: 1.33 - 2.08]; P = 0.011), but not Dogon adults. Conclusion: These data show that the malaria-resistant Fulani have a higher percentage of activated MBCs compared to the Dogon, and that P. falciparum infection is associated with a higher percentage of plasma cells in the Fulani compared to the Dogon, findings that may account for the higher levels of P. falciparum antibodies in the Fulani. JF - Malaria Journal AU - Portugal, Silvia AU - Doumtabe, Didier AU - Traore, Boubacar AU - Miller, Louis H AU - Troye-Blomberg, Marita AU - Doumbo, Ogobara K AU - Dolo, Amagana AU - Pierce, Susan K AU - Crompton, Peter D AD - Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, MD 20852, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 162 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 11 IS - 1 SN - 1475-2875, 1475-2875 KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Microbiology Abstracts C: Algology, Mycology & Protozoology KW - Parasites KW - Human diseases KW - Mali KW - Immunological memory KW - Malaria KW - Lymphocytes KW - Infection KW - Public health KW - Flow cytometry KW - Serological studies KW - Ethnic groups KW - Immunoglobulins KW - Data processing KW - Lymphocytes B KW - Sympatric populations KW - Memory cells KW - Plasmodium falciparum KW - Blood KW - USA KW - Antibodies KW - Plasma cells KW - K 03400:Human Diseases KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08524:Public health, medicines, dangerous organisms UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1257750765?accountid=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=Malaria+Journal&rft.atitle=B+cell+analysis+of+ethnic+groups+in+Mali+with+differential+susceptibility+to+malaria&rft.au=Portugal%2C+Silvia%3BDoumtabe%2C+Didier%3BTraore%2C+Boubacar%3BMiller%2C+Louis+H%3BTroye-Blomberg%2C+Marita%3BDoumbo%2C+Ogobara+K%3BDolo%2C+Amagana%3BPierce%2C+Susan+K%3BCrompton%2C+Peter+D&rft.aulast=Portugal&rft.aufirst=Silvia&rft.date=2012-01-01&rft.volume=11&rft.issue=1&rft.spage=162&rft.isbn=&rft.btitle=&rft.title=Malaria+Journal&rft.issn=14752875&rft_id=info:doi/10.1186%2F1475-2875-11-162 L2 - http://www.malariajournal.com/content/11/1/162 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-12-01 N1 - Number of references - 17 N1 - Last updated - 2015-10-28 N1 - SubjectsTermNotLitGenreText - Flow cytometry; Parasites; Blood; Antibodies; Serological studies; Human diseases; Malaria; Lymphocytes; Public health; Data processing; Lymphocytes B; Sympatric populations; Immunological memory; Memory cells; Infection; Plasma cells; Ethnic groups; Immunoglobulins; Plasmodium falciparum; USA; Mali DO - http://dx.doi.org/10.1186/1475-2875-11-162 ER - TY - JOUR T1 - The effects of oviposition-site deprivation on Anopheles gambiae reproduction AN - 1257747941; 17436656 AB - Background: The African malaria mosquito, Anopheles gambiae, depends on availability of suitable surface water for oviposition. Short and long dry spells occur throughout the year in many parts of its range that limit its access to oviposition sites. Although not well understood, oviposition-site deprivation has been found to rapidly reduce egg batch size and hatch rate of several mosquito species. We conducted laboratory experiments to assess these effects of oviposition-site deprivation on An. gambiae and to evaluate the role of nutrition and sperm viability as mediators of these effects. Methods: Anopheles gambiae adults (1-2 d old) from the G3 laboratory colony were assigned to the following treatment groups: oviposition-deprived (fed once and then deprived of oviposition site for 7 or 14 d), multiple-fed control (fed regularly once a week and allowed to lay eggs without delay), and age matched blood-deprived control (fed once, three days before water for oviposition was provided). Egg batch size and hatch rate were measured. In the second experiment two additional treatment groups were included: oviposition-deprived females that received either a second (supplemental) blood meal or virgin males (supplemental mating) 4 days prior to receiving water for oviposition. Results: An. gambiae was highly sensitive to oviposition-site deprivation. Egg batch size dropped sharply to 0-3.5 egg/female within 14 days, due to reduced oviposition rate rather than a reduced number of eggs/batch. Egg hatch rate also fell dramatically to 0-2% within 7 days. The frequency of brown eggs that fail to tan was elevated. A supplemental blood meal, but not 'supplemental insemination,' recovered the oviposition rate of females subjected to oviposition-site deprivation. Similarly, a supplemental blood meal, but not 'supplemental insemination,' partly recovered hatch rate, but this increase was marginally significant (P < 0.069). Conclusions: Even a short dry spell resulting in oviposition-site deprivation for several days may result in a dramatic decline of An. gambiae populations via reduced fecundity and fertility. However, females taking supplemental blood meals regain at least some reproductive success. If mosquitoes subjected to oviposition-site deprivation increase the frequency of blood feeding, malaria transmission may even increase during a short dry spell. The relevance of oviposition-site deprivation as a cue to alter the physiology of An. gambiae during the long dry season is not evident from these results because no reduction in hatch rate was evident in wild M-form An. gambiae collected in the dry season in the Sahel by previous studies. JF - Parasites & Vectors AU - Dieter, Kathryne L AU - Huestis, Diana L AU - Lehmann, Tovi AD - Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 12735 Twinbrook Parkway, Room 2W-09-C, Rockville, MD, 20852, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 235 PB - BioMed Central Ltd., Floor 6 London WC1X 8HL United Kingdom VL - 5 IS - 1 SN - 1756-3305, 1756-3305 KW - ASFA 1: Biological Sciences & Living Resources; ASFA 3: Aquatic Pollution & Environmental Quality; Ecology Abstracts; Entomology Abstracts KW - Anopheles gambiae KW - Dry season KW - Drought KW - Hatch rate KW - Malaria KW - Reproduction KW - Seasonality KW - Vectorial capacity KW - Oviposition KW - Fecundity KW - Parasites KW - Fertility KW - Human diseases KW - Surface water KW - Sperm KW - Blood meals KW - Biological fertilization KW - Nutrition KW - Eggs KW - Public health KW - Mating KW - Colonies KW - Aquatic insects KW - Feeding KW - Vectors KW - Pest control KW - Blood KW - Africa KW - Breeding success KW - D 04040:Ecosystem and Ecology Studies KW - Q1 08484:Species interactions: parasites and diseases KW - Q5 08524:Public health, medicines, dangerous organisms KW - Z 05330:Reproduction and Development UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1257747941?accountid=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=Parasites+%26+Vectors&rft.atitle=The+effects+of+oviposition-site+deprivation+on+Anopheles+gambiae+reproduction&rft.au=Dieter%2C+Kathryne+L%3BHuestis%2C+Diana+L%3BLehmann%2C+Tovi&rft.aulast=Dieter&rft.aufirst=Kathryne&rft.date=2012-01-01&rft.volume=5&rft.issue=1&rft.spage=235&rft.isbn=&rft.btitle=&rft.title=Parasites+%26+Vectors&rft.issn=17563305&rft_id=info:doi/10.1186%2F1756-3305-5-235 L2 - http://www.parasitesandvectors.com/content/5/1/235 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-12-01 N1 - Number of references - 25 N1 - Last updated - 2015-10-28 N1 - SubjectsTermNotLitGenreText - Human diseases; Reproduction; Malaria; Pest control; Dry season; Biological fertilization; Aquatic insects; Oviposition; Public health; Feeding; Parasites; Fertility; Surface water; Vectors; Blood meals; Sperm; Nutrition; Eggs; Mating; Blood; Colonies; Fecundity; Breeding success; Anopheles gambiae; Africa DO - http://dx.doi.org/10.1186/1756-3305-5-235 ER - TY - JOUR T1 - Impact of cellular autophagy on viruses: Insights from hepatitis B virus and human retroviruses AN - 1238109787; 17379270 AB - Autophagy is a protein degradative process important for normal cellular metabolism. It is apparently used also by cells to eliminate invading pathogens. Interestingly, many pathogens have learned to subvert the cell's autophagic process. Here, we review the interactions between viruses and cells in regards to cellular autophagy. Using findings from hepatitis B virus and human retroviruses, HIV-1 and HTLV-1, we discuss mechanisms used by viruses to usurp cellular autophagy in ways that benefit viral replication. JF - Journal of Biomedical Science AU - Tang, Sai-Wen AU - Ducroux, Aurelie AU - Jeang, Kuan-Teh AU - Neuveut, Christine AD - Molecular Virology Section, Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, 20892-0460, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 92 PB - S. Karger AG, P.O. Box Basel CH-4009 Switzerland VL - 19 IS - 1 SN - 1423-0127, 1423-0127 KW - Biotechnology and Bioengineering Abstracts; Virology & AIDS Abstracts KW - Retrovirus KW - Hepatitis B virus KW - Replication KW - Reviews KW - Human T-lymphotropic virus 1 KW - Human immunodeficiency virus 1 KW - Protein turnover KW - Pathogens KW - Phagocytosis KW - V 22360:AIDS and HIV KW - W 30940:Products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1238109787?accountid=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+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 L2 - http://www.jbiomedsci.com/content/19/1/92 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-12-01 N1 - Number of references - 151 N1 - Last updated - 2013-09-20 N1 - SubjectsTermNotLitGenreText - Replication; Reviews; Protein turnover; Pathogens; Phagocytosis; Retrovirus; Hepatitis B virus; Human immunodeficiency virus 1; Human T-lymphotropic virus 1 DO - http://dx.doi.org/10.1186/1423-0127-19-92 ER - TY - JOUR T1 - Social representations of Human Papillomavirus in Bogota, Colombia AN - 1230586878; 4371192 AB - Identifying DNA of Human Papillomavirus (HPV) has been proposed as a new screening method for cervical cancer control. Conventionally, health education for screening programs is based on scientific information without considering any community cognitive processes. We examine HPV social representations of 124 men and women from diverse educational status living in Bogota, Colombia. The social representation of HPV involves a series of figurative nuclei derived from meanings linked to scientific information. While women focused on symbols associated to contagion, men focused on its venereal character. Figurative nuclei also included long-term uncertainty, need or urgent treatment, and feelings of imminent death associated with cancer and chronic sexually transmitted infections. The social representation of HPV impeded many participants from clearly understanding written information about HPV transmission, clearance, and cancer risk; they are built into a framework of values, which must be deconstructed to allow women full participation in HPV screening programs. Reprinted by permission of Harwood Academic Publishers, Taylor and Francis Ltd JF - Medical anthropology AU - Wiesner, Carolina AU - Acosta, Jesus AU - Diaz del Castillo, Adriana AU - Tovar, Sandra AD - Colombian National Cancer Institute Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - 77 EP - 92 VL - 31 IS - 1 SN - 0145-9740, 0145-9740 KW - Anthropology KW - Human papillomavirus KW - Bogota KW - Risk KW - Uncertainty KW - Medical anthropology KW - Health education KW - DNA KW - Colombia KW - Sexually transmitted diseases KW - Cancer KW - Social representations UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1230586878?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Medical+anthropology&rft.atitle=Social+representations+of+Human+Papillomavirus+in+Bogota%2C+Colombia&rft.au=Wiesner%2C+Carolina%3BAcosta%2C+Jesus%3BDiaz+del+Castillo%2C+Adriana%3BTovar%2C+Sandra&rft.aulast=Wiesner&rft.aufirst=Carolina&rft.date=2012-01-01&rft.volume=31&rft.issue=1&rft.spage=77&rft.isbn=&rft.btitle=&rft.title=Medical+anthropology&rft.issn=01459740&rft_id=info:doi/10.1080%2F01459740.2011.633947 LA - English DB - International Bibliography of the Social Sciences (IBSS) N1 - Date revised - 2013-06-12 N1 - Last updated - 2013-09-16 N1 - SubjectsTermNotLitGenreText - 11909 11943 10689; 7871 1077; 1939 3617 6220; 3254 5460 1615 8573 11325; 5779 4049; 11581 3617 6220; 13078; 11035; 94 386 14 DO - http://dx.doi.org/10.1080/01459740.2011.633947 ER - TY - JOUR T1 - Identification of Pigment Epithelium-Derived Factor Protein Forms with Distinct Activities on Tumor Cell Lines AN - 1221145566; 17366044 AB - Purpose. Pigment epithelium-derived factor (PEDF) is a multifunctional serpin. The purpose of this study is to identify PEDF protein forms and investigate their biological activities on tumor cell lines. Methods. Recombinant human PEDF proteins were purified by cation- and anion-exchange column chromatography. They were subjected to SDS-PAGE, IEF, deglycosylation, heparin affinity chromatography, and limited proteolysis. Cell viability, real-time electrical impedance of cells, and wound healing assays were performed using bladder and breast cancer cell lines, rat retinal R28, and human ARPE-19 cells. Results. Two PEDF protein peaks were identified after anion-exchange column chromatography: PEDF-1 eluting with lower ionic strength than PEDF-2. PEDF-1 had higher pI value and lower apparent molecular weight than PEDF-2. Both PEDF forms were glycosylated, bound to heparin, and had identical patterns by limited proteolysis. However, PEDF-2 emerged as being highly potent in lowering cell viability in all tumor cell lines tested, and in inhibiting tumor and ARPE-19 cell migration. In contrast, PEDF-1 minimally affected tumor cell viability and cell migration but protected R28 cells against death caused by serum starvation. Conclusion. Two distinct biochemical forms of PEDF varying in overall charge have distinct biological effects on tumor cell viability and migration. The existence of PEDF forms may explain the multifunctional modality of PEDF. JF - Journal of Biomedicine and Biotechnology AU - Subramanian, P AU - Deshpande, M AU - Locatelli-Hoops, S AU - Moghaddam-Taaheri, S AU - Gutierrez, D AU - Fitzgerald, D P AU - Guerrier, S AU - Rapp, M AU - Notario, V AU - Becerra, S P AD - Section of Protein Structure and Function, LRCMB, National Eye Institute, NEI, Bethesda, MD 20892-0608, USA, becerrap@nei.nih.gov Y1 - 2012/01// PY - 2012 DA - Jan 2012 PB - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States VL - 2012 SN - 1110-7243, 1110-7243 KW - Biotechnology and Bioengineering Abstracts KW - Affinity chromatography KW - Tumor cell lines KW - W 30925:Genetic Engineering UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1221145566?accountid=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+Biomedicine+and+Biotechnology&rft.atitle=Identification+of+Pigment+Epithelium-Derived+Factor+Protein+Forms+with+Distinct+Activities+on+Tumor+Cell+Lines&rft.au=Subramanian%2C+P%3BDeshpande%2C+M%3BLocatelli-Hoops%2C+S%3BMoghaddam-Taaheri%2C+S%3BGutierrez%2C+D%3BFitzgerald%2C+D+P%3BGuerrier%2C+S%3BRapp%2C+M%3BNotario%2C+V%3BBecerra%2C+S+P&rft.aulast=Subramanian&rft.aufirst=P&rft.date=2012-01-01&rft.volume=2012&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomedicine+and+Biotechnology&rft.issn=11107243&rft_id=info:doi/10.1155%2F2012%2F425907 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-11-01 N1 - Number of references - 1 N1 - Last updated - 2014-02-21 N1 - SubjectsTermNotLitGenreText - Tumor cell lines DO - http://dx.doi.org/10.1155/2012/425907 ER - TY - JOUR T1 - Prioritizing PubMed articles for the Comparative Toxicogenomic Database utilizing semantic information. AN - 1178668252; 23160415 AB - The Comparative Toxicogenomics Database (CTD) contains manually curated literature that describes chemical-gene interactions, chemical-disease relationships and gene-disease relationships. Finding articles containing this information is the first and an important step to assist manual curation efficiency. However, the complex nature of named entities and their relationships make it challenging to choose relevant articles. In this article, we introduce a machine learning framework for prioritizing CTD-relevant articles based on our prior system for the protein-protein interaction article classification task in BioCreative III. To address new challenges in the CTD task, we explore a new entity identification method for genes, chemicals and diseases. In addition, latent topics are analyzed and used as a feature type to overcome the small size of the training set. Applied to the BioCreative 2012 Triage dataset, our method achieved 0.8030 mean average precision (MAP) in the official runs, resulting in the top MAP system among participants. Integrated with PubTator, a Web interface for annotating biomedical literature, the proposed system also received a positive review from the CTD curation team. JF - Database : the journal of biological databases and curation AU - Kim, Sun AU - Kim, Won AU - Wei, Chih-Hsuan AU - Lu, Zhiyong AU - Wilbur, W John AD - National Center for Biotechnology Information, National Library of Medicine, National Institutes of Health, Bethesda, MD 20894, USA. Y1 - 2012 PY - 2012 DA - 2012 SP - 1 VL - 2012 KW - Index Medicus KW - Models, Theoretical KW - Periodicals as Topic KW - Databases, Factual KW - Toxicogenetics KW - PubMed KW - Semantics UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1178668252?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Database+%3A+the+journal+of+biological+databases+and+curation&rft.atitle=Prioritizing+PubMed+articles+for+the+Comparative+Toxicogenomic+Database+utilizing+semantic+information.&rft.au=Kim%2C+Sun%3BKim%2C+Won%3BWei%2C+Chih-Hsuan%3BLu%2C+Zhiyong%3BWilbur%2C+W+John&rft.aulast=Kim&rft.aufirst=Sun&rft.date=2012-01-01&rft.volume=2012&rft.issue=&rft.spage=bas042&rft.isbn=&rft.btitle=&rft.title=Database+%3A+the+journal+of+biological+databases+and+curation&rft.issn=1758-0463&rft_id=info:doi/10.1093%2Fdatabase%2Fbas042 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2013-04-24 N1 - Date created - 2012-11-19 N1 - Date revised - 2017-01-13 N1 - SuppNotes - Cited By: J Biomed Inform. 2002 Aug;35(4):247-59 [12755519] Database (Oxford). 2012;2012:bas037 [23180769] Proc Natl Acad Sci U S A. 2004 Apr 6;101 Suppl 1:5228-35 [14872004] BMC Bioinformatics. 2005;6:51 [15760478] BMC Bioinformatics. 2005;6 Suppl 1:S8 [15960842] Brief Bioinform. 2005 Dec;6(4):357-69 [16420734] AMIA Annu Symp Proc. 2006;:754-8 [17238442] Pac Symp Biocomput. 2008;:652-63 [18229723] BMC Bioinformatics. 2008;9 Suppl 3:S3 [18426548] Bioinformatics. 2008 Jul 1;24(13):i268-76 [18586724] J Biomed Inform. 2008 Aug;41(4):580-7 [18272430] Genome Biol. 2008;9 Suppl 2:S1 [18834487] Nucleic Acids Res. 2009 Jul;37(Web Server issue):W135-40 [19417065] Nucleic Acids Res. 2011 Jan;39(Database issue):D1067-72 [20864448] PLoS One. 2011;6(3):e14780 [21468321] BMC Bioinformatics. 2011;12 Suppl 8:S9 [22151252] BMC Bioinformatics. 2011;12 Suppl 8:S1 [22151647] Bioinformatics. 2012 Feb 15;28(4):597-8 [22199390] Bioinformatics. 2012 Jun 15;28(12):1633-40 [22500000] Database (Oxford). 2012;2012:bas041 [23160414] Pac Symp Biocomput. 2004;:238-49 [14992507] N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.1093/database/bas042 ER - TY - JOUR T1 - Introduction TT - Introduction AN - 1126537855; 201231182 AB - Abstract not available. JF - Politique etrangere AU - Nocetti, Julien AD - Chercheur associe, Centre Russie/NEI, IFRI Y1 - 2012///0, PY - 2012 DA - 0, 2012 SP - 246 EP - 248 PB - IFRI, Paris France IS - 2 SN - 0032-342X, 0032-342X KW - Politics KW - International Relations KW - Political Power KW - Internet KW - article KW - 9221: politics and society; politics and society UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1126537855?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Awpsa&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Politique+etrangere&rft.atitle=Introduction&rft.au=Nocetti%2C+Julien&rft.aulast=Nocetti&rft.aufirst=Julien&rft.date=2012-01-01&rft.volume=&rft.issue=2&rft.spage=246&rft.isbn=&rft.btitle=&rft.title=Politique+etrangere&rft.issn=0032342X&rft_id=info:doi/ LA - French DB - Worldwide Political Science Abstracts N1 - Date revised - 2012-11-01 N1 - Last updated - 2016-09-28 N1 - SubjectsTermNotLitGenreText - Politics; Internet; Political Power; International Relations ER - TY - JOUR T1 - Russia: Will the Web Reinvent Policy? TT - Russie: Le Web reinvente-t-il la politique? AN - 1126530193; 201230893 AB - The Web has seen a spectacular development in Russia, opening an intermediary political space through which protesters against the regime have been able to coalesce, as shown by the events in late 2011 and early 2012. As use of the Web in this way becomes more common, authorities are adapting by working to integrate digital means into the governance of the country through sophisticated network controls. In Russia in 2012, policy goes digital and digital gets politicized. Adapted from the source document. JF - Politique etrangere AU - Nocetti, Julien AD - Chercheur associe au centre Russie/NEI de I' Ifri Y1 - 2012///0, PY - 2012 DA - 0, 2012 SP - 277 EP - 289 PB - IFRI, Paris France IS - 2 SN - 0032-342X, 0032-342X KW - Russia KW - Governance KW - article KW - 9181: politics and communication; politics and communication UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1126530193?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Awpsa&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Politique+etrangere&rft.atitle=Russia%3A+Will+the+Web+Reinvent+Policy%3F&rft.au=Nocetti%2C+Julien&rft.aulast=Nocetti&rft.aufirst=Julien&rft.date=2012-01-01&rft.volume=&rft.issue=2&rft.spage=277&rft.isbn=&rft.btitle=&rft.title=Politique+etrangere&rft.issn=0032342X&rft_id=info:doi/ LA - French DB - Worldwide Political Science Abstracts N1 - Date revised - 2012-11-01 N1 - Last updated - 2016-09-28 N1 - SubjectsTermNotLitGenreText - Russia; Governance ER - TY - JOUR T1 - Associations of Television Viewing With Eating Behaviors in the 2009 Health Behaviour in School-aged Children Study AN - 1125260578; 16669199 AB - OBJECTIVE: To examine associations of television viewing with eating behaviors in a representative sample of US adolescents. DESIGN: Cross-sectional survey. SETTING: Public and private schools in the United States during the 2009-2010 school year. PARTICIPANTS: A total of 12 642 students in grades 5 to 10 (mean [SD] age, 13.4 [0.09] years; 86.5% participation). Main Exposures Television viewing (hours per day) and snacking while watching television (days per week). MAIN OUTCOME MEASURES: Eating ( greater than or equal to 1 instance per day) fruit, vegetables, sweets, and sugary soft drinks; eating at a fast food restaurant ( greater than or equal to 1 d/wk); and skipping breakfast ( greater than or equal to 1 d/wk). RESULTS: Television viewing was inversely related to intake of fruit (adjusted odds ratio, 0.92; 95% CI, 0.88-0.96) and vegetables (0.95; 0.91-1.00) and positively related to intake of candy (1.18; 1.14-1.23) and fast food (1.14; 1.09-1.19) and skipping breakfast (1.06; 1.02-1.10) after adjustment for socioeconomic factors, computer use, and physical activity. Television snacking was related to increased intake of fruit (adjusted odds ratio, 1.06; 95% CI, 1.02-1.10), candy (1.20; 1.16-1.24), soda (1.15; 1.11-1.18), and fast food (1.09; 1.06-1.13), independent of television viewing. The relationships of television viewing with fruit and vegetable intake and with skipping breakfast were essentially unchanged after adjustment for television snacking; the relationships with intake of candy, soda, and fast food were moderately attenuated. Age and race/ethnicity modified relationships of television viewing with soda and fast food intake and with skipping breakfast. CONCLUSION: Television viewing was associated with a cluster of unhealthy eating behaviors in US adolescents after adjustment for socioeconomic and behavioral covariates. JF - Archives of Pediatrics & Adolescent Medicine AU - Lipsky, Leah M AU - Iannotti, Ronald J AD - Author Affiliations: Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, Maryland Y1 - 2012 PY - 2012 DA - 2012 SP - 465 EP - 472 PB - American Medical Association, 515 N. State St. Chicago IL 60610 United States VL - 166 IS - 5 SN - 1072-4710, 1072-4710 KW - Health & Safety Science Abstracts KW - Fruits KW - USA KW - Age KW - Schools KW - Behavior KW - Physical activity KW - Television KW - Socioeconomics KW - Adolescents KW - Ethnic groups KW - H 0500:General UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1125260578?accountid=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=Archives+of+Pediatrics+%26+Adolescent+Medicine&rft.atitle=Associations+of+Television+Viewing+With+Eating+Behaviors+in+the+2009+Health+Behaviour+in+School-aged+Children+Study&rft.au=Lipsky%2C+Leah+M%3BIannotti%2C+Ronald+J&rft.aulast=Lipsky&rft.aufirst=Leah&rft.date=2012-01-01&rft.volume=166&rft.issue=5&rft.spage=465&rft.isbn=&rft.btitle=&rft.title=Archives+of+Pediatrics+%26+Adolescent+Medicine&rft.issn=10724710&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2013-06-28 N1 - SubjectsTermNotLitGenreText - Fruits; Age; Schools; Behavior; Physical activity; Television; Socioeconomics; Ethnic groups; Adolescents; USA ER - TY - JOUR T1 - Confronting The Urgent Challenge Of Diabetes: An Overview AN - 1125219973; 201207613 AB - The rising tide of diabetes has an unacceptable human and societal toll. Rates of all major forms of diabetes are increasing at enormous individual and societal cost: 8.3 percent of the US population is afflicted today, and financial costs reached $174 billion for 2007. A major cause of blindness, renal failure, amputation, and cardiovascular disease, diabetes also increases the risk of cancer and dementia and more than doubles individual health care costs. Control of glucose, blood pressure, and lipids improves outcomes. Yet diabetes management is nonetheless suboptimal, particularly in disproportionately affected poor and minority populations. Safer, less burdensome, and more personalized approaches to therapy are needed. People at high risk for type 2 diabetes must be identified if society is to realize the benefits of therapies proven to delay or prevent the disease. We have many of the tools we need to address this challenge, and we must apply them now. Adapted from the source document. JF - Health Affairs AU - Fradkin, Judith E AD - Division of Diabetes, Endocrinology, and Metabolic Diseases, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, in Bethesda, Maryland jf58s@nih.gov Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 12 EP - 19 PB - Project HOPE, Bethesda MD VL - 31 IS - 1 SN - 0278-2715, 0278-2715 KW - Risk KW - Management KW - Heart Diseases KW - Blood Pressure KW - Senility KW - United States of America KW - Cancer KW - Health Care Costs KW - Diabetes KW - article KW - 6140: illness & health care UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1125219973?accountid=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=Health+Affairs&rft.atitle=Confronting+The+Urgent+Challenge+Of+Diabetes%3A+An+Overview&rft.au=Fradkin%2C+Judith+E&rft.aulast=Fradkin&rft.aufirst=Judith&rft.date=2012-01-01&rft.volume=31&rft.issue=1&rft.spage=12&rft.isbn=&rft.btitle=&rft.title=Health+Affairs&rft.issn=02782715&rft_id=info:doi/10.1377%2Fhlthaff.2011.1150 LA - English DB - Social Services Abstracts N1 - Date revised - 2012-11-01 N1 - Last updated - 2016-09-28 N1 - SubjectsTermNotLitGenreText - Diabetes; Risk; Heart Diseases; Blood Pressure; Senility; Health Care Costs; Management; Cancer; United States of America DO - http://dx.doi.org/10.1377/hlthaff.2011.1150 ER - TY - JOUR T1 - Reproductive consequences of developmental phytoestrogen exposure AN - 1093461909; 16474097 AB - Phytoestrogens, estrogenic compounds derived from plants, are ubiquitous in human and animal diets. These chemicals are generally much less potent than estradiol but act via similar mechanisms. The most common source of phytoestrogen exposure to humans is soybean-derived foods that are rich in the isoflavones genistein and daidzein. These isoflavones are also found at relatively high levels in soy-based infant formulas. Phytoestrogens have been promoted as healthy alternatives to synthetic estrogens and are found in many dietary supplements. The aim of this review is to examine the evidence that phytoestrogen exposure, particularly in the developmentally sensitive periods of life, has consequences for future reproductive health. JF - Reproduction AU - Jefferson, Wendy N AU - Patisaul, Heather B AU - Williams, Carmen J AD - Reproductive Medicine Group, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences, National Institutes of Health, NIEHS/NIH/DHHS, PO Box 12233, MD E4-05, Research Triangle Park, North Carolina 27709, USA , Department of Biology, North Carolina State University, Raleigh, North Carolina 27695, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 247 EP - 260 PB - Portland Press Ltd., 59 Portland Place London W1N 3AJ United Kingdom VL - 143 IS - 3 SN - 1470-1626, 1470-1626 KW - Health & Safety Science Abstracts KW - Chemicals KW - Dietary supplements KW - Diets KW - Estrogens KW - Reproduction KW - Reviews KW - infant formulas KW - H 6000:Natural Disasters/Civil Defense/Emergency Management UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1093461909?accountid=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=Reproduction&rft.atitle=Reproductive+consequences+of+developmental+phytoestrogen+exposure&rft.au=Jefferson%2C+Wendy+N%3BPatisaul%2C+Heather+B%3BWilliams%2C+Carmen+J&rft.aulast=Jefferson&rft.aufirst=Wendy&rft.date=2012-01-01&rft.volume=143&rft.issue=3&rft.spage=247&rft.isbn=&rft.btitle=&rft.title=Reproduction&rft.issn=14701626&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Last updated - 2012-10-19 N1 - SubjectsTermNotLitGenreText - infant formulas; Chemicals; Diets; Estrogens; Dietary supplements; Reviews; Reproduction ER - TY - JOUR T1 - Close ties: an exploratory Colored Eco-Genetic Relationship Map (CEGRM) study of social connections of men in Familial Testicular Cancer (FTC) families AN - 1093458883; 17143840 AB - Background: Testicular cancer, while rare compared with other adult solid tumors, is the most common cancer in young men in northern Europe and North America. Risk factors include white race, positive family history, contralateral testicular cancer, cryptorchidism, infertility and testicular microlithiasis. As the genetic causes of familial clusters (Familial Testicular Cancer or FTC) are being sought, it is also important to understand the psycho-social experiences of members of FTC families. Methods: This is a cross-sectional examination via the Colored Eco-Genetic Relationship Map (CEGRM) of social connections reported by 49 men in FTC families participating in NCI research study 02-C-178. Results: The CEGRM was acceptable and feasible for use with men in FTC families, and valuable in understanding their social connections. These men have largely adjusted to the TC history in themselves and/or their relatives. They have considerable social and emotional support from family and friends, although there is wide variability in sources and types. Conclusions: The CEGRM focuses on men's social connections and close emotional bonds in FTC families. This action-oriented process of placing colored symbols on significant relationships uncovered previously under-appreciated emotions accompanying men's social exchanges. Most men in FTC families succeed in re-establishing a sense of normalcy in their lives and social connections, in the aftermath of a testicular cancer diagnosis. JF - Hereditary Cancer in Clinical Practice AU - Peters, June A AU - Kenen, Regina AU - Hoskins, Lindsey M AU - Glenn, Gladys M AU - Kratz, Christian AU - Greene, Mark H AD - Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, US Department of Health and Human Services, 6120 Executive Blvd, Rockville, MD, 20852 USA Y1 - 2012 PY - 2012 DA - 2012 SP - 2 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 10 IS - 1 SN - 1897-4287, 1897-4287 KW - Risk Abstracts KW - Cancer KW - Genetics KW - Historical account KW - Males KW - Risk factors KW - Tumors KW - infertility KW - North America KW - Europe KW - R2 23060:Medical and environmental health UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1093458883?accountid=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=Hereditary+Cancer+in+Clinical+Practice&rft.atitle=Close+ties%3A+an+exploratory+Colored+Eco-Genetic+Relationship+Map+%28CEGRM%29+study+of+social+connections+of+men+in+Familial+Testicular+Cancer+%28FTC%29+families&rft.au=Peters%2C+June+A%3BKenen%2C+Regina%3BHoskins%2C+Lindsey+M%3BGlenn%2C+Gladys+M%3BKratz%2C+Christian%3BGreene%2C+Mark+H&rft.aulast=Peters&rft.aufirst=June&rft.date=2012-01-01&rft.volume=10&rft.issue=1&rft.spage=2&rft.isbn=&rft.btitle=&rft.title=Hereditary+Cancer+in+Clinical+Practice&rft.issn=18974287&rft_id=info:doi/10.1186%2F1897-4287-10-2 L2 - http://www.hccpjournal.com/content/10/1/2 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-10-01 N1 - Number of references - 75 N1 - Last updated - 2012-10-19 N1 - SubjectsTermNotLitGenreText - Genetics; Historical account; infertility; Risk factors; Males; Tumors; Cancer; North America; Europe DO - http://dx.doi.org/10.1186/1897-4287-10-2 ER - TY - JOUR T1 - Collection = Connection: The Library Collection Management Blog AN - 1081862165; 201209934 AB - The Collection=Connection: The Library Collection Management Blog (http://www.collectionconnection.alcts.ala.org) is reviewed. The blog is sponsored by the Collection Management Section of the Association of Library Collections and Technical Services, a division of the American Library Association. The blog was launched on March 22, 2011 and its purpose is to present new ideas about library collections and to provide a forum to discuss changes in the practice of collection management and development. Collection Connection has a great deal of potential but is still embryonic in content. Adapted from the source document. JF - Technical Services Quarterly AU - Landesman, Betty AD - National Institutes of Health Library, Bethesda, MD Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 85 EP - 86 PB - Taylor & Francis, Philadelphia PA VL - 29 IS - 1 SN - 0731-7131, 0731-7131 KW - Reviews KW - Blogs KW - Collection management KW - article KW - 9.12: TECHNICAL SERVICES - COLLECTION DEVELOPMENT UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1081862165?accountid=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=Technical+Services+Quarterly&rft.atitle=Collection+%3D+Connection%3A+The+Library+Collection+Management+Blog&rft.au=Landesman%2C+Betty&rft.aulast=Landesman&rft.aufirst=Betty&rft.date=2012-01-01&rft.volume=29&rft.issue=1&rft.spage=85&rft.isbn=&rft.btitle=&rft.title=Technical+Services+Quarterly&rft.issn=07317131&rft_id=info:doi/10.1080%2F07317131.2012.624904 LA - English DB - Library & Information Science Abstracts (LISA) N1 - Date revised - 2012-10-01 N1 - Last updated - 2016-09-27 N1 - SubjectsTermNotLitGenreText - Collection management; Blogs; Reviews DO - http://dx.doi.org/10.1080/07317131.2012.624904 ER - TY - JOUR T1 - A parsimonious geomorphological unit hydrograph for rainfall-runoff modelling in small ungauged basins AN - 1034818225; 17032703 AB - In this study, a parsimonious hydrological modelling algorithm is proposed based on the automated DEM-based geomorphic characterization of runoff dynamics in scarcely monitored river basins. The proposed approach implements the instantaneous unit hydrograph (IUH) concept, estimated using the width function (WF), for characterizing the travel time distribution using just one parameter, the river network flow velocity. Hillslope velocities are defined using spatially-distributed empirical formulas based on slope and soil-use information extrapolated from digital topographic data. Case studies are presented for testing model performance and comparing simulated and observed hydrographs of 25 selected flood events, as well as investigating the differences with the geomorphological instantaneous unit hydrograph (GIUH) model results. The calibration of the WFIUH channel flow velocity parameter using the concentration time is investigated providing interesting insights for the use of such a method for hydrological prediction in ungauged basins. JF - Hydrological Sciences Journal/Journal des Sciences Hydrologiques AU - Grimaldi, S AU - Petroselli, A AU - Nardi, F AD - Dipartimento per l'Innovazione nei sistemi Biologici, Agroalimentari e Forestali (DIBAF Department), University of Tuscia, Viterbo, Italy,Honors Center of Italian Universities (H2CU), Sapienza University of Rome, Roma, Italy,Department of Mechanical and Aerospace Engineering, Polytechnic Institute of New York University, Six MetroTech Center, Brooklyn, New York, USA Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - 73 EP - 83 PB - Taylor & Francis Group Ltd., 2 Park Square Oxford OX14 4RN United Kingdom VL - 57 IS - 1 SN - 0262-6667, 0262-6667 KW - Water Resources Abstracts; ASFA 2: Ocean Technology Policy & Non-Living Resources; Aqualine Abstracts; Meteorological & Geoastrophysical Abstracts; Environment Abstracts KW - Prediction KW - Rainfall KW - Algorithms KW - Automation KW - Basins KW - River networks KW - Freshwater KW - Unit hydrographs KW - Hydrologic Models KW - Geomorphology KW - Stormwater runoff KW - Floods KW - Slopes KW - Channel Flow KW - Modelling KW - Instantaneous unit hydrographs KW - Fluvial morphology KW - Flow in channels KW - Hydrologic analysis KW - Mathematical models KW - River discharge KW - Velocity KW - River basins KW - Channels KW - Channel flow KW - Rainfall-runoff modeling KW - Unit Hydrographs KW - Runoff KW - SW 5010:Network design KW - Q2 09262:Methods and instruments KW - M2 556:General (556) KW - AQ 00005:Underground Services and Water Use KW - ENA 15:Renewable Resources-Terrestrial UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1034818225?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aaqualine&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Hydrological+Sciences+Journal%2FJournal+des+Sciences+Hydrologiques&rft.atitle=A+parsimonious+geomorphological+unit+hydrograph+for+rainfall-runoff+modelling+in+small+ungauged+basins&rft.au=Grimaldi%2C+S%3BPetroselli%2C+A%3BNardi%2C+F&rft.aulast=Grimaldi&rft.aufirst=S&rft.date=2012-01-01&rft.volume=57&rft.issue=1&rft.spage=73&rft.isbn=&rft.btitle=&rft.title=Hydrological+Sciences+Journal%2FJournal+des+Sciences+Hydrologiques&rft.issn=02626667&rft_id=info:doi/10.1080%2F02626667.2011.636045 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-08-01 N1 - Last updated - 2014-05-05 N1 - SubjectsTermNotLitGenreText - Fluvial morphology; Mathematical models; Channel flow; Geomorphology; River discharge; River basins; Runoff; Modelling; Instantaneous unit hydrographs; Flow in channels; Hydrologic analysis; Floods; Algorithms; Rainfall-runoff modeling; River networks; Unit hydrographs; Channels; Prediction; Stormwater runoff; Rainfall; Velocity; Basins; Hydrologic Models; Automation; Unit Hydrographs; Slopes; Channel Flow; Freshwater DO - http://dx.doi.org/10.1080/02626667.2011.636045 ER - TY - JOUR T1 - A Bayesian approach to mixture cure models with spatial frailties for population-based cancer relative survival data AN - 1031279059; 4317954 AB - As the treatments of cancer progress, a certain number of cancers are curable if diagnosed early. In population-based cancer survival studies, cure is said to occur when mortality rate of the cancer patients returns to the same level as that expected for the general cancer-free population. The estimates of cure fraction are of interest to both cancer patients and health policy makers. Mixture cure models have been widely used because the model is easy to interpret by separating the patients into two distinct groups. Usually parametric models are assumed for the latent distribution for the uncured patients. The estimation of cure fraction from the mixture cure model may be sensitive to misspecification of latent distribution. We propose a Bayesian approach to mixture cure model for population-based cancer survival data, which can be extended to county-level cancer survival data. Instead of modeling the latent distribution by a fixed parametric distribution, we use a finite mixture of the union of the lognormal, loglogistic, and Weibull distributions. The parameters are estimated using the Markov chain Monte Carlo method. Simulation study shows that the Bayesian method using a finite mixture latent distribution provides robust inference of parameter estimates. The proposed Bayesian method is applied to relative survival data for colon cancer patients from the Surveillance, Epidemiology, and End Results (SEER) Program to estimate the cure fractions. JF - Canadian journal of statistics AU - Tiwari, Ram C AU - Yu, Binbing AD - National Institute on Aging, USA Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - 40 EP - 54 VL - 40 IS - 1 SN - 0319-5724, 0319-5724 KW - Economics KW - Monte Carlo simulation KW - Distribution KW - Survival KW - Population KW - Health policy KW - Estimation KW - Data analysis KW - Cancer KW - Bayesian method UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1031279059?accountid=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=A+Bayesian+approach+to+mixture+cure+models+with+spatial+frailties+for+population-based+cancer+relative+survival+data&rft.au=Tiwari%2C+Ram+C%3BYu%2C+Binbing&rft.aulast=Tiwari&rft.aufirst=Ram&rft.date=2012-01-01&rft.volume=40&rft.issue=1&rft.spage=40&rft.isbn=&rft.btitle=&rft.title=Canadian+journal+of+statistics&rft.issn=03195724&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 - 4403 7854; 9846; 1512 3865 4025; 5788 11888 10472; 3641 12233; 8268 12265 3865 4025 10214 12224 971 12228 10919; 3279 971 3286; 1939 3617 6220; 12430 ER - TY - JOUR T1 - Lipoprotein biosynthesis by prolipoprotein diacylglyceryl transferase is required for efficient spore germination and full virulence of Bacillus anthracis AN - 1028079468; 16161235 AB - Bacterial lipoproteins play a crucial role in virulence in some Gram-positive bacteria. However, the role of lipoprotein biosynthesis in Bacillus anthracis is unknown. We created a B.anthracis mutant strain altered in lipoproteins by deleting the lgt gene encoding the enzyme prolipoprotein diacylglyceryl transferase, which attaches the lipid anchor to prolipoproteins. 14C-palmitate labelling confirmed that the mutant strain lacked lipoproteins, and hydrocarbon partitioning showed it to have decreased surface hydrophobicity. The anthrax toxin proteins were secreted from the mutant strain at nearly the same levels as from the wild-type strain. The TLR2-dependent TNF- alpha response of macrophages to heat-killed lgt mutant bacteria was reduced. Spores of the lgt mutant germinated inefficiently in vitro and in mouse skin. As a result, in a murine subcutaneous infection model, lgt mutant spores had markedly attenuated virulence. In contrast, vegetative cells of the lgt mutant were as virulent as those of the wild-type strain. Thus, lipoprotein biosynthesis in B.anthracis is required for full virulence in a murine infection model. JF - Molecular Microbiology AU - Okugawa, Shu AU - Moayeri, Mahtab AU - Pomerantsev, Andrei P AU - Sastalla, Inka AU - Crown, Devorah AU - Gupta, Pradeep K AU - Leppla, Stephen H AD - Laboratory of Bacterial Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 96 EP - 109 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 83 IS - 1 SN - 0950-382X, 0950-382X KW - Biotechnology and Bioengineering Abstracts; Toxicology Abstracts; Microbiology Abstracts B: Bacteriology KW - Macrophages KW - Skin KW - Hydrocarbons KW - Gram-positive bacteria KW - Lipids KW - Spore germination KW - Animal models KW - Enzymes KW - Hydrophobicity KW - Bacillus anthracis KW - Infection KW - Vegetative cells KW - Toxins KW - Virulence KW - Lipoproteins KW - Anthrax KW - Tumor necrosis factor- alpha KW - J 02410:Animal Diseases KW - X 24370:Natural Toxins KW - W 30940:Products UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028079468?accountid=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=Lipoprotein+biosynthesis+by+prolipoprotein+diacylglyceryl+transferase+is+required+for+efficient+spore+germination+and+full+virulence+of+Bacillus+anthracis&rft.au=Okugawa%2C+Shu%3BMoayeri%2C+Mahtab%3BPomerantsev%2C+Andrei+P%3BSastalla%2C+Inka%3BCrown%2C+Devorah%3BGupta%2C+Pradeep+K%3BLeppla%2C+Stephen+H&rft.aulast=Okugawa&rft.aufirst=Shu&rft.date=2012-01-01&rft.volume=83&rft.issue=1&rft.spage=96&rft.isbn=&rft.btitle=&rft.title=Molecular+Microbiology&rft.issn=0950382X&rft_id=info:doi/10.1111%2Fj.1365-2958.2011.07915.x LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Document feature - figure 9 N1 - Last updated - 2016-04-29 N1 - SubjectsTermNotLitGenreText - Macrophages; Skin; Hydrocarbons; Lipids; Gram-positive bacteria; Spore germination; Animal models; Enzymes; Hydrophobicity; Infection; Vegetative cells; Toxins; Virulence; Lipoproteins; Anthrax; Tumor necrosis factor- alpha; Bacillus anthracis DO - http://dx.doi.org/10.1111/j.1365-2958.2011.07915.x ER - TY - JOUR T1 - Patient-Derived Xenografts of Non Small Cell Lung Cancer: Resurgence of an Old Model for Investigation of Modern Concepts of Tailored Therapy and Cancer Stem Cells AN - 1028035321; 16827751 AB - Current chemotherapy regimens have unsatisfactory results in most advanced solid tumors. It is therefore imperative to devise novel therapeutic strategies and to optimize selection of patients, identifying early those who could benefit from available treatments. Mouse models are the most valuable tool for preclinical evaluation of novel therapeutic strategies in cancer and, among them, patient-derived xenografts models (PDX) have made a recent comeback in popularity. These models, obtained by direct implants of tissue fragments in immunocompromised mice, have great potential in drug development studies because they faithfully reproduce the patient's original tumor for both immunohistochemical markers and genetic alterations as well as in terms of response to common therapeutics They also maintain the original tumor heterogeneity, allowing studies of specific cellular subpopulations, including their modulation after drug treatment. Moreover PDXs maintain at least some aspects of the human microenvironment for weeks with the complete substitution with murine stroma occurring only after 2-3 passages in mouse and represent therefore a promising model for studies of tumor-microenvironment interaction. This review summarizes our present knowledge on mouse preclinical cancer models, with a particular attention on patient-derived xenografts of non small cell lung cancer and their relevance for preclinical and biological studies. JF - Journal of Biomedicine and Biotechnology AU - Moro, Massimo AU - Bertolini, Giulia AU - Tortoreto, Monica AU - Pastorino, Ugo AU - Sozzi, Gabriella AU - Roz, Luca AD - Tumor Genomics Unit, Department of Experimental Oncology and Molecular Medicine, IRCCS Foundation National Cancer Institute, Via Venezian 1, 20133 Milan, Italy, luca.roz@istitutotumori.mi.it Y1 - 2012/01// PY - 2012 DA - Jan 2012 PB - Hindawi Publishing Corporation, P.O. Box 3079 Cuyahoga Falls OH 44223 United States VL - 2012 SN - 1110-7243, 1110-7243 KW - Biotechnology and Bioengineering Abstracts KW - Animal models KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028035321?accountid=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+Biomedicine+and+Biotechnology&rft.atitle=Patient-Derived+Xenografts+of+Non+Small+Cell+Lung+Cancer%3A+Resurgence+of+an+Old+Model+for+Investigation+of+Modern+Concepts+of+Tailored+Therapy+and+Cancer+Stem+Cells&rft.au=Moro%2C+Massimo%3BBertolini%2C+Giulia%3BTortoreto%2C+Monica%3BPastorino%2C+Ugo%3BSozzi%2C+Gabriella%3BRoz%2C+Luca&rft.aulast=Moro&rft.aufirst=Massimo&rft.date=2012-01-01&rft.volume=2012&rft.issue=&rft.spage=&rft.isbn=&rft.btitle=&rft.title=Journal+of+Biomedicine+and+Biotechnology&rft.issn=11107243&rft_id=info:doi/10.1155%2F2012%2F568567 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Number of references - 1 N1 - Last updated - 2014-02-21 N1 - SubjectsTermNotLitGenreText - Animal models DO - http://dx.doi.org/10.1155/2012/568567 ER - TY - JOUR T1 - The CMG (CDC45/RecJ, MCM, GINS) complex is a conserved component of the DNA replication system in all archaea and eukaryotes AN - 1028030123; 16884959 AB - Background: In eukaryotes, the CMG (CDC45, MCM, GINS) complex containing the replicative helicase MCM is a key player in DNA replication. Archaeal homologs of the eukaryotic MCM and GINS proteins have been identified but until recently no homolog of the CDC45 protein was known. Two recent developments, namely the discovery of archaeal G INS- a ssociated n uclease (GAN) that belongs to the RecJ family of the DHH hydrolase superfamily and the demonstration of homology between the DHH domains of CDC45 and RecJ, show that at least some Archaea possess a full complement of homologs of the CMG complex subunits. Here we present the results of in-depth phylogenomic analysis of RecJ homologs in archaea. Results: We confirm and extend the recent hypothesis that CDC45 is the eukaryotic ortholog of the bacterial and archaeal RecJ family nucleases. At least one RecJ homolog was identified in all sequenced archaeal genomes, with the single exception of Caldivirga maquilingensis. These proteins include previously unnoticed remote RecJ homologs with inactivated DHH domain in Thermoproteales. Combined with phylogenetic tree reconstruction of diverse eukaryotic, archaeal and bacterial DHH subfamilies, this analysis yields a complex scenario of RecJ family evolution in Archaea which includes independent inactivation of the nuclease domain in Crenarchaeota and Halobacteria, and loss of this domain in Methanococcales. Conclusions: The archaeal complex of a CDC45/RecJ homolog, MCM and GINS is homologous and most likely functionally analogous to the eukaryotic CMG complex, and appears to be a key component of the DNA replication machinery in all Archaea. It is inferred that the last common archaeo-eukaryotic ancestor encoded a CMG complex that contained an active nuclease of the RecJ family. The inactivated RecJ homologs in several archaeal lineages most likely are dedicated structural components of replication complexes. Reviewers: This article was reviewed by Prof. Patrick Forterre, Dr. Stephen John Aves (nominated by Dr. Purificacion Lopez-Garcia) and Prof. Martijn Huynen. For the full reviews, see the Reviewers' Comments section. JF - Biology Direct AU - Makarova, Kira S AU - Koonin, Eugene V AU - Kelman, Zvi AD - National Center for Biotechnology Information, NLM, National Institutes of Health, Bethesda, Maryland 20894, USA Y1 - 2012///0, PY - 2012 DA - 0, 2012 SP - 7 PB - BioMed Central Ltd., Middlesex House London W1T 4LB United Kingdom VL - 7 IS - 1 SN - 1745-6150, 1745-6150 KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - Genomes KW - Phylogeny KW - DNA biosynthesis KW - Methanococcales KW - Archaea KW - Replication KW - Thermoproteales KW - Nuclease KW - Caldivirga maquilingensis KW - Aves KW - hydrolase KW - Crenarchaeota KW - Homology KW - Reviews KW - Cdc45 protein KW - DNA helicase KW - Evolution KW - J 02310:Genetics & Taxonomy KW - N 14820:DNA Metabolism & Structure UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1028030123?accountid=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=Biology+Direct&rft.atitle=The+CMG+%28CDC45%2FRecJ%2C+MCM%2C+GINS%29+complex+is+a+conserved+component+of+the+DNA+replication+system+in+all+archaea+and+eukaryotes&rft.au=Makarova%2C+Kira+S%3BKoonin%2C+Eugene+V%3BKelman%2C+Zvi&rft.aulast=Makarova&rft.aufirst=Kira&rft.date=2012-01-01&rft.volume=7&rft.issue=1&rft.spage=7&rft.isbn=&rft.btitle=&rft.title=Biology+Direct&rft.issn=17456150&rft_id=info:doi/10.1186%2F1745-6150-7-7 L2 - http://www.biology-direct.com/content/7/1/7 LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-07-01 N1 - Number of references - 38 N1 - Last updated - 2016-04-13 N1 - SubjectsTermNotLitGenreText - Phylogeny; Genomes; hydrolase; DNA biosynthesis; Homology; Replication; Reviews; Nuclease; Cdc45 protein; DNA helicase; Evolution; Aves; Methanococcales; Crenarchaeota; Archaea; Thermoproteales; Caldivirga maquilingensis DO - http://dx.doi.org/10.1186/1745-6150-7-7 ER - TY - JOUR T1 - Tandem autologous stem cell transplantation in multiple myeloma after high-dose chemotherapy with two separate collections: single institution experience. AN - 1024096061; 22668021 AB - Presented is a retrospective analysis of multiple myeloma patients transplanted at our institution between November 1993 and August 2007. The objective of this analysis was to assess the feasibility and toxicity of tandem autologous stem cell transplantation (T-ASCT) when stem cells were harvested before first and before second transplantation separately. A total of 90 patients transplanted in our center were analyzed, of whom 43 patients were in tandem transplantation group.The overall response rate (ORR) was 83.7% and 95.1%, estimated five-year overall survival (OS) was 40.1% and 60.0%, probability of five-year event-free survival (EFS) was 18.2% and 25.6%, transplant related mortality (TRM) was 6.3% and 4.6% in the single and tandem transplant group, respectively. In multivariable analysis of all 90 patients, tandem transplantation and ORR attained after induction therapy were favourable prognostic factors for OS (p=0.024 and p=0.002) and EFS (p=0.036 and p=0.008), respectively. In conclusion, tandem transplantation with two separate stem cell harvests, performed separately before the each transplantation, is feasible in majority of patients with acceptable toxicity. JF - Neoplasma AU - Ladicka, M AU - Ballova, V AU - Drgona, L AU - Vranovsky, A AU - Lakota, J AD - Bone Marrow Transplantation Unit, National Cancer Institute, Bratislava, Slovakia. Y1 - 2012 PY - 2012 DA - 2012 SP - 551 EP - 558 VL - 59 IS - 5 SN - 0028-2685, 0028-2685 KW - Vincristine KW - 5J49Q6B70F KW - Dexamethasone KW - 7S5I7G3JQL KW - Doxorubicin KW - 80168379AG KW - Index Medicus KW - Dexamethasone -- therapeutic use KW - Transplantation Conditioning KW - Combined Modality Therapy KW - Humans KW - Prognosis KW - Retrospective Studies KW - Aged KW - Transplantation, Autologous KW - Survival Rate KW - Vincristine -- therapeutic use KW - Adult KW - Doxorubicin -- therapeutic use KW - Middle Aged KW - Female KW - Male KW - Remission Induction KW - Multiple Myeloma -- therapy KW - Hematopoietic Stem Cell Transplantation KW - Antineoplastic Combined Chemotherapy Protocols -- therapeutic use KW - Multiple Myeloma -- mortality UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1024096061?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Atoxline&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Neoplasma&rft.atitle=Tandem+autologous+stem+cell+transplantation+in+multiple+myeloma+after+high-dose+chemotherapy+with+two+separate+collections%3A+single+institution+experience.&rft.au=Ladicka%2C+M%3BBallova%2C+V%3BDrgona%2C+L%3BVranovsky%2C+A%3BLakota%2C+J&rft.aulast=Ladicka&rft.aufirst=M&rft.date=2012-01-01&rft.volume=59&rft.issue=5&rft.spage=551&rft.isbn=&rft.btitle=&rft.title=Neoplasma&rft.issn=00282685&rft_id=info:doi/10.4149%2Fneo_2012_071 LA - English DB - ProQuest Environmental Science Collection N1 - Date completed - 2012-09-27 N1 - Date created - 2012-07-06 N1 - Date revised - 2017-01-13 N1 - Last updated - 2017-01-18 DO - http://dx.doi.org/10.4149/neo_2012_071 ER - TY - JOUR T1 - Assessing the accuracy of a multiphase diagnosis procedure for dementia AN - 1021121462; 4305255 AB - Multiphase (stage) designs that involve more than two phases are increasingly used by clinicians and psychologists for diagnosis and screening of dementia and many other diseases, e.g. colorectal or breast cancer. The multiphase design is an extension of the commonly used two-phase design, where an inexpensive initial screening test is followed by a gold standard. In a typical three-phase design, the screening test in phase 1 usually has high sensitivity but relatively low specificity. Phase 2 consists of a repeated application of the initial screening test and/or a more confirmatory test and then the gold standard test is used in phase 3. In such designs, both the verification process and the accuracy of each screening test may depend on patients characteristics. In addition, multiple-screening tests are correlated and composite decision rules may be used. However, no estimation methods exist for assessing the accuracy of a multiphase diagnosis procedure. To address these problems, we develop a method of estimating the diagnostic accuracy for each individual test and for the whole diagnostic procedure in a multiphase design in the presence of verification bias. Simulation studies are carried out to evaluate the performance of the method proposed and to compare different strategies of combining sequential tests. The method proposed is applied to data from a multiphase study of dementia. Reprinted by permission of Blackwell Publishers JF - Journal of the Royal Statistical Society AU - Yu, Binbing AU - Zhou, Chuan AD - National Institute on Aging ; University of Washington Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - 67 EP - 81 VL - 61 IS - 1 SN - 0035-9254, 0035-9254 KW - Economics KW - Measurement KW - Estimation KW - Medical treatment KW - Performance KW - Dementia KW - Bias KW - Design UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1021121462?accountid=14244 L2 - http://vb3lk7eb4t.search.serialssolutions.com/?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&rfr_id=info:sid/ProQ%3Aibss&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.jtitle=Journal+of+the+Royal+Statistical+Society&rft.atitle=Assessing+the+accuracy+of+a+multiphase+diagnosis+procedure+for+dementia&rft.au=Yu%2C+Binbing%3BZhou%2C+Chuan&rft.aulast=Yu&rft.aufirst=Binbing&rft.date=2012-01-01&rft.volume=61&rft.issue=1&rft.spage=67&rft.isbn=&rft.btitle=&rft.title=Journal+of+the+Royal+Statistical+Society&rft.issn=00359254&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 - Dementia; 7890 5792 10484; 3458 2991 9429 9416 2153; 4403 7854; 1565 1362 2688 2449 10404; 9390; 7854 ER - TY - JOUR T1 - Lung Manifestations in an Autopsy-Based Series of Pulmonary or Disseminated Nontuberculous Mycobacterial Disease AN - 1020850882; 16669280 AB - BACKGROUND: Comparisons of lung manifestations in primary pulmonary vs disseminated nontuberculous mycobacterial disease have not been well described. The clinical, histopathologic, and radiologic disease manifestations of primary pulmonary or disseminated nontuberculous mycobacterial disease were compared in an autopsy series. METHODS: Medical and microbiologic records, autopsy reports, histopathologic slides of the lungs, and chest CT scans were reviewed on patients at the National Institutes of Health with nontuberculous mycobacterial disease who died between 1996 and 2010. RESULTS: The 11 patients with primary pulmonary nontuberculous mycobacterial disease were predominantly female (n = 9), with symptom onset at median 50 (range 35, 71) years and time from onset until death of 12 (3, 34) years. Bronchiectasis with cavity formation and necrotizing bronchocentric granulomatous inflammation predominated but extrapulmonary infection was absent. The five patients with disseminated disease and systemic immune defects were all men with age at onset of 2 (0.33, 33) years and time from onset of disease until death of 9 (1, 31) years. Miliary nodules and/or consolidation with poorly formed granulomatous inflammation were noted in the three disseminated patients with mycobacterial lung involvement. Significant extrapulmonary infection was noted in all five with a relative paucity of lung findings. CONCLUSIONS: Nontuberculous mycobacteria can cause progressive, fatal disease. Primary pulmonary disease is bronchocentric and lacks extrathoracic infection consistent with impaired airway surface defenses. In contrast, fatal disseminated infections involving the lung have hematogenous spread, extensive extrathoracic disease, and a distinct pulmonary histopathology consistent with systemic immune dysfunction. JF - Chest AU - O'Connell, Meghan L AU - Birkenkamp, Kate E AU - Kleiner, David E AU - Folio, Les R AU - Holland, Steven M AU - Olivier, Kenneth N AD - Laboratory of Clinical Infectious Diseases (Mss O'Connell and Birkenkamp and Drs Holland and Olivier), National Institute of Allergy and Infectious Diseases Y1 - 2012 PY - 2012 DA - 2012 SP - 1203 EP - 1209 PB - American College of Chest Physicians, 3300 Dundee R. Northbrook IL 60062 United States VL - 141 IS - 5 SN - 0012-3692, 0012-3692 KW - Microbiology Abstracts B: Bacteriology KW - Age KW - Autopsy KW - Bronchiectasis KW - Cavities KW - Chest KW - Computed tomography KW - Disseminated infection KW - Inflammation KW - Lung diseases KW - Nodules KW - Respiratory tract KW - Mycobacterium KW - J 02400:Human Diseases UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1020850882?accountid=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=Chest&rft.atitle=Lung+Manifestations+in+an+Autopsy-Based+Series+of+Pulmonary+or+Disseminated+Nontuberculous+Mycobacterial+Disease&rft.au=O%27Connell%2C+Meghan+L%3BBirkenkamp%2C+Kate+E%3BKleiner%2C+David+E%3BFolio%2C+Les+R%3BHolland%2C+Steven+M%3BOlivier%2C+Kenneth+N&rft.aulast=O%27Connell&rft.aufirst=Meghan&rft.date=2012-01-01&rft.volume=141&rft.issue=5&rft.spage=1203&rft.isbn=&rft.btitle=&rft.title=Chest&rft.issn=00123692&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-06-01 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Cavities; Autopsy; Age; Bronchiectasis; Disseminated infection; Computed tomography; Lung diseases; Chest; Nodules; Respiratory tract; Inflammation; Mycobacterium ER - TY - JOUR T1 - CB1 -- Cannabinoid Receptor Antagonist Effects on Cortisol in Cannabis-Dependent Men AN - 1018376406; 201210697 AB - Background: The endocannabinoid system modulates the hypothalamic-pituitary-adrenal (HPA) axis, but the effect of cannabinoid type 1 (CB1) receptor antagonism following chronic CB1 receptor stimulation in humans is unknown. Objectives: To evaluate effects of the CB1 receptor antagonist rimonabant on the HPA axis in cannabis-dependent individuals. Methods: Fourteen daily cannabis smokers received increasingly frequent 20 mg oral delta-9-tetrahydrocannabinol (THC) doses (60-120 mg/day) over 8 days to standardize cannabis tolerance. Concurrent with the last THC dose, double-blind placebo or rimonabant (20 or 40 mg) was administered. Cannabinoid, rimonabant, and cortisol plasma concentrations were measured 1.5 hours prior to rimonabant administration and 2.0, 5.5, and 12.5 hours post-dose. Results: Ten participants completed before premature study termination due to rimonabant's withdrawal from development. Five participants received 20 mg, three received 40 mg, and two placebo. There was a significant positive association between rimonabant concentration and change in cortisol concentration from baseline (r = .53, p 40 mg might elicit cortisol changes, confirming a role for CB1 receptors in modulating the HPA axis in humans. Adapted from the source document. JF - The American Journal of Drug and Alcohol Abuse AU - Goodwin, Robert S AU - Baumann, Michael H AU - Gorelick, David A AU - Schwilke, Eugene AU - Schwope, David M AU - Darwin, William D AU - Kelly, Deanna L AU - Schroeder, Jennifer R AU - Ortemann-Renon, Catherine AU - Bonnet, Denis AU - Huestis, Marilyn A AD - Chemistry and Drug Metabolism, Intramural Research Program, National Institute on Drug Abuse, National Institutes of Health Y1 - 2012/01// PY - 2012 DA - January 2012 SP - 114 EP - 119 PB - Taylor & Francis Inc., Philadelphia, PA VL - 38 IS - 1 SN - 0095-2990, 0095-2990 KW - cortisol, rimonabant, cannabis, antagonist, withdrawal KW - Stimulation KW - Cortisol KW - Cannabis KW - Dosage KW - Concentration KW - Premature KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1018376406?accountid=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=CB1+--+Cannabinoid+Receptor+Antagonist+Effects+on+Cortisol+in+Cannabis-Dependent+Men&rft.au=Goodwin%2C+Robert+S%3BBaumann%2C+Michael+H%3BGorelick%2C+David+A%3BSchwilke%2C+Eugene%3BSchwope%2C+David+M%3BDarwin%2C+William+D%3BKelly%2C+Deanna+L%3BSchroeder%2C+Jennifer+R%3BOrtemann-Renon%2C+Catherine%3BBonnet%2C+Denis%3BHuestis%2C+Marilyn+A&rft.aulast=Goodwin&rft.aufirst=Robert&rft.date=2012-01-01&rft.volume=38&rft.issue=1&rft.spage=114&rft.isbn=&rft.btitle=&rft.title=The+American+Journal+of+Drug+and+Alcohol+Abuse&rft.issn=00952990&rft_id=info:doi/10.3109%2F00952990.2011.600398 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-06-01 N1 - Last updated - 2016-09-27 N1 - CODEN - AJDABD N1 - SubjectsTermNotLitGenreText - Cortisol; Dosage; Cannabis; Concentration; Stimulation; Premature DO - http://dx.doi.org/10.3109/00952990.2011.600398 ER - TY - JOUR T1 - Sugars in diet and risk of cancer in the NIH-AARP Diet and Health Study? AN - 1017961390; 16689646 AB - Prospective epidemiologic data on the effects of different types of dietary sugars on cancer incidence have been limited. In this report, we investigated the association of total sugars, sucrose, fructose, added sugars, added sucrose and added fructose in the diet with risk of 24 malignancies. Participants (n = 435,674) aged 50-71 years from the NIH-AARP Diet and Health Study were followed for 7.2 years. The intake of individual sugars was assessed using a 124-item food frequency questionnaire (FFQ). Cox proportional hazards regression was used to estimate hazard ratios (HR) and 95% confidence intervals (CI) in multivariable models adjusted for confounding factors pertinent to individual cancers. We identified 29,099 cancer cases in men and 13,355 cases in women. In gender-combined analyses, added sugars were positively associated with risk of esophageal adenocarcinoma (HRQ5 vs. Q1: 1.62, 95% CI: 1.07-2.45; ptrend = 0.01), added fructose was associated with risk of small intestine cancer (HRQ5 vs. Q1: 2.20, 95% CI: 1.16-4.16; ptrend = 0.009) and all investigated sugars were associated with increased risk of pleural cancer. In women, all investigated sugars were inversely associated with ovarian cancer. We found no association between dietary sugars and risk of colorectal or any other major cancer. Measurement error in FFQ-reported dietary sugars may have limited our ability to obtain more conclusive findings. Statistically significant associations observed for the rare cancers are of interest and warrant further investigation. JF - International Journal of Cancer AU - Tasevska, Natasa AU - Jiao, Li AU - Cross, Amanda J AU - Kipnis, Victor AU - Subar, Amy F AU - Hollenbeck, Albert AU - Schatzkin, Arthur AU - Potischman, Nancy AD - Applied Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD, tasevskan@gmail.com Y1 - 2012/01/01/ PY - 2012 DA - 2012 Jan 01 SP - 159 EP - 169 PB - Wiley-Blackwell, 111 River Street Hoboken NJ 07030-5774 United States VL - 130 IS - 1 SN - 1097-0215, 1097-0215 KW - Health & Safety Science Abstracts; Risk Abstracts KW - Cancer KW - Diets KW - Ovarian carcinoma 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/1017961390?accountid=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=Sugars+in+diet+and+risk+of+cancer+in+the+NIH-AARP+Diet+and+Health+Study%3F&rft.au=Tasevska%2C+Natasa%3BJiao%2C+Li%3BCross%2C+Amanda+J%3BKipnis%2C+Victor%3BSubar%2C+Amy+F%3BHollenbeck%2C+Albert%3BSchatzkin%2C+Arthur%3BPotischman%2C+Nancy&rft.aulast=Tasevska&rft.aufirst=Natasa&rft.date=2012-01-01&rft.volume=130&rft.issue=1&rft.spage=159&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Cancer&rft.issn=10970215&rft_id=info:doi/10.1002%2Fijc.25990 L2 - http://onlinelibrary.wiley.com/doi/10.1002/ijc.25990/abstract LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2012-08-10 N1 - SubjectsTermNotLitGenreText - Diets; ovarian carcinoma; Ovarian carcinoma; Cancer DO - http://dx.doi.org/10.1002/ijc.25990 ER - TY - JOUR T1 - Temporal shifts in the skin microbiome associated with disease flares and treatment in children with atopic dermatitis AN - 1014108218; 16669332 AB - Atopic dermatitis (AD) has long been associated with Staphylococcus aureus skin colonization or infection and is typically managed with regimens that include antimicrobial therapies. However, the role of microbial communities in the pathogenesis of AD is incompletely characterized. To assess the relationship between skin microbiota and disease progression, 16S ribosomal RNA bacterial gene sequencing was performed on DNA obtained directly from serial skin sampling of children with AD. The composition of bacterial communities was analyzed during AD disease states to identify characteristics associated with AD flares and improvement post-treatment. We found that microbial community structures at sites of disease predilection were dramatically different in AD patients compared with controls. Microbial diversity during AD flares was dependent on the presence or absence of recent AD treatments, with even intermittent treatment linked to greater bacterial diversity than no recent treatment. Treatment-associated changes in skin bacterial diversity suggest that AD treatments diversify skin bacteria preceding improvements in disease activity. In AD, the proportion of Staphylococcus sequences, particularly S. aureus, was greater during disease flares than at baseline or post-treatment, and correlated with worsened disease severity. Representation of the skin commensal S. epidermidis also significantly increased during flares. Increases in Streptococcus, Propionibacterium, and Corynebacterium species were observed following therapy. These findings reveal linkages between microbial communities and inflammatory diseases such as AD, and demonstrate that as compared with culture-based studies, higher resolution examination of microbiota associated with human disease provides novel insights into global shifts of bacteria relevant to disease progression and treatment. JF - Genome Research AU - Kong, Heidi H AU - Oh, Julia AU - Deming, Clay AU - Conlan, Sean AU - Grice, Elizabeth A AU - Beatson, Melony A AU - Nomicos, Effie AU - Polley, Eric C AU - Komarow, Hirsh D AU - Murray, Patrick R AU - Turner, Maria L AU - Segre, Julia A AD - Dermatology Branch, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland 20892, USA Y1 - 2012///0, PY - 2012 DA - 0, 2012 SP - 850 EP - 859 PB - Cold Spring Harbor Laboratory Press, Fulfillment & Distribution Dept. Woodbury NY 11797-2924 United States VL - 22 IS - 5 SN - 1088-9051, 1088-9051 KW - Genetics Abstracts; Microbiology Abstracts A: Industrial & Applied Microbiology; Biochemistry Abstracts 2: Nucleic Acids KW - Streptococcus KW - Skin KW - Commensals KW - Infection KW - Children KW - Corynebacterium KW - Antimicrobial agents KW - Colonization KW - DNA sequencing KW - Inflammatory diseases KW - Skin diseases KW - Community structure KW - DNA KW - Sampling KW - Propionibacterium KW - Staphylococcus aureus KW - rRNA 16S KW - Atopic dermatitis KW - A 01340:Antibiotics & Antimicrobials KW - N 14815:Nucleotide Sequence KW - G 07770:Bacteria UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1014108218?accountid=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=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 revised - 2012-05-01 N1 - Last updated - 2016-02-04 N1 - SubjectsTermNotLitGenreText - Skin; Commensals; Children; Infection; Antimicrobial agents; Colonization; DNA sequencing; Skin diseases; Inflammatory diseases; Community structure; DNA; Sampling; Atopic dermatitis; rRNA 16S; Streptococcus; Staphylococcus aureus; Propionibacterium; Corynebacterium ER - TY - JOUR T1 - Cognitive and socioemotional caregiving in developing countries AN - 1011850814; 4291667 AB - Enriching caregiving practices foster the course and outcome of child development. This study examined 2 developmentally significant domains of positive caregiving - cognitive and socioemotional - in more than 127,000 families with under-5 year children from 28 developing countries. Mothers varied widely in cognitive and socioemotional caregiving and engaged in more socioemotional than cognitive activities. More than half of mothers played with their children and took them outside, but only a third or fewer read books and told stories to their children. The GDP of countries related to caregiving after controlling for life expectancy and education. The majority of mothers report that they do not leave their under-5s alone. Policy and intervention recommendations are elaborated. Reprinted by permission of the University of Chicago Press. © All rights reserved JF - Child development AU - Putnick, Diane L AU - Bornstein, Marc H AD - US National Institutes of Health Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - 46 EP - 61 VL - 83 IS - 1 SN - 0009-3920, 0009-3920 KW - Sociology KW - Emotions KW - Socioeconomic status KW - Caring KW - Child care KW - Developing countries KW - Child development KW - Cognition KW - Child welfare UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1011850814?accountid=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=Cognitive+and+socioemotional+caregiving+in+developing+countries&rft.au=Putnick%2C+Diane+L%3BBornstein%2C+Marc+H&rft.aulast=Putnick&rft.aufirst=Diane&rft.date=2012-01-01&rft.volume=83&rft.issue=1&rft.spage=46&rft.isbn=&rft.btitle=&rft.title=Child+development&rft.issn=00093920&rft_id=info:doi/10.1111%2Fj.1467-8624.2011.01673.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 - 2208 2212; 2039 13521; 4196; 2449 10404; 2197 2212 6075 3483; 3480 2958 12092; 11988 4011 3974 9390 11932 2328 11935 5837 2360 2688 2449 10404 11936; 2192 DO - http://dx.doi.org/10.1111/j.1467-8624.2011.01673.x ER - TY - JOUR T1 - Housing quality and access to material and learning resources within the home environment in developing countries AN - 1011846466; 4291669 AB - This study examined home environment conditions (housing quality, material resources, formal and informal learning materials) and their relations with the Human Development Index (HDI) in 28 developing countries. Home environment conditions in these countries varied widely. The quality of housing and availability of material resources at home were consistently tied to HDI; the availability of formal and informal learning materials a little less so. Gross domestic product (GDP) tended to show a stronger independent relation with housing quality and material resources than life expectancy and education. Formal learning resources were independently related to the GDP and education indices, and informal learning resources were not independently related to any constituent indices of the overall HDI. Reprinted by permission of the University of Chicago Press. © All rights reserved JF - Child development AU - Bradley, Robert H AU - Putnick, Diane L AD - Arizona State University ; US National Institutes of Health Y1 - 2012/01// PY - 2012 DA - Jan 2012 SP - 76 EP - 91 VL - 83 IS - 1 SN - 0009-3920, 0009-3920 KW - Sociology KW - Learning KW - Home KW - Socioeconomic status KW - Housing KW - Informal groups KW - Level of education KW - Social environment KW - Gross domestic product KW - Developing countries UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1011846466?accountid=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=Housing+quality+and+access+to+material+and+learning+resources+within+the+home+environment+in+developing+countries&rft.au=Bradley%2C+Robert+H%3BPutnick%2C+Diane+L&rft.aulast=Bradley&rft.aufirst=Robert&rft.date=2012-01-01&rft.volume=83&rft.issue=1&rft.spage=76&rft.isbn=&rft.btitle=&rft.title=Child+development&rft.issn=00093920&rft_id=info:doi/10.1111%2Fj.1467-8624.2011.01674.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 - 7278 12929 7073; 7353 4049; 5943 5706; 11829 6077 4309; 6045 5706; 11988 4011 3974 9390 11932 2328 11935 5837 2360 2688 2449 10404 11936; 6513 5676; 5627 8503 10242 3872 554 971; 3480 2958 12092 DO - http://dx.doi.org/10.1111/j.1467-8624.2011.01674.x ER - TY - JOUR T1 - Mobile phone use and glioma risk: comparison of epidemiological study results with incidence trends in the United States AN - 1011202444; 16483257 AB - OBJECTIVE: In view of mobile phone exposure being classified as a possible human carcinogen by the International Agency for Research on Cancer (IARC), we determined the compatibility of two recent reports of glioma risk (forming the basis of the IARC's classification) with observed incidence trends in the United States. Design Comparison of observed rates with projected rates of glioma incidence for 1997-2008. We estimated projected rates by combining relative risks reported in the 2010 Interphone study and a 2011 Swedish study by Hardell and colleagues with rates adjusted for age, registry, and sex; data for mobile phone use; and various latency periods. Setting US population based data for glioma incidence in 1992-2008, from 12 registries in the Surveillance, Epidemiology, and End Results (SEER) programme (Atlanta, Detroit, Los Angeles, San Francisco, San Jose-Monterey, Seattle, rural Georgia, Connecticut, Hawaii, Iowa, New Mexico, and Utah). Participants Data for 24 813 non-Hispanic white people diagnosed with glioma at age 18 years or older. RESULTS: Age specific incidence rates of glioma remained generally constant in 1992-2008 (-0.02% change per year, 95% confidence interval -0.28% to 0.25%), a period coinciding with a substantial increase in mobile phone use from close to 0% to almost 100% of the US population. If phone use was associated with glioma risk, we expected glioma incidence rates to be higher than those observed, even with a latency period of 10 years and low relative risks (1.5). Based on relative risks of glioma by tumour latency and cumulative hours of phone use in the Swedish study, predicted rates should have been at least 40% higher than observed rates in 2008. However, predicted glioma rates based on the small proportion of highly exposed people in the Interphone study could be consistent with the observed data. Results remained valid if we used either non-regular users or low users of mobile phones as the baseline category, and if we constrained relative risks to be more than 1. CONCLUSIONS: Raised risks of glioma with mobile phone use, as reported by one (Swedish) study forming the basis of the IARC's re-evaluation of mobile phone exposure, are not consistent with observed incidence trends in US population data, although the US data could be consistent with the modest excess risks in the Interphone study. JF - British Medical Journal AU - Little, M P AU - Rajaraman, P AU - Curtis, R E AU - Devesa, S S AU - Inskip, P D AU - Check, D P AU - Linet, M S AD - Radiation Epidemiology Branch, National Cancer Institute, Rockville, MD 20852-7238, USA Y1 - 2012 PY - 2012 DA - 2012 SP - e1147 PB - British Medical Association, BMA House Square London WC1H 9JP United Kingdom VL - 344 SN - 0959-8138, 0959-8138 KW - CSA Neurosciences Abstracts; Risk Abstracts; Health & Safety Science Abstracts KW - Age KW - Brain tumors KW - Cancer KW - Carcinogens KW - Cellular telephones KW - Classification KW - Data processing KW - Epidemiology KW - Geriatrics KW - Glioma KW - Risk assessment KW - Risk factors KW - Rural areas KW - cellular telephones KW - classification KW - glioma KW - USA, Connecticut KW - USA, California, Los Angeles KW - USA, Michigan, Detroit KW - USA, California, San Francisco KW - USA, Utah KW - USA, New Mexico KW - USA, Iowa KW - INE, USA, Washington, Seattle KW - USA, Georgia, Atlanta KW - H 6000:Natural Disasters/Civil Defense/Emergency Management KW - R2 23060:Medical and environmental health KW - N3 11027:Neurology & neuropathology UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1011202444?accountid=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+Medical+Journal&rft.atitle=Mobile+phone+use+and+glioma+risk%3A+comparison+of+epidemiological+study+results+with+incidence+trends+in+the+United+States&rft.au=Little%2C+M+P%3BRajaraman%2C+P%3BCurtis%2C+R+E%3BDevesa%2C+S+S%3BInskip%2C+P+D%3BCheck%2C+D+P%3BLinet%2C+M+S&rft.aulast=Little&rft.aufirst=M&rft.date=2012-01-01&rft.volume=344&rft.issue=&rft.spage=e1147&rft.isbn=&rft.btitle=&rft.title=British+Medical+Journal&rft.issn=09598138&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-05-01 N1 - Last updated - 2013-04-05 N1 - SubjectsTermNotLitGenreText - Risk assessment; Brain tumors; Age; Data processing; Epidemiology; Classification; Risk factors; Geriatrics; Cellular telephones; Carcinogens; Glioma; glioma; cellular telephones; classification; Cancer; Rural areas; USA, Utah; USA, California, Los Angeles; USA, New Mexico; USA, Michigan, Detroit; USA, Iowa; USA, Connecticut; USA, Georgia, Atlanta; INE, USA, Washington, Seattle; USA, California, San Francisco ER - TY - JOUR T1 - Depression treatment preferences among Japanese undergraduates: Using conjoint analysis AN - 1010709037; 201209189 AB - Background: Treatment preferences may contribute to seeking and adhering to professional help for depression. Few studies have considered practical barriers and controlled for individual difference factors. Objective: To clarify depression treatment preferences among Japanese undergraduates while considering practical barriers and controlling for individual difference factors. Methods: This was a cross-sectional study of 985 undergraduates. Depression treatment preferences were assessed by presenting them with nine hypothetical clinics. Conjoint analysis was performed using a random effect ordered probit model, controlling for the effects of gender, age, department, lifetime use of healthcare services, perceived etiology of depression, stigma towards depression, transportation time, opening hours, and treatment options. Results: Transportation time and treatment options had the greatest average discrete changes than other factors. Although information is presented about treatment costs in the order medication (3,000 yen), psychotherapy (7,000 yen) and combination (10,000 yen), the order of predicted probabilities for positive ratings was combination (61.4%), psychotherapy (54.9%) and medication (23.2%). Sensitivity analyses showed similar results. Conclusion: Transportation time and treatment options have greater utility than other factors, and a combination of psychotherapy and medication is the most preferred treatment option despite having the highest treatment costs. Efforts to overcome these effects could help increase depression treatment preferences. [Reprinted by permission of Sage Publications Ltd., copyright holder.] JF - International Journal of Social Psychiatry AU - Okumura, Yasuyuki AU - Sakamoto, Shinji AD - Department of Social Psychiatry, National Institute of Mental Health, National Centre of Neurology and Psychiatry, Japan Y1 - 2012///0, PY - 2012 DA - 0, 2012 SP - 195 EP - 203 PB - Sage Publications, London UK VL - 58 IS - 2 SN - 0020-7640, 0020-7640 KW - adherence attitudes discrete choice experiments help seeking mental health literacy KW - Depression KW - Psychotherapy KW - Transport KW - Treatment preferences KW - Conjoint analysis KW - Undergraduate students KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1010709037?accountid=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=International+Journal+of+Social+Psychiatry&rft.atitle=Depression+treatment+preferences+among+Japanese+undergraduates%3A+Using+conjoint+analysis&rft.au=Okumura%2C+Yasuyuki%3BSakamoto%2C+Shinji&rft.aulast=Okumura&rft.aufirst=Yasuyuki&rft.date=2012-01-01&rft.volume=58&rft.issue=2&rft.spage=195&rft.isbn=&rft.btitle=&rft.title=International+Journal+of+Social+Psychiatry&rft.issn=00207640&rft_id=info:doi/10.1177%2F0020764010390437 LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-05-01 N1 - Last updated - 2016-09-27 N1 - CODEN - IJSPAG N1 - SubjectsTermNotLitGenreText - Depression; Treatment preferences; Psychotherapy; Undergraduate students; Transport; Conjoint analysis DO - http://dx.doi.org/10.1177/0020764010390437 ER - TY - JOUR T1 - Affective prosody labeling in youths with bipolar disorder or severe mood dysregulation AN - 1010707830; 201208177 AB - Background: Accurate identification of nonverbal emotional cues is essential to successful social interactions, yet most research is limited to emotional face expression labeling. Little research focuses on the processing of emotional prosody, or tone of verbal speech, in clinical populations. Methods: Using the Diagnostic Analysis of Nonverbal Accuracy, the current study examined whether youths with pediatric-onset bipolar disorder (BD) and/or those with chronic and severe irritability (i.e. the severe mood dysregulation phenotype) are impaired in their ability to identify the emotional prosody of a spoken sentence with neutral content. Results: Youths with severe mood dysregulation (n=67) performed more poorly than healthy comparison children (n=57), even when the sample was limited to unmedicated patients. Medicated BD youths (n=52) exhibited impairment relative to healthy comparison children. No interactions between group and emotion were observed, suggesting that emotional prosody labeling problems may represent a general deficit in chronically irritable youths and in medicated youths with BD. Conclusion: In concert with previously documented facial emotion labeling deficits, difficulties ascertaining the correct emotional tone of a spoken sentence may contribute to emotion dysregulation in chronically irritable children, and possibly also in youths with BD. Adapted from the source document. JF - The Journal of Child Psychology and Psychiatry AU - Deveney, Christen M AU - Brotman, Melissa A AU - Decker, Ann Marie AU - Pine, Daniel S AU - Leibenluft, Ellen AD - Emotion and Development Branch, National Institute of Mental Health, National Institutes of Health, US Department of Health and Human Services, Bethesda, MD, USA Y1 - 2012///0, PY - 2012 DA - 0, 2012 SP - 262 EP - 270 PB - Blackwell Publishing, Oxford UK VL - 53 IS - 3 SN - 0021-9630, 0021-9630 KW - Chronically KW - Bipolar affective disorder KW - Moods KW - Young people KW - Children KW - Prosody KW - article UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1010707830?accountid=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=Affective+prosody+labeling+in+youths+with+bipolar+disorder+or+severe+mood+dysregulation&rft.au=Deveney%2C+Christen+M%3BBrotman%2C+Melissa+A%3BDecker%2C+Ann+Marie%3BPine%2C+Daniel+S%3BLeibenluft%2C+Ellen&rft.aulast=Deveney&rft.aufirst=Christen&rft.date=2012-01-01&rft.volume=53&rft.issue=3&rft.spage=262&rft.isbn=&rft.btitle=&rft.title=The+Journal+of+Child+Psychology+and+Psychiatry&rft.issn=00219630&rft_id=info:doi/10.1111%2Fj.1469-7610.2011.02482.x LA - English DB - Applied Social Sciences Index & Abstracts (ASSIA) N1 - Date revised - 2012-05-01 N1 - Last updated - 2016-09-27 N1 - CODEN - JPPDAI N1 - SubjectsTermNotLitGenreText - Young people; Prosody; Moods; Children; Bipolar affective disorder; Chronically DO - http://dx.doi.org/10.1111/j.1469-7610.2011.02482.x ER - TY - JOUR T1 - Ablation of the transcriptional regulator Id1 enhances energy expenditure, increases insulin sensitivity, and protects against age and diet induced insulin resistance, and hepatosteatosis AN - 1008844950; 16198563 AB - Obesity is a major health concern that contributes to the development of diabetes, hyperlipidemia, coronary artery disease, and cancer. Id proteins are helix-loop-helix transcription factors that regulate the proliferation and differentiation of cells from multiple tissues, including adipocytes. We screened mouse tissues for the expression of Id1 and found that Id1 protein is highly expressed in brown adipose tissue (BAT) and white adipose tissue (WAT), suggesting a role for Id1 in adipogenesis and cell metabolism. Id1-/- mice are viable but show a significant reduction in fat mass (P<0.005) over the life of the animal that was not due to decreased number of adipocytes. Analysis of Id1-/- mice revealed higher energy expenditure, increased lipolysis, and fatty acid oxidation, resulting in reduced triglyceride accumulation in WAT compared to Id1+/+ mice. Serum levels of triglycerides (193.9 plus or minus 32.2 vs. 86.5 plus or minus 33.8, P<0.0005), cholesterol (189.4 plus or minus 33.8 vs. 110.6 plus or minus 8.23, P<0.0005) and leptin (1263 plus or minus 835 vs. 222 plus or minus 260, P<0.005) were significantly lower in aged Id1-/- mice compared to Id1+/+ mice. Id1-deficient mice have higher resting (P<0.005) and total (P<0.05) O2 consumption and lower respiratory exchange ratio (P<0.005), confirming that Id1-/- mice use a higher proportion of lipid as an energy source for the increased energy expenditure. The expression of PGC1 alpha and UCP1 were 2- to 3-fold up-regulated in Id1-/- BAT, suggesting that loss of Id1 increases thermogenesis. As a consequence of higher energy expenditure and reduced fat mass, Id1-/- mice displayed enhanced insulin sensitivity. Id1 deficiency protected mice against age- and high-fat-diet-induced adiposity, insulin resistance, and hepatosteatosis. Our findings suggest that Id1 plays a critical role in the regulation of energy homeostasis and could be a potential target in the treatment of insulin resistance and fatty liver disease.-Satyanarayana, A., Klarmann, K. D., Gavrilova, l O., Keller, J. R. Ablation of the transcriptional regulator Id1 enhances energy expenditure, increases insulin sensitivity, and protects against age and diet-induced insulin resistance and hepatosteatosis. JF - FASEB Journal AU - Satyanarayana, Ande AU - Klarmann, Kimberly D AU - Gavrilova, Oksana AU - Keller, Jonathan R AD - Basic Research Program, SAIC-Frederick, Center for Cancer Research, National Cancer Institute-Frederick, Frederick, Maryland, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 309 EP - 323 PB - Federation of American Societies for Experimental Biology, 9650 Rockville Pike Bethesda MD 20814 United States VL - 26 IS - 1 SN - 0892-6638, 0892-6638 KW - Environment Abstracts KW - Sensitivity KW - Age KW - insulin KW - adipose tissues KW - obesity KW - Mice KW - Cancer KW - Bioaccumulation KW - Proteins KW - ENA 03:Energy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008844950?accountid=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=Ablation+of+the+transcriptional+regulator+Id1+enhances+energy+expenditure%2C+increases+insulin+sensitivity%2C+and+protects+against+age+and+diet+induced+insulin+resistance%2C+and+hepatosteatosis&rft.au=Satyanarayana%2C+Ande%3BKlarmann%2C+Kimberly+D%3BGavrilova%2C+Oksana%3BKeller%2C+Jonathan+R&rft.aulast=Satyanarayana&rft.aufirst=Ande&rft.date=2012-01-01&rft.volume=26&rft.issue=1&rft.spage=309&rft.isbn=&rft.btitle=&rft.title=FASEB+Journal&rft.issn=08926638&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-05-07 N1 - SubjectsTermNotLitGenreText - Sensitivity; Age; Bioaccumulation; insulin; obesity; adipose tissues; Proteins; Mice; Cancer ER - TY - JOUR T1 - 11C-Acetate PET/CT in Localized Prostate Cancer: A Study with MRI and Histopathologic Correlation AN - 1008839211; 16524034 AB - This work characterizes the uptake of 11C-acetate in prostate cancer (PCa), benign prostate hyperplasia, and normal prostate tissue in comparison with multiparametric MRI, whole-mount histopathology, and clinical markers to evaluate the potential utility of 11C-acetate for delineating intraprostatic tumors in a population of patients with localized PCa. METHODS: Thirty-nine men with presumed localized PCa underwent dynamic-static abdominal-pelvic 11C-acetate PET/CT for 30 min and 3-T multiparametric MRI before prostatectomy. PET/CT images were registered to MR images using pelvic bones for initial rotation-translation, followed by manual adjustments to account for prostate motion and deformation from the MRI endorectal coil. Whole-mount pathology specimens were sectioned using an MRI-based patient-specific mold resulting in improved registration between the MRI, PET, and pathology. 11C-acetate PET standardized uptake values were compared with multiparametric MRI and pathology. RESULTS: 11C-acetate uptake was rapid but reversible, peaking at 3-5 min after injection and reaching a relative plateau at approximately 10 min. The average maximum standardized uptake value (10-12 min) of tumors was significantly higher than that of normal prostate tissue (4.4 plus or minus 2.05 [range, 1.8-9.2] vs. 2.1 plus or minus 0.94 [range, 0.7-3.4], respectively; P < 0.001); however, it was not significantly different from that of benign prostatic hyperplasia (4.8 plus or minus 2.01 [range, 1.8-8.8]). A sector-based comparison with histopathology, including all tumors greater than 0.5 cm, revealed a sensitivity and specificity of 61.6% and 80.0%, respectively, for 11C-acetate PET/CT and 82.3% and 95.1%, respectively, for MRI. The 11C-acetate accuracy was comparable to that of MRI when only tumors greater than 0.9 cm were considered. In a small cohort (n = 9), 11C-acetate uptake was independent of fatty acid synthase expression using immunohistochemistry. CONCLUSION: 11C-acetate PET/CT demonstrates higher uptake in tumor foci than in normal prostate tissue; however, 11C-acetate uptake in tumors is similar to that in benign prostate hyperplasia nodules. Although 11C-acetate PET/CT is not likely to have utility as an independent modality for evaluation of localized PCa, the high uptake in tumors may make it useful for monitoring focal therapy when tissue damage after therapy may limit anatomic imaging methods. JF - Journal of Nuclear Medicine AU - Mena, Esther AU - Turkbey, Baris AU - Mani, Haresh AU - Adler, Stephen AU - Valera, Vladimir A AU - Bernardo, Marcelino AU - Shah, Vijay AU - Pohida, Thomas AU - McKinney, Yolanda AU - Kwarteng, Gideon AU - Daar, Dagane AU - Lindenberg, Maria L AU - Eclarinal, Philip AU - Wade, Revia AU - Linehan, WMarston AU - Merino, Maria J AU - Pinto, Peter A AU - Choyke, Peter L AU - Kurdziel, Karen A AD - Molecular Imaging Program, National Cancer Institute, National Institutes of Health, Bethesda, Maryland Y1 - 2012 PY - 2012 DA - 2012 SP - 538 EP - 545 PB - Society of Nuclear Medicine VL - 53 IS - 4 SN - 0161-5505, 0161-5505 KW - Biotechnology and Bioengineering Abstracts KW - Benign KW - Computed tomography KW - Fatty-acid synthase KW - Hyperplasia KW - Immunohistochemistry KW - Magnetic resonance imaging KW - Molds KW - Nodules KW - Nuclear medicine KW - Pelvis KW - Prostate KW - Prostate cancer KW - Tumors KW - W 30910:Imaging UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008839211?accountid=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+Nuclear+Medicine&rft.atitle=11C-Acetate+PET%2FCT+in+Localized+Prostate+Cancer%3A+A+Study+with+MRI+and+Histopathologic+Correlation&rft.au=Mena%2C+Esther%3BTurkbey%2C+Baris%3BMani%2C+Haresh%3BAdler%2C+Stephen%3BValera%2C+Vladimir+A%3BBernardo%2C+Marcelino%3BShah%2C+Vijay%3BPohida%2C+Thomas%3BMcKinney%2C+Yolanda%3BKwarteng%2C+Gideon%3BDaar%2C+Dagane%3BLindenberg%2C+Maria+L%3BEclarinal%2C+Philip%3BWade%2C+Revia%3BLinehan%2C+WMarston%3BMerino%2C+Maria+J%3BPinto%2C+Peter+A%3BChoyke%2C+Peter+L%3BKurdziel%2C+Karen+A&rft.aulast=Mena&rft.aufirst=Esther&rft.date=2012-01-01&rft.volume=53&rft.issue=4&rft.spage=538&rft.isbn=&rft.btitle=&rft.title=Journal+of+Nuclear+Medicine&rft.issn=01615505&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Magnetic resonance imaging; Molds; Tumors; Nodules; Fatty-acid synthase; Pelvis; Hyperplasia; Prostate cancer; Computed tomography; Nuclear medicine; Prostate; Immunohistochemistry; Benign ER - TY - JOUR T1 - Potential of PET to Predict the Response to Trastuzumab Treatment in an ErbB2-Positive Human Xenograft Tumor Model AN - 1008838877; 16524022 AB - Currently, an alteration in the gross volume of a tumor is used to assess its response to trastuzumab; however, this approach provides only a late indication of response. Tissue-sample ex vivo assays are potentially valuable, but their procurement through biopsies is invasive and might be biased by tumor heterogeneity. We studied the feasibility of using PET to quantify changes in ErbB2 (HER2/neu) expression and to predict the response to trastuzumab in BT474 breast cancer xenografts with N-[2-(4-18F-fluorobenzamido)ethyl]maleimide (18F-FBEM)-HER2:342 Affibody. METHODS: Mice bearing BT474 tumors were given trastuzumab (50 mg/kg loading dose, 25 mg/kg maintenance dose, administered intraperitoneally twice a week) or saline (control) for a total of 5 doses. Tumor size was monitored twice a week. Animals were scanned before the treatment, at 48 h, and 2 wk after the beginning of therapy. After the final scan, PET results were correlated with tumor response and immunohistochemical assessment of ErbB2 level, as well as with vasculature in the treated tumors. RESULTS: Analysis of PET images indicated that tracer uptake was significantly reduced after 1 dose of trastuzumab, compared with baseline, suggesting applicability as an early indicator of changes in ErbB2 expression. After 5 doses of trastuzumab, the overall decrease in 18F-FBEM-HER2:342 Affibody uptake also correlated with tumor response and downregulation of ErbB2 expression by immunohistochemical assessment. However, individual animals had different responses. There was a correlation between bigger PET changes and a higher vessel count in the tumors, suggesting that an increased number of vessels could lead to better trastuzumab delivery. We confirmed that the difference in average vessel count in the tumors was not related to the size of the tumors and therefore was not due to the selection of more vascular tumors. This finding is consistent with previous findings demonstrating that the number of vessels in a tumor could be a useful prognostic marker for treatment response. CONCLUSION: Our data suggest that Affibody-based PET can noninvasively provide specific information on changes in receptor expression and could be a valuable strategy for predicting tumor response to trastuzumab. JF - Journal of Nuclear Medicine AU - Kramer-Marek, Gabriela AU - Gijsen, Merel AU - Kiesewetter, Dale O AU - Bennett, Ruth AU - Roxanis, Ioannis AU - Zielinski, Rafal AU - Kong, Anthony AU - Capala, Jacek AD - Radiation Oncology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland Y1 - 2012 PY - 2012 DA - 2012 SP - 629 EP - 637 PB - Society of Nuclear Medicine VL - 53 IS - 4 SN - 0161-5505, 0161-5505 KW - Biotechnology and Bioengineering Abstracts KW - Animal models KW - Biopsy KW - Breast cancer KW - Data processing KW - ErbB-2 protein KW - Invasiveness KW - Models KW - Nuclear medicine KW - Tracers KW - Tumors KW - Xenografts KW - trastuzumab KW - W 30900:Methods UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008838877?accountid=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+Nuclear+Medicine&rft.atitle=Potential+of+PET+to+Predict+the+Response+to+Trastuzumab+Treatment+in+an+ErbB2-Positive+Human+Xenograft+Tumor+Model&rft.au=Kramer-Marek%2C+Gabriela%3BGijsen%2C+Merel%3BKiesewetter%2C+Dale+O%3BBennett%2C+Ruth%3BRoxanis%2C+Ioannis%3BZielinski%2C+Rafal%3BKong%2C+Anthony%3BCapala%2C+Jacek&rft.aulast=Kramer-Marek&rft.aufirst=Gabriela&rft.date=2012-01-01&rft.volume=53&rft.issue=4&rft.spage=629&rft.isbn=&rft.btitle=&rft.title=Journal+of+Nuclear+Medicine&rft.issn=01615505&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2012-06-18 N1 - SubjectsTermNotLitGenreText - Tracers; Invasiveness; Data processing; ErbB-2 protein; Animal models; Breast cancer; Nuclear medicine; Biopsy; Xenografts; Tumors; trastuzumab; Models ER - TY - JOUR T1 - Systemic SIRT1 insufficiency results in disruption of energy homeostasis and steroid hormone metabolism upon high-fat-diet feeding AN - 1008833773; 16297536 AB - SIRT1 is a highly-conserved NAD+-dependent protein deacetylase that plays essential roles in the regulation of energy metabolism, genomic stability, and stress response. Although the functions of SIRT1 in many organs have been extensively studied in tissue-specific knockout mouse models, the systemic role of SIRT1 is still largely unknown as a result of severe developmental defects that result from whole-body knockout in mice. Here, we investigated the systemic functions of SIRT1 in metabolic homeostasis by utilizing a whole-body SIRT1 heterozygous mouse model. These mice are phenotypically normal under standard feeding conditions. However, when chronically challenged with a 40% fat diet, they become obese and insulin resistant, display increased serum cytokine levels, and develop hepatomegaly. Hepatic metabolomic analyses revealed that SIRT1 heterozygous mice have elevated gluconeogenesis and oxidative stress. Surprisingly, they are depleted of glycerolipid metabolites and free fatty acids, yet accumulate lysolipids. Moreover, high-fat feeding induces elevation of serum testosterone levels and enlargement of seminal vesicles in SIRT1 heterozygous males. Microarray analysis of liver mRNA indicates that they have altered expression of genes involved in steroid metabolism and glycerolipid metabolism. Taken together, our findings indicate that SIRT1 plays a vital role in the regulation of systemic energy and steroid hormone homeostasis.-Purushotham, A., Xu, Q., Li, X. Systemic SIRT1 insufficiency results in disruption of energy homeostasis and steroid hormone metabolism upon high-fat-diet feeding. JF - FASEB Journal AU - Purushotham, Aparna AU - Xu, Qing AU - Li, Xiaoling AD - Laboratory of Signal Transduction, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 656 EP - 667 PB - Federation of American Societies for Experimental Biology, 9650 Rockville Pike Bethesda MD 20814 United States VL - 26 IS - 2 SN - 0892-6638, 0892-6638 KW - Environment Abstracts KW - Diets KW - insulin KW - feeding KW - Mice KW - steroids KW - Organs KW - steroid hormones KW - Fatty acids KW - Metabolism KW - ENA 03:Energy UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008833773?accountid=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 revised - 2012-04-01 N1 - Last updated - 2012-05-07 N1 - SubjectsTermNotLitGenreText - Diets; insulin; Fatty acids; steroid hormones; feeding; Mice; steroids; Organs; Metabolism ER - TY - JOUR T1 - YbxF and YlxQ are bacterial homologs of L7Ae and bind K-turns but not K-loops AN - 1008833251; 16474107 AB - The archaeal protein L7Ae and eukaryotic homologs such as L30e and 15.5kD comprise the best characterized family of K-turn-binding proteins. K-turns are an RNA motif comprised of a bulge flanked by canonical and noncanonical helices. They are widespread in cellular RNAs, including bacterial gene-regulatory RNAs such as the c-di-GMP-II, lysine, and SAM-I riboswitches, and the T-box. The existence in bacteria of K-turn-binding proteins of the L7Ae family has not been proven, although two hypothetical proteins, YbxF and YlxQ, have been proposed to be L7Ae homologs based on sequence conservation. Using purified, recombinant proteins, we show that Bacillus subtilis YbxF and YlxQ bind K-turns (Kd similar to 270 nM and similar to 2300 nM, respectively). Crystallographic structure determination demonstrates that both YbxF and YlxQ adopt the same overall fold as L7Ae. Unlike the latter, neither bacterial protein recognizes K-loops, a structural motif that lacks the canonical helix of the K-turn. This property is shared between the bacterial and eukaryal family members. Comparison of our structure of YbxF in complex with the K-turn of the SAM-I riboswitch and previously determined structures of archaeal and eukaryal homologs bound to RNA indicates that L7Ae approaches the K-turn at a unique angle, which results in a considerably larger RNA-protein interface dominated by interactions with the noncanonical helix of the K-turn. Thus, the inability of the bacterial and eukaryal L7Ae homologs to bind K-loops probably results from their reliance on interactions with the canonical helix. The biological functions of YbxF and YlxQ remain to be determined. JF - RNA AU - Baird, Nathan J AU - Zhang, Jinwei AU - Hamma, Tomoko AU - Ferre-D'Amare, Adrian R AD - Laboratory of RNA Biophysics and Cellular Physiology, National Heart, Lung and Blood Institute, Bethesda, Maryland 20892-8012, USA Y1 - 2012 PY - 2012 DA - 2012 SP - 759 EP - 770 PB - Cold Spring Harbor Laboratory Press, Fulfillment & Distribution Dept. Woodbury NY 11797-2924 United States VL - 18 IS - 4 SN - 1355-8382, 1355-8382 KW - Microbiology Abstracts B: Bacteriology; Biochemistry Abstracts 2: Nucleic Acids KW - Bacillus subtilis KW - RNA KW - Gene regulation KW - Conserved sequence KW - Lysine KW - Riboswitches KW - J 02330:Biochemistry KW - N 14830:RNA UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008833251?accountid=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=RNA&rft.atitle=YbxF+and+YlxQ+are+bacterial+homologs+of+L7Ae+and+bind+K-turns+but+not+K-loops&rft.au=Baird%2C+Nathan+J%3BZhang%2C+Jinwei%3BHamma%2C+Tomoko%3BFerre-D%27Amare%2C+Adrian+R&rft.aulast=Baird&rft.aufirst=Nathan&rft.date=2012-01-01&rft.volume=18&rft.issue=4&rft.spage=759&rft.isbn=&rft.btitle=&rft.title=RNA&rft.issn=13558382&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2013-09-09 N1 - SubjectsTermNotLitGenreText - RNA; Gene regulation; Lysine; Conserved sequence; Riboswitches; Bacillus subtilis ER - TY - JOUR T1 - A conserved membrane-binding domain targets proteins to organelle contact sites AN - 1008827147; 16297660 AB - Membrane contact sites (MCSs), where the membranes of two organelles are closely apposed, are regions where small molecules such as lipids or calcium are exchanged between organelles. We have identified a conserved membrane-binding domain found exclusively in proteins at MCSs in Saccharomyces cerevisiae. The synaptotagmin-like-mitochondrial-lipid binding protein (SMP) domain is conserved across species. We show that all seven proteins that contain this domain in yeast localize to one of three MCSs. Human proteins with SMP domains also localize to MCSs when expressed in yeast. The SMP domain binds membranes and is necessary for protein targeting to MCSs. Proteins containing this domain could be involved in lipid metabolism. This is the first protein domain found exclusively in proteins at MCSs. JF - Journal of Cell Science AU - Toulmay, Alexandre AU - Prinz, William A AD - Laboratory of Cell and Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA PY - 2012 SP - 49 EP - 58 PB - Company of Biologists, 140 Cowley Road Cambridge CB4 0DL United Kingdom VL - 125 IS - 1 SN - 0021-9533, 0021-9533 KW - Environment Abstracts KW - Yeasts KW - Membranes KW - Calcium KW - Lipids KW - Proteins KW - Metabolism KW - Saccharomyces cerevisiae KW - ENA 21:Wildlife UR - http://libproxy.lib.unc.edu/login?url=http://search.proquest.com/docview/1008827147?accountid=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=Journal+of+Cell+Science&rft.atitle=A+conserved+membrane-binding+domain+targets+proteins+to+organelle+contact+sites&rft.au=Toulmay%2C+Alexandre%3BPrinz%2C+William+A&rft.aulast=Toulmay&rft.aufirst=Alexandre&rft.date=2012-01-01&rft.volume=125&rft.issue=1&rft.spage=49&rft.isbn=&rft.btitle=&rft.title=Journal+of+Cell+Science&rft.issn=00219533&rft_id=info:doi/ LA - English DB - ProQuest Environmental Science Collection N1 - Date revised - 2012-04-01 N1 - Last updated - 2016-01-21 N1 - SubjectsTermNotLitGenreText - Yeasts; Calcium; Membranes; Lipids; Proteins; Metabolism; Saccharomyces cerevisiae ER -